1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899
THE ATHLETE’S SHOULDER
ISBN: 978-0-443-06701-3
Copyright © 2009, 1994 by Churchill Livingstone, an imprint of 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. Permissions may be sought directly from Elsevier’s Rights Department: phone: (+1) 215 239 3804 (US) or (+44) 1865 843830 (UK); fax: (+44) 1865 853333; e-mail:
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Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate. 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 the practitioner, relying on his or her experience and knowledge of the patient, 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 Editors assume any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book. The Publisher Library of Congress Cataloging-in-Publication Data The athlete’s shoulder/[edited by] Kevin E. Wilk, Michael M. Reinold, James R. Andrews. — 2nd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-0-443-06701-3 1. Shoulder—Wounds and injuries. 2. Sports injuries. I. Wilk, Kevin E. II. Reinold, Michael M. III. Andrews, James R. (James Rheuben). IV. Title. [DNLM: 1. Shoulder—injuries. 2. Athletic Injuries—therapy. 3. Rotator Cuff— injuries. 4. Shoulder Joint—injuries. WE 810 A871 2009] RD557. 5. A83 2009 617. 5’ 72044—dc22 2008002907
Acquisitions Editor: Daniel Pepper Developmental Editor: Angela Norton Publishing Services Manager: Frank Polizzano Project Manager: Jeff Gunning Design Direction: Lou Forgione
Printed in the United States of America
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Contributors
Robert Afra, M.D.
John C. Austin, M.D.
Assistant Professor, Chief of Sports Medicine, Department of Orthopaedic Surgery, University of California, San Diego, San Diego, California Mini-Open Rotator Cuff Repair
Northwest Orthopaedic Surgery and Sports Medicine, Hillsboro, Oregon Posterior Shoulder Instability
David W. Altchek, M.D.
Clinical Professor, Department of Physical Therapy, University of Delaware, Newark, Delaware Injuries and Rehabilitation of the Overhead Female Athlete’s Shoulder
Michael J. Axe, M.D.
Attending Orthopaedic Surgeon, Sports Medicine and Shoulder Service, Hospital for Special Surgery, New York, New York Bankart Lesions: Diagnosis and Treatment with Arthroscopic and Open Approaches
David S. Bailie, M.D. Vice President, The Orthopedic Clinic Association, Scottsdale, Arizona Shoulder Arthroplasty in the Athletic Shoulder
Ammar Anbari, M.D. Orthopedic and Shoulder Surgery, Sports Medicine, Norwich Orthopedic Group, North Franklin, Connecticut Arthroscopic Rotator Cuff Repair
Champ L. Baker, Jr., M.D. Staff Physician, The Hughston Clinic, Columbus; Clinical Assistant Professor, Department of Orthopaedics, Medical College of Georgia, Augusta, Georgia Neurovascular Compression Syndromes of the Shoulder
James R. Andrews, M.D. Medical Director, The American Sports Medicine Institute; Clinical Professor of Surgery, Division of Orthopaedic Surgery, University of Alabama at Birmingham School of Medicine, Birmingham, Alabama; Clinical Professor, Department of Surgery, University of South Carolina School of Medicine, Columbia, South Carolina; Clinical Assistant Professor, Department of Surgery, Florida State University College of Medicine, Tallahassee, Florida Operative Arthroscopy of the Shoulder; Internal Impingement; Open Repair of the Rotator Cuff; Shoulder Injuries in Baseball
Champ L. Baker III, M.D. Resident, Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Neurovascular Compression Syndromes of the Shoulder
Christopher W. Baker, M.D., M.P.H. Chief Resident, Department of Orthopedics, UMass Memorial Medical Center, Worcester, Massachusetts Tensile Failure of the Rotator Cuff; Shoulder Injuries in Football
Robert A. Arciero, M.D. Professor, Department of Orthopaedic Surgery, University of Connecticut School of Medicine; Chief, Sports Medicine Division, Department of Orthopaedic Surgery, and Director, Orthopaedic Sports Medicine Fellowship Program, UConn Medical Center, Farmington, Connecticut Management of the First-Time Shoulder Dislocation in the Athlete
John-Erik Bell, M.D. Assistant Professor, Shoulder, Elbow, and Sports Medicine, Department of Orthopaedic Surgery, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire Subacromial Impingement
J. Gregory Bennett, P.T., D.Sc., M.S. Peter D. Asnis, M.D.
Excel Physical Therapy, Fairfax; Adjunct Faculty, Advanced Orthopedics, Marymount University, Arlington, Virginia The Decelerator Mechanism: Eccentric Muscular Contraction Applications at the Shoulder
Instructor in Orthopaedic Surgery, Harvard Medical School; Assistant in Orthopaedic Surgery, Massachusetts General Hospital, Boston, Massachusetts Pediatric Shoulder Injuries v
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CONTRIBUTORS
Eric M. Berkson, M.D.
Richard B. Caspari, M.D. (deceased)
Clinical Associate Orthopaedic Surgery, Massachusetts General Hospital, Boston, Massachusetts Pediatric Shoulder Injuries
Clinical Professor, Division of Orthopedic Surgery, Virginia Commonwealth University Medical College of Virginia School of Medicine; Director, Orthopedic Research of Virginia, Richmond, Virginia Arthroscopic Techniques of the Shoulder
James Bicos, M.D. Orthopaedic Surgeon, Sports Medicine, St. Vincent Hospital, Minneapolis, Minnesota Management of the First-Time Shoulder Dislocation in the Athlete
Louis U. Bigliani, M.D.
Theresa A. Chiaia, B.S., B.S.P.T. Section Manager, Sports Rehabilitation and Performance Center, Hospital for Special Surgery, New York, New York Female Shoulder Injuries
Attending Orthopaedic Surgeon, Columbia University Medical Center; Frank E. Stinchfield Professor and Chairman, Director of Orthopaedic Surgery Service, Chief of the Center for Shoulder, Elbow, and Sports Medicine, New York Presbyterian Hospital, New York, New York Subacromial Impingement
William G. Clancy, Jr., M.D.
James L. Bond, M.D.
The Center for Advanced Orthopaedics, Chillicothe, Ohio Arthroscopic Rotator Cuff Repair
Clinical Faculty, Department of Orthopedics, Division of Sports Medicine, University of Oklahoma; Orthopedic Surgeon, Oklahoma Sports and Orthopedics Institute, Norman, Oklahoma Partial Articular Supraspinatus Tendon Avulsion (PASTA) Lesions of the Rotator Cuff
Angie Botto-van Bemden, Ph.D. Director of Research, Uribe, Hechtman, Zvijac Sports Medicine Institute (UHZSMI), Coral Gables, Florida Multidirectional Instability of the Shoulder
Joe P. Bramhall, M.D. Director of Sports Medicine, Team Physician, Orthopedic Surgeon, Texas A&M Department of Athletics, College Station, Texas Operative Arthroscopy of the Shoulder
Brian D. Busconi, M.D.
Orthopaedic Surgeon, Andrews Sports Medicine Center, Birmingham, Alabama Soft Tissue Injuries of the Shoulder; Brachial Plexus Injuries
Brian S. Cohen, M.D.
David A. Cortese, M.D. Orthopedic Surgeon, Kaiser Permanente, Vancouver, Washington Superior Labral Anterior-Posterior Lesions of the Shoulder
Andrew J. Cosgarea, M.D. Professor, Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine; Director, Division of Sports Medicine and Shoulder Surgery, Johns Hopkins Hospital, Baltimore, Maryland Suprascapular Nerve Entrapment
Ken Crenshaw, A.T.C., C.S.C.S., B.S. Head Athletic Trainer, Arizona Diamondbacks, Phoenix, Arizona Conditioning of the Shoulder Complex for Specific Sports
Associate Professor of Orthopedics and Physical Rehabilitation, University of Massachusetts Medical School; Chief of Sports Medicine, UMass Memorial Medical Center, Worcester, Massachusetts Tensile Failure of the Rotator Cuff; Shoulder Injuries in Football
Elsie Culham, P.T., Ph.D.
E. Lyle Cain, M.D.
Professor, Armstrong Atlantic State University, Savannah, Georgia; Professor Emeritus, University of Wisconsin– Lacrosse, Lacrosse, Wisconsin; Sports Physical Therapist, Gundersen Lutheran Sports Medicine, Lacrosse, Wisconsin, and Coastal Therapy, Savannah, Georgia The Shoulder in Swimming; Isokinetic Testing and Rehabilitation of the Shoulder Complex
Fellowship Director, American Sports Medicine Institute; Orthopaedic Surgeon, Andrews Sports Medicine and Orthopaedic Center, Birmingham, Alabama Open Repair of the Rotator Cuff; Adhesive Capsulitis of the Shoulder; Shoulder Injuries in Baseball
William G. Carson, Jr., M.D. Assistant Professor of Orthopaedics, University of South Florida College of Medicine, Tampa, Florida Normal Arthroscopic Anatomy of the Shoulder
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Professor and Director, School of Rehabilitation Therapy, Queen’s University, Kingston, Ontario, Canada Functional Anatomy of the Shoulder Complex
George J. Davies, D.P.T., M.Ed., P.T., S.C.S., A.T.C., L.A.T., C.S.C.S., F.A.P.T.A.
Kathleen Devine, M.P.H., P.T. Owner, Advanced Health Systems, Sarasota, Florida Shoulder Injuries in Baseball
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CONTRIBUTORS
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David Donatucci, M.Ed.
Rafael Escamilla, Ph.D., P.T.
Human Performance Center, Bradenton, Florida Conditioning of the Shoulder Complex for Specific Sports
Professor, Department of Physical Therapy, California State University–Sacramento; Physical Therapist, Results Physical Therapy and Training Center, Sacramento, California Electromyographic Activity During Upper Extremity Sports; Open- and Closed-Chain Rehabilitation for the Shoulder Complex
Mark C. Drakos, M.D. Sports Medicine Fellow, Hospital for Special Surgery, New York, New York Anterior Instability of the Shoulder
Jeffrey R. Dugas, M.D. Orthopaedic Surgeon, Andrews Sports Medicine and Orthopaedic Center, Birmingham, Alabama Internal Impingement
Shouchen Dun, M.S. Project Engineer, DePuy Orthopaedics, Inc., Warsaw, Indiana Biomechanics of the Shoulder During Sports
Brian J. Eckenrode, P.T., M.S.P.T., O.C.S. Advanced Clinician I, University of Pennsylvania Health System, Philadelphia, Pennsylvania Clinical Biomechanics of the Shoulder Complex
Sara L. Edwards, M.D. Orthopaedic Surgeon, Alta Bates Summit Medical Center, Oakland, California Subacromial Impingement
Marsha Eifert-Mangine, Ed.D., P.T., A.T.C. Assistant Professor, Department of Health Sciences, College of Mt. St. Joseph, Cincinnati, Ohio; Assistant Director of Research/Physical Therapist, NovaCare Rehabilitation, Florence, Kentucky Alternative Techniques for the Motion-Restricted Shoulder
Todd S. Ellenbecker, D.P.T., M.S., S.C.S., O.C.S., C.S.C.S.
Sue Falsone, P.T., M.S., S.C.S., A.T.C., C.S.C.S. Adjunct Professor, Department of Interdisciplinary Health Sciences, Arizona School of Health Sciences, A.T. Still University, Mesa; Director of Performance Physical Therapy, Athletes’ Performance, Core Performance, Tempe, Arizona Core Stabilization: Integration with Shoulder Rehabilitation
Glenn S. Fleisig, Ph.D. Adjunct Professor, Department of Biomedical Engineering, University of Alabama at Birmingham; Smith & Nephew Chair of Research, American Sports Medicine Institute, Birmingham, Alabama Biomechanics of the Shoulder During Sports
Michael B. Fox, B.A., B.S., P.T., S.C.S. Adjunct Faculty, New York University; Owner, Sports Therapy and Rehabilitation, New York, New York Cervicogenic Shoulder Pain
Tandy R. Freeman, M.D. Orthopedic Surgeon, Mary Shiels Hospital, Dallas, Texas; Orthopedic Surgeon, Dallas Orthopedic Clinic, Dallas, Texas; Director of Medical Services, Justin Sports Medicine Team, Professional Rodeo Cowboys Association, Colorado Springs, Colorado; Medical Director, Professional Bull Riders, Inc., Pueblo, Colorado Brachial Plexus Injuries
Clinic Director, Physiotherapy Associates, Scottsdale, Arizona; Scottsdale Sports Clinic, National Director of Clinical Research, Physiotherapy Associates; and Director of Sports Medicine, APT Tour, Ponte Vedra Beach, Florida Shoulder Arthroplasty in the Athletic Shoulder; Shoulder Injuries in Tennis; The Shoulder in Swimming; Isokinetic Testing and Rehabilitation of the Shoulder Complex
Gregory Gebauer, M.D., M.S.
Matthew J. Ernst, M.P.T., O.C.S.
Adjunct Faculty, New York University; Owner, Sports Therapy and Rehabilitation, New York, New York Cervicogenic Shoulder Pain
Adjunct Faculty, Physical Therapy Department, College of Mt. St. Joseph, Cincinnati, Ohio; Partner, Department of Physical Therapy, Oxford Physical Therapy Centers, Florence, Kentucky Alternative Techniques for the Motion-Restricted Shoulder
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Resident, Department of Orthopaedic Surgery, Johns Hopkins Hospital, Baltimore, Maryland Suprascapular Nerve Entrapment
William B. Geissler, M.D. University Orthopaedics, Jackson, Mississippi Arthroscopic Techniques of the Shoulder
Benjamin Gelfand, B.S., P.T., S.C.S.
Thomas J. Gill, M.D. Associate Professor of Orthopedic Surgery, Harvard Medical School; Chief, Sports Medicine Service,
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CONTRIBUTORS
Massachusetts General Hospital; Medical Director, Boston Red Sox; Head Team Physician, New England Patriots; Team Physician, Boston Bruins, Boston, Massachusetts Shoulder Injuries in Football; Pediatric Shoulder Injuries
Bruce Greenfield, P.T., Ph.D., O.S.C. Assistant Professor, Emory University, Atlanta, Georgia Proprioceptive Neuromuscular Facilitation for the Shoulder
Jo A. Hannafin, M.D., Ph.D. Professor of Orthopaedic Surgery, Weill Medical College of Cornell University; Attending Orthopaedic Surgeon and Orthopaedic Director, Womens Sports Medicine Center, Hospital for Special Surgery, New York, New York Female Shoulder Injuries
Kevin Harmon, B.S. (Sports Medicine) Assistant Athletic Trainer, Texas Rangers Baseball Team, Arlington, Texas Conditioning of the Shoulder Complex for Specific Sports
Samer S. Hasan, M.D., Ph.D. Cincinnati Sports Medicine and Orthopaedic Center, Cincinnati, Ohio Posterior Shoulder Instability
Richard J. Hawkins, M.D. Clinical Professor, Department of Orthopaedics, University of Colorado School of Medicine, Denver, Colorado, and University of Texas Southwestern Medical School, Dallas, Texas; Medical Director and Program Director, Steadman Hawkins Clinic of the Carolinas Fellowship, Steadman Hawkins Clinic of the Carolinas, Spartanburg, South Carolina Clinical Examination of the Shoulder Complex; Open Repair of the Rotator Cuff
Christopher Hughes, P.T., Ph.D., O.C.S., C.S.C.S Professor, School of Physical Therapy, Slippery Rock University, Slippery Rock; North Hills Orthopaedic and Sports Physical Therapy, Sewickley, Pennsylvania Neuromuscular Control Exercises for Shoulder Instability
Airelle O. Hunter-Giordano, P.T., D.P.T., O.C.S., S.C.S., C.S.C.S. Clinical Faculty, Department of Physical Therapy, University of Delaware; Associate Director of Sports PT, University of Delaware Physical Therapy Clinic, Newark, Delaware Injuries and Rehabilitation of the Overhead Female Athlete’s Shoulder
Wendy J. Hurd, P.T., Ph.D., S.C.S. Post-Doctoral Research Fellow, Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota Injuries and Rehabilitation of the Overhead Female Athlete’s Shoulder
James J. Irrgang, Ph.D., P.T., A.T.C. Associate Professor and Director of Clinical Research, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine; Physical Therapist, Center for Sports Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania Shoulder Outcome Measures
Ron M. Johnson, P.T., M.P.T., S.C.S., L.A.T., A.T.C., C.S.C.S. Facility Director, Excel Sports Therapy, Gulf Coast Rehabilitation, P.C., Shiner, Texas Conditioning, Training, and Rehabilitation for the Golfer’s Shoulder
Michael A. Keirns, Ph.D., P.T., S.C.S., A.T.C., C.S.C.S.
Cincinnati Sports Medicine and Orthopaedic Center, Cincinnati, Ohio Posterior Shoulder Instability
Associate Professor, Regis University, Denver, Colorado; Facility Director and Senior Group Leader, Physiotherapy Associates at Greenwood Athletic Club, Greenwood Village, Colorado Nonoperative Treatment of Shoulder Impingement
Steven Hoffman, M.S., P.T., A.T.C., S.C.S.
Martin J. Kelley, P.T., D.P.T., O.C.S.
Clinical Instructor in Physical Therapy, Slippery Rock University, Slippery Rock, Pennsylvania; Chatham University; Washington University in St. Louis, St. Louis, Missouri; and West Virginia University, Morgantown, West Virginia; Owner, North Hills Orthopedic and Sports Physical Therapy, Sewickley, Pennsylvania Neuromuscular Control Exercises for Shoulder Instability
Musculoskeletal Team Leader, University of Pennsylvania Health System, Philadelphia, Pennsylvania Clinical Biomechanics of the Shoulder Complex
Timothy P. Heckman, P.T.
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W. Ben Kibler, M.D. Medical Director, Lexington Clinic Sports Medicine Center and Shoulder Center of Kentucky, Lexington, Kentucky The Role of the Scapula in Rehabilitation
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CONTRIBUTORS
David Kingsley, B.S. (BiomedEng)
Leonard C. Macrina, M.S.P.T., S.C.S., C.S.C.S.
Graduate Research Assistant, University of Southern Mississippi, Hattiesburg, Mississippi Biomechanics of the Shoulder During Sports
Physical Therapist, Champion Sports Medicine, Birmingham, Alabama Nonoperative Rehabilitation for Traumatic and Congenital Glenohumeral Instability; Strength and Conditioning for the Preadolescent and Adolescent Athlete
Michael J. Kissenberth, M.D., B.S. (Biol) Assistant Clinical Professor of Orthopaedic Surgery and Medical Director, Orthopaedic Sports Medicine Service, Greenville Hospital System, Steadman Hawkins Clinic of the Carolinas, Greenville, South Carolina Clinical Examination of the Shoulder Complex
Stephen M. Kocaj, M.D. Department of Sports Medicine, Morristown Memorial Hospital, Morristown, New Jersey Adhesive Capsulitis of the Shoulder
Jeff G. Konin, Ph.D., A.T.C., P.T. Associate Professor, Department of Orthopaedic and Sports Medicine, University of South Florida College of Medicine; Executive Director, Sports Medicine and Athletic Related Trauma (SMART) Institute, Tampa, Florida Taping, Padding, and Bracing for the Shoulder Complex
Sanford S. Kunkel, M.D. Orthopaedic Surgeon, Indiana Orthopaedic Hospital, Indianapolis, Indiana Open Repair of the Rotator Cuff
Thomas J. Kuster III, M.S., A.T.C., N.A.S.M.-P.E.S. Assistant Athletic Director for Sports Medicine, James Madison University, Harrisonburg, Virginia Taping, Padding, and Bracing for the Shoulder Complex
David G. Lemak, M.D. Co-Director, Sports Medicine Fellowship, Lemak Sports Medicine, Brookwood Medical Center, Birmingham, Alabama Calcific Tendinitis
Lawrence J. Lemak, M.D. Director, Sports Medicine Fellowship, Lemak Sports Medicine, Brookwood Medical Center, Birmingham, Alabama Calcific Tendinitis
Scott M. Lephart, Ph.D., A.T.C. Associate Professor and Chair, Department of Sports Medicine and Nutrition, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania Sensorimotor Contribution to Shoulder Joint Stability
Terry R. Malone, P.T., Ed.D., A.T.C., F.A.P.T.A. Professor, Department of Rehabilitation Sciences and Physical Therapy, University of Kentucky, Lexington, Kentucky Standardized Shoulder Examination—Clinical and Functional Approaches
Robert E. Mangine, M.Ed., P.T., A.T.C. Clinical Instructor, Department of Orthopedics, University of Cincinnati; Director of Sports Clinical Residency, NovaCare Rehabilitation, Cincinnati, Ohio Alternative Techniques for the Motion-Restricted Shoulder
Robert Manske, D.P.T., M.Ed., P.T., S.C.S., A.T.C., C.A.T., C.S.C.S. Associate Professor, Wichita State University; Sports Physical Therapist, Via Christi Medical Center, Wichita, Kansas The Shoulder in Swimming
James W. Matheson, D.P.T., M.S., P.T., S.C.S., O.C.S. Therapy Partners, Inc., Burnsville, Minnesota The Shoulder in Swimming
Augustus D. Mazzocca, M.S., M.D. Assistant Professor, Department of Orthopaedic Surgery, University of Connecticut School of Medicine; Director of Clinical Biomechanics and Bioskills Laboratory, Department of Orthopaedic Surgery, UConn Health Center, Farmington, Connecticut Management of the First-Time Shoulder Dislocation in the Athlete; Acromioclavicular Joint Injuries
Mark D. Miller, M.D. Professor of Orthopaedic Surgery and Head, Division of Sports Medicine, University of Virginia, Charlottesville; Team Physician, James Madison University, Harrisonburg, Virginia Taping, Padding, and Bracing for the Shoulder Complex
Joseph B. Myers, Ph.D., A.T.C. Thomas N. Lindenfeld, M.D. Cincinnati Sports Medicine and Orthopaedic Center, Cincinnati, Ohio Posterior Shoulder Instability
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Assistant Professor, Department of Exercise and Sport Science, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina Sensorimotor Contribution to Shoulder Joint Stability
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CONTRIBUTORS
Larry Nassar, B.S., D.O. Associate Professor, College of Osteopathic Medicine, Department of Radiology, Division of Sports Medicine, Michigan State University, East Lansing, Michigan The Artistic Gymnast’s Shoulder
Stephen J. O’Brien, M.D., M.B.A Associate Professor of Orthopaedic Surgery, Weill Medical College of Cornell University; Associate Attending Orthopaedic Surgeon, Hospital for Special Surgery, New York, New York Anterior Instability of the Shoulder
Adam C. Olsen, P.T., A.T.C. Medical/Rehabilitation Coordinator, St. Louis Cardinals, Jupiter, Florida Interval Sport Programs for the Shoulder
Judson W. Ott, M.D. Orthopaedic Surgeon, Medical Associates, Dubuque, Iowa Soft Tissue Injuries of the Shoulder
Russell M. Paine, P.T., B.S. (Biol, PhysTher) Director of Rehabilitation, Memorial Hermann Sports Medicine; Team Physical Therapist, Houston Rockets, Houston, Texas Conditioning, Training, and Rehabilitation for the Golfer’s Shoulder
Christ J. Pavlatos, M.D.
Massachusetts General Hospital; Adjunct Faculty, Northeastern University College of Professional Studies, Boston, Massachusetts Internal Impingement; Nonoperative Rehabilitation for Traumatic and Congenital Glenohumeral Instability; Strength and Conditioning for the Preadolescent and Adolescent Athlete; Biomechanical Considerations in Shoulder Rehabilitation Exercises; Interval Sport Programs for the Shoulder
Scott B. Reynolds, M.D. Orthopaedic Surgeon, Nebraska Orthopaedic Associates, Omaha, Nebraska Normal Arthroscopic Anatomy of the Shoulder; Operative Arthroscopy of the Shoulder; Arthroscopic Techniques of the Shoulder
Gordon Riddle, P.T., D.P.T., A.T.C., C.S.C.S. Adjunct Professor and Clinical Instructor, School of Physical Therapy, Slippery Rock University, Slippery Rock; Physical Therapist, North Hills Orthopaedic and Sports Physical Therapy, Sewickley, Pennsylvania Neuromuscular Control Exercises for Shoulder Instability
Tara Ridge, M.S., P.T., S.C.S. UPMC Center for Sports Medicine, Pittsburgh, Pennsylvania Shoulder Outcome Measures
E. Paul Roetert, Ph.D.
Orthopaedic Surgeon, Libertyville, Illinois Acromioclavicular Joint Injuries
Managing Director, Player Development, United States Tennis Association, Boca Raton, Florida Shoulder Injuries in Tennis
Malcolm Peat, M.B.E., M.C.S.P., M.Sc., M.D. (Hon), Ph.D.
Anthony A. Romeo, M.D.
Executive Director of the International Centre for the Advancement of Community Based Rehabilitation (ICACBR), Faculty of Health Sciences, Queen’s University, Kingston, Ontario, Canada Functional Anatomy of the Shoulder Complex
Matthew Rappé, M.D. Knoxville Orthopaedic Clinic, Knoxville, Tennessee Open Repair of the Rotator Cuff
Jamie Reed, A.T.C. Head Athletic Trainer, Texas Rangers Baseball Team, Arlington, Texas Conditioning of the Shoulder Complex for Specific Sports
Michael M. Reinold, P.T., D.P.T., A.T.C., C.S.C.S. Rehabilitation Coordinator/Assistant Athletic Trainer, Boston Red Sox Baseball Team, Coordinator of Rehabilitation Research and Education, Department of Orthopedic Surgery, Division of Sports Medicine,
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Associate Professor of Orthopedics, Department of Sports Medicine, Rush University Medical Center, Chicago, Illinois Arthroscopic Rotator Cuff Repair
Omar Ross, B.S., M.S., P.T./D.P.T., A.T.C. Adjunct Professor and Clinical Instructor, School of Physical Therapy, Slippery Rock University, Slippery Rock; Physical Therapist, North Hills Orthopaedic and Sports Physical Therapy, Sewickley, Pennsylvania Neuromuscular Control Exercises for Shoulder Instability
J.R. Rudzki, M.D. Sports Medicine and Shoulder Service, Hospital for Special Surgery, New York, New York Bankart Lesions: Diagnosis and Treatment with Arthroscopic and Open Approaches
Stanley Rutkowski, B.S., B.A., P.T. Clinical Supervisor, New York University; Clinical Supervisor, Sports Therapy and Rehabilitation, New York, New York Cervicogenic Shoulder Pain
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CONTRIBUTORS
Marc Safran, M.D. Professor of Orthopaedic Surgery and Associate Director, Sports Medicine, Stanford University, Stanford, California Shoulder Injuries in Tennis
William Sands, Ph.D., F.A.C.S.M., C.-A.R.S., N.R.E.M.T. Performance Services, U.S. Olympic Committee, Colorado Springs, Colorado The Artistic Gymnast’s Shoulder
Edgar T. Savidge, P.T., D.P.T., O.C.S. Senior Physical Therapist, MGH Sports Physical Therapy, Boston, Massachusetts Biomechanical Considerations in Shoulder Rehabilitation Exercises
Dorothy F. Scarpinato, M.D. Orthopaedic Surgeon, Central Orthopaedic Group, Plainview, New York Operative Arthroscopy of the Shoulder
Anthony Schepsis, M.D. Professor of Orthopedic Surgery, Boston University School of Medicine; Director of Sports Medicine, Boston University Medical Center, Boston, Massachusetts Mini-Open Rotator Cuff Repair
Martin L. Schwartz, M.D. Clinical Professor of Radiology, University of Alabama at Birmingham School of Medicine; Chairman, Department of Radiology, St. Vincent’s Birmingham, Birmingham, Alabama Diagnostic Imaging of the Shoulder Complex
Monique A. Sheridan, B.A. Medical Student, University of Maryland School of Medicine; Formerly Ludwig Research Fellow, Women’s Sports Medicine Center, Hospital for Special Surgery, New York, New York Female Shoulder Injuries
James F. Silliman, M.D. President, Steadman Hawkins Clinic of the Carolinas; Program Medical Director, Musculoskeletal Institute of Greenville Hospital System, Greenville, South Carolina Clinical Examination of the Shoulder Complex
Stephen J. Snyder, M.D. Orthopedic Surgeon, Practice Limited to Shoulder Arthroscopy, Southern California Orthopedic Institute, Van Nuys, California Partial Articular Supraspinatus Tendon Avulsion (PASTA) Lesions of the Rotator Cuff; Superior Labral Anterior-Posterior Lesions of the Shoulder
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Lynn Snyder-Mackler, P.T., S.C.D., F.A.P.T.A., S.C.D. Alumni Distinguished Professor, Department of Physical Therapy, University of Delaware, Newark, Delaware Injuries and Rehabilitation of the Overhead Female Athlete’s Shoulder
Samuel A. Taylor, M.D. Orthopaedic Surgery Resident, Hospital for Special Surgery, New York, New York Anterior Instability of the Shoulder
D. Dean Thornton, M.D. Clinical Assistant Professor of Radiology, Department of Radiology, University of Alabama at Birmingham; Musculoskeletal Radiologist, Radiology Associates of Birmingham PC, Birmingham, Alabama Diagnostic Imaging of the Shoulder Complex
Albert Tom, M.D. Sports Fellow, University of Connecticut, Farmington, Connecticut Acromioclavicular Joint Injuries
John Tomberlin, P.T., O.C.S., F.A.A.O.M.P.T. Director of Mercy SportsCare, Department of Rehabilitation Services, Mercy Medical Center, Cedar Rapids, Iowa Neurodynamic Techniques for the Athlete’s Shoulder
Tim L. Uhl, Ph.D. Associate Professor, Department of Rehabilitation Sciences, University of Kentucky College of Health Science, Lexington, Kentucky The Role of the Scapula in Rehabilitation
John Uribe, M.D. Professor and Chairman, Department of Orthopaedics, Florida International University, Miami, Florida Multidirectional Instability of the Shoulder
Nikhil N. Verma, M.D. Assistant Professor, Department of Orthopaedic Surgery, Rush Medical College, Chicago, Illinois Arthroscopic Rotator Cuff Repair
Mark Verstegen, B.S., M.S. Director of Performance, Player Safety, and Welfare, NFL Players Association; President and Founder, Athletes’ Performance, Andrews Institute/Home Depot Center, Arizona State University, Tucson; Creator, Core Performance System, Tempe, Arizona Core Stabilization: Integration with Shoulder Rehabilitation
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CONTRIBUTORS
Michael L. Voight, P.T., D.H.Sc., O.C.S., S.C.S., A.T.C., C.S.C.S. Professor, School of Physical Therapy, Belmont University, Nashville, Tennessee Plyometrics for the Shoulder Complex
Ilya Voloshin, M.D. Orthopaedic Surgeon, Boston University Medical School, Boston, Massachusetts Mini-Open Rotator Cuff Repair
Robert Y. Wang, M.D., F.R.C.S.C. York Central Hospital, Richmond Hill, Ontario, Canada Orthopaedic Sports Medicine Fellow, New England Musculoskeletal Institute, UConn Health Center, Farmington, Connecticut Management of the First-Time Shoulder Dislocation in the Athlete
Alabama; Adjunct Assistant Professor, Programs in Physical Therapy, Marquette University, Milwaukee, Wisconsin Functional Anatomy of the Shoulder Complex; Internal Impingement; Soft Tissue Injuries of the Shoulder; Adhesive Capsulitis of the Shoulder; Shoulder Injuries in Baseball; Nonoperative Rehabilitation for Traumatic and Congenital Glenohumeral Instability; Isometric Testing and Rehabilitation of the Shoulder Complex; Plyometrics for the Shoulder Complex; Interval Sport Programs for the Shoulder
Kyle Yamashiro, P.T.
Craig A. Wassinger, Ph.D., P.T.
Medical Adjunct Faculty/Physical Therapist, Department of Athletics, California State University–Sacramento; Physical Therapist and CEO/Rehab Consultant, Oakland Athletics, Results Physical Therapy and Training Center, Sacramento, California Open- and Closed-Chain Rehabilitation for the Shoulder Complex
University of Otago, Dunedin, New Zealand Sensorimotor Contribution to Shoulder Joint Stability
Bashir Zikria, M.D.
Julie M. Whitman, D.Sc., M.P.T., B.S. (Biol) Assistant Professor, School of Physical Therapy, Regis University, Denver, Colorado Nonoperative Treatment of Shoulder Impingement
Kevin E. Wilk, P.T., D.P.T. Vice President Education, Physiotherapy Associates; Associate Clinical Director, Champion Sports Medicine, Physiotherapy Associates Clinic, Birmingham, Alabama; Rehabilitation Consultant, Tampa Bay Rays Baseball Team, Tampa Florida; Director Rehabilitation Research, American Sports Medicine Institute, Birmingham,
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Assistant Professor, Johns Hopkins Medicine, Lutherville, Maryland Multidirectional Instability of the Shoulder
John Zvijac, M.D. Professor, Department of Exercise Science and Sports Medicine, and Voluntary Associate Professor, Department of Orthopaedics/Rehabilitation, University of Miami Miller School of Medicine, Miami; Courtesy Professor, Department of Exercise and Sports Science, Florida International University, Miami; Team Physician, Tampa Bay Buccaneers, Tampa, Florida Multidirectional Instability of the Shoulder
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Preface
The shoulder joint continues to be one of the most intriguing joints in the human body. The interest in the shoulder joint in the orthopedic and sports medicine communities has stemmed from its functional and anatomic complexity, the precision of its biomechanics, and the wide variety of possible lesions affecting this structure. In the preface to the first edition of this textbook, we noted that increasing interest in the shoulder had led to “a proliferation of knowledge, enlightening research, improved awareness, and enhanced critical thinking regarding our recognition and treatment of shoulder joint disorders.” Since that time, almost 15 years ago, we have seen an even greater amount of interest and effort directed toward further understanding of the shoulder and its complex and intricate actions. The shoulder complex is a commonly injured region of the body, not only during sports but also as a result of work-related activities, overuse or disuse, and age-related degeneration. Accordingly, our goal in preparing this second edition was to make The Athlete’s Shoulder a comprehensive textbook addressing not only the most recent advances in sports-related shoulder disorders but also those occurring in the active orthopedic patient. Many iverse topics, including instabilities, labral lesions, rotator cuff lesions, neurovascular syndromes, total joint replacement, and biomechanics of specific sports, are discussed, and rehabilitation techniques are described in detail. Also included are several new chapters that overview current topics and recent advances in research in areas such as superior labral anterior-posterior (SLAP) tears, internal impingement, and articular-sided partial rotator cuff lesions. Several additional chapters are dedicated to various topics in surgery and rehabilitation. Each chapter has been updated and revised to contain the latest information available. This book is intended to not only increase the readers’ knowledge of the shoulder joint but also improve their understanding of the shoulder complex. The book is organized into six basic sections. The first, on the basic science of the shoulder complex, thoroughly discusses anatomy and biomechanics. This is followed by the examination section, which includes physical examination and diagnostic imaging of the shoulder. The third section describes recent arthroscopic surgical techniques. The fourth section discusses the recognition and treatment of various pathologies, including the appropriate surgical and rehabilitation approaches to these pathologies. The fifth section focuses on injuries in various sports and specific patient populations, such as baseball, golf, and the pediatric athlete. The last section discusses specific topics in rehabilitation. Although concise in format, the chapters provide the reader with a reference that includes historical perspective, functional anatomy, evaluation, and current treatment options. This text is not intended to be a “cookbook,” but rather is presented as a resource that enhances the practitioner’s expertise in the examination and treatment of shoulder injuries. The way we think about and look at the shoulder has changed over the years, and we are sure that this trend will continue. The challenge has been to prepare a text that discusses current and advanced concepts in an area in which knowledge is expanding daily. It is our hope that this book meets this challenge—and that it enables the reader to look into the future of shoulder treatment. We hope that this second edition of The Athlete’s Shoulder stimulates interest, provokes thought, inspires additional research, and enhances the care of shoulder patients in the future. We offer this textbook to clinicians, physicians, physical therapists, athletic trainers, and others involved in caring for shoulder patients. May it help you to discover more about the enormously fascinating shoulder joint, a truly complex functional structure that, once you begin exploring, becomes even more intriguing and complex in its interrelationships. The contributors to this book represent the leaders in shoulder care, and we greatly appreciate their contributions. Their work in the fields of orthopedics and sports medicine related to the shoulder has been invaluable to the continued advancement of understanding and treatment of shoulder pathology. Kevin E. Wilk, P.T., D.P.T. Michael M. Reinold, P.T., D.P.T., A.T.C., C.S.C.S. James R. Andrews, M.D.
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Acknowledgments
To Kevin Wilk, Glenn Fleisig, and Jim Andrews: Your mentorship, guidance, and friendship have been an invaluable gift to me. You have served as excellent role models and engraved in me the values of work ethic, team work, and leadership. I can’t thank you enough for sharing your knowledge and helping me to open so many doorways. To my family, especially Sandi, Mom, Dad, Lance, and Lucy: Thank you for your love, encouragement, patience, and understanding throughout my life. By following the values you have instilled and examples you have set, I have always been provided with motivation needed for me to be my best. Your strength and perseverance through life’s ups and downs continue to provide a driving force in everything I do, even from a distance. To all my past students, colleagues, patients, and players: Thank you for supplying the motivation to challenge myself to further my understanding of the shoulder. To everyone at Elsevier who was involved with this project, especially Jeff Gunning, Julia Bartz, and Angela Norton: This book would not have happened without your help and persistence.
Michael M. Reinold
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CHAPTER 1 Functional Anatomy of the
Shoulder Complex Malcolm Peat, Elsie Culham, and Kevin E. Wilk
The glenohumeral joint is the most complex joint in the human body. The glenohumeral joint combined with the scapulothoracic, sternoclavicular, and acromioclavicular joints comprise the shoulder joint complex. All these joints are critical to normal pain-free function. The glenohumeral joint has the greatest amount of motion of any joint in the human body.
COMPONENTS Sternoclavicular Joint The sternoclavicular joint is the only joint connecting the shoulder complex to the axial skeleton.9,10 Although the structure of this synovial joint is classified as plain, its function most closely resembles a ball-and-socket articulation.4,11,12 The articular surfaces lack congruity. Approximately one half of the large, rounded medial end of the clavicle protrudes above the shallow sternal socket. An intra-articular disc is attached to the upper portion of this nonarticular segment of the clavicle. The articular surface is saddle-shaped, anteroposteriorly concave, and downwardly convex.2,4
The overall function of the upper extremity is related to the shoulder complex, with the ultimate purpose of this mechanism being the placement and full use of the hand. The joint mechanisms of the limb permit the placement, functioning, and control of the hand directly in front of the body, where the functions can be observed.1 Manipulation of the hand is controlled by the shoulder complex, which positions and directs the humerus, the elbow, which positions the hand in relation to the trunk, and the radioulnar joints, which determine the position of the palm.2,3 Sports that involve actions such as throwing, using a racket, and swimming require excessive glenohumeral joint motion. For example, the excessive motion required to throw a baseball is accomplished through the integrated and synchronized motion of the various joints in the upper quadrant, most significantly the glenohumeral and scapulothoracic joints.
The medial end of the clavicle is bound to the sternum, the first rib and its costal cartilage. Ligaments strengthen the capsule anteriorly, posteriorly, superiorly, and inferiorly. The main structures stabilizing the joint, resisting the tendency for medial displacement of the clavicle and limiting clavicular movement, are the articular disc and the costoclavicular ligament (Fig. 1-1).4,13 The articular disc is a strong, almost circular fibrocartilage that completely divides the joint cavity.14 The disc is attached superiorly to the upper medial end of the clavicle and passes downward between the articular surfaces to the sternum and first costal cartilage.4 This arrangement permits the disc to function as a hinge, a mechanism that contributes to the total range of joint movement. The areas of compression between the articular surfaces and intraarticular disc vary with movements of the clavicle. During elevation and depression, most motion occurs between the clavicle and articular disc (Fig. 1-2A and B). During protrusion and retraction, the greatest movement occurs between the articular disc and sternal articular surface (see Fig. 1-2C and D).2 The combination of taut ligaments, pressure on the disc and articular surfaces is important for maintaining stability in the plane of motion.
The shoulder complex provides the upper limb with a range of motion exceeding that of any other joint mechanism.4 This range of motion is greater than that required for most daily functional activities. For example, use of the hand in limited activities of daily living is possible when the shoulder complex is immobilized with the humerus held by the side. Compensation for absent shoulder motion is provided by the cervical spine, elbow, wrist, and finger joint mechanisms.5,6 The shoulder complex consists of four joints that function in a precise, coordinated, synchronous manner. Position changes of the arm involve movements of the clavicle, scapula, and humerus. These movements are the direct result of the complex mechanism comprised of the sternoclavicular, acromioclavicular, and glenohumeral joints and the scapulothoracic gliding mechanism.4,7,8
The articular disc also stabilizes the joint against forces applied to the shoulder, which are transmitted medially through the clavicle to the sternum. Without this attachment, the 3
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THE ATHLETE’S SHOULDER
The joint capsule is supported by oblique anterior and posterior sternoclavicular ligaments. Both ligaments pass downward and medially from the sternal end of the clavicle to the anterior and posterior surfaces of the manubrium and limit anteroposterior movement of the clavicle. An interclavicular ligament runs across the superior aspect of the sternoclavicular joint, joining the medial ends of the clavicles. This ligament, with deep fibers attached to the upper margin of the manubrium, provides stability to the superior aspect of the joint.4,9
Clavicle
Disc
The sternoclavicular joint allows elevation and depression, protraction and retraction, and long-axis rotation of the clavicle. The axis for both angular movements lies close to the clavicular attachment of the costoclavicular ligament.9 Costoclavicular ligament
Acromioclavicular Joint
Figure 1-1. Sternoclavicular joint showing major ligamentous structures influencing stability.
clavicle would tend to override the sternum, resulting in medial dislocation. Forces acting on the clavicle are most likely to cause fractures of the bone medial to the attachment of the coracoclavicular ligament but rarely cause dislocation of the sternoclavicular joint.5 The costoclavicular ligament is a strong bilaminar structure attached to the inferior surface of the medial end of the clavicle and first rib. The anterior component of the ligament passes upward and laterally; the posterior aspect upward and medially. The ligament is a major stabilizing structure and strongly binds the medial end of the clavicle to the first rib. The ligament becomes taut when the arm is elevated or the shoulder protracted.4
The acromioclavicular joint is a synovial plane joint between the small, convex, oval facet on the lateral end of the clavicle and a concave area on the anterior part of the medial border of the acromion process of the scapula.4,9 The joint line is oblique and slightly curved. The curvature of the joint permits the acromion, and thus the scapula, to glide forward or backward over the lateral end of the clavicle. This movement keeps the glenoid fossa continually facing the humeral head. The oblique nature of the joint is such that forces transmitted through the arm will tend to drive the acromion process under the lateral end of the clavicle, with the clavicle overriding the acromion (Fig. 1-3). The joint also contains a fibrocartilaginous disc that is variable in size and does not completely separate the joint into two compartments.9,14 The acromioclavicular joint is
Taut ligament
Taut ligament
Contact Contact
Depression
Elevation
B
A
Taut ligament Figure 1-2. Sternoclavicular joint illustrating compression of articular disc. A, Depression. B, Elevation. C, Retraction. D, Protrusion. (From Dempster WT: Mechanisms of shoulder movement. Arch Phys Med Rehabil 46:49, 1965.)
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Contact
Contact
Taut ligament
C
Retraction
D
Protrusion
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
5
The primary function of this ligament is to prevent overriding of the clavicle on the acromion.5,17
Acromion
Clavicle
Figure 1-3. Acromioclavicular joint surfaces.
important because it contributes to total arm movement in addition to transmitting forces between the clavicle and acromion.4,15 The acromioclavicular joint has a capsule and superior acromioclavicular ligament that strengthen the upper aspect of the joint.4,11 The main ligamentous structure stabilizing the joint and binding the clavicle to the scapula is the coracoclavicular ligament. Although this ligament is placed medially and is separate from the joint, it forms the most efficient means of preventing the clavicle from losing contact with the acromion.4,5,8,9,15,16 The coracoclavicular ligament consists of two parts, the trapezoid and the conoid. These two components, functionally and anatomically distinct, are united at their corresponding borders. Anteriorly, the space between the ligaments is filled with adipose tissue and, frequently, a bursa. A bursa also lies between the medial end of the coracoid process and the inferior surface of the clavicle. In up to 30% of subjects, these bony components may be opposed closely and may form a coracoclavicular joint.2,16 The coracoclavicular ligament suspends the scapula from the clavicle and transmits the force of the upper fibers of the trapezius to the scapula.2 The trapezoid ligament, the anterolateral component of the coracoclavicular ligament, is broad, thin, and quadrilateral. It is attached from below to the superior surface of the coracoid process. The ligament passes laterally almost horizontally in the frontal plane and is attached to the trapezoid line on the inferior surface of the clavicle.4,9
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The conoid ligament is located partly posteriorly and medially to the trapezoid ligament. It is thick and triangular, with its base attached from above to the conoid tubercle on the inferior surface of the clavicle. The apex, which is directed downward, is attached to the “knuckle” of the coracoid process (i.e., medial and posterior edge of the root of the process). The conoid ligament is oriented vertically and twisted on itself.4,17 The ligament limits upward movement of the clavicle on the acromion. When the arm is elevated, the rotation of the scapula causes the coracoid process to move and increases the distance between the clavicle and coracoid process. This movement increases the tension on the conoid ligament, resulting in dorsal (posterior) axial rotation of the clavicle. Viewed from above, the clavicle has a shape resembling a crank. The taut coracoclavicular ligament acts on the outer curvature of the cranklike clavicle and effects a rotation of the clavicle on its long axis.11,18 This clavicular rotation allows the scapula to continue to rotate and increase the degree of arm elevation. During full elevation of the arm, the clavicle rotates 50 degrees axially.11 When the clavicle is prevented from rotating, the arm can be abducted actively to only 120 degrees.4,8 Movement of the acromioclavicular joint is an important component of total arm movement. A principal role of the joint in the elevation of the arm is to permit continued lateral rotation of the scapula after about 100 degrees of abduction when sternoclavicular movement is restrained by the sternoclavicular joint ligaments. The acromioclavicular joint has three degrees of freedom. Movement can occur between the acromion and lateral end of the clavicle about a vertical axis, around a frontal axis, or about a sagittal axis. Functionally, the two main movements at the acromioclavicular joint, however, are a gliding movement as the shoulder joint flexes and extends and an elevation and depression movement to conform with changes in the relation between the scapula and humerus during abduction.5,9,16
Glenohumeral Joint The glenohumeral joint is a multiaxial ball-and-socket synovial joint. This type of joint geometry permits a tremendous amount of motion; however, the inherent stability is minimal (Fig. 1-4). The articular surfaces, head of the humerus, and glenoid fossa of the scapula, although reciprocally curved, are oval and are not sections of true spheres.4 Because the head of the humerus is larger than the glenoid fossa, only part of the humeral head can be in articulation with the glenoid fossa in any position of the joint. At any given time, only 25% to 30% of the humeral head is in contact with the glenoid fossa.19-21 The surfaces are not congruent, and the joint is loose-packed. Full congruence and the close-packed position are obtained when the humerus is in full elevation.22,23
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THE ATHLETE’S SHOULDER
Other investigators have also reported bilateral differences in retroversion in overhead athletes, in whom the throwing side exhibits greater retroversion.27-29 The glenoid fossa is somewhat pear-shaped and resembles an inverted comma (Fig. 1-5). The surface area is 25% to 33%, the vertical diameter 75%, and the transverse diameter 55% of that of the humeral head.25 In 75% of subjects, the glenoid fossa is retroverted an average of 7.4 degrees in relation to the plane of the scapula.30,31 Furthermore, the glenoid fossa has a slight upward tilt of about 5 degrees in reference to the medial border of the scapula32; we refer to this as the inclination angle. It has been suggested that this relation is important in maintaining horizontal stability of the joint and counteracting any tendency toward anterior displacement of the humeral head.25,30,31 However, this concept has not been supported by subsequent studies.33,34 The articular cartilage lining the glenoid fossa is thickest in the periphery and thinnest in the central region. Figure 1-4. Osseous structure of the glenohumeral joint. The large convex humeral head is in a relatively small glenoid fossa.
The design characteristics of the joint are typical of an incongruous joint. The surfaces are asymmetrical, the joint has a movable axis of rotation, and muscles related to the joint are essential in maintaining stability of the articulation (Box 1-1).9 The humeral articular surface has a radius of curvature of 35 to 55 mm. The humeral head and neck make an angle of 130 to 150 degrees with the shaft and are retroverted about 20 to 30 degrees with respect to the transverse axis of the elbow.24,25
Because of the amount of pathology involving the acromion and head of the humerus, the acromion has been studied extensively. Bigliani and Morrison35 have classified the shapes of the acromion into three categories. Type I acromions are those with a flat undersurface and have the lowest risk for impingement syndrome and its sequelae. Type II acromions have a curved undersurface and type III acromions have a hooked undersurface (Fig. 1-6). Type III has the highest correlation with impingement syndromes, rotator cuff pathologies or both. Nicholson and associates36 have reported that the shape of the acromion is congenital and does not develop over time. The acromions have epiphysis and occasionally may not fuse, leading to acromion deformity, often referred to as os acromiale.37
The topic of retroversion has received increased attention because of the implications of its effect on glenohumeral joint motion. Nowhere is this point more evident than with the overhead athlete, who exhibits excessive external rotation and a limitation of internal rotation. Crockett and colleagues26 have studied professional baseball pitchers and noted a bilateral difference in humeral retroversion. The investigators noted a 17-degree difference, with the throwing shoulder exhibiting greater external rotation and loss of internal rotation. This difference was not observed in the control group of non–overhead throwing athletes. Box 1-1. Stability
Factors Contributing to Glenohumeral
Osseous configuration (joint geometry) Glenoid labrum Glenohumeral capsule Neuromuscular system Negative intra-articular pressure
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Figure 1-5. Lateral view of the glenoid fossa. Note the pear-shaped appearance and similarity to an inverted comma.
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
A
7
increase the depth of the concave surface substantially, and that the glenoid labrum is no more than a fold of capsule composed of dense fibrous connective tissue that stretches out anteriorly with external rotation and posteriorly with internal rotation of the humerus.40 The main function of the labrum may be to serve as an attachment for the glenohumeral ligaments.4,40 When that attachment is compromised, it represents a Bankart lesion, in which the capsular-labral complex is detached from the glenoid rim (Fig. 1-7; see Fig. 1-6).
Capsule
B
C Figure 1-6. Acromial shapes. A, Type 1, flat acromion. B, Type II, curved acromion. C, Type III, hooked acromion.
The resting position of the scapula in reference to the trunk is anteriorly rotated about 30 to 40 degrees,21,38 with respect to the frontal plane as viewed from above. This has been referred to as the scapular plane. The scapula is also rotated upward about 3 degrees and tilted forward approximately 20 degrees.38,39
The capsule surrounds the joint and is attached medially to the margin of the glenoid fossa beyond the labrum. Laterally, it is attached to the circumference of the anatomic neck, and the attachment descends about 1⁄2 inch onto the shaft of the humerus. The capsule is loose-fitting, allowing the joint surfaces to be separated 2 to 3 mm by a distractive force.4 Matsen and colleagues42 have shown 22 mm of inferior, 6 mm anterior, and 7 mm posterior translation in normal subjects. The capsule is relatively thin and, by itself, would contribute little to the stability of the joint. The integrity of the capsule and maintenance of the normal glenohumeral relationship depend on the reinforcement of the capsule by ligaments and attachment of the muscle tendons of the rotator cuff mechanism.4,9,16 The superior part of the capsule, together with the superior glenohumeral ligament, is important in strengthening
Glenoid Labrum The glenoid labrum consists of fibrocartilage and fibrous tissue.4,40 This rim of fibrocartilaginous tissue attaches around the margin of the glenoid fossa.40 The inner surface of the labrum is covered with synovium; the outer surface attaches to the capsule and is continuous with the periosteum of the scapular neck. The shape of the labrum adapts to accommodate rotation of the humeral head, adding flexibility to the edges of the glenoid fossa. The tendons of the long head of the biceps brachii muscle contribute to the structure and reinforcement of the labrum. The long head of the biceps brachii attaches to the superior region of the labrum. The width and thickness of the glenoid labrum vary. The anterior labrum appears thicker and at times larger than the posterior labrum. It has been suggested40 that the labrum protects the edges of the glenoid, assists in lubrication of the joint, and deepens the glenoid cavity, thus contributing to stability of the joint.4,5,9,41 Others have stated that the labrum does not
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A
B Figure 1-7. Capsular-labral complex defect, often described as a Bankart lesion. A, Lateral capsular flap reattached to glenoid rim. B, Added strength from double-breasting the medial capsule, reinforcing the entire glenoid rim from 2:00 to 6:00.
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THE ATHLETE’S SHOULDER
the superior aspect of the joint and resisting the effect of gravity on the dependent limb.4,43 Anteriorly, the capsule is strengthened by the anterior glenohumeral ligaments and attachment of the subscapularis tendon (Fig. 1-8).44 Posteriorly, the capsule is strengthened by the attachment of the teres minor and infraspinatus tendons.45 Inferiorly, the capsule is relatively thin and weak and contributes little to the stability of the joint. The inferior part of the capsule is subjected to considerable strain because it is stretched tightly across the head of the humerus when the arm is elevated. The inferior part of the capsule, the weakest area, is lax and lies in folds when the arm is adducted. Kaltsas46 has compared the collagen structure of the shoulder joint capsule with that of the elbow and hip. When the joint capsules were subjected to a mechanical force, the shoulder joint capsule showed a greater capacity to stretch than to rupture. When the capsule was tested to failure, the structure ruptured anteroinferiorly.46,47 Also, Reeves47 has demonstrated that the force required to cause glenohumeral joint dislocation is less in those younger than 20 years and greater in those older than 50 years. O’Brien and coworkers48 have described the glenohumeral capsule and its ligamentous structures and noted that the anterior capsule is comprised of three ligamentous portions—the superior glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and inferior glenohumeral ligament complex (IGHLC) (Fig. 1-9). The IGHLC is comprised of the anterior band (AB), posterior band (PB), and axillary pouch (AP). The study noted that during abduction and external rotation, the anterior band acts as a hammock, resulting in anterior displacement of
Coracohumeral
Superior glenohumeral
Middle glenohumeral Inferior glenohumeral
Figure 1-8. Coracohumeral and glenohumeral ligaments. Note the deficiencies between the glenohumeral ligaments and the Z arrangement of the three components of the ligament.
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B SG HL P
M G H
PC
A L
A B
PB AP IG H L C
Figure 1-9. Glenohumeral joint capsule. Note the superior glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and inferior glenohumeral ligament complex (IGHLC). AB, anterior band; AP, axillary pouch; PB, posterior band.
the humerus (see Fig. 1-9). Conversely, with abduction internal rotation, the posterior band functions as a ligamentous restraint to posterior displacement. The axillary pouch functions as a redundancy to the capsule, allowing excessive mobility. Fealy and colleagues49 have examined the glenohumeral joint in 51 fetal shoulders ranging from 9 to 40 weeks of gestation. The authors noted distinct capsules with ligaments present, especially a prominent inferior glenohumeral ligament complex. A coracohumeral ligament and rotator cuff interval were also present. Johnston23 has stated that, with the arm by the side, the capsular fibers are oriented with a forward and medial twist. This twist increases in abduction and decreases in flexion. The capsular tension in abduction compresses the humeral head into the glenoid fossa. As abduction progresses, the capsular tension exerts an external rotation moment. This external rotation untwists the capsule and allows further abduction. The external rotation of the humerus that occurs during coronal plane abduction may therefore be assisted by the configuration of the joint capsule.23 The capsule is lined by a synovial membrane attached to the glenoid rim and anatomic neck inside the capsular attachments.4 The tendon of the long head of the biceps brachii muscle passes from the supraglenoid tubercle over
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
the superior aspect of the head of the humerus and lies within the capsule, emerging from the joint at the intertubercular groove (Fig. 1-10). The tendon is covered by a synovial sheath to facilitate movement of the tendon within the joint. The structure is susceptible to injury at the point at which the tendon arches over the humeral head, and the surface on which it glides changes from bony cortex to articular cartilage.5
TABLE 1-1 Stability of the Glenohumeral Joint Position
Structure
Dependent
Coracohumeral ligament Superior glenohumeral ligament Supraspinatus muscle
Elevation (degrees) Lower range (0-45)
Coracohumeral Ligament The coracohumeral ligament is an important ligamentous structure in the shoulder complex.43 The ligament is attached to the base and lateral border of the coracoid process and passes obliquely downward and laterally to the humerus, blending with the supraspinatus muscle and the capsule. Laterally, the ligament separates into two components that insert into the greater and lesser tuberosities, creating a tunnel through which the biceps tendon passes.50 Inferiorly, the coracohumeral ligament blends with the superior glenohumeral ligament. The anterior border of the ligament is distinct medially and merges with the capsule laterally. The posterior border is indistinct and blends with the capsule.4,9 It has been suggested that the downward pull of gravity on an adducted arm is counteracted largely by the superior capsule, coracohumeral ligament, and inferior glenohumeral ligament (Table 1-1).50,51 As the arm is abducted, the restraining force is shifted to the inferior structures and the primary restraining force is the inferior glenohumeral ligament.52 Because the coracohumeral ligament is located anteriorly to the vertical axis about which the humerus rotates axially, the ligament checks lateral rotation during arm elevation between 0 and 60 degrees. When
9
Anterior capsule Superior glenohumeral ligament Coracohumeral ligament Middle glenohumeral ligament Subscapularis, infraspinatus, and teres minor muscles
Middle range (45-75) Middle glenohumeral ligament (MGHL) Supscapularis muscle (decreasing importance) Infraspinatus and teres minor muscles Inferior glenohumeral ligament (superior band) Upper range (⬎75)
Inferior glenohumeral ligament (anterior band; axillary pouch)
Throughout elevation Dynamic activity of rotator cuff
the humerus, in a position of neutral rotation, is elevated in the sagittal plane, the movement is limited to approximately 75 degrees by the coracohumeral ligament. For elevation to continue, the humerus is medially rotated and moves toward the scapular plane by the dynamic tension in this ligament.22
Glenohumeral Ligaments The three glenohumeral ligaments lie on the anterior and inferior aspect of the joint . They are described as being thickened parts of the capsule.4 The superior glenohumeral ligament passes laterally from the superior glenoid tubercle, upper part of the glenoid labrum, and base of the coracoid process to the humerus, between the upper part of the lesser tuberosity and anatomic neck.50,51 The ligament lies anterior to and partly under the coracohumeral ligament. The superior glenohumeral ligament, together with the superior joint capsule and rotator cuff muscles, assist in preventing downward displacement of the humeral head.51,53
Anterior
Medial
Figure 1-10. Attachments of the glenohumeral ligaments to the humerus.
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The middle glenohumeral ligament has a wide attachment, extending from the superior glenohumeral ligament along the anterior margin of the glenoid fossa down as far as the junction of the middle and inferior thirds of the glenoid rim.51 From this attachment, the ligament passes laterally, gradually enlarges, and attaches to the anterior aspect of the anatomic neck and lesser tuberosity of the humerus. The ligament lies under the tendon of the subscapularis muscle and is intimately attached to it.25,50 Note
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THE ATHLETE’S SHOULDER
the large variation in size of the middle glenohumeral ligament; it can be 2 cm wide but is absent in some individuals. This structure exhibits the greatest amount of structural variation. The middle glenohumeral ligament and subscapularis tendon limit lateral rotation from 45 to 75 degrees of abduction and are important anterior stabilizers of the glenohumeral joint, particularly effective in the lower to middle ranges of abduction (see Table 1-1).
Inside the glenohumeral joint capsule is negative pressure in comparison with outside the joint capsule. This is referred to as negative intra-articular pressure and provides a stabilizing effect on the shoulder joint.54 Wulker and colleagues55 have demonstrated that venting the capsule (creating a cut into the capsule, thus eliminating the negative intra-articular pressure) may increase translation of the humerus on the glenoid by 19% to 50%.
The inferior glenohumeral ligament is the thickest of the glenohumeral structures and is the most important stabilizing structure of the shoulder in the overhead athlete. The ligament attaches to the anterior, inferior, and posterior margins of the glenoid labrum and passes laterally to the inferior aspects of the anatomic and surgical necks of the humerus.4,25 The ligament can be divided into three distinct portions—the anterior band, axillary pouch, and posterior band (see Fig. 1-9).48 The inferior part is thinner and broader and is termed the axillary pouch. The anterior band strengthens the capsule anteriorly and supports the joint most effectively in the upper ranges (more than 75 degrees) of abduction.48 The anterior band of the inferior glenohumeral ligament provides a broad buttresslike support for the anterior and inferior aspects of the joint, preventing subluxation in the upper part of the range (see Table 1-1).51
Rotator Cuff: Dynamic Stability
O’Brien and associates48 have demonstrated that with the arm abducted to 90 degrees and externally rotated, the anterior band of the inferior glenohumeral ligament complex wraps around the humeral head like a hammock to prevent anterior humeral head migration. This structure provides stability during the throwing motion, tennis serve motion, freestyle stroke, or any overhead arm position. Tightening of the inferior glenohumeral ligament during coronal plane abduction limits elevation to an average of 90 degrees. To continue to elevate, the humerus must move toward the scapular plane and laterally rotate. Gagey and coworkers22 have stated that both movements occur because of dynamic tension in the inferior glenohumeral ligament. The coracohumeral and glenohumeral ligaments viewed from the front form a Z pattern . This arrangement creates potential areas of capsular weakness above and below the middle glenohumeral ligament. The subscapularis bursa communicates with the joint cavity through the superior opening, or foramen of Weitbrecht, between the superior and middle glenohumeral ligaments. Ferrari50 has also reported the presence of an inferior subscapular bursa, between the middle and inferior glenohumeral ligaments. This bursa was present in all 14 specimens in those younger than 55 years and could be seen up to the age of 75 years. When the middle glenohumeral ligament is attenuated or absent, this anterior defect is enhanced and may contribute to anterior instability of the joint.50
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The rotator cuff is the musculotendinous complex formed by the attachment to the capsule of the supraspinatus muscle superiorly, the subscapularis muscle anteriorly, and the teres minor and infraspinatus muscles posteriorly. These tendons blend intricately with the fibrous capsule and the adjacent rotator cuff tendon.56 They provide active support for the joint and can be considered true dynamic ligaments that provide dynamic stability.8 The capsule is less well protected inferiorly because the tendon of the long head of the triceps brachii muscle is separated from the capsule by the axillary nerve and posterior circumflex humeral artery.4 The rotator cuff tendons insert into a large contact point onto the greater and lesser tuberosities of the humerus and not a small insertion point, as was once thought. Dugas and associates57 have reported that the rotator cuff inserts less than 1 mm from the articular margin. Curtis and coworkers58 later reported that the insertional anatomy in cadaveric shoulders exhibits a consistent pattern and noted interdigitation of the muscles, particularly between the supraspinatus and infraspinatus. The average insertional lengths and widths for the rotator cuff muscles were as follows: supraspinatus 23 ⫻ 16 mm, subscapularis 40 ⫻ 20 mm, infraspinatus 29 ⫻ 19 mm, and teres minor 29 ⫻ 11 mm. Bassett and colleagues59 have studied the cross-sectional area of the rotator cuff muscles as they cross the glenohumeral joint capsule (Table 1-2); they found that the larger the cross-sectional area, the more significant the contribution to shoulder stability. Miller and associates60 have described a space between the supraspinatus and infraspinatus and referred to this area as the posterior rotator cuff interval. They went on to discuss the importance of releasing this area when rotator cuff repairs are performed in specific types of patients who exhibit supraspinatus retraction and scarring. It is generally accepted that the deltoid and the rotator cuff muscles are prime movers of glenohumeral abduction.61-63 These muscles have been found to contribute equally to torque production in functional planes of motion.63 With the arm at the side, the directional force of the deltoid muscle is almost vertical.25,64 Thus, most of the deltoid force will cause a superior shear force of the humeral head that, if unopposed, would cause the humeral head to contact the coracoacromial arch, resulting in impingement of soft
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
TABLE 1-2 Cross-Sectional Area of Rotator Cuff Muscles Crossing the Glenohumeral (GH) Joint Capsule
Muscle
Contribution of Muscle Area (cm2) Crossing GH Joint (%)
Biceps (LH)
2.01
2
Biceps (SH)
1.11
2
Deltoid
18.2
17.7
5.0
5
Infraspinatus and teres minor
13.7
13
Latissimus dorsi
12.0
11.7
Pectoralis major
13.3
13
Subscapularis
16.3
16
Supraspinatus
5.7
5.6
Teres major
8.77
8.5
Triceps
3.0
3.8
Deltoid (posterior)
From Bassett R, Browne A, Morrey BF, et al: Glenohumeral muscle force and moment mechanics in a position of shoulder instability. J Biomech 23:405, 1990.
tissues.65 The force vectors of the infraspinatus, subscapularis, and teres minor muscles are such that each tends to have a compressive component as well as a rotational force.39,65 Each muscle’s compressive force offsets the superior shear force of the deltoid.39 The infraspinatus, teres minor, and subscapularis thus form a force coupled with the deltoid and act to stabilize the humeral head on the glenoid fossa, allowing the deltoid and supraspinatus to act as abductors of the humerus.66 We often refer to the rotator cuff muscles as the compressive cuff. In studies on a mechanical model, Comtet and coworkers61 have determined that the depressor forces are at their maximum between 60 and 80 degrees of elevation and disappear beyond 120 degrees. The supraspinatus has a small superior shear component, but its main function is compression because of the horizontal orientation of the muscle fibers39; thus, it opposes the upward superior shear action of the deltoid. Lesions of the rotator cuff mechanism can occur as a response to repetitious activity over time or to overload activity that causes a spontaneous lesion.67 Stress applied to a previously degenerated rotator cuff may cause the cuff to rupture. Often, this stress also tears the articular capsule, resulting in a communication between the joint cavity and subacromial bursa. Rotator cuff tears result in considerably reduced force of elevation of the glenohumeral joint. In attempting to elevate the arm, the patient shrugs the shoulder. If the arm is abducted passively to 90 degrees, the patient should be able to maintain the arm in the abducted position.9
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11
The space between the supraspinatus and superior border of subscapularis has been termed the rotator interval. This space is triangular, with its base located medially at the coracoid process. The rotator interval contains the coracohumeral ligament, superior glenohumeral ligament, glenohumeral capsule, and biceps tendon.68-72 The medial aspect consists of two layers and the lateral portion is composed of four layers. The superficial layer of the medial rotator interval is comprised of the coracohumeral ligament and the deep layer consists of the superior glenohumeral ligament and joint capsule. The coracohumeral ligament also represents the superficial layer of the lateral portion of the rotator interval. The second layer is composed of the fibers of the supraspinatus and subscapularis. The third layer consists of the deep fibers of the coracohumeral ligament and the fourth layer is the superior glenohumeral ligament and lateral capsule.68,69 The size of the rotator cuff interval varies. The larger the interval, the greater the inferior and posterior laxity.72 The function of the long head of the biceps is controversial. Some believe that it contributes to the stability of the glenohumeral joint by preventing upward migration of the head of the humerus during powerful elbow flexion and forearm supination. Lesions of the long head of the biceps, therefore, may produce instability and shoulder dysfunction.73 Conversely, other physicians74-76 have reported performing biceps tenotomy in patients with refractory biceps pain. Once the biceps was released, pain was eliminated in over 70% of patients and no functional limitations, instability, or weakness were reported. Thus, the function of the proximal long head of the biceps brachii is still being debated. The scapula plays a vital role in normal shoulder function. Normal scapulothoracic joint motion and rhythm are critical to pain-free normal shoulder function. Numerous muscles about the scapula play a critical role in accomplishing this function. The trapezius muscle is the largest and most superficial scapulothoracic muscle. This muscle originates from the spinous processes of the C7 through T12 vertebrae. The muscle is classified into upper, middle, and lower fibers. Insertion of the upper fibers is over the distal third of the clavicle. The lower cervical and upper thorax fibers insert over the acromion and spine of the scapula. The lower portion of the trapezius inserts into the base of the spine of the scapula. The rhomboids function similarly as the midportion of the trapezius.77 The origin of the rhomboids is from the lower ligamentum nuchae, C7 and T1 for the rhomboid minor and T2 through T5 for the rhomboid major. The rhomboid minor inserts onto the posterior portion of the medial base of the spine of the scapula. The rhomboid major inserts onto the medial border of the scapula. The levator scapulae muscle proceeds from its origin on the transverse processes from C1 through C3 (and sometimes C4) and inserts onto the superior angle of the scapula. The serratus anterior takes its origin from the ribs on the lateral wall of the thoracic cage.
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THE ATHLETE’S SHOULDER
The serratus has three divisions, upper, middle and lower. The upper fibers originate from ribs 1 and 2, the middle fibers from ribs 2 through 4, and the lower from ribs 5 through 9. The serratus anterior muscle orientation is in individual slips from each rib. The serratus inserts onto the superior angle, medial border, and inferior angle of the scapula, respectively. The pectoralis minor runs from the second through fifth ribs upward to the medial base of coracoid. Somewhat frequently, approximately 15% incidence, there will be an aberrant slip from the pectoralis minor to the humerus, glenoid, clavicle, or scapula.78,79 The subclavius muscle is a small muscle that originates from the first rib and inserts as a muscle onto the inferior surface of the medial third of the clavicle. This muscle stabilizes the sternoclavicular joint.
Coracoacromial Arch The coracoacromial ligament is triangular with the base attached to the lateral border of the coracoid process (Fig. 1-11). The ligament passes upward, laterally, and slightly posteriorly to the superior aspect of the acromion process.4,80 Superiorly, the ligament is covered by the deltoid muscle. Posteriorly, the ligament is continuous with the fascia that covers the supraspinatus muscle. Anteriorly, the coracoacromial ligament has a sharp, well-defined, free border. Together with the acromion and the coracoid processes, the ligament forms an important protective arch over the glenohumeral joint.9 The arch forms a secondary restraining socket for the humeral head, protecting the joint from trauma from above and preventing upward
dislocation of the humeral head. The supraspinatus muscle passes under the coracoacromial arch, lies between the deltoid muscle and the capsule of the glenohumeral joint, and blends with the capsule. The supraspinatus tendon is separated from the arch by the subacromial bursa (see Fig. 1-11).9 The space between the inferior acromion and head of the humerus (subacromial distance) has been measured on radiographs and is used as an indicator of proximal humeral subluxation.81,82 The distance was found to be between 9 and 10 mm in 175 asymptomatic shoulders and was greater in men than in women.81 A distance of less than 6 mm was considered pathologic and was thought to be indicative of supraspinatus tendon attenuation or rupture.81 During elevation, with internal rotation of the arm in abduction and flexion, the greater tuberosity (the supraspinatus tendon) of the humerus may apply pressure against the anterior edge and inferior surface of the anterior third of the acromion and coracoacromial ligament. This is in part because of the anterior orientation of the supraspinatus tendon. In some cases, the impingement also may occur against the acromioclavicular (AC) joint. This often occurs when the AC joint exhibits degenerative joint disease or spurring, or both. Most upper extremity functions are performed with the hand placed in front of the body, not lateral to it. When the arm is raised forward in flexion, the supraspinatus tendon passes under the anterior edge of the acromion and acromioclavicular joint. For this movement, the critical area for wear is centered on the supraspinatus tendon and also may involve the long head of the biceps brachii muscle. Flatow and colleagues83 have examined the concept of impingement, compression between the supraspinatus and acromion. The investigators measured the distance between the undersurface of the acromion and humeral head at various degrees of abduction. At 0 degrees adduction (arm at the side), the acromiohumeral space was approximately 11 mm, at 90 degrees of abduction it was 5.7 mm, and at 120 degrees of abduction less than 5 mm (4.8 mm). Furthermore, the investigators placed Fuji contact film, which measures pressure per square area, on the acromion and humeral head. They found that with arm abduction from 60 degrees to full elevation, there was contact between the acromion and humeral head. Therefore, Flatow and associates83 have reported that contact between the humeral head and acromion is normal.
Bursae
Figure 1-11. Coracoacromial ligament and its relation to the humeral head.
Ch01_001-016-F06701.indd 12
Several bursae are found in the shoulder region.4 Two bursae particularly important to the clinician are the subacromial and subscapular bursae.15 Other bursae located in relation to the glenohumeral joint structures are between the infraspinatus muscle and capsule, on the superior surface of the acromion, between the coracoid process and
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FUNCTIONAL ANATOMY OF THE SHOULDER COMPLEX
capsule, under the coracobrachialis muscle, between the teres major and long head of the triceps brachii muscles, and in front of and behind the tendon of the latissimus dorsi muscle. Because bursae are located where motion is required between adjacent structures, they have a major function in the shoulder mechanism. The subacromial bursa (Fig. 1-12) is located between the deltoid muscle and capsule, extending under the acromion and coracoacromial ligament and between them and the supraspinatus muscle. The bursa adheres to the coracoacromial ligament and to the acromion above and rotator cuff below. The bursa does not frequently communicate with the joint; however, a communication may develop if the rotator cuff is ruptured.80 The subacromial bursa is important for allowing gliding between the acromion and deltoid muscle and rotator cuff. It also reduces friction on the supraspinatus tendon as it passes under the coracoacromial arch.9,80 Often, with repetitive overhead motion, the bursae may become inflamed and thickened, which may decrease the critical space in the subacromial region. The subscapular bursa lies between the subscapularis tendon and neck of the scapula. It protects this tendon where it passes under the base of the coracoid process and over the neck of the scapula. The bursa communicates with the joint cavity between the superior and middle glenohumeral ligaments9,51 and often between the middle and inferior glenohumeral ligaments.40,50
Vascular Supply The rotator cuff is a frequent site of pathologic conditions, usually degenerative and often in response to fatigue stress.17 Because degeneration may occur even with normal activity levels, the nutritional status of the glenohumeral structures is of great importance. The blood supply to the Acromion
Deltoid Subacromial bursa Supraspinatus
13
rotator cuff comes from the posterior humeral circumflex and suprascapular arteries.4 These arteries supply principally the infraspinatus and teres minor muscle areas of the cuff. The anterior aspect of the capsular ligamentous cuff is supplied by the anterior humeral circumflex artery and occasionally by the thoracoacromial, suprahumeral, and subscapular arteries. Superiorly, the supraspinatus muscle is supplied by the thoracoacromial artery. The supraspinatus tendon has a region of relative avascularity 1 cm proximal to the humeral insertion, often including its insertion into the humerus.84,85 Rothman and Parke85 have reported hypovascularity in the tendon in 63% of 72 shoulders studied. In a study by Rathbun and MacNab,84 an avascular area was found in all specimens and was unrelated to age. Abduction of the arm resulted in relaxation of the tension on the supraspinatus muscle and complete filling of vessels throughout the tendon. In addition, with increasing age, the area of avascularity also increases67; thus, the potential for healing decreases with age. The other cuff tendons generally demonstrate good vascularity, except for an occasional zone of hypovascularity in the superior portion of the insertion of the infraspinatus tendon.84,85
Articular Neurology Innervation of the shoulder region is derived from C5, C6, and C7; C4 also may add a minor contribution. The nerves supplying the ligaments, capsule, and synovial membrane are axillary, suprascapular, subscapular, and musculocutaneous nerves. Branches from the posterior cord of the brachial plexus also may supply the joint structures. Occasionally, the shoulder may receive a greater supply from the axillary nerve than from the musculocutaneous nerve; the reverse may also be true. The complex overlapping innervation pattern makes denervation of the joint difficult. The nerve supply follows the small blood vessels into periarticular structures.4,5 The skin on the anterior region of the shoulder complex is supplied by the supraclavicular nerves from C3 and C4 and by the terminal branches of the sensory component of the axillary nerve. The articular structures on the anterior aspect of the glenohumeral joint are supplied by the axillary nerve and, to a lesser degree, by the suprascapular nerves. The subscapular nerve and posterior cord of the brachial plexus may also innervate the anterior aspect of the joint after piercing the subscapularis muscle.4,5,9 The supraclavicular nerves supply the skin on the superior and upper posterior aspects of the shoulder region. The lower, posterior, and lateral aspects of the shoulder are supplied by the posterior branch of the axillary nerve.
Figure 1-12. Supraspinatus tendon and related structures.
Ch01_001-016-F06701.indd 13
The periarticular structures on the superior aspect of the joint obtain part of their innervation from the suprascapular nerve. The axillary and musculocutaneous nerves
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14
THE ATHLETE’S SHOULDER
and the lateral pectoral nerve may also contribute to the innervation of the superior aspect of the joint. Posteriorly, the main nerve supply is from the suprascapular nerve, which supplies the proximal part of the joint, and the axillary nerve, which supplies the distal region.3-5,9 The acromioclavicular joint is innervated by the lateral supraclavicular nerve from the cervical plexus (C4) and by the lateral pectoral and suprascapular nerves from the brachial plexus (C5 and C6). The sternoclavicular joint is innervated by branches from the medial supraclavicular nerve from the cervical plexus (C3 and C4) and subclavian nerve from the brachial plexus (C5 and C6).4,9
SUMMARY The shoulder complex is more mobile than any other joint mechanism of the body because of the combined movement at the glenohumeral and scapulothoracic articulations. This wide range of motion permits positioning of the hand in space, allowing performance of numerous gross and skilled functions. Shoulder complex stability is also required during dynamic activity, particularly when the distal extremity encounters resistance. The glenohumeral joint is inherently unstable because of the shallowness of the glenoid fossa as well as the disproportionate size and lack of congruency between the articular surfaces. During dynamic activities, stabilization of the humeral head on the glenoid fossa depends on an intact capsule and glenohumeral ligaments, as well as on coordinated and synchronous activity in the deltoid and rotator cuff muscles. Injury or disease of any of these structures can lead to instability and impingement of subacromial structures, resulting in pain and dysfunction in the shoulder region.
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35. Bigliani LU, Morrison DS, April EW: The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 10:228, 1986. 36. Nicholson GP, Goodman DA, Flatow EL: The cromion: Morphologic condition and and age-related changes. A study of 420 scapulas. J Shoulder Elbow Surg 5:1, 1996. 37. Lieberson F: Os acromiale—a contested anomaly. J Bone Joint Surg 19:683, 1937. 38. Laumann U: Kinesiology of the Shoulder Joint. In Kolbel R (ed): Shoulder Replacement. Berlin, Springer-Verlag, 1987. 39. Morrey BF, An KN: Biomechanics of the shoulder. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, p 235. 40. Moseley HF, Overgaard B: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder: Morphological and clinical studies with special reference to the glenoid labrum and the gleno-humeral ligaments. J Bone Joint Surg Br 44:913, 1962. 41. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics, and tennis. Clin Sports Med 2:247, 1983. 42. Matsen FA, Harryman DT, Didles JA: Mechanics of glenohumeral instability. In Hawkins RJ (ed): Clinics in Sports Medicine: Basic Science and Clinical Application in the Athlete’s Shoulder. Philadelphia, WB Saunders, 1991. 43. Basmajian JV, Bazant FJ: Factors preventing downward dislocation of the adducted shoulder joint. J Bone Joint Surg Am 41:1182, 1959. 44. Ovesen J, Nielsen S: Anterior and posterior shoulder instability: A cadaver study. Acta Orthop Scand 57:324, 1986. 45. Ovesen J, Nielsen S: Posterior instability of the shoulder: A cadaver study. Acta Orthop Scand 57:436, 1986. 46. Kaltsas DS: Comparative study of the properties of the shoulder joint capsule with those of other joint capsules. Clin Orthop 173:20, 1983. 47. Reeves B: Experiments on the tensile strength of the anterior capsular structures of the shoulder in man. J Bone Joint Surg Br 50:858, 1968. 48. O’Brien SJ, Neeves MC, Arnoczky SN, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:451, 1990. 49. Fealy S, Dodeo SA, Dicarlo EF, O’Brien SJ: The developmental anatomy of the glenohumeral joint. J Shoulder Elbow Surg 9:217, 2000. 50. Ferrari DA: Capsular ligaments of the shoulder: Anatomical and functional study of the anterior superior capsule. Am J Sports Med 18:20, 1990. 51. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208, 1981. 52. Bowen MK, Warren RF: Ligamentous control of shoulder stability based on selective cutting and static translation experiments. Clin Sports Med 10:757, 1991. 53. Schwartz E, Warren RF, O’Brien SJ, et al: Posterior shoulder instability. Orthop Clin North Am 18:409, 1987. 54. Hurchler C, Wulker N, Mendilia M: The effect of negative intraarticular pressure and rotator cuff force on glenohumeral translation during simulated active elevation. Clin Biomech 15:306, 2000.
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55. Wulker N, Rossig S, Korell M, Thren K; Dynamic stability of the glenohumeral joint. A biomechanical study. Sportverletz Sportschaden 9:1, 1995. 56. Clark JM, Harryman DT 2nd: Tendons, ligamentous and capsule of the rotator cuff. J Bone Joint Surg Am 74:713, 1992. 57. Dugas JR, Campbell DA, Warren RF, et al: Anatomy and dimensions of rotator cuff insertions. J Shoulder Elbow Surg 11:98, 2002. 58. Curtis AS, Burbank KM, Tierney JJ, et al: The insertional footprint of the rotator cuff: An anatomic study. Arthroscopy 22:609, 2006. 59. Bassett R, Browne A, Morrey BF, et al: Glenohumeral muscle force and moment mechanics in a position of shoulder instability. J Biomech 23:405, 1990. 60. Miller SL, Gladstone JN, Cleeman E, et al: Anatomy of the posterior rotator interval: Implications for cuff mobilization. Clin Orthop Relat Res 408:152, 2003. 61. Comtet JJ, Herberg G, Naasan IA: Biomechanical basis of transfers for shoulder paralysis. Hand Clin 5:1, 1989. 62. deLuca CJ, Forrest WJ: Force analysis of individual muscles acting simultaneously on the shoulder joint during isometric abduction. J Biomech 6:385, 1973. 63. Howell SM, Imobersteg AM, Seger DH, Marone PJ: Clarification of the role of the supraspinatus muscle in shoulder function. J Bone Joint Surg Am 68:398, 1986. 64. Lucas DB: Biomechanics of the shoulder joint. Arch Surg 107:425, 1973. 65. Poppen NK, Walker PS: Forces at the glenohumeral joint in abduction. Clin Orthop 135:165, 1978. 66. Saha AK: Mechanism of shoulder movements and a plea for the recognition of “zero position” of the glenohumeral joint. Clin Orthop 173:3, 1983. 67. Brewer BJ: Aging of the rotator cuff. Am J Sports Med 7:102, 1979. 68. Hunt SA, Kwon YW, Zuckerman JD: The rotator interval: Anatomy, pathology, and strategies for treatment. J Am Acad Orthop Surg 15:4, 2007. 69. Jost B, Koch PP, Gerber C: Anatomy and functional aspects of the rotator interval. J Shoulder Elbow Surg 9:336, 2000. 70. Nobuhara K, Ikeda H: Rotator interval lesion. Clin Orthop 223:44, 1987. 71. Fitzpatrick MJ, Powell SE, Tibone JE, Warren RF: The anatomy, pathology, and definitive treatment of rotator interval lesions: Current concepts. Arthroscopy 19:70, 2003. 72. Harryman DT, Sidles JA, Harris SL, Matsen FA: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53, 1992. 73. Kumar VP, Satku K, Balasubramaniam P: The role of the long head of biceps brachii in the stabilization of the head of the humerus. Clin Orthop 244:172, 1989. 74. Kelly Am, Drakos MC, Fealy S, et al: Arthroscopic release of the long head of the biceps tendon: Functional outcome and clinical results. Am J Sports Med 33:208, 2005. 75. Walch G, Edwards TB, Boulahia A, et al: Arhtroscopic tentomy of the long head of the biceps in the treatment of rotator cuff tears: Clinical and radiographic results of 307 cases. J Shoulder Elbow Surg 14:238, 2005. 76. Boileau P, Baque F, Valerio L, et al: Isolated arthroscopic biceps tentomy or tendodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am 89:747, 2007.
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77. Inman VT, Saunders JB, Abbott LC: Observations on the function of the shoulder joint. J Bone Joint Surg 26:1, 1944. 78. Lambert AE: A rare variation in the pectoralis minor muscle. Anat Rec 31:193, 1925. 79. Vare AM, Indurak GM: Some anomalous findings in the axillary muscles. J Anat Soc India 14:34, 1965. 80. Rothman RH, Marvel JP, Heppenstall RB: Anatomic considerations in the glenohumeral joint. Orthop Clin North Am 6:341, 1975. 81. Petersson CJ, Redlund-Johnell I: The subacromial space in normal shoulder radiographs. Acta Orthop Scand 55:57, 1984. 82. Weiner DS, MacNab I: Superior migration of the humeral head: A radiological aid in the diagnosis of tears of the rotator cuff. J Bone Joint Surg Br 52:524, 1970. 83. Flatow EL, Soslowsky LJ, Tcker JB, et al: Excursion of the rotator cuff under the acromion. Patterns of subacromial contact. Am J Sports Med 22:779, 1994. 84. Rathbun JB, MacNab I: The microvascular pattern of the rotator cuff. J Bone Joint Surg Br 52:540, 1970. 85. Rothman RH, Parke WW: The vascular anatomy of the rotator cuff. Clin Orthop 41:176, 1965.
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Suggested Readings Hawkins RJ, Abrams JS: Impingement syndrome in the absence of rotator cuff tear (states 1 and 2). Orthop Clin North Am 18:373, 1987. Neer CS: Impingement lesions. Clin Orthop 173:70, 1983. Neviaser TJ: The role of the biceps tendon in the impingement syndrome. Orthop Clin North Am 18:383, 1987. Ovesen J, Nielsen S: Stability of the shoulder joint: Cadaver study of stabilizing structures. Acta Orthop Scand 56:149, 1985. Porterfield JA, DeRosa C: Musculature of the shoulder complex. In Porterfield JA, DeRosa C (eds): Mechanical Shoulder Disorders. Philadelphia, WB Saunders, 2004, p 47. Post M, Cohen J: Impingement syndrome: A review of late stage II and early stage III lesions. Clin Orthop 207:126, 1986. Watson MS: Classification of the painful arc syndromes. In Bayley JI, Kessel L (eds): Shoulder Surgery. New York, Springer-Verlag, 1982.
9/19/08 7:05:47 PM
CHAPTER 2 Clinical Biomechanics
of the Shoulder Complex Brian J. Eckenrode and Martin J. Kelley
PLANES OF MOTION
Shoulder function is the result of the complex interplay of the muscular, osseous, and supporting structures of the shoulder girdle. The lower extremity and trunk initiate and accumulate forces expressed at the shoulder and distal upper extremity. Ultimately, the shoulder positions the hand for precise movements necessary for activities of daily living and athletic performance.
Motion of the shoulder complex is described in relation to the cardinal planes—sagittal, coronal, and horizontal (Fig. 2-1). Shoulder flexion and extension occur in the sagittal plane, abduction and adduction in the coronal plane, and horizontal abduction and adduction in the horizontal plane. Internal and external rotation occur through the long axis of the humerus, affording a high degree of mobility in an infinite number of planes. This is typically assessed at 90 degrees of coronal plane abduction or with the arm at the side.
The articulations of the shoulder complex provide the shoulder with a range of motion that far exceeds that of any other joint. This movement is dependent on controlled and synchronous motion of all joints of the shoulder.1
The American Academy of Orthopaedic Surgeons (AAOS) no longer differentiates the plane of motion in which the arm is brought overhead; instead, they have adopted the term elevation.8 For the purposes of this chapter, shoulder elevation will be used to describe the flexion or abduction of the shoulder complex in the plane of the scapula or cardinal planes. Flexion and abduction will be specifically designated where applicable.
RESTING POSITION Ideally, the shoulder girdle musculature should be well balanced with respect to muscle strength and length to allow proper osseous orientation for optimal upper extremity function. Shoulder girdle suspension is reliant on the sternoclavicular ligaments,2 upper trapezius,3,4 levator scapulae, sternocleidomastoid, fascia,5 and atmospheric pressure.
Plane Of The Scapula In the resting position, the concave ventral surface of the scapula floats on the convex posterior thoracic wall, thus directing the glenoid fossa anteriorly approximately 30 to 45 degrees anterior to the coronal plane. This is referred to as the plane of the scapula (Fig. 2-2).11-13 The scapula has a slight anterior tilt in the sagittal plane,14 and the glenoid fossa exhibits a slight upward inclination in the resting position.15,16
The resting position of the shoulder girdle also depends on thoracic spine alignment and muscular linkages from the thoracic and cervical spine to the shoulder’s bony components.6,7 Shoulder girdle resting position is highly variable, depending on postural habits, hand dominance, occupation, muscle tone, and age.8 For example, the dominant shoulder of a competitive baseball pitcher tends to exhibit increased anterior tilt, depression, and abduction of the scapula compared with the nondominant side. The repetitive throwing cycle may result in abnormal and pathologic alterations. Burkhart and colleagues9 have described the asymmetrical malposition of the scapula in the throwing athletes as the SICK scapula (scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement). Altered scapular position may produce scapular dyskinesis dynamically in the throwing cycle, affecting glenohumeral and acromioclavicular joint kinematics. This syndrome often manifests itself with pain and impaired throwing accuracy and velocity, along with altered scapular kinematics.10
Motion in the scapular plane is actually arm movement relative to the scapula as opposed to the trunk. This suggests that the plane of the scapula is not truly fixed, because the scapula translates forward during elevation.4 There are several unique biomechanical and anatomic features of scapular plane elevation:81 1. The joint surfaces have greater conformity.12,17 2. During elevation the inferior capsuloligamentous complex and rotator cuff tendons remain untwisted, because humeral rotation is not required (Fig. 2-3). 17
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THE ATHLETE’S SHOULDER Flexion Plane of scapula Horizontal adduction
Internal rotation Abduction
B
External rotation
Coronal abduction
Horizontal abduction
A
Extension
C
Figure 2-1. Motion of the shoulder complex. A, Planes of motion (superior view). B, Humeral external and internal rotation at 90 degrees of coronal plane abduction. C, Pure glenohumeral rotation at neutral and functional internal rotation. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 68.)
3. The supraspinatus and deltoid are optimally aligned for elevation. 4. Most functional activities are performed in this plane.18 These characteristics, specific to the scapular plane, can greatly enhance shoulder rehabilitation. By performing strengthening exercise in the plane of the scapula, rotator
cuff muscle strength can be optimized whereas unwanted passive tension on the rotator cuff tendons and capsuloligamentous complex (CLC) can be minimized. In the athlete with shoulder instability, the clinician can strengthen and perform range-of-motion exercises in the scapular plane, reducing potential anterior and posterior translation by eliminating stress on the deficient static restraints.
OSTEOKINEMATICS AND ARTHROKINEMATICS Scapulothoracic Joint
Figure 2-2. Scapular orientation in the plane of the scapula. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 65.)
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Scapulothoracic joint function enhances arm-trunk motion and glenohumeral stability as the scapula orients the glenoid to the humeral head. It also serves as a protective mechanism, because the joint and surrounding musculature absorb energy with a fall onto an outstretched arm.8 Kibler10 has described five distinct roles of the scapula: (1) it represents a stable part of the glenohumeral articulation; (2) allows for retraction and protraction along the thoracic wall; (3) elevates the acromion to decrease
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
A
19
B
Figure 2-3. Inferior view of the glenohumeral joint and capsuloligamentous complex. A, Scapular plane abduction. B, Coronal plane abduction. (From Johnston TB: The movements of the shoulder joint. A plea for the use of the “Plane of the Scapula” as the plane of reference in movements occurring at the humero-scapular joint. Br J Surg 25:252, 1937.)
impingement and coracoacromial arch compression in the throwing and serving motion; (4) serves as a base for muscle attachment; and (5) functions as a link in the proximal to distal sequencing of the kinetic chain. The failure of the scapula to perform these roles causes inefficient physiology and biomechanics, and therefore, inefficient shoulder function.10
Elevation and Depression Although gliding occurs between the scapula and thorax, the true fulcrum for motion is the sternoclavicular joint.8 Scapular elevation, movement of the scapula superiorly on the thorax (see Fig. 2-4),21 occurs primarily from activation of the upper trapezius4 and levator scapulae22; the rhomboid elevates with retraction.
The scapula is suspended on the axial skeleton by the sternoclavicular ligaments, indirectly through the clavicle,2 descending axioscapular muscles,3,5 coracoclavicular ligaments, atmospheric pressure,4 and fascia.5 Glenohumeral joint stability is maximized as the glenoid adjusts to support the humeral head.19 At rest, the scapula is positioned in the scapular plane. Scapular movement is primarily mediated by the oblique axioscapular muscles. The scapulothoracic joint is described with five degrees of freedom, three rotations and two translations (Fig. 2-4).20
Depression is movement of the scapula inferiorly on the thorax, and occurs in conjunction with scapular anterior or posterior tilting (see Fig. 2-4). Contraction of the pectoralis minor and serratus anterior causes depression and anterior tilting (protraction), whereas depression and posterior tilting are mediated by the lower trapezius.8 When a patient assumes the prone position, the shoulder girdle falls into a relatively elevated and protracted state. This is why muscle testing of the middle and lower trapezius requires manual setting of the scapula into an anatomic position.
Figure 2-4. Motions of the scapulothoracic joint. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 75.)
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THE ATHLETE’S SHOULDER
Abduction and Adduction Abduction is the movement of the medial border of the scapula away from the vertebral column (see Fig. 2-4).21 This motion is powered by the serratus anterior and pectoralis minor.3 The pectoralis major contributes to abduction by pulling on the fixed humerus, which then moves the scapula.8 Adduction is defined as movement of the medial border of the scapula toward the vertebral column (see Fig. 2-4).21 The rhomboids,22 middle trapezius,3 and lower trapezius23 are responsible for adduction.24 The levator scapulae are inactive unless elevation occurs. Posterior and Anterior Tilt Posterior and anterior tilt is scapular rotation about an oblique medial-lateral axis.25 Posterior tilt occurs as the acromion moves backward and anterior tilt occurs as the acromion moves forward (Fig. 2-5). Internal and External Rotation Internal and external rotation are described as scapular rotation about an oblique superior-inferior axis.25 External rotation can be visualized as the acromion moving posteriorly with the medial border of the scapula moving in an anterior direction; internal rotation can be visualized as the acromion moves anteriorly while the medial border moves posteriorly (see Fig. 2-5). Downward (Medial) and Upward (Lateral) Rotation Scapular downward and upward rotation occurs about an axis in the scapular body.25 Downward rotation is defined by rotation of both the glenoid downward and the inferior
Internal rotation
Anterior tilting
External rotation Posterior tilting
Upward rotation
Downward rotation Figure 2-5. Scapular variables of posterior tilt, upward rotation, and external rotation. (From Dayanidhi S, Orlin M, Kozin S, et al: Scapular kinematics during humeral elevation in adults and children. Clin Biomech (Bristol, Avon) 20:600-606, 2005.)
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angle of the scapula toward the spine (see Fig. 2-4). This is mediated by the rhomboids, levator scapulae, and pectoralis minor.4 Upward rotation is the rotation of the glenoid superiorly and movement of the inferior angle away from the spine. This motion is considered critical to shoulder performance. The scapula’s axis of rotation has been found to be slightly inferior to the scapular spine, approximately equidistant from the axillary and vertebral borders.26 A number of investigations have used three-dimensional techniques to quantify scapular movement relative to the thorax.27-32 McClure and associates31 have reported a mean ratio of glenohumeral to scapulothoracic motion of 1.7:1 in eight healthy shoulders in vivo using bone pin insertion directly into the scapula. During scapular plane elevation, the scapula was found to rotate upwardly (mean 50 degrees), rotate externally (mean 24 degrees), and tilt posteriorly (mean 30 degrees), whereas the clavicle elevated (mean 10 degrees) and retracted (mean 21 degrees). It was also found that scapular upward rotation and clavicular rotation occur approximately linearly throughout humeral elevation, especially beyond 50 degrees of elevation. Posterior tilting and external rotation motions were nonlinear, with the majority of these motions not occurring until after 90 degrees of arm elevation. Ebaugh and coworkers33 have reported that beyond 90 degrees elevation, the scapula moves into an anterior tilt, with external rotation motion having reached a plateau. These findings are similar to those of Ludewig, Lukasiewicz, Ebaugh, and their colleagues.29,30,33,34 Clinical assessment of scapular rotation during arm elevation should be examined as this is essential for normal shoulder function. The scapula should begin to migrate into lateral rotation by 60 degrees of elevation.8 If delayed, abnormal scapulohumeral rhythm may exist, possibly resulting in rotator cuff and bursa impingement because the glenoid and acromion have not begun their superior travel as the greater tuberosity approaches. Scapulohumeral Rhythm Proper scapular motion and stability are considered to be crucial to normal function of the shoulder31; therefore, scapulohumeral rhythm is an essential concept in the understanding of shoulder function. This phenomenon describes the relationship of motion between the scapula and humerus; however, the sternoclavicular and acromioclavicular joints also influence scapulohumeral rhythm. With active humeral elevation up to 30 degrees in the coronal or scapular abduction planes and up to 60 degrees of sagittal plane flexion, the scapula seeks a position of stability. This initial phase, called the setting phase, is variable and individualized.35 The scapula continues to rotate laterally around 60 degrees elevation,17 stabilizing against the thoracic wall with little superior or inferior migration. During
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
the first 90 degrees of motion, significant superior acromioclavicular joint migration occurs, corresponding to the clavicular elevation. At approximately 100 degrees of elevation, the coracoclavicular ligament begins to tighten, pulling on the posterior lip of the clavicle and producing clavicular upward rotation.36 The scapula continues to rotate, causing the center of rotation to shift toward the glenoid, resulting in medial and continued superior movement of the glenoid and lateral migration of the scapular inferior angle.16 Along with lateral rotation, the scapula orients the glenoid fossa anteriorly toward the sagittal plane.8 The scapula posteriorly tilts as the superior angle moves away from the thoracic wall with concomitant movement of the inferior angle toward the thoracic wall. Ten more degrees of acromioclavicular contribution occur after 135 degrees. In all, the scapula rotates approximately 60 degrees.3,14 Following the initial phase, the humerus and scapula maintain a particular relationship during arm elevation, described as a ratio of movement. This ratio has been investigated and quantified radiographically, goniometrically, and through the use of three-dimensional techniques. The classic work by Inman and colleagues35 has found a 2:1 ratio during both sagittal plane flexion and coronal plane abduction between 30 and 170 degrees of motion. Other studies have examined elevation of the glenohumeral joint in the scapular plane. Saha13 has reported a ratio of 2.3:1, similar to the findings by Inman and associates. Freedman and Munro15 have observed a 3:2 ratio from 0 to 135 degrees, with a decreased scapulothoracic contribution from 135 degrees to maximum elevation. Doody and coworkers14 have goniometrically determined a 1.74:1 ratio from 0 to 180 degrees, with varied inputs from the scapulothoracic and glenohumeral joints at different stages; the former contributes more during the middle phases of abduction (90 to 140 degrees). Poppen and Walker16 have discovered a 4.3:1 ratio from 0 to 30 degrees, followed by a 1.25:1 or 5:4 ratio from 30 to 180 degrees of elevation. McClure and colleagues31 have reported a mean ratio of glenohumeral-to-scapulothoracic motion of 1.7:1 in eight healthy shoulders in vivo using bone pin insertion directly into the scapula. McQuade and Smidt32 have demonstrated that during dynamic humeral elevation, the scapulohumeral rhythm changes, depending on the phase of elevation and amount of external load on the arm. For unloaded elevation, the scapulohumeral rhythm ranges from 7.9:1 to 2.9:1, for light load elevation, 3.1:1 to 4.3:1; and for heavy load elevation, 1.9:1 to 4.5:1. Graichen and associates37 have noted a ratio of 1.5:1 at 60 degrees to 2.4:1 at 120 degrees for passive scapular plane abduction, using open magnetic resonance imaging and three-dimensional image processing. Passive elevation follows a pattern similar to that of active elevation, except that the scapula tends to move into a position
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21
of internal rotation,33 with less upward rotation early and more upward rotation in the last two phases.32 Borstad and Ludewig27 have examined the effect of eccentric versus concentric control on three-dimensional scapular kinematics. They found a decrease in scapular anterior tilt and increase in scapular internal rotation during the eccentric phase of arm elevation at 80, 100, and 120 degrees. No significant difference was noted in scapular position with eccentric and concentric trials for any scapular variable below 80 degrees. Overhead shoulder function, especially eccentric lowering, may alter scapular kinematics and predispose athletes to injury. Throwing athletes demonstrate increased scapular upward rotation, internal rotation, and retraction.38 This adaptation may allow for clearance of the subacromial space and improve throwing performance. The results for scapulohumeral rhythm vary somewhat because of the type of measurement technique used (Table 2-1). However, the relationship between glenohumeral and scapulothoracic motion is critical and is generally considered to be 2:1, culminating in 120 and 60 degrees, respectively. Caution is required when comparing passive and active glenohumeral-to-scapulothoracic ratios and their phases of contribution.8 During passive motion, the muscles that drive the scapula are inactive; thus, initiation of scapular movement will lag compared with active motion, being dependent on the glenohumeral capsuloligamentous structure’s elasticity and expansion. This explains why during passive movement, scapular motion may not be detected until 70 to 90 degrees. Viewed another way, scapular upward rotation is partly related to tension developed in the CLC during elevation. Patients with hyperelastic tissue or instability probably demonstrate less upward scapular rotation during active elevation because there is more “play” in the CLC. The scapula will move earlier with
TABLE 2-1 Comparison of Ratios of Active Glenohumeral to Scapulothoracic Rhythm in the Plane of Scapula Study, Year
Ratio ( Average)
Inman et al, 194435
2:1
Saha, 1961
13
2.3:1
Freedman and Munro, 196615 3:2 Doody et al, 197014
1.74:1
Poppen and Walker, 1976 McClure et al, 2001
16
31
Graichen et al, 2000
1.7:1
37
McQuade and Smidt, 1998
1.25:1 or 5:4 1.5:1 to 2.4:1
32
7.9:1 to 2.1:1 (passive range of motion); 1.9:1 to 4.5:1 (with load)
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THE ATHLETE’S SHOULDER
movement of the humerus if adhesions exist in the capsuloligamentous complex. Therefore, passive rather than active assessment of scapulohumeral rhythm tends to be more sensitive in determining restrictions of the capsuloligamentous complex. Effect of Shoulder Pathology on Shoulder Rhythm. Quantitative scapular kinematics studies have shown abnormal scapular motion associated with certain pathologies.39,40 Unfortunately, the equipment used to attain these measurements is not clinically applicable. The clinician is left with visual inspection and linear measurements that have low reliability.41 Active movement assessment of the shoulder complex is necessary to determine whether a dysfunctional scapulohumeral rhythm exists, because this is often associated with muscular weakness or abnormal activation patterns.8 Dramatic or subtle scapular dyskinesia may be visualized on active arm elevation in the sagittal plane, possibly indicating a nerve palsy, instability, or motor dyskinesia (Fig. 2-6). Weakness of the rotator cuff muscles typically results in compensation by the patient shrugging or excessive scapular elevation. Pain or contracture of the glenohumeral capsuloligamentous complex will manifest during active arm motion by increased scapular elevation and lateral rotation. Shoulder pathology has been demonstrated to have an adverse effect on scapulothoracic rhythm. Paletta and coworkers,39 using a two-plane radiograph series, found that
subjects with shoulder instability and subjects with a rotator cuff tear demonstrate altered glenohumeral-scapulothoracic motion relationships. Mell and colleagues42 have reported that shoulder kinematics are altered in subjects with a rotator cuff tear. The scapula was found to elevate more for the same amount of humeral elevation than in normal shoulders or shoulders with tendonopathy. The presence of this kinematic alteration in cuff tear patients and not in tendinosis patients suggests that it is related to loss of cuff strength and function rather than pain. In shoulders with known instability, Von Eisenhart-Rothe and colleagues43 have demonstrated an increase in scapular internal rotation in the transverse plane and a malcentering of the humeral head in the direction of the instability. Their study suggested that scapular positioning is relevant for humeral head decentering and should be considered in the treatment of different forms of atraumatic shoulder instability. Lukasiewicz and associates30 have reported that subjects with impingement syndrome demonstrate significantly less posterior tilt, greater superior translation at the horizontal, and maximal elevation when compared with nonimpaired individuals. Ludewig and Cook34 have demonstrated decreased posterior tilt, external rotation, and upward rotation in subjects with impingement. The presence of posterior tilting may be important functionally to allow for clearance of the humeral head and rotator cuff tendons under the anterior aspect of the acromion during elevation.31 Limited scapular posterior tilt could result from a shortened pectoralis minor, restricted scapular mobility, and inadequate shoulder complex muscle activity. Altered kinematics may result as patients tend to rotate the scapula to a greater degree to avoid impingement and reduce the requirement for elevation at the glenohumeral joint.42 Effect of Posture on Shoulder Rhythm. Scapulohumeral rhythm and strength may also be influenced by postural changes and adaptively shortened muscular structures. Increased thoracic kyphosis may lead to a decrease in posterior tilt and lateral scapular rotation with humeral elevation.44 Smith and coworkers45 have found a reduction in isometric shoulder strength in protracted and retracted scapular positions when compared with neutral, suggesting compromised shoulder muscle function and deviation from normal resting scapular position.
Figure 2-6. Patient with a long thoracic nerve palsy. Note the prominence of the medial border of the scapula, with active elevation of the right shoulder.
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During active arm elevation, the pectoralis minor becomes passively lengthened by scapular upward rotation, external rotation, and posterior tilting.31,34 Individuals with a shortened pectoralis minor exhibited decreased scapular upward rotation, external rotation, and posterior tilting during elevation.46 The finding of a short pectoralis minor muscle suggests an increased risk for impingement in this
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
23
population and may contribute to altered mechanics in throwers.9 Deviating patterns of external rotation or the inability to rotate the humerus externally change the scapulohumeral rhythm substantially.47 Anterior tightening procedures, such as the Putti-Platt or Magnuson-Stack procedure or a tight Bankart repair, are likely to result in a loss of external rotation and elevation.48 Athletes with limited external rotation range of motion tend to exhibit an altered scapulohumeral rhythm, which may affect throwing performance and overhead function. Excessive restriction of external rotation caused by an overtightened anterior-inferior CLC increases posterior translation, exacerbating wear on the posterior glenoid and ultimately leading to the long-term complication of secondary osteoarthritis.48-50
Sternoclavicular Joint The sternoclavicular joint represents the single bony articulation between the axial skeleton and upper extremity. This is a monumental responsibility, particularly because the amount of articular contact is the least of all the major joints in the body.51 The sternoclavicular joint serves as the pivot point for scapular elevation-depression and abduction-adduction. Clavicular elevation and depression occur through an axis in the sagittal plane. The sternoclavicular joint is reported to allow for 45 to 60 degrees of elevation and 5 degrees of depression.14,52 Elevation is limited by tension on the costoclavicular ligament.2,4,51,53,54 Depression of the sternoclavicular joint is limited by the superior joint capsule and interclavicular ligament, and contact between the clavicle and first rib.21 Although only 5 degrees of active depression is available, greater excursion results, particularly when the clavicular suspensory muscles are lacking. Clavicular protraction and retraction occur through an axis in the transverse plane,4 allowing approximately 15 degrees of motion in each direction.52 Because the axis is oblique, retraction is accompanied by elevation and protraction is combined with depression.2 Protraction is limited by the posterior fibers of the costoclavicular ligament, posterior sternoclavicular capsule, and posterior fibers of the interclavicular ligament.51,55 Retraction is restricted by the anterior costoclavicular fibers and anterior sternoclavicular capsule (Fig. 2-7). Rotation occurs through the longitudinal axis of the clavicle. During flexion and abduction, Inman and colleagues35 have demonstrated approximately 40 degrees of upward rotation, as defined by the direction of the anterior edge of the clavicle. The upward rotation motion begins at approximately 90 degrees of elevation, and becomes increasingly greater at the end range. Tension of the coracoclavicular ligaments regulates this upward rotation. As the scapula moves into elevation, the base of the coracoid process, which
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A
B
C
D
Figure 2-7. Sternoclavicular motion through two axes. Illustrated are depression (A) and elevation (B) through the sagittal axis, and retraction (C) and protraction (D) through the superomedial to inferolateral oblique axis. (From Dempster WT: Mechanisms of shoulder movement. Arch Phys Med Rehabil 46:49-70, 1965.)
is the insertion of the coracoclavicular ligaments, begins to move distally. This produces a downward pull on the posterior clavicle, thus causing upward rotation. Approximately 10 degrees of downward rotation are available. Even with trauma to the sternoclavicular joint, close to normal range of motion and full function are achieved, but pain acts as the limiting factor. In patients with hypomobility of this joint, shoulder elevation may be limited to 100 degrees, with abduction and internal rotation the most painful movements.
Acromioclavicular Joint The acromioclavicular joint is a plane-type joint formed by the articulation of the distal clavicle with the acromion of the scapula. Three degrees of freedom are available at the acromioclavicular joint; however, they rarely occur individually.52 Motion occurs in a vertical, anterior-posterior, and medial-lateral direction (Fig. 2-8). The vertical axis allows the scapular vertebral border to “wing” and the glenoid fossa to face anteriorly.51,52 The acromion glides forward and backward as the scapula’s medial border swings away from and into the thorax— scapular internal and external rotation. This motion is checked by tension in the conoid and trapezoid ligaments. Motion about the anteroposterior axis results in enlarging or shrinking the angle formed by the clavicle and spine of the scapula in the frontal plane.21 This axis allows for scapular abduction and adduction, as described by Mosley.52 An axis through the coronal plane permits anterior tilting of the superior angle, causing the inferior angle
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THE ATHLETE’S SHOULDER Vertical axis
Winging of vertebral border (50° max.)
Sagittal (anteroposterior) axis
A
Inman and coworkers35 have warned against screw fixation negating acromioclavicular joint motion. Several investigators have found screw fixation or coracoclavicular ossification to have little or no effect on shoulder elevation.58,59 In fact, when Kirschner wires were attached to the clavicle of a patient whose distal clavicle was fixated to the coracoid by a screw, full clavicular rotation was observed.60 Kennedy and Cameron58 have reported that patients older than 50 years have less satisfactory results and painful end range abduction with screw fixation. It was concluded that this group relies more on the coracoclavicular ligamentous play than younger patients.
Glenohumeral Joint
Frontal axis
B
C Figure 2-8. Three axes of motion shown through the acromioclavicular joint. A, Vertical axis allows the glenoid to face toward the sagittal or coronal plane. B, Sagittal axis allows slight medial and lateral rotation. C, Coronal axis allows anterior and posterior tilting. (From Moseley HF: The clavicle: Its anatomy and function. Clin Orthop 58:17-27, 1958.)
to lift posteriorly. Anterior tilting is restricted by the anterior acromioclavicular and trapezoid ligaments, whereas posterior tilting is restricted by the thorax and posterior acromioclavicular and conoid ligaments.51 Inman and associates35 have demonstrated that approximately 10 degrees of motion occur at the acromioclavicular joint during the first 30 degrees of flexion and abduction, and then again in the last 45 degrees of motion. The acromioclavicular joint contributes greater motion at the end range of elevation,3 although total motion is restricted to about 5 to 8 degrees per axis.56 When irritation of this joint exists, clinical findings reveal pain at all shoulder end ranges, particularly during horizontal adduction. The acromioclavicular joint may compensate for lost motion in the presence of glenohumeral joint restriction.57
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The glenohumeral joint is a classic ball-and-socket joint between the humeral head and glenoid fossa of the scapula, and is the most mobile joint in the body.1,21,61 This high level of mobility challenges the inherent stability, as evidenced by the articulation between the larger convex humeral head and shallow concave glenoid fossa. This joint is an intricate complex with a sometimes fragile system of checks and balances; its vulnerability is demonstrated by the number of patients seen with pathology of associated static and dynamic components. The glenohumeral joint has three axes of motion along the cardinal planes of the body: sagittal, frontal, and horizontal. Sagittal plane flexion and frontal plane abduction require concomitant humeral rotation. The humerus externally rotates with abduction11,12,4,,62 and internally rotates with flexion.23,63,64 With scapular plane elevation, no external rotation is required.14 Only 25% to 30% of the humeral head is covered by the glenoid surface in any given anatomic position.11 The average humeral head diameter is 44 mm compared with a glenoid diameter of 25 mm. The fossa is deepened by a 2-mm ridge of labral fibrocartilage tissue.65 Although the bony surfaces of the humeral head and glenoid fossa have slightly different curvatures, their cartilaginous articular surfaces have approximately the same radius of curvature.21,66-68 The radius of curvature quantifies the amount of curve in a surface by describing the radius of the circle from which the surface is derived. These surfaces have similar curvatures; thus, there is a high degree of congruence, which helps disperse loads across a larger surface area, reducing articular surface stress. The concept of glenohumeral motion occurring with a certain degree of rotation (spin), roll, and glide is well accepted (Fig. 2-9). MacConnail and Basmajian64 have developed the term roll-gliding to describe joint motion between incongruent, concave, and convex surfaces. The direction of rolling and gliding components is dependent on whether the concave or convex surface is moving. The convex-concave theory of arthrokinematics dictates that if a convex surface
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
initial phase, the humerus center of rotation remains constant, moving 1 to 2 mm upward or downward relative to the glenoid center. It was concluded that after the initial rise, the humeral head will rotate or spin on a more or less fixed center, with little if any excursion. Harryman and associates72,73 have reported an average superior migration of 0.7 mm during abduction and 0.8 mm during flexion. A
B
Using a three-dimensional technique of stereophotogrammetry on cadaver shoulders, Kelkar and coworkers74 have found an average vertical excursion of 1.29 mm occurring through an arc of 180 degrees of scapular plane abduction and an average of 0.94 mm of superior glide in the first 30 degrees of motion (Fig. 2-10). In support of Poppen and Walker’s findings,16 they concluded that the initial superior rise occurs because of the dependent (inferior) state of the humerus when unloaded but after 30 degrees, pure glenohumeral joint rotation occurs. Yamaguchi and colleagues75 have demonstrated a progressive superior translation of the humeral head on the glenoid, with increasing arm elevation in patients with symptomatic and asymptomatic rotator cuff tears. The symptomatic and asymptomatic rotator cuff tear groups exhibit an increase in superior head migration from 30 to 150 degrees during scapular plane elevation, as well as a disruption of normal glenohumeral kinematics. However, shoulder pain is not always present with the superior migration.
C
moves on a concave surface, then gliding occurs in the opposite direction to the rolling; if a concave surface moves on a convex surface, then rolling and gliding occur in the same direction. The more congruent the surfaces, the more gliding occurs and the more incongruent, the more rolling takes place.69 The disproportion between the glenohumeral articular surfaces would then dictate that rolling dominates. In other investigations, however, these findings were not validated. There has been much debate regarding the translatory motion of the glenohumeral joint. Calliet6 and Saha13,70 have stated that humeral head rolling on the glenoid is the predominant motion and that this is accompanied by some amount of gliding. Perry5 has stated that gliding is the primary component motion and that rolling is not significant to glenohumeral motion, other than the first 3 mm of superior excursion. Howell and colleagues71 have noted that rotation is the dominant movement, with gliding as the initial movement. Poppen and Walker16 have radiographically determined the initial 30 degrees of scapular plane elevation; often, from 30 to 60 degrees, the humeral head glides upward on the glenoid fossa approximately 3 mm. After this
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It is important for the clinician to realize that the humeral head does not truly“depress”with elevation, and that gliding is both superior and inferior.8 The humeral head center of rotation remains relatively constant with the center of the glenoid. What changes, through rotation and subtle gliding of 1 to 2 mm (roll-glide), is the humeral articular contact point moving inferiorly to superiorly on the humeral head.16,74,76 The greater tubercle “depressing”
1
0 Translation (mm)
Figure 2-9. Three types of articular movement occur at the glenohumeral joint. A, Rotation. B, Rolling. C, Gliding. (From Matzen FA III, Zuckerman J: Biomechanics of the shoulder. In Frankel VH, Mordin M [eds]: Basic Biomechanics of the Musculoskeletal System, 2nd ed. Philadelphia, Lea & Febiger, 1989, p 231.)
–1
–2
–3 0
30
60
90
120
150
180
Arm elevation (degrees) Figure 2-10. Normal superior glide during plane of the scapula abduction. (From Kelkar R, Flatow E, Bigliani L, et al: A stereophotogrammetric method to determine the kinematics of the glenohumeral joint. Adv Bioeng 19:143, 1992.)
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(as the humerus elevates) during palpation must not be mistaken for a sign of humeral head inferior gliding. Instead, greater tubercle movement represents medial migration beneath the acromion. Controversy also exists regarding the translation or gliding of the humeral head in the anterior and posterior directions. Howell and associates71 have radiographically evaluated anterior and posterior translation with the arm positioned in varying degrees of horizontal adduction/abduction and rotation (Fig. 2-11). It was concluded that the humeral head normally translates 4 mm posteriorly in 90 degrees of abduction, full external rotation, and maximal horizontal abduction, but subjects with known anterior instability demonstrate anterior, not posterior, translation in the same position. Harryman and coworkers73 have performed a biomechanical analysis on cadavers using telemetry; they found approximately 3.8 mm of anterior translation with flexion and 5 mm of posterior translation with extension. With tightening of the posterior capsule, there is a significant increase in anterior translation and, to some extent, superior humeral head translation. Additionally, it was noted that external rotation and internal rotation, performed with the humerus at the side, produces posterior and anterior gliding, respectively. Werner and colleagues77 have examined the effects of capsular tightening on humeral head translation in cadavers. The capsular plication causes a translation directed away from the plication site. Moore and associates78 have studied the kinematics of glenohumeral joint translation, with varying degrees of internal and external rotation at 90 degrees abduction. With increasing external rotation, anterior translation decreases and the humeral head moves in the posterior direction.
–4 mm extension (ext. rot.)
Figure 2-11. Axillary view (inferior through the glenohumeral joint) in 90 degrees of abduction, full external rotation, and horizontal abduction. The geometric center of the humeral head is 4 mm posterior to the center of the glenoid fossa, demonstrating normal posterior, not anterior, translation. ext. rot., external rotation. (From Howell SM, Galinat BJ, Renzi AJ, Marone PJ: Normal and abnormal mechanics of the glenohumeral joint in the horizontal plane. J Bone Joint Surg Am 70:227-232,1988.)
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These studies have concluded that the direction of translation is dictated by tightening of the capsuloligamentous complex opposite the side of translation (Fig. 2-12). Shoulder movement causes the static restraints to become taut; they not only serve to counteract but to reverse humeral head movement. If the static restraints are stretched or their attachments compromised, abnormal translation occurs.8 For example, in the presence of a Bankart lesion or loose anterior and inferior capsule, the humeral head would translate anteriorly when placed in abduction and external rotation, as opposed to posteriorly. In summary, an initial superior glide occurs with elevation, not inferior, until the head centers and rotation occurs. During shoulder extension and external rotation, the humeral head glides posteriorly and, with shoulder flexion and internal rotation, the humeral head glides anteriorly.21,67,73,79-81 This is likely because of the constraints of the capsular tissue and glenohumeral ligaments. These findings contradict the traditionally taught kinematics—the concave-convex rule.21 Performing joint glides to re-establish proper joint mechanics based on the traditionally accepted idea of joint motions is questionable. Joint mobilization is essential for relieving pain, producing muscular relaxation, and increasing joint range of motion. These techniques are effective because directional mobilizations “stretch” isolated portions of the capsuloligamentous complex. By improving capsuloligamentous pliability in any direction, regardless of the directions in which the humeral head translates during motion, proper joint mechanics and range of motion are restored in all ranges of motion and planes.8
STABILITY Stability of the glenohumeral joint is provided by the articulating surfaces, capsular and ligamentous structures, and synchronous activity of the rotator cuff, biceps, deltoid, and scapular muscles.82 Stability or instability research has been based primarily on cadaveric and operative investigations. Focus has been on anterior instability because this is most commonly seen, followed by posterior instability and inferior instability. Four structures are considered to be the main factors in stability of the shoulder—articular surfaces, labrum, capsuloligamentous complex, and rotator cuff. Scapular muscle function will be discussed separately. Related factors will also be addressed in this section.
Articular Surfaces The glenohumeral articular surfaces have been shown to provide static stability to the joint.83 The surface of the glenoid fossa has been found to be one third to one quarter that of the humeral head,70,84-87 and this difference in the size of the articular surfaces allows a large degree of
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27
Superior (90° sup) 10 mm
5 Abd Flex Posterior (180°)
Anterior (0°) 10 mm
5
ER 0
ER 90 ER 45
5
10 mm
IR 0
IR 90
IR 45
5
10 mm Inferior (90° inf) Translation
SD
Direction
Abd
3.8 mm
2.2 mm
83° sup
Flex
7.3 mm
3.2 mm
18° sup
ER 0
0.9 mm
0.4 mm
19° inf
ER 45
4.3 mm
2.3 mm
145° inf
ER 90
5.6 mm
1.8 mm
160° inf
IR 0
6.1 mm
4.0 mm
22° inf
IR 45
8.0 mm
3.9 mm
16° inf
IR 90
12.0 mm
8.2 mm
5° inf
Figure 2-12. Translation at the end of several movements with intact capsule. The values indicated are mean translations in the actual directions (directions are defined relative to a strictly anterior direction: 0 degrees, posterior direction; 180 degrees, superior and inferior parts, respectively). Abd, abduction; Flex, flexion; ER 0, external rotation at 0 degrees of abduction; ER 45, external rotation at 45 degrees of abduction; ER 90, external rotation at 90 degrees of abduction; IR 0, internal rotation at 0 degrees of abduction; IR 45, internal rotation at 45 degrees of abduction; IR 90, internal rotation at 90 degrees of abduction. (From Werner CM, Nyffeler RW, Jacob HA, Gerber C: The effect of capsular tightening on humeral head translations. J Orthop Res 22:194-201, 2004.)
mobility. Saha,36 using cadaveric radiographic studies, has determined that the normal glenoid is retroverted approximately 7.4 degrees, serving to discourage anterior humeral translation. Of 21 shoulders with anterior instability, 80% demonstrated 2 to 10 degrees of glenoid anteversion. A corresponding increase in humeral retroversion was believed to predispose the joint to anterior instability. Basmajian and Bazant57 have discovered that a 5-degree superior tilt of the glenoid assists in preventing inferior humeral migration.
resulting in a misleadingly flat glenoid shape on radiographs.88
Congruence can be defined as the difference in the radii of the humeral head and glenoid articulating surfaces.82 The closer this difference is to zero, the more congruent is the joint. Soslowsky and coworkers83 have demonstrated excellent congruency between the glenoid and humeral head using three-dimensional stereophotogrammetry to quantify the articular geometry in 32 cadavers. They found an average ratio of the radii of curvature between the two surfaces of 0.99 ⫾ 0.05. This conformity of surfaces dictates that pure rotation with minimal translation occurs at this joint.74 The articulating cartilage surfaces are much more conforming than the underlying bone surfaces,
The glenoid labrum is a wedge-shaped ring of fibrocartilage that encircles the bony glenoid, deepening the glenoid cavity and serving to bridge bone to the glenohumeral ligaments and biceps tendon (Fig 2-13). Using cadavers, Howell and Galinet65 have found the average depth of the socket and labrum to be 9 mm superiorly-inferiorly and 5 mm anteriorly-posteriorly. The labrum was found to contribute approximately 50% of the total depth of the socket, and detachment of the labrum anteriorly, as in a Bankart lesion, may reduce the depth of the socket in the anterior-posterior direction. Regional variation in the labrum exists; the inferior portion is immobile and firmly
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A built-in safeguard promoting articular stability, often forgotten, is the effect of scapular motion.8 Scapular mobility allows the glenoid to adjust, providing a stable osseous platform for the humeral head.89 This movable base may compensate for articular deficiencies.
Labrum
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produce anterior glenohumeral dislocation clinically requires inferior glenohumeral ligament plastic deformation in addition to the Bankart lesion. Resection of the glenoid labrum has been reported to reduce the effectiveness of compression-stabilization by approximately 10% to 20%.95 Chondral-labral defects reduce the height of the glenoid, which in turn significantly reduces the stability ratio.96 Compression by muscle activity and capsuloligamentous tightening increases the stability of the labrum.94 Rodosky and associates,97 using dynamic cadaveric shoulder models, have created superior labral lesions and found that these shoulders show a decreased ability to resist external rotation when abducted and internally rotated. Superior labral defects have been found to decrease torsional rigidity and increase inferior glenohumeral ligament strain, which contributes to anterior instability.88
Capsuloligamentous Complex
Figure 2-13. Labral insertion to the glenoid rim. (From O’Brien SJ, Arnoczky SP, Warren RF, Rozbruch RA: Developmental anatomy of the shoulder and anatomy of the glenohumeral joint. In Rockwood CA, Matsen FA (eds): The Shoulder. Philadelphia, WB Saunders, 1990, p 14.)
attached to the glenoid and the superior portion is attached more loosely, allowing for substantial range of motion of the glenohumeral joint.88 The labrum is the weak link (younger than 30 years) when a continuous progressive low load is exerted across the anterior capsular mechanism.90 Hara and colleagues91 have reported that the anterior-inferior portion of the labrum is relatively weak, consistent with clinical findings of lesions commonly identified in anterior shoulder dislocation. Bankart,92 Rowe,93 and Rowe and Sakellarides,19 proponents of labral stability influence, have emphasized the importance of the labrum linking the capsule to the glenoid bony rim as opposed to a buttress effect, in which the labrum acts as a physical block to humeral head displacement. Recurrent instability tends to erode the articular cartilage of the anterior inferior glenoid rim and decreases concavity.88 With the labrum intact, the humeral head resists tangential forces as much as 60% of the compressive load.94 The amount of humeral head translation needed to
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The glenohumeral joint capsule provides passive stability at the extremes of glenohumeral motion.77 The capsule does not only limit rotation and prevent excessive translations, but also causes a coaptation and obligate translation of the humeral head on the glenoid at the end of passive movements. The glenohumeral ligaments and coracohumeral ligaments reinforce the capsule and serve as static restraints (Fig. 2-14).98-104 Ligaments attach bone to bone and act to guide and limit motion, with their constraining function evident as these structures become taut. Essentially, ligaments fulfill a dual stabilizing role—to provide a barrier against translation103 and to increase articular compressive forces as they tighten.51 The extreme of this is seen in the presence of capsular adhesions. In the presence of fibrotic capsuloligamentous tissue, glenohumeral articular compression can be so oppressive that normal rotation is obliterated.8 The role of any specific component of the stabilizing system varies with glenohumeral joint position and direction of the opposing force.88 A functional interplay or interdependence exists between anterior and posterior and superior and inferior components of the capsuloligamentous system. This circle concept of capsuloligamentous stability implies that excessive translation in one direction may damage the restraints on both the same and opposite sides of the joint.105 The capsule is a continuous structure; injury or repair to one region of the capsule may have an adverse effect on the properties of the neighboring regions and on joint function.106 Coracohumeral Ligament The coracohumeral ligament (CHL) is intimately related to the rotator cuff and actually reinforces the supraspinatus superiorly and inferiorly.107 The CHL and superior glenohumeral ligament join to make up the rotator cuff interval, which bridges the supraspinatus and subscapularis
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Figure 2-14. Lateral view of the glenoid showing the capsuloligamentous complex attachments in relation to the deep muscles and tendons. (From Turkel SJ, Panio MW, Marshal JL: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981.)
(Fig. 2-15).23,73 The rotator cuff interval is the primary restraint against inferior and posterior translation of the adducted shoulder. Sectioning the interval increases anterior and posterior translation, whereas imbricating it significantly reduces translation in both directions. Harryman and coworkers73 have found that tightening the rotator cuff interval leads to an 8-degree loss of flexion and an 18-degree loss of extension. This is consistent with the study by Terry and colleagues,102 who found the CHL to be a primary restraint in flexion and extension. Harryman and associates73 have also found external rotation performed with the arm adducted decreased by 38 degrees and adduction by 8 degrees when the interval was imbricated. Gerber and coworkers,108 using cadavers, have found that Supraspinatus
closure of the rotator interval limits external rotation of the adducted arm by a mean of 30.1 degrees (56.4% of normal), whereas it had no significant effect on external rotation of the abducted arm. In addition to preventing inferior instability with the arm at the side, the CHL restricts external rotation and extension.72,85,100,102,109 The significance of the coracohumeral ligament is not only important in stability but in the presence of supraspinatus pathology. Because the CHL limits external rotation when the arm is adducted, exercising into excessive external rotation while the arm is adducted should be approached with caution. The passive tension developed in the CHL translates directly to the compromised supraspinatus,
CHL Coracoid
Coracoid
Supraspinatus RI capsule
Biceps SGHL
Subscapularis
A
Biceps in intertubercular groove
B
Subscapularis
Figure 2-15. Schematic of the rotator cuff interval. A, Anterior view. B, Cross-sectional lateral view. CHL, coracohumeral ligament; RI, rotator interval; SGHL, superior glenohumeral ligament. (From Fitzpatrick MJ, Powell SE, Tibone JE, Warren RF: The anatomy, pathology, and definitive treatment of rotator interval lesions: Current concepts. Arthroscopy 19:70-79, 2003.)
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THE ATHLETE’S SHOULDER
causing pain or further disruption.8 Additionally, release of the interval and subsequent suturing during a rotator cuff repair need to be respected by limiting postoperative external rotation motion when the arm is at the side. Superior Glenohumeral Ligament The superior glenohumeral ligament (SGHL) prevents inferior displacement of the humeral head,84,110 limits external rotation at 0 degrees of rotation,100,102,104 and acts as a restraint during extension. A lesion of the rotator cuff interval, which is associated with anterior and inferior instability of the glenohumeral joint,111 may be caused by a deficiency in the superior glenohumeral ligament. The SGHL and anterior band of the coracohumeral ligament also serve as restraints up to 50 degrees abduction and external rotation.112 Both ligaments have been implicated as the source of fatigue pain when a mild downward load is placed on the arm.113 Following shoulder surgery, and in the presence of reflex inhibition, tension that develops in these ligaments may partly explain postoperative pain.8 Once these ligaments have stretched, as in hemiplegia, it is difficult to regain stability.57 Middle Glenohumeral Ligament Turkel and associates104 have investigated the stabilizing mechanisms of the glenohumeral joint that prevent anterior dislocation by sequentially incising the glenohumeral anterior and posterior soft tissue structures. The subscapularis was initially cut, followed by the SGHL, middle glenohumeral ligament (MGHL), and inferior glenohumeral ligament (IGHL). It was found that anterior dislocation occurs at neutral when externally rotated, with the subscapularis muscle providing primary stability. At 45 degrees of abduction, primary stability is provided by the subscapularis, MGHL, and anterosuperior fibers of the IGHL. Approaching 90 degrees of abduction, the inferior glenohumeral ligament prevents dislocation during external rotation. At 90 degrees of abduction and full external rotation, the joint remains stable, until the posterior cuff was cut, which resulted in anterior dislocation. This study104 was performed with scapular fixation while abducting the humerus to 90 degrees, which does not take into consideration scapular rotation; 90 degrees in this investigation corresponds to approximately 120 to 135 degrees of true shoulder elevation.8 A limitation of this study was that it did not introduce horizontal abduction or apply any anterior force. Gerber and coworkers108 have studied the effect of capsular contractures on the passive range of movement of the glenohumeral joint. Their data suggest that anterior plications restrict external rotation, whereas posterior plications restrict internal rotation. Plications of the superior aspect of the capsule are largely responsible for restrictions of motion with the arm in an adducted position. Conversely, plications of the inferior aspect of the capsule have more influence on motion of the abducted arm. The results of this study have demonstrated that contracture of the
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posterosuperior aspect of the capsule may limit internal rotation and flexion, whereas contracture of the anteroinferior aspect of the capsule, including the anteroinferior glenohumeral ligament complex, increasingly limits motion with increasing abduction of the arm. Contracture of the posterior aspect of the capsule plays an important role in limiting internal rotation, flexion, and abduction, even without inferior plication. The MGHL was found to have stabilizing effects at 0 and 45 degrees of abduction.8 External rotation at these positions causes tightening of the MGHL, providing a barrier against anterior displacement.104,114 Turkel and colleagues104 have reported that this ligament is loose at 90 degrees of abduction and full external rotation. Other investigations have shown that the MGHL, along with the SGHL, is similar to the IGHL in regard to abduction and external rotation,100,115 and that the MGHL is found to tighten during flexion combined with external rotation.102 The MGHL also functions to support the arm and provide anterosuperior stability.112 Inferior Glenohumeral Ligament The IGHL is the thickest of the glenohumeral ligaments, with an anterior band, posterior band, and axillary pouch. As with the other glenohumeral ligaments, the IGHL’s ability to restrict motion depends on humeral elevation and rotation. At 0 degrees abduction, the anterior band becomes the primary stabilizer,112 tightening when the humerus is externally rotated at neutral and when the humerus is abducted without external rotation.102 When external rotation is performed at 90 degrees of abduction, the entire IGHL tightens while the superior or anterior band wraps snugly across the humeral head, checking anterior displacement.99,102,104,114,116 O’Connell and colleagues100 have found the greatest amount of strain through the IGHL at 90 degrees of abduction and full external rotation. Kuhn and associates117 have suggested that the inferior glenohumeral ligament is the most important restraint to external rotation in both the neutral and abducted positions. The clinical implication is that external rotation may contribute to failure of the inferior glenohumeral ligament in patients with shoulder instability. The IGHL has the ability to stretch considerably before ligament failure, suggesting that lateral translation of the humeral head is possible under loads that would allow the head to override the glenoid rim.88,118 This supports the clinical finding that certain patients can sublux without disruption of the capsule or its insertion sites. Repetitive loading of the inferior glenohumeral ligament at increasing levels of subfailure strain shows a dramatic increase in peak force with elongation, suggesting that the capsule may be subject to plastic deformation, especially after trauma.101,119 The IGHL appears to be a single identifiable complex that stabilizes against abnormal anterior and posterior humeral
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CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
31
head translation, becoming taut with external and internal rotation, respectively, during arm elevation.99 Conversely, it can be appreciated how adhesions or contracture of this structure could limit external rotation, internal rotation, and elevation.
internally rotated in the abducted position.8 The posterior rotator cuff and capsule are the primary restraints against posterior instability; the anterior capsuloligamentous complex assists with posterior stability and the posterior structure assists with anterior stability.102
Internal rotation performed at 90 degrees of abduction causes the posterior band and axillary pouch to fan out and cradle the humeral head posteriorly, restricting posterior subluxation of the humeral head.99,114 Tightness of the posterior capsular ligamentous structures has been hypothesized to cause glenohumeral internal rotation deficit (GIRD) and a higher incidence of SLAP (superior labral anterior-posterior) lesions.120 GIRD is defined as the loss (in degrees) of glenohumeral internal rotation of the throwing shoulder compared with the nonthrowing shoulder, as measured in the supine position at 90 degrees of abduction. SLAP lesions were first described by Snyder and coworkers.121 Andrews and colleagues122 have hypothesized that during the follow-through phase of pitching, the biceps contracts eccentrically to decelerate the extending elbow. The resulting force might transmit proximally to the glenoid tubercle and stress, if not tear, the anterosuperior labrum. Burkhart and Morgan123 have proposed that pitchers and overhead athletes develop SLAP lesions because of the peel back mechanism. In a series of 53 overhead athletes who had surgery for type II SLAP lesions, they quantified a loss of internal rotation at 90 degrees of abduction of 25 degrees or greater. They proposed that the tight posteroinferior capsule wraps inferiorly when the arm is in the late cocking phase (90 degrees of abduction and full external rotation [ER]), resulting in the humeral head to shift or be pushed superiorly and posteriorly.123 Additionally, the long head of the biceps is oriented vertically and posteriorly and, as it contracts, it causes the posterior-superior labrum to peel back over the glenoid rim.
Dynamic Stability
Conclusion Understanding the unique position-related constraining characteristics of the glenohumeral ligaments, the clinician can gain insight into capsuloligamentous pathology and anatomic appreciation of the unstable shoulder. The interdependency of the capsuloligamentous-labral complex becomes evident when examining the literature; thus, it can be concluded that the complex should be considered a functional unit.8 With regard to anterior stability with the arm at 0 degrees abduction, the SGHL and MGHL are the primary restraints, with the posterior capsule as the secondary restraint.124 At 45 degrees of abduction, the primary restraint is the MGHL, with secondary restraints being the posterior capsule, IGHL, and MGHL. With the arm at 90 degrees, the primary restraint is the IGHL and secondary restraints are the MGHL and posterior capsule. The IGHL appears to function in a dual role; it is the main restraint against anterior humeral head displacement when in external rotation at 90 degrees of abduction and also forms a substantial posterior barrier when the arm is
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The dynamic system of the glenohumeral joint is the fourth line of defense against shoulder instability (see Fig. 2-13). The musculotendinous units surrounding the glenohumeral joint assist the static restraints in stabilizing responsibilities, while also providing the power for motion. Under normal conditions, forces transmitted by the supraspinatus, infraspinatus, teres minor, and subscapularis provide significant stability to the glenohumeral joint. This is achieved in several ways: 1. Contraction of these muscles centralizes the humeral head in the glenoid by increasing compressive forces.11,16,35,70,79,98 2. The tension developed across the cuff tendons during a contraction squeezes the humeral head preventing anterior and posterior displacement.70 3. Passive tension of the tendons provides some stability.101,104 Active stability is achieved through coordinated shoulder muscle activity that compresses the humeral head into the glenoid and allows concentric rotation of the humeral head on the glenoid (Fig. 2-16).16,71,92,115,125-127 This mechanism, termed concavity-compression, depends on both shoulder muscle forces and the shape of the articular surfaces, principally the glenoid.94 The shoulder muscles may be the primary stabilizers of the glenohumeral joint during the midranges of motion, in which the capsuloligamentous structures are lax. Concavity-compression may also be important at the end ranges of motion, because glenohumeral joint forces are increased.127-129 Shoulder muscle activity protects the capsuloligamentous structures at the end ranges by limiting the joint’s range of motion130 and decreasing strain on these structures.
Figure 2-16. Dynamic effect of the rotator cuff causing compression as well as superior, anterior, and posterior barrier effects. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 85.)
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The effectiveness of the concavity-compression mechanism depends on characteristics of the shoulder muscle forces and the articular surfaces.94 Muscle forces acting on the shoulder joint can be divided into three components— compressive forces, superiorly-inferiorly directed forces, and anteriorly-posteriorly directed forces. The compressive forces stabilize the glenohumeral joint and the anteriorly, posteriorly, inferiorly, and superiorly directed forces, or translational forces, destabilize the glenohumeral joint.127 Glenohumeral joint stability may be quantified by the ratio between the translational forces in any direction and the compressive forces.96 As the ratio between the translational forces and compressive forces decreases, stability of the glenohumeral joint increases, and vice versa.95 Glenohumeral joint stability through concavity-compression is greater in neutral than in an abducted position, which may contribute to the dislocation of the shoulder anteriorly. The rotator cuff muscles and long head of the biceps actively compress the humeral head into the glenoid cavity, along with the outer sleeve of the shoulder muscles, such as the deltoid, pectoralis major, and latissimus dorsi. Shoulders with weakened or deficient rotator cuff mechanisms are likely to have compromised stability from impaired concavity-compression.88 Although the rotator cuff muscles, along with the deltoid, are considered stabilizers of the glenohumeral joint, the subscapularis is considered important for anterior integrity. DePalma and colleagues131 have advocated that the role of the subscapularis is to provide a “dynamic buttress” effect. Morrey and Chao98 have calculated forces at the glenohumeral joint during 90 degrees of coronal plane abduction in external rotation and determined that the anterior shear force increases from 12 to 42 kg in the unloaded upper extremity when the arm moves into 30 degrees of horizontal abduction. The combined tensile strength of the subscapularis and capsuloligamentous complex is calculated as 120 kg,90 allowing stability of the glenohumeral joint to be maintained. Anterior shear increases under higher speeds and greater loads and, when the force exceeds the tensile strength of the anterior structures, dislocation occurs.8 With an incompetent capsuloligamentous complex, the subscapularis muscle becomes the primary structure to stabilize against the impeding translation. This becomes increasingly difficult for the subscapularis with subsequent dislocations because evidence of tendon lengthening has been reported.131-133 Inherent lengthening of this structure leads to inefficient translation of tension from the muscle to bone and the buttress effect is lost. Turkel and coworkers’104 sequential incising study has revealed a significant increase (mean 18 degrees) in external rotation in the neutral position once the subscapularis is cut. No significant increase in anterior translation is noted at 45 and 90 degrees of abduction and the joint cannot be dislocated. These findings were similar to those of Oversen and Nielsen.101 Interestingly, the inferior border of the subscapularis was noted to rise above the inferior humeral
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head at 90 degrees of abduction and external rotation; thus, the subscapularis is an ineffective barrier against dislocation in this position. This finding provides insight as to why patients with a deficient CLC, Bankart lesion, or both recurrently dislocate in the abducted and externally rotated position, even though they possess significant strength of the subscapularis.8 Karduna and associates125 have concluded that activation of the rotator cuff muscles serves to limit rotation and translation of the glenohumeral joint compared with passive positioning. Cain and coworkers,130 using abducted cadaveric shoulders under passive external rotation, have demonstrated that the strain on the inferior glenohumeral ligament is decreased by increasing the force applied to the tendons of the infraspinatus and teres minor. However, muscle forces may promote anterior humeral head translation in the apprehension position, and predispose the glenohumeral joint to anterior instability when other stabilizing mechanisms are not functioning normally.134 Graichen and colleagues79 have found a decrease in glenohumeral translation with active shoulder motion because muscular activity centralizes that humeral head when compared with passive motion. A 50% decrease in the rotator cuff muscle force results in an almost 50% increase in anterior displacement of the humeral head in response to external loading at all glenohumeral joint positions.129 Mild recruitment of the internal rotators, including the subscapularis, has been shown to create an anterior translation constraint in the apprehension position.135 The role of the posterior rotator cuff structures is to assist dynamically in anterior stability of the glenohumeral joint. Cain and associates130 have demonstrated that the posterior cuff, particularly the infraspinatus and teres minor, pull the humeral head posteriorly when contracting, therefore reducing the anterior shear. Lee and coworkers136 have found that the infraspinatus and teres minor generate posterior shear forces and increase compressive forces in the anterior instability position, thereby enhancing joint stability. Conversely, the supraspinatus generates a large anterior shear force in the apprehension position, which may destabilize the joint anteriorly. Combined contraction of the subscapularis and infraspinatus forms a force couple, providing stability throughout the midranges of elevation.88 Electromyography has demonstrated that the subscapularis and infraspinatus contract to stabilize the glenohumeral joint in abduction at 60 to 150 degrees.131 This type of activity, in conjunction with known decreased tensile strength of the rotator cuff,90 explains the high incidence of rotator cuff tears in individuals older than 45 years when they anteriorly dislocate137; excessive translation in the presence of a degenerative cuff causes tearing. Tear location has the most significant effect on stability in the inferior and anterior directions for smaller tears and on the anterior direction for larger tears.88
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Passive tension of the posterior cuff may also play a role in stability. With incision of the infraspinatus and teres minor, significant posterior displacement occurs.101 It could logically be concluded that if passive tension of these muscles maintains significant stability, then active contraction would further enhance stability.8 Saha70 concluded the infraspinatus and teres minor are horizontal steerers that maintain stability. The importance of the posterior rotator cuff and deltoid to posterior stability is seen clinically; patients with posterior instability have responded well with external rotation strengthening.138 This is particularly true if the patient is a subluxator as opposed to a dislocator.139
humeral head translation and the effect of capsular venting and found a slight increase in anterior translation during flexion and horizontal adduction. Matsen and coworkers132 have described this phenomenon as disruption of “finite joint volume.” Finite joint volume combined with the adhesion-cohesion mechanism enhances joint stability.8 Adhesion is described as fluid holding to a surface, whereas cohesion is the joining of two surfaces by fluid. Adhesion-cohesion is best demonstrated by wet microscope slides sticking together but able to slide on one another. The glenohumeral joint mimics this phenomenon at the contact area between the humerus and glenoid.
Lee and An140 have quantified the contribution of the deltoid muscle to glenohumeral joint stability. At 60 degrees of abduction in the scapular plane, deltoid activity increases glenohumeral joint stability; however, at 60 degrees of abduction in the coronal plane, deltoid activity is found to decrease glenohumeral joint stability. Strengthening the middle and posterior portions of the deltoid may provide more stability to a patient with anterior instability, because they may work to generate higher compressive force and lower shear force than the anterior head.
To summarize, the interplay of the various active and passive components contributes to the stability of the glenohumeral joint. The IGHL appears to be the primary structure in providing anterior stability, with the subscapularis contributing to anterior stability through the compressive forces imparted on the joint. The labrum is significant, being the weak link in the chain attaching the IGHL to the bony glenoid rim.8 Regardless of the direction of shoulder instability, efficient control of the rotator cuff is essential to function. Posterior stability is dependent on the anterior capsule and structures. Accepting the capsuloligamentous-labral complex as a functional unit explains why global laxity of this complex leads to multidirectional instability and why a capsular shift surgical procedure is required to address global laxity. Finally, atmospheric pressure and the adhesioncohesion mechanism also add to the stability of the shoulder joint. The clinician needs to consider all factors related to glenohumeral instability to implement safe and effective treatment during conservative and postoperative rehabilitation of the athlete.
The superior labrum serves as an attachment for the long head of the biceps and the superior glenohumeral ligament.61 The long head of the biceps tendon has an important role as a dynamic restraint to external rotation in the abducted shoulder.117 It has been suggested that the biceps becomes more important than the rotator cuff as an anterior stabilizer with decreased stability of the capsuloligamentous structures.141 Injury may represent a traction phenomenon, secondary to activity in the biceps, or possibly a compression phenomenon.88 Repetitive movement into extreme external rotation may excessively load the biceps tendon and predispose the overhead athlete to a biceps-labral complex injury, as noted earlier.142 As long as the scapula is positioned so that the glenoid fossa accepts the net forces acting on the humeral head, the glenohumeral joint will remain stable.88 A redundant capsule may allow excessive glenohumeral angles that exceed the scapulohumeral balancing mechanism,143 allowing instability to occur before the capsuloligamentous structures have sufficiently tightened to provide restraint.
Other Stabilizing Factors Other forces that influence shoulder stability are atmospheric pressure and the adhesion-cohesion mechanism. Normal negative intra-articular pressure has been demonstrated to contribute to the stability of the glenohumeral joint.78 Kumar and Balasubramaniam144 have radiographically demonstrated significant inferior subluxation following percutaneous puncture of the capsule without dependence on muscle suspension, allowing atmospheric air to enter the joint. Harryman and associates72 have evaluated
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MUSCLE ACTIVITY Oatis21 has classified the muscles of the shoulder complex into axioscapular, axioclavicular, scapulohumeral, and axiohumeral muscles. Box 2-1 presents a listing of these categories.
Axioscapular and Axioclavicular Muscles of the axioscapular and axioclavicular groups all attach to both the axioskeleton and scapula or clavicle.21 These muscles act on the sternoclavicular and scapulothoracic joints, and ultimately on the acromioclavicular joint. They provide a stable yet mobile base from which the glenohumeral joint and associated muscles can function. Loss of these muscles, particularly the trapezius or serratus anterior, consequently affects scapulohumeral rhythm and shoulder function. Functional stability of the scapula requires optimal positioning, smooth muscular balance in the force couple around the scapula, and correct timing of muscle activity of the scapula
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BOX 2-1.
Muscles Acting on the Shoulder Complex
Axioscapular and Axioclavicular
Teres minor
Trapezius
Subscapularis
Serratus anterior
Teres major
Levator scapulae
Coracobrachialis
Rhomboid major
Axiohumeral
Rhomboid minor
Pectoralis major
Pectoralis major
Latissimus dorsi
Subclavius
Other
Sternocleidomastoid
Biceps brachii
Scapulohumeral
Triceps brachii
Deltoid
Coracobrachialis
Supraspinatus
Omohyoid
Infraspinatus
rotators.145 A force couple is defined as equal forces producing a rotation by pulling in the opposite direction. The serratus anterior and trapezius force couple is a key component for normal function of the shoulder (Fig. 2-17). This force couple serves four paramount functions:8 (1) rotates the scapula, maintaining the glenoid surface in an appropriate position; (2) through scapular rotation, positions the deltoid to maintain efficient length, thereby enhancing power and stability (without scapular rotation, only 90 degrees of active abduction is available35,146); (3) prevents impingement of the subacromial structures on the coracoacromial arch; and (4) provides a stable base, enabling the axiohumeral and scapulohumeral muscles to move the arm against resistance.88 Trying to move the humerus without the trapezius, serratus, or both is analogous to trying to push against a solid wall while on roller skates.8 This force couple can be divided into upper and lower components, both of which function in all planes of elevation. The upper component is comprised of the upper trapezius, levator scapulae, and upper portion of the serratus anterior. The lower component is comprised of the lower trapezius and lower portion of the serratus anterior.35 For the upper component, the upper trapezius and levator scapulae act to elevate the scapula during shoulder elevation. Activity of the upper trapezius, which is fairly constant in flexion and abduction, continues in a linear fashion as the scapula rotates about its axis.35,147 The upper trapezius is active as a scapular elevator and rotator through its insertion at the acromion. The fibers of the upper portion of the serratus anterior also assist in upward rotation.
Figure 2-17. Serratus anterior (SA) and trapezius force couple generating scapular rotation. LS, levator scapulae; LT, lower trapezius; MT, middle trapezius; UT, upper trapezius. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 100.)
For the lower component, the lower trapezius pulls inferiorly from its insertion at the base of the scapular spine to direct
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the glenoid upward. The lower trapezius contribution increases with increasing abduction. In flexion, activity plateaus between 70 and 120 degrees, after which activity significantly increases to coincide with the abduction curve.35,147 The force couple is now complete as the serratus anterior lower fibers pull the inferior angle forward and laterally. The scapula translates forward on the thoracic wall, directing the glenoid toward the sagittal plane, with the serratus anterior pulling the scapula forward. Progressive activity of the serratus anterior with humeral elevation should contribute to posterior tipping and external rotation of the scapula, as well as upward rotation.29 Electromyographic activity is equal for the scapular rotators at end range flexion and abduction, because the scapula always achieves the same terminal position with elevation, regardless of plane.148 The differences of scapular migration between flexion and coronal plane abduction are explained by the differences in activity of the lower trapezius, middle trapezius, and rhomboids; all have greater action potential values in abduction.8 The downward and medially directed fibers of the lower trapezius may assist in producing posterior tipping and external rotation moments as the humerus is elevated. Individuals with impingement have been shown to exhibit decreased levels of serratus anterior activity and scapular upward rotation34 and a delay in middle and lower trapezius activation.145 A delayed response of the middle and lower trapezius muscles compared with the upper trapezius may lead to supremacy of the upper trapezius muscle, causing an abnormality in scapulohumeral rhythm. The upper and lower trapezius and serratus anterior muscles play a role in the production of scapular upward rotation throughout the range.33 Clinically, a long thoracic nerve palsy is more common, and results in greater functional impairment, than a spinal accessory nerve palsy.8 A prolonged, complete trapezius palsy can be debilitating because of the loss of scapular suspension and subsequent depression of the shoulder girdle (Fig. 2-18). A patient with an isolated spinal accessory nerve palsy will demonstrate weak sagittal plane motion, but frontal plane abduction will be significantly impaired. With a complete long thoracic nerve palsy, patients typically will be unable to flex or abduct the involved shoulder fully. A synergy also exists between the scapular adductors, particularly the middle and lower trapezius, with the motion of external rotation. When resisting shoulder external rotation in neutral, the trapezius and rhomboids work to stabilize the vertebral border of the scapula.8 In individuals with a spinal accessory nerve palsy, this relation becomes evident. Resisted external rotation results in a flip sign because the middle and lower trapezius cannot oppose the pull of the external rotators from their fixed origins.149,150 Clinically, we have seen up to a 25% reduction of internal and external torque output in patients with a
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Figure 2-18. Patient with chronically denervated trapezius. Note shoulder girdle depression caused by loss of trapezius suspension effect.
serratus anterior or trapezius nerve palsy caused by loss of this synergy. Recognition of scapulothoracic contribution to shoulder function is imperative. The clinician must evaluate for scapulothoracic muscle dysfunction because significant impairment of these muscles often exists in the presence of shoulder pathology. A muscular imbalance from weakness or shortening can result in impaired stabilization of the scapula. This concept becomes especially important for the thrower, who depends on the proper coordination and sequencing of the entire shoulder complex.
Scapulohumeral Muscles The scapulohumeral muscles provide motion and dynamic stabilization to the glenohumeral joint.10,19,21 These muscles are crucial for function of the shoulder complex because the glenohumeral joint contributes to a significant amount of motion. In the normal shoulder, the middle deltoid is active in all planes of elevation,128,151-153 whereas the anterior and posterior heads command flexion and extension, respectively.8 Although the anterior fibers dominate motion in flexion, the middle fibers become more involved at 60 degrees.147 This occurs because of relative humeral realignment toward the scapular plane as the scapula translates forward over the thoracic wall. Also, the obligatory internal rotation with flexion moves the deltoid’s insertion forward, providing the middle deltoid with a more efficient line of pull. Poppen and Walker128 have found that as the line of pull improves, so does the deltoid moment arm. The improvement in the line of pull and moment arm during abduction would be meaningless to the deltoid if the scapula did not rotate, functionally lengthening the deltoid. Without scapular rotation, the deltoid would excessively shorten by 90 degrees of abduction and the arm could not actively raise past this point; this is called active insufficiency.35,146 The deltoid is able to maximize function by a complex interplay of mechanical adjustments as the insertion rises overhead and the scapula rotates.
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The other component of the scapulohumeral muscles is the rotator cuff, which provides the core dynamic control about the glenohumeral joint. Comprised of four muscles and associated tendons, the rotator cuff dynamically maintains articular congruity, thus providing the larger and more powerful shoulder muscles with the ability to move against great resistance.8 The dynamic effect of the supraspinatus is to stabilize the humeral head in the glenoid fossa centrally.5,11,35,70,98,128,154 This muscle also provides a depressive force because of tendon compression of the superior humeral head.155,156 A dysfunctional rotator cuff is unable to mitigate the upward shear from the deltoid, leading to impingement of the supraspinatus tendon and subacromial bursa against the coracoacromial arch.42 This mechanism may lead to humeral head superior migration in patients with chronic rotator cuff tears.157-159 Fatigue of the deltoid and rotator cuff complex also has been found to produce abnormal glenohumeral kinematics of superior migration of the humeral head on the glenoid.160 The second force couple of the shoulder complex is from the action of the deltoid, supraspinatus, infraspinatus, teres minor, and subscapularis (Fig. 2-19). The line of pull to the glenoid face of the infraspinatus and subscapularis has been estimated at 45 degrees, and the teres minor at 55 degrees.5 These three muscles have a negligible moment arm as abductors.33 Their responsibility in the force couple is to exert a predominantly downward shear, which peaks at 60 degrees of elevation, as well as a compressive load.3,35,70 As the deltoid draws the humeral head upward, the depressors tug downward, allowing humeral rotation while maintaining glenohumeral joint conformity.74,128 Compromise of the humeral head depressors results in an
imbalanced struggle against the opposing deltoid shear, leading to superior humeral head displacement, loss of the effective fulcrum, and impaired strength. The supraspinatus and deltoid are in optimal alignment in the scapular plane.12 The supraspinatus is active in all planes of elevation,35,147,151,153 contrary to its originally being regarded as the isolated initiator of abduction. This has been clearly disproved by electromyographically induced nerve palsy studies162-164 and clinical observations.165,166 In fact, 40% to 60% of elevation torque output has been attributed to the supraspinatus and infraspinatus.167 With scapular plane elevation of the glenohumeral joint, the supraspinatus pulls the humeral head into the glenoid cavity and remains active during the movement.168 Scepi and colleagues168 have determined that at the beginning of scapular plane elevation, the anterior portion of the deltoid works synergistically with the supraspinatus. There remains some controversy over the stabilizing versus abducting effect. Celli and associates169 have defined a stabilizer as a structure that demonstrates constant activity by electromyography compared with a mover, whose activity increases with motion. It was found that the deltoid is the abducting force (mover) whereas the supraspinatus is a stabilizer. Ito147 has found a linear progression of electrical activity in the supraspinatus and deltoid during abduction. The infraspinatus and teres minor have also been found to be active throughout elevation,35,151,153 fulfilling two responsibilities—force couple requirements and serving as a posterior barrier against translation. The infraspinatus also contributes to the generation of abduction glenohumeral torque and stabilization of the humeral head against superior subluxation.170 The infraspinatus demonstrates a linear progression in activity throughout coronal35 and scapular plane abduction.70,147 Activity differs somewhat in flexion, being higher and peaking at between 60 and 120 degrees. Activity is enhanced because of muscle demand created when the elbow is flexed to 90 degrees, producing a moment toward internal rotation.8 The subscapularis acts synergistically with the posterior cuff muscles to depress and compress the humeral head and is more active in abduction than flexion. Significant activity of the teres minor and infraspinatus is noted in full external rotation and horizontal extension.171-173 This is the late cocking phase position in throwing and is advocated for strengthening the posterior cuff muscles.174 Strong eccentric activity occurs in the subscapularis during the late cocking phase of throwing.171,175 Further discussion of the throwing cycle and pitching mechanics will be presented in subsequent chapters..
Figure 2-19. Deltoid and rotator cuff force couple. (From Kelley MJ, Clark WA: Orthopedic Therapy of the Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1995, p 92.)
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Clinically, strengthening of the posterior cuff muscles is essential for rehabilitating the nonoperative and postoperative athlete. Proper strength and balance of these muscles are key components of optimal shoulder function.
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Axiohumeral Muscles The axiohumeral muscles, pectoralis major and latissimus dorsi, attach the thorax to the humerus.21 They have large physiologic cross-sectional areas and are believed to provide additional strength to shoulder movement.113 Controversy exists regarding activity of the latissimus dorsi and pectoralis muscles in unresisted rotation.8 These muscles produce the forces required to accelerate the arm and object velocity.
Other Muscles The biceps brachii, coracobrachialis, and triceps brachii also act on the shoulder joint. The biceps, although predominantly an elbow flexor and forearm supinator, can be an effective elevator and functions to stabilize the humeral head in the glenoid, preventing upward migration.85,146,176 Also, humeral external rotation places the long head laterally, causing it to act like a pulley and assisting in arm elevation.
SUMMARY This chapter has discussed the biomechanics and principals behind the function of the shoulder complex. There is an impressive interdependency among muscle action, ligamentous stability, and osseous orientation to shoulder function. Understanding this relationship is paramount to the successful diagnosis and treatment of shoulder pathology and dysfunction. References 1. Culham E, Peat M: Functional anatomy of the shoulder complex. J Orthop Sports Phys Ther 18:342-350, 1993. 2. Bearn JG: Direct observations on the function of the capsule of the sternoclavicular joint in clavicular support. J Anat 101:159-170, 1967. 3. Bateman J: The Shoulder and Neck. Philadelphia, WB Saunders, 1971. 4. Steindler A: Kinesiology of the Human Body Under Normal and Pathological Conditions. Springfield, Ill, Charles C Thomas, 1955. 5. Perry J: Biomechanics. In Rowe C (ed): The Shoulder. New York, Churchill-Livingstone, 1988. 6. Calliet R: Shoulder Pain. Philadelphia, FA Davis, 1977. 7. Kebaetse M, McClure P, Pratt NA: Thoracic position effect on shoulder range of motion, strength, and three-dimensional scapular kinematics. Arch Phys Med Rehabil 80:945-950, 1999. 8. Kelley M, Clark W: Orthopedic Therapy of the Shoulder. Philadelphia, JB Lippincott, 1995. 9. Burkhart SS, Morgan CD, Kibler WB; The disabled throwing shoulder: Spectrum of pathology. Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 19:641-661, 2003. 10. Kibler WB: The role of the scapula in athletic shoulder function. Am J Sports Med 26:325-337, 1998.
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11. Codman E: The Shoulder. Boston, Thomas Todd, 1934. 12. Johnston T: The movements of the shoulder joint. A plea for the use of the “Plane of the Scapula” as the plane of reference in movements occurring in the humero-scapular joint. Br J Surg 25:252, 1937. 13. Saha AK: Theory of Shoulder Mechanism: Descriptive and Applied. Springfield, Ill, Charles C Thomas, 1961. 14. Doody SG, Freedman L, Waterland JC: Shoulder movements during abduction in the scapular plane. Arch Phys Med Rehabil 51:595-604, 1970. 15. Freedman L, Munro RR.: Abduction of the arm in the scapular plane: Scapular and glenohumeral movements. A roentgenographic study. J Bone Joint Surg Am 48:1503-1510, 1966. 16. Poppen NK, Walker PS: Normal and abnormal motion of the shoulder. J Bone Joint Surg Am 58:195-201, 1976. 17. Dvir Z, Berme N: The shoulder complex in elevation of the arm: A mechanism approach. J Biomech 11:219-225, 1978. 18. McGregor L: Rotation at the shoulder: A critical injury. Br J Surg 24:425-438, 1937. 19. Rowe CR, Sakellarides HT: Factors related to recurrences of anterior dislocations of the shoulder. Clin Orthop 20:40-48, 1961. 20. Michener LA, McClure PW, Karduna AR: Anatomical and biomechanical mechanisms of subacromial impingement syndrome. Clin Biomech (Bristol, Avon) 18:369-379, 2003. 21. Oatis CA: Kinesiology: The Mechanics and Pathomechanics of Human Movement. Philadelphia, Lippincott Williams & Wilkins, 2004. 22. De Freitas V, Vitti M, Furlani J: Electromyographic study of levator scapulae and rhomboideus major muscles in movements of the shoulder and arm. Electromyogr Clin Neurophysiol 20:205-216, 1980. 23. Duchenne G, Kaplan E: Physiology of Motion. Philadelphia, JB Lippincott, 1949. 24. Kendall F, McCreary E: Muscle Testing and Function, 3rd ed. Baltimore, Williams & Wilkins, 1982. 25. Karduna AR, McClure PW, Michener LA: Scapular kinematics: Effects of altering the Euler angle sequence of rotations. J Biomech 33:1063-1068, 2000. 26. van der Helm FC: A finite element musculoskeletal model of the shoulder mechanism. J Biomech 27:551-569, 1994. 27. Borstad JD, Ludewig PM: Comparison of scapular kinematics between elevation and lowering of the arm in the scapular plane. Clin Biomech (Bristol, Avon) 17:650-659, 2002. 28. Karduna AR, McClure PW, Michener LA, Sennett B: Dynamic measurements of three-dimensional scapular kinematics: A validation study. J Biomech Eng 123:184-190, 2001. 29. Ludewig PM, Cook TM, Nawoczenski DA: Three-dimensional scapular orientation and muscle activity at selected positions of humeral elevation. J Orthop Sports Phys Ther 24:57-65, 1996. 30. Lukasiewicz AC, McClure P, Michener L, et al: Comparison of three-dimensional scapular position and orientation between subjects with and without shoulder impingement. J Orthop Sports Phys Ther 29:574-583, 1999. 31. McClure PW, Michener LA, Sennett BJ, Karduna AR: Direct three-dimensional measurement of scapular kinematics during dynamic movements in vivo. J Shoulder Elbow Surg 10:269-277, 2001. 32. McQuade KJ, Smidt GL: Dynamic scapulohumeral rhythm: The effects of external resistance during elevation of the
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arm in the scapular plane. J Orthop Sports Phys Ther 27:125-133, 1998. Ebaugh DD, McClure PW, Karduna AR: Three-dimensional scapulothoracic motion during active and passive arm elevation. Clin Biomech (Bristol, Avon) 20:700-709, 2005. Ludewig PM, Cook TM: Alterations in shoulder kinematics and associated muscle activity in people with symptoms of shoulder impingement. Phys Ther 80:276-291, 2000. Inman V, Saunder J, Abbot L: Observations on the function of the shoulder joint. J Bone Joint Surg 26:1, 1944. Saha AK: Mechanism of shoulder movements and a plea for the recognition of “zero position” of glenohumeral joint. Indian J Surg 12:153-165, 1950. Graichen H, Stammberger T, Bonel H, et al: Magnetic resonance-based motion analysis of the shoulder during elevation. Clin Orthop Relat Res (370):154-163, 2000. Myers JB, Laudner KG, Pasquale MR, et al: Scapular position and orientation in throwing athletes. Am J Sports Med 33:263-271, 2005. Paletta GA Jr, Warner JJ, Warren RF, et al: Shoulder kinematics with two-plane x-ray evaluation in patients with anterior instability or rotator cuff tearing. J Shoulder Elbow Surg 6:516-527, 1997. Warner JJ, Micheli LJ, Arslanian LE, et al: Scapulothoracic motion in normal shoulders and shoulders with glenohumeral instability and impingement syndrome. A study using Moire topographic analysis. Clin Orthop Relat Res (285):191-199, 1992. Kibler WB, Uhl TL, Maddux JW, et al: Qualitative clinical evaluation of scapular dysfunction: a reliability study. J Shoulder Elbow Surg 11:550-556, 2002. Mell AG, LaScalza S, Guffey P, et al: Effect of rotator cuff pathology on shoulder rhythm. J Shoulder Elbow Surg 14(Suppl):58S-64S, 2005. von Eisenhart-Rothe R, Matsen FA 3rd, Eckstein F, et al: Pathomechanics in atraumatic shoulder instability: Scapular positioning correlates with humeral head centering. Clin Orthop Relat Res (433):82-89, 2005. Finley MA, Lee RY: Effect of sitting posture on threedimensional scapular kinematics measured by skinmounted electromagnetic tracking sensors. Arch Phys Med Rehabil 84:563-568, 2003. Smith J, Kotajarvi BR, Padgett DJ, Eischen JJ: Effect of scapular protraction and retraction on isometric shoulder elevation strength. Arch Phys Med Rehabil 83:367-370, 2002. Borstad JD, Ludewig PM: The effect of long versus short pectoralis minor resting length on scapular kinematics in healthy individuals. J Orthop Sports Phys Ther 35:227-238, 2005. Stokdijk M, Eilers PH, Nagels J, Rozing PM: External rotation in the glenohumeral joint during elevation of the arm. Clin Biomech (Bristol, Avon) 18:296-302, 2003. Ahmad CS, Wang VM, Sugalski MT, et al: Biomechanics of shoulder capsulorrhaphy procedures. J Shoulder Elbow Surg 14(Suppl):12S-18S, 2005. Hawkins RJ, Angelo RL: Glenohumeral osteoarthrosis. A late complication of the Putti-Platt repair. J Bone Joint Surg Am 72:1193-1197, 1990. Lusardi DA, Wirth MA, Wurtz D, Rockwood CA Jr: Loss of external rotation following anterior capsulorrhaphy of the shoulder. J Bone Joint Surg Am 75:1185-1192, 1993.
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51. Dempster WT: Mechanisms of shoulder movement. Arch Phys Med Rehabil 46:49-70, 1965. 52. Moseley HF: The clavicle: Its anatomy and function. Clin Orthop 58:17-27, 1958. 53. Cave A: The nature and morphology of the costoclavicular ligament. J Anat 95:170-179, 1961. 54. McArdle PJ, Kalbassi R, Ilankovan V: Stability of the sternoclavicular joint. A retrospective study. Br J Oral Maxillofac Surg 41:12-15, 2003. 55. Spencer EE, Kuhn JE, Huston LJ, et al: Ligamentous restraints to anterior and posterior translation of the sternoclavicular joint. J Shoulder Elbow Surg 11:43-47, 2002. 56. Shaffer BS: Painful conditions of the acromioclavicular joint. J Am Acad Orthop Surg 7:176-188, 1999. 57. Basmajian J, Bazant F: Factors preventing downward dislocation of the adducted shoulder joint. An electromyographic and morphological study. Am J Orthop 41A:1182-1186, 1959. 58. Kennedy JC, Cameron H: Complete dislocation of the acromio-clavicular joint. J Bone Joint Surg Br 36:202-208, 1954. 59. Rockwood CA, Young DC: Disorders of the acromioclavicular joint. In Rockwood CA, Matsen FA 3rd (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 413-416. 60. Kapandji I: The Physiology of Joints, vol 1. Baltimore, Williams & Wilkins, 1970. 61. Curl LA, Warren RF: Glenohumeral joint stability. Selective cutting studies on the static capsular restraints. Clin Orthop Relat Res (330):54-65, 1996. 62. DePalma A: Surgery of the Shoulder. New York, JB Lippincott, 1973. 63. Blakely RL, Palmer ML: Analysis of rotation accompanying shoulder flexion. Phys Ther 64:1214-1216, 1984. 64. MacConail M, Basmajian J: Muscles and Movements: A Basis for Human Kinesiology. Baltimore, Williams & Wilkins, 1969. 65. Howell SM, Galinat BJ: The glenoid-labral socket. A constrained articular surface. Clin Orthop Relat Res (243): 122-125, 1989. 66. Iannotti JP, Gabriel JP, Schneck SL, et al: The normal glenohumeral relationships. An anatomical study of one hundred and forty shoulders. J Bone Joint Surg Am 74:491-500, 1992. 67. Soslowsky LJ, Flatow EL, Bigliani LU, et al: Quantitation of in situ contact areas at the glenohumeral joint: A biomechanical study. J Orthop Res 10:524-534, 1992. 68. Van der Helm FC, Veeger HE, Pronk GM, et al: Geometry parameters for musculoskeletal modelling of the shoulder system. J Biomech 25:129-144, 1992. 69. Kaltenborn F: Mobilization of the Extremity Joints. Examination and Basic Treatment Techniques. Oslo, Olaf Bokhandel, 1980. 70. Saha AK: Dynamic stability of the glenohumeral joint. Acta Orthop Scand 42:491-505, 1971. 71. Howell SM, Galinat BJ, Renzi AJ, Marone PJ: Normal and abnormal mechanics of the glenohumeral joint in the horizontal plane. J Bone Joint Surg Am 70:227-232, 1988. 72. Harryman DT 2nd, Sidles JA, Clark JM, et al: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334-1343, 1990. 73. Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53-66, 1992.
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74. Kelkar R, Flatow E, Bigliani L, et al: A stereophotogrammetric method to determine the kinematics of the glenohumeral joint. Adv Bioeng 19:143-145, 1992. 75. Yamaguchi K, Sher JS, Andersen WK, et al: Glenohumeral motion in patients with rotator cuff tears: A comparison of asymptomatic and symptomatic shoulders. J Shoulder Elbow Surg 9:6-11, 2000. 76. Nobuhara K: The Shoulder: Its Function and Clinical Aspects. Tokyo, Igaku-Shoin, 1977. 77. Werner CM, Nyffeler RW, Jacob HA, Gerber C: The effect of capsular tightening on humeral head translations. J Orthop Res 22:194-201, 2004. 78. Moore SM, Musahl V, McMahon PJ, Debski RE: Multidirectional kinematics of the glenohumeral joint during simulated simple translation tests: Impact on clinical diagnoses. J Orthop Res 22:889-894, 2004. 79. Graichen H, Stammberger T, Bonel H, et al: Glenohumeral translation during active and passive elevation of the shoulder—a 3D open-MRI study. J Biomech 33:609-613, 2000. 80. Moseley HF, Overgaard D: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 44:913-927, 1962. 81. Novotny JE, Woolley CT, Nichols CE 3rd, Beynnon BD: In vivo technique to quantify the internal-external rotation kinematics of the human glenohumeral joint. J Orthop Res 18:190-194, 2000. 82. Bigliani LU, Kelkar R, Flatow EL, et al: Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res (330):13-30, 1996. 83. Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC: Articular geometry of the glenohumeral joint. Clin Orthop (285): 181-190, 1992. 84. Jobe CM, Iannotti JP: Limits imposed on glenohumeral motion by joint geometry. J Shoulder Elbow Surg 4:281-285, 1995. 85. Kent BE: Functional anatomy of the shoulder complex. Phys Ther 51:867-874, 1971. 86. Peat M: Functional anatomy of the shoulder complex. Phys Ther 66:1855-1865, 1986. 87. Sarrafian SK: Gross and functional anatomy of the shoulder. Clin Orthop Relat Res (173):11-19, 1983. 88. Abboud JA, Soslowsky LJ: Interplay of the static and dynamic restraints in glenohumeral instability. Clin Orthop Relat Res (400):48-57, 2002. 89. Rowe CR: The Shoulder. New York, Churchill-Livingstone, 1988. 90. Reeves B: Experiments on the tensile strength of the anterior capsular structures of the shoulder in man. J Bone Joint Surg Br 50:858-865, 1968. 91. Hara H, Ito N, Iwasaki K: Strength of the glenoid labrum and adjacent shoulder capsule. J Shoulder Elbow Surg 5:263-268, 1996. 92. Bankart A: The pathology and treatment of recurrent dislocation of the shoulder. Br J Surg 26:23-29, 1938. 93. Rowe CR, Patel D, Southmayd WW: The Bankart procedure: A long-term end-result study. J Bone Joint Surg Am 60: 1-16, 1978. 94. Lippitt SB, Vanderhoof JE, Harris SL, et al: Glenohumeral stability from concavity-compression: A quanitative analysis. J Shoulder Elbow Surg 2: 27-34, 1993.
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95. Halder AM, Kuhl SG, Zobitz ME, et al: Effects of the glenoid labrum and glenohumeral abduction on stability of the shoulder joint through concavity-compression: An in vitro study. J Bone Joint Surg Am 83:1062-1069, 2001. 96. Lazarus MD, Sidles JA, Harryman DT 2nd, Matsen FA 3rd: Effect of a chondral-labral defect on glenoid concavity and glenohumeral stability. A cadaveric model. J Bone Joint Surg Am 78:94-102, 1996. 97. Rodosky MW, Harner CD, Fu FH: The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am J Sports Med 22:121-130, 1994. 98. Morrey BF, Chao EY: Recurrent anterior dislocation of the shoulder. In Dumbleton J, Black J (eds): Clinical Biomechanics. London, Churchhill Livingstone, 1981. 99. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 100. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 18:579-584, 1990. 101. Ovesen J, Nielsen S: Anterior and posterior shoulder instability. A cadaver study. Acta Orthop Scand 57:324-327, 1986. 102. Terry GC, Hammon D, France P, Norwood LA: The stabilizing function of passive shoulder restraints. Am J Sports Med 19:26-34, 1991. 103. Townley CO: The capsular mechanism in recurrent dislocation of the shoulder. J Bone Joint Surg Am 32:370-380, 1950. 104. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 105. Flatow EL, Warner JI: Instability of the shoulder:complex problems and failed repairs: Part I. Relevant biomechanics, multidirectional instability, and severe glenoid loss. Instr Course Lect 47:97-112, 1998. 106. Moore SM, McMahon PJ, Azemi E, Debski RE: Bi-directional mechanical properties of the posterior region of the glenohumeral capsule. J Biomech 38:1365-1369, 2005. 107. Clark JM, Harryman DT 2nd: Tendons, ligaments, and capsule of the rotator cuff. Gross and microscopic anatomy. J Bone Joint Surg Am 74:713-725, 1992. 108. Gerber C, Werner CM, Macy JC, et al: Effect of selective capsulorrhaphy on the passive range of motion of the glenohumeral joint. J Bone Joint Surg Am 85:48-55, 2003. 109. Ferrari DA: Capsular ligaments of the shoulder. Anatomical and functional study of the anterior superior capsule. Am J Sports Med 18:20-24, 1990. 110. Bowen MK, Warren RF: Ligamentous control of shoulder stability based on selective cutting and static translation experiments. Clin Sports Med 10:757-782, 1991. 111. Nobuhara K, Ikeda H: Rotator interval lesion. Clin Orthop Relat Res (223):44-50, 1987. 112. Burkart AC, Debski RE: Anatomy and function of the glenohumeral ligaments in anterior shoulder instability. Clin Orthop Relat Res (400):32-39, 2002. 113. Basmajian J: Muscles Alive, 4th ed. Baltimore, Williams & Wilkins, 1979. 114. Gagey OJ, Boisrenoult P: Shoulder capsule shrinkage and consequences on shoulder movements. Clin Orthop Relat Res (419):218-222, 2004.
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115. Blasier RB, Guldberg MS, Rothman ED: Anterior shoulder stability: Contributions of rotator cuff forces and the capsular ligaments in a cadaver model. J Shoulder Elbow Surg 1:140-150, 1992. 116. O’Brien SJ, Schwartz RS, Warren RF, Torzilli PA: Capsular restraints to anterior-posterior motion of the abducted shoulder: A biomechanical study. J Shoulder Elbow Surg 4:298-308, 1995. 117. Kuhn JE, Huston LJ, Soslowsky LJ, et al: External rotation of the glenohumeral joint: Ligament restraints and muscle effects in the neutral and abducted positions. J Shoulder Elbow Surg 14(Suppl):39S-48S, 2005. 118. Bigliani LU, Pollock RG, Soslowsky LJ, et al: Tensile properties of the inferior glenohumeral ligament. J Orthop Res 10:187-197, 1992. 119. Pollock RG, Wang VM, Bucchieri JS, et al: Effects of repetitive subfailure strains on the mechanical behavior of the inferior glenohumeral ligament. J Shoulder Elbow Surg 9:427-435, 2000. 120. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 19:404-420, 2003. 121. Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274-279, 1990. 122. Andrews JR, Kupferman SP, Dillman CJ: Labral tears in throwing and racquet sports. Clin Sports Med 10:901-911, 1991. 123. Burkhart SS, Morgan CD: The peel-back mechanism: Its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair rehabilitation. Arthroscopy 14:637-640, 1998. 124. Wilk KE, Andrews JR, Arrigo CA: The physical examination of the glenohumeral joint: Emphasis on the stabilizing structures. J Orthop Sports Phys Ther 25:380-389, 1997. 125. Karduna AR, Williams GR, Williams JL, Iannotti JP: Kinematics of the glenohumeral joint: Influences of muscle forces, ligamentous constraints, and articular geometry. J Orthop Res 14:986-993, 1996. 126. Kelkar R, Wang VM, Flatow EL, et al: Glenohumeral mechanics: A study of articular geometry, contact, and kinematics. J Shoulder Elbow Surg 10:73-84, 2001. 127. Labriola JE, Lee TQ, Debski RE, McMahon PJ: Stability and instability of the glenohumeral joint: The role of shoulder muscles. J Shoulder Elbow Surg 14(Suppl): 32S-38S, 2005. 128. Poppen NK, Walker PS: Forces at the glenohumeral joint in abduction. Clin Orthop Relat Res (135):165-170, 1978. 129. Wuelker N, Korell M, Thren K: Dynamic glenohumeral joint stability. J Shoulder Elbow Surg 7:43-52, 1998. 130. Cain PR, Mutschler TA, Fu FH, Lee SK: Anterior stability of the glenohumeral joint. A dynamic model. Am J Sports Med 15:144-148, 1987. 131. DePalma AF, Cooke AJ, Prabhakar M: The role of the subscapularis in recurrent anterior dislocations of the shoulder. Clin Orthop Relat Res 54:35-49, 1967. 132. Matsen FA 3rd, Thomas SC, Rockwood CA: Anterior glenohumeral instability. In Rockwood CA, Matsen FA 3rd (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 526-622. 133. Symeonides PP: The significance of the subscapularis muscle in the pathogenesis of recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 54:476-483, 1972.
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134. Labriola JE, Jolly JT, McMahon PJ, Debski RE: Active stability of the glenohumeral joint decreases in the apprehension position. Clin Biomech (Bristol, Avon) 19:801-809, 2004. 135. McQuade KJ, Murthi AM: Anterior glenohumeral force/ translation behavior with and without rotator cuff contraction during clinical stability testing. Clin Biomech (Bristol, Avon) 19:10-15, 2004. 136. Lee SB, Kim KJ, O’Driscoll SW, et al: Dynamic glenohumeral stability provided by the rotator cuff muscles in the mid-range and end-range of motion. A study in cadavera. J Bone Joint Surg Am 82:849-857, 2000. 137. Hawkins RJ, Misamore GW, Hobeika PE: Surgery for full-thickness rotator-cuff tears. J Bone Joint Surg Am 67: 1349-1355, 1985. 138. Schwartz E, Warren RF, O’Brien SJ, Fronek J: Posterior shoulder instability. Orthop Clin North Am 18:409-419, 1987. 139. Detrisac D, Johnson L: Arthroscopic Shoulder Anatomy. Thorofare, NJ, Slack, 1986. 140. Lee SB, An KN: Dynamic glenohumeral stability provided by three heads of the deltoid muscle. Clin Orthop Relat Res (400):40-47, 2002. 141. Itoi E, Newman SR, Kuechle DK, et al: Dynamic anterior stabilisers of the shoulder with the arm in abduction. J Bone Joint Surg Br 76:834-836, 1994. 142. Morgan CD, Burkhart SS, Palmeri M, Gillespie M: Type II SLAP lesions: Three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14: 553-565, 1998. 143. Neer CS 2nd, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am 62:897-908, 1980. 144. Kumar VP, Balasubramaniam P: The role of atmospheric pressure in stabilising the shoulder. An experimental study. J Bone Joint Surg Br 67:719-721, 1985. 145. Cools AM, Witvrouw EE, Declercq GA, et al: Scapular muscle recruitment patterns: Trapezius muscle latency with and without impingement symptoms. Am J Sports Med 31:542-549, 2003. 146. Ito N: Electromyographic study of shoulder joint. Nippon Seikeigeka Gakkai Zasshi 54:1529-1540, 1980. 147. Laumann U: Kinesiology of the shoulder joint. In Kôlbel R, Helbig B, Blauth W (eds): Shoulder Replacement. Berlin, Springer-Verlag, 1987, pp 23-31. 148. Kelley M: Clinical evaluation of the shoulder. In Mackin E, Callahan A, Skirven T (eds): Rehabilitation of the Hand and Upper Extremity, 5th ed. St. Louis, Mosby, 2002, pp 1311-1350. 149. Kelley M, Brenneman S: The scapular flip sign: An examination sign to identify the presence of a spinal accessory nerve palsy. Presented at the APTA Combined Sections Meeting, New Orleans, February 2000. 150. Nuber GW, Bowman ID, Perry JP, et al: EMG analysis of classical shoulder motion. Trans Orthop Res Soc 11, 1986. 151. Shevlin MG, Lehmann JF, Lucci JA: Electromyographic study of the function of some muscles crossing the glenohumeral joint. Arch Phys Med Rehabil 50:264-270, 1969. 152. Sugahara R: Electromyographic study of shoulder movements. Jpn J Rehab Med 11:41-52, 1974.
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153. Lucas DB: Biomechanics of the shoulder joint. Arch Surg 107:425-432, 1973. 154. Radin EL: Biomechanics and functional anatomy. In Post M (ed): The Shoulder: Surgical and Nonsurgical Management, 2nd ed. Philadelphia, Lea & Febiger, 1988, pp 54-60. 155. Matsen FA 3rd: Biomechanics of the shoulder. In Frankel VH, Nordin M (eds): Basic Biomechanics of the Skeletal System. Philadelphia, Lea & Febiger, 1980, pp 221-242. 156. Zuckerman JD, Matsen FA 3rd: Biomechanics of the shoulder. In Zuckerman JD, Matsen FA 3rd (eds): Basic Biomechanics of the Musculoskeletal System. Philadelphia, Lea & Febiger, 1989, pp 225-247. 157. Deutsch A, Altchek DW, Schwartz E, et al: Radiologic measurement of superior displacement of the humeral head in the impingement syndrome. J Shoulder Elbow Surg 5: 186-193, 1996. 158. Hawkins RJ, Bell RH, Hawkins RH, Koppert GJ: Anterior dislocation of the shoulder in the older patient. Clin Orthop Relat Res (206):192-195, 1986. 159. Weiner DS, Macnab I: Superior migration of the humeral head. A radiological aid in the diagnosis of tears of the rotator cuff. J Bone Joint Surg Br 52:524-527, 1970. 160. Chen SK, Simonian PT, Wickiewicz TL, et al: Radiographic evaluation of glenohumeral kinematics: A muscle fatigue model. J Shoulder Elbow Surg 8:49-52, 1999. 161. De Duca CJ, Forrest WJ: Force analysis of individual muscles acting simultaneously on the shoulder joint during isometric abduction. J Biomech 6:385-393, 1973. 162. Colachis SC Jr, Strohm BR: Effect of suprascapular and axillary nerve blocks on muscle force in upper extremity. Arch Phys Med Rehabil 52:22-29, 1971. 163. Colachis SC, Jr., Strohm BR, Brechner VL: Effects of axillary nerve block on muscle force in the upper extremity. Arch Phys Med Rehabil 50:647-654, 1969. 164. Howell SM, Imobersteg AM, Seger DH, Marone PJ: Clarification of the role of the supraspinatus muscle in shoulder function. J Bone Joint Surg Am 68:398-404, 1986.
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165. Markhede G, Monastyrski J, Stener B: Shoulder function after deltoid muscle removal. Acta Orthop Scand 56: 242-244, 1985. 166. Staples OS, Watkins AL: Full active abduction in traumatic paralysis of the deltoid. J Bone Joint Surg 25:85, 1943. 167. Kuhlman JR, Iannotti JP, Kelly MJ, et al: Isokinetic and isometric measurement of strength of external rotation and abduction of the shoulder. J Bone Joint Surg Am 74: 1320-1333, 1992. 168. Scepi M, Faure JP, Ridoux N, et al: A three-dimensional model of the shoulder girdle. Forces developed in deltoid and supraspinatus muscles during abduction. Surg Radiol Anat 26:290-296, 2004. 169. Celli L, Balli A, de Luise G, Rovesta C: Some new aspects of the functional anatomy of the shoulder. Ital J Orthop Traumatol 11:83-91, 1985. 170. Mura N, O’Driscoll SW, Zobitz ME, et al: The effect of infraspinatus disruption on glenohumeral torque and superior migration of the humeral head: A biomechanical study. J Shoulder Elbow Surg 12:179-184, 2003. 171. Jobe FW, Moynes DR, Tibone JE, Perry J. An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 172. Kadefors R, Petersen I, Herberts P: Muscular reaction to welding work: An electromyographic investigation. Ergonomics 19:543-548, 1976. 173. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics, and tennis. Clin Sports Med 2:247-270, 1983. 174. Blackburn T, McLeod W, White B, Wofford L: Analysis of posterior rotator cuff exercise. Athl Train 25:40-45, 1990. 175. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the shoulder in throwing and pitching. A preliminary report. Am J Sports Med 11:3-5, 1983. 176. Kumar VP, Satku K, Balasubramaniam P: The role of the long head of biceps brachii in the stabilization of the head of the humerus. Clin Orthop Relat Res (244):172-175, 1989.
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CHAPTER 3 Standardized Shoulder Examination—
Clinical and Functional Approaches Terry R. Malone
This chapter addresses the components of a standardized examination process for the shoulder. This process requires attention to detail, recognizing the function of the shoulder as that of multiple joints functioning in a complex rather than individual actions at single joints. Most evaluation schemes have been derived through the particular emphases of the individual practitioner.1-4 Most involve an anatomic inspection moving toward a functional examination through range of motion and neurologic assessment, followed by specific tests for particular structures. Fortunately, the contemporary clinician is able to increase the information in this database to include assessment of strength and evaluation of function through a number of techniques. This chapter presents a schema for clinical assessment and a functional process of shoulder evaluation. It is a selective approach, with the focus on clinical tests with higher predictive qualities and how best to apply the results to establish diagnoses and treatment regimens. Radiographic, magnetic resonance imaging, arthrotomographic, and ultrasonographic modes of assessment are discussed in other chapters.
Is the pain acute or chronic? When does it hurt? Do you have pain at night? Do you have pain at rest? What type of pain is present? What has been the effect of treatment: such as rest, heat, ice, and exercise? Have you tried an anti-inflammatory drug? In both sports and work, what do you wish to do, and what are you unable to do? Have you had this problem before? Is there a medical history of diabetes in your family? These are examples of the types of questions that should be asked to get a picture of the condition before proceeding into an objective assessment. Also, as you begin your objective evaluation, it is important to have the person point with one finger to the area of pain. This enables you to determine the location and begin the process of evaluation for referral of pain rather than structure only. Screen. Be certain to look at the cervical spine, because many shoulder problems are related to underlying nerve roots of segmental facilitation and are easily misinterpreted as a peripheral problem. I always look to the capsule after ruling out the spine, particularly in athletes, because capsular insufficiency is common and often missed. The great challenge is to appreciate the need for motion and the changes in the thrower that enable him or her to be successful but also different.
A recommended schema for shoulder evaluation is presented that describes the tests commonly used in the clinical and manual examination of the musculoskeletal shoulder complex. Additional portions of this chapter describe strength assessment—static and dynamic—and culminate in a discussion of functional assessments.
EXAMINATION SCHEMA
General Evaluation Sequence. Clinicians must develop a process that works for them and, in their particular setting, provides information to assess the patient on the initial visit and also allows them to assess treatment effectiveness at ensuing clinical visits. This objective standardized scheme is described in Box 3-1 (also discussed elsewhere in this text). I will focus on the recommended clinical screening process and on the difficult problems of strength assessment and functional performance that is so important for the athlete.
Clinicians must develop an evaluation form or sequence to enable them to be effective and efficient. A written form is helpful to keep the clinician focused and to avoid becoming too findings-oriented. There might be a greater likelihood of reaching a conclusion when an expected positive examination result is confirmed using our hands. The following series of tenets may help in developing an evaluation form or sequence. Initiating the Evaluation. The evaluation should begin with the patient’s subjective description of the chief complaint, such as by asking the following questions:
Clinical Shoulder Screen During the past decade, clinical examination has evolved through the validation of tests to determine whether they are useful. As greater appreciation for the capsule labral complex and interactions of the scapula has been gained, more detailed scrutiny of popular assessment techniques has enabled clinicians to select and apply manual skills for
Why are you here in the clinic? What was the onset of this problem, abrupt or insidious? What is the level of pain? How long has it been hurting? 45
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BOX 3-1.
Objective Standardized Scheme
Observation—position and movement of scapula; rightleft comparisons; scapular slide test when obviously altered or different scapular patterns observed Active motion—elevation, external rotation at side, back scratch for internal rotation (composite movement); recognition of expected compensations in the throwing shoulder (loss of internal rotation and increased external rotation) Palpation—primary bony articulations and prominences Passive motion—done when differences seen actively Resisted motion Joint play Orthopedic tests—used as battery and sequenced; initial screen pattern Strength—isometric through dynamic assessment
applies an inferiorly directed stress through the upper arm to minimize the effect of the biceps and triceps. A markedly large displacement is typical bilaterally in the patient with multidirectional instability. Although there are no specific references related to independent validity of this test, it appears to be valuable as part of an overall assessment and when used as part of a battery of tests.5 Load and Shift Test—Anterior and Posterior Capsule. The load and shift test is designed to assess the anterior and posterior capsules of the glenohumeral joint performed while the subject is in a neutral sitting or supine posture. The examiner stabilizes the scapula with one hand, while displacing or gliding the humeral head with the other, assessing the displacement anteriorly and posteriorly. Hawkins and Schutte6 have provided a grading scale of this process; grade 1 is minimal motion and grade 3 manifests with the head riding up and over the glenoid rim. The validity of this test in demonstrating the presence of a Bankart lesion (anterior instability) is greater than 90% (sensitivity, 90.9%; specificity, 93.3%).7
Functional performance
determining structural problems more effectively. The process of this shoulder screen is to divide patients into two groups and then divide each of these into two subgroupings (Table 3-1). The screen is sequenced to assess the capsule initially. This can help determine whether the patient has presented with an instability or whether there is an underlying instability that has led to a secondary problem related to capsular incompetency. I recommend doing a series of capsular tests begun in the seated position.
Capsular Tests—Recommended Sequence Sulcus Sign (Superior Capsule). The sulcus sign is designed to assess the superior capsular restraints, including the superior glenohumeral ligament and coracohumeral ligament, in an adducted neutral posture. The examiner TABLE 3-1 Shoulder Screen INSTABILITY-RELATED (CAPSULAR TESTS POSITIVE)
NOT INSTABILITY-RELATED (CAPSULAR TESTS NEGATIVE)
Traumatic Instability
Atraumatic Trauma Instability Onset Insidious Onset
Rehabilitation potential limited
Good rehabilitation potential
Defined injury
Less defined process Rehabilitation potential specific to injury and process
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Apprehension Test—Anterior-Inferior Capsule. The apprehension test is performed with the patient sitting, standing, or supine. The examiner passively moves the humerus into maximal external rotation with the arm at 90 degrees abduction. The examiner may also add an anterior push to the posterior humeral head during the test as well. Lo and colleagues8 have reported a high specificity (99%) and moderate sensitivity (53%) with this maneuver to confirm anterior instability. An important discriminator for this test is to document apprehension, not pain; for example, if one places significant loading into external rotation, end-range tension is often reported as painful. Unfortunately, in my experience, examiners often report this as a positive test, which was not the original intent.9 Relocation Test—Anterior-Inferior Capsule. When the apprehension test is deemed positive, many examiners will then use the relocation test to further confirm or complement the apprehension test results. The patient is in a supine position and the examiner places one hand over the humeral head and applies a posterior force to maintain the humeral head in a posterior position. The examiner then externally rotates the humerus in the 90-degree abducted position, repeating the apprehension test, to determine whether the previous apprehension action is eliminated. Speer and associates9 have examined the relocation test in relation to surgical findings of anterior-inferior instability and found a specificity of 58% and a sensitivity of only 30%. They noted that patients often confuse pain and apprehension, greatly diminishing the actual selectivity of this and the apprehension test. Posterior Drawer Test—Posterior Capsule. The posterior drawer test is accomplished with the patient in a supine position while the examiner grasps the forearm and flexes
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the elbow approximately 120 degrees. The shoulder is then flexed approximately 90 degrees; the other hand of the examiner is placed under the scapula to enable palpation of the humeral head when a posterior force is applied through the humerus. The patient often does not have a strong reaction other than possibly sensing the humerus as slipping posteriorly. There are no specific references of the values associated with this test; many clinicians only use it if the subjective complaints of the patient indicate posterior instability. Some clinicians modify the loading process by adding a crossing of the arm over the chest to assess the actual slipping of the humeral head further. Again, no specific sensitivity/specificity data are available for this test. Capsular Assessment Interpretation Instability Related (Capsular Tests Positive). The completion of this sequence delineates the capsule as the superior (sulcus), anterior (load and shift), anterior-inferior (apprehension and relocation), and posterior (load and shift and posterior drawer) segments are evaluated. If the patient has a large sulcus, it is normally bilateral and the other tests will demonstrate significant motion as well. This is the classic multidirectional (atraumatic) instability patient who responds well to rehabilitation at a relatively high rate, a 70% or higher success rate in my experience. The patient with a positive apprehension test, not pain, has a problem usually related to a traumatic instability and has a limited response to rehabilitation. There may be the rare case of the patient who was born with a loose capsule that is then torn loose. However, these capsular tests efficiently categorize most problems as being related to instability and define the type of instability, which then helps predict rehabilitation success or failure and overall outcomes. Also, patients are often seen who have a positive instability assessment but have developed secondary problems in their attempt to live with the underlying instability. Thus, although the second portion of the shoulder screen is designed for patients without instability, we frequently have positive findings in both instability and what may be perceived as not instability tests. We sometimes describe this as having “fleas and lice.” The clinician is always urged to screen the capsule initially unless an obvious deformity prevents this. Not Instability Related (Capsular Tests Negative). The second phase of the screen is usually begun with the patient in the supine position as the process continues from the posterior drawer or apprehension test and the assessment of specific structures is initiated. (The problem has been determined not to be related to instability after completion of the capsular screen.) The acromioclavicular joint is palpated first and then tested specifically. Specific structures are now examined, with the patient’s subjective comments helping direct the flow of examination. Typically, if the patient has experienced trauma, the examination will focus on what is related to the specific force. However, when not related to trauma, the following sequence or screen pattern is efficient.
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Acromioclavicular and Labral Assessment Palpation and Crossed Arm Adduction. The patient is supine and the examiner palpates the acromioclavicular (AC) joint while the other hand passively grasps the flexed elbow and crosses the humerus across the body. The test is positive if significant pain is reported, particularly at the end range. The sensitivity has been reported to be 77%, with a specificity of 79%.10 Active Compression (O’Brien) Test. This test is done to assess AC and superior labral anterior-posterior (SLAP) lesions. The patient is standing or sitting and the examiner is at his or her side. The patient elevates the shoulder to 90 degrees (elbow extended) and then moves it (horizontal adduction) across the body to 10 to 15 degrees past midline. He or she is then asked to rotate the thumb downward; the examiner places a downward force on the humerus that the patient resists. This test is then repeated with the thumb up. Positive test results are significant pain as the patient resists the downward force. A positive test for the AC joint is pain on the top of the shoulder during both tests while a superior labral pathology is suspected if the test is only positive with the thumb down and significantly lessened when repeated with the thumb upward. The specificity of this test for labral pathology is relatively high (more than 90%) but is more limited in sensitivity (41%), with slightly higher values for AC assessments.10,11 Labral Tests Crank Test. This test is performed with the patient supine and the arm elevated in the scapular plane to approximately 160 degrees, with the elbow flexed slightly. The examiner then applies compression (axial load) through the elbow while internally and externally rotating the humerus. Pain is most common during external rotation and is often correlated with the patient complaining of pain during functional shoulder activities. Lui and coworkers5 have reported specificity and sensitivity as greater than 90%. Biceps Load I and II; Pain Provocation Tests. Several labral tests that use the biceps to bias labral loading have been reported. All these tests usually begin with the humerus in a 90-degree apprehension position, with additional pronation and supination of the forearm. Mimori and colleagues12 have reported a 100% sensitivity and a 90% specificity, whereas Kim and associates13 have reported a sensitivity of 90.9% and a specificity of 96.6% for these tests for SLAP lesions. Labral pathology is commonly the result of injury superimposed onto the labrum, allowing it to experience loads that are normally controlled by other structures. Liu and Henry14 have used this approach in evaluation of the labrum by grouping the positive load and shift test (capsular incompetency) with apprehension, relocation, sulcus, and crank tests; they reported a sensitivity of 90% and a specificity of 85%.
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At this point in the screen, we have evaluated the capsule (determined whether the problem is instabilityrelated and the type, if instability) and specific structures, the acromioclavicular joint, and labrum. The next assessment usually involves impingement signs and tests.
Impingement Testing Numerous impingement tests have been developed to elicit the pinching of tissues between the acromion and humeral head (classic external impingement). Many of these tests are plagued by being positive secondary to other conditions causing the impingement; thus, clinicians must always be wary of an easy assumption. Neer’s Sign. The patient is standing or sitting with the arm elevated overhead to the end range. The examiner forces the arm into maximal elevation, with slight overpressure. The test is considered positive with pain at the end range of motion. Some clinicians modify this examination by altering the position of the scapula to decrease pain (retraction), to increase pain (protraction), or increase pain (humeral internal rotation). Calis and colleagues15 have reported sensitivity values of 89% but a specificity of 31%. I often do the initial test in neutral humeral rotation and then repeat with internal rotation if the initial test was positive. The underlying assumption is that the second test should be more painful. The scapular position can similarly be altered but may be more difficult to control than humeral rotation, but it is also reassuring to be able to demonstrate a decrease in pain through proper positioning of the scapula to document likely rehabilitation success. Hawkin’s (Kennedy) Test. The patient is standing and the flexed arm is elevated to 90 degrees in the scapular plane. The examiner is at the patient’s side and internally rotates the humerus. A positive test is the response of pain with end-range rotation. When positive, this test can be modified by asking the patient to retract the scapula and repeat with scapular retraction being maintained. If the response is minimized, rehabilitation may include a focus on scapular or proximal musculature. Calis and associates15 have reported a sensitivity of 92% but specificity values of 25%. If this is the only positive test for impingement, the therapist should carefully evaluate the AC joint further, because a level of cross-arm adduction can occur and may be painful in those with AC pathology. Painful Arc Test. The patient is standing or seated and asked to abduct the arm actively away from the body (abduction plane) in a smooth rhythmic fashion. If the patient perceives pain in the 60- to 120-degree portion of the movement, but has pain-free movement above the painful arc, a positive test is recorded. This test can be modified to increase pain perception by adding a level of
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humeral internal rotation during the maneuver. This test was reported to have a sensitivity of 33% but a specificity of 81%.15 Rather than relying on a single test, the clinician is urged to use a combination of tests to achieve acceptable sensitivity and specificity values. By combining these three assessments, actual pathology can be more effectively determined, similar to that described previously for the labral tests by Liu and Henry.14 Just as with labral pathology, it is vital to recognize that impingement is often an accompanying diagnosis because of other causative factors.
Internal Impingement In the throwing athlete, the term internal impingement has been created to describe the condition in which the athlete reports pain at maximal external rotation associated with the throwing motion, also known as posterior impingement. The athlete is standing or seated and the arm is positioned at 90 degrees. The arm is then maximally externally rotated, and pain at the end range is considered positive if it replicates the chief complaint of what the athlete has perceived during throwing. Meister and coworkers16 have demonstrated a sensitivity of 75% and a specificity of 85% but these values were both greater than 90% if the onset was gradual and in an overhead thrower. At this point, the focus normally proceeds to individual musculotendinous structures. The reader is urged to review specific texts related to the intricacies of this process, such as Muscles: Testing and Function. Only a summary of the screening assessment will be presented here that relates to the most commonly involved muscle-tendon units in the overhead athlete.
Rotator Cuff Assessment (Primarily Supraspinatus and Infraspinatus) Integrity of the superior rotator cuff musculature is assessed through various loading techniques attempting to determine the supraspinatus and infraspinatus levels of function. Most clinicians use a combination of tests of active (movement to a position with additional resistance) and holding of a position (lag signs) to assess the function of these structures. Quantification of these tests is always a challenge because complete disruptions are often relatively easy to confirm, whereas combinations and partial disruptions are more difficult to delineate. Drop Arm Test. This classic test is designed to determine the function of the supraspinatus. The patient stands and elevates the arm to shoulder height in the scapular plane. The full can test is done with the thumb up while the empty can test is done with the thumb down. The examiner
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adds a downward force while the patient maintains the elevated position. Itoi and colleagues17 have reported that using the combination of pain and weakness yields a sensitivity of 86% and 89% with a specificity of 57% and 50%, respectively, for the full can and empty can positions. Note that the thumb down—empty can test—has a tendency of increasing pain but not improving diagnostic values. A modification that I often use is to make the patient lower the arm slowly against some downward force to assess the eccentric function of the supraspinatus. I frequently have seen this to be difficult for patients with small or possibly partial tears, which may be helpful in further reinforcing the likelihood of involvement. Significant weakness correlates highly with supraspinatus tears, particularly large tears. It is less reliable when it is more of a painful response rather than true weakness. In this case, the use of an injection to ablate pain can be helpful. I have examined a series of 25 patients with suspected involvement of the supraspinatus through the use of a posterior shoulder injection, xylocaine and corticosteroid. Isometric strength of the external rotators and abductors was measured before and after injection. If pain was ablated and strength increased, impingement is indicated, whereas ablation of pain but no resulting increase in strength indicates rotator cuff tear. Resisted External Rotation. The patient is seated with the arm in neutral position while the elbow is typically flexed 90 degrees. The examiner applies a force in the direction of internal rotation and the patient is asked to resist the force. The examiner compares right with left for determination of the normal. Significant weakness provides good sensitivity (more than 90%) but lower specificity (75%).18 Lag Signs of the Rotator Cuff. The use of positioning that requires stabilization against gravity is useful to elicit the lack of function of the cuff musculature. European researchers have used the hornblower’s sign (positioning of the arm to allow blowing of a horn) and maintaining external rotation while elevating the arm in the scapular plane to delineate this process; U.S. researchers refer to this as the lag sign. The most common sequence used is positioning the arm in the scapular plane and then passively positioning the humerus into external rotation maximally and asking the patient to maintain the rotation. Some examiners prefer to do this at 20 to 30 degrees of scapular abduction and others prefer higher levels of abduction. If higher abduction is used, the examiner must provide support under the elbow because supraspinatus involvement will preclude appropriate external rotation assessment when a significant tear of the supraspinatus is present. Hertel and colleagues19 have quantified the amount of drop and showed that if more than 10 degrees of drop is seen, patients are found to have combined tears of the
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supraspinatus and infraspinatus. These lag tests can thus have high sensitivities when significantly positive (more than 90%). Multiple variations of the tests are commonly described in textbooks and articles. The clinician is urged to read with a critical eye and apply a battery of tests whenever possible to better define pathology. Rehabilitation success is related to the actual structural involvement. Consequently, the better the evaluation, the greater the opportunity for predicting the nature of required care. I often proceed with strength and functional assessments after completion of the screen in the athlete, because dynamic function requires the synchronous interactions of active and passive elements, which are not assessed through traditional orthopedic examination and screening.
Strength Assessment Our assessment of muscular output is typically performed noninvasively. Thus, although muscle tissue is generating tension through its attachments by tendon to the skeletal system, the absolute tension-generating capacity of the muscle is not measured. Instead, changes in multiple components of the ability of the muscle to generate tension and alterations in the skeletal system, and corresponding changes in length-tension ratios, rotational orientation, compression, leverage, and angulation, are assessed.20,21 The operational definition of strength is delineated by the assessment methodology, which determines whether force, torque, power, and/or work values are measured. Some have recommended isometric assessment as the most appropriate method to minimize some of the alterations described earlier.22 The shoulder is a dynamic joint, because it completely depends on musculature for its stability and functional patterns. Although fraught with dangers, combining isometric assessment of individual muscle functions with dynamic assessment of movement patterns provides a clearer understanding of the tissues involved and appropriate intervention.
MUSCLE ACTIONS Characteristics of muscle action are presented in Table 3-2. The assessment of muscle action is best described as muscle activation, with the external load determining the observed function. This means that an object will be lowered with control, held in place, or raised by the applied muscular action. This obviates the problem of describing an eccentric activity as a muscle contraction when actually the muscle fibers are controllably lengthening. It is important for the clinician to determine whether the patient is describing difficulties with concentric or eccentric actions, because the inherent stability and functioning of the
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TABLE 3-2 Characteristics of Muscle Actions Type
Action
Level of Output/Unit Area Metabolic Demands
Isometric
Tension-producing, no motion
Moderate
Intensity-related
Isotonic
Movement of a resistance (weight) through a range of motion
Low/moderate
High
Isokinetic
Machine-controlled speed of motion
Low/moderate
High
Isotonic
Weight being lowered through a range of motion
Low
Low
Isokinetic
Machine-controlled speed of motion “driving” the muscle to a length while activated
High
Low (?) (best guess)
Concentric
Eccentric
shoulder complex require a controlled sequence of all three types of muscle activity or activation.
validity25 but, again, prevent assessment of the dynamic shoulder.
In general terms, eccentric contractions generate the highest tension per unit area of muscle, followed by isometric and concentric actions. Isometric assessment or action may be the best opportunity to assess tension capability of the active component of the musculature but may be of limited value in predicting functional capacity. Concentric actions can be performed isotonically or isokinetically but are frequently misinterpreted because of the inhibitory effects of effusion, pain, and altered recruitment.21,23
Cable Tensiometry. Cable tensiometers assess isometric output through a perpendicular tension assessment developed by Clarke.26 These devices have not gained wide acceptance in clinical settings and have been used primarily in a testing situation; they are generally not used for function or rehabilitation of patients.
Isometric Techniques Manual Muscle Testing Manual muscle testing is a frequently used system of manually applying loads against gravity or with gravity minimized to determine the voluntary response of the patient. Patients must be urged to be consistent in how they assess (make or break) and in their position of evaluation (midrange or locked) to minimize differing results.24 Problems of manual muscle testing include assessment of athletes who surpass normal and the tremendous difficulty in intertester reliability. The length of time allowed to generate tension and the ability to reproduce this on a repeated basis, coupled with the problems of multijoint muscle assessment, make manual muscle testing useful for screening patients but of limited value in attempting to assess muscular output objectively in the dynamic shoulder. Hand-Held Dynamometry. A number of hand-held dynamometers have been developed to enhance the objectivity of a manual examination. These devices have been shown to be acceptable clinically in terms of reliability and
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Isotonic Assessment Isotonic weight lifting involves the movement of a weight through a range of motion in raising (concentric) and lowering (eccentric). Problems include limitations by the neural drive through the central nervous system and inhibitions that may occur through the peripheral system. This includes the person’s ability to recruit muscle and his or her ability to use it in different formats, including concentric and eccentric patterns. This leads to the difficulty of endurance and repeatability of actions. The isotonic movement is limited to the weakest link, which is typically the maximal concentric pattern, such as 90 degrees of abduction at the glenohumeral joint. Factors vital to isotonic assessment include lever arm length and speed of movement. The perpendicular distance from the axis of rotation dictates the force required for the movement, whereas the person’s ability to move quickly and smoothly provides much information about the functional capability of the dynamic shoulder. A stronger individual can accelerate a particular weight in a freer and more controlled pattern than a weaker individual; however, this also requires looking closely at substitution and requirement of synchronous action before automatically accepting the performance of the stronger individual as being adequate. Inherent in the isotonic assessment are fatigue and completion of range of motion during testing.
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Isotonic measurements may reflect function, particularly in activities that require fairly slow movements. However, the average speed of isotonic assessment is approximately 60 deg/sec, and concentric assessment may not reflect eccentric performance.21,22,27 Clinicians will continue to use isotonic assessment but should recognize that it primarily reflects concentric performance unless additional loading is provided during assessment. I recommend this, particularly when assessing the supraspinatus and external rotators, because these are often functioning in an eccentric, stabilizing, and reducing pattern.
Isokinetic Assessment
51
must be determined. Assessment of strength is a multifaceted problem caused by the inability to take direct measurements and by the effects of such factors as neural drive, inhibition, pain, or changing lever arms. Although the ability to measure output has improved substantially, techniques directly related to function have not been developed. Because the shoulder joint is dynamic, caution must be exercised when interpreting muscular assessment results. Clinicians are urged not to overinterpret and use single pieces of data that are often provided by isokinetic devices.
FUNCTIONAL ASSESSMENT
Isokinetic exercise devices involve speed-controlled movements as the patient accelerates a lever arm to a predetermined maximal velocity and then moves through a range of motion and decelerates at the end of the range to the terminal position.28,29 One of the primary advantages of this type of assessment is the ability to evaluate individual muscle patterns in a dynamic orientation while providing some inherent stability to the testing positions. The information collected from these machines is in a machinespecific format; different machines handle the collected data through different software programs.30
Performance evaluation is a critical part of the evaluation schema. It is not unusual for no problem to be determined through clinical evaluation until more detailed information about dynamic shoulder function is obtained. This is why many practitioners now use the term clinical stability rather than functional stability. Functional stability requires neuromuscular integration and synchronous activity to enable the performance of high-demand dynamic movements.
Another use of isokinetics involves the evaluation of eccentric actions. Isokinetic (speed-controlled) eccentric actions can be performed two ways—by overcoming a predetermined load and having the lever arm drive the extremity at the predetermined velocity, or by having the individual work against a passively moving lever arm at the predetermined velocity. The neurophysiology of these actions may be different from the eccentric activity seen with isotonic actions, and again these actions are machinespecific in their interpretation. There is a different pattern of torque production with isokinetic concentric activity decreasing as speed increases compared with a relative plateau seen with eccentric peak torque assessment.21
The evaluation of performance should be directed toward the activities required of work or desired athletic pursuit, which is generally why the patient has come for evaluation. Thus, the evaluation of function should be patient specific. As noted, the clinician must attempt to determine not only the location of pain but also the actions of structures at that point in the functional pattern. Concentric pain usually indicates musculotendinous junction problems or impingement of bony, labral, or soft tissues. Eccentric pain is typically related to tendinous lesions or high-demand decelerative efforts to provide dynamic stability. Although this sounds fairly simplistic, the interpretation of functional activities can be extremely difficult and challenging for experienced as well as inexperienced clinicians.
Although clinicians have grown accustomed to the interpretation of isokinetic exercise being performance oriented, minimally true patterns of function or performance are being evaluated. The limitations of isokinetic assessment with open and closed kinetic patterns and with functional levels in speed being somewhat inconsistent must be recognized. For isokinetic assessment to have meaning, a standardized protocol for the evaluation should be followed.31 Evaluation via isokinetics should be accomplished only after the clinician has determined what he or she wishes to evaluate and the type of contraction that would be most appropriate, enabling meaningful information to be obtained. Thus, which plane of motion to evaluate and which would be the most appropriate testing position
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CONCLUSIONS The difficulty of assessing these components, which function in a dynamic pattern about this soft tissue structure, must be recognized. Shoulder evaluation must be systematic and activity specific. I recommend the use of a systematic screen that initially clears the capsule before specific structures are examined. As noted, not all problems are related to a single structure, which leads to difficulty in isolating pathology and best establishing the treatment sequence. Clinicians have a tendency to apply a single protocol of treatment that may not address all patterns or involved structures. The following case study exemplifies this problem.
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CASE STUDY A 15-year-old female swimmer with a 6-month history of bilateral shoulder pain (right greater than left) presented to our clinic with the previous diagnosis of impingement. Her treatment had included strengthening (internal rotators and external rotators), anti-inflammatories, and rest. Continued problems led her to receive bilateral corticosteroid injections with minimal response. Her radiographs had been negative and she had just been told that it is common for swimmers in her age group to continue to have such problems. We observed a healthy 15-year-old swimmer whose right shoulder was visibly lower than the left, as was the scapular position, with the right demonstrating a somewhat more protracted rest position; she had forward head posture and a very strong bilateral internal rotation bias. Her present swimming routine involved 3000 to 5000 meters in the morning followed by 3000 to 5000 meters in the afternoon, with most of these strokes being freestyle. Her routine had included the use of hand paddles during the past 6 to 8 months, when she also developed her impingement problems. Range-of-motion evaluations, both active and passive, revealed an internal rotation limitation of approximately 10 degrees bilaterally, but she moved her scapulae and trunk to achieve the additional movement. Her instability assessment revealed a positive posterior apprehension test on the right, as well as a similar apprehension relation on the right. She had some posterior labral tenderness on the right during testing and also exhibited positive impingement bilaterally.
STRENGTH ASSESSMENT Her manual muscle test revealed weak external rotators with very strong internal rotators. Her isokinetic assessment (prone data) revealed a 42% external rotation–to–internal rotation ratio.
FUNCTIONAL ASSESSMENT Her activities obviously revolved around swimming and her associated training techniques. She had been doing a strengthening routine but continued to emphasize internal rotators rather than attempting to correct the imbalance with her external rotators. It was important when testing her to do the testing in a prone position to duplicate her functional positions. Our assessment led to the recognition that she does have impingement, but it is secondary to lack of humeral head
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control associated with instability. She also has an activityrelated problem with swimming, particularly with emphasis on the use of hand paddles. As her external rotation strength was enhanced and her use of hand paddles eliminated, her symptoms began to resolve rapidly. She became essentially asymptomatic when a 50% external rotation–to–internal rotation ratio was achieved. Frequently, a person who has some instability and impingement overlap may do fairly well if dynamic control is enhanced. As with most clinical activities, evaluation is the key. Proper rehabilitation and interventions can be provided only when the specific structure is enhanced within an overall context. The goal of the clinical examination must be to establish the nature and severity of the injury or pathology and dysfunction, and to address these most appropriately.
References 1. Andrews JR, Gillogly S: Physical examination of the shoulder in throwing athletes. In Zarins B, Andrews JR, Carson WG (eds): Injuries to the Throwing Arm. Philadelphia, WB Saunders, 1985, pp 51-65. 2. Cyriax J: Textbook of Orthopaedic Medicine, 8th ed. Philadelphia, Bailliere Tindall, 1982. 3. Hoppenfeld S: Physical Examination of the Spine and Extremities. East Norwalk, Conn, Appleton-Century-Crofts, 1976. 4. Magee DJ: Orthopaedic Physical Assessment. 4th ed. Philadelphia, WB Saunders, 2002. 5. Liu SH, Henry MH, Shapiro MS, et al: Diagnosis of glenoid labral tears: A comparison between magnetic resonance imaging and clinical examinations. Am J Sports Med 24: 149-154, 1996. 6. Hawkins RJ, Schutte JP: The assessment of glenohumeral translation using manual and fluoroscopic techniques. Orthop Trans 12:727-728, 1988. 7. Neer CS, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897-908, 1980. 8. Lo IK, Nonweiler B, Woolfrey M, et al: An evaluation of the apprehension, relocation, and surprise tests for anterior shoulder instability. Am J Sports Med 32:301-307, 2004. 9. Speer KP, Hannafin JA, Altchek DW, et al.: An evaluation of the shoulder relocation test. Am J Sports Med 22:177-183, 1994. 10. Chronopoulos E, Kim TK, Park HB: Diagnostic value of physical tests for isolated chronic acromioclavicular lesions. Am J Sports Med 32:655-661, 2004. 11. O’Brien S, Pagnani M: The active compression test: A new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med 26:610-613, 1998. 12. Mimori K, Muneta T, Nakagawa T, et al: A new pain provocation test for superior labral tears of the shoulder. Am J Sports Med 27:137-142, 1999.
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13. Kim SH, Ha KI, Ahn JH, et al: Biceps load test. II: A clinical test for SLAP lesions of the shoulder. Arthroscopy 17:160164, 2001. 14. Liu S, Henry M: A prospective evaluation of a new physical examination in predicting glenoid labral tears. Am J Sports Med 24:721-725, 1996. 15. Calis M, Akgun K, Birtane M, et al: Diagnostic values of clinical diagnostic tests in subacromial impingement syndrome. Ann Rheum Dis 59:44-47, 2000. 16. Meister K, Buckley B, Batts J: The posterior impingement sign: diagnosis of rotator cuff and posterior labral tears secondary to internal impingement in overhead athletes. Am J Orthop 33:412-415, 2004. 17. Itoi E, Kido T, Sano A, et al: Which is more useful, the “full can test” or the “empty can test” in detecting the torn supraspinatus tendon? Am J Sports Med 27:65-68, 1999. 18. Lyons A, Tomlinson J: Clinical diagnosis of tears of the rotator cuff. J Bone Joint Surg Br 74:414-415, 1992. 19. Hertel R, Ballmer FT, Lombert SM, et al: Lag signs in the diagnosis of the rotator cuff rupture. J Shoulder Elbow Surg 5: 307-313, 1996. 20. Williams M, Lissner HR: Biomechanics of Human Movement. Philadelphia, WB Saunders, 1966. 21. Malone TR: Muscle injury and rehabilitation. In Sports Injury Management, vol 1, no. 3. Baltimore, Williams & Wilkins, 1988, pp 43-74.
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22. Rothstein JM: Measurement in Physical Therapy. New York, Churchill Livingstone, 1985. 23. DeAndrade J, Grant C: Joint distension and reflex inhibition in the knee. J Bone Joint Surg 47:313-322, 1965. 24. Poland J, Hobart D, Payton O: The Musculoskeletal System. Garden City, NY, Medical Examination Publishers, 1981. 25. Bohannon R: Test-retest reliability of hand-held dynamometry during a single session of strength assessment. Phys Ther 66:206-209, 1986. 26. Clarke HH: Cable Tension Strength Test: A Manual. Springfield, Mass, Stuart E. Murphy, 1953. 27. Sanders M, Sanders B: Mobility: Active-resistive training. In Gould J, Davies G (eds): Orthopaedic and Sports Physical Therapy. St. Louis, Mosby, 1985, pp 228-241. 28. Davies G: A Compendium of Isokinetics in Clinical Usage, 2nd ed. LaCrosse, Wis, S&S Publishers, 1985. 29. Lesmes GR, Costill DL, Coyle EF, Fink WJ: Muscle strength and power change during maximal isokinetic training. Med Sci Sports 10:266-269, 1978. 30. Malone TR: Evaluation of isokinetic equipment. In Sports Injury Management, vol 1, no. 1. Baltimore, Williams & Wilkins, 1988, pp 1-90. 31. Wilk KE, Arrigo CA, Andrews JR: Standardized isokinetic testing protocol for the throwing shoulder: The throwers’ series. Isokin Exerc Sci 1:63-71, 1991.
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CHAPTER 4 Clinical Examination of the
Shoulder Complex Michael J. Kissenberth, James F. Silliman, and Richard J. Hawkins
An accurate and thorough examination can only be performed in a relaxed environment. The patient should be clothed so that he or she is relaxed, but the examiner should have adequate visibility of both shoulder girdles and the upper trunk. The examination is performed with the patient standing, sitting, supine, or prone, as necessary. The history often influences the clinician to focus on a specific aspect of the examination, but an organized screening examination should be performed on every patient. Because of the interaction of the many factors contributing to the symptom complex in these athletes, it is essential to have a thorough understanding of the entire shoulder girdle, especially the glenohumeral and scapulothoracic interplay. The athlete’s shoulder creates many diagnostic dilemmas because of the fine balance between extreme mobility and instability.
Successful management of any clinical problem begins with an accurate history and physical examination. This chapter will describe physical examination of the athlete’s shoulder. Overhead athletes who swim, throw, and serve present with special problems. The extreme forces that act on the shoulder girdle during these activities cannot be re-created in a typical examination. With new technology for assessment, such as motion analysis, we now know that these forces often exceed the physiologic limits of the capsuloligamentous restraints of the rotator cuff.1 If the rate of injury (overuse) exceeds that of repair, impairment and dysfunction result.2 As we have advanced in our understanding of the throwing shoulder, we also see loss of internal rotation and posterior capsular tightness as an early manifesting symptom. Pain is often the most common manifesting symptom.3 The emphasis on the cause of this pain has evolved from biceps3,4 and rotator cuff impingement tendinitis5-9 to anterior instability and posterior capsular tightness, with obvious overlap among these causes in many athletes.
We suggest an organized, thorough, and consistent format when examining an athlete’s shoulder. Re-creation of the patient’s symptoms with certain maneuvers may help the examiner arrive at an accurate diagnosis. Great variability exists from patient to patient in regard to range of motion, joint laxity, and strength. Often, certain sports require emphasis on different aspects of these facets. For example, gymnastics demands hypermobile or hyperlax joints, and weightlifting demands excess strength. Often, the final question before beginning the examination is to ask the patient to point with one finger and touch the area where the problem is located. The examination proceeds in the following sequence, remembering that presentation can be in the acute setting immediately after an injury or, more often, in a chronic situation presenting to the clinic or office.
Prior to beginning the clinical examination, it is imperative to obtain a chief complaint, an accurate history, and a full understanding of the athlete’s sport, level of participation, position played, motivation, and expectations. For example, a baseball pitcher who has thrown many pitches may have tendinosis, labral tears, or subtle anterior instability. A football player who falls and has a traumatic injury may have dislocated the shoulder or fractured the clavicle. A thorough understanding of the initial event or injury is helpful in the initial development of a differential diagnosis. Communication with the family and athletic trainer is also helpful in obtaining additional objective information and feedback regarding the athlete and the injury. It is essential to ask the patient if he or she has had any prior treatment to include periods of rest, injection, physical therapy, and medication. The location and response to the injection can provide valuable information before beginning the examination. Often, the athlete arrives with a magnetic imaging resonance (MRI) scan and a presumptive diagnosis based on the MRI reading. Although this is often helpful information, the MRI scan can often lead the physician down the wrong path and should not influence the initial examination. We recommend waiting to review the MRI scan until after the history and examination have been completed.
INITIAL EVALUATION Cursory Impression On first visualizing the athlete, an initial cursory impression encompassing many factors is formed. For example, a large muscular individual with a mesomorph frame obviously suggests someone in a strength-type of sport, such as weightlifting or football. A petite young woman might well suggest involvement in gymnastics. In analyzing these patients, we may see those who have an acute injury presenting with significant pain, which influences our approach to the situation. The older athlete presenting to the office in a business suit presents a different impression 55
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than the 6-foot 10-inch basketball player who walks into the athletic clinic directly from practice.
Inspection Inspection should be performed from different perspectives— that is, from the front, side, back, and top—noting attitude (symmetry), muscles (wasting or hypertrophy), deformities (e.g., scars, lumps, bumps), any evidence of discoloration such as bruising and swelling. The way the athlete carries the upper trunk and shoulders provides clues as to the diagnosis. For example, an athlete with a painful shoulder may show asymmetry between the trapezius contours when looking from the front and back. Dominance may lead to asymmetry between the sizes and contours of the different shoulder girdle muscles. The symmetry of the borders of the clavicle, acromioclavicular joint, and sternoclavicular joints should also be noted. Deformities in these areas are often revealing. Scars should be inspected, not only as evidence of previous surgical procedures, but also for widening or spreading of the scars, which may denote a collagen abnormality, as seen in patients with multidirectional instability.10 Evidence of wasting of different muscles or muscle groups may suggest certain diagnoses. Deltoid wasting may appear as prominence and squaring of the acromial borders. Supraspinatus and infraspinatus wasting can be related to rotator cuff tear11 or, rarely, to suprascapular nerve injury (Fig. 4-1).12 In particular, infraspinatus atrophy is often a sign of a large rotator cuff tear in an older patient; however, in a throwing athlete, a cyst in the spinoglenoid notch causing compression on the suprascapular nerve must be considered.13 Occasionally, hypertrophy of a muscle such as the trapezius may be caused by muscle spasm. A patient with a recent injury may have bruising, with associated discoloration. Swelling and discoloration are uncommon in chronic complaints but often manifest with acute trauma.
Figure 4-1. Supraspinatus and infraspinatus atrophy. Atrophy is caused by compression of the suprascapular nerve.
From behind the standing patient, the scapulothoracic joint with forward flexion and abduction is observed. Scapular winging can be demonstrated by asking the patient to elevate the arms forward at about half speed, with maximum winging usually demonstrated by applying resistance at about 30 degrees of forward elevation. The patient can also be asked to perform a wall push-up (Fig. 4-2). Ligamentous laxity can be observed with extension of the elbow or a thumb-to-forearm examination (Fig. 4-3).
Observation Before focusing on range of motion about the shoulder, it is helpful to appreciate glenohumeral and scapulothoracic synchrony. Beginning at 30 degrees of abduction, every 30 degrees of glenohumeral abduction relate to 12 degrees of scapular rotation.14-16 Dyskinesia or asynchrony of this coupled mechanism can be related to loss of range of motion or guarding. Weakness of the scapular stabilizers with resultant scapular winging can be part of the symptom complex of anterior shoulder pain, especially in the throwing athlete. It is common for the throwing athlete or patients with subtle forms of multidirectional and posterior instability to have scapular winging. This is usually not related to a neurologic deficit but rather to dyskinesia of the scapulothoracic articulation.
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Figure 4-2. Scapular winging. Winging is present bilaterally by applying resistance at 30 degrees of forward elevation.
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A
Palpation As noted, it is helpful to ask the patient to point with one finger and touch the area of maximum tenderness. Thorough palpation of the shoulder girdle is now performed, noting warmth, tenderness, deformity, and crepitus. It is often helpful, as confidence of the patient is gained, to wait and palpate the area of maximum tenderness at the end of this part of the examination. Starting from the back, palpation of the cervical spinous processes, scapular spine, medial border of the scapula, and scapular angle may reveal tender areas. Scapulothoracic bursitis at the inferior medial angle of the scapula may manifest in baseball pitchers.17,18 Superior angle tenderness and snapping in the tennis serve are common manifesting complaints. The posterior cuff and joint capsule should be palpated deep to the infraspinatus muscle belly. The posterior cuff is often tender, not only with posterior instability but also with internal impingement.13 Posterior capsular ossification can lead to significant pain and dysfunction during the throwing motion.19 Palpation of the rhomboids, latissimus, supraspinatus, and infraspinatus can provide an assessment of their tone. Palpation of the quadrilateral space below the posterior joint is an important area to localize and palpate, especially in overhead athletes, because of possible compression of the neurovascular structures when the arm is in maximum abduction and external rotation, the cocking position.20 The quadrilateral space is bordered by the teres minor superiorly, the teres major inferiorly, the humerus laterally, and the long head of the triceps medially. Clinical findings include vague pain and paresthesias around the shoulder and pinpoint tenderness at the quadrilateral space. From the back, the location of the bicipital tendons can be palpated simultaneously to ascertain tenderness (Fig. 4-4).
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B
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Figure 4-3. Ligamentous laxity and hypermobility. These can be appreciated from observing the patient’s hyperextensible elbows (A) or the thumb-to-forearm examination (B).
The clinician can locate the bicipital groove by directing his or her fingers anteriorly and distally to the acromioclavicular joint, with the patient’s arm in approximately 10 degrees of internal rotation. Moving to the front of the standing or seated patient and palpating the sternoclavicular joint statically, and with arm rotation, may reveal tenderness, crepitus, or even instability. The clavicle and acromioclavicular joint are also palpated in this way. It is important to palpate the acromion and not to forget about the symptomatic os acromiale. A common injury in the collision athlete, especially in football, is to the acromioclavicular joint.21 Acutely, athletes can present with a wide range of severity of injury and deformity to this joint, with varying degrees of
Figure 4-4. Bicipital groove palpation. Palpating both grooves at the same time serves as a good comparison examination for tenderness.
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prominence of the outer clavicle. The classification scheme of Rockwood and Green22 is useful for appropriate management. Chronic injury to the acromioclavicular joint can lead to hypertrophy, pain, instability, and degenerative joint disease. A symptomatic acromioclavicular (AC) joint is often tender to palpation and the cross-arm adduction test is used as a provocative maneuver to elicit pain at this joint.23 The arm is forcibly adducted across the chest wall, producing pain on top of the shoulder (Fig. 4-5). This test can be positive with labral tears and with cuff pathology, so it is important to have the patient indicate where this test causes pain. Pain felt deep in the shoulder may occur because of a superior labral anterior-posterior (SLAP) tear (see later). The Paxinos test can also help diagnose AC joint pathology. This is accomplished by compressing the AC joint with the index finger anterior to the clavicle and the thumb on the posterior edge of the acromion.24 Injection of 5 mL of 1% lidocaine directly into the joint, with relief of the symptomatology in the cross-arm test, can assist in the diagnosis of primary acromioclavicular pathology. The subacromial arch is assessed initially with palpation of the greater tuberosity and supraspinatus insertion (Codman’s point). With circumduction of the arm, an appreciation of the crepitus is important, especially in rotator cuff disease and degenerative joint disease of the glenohumeral joint. A positive clunk test or labral grinding can suggest labral pathology.25 Palpable crepitus or grinding, with the arm abducted to 90 degrees and the humeral head translated to the anterior rim of the glenoid with a
Figure 4-5. Cross-body adduction test for acromioclavicular joint pathology.
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posterior force (prone or seated), and rotation of the arm, is considered positive (Fig. 4-6). Attention to the contralateral shoulder is also important and useful in palpating painful areas to use as a comparison and to validate clinical findings. There will likely be physiologic adaptations to the throwing shoulder in regards to muscle girth and range of motion (excessive external rotation) that must be taken into account during the examination.
Range-of-Motion Assessment The rhythm and synchrony of scapulothoracic and glenohumeral motion have been discussed. Athletes are often selectively or generally hypermobile in performing their different movements. For example, accomplished baseball pitchers sometimes show extremes of external rotation at the expense of internal rotation.18 However, the total arc of rotation (external rotation plus internal rotation) usually remains similar to that of the contralateral shoulder (Fig. 4-7). Pathology and glenohumeral internal rotation deficit (GIRD) may exist if the total arc of motion is 25 degrees less than that of the contralateral shoulder (Fig. 4-8).13 A pitcher will usually have excessive external rotation and a concomitant loss of internal rotation. As long as the total arc of motion is similar to that of the contralateral shoulder, an internal rotation deficit does not exist. The quality of the examination is often improved
Figure 4-6. Crank test. This test is performed by placing the abducted arm to 90 degrees, translating the humeral head anteriorly by posterior force, and palpating and feeling for crepitus, or grinding, on the anterior rim of the glenoid.
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A
59
B
Figure 4-7. Total arc of motion. A, Maximum external rotation. B, Maximum internal rotation. With the patient in the supine position, with the shoulder abducted to 90 degrees, maximum external and internal rotation are recorded. The scapula is stabilized. The other shoulder is compared and a difference of more than 25 degrees can be a sign of a glenohumeral internal rotation deficit (GIRD).
by using a worksheet to record range of motion. Examination for different ranges in different circumstances can be performed with the patient standing, sitting, or supine, depending on clinician preference. From behind the standing patient, active forward elevation is observed. The patient is allowed to flex his or her arm in the plane that is most comfortable, usually somewhere between the sagittal and scapular planes, and with the thumbs pointing upward (Fig. 4-9). Once the patient has achieved maximum active range, passive range is assessed by stressing the arm into forward elevation. This represents the classic impingement sign (see later). The passive range is recorded bilaterally in degrees. External rotation is evaluated with the arm at the side and at 90 degrees of abduction in much the same manner. Internal rotation is measured by determining where the abducted thumb reaches in reference to spinal vertebrae (Fig. 4-10). These four motions—forward elevation, external rotation at neutral and 90 degrees, and internal rotation—should be the motions selected for documentation in the athlete, according
A
to the American Shoulder and Elbow Surgeons (ASES). Strength assessment is described in the next section, but it is determined as range-of-motion testing is performed.
Strength Assessment Strength is easy to assess from behind the standing or sitting patient and can be performed in concert with rangeof-motion assessment. Unfortunately, the presence of pain may preclude a reliable assessment of strength. The routine strengths to be assessed in the athlete’s shoulder consist of forward elevation, external rotation, internal rotation, and abduction. Strength assessment is performed while testing and comparing the opposite normal side. As with all muscle testing, the muscle being tested should be given the mechanical advantage. All muscle testing should be graded using the 0 to 5 rating system (Table 4-1). Forward elevation strength (anterior deltoid) is assessed with resistance applied to the forward-flexed arm at approximately 70 to 80 degrees. External rotation strength
B
Figure 4-8. Arc of motion. A, Maximum external rotation. B, Maximum internal rotation. Note the increased external rotation that is usually seen in a thrower and the internal rotation deficit that may be present.
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A
Figure 4-9. Forward elevation.
assesses the strength of the rotator cuff, which contributes 30 to 40 degrees of the power of elevation and 80% to 90% of the power of external rotation.26 Abduction strength is also assessed in the coronal plane, and weakness may be suggestive of deltoid or cuff deficiency. At this point in the examination, there is some confluence of testing, because strength tests become part of the special diagnostic tests used to determine rotator cuff pathology, instability, and overuse throwing conditions. Therefore, specific shoulder muscle tests will be described later in this chapter.
IMPINGEMENT AND ROTATOR CUFF PATHOLOGY Impingement syndrome and rotator cuff pathology are common conditions affecting the overhead athlete and can frequently result in pain, weakness, instability, or a combination of symptoms. Pain in rotator cuff pathology often involves night pain and difficulty lying on the affected extremity. After completing the initial part of the examination, specific tests can be used to evaluate the integrity of the rotator cuff musculotendinous structures. The three impingement signs are assessed in forced elevation, forced internal rotation, and the classic painful arc. From the front of the seated or standing patient, passively stressed maximum forward elevation, which elicits pain as the rotator cuff opposes the anterior acromial arch, is the classic Neer’s impingement sign (Fig. 4-11).6,8 The Hawkins sign is elicited by placing the arm in 90 degrees of forward flexion, with the elbow flexed to 90 degrees. Pain with
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B Figure 4-10. Active rotation. A, Active external rotation. B, Active internal rotation.
forced internal rotation of the arm can be provoked by opposing the rotator cuff on the acromion and coracoacromial ligament; this is another impingement sign (Fig. 4-12).5,27 A painful arc in the abducted position in the coronal plane is also an impingement sign. This pain is often increased with resistance and by placing the arm posterior to the plane of TABLE 4-1 Rating System for Muscle Testing Grade
Descriptive Term
0, zero
Nothing
1, trace
Trace
2, poor
Gravity eliminated
3, fair
Against gravity
4, good
Near-normal
5, excellent
Normal
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Figure 4-13. Painful arc sign for impingement. Figure 4-11. Neer’s impingement sign.
signs of impingement.3 These signs are 88% to 92% sensitive, but are all somewhat nonspecific. The yield from the impingement sign is improved by evaluation of an injection test. The subacromial space is injected with 10 mL of 1% lidocaine, and the impingement tests are repeated. Abatement of pain postinjection suggests subacromial pathology.28 It is important to document the percentage of improvement after any injection because it is a prognostic indicator for surgery and provides helpful information at follow-up visits.
Figure 4-12. Hawkins’ sign.
the scapula in the coronal plane (Fig. 4-13). The stressed cross-arm adduction test can be performed and is suggestive of acromioclavicular pathology, as described earlier. Traumatic osteolysis of the distal clavicle seen in weightlifters can manifest with this positive sign, and frequently with
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The following tests can evaluate the strength and integrity of the rotator cuff. They involve standard strength testing of the specific muscles and lag tests to demonstrate weak musculotendinous units. The supraspinatus test, as described by Jobe and Jobe,17 isolates and assesses the strength of the supraspinatus tendon (Fig. 4-14). The strength of elevation is assessed at 90 degrees of forward flexion in the scapular plane, with the thumbs pointed to the floor. Downward pressure is resisted by the patient.17,29 This test is supposedly specific for evaluation of the supraspinatus function and reasonably accurate for assessment of rotator cuff strength and integrity. Unfortunately, many patients have pain, precluding the reliability of such a test. Because this test can be painful, the full can test has been described as an alternative. The thumbs are pointed up and the test is repeated as described for the Jobe test (Fig. 4-15). Resisted external rotation is then performed with the elbows flexed at the sides to assess the strength of the infraspinatus
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Figure 4-14. Jobe test for supraspinatus function.
tendon (Fig. 4-16). As with all strength tests, the normal shoulder is used as a comparison, and asymmetrical strength is documented and considered a significant finding. An external rotation lag test is used to demonstrate weakness of the infraspinatus and, when positive, is indicative of a significant tear in the musculotendinous unit. This test is accomplished by placing the patient’s shoulder at the side in neutral abduction and externally rotating the forearm; the patient then is asked to hold that position.30,31 With a fullthickness rotator cuff tear or dysfunction involving the supraspinatus and infraspinatus, the forearm will spontaneously rotate back to neutral. This test can also be performed with the shoulder in 90 degrees of elevation in the scapular plane, with the elbow flexed to 90 degrees; this is called a drop sign. The patient is then asked to maintain this position. The sign is positive if a lag or drop occurs.
Figure 4-16. External rotation (infraspinatus) motor testing.
Gerber has popularized the liftoff test to evaluate subscapularis strength and integrity. The patient is asked to lift the back of his or her hand away from the lumbar spine; this may suggest an intact subscapularis (Fig. 4-17). If performed properly, this test is reliable to identify a subscapularis
Figure 4-15. Supraspinatus thumbs up test.
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Figure 4-17. Liftoff test for subscapularis integrity.
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rupture; however, the patient will often recruit the triceps, which can lead to a false-negative test result. Technique is critical; it is necessary for the patient to keep the upper arm relaxed while performing the test. There are several variations. The same liftoff test can be performed like a lag test (internal rotation lag sign) by positioning the patient’s hand away from the small of the back and then asking the patient to hold that position. If the hand spontaneously returns to the small of the back, it is highly suggestive of subscapularis dysfunction (Fig. 4-18). The belly press test has been described as an alternative to the liftoff test, especially for patients with internal rotation contractures.20 This test is performed by having the patient place both hands on the upper abdomen and attempting to keep the arm in maximum internal rotation, with and without resistance. With a normal subscapularis, the elbow stays anterior and does not drop backward (Fig. 4-19). Both these tests have been validated for the determination of subscapularis integrity and should be parts of all shoulder examinations.
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A
BICEPS AND SLAP CONDITIONS Much attention has been given to the biceps and superior labral structures in the throwing athlete recently. There is often a mixed picture, with positive SLAP and biceps findings in patients with rotator cuff problems and those with instability. Therefore, we will describe the tests for extraarticular biceps involvement and intra-articular SLAP tears separately—these tests are performed as part of a comprehensive shoulder examination. Biceps tendon involvement
B Figure 4-19. Belly press test for subscapularis integrity. A, Intact subscapularis. B, Deficient subscapularis. Electromyographic studies have shown that this is a better test for the upper subscapularis tendon.
may be evaluated with the tests of Speed and Yergason.29 Speed’s test is performed with the shoulder in forward flexion, elbow extended, and hand supinated with applied resistance (Fig. 4-20). Pain in this position from the area of the bicipital groove is a positive finding suggestive of bicipital tendinitis.32 Resisted supination with the elbow flexed to 90 degrees is Yergason’s test.8 Once again, pain in the bicipital region with this maneuver is considered positive for biceps tendon involvement (Fig. 4-21). These are not strength tests and, if positive, are suggestive of extra-articular biceps involvement. An arthroscopic analysis of the Speed’s test has shown a specificity of 14% and a sensitivity of 90%.33 Figure 4-18. Internal rotation lag test. This is a modification of the liftoff test.
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SLAP lesions have been discussed by Snyder and associates34 and several tests were described in an attempt to
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diagnose tears to the superior labrum on physical examination accurately. As noted, much attention has been given to SLAP tears in baseball pitchers and to understanding the disabled throwing shoulder. Burkhart and colleagues13 have advanced our understanding of SLAP tears; they hypothesized that posterior capsular contracture initiates the cascade of events that eventually lead to a positive peel back of the posterior superior labrum in the late cocking phase of throwing. It is important to evaluate the arc of rotation and loss if internal rotation closely in any thrower, especially those presenting with signs and symptoms of a SLAP tear. The SLAP lesion can also be an acute injury that can be caused by a traction type of injury or a compressionshear type of injury from the humeral head. In general, the examination tests described to identify superior labral lesions attempt to pull on the torn structures with tension and rotation or push on the torn structures with the humeral head. Patients with SLAP tears often complain of a deep pain in the shoulder. The tests are positive if this deep pain is produced during the provocative maneuver. As with all tests, diagnostic injections are critical to confirm the presumed diagnosis. Figure 4-20. Speed’s test for long head of biceps pathology.
The active compression test described by O’Brien is one of the more commonly performed tests. It is accomplished by standing behind the patient. The patient is asked to forwardflex the arm to 90 degrees, with the elbow in full extension against resistance (Speed’s test). The arm is then adducted 10 to 15 degrees medially to the sagittal plane of the body, with the arm internally rotated (thumb down), and resistance is again applied. With the arm in the same position, the test is repeated with the palm facing upward. The test is considered positive if pain is elicited during the maneuver with the thumb pointing down and relieved with the palm facing up (Fig. 4-22).35 This test will often be positive with impingement and with acromioclavicular pathology, so it is important to ask the patient to localize the pain during the test. The results have been shown to be positive in 95% of patients with superior labral pathology. Often, we have also found the test positive with other labral pathology. The O’Driscoll SLAP test is performed with the patient supine or upright. The shoulder is maximally abducted and externally rotated. From this position, a moving valgus stress is applied in an attempt to push the humerus against the superior labrum.20 Pain is considered a positive response. This is similar to the compression-rotation test as described by Snyder and coworkers,34 except that the arm is placed in maximum abduction and external rotation. We have found this test to be sensitive but not specific. The crank test, as described earlier, may also be found positive in SLAP tears.
Figure 4-21. Yergason’s test for biceps pathology.
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There are many alternative SLAP tests and most produce fairly good sensitivities and specificities, but it must be stressed that none of the tests is absolutely diagnostic of a
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A
B
Figure 4-22. O’Brien’s active compression test for superior labral anterior-posterior (SLAP) lesions. A, Test performed with palm down. B, Test repeated with palm up.
SLAP tear. Any of the positive tests can be repeated after the injection of 10 mL of 1% lidocaine into the glenohumeral joint. Abatement of pain after the injection is further confirmation of intra-articular involvement. The results of these tests, with an accurate history and comprehensive examination, can be helpful in arriving at an accurate diagnosis.
GLENOHUMERAL STABILITY ASSESSMENT Glenohumeral instability is assessed by provocative maneuvers, such as an apprehension sign. It is also assessed by translation, anteriorly and posteriorly, of the humeral head in the glenoid fossa, as well as inferior translation with a sulcus sign. During these maneuvers, it is important to ask the patient whether there is any reproduction of the symptom complex. It is not uncommon for the throwing athlete to present with shoulder pain and have an underlying degree of subtle anterior instability. Similarly, it is not uncommon for the hyperlax and hypermobile patient to have an element of multidirectional instability. Many patients also present with arm weakness or heaviness, the so-called dead arm syndrome.36-38 Therefore, it is imperative to consider the patient’s pain symptoms during the examination as an important aspect of any provocative testing. Initially, the patient should be as relaxed as possible. It is often prudent to begin the stability assessment with the
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contralateral or uninvolved shoulder to gain the patient’s confidence during the examination. The stability assessment begins with the load and shift examination. When assessing the amount of translation, it is important to ensure that the humeral head is initially reduced concentrically into the glenoid fossa (i.e., loaded). In patients with significant laxity, the humeral head may have a resting position that is nonconcentric. Hence, at the commencement of any stress testing, the humeral head must be grasped and pushed into the glenoid fossa to ensure its reduction in neutral position.39 Once the humeral head is loaded, directional stresses may be applied. To perform this maneuver, the examination initially involves assessment of the patient sitting and the examiner located beside and behind the side to be examined. The examiner places his or her hand over the shoulder and scapula to steady the limb girdle and then, with the opposite hand, grasps the humeral head. As the head is loaded, anterior and posterior stresses are applied and the amount of translation is noted (Fig. 4-23). Next, the elbow is grasped and inferior traction is applied. The area adjacent to the acromion is observed and dimpling of the skin may indicate a sulcus sign (Fig. 4-24). A positive sulcus sign may be seen in patients with multidirectional instability (MDI), but also can be positive in patients with combined labral and rotator interval lesions. It is important to differentiate between generalized laxity and instability. A positive test should reproduce the patient’s symptoms. An increased sulcus sign as compared with the asymptomatic shoulder is helpful and should be documented by recording how much the humeral head is translated inferiorly from the acromion (in millimeters). If a positive sulcus sign is identified, the test should then be repeated with the arm externally
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A Figure 4-24. Sulcus sign.
B Figure 4-23. Determining the amount of translation. A, Sitting anterior load shifting. B, Sitting posterior load shifting.
A
rotated 20 to 30 degrees; if still positive, it can be suggestive of a rotator interval deficiency. Glenohumeral translation is also assessed with the patient supine. The arm is grasped in the position of approximately 20 degrees of abduction and forward flexion in neutral rotation. The humeral head is loaded and posterior and anterior stresses are applied. Inferior stress is applied again, noting the sulcus sign (Fig. 4-25). The accuracy of this test will depend not only on the examiner’s skill but on the ability of the patient to relax. In some patients with associated tendinitis, it is too painful to grasp the humeral head between the thumb and fingers. In this situation,
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B Figure 4-25. Load shift test. A, Supine anterior load shift test B, Posterior load shift test.
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grasping the upper arm distally to the shoulder may be the only method of assessing translation but is less reliable. It is helpful to have a grading system of translations so that the translation can be understood in relation to any instability pattern that may or may not be present. It is impractical to use distances or percentages. Two important situations may occur during this examination. First, the examiner may feel the humeral head ride up to the face of the glenoid but not over the rim (grade I). Second, the head may be felt riding over the rim but reduces when the stress is released (grade II). In some cases, at least under anesthesia, once the stress is released, the head sometimes remains dislocated. For purposes of simplicity, this should probably not receive a separate grade. It is important during these maneuvers to ask the patient if this in any way reproduces the symptom complex. If affirmative, this might be a significant clue toward diagnosis and direction of instability, especially for posterior instability. Anterior and posterior drawer tests have also been described.40 These are variations of the glenohumeral translation test analogous to the Lachman test of the knee. They are performed with the patient in the supine position to make measurements more reliable. The affected shoulder is held in 80 to 120 degrees of abduction, 0 to 20 degrees of forward flexion, and 0 to 30 degrees of lateral rotation. While pressing the scapular spine forward with counterpressure on the coracoid process, the relative movement between the fixed scapula and the moveable humerus can be appreciated. Occasionally, a positive grind test can be felt during this maneuver, noting labral pathology. The posterior drawer test is performed with the elbow at 120 degrees of flexion and the shoulder in 80 to 120 degrees of abduction and 20 to 30 degrees of forward flexion. Again, the scapula is stabilized, and a posterior directed force is placed on the humeral head with the thumb.
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of the arm when subluxation or dislocation occurs is abduction in external rotation. The apprehension test for anterior instability can be performed with the patient in the supine or seated position, although maximum muscle relaxation is best achieved with the patient supine. With the patient sitting, the examiner stands behind the shoulder to be examined. To assess the patient’s left shoulder, the examiner raises the patient’s arm to 90 degrees of abduction and begins to rotate the humerus externally. The right hand of the examiner is placed over the humeral head, with the thumb pushing from posterior for extra leverage and with the fingers anterior to control for any sudden instability episode that may occur (Fig. 4-26). With increasing external rotation and controlled general forward pressure exerted against the humeral head, an impending feeling of anterior instability may be produced— an apprehension sign. An apprehensive look may appear on the patient’s face as he or she contracts his or her muscles to prevent dislocation or, if the stress is continued, he or she may volunteer that the shoulder feels like it will come out. Pain alone is not a positive apprehension sign, although it is often present. The apprehension test can be repeated with the patient supine (Fig. 4-27). The shoulder to be examined is positioned so that the scapula is supported by the edge of the examining table and the proximal humerus is then stressed in varying degrees of abduction and external rotation, again attempting to reproduce impending instability. In the supine position, the body acts as a counterweight. The
Significant expansion of information about the athlete’s shoulder has come from advances in arthroscopy.41 During arthroscopy, particularly under general anesthesia, an appreciation of glenohumeral translation can be obtained. This is sometimes important when completing the examination of the athlete who has a confusing diagnosis and has arrived at the stage of surgical reconstruction.42 The next phase of stability assessment is to attempt reproduction of the symptom complex by eliciting apprehension with certain provocative positions of impending subluxation or dislocation. This is especially applicable for anterior instability. The apprehension test is an evaluation of the patient’s sense of pending anterior subluxation or dislocation with the arm in stressed external rotation abduction.38,43 The role of pain needs to be interpreted, because frequently a patient may not be apprehensive in this position but may only experience pain. The usual position
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Figure 4-26. Apprehension sign for anterior instability in the sitting position.
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not with apprehension. A positive relocation test for pain located in the posterior aspect of the shoulder is suggestive of internal impingement between the posterosuperior labrum and infraspinatus tendon. This is an important differentiation because the problem is likely the result of posterior capsular tightness and not anterior instability. The positive relocation test allows greater external rotation in the abducted position, with less pain.
Figure 4-27. Apprehension sign for anterior instability in the supine position.
edge of the table serves as the fulcrum and the arm as the lever. When the apprehensive position is located, note is taken of the amount of external rotation. With the arm in this position, a posterior stress may be exerted on the proximal humerus and the apprehension may disappear, allowing external rotation before emergence of the apprehension sign. The relocation test can be done and has two possible results—at the apprehension point, the humeral head is subluxated slightly and pushing it posteriorly causes reduction, or the posteriorly directed pressures act as a supportive buttress anteriorly to give the patient more confidence, preventing apprehension (Fig. 4-28). The relocation test was originally described in the presence of pain only and
Figure 4-28. Relocation test for internal impingement. The relocation maneuver eliminates pain in the posterior shoulder and permits increased external rotation. For anterior instability, the relocation maneuver eliminates apprehension.
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If the arm is suddenly released when stressed with external rotation and abduction, the patient has a substantial increase in pain, which may be referred to as a release test. This may be caused by the humeral head jumping forward on release of the posteriorly applied stress. The pain can also be augmented with external rotation and abduction by pulling forward on the back of the arm (augmentation test). These findings may be present but are not necessarily related to nor represent the classic apprehension sign. Their value, however, is in the differentiation of impingement or anterior subluxation as the source of pain. Posterior instability may present with subluxation rather than dislocation. Pain may also be a contributing factor. Most patients can demonstrate the position that reproduces their symptoms. Having ascertained the compromising maneuver, the examiner may attempt to reproduce the instability by manually duplicating the stresses. Because this is usually a painless subluxation that easily reduces, posterior apprehension is not commonly present and, therefore, is not a reliable sign. With posterior stresses, patients who are painful may resist, which is sometimes erroneously interpreted as apprehension. The Jahnke or jerk test, when positive, is excellent for diagnosing posterior instability patterns. The examiner adducts and internally rotates the shoulder and then applies a posterior stress. If unstable, the humeral head will subluxate posteriorly. Next, the shoulder is brought back from horizontal adduction while maintaining a posterior force on the humerus from the elbow. As the shoulder returns to neutral, a clunk or visible reduction may be felt and heard as the shoulder reduces (Fig. 4-29).20 In posterior instability, the patient who cannot demonstrate the instability may present a diagnostic challenge. It is not uncommon for the patient only to demonstrate pain on posterior stress testing of the shoulder, without any obvious translational abnormalities. This subset of patients may have only a labral tear, without significant capsular redundancy. At times, a click may be felt on posterior stress testing suggesting a posterior labral tear. Therefore, pain reproducing the patient’s symptoms may provide the only diagnostic clue. Patients with inferior instability may state that the distal traction on the arm reproduces their symptom complex, suggesting underlying multidirectional instability.44,45 Comparison with the contralateral extremity is always performed following the examination.
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and wrist are noted. Evaluation of muscle mass and tone, and strength, is performed during the palpation part of the examination. The addition of evaluation of wrist extension, finger abduction and adduction, thumb abduction, and elbow extension can provide a quick assessment of the health of the cervical roots. Cervical spine radiculopathy can mimic that of intrinsic shoulder disease (e.g., C5 radiculopathy can mimic a rotator cuff tear).46-48 Spurling’s test is helpful to determine cervical disease (Fig. 4-30). The neck is flexed and rotated to one side, with corresponding compression to elicit pain.49 In the absence of tenderness of the posterior cervical spinous processes to palpation, and in the presence of a negative Spurling’s test, cervical spine pathology and radiculopathy can usually be excluded.
VASCULAR EXAMINATION A
The vascular examination consists of palpation of the pulses at the wrist and elbow, along with an assessment of vascular changes from dystrophy, such as swelling, discoloration, and lack of sweating. There are also tests to determine thoracic outlet syndrome. Adson’s maneuver is performed with the shoulders extended, breath held, neck extended, and chin turned to the same side. The arm is in a slightly abducted and extended position. Diminution of a palpable pulse at the wrist is considered positive for thoracic outlet syndrome (Fig. 4-31). Other thoracic outlet tests are less
B Figure 4-29. Jerk (Jahnke) test for posterior instability. A, Shoulder is adducted with posterior force on the shoulder. B, Clunk or visible reduction as shoulder is brought back to neutral.
NEUROLOGIC EXAMINATION Any athlete who presents with shoulder pain and/or weakness should have a thorough neurologic examination. It is however, common for many athletes who throw, swim, and serve to present with dysesthesias in their extremities. For example, this is a common presentation with instability patterns. The timing of performing a neurologic examination may vary. It is frequently helpful to carry out the examination during range-of-motion assessment because strength testing is done almost concurrently, and it seems appropriate to complete the sensory and reflex examinations at that time. Normally, a dermatomal sensory examination is performed in the usual manner. Deep tendon reflexes at the elbow
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Figure 4-30. Spurling’s test.
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A
Figure 4-31. Adson’s maneuver for thoracic outlet syndrome.
reliable; perhaps the most helpful is provocative testing. The Roos test is performed with the patient standing or sitting, with both shoulders in abduction and external rotation. With the arms above the head, the patient is asked to open and close each fist repetitively to reproduce the symptoms distal to the forearm (Fig. 4-32).50 This often causes an aching fatigue, suggestive of thoracic outlet syndrome.
SUMMARY Athletes with shoulder injuries often present a diagnostic dilemma. If the examiner systematically approaches the history to classify the patient as having specific symptom patterns and performs a thorough physical examination, paying particular attention to how the assessment relates to the patient’s symptomatology, an accurate diagnosis can usually be made. Specifically, the initial event or injury is a critical aspect of the history and a thorough understanding is helpful before beginning the examination. Management techniques are obviously predicated on an accurate diagnosis. Often, patients can relate the exact mechanism of injury and actually have a clear understanding of their symptom pattern. However, with increasing demands from an athletic population, many patients present with unclear histories of their symptoms. The importance of using injections and comparing with the asymptomatic shoulder to confirm examination findings cannot be overstated. If care is taken during the examination to be thorough and organized, the correct diagnosis can be reached.
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B Figure 4-32. Roos test for thoracic outlet syndrome.
References 1. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220, 1988. 2. Jobe FW, Bradley JP: Rotator cuff injuries in baseball: Prevention and rehabilitation. Sports Med 6:377, 1988. 3. Butters KP, Rockwood CA Jr: Office evaluation and management of the shoulder impingement syndrome. Orthop Clin North Am 19:755, 1988. 4. Nirschl RP: Shoulder tendinitis. In Pettrone FA (ed): Symposium on Upper Extremity Injuries in Athletes (American Academy of Orthopaedic Surgeons). St. Louis, Mosby, 1986.
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5. Hawkins RJ, Hobeika P: Impingement syndrome in the athletic shoulder. Clin Sports Med 2:391, 1983. 6. Neer CS II: Impingement lesions. Clin Orthop 173:70, 1983. 7. Neer CS II: Anterior acromioplasty for the chronic impingement syndrome in the shoulder. J Bone Joint Surg Am 54:41, 1972. 8. Neer CS II, Welsh RP: The shoulder in sports. Orthop Clin North Am 8:583, 1977. 9. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics and tennis. Clin Sports Med 2:247, 1983. 10. Hawkins RJ, Bell RH: Collagen analysis in patients with multidirectional instability. Presented at the AOSSM Specialty Day Meeting, Anaheim, CA, March 1991. 11. Hawkins RJ, Hobeika P: Physical examination of the shoulder. Orthopedics 10:1270, 1983. 12. Drez D Jr: Suprascapular neuropathy in the differential diagnosis of rotator cuff injuries. Am J Sports Med 4:43, 1976. 13. Burkart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 19:404, 2003. 14. Codman EA: Normal motions of the shoulder joint. In Codman EA (ed): The Shoulder. Boston, Thomas Todd, 1934, p 32. 15. Freeman L, Monroe RR: Abduction of the arm in the scapular plane: Scapular and glenohumeral movement. J Bone Joint Surg Am 48:1503, 1966. 16. Poppen NK, Walker PS: Normal and abnormal motion of the shoulder. J Bone Joint Surg Am 58:195, 1976. 17. Jobe FW, Jobe CM: Painful athletic injuries of the shoulder. Clin Orthop 173:117, 1983. 18. Sisto DJ, Jobe FW: The operative treatment of scapulothoracic bursitis in professional pitchers. Am J Sports Med 14:192, 1986. 19. Lombardo SJ, Jobe FW, Kerlan RK, et al: Posterior shoulder lesions in throwing athletes. Am J Sports Med 5:106, 1977. 20. Krishnan SG, Hawkins RJ, Warren R: The Shoulder in the Overhead Athlete. Philadelphia, Lippincott Williams & Wilkins, 2004. 21. Hoyt WA Jr: Etiology of shoulder injuries in athletes. J Bone Joint Surg Am 49:755, 1967. 22. Rockwood CA, Green DP: Fractures in Adults. Philadelphia, JB Lippincott, 1984. 23. Shields CL, Glousman RE: Open management of rotator cuff tears. In Grana WA (ed): Advances in Sports Medicine and Fitness, vol 2. Chicago, Year Book, 1989, p 223. 24. Walton J, Mahajan S, Paxinos A, et al: Diagnostic value of tests for acromioclavicular joint pain. J Bone Joint Surg Am 86:807, 2004. 25. Hurley JA, Anderson TE: Shoulder arthroscopy: Its role in evaluating shoulder disorders in the athlete. Am J Sports Med 18:480, 1990. 26. Colachis SC Jr, Strohm BR: Effect of suprascapular and axillary nerve blocks and muscle force in upper extremity. Arch Phys Med Rehabil 52:22, 1971. 27. Hawkins RJ, Kennedy JC: Impingement syndrome in athletes. Am J Sports Med 8:151, 1980. 28. Scheib JS: Diagnosis and rehabilitation of the shoulder impingement syndrome in the overhead and throwing athlete. Rheum Dis Clin North Am 16:971, 1990.
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29. Yergason RM: Supraspinatus sign. J Bone Joint Surg 13:60, 1931. 30. Tennent TD, Baech WR, Meyers JF: A review of the special tests associated with shoulder examination, Part I: The rotator cuff tests. Am J Sports Med 31:154, 2003. 31. Tennent TD, Baech WR, Meyers JF: A review of the special tests associated with shoulder examination, Part II: laxity, instability, and superior labral anterior and posterior (SLAP) lesions. Am J Sports Med 31:301, 2003. 32. Crenshaw AII, Kilgore WE: Surgical treatment of bicipital tenosynovitis. J Bone Joint Surg Am 48:1496, 1966. 33. Bennett WF: Specificity of the Speed’s test: Arthroscopic technique for evaluating the biceps tendon at the level of the bicipital groove. Arthroscopy 14:789, 1998. 34. Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274, 1990. 35. O’Brien SJ, Pagnani MJ, Fealy S, et al: The active compression test: A new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sports Med 26:610, 1998. 36. Hastings DE, Coughlin LP: Recurrent subluxation of the glenohumeral joint. Am J Sports Med 9:352, 1981. 37. Protzman RR: Anterior instability of the shoulder. J Bone Joint Surg Am 62:909, 1980. 38. Rowe CR, Zarins B: Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am 63:863, 1981. 39. Hawkins RJ, Schutte JP, Huckell GH, Abrams J: The assessment of glenohumeral translation using manual and fluoroscopic techniques. Orthop Trans 12:727, 1988. 40. Gerber C, Ganz R: Clinical assessment of instability of the shoulder with special reference to anterior and posterior drawer tests. J Bone Joint Surg Br 66:551, 1984. 41. Pappas AM, Goss TP, Kleinman PK: Symptomatic shoulder instability due to lesions of the glenoid labrum. Am J Sports Med 11:279, 1983. 42. Cofield RH, Irving JF: Evaluation and classification of shoulder instability with special reference to examination under anesthesia. Clin Orthop 223:32, 1987. 43. Zarins B, Rowe CR: Current concepts in the diagnosis and treatment of shoulder instability in athletes. Med Sci Sports Exerc 16:444, 1984. 44. Neer CS II: Involuntary inferior and multidirectional instability of the shoulder: Etiology, recognition and treatment. Instr Course Lect 34:232, 1985. 45. Neer CS II, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897, 1980. 46. Bateman JE: Neurologic painful conditions affecting the shoulder. Clin Orthop 173:44, 1983. 47. Bennett RM: The painful shoulder. A four-article symposium. Postgrad Med 73:153, 1983. 48. Bowling RW, Rockar PA Jr, Erhard R: Examination of the shoulder complex. Phys Ther 66:1866, 1986. 49. Spurling RG, Scoville WB: Lateral rupture of the cervical intervertebral discs. Surg Gynecol Obstet 78:350, 1944. 50. Roos DB: Congenital anomalies associated with thoracic outlet syndrome. Anatomy, symptoms, diagnosis, and treatment. Am J Surg 132:771, 1976.
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CHAPTER 5 Diagnostic Imaging of the
Shoulder Complex Martin L. Schwartz and D. Dean Thornton
Evaluation of shoulder disorders has become much easier because of advances in imaging techniques. Continued refinement of magnetic resonance imaging (MRI) and computed tomography (CT) hardware and software have significantly improved the sensitivity and specificity of diagnosing pathologic conditions of the shoulder. Increasingly accurate imaging diagnosis of shoulder disorders has decreased the number of unnecessary arthroscopic procedures while providing important information that guides appropriate surgical intervention. This chapter will present the state of the art shoulder imaging available to the orthopedic surgeon, sports medicine physician, and radiologist.
Included in this study are internal and external rotation views, an axillary view, and weight-bearing views. CT is an excellent imaging technique for evaluation of bony abnormalities such as fractures; however, like conventional radiographs, it provides limited information regarding soft tissues. With the widespread availability of multislice helical CT scanners, sophisticated reconstructed images can be obtained in two and three dimensions (2D and 3D). A slice thickness as small as 1 mm can be used and yields highquality reconstructed images. Generally, the examination is performed with the shoulder in external rotation and the patient supine. Two-dimensional reconstructed images are usually performed in the oblique sagittal and coronal planes. Three-dimensional reconstructions allow for image rotation into any plane. Postprocessed images can be viewed on workstations with multiple window levels.
IMAGING TECHNIQUES After a thorough clinical examination of the shoulder, conventional radiographs should be obtained, with a minimum of three views—anteroposterior internal and external rotation, as well as axillary views. Additional views may be obtained depending on the specific pathology involved. At our institution, the thrower’s series consists of five radiographs; these include the West Point, axillary, Stryker notch, and internal and external rotation views. Occasionally, an acromial profile view is added. These radiographs should enable the clinician to evaluate the skeletal structures and to exclude most common fractures and dislocations. It must be stressed that conventional radiographs of the shoulder are of limited benefit in the evaluation of soft tissues, with the exception of calcification in the rotator cuff. If conventional radiographs are negative, the next diagnostic imaging test required will vary according to the specific condition that the clinician needs to confirm based on the mechanism of injury and physical examination.
MRI is the most powerful imaging tool available to the clinician when there are questions regarding the status of the osseous and soft tissue components of the shoulder. MRI can provide an overview of pathology when there is uncertainty in the clinical examination results. MRI can also be directed to answer specific clinical questions. There are many options to consider when referring a patient for MRI. There are differing levels of magnet strength and quality; most current MR scanners offer 1.5-tesla (T) imaging. Older MR units may be 1.0 T, but more powerful 3.0-T scanners are becoming increasingly common in larger centers. Claustrophobic or large patients may require the use of an open MR unit, which can range in strength from 0.2 to 0.7 T. Newer, even higher strength (up to 1.5 T), open MR units are becoming available. There is a correlation between magnet strength and image quality, but even lowfield strength magnets can produce good images if used properly. In general, a high-field MRI unit should be used whenever possible.1 MRI allows for direct imaging of the important soft tissue structures of the shoulder, such as the rotator cuff, labrum, and glenohumeral ligaments, while providing information about osseous structures that is complementary to that obtained by radiography and CT. The cross-sectional nature of MRI allows for the examination of anatomic structures in multiple planes.
Conventional arthrography is seldom used in isolation because of the advances in MR arthrography. It can be useful for patients who have a contraindication to MRI, such as those with a cardiac pacemaker or other device that is not MRI compatible. The procedure is performed using sterile technique and fluoroscopic guidance, with the patient in the supine position and the shoulder in external rotation. Following administration of a local anesthetic, a 22-gauge spinal needle is placed into the joint. For single-contrast arthrography, approximately 15 mL of iodinated contrast is injected into the joint. For double-contrast arthrography, injection of 6 mL of contrast is followed by injection of 12 mL of air. Five radiographs are obtained after controlled exercise.
MR arthrography is another important tool that can be used in the diagnostic evaluation of the shoulder. The addition of intra-articular contrast provides another layer of detail to the MR examination. Shoulder arthrography is 73
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performed in the customary way, using a dilute solution of gadolinium. Injection of contrast accomplishes several purposes. It ensures the presence of joint fluid, which outlines intra-articular structures such as the labrum and makes them more conspicuous. The joint is distended, which forces fluid into the tears and leaks that are being sought (e.g., rotator cuff tears, labral tears, capsular disruptions). The unique MR properties of gadolinium allow for the detection of small amounts of contrast on MRI, with differentiation from other fluid around the joint that may be present. Performed properly, MR arthrography is a quick and easy way to obtain additional information from the shoulder MRI examination.
imaging is required. Complex humeral fractures can be further evaluated using CT3,4 and, to a lesser degree, MRI. Newer, multislice, helical CT scanners can provide not only high-quality axial images but can also produce 2D and 3D reconstructed views in any plane. The reconstructed images allow the surgeon to visualize and manipulate these fractures using sophisticated software and high-quality monitors. MRI is particularly useful for occult fractures in which radiographs are negative. A typical low-signal pattern is seen on T1-weighted images, with increased T2 signal on short tau inversion recovery (STIR) or T2-weighted fat-suppressed images. The fracture lines can range from simple and linear to complex and stellate.
In those patients who cannot undergo MRI of the shoulder for some reason (e.g., cardiac pacemaker, large body habitus), CT arthrography can provide much of the same diagnostic information. Conventional arthrography is first performed using a single-contrast or air contrast technique. As with MR arthrography, the intra-articular contrast outlines the important anatomic structures and exposes tears and leaks to greater advantage. Transverse CT scans are then acquired through the region of interest. Multiplanar reconstruction images can be produced, which can approximate the appearance of the images obtained by MRI.
Dislocations, particularly posterior in position, can be problematic with conventional radiograph analysis. Subtle dislocations or subluxations can be missed if only anteroposterior internal and external rotation views are obtained. For this reason, an axillary view should be obtained when dislocation is suspected (Fig. 5-1). In the acute setting, CT can be helpful in identifying subtle dislocations as well any associated fractures of the humeral head or glenoid (see Fig. 5-1). CT and MRI can both be useful in the evaluation of the osseous and soft tissue changes associated with chronic dislocation.
Sonography or ultrasound (US) of the shoulder can provide some useful information to the clinician. Partial or fullthickness rotator cuff tears can be identified accurately with US. Advantages of US include its relatively low cost compared with MRI and lack of ionizing radiation used for radiography and fluoroscopy. There are, however, several important limitations of US in the examination of the athlete’s shoulder. Evaluation of structures other than the rotator cuff is limited. Specifically, the labroligamentous structures are not well demonstrated. The sonographic examination of the shoulder can be difficult and is highly operator dependent. In general, clinicians are not as comfortable viewing shoulder US images as they are with radiography or MRI.
IMAGING OF SPECIFIC PATHOLOGIC CONDITIONS Fracture and Dislocation In 1970, Neer2 published his classic paper on acute proximal humeral fractures, showing that the prognosis depended not only on the number of fracture fragments but also on the amount of displacement and angulation. Minimally displaced fractures could be treated without surgery; however, significant separation of fragments or rotation required surgery to prevent chronic changes and loss of function. If a fracture or dislocation is suspected after physical examination, conventional radiographs should be obtained. Most fractures will be obvious on this examination, and no further
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MR arthrography is the diagnostic imaging test of choice for patients with chronic dislocation to evaluate the glenoid labrum and capsular structures. Often, chronic injuries to the labrum and bony glenoid are seen. MR arthrography can also be used in cases of acute dislocation in which specific labral and capsular changes occur. These findings will be discussed later in the chapter.
Bone and Articular Cartilage Abnormalities Osteoarthritis is a common condition seen in the shoulder. Loss of articular cartilage leads to osteophyte formation, subchondral cysts, and synovitis. Radiographs (and CT) will show joint space narrowing, sclerosis of the subchondral bone, subchondral cysts, and osteophyte formation. MRI demonstrates a subchondral low signal on T1-weighted images, with increased T2 signal caused by cystic changes. Other conditions that mimic these findings include inflammatory arthritis, synovitis, septic arthritis, and neuropathic arthritis. The findings can be seen in conjunction with other shoulder pathology, such as rotator cuff tears. Avascular necrosis (AVN) or osteonecrosis most often occurs in the superomedial portion of the humeral head. On MRI, the finding of low-signal serpiginous lines in the subchondral bone in this location is virtually diagnostic (Fig. 5-2). With advanced cases, there may be flattening of the humeral head, which may progress to collapse similar to that seen in the hip. Osteochondral lesions are seen in conjunction with shoulder trauma.5 Both the articular cartilage and underlying
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B
Figure 5-1. Posterior shoulder dislocation. A, Anteroposterior radiograph. There is a subtle indentation on the humeral head (arrow), but the findings are equivocal. B, Axillary view. The posterior dislocation of the humeral head is clearly seen. The anterior humeral head is impacted against the posterior rim of the glenoid (arrow). C, Axial computed tomography (CT) scan in a different patient. A fracture of the lesser tuberosity (arrow) may accompany posterior dislocation.
bone may be injured. This finding is most commonly demonstrated in the anterior glenoid, but can occur posteriorly or on the humeral head. The abnormality can range in size from just a few millimeters to a large area of several centimeters of cartilage loss. The best imaging modality for these abnormalities is to use a cartilage-sensitive MRI sequence (gradient or fat-suppressed proton density) in the axial and coronal planes, intra-articular contrast, or both (Fig. 5-3). The reactive changes in the underlying subchondral bone can best be seen on T2 fat-suppressed images.
fat-suppressed images.6 The loose bodies can range in size from a few millimeters to more than 1 cm. They can occur anywhere in the joint space but are most commonly observed anteriorly and inferiorly (Fig. 5-4). Care must be taken not to mistake air bubbles inadvertently introduced at the time of joint injection for loose bodies. These are usually located in a nondependent position anterior in the joint with the patient supine on the MRI table.
Loose bodies can be seen when an injury to the cartilage or bone has occurred. Both cartilaginous and bony loose bodies are best detected using MR arthrography with T1
The diagnosis of adhesive capsulitis is usually based on the clinical examination. Often, patients presenting with this condition have undergone previous surgery, have had
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A
B
Figure 5-2. Avascular necrosis of the humeral head. A, Coronal proton density MR image. A serpiginous low-signal line is present in the subchondral bone of the humeral head (arrow). B, Coronal short tau inversion recovery (STIR) image. Bone marrow edema is found around the low-signal abnormality. Note also the mild flattening of the humeral head (arrow).
Figure 5-3. Osteochondral lesion of the glenoid; coronal T2-weighted fat-suppressed magnetic resonance arthrogram. Focal chondral defect in the anterior inferior glenoid is associated with subchondral edema (arrow).
Figure 5-4. Loose bodies; axial T1 magnetic resonance arthrogram. Multiple small osteochondral bodies (arrow) are present in the subscapular recess of the joint space.
multiple joint injections, or are chronic dislocators. Imaging confirmation is obtained when the patient undergoes joint injection for MR arthrography. The total volume of the joint space is reduced, limiting the quantity of contrast that can be injected. The patient will also complain of pain
during the injection, especially when the volume end point is reached. MRI shows an irregular, small, axillary recess that is markedly reduced in volume.7,8 If the patient has a contraindication to MRI, a conventional arthrogram can be obtained to confirm the diagnosis.
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Bennett Lesion When an individual presents with posterior shoulder pain, particularly with overhead motion, a Bennett lesion should be considered. This condition, also referred to as thrower’s exostosis, results from posterior capsular traction on the glenoid. Calcification is found adjacent to the posterior glenoid, but this finding can be subtle and is often hard to visualize on conventional radiographs. MRI shows an area of very low signal adjacent to the posterior glenoid.9 CT can be diagnostic, with the calcification nicely demonstrated as conforming to the contour of the glenoid or in the adjacent capsular soft tissues (Fig. 5-5).10,11
Labral Injury Most glenoid labrum abnormalities are caused by shoulder trauma, particularly dislocation. The humeral head moves anteriorly or posteriorly relative to the glenoid, affecting the labrum and stretching capsular structures. MR arthrography has become the imaging procedure of choice for diagnosis of these conditions. Most complex labral injuries involve the anterior labrum and will be discussed later. A Bankart lesion is defined as an anterior labral disruption with tearing of the attached periosteum, usually as a result of anterior dislocation. On MR arthrography, contrast flows into the defect created by the absence of the anterior labrum.12 There is often a Hill-Sachs fracture of the posterolateral aspect of the humeral head. If the bony glenoid is involved the abnormality is then referred to as a bony Bankart lesion. The abduction external rotation (ABER)
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sequence can often demonstrate this abnormality as the labrum and periosteum are pulled away from the glenoid by the traction placed on these structures in this position (Fig. 5-6).13 There are several Bankart variants that involve the anterior labrum; these are based on the type of detachment of the anterior labrum and capsule from the glenoid. A Perthes lesion involves detachment of the anterior labrum from the glenoid, with preservation of an intact attachment to the periosteum (unlike in the Bankart lesion).14 The anterior labrum, although detached, may remain in place, making the tear difficult to see on routine MR sequences. Again, the ABER view is often the most helpful in diagnosing this problem because it accentuates the separation between labrum and glenoid (Fig. 5-7). The anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion involves an anterior labral detachment with rotation of the labrum 90 degrees medially and an avulsion of the inferior glenohumeral labroligamentous complex, with an intact periosteum still attached to the labrum.15 If chronic, the labrum may scar down in this medially displaced location (Fig. 5-8). Axial MR arthrographic and ABER sequences are most helpful to visualize these findings. The Bankart lesion and its variants involve some degree of anterior instability. The glenolabral articular disruption (GLAD) lesion consists of an articular cartilage defect in the anterior glenoid, with a partial tear of the anterior labrum (Fig. 5-9).15 Axial and coronal MR arthrographic images often show both
B
Figure 5-5. Bennett lesion. A, Axial T1 magnetic resonance arthrogram. A focus of low signal (arrow) is found at the posterior capsular insertion on the glenoid. B, Axial computed tomography (CT) scan. This confirms the calcific nature of the low signal (arrow).
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A
A
B
B
Figure 5-6. Bankart lesion. A, Axial T1 magnetic resonance arthrogram. The anterior labrum is torn and detached from the anterior glenoid (arrow). B, Abduction external rotation (ABER) T1 fat-suppressed magnetic resonance arthrogram. The ABER position puts traction on the anterior labroligamentous structures. Note the increased separation of the anterior labrum (arrow) from the glenoid.
Figure 5-7. Perthes lesion. A, Axial T1 magnetic resonance arthrogram. No definite abnormality is seen in this patient suspected of having a labral tear. B, Abduction external rotation (ABER) T1 fat-suppressed magnetic resonance arthrogram. The ABER position reveals the anterior labral tear, although the labrum remains attached to the scapular periosteum (arrow).
abnormalities, especially if cartilage protocols are used. This lesion is considered stable.
whether the bony glenoid is involved. There may be a reverse Hill-Sachs lesion of the anteromedial humeral head in these patients. The posterior band of the inferior glenohumeral ligament and the posterior capsule may also be affected. Axial and ABER images show detachment of the labrum from the glenoid, with contrast filling the space (Fig. 5-10). Posterior labral tears also occur in association with glenoid dysplasia.16
Posterior labral tears are generally caused by posterior dislocations of the humeral head. The most common mechanism of injury is the result of a direct anterior blow to the humeral head or a seizure. These are often called reverse Bankart or bony Bankart lesions, depending on
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A Figure 5-8. Anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion; axial T1 magnetic resonance arthrogram. In this patient, with a history of recurrent anterior shoulder dislocation, the anterior labrum is deformed and displaced medially (white arrow) along the anterior margin of the glenoid. Note the Hill-Sachs deformity of the posterior humeral head (black arrow), confirming the history of dislocation.
B Figure 5-10. Posterior labral tear. A, Axial T1 magnetic resonance arthrogram. There is a tear of the posterior labrum (arrow), with contrast extending through the tear into a small paralabral cyst. B, Axial gradient sequence. In a different patient, a posterior labral tear is associated with a large paralabral cyst that extends to the spinoglenoid notch (arrow).
Figure 5-9. Glenolabral articular disruption (GLAD) lesion; axial T1 magnetic resonance arthrogram. A small, focal, chondral defect of the anterior glenoid (arrow) is associated with a partial nondisplaced tear of the anterior labrum.
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Superior labral anterior-posterior (SLAP) lesions can be simple or complex.17 There are nine different classifications of SLAP lesions, depending on the adjacent structures involved. Types I to IV involve tears of the superior labrum with or without involvement of the biceps tendon or biceps anchor. Types V to IX show extension into different adjacent soft tissues. On coronal MR images, contrast is seen entering the tear of the superior labrum, with associated increased signal
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in adjacent structures on T2-weighted images (Fig. 5-11). Care must be taken not to mistake the normal sublabral foramen that can exist between the superior labrum and glenoid for a SLAP lesion. Approximately 3% to 5% of all labral tears are associated with a paralabral cyst. Occasionally, the labral tear will heal but the cyst will persist. The cysts can vary in size, ranging from a few millimeters to several centimeters in the dissecting type.18 If there is a connection between the labral
tear and the cyst, some contrast may be seen in the cyst as high signal on T1-weighted fat-suppressed images. The cyst will be low signal on T1-weighted fat-suppressed images if there is no connection. Both will show high signal on T2-weighted images. A paralabral cyst associated with a superior labral tear may extend to the suprascapular notch. If the cyst compresses the suprascapular nerve, pain and weakness can develop in the supraspinatus and infraspinatus muscles. If the cyst relates to a posterior labral tear, it may extend to the spinoglenoid notch, where it may affect the nerve supply to the infraspinatus only (Fig. 5-10).
Glenohumeral Ligament Injury The inferior glenohumeral ligament (IGHL) is the most commonly torn ligament in the shoulder joint. IGHL tears usually occur with anterior dislocations because they also affect the inferior joint space. The IGHL forms the axillary pouch or recess and, when torn, the fibers are discontinuous on coronal MR arthrographic images. There may be extravasation of contrast into the adjacent soft tissues. Occasionally, the ligament is just sprained and not completely torn, resulting in stretching or thickening of the IGHL without disruption. These findings can also be seen on noncontrast MR images, particularly when using the ABER view.19
A
The humeral avulsion of the glenohumeral ligament (HAGHL) lesion occurs when the IGHL is torn from the humerus or when there is an avulsion fracture at the humeral attachment. This lesion occurs with anterior-inferior dislocation of the humeral head. The IGHL fibers are discontinuous at the humeral interface and the normally U-shaped axillary recess becomes J-shaped (Fig. 5-12).20 If there is bony avulsion, there will be edema in the donor site and a piece of bone will be visualized on coronal or axial images. Rarely, the IGHL will rupture in its midsubstance, with discontinuity of the axillary recess on coronal images. Middle and superior glenohumeral ligament tears are uncommon. When present, they are best visualized on axial and sagittal MR arthrographic images. Posterior capsule injuries are also unusual but can occur with posterior dislocation.
Biceps Tendon Injury
B Figure 5-11. Superior labral anterior-posterior (SLAP) lesion. A, Coronal T2 fat-suppressed image. A linear high signal extends into the substance of the superior labrum (arrow). B, Coronal T1 fat-suppressed magnetic resonance arthrogram. Intra-articular contrast extends into the superior labral tear (arrow), increasing its conspicuity.
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Biceps tendinosis occurs when there is degeneration of the long head of the biceps caused by chronic microtrauma or acute injury.21 The tendon remains intact but may be thickened to greater than 5 mm in diameter. The patient typically complains of shoulder pain radiating into the upper arm, especially during overhead motion. This condition may be seen in conjunction with rotator cuff disease. MRI shows a thickened tendon on axial, coronal, or sagittal images, with increased T1 and T2 signals. The tendon of the long head of the biceps may also rupture, usually because of repetitive microtrauma.22 This
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Figure 5-12. Humeral avulsion of the glenohumeral ligament (HAGL) lesion; coronal T1 fat-suppressed magnetic resonance arthrogram. The inferior glenohumeral ligament (arrow) has been avulsed from its humeral attachment. Note the intra-articular contrast extending through the capsular defect.
Figure 5-13. Biceps tendon dislocation; axial T1 magnetic resonance arthrogram. A full-thickness tear of the subscapularis tendon (white arrow) has allowed medial dislocation of the biceps tendon (black arrow) into the anterior joint space. Note the empty bicipital groove.
condition often occurs with rotator cuff disease23 and bony encroachment from the acromioclavicular (AC) joint. The biceps muscle belly may retract distally, leading to the Popeye sign. A tear or gap in the tendon may be seen on MRI, with or without retraction. If there is significant retraction, the empty tendon sheath and bicipital groove will be identified on axial MR arthrographic images.
Primary extrinsic impingement occurs when the coracoacromial arch exerts pressure on the subacromial bursa and/or tendons of the rotator cuff, primarily the supraspinatus. The coracoacromial arch is composed of the following structures, from anterior to posterior: the coracoid process, the coracoacromial ligament, the distal clavicle, the AC joint, and the acromion. Impingement can occur at any of these locations (Fig. 5-14).27 Most commonly, there is hypertrophic degenerative change at the AC joint, producing capsular distention and distal clavicle osteophytes, both of which can extend inferiorly to encroach on the supraspinatus. The coracoacromial ligament may be thickened or produce traction on the acromion, resulting in a prominent anterior acromial spur (Fig. 5-15). The anterior acromial ossification center may fail to fuse, resulting in an os acromiale. If excessively mobile, the os acromiale can undergo inferior displacement with deltoid contraction.28 Other conditions, such as a type III acromion with an anterior hook, downsloping acromion, or low-lying acromion, can also produce encroachment on the cuff.29
Biceps tendon dislocation occurs after the loss of its stabilizing structures. The subscapularis tendon and coracohumeral ligament are the main stabilizers of the biceps tendon. A shallow bicipital groove also predisposes to dislocation. If the subscapularis tendon is intact, the dislocation is medial but on the same anterior plane as the bicipital groove.24 The tendon can dislocate medially and posteriorly all the way to the anterior labrum if the subscapularis tendon is torn (Fig. 5-13).25 MRI shows a round or oval low-signal structure outside the bicipital groove, which is left empty.
Shoulder Impingement and Rotator Cuff Abnormalities Evaluation of the rotator cuff is the most common indication for shoulder MRI. The power of MRI is its ability to answer many questions that the clinician may have regarding the status of the cuff. Not only can MRI accurately depict the status of the rotator cuff, but it can also demonstrate the potential underlying causative factors for the abnormality. Shoulder impingement is a clinical diagnosis made by clinicians. MRI can, however, provide important information to support this diagnosis.26,27
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Secondary extrinsic impingement is usually seen in athletes involved in throwing or overhead arm motion sports, such as baseball, football, tennis, or swimming. Such athletes are more susceptible to glenohumeral ligamentous instability. This instability can allow for superior migration of the humeral head during range of motion, producing impingement against the coracoacromial arch, which may appear anatomically normal.30 Internal impingement, or posterosuperior glenoid impingement, is another clinical entity associated with overhead
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AC Ac
to a rotator cuff abnormality, the posterosuperior glenoid labrum may suffer fraying or a discrete tear, and cystic changes may be found in the posterior humeral head.31 (Fig. 5-16) The use of the ABER position accentuates these abnormalities.32 The elbow is raised above the head with the hand positioned behind the head, resulting in
CI CA
Co
Figure 5-14. Coracoacromial arch; sagittal T1 magnetic resonance arthrogram. The coracoacromial arch is formed by the coracoid (Co), coracoacromial ligament (CA), distal clavicle (Cl), AC joint (AC), and acromion (Ac). An inferior distal clavicle osteophyte encroaches on the supraspinatus tendon (arrowhead).
A
Figure 5-15. Anterior acromial spur; sagittal T1 magnetic resonance arthrogram. Traction at the attachment of the coracoacromial ligament has produced a prominent spur (white arrow). Note the underlying tear of the supraspinatus tendon (black arrow).
sports. With the arm in the overhead position, the humerus is abducted and externally rotated. In this position, the undersurface of the supraspinatus and anterior infraspinatus may become entrapped between the greater tuberosity and the posterosuperior rim of the glenoid. In addition
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B Figure 5-16. Internal impingement. A, Coronal T2 fat-suppressed magnetic resonance arthrogram. In this baseball pitcher, there is increased signal in the supraspinatus tendon (arrow), with cystic change in the humeral head. B, Abduction external rotation (ABER) T1 fat-suppressed magnetic resonance arthrogram. In the overhead position, there is interposition of the supraspinatus tendon (arrow) between the greater tuberosity and posterosuperior glenoid. A partial articular surface tear of the supraspinatus is revealed in this position.
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abduction and external rotation of the humerus. The ABER position approximates the overhead position responsible for this pathology. As a consequence of impingement, the subacromial bursa may become distended and inflamed. Visualization of more than a minimal amount of fluid in the bursa suggests subacromial bursitis. This fluid appears as high signal intensity on T2-weighted images. Fluid may extend into the subdeltoid bursa. Recent subacromial injection can also produce high signal in this location and should not be confused with bursitis. If possible, MRI should be performed before or at least 24 hours after subacromial injection to avoid confusion. A potential mimic of the impingement syndrome is calcific tendinitis. Any of the rotator cuff tendons may be involved, but the supraspinatus is the most commonly affected. In this condition, calcium hydroxyapatite deposition occurs in the tendon. The calcification may then extend into the subacromial or subdeltoid bursa or the glenohumeral joint. The calcification is usually best seen on radiographs; CT can be used in cases of very faint calcification. On MRI, calcification is low signal on all sequences. Distinguishing low-signal calcification from a low-signal tendon can sometimes be difficult. Ideally, shoulder MRI examinations should be interpreted with access to shoulder radiography. The calcification may be associated with edema within the tendon (tendinitis) or in the adjacent bursa (bursitis) (Fig. 5-17).
Figure 5-17. Calcific tendinitis; coronal T2 fat-suppressed magnetic resonance arthrogram. A globular low signal within the supraspinatus tendon (arrows) was confirmed on radiographs (not shown) as calcification. Note the small amount of fluid in the subacromial bursa and the edema in the supraspinatus muscle.
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Fluoroscopic or CT guidance can be used to aspirate the calcification in difficult cases. The tendons of the rotator cuff can undergo a spectrum of abnormalities, ranging from senescent degeneration to a full-thickness tear, with associated atrophy. Degenerative changes in the tendon are best described using the term tendinosis (or tendinopathy). Tendinitis is a clinical term with imaging features that overlap with those of tendinosis. The normal rotator cuff tendon is predominately low signal on all sequences. Tendinosis is seen as a mildly increased signal on T1-weighted or proton density (PD) sequences within the tendon, without the high signal on T2-weighted images that indicates fluid (Fig. 5-18).33 The tendon may be thickened. Tendinosis may or may not be seen in association with subacromial bursitis. Radiographic signs of rotator cuff tear are insensitive but include elevation of the humeral head, with decreased acromiohumeral distance. On standard MRI, a rotator cuff tear is identified by high T2 (bright) signal intensity within the tendon.26 There is usually some degree of underlying tendinosis unless a discrete traumatic event has occurred. With MR arthrography, contrast will enter any tear that communicates with the joint space. Partial-thickness tears of the rotator cuff may extend to the articular or bursal surface, or remain intrasubstance. Articular surface (or undersurface) tears are most common and tend to occur in one of two locations—the critical zone, which is about
Figure 5-18. Supraspinatus tendinosis; coronal T2 fat-suppressed magnetic resonance arthrogram. A mild increased signal is present in the supraspinatus tendon (arrow). No bright fluid signal intensity defect is present to suggest a tear. A very small amount of fluid is present in the subacromial bursa.
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1 cm proximal to the insertion onto the greater tuberosity, or at the attachment onto the tuberosity itself (Fig. 5-19). Contrast will extend into articular surface tears on MR arthrography, providing increased sensitivity over standard MRI. Bursal surface tears are often associated with subacromial bursitis (Fig. 5-20). Such tears are important to identify on MRI because they will not be visualized at arthroscopy. Pure intrasubstance tears of the cuff are uncommon; they are generally seen as extensions of an articular or bursal surface tear. Partial-thickness tears can be graded according to the percentage of the tendon thickness involved. Full-thickness tears of the rotator cuff are identified by discontinuity of tendon fibers extending from the articular to bursal surfaces. The tendon gap will exhibit high T2 signal throughout. On MR arthrography, contrast will extend from inside the joint through the tear into the subacromial or subdeltoid bursa (Fig. 5-21). Visualization of contrast in the bursa provides reliable evidence of a full-thickness defect in the tendon, again with increased sensitivity compared with standard MRI.34 In the setting of a rotator cuff tear on standard MRI, it can be difficult to determine whether fluid in the subacromial bursa is related to bursitis or extension of intra-articular fluid through a full-thickness defect. Absence of contrast in the subacromial bursa in this setting provides reassurance that the tear is not a full-thickness tear. Full-thickness tears may involve only a portion of the involved tendon or the tendon in its entirety (complete tear).
Figure 5-19. Partial tear supraspinatus tendon, articular surface; coronal T2 fat-suppressed magnetic resonance arthrogram. Focal high T2 signal is present in the distal supraspinatus tendon (arrow) at its attachment onto the greater tuberosity. The tear extends to the articular surface and involves 25% to 50% of the tendon thickness.
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Figure 5-20. Partial-thickness tear of the supraspinatus tendon, bursal surface; coronal T2 fat-suppressed magnetic resonance arthrogram. High T2 signal fills a bursal-sided partial tear (white arrow) of the supraspinatus tendon. The tear is associated with subacromial bursitis (black arrow).
Figure 5-21. Full-thickness tear of the supraspinatus tendon; coronal T1 fat-suppressed magnetic resonance arthrogram. Intra-articular contrast extends through a full-thickness tear of the supraspinatus tendon (arrow) into the subacromial bursa. Mild retraction of the tendon is present.
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The size of the tendon gap and degree of retraction of the tendon are important factors when operative repair is being considered. Another factor to consider is the acuity of the tear. Fatty atrophy of the rotator cuff muscle in question suggests a chronic process, with a corresponding decrease in likelihood of a satisfactory postoperative result. Massive rotator cuff tears involve two or more tendons (Fig. 5-22). These tears are seen in long-standing degenerative changes
85
in older patients or in cases of substantial trauma, usually in younger patients. The subscapularis tendon may be injured as a result of impingement or acute trauma, such as anterior shoulder dislocation. Full-thickness or even high-grade partialthickness tears of the subscapularis can allow for medial subluxation or dislocation of the biceps tendon out of the bicipital groove (see Fig. 5-13). The teres minor is rarely a source of clinical concern.
Muscle Injuries Pectoralis major musculotendinous abnormalities can present as anterior shoulder pain. The pectoralis major tendon inserts on the proximal humerus on the lateral lip of the intertubercular groove. The most common injuries of the pectoralis major are avulsion of the tendon at the bony attachment and partial tear at the musculotendinous junction.35,36 The degree of retraction, percentage of tendon involved, and status of the muscle can be assessed on MRI in a similar manner as with the rotator cuff (Fig. 5-23). The teres major and latissimus dorsi muscles are uncommon sources of shoulder pain. Strain is the most common injury involving these muscles (Fig. 5-24), although injury at the musculotendinous junction of the latissimus dorsi may occur.37 A
B Figure 5-22. Massive rotator cuff tear; coronal T1 fat-suppressed magnetic resonance arthrogram. A, There is a complete full-thickness tear of the supraspinatus tendon (arrow), with retraction to the level of the glenoid. B, A more posterior image shows that the infraspinatus tendon (arrow) is also completely torn and retracted.
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Figure 5-23. Pectoralis major tendon tear; axial T2-weighted image. There is a complete tear of the musculotendinous junction of the pectoralis major (black arrow), but the distal tendon attachment to the humerus (white arrow) remains intact.
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IS
Tm
TM
A
B
Figure 5-24. Muscle strains. A, Coronal proton density (PD) image. There is high signal throughout the teres major (TM) muscle. The infraspinatus (IS) and teres minor (Tm) muscles are labeled for reference. B, Axial T2 fat-suppressed image. High T2 signal and focal disruption of muscle fibers in the latissimus dorsi muscle (arrow) indicate strain, with a partial tear.
References 1. Magee T, Shapiro M, Williams D: Comparison of highfield-strength versus low-field-strength MRI of the shoulder. AJR Am J Roentgenol 181:1211-1215, 2003. 2. Neer CS: Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am 52:1077-1089, 1970. 3. Kilcoyne RF, Shuman WP, Matsen FA 3rd, et al: The Neer classification of displaced proximal humeral fractures: spectrum of findings on plain radiographs and CT scans. AJR Am J Roentgenol 154:1029-1033, 1990. 4. Newberg AH: Computed tomography of joint injuries. Radiol Clin North Am 28:445-460, 1990. 5. Potter HG, Foo LF: Magnetic resonance imaging of articular cartilage: Trauma, degeneration, and repair. Am J Sports Med 34:661-677, 2006. 6. Steinbach LS, Palmer WE, Schweitzer ME: Special focus session. MR arthrography. Radiographics 22:1223-1246, 2002. 7. Emig EW, Schweitzer ME, Karasick D, Lubowitz J: Adhesive capsulitis of the shoulder: MR diagnosis. AJR Am J Roentgenol 164:1457-1459, 1995. 8. Connell D, Padmanabhan R, Buchbinder R: Adhesive capsulitis: Role of MR imaging in differential diagnosis. Eur Radiol 12:2100-2106, 2002. 9. Connor PM, Banks DM, Tyson AB, et al: Magnetic resonance imaging of the asymptomatic shoulder of overhead athletes: A 5-year follow-up study. Am J Sports Med 31:724-727, 2003. 10. De Maeseneer M, Jaovisidha S, Jacobson JA, et al: The Bennett lesion of the shoulder. J Comput Assist Tomogr 22: 31-34, 1998.
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11. Ferrari JD, Ferrari DA, Coumas J, Pappas AM: Posterior ossification of the shoulder: The Bennett lesion. Etiology, diagnosis, and treatment. Am J Sports Med 22:171-175, 1994. 12. Matheson GO: Evaluating the dislocated shoulder joint with MRI and arthroscopy. Clin J Sport Med 14:148-151, 2004. 13. Cvitanic O, Tirman PF, Feller JF, et al: Using abduction and external rotation of the shoulder to increase the sensitivity of MR arthrography in revealing tears of the anterior glenoid labrum. AJR Am J Roentgenol 169: 837-844, 1997. 14. Wischer TK, Bredella MA, Genant HK, et al: Perthes lesion (a variant of the Bankart lesion): MR imaging and MR arthrographic findings with surgical correlation. AJR Am J Roentgenol 178:233-237, 2002. 15. Waldt S, Burkart A, Imhoff AB, et al: Anterior shoulder instability: Accuracy of MR arthrography in the classification of anteroinferior labroligamentous injuries. Radiology 237:578-583, 2005. 16. Harper KW, Helms CA, Haystead CM, Higgins LD: Glenoid dysplasia: Incidence and association with posterior labral tears as evaluated on MRI. AJR Am J Roentgenol 184: 984-988, 2005. 17. Tuite MJ, Rutkowski A, Enright T, et al: Width of high signal and extension posterior to biceps tendon as signs of superior labrum anterior to posterior tears on MRI and MR arthrography. AJR Am J Roentgenol 185:1422-1428, 2005. 18. Tung GA, Entzian D, Stern JB, Green A: MR imaging and MR arthrography of paraglenoid labral cysts. AJR Am J Roentgenol 174:1707-1715, 2000.
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19. Takubo Y, Horii M, Kurokawa M, et al: Magnetic resonance imaging evaluation of the inferior glenohumeral ligament: Non-arthrographic imaging in abduction and external rotation. J Shoulder Elbow Surg 14:511-515, 2005. 20. Chung CB, Sorenson S, Dwek JR, Resnick D: Humeral avulsion of the posterior band of the inferior glenohumeral ligament: MR arthrography and clinical correlation in 17 patients. AJR Am J Roentgenol 183:355-359, 2004. 21. Patton WC, McCluskey GM 3rd; Biceps tendinitis and subluxation. Clin Sports Med 20:505-529, 2001. 22. Zanetti M, Weishaupt D, Gerber C, Hodler J: Tendinopathy and rupture of the tendon of the long head of the biceps brachii muscle: Evaluation with MR arthrography. AJR Am J Roentgenol 170:1557-1561, 1998. 23. Beall DP, Williamson EE, Ly JQ, et al: Association of biceps tendon tears with rotator cuff abnormalities: Degree of correlation with tears of the anterior and superior portions of the rotator cuff. AJR Am J Roentgenol 180:633-639, 2003. 24. Cervilla V, Schweitzer ME, Ho C, et al: Medial dislocation of the biceps brachii tendon: Appearance at MR imaging. Radiology 180:523-526, 1991. 25. Chan TW, Dalinka MK, Kneeland JB, Chervrot A: Biceps tendon dislocation: Evaluation with MR imaging. Radiology 179:649-652, 1991. 26. Reinus WR, Shady KL, Mirowitz SA, Totty WG: MR diagnosis of rotator cuff tears of the shoulder: Value of using T2-weighted fat-saturated images. AJR Am J Roentgenol 164:1451-1455, 1995. 27. Seeger LL, Gold RH, Bassett LW, Ellman H: Shoulder impingement syndrome: MR findings in 53 shoulders. AJR Am J Roentgenol 150:343-347, 1988. 28. Park JG, Lee JK, Phelps CT: Os acromiale associated with rotator cuff impingement: MR imaging of the shoulder. Radiology 193:255-257, 1994.
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29. Peh WC, Farmer TH, Totty WG: Acromial arch shape: Assessment with MR imaging. Radiology 195:501-505, 1995. 30. Jobe FW, Kvitne RS, Giangarra CE: Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18:963-975, 1989. 31. Giaroli EL, Major NM, Higgins LD: MRI of internal impingement of the shoulder. AJR Am J Roentgenol 185: 925-929, 2005. 32. Roger B, Skaf A, Hooper AW, et al: Imaging findings in the dominant shoulder of throwing athletes: Comparison of radiography, arthrography, CT arthrography, and MR arthrography with arthroscopic correlation. AJR Am J Roentgenol 172:1371-1380, 1999. 33. Kjellin I, Ho CP, Cervilla V, et al: Alterations in the supraspinatus tendon at MR imaging: Correlation with histopathologic findings in cadavers. Radiology 181:837-841, 1991. 34. Ferrari FS, Governi S, Burresi F, et al: Supraspinatus tendon tears: Comparison of US and MR arthrography with surgical correlation. Eur Radiol 12:1211-1217, 2002. 35. Lee J, Brookenthal KR, Ramsey ML, et al: MR imaging assessment of the pectoralis major myotendinous unit: An MR imaging-anatomic correlative study with surgical correlation. AJR Am J Roentgenol 174:1371-1375, 2000. 36. Connell DA, Potter HG, Sherman MF, Wickiewicz TL: Injuries of the pectoralis major muscle: Evaluation with MR imaging. Radiology 210:785-791, 1999. 37. Schickendantz MS, Ho CP, Keppler L, Shaw BD: MR imaging of the thrower’s shoulder. Internal impingement, latissimus dorsi/subscapularis strains, and related injuries. Magn Reson Imaging Clin North Am 7:39-49, 1999.
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CHAPTER 6 Normal Arthroscopic Anatomy
of the Shoulder William G. Carson, Jr. and Scott B. Reynolds
Diagnostic and operative arthroscopy of the shoulder has been well established for the treatment of various shoulder disorders.1-18 Diagnostic and surgical techniques, as well as the arthroscopic anatomy of the shoulder, have been well described.3,5,7,9,14,19-27 Surgical techniques include glenoid labrum resections,2,11,15 certain rotator cuff débridements, and impingement releases,1,28-33 for the débridement of a degenerative shoulder17 or for the resection of a degenerative acromioclavicular joint.16,18 Arthroscopic techniques have also been developed for arthroscopic Bankart repairs34,35 and for arthroscopic staple capsulorrhaphy of the shoulder for recurrent anterior instability.36-40 Additionally, techniques for superior labral anterior-posterior (SLAP) repairs,41 posterior labral repairs,42 and rotator cuff repairs43,44 have also been developed. Techniques to address other forms of shoulder pathology are continuing to be delineated. A knowledge of the normal anatomy of the shoulder as viewed arthroscopically is an essential prerequisite for orthopedic surgeons performing any of these surgical procedures. This section describes the normal arthroscopic anatomy of the shoulder.
from an imaginary vertical line. It attaches to the supraglenoid tubercle at the posterosuperior aspect of the glenoid and, in this area, is related to and appears to be continuous with the glenoid labrum (Fig. 6-3). This attachment of the biceps tendon at the superior labrum is involved in the SLAP lesions commonly seen in overhead throwing athletes. The patient’s arm can be externally rotated to facilitate visualization of the biceps tendon, which can be followed anteriorly to portions of the bicipital groove. The normal biceps tendon should appear glistening and smooth and free of any adhesions, fraying, synovitis, or partial tearing.
Humeral Head and Glenoid After inspection of the biceps tendon is complete and proper orientation is once again obtained, the articular surfaces of the humeral head (superiorly) and the glenoid (inferiorly) are examined. Both these articular surfaces are covered by hyaline cartilage. With the patient positioned in the lateral decubitus position, approximately one third of the articular surface of the humeral head can be seen, which is oriented in 30 degrees of retroversion. Examination of the entire articular surface of the humeral head is facilitated by rotating the arthroscope superiorly and moving the humeral head into internal and external rotation. Anteriorly, the articular surface of the humeral head extends to the level of the humeral neck and is near the insertion of the subscapularis. However, there can be variations in the humeral head’s articular surface extension posteriorly to the soft tissues. Posteriorly, the rotator cuff attaches lateral to the actual extent of the articular cartilage, and thus a bare area of bone can be visualized. This bare area is located, for the most part, straight posteriorly and should not be confused with the Hill-Sachs lesion, which is located more posterolaterally. The size of the normal bare area can vary, but this normal area is usually smooth and rounded without evidence of fraying or degeneration, indicative of possible trauma. Also, the bare area is often characterized by different blood vessels that can be seen coursing through it.
STRUCTURAL ANATOMIC CONSIDERATIONS The arthroscopic anatomy and its various relationships, as shown in the figures for this chapter, are representative of those seen with the patient in the lateral decubitus position, with the shoulder superior. The arm is abducted approximately 45 degrees and forward flexed 15 degrees.3-5,23 Most of the photographs and illustrations represent a posterior portal, which is the preferred approach for diagnostic arthroscopy of the shoulder. This posterior portal is located approximately 3 cm inferior to and slightly medial to the posterolateral corner of the acromion (Fig. 6-1). This point corresponds to the soft spot on the posterior aspect of the shoulder that comprises the relative interval between the infraspinatus and teres minor muscles (Fig. 6-2).
Biceps Tendon
The glenoid is a bean- or pear-shaped cavity approximately one fourth the size of the humeral head. Its surface is longer in the superior-to-inferior dimension than in the anterior-to-posterior dimension. The articular surface clinically appears to be thicker near its periphery than in its central portions.
The long head of the biceps tendon is usually the first structure identified after the arthroscope has been inserted into the shoulder through a posterior portal. This provides proper orientation and, with the patient positioned in the lateral decubitus position, the long head of the biceps tendon is oriented approximately 10 to 15 degrees away 91
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Glenoid Labrum The glenoid labrum is a wedge-shaped structure that borders the glenoid cavity and appears to provide inherent stability to the glenohumeral joint, thus restricting anterior and posterior excursion of the humerus (see Fig. 6-3).45,46 The glenoid labrum consists of hyaline cartilage, fibrocartilage, and fibrous tissue.45-51 This fibrocartilaginous rim of tissue surrounds the glenoid circumferentially and portions of the labrum appear to overlap the articular surface of the glenoid or articular surface. This overlap portion of the glenoid labrum appears to deepen the glenoid, providing some inherent stability to the glenohumeral joint, primarily by restricting anterior excursion. The glenoid surface of the labrum is continuous with the hyaline cartilage of the glenoid cavity, whereas the capsular surface blends with the joint capsule and glenohumeral ligaments. There can be variations in the width or thickness of the glenoid labrum, particularly at the different locations of the glenoid as it relates to the glenoid rim. Thus, the anterior glenoid may appear to be thicker than the posterior aspect of the glenoid labrum in some individuals. At times, particularly anteriorly, the glenoid labrum can appear to be large and almost hypermobile; occasionally it appears to be analogous to a meniscus that can be seen arthroscopically in the knee joint. At other times, the glenoid labrum can be smaller and appears to be more firmly attached to the edge of the glenoid and to blend more with the actual hyaline cartilage surface. One common anatomic variant of the anterior labrum is the Buford complex, which involves a cordlike middle glenohumeral ligament that attaches to the superior labrum; also, the anterior labrum above the midglenoid notch is absent.52
Figure 6-1. Arthroscope in place through a posterior portal in a right shoulder.
B A
The normal glenoid labrum should appear to be smooth and lack any fraying, partial tearing, or excessive hypermobility. The usual inspection of the glenoid begins at the insertion of the biceps tendon, which appears to insert through the superior portion of the labrum into the supraglenoid tubercle. With traction placed on the arm with the traction apparatus, portions of the inferior glenoid rim can be visualized. Slight retraction and posterior rotation
Figure 6-2. Relative interval between infraspinatus and teres minor muscles. This cadaveric specimen shows the relative interval between the infraspinatus (A) and teres minor (B) muscles traversed by the arthroscope when establishing a posterior portal.
B Figure 6-3. Biceps tendon and other structures. A, Arthroscopic view of a right shoulder with the patient in lateral decubitus position and the arm abducted 45 degrees. Structures that can be identified are the long head of the biceps tendon (A), superior glenohumeral ligament (B), anterior portion of the glenoid labrum (C), and humeral head (D). B, Biceps tendon is oriented in a vertical direction (A). The supraspinatus portion of the rotator cuff (B) is just superior and intimately related to the biceps tendon in this view.
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D B A
A C
A
B
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of the arthroscope will allow examination of the posterior rim of the glenoid labrum from a posterior arthroscopic portal. The arthroscope can be changed to an anterior portal for better visualization of the more posterior portions of the glenoid rim.
Glenohumeral Ligaments The terms superior, middle, and inferior glenohumeral ligaments are used to describe the different thickenings of the anterior and inferior capsule of the shoulder joint. These glenohumeral ligaments are not free-standing distinct ligaments that can be seen, for example, in the ankle or the knee joint; they simply represent the different portions or thickenings of the capsule of the shoulder. There can be much variation in the thickness or presence of the superior, middle, and inferior glenohumeral ligaments. These glenohumeral ligaments stabilize the anterior and inferior portions of the shoulder capsule.47,50,53-56 When viewed arthroscopically, the glenohumeral ligaments are displaced anteriorly because of fluid distention within the shoulder joint. In actuality, these ligaments normally lie closer to the glenoid labrum (Fig. 6-4). Occasionally, they will be seen to have distinct labral origins rather than their usual capsular origins originating off the edge of the glenoid labrum. The superior glenohumeral ligament, together with the coracohumeral ligament, stabilizes the shoulder joint when the arm is in the abducted dependent position.50,53 This ligament has two proximal attachments—one to the superior aspect of the labrum conjoined with the biceps tendon and one to the
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base of the coracoid.56 This ligament courses laterally to insert on the anterior aspect of the anatomic neck of the humerus. The superior glenohumeral ligament can occasionally be seen near the insertion of the biceps tendon into the superior aspect of the glenoid; however, it may be hidden behind the biceps tendon or may appear to be absent. The middle glenohumeral ligament stabilizes the glenohumeral joint when the shoulder is abducted 45 degrees.56 Although the attachments of this ligament are wide, they may be difficult to visualize arthroscopically. However, the middle portion of the ligament can usually be seen just posterior to the subscapularis tendon, with which it occasionally appears to fuse. The middle glenohumeral ligament extends from just beneath the superior glenohumeral ligament, along the anterior border of the glenoid, to the junction of the middle and inferior third of the glenoid rim, except in cases of a Buford complex, as previously described. It blends with the capsule of the anteroinferior aspect of the shoulder joint and inserts near the lesser tuberosity over the anterior aspect of the anatomic neck of the humerus. The inferior glenohumeral ligament consists of an anterior and posterior band. The anterior band provides stability when the arm is abducted and externally rotated, whereas the posterior band stabilizes the shoulder in abduction and internal rotation.57 This triangular ligament arises from the anteroinferior and posteroinferior margins of the glenoid and inserts into the inferior aspect of the surgical neck of the humerus. Both the anterior and posterior bands can be seen arthroscopically when the arm is in abduction.
Subscapularis Tendon and Recess
C
A
D
E
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Figure 6-4. Intra-articular structures that can be visualized arthroscopically in a right shoulder. These include the long head of the biceps tendon (A), superior glenohumeral ligament (B), subscapularis tendon (C), middle glenohumeral ligament (D), and inferior glenohumeral ligament (E).
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With the arm in the abducted position, the posterosuperior aspect of the subscapularis tendon can be seen over the anterior aspect of the shoulder between the superior and middle glenohumeral ligaments (Fig. 6-5). At times, however, the subscapularis tendon may be obscured by or appear to blend with the middle glenohumeral ligament. When viewed in most anatomy textbooks or when viewed grossly at the time of open or arthrotomy surgery to the shoulder, the subscapularis muscle and tendon usually appear to be a broad flat structure extending from the more medial aspects of the anterior aspect of the scapula to insert onto the lesser tuberosity of the humerus. However, at the time of arthroscopic surgery, with the patient’s arm abducted approximately 45 degrees, and when viewed from a posterior arthroscopic portal, only the posterosuperior edge of the tendon can be seen, which now appears to be a distinct ropelike banded structure, different from that normally seen in anatomy textbooks (Fig. 6-6). The subscapularis recess is found over the anterior aspect of the shoulder in the area of the middle glenohumeral ligament. There can be much variation in the appearance of the relationship of the middle glenohumeral ligament to the recess, which occasionally can appear to be absent.
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A A B Figure 6-5. Posterosuperior aspect of the subscapularis tendon. A, Subscapularis tendon (A), middle glenohumeral ligament (B), and anterior aspect of glenoid labrum (C) in a right shoulder. B, Arthroscopic view of subscapularis tendon (A) and middle glenohumeral ligament (B) in a right shoulder.
B C
A
Rotator Cuff Arthroscopic evaluation of the rotator cuff begins by identifying the biceps tendon and obtaining proper orientation. The supraspinatus portion of the rotator cuff can be seen just superior to the biceps tendon (Fig. 6-7A). To visualize the more posterior portions of the rotator cuff, the arthroscope is
B
retracted and directed superiorly and slightly posteriorly to reveal the insertion of the tendinous portion of the infraspinatus and teres minor into the humeral head (see Fig. 6-7B). Arthroscopically, the more posterior portions of the rotator cuff inserting into the humeral head and moving toward the glenoid surface are visualized, the posterior portions of the rotator cuff appear to blend with the posterior capsule. The rotator cuff should be one continuous structure and free of any partial tears, complete tears, or fraying. The attachment of the rotator cuff should be firm, and no bone should be visualized beneath the insertion site.
A
B
When viewed arthroscopically, the articular surface of an intact rotator cuff will have an arching cable-like thickening of the capsule surrounding a thinner crescent of tissue that inserts on the greater tuberosity.58,59 This cable-like structure extends from the biceps to the inferior margin of the infraspinatus, spanning the supraspinatus and infraspinatus insertions at the avascular zone margin. The rotator cable potentially serves a protective role, allowing stress to be transferred along the cable and thereby protecting the thinner, avascular, crescent tissue attachment of the cuff.
Rotator Interval The rotator interval is the space between the supraspinatus and subscapular tendons. This interval is easily identified arthroscopically while viewing the posterior portal. During arthroscopy, the interval is defined as the triangular space outlined by the anterior edge of the supraspinatus tendon, superior edge of the subscapularis tendon, and anterior rim of the glenoid. This space is the location of the standard anterior portal. Plication of this interval is sometimes done while treating certain types of instability patterns.60
Superior Recess and Subacromial Space Figure 6-6. Posterosuperior edge of subscapularis tendon and biceps tendon. This cadaveric specimen shows the posterosuperior edge of the subscapularis tendon (A) and biceps tendon (B) when viewed from a posterior arthroscopic portal.
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The superior recess is located superior to and slightly anterior to the superior aspect of the glenoid and to the insertion of the biceps tendon (Fig. 6-8).
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B
A
A
A
B
Figure 6-7. Rotator cuff. A, Arthroscopic view of the biceps tendon (A) and supraspinatus portion of the rotator cuff (B) in a right shoulder. B, Arthroscopic view of the more posterior portions of the rotator cuff (infraspinatus and teres minor) in a right shoulder (A).
The subacromial space, or subacromial bursa, is the area inferior to the distal clavicle, acromioclavicular joint, and acromion and superior to the humeral head and rotator cuff. This subacromial space is bordered superiorly by the subacromial arch that consists of the undersurface of the acromion, outer end of the clavicle, acromioclavicular joint, and coracoacromial ligament, which forms a fibrous roof. The base of the subacromial space is the greater tuberosity of the humerus and the insertion of the rotator cuff. The subacromial bursa forms the actual joint cavity (Fig. 6-9). The subacromial bursa attaches superiorly to the undersurface of the acromion and below to the greater tuberosity at the insertion of the rotator cuff tendons.61 Arthroscopic visualization of the subacromial bursa is sometimes difficult; many clinicians believe that visualization of this subacromial bursa should always be difficult if the
patient has an impingement syndrome29 or other pathology in the subacromial space. If a normal-appearing bursa is seen, the patient’s problems are probably not related to the subacromial space nor to an impingement problem. Structures that should be visualized in the subacromial space are the inferior surface of the acromion, the acromioclavicular joint, the superior portion of the coracoacromial ligament, the superior surface of the rotator cuff, and the bursa itself. On entering the subacromial bursa through a posterior portal, a bursal curtain or sheet is often encountered, which can make visualization difficult (Fig. 6-10). The arthroscope has to be passed well anterior to this bursa shelf for the actual subacromial space itself to be visualized. Once in the subacromial space, it is possible to identify the inferior surface of the acromion, which is covered by periosteum and extended fibers from the coracoacromial ligament and
C
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E
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Figure 6-8. Superior recess. This is located just above the biceps tendon insertion or to the left of the biceps tendon (A) in this arthroscopic view of a right shoulder.
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Figure 6-9. Subacromial space structures. These include the bursa (A), rotator cuff (B), acromion (C), coracoacromial ligament (D), and acromioclavicular joint (E).
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B A
A
Figure 6-12. Superior surface of the rotator cuff. This arthroscopic subacromial space visualization shows the superior surface of the rotator cuff (A) in a right shoulder. Figure 6-10. Arthroscopic view of bursal shelf or curtain. The bursal shelf (A) is normally seen on visualization of the subacromial space (B) in a right shoulder.
therefore has a softer appearance as compared with a bony appearance. Also, it is possible to visualize clearly the superior portion of the coracoacromial ligament (Fig. 6-11). The superior surface of the rotator cuff should be inspected carefully for any evidence of partial tearing or full-thickness tears and should have a smooth homogenous appearance (Fig. 6-12). Portions of the inferior surface of the acromioclavicular joint can usually be visualized arthroscopically. However, it
may be obscured by a large fat pad covering the inferior surface of this joint. The subacromial bursa is a reasonably large space, and in the absence of any pathologic processes, most structures described can be viewed arthroscopically. In the presence of pathologic processes such as subacromial bursitis or inflammation, or with partial or complete rotator cuff tears, the subacromial space at times can be almost obliterated by hypertrophic bursal tissue. In such cases, visualization is almost impossible until a space is created, with the motorized instrumentation performed arthroscopically.
SUMMARY
B A
Diagnostic and operative arthroscopy of the shoulder is a reasonably demanding surgical procedure. Attention to detail is required to perform a safe, reproducible, and systematic arthroscopic evaluation. The structures described in this chapter should be visualized on each arthroscopic evaluation of the shoulder, which should be performed systematically to ensure an accurate and reproducible examination.
References
Figure 6-11. Superior portion of the coracoacromial ligament. This arthroscopic subacromial space visualization shows the inferior surface of the acromion (A) and superior edge of coracoacromial ligament (B) in a right shoulder.
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1. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117, 1985. 2. Andrews JR, Carson WG, McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337, 1985. 3. Andrews JR, Carson WG: Shoulder joint arthroscopy. Orthopedics 6:1157, 1983.
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4. Andrews JR, Carson WG: Operative arthroscopy of the shoulder in the throwing athlete. In Zarins B, Andrews JR, Carson WG (eds): Injuries to the Throwing Arm. Philadelphia, WB Saunders, 1985, p 84. 5. Andrews JR, Carson WG: Arthroscopic surgery of the shoulder. In Parisien JS (ed): Arthroscopic Surgery. New York, McGraw-Hill, 1987, p 231. 6. Gross RM, Fitzgibbons TC: Shoulder arthroscopy: A modified approach. Arthroscopy 1:156, 1985. 7. Neviarser TJ: Arthroscopy of the shoulder. Orthop Clin North Am 18:361, 1987. 8. Ogilvie-Harris DJ, Wiley AM: Arthroscopic surgery of the shoulder. J Bone Joint Surg Br 68:201, 1986. 9. Johnson LL: Shoulder arthroscopy. In Johnson LL (ed): Arthroscopic Surgery. St. Louis, Mosby, 1986, p 1301. 10. McFlynn FJ, Caspari RB: Arthroscopic findings in the subluxing shoulder. Clin Orthop 183:173, 1984. 11. Snyder SJ, Kargel RP, DelPizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274, 1990. 12. Wheeler JH, Ryan JB, Arciero RA, Moliman RN: Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy 5:213, 1989. 13. Buss DD, Warren RF, Galinat BJ: Indications for shoulder arthroscopy. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 465. 14. Andrews JR, Heckman MM: Shoulder arthroscopy, operating room set-up. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 473. 15. Snyder SJ, Ramer RD, Walbert E: Labral lesions. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 491. 16. Meyers JF: Arthroscopic debridement of the acromioclavicular joint and distal clavicle resection. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 557. 17. Matthews LS, Wolock BS, Martin DF: Arthroscopic management of degenerative arthritis of the shoulder. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 567. 18. Gartsman GM, Combs AH, Davis PF, Tullos HS: Arthroscopic acromioclavicular joint resection. An anatomical study. Am J Sports Med 19:2, 1991. 19. Andrews JR, Carson WG, Ortega K: Arthroscopy of the shoulder: Technique and normal anatomy. Am J Sports Med 12:1, 1984. 20. Matthews LS, Zarins B, Michael RH, Helfet DL: Anterior portal selection for shoulder arthroscopy. Arthroscopy 1:33, 1985. 21. Carson WG: Arthroscopy of the shoulder: Normal anatomy. In Zarins B, Andrews JR, Carson WG (eds): Injuries to the Throwing Arm. Philadelphia, WB Saunders, 1985, p 83. 22. Wolf EM: Anterior portals for shoulder arthroscopy. Arthroscopy 5:201, 1989. 23. Andrews JR, Carson WG: Arthroscopic anatomy of the shoulder. Shoulder surgery in the athlete. In Jackson DW (ed): Techniques in Orthopaedics. Rockville, Md, Aspen Systems, 1985, p 25. 24. Blanchut PA, Day B: Arthroscopic anatomy of the shoulder. Arthroscopy 5:1, 1989. 25. Matthews LS, Fadale PD: Subacromial anatomy for the arthroscopist. Arthroscopy 5:36, 1989. 26. Arnoczky SP, Altchek DW, O’Brien SJ: Anatomy of the shoulder. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 425.
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27. Souryal TO, Baker CL: Anatomy of the supraclavicular fossa portal in shoulder arthroscopy. Arthroscopy 6:297, 1990. 28. Ellman H: Arthroscopic subacromial decompression. Analysis of one- to three-year results. Arthroscopy 3:173, 1987. 29. Ellman H: Arthroscopic acromioplasty. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 543. 30. Snyder SJ, Pachelli AF, DelPizzo W et al: Partial-thickness rotator cuff tears: Results of arthroscopic treatment. Arthroscopy 7:1, 1991. 31. Levy HJ, Uribe JW, Delaney LG: Arthroscopic-assisted rotator cuff repair: Preliminary result. Arthroscopy 6:55, 1990. 32. Paulos LE, Franklin JL, Beck CL: Arthroscopic management of rotator cuff tears. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 529. 33. Levy JH, Gardner RD, Lemak LJ: Arthroscopic subacromial decompression in the treatment of full thickness rotator cuff tears. Arthroscopy 7:8, 1991. 34. Caspari RB, Savoie FH: Arthroscopic reconstructions of the shoulder: The Bankart repair. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 507. 35. Morgan CD, Bodenstab AB: Arthroscopic Bankart suture repair: Technique and early results. Arthroscopy 3:111, 1987. 36. Hawkins RB: Arthroscopic stapling repair for shoulder instability: A retrospective study of 50 cases. Arthroscopy 5:122, 1989. 37. Detrisac DA: Arthroscopic shoulder staple capsulorrhaphy for traumatic anterior instability. In McGinty JB (ed): Operative Arthroscopy. New York, Raven Press, 1991, p 517. 38. Matthews LS, Vetter WL, Oweida SJ, et al: Arthroscopic staple capsulorrhaphy for recurrent anterior shoulder instability. Arthroscopy 4:106, 1988. 39. Wiley AM: Arthroscopy for shoulder instability and a technique for arthroscopic repair. Arthroscopy 4:25, 1988. 40. Matthews LS, Helfet DL, Spearman J, Oweida S: Arthroscopic staple capsulorrhaphy for anterior instability of the shoulder. Arthroscopy 2:116, 1986. 41. Burkhart SS, Morgan C: SLAP lesions in the overhead athlete. Orthop Clin North Am 32:431, 2001. 42. Goubier JN, Iserin A, Augereau B: The posterolateral portal: A new approach for shoulder arthroscopy. Arthroscopy 17:1000, 2001. 43. Cole BJ, El Attrache NS, Anbari A: Arthroscopic rotator cuff repairs: An anatomic and biomechanical rationale for different suture–anchor repair configurations. Arthroscopy 23:662, 2007. 44. Burkhart SS: A stepwise approach to arthroscopic rotator cuff repair based on biomechanical principals. Arthroscopy 16:82, 2000. 45. Bankart ASB: The pathology and treatment of recurrent dislocation of the shoulder joint. Br J Surg 26:23, 1938. 46. DePalma AF: Surgery of the Shoulder. Philadelphia, JB Lippincott, 1973. 47. Bost FC, Inman VT: The pathological changes in recurrent dislocation of the shoulder. A report of Bankart’s operative procedure. J Bone Joint Surg Am 24:595, 1942. 48. Dutoit GT, Roux D: Recurrent dislocation of the shoulder. A twenty-four year study of the Johannesburg stapling operation. J Bone Joint Surg Am 38:1, 1956. 49. Warwick R, Williams P (eds): Gray’s Anatomy of the Human Body. Philadelphia, WB Saunders, 1973. 50. Mosely JF, Overgaard B: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 44:913, 1962.
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51. Rowe CR, Patell D, Southmayd WW: The Bankart procedure. a long-term, end-results study. J Bone Joint Surg Am 60:1, 1978. 52. Williams MM, Snyder SJ, Buford D Jr.: The Buford complex: The cord-like middle glenohumeral ligament and absent anterosuperior labrum complex: A normal anatomic capsulolabral variant. Arthroscopy 10:241, 1994. 53. Basmajian JV, Bazant FJ: Factors preventing downward dislocation of the adducted shoulder. J Bone Joint Surg Am 41:1182, 1959. 54. Rowe DR, Zarins B: Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am 63:863, 1981. 55. Schlemm F: Über die verstarkungsbander am schultergelenk. Arch Anat 45, 1853. 56. Turkel SJ, Panio MW, Marshall JL, et al: Stabilizing mechanism preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208, 1981.
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57. O’Brien SJ, Schwartz RS, Warren RF, Torzilli PA: Capsular restraints to anterior-posterior motion of the abducted shoulder: A biomechanical study. J Shoulder Elbow Surg 4:298, 1995. 58. Clark JM, Harryman DT II: Tendons, ligaments, and capsule of the rotator cuff. J Bone Joint Surg Am 74:713, 1992. 59. Burkhart SS, Esch JC, Jolson RC: The rotator crescent and rotator cable: An anatomic description of the shoulder’s “suspension bridge.” Arthroscopy 9:611,1993. 60. Field LD, Warren RF, O’Brien SJ, et al: Isolated closure of rotator interval defects for shoulder instability. Am J Sports Med 23:557, 1995. 61. Ellman H: Arthroscopic subacromial decompression. In Parisien JS (ed): Arthroscopic Surgery. New York, McGraw-Hill, 1988, p 243.
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CHAPTER 7 Operative Arthroscopy of the Shoulder Scott B. Reynolds, Joe P. Bramhall, Dorothy F. Scarpinato, and James R. Andrews
Understanding the management of the athlete’s shoulder has been difficult and controversial. With the different technological advances and convergence of ideas from orthopedic surgeons who perform shoulder surgery, a better understanding of the pathology and treatment is continuing to evolve. Surgical treatment, in general, should be as conservative as possible. Operative arthroscopy has its role, especially after conservative treatment fails. For other more severe cases, open operative intervention still has a place in the treatment armamentarium.
8 mm of the anterior acromion, extending medially to the acromioclavicular joint and beveled posteriorly for about 2 cm. This is a technically demanding procedure, and care should be taken to control bleeding.
This section addresses special considerations for the indications and contraindications for arthroscopic examination of the athlete’s shoulder and its use for treatment of the throwing athlete’s shoulder. The actual recognition and treatment of each of these pathologies are addressed in other chapters in this text.
Arthroscopic decompression of the subacromial space has minimal morbidity because the insertion of the deltoid is not violated.4 It also allows for early rehabilitation, which in turn allows for an earlier return to competition.
If there is partial tearing of the superior surface of the rotator cuff, this may be débrided to healthy bleeding tissue or repaired. At this time, the humeral head is rotated to assess the adequacy of the amount of space available between the acromion and rotator cuff.
Secondary Compressive Cuff Disease Impingement may be secondary to another underlying problem, such as glenohumeral instability.4 The correct diagnosis is mandatory, because treatment includes alleviating the primary problem. The patient may present only with a complaint of pain; therefore, a thorough history and physical examination must be performed. Emphasis should be placed on comparing range of motion and anteriorposterior translation of the humeral head to the opposite shoulder. Generalized ligamentous laxity should be noted. A special test that is helpful to determine anterior capsular laxity is Lachman’s test of the shoulder, which is similar to Lachman’s test of the knee for anterior cruciate ligament laxity. With the patient supine and the shoulder abducted 90 degrees and externally rotated about 45 degrees, an anterior force is applied to the humeral head to assess the anterior translation of the glenohumeral joint and end point of the anterior capsule.
COMPRESSIVE CUFF DISEASE Primary Compressive Cuff Disease Primary compressive cuff disease can be a primary cause for cuff disease when associated with a type III hooked acromion,1 degenerative spurs, os acromiale or, in some cases, a congenitally thickened coracoacromial ligament. It can also be caused by the prominence of a degenerated acromioclavicular joint. Compressive cuff disease results in an outside-in type of rotator cuff tear. Overhead sports movements that require using the arm in a 90-degree or greater horizontally abducted position, with rotation into internal and horizontal adduction, are likely to produce impingement symptoms. These are reproducible on physical examination by forceful forward flexion (positive impingement sign).2 Pain relief by injecting 1% lidocaine into the subacromial space helps confirm the diagnosis. Most patients respond to a conservative program of active rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and progressive rotator cuff strengthening and stretching exercises.3
If anterior laxity is evident, the compressive cuff disease may be secondary to anterior shoulder laxity. If only mild instability is present, treatment options in this situation include rehabilitation, with an emphasis on dynamic stabilization by muscular strengthening. If this fails, arthroscopic or open stabilization may be warranted. Primary rotator cuff failure from tensile overload may also cause secondary impingement. This failure occurs because of repetitive tensile overloading of the cuff, as is seen in the deceleration phase of throwing. These forces encountered in athletic activity may ultimately exceed the ability
If the athlete’s symptoms are not relieved by nonoperative measures, surgical treatment may be warranted. Arthroscopy of the subacromial space may reveal bursitis that can be easily débrided with a motorized resector. An acromioplasty is performed using a motorized burr, removing approximately 99
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of the dynamic stabilizers and anterior static stabilizers of the rotator cuff to compensate, which may lead to a secondary impingement phenomenon of the rotator cuff.4 Again, rehabilitation may be the first line of treatment; if this fails, arthroscopic débridement of the tensile tear is performed, along with anterior stabilization, decompression of the coracoacromial arch, or both, as necassary.
INTERNAL IMPINGEMENT Internal impingement is a concept that has developed as our understanding of the thrower’s shoulder has evolved. Walch and colleagues5 had initially described pinching of the posterosuperior rotator cuff between the posterosuperior glenoid labrum and greater tuberosity as the arm is abducted and externally rotated. Jobe6 has hypothesized that internal impingement is exacerbated in overhead throwing athletes with anterior microinstability. Burkhart and associates7 have emphasized that type II superior labral anterior-posterior (SLAP) lesions are a major pathology associated with the symptoms of internal impingement. The arthroscopic findings associated with internal impingement include a combination of injuries involving partial-thickness, articular-sided, rotator cuff tears in the posterior supraspinatus and anterior infraspinatus.8-10 There is also typical pathology of the posterior superior labrum and changes on the posterior humeral head, including an expanded bare area and cyst formation.5,6,11 In addition, most shoulders are believed to have a component of anterior microinstability, 6,12,13 which worsens the internal impingement, or a tight posteroinferior capsule,7 resulting in posterosuperior glenohumeral translation and anteroinferior pseudolaxity. The implications and treatment of these findings will be discussed in further detail in later chapters.
TENSILE LESIONS
rotation weakness from the abducted position. Magnetic resonance imaging may reveal a partial undersurface tear of the rotator cuff. Initially, the athlete is started on a rehabilitation program, with emphasis on strengthening the rotator cuff. If there is no improvement over 2 to 3 months, arthroscopy may be performed, which will reveal a partial tearing of the undersurface of the rotator cuff at or near its insertion into the humeral head. Arthroscopic débridement with a motorized shaver is performed to healthy, bleeding tissue.3,8 If the tear involves more than 50% thickness of the tendon insertion, repairing the tear is often recommended.14-16 Next, inspection of the subacromial space is performed. Frequently, there are no signs of impingement intraoperatively but, in chronic cases, secondary impingement may be present, with further tearing of the outer surface of the rotator cuff. In these cases, subacromial decompression with an acromioplasty should be performed (Fig. 7-1). Andrews and colleagues8 have reported on 34 athletes with partial tears who underwent arthroscopic débridement. Of these, 76% had excellent results and 9% had good results, and all were able to return to their previous athletic activities; 15% were rated as poor results and were not able to return to competitive throwing. Débridement of partial rotator cuff tears appears to reduce the pain in the athlete’s shoulder sufficiently to enable him or her to engage in a program of progressive strengthening exercises3 and to make a gradual return to competitive throwing, which usually takes 6 months or longer. Biceps-labral complex tears are believed to occur during the deceleration and follow-through phase of throwing. Large forces are placed on the proximal attachment of the biceps tendon at or near 90 degrees of abduction; the
The tensile lesions usually seen in the athlete’s shoulder occur as undersurface rotator cuff tears, biceps-labral complex tears, or both. The mechanism of injury in a primary tensile rotator cuff tear is deceleration of the rotator cuff as it resists horizontal adduction and internal rotation, anterior translation, and distraction forces seen during the deceleration phase of throwing. This results in eccentric tensile overload failure. Partial tears usually develop secondary to repetitive microtrauma.3 These are found in the region of the undersurface of the supraspinatus tendon and may extend posteriorly to the area of the infraspinatus tendon. These tears may also be found isolated to the infraspinatus tendon and posterior cuff capsule. It is not uncommon, especially in throwing athletes, for the athlete to experience pain only during the pitching motion. On physical examination, tenderness may be elicited over the supraspinatus or infraspinatus tendons, or both. If weakness is present; it is usually found by testing for external
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Figure 7-1. Acromioplasty—postarthroscopic subacromial decompression.
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humerus internally rotates at the same time as deceleration of elbow extension is occurring.17,18 There may also be some type of concurrent entrapment of the biceps-labral complex associated with glenohumeral laxity. Physical examination may reveal a popping or catching when the arm is in full abduction and external rotation, brought out by circumducting the humeral head on the glenoid—the clunk test. This test is performed with the patient in the supine position.18 The examiner’s hand lies posterior to the humeral head, applying an anterior directed force, while the opposite hand rests on the distal humerus, rotating the humerus. The patient’s arm is brought into the full overhead abducted position, assessing for a clunk or grind in the shoulder, suggesting a labral tear. At arthroscopy, a tear of the labrum in the anterosuperior quadrant at the insertion of the long head of the biceps is evident (Fig. 7-2). A partial tear of the biceps tendon near its origin may also be evident. Andrews and coworkers17 have suggested a mechanism for the anterosuperior glenoid labral tear. In 73 shoulder arthroscopies performed in pitchers and throwing athletes with labral tears, 83% had glenoid labral tearing at the biceps-labral complex anterosuperiorly; electrical stimulation of the biceps in 5 patients at arthroscopy produced tension in the biceps tendon and lifting up of the superior labrum off the glenoid. It was hypothesized that this eccentric contraction may cause tearing of the anterosuperior labrum.17 Treatment for this lesion usually entails limited arthroscopic débridement of the labral tear, if stable, as well as the biceps tendon if it is partially torn.3 If unstable, the labral tear should be repaired. Infrequently, the tear may propagate into the superior attachment of the middle and inferior glenohumeral ligaments, with the subsequent development of instability. If this is the case, the lesion should be repaired. Arthroscopic débridement is followed by rehabilitation.
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ROTATOR CUFF TEARS As noted, proposed mechanisms for rotator cuff tears in overhead throwing athletes have included eccentric tendon failure caused by overuse, secondary impingement from instability, and internal impingement of the rotator cuff on the posterior superior labrum.5,6,8,19-22 Most likely, these mechanisms all overlap somewhat and contribute to each individual’s rotator cuff injury to a different degree. In addition, a traumatic injury can result in an acute rotator cuff tear, although this is less common in the young athlete. Rotator cuff tears include a spectrum ranging from partialthickness to full-thickness tears, both of which can be managed arthroscopically with débridement or repair. It is generally agreed that any full-thickness tear should be repaired. Management of partial-thickness tears has been somewhat more controversial and continues to evolve. Results of rotator cuff débridement for partial tears have been favorable, but tears of more than 50% thickness are usually repaired.8,14-16,23,24 Arthroscopically, the depth of a tear is determined by estimating the distance of the intact cuff from the articular surface. That distance is then considered as a percentage of 14 mm, which is the size of the average supraspinatus footprint as determined by Dugas and colleagues.25 Again, the topic of rotator cuff tears in athletes will be discussed in more detail in later chapters.
GLENOHUMERAL LAXITY Generally, the diagnosis of shoulder laxity can be made on the basis of the history and physical findings. The athlete may have a history of documented anterior dislocation with subsequent redislocations, or the athlete may present only with the complaint of pain, clicking, or the so-called dead arm syndrome.26 In this syndrome, the athlete feels a sudden sharp or paralyzing pain when the shoulder is externally rotated forcibly in the abducted overhead position. The most reliable finding on physical examination is the apprehension test, in which the abducted arm is rotated externally while forward pressure is exerted on the humeral head. This pushes the humeral head forward against the anterior capsule. If the patient experiences pain and apprehension, this suggests anterior instability.
Figure 7-2. Biceps-labral complex tear.
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Approximately 50% of patients with shoulder subluxation are unaware of it.26 Therefore, physical examination, radiography, and arthroscopy become important aids in the diagnosis.27-29 After the patient is administered general anesthesia, the shoulder is examined and compared with the contralateral shoulder. Range of motion and anteriorposterior translation are assessed, and the clunk test is carried out. Next, diagnostic arthroscopy is performed to assess redundancy of the anterior capsule and glenohumeral ligaments.28,30 The glenoid labrum is evaluated and
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probed, looking for tears and detachment. A detachment of the inferior glenohumeral ligament–labral complex from the lower one half of the glenoid margin is most often associated with anterior instability.27-29 Under direct visualization using the arthroscope, the humeral head is pushed anteriorly, posteriorly, and inferiorly, and the amount of translation or subluxation is noted. This is helpful in deciding the main direction of instability, although it may be difficult to measure humeral head subluxation with arthroscopy. Also, the presence of a drive-through sign seen arthroscopically helps confirm the diagnosis of instability. The drive-through test is performed by sweeping the scope from superior to inferior between the glenoid and humeral head. If the scope can easily be driven through, the test is positive. If the labrum is torn, repair may be done arthroscopically or with an open procedure. A decision must be made regarding the treatment plan. Athletes with mild instability may be tried with strengthening exercises first29; if this fails, further intervention may be warranted. Athletes with moderate to severe instability may require an arthroscopic or open stabilization procedure. If there is an early true Bankart lesion, arthroscopic repair may be performed as described by Caspari,31 Johnson,32 and Morgan and Bodenstab.33 Postoperatively, the shoulder is immobilized in the adducted and internally rotated position in a shoulder immobilizer for 4 weeks to ensure soft tissue healing. At the American Academy of Orthopaedic Surgeons meeting in 1989, Caspari31 reported a 4% resubluxation rate for the arthroscopic Bankart repair, with 90% good or excellent results. Regardless of this early enthusiasm for the arthroscopic repair of the unstable shoulder, some surgeons still do not recommend this procedure for athletes returning back to contact sports.
such as in throwing, tennis, and swimming.35 It may also be caused by forceful entrapment associated with an avulsion sprain of the biceps-labrum complex between the humeral head and glenoid rim, such as a player diving to catch a baseball on the outstretched arm (Fig. 7-3). A significant percentage of labral tears in the throwing athlete involve the anterosuperior portion near the insertion of the long head of the biceps tendon and are not associated with instability.36 Pappas and associates37 have noted a functional instability from the torn hypermobile labrum. There was no increase in glenohumeral translation, but the patient felt insecure about the shoulder. It was theorized that there is clicking, catching, or locking in the joint secondary to the intermittent interposition of a partially attached fragment or bucket-handle tear between the glenoid and humeral head (Fig. 7-4). One must always be cautious because these functional tears may represent occult laxity and lead to overt instability. Arthroscopy is indicated for the athlete with persistent shoulder pain, symptoms of catching, and demonstrate a positive clunk test on physical examination.35 Andrews and Carson11 reported on arthroscopy in 73 athletes with labral tears and found 83% with anterosuperior tears. After arthroscopic débridement, 88% had good to excellent results at 13.5 months’ follow-up. Arthroscopic repair is indicated for unstable labral tears and will be discussed further in later chapters.
THROWER’S EXOSTOSIS The finding of a posterior glenoid exostosis in throwers with shoulder pain was first described in 1941 by Bennett, who studied a group of professional baseball players.3 The exostosis is located at approximately the 8-o’clock position on a right glenoid and is probably a secondary reaction associated
There is increasing experience regarding arthroscopic treatment of posterior instability. Treatment considerations are the same as those for anterior instability.34 Most athletes will respond to an aggressive exercise program, especially those with generalized ligamentous laxity. Arthroscopy should be considered for those who fail an adequate trial of conservative therapy. Again, a thorough examination under general anesthesia is mandatory. With current techniques, reverse Bankart lesions can be treated and repaired arthroscopically.
GLENOID LABRAL TEARS Not all labral tears are associated with instability.27 SLAP tears may occur with throwing and racquet sports or with some other type of deceleration injury. The mechanism of labral tearing can be caused by repetitive overhead activity,
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Figure 7-3. Anterior glenoid labral tear.
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needed before surgery is indicated. Diagnostic and operative arthroscopy has its role in the treatment armamentarium but caution must be exercised; treatment must be aggressive enough to return the athlete to competition in the shortest period of time but also conservative enough that it does not compromise the athlete’s subsequent performance. There are many factors to consider in the treatment process, thus making the definitive decision a difficult one. This chapter has briefly described the different lesions that may be encountered in the athlete’s shoulder and their arthroscopic management. These lesions are not mutually exclusive but may occur together or secondary to an underlying problem, which must be identified. The following chapter in this section discuss these pathologies in detail and explain different treatment options. Figure 7-4. Anterior glenoid labral tear.
References
with repeated microtrauma and tearing of the posterior and inferior capsule off its glenoid insertion.3 For many years, it was believed that the exostosis was calcification in the long head of the triceps tendon insertion. Arthroscopic resection of this lesion with posterior capsular release has been performed on many pitchers and relieved their symptoms, allowing them to return to competitive pitching.
ACROMIOCLAVICULAR JOINT INJURIES Athletes who lift weights as part of their training program and weightlifters are prone to acromioclavicular joint injuries. These include osteolysis of the distal clavicle secondary to longitudinal shear or compressive forces across the joint and partial or complete acromioclavicular separations secondary to post-traumatic injury to the joint. The athlete usually complains of a dull ache or pain over the acromioclavicular joint. Conservative treatment is tried first, consisting of an NSAID, physical therapy, modification of physical activity and, finally, steroid injection into the joint. If this fails, arthroscopic débridement of the acromioclavicular joint may be performed, with decompression on the acromion and clavicular side of the joint.
CONCLUSIONS AND SUMMARY The athlete with shoulder pathology should be treated conservatively and aggressively at the same time. Usually, the diagnosis is established with the history and physical examination. Ancillary tests are important and may be needed to confirm or substantiate the clinical impressions. Depending on the pathology and time constraints of the athlete, most are first placed on a rehabilitation program. Three months of conservative treatment are generally
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1. Bigliani LU, Morrison DS, April EW: The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 10:216, 1986. 2. Hawkins RJ, Kennedy JC: Impingement syndrome in athletes. Am J Sports Med 8:151, 1980. 3. Andrews JR, Angelo RL: Shoulder arthroscopy for the throwing athlete. In Paulos LE, Tibone JE (eds): Operative Techniques in Shoulder Surgery. Rockville, Md, Aspen, 1991, p 79. 4. Jobe FW, Glousman RE: Rotator cuff dysfunction and associated glenohumeral instability in the throwing athlete. In Paulos LE, Tibone JE (eds): Operative Techniques in Shoulder Surgery. Rockville, Md, Aspen, 1991, p 85. 5. Walch G, Boileau J, Noel E, Donnell ST: Impingement of the deep surface of the supraspinatus tendon on the posterior superior glenoid rim: An arthroscopic study. J Shoulder Elbow Surg 1:238, 1992. 6. Jobe CM: Posterior superior glenoid impingement: expanded spectrum. Arthroscopy 11:530, 1995. 7. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology, Part 1: Pathoanatomy and biomechanics. Arthroscopy 19:404, 2003. 8. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117, 1985. 9. Meister K, Andrews JR: Classification and treatment of rotator cuff injuries in the overhead athlete. J Orthop Sports Phys Ther 18:413, 1993. 10. Paley KJ, Jobe FW, Pink MM, et al: Arthroscopic findings in the overhead throwing athlete: Evidence for posterior internal impingement of the rotator cuff. Arthroscopy 16:35, 2000. 11. Andrews JR, Carson WG: The arthroscopic treatment of glenoid labrum tears in the throwing athlete. Orthop Trans 8:44, 1984. 12. Gross ML, Brenner SL, Esformes I, Sonzogni JJ: Anterior shoulder instability in weight lifters. Am J Sports Med 21:599, 1993. 13. Davidson RA, El Attrache NW, Jobe CM, Jobe FW: Rotator cuff and posterior-superior glenoid labrum injury associated
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14.
15. 16.
17.
18.
19.
20.
21.
22. 23. 24.
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with increased glenohumeral motion: A new site of impingement. J Shoulder Elbow Surg 4:384, 1995. Conway JE: Arthroscopic repair of partial-thickness rotator cuff tears and SLAP lesions in professional baseball players. Orthop Clin North Am 32:443, 2001. Gartsman GM, Milne JC: Articular surface partial-thickness rotator cuff tears. J Shoulder Elbow Surg 4:409, 1995. Millstein ES, Snyder SJ: Arthroscopic management of partial, full-thickness, and complex rotator cuff tears: Indications, techniques, and complications. Arthroscopy 19:189, 2003. Andrews JR, Carson WG, McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337, 1985. Andrews JR, Carson WG, Ortega K: Arthroscopy of the shoulder: Technique and normal anatomy. Am J Sports Med 12:1, 1984. Nirschl RP. Shoulder tendonitis. In Pettrone FA (ed): Symposium on Upper Extremity Injuries in Athletes (American Academy of Orthopaedic Surgeons). St. Louis, Mosby, 1986, pp 322-337. Jobe FK, Kvitne RS: Shoulder pain in the overhead or throwing athlete: The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18:963, 1989. Jobe FK, Pink MM: Classification and treatment of shoulder dysfunction in the overhead athlete. J Orthop Sports Phys Ther 18:427, 1993. Jobe CM: Superior glenoid impingement: Current concepts. Clin Orthop 330:98, 1996. Altchek DW, Carson EW: Arthroscopic acromioplasty: Current status. Orthop Clin North Am 28:157, 1997. Snyder SJ, Pachelli AF, Del Pizzo W, et al: Partial thickness rotator cuff tears: Results of arthroscopic treatment. Arthroscopy 7:1, 1991.
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25. Dugas JR, Cambell DA, Warren RF, et al: Anatomy and dimensions of rotator cuff insertions. J Shoulder Elbow Surg 11:498, 2002. 26. Zarins B, Rowe CR: Current concepts in the diagnosis and treatment of shoulder instability in athletes. Med Sci Sports Exerc 16:444, 1984. 27. Ellman H: Shoulder arthroscopy: Current indications and techniques. Orthopedics 11:45, 1988. 28. McGlynn FJ, Caspari RB: Arthroscopic Findings in the Subluxating Shoulder. Rockville, Md, Aspen, 1991. 29. O’Brien SJ, Warren RF, Schwartz E: Anterior shoulder instability. Orthop Clin North Am 18:395, 1987. 30. Yahiro MA, Matthews LS: Arthroscopic stabilization procedures for recurrent anterior shoulder instability. Orthop Rev 18:1161, 1989. 31. Caspari RB: Arthroscopic reconstruction for anterior shoulder instability. In Paulos LE, Tibone JE (eds): Operative Techniques in Shoulder Surgery. Rockville, Md, Aspen, 1991, p 57. 32. Johnson LL: Shoulder arthroscopy. In Johnson LL (ed): Arthroscopic Surgery, Principles and Practice. St. Louis, Mosby, 1986. 33. Morgan CD, Bodenstab AB: Arthroscopic Bankart suture repair: Technique and early results. Arthroscopy 3:111, 1987. 34. Schwartz E, Warren RF, O’Brien SJ, Fronek J: Posterior shoulder instability. Orthop Clin North Am 18:409, 1987. 35. Andrews JR, Kupferman SP, Dillman CJ: Labral tears in throwing and racquet sports. Clin Sports Med 10:901, 1991. 36. Andrews JR, Gidumal RH: Shoulder arthroscopy in the throwing athlete: Perspectives and prognosis. Arthroscopy 6:565, 1987. 37. Pappas AM, Goss TP, Kleinman PK: Symptomatic shoulder instability due to lesions of the glenoid labrum. Am J Sports Med 11:279, 1983.
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CHAPTER 8 Arthroscopic Techniques
of the Shoulder William B. Geissler, Richard B. Caspari, and Scott B. Reynolds
shoulder.2 The patient is further stabilized with tape running from the side rails across the pelvis. After the anesthesiologist has checked the position of the head, it is covered and lightly taped to prevent any displacement during the procedure (Fig. 8-1). A skin traction device is applied to the forearm after the patient has been prepared and draped, and the arm is suspended by an overhead rope and pulley traction apparatus. The arm is placed in approximately 30 to 40 degrees of abduction and 20 degrees of forward flexion. The arm is suspended by 10, 15 or, rarely, 20 pounds of traction, which provides distraction and inferior subluxation of the humerus. This displacement allows the surgeon to see and work in the anteroinferior area of the glenoid, where most pathology related to anterior instability is located. In the beach chair position, the patient is placed as if sitting in a chair.3 The head must be carefully supported in a neutral position to prevent hyperextension. The body is again supported and stabilized in place. The operative arm is draped free to allow full access to the shoulder. Temporary traction may be applied by a surgical assistant, if required, during the procedure.
The techniques of diagnostic and surgical shoulder arthroscopy have become a valuable adjunct in the management of shoulder disorders. A thorough understanding of the anatomy of the shoulder girdle is mandatory as the complexity of arthroscopic shoulder procedures continues to expand. Precise placement of arthroscopic portals is imperative in the shoulder because of the proximity of many neurovascular structures and the muscles that are perforated. This chapter reviews the operative technique and anatomy pertaining to establishing the various portals for arthroscopic surgery of the shoulder.
OPERATIVE TECHNIQUE The importance of the operating room setup cannot be overemphasized for a successful and efficient arthroscopic shoulder procedure. The procedure may be performed under general endotracheal anesthesia or interscalene block. Most surgeons prefer general endotracheal anesthesia, particularly if the lateral decubitus position is used. Intubation in this position is difficult if the patient becomes uncomfortable and may require re-preparing and draping. Interscalene blocks are more frequently used when the patient is placed in the beach chair position. This allows the patient to help position himself or herself for the procedure, and the anesthesiologist has more optimal access to the patient’s airway if the need should arise.
In both positions, the monitor, light, and power equipment source are placed opposite the patient’s shoulder in front of the surgeon. The scrub nurse and Mayo stand can be situated just in front of the surgeon toward the foot of the table for both positions, or at the head of the operating table for the lateral decubitus position (Fig. 8-2). Using these setups, the surgeon has easy access to the whole shoulder without having to move any equipment or personnel.4 The scrub nurse is in the ideal position to pass instruments and to assist the surgeon when needed. The standard-sized instruments that are used for the knee may be used for the shoulder.
Vital information is gained from examination of the shoulder under anesthesia, and this opportunity should not be missed. The shoulder girdle muscles are relaxed, allowing the examiner to translocate the humeral head on the glenoid freely and measure any existing instability. The evaluation also should include range of motion of both shoulders, noting any limitations in passive motion suggestive of adhesive capsulitis. Occasionally, increased external rotation in abduction is observed, reflecting anterior capsular laxity and possible anterior instability. In cases of shoulder subluxation, the information obtained from the clinical examination is correlated with the arthroscopic findings to confirm the diagnosis.1 After the clinical examination, the patient is placed in the lateral decubitus or beach chair position, depending on the surgeon’s preference. In the lateral decubitus position, the patient is placed on his or her side with the affected shoulder up. The patient is supported by an inflatable beanbag or kidney rests, or both. It is important to tilt the patient back 30 degrees to allow easier access to the front of the
EXTERNAL ANATOMY Knowledge of the external anatomy and palpable landmarks of the shoulder is essential for precise portal placement. Palpable bony landmarks include the clavicle and coracoid anteriorly, the acromion laterally, and the scapular spine posteriorly. The coracoid is located just inferior to the palpable acromioclavicular joint. It is important to note the location of the coracoid when making an anterior portal because the neurovascular bundle runs medial to it. The posterior lateral corner of the acromion is almost always palpable, no matter how large or obese the patient. This is 105
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Figure 8-1. Patient positioning. The patient is placed in the lateral decubitus position and slanted back 30 degrees for easier access to the front of the shoulder. Figure 8-3. External anatomy and relative positions of arthroscopic portals. The letter “X” anteriorly marks the coracoid process. Note the position of the posterior portal medial to the posterolateral edge of the acromion.
It is important to maintain a portal in the shoulder once it has been established, because the chance of reintroducing an instrument or cannula exactly through the same hole in the tissue is remote.5 Attempts to re-establish a previous portal not only lead to unnecessary soft tissue damage but also promote extravasation of irrigation fluid into the soft tissues, obliterating bony landmarks. Therefore, interchangeable cannula systems are used that allow passage of the arthroscope and motorized instruments through the same cannula.
Figure 8-2. Lateral decubitus position. The arm is suspended 30 to 40 degrees. Note the Mayo stand at the head of the table. The light source and camera cords are passed under the arm and the shaver above.
an important landmark, because the placement of the initial posterior portal is based on its location. The shoulder is surrounded by a thick, soft tissue envelope that can make palpation of landmarks difficult, particularly in obese or well-muscled individuals. It is often helpful to draw the bony landmarks on the shoulder skin to help maintain proper orientation. These should be palpated and drawn before the introduction of irrigation fluid, which may extravasate and further obliterate identification of these landmarks (Fig. 8-3).
PORTALS AND ANATOMY Establishing a portal in the shoulder involves perforation of several layers of tissue. Also, in some patients, the shoulder joint lies a considerable distance from the skin.
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Langer’s lines are observed during skin incisions for portal placement. The anterior and posterior portal skin incisions are vertical, aiming at the axillary fold. The lateral portal incision is horizontal, and the superior portal incision is established in the anteroposterior direction. When making an incision for a portal, only the skin is cut, avoiding deep plunges with the knife.
Posterior Portal The posterior portal is the most frequently used portal for shoulder arthroscopy. It allows almost complete visualization of the entire glenohumeral joint. Precise positioning of the posterior portal is important, because improper placement can make viewing of the joint difficult and will displace the normal position of the anterior portal if the inside-out technique is used. The posterior portal is located approximately 2 cm distal and 1 cm medial to the posterolateral corner of the acromion. This portion of the acromion is almost always palpable, regardless of the size of the patient. It is important to avoid the tendency to stray laterally down the arm and to remain 1 cm medial to the edge of the acromion when
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ARTHROSCOPIC TECHNIQUES OF THE SHOULDER
making this portal. The portal is located in the usually palpable soft spot of the shoulder. The glenohumeral joint may be insufflated with irrigation solution before insertion of the cannula, depending on the surgeon’s preference. After the skin is incised, a sharp cannula is inserted and directed toward the coracoid on the opposite side of the shoulder. The cannula passes through the deltoid muscle and a portion of the subdeltoid bursa. It then perforates the muscular belly of the infraspinatus or passes between the interval of this muscle and the teres minor. The cannula finally pierces the capsule and synovium to enter the joint. The posterior portal is relatively safe when placed in the correct position. The axillary nerve passes below the teres minor through the quadrilateral space to innervate it and the deltoid. The nerve becomes at risk if the cannula is advanced too far inferiorly, passing below rather than above the teres minor. The suprascapular nerve passes around the scapular spine after it has innervated the supraspinatus to supply the infraspinatus muscle. The nerve passes 2 cm medial to the posterior edge of the glenoid. It becomes at risk if the cannula is advanced too far medially along the glenoid neck.
Anterior Portal The anterior portal is used mainly to pass instrumentation into the joint. The anterior glenoid neck and labrum, articular surface of the rotator cuff, and intra-articular portion of the biceps tendon are easily accessible through this portal. The arthroscope may be placed through the anterior portal to evaluate pathology of the glenohumeral joint further if not properly seen from the posterior portal. This is particularly helpful when judging the effectiveness of the anterior inferior glenohumeral ligament from a different perspective in patients with a history of shoulder subluxation, as well as when viewing posterior shoulder pathology. The anterior portal may be made in one of two ways. One method is to pass the arthroscope from the posterior portal across the joint to the desired location on the anterior capsule. The desired location on the capsule lies within a triangle bounded by three easily identifiable landmarks. The triangle is formed by the biceps tendon superiorly, the intra-articular portion of the subscapularis inferiorly, and the anterior glenoid medially. The arthroscope is advanced against the anterior capsule and withdrawn from its sheath. A sharp obturator is placed in the sheath, and this is passed through the capsule to tent the skin anteriorly. A small skin incision is made, and a cannula is placed over the obturator as it exits the skin. Most cannulas are slightly larger than the arthroscopic sheath and slide snugly over it. The cannula then follows the obturator as it is withdrawn posteriorly to enter the joint. The obturator is removed, and the arthroscope is replaced back into its sheath. Using this method, the cannula passes through the rotator cuff interval between the subscapularis inferiorly and the
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supraspinatus superiorly. It then pierces the anterior deltoid to exit the skin. Once this portal has been established, it should never be lost because of the risk of extravasation of fluid into the soft tissues. The anterior portal may also be established directly by passing a spinal needle from the anterior shoulder into the joint. If the position of the needle is satisfactory intra-articularly, a cannula is passed through a small skin incision, reproducing the tract of the needle into the joint. This method is more difficult because of the thick, soft tissue envelope of the shoulder, and following the exact path of the spinal needle with a cannula is not easy. Occasionally, this method is required when the arthroscope sheath cannot be advanced across the joint secondary to improper placement of the original posterior portal or severe adhesive capsulitis. The anterior portal is relatively safe if properly placed and close attention is paid to the palpable external landmarks. Whether the inside-out or direct method of portal placement is used, the position of the portal must always be lateral to the palpable coracoid. The conjoined tendon inserts on the coracoid. The musculocutaneous nerve runs along the medial border of the conjoined tendon approximately 3 to 7 cm inferior to the coracoid. Any portal placed medial to the coracoid places this nerve at unnecessary risk. The anterior portal should also not be placed below the subscapularis tendon. The axillary nerve passes below the subscapularis to innervate the deltoid and will be at jeopardy if the portal is placed too inferiorly.
Subacromial Portals A thorough arthroscopic examination of the shoulder includes the glenohumeral joint and subacromial space. Subacromial portals are useful to examine the superior surface of the rotator cuff for full- or partial-thickness tears and the undersurface of the acromion for signs of impingement. Arthroscopic subacromial decompression, distal clavicle resection, and débridement or repair of the rotator cuff are procedures that can usually be performed through these portals. A considerable amount of irrigation fluid may be extravasated into the soft tissues after arthroscopy of the subacromial space. Thus, the subacromial space is usually approached after examination of the glenohumeral joint. The arthroscope sheath with a sharp obturator is placed through the original skin incision for the posterior glenohumeral portal and tracked subcutaneously toward the posterior edge of the acromion. It is then advanced under the acromion into the subacromial space, aiming for the anterolateral corner of the acromion. The undersurface of the acromion should be palpated with the arthroscope sheath to confirm its position in the subacromial space. The sharp obturator is replaced with the arthroscope and inflow is provided through the scope sheath with an infusion
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pump or through a separate anterior portal. Typically, an irrigation pump is used to supply inflow through the arthroscope sheath. If not, a second portal for inflow is usually required because bleeding into the subacromial space can be profuse and a high flow rate may be required. To establish the anterior inflow portal, the arthroscope sheath and obturator are advanced past the anterior acromion and out the previous skin incision for the anterior glenohumeral portal. A cannula is placed over the arthroscope sheath and guided into the subacromial space as the sheath is retracted. This portal can also be used as a working portal for distal clavicle excision or for suture management during a rotator cuff repair. An additional working portal is frequently made laterally to the acromion to pass instrumentation or the arthroscope. The position of this portal is approximately 3 cm distal to the anterolateral corner of the acromion (Fig. 8-4). An incision is made just through the skin to avoid any possible injury to the underlying deltoid muscle or the axillary nerve. A blunt obturator is passed obliquely and can be seen to enter the subacromial space with the arthroscope. The position of this portal places the instrumentation parallel to the anterior acromion and in an ideal position to resect the coracoacromial ligament, if required. The position of the axillary nerve should always be kept in mind when making this portal because it runs 5 cm distally to the lateral edge of the acromion under the deltoid to supply this muscle.
Additional Portals Although the portals previously described are the most commonly used during shoulder arthroscopy, additional portals can be used. Accessory portals for anchor placement and suture passage are necessary for various labral repairs. These portals include the 5 o’clock portal, anterosuperolateral portal, Port of Wilmington portal, posterolateral portal,6 and Nevaiser’s portal.7 The 5 o’clock portal, established about 1 cm inferiorly and 2 to 3 cm laterally to the anterior
portal through the most lateral portion of the subscapularis tendon, is helpful for the placement of anchors along the anteroinferior glenoid during a Bankart repair. The anterosuperolateral portal is located approximately 1 to 2 cm laterally to the anterolateral corner of the acromion. The Port of Wilmington portal is established approximately 1 cm anteriorly and 1 cm laterally to the posterolateral corner of the acromion. These two portals are essential for anchor placement during repair of SLAP lesions. The anterosuperolateral portal is also useful for placing medial row anchors during double-row rotator cuff repairs. The posterolateral portal is placed about 1 cm inferiorly and 2 to 3 cm laterally to the posterior portal, entering through the lateral portion of the posterior cuff. This allows access to the posteroinferior glenoid for anchor placement during repair of posterior Bankart lesions. Finally, Nevaiser’s portal is located just posteriorly and medially to the acromioclavicular joint, through the palpable soft spot in this area. This portal can be useful for rotator cuff repairs, as well as for passage of sutures during SLAP repairs. All these portal locations are established with an outside-in technique after localizing with a spinal needle. The exact angle and location are adjusted based on the placement of the spinal needle.
SUMMARY A knowledge of shoulder arthroscopy is imperative as it continues to evolve and become popular for the diagnosis and management of shoulder disorders. Arthroscopy of the shoulder has helped advance the understanding of various shoulder maladies, such as the complex relationship between impingement and instability in the throwing athlete. As with any surgical technique, a thorough knowledge of the anatomy of the shoulder girdle relative to portal placement is essential before undertaking this successful procedure.
References
Figure 8-4. Ideal position of lateral subacromial portal. This is initially determined with a spinal needle. The position of the needle in the subacromial space is viewed arthroscopically and modified accordingly.
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1. McGlynn FJ, Caspari RB: Arthroscopic findings in the subluxating shoulder. Clin Orthop Relat Res 183:173-178, 1984. 2. Caspari RB: Shoulder arthroscopy: A review of the present state of the art. Contemp Orthop 4:523, 1982. 3. Skyhar MJ, Altchek DW, Warren RF et al: Shoulder arthroscopy with the patient in the beach-chair position. Arthroscopy 4:256-259, 1988. 4. Caspari RB: Instrumentation and operating room organization for arthroscopy of the shoulder. In McGinty JB (ed): Arthroscopic Surgery Update, Techniques in Orthopaedics. Rockville, Md, Aspen, 1985, p 155. 5. Andrews JR, Carson WG: Shoulder joint arthroscopy. Orthopedics 6:1157, 1983. 6. Lo IK, Lind CC, Burkhart SS: Glenohumeral arthroscopy portals established using an outside-in technique: Neurovascular anatomy at risk. Arthroscopy 20:596-602, 2004. 7. Nord KD, Masterson JP, Mauck BM: Superior labrum anterior posterior (SLAP) repair using the Neviaser portal. Arthroscopy 20(Suppl 2):129-133, 2004.
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CHAPTER 9 Tensile Failure of the Rotator Cuff Christopher W. Baker and Brian D. Busconi
Rotator cuff injury in the athlete can have several different causes. Factors related to the development of rotator cuff tears can be classified as intrinsic (changes to cuff vasculature or the normal aging process), extrinsic (impingement caused by abnormalities in the subacromial arch), or traumatic (excessive tensile load to the rotator cuff caused by a single traumatic event or repetitive microtrauma).1 This latter mechanism, which can lead to the injury complex known as primary tensile failure of the rotator cuff,1,2 is most typically seen in the throwing or overhead athlete participating in sports such as baseball, tennis, volleyball, and team handball. It is a complex problem that can create a significant clinical challenge.1,3
pitching motion have divided it into six phases, separated by reproducible points within the motion. These phases include the wind-up, early cocking (stride), late cocking, acceleration, deceleration, and follow-through.9 It is during this throwing motion that the shoulder and tissues surrounding it are subjected to extreme stress, position, and force.3,7,8 The late cocking, acceleration, and deceleration phases generate the largest forces and account for most injuries.5,9 The shoulder is maintained in about 90 to 110 degrees of abduction throughout the throw, but ranges from 30 degrees of abduction at maximal cocking to 10 degrees of adduction at follow-through. External rotation is maximized at around 175 degrees during the late cocking phase and moves to around 105 degrees of internal rotation during the throw. This can generate arm angular velocities in excess of 7000 to 8000 deg/sec and rotational torques more than 70 N•m, with shear forces ranging from 300 to 400 N and compressive forces more than 1000 N.6,11 During deceleration, forces can approach ⫺500,000 deg/sec2. The extreme range of external rotation, coupled with the tremendously high joint forces, can exceed the physiologic limits of the joint, leading to failure.
The repetitive throwing motion is a dynamic activity that places extraordinary stresses on the athlete’s shoulder, capsuloligamentous complex and, in particular, rotator cuff.1,3-7,9 Remarkably high forces are generated by the cuff musculature, specifically during the deceleration phase of throwing, to slow the rapidly moving shoulder. These forces, applied repetitively with the throwing motion, are believed to be primary factors underlying the mechanism for tensile rotator cuff failure.
FORCES AND MUSCLE ACTIVITY
Electromyography data collected throughout the phases of the throwing motion have allowed for the evaluation of muscular firing patterns.5,8,9 During the wind-up phase, muscle activity is low, below 21% of maximal voluntary contraction. Small forces are placed on the shoulder and few injuries occur during wind-up. During the early cocking phase, muscle activity increases. The serratus anterior and trapezius muscles demonstrate moderate to high activity and, in concert with the middle deltoid and supraspinatus, help keep the humeral head congruent with the glenoid. The late cocking and acceleration phases are when the shoulder begins to experience an increase in forces. It is also when the shoulder is maximally externally rotated and horizontally abducted.3 The subscapularis, pectoralis major, and latissimus dorsi all demonstrate high to very high activity and provide stability to the joint. The action of the deltoid begins to diminish ,and the rotator cuff muscles increase their activity. The infraspinatus and teres minor show very high activity, whereas the supraspinatus is the least active. The rotator cuff muscles provide a compressive force, contributing to the stability of the joint. During deceleration and follow-through, the excess kinetic energy not transferred to the ball is dissipated
The shoulder is the most mobile joint in the body. It is designed to provide stability, which allows a wide range of motion in multiple directions. Motion is determined by glenohumeral configuration, soft tissue flexibility, and a balance between dynamic (muscle) and static (ligament, tendon) shoulder stabilizers.1,10 This leads to a delicate equilibrium of stability and mobility, especially in the overhead athlete who is trying to generate a tremendous amount of energy.4 The athlete must maximally accelerate and decelerate the arm over a short period of time while maintaining precise control over the object being thrown.9 This places extreme demands on the shoulder. The baseball pitch is the biomechanical model most used for many overhead throwing motions.3 This motion is a kinetic chain activity in which energy derived from the lower extremity is transferred through the pelvis and trunk rotationally, with subsequent release through the upper extremity. As a segment of the body undergoes acceleration, the succeeding segment is left behind.5 High-speed cinematography and three-dimensional analysis of the 111
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through the shoulder. This is characterized by a powerful deceleration force provided by the posterior musculature. Opposing muscles tend to fire simultaneously to accomplish this control. The teres minor demonstrates the highest activity of the posterior musculature, and the middle and posterior heads of the deltoid are the most active antagonists. The subscapularis also demonstrates high activity as well in maintaining humeral head position and preventing subluxation. Injury to the rotator cuff can occur during the deceleration phase as it resists horizontal adduction, internal rotation, anterior translation, and distraction forces. This repetitive action may result in microtrauma over time and lead to tensile failure of the rotator cuff.7
PATHOGENESIS OF TENSILE FAILURE With repeated injury, articular-sided partial-thickness tears and intratendinous tears can develop in the rotator cuff.7,12 This has been referred to as primary tensile failure of the rotator cuff.2 As noted, the rotator cuff is exposed to tremendous forces during the deceleration phase. The rotator cuff must not only offset these high-energy forces but also stabilize the humeral head within the glenoid. These eccentric tensile forces can overload the rotator cuff tendons, resulting in microtraumatic injuries, which accumulate with repetitive throwing.8 This is typically believed to occur during the deceleration phase as the rotator cuff musculature resists horizontal adduction, internal rotation, anterior translation, and distraction forces.1 It usually involves the undersurface of the posterior half of the supraspinatus and superior half of the infraspinatus. Once believed to be caused exclusively by repetitive microtrauma, it is now believed to be multifactorial in origin. Intrinsic factors, such as age-related changes in vascularity of the cuff or other metabolic alterations, may play a role in the development of partial-thickness articular-sided tears.1 Similarly, the structure of the tendon itself may also be a contributing factor. The rotator cuff tendon is composed of five layers, which predisposes it to the development of internal shear forces.12 The bursal side is more resistant to rupture and elongates with a tensile load, whereas the articular side does not stretch and tears easily. Cadaveric studies have shown that partial-thickness articular-sided tears will develop at only 15 degrees of shoulder abduction, and that tendon failure can occur at 90 degrees and more of abduction. Propagation of the tear from the articular side to the bursal side may also occur at increasing degrees of abduction, such as in overhead athletes who undergo repetitive strains at extremes of motions. Extrinsic factors may also be involved in the development of partial-thickness, articular-sided, rotator cuff pathology in the overhead athlete. Subacromial impingement, as a result of narrowing of the supraspinatus outlet by anatomic variations in the coracoacromial arch, may cause
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partial tears by irritation of the cuff. Although originally believed to be primarily a source of bursa-sided tears, finite element models have demonstrated that external impingement can result in high enough stress to cause not only bursa-sided tears, but intratendinous and articularsided tears as well.1,12 Similarly, subacromial impingement may play a role in aggravating many partial-thickness tears. However, bursa-sided tears are still more commonly associated with subacromial impingement. Internal impingement may also be a contributing factor in the development of articular-sided rotator cuff tears. Internal impingement is abnormal contact between the posterosuperior aspect of the glenoid and the undersurface of the rotator cuff.5,12 This can be the result of many factors, including anterior instability, posterior capsular tightness, decreased humeral retroversion, tension overload, poor throwing mechanics, and scapular muscle imbalance. Repetitive throwing may cause progressive injury or attenuation of the static stabilizers of the shoulder joint, leading to increased glenohumeral translation.1 Consequently, increased rotator cuff activity is required to counteract this increased humeral translation or subluxation.7 Over time, these dynamic stabilizers may fatigue, allowing the rotator cuff to impinge on the coracoacromial arch, with resultant rotator cuff injury. However, many overhead athletes will have adaptive ligamentous laxity of the shoulder to begin with.12 Therefore, it is important to be able to differentiate which components of the clinical picture are adaptive and which are pathologic in development. As noted, the pathogenesis of articular-sided, partialthickness, rotator cuff tears is likely multifactorial. Interactions between trauma, intrinsic, and extrinsic factors may all contribute to the development of primary tensile failure of the rotator cuff.1,5,7,8,12
DIAGNOSIS The vast majority of athletes with partial-thickness rotator cuff tears will present with a chief complaint of shoulder pain and diagnosis may be extremely challenging, because many conditions manifest with this finding.1,3,9,12 A careful and complete history that details the precise occurrence and precipitation of symptoms is necessary. The pain of a rotator cuff tear is classically described as persisting, even at rest, or as night pain. The location of pain may help delineate the causative factor. Anterior pain may be associated with subscapularis, biceps tendon, or capsulolabral injury, anterolateral pain is commonly seen with supraspinatus injury, and posterior pain can be seen with infraspinatus or capsulolabral injury.5,8 Instability symptoms may include a feeling of the arm going dead or a sensation of subluxation. The examiner should determine which phase of the throwing motion reproduces symptoms. Patients with anterior instability will experience pain, dead arm, or
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subluxation symptoms during the late cocking or early acceleration phase. Posterior subluxation typically manifests with pain during the follow-through phase. Pain related to certain precipitating activities might suggest a diagnosis of tendonitis or impingement. However, these distinctions are not always clear, making diagnosis difficult. A thorough physical examination is crucial and should attempt to isolate the structures that are responsible for the symptoms. The cervical spine, including range of motion, tenderness, and Spurling’s maneuver, should always be assessed to ensure that the pain is not radicular in nature.12 Inspection for asymmetry and atrophy are initial steps. Atrophy, especially of the infraspinatus fossa, may indicate chronic rotator cuff dysfunction or suprascapular nerve injury.9 Scapular dyskinesis may be a primary or secondary problem, and may be caused by fatigue or intra-articular glenohumeral pathology.3 Documentation of active and passive range of motion and muscle strength should also be preformed. Increased external rotation of the dominant shoulder compared with the nondominant arm may be a normal manifestation. Some throwers will also demonstrate a normal loss of internal rotation, which is also a common finding in an injured pitcher. Tenderness over the supraspinatus insertion or over the subacromial bursa would direct attention to impingement of the rotator cuff. Marked improvement in symptoms with local anesthetic infiltration of the bursa would support the subacromial space as the primary area of pathology. Loss of supraspinatus muscle strength, with resolution of pain after subacromial injection, suggests the presence of a full-thickness rotator cuff tear, whereas maintenance of strength after injection suggests inflammation or an articular surface or intratendinous tear. Ligamentous stability is tested in the anterior, posterior, and inferior directions and is mandatory in the young athlete because of the possibility of a coexistent internal impingement.12 These tests are performed on both shoulders and the results compared. The sulcus sign, Jobe’s test, and apprehension and relocation tests may all be performed, but may be difficult to interpret by inexperienced clinicians.3,9 The O’Brien test may help distinguish biceps tendon lesions, and impingement tests may delineate acromioclavicular pathology. A thorough neurovascular examination should also be performed distally in all cases. Radiographic studies complete the evaluation, even though they are frequently unrevealing. Os acromiale, subacromial spurs, and markedly curved or hook-shaped acromions may play a role in extrinsic rotator cuff impingement and can be detected with x-ray.5,8,12 Similarly, the anteroposterior view (x-ray) should be assessed for bony Bankart or Hill-Sachs lesions.9 Historically, arthrography and bursography have been used to aid in the diagnosis of partialthickness tears, but their accuracy has come under scrutiny. As a result, ultrasound and magnetic resonance imaging
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(MRI) are being used more often. Ultrasound has been reported to have a high sensitivity and specificity for the diagnosis of partial-thickness tears, but is extremely user dependent, making it less available. MRI, with multiple techniques available, demonstrates similar accuracy rates as ultrasound when diagnosing partial-thickness tears, and has the added benefit of being able to diagnose concomitant pathologic lesions. Despite a thorough examination and appropriate imaging, diagnostic arthroscopy may still be needed to diagnose a partial-thickness rotator cuff tear accurately.
TREATMENT OPTIONS For the throwing athlete suspected of having an isolated, partial-thickness, rotator cuff tear, the initial approach to management is nonoperative.5,8,9,12 This includes modification of activities, such as avoidance of overhead painprovoking maneuvers, and a short course of nonsteroidal anti-inflammatory drugs (NSAIDs).This is followed by a dedicated physical therapy program, with attention directed toward maintaining or regaining normal shoulder kinematics. This includes stretching, use of cryotherapy, and gradual range-of-motion (ROM) and strengthening exercises addressing the rotator cuff and scapular stabilizers. Corticosteroid injections can also be used, but multiple injections should be approached with caution because they could damage the rotator cuff tendon and should be completely avoided in the young athlete.1 For those athletes with concurrent shoulder instability or internal impingement, a similar initial course consisting of activity modification, NSAIDs, and physical therapy is used. Despite conservative measures, spontaneous healing of partial-thickness tears is unlikely and most progress to full-thickness tears. The absolute indications for surgical treatment of partialthickness rotator cuff tears continue to evolve.1,12 Operative treatment is typically reserved for patients with persistent symptoms who have failed conservative management, usually after 3 to 6 months.5,8 Additional factors are also considered, including the type and extent of the tear, occupation and activity level of the patient, and presence of additional intra-articular pathology. The timing can vary and multiple surgical options are available, ranging from simple débridement to repair.
SUMMARY Extraordinary stresses are placed on the athlete’s shoulder during the throwing motion. The rotator cuff serves to help maintain the glenohumeral relationship during the early phase of throwing, and decelerate the arm during the latter stages. A number of structures are subjected to these extreme forces, especially during the deceleration phase of the throwing motion. It is during this phase that the rotator
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cuff is most vulnerable to injury. Tensile failure of the rotator cuff (partial-thickness articular-sided tears) typically occurs during this phase. Initially believed to be traumatic in nature, it is now believed that there are a number of causative factors. Diagnosis can be difficult, and a thorough physical examination supplemented with radiographic imaging are necessary. Nonoperative treatment remains central to the management of these injuries.
References 1. Fukuda H: The management of partial-thickness tears of the rotator cuff. J Bone Joint Surg Br 85:3-11, 2003. 2. Andrews JR: The athlete’s shoulder: biomechanics, diagnosis and treatment. Presented at the American College of Sports Medicine Annual Meeting (Joseph B. Wolffe Memorial Lecture). Salt Lake City, Utah, May 22, 1990. 3. Limposvati O, Elattrache NS, Jobe FW: Understanding shoulder and elbow injuries in baseball. J Am Acad Orthop Surg 15:139-147, 2007. 4. Van Der Hoeven H, Kibler WB: Shoulder injuries in tennis players. Br J Sports Med 40:435-440, 2006.
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5. Park SS, Loebenberg ML, Rokito AS, Zuckerman JD: The shoulder in baseball pitching: biomechanics and related injuries—part 1. Bull Hosp Jt Dis 61:68-79, 2002-2003. 6. Borsa PA, Dover GC, Wilk KE, Reinold MM: Glenohumeral range of motion and stiffness in professional baseball pitchers. Med Sci Sports Exerc 38:21-26, 2006. 7. Mazoue CG, Andrews JR: Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med 34:182-189, 2006. 8. Park SS, Loebenberg ML, Rokito AS, Zuckerman JD: The shoulder in baseball pitching: biomechanics and related injuries—part 2. Bull Hosp Jt Dis 61:80-88, 2002-2003. 9. Altchek DW, Dines DM: Shoulder injuries in the throwing athlete. J Am Acad Orthop Surg 3:159-165, 1995. 10. Baltaci G, Tunay VB: Isokinetic performances at diagonal pattern and shoulder mobility in elite overhead athletes. Scand J Med Sci Sports 14:231-238, 2004. 11. Sabick MB, Torry MR, Kim YK, Hawkins RJ: Humeral torque in professional baseball pitchers. Am J Sports Med 32: 892-898, 2004. 12. Matava MJ, Purcell DB, Rudzki JR: Partial-thickness rotator cuff tear. Am J Sports Med 33:1405-1417, 2005.
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CHAPTER 10 Subacromial Impingement Sara L. Edwards, John-Erik Bell, and Louis U. Bigliani
Subacromial impingement is a common disorder of the shoulder that requires further investigation to understand the cause and treatment options. Knowledge of the pathogenesis of the condition has expanded greatly since Neer’s original ideas 40 years ago. In recent years, several different factors have been identified that contribute to impingement and rotator cuff disease. The purpose of this chapter is to discuss the mechanism behind subacromial impingement and emphasize new research about this disease, as well as treatment methods and their applications to the overhead athlete.
continued insult, stage II develops, identified by permanent histologic changes of fibrosis and tendinosis of the affected tendons. This is often the stage at which patients present to the orthopedic surgeon. If allowed to progress, stage III develops, with either a partial or complete rupture of the rotator cuff and biceps tendons and associated pathologic changes in the acromion and acromioclavicular joint. Stage III is not commonly seen in the general population younger than 40 years. However, in the overhead athlete, an individual may progress through each stage more rapidly. These patients can present with impingement pathology at an earlier age than usual. If left untreated for long periods, these shoulders may undergo chronic arthritic changes caused by unopposed superior migration of the humeral head into the acromion, a process known as cuff tear arthropathy. Stage II of outlet impingement, before the development of a complete rotator cuff tear, represents the population most frequently seen by orthopedic surgeons and will be the focus of this chapter.
CAUSES AND PATHOLOGY The cause of rotator cuff pathology has been the source of much controversy. Although rotator cuff tears were first described by Smith in 1834, disagreement remains as to which factors are principally responsible for this disease.1 Extrinsic factors, or the mechanical wear of the rotator cuff under the coracoacromial arch, have been described as the primary cause. Other intrinsic biologic forces, such as vascular supply to the tendons, aging, inflammation, and the development of degenerative tendinopathy have been identified as potential causes of external impingement. Studies have shed light on other factors that may lead to external compression injury, including poor posture, muscle weakness, subtle tissue contractures, and altered scapular or glenohumeral kinematics.2 Therefore, it is reasonable to conclude that the cause of subacromial impingement is variable and multifactorial.
As understanding of subacromial impingement has expanded, it has become clear that several mechanisms that contribute to rotator cuff injury may be occurring simultaneously. These mechanisms have been divided into two groups, intrinsic and extrinsic factors. Intrinsic causes represent overload, aging, and inflammatory processes that degrade the integrity of the tendons. Extrinsic injury represents direct compression. Compression under the coracoacromial arch, initially named by Neer as outlet impingement, is also known as subacromial impingement, classic impingement, or external impingement. More recently, another compression injury to the articular side of the rotator cuff and posterosuperior glenoid rim and humerus has been described, known as internal impingement (see Chapter 11).
Abnormal morphology of the acromion and the link to impingement syndrome were described by Neer in 1972. He isolated the undersurface of the anterior one third of the acromion rather than its lateral or posterior aspect as the area responsible for mechanical wear on the structures in the subacromial space. Neer identified the coracoacromial ligament and acromioclavicular joint as structures that also contribute to impingement on the rotator cuff.3,4
The acromion, coracoacromial ligament, and coracoid are the components of the coracoacromial arch. The coracoacromial arch superiorly and the humerus inferiorly serve as rigid boundaries for the soft tissue contents of the subacromial space. To achieve forward elevation above 90 degrees, the rotator cuff must pass under this arch. There is always contact between the cuff and arch, because the subacromial space is a relative space. Prior investigation has demonstrated anterolateral contact present at 0 degrees of elevation, which shifts medially with forward elevation. The humerus contacts the undersurface of the supraspinatus from proximal to distal with forward elevation. The primary point of contact on the bursal side is at the supraspinatus
The pathology may involve one or more of the rotator cuff tendons and the long head of the biceps. Neer outlined three progressive stages. Stage I is characterized by edema and hemorrhage of the subacromial bursa. Stage I usually occurs in younger patients and is difficult to distinguish from an acute partial tear of the rotator cuff without imaging studies. This stage is reversible with conservative treatment. With 115
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insertion throughout forward elevation. The subacromial bursa facilitates this motion and contact. It is a unique anatomic arrangement that exposes the soft tissues to wear and degeneration as the arm is elevated and rotated during range of motion of the shoulder. Furthermore, the impingement may be accelerated by any anatomic architectural changes in the acromion or acromioclavicular joint that reduce the volume of the subacromial space.
ANATOMY Normal Anatomy The development and function of the acromion are unique in humans. Studies of human embryos have shown that the acromion is identifiable by 5 or 6 weeks of age and is composed of cartilage at birth. The centers of ossification in the acromion, usually two, are the last to appear in the scapula; these appear during puberty or adolescence and usually fuse between 18 and 25 years of age.5,6 One variation that has been well outlined is failure of ossification, referred to as os acromiale. This anomaly may be present in up to 8% of cases and is often bilateral.7,8 The acromion is positioned above the superior aspect of the shoulder as the lateral extension of the spine of the scapula. It is defined posteriorly at the acromial angle, where the acromion and crest of the spine of the scapula converge. The posterior extent and lateral border of the acromion are easily defined with palpation. Anteriorly, at the tip, is the attachment of the coracoacromial ligament, where spur formation may be found. The coracoacromial ligament is located superior to the subacromial space. This ligament is a broad fan-shaped structure between the anterior aspect of the acromion and lateral tip of the coracoid. The acromioclavicular joint involves the medial aspect of the acromion and lateral aspect of the clavicle; it is the only diarthrodial articulation of the acromion. The opposing articular surfaces of the acromioclavicular joint may vary in their angulation when viewed anteriorly, and the surfaces are separated by an intra-articular disc in the early stages of life. Degeneration of the acromioclavicular joint occurs with age, and the formation of inferior osteophytes on the acromial or clavicular side increases in frequency with advancing years.9-11 The long head of the biceps and tendons of the rotator cuff pass through the subacromial space; these include the supraspinatus, infraspinatus, and teres minor muscles, which insert onto the greater tuberosity of the humerus. The subscapularis muscle inserts onto the lesser tuberosity. The rotator interval is created between the subscapularis and supraspinatus tendons. All four rotator cuff tendons interlace with each other over the humeral head before inserting. This continuity allows a functional interaction of the rotator cuff
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muscles and the ability to contribute to all motions of the glenohumeral joint. Subjacent to the anterior aspect of the supraspinatus lies the tendon of the long head of the biceps, which courses between the lesser and greater tuberosity in the bicipital groove. The subacromial bursa lies superior to the rotator cuff tendons, extending from the medial aspect of the acromion to the proximal one third of the humerus, underlying the deltoid muscle as it extends distally. The bursa is believed to have a lubricating effect by reducing friction of the rotator cuff under the coracoacromial (CA) arch. The vascular supply to the rotator cuff muscles and tendons includes contributions from the suprascapular, anterior and posterior humeral circumflex, thoracoacromial, and subscapular arteries. A region of hypovascularity in the supraspinatus tendon corresponds to the critical area, where rotator cuff pathology is usually initiated.12-15
Variations in Architecture Associated with Rotator Cuff Pathology Classically, external impingement occurs in the supraspinatus outlet as the arm is elevated from 70 to 120 degrees, also known as the impingement arc. It has been recognized that compression can occur at any point under this arch, and that processes that diminish the size or increase the rigidity of the outlet structures will exacerbate impingement.16 Conversely, measures taken to enlarge the outlet will relieve symptoms. The subacromial decompression enlarges the outlet in three ways: (1) by removing the prominent anterior acromion; (2) by releasing a tight coracoacromial ligament; and (3) by removing the bulky, thickened subacromial bursa. Prominent inferior osteophytes from the acromioclavicular joint may also contribute and are removed as necessary. Native anatomy can vary substantially. As Neer noted in his original paper on the subject, individual variation in the shape or slope of the acromion may affect the progression of impingement lesions.4 Bigliani and colleagues17 have studied the shape of the acromion in 140 cadaver shoulders to determine the relationship to full-thickness tears of the rotator cuff. The overall incidence of full-thickness tears in this elderly population was 34%. Three types of acromions were identified—type I (flat) in 17%, type II (curved) in 43%, and type III (hooked) in 39% (Fig. 10-1). The type III acromion was present in 70% of patients with rotator cuff tears, whereas only 3% of type I acromions were associated with a tear. Also, anterior acromial spurs were noted in 14% of those in the series overall but in 70% of patients with rotator cuff tears. It is important to distinguish between spurs, which are probably acquired, and variations of the native acromial architecture. Clinically, the same investigators examined acromial morphology using the supraspinatus outlet view in 200 consecutive patients with different shoulder problems.18
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A
B
C Figure 10-1. Variations of acromial morphology. A, Type I, flat. B, Type II, curved. C, Type III, hooked.
The incidence of acromial type correlated closely to the anatomic study—18% type I, 41% type II, and 41% type III. In patients with an arthrogram positive for a full-thickness rotator cuff tear, 80% had a type III acromion. In another group of 50 patients who underwent open subacromial decompression, 6% had a type I, 28% had a type II, and 66% had a type III acromion. Of this symptomatic group, 70% had a full-thickness rotator cuff tear. The findings of this study established a correlation between the type III acromion and rotator cuff tears and confirmed the importance of the supraspinatus outlet radiographic view for evaluation of the acromion. Other investigators have demonstrated a significant correlation between a hooked morphology and decreased Constant-Murley score.19 Other investigators have investigated the slope of the acromion.20 Aoki and coworkers21 have developed a technique for measuring the acromial slope using the supraspinatus outlet view of the scapula. Their investigation of skeletal shoulders has revealed that a flatter acromial slope may be associated with the presence of a spur and narrowing of the supraspinatus outlet. When applied clinically, patients with stage II impingement compared with normal patients had a significantly flatter acromial slope. In addition to acromial morphology, other anatomic factors have been associated with impingement of the rotator
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cuff. Many clinicians have described the occurrence of inferiorly protruding osteophytes from the anterior aspect of the acromion and inferior aspect of the acromioclavicular joint, which may compromise the integrity of the rotator cuff tendons when they pass below these structures.3,18,22 The anterior bony prominence, or traction spur, represents an enthesopathic reaction to the humerus repeatedly abutting the undersurface of the coracoacromial ligament. Chambler and colleagues23 have suggested that humeral contact from overhead motion causes rapid alterations in tension within the substance of the coracoacromial ligament that may provoke an adaptive change at the enthesis, leading to spur formation. Also, several series involving overhead athletes have suggested that the coracoacromial ligament is a primary source of pathology in this population. Suenaga16 has demonstrated in histologic studies that some patients have hypertrophic fibrocartilaginous changes within the coracoacromial ligament while having a normal-appearing acromial undersurface during arthroscopy. Soslowsky and associates24 have found that shoulders with rotator cuff tears have shortening and thickening of the anterolateral band of the coracoacromial ligament compared with shoulders with intact rotator cuff tendons. The subacromial bursa has also been implicated in the pathogenesis of rotator cuff disease and impingement. There is a rich supply of nerve fibers in the bursa compared with that in other tissues in the subacromial space, which may be responsible for the pain associated with impingement syndrome. Increased inflammatory cytokine expression has been identified in patients with subacromial bursitis compared with control patients. Developmental problems, such as failure of fusion of the acromial epiphyses, may alter the structure of the undersurface of the acromion and decrease the volume of the subacromial space.8,25,26 Although this may lead to bursal and rotator cuff lesions, coracoid impingement should be distinguished from the much more common form of subacromial, or outlet, impingement that typically is initiated in the supraspinatus tendon.
IMPINGEMENT IN THE ATHLETIC SHOULDER: PATHOPHYSIOLOGY AND CLINICAL CORRELATION Reports concerning injuries of the rotator cuff in athletes have increased tremendously during the past 30 years.27-38 There is a greater awareness about overuse syndromes and the impact that repetitive motions have on the rotator cuff, particularly those motions occurring above the horizontal plane. As a result, impingement and its pathophysiology have been well described in this population. Occasionally, the pathology is caused by an acute traumatic episode.37 Frequently, microtrauma to the subacromial bursa and
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rotator cuff tendons abutting the coracoacromial arch during repeated overhead motion will cause pain and a decrease or complete loss in function.29,33,34,38-41 Furthermore, involvement of the biceps tendon and the tendon’s association with impingement of the supraspinatus tendon have been well defined.4 The function of the rotator cuff muscles and motion of the shoulder in overhead sports have also been delineated.42,43 The rotator cuff muscles serve to compress the humeral head dynamically into the glenoid, providing stability during motion of the glenohumeral joint. The complex shoulder motions and the muscles involved in athletics have also been described in detail.44,45 In general, many overhead motions in sports, such as throwing a ball, serving in tennis, and swimming require maximal abduction with external rotation. This subjects subacromial bursa and rotator cuff tendons to wear under the anterior acromion and coracoacromial ligament as the arm accelerates forward. The bursa is a reactive membrane and this external mechanical stimulus may initiate a response of intrinsic factors, leading to inflammation and cuff disease. Impingement also may be seen if the rotator cuff muscles are weak and fail to stabilize the humeral head in the glenoid for proper mechanics. As a result, the action of the deltoid muscle will not be counterbalanced and the humeral head may translate superiorly into the coracoacromial arch. Tightness of the posterior capsule is known to limit glenohumeral internal rotation and create obligate anterior and superior humeral translation during flexion.46-48 Scapular mechanics also plays a role in some individuals in the contribution to subacromial impingement. Weakness of the dorsal scapular stabilizers and tightness of the pectoralis minor and short head of the biceps lead to scapular protraction and anterior tilting. This protracted and anteriorly tilted posture causes the scapula to tilt forward and places the acromion in a more horizontal position; thus, there is relative lowering of the roof of the coracoacromial arch and a decrease in the supraspinatus outlet space.49 Although extrinsic factors are a component of the disease, intrinsic factors have been demonstrated. Inflammatory mediators have been demonstrated by a number of researchers in both bursal and tendon tissues of patients with symptomatic impingement.50-53 Amyloid deposition has been demonstrated in patients with chronic pain, suggesting a degenerative component.54 Studies examining the stumps of torn tendons have demonstrated thinning and disorientation of collagen fibers, also suggesting a degenerative process.55 The debate among researchers as to whether rotator cuff disease is the result of an extrinsic mechanical force or an intrinsic problem within the tissue seems to indicate that multiple processes can be responsible at the same time. What seems likely is that repeated overhead motion in a
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constricting space mechanically presses the tissue and sets off a reaction that is inflammatory in nature. This increase in inflammatory mediators and cytokines has been demonstrated by various researchers. It is the contribution of mechanical and molecular factors to tissue weakened from previous insults that causes failure.
EVALUATION A complete evaluation, including a thorough history and physical examination, is required for all patients presenting with shoulder pain. Symptoms suggestive of impingement include pain with overhead activities, such as combing the hair and reaching high shelves. Pain with internal rotation is a common complaint. Night pain while lying on the affected side is also a frequent problem. Patients may locate the pain to the anterior shoulder or lateral deltoid, because the subacromial bursa extends beyond the lateral border of the acromion. Overhead athletes with impingement and cuff pathology secondary to subtle anterior instability are usually young and complain of pain and decreased throwing velocity. The physical examination should begin with inspection, looking for abnormal posture and signs of wasting or scapular winging that suggest neurologic injury or entrapment. The cervical spine should be examined, looking for evidence of degenerative disc disease, arthritis, or radicular pain. Range of motion is documented for forward elevation in the plane of the scapula, external rotation with the arm at the side and in 90 degrees of abduction, and internal rotation to the highest vertebral level. Ranges are compared with those of the contralateral shoulder. It is not unusual to see excessive external rotation in an overhead athlete, but with overall decreased range of rotation when compared with the nondominant extremity. Tests specific for impingement include Neer’s sign; this is measured by passively elevating the arm in the plane of the scapula while the examiner stabilizes the scapula with a hand. A positive test elicits pain between 70 and 120 degrees of elevation. Hawkins’ test is performed with the shoulder flexed 90 degrees and internally rotated (Fig. 10-2). Anatomic studies have validated both tests for placing the rotator cuff in contact with the undersurface of the coracoacromial arch and clinical studies have confirmed their high sensitivity, although specificity is low.56 The sensitivity of Hawkins’ test was 92% in two independent studies.57,58 Not to be confused with his impingement sign, Neer’s impingement test involves the injection of 10 mL of lidocaine into the subacromial space, followed by performance of the provocative motion. A positive test will relieve pain in those with impingement and calcific tendinitis but will continue to be painful if other causes are responsible. This test has been shown to be an independent predictor of good outcome after arthroscopic subacromial decompression.59,60
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Figure 10-2. Hawkins’ impingement test.
Figure 10-3. Scapular Y view demonstrating anterior spur.
Patients with impingement generally have good ranges of motion and strength. A positive drop arm test, liftoff test, hornblower’s sign, and external and internal rotation lag signs should alert the clinician to a complete rotator cuff tear. Significant loss of passive range of motion is a feature of adhesive capsulitis, not primary impingement, although the two may coexist. Subtle instability can be detectable through a positive relocation test on examination.
axial view is good for identifying bicep tendon and subscapularis pathology.
When treating an athlete with impingement syndrome, the anatomy of the coracoacromial arch should be considered as part of the evaluation. Radiographic evaluation can identify any bony abnormality or spur that may be the source of the pathology. Spur formation usually occurs in older patients older than 40 years, but we have seen them in younger overhead athletes who compress the humerus and cuff against the coracoacromial ligament. Spur formation occurs in the insertion of the coracoacromial ligament into the undersurface of the acromion. Diagnostic studies include the anteroposterior (AP) view in the plane of the scapula and supraspinatus outlet and an axillary lateral view. The AP view helps distinguish between other sources of pain, such as calcific tendinitis and arthritis. The supraspinatus outlet view can alert the clinician to altered acromial morphology or acromial spurs (Fig. 10-3). The axillary lateral view can demonstrate an os acromiale if present. In the early stages, routine magnetic resonance imaging (MRI) is not recommended. However, if symptoms persist or if significant rotator cuff pathology is suspected by clinical examination, MRI is recommended. MRI is useful to identify inflammation. The coronal and sagittal oblique views will demonstrate bursitis and cuff pathology (Fig. 10-4). Acromial morphology, such as the presence of a spur or failure of formation, can be better identified as well. The
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TREATMENT The initial management of a patient with subacromial impingement is conservative. Avoidance of provocative activities, anti-inflammatory medication, and physical therapy should be the initial modes of treatment.60 Physical therapy
Figure 10-4. Sagittal oblique magnetic resonance imaging scan demonstrating anterior spur and inflamed bursa.
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plays an integral role in the treatment of impingement, both in preventing surgery and for postoperative rehabilitation. Conservative measures in patients with type I acromions had a success rate of 89% in one series.61 Targeted therapy on scapular stabilizers and humeral head compressors has been shown to improve range of motion and decrease pain significantly.62 Traditionally, only anecdotal evidence existed regarding steroid injections for the treatment of impingement. Their effectiveness in the short term has now been validated in randomized, double-blinded clinical studies.63 However, the accuracy of injection placement has come into question, with one study demonstrating that only 70% of injections reach the subacromial space, as verified by bursography.64 Furthermore, there is little information about the content of the injections and the efficacy of different synthetic steroids. We prefer a combination of 2 mL of methylprednisolone (Depo-Medrol), 4 mL of 1% lidocaine, and 4 mL of 0.25% bupivacaine (Marcaine) injected through the anterior or posterolateral portal site. Although there are no quantitative data, it is generally believed that repeated injections should be avoided because of the potentially adverse effects on tendon integrity.65,66
Surgical Treatment As Neer solidified his theory of impingement, he advocated the anterior acromioplasty, recognizing that only a small anterior portion of bone is involved. This procedure remains the basis for how treatment is carried out today. The main advantages of the anterior acromioplasty are limited removal of bone and greater preservation of the deltoid muscle origin. The treatment of impingement in an older patient also includes the débridement of the subacromial bursa, coracoacromial ligament release and, if necessary, resection of osteophytes at the acromioclavicular joint. Ellman first described performing this operation through the arthroscope in 1985.67 The follow-up in this study reported good to excellent results in 88% of patients based on the UCLA shoulder rating scale. Since that time, prospective randomized studies comparing open with arthroscopic acromioplasty have found both methods to be reliable, with only minor differences.68-70 The role of the coracoacromial ligament in impingement has been given more attention in the athlete (Fig. 10-5). Most overhead motions in sports begin with abduction and external rotation, followed by forward flexion and internal rotation. With repetition of these motions, pain and decreased function may result from mechanical wear on the bursa and rotator cuff as they pass below the leading edge of the coracoacromial ligament and anterior acromion. Surgical resection of the coracoacromial ligament without acromioplasty has uniformly provided these patients with pain relief, but has not allowed most of those athletes to return to their previous level of function.71 This phenomenon has been
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Figure 10-5. Coracoacromial ligament.
noticed particularly in pitchers. The less than ideal outcome following isolated coracoacromial ligament resection and decompression should not imply that the addition of an anterior acromioplasty will lead to an improved outcome in these patients. Tibone and colleagues39 have studied 45 athletes with incomplete or complete rotator cuff tears; they found that 80% of patients with incomplete tears treated with an anterior acromioplasty have improved pain relief, but an overall good result was seen in only 50%. More recent long-term studies by Stephens and associates have reported the 6- to 10-year follow-up of arthroscopic acromioplasty for chronic impingement; 81% of patients had good to excellent results. However, one third of athletes were not able to return to overhead and throwing sports. It was hypothesized that occult instability may have been a factor in these patients and suggests ruling this out before surgery; it was also suggested that throwers be considered as a separate clinical group from the general population with impingement. In the athletic population, anterior instability follows impingement pathology as the second most common shoulder problem.40 Instability may lead to subluxation of the humeral head, causing mechanical impingement secondarily. Whether or not impingement is the primary or secondary cause for rotator cuff pathology in an athlete with shoulder pain, early intervention with a specifically designed rehabilitation program can alleviate symptoms and restore function.36,72,73 It is our recommendation that true impingement in the older athlete be treated with bursectomy, limited anterior acromioplasty, and CA ligament resection (Fig. 10-6). In young overhead athletes with isolated impingement, bursectomy and partial longitudinal anterior band CA ligament resection should be performed without acromioplasty.
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A
B Figure 10-6. Coracoacromial ligament excision. A, Defining the spur. B, Post–spur excision.
SUMMARY Variations in the architecture of the coracoacromial arch can lead to a clinically symptomatic rotator cuff lesion. Differences in the shape and slope of the acromion and the presence of anterior acromial spurs or inferior protruding acromioclavicular osteophytes may decrease the volume of the subacromial space, leading to impingement. Treatment should be focused initially on nonoperative modalities, such as rest, anti-inflammatory medications, and physical therapy, with surgical decompression used as a final option.
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7. Grant JCB: The upper limb. In Grant JCB (ed): A Method of Anatomy, 2nd ed. Baltimore, Williams & Wilkins, 1940. 8. Lieberson E: Os acromiale: A contested anomaly. J Bone Joint Surg 19:683, 1937. 9. DePalma AF: Surgical anatomy of acromioclavicular and sternoclavicular joints. Surg Clin North Am 43:1541, 1963. 10. Moseley HF: The clavicle and its articulations. In Moseley HF (ed): Shoulder Lesions, 2nd ed. New York, Hoeber, 1953. 11. Petersson CJ: Degeneration of the acromioclavicular joint: a morphological study. Acta Orthop Scand 54:434, 1983. 12. Lindblom K: On pathogenesis of ruptures of the tendon aponeurosis of the shoulder joint. Acta Radiol 20:563, 1939. 13. Moseley HF, Goldie I: The arterial pattern of the rotator cuff of the shoulder. J Bone Joint Surg Br 45:780, 1963. 14. Rathbun JB, Macnab I: The microvascular pattern of the rotator cuff. J Bone Joint Surg Br 52:540, 1970. 15. Rothman RH, Parke WW: The vascular anatomy of the rotator cuff. Clin Orthop Relat Res 41:176, 1965. 16. Suenaga N: The correlation between burscopic and histologic findings of the acromion undersurface in patients with subacromial impingement syndrome. Arthroscopy 18:16, 2002. 17. Bigliani LU, Morrison DS, April EW: The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 10:228, 1986. 18. Morrison DS, Bigliani LU: The clinical significance of variations in acromial morphology. Orthop Trans 11:234, 1987. 19. Constant CR, Murley AH: A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res 214:160, 1987. 20. Aoki M, Ishii I, Usui M: The slope of the acromion and rotator cuff impingement. Orthop Trans 10:228, 1986. 21. Aoki M, Ishii I, Usui M: Clinical application for measuring the slope of the Acromion. In Post M, Hawkins RJ, Morrey BF (eds): Surgery of the Shoulder. St. Louis, Mosby Year Book, 1990, pp 200. 22. Petersson CJ, Gentz CF: Ruptures of the supraspinatus tendon: The significance of distally pointing acromioclavicular osteophytes. Clin Orthop Relat Res 174:143, 1983. 23. Chambler AF, Pitsillides AA, Emery RJ: Acromial spur formation in patients with rotator cuff tears. J Shoulder Elbow Surg 12:314, 2003. 24. Soslowsky LJ, An CH, Johnston SP, Carpenter JE.: Geometric and mechanical properties of the coracoacromial ligament and their relationship to rotator cuff disease. Clin Orthop Relat Res 304:1, 1994. 25. Bigliani LU, Norris TR, Fischer J, et al: The relationship between the unfused acromial epiphysis and subacromial lesions. Orthop Trans 7:138, 1983. 26. DePalma MJ, Johnson EW: Detecting and treating shoulder impingement syndrome. Phys Sport Med 31:25, 2003. 27. Bateman JE: Cuff tears in athletes. Orthop Clin North Am 1:721, 1973. 28. Bigliani LU, D’Alessandro DF, Duralde XA, et al: Anterior acromioplasty for subacromial impingement in patients younger than 40 years of age. Clin Orthop Relat Res 246:111, 1989. 29. Cofield RH, Simonet WT: The shoulder in sports. Mayo Clin Proc 59:157, 1984. 30. Fowler P: Swimmer problems. Am J Sports Med 7:141, 1979. 31. Fu FH, Harner CD, Klein AH: Shoulder impingement syndrome: A critical review. Clin Orthop Relat Res 269:162, 1991.
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32. Gainor BJ, Piotrowski G, Puhl J, et al: The throw: biomechanics and acute injury. Am J Sports Med 8:114, 1980. 33. Hawkins RJ, Kennedy JC: Impingement syndrome in athletes. Am J Sports Med 8:151, 1980. 34. Jackson DW: Chronic rotator cuff impingement in the throwing athlete. Am J Sports Med 4:231, 1976. 35. Jackson DW: Problems among the inexperienced and experienced athlete. Am J Sports Med 7:142, 1979. 36. Jobe FW: Impingement problems in athletes. ICLS 38:205, 1989. 37. Neer CS, Welsh RP: The shoulder in sports. Orthop Clin North Am 8:583, 1977. 38. Penny JN, Welsh RP: Shoulder impingement syndromes in athletes and their surgical management. Am J Sports Med 9:11, 1981. 39. Tibone JE, Elrod B, Jobe FW, et al: Surgical treatment of tears of the rotator cuff in athletes. J Bone Joint Surg Am 68:887, 1986. 40. Jobe FW, Jobe CM: Painful athletic injuries of the shoulder. Clin Orthop Relat Res 173:117, 1983. 41. Norwood LA, Del Pizzo W, Jobe FW, et al: Anterior shoulder pain in baseball pitchers. Orthop Trans 2:20, 1978. 42. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220, 1988. 43. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics, and tennis. Clin Sports Med 2:247, 1983. 44. Jobe FW, Tibone JE, Perry J, et al: An EMG analysis of the shoulder in throwing and pitching: A preliminary report. Am J Sports Med 11:3, 1983. 45. Tullos HS, King JW: Throwing mechanism in sports. Orthop Clin North Am 1:709, 1973. 46. Tyler TF: Quantification of posterior capsule tightness and motion loss in patients with subacromial impingement. Am J Sports Med 28:668, 2000. 47. Harryman DT: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334, 1990. 48. Graichen H: Three-dimensional analysis of shoulder girdle and supraspinatus motion patterns in patients with impingement syndrome. J Orthop Res 19:1192, 2001. 49. Solem-Bertoft E, Thuomas KA, Westerberg CE: The influence of scapular retraction and protraction on the width of the subacromial space: An MRI study. Clin Orthop Relat Res 296:99, 1993. 50. Sakai H: Immunolocalization of cytokines and growth factors in subacromial bursa of rotator cuff tear patients. Kobe J Med Sci 47:25, 2001. 51. Yoshida M: Pathologic gene expression in adhesive subacromial bursae of the human shoulder. Clin Orthop 412:57, 2003. 52. Yanagisawa K: Vascular endothelial growth factor expression in the subacromial bursa is increased in patients with impingement syndrome. J Orthop Res 19:448, 2001. 53. Blaine TA, Kim YS, Voloshin I, et al: The molecular physiology of subacromial bursitis in rotator cuff disease. J Shoulder Elbow Surg 14(Suppl S):84S, 2005.
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54. Cole AS: Localized deposition of amyloid in tears of the rotator cuff. J Bone Joint Surg Br 83:561, 2001. 55. Hashimoto T, Nobuhara K, Hamada T: Pathologic evidence of degeneration as a primary cause of rotator cuff tear. Clin Orthop Relat Res 415:111, 2003. 56. Valadie AL: Anatomy of provocative tests for impingement syndrome of the shoulder. J Shoulder Elbow Surg 9:561, 2001. 57. MacDonald PB, Clark P, Sutherland K: An analysis of the diagnostic accuracy of the Hawkins and Neer subacromial impingement signs. J Shoulder Elbow Surg 9:299, 2000. 58. Calis M: Diagnostic values of clinical diagnostic tests in subacromial impingement syndrome. Ann Rheum Dis 59:44, 2000. 59. Mair SD: Can the impingement test predict outcome after arthroscopic subacromial decompression? J Shoulder Elbow Surg 8:231, 1999. 60. Morrison DS, Frogameni AD, Woodworth P: Non-operative treatment of subacromial impingement syndrome. J Bone Joint Surg Am 79:732, 1997. 61. Wang JC: The relationship between acromial morphology and conservative treatment of patients with impingement syndrome. Orthopaedics 23:557, 2000. 62. Walther M: The subacromial impingement syndrome of the shoulder treated by conventional physiotherapy, self-training, and a shoulder brace: Results of a prospective, randomized study. J Shoulder Elbow Surg 13:417, 2004. 63. Blair B: Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am 78:1685, 1996. 64. Yamakado K: The targeting accuracy of subacromial injection to the shoulder: An arthrographic evaluation. Arthroscopy 18:887, 2002. 65. Akpinar S: Effects of methylprednisolone and betamethasone injections on the rotator cuff: An experimental study in rats. Adv Ther 19:194, 2002. 66. Tillander B: Effect of steroid injection on the rotator cuff: An experimental study in rats. J Shoulder Elbow Surg 8:271, 1999. 67. Ellman H: Arthroscopic subacromial decompression: Analysis of one- to three-year results. Arthroscopy 18:173, 1987. 68. Husby T: Open versus arthroscopic subacromial decompression: A prospective, randomized study of 34 patients followed for 8 years. Acta Orthop Scand 74:408, 2003. 69. Spangehl MJ: Arthroscopic versus open acromioplasty: A prospective, randomized blinded study. J Shoulder Elbow Surg 11:101, 2002. 70. Lindh M, Norlin R: Arthroscopic subacromial decompression versus open acromioplasty. A two-year follow-up study. Clin Orthop Relat Res 290:174, 1993. 71. Tibone JE, Jobe FW, Kerlan RK, et al. Shoulder impingement syndrome in athletes treated by anterior acromioplasty. Clin Orthop Relat Res 198:134, 1985. 72. Pappas AM, Zawacki RM, McCarthy CF: Rehabilitation of the pitching shoulder. Am J Sports Med 13:223, 1988. 73. Jobe FW, Moynes DR: Delineation of diagnostic criteria and a rehabilitation program for rotator cuff injuries. Am J Sports Med 10:336, 1982.
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CHAPTER 11 Internal Impingement Michael M. Reinold, Kevin E. Wilk, Jeffrey R. Dugas, and James R. Andrews
Internal impingement is one of the most common shoulder pathologies seen in overhead athletes. Walch and colleagues1 first described internal impingement as contact between the articular side of the supraspinatus and/or infraspinatus tendon and the posterosuperior rim of the glenoid when the arm is abducted to 90 degrees and externally rotated, as seen during the late cocking and early acceleration phases of the overhead throwing motion (Fig. 11-1). This pathology differs from classic shoulder impingement, as described by Neer,2,3 which involves contact between the bursal side of the rotator cuff, usually the supraspinatus tendon, and the coracoacromial arch during arm elevation. Walch and coworkers1 noted this contact of the tendon in this area in 17 overhead athlete patients; Andrews and associates4 described this undersurface rotator cuff fraying in overhead athletes almost a decade earlier and, at the time, it was hypothesized that these lesions occur from excessive traction on the cuff from repetitive throwing.
Anatomic Theory Several authors have shown that there is contact between the posterior rotator cuff and glenoid rim and labrum with abduction and external rotation of the shoulder, which has been theorized to be a normal occurrence for the overhead athlete. Jobe and Sidles5 have demonstrated this on cadaver shoulders. Using magnetic resonance imaging (MRI), Halbrecht and colleagues6 have examined 10 asymptomatic college baseball pitchers in the abducted externally rotated position. All 10 pitchers demonstrated contact of the rotator cuff on the posterosuperior glenoid on the throwing shoulder; however, none exhibited this contact on the nonthrowing shoulder. It is still unknown whether contact itself is the same as pathologic internal impingement. The rationale for this theory of why contact occurs on the throwing shoulder and not the other side may be caused by bilateral anatomic differences in range of motion, laxity, humeral retroversion, or a combination of these factors. All these characteristics have been shown to be altered on the dominant side of overhead athletes (see later). Although contact has been shown to occur in the asymptomatic athlete, it is still unknown whether this is a normal occurrence in all overhead athletes or if the subjects involved in the studies cited demonstrated the specific characteristics that predispose the athlete to internal impingement. It is possible that contact of the rotator cuff on the glenoid is a normal occurrence in the overhead athlete because of the unique anatomic characteristics of the thrower’s shoulder. Consequently, with chronic repetitive contact, symptomatic internal impingement may arise as articular-sided rotator cuff partial tearing and labral pathology develop, after concomitant injuries to the labrum and capsule that affect the static stability of the shoulder, or both.
Since this original description, several theories have been proposed and new research has shed light on the mechanisms and consequences of internal impingement. The repetitive contact (or rubbing) between the tendon and glenoid rim during the throwing motion has been shown to result in undersurface partial-thickness rotator cuff tearing, posterosuperior glenoid labrum fraying or detachment, and cystic changes on the posterolateral aspect of the humeral head. Internal impingement, once considered simply impingement of the undersurface of the rotator cuff on the glenoid rim, now encompasses a broad spectrum of interrelated pathologies, including partial-thickness, articularsided, rotator cuff tears, capsular instability, superior labral anterior-posterior (SLAP) lesions, and occasional humeral head cystic changes. The purpose of this chapter is to discuss the pathology and pathomechanics of internal impingement. Using this background, we will review the examination, surgical intervention, and rehabilitation principles of caring for the athlete with internal impingement.
Anterior Laxity Theory The second proposed theory is the anterior laxity or instability theory. The anterior capsule undergoes significant tensile stress in the late cocking and early acceleration phases of the throwing motion. This stress can lead to gradual stretching of the capsular collagen over time, leading to increased anterior capsular laxity. Several clinicians7-11 have proposed that this repetitive strain on the anterior capsule in overhead athletes causes anterior capsular laxity over time. Mihata and associates12 have demonstrated in the cadaveric model that excessive external rotation (ER)
PATHOLOGY Numerous theories have been proposed to explain internal impingement in the overhead athlete. We will briefly discuss these theories, with the current scientific rationale for each. 123
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colleagues14 have subsequently shown that increasing the capsular elasticity by 30% produces an increase in external rotation of 18 degrees. Regardless of the answer, there is little doubt that increased anterior capsular laxity produces significant changes in the biomechanics of the shoulder throughout the throwing motion. Jobe15 and Davidson and associates16 have also described how improper throwing mechanics may also play a role in increasing anterior translation. Hyperangulation (excessive horizontal abduction), or opening up during the acceleration phase, causes the humerus to move posteriorly to the plane of the scapula, which may lead to increased strain on the anterior structures (Fig. 11-2).
Figure 11-1. Internal impingement. Shown is articular-sided impingement of the infraspinatus and/or supraspinatus on the posterosuperior glenoid rim.
If increases in anterior capsular laxity can lead to internal impingement, can reversing such changes decrease the likelihood of injury? This clinical question remains to be answered. Alberta and coworkers17 have measured rotation and translation in six intact cadaveric specimens. Measurements were repeated after stretching the anterior capsule and after plicating the anterior capsule in an attempt to reproduce the normal condition. It was found that with stretching of the anterior capsule, increased external rotation results, without a resultant posterior superior migration. Plication subsequently reduces external rotation and anterior translation, along with moving the center of rotation posteriorly and inferiorly (away from the rotator cuff and labrum) in external rotation.
results in elongation of the anterior band of the inferior glenohumeral ligament complex. Consequently, a significant increase in anterior and inferior capsular translation is noted. This acquired laxity from repetitive throwing may not manifest as gross anterior instability, although it is commonly believed that microinstability may be present (see later). This has been theorized to allow the humeral head to translate anteriorly during the cocking phase of throwing. Even if the amount of anterior translation is negligible, any further anterior displacement may cause—or increase—the undersurface of the posterior rotator cuff musculature to impinge on the posterosuperior glenoid rim. Thus, any amount of increased anterior translation may amplify the amount of internal impingement observed.
Posterior Capsular Tightness Theory Another theory is the posterior glenohumeral capsular tightness theory, proposed by Burkhart and colleagues,18 who hypothesized that the posterior capsule may become tight, causing a loss of glenohumeral internal rotation and posterosuperior humeral head translation. To date, no clinical data have shown this to be present. These researchers
A common debate among experienced clinicians centers around which occurs first, the increase in external rotation or the increase in capsular laxity. Fitzpatrick and coworkers13 have demonstrated that with increased capsular laxity, increases in external rotation occur. Schneider and Scapular axis
Scapular axis
o o –40
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Figure 11-2. Hyperangulation of the shoulder during throwing. A, Arm in the scapular plane. B, Arm posterior to the scapular plane.
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o
Arm axis
o 40 30 –
Body axis
A
Body axis
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Arm axis
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coined the term glenohumeral internal rotation deficit (GIRD), which means that in the throwing shoulder, the athlete demonstrates a loss of 20 degrees or more of internal rotation compared with the opposite (nonthrowing) shoulder. The unique range-of-motion (ROM) characteristics of the shoulder in overhead throwing athletes have been well defined.11,19-26 These studies have shown that asymptomatic baseball pitchers normally exhibit increased ER and decreased internal rotation (IR) at 90 degrees abduction in the throwing shoulder. Wilk and associates11 have studied the shoulder passive ROM characteristics in 372 professional baseball players. They reported a mean of 129 ± 10 degrees of ER and 61 ± 9 degrees of IR in the throwing shoulder at 90 degrees abduction. It was noted that ER is 7 degrees more and IR 7 degrees less in the dominant arm when compared with the nondominant arm. The concept of total motion was introduced in this study; this is the total value of external and internal rotation ROM (at 90 degrees abduction) added together (Fig. 11-3). It was also noted that there is no significant difference in total motion bilaterally, despite alterations in external and internal rotation. These ROM characteristics have been shown in studies by several clinicians in baseball20-22 and tennis players.24
IR
ER
IR
ER Figure 11-3. Total motion concept. The overhead athlete presents with excessive external rotation (ER) and a limitation of internal rotation (IR). This same arc is present on the nondominant shoulder, but is shifted toward internal rotation.
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It is well recognized and reported that ROM adaptations are normal in the overhead throwing athlete. However, the precise cause of this adaptation has not been established. Several clinicians have documented humeral retroversion in the thrower’s shoulder and attribute the altered ROM to bony adaptations.23,27,28 Crockett and coworkers23 have demonstrated that the average humeral retroversion in asymptomatic throwers is almost 40 degrees, whereas symptomatic throwers have an average of only 24 degrees of retroversion. Thus, the bilateral difference in retroversion is 16 degrees. Athletes who have never participated in throwing sports have an average bilateral humeral retroversion of 24 degrees, which is equal bilaterally. Meister and colleagues26 have shown that the maximum increases in humeral retroversion occur between ages 12 and 13 years. Thus, it appears that the loss of IR in baseball players may be a normal occurrence caused by humeral retroversion as the athlete is developing. Clinically, it is our belief that a loss of IR or GIRD is not problematic, regardless of the differential amount of IR bilaterally, if total motion is equal bilaterally. However, if there is a loss of total motion and IR, we think that the athlete may be more susceptible to injury. Reinold and associates29 have recently analyzed ROM before and after pitching and noted that the throwing shoulder has a significant decrease of IR and total motion (⫺10 degrees for both) immediately after pitching. These changes are still present 24 hours after pitching. Furthermore, there are no significant changes on the nondominant shoulder. The acute loss of motion was attributed to microscopic muscle damage caused by eccentric contractions of the posterior shoulder musculature. Eccentric muscular contractions have been correlated with a rise in passive muscular tension and a loss of joint ROM.30 It is our experience that baseball players often describe generalized tightness in the musculature of their posterior shoulder after pitching. The muscles responsible for ER of the shoulder exhibit high eccentric muscle activity31-34 during the throwing motion as the shoulder internally rotates between 6000 and 7000 deg/sec.35-37 Previous studies examining the effect of repetitive eccentric contractions have shown a subsequent loss of joint ROM in the upper and lower extremities following testing.39-41 The theory of posterior capsular tightness has also been questioned by other researchers20,21 who have found that ROM in baseball pitchers, specifically a loss of IR, does not correlate with an alteration in posterior glenohumeral translation. Borsa and coworkers20 have studied glenohumeral translation in a series of 43 healthy professional baseball pitchers. They reported that posterior translation is twice that of anterior translation. There is also no difference between the amount of translation of the dominant and nondominant shoulder. However, they were unable to show a correlation between IR range of motion and posterior laxity.
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Thus, it appears that a loss of IR on the throwing shoulder is normal and related to a certain degree of bony retroversion. The eccentric muscle activities involved in baseball pitching may be responsible for an acute loss of IR immediately following pitching. It does not appear that players with a significant decrease in IR on the dominant shoulder have an associated loss of posterior glenohumeral translation. Currently, it is difficult to say whether posterior capsular tightness occurs in overhead athletes or this plays a role in internal impingement. Further research is required to explore this theory in greater detail.
Microinstability–Over-rotation Theory Another theroy represents a combination of the theories discussed, which all relate to microinstability and overrotation of the throwing shoulder. This theory states that internal impingement is a mixture of several pathologic entities, including partial-thickness, articular-sided, rotator cuff tearing and superior labral degeneration and tearing (SLAP tears), which are a result of a combination of capsular microinstability, excessive external rotation, and humeral retroversion. Although contact of the undersurface of the rotator cuff may be a normal anatomic occurrence, any concomitant microinstability, rotator cuff weakness, or other loss of static or dynamic stability from the act of throwing may facilitate the development of pathologic internal impingement. This would explain why internal impingement is only seen on the dominant throwing side and not on the nonthrowing shoulder. As previously noted, macroinstability, or dislocation, is distinctly uncommon in the overhead throwing athlete. Microinstability may be defined as any rotational or directional pathologic laxity that leads to abnormal mechanics within the shoulder, without frank dislocation. Such rotational or directional laxity can lead to partial rotator cuff tearing, labral detachment or fraying, further capsular damage, or combinations of these injuries. It has been theorized that repetitive pitching causes acquired anterior laxity as the anterior capsule undergoes significant stress. If the repetitive strain on the anterior capsule from pitching causes an increase in anterior microinstability, internal impingement is likely to occur. Rizio and colleagues42 have recently studied the effects of anterior capsular laxity on superior labral strain. They simulated anterior instability in the cadaveric model and noted that posterosuperior labral strain increases significantly by 160% during the late cocking phase of throwing in shoulders with anterior instability. As noted, even though there are significant differences in external rotation, the total arc of motion of the throwing shoulder is not significantly different from that of the nonthrowing shoulder. In the throwing shoulder, the total arc is spun back into an externally rotated position. The cause
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of this spin back is likely a combination of soft tissue and bony adaptive changes, including humeral retroversion, which occur in the thrower’s shoulder over many years. These findings have led various clinicians to conclude that bony adaptations are potentially protective against internal impingement in the throwing athlete. In other words, if a throwing shoulder does not develop the protective osseous retroversion, the anterior capsule must stretch to accommodate the requirements of throwing, leading to anterior capsular stretch and internal impingement. Thus, it is our opinion that it is important to identify players who do not have a spin back total arc of motion, because they may have decreased retroversion and be predisposed to developing anterior microinstability and internal impingement. Several theories have been discussed whose conclusions, in all likelihood, have a certain effect on the development of internal impingement. Regardless, it appears that the term internal impingement itself should be considered as a collective group of findings, including articular-sided rotator cuff partial tearing, superior labral degeneration and tearing, and other associated pathologies.
EXAMINATION Clinical examination of the athlete with internal impingement includes a standard shoulder evaluation (see Chapters 3 and 4). We will describe some components of the examination that are important to discuss when dealing with players with internal impingement. Because of associated pathologies, the clinical examination of the thrower with internal impingement should include assessments of range of motion, capsular laxity, superior labrum, and static and dynamic stabilizers of the shoulder. The injured thrower with internal impingement generally presents with pain while throwing. Subjectively, the player may complain that it is “difficult to warm up” or “get loose.” There is often a loss of velocity and lack of command while pitching. Common complaints in throwers with internal impingement include pain during the late cocking and early acceleration phases of throwing. This pain is often posterosuperior but can also be anterior or even vague in nature because of the combination of pathologies typically present with internal impingement. Pain to palpation at the posterior glenohumeral joint line is also a common physical examination finding. These symptoms, while throwing, can be re-created on physical examination using the internal impingement sign as described by Meister and associated.43 With the athlete supine, the arm is passively abducted to 90 degrees and maximally externally rotated, similar to a classic apprehension test. This maneuver is designed to rotate the humeral head into the position of internal impingement, re-creating symptoms. In this position, the athlete will experience
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discomfort in the posterosuperior aspect of the shoulder and often report a vague deep discomfort. This internal impingement sign is considered positive if relocation of the humeral head causes a decrease in symptoms (Fig. 11-4). This is performed by exerting a posterior force on the humeral head similar to the apprehension or relocation test for anterior instability. The fact that this relocation test is indicative of internal impingement lends credibility to the theory that anterior capsular laxity and microinstability are likely contributing factors to internal impingement. Establishing the athlete’s passive ROM is also important. Asymptomatic throwers should display total motion that is equal bilaterally. It is important to note whether a player has an increase or decrease in total motion. As noted, chronic repetitive eccentric muscle trauma of the posterior rotator cuff from pitching may result in a loss of internal rotation and sometimes horizontal adduction. If a player has a significant increase in total motion in comparison with his nondominant shoulder, the athlete probably has a certain degree of laxity present. Thus, examination of the athlete’s static stabilizers is important. The typical capsular examination is performed with the athlete supine. This includes drawer and fulcrum testing at 90 degrees of abduction. In addition to side to side differences, the end feel of the ligamentous restraints to translation should be noted. Because of the close association of superior labral pathology, testing for SLAP tears should also be conducted. It is our opinion that testing for SLAP tears in the overhead athlete should include special tests that reproduce the thrower’s motion and the peel-back mechanism, which include the supinated external rotation,45 pronated load,44 and biceps load tests.46,47 Often, other SLAP tests that do not reproduce the peel-back mechanism, such as the
A
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O’Brien test, may not reveal the pathology present or may produce a false-positive test because of rotator cuff overload in this provocative position. Most throwers exhibit a typical muscular strength pattern in the throwing shoulder. Wilk and colleagues48,49 using isokinetic testing, have reported that the thrower’s shoulder’s external rotators were approximately 5% to 7% weaker than those of the nonthrowing shoulder. The internal rotators were 15% to 20% stronger. The ER/IR unilateral ratio was 66% to 72% Athlete’s with internal impingement will often exhibit weakness with external rotation and full or empty can testing. Scapula position may also have an effect on range of motion. It has been reported that the thrower exhibits a dropped shoulder and scapula on the throwing side. Basten and associates50 have reported that the thrower scapula exhibits a more protracted and anteriorly tilted posture at rest when compared with the opposite side. Macrina and coworkers51 have noted that following throwing and fatigue, the throwing shoulder’s scapula exhibits greater protraction and anterior tilting compared with that before throwing. This anteriorly tilted posture may contribute to the loss of internal rotation exhibited by the thrower.
RADIOGRAPHIC DIAGNOSIS From a diagnostic standpoint, each patient should undergo standard throwers’ series plain radiography, including AP views, internal and external rotation, and West Point, axillary, and subacromial outlet views. MRI is used for the confirmation of suspected shoulder pathology. In the vast majority of throwers, the diagnosis of labral pathology is made on the basis of clinical history and physical
B
Figure 11-4. Internal impingement sign. The examiner passively positions the arm into external rotation (A) and pain is felt posterosuperiorly. The examiner may then exert a force on the anterior shoulder to relocate the shoulder (B) and symptoms are diminished.
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examination. Sophisticated and sensitive radiographic tests such as MRI are used to confirm the suspected pathology. The use of MRI for diagnostic purposes has increased in popularity in recent years, and the accuracy of these tests are highly correlated with the experience of the radiologist reading the results and the quality of the examination itself. As with any MRI, the strength of the magnet is one of the determinants of image quality. The use of intra-articular contrast increases the accuracy of diagnosis in the hands and eyes of many clinicians. Figure 11-5 shows the typical appearance of a type II SLAP lesion on contrast-enhanced MRI. Figure 11-6 shows the ABER (abduction external rotation) view, which is done with the arm in the position of internal impingement. This sequence of images is particularly useful in throwers with symptoms of internal impingement—posterior superior shoulder pain in the late cocking and early acceleration phases of throwing.
TREATMENT Nonoperative Management Nonoperative management of internal impingement is the primary treatment for this pathology, and is successful in the vast majority of cases. The rehabilitation program is a multiphase sequential approach. The athlete is initially instructed to abstain from throwing, generally from 2 to 6 weeks, depending on the severity and chronicity of symptoms. In the acute phase, the patient presents with the main complaint of pain and possible stiffness. In addition, the patient exhibits loss of motion and weakness of
Figure 11-6. ABER (abduction external rotation) view demonstrating internal impingement. The typical undersurface fraying that occurs in the infraspinatus can be seen.
the external rotators and specific scapular muscles. In this phase, treatment is focused on diminishing pain and inflammation. A common modality that we have found to be effective is iontophoresis using a long-duration patch such as the Empi Action Patch (Empi, St. Paul, Minn) or Hybresis patch (IOMED, St. Paul, Minn). Phonophoresis, ice, and nonsteroidal anti-inflammatory drugs (NSAIDs) may be used to reduce pain and inflammation as well. The athlete often exhibits a loss of internal rotation motion and horizontal adduction. We believe this internal rotation deficit is caused by inflammation and tightness of the external rotators and posterior musculature. The stretches we have athletes perform include the sleeper stretch (Fig. 11-7), supine horizontal adduction stretch (Fig. 11-8), supine horizontal adduction with internal rotation (Fig. 11-9), and passive ROM into internal rotation (Fig. 11-10). These stretches can be aggressive on the rotator cuff and should be performed in a controlled fashion. A sensation of stretching should be felt in the posterior aspect of the shoulder, not at the rotator cuff insertion. The goals of these stretches are to restore the athlete’s normal spun back total motion in comparison with the nonthrowing shoulder and to improve the athletes’ end range elasticity of the external rotators.
Figure 11-5. Magnetic resonance imaging scan of a typical type II superior labral anterior-posterior (SLAP) lesion.
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In addition, muscular strengthening exercises are used to restore strength, muscular balance, and proprioception. In most overhead athletes, we emphasize the external rotators, scapular retractors, scapular depressors, core, and legs. Additionally, scapular strengthening exercises include prone horizontal abduction, prone horizontal
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Figure 11-7. Sleeper stretch.
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Figure 11-10. Passive range of motion into internal rotation stretch.
abduction at 120 degrees with external rotation (prone full can), prone extensions at 30 degrees of abduction, and prone rowing into external rotation. Total armstrengthening exercises are performed, including arm, forearm, and wrist exercises.
Figure 11-8. Supine horizontal adduction stretch.
Figure 11-9. Supine horizontal adduction with internal rotation stretch.
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Because we think that microinstability is a contributing factor to internal impingement, the goal of rehabilitation is to enhance dynamic stabilization of the shoulder. Rhythmic stabilization exercises are performed to improve proprioception, neuromuscular control, and muscular balance (Fig. 11-11). To strengthen and enhance the neuromuscular control of the external rotators, electrical muscle stimulation (300PV, Empi, St Paul, Minn) is applied (Fig. 11-12) during exercises such as standing tubing external rotation, side-lying external rotation, prone external rotation, and other rotator cuff–strengthening exercises.
Figure 11-11. Rhythmic stabilization exercises.
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exercises are progressed to incorporate perturbations before the initiation of throwing. The perturbation drills are performed with exercise tubing at 90 degrees of abduction and with a plyometrics ball (Fig. 11-17). The goal of the perturbation drills is to improve the patient’s end range stabilization. When the patient is pain free and exhibits excellent end range stability, an interval throwing program may be implemented. The return to activity phase is focused on the initiation of an interval throwing program.54 The interval throwing program is performed every other day, three times weekly, and in conjunction with a stretching, strengthening, and plyometrics program. The interval throwing is initiated at 45 feet and the distance is gradually increased to 120 feet and occasionally to 180 feet. Throwing programs are highly individualized based on the specific athlete, season, and goals; Chapter 58 discusses interval sports programs. Once the long toss program is successfully completed, a mound throwing program is initiated. When the mound program is completed, a gradual return to competition is carried out. Figure 11-12. Neuromuscular electrical stimulation applied to the infraspinatus during tubing external rotation exercises.
In the second subacute phase, the entire shoulder complex is emphasized. The patient is placed on the thrower’s ten program (Fig. 11-13),52,53 which focuses on all the muscles involved in the act of throwing. The scapula and core exercises are performed daily; one day the exercises are performed on the table and the alternating day on a physioball (Fig. 11-14). We prefer this method because it alters the challenges onto the shoulder complex. Other scapular exercises performed during this phase include side-lying neuromuscular control drills (Fig. 11-15) and plank exercises (Fig. 11-16). Additionally, during this phase, stretching and range of motion are performed to maintain the athlete’s total motion. The next phase represents the advanced strengthening phase. During this phase, the exercise intensity, velocity, and volume are all increased to prepare the athlete for the upcoming initiation of a formal interval throwing program. The exercises performed in this phase include stretching, range of motion, thrower’s ten program, dynamic stabilization drills advanced manual resistance and reactive neuromuscular control drills are initiated. These drills include proprioceptive neuromuscular fasciculation (PNF) patterns, tubing with manual resistance, and plyometrics. The plyometrics program that we use includes one- and two-hand throws, wall drills, and Plyoball bounce-back drills. (For a detailed description of plyometric exercises, see Chapter 55.) The plyometrics drills are initiated with twohand throws first and then progress to one-hand throws. The goal of plyometrics is to increase the loads onto the shoulder and entire upper extremity progressively. Manual
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Surgical Intervention for Internal Impingement Operative management of internal impingement should only be considered after failure of nonoperative measures. When a thrower is unable to return to competition despite adequate rest and rehabilitation, surgical management may be considered. The procedure should be tailored to the athlete, because each shoulder is unique and requires individualized management. The first part of any surgical procedure on the thrower’s shoulder is a thorough examination under anesthesia. This should include evaluation and documentation of ROM of the throwing and nonthrowing shoulders. This will give the surgeon a definitive assessment of the amount of spin back and amount of retroversion and total arc of motion. This will later guide the surgeon with regard to the need for capsular release or tightening. Diagnostic arthroscopy is then carried out through a standard posterior portal. This will allow complete access to the glenohumeral joint. The articular surfaces of the glenoid and humerus are assessed. The presence or absence of loose bodies is noted. The undersurface of the supraspinatus and infraspinatus are visualized, and the presence or absence of fraying or detachment is noted. The labrum and biceps tendon anchor are also well visualized through this portal. The anterior recess of the shoulder and subscapularis tendon are also seen. Next, an anterior portal is established under direct vision. The arthroscope is placed through this portal for better visualization of the posterior aspect of the rotator cuff, capsule, and labrum. Switching between portals, the surgeon can determine whether there is any labral detachment throughout the entire circumference of the labrum.
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1A. Diagonal pattern D2 extension: Involved hand will grip tubing handle overhead and out to the side. Pull tubing down and across your body to the opposite side of leg. During the motion, lead with your thumb. Perform _______ sets of _______ repetitions _______ daily.
1B. Diagonal pattern D2 flexion: Gripping tubing handle in hand of involved arm, begin with arm out from side 45° and palm facing backward. After turning palm forward, proceed to flex elbow and bring arm up and over involved shoulder. Turn palm down and reverse to take arm to starting position. Exercise should be performed _______ sets of _______ repetitions _______ daily.
2A. External rotation at 0° abduction: Stand with involved elbow fixed at side, elbow at 90° and involved arm across front of body. Grip tubing handle while the other end of tubing is fixed. Pull out arm, keeping elbow at side. Return tubing slowly and controlled. Perform _______ sets of _______ repetitions _______ times daily.
2B. Internal rotation at 0° abduction: Standing with elbow at side fixed at 90° and shoulder rotated out. Grip tubing handle while other end of tubing is fixed. Pull arm across body keeping elbow at side. Return tubing slowly and controlled. Perform _______ sets of _______ repetitions _______ times daily.
If a tear in the labrum is present, the next determination is whether or not the tear should be simply débrided or repaired. Inner rim bucket-handle tears (type III SLAP) can usually be débrided back to a stable rim. If the labrum is detached from the glenoid rim, arthroscopic repair of the labrum can be carried out after adequate preparation of the bony attachment. These repairs are generally done using suture anchors implanted into the glenoid rim. It is
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Figure 11-13. The thrower’s ten exercise program. This program is designed to exercise the major muscles necessary for throwing; its goal is to be an organized and concise exercise program. Also, all exercises are specific to the thrower and designed to improve the strength, power, and endurance of the shoulder’s complex musculature. ABD, abduction.
important to place the anchors on the margin of the articular cartilage, not down the neck of the glenoid, to obtain adequate re-approximation of the labrum to the glenoid surface. The suture from the anchor is then passed beneath the detached portion of the labrum and an arthroscopic knot is tied to fix the labrum back to the glenoid firmly. Multiple anchors are generally used. Text continued on page 135
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2C. (Optional) External rotation at 90° abduction: Stand with shoulder abducted 90°. Grip tubing handle while the other end is fixed straight ahead, slightly lower than the shoulder. Keeping shoulder abducted, rotate shoulder back keeping elbow at 90°. Return tubing and hand to start position. I. Slow speed sets: (Slow and controlled) Perform _______ sets of _______ repetitions _______ times daily. II. Fast speed sets: Perform _______ sets of _______ repetitions _______ times daily.
2D. (Optional) Internal rotation at 90° abduction: Stand with shoulder abducted to 90°, externally rotated 90° and elbow bent to 90°. Keeping shoulder abducted, rotate shoulder forward, keeping elbow bent at 90°. Return tubing and hand to start position. I. Slow speed sets: (Slow and controlled) Perform _______ sets of _______ repetitions _______ times daily. II. Fast speed sets: Perform _______ sets of _______ repetitions _______ times daily.
3. Shoulder abduction to 90°: Stand with arm at side, elbow straight, and palm against side. Raise arm to the side, palm down, until arm reaches 90° (shoulder level). Perform _______ sets of _______ repetitions _______ times daily.
4. Scaption, external rotation: Stand with elbow straight and thumb up. Raise arm to shoulder level at 30° angle in front of body. Do not go above shoulder height. Perform _______ sets of _______ repetitions _______ times daily.
5. Sidelying external rotation: Lie on uninvolved side, with involved arm at side of body and elbow bent to 90°. Keeping the elbow of involved arm fixed to side, raise arm and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
Figure 11-13 cont’d.
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6A. Prone horizontal abduction (neutral): Lie on table, face down, with involved arm hanging straight to the floor, and palm facing down. Raise arm out to the side, parallel to the floor. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
6B. Prone horizontal abduction (full ER, 100° ABD): Lie on table face down, with involved arm hanging straight to the floor, and thumb rotated up (hitchhiker). Raise arm out to the side with arm slightly in front of shoulder, parallel to the floor. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
6C. Prone rowing: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, and bring dumbbell as high as possible. Hold at the top for 2 seconds, then slowly lower. Perform _______ sets of _______ repetitions _______ times daily.
6D. Prone rowing into external rotation: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, up to the level of the table. Pause one second. Then rotate shoulder upward until dumbbell is even with the table, keeping elbow at 90°. Hold at the top for 2 seconds, then slowly lower taking 2-3 seconds. Perform _______ sets of _______ repetitions _______ times daily.
7. Press-ups: Seated on a chair or table, place both hands firmly on the sides of the chair or table, palm down and fingers pointed outward. Hands should be placed equal with shoulders. Slowly push downward through the hands to elevate your body. Hold the elevated position for 2 seconds and lower body slowly. Perform _______ sets of _______ repetitions _______ times daily. Figure 11-13 cont’d.
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8. Push-ups: Start in the down position with arms in a comfortable position. Place hands no more than shoulder width apart. Push up as high as possible, rolling shoulders forward after elbows are straight. Start with a push-up into wall. Gradually progress to table top and eventually to floor as tolerable. Perform _______ sets of _______ repetitions _______ times daily.
9A. Elbow flexion: Standing with arm against side and palm facing inward, bend elbow upward turning palm up as you progress. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
9B. Elbow extension (abduction): Raise involved arm overhead. Provide support at elbow from uninvolved hand. Straighten arm overhead. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
10A. Wrist extension: Supporting the forearm and with palm facing downward, raise weight in hand as far as possible. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
10B. Wrist flexion: Supporting the forearm and with palm facing upward, lower a weight in hand as far as possible and then curl it up as high as possible. Hold for 2 seconds and lower slowly. Figure 11-13 cont’d.
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10C. Supination: Forearm supported on table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm up. Hold for a 2 count and return to starting position. Perform _______ sets of _______ repetitions _______ times daily.
10D. Pronation: Forearm should be supported on a table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm down. Hold for a 2 count and return to starting position. Perform _______ sets of _______ repetitions _______ times daily. Figure 11-13 cont’d.
Undersurface rotator cuff pathology can be addressed through the same two working portals. Simple fraying of the undersurface of the supraspinatus or infraspinatus can be débrided using a shaver. Partial-thickness detachment from the greater tuberosity can be repaired using smallsuture transtendon anchors placed through an accessory portal or through the working portals if the area of the tear is accessible. Once the labral or rotator cuff pathology has been addressed, attention can be shifted to the capsule. Based on the clinical evaluation of the athlete and the examination under anesthesia, remembering the total arc concept, a decision can be made as to which anatomic aspect of the capsule should be addressed. If the clinical picture of rotational microinstability is present, anterior plication or thermal shrinkage can be carried out to decrease external
A
B
Figure 11-14. Prone horizontal abduction flips with a Plyoball.
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Figure 11-15. Side-lying neuromuscular control drills for the scapular. A, Scapular retraction and protraction. B, Scapular elevation and depression.
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Figure 11-16. Plank exercises for neuromuscular control of the shoulder and scapula stabilizers.
rotation and internal impingement. It is rare that a thrower requires closure of the rotator interval, because this may severely limit capsular mobility anteriorly. If it is believed that the posterior capsule is overly voluminous, plication or thermal shrinkage can be performed to decrease capsular volume.
A
If capsular plication is to be carried out, the location of plication is identified and the amount of tissue to be plicated is determined, based on the amount of tightening desired. Sutures can be passed through the capsule alone or through the labrum as well, depending on the amount of tightening desired. Again, arthroscopic passing and tying techniques are used to complete these types of procedures. If thermal shrinkage is the modality of choice, a monopolar device should be used in a linear striping pattern extending from the glenoid to the humeral head, and separated by several millimeters of unshrunk tissue. Only the areas of interest should be treated with the shrinkage probe. Careful assessment of the posterior capsule should be made before deciding whether release of the posterior capsule is indicated. A loss of internal rotation is often treated successfully with a proper stretching program for the posterior musculature. If it is necessary to perform a capsular release to improve internal rotation, although not commonly performed, this can be carefully done using an electrocautery or arthroscopic cutting device. Typically, the capsule is released from the posterior portal inferiorly toward the posterior band of the inferior glenohumeral ligament. Careful attention should be paid to remaining as close as possible to the glenoid rim to prevent injury to the nearby axillary nerve. Once the intra-articular pathology has been addressed, the arthroscope can be directed into the subacromial space through the same standard posterior portal. The dorsal side of the rotator cuff can be visualized after resection of
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B Figure 11-17. Wall dribbles using a plyometric ball (A) and incorporating end-range perturbations (B).
the subacromial bursa. If necessary, acromioplasty can also be performed through these same portals. If any rotator cuff repair has been performed, the sutures are typically tied in the subacromial space over the dorsal side of the cuff. Regardless of which surgical procedure or technique is performed, communication with the physical therapist or
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athletic trainer is of paramount importance. The rehabilitation team should be informed as to exactly what was done to the shoulder and what to expect with regard to early and long-range rehabilitation goals, such as ROM, glenohumeral translation, and any prohibited motions, modalities, and braces or restraints that may be needed. Only through direct communication will these procedures yield a high degree of success. In some cases of chronic microinstability, long-standing pathomechanics may lead to worsening injuries and subsequent severe capsular, labral, and rotator cuff pathologies. Because the capsule and glenohumeral ligaments limit and allow rotational motion in the shoulder, complete rotator cuff tearing, capsular injury, or disruption of the glenohumeral ligament(s) is a careerthreatening injury to the thrower. Repair of the thin, friable, capsular layer of the shoulder is technically difficult and, from a recovery and rehabilitation standpoint, it is difficult to regulate return of motion. Therefore, it is important to establish good habits in terms of stretching, throwing mechanics, and injury prevention for the thrower. The following section will delineate some of the intrinsic aspects of postsurgical recovery from a rehabilitation standpoint.
137
is a common cause of symptoms while the athlete is trying to progress through the rehabilitation and throwing stages of rehabilitation. Muscle training drills and exercises are performed immediately following surgery. These are done in the form of isometrics. We allow isometrics for the first 7 to 10 days in a submaximal and subpainful manner. At approximately 10 to 14 days postoperatively, a light isotonic program will be allowed. We emphasize external rotation and scapular strengthening muscles. At week 5, the athlete is allowed to progress to the full thrower’s ten program. Plyometrics is allowed at approximately 8 weeks postoperatively. These plyometrics drills are permitted using two hands and restricting the amount of external rotation. After 10 to 14 days, two-hand plyometrics drills are progressed by incorporating one-hand drills. An aggressive strengthening program is allowed, starting at week 12 and progressing to week 16. The program is adjusted according to the patient’s response to the strengthening program and response to the surgery. A gradual return to throwing is instituted at week 16.54 A return to contact sports is usually allowed at 6 to 8 months and to overhead sports by 9 to 12 months.
Following Thermal Capsular Shrinkage
POSTOPERATIVE REHABILITATION Following Capsular Plication Immediately following capsular plication surgery, we allow immediate restricted passive range of motion, but not overaggressive stretching. We do not allow excessive external rotation, elevation, or shoulder extension. Gentle passive and active-assisted range of motion are allowed during the first 2 weeks with a goal of immediate motion to stimulate proliferation of collagen tissue. At week 3, we allow internal and external rotation to be performed at 45 degrees of abduction. We allow external rotation to approximately 30 degrees. Internal rotation can be performed to touch the side. Active-assisted flexion is allowed to 90 degrees and gradually progressed past 90 degrees during week 4. At week 5, we allow internal and external rotation to be performed at 90 degrees of abduction. Our goal is to have 75 degrees of external rotation by week 6 and to have 90 degrees of external rotation at 90 degrees of abduction by week 8. Usually, by weeks 6 to 8, flexion is 170 to 180 degrees. In the case of the overhead athlete, particularly the pitcher, we want to achieve a gain of external rotation to approximately 115 degrees. This goal is usually achieved gradually, and no earlier than week 12. We do not typically stretch the athlete aggressively past 115 to 120 degrees of external rotation; rather, we let the athlete regain normal motion through functional activities within the rehabilitation program, such as plyometrics. Not restoring full external rotation in the overhead athlete
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Guidelines for rehabilitation following thermal capsular shrinkage of the shoulder are similar to those following plication, but there a few specific precautions.55,56 The rehabilitation program must be carried out cautiously during the first 4 to 6 weeks so that the athlete does not stretch excessively. Hecht and colleagues57 have demonstrated that during the first 8 weeks following a thermal procedure, the collagen tissue is extremely vulnerable to being stretched out. Thus, during the first 6 to 8 weeks, the rehabilitation specialist must be cautious about overaggressive ROM exercises. Schaefer and associates58 have demonstrated that overaggressive activities during the first 8 weeks following thermal application to patellar tendons in rabbits caused an overall increase in resting length of the tendon. Hayashi and coworkers59 have demonstrated that an inflammatory reaction is present for at least 8 weeks and may be present as long as 3 to 6 months after a thermal procedure. Often, this inflammatory reaction can lead to joint stiffness and soreness, which may limit the patient’s progression in regards to motion. Rehabilitation following a thermal capsular shrinkage must be modified and adjusted according to the patient’s response to surgery. The program needs to be assessed and adjusted weekly; not all patients appear to respond in the same manner following this surgical procedure. Another factor to consider is a concomitant procedure performed at the time of thermal capsular shrinkage.56,60 Frequently, a SLAP repair or a rotator cuff débridement is performed concomitantly with the thermal capsular shrinkage to address internal impingement.
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Following Anterior Capsular Shift Procedure An open capsular shift procedure may be another procedure performed to address shoulder instability. This requires a delicate balance between the surgical procedure and postoperative rehabilitation program. Our experience with this type of surgical procedure is to be somewhat aggressive with postoperative management. We use two rehabilitation protocols based on the goals of each patient. Most general orthopedic patients will progress cautiously to avoid overstressing their healing tissue. An accelerated rehabilitation approach based on immediate restricted motion and a gradual return to the motion is necessary for overhead athletes. During weeks 1 through 3, active-assisted ROM for ER and IR is performed with the arm in 30 degrees of abduction to patient tolerance. During weeks 2 to 4, ROM and stretching gradually progress. Active-assisted ER and IR ROM exercises are performed at 45 degrees of abduction, with the goal of 45 degrees of motion (ER and IR) by week 4. During this time, tubing exercises may be initiated for the shoulder’s internal and external rotators; rhythmic stabilization drills and co-contractions also are performed. ER-IR stretching is performed at 90 degrees of abduction at week 4 for overhead athletes and week 6 for the general orthopedic patient. At week 8, the overhead athlete should exhibit full motion (90 degrees of ER and 45 to 55 degrees of horizontal abduction) and gradually progress to full thrower’s motion between weeks 8 and 12. For general orthopedic patients, we often restore approximately 80% to 90% of their motion by week 10 and allow time and functional activities to regain their remaining motion. A return to unrestricted sports usually occurs between 6 and 9 months, depending on the patient’s sport, position, skill level, and rate of progression.
Following Superior Labral Surgery The specific rehabilitation program following surgical intervention involving the superior glenoid labrum is dependent on the severity of the pathology and type of SLAP lesion, exact surgical procedure performed (débridement versus repair), and other concomitant procedures performed because of the underlying glenohumeral joint instability that is often present. Overall, emphasis should be placed on restoring and enhancing dynamic stability of the glenohumeral joint, while at the same time ensuring that adverse stresses are not applied to healing tissue.44 Before rehabilitation, we think that it is imperative that the mechanism of injury be fully understood. For patients who sustained a SLAP lesion via a compressive injury, such as a fall on an outstretched hand, weight-bearing exercises should be avoided to minimize compression and sheer on the superior labrum. Patients with traction injuries should
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avoid heavy resisted or excessive eccentric biceps contractions. Furthermore, patients with peel-back lesions, such as overhead athletes, should avoid excessive amounts of shoulder external rotation while the SLAP lesion is healing. Thus, the mechanism of injury is an important factor to assess individually when determining appropriate rehabilitation guidelines for each patient. Although the efficacy of rehabilitation following SLAP repairs has not been documented, the following sections will provide an overview of the rehabilitation guidelines based on our clinical experience and studies on the mechanics of the glenoid labrum and pathomechanics of SLAP lesions.44,45,61-65 Débridement of Types I and III SLAP Lesions Types I and III SLAP lesions normally undergo a simple arthroscopic débridement of the frayed labrum without an anatomic repair.44 This program can be somewhat aggressive in restoring motion and function because the biceps labral anchor to the glenoid rim is stable and intact. The rate of progression during the course of postoperative rehabilitation is based on the presence and extent of concomitant lesions and patient tolerance. If, for example, significant rotator cuff fraying (partial-thickness tear) is present and treated with arthroscopic débridement, the rehabilitative program must be appropriately adapted. Generally, a sling is worn for comfort during the first 3 to 4 days following surgery. Active-assisted range of motion and passive rangeof-motion (PROM) exercises are initiated immediately following surgery, with full PROM expected within 10 to 14 days postoperatively. Flexion ROM exercises are performed to tolerance. ER and IR in the scapular plane are initiated at 45 degrees of glenohumeral abduction and advanced to 90 degrees of abduction, usually by postoperative day 4 or 5. ROM exercises may be done early because an anatomic repair has not been performed. Shoulder musculature training may begin during the first week, with the patient performing submaximal isometrics. Light isotonic strengthening for the shoulder and scapular musculature, with the exception of the biceps, is initiated during week 2. This includes ER-IR exercise tubing, sidelying ER, prone rowing, prone horizontal abduction, and prone ER. Active elevation exercises such as scapular plane elevation (full can) and lateral raises are also included. Light biceps resistance is usually not initiated until 2 weeks following surgery in an attempt to prevent débridement site irritation. Furthermore, early overaggressive elbow flexion and forearm supination exercises should be done cautiously, particularly eccentric exercises. The individual is advanced to controlled weight-training activities between postoperative weeks 4 and 6. In athletes, plyometrics exercises may be used and are initiated between weeks 4 and 5 to train the upper extremity to absorb and develop external forces. The athlete is allowed to begin a
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gradual return to sport-specific activities between postoperative weeks 7 and 10, usually with an interval sport program. The rate of return to overhead sports is often dependent on the extent of concomitant injuries. For example, an athlete with rotator cuff débridement involving 20% to 30% penetration of the rotator cuff will usually begin an interval sport program following these guidelines, whereas an athlete with more extensive pathology may need to delay initiation of the interval sport program for up to 4 months. Repair of Type II SLAP Lesions Injuries that involve detachment of the glenoid labrum– biceps complex from the glenoid rim have various causes. This type of injury may be caused by a fall, traction force, motor vehicle accident, or during sports.44 Overhead throwing athletes commonly present with a type II SLAP lesion with the biceps tendon detached from the glenoid rim. Frequently, a peel-back lesion is also present.63 The initial rehabilitative concern is to ensure that forces and loads on the repaired labrum are appropriately controlled. We think that it is important to determine the extent of the lesion and understand its exact location and number of suture anchors when devising an appropriate rehabilitation program. For example, the rate of rehabilitation progression would be slower for a SLAP repair completed with three anchors rather than one anchor, based on the extent of the pathology and tissue involvement. Postoperative rehabilitation is delayed to allow healing of the more extensive anatomic repair required to re-attach the biceps tendon anchor in a type II lesion, in comparison with types I and II lesions. The patient is instructed to sleep in a shoulder immobilizer and wear a DonJoy Ultra Sling (DonJoy, Vista, Calif) during the daytime for the first 4 weeks following surgery to protect the healing structures from excessive amounts of motion. Gradual range of motion in a protective range is performed for the first 4 weeks below 90 degrees of elevation to avoid strain on the labral repair. During the first 2 weeks, internal and external rotation ROM exercises are performed passively in the scapular plane to approximately 10 to 15 degrees of ER and 45 degrees of IR. Initial ER ROM exercises are performed cautiously to minimize strain on the labrum through the peel-back mechanism. At postoperative week 4, the patient is instructed to begin internal and external rotation ROM activities at 90 degrees of shoulder abduction, and flexion motion can be performed above 90 degrees of elevation. Motion is gradually increased to restore full range of motion (90 to 100 degrees of ER at 90 degrees of abduction) by 8 weeks and progressed to a thrower’s motion (approximately 115 to 120 degrees of ER) through week 12. Restoration of motion is usually accomplished with minimal difficulty. Isometric exercises are performed immediately postoperatively. These exercises are performed submaximally and designed to prevent shoulder atrophy. No biceps
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contractions are permitted for 8 weeks following repair. ER-IR tubing exercises are initiated at weeks 3 to 4 and progressed to include lateral raises, full can, prone rowing, and prone horizontal abduction by week 6. As the patient progresses, a full isotonic exercise program, such as the thrower’s ten program, is initiated by weeks 7 to 8. Emphasis is placed on strengthening exercises for the external rotators and scapular stabilizers. No resisted biceps activity (both elbow flexion and forearm supination) is allowed for the first 8 weeks to protect healing of the biceps anchor. Aggressive strengthening of the biceps is avoided for 12 weeks following surgery. Furthermore, weight-bearing exercises are usually not performed for at least 8 weeks to avoid compression and shearing forces on the healing labrum. Two-hand plyometrics, as well as more advanced strengthening activities, are allowed between 10 and 12 weeks, progressing to the initiation of an interval sport program at postoperative week 16. The same criteria described earlier are used to determine whether an interval sport program can be initiated. Return to play following the surgical repair of a type II SLAP lesion typically occurs at approximately 9 to 12 months following surgery.
SUMMARY Our understanding of the mechanisms and consequences of internal impingement has been greatly enhanced over the last several years. It is now accepted that internal impingement encompasses a broad spectrum of pathologies, including articular-sided partial-thickness tears of the rotator cuff, superior labral degeneration and tears, and microinstability. Examination, surgical intervention, and rehabilitation should consider each of these underlying pathologies.
References 1. Walch G, Liotard JP, Boileau P, Noel E: Postero-superior glenoid impingement. Another shoulder impingement. Rev Chir Orthop Reparatrice Appar Mot 77:571-574, 1991. 2. Neer CS 2nd: Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am. Jan 54:41-50, 1972. 3. Neer CS 2nd: Impingement lesions. Clin Orthop Relat Res (173):70-77, 1983. 4. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117-122, 1985. 5. Jobe CM, Sidles J: Evidence for a superior glenoid impingement upon the rotator cuff. J Shoulder Elbow Surg 2:S19, 1993. 6. Halbrecht JL, Tirman P, Atkin D: Internal impingement of the shoulder: Comparison of findings between the throwing and nonthrowing shoulders of college baseball players. Arthroscopy 15:253-258, 1999.
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7. Jobe FW, Kvitne RS, Giangarra CE: Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18:963-975, 1989. 8. Jobe FW, Giangarra CE, Kvitne RS, Glousman RE: Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med 19:428-434, 1991. 9. Kvitne RS, Jobe FW: The diagnosis and treatment of anterior instability in the throwing athlete. Clin Orthop Relat Res (291):107-123, 1993. 10. Kvitne RS, Jobe FW, Jobe CM: Shoulder instability in the overhand or throwing athlete. Clin Sports Med 14:917-935, 1995. 11. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30:136-151, 2002. 12. Mihata T, Lee Y, McGarry MH, et al: Excessive humeral external rotation results in increased shoulder laxity. Am J Sports Med 32:1278-1285, 2004. 13. Fitzpatrick MJ, Tibone JE, Grossman M, et al: Development of cadaveric models of a thrower’s shoulder. J Shoulder Elbow Surg 14(Suppl S):49S-57S, 2005. 14. Schneider DJ, Tibone JE, McGarry MH, et al: Biomechanical evaluation after five- and ten-millimeter anterior glenohumeral capsulorrhaphy using a novel shoulder model of increased laxity. J Shoulder Elbow Surg 14:318-323, 2005. 15. Jobe CM: Superior glenoid impingement. Current concepts. Clin Orthop Relat Res (330):98-107, 1996. 16. Davidson PA, Elattrache NS, Jobe CM, Jobe FW: Rotator cuff and posterior-superior glenoid labrum injury associated with increased glenohumeral motion: A new site of impingement. J Shoulder Elbow Surg 4:384-390, 1995. 17. Alberta FG, Elattrache NS, Mihata T, et al: Arthroscopic anteroinferior suture plication resulting in decreased glenohumeral translation and external rotation. Study of a cadaver model. J Bone Joint Surg Am 88:179-187, 2006. 18. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 19:404-420, 2003. 19. Bigliani LU, Codd TP, Connor PM, et al: Shoulder motion and laxity in the professional baseball player. Am J Sports Med 25:609-613, 1997. 20. Borsa PA, Wilk KE, Jacobson JA, et al: Correlation of range of motion and glenohumeral translation in professional baseball pitchers. Am J Sports Med 33:1392-1399, 2005. 21. Borsa PA, Dover GC, Wilk KE, Reinold MM: Glenohumeral range of motion and stiffness in professional baseball pitchers. Med Sci Sports Exerc 38:21-26, 2006. 22. Brown LP, Niehues SL, Harrah A, et al: Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 16:577-585, 1988. 23. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 30:20-26, 2002. 24. Ellenbecker TS, Roetert EP, Bailie DS, et al: Glenohumeral joint total rotation range of motion in elite tennis players and baseball pitchers. Med Sci Sports Exerc 34:2052-2056, 2002. 25. Johnson L: Patterns of Shoulder Flexibility Among College Baseball Players. J Athl Train 27:44-49, 1992. 26. Meister K, Day T, Horodyski M, et al: Rotational motion changes in the glenohumeral joint of the adolescent/Little League baseball player. Am J Sports Med 33:693-698, 2005.
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27. Osbahr DC, Cannon DL, Speer KP: Retroversion of the humerus in the throwing shoulder of college baseball pitchers. Am J Sports Med 30:347-353, 2002. 28. Reagan KM, Meister K, Horodyski MB, et al: Humeral retroversion and its relationship to glenohumeral rotation in the shoulder of college baseball players. Am J Sports Med 30:354-360, 2002. 29. Reinold MM, Wilk KE, Macrina LC, et al: Changes in shoulder and elbow passive range of motion after pitching in professional baseball players. Am J Sports Med 36:523-527, 2008. 30. Proske U, Morgan DL: Muscle damage from eccentric exercise: mechanism, mechanical signs, adaptation and clinical applications. J Physiol 537(Pt 2):333-345, 2001. 31. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220-226, 1988. 32. Gowan ID, Jobe FW, Tibone JE, et al: A comparative electromyographic analysis of the shoulder during pitching. Professional versus amateur pitchers. Am J Sports Med 15: 586-590, 1988. 33. Jobe FW, Moynes DR, Tibone JE, Perry J: An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 34. Sisto DJ, Jobe FW, Moynes DR, Antonelli DJ: An electromyographic analysis of the elbow in pitching. Am J Sports Med 15:260-263, 1987. 35. Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 18:402-408, 1993. 36. Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233-239, 1995. 37. Fleisig GS, Barrentine SW, Escamilla RF, Andrews JR: Biomechanics of overhand throwing with implications for injuries. Sports Med 21:421-437, 1996. 38. Yanagisawa O, Niitsu M, Takahashi H, Itai Y: Magnetic resonance imaging of the rotator cuff muscles after baseball pitching. J Sports Med Phys Fitness 43:493-499, 2003. 39. Jamurtas AZ, Theocharis V, Tofas T, et al: Comparison between leg and arm eccentric exercises of the same relative intensity on indices of muscle damage. Eur J Appl Physiol 95:179-185, 2005. 40. Prasartwuth O, Taylor JL, Gandevia SC: Maximal force, voluntary activation and muscle soreness after eccentric damage to human elbow flexor muscles. J Physiol 567 (Pt 1):337-348, 2005. 41. Reisman S, Walsh LD, Proske U: Warm-up stretches reduce sensations of stiffness and soreness after eccentric exercise. Med Sci Sports Exerc 37:929-936, 2005. 42. Rizio L, Garcia J, Renard R, Got C: Anterior instability increases superior labral strain in the late cocking phase of throwing. Orthopedics 30:544-550, 2007. 43. Meister K, Buckley B, Batts J: The posterior impingement sign: Diagnosis of rotator cuff and posterior labral tears secondary to internal impingement in overhand athletes. Am J Orthop 33:412-415, 2004. 44. Wilk KE, Reinold MM, Dugas JR, et al: Current concepts in the recognition and treatment of superior labral (SLAP) lesions. J Orthop Sports Phys Ther 35:273-291, 2005. 45. Myers TH, Zemanovic JR, Andrews JR: The resisted supination external rotation test: A new test for the diagnosis of
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46.
47.
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51.
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53.
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superior labral anterior posterior lesions. Am J Sports Med 33:1315-1320, 2005. Kim SH, Ha KI, Han KY: Biceps load test: A clinical test for superior labrum anterior and posterior lesions in shoulders with recurrent anterior dislocations. Am J Sports Med 27:300-303, 1999. Kim SH, Ha KI, Ahn JH, et al: Biceps load test II: A clinical test for SLAP lesions of the shoulder. Arthroscopy 17:160164, 2001. Wilk KE, Andrews JR, Arrigo CA, et al: The strength characteristics of internal and external rotator muscles in professional baseball pitchers. Am J Sports Med 21:61-66, 1993. Wilk KE, Andrews JR, Arrigo CA: The abductor and adductor strength characteristics of professional baseball pitchers. Am J Sports Med 23:778, 1995. Bastan M, Reinold MM, Wilk KE, Crenshaw K: Scapular position in professional baseball pitchers: A three-dimension clinical measure. J Orthop Sports Phys Ther 36:A67, 2006. Macrina LC, Wilk K, Geus J, Porterfield R: The effect of pitching on scapula position on professional baseball players. J Orthop Sports Phys Ther 37:A69, 2007. Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34:385-394, 2004. Reinold MM, Macrina LC, Wilk KE, et al: Electromyographic analysis of the supraspinatus and deltoid muscles during 3 common rehabilitation exercises. J Athl Train 42:464-469, 2007. Reinold MM, Wilk KE, Reed J, et al: Interval sport programs: Guidelines for baseball, tennis, and golf. J Orthop Sports Phys Ther 32:293-298, 2002. Wilk KE, Reinold MM, Dugas JR, Andrews JR: Rehabilitation following thermal-assisted capsular shrinkage of the glenohumeral joint: current concepts. J Orthop Sports Phys Ther 32:268-292, 2002.
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56. Reinold MM, Wilk KE, Hooks TR, et al: Thermal-assisted capsular shrinkage of the glenohumeral joint in overhead athletes: A 15- to 47-month follow-up. J Orthop Sports Phys Ther 33:455-467, 2003. 57. Hecht P, Hayashi K, Lu Y, et al: Monopolar radiofrequency energy effects on joint capsular tissue: potential treatment for joint instability. An in vivo mechanical, morphological, and biochemical study using an ovine model. Am J Sports Med 27:761-771, 1999. 58. Schaefer SL, Ciarelli MJ, Arnoczky SP, Ross HE: Tissue shrinkage with the holmium:yttrium aluminum garnet laser. A postoperative assessment of tissue length, stiffness, and structure. Am J Sports Med 25:841-848, 1997. 59. Hayashi K, Markel MD, Thabit G 3rd, et al: The effect of nonablative laser energy on joint capsular properties. An in vitro mechanical study using a rabbit model. Am J Sports Med 23:482-487, 1995. 60. Levitz CL, Dugas J, Andrews JR: The use of arthroscopic thermal capsulorrhaphy to treat internal impingement in baseball players. Arthroscopy 17:573-577, 2001. 61. Andrews JR, Carson WG, Jr., McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337-341, 1985. 62. Nam EK, Snyder SJ: The diagnosis and treatment of superior labrum, anterior and posterior (SLAP) lesions. Am J Sports Med 31:798-810, 2003. 63. Burkhart SS, Morgan CD: The peel-back mechanism: Its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair rehabilitation. Arthroscopy 14:637-640, 1998. 64. Morgan CD, Burkhart SS, Palmeri M, Gillespie M: Type II SLAP lesions: Three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14:553-565, 1998. 65. Burkhart SS, Morgan C: SLAP lesions in the overhead athlete. Orthop Clin North Am 32:431-441, 2001.
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CHAPTER 12 Partial Articular Supraspinatus Tendon
Avulsion (PASTA) Lesions of the Rotator Cuff Stephen J. Snyder and James L. Bond
not address significant bursal-sided fraying and fragmentation. It is paramount, then, for the surgeon to develop a thoughtful approach to PASTA lesions.
Partial-thickness rotator cuff tears (PTRCTs) are probably the most common form of rotator cuff disease. In cadaveric studies, the reported incidence of PTRCTs is between 17% and 37% of the population,1-4 with most occurring in the fifth and sixth decades of life. Before magnetic resonance imaging (MRI) and diagnostic shoulder arthroscopy, PTRCTs were difficult to recognize, much less diagnose and treat. Therefore, most scientific and clinical research has focused on full-thickness rotator cuff tears (FTRCTs). With an increase in the recognition of PTRCTs, however, there has been an increased emphasis on diagnosis, classification, and treatment.
PATHOGENESIS An understanding of the rotator cuff anatomy in normal and pathologic states is essential for the appropriate treatment of PASTA lesions. Although no study has fully elucidated one specific cause, most clinicians agree that intrinsic, extrinsic, and traumatic factors are all possible causes of PASTA tears.
PTRCTs are usually classified according to their location (articular, bursal, or complete) and arthroscopic appearance. The partial articular supraspinatus tendon avulsion (PASTA) variety of PTRCTs is significantly more common and typically more significant than its bursal-sided or intratendinous counterparts.5-11 Payne and colleagues12 have found that PASTA lesions comprise 91% of all partial-thickness tears. PASTA lesions are also more commonly associated with overhead athletes and younger patients.12-15
Intrinsic factors include changes in rotator cuff vascularity, metabolic changes associated with aging, or both. The primary vascular supply of the supraspinatus tendon is the suprascapular artery. There are lesser contributions from the subscapular artery and some osseous contributions from the circumflex arteries. The size of the vessels decreases from medial to lateral as they travel along their musculotendinous units. Interestingly, several studies have elegantly revealed that the vessels are larger and more prevalent on the bursal side of the cuff. The articular surface of the cuff is relatively hypovascular, leading many clinicians to believe that the pathology behind PASTA lesions may be associated more with a lack of vascularity rather than impingement syndrome.17,18 In support of this concept, histologic changes on the acromial undersurface of cadaveric acromions are common with bursal surface tears but not with articular surface tears.19
The natural history of PASTA lesions is not completely understood. There is little doubt, though, that this type of tendon disruption is often associated with unacceptable pain and disability and that to return the patient back to the best possible function, surgical treatment is often necessary. In a study of 40 shoulders, 28% progressed to FTRCTs in 1 year when treated nonoperatively, whereas 10% healed spontaneously.16 In another study, Fukuda and associates3 examined histologic sections of PASTA lesions and found no evidence of tissue repair. This seems to suggest that although some PASTA lesions have the potential for healing, most continue to enlarge with time.
Histologic studies have also noted that collagen is thinner and not as well organized on the articular cuff surface when compared with the corresponding layers on the bursal side of the rotator cuff.17 This lack of organization appears to correlate with a lack of strength. In a biomechanical study, Nakajima and coworkers20 have argued that the articular cuff is only one half as strong as the bursal cuff tissue. All these factors seem to contribute to and perhaps explain the clinical observation that PASTA lesions occur more often than their bursal-sided counterparts.
Operative treatment of PASTA lesions, on the other hand, presents a conundrum. There is no firm evidence that arthroscopic débridement stimulates tendon healing and patients seldom have associated impingement signs. Therefore, subacromial decompression may be of limited value. Additionally, there is usually a significant portion of healthy tendon on the bursal side that remains anatomically attached. If the surgeon chooses to incise this normal-appearing bursal cuff, she or he destroys the natural footprint. Use of the in situ transtendon technique, however, allows the bursal portion of the tendon to remain intact, but this technique is more difficult and may
In contrast to the intrinsic theories, there are some clinicians who argue for extrinsic and traumatic explanations as the primary factor in the pathogenesis of PASTA lesions. Gartsman and Milne15 have argued that coracoacromial arch narrowing can cause extrinsic impingement 143
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and differential shear stresses that affect the articular and bursal surfaces of the cuff. They noted that these shear stresses can cause a laminated disrepair on articular, bursal, and intratendinous aspects of the cuff. Trauma, on the other hand, is commonly associated with PASTA lesions. As mentioned, the repetitive microtrauma associated with the overhead athlete preferentially causes an articular surface tear.6 Several clinicians have demonstrated what has been termed by Walch and colleagues21 as internal impingement, which is slight anterior glenohumeral instability associated with articular-sided rotator cuff lesions in the overhead athlete. During the throwing motion, the anterior instability leads to articular surface tears in the absence of extrinsic impingement.22 Overhead athletes may experience posterior shoulder pain secondary to repetitive contact between the undersurface of the supraspinatus and posterosuperior glenoid during the late cocking phase of the throwing motion. Many clinicians have stated that internal impingement is exacerbated by fatigue of the dynamic stabilizers within the shoulder, coupled with excessive external rotation secondary to an overstretched anterior capsule and the repetitive pathologic microtrauma that results. There is no complete consensus about the internal impingement theory, however, some clinicians have observed PASTA lesions in an otherwise stable shoulder with no pathologic laxity. The anatomy of the rotator cuff insertion or anatomic footprint has become a widely debated topic in the recent literature; this is obviously relevant for PASTA repairs. In a study of 17 cadaveric rotator cuff footprints, Ruotolo and associates23 have noted that the supraspinatus tendon insertion is, on average, 1.7 mm from the articular margin. Additionally, studies have shown that if the cuff insertion is more than 7 mm from its articular margin insertion, the corresponding tear in the rotator cuff is greater than 50% of the supraspinatus tendon thickness.24 Knowledge of these measurements is crucial when assessing and treating PASTA lesions.
CLINICAL DIAGNOSIS Diagnosis of PASTA lesions can be difficult. Physical examination findings can be nonspecific and therefore must be correlated with imaging modalities. Lesions found on imaging studies that do not correlate with clinical findings may be insignificant. Sher and coworkers,25 in their MRI evaluation of asymptomatic individuals, have shown that not all PASTA tears are symptomatic; this further reveals our minimal understanding of the natural history of PASTA lesions. There is no doubt, however, that PASTA lesions can be a significant source of pain, particularly in the arc of motion between 60 and 120 degrees.6 Resistance to abduction
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with the shoulder positioned in 90 degrees of abduction (Jobe’s test) generally provokes pain. External rotation and abduction lag signs are uniformly negative. Weakness and positive lag tests should alert the examiner away from a PASTA lesion toward a more probable FTRCT.26 Despite the argument against external impingement as the pathologic factor behind PASTA lesions, impingement signs as described by Neer (pain with passive forward flexion) and Hawkins (pain with internal rotation of the humerus, with the arm in 90 degrees of forward flexion) are typically positive.15 Strength is commonly preserved, but pain may limit the amount of resistance that the patient can generate. Maintenance of strength in the absence of pain after subacromial injection suggests cuff inflammation, bursitis, or some type of PTRCT. In the overhead athlete, the clinician should always evaluate for subtle signs of shoulder instability, because internal impingement may be evident. There may be varying degrees of glenohumeral joint contracture with loss of internal rotation and an increase in external rotation in the dominant shoulder. Apprehension testing—external rotation force applied to the shoulder in 90 degrees of abduction and external rotation while the patient is lying in the supine position—may be positive. The relocation test, applying a posterior force to the anterior humeral head while performing the apprehension test, is a good method for eliciting subtle amounts of anterior translation of the humeral head.21 It should be noted, however, that the presence of pain without apprehension is an unreliable indicator of anterior instability and is associated with many other pathologic conditions within the shoulder. Internal impingement is commonly associated with pain at the posterior joint line, particularly with apprehension testing. Similar to the physical examination, the clinical course of patients with PASTA lesions is difficult to distinguish from that of patients with other shoulder conditions, such as impingement, biceps tendinopathy, and labral pathology. In fact, biceps tendinopathy, posterosuperior labral degeneration, or both can occur concomitantly in as many as 30% of PASTA lesions.5,21,27 Despite the difficulty in diagnosis, many patients improve with 6 months of conservative treatment
IMAGING STUDIES Because no single study is particularly accurate for the assessment of PASTA lesions, the clinician should use a wide variety of imaging modalities, such as radiography, ultrasound, arthrography, and MRI. Although radiographs are rarely helpful for the diagnosis of a PASTA lesion, they are important for evaluating any patient with shoulder pain and helpful for diagnosing acromioclavicular lesions or glenohumeral arthritis.4 The presence of changes in the
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greater tuberosity, such as notching, sclerosis, and subchondral cystic formations, may be seen in conjunction with generalized rotator cuff pathology.28 Standard x-ray views include an anteroposterior view of the shoulder, an axillary lateral view, and a supraspinatus outlet view. The supraspinatus outlet view best demonstrates a curved or hooked acromial morphology, which is seen in some individuals with PTRCTs resulting from supraspinatus outlet narrowing. An os acromiale, which can cause impingement symptoms, can be seen on an axillary lateral film. Degenerative changes of the acromioclavicular joint are seen with a 15-degree cephalic tilt anteroposterior (Zanca) view. An apical oblique (Garth) or West Point axillary view may be added if glenohumeral instability is suspected. Conventional arthrography has historically been used for the evaluation of the rotator cuff. The initial proponents touted sensitivity as high as 83% but other studies have reported arthrography to be much less valuable.6 Gartsman and Milne15 have reported that arthrography detected only 7 of 46 arthroscopically proved PASTA lesions. Walch and colleagues21 have reported positive arthrograms in only 8 of 17 surgically proved articular surface tears. As a result of these findings, other modalities have largely replaced arthrography in the detection of PASTA lesions. Ultrasound evaluation of rotator cuff integrity has proved to be a valuable tool for FTRCTs. Wiener and Seitz29 have reported a sensitivity of 94% and specificity of 93% for the diagnosis of PTRCTs, especially in patients with pacemakers. Sonography is well tolerated by the patient and is cost effective. The limitation of ultrasound, however, continues to be its reliance on experienced personnel for accurate interpretation. This operator dependence was shown by the somewhat low 41% detection rate in the study by Brenneke and Morgan.30 These limitations are particularly relevant for subtle PASTA lesions. With the development of various techniques, such as contrast arthrography, and differential arm position, such as abduction–external rotation (ABER) views, MRI improved the ability to characterize subtle cuff abnormalities. The typical pathology of a PASTA lesion on MRI is an increased signal on the articular side of the rotator cuff on T1- and T2-weighted images, consistent with a focal defect. The defect does not extend across the entirety of the tendon (Fig. 12-1). This may seem straightforward, but previous MRI reports have been disappointing in their predictive value. Gartsman and Milne15 have reported a false-negative rate of 83% in a study of arthroscopically visualized PASTA lesions. The clinical relevance is further limited by the fact that many asymptomatic individuals have abnormal rotator cuffs on MRI, especially in patients older than 40 years.25
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PASTA lesion
Figure 12-1. T2-weighted magnetic resonance imaging scan with gadolinium enhancement of a partial articular supraspinatus tendon avulsion (PASTA) tear (arrows). The lattermost aspect of the footprint of the supraspinatus is still attached.
As a result of these issues, fat suppression, positional variation, and contrast arthrography have all been used to increase diagnostic accuracy. Unfortunately, any one of these techniques used in isolation has not seemed to increase the accuracy for detecting a PASTA detection.31-33 A recent study, however, has reported accuracy as high as 91% if all these MRI methods are used.34 The ABER view is also a useful adjunct for labral lesions, which are commonly associated with PASTA lesions, especially in throwers. Regardless of recent findings, MRI findings suggestive of a PASTA lesion should be interpreted cautiously. They should be used only as an adjunct to the clinical evaluation when determining treatment options.
CLASSIFICATION A classification system of PASTA lesions as a distinct entity does not exist. Any classification system of rotator cuff pathology, however, should begin with Neer.35 This system categorized cuff abnormalities as a continuum ranging from stage I (inflammation, hemorrhage, edema) through stage II (tendon fibrosis), into stage III (tendon tearing). PTRCTs of any variety were not addressed by this classification. Therefore, Ellman36 has proposed a more detailed classification scheme that includes partial cuff tears. In this system, lesions are classified according to location (articular surface, bursal surface, or intratendinous) and depth of the tear. Grade I tears are smaller than 3 mm, grade II tears are between 3 and 6 mm, and grade III tears involve more than one half the cuff thickness (average cuff thickness, 9 to 12 mm).
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Snyder and colleagues4,27 have classified PTRCTs according to their location (articular, bursal, or complete) and arthroscopic appearance (grades 0 to 4). Grade 0 represents a normal cuff with smooth covering. Grade 1 signifies minimal superficial fraying in an area smaller than 1 cm. Grade 2 represents fraying and failure of rotator cuff fibers smaller than 2 cm. Grade 3 includes fraying and fragmentation of the whole surface of a tendon (usually the supraspinatus) smaller than 3 cm. Grade 4 lesions contain a sizable flap tear that often encompasses more than a single tendon and is larger than 3 cm. Conway37 has extended the classification of PTRCTs to include an intratendinous extension, or partial articular tears with intratendinous extension (PAINT) lesion. Extrapolating from the literature on PTRCTs, many surgeons treat PASTA lesions according to the 50% rule, because tears involving more than one half of the tendon thickness are a significant threat to cuff integrity. Thus, the presence of an Ellman or Snyder grade III PTRCT is considered an indication for surgical repair in a symptomatic patient. Clinical data, although limited, appear to support this protocol.10,13,38 It is important to note, however, that determining the cause behind the pathology of a PASTA lesion will ensure the most appropriate treatment plan.15
TREATMENT No algorithm for treatment of PASTA lesions exists. As noted, the PASTA tear may be one of several different lesions in the same shoulder. The lesion may be a red herring, especially in an active patient older than 40 years, or it may be the primary pain generator. Therefore, the treatment algorithm demands a thoughtful approach from the surgeon.
Nonoperative Treatment For most patients with a PASTA lesion, activity modification with avoidance of overhead and other activity that provokes pain should be the initial recommendation. Nonsteroidal anti-inflammatory drugs (NSAIDs) may also help in reduction of the pain and inflammation. A physical therapy program directed toward regaining the complete shoulder range of motion should be initiated.39 Most stretches can be performed at the patient’s side to avoid the zone of impingement (60 to 120 degrees of abduction). Subacromial and/or intra-articular corticosteroid injections can also be helpful if used with great caution. No more than two injections should be given because of the potential deleterious effects on the tendons, particularly in the throwing athlete. Overhead athletes should pay particular attention on stretching out the contracted posterior capsule. Eccentric and plyometric strengthening should be included in the rehabilitation program to mimic the deceleration and
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follow-through phase of the throwing motion. Attention to a core-strengthening program is beneficial because it reduces the degree of effort that the shoulder and arm must exert during the throwing motion. Throwing mechanics must be studied and a throwing program should be instigated in regard to the new throwing motion. Finally, rehabilitation of the parascapular musculature may serve to restore normal scapulothoracic mechanics and minimize dynamic impingement secondary to scapulothoracic dyskinesis.37,40,41 Like the natural history of PASTA lesions, the success of nonoperative treatment is unknown, because there are currently no randomized prospective studies that have assessed the results of treatment with respect to patient age, tear size, location, and cause. The literature does suggest, however, that PASTA lesions frequently progress to FTRCTs. Yamanaka and Matsumoto16 have followed 40 PASTA lesions nonoperatively for 2 years and found a progression of the tear in 80% of patients. A decrease in size of the tear occurred in 10% and a disappearance of the tear occurred in the other 10%. This seems to suggest that conservative management may not be the best option.
Operative Treatment Although the effectiveness of nonoperative treatment has yet to be reported in the literature, it is generally accepted that clinical symptoms after 6 months of conservative measures is an indication to move ahead with operative intervention. Other factors, however, such as high-level athletic participation, might require earlier intervention. Various surgical techniques such as arthroscopic débridement, arthroscopic débridement with acromioplasty, rotator cuff repair with and without acromioplasty, and transtendon intra-articular rotator cuff repair with and without acromioplasty are options for the treating physician. Some surgeons may even prefer open versus mini–open repair of the PASTA lesion. Regardless of preferred technique, it is important to discuss all these options with the patient preoperatively. In our experience, arthroscopic repair provides a distinct advantage over open procedures because it allows a unique examination of the pathologic lesion and its repair while introducing minimal trauma to healthy tissues. Results of the arthroscopic débridement–only technique have been reported.42-50 Andrews, Budoff, and coworkers42,43 have reported 85% to 89% good to excellent results on overhead athletes, with follow-up of 13 to 93 months; 77% to 100% of patients had associated labral lesions and 25% had abnormalities in the long head of the biceps tendon. Whether the surgeon should combine débridement of the PASTA lesion with concomitant subacromial decompression is controversial. Few studies have examined a uniform population with similar pathologic changes. Snyder and colleagues,27 however, have retrospectively reviewed 31 patients and reported 84% good to excellent results; in this study, 13 patients did not undergo subacromial decompression
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and there was no significant difference in the outcome of this cohort of patients. Although these studies have reported good results, there is some question as to whether arthroscopic débridement alone is enough treatment for a PASTA tear. Ryu5 has reported 86% satisfactory results in the treatment of 35 PTRCTs by arthroscopic subacromial decompression but was disappointed that only 1 of the 4 patients with PASTA tears achieved a satisfactory result. These results were contrasted with those of patients who had bursal surface–only lesions. In this cohort, 94% reported a satisfactory result. In view of these results, it was suggested that articular-sided PTRCTs might achieve better results with repair rather than with débridement alone. In an effort to answer the débridement versus repair question scientifically, Weber10 has compared arthroscopic débridement and acromioplasty with arthroscopic acromioplasty and mini–open repair. The arthroscopic débridement group had 14 good and no excellent results, whereas the mini–open repair achieved 28 good and 3 excellent results. These findings seem to confirm that lesions of more than 50% of the tendon thickness in symptomatic individuals should be repaired, An accurate measurement of cuff thickness, however, has yet to be determined. Miller and Lewis13 have further studied the results of open repair; they used the thickness of the cuff tear as their primary criterion for open repair in 55 patients. In the patients with less than 50% of tendon involvement, arthroscopic subacromial decompression and cuff débridement alone was performed. In the 24 patients with more extensive tears and more than 50% involvement, the cuff was repaired by a mini–open repair or arthroscopic technique, in 20 and 4 patients, respectively. With this protocol, 95% had satisfactory results at 1-year follow-up. It was concluded that cuff repair should be carefully considered for active patients with involvement of the dominant arm and for tears extending through more than 50% of the cuff thickness. Fukuda41 has also reported on open anterior acromioplasty with repair and reported 92% satisfactory results at a longer follow-up of 34 months. Although open repair of PASTA tears has achieved good results in the literature, this technique is severely compromised by the inability to visualize the articular surface of the cuff directly. Our preferred treatment algorithm is as follows. The initial step in the treatment of a PASTA lesion is a thorough examination of the glenohumeral joint. We prefer to use the lateral decubitus position, but the beach chair modification has been used with equal success. With the arm in 15 pounds of traction and approximately 60 degrees of abduction, an excellent view of the articular cuff using a standard 30-degree arthroscope can be obtained. Hill-Sachs, labral, and other lesions that are commonly associated with PASTA tears should be carefully considered during glenohumeral arthroscopy. Matava and associates51 have reported good success with a
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dynamic assessment of a PASTA lesion, in which the arm is placed in 90 degrees of external rotation and abduction to assess the presence of impingement of the undersurface of the supraspinatus and infraspinatus against the posterosuperior cuff and labrum. Once the diagnosis of a PASTA tear is made arthroscopically, there is no reliable method to measure the thickness of the remaining bursal cuff (Fig. 12-2). Thus, the surgeon must use all the clinical information gathered in the preoperative assessment to determine the most appropriate treatment for each case. The supraspinatus outlet radiograph is important for predicting the likelihood of an impingement lesion and subsequent need for decompression surgery. MRI, especially if enhanced by gadolinium, is the best method to estimate the thickness of the tendon defect. Based on the MRI measurements, the surgeon can assess the probability of needing a complete resection versus a transtendon repair. In our practice, if 30% to 40% of the cuff tendon remains intact on the bursal side, we perform a PASTA transtendon repair. If less than 25% to 30% of good-quality bursal tendon remains, we complete the tear and repair the entire tendon as if it were a FTRCT. When we encounter a PASTA lesion, we place a marking suture on the articular surface (0 polydioxanone suture) and cover the marking suture with a Suture Saver (Linvatec, Largo, Fla) on the bursal surface (Fig. 12-3). This technique protects the marking suture during the bursectomy and allows the corresponding bursal surface to be observed easily (Fig. 12-4). When the top of the tendon is damaged in the same location on both the articular and bursal sides, it is likely that the vitality of the remaining tendon is compromised; therefore, the takedown method of cuff repair coupled with a subacromial smoothing is necessary. A blunt obturator can be inserted into the bursa in the same direction as the spinal needle to palpate
A4 RCT tear
Figure 12-2. Type A4 or partial articular supraspinatus tendon avulsion (PASTA) cuff tear. This is characterized by having a significant articular-sided flap of torn tendon. RCT, rotator cuff tear.
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Figure 12-3. Marking suture placed through the articular side of the partial articular supraspinatus tendon avulsion (PASTA) lesion.
the area of injury and evaluate the amount of viable bursal tendon. If the bursal remnant is felt to be less than 30%, the thinned area of cuff tendon is opened, using electrocautery to peel the thin leaf of tendon off the bone. A shaver and square-tipped basket punch can then trim the feathered edge (Fig. 12-5). It is important to resect enough tissue to provide a robust edge, but never remove so much that the
Figure 12-4. Illustration of how the marking suture correlates the articular-side lesion with its bursal counterpart. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
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Figure 12-5. Preparation for a full-thickness cuff repair. The thin remnant of the bursal-sided cuff is peeled off the tuberosity and the feathered edge is removed.
free edge of the tendon rests medial to the articular cartilage of the humeral head. The remainder of the procedure is similar to the standard suture anchor repair of FTRCTs. We view the lesion from the lateral acromial portal (LAP) while inserting a spinal needle percutaneously next to the acromion to determine the proper position and angle for placement of a Revo anchor (Linvatec, Largo, Fla). The anchor is loaded with two strands of no. 2 Ethibond (Ethicon, Johnson & Johnson, Piscataway, NJ) suture and one strand of Herculine suture (Linvatec, Largo, Fla), with the Herculine suture between the two strands of Ethibond. The angle of insertion is approximately 45 degrees below the subchondral bone, which is critical to the success of the repair. If the angle is too vertical, the anchor will enter the softer bone of the greater tuberosity rather than the dense subchondral bone of the humeral head, risking anchor failure. Once the proper anchor placement and insertion angle are determined, a small punch is used to create a pilot hole. The anchor is then placed into the subchondral bone, ensuring that the horizontal depth guideline is seated completely below the bone and the dashed vertical guide mark is directed toward the cuff. We choose to begin passing sutures through the tendon by retrieving the posterior suture out from the anterior cannula with a crochet hook. The appropriate suture hook is then passed through the cuff from the posterior portal. The hook is passed through the cuff from top to bottom, 6 mm posterior to the anchor and 1 to 1.5 cm medial to the free edge of the tendon. A shuttle is then fed through the tendon and grasped with a clamp from the anterior canula. Once secured, the shuttle is carried out the anterior cannula and loaded with
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the posterior Ethibond suture, which is carried back through the tendon. The partner of the posterior Ethibond suture is then retrieved with the crochet hook and stored in a Suture Saver outside the posterior cannula. These steps are repeated with the middle Herculine suture. After a Suture Saver is placed around the Herculine suture pair and placed outside the posterior cannula, the anterior suture is carried out the posterior portal with the crochet hook. The proper suture hook is again introduced, but this time through the anterior cannula. The hook is passed through the cuff from top to bottom, 6 mm anterior to the anchor and approximately 1 cm medial to the cuff edge. A shuttle is pulled out the posterior cannula, loaded with the anterior Ethibond suture, and pulled back through the anterior aspect of the cuff lesion. The partner of the anterior suture is retrieved with the crochet hook and tied down to the anchor with a sliding knot and three alternating half-hitches. The scope is then transferred to the anterior portal and the Herculine sutures are pulled out through the lateral portal and tied down to the anchor. Finally, the posterior sutures are retrieved out the lateral portal and tied down to the anchor. The cuff is visualized and palpated to ensure stability and the portals are closed with a single, absorbable, subcutaneous suture. When a significant articular-sided cuff tear is present and a healthy portion of bursal tendon is intact, we prefer to repair the torn portion while leaving the bursal attachment in place. This technique is known as the PASTA repair, or transtendon technique. There are many ostensible benefits to performing this method of repair but the most significant is that the bursal portion of the tendon is left attached, thereby lessening the stress on the sutures after surgery. To qualify for a PASTA repair, there should be at least 30% of normal tendon remaining, with little or no bursal-sided cuff damage. The PASTA repair is carried out as follows. The glenohumeral diagnostic arthroscopy is performed and all frayed fragments of the torn cuff are removed. The footprint is débrided to provide a clean bony interface for tendon healing. The marking suture is passed through the center of the tear, and the scope is moved to the subacromial space. With PASTA tears, there are usually no signs of impingement and so decompression is unnecessary. If this is confirmed on bursoscopy, the scope is placed back into the glenohumeral joint and a spinal needle introduced into the joint to establish the ideal position and angle of the first Revo anchor. We begin the repair at the anterior edge of the tear. The needle is used to penetrate the cuff as close to the remaining attachment as possible. It is usually helpful to move the arm into slightly less abduction for insertion of the anchor. A smooth 5/64-cm K wire is introduced following the path chosen by the spinal needle (Fig. 12-6). The Super-Revo anchor is then placed through the bursal cuff as close to the bone attachment as possible (Fig. 12-7). The anchor is then advanced down until the horizontal
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Figure 12-6. Illustration of how the spinal needle and K wire can be used to gauge the best position for the Super-Revo anchors to enter the prepared bone. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
guideline is below the surface of the bone. The vertical hash marks are oriented so that they face the torn tendon edge if simple sutures are desired (Fig. 12-8). They are oriented perpendicularly to the edge of the tear if horizontal mattress stitches are planned. In other words, if the eyelet of the anchor is aligned parallel to the torn cuff edge
Figure 12-7. Super-Revo anchor inserted through the bursal cuff remnant and placed down to horizontal seating line. The Super-Revo anchor separates the fibers of the bursal cuff remnant but does not seem to damage it.
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edge of the flap tear (Fig. 12-9). A Shuttle Relay Suture Passer (Linvatec, Largo, Fla) is passed through the spinal needle, pulled out through the anterior cannula (Fig. 12-10), loaded with the anterior suture, carried out the lateral puncture, and clamped to its opposite tail (Fig. 12-11). This process is repeated as needed to close the tear completely.
Figure 12-8. Use of two sutures. When two sutures are used, it is helpful to color one half of each suture with a purple marker to avoid confusion.
and each limb of the suture is passed through the flap tear 8 mm apart on each side of the anchor, a mattress stitch pattern results that provides excellent juxtaposition of the torn tendon down to bone. If the simple suture technique is used, the suture that exits nearest to the torn tendon edge is retrieved out through the anterior cannula and a spinal needle is inserted 5 mm anterior to the anchor insertion and 5 mm medial to the
A
B
Figure 12-9. First green suture is retrieved out through the anterior cannula with a crochet hook.
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Figure 12-10. Simple suture technique. A, Insertion of the spinal needle through the torn portion of the cuff. A Shuttle Relay Suture Passer (Linvatec, Largo, Fla) is pushed through the spinal needle, and grasped with a clamp from the anterior portal. B, Suture passer grasped from the anterior portal. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
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The arthroscope is then reintroduced into the subacromial space from the posterior portal. The sutures are located and retrieved through a crystal cannula in the lateral portal (Fig. 12-12). If the sutures slide easily, they are tied with a Samsung Medical Center (SMC) sliding-locking knot and three half-hitches. Often, however, the sutures do not slide easily and a Revo knot must be used (Fig. 12-13). After a PASTA repair, we place patients in an UltraSling (DonJoy, Vista, Calif) for 4 weeks. Because the cuff is never detached from the bone, we have not found it necessary to protect the shoulder as long as is needed for the takedown method and FTRCT repairs. The transtendon repair technique is an excellent example of the modern advantages afforded by the arthroscope. It restores the normal footprint of the rotator cuff and provides secure fixation down to bone, with minimal invasion of normal tissues (Fig. 12-14). In a study by Lo and Burkhart,52 good to excellent results were reported at minimum 1-year follow-up on all 25 patients who underwent transtendon fixation for PASTA lesions. Further studies have confirmed good results in longer follow-up (25 to 57 months); Ide and coworkers53 have reported 16 good and excellent results, with no poor results, in a cohort of 17 patients after transtendon PASTA repair.
Figure 12-12. Sutures being pulled out the lateral portal through a crystal cannula to allow knot tying. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. (In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
It appears that arthroscopic transtendon repair is a safe and effective means of PASTA repair. However, future studies still need to address the lack of randomized prospective studies with regard to PASTA lesions. Similarly, clinical outcome studies need to focus on a mechanismbased tear classification and on obtaining a more detailed
Figure 12-11. Shuttle Relay Suture Passer (Linvatec, Largo, Fla) with green suture. This is carried through the cuff to the bursal side.
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Figure 12-13. Completed repair may use various stitches. These include mattress, double-simple, and simple sutures, depending on the configuration of suture passage through the partial articular supraspinatus tendon avulsion (PASTA) tear. (From Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ [ed]: Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229.)
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11.
12.
Super-Revo anchors
13.
Healed cuff 6 mo. after PASTA repair
14.
15. 16. Figure 12-14. Transtendon repair technique using Super-Revo anchors (arrows). This magnetic resonance imaging scan with gadolinium enhancement documents the excellent healing in this partial articular supraspinatus tendon avulsion (PASTA) lesion at 6 months postoperatively.
17.
18. 19.
natural history for PASTA tears. Perhaps the indications of operative intervention may then be more precise, providing a better evidence-based algorithm to help the surgeon know exactly when to use these exciting surgical techniques.
20.
21. References 1. Fukuda H, Craig EV, Yamanaka K, Hamada K: Partialthickness cuff tears. In Burkhead WZ Jr (ed): Rotator Cuff Disorders. Baltimore, Williams & Wilkins, 1996, pp 174-181. 2. Fukuda H, Mikasa M, Yamanaka K: Incomplete thickness rotator cuff tears diagnosed by subacromial bursography. Clin Orthop 223:51-58, 1987. 3. Fukuda H, Mikasa M, Ogawa K, et al: The color test: An intraoperative staining test for joint-side rotator cuff tearing and its extension. J Shoulder Elbow Surg 1:86-90, 1992. 4. Snyder SJ: Arthroscopic repair of partial articular supraspinatus tendon avulsions: PASTA lesions of the rotator cuff tendon. In Snyder SJ (ed): Shoulder Arthroscopy. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 219-229. 5. Ryu RKN: Arthroscopic subacromial decompression: A clinical review. Arthroscopy 8:141-147, 1992. 6. Itoi E, Tabata S: Incomplete rotator cuff tears: Results of operative treatment. Clin Orthop 284:128-135, 1992. 7. Gartsman GM: Arthroscopic acromioplasty for lesions of the rotator cuff. J Bone Joint Surg Am 72:169-180, 1990. 8. Gartsman GM: Arthroscopic treatment of rotator cuff disease. J Shoulder Elbow Surg 4:228-241, 1995. 9. Ellman H: Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop 254:64-74, 1990. 10. Weber SC: Arthroscopic debridement and acromioplasty versus mini-open repair in the management of significant
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22. 23.
24.
25.
26.
27.
28.
29.
partial-thickness tears of the rotator cuff. Orthop Clin North Am 28:79-82, 1997. Olsewski JM, Depew AD: Arthroscopic subacromial decompression and rotator cuff debridement for stage II and stage III impingement. Arthroscopy 10:61-68, 1994. Payne LZ, Altchek DW, Craig EV, Warren RF: Arthroscopic treatment of partial rotator cuff tears in young athletes: A preliminary report. Am J Sports Med 25:299-305, 1997. Miller DV, Lewis JM: Surgical management of partial rotator cuff tears. Presented at the Second Annual Meeting of the American Orthopaedic Society for Sports Medicine, Lake Buena Vista, Fla, June 1996. Andrews JR, Broussard TS, CarsonWG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117-122, 1985. Gartsman GM, Milne JC: Articular surface partial-thickness rotator cuff tears. J Shoulder Elbow Surg 4:409-415, 1995. Yamanaka K, Matsumoto T: The joint side tear of the rotator cuff: A follow-up study by arthrography. Clin Orthop 304:68-73, 1994. Clark JM, Harryman DT II: Tendons, ligaments, and capsule of the rotator cuff: Gross and microscopic anatomy. J Bone Joint Surg Am 74:713-725, 1992. Lohr JF, Uhthoff HK: The microvascular pattern of the supraspinatus tendon. Clin Orthop 254:35-38, 1990. Ozaki J, Fujimoto S, Nakagawa Y, et al: Tears of the rotator cuff of the shoulder associated with pathological changes in the acromion: A study in cadavera. J Bone Joint Surg Am 70:1224-1230, 1988. Nakajima T, Rokuuma N, Hamada K, et al: Histologic and biomechanical characteristics of the supraspinatus tendon: Reference to rotator cuff tearing. J Shoulder Elbow Surg 3:79-87, 1994. Walch G, Boileau P, Noel E, Donell ST: Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: An arthroscopic study. J Shoulder Elbow Surg 1:238-245, 1992. Jobe CM: Superior glenoid impingement. Orthop Clin North Am 28:137-143, 1997. Ruotolo C, Fow JE, Nottage WM : The supraspinatus footprint: An anatomic study of the supraspinatus insertion. Arthroscopy 20:246-249, 2004. Sakurai G, Ozaki j, Tomita Y, et al: Incomplete tears of the subscapularis tendon associated with tears of the supraspinatus tendon: Cadaveric and clinical studies. J Shoulder Elbow Surg 7:510-515, 1998. Sher JS, Uribe JW, Posada A, et al: Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg Am 77:10-15, 1995. Hertel R, Ballmer FT, Lambert SM, Gerber C: Lag signs in the diagnosis of rotator cuff rupture. J Shoulder Elbow Surg 5:307-313, 1996. Snyder SJ, Pachelli AF, Del Pizzo W, et al: Partial-thickness rotator cuff tears: Results of arthroscopic treatment. Arthroscopy 7:1-7, 1991. Nakagawa S, Yoneda M, Hayashida K, et al: Greater tuberosity notch: An important indicator of articular-sided partial rotator cuff tears in the shoulders of throwing athletes. Am J Sports Med 29:762-770, 2001. Wiener SN, Seitz WH Jr: Sonography of the shoulder in patients with tears of the rotator cuff: Accuracy and value
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30.
31.
32.
33.
34.
35. 36. 37.
38.
39.
40.
41.
for selecting surgical options. AJR Am J Roentgenol 160:103-107, 1993. Brenneke SL, Morgan CJ: Evaluation of ultrasonogrophy as a diagnostic technique in the assessment of rotator cuff tendon tears. Am J Sports Med 20:287-289, 1992. Quinn SF, Sheley RC, Demlow TA, Szumowski J: Rotator cuff tendon tears: Evaluation with fat-suppressed MR imaging with arthroscopic correlation in 100 patients. Radiology 195:497-500, 1995. Reinus WR, Shady KL, Mirowitz SA, Totty WG: MR diagnosis of rotator cuff tears of the shoulder: Value of using T2-weighted fat-saturated images. AJR Am J Roentgenol 164:1451-1455, 1995. Hodler J, Kursunoglu-Brahme S, Snyder SJ: Rotator cuff disease: Assessment with MR arthrography versus standard MR imaging in 36 patients with arthroscopic confirmation. Radiology 182:431-436, 1992. Meister K, Thesing J, Montgomery WJ, et al: MR arthrography of partial-thickness tears of the undersurface of the rotator cuff: An arthroscopic correlation. Skeletal Radiol 33:136-141, 2004. Neer CS II: Impingement lesions. Clin Orthop 173:70-77, 1983. Ellman H: Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop Relat Res 254:64-74, 1990. Conway JE: Arthroscopic repair of partial-thickness rotator cuff tears and SLAP lesions in professional baseball players. Orthop Clin North Am 32:443-456, 2001. Williams GR Jr, Iannotti JP, Rosenthal A, et al: Anatomic, histologic, and magnetic resonance imaging abnormalities of the shoulder. Clin Orthop 330:66-74, 1996. Gotoh M, Hamada K, Yamakawa H, et al: Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases. J Orthop Res 16:618-621, 1998. Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233-239, 1995. Fukuda H: The management of partial-thickness tears of the rotator cuff. J Bone Joint Surg Br 85:3-11, 2003.
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42. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: A preliminary report. Arthroscopy 1:117-122, 1985. 43. Budoff JE, Nirschl RP, Guidi EJ: Debridement of partialthickness tears of the rotator cuff without acromioplasty: Long-term follow-up and review of the literature. J Bone Joint Surg Am 80:733-748, 1998. 44. Paulos LE, Franklin JL: Arthroscopic shoulder decompression development and application: A five-year experience. Am J Sports Med 18:180-189, 1990. 45. Wright SA, Cofield RH: Management of partial-thickness rotator cuff tears. J Shoulder Elbow Surg 5:458-466, 1996. 46. Traughber PD, Goodwin TE: Shoulder MRI: Arthroscopic correlation with emphasis on partial tears. J Comput Assist Tomogr 16:129-133, 1992. 47. Morrison DS: Conservative management of partial-thickness rotator cuff lesions. In Burkhead WZ Jr (ed): Rotator Cuff Disorders. Baltimore, Williams & Wilkins, 1996, pp 249-257. 48. Ogilvie-Harris DJ, Wiley AM: Arthroscopic surgery of the shoulder: A general appraisal. J Bone Joint Surg Br 68: 201-207, 1986. 49. Esch JC, Ozerkis LR, Helgager JA, et al: Arthroscopic subacromial decompression: Results according to the degree of rotator cuff tear. Arthroscopy 4:241-249, 1988. 50. Altchek DW, Warren RF, Wickiewicz TL, et al: Arthroscopic acromioplasty: Technique and results. J Bone Joint Surg Am 72:1198-1207, 1990. 51. Matava MJ, Purcell DB, Rudski JR: Partial-thickness rotator cuff tears. Am J Sports Med 33:1405-1417, 2005. 52. Lo IK, Burkhart SS: Transtendon arthroscopic repair of partial-thickness, articular surface tears of the rotator cuff. Arthroscopy 20:214-20, 2004. 53. Ide J, Maeda S, Takagi K: Arthroscopic transtendon repair of partial-thickness articular-side tears of the rotator cuff: Anatomical and clinical study. Am J Sports Med 33: 1672-1679, 2005. 54. McConville OR, Ianotti JP: Partial-thickness tears of the rotator cuff: Evaluation and management. J Am Acad Orthop Surg 7:32-43, 1999.
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CHAPTER 13 Calcific Tendinitis David G. Lemak and Lawrence J. Lemak
Calcific tendinitis is the diagnosis given to shoulder pain often associated with tenderness to palpation at the greater tuberosity of the humerus, subacromial impingement, or radiographic evidence of calcific deposits in the rotator cuff tendon (Fig. 13-1). It has been attributed to cell-mediated calcification and subsequent spontaneous phagocytic resorption.1 Some patients present in the active resorptive phase when acute severe pain is present. However, most cases are diagnosed incidentally or during the workup of chronic and vague shoulder pain. The primary treatment of calcific tendinitis consists of conservative management including physical therapy, antiinflammatory medications, and occasionally a subacromial injection of corticosteroid if accompanied by subacromial impingement. More aggressive treatment may include extracorporeal shock wave therapy, needling and lavage, and surgical débridement.
been attributed to patients having a more rapid diagnosis and earlier treatment with physical therapy, combined with active rest. Several causative factors have been attributed to the development of calcific tendinitis. Zones of stress, areas of increased pressure, hypoxemia, and degeneration have all been associated with this condition. Two distinct processes have been attributed to the development of calcific tendinitis—degenerative calcification and reactive calcification.6
Degenerative Calcification Many clinicians think that the rotator cuff degenerates and subsequently becomes calcific. During the fourth and fifth decades, the fascicles of the tendon undergo thinning and fibrillation. These thinned fascicles are often hypocellular and have irregular organization.6 Necrosis of the tenocytes have been associated with intracellular accumulation of calcium, often in microspheroliths of psammomas.11 These theories support Codman’s original idea that degeneration of the cuff precedes calcification.
HISTORICAL PERSPECTIVE In 1907, Painter2 described a condition associated with subdeltoid bursitis in patients with radiographic evidence of calcific deposits in the rotator cuff. Codman,3 in 1934, attributed calcification of the rotator cuff tendon to degeneration of its fibers. In 1978, Bateman4 noted that deposits of calcification arise in an area of hypovascularization and a “zone of stress” in the supraspinatus tendon. Brewer5 thought that the calcification was attributed to aging of the rotator cuff. Most recently, Uhthoff and Loehr6 have described the progressive stages of the disease ultimately associated with tendon reconstitution, a process analogous to that described by Lippmann7 in 1961.
Uhthoff6 has noted several discrepancies with this theory. First, the incidence of calcific tendinitis peaks in the fifth decade, unlike degenerative calcification, which increases with age. Similarly, degenerative diseases never exhibit a potential for self healing. Lastly, the histologic features of calcific tendinitis and degenerative calcification are different.
Reactive Calcification The process of reactive calcification has received support in the recent literature. Uhthoff6 has noted that the process of calcification is actively mediated by cells in a viable environment and has named three distinct stages in the evolution of this disease process—the precalcific, calcific, and postcalcific stages. Although these are distinct stages, they evolve in a continuum of the disease process.
PATHOGENESIS The cause of calcific tendinitis of the rotator cuff is still unknown; however, several theories have been proposed. It should be noted that it is uncommon to find this disease in patients younger than 30 years and that the process peaks in the fifth decade.6 Some investigations have shown an increased incidence in patients with diabetes mellitus,8 and women have been shown to be afflicted more often than men. There is a 10% incidence of bilateral involvement,9 and 25% of patients have concomitant rotator cuff tears.10 Most clinicians have found that the incidence of calcific tendinitis has decreased recently. This has
In the precalcific stage, the site of predilection for calcification undergoes fibrocartilaginous transformation. There is metaplasia of tenocytes into chondrocytes. Patients exhibit little or no pain during this stage of the disease.6 The next stage is known as the calcific stage. This stage is subdivided into the formative, resting, and resorptive 155
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associated with acute and often severe pain. The deposits have a thick creamy appearance that is often under pressure. Spontaneous rupture occurs most frequently into the subacromial space; however, two cases of rupture into the glenohumeral joint have been reported.6 The postcalcific phase occurs as a continuum of the resorptive phase. Here, granulation tissue containing fibroblasts and vascular channels begin to remodel the foci previously occupied by calcium. There is positive staining for type III collagen, which is subsequently replaced with type I collagen. This reconstitution phase may or may not be associated with pain.6 A
EVALUATION 5-mm Shaver
Extruded calcium deposit
B
Rotator cuff
Figure 13-1. Radiographic evidence of calcific deposits in a rotator cuff tendon. A, Arthroscopic view of supraspinatus muscle exhibiting calcific deposit extruding into subacromial space. B, Diagrammatic representation of arthroscopic view.
phases;12 Uhthoff’s formative and resorptive phases are analogous to the early and late phases of increment, respectively, originally described by Lippmann in 1961.7 The hallmark of the formative phase is the deposition of calcium crystals in the matrix vesicles. These coalesce into larger foci of calcification.13 Fibrocartilaginous septa separate the individual foci and gradually erode as the foci enlarge. The septa are generally devoid of vascular channels and inconsistently stain for type II collagen. The gross appearance of the deposits during this stage is chalklike. There may or may not be pain present during this phase.6
The diagnosis of calcific tendinitis is based on the physical examination findings and radiographic evidence of calcific deposits in the rotator cuff tendon. A routine physical examination of the shoulder should be performed. The range of motion, impingement testing, and cross-arm evaluation for acromioclavicular joint disease should be included. The motor strength of the rotator cuff should be evaluated, as well as any evidence of glenohumeral joint instability. The radiographic evaluation is of utmost importance for this diagnosis. A standard thrower’s series of radiographs for the shoulder should be evaluated. This includes anteroposterior (AP), AP internal and external, scapular Y, and axillary radiographs. Deposits within the supraspinatus can easily be viewed on the AP views (Fig. 13-2). Deposits in the infraspinatus or teres minor can be seen on the internal rotation radiograph. Those in the subscapularis are best seen on the AP external radiograph.6 Magnetic resonance imaging (MRI) is not usually indicated for the assessment of calcific tendinitis, except when the clinical findings indicate a concomitant rotator cuff tear. Although computed tomography is not routinely used, it may be beneficial in the resorptive phase when deposits can be difficult to see.
The resting phase is histologically identified by the presence of fibrocartilaginous tissue that borders the foci. The presence of this tissue indicates that the calcium deposition at that site has concluded. There may or may not be pain present during the resting phase.6 During the resorptive phase, the histologic appearance of thin-walled vascular channels occur at the periphery of foci. Subsequently, macrophages and multinucleated giant cells phagocytose the deposits. This phase is consistently
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Figure 13-2. Radiographic anteroposterior view of a right shoulder with calcific tendinitis.
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DePalma and Kruper8 have described two radiographic forms of calcific tendinitis. Type I shows a fluffy appearance of the deposits, with poorly defined margins. This is commonly seen in the resorptive phase when patients present in acute pain. Type II is characterized by discrete deposits, with well-delineated borders. These deposits are commonly seen in the subacute and chronic stages of the disease.
TREATMENT It is important to distinguish which phase of the disease process is involved when treatment options are discussed with the patient. More than 90% of patients will respond to conservative treatment and will never require more advanced therapy or surgical intervention. An effective physical therapy program to restore range of motion and a short course of anti-inflammatory mediations will often alleviate the symptoms of calcific tendinitis. If the patient presents with concomitant subacromial impingement, a corticosteroid injection into the subacromial space may also be helpful for relieving pain. There has been some evidence to support therapeutic ultrasound for the alleviation of pain associated with calcific tendinitis. A randomized double-blind study14 has shown that patients treated with ultrasound versus placebo have a greater decrease in pain and an improved quality of life after therapeutic ultrasound is used. In addition, there is a significant reduction in the radiographic size of the deposits. When patients present with pain during the resorptive phase, needling and lavage therapy is often recommended. This can be performed in the operating room or radiology suite. Two large-bore needles are used for inflow and outflow.6 Ultrasound or fluoroscopy may be used for localization of the deposits. The deposits under pressure are decompressed after localization, and copious irrigation of the subacromial space is performed. This reduction of intratendinous pressure will often alleviate pain. Extracorporeal shock wave therapy (ECSWT) has been widely used and studied in Europe with varying results. In 1999, Loew and colleagues15 randomly assigned patients to a control group, low-dose energy group, highdose energy group, and two-dose high-energy group for treatment with ECSWT. Results showed an energydependent success, with relief of pain ranging from 5% in the control group to 58% in the two-dose high-energy group. The improvements in Constant-Murley scores and radiographic dissolution of calcific foci were also noted to be dose dependent. Rompe and associates16 have compared surgical extirpation with high-energy ECSWT treatment in patients with
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chronic calcific tendinitis. It was noted that surgical treatment has superior results in patients with homogeneous deposits. However, in those with inhomogeneous deposits, ECSWT is equivalent to surgery in providing pain relief. It was concluded that ECSWT should be given priority because of its noninvasiveness. Daecke and coworkers17 have evaluated the long-term effect of ECSWT for the treatment of chronic calcific tendinitis. A prospective study of 115 patients at the 4-year follow-up found that although ECSWT has a high failure rate—20% required surgical intervention—70% of patients had success without having long-term complications. This was therefore recommended as a noninvasive treatment of calcific tendinitis of the rotator cuff.
Surgical Treatment Although conservative treatment will resolve symptoms in most patients, some will fail to improve. They continue to have progression of symptoms that affect their activities of daily living. Surgical intervention can be used in the chronic formative phase when conservative treatments have failed. Traditionally, an open deltoid-splitting approach was used via an anterior approach to the shoulder. However, advances in arthroscopic techniques will likely make this a treatment of the past. Treatment with arthroscopic surgery has several advantages. It will probably have less morbidity because of its less invasive nature, may have a better cosmetic outcome, and may offer the advantage of decreased rehabilitation time.18 Fluoroscopy or ultrasound may be needed for assistance in localization of the deposits. Once needle localization has been achieved, a longitudinal incision can be made at the level of the deposit on the bursal surface of the rotator cuff tendon. The chalky calcific deposit is removed from the subacromial space and copious lavage is performed. Any significant disruption of the tendon can be concomitantly repaired at the time of surgical débridement. This may require a side-to-side suture repair or suture anchor to the greater tuberosity. Acromioplasty should only be performed if subacromial impingement occurs in conjunction with the calcific tendinitis.19 A sling should be used for comfort, and physical therapy should be initiated immediately to achieve range of motion and prevent arthrofibrosis.
SUMMARY Calcific tendinitis is usually a self-limited disease process that is often treated successfully with conservative measures. If unsuccessful, surgical intervention may be indicated. Arthroscopic excision of the calcific deposits, with copious irrigation of the subacromial space during the chronic formative phase, is recommended for patients
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who fail conservative measures. An acromioplasty should not be performed unless concomitant subacromial impingement is present.
References 1. Uhthoff HK, Sarkar K: Calcifying tendinitis. In Rockwood CA Jr, Matsen FA III (eds): The Shoulder, vol 2. Philadelphia: WB Saunders, 1990, pp 774-790. 2. Painter C: Subdeltoid bursitis. Boston Med Surg J 156: 345-349, 1907. 3. Codman EA: The shoulder: rupture of the supraspinatus tendon and other lesions in or about the subacromial bursa. Boston, Thomas Todd, 1934, pp 178-215. 4. Bateman JE: The Shoulder and Neck. Philadelphia, WB Saunders, 1978. 5. Brewer BJ: Aging of the rotator cuff. Am J Sports Med 7:102-110, 1979. 6. Uhthoff HK, Loehr JW: Calcific tendinopathy of the rotator cuff: Pathogenesis, diagnosis, and management. J Am Acad Orthop Surg 5:183-191, 1997. 7. Lippmann RK: Observations concerning the calcific cuff deposit. Clin Orthop 20:49-60, 1961. 8. DePalma AF, Kruper JS: Long term study of shoulder joints afflicted with and treated for calcific tendinitis. Clin Orthop 20:61-72, 1961. 9. Hurt G, Baker CL: Calcific tendinitis of the shoulder. Orthop Clin North Am 34:567-575, 2003. 10. Jim YP, Hsu HC, Chang CY, et al: Coexistince of calcific tendinitis and rotator cuff tear: An arthographic study. Skeletal Radiol 22:183-185, 1993.
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11. Mohr W, Bilger S: Morphologische Grundstrukturen der Dalzifiaierten. Tendopathie and ihre Bedeutung fur die Pathogenese. Z Rheumatol 49:346-355, 1990. 12. Uhthoff HK, Sarkar K, Maynard JA: Calcifying tendinitis: A new concept of its pathogenesis. Clin Orthop 118: 164-168, 1976. 13. Sarkar K, Uhthoff HK: Ultrastructural localization of calcium in calcifying tendinitis. Arch Pathol Lab Med 102:266-269, 1978. 14. Ebenlichler GR, Erdogmus CB, Resch KL, et al: Ultrasound therapy for calcific tendinitis of the shoulder. N Engl J Med 340:1533-1538, 1999. 15. Loew M, Daecke W, Kusnierczak D, et al: Shock-wave therapy is effective for chronic calcifying tendinitis of the shoulder. J Bone Joint Surg Br 8:863-867, 1999. 16. Rompe JD, Zoellner J, Bernhard N: Shock wave therapy versus conventional surgery in the treatment of calcifying tendinitis of the shoulder. Clin Orthop Relat Res 387:72-82, 2001. 17. Daecke W, Kusnierczak D, Loew M: Long-term effects of extracorporeal shock wave therapy in chronic calcific tendinitis of the shoulder. J Shoulder Elbow Surg 11:476-480, 2002. 18. Ark JW, Flock TJ, Flatow EL, Bigliani LV: Arthroscopic treatment of calcific tendinitis of the shoulder. Arthroscopy 8:183-188, 1992. 19. Jerosch J, Strauss JM, Schmiel S: Arthroscopic treatment of calcific tendinitis of the shoulder. J Shoulder Elbow Surg 7:30-37, 1998.
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CHAPTER 14 Open Repair of the Rotator Cuff Matthew Rappé, E. Lyle Cain, Sanford S. Kunkel, Richard J. Hawkins, and James R. Andrews
sterile fashion, draping the upper extremity free. A sterile stockinette is used to drape the lower arm.
Management of a rotator cuff tear in an athlete continues to present a unique and challenging problem. The treatment for rotator cuff tears, especially in athletes, continues to evolve. Ten years ago, at our institutions, the vast majority of rotator cuff tears in athletes were fixed through an open or mini-open approach. Arthroscopic techniques and tools have vastly improved and our comfort level with these techniques has increased in the last 10 years, so the treatment algorithm has changed. We now treat most rotator cuff tears arthroscopically and reserve open repairs for contact athletes with two or more tendon tears. Although it is important to understand how to perform a standard open rotator cuff repair with detachment of the anterior deltoid through a deltopectoral approach, we seldom perform this operation for fear of late deltoid avulsion, a disastrous consequence.1-3 If deemed necessary to perform an open repair for improved security of the repair, we will perform the repair through a series of windows to preserve the deltoid attachment and function.3 For the purposes of this chapter, we will outline the mini-open approach through multiple windows, as well as the standard open approach.
Bony landmarks are outlined and a standard posterior portal is created within the soft spot. Under direct arthroscopic visualization, an anterior portal is created through the rotator cuff interval. Any intra-articular procedure, such as loose body excision, labrum débridement, or labral repair, is carried out. We then perform a standard bursoscopy, removing any bursa and, in the case of a rotator cuff tear, would proceed with a standard arthroscopic subacromial decompression. If a complete tear of the supraspinatus and infraspinatus exists in a contact athlete, we would proceed with a standard mini-open repair. Although this is discussed elsewhere in this text (see Chapter 15), we will describe this operation briefly. We create a transverse skin incision approximately 3 to 4 cm at the edge of the lateral acromion. We then perform a deltoid splitting approach in the raphe between the anterior and middle thirds of the deltoid. Next, we identify the rotator cuff tear, mobilize as necessary, and place multiple modified Mason-Allen sutures through the cuff tear (Fig. 14-1).
The treatment goals in rotator cuff surgery have not changed, even though the technology used may be different. In the athlete, the primary goal for rotator cuff repair is usually to relieve pain; the secondary goal is to improve function. In the contact athlete, the cause of a rotator cuff tear is generally secondary to an isolated trauma; this differs greatly from the cause of a tear in the competitive overhead athlete. The goal for both groups of injured athletes is to return the athlete to his or her previous level of competition.
The rotator cuff footprint is roughened and anchors are placed within the medial aspect of the footprint (Fig. 14-2). The sutures from these anchors are then brought through the cuff medially to the Mason-Allen sutures previously placed (Fig. 14-3). Standard transosseous tunnels are created using an air-driven device (Curvetek, Biomet Sports Medicine, Warsaw, Ind; Fig. 14-4). The sutures within the transosseous tunnels are tied to themselves and the medial anchor sutures are secured (Fig. 14-5). We repair the tear using two rows of repair, if possible, similar to the method used for a complete full-thickness tear of the subscapularis, but the approach is different. We leave the patient in the lateral position and carry out the procedure using a limited deltopectoral approach centered just lateral to the coracoid. We identify the tear and secure it to the tuberosity in the same fashion as for the miniopen repair described earlier. If all three tendons are involved, we will create both these incisions and repair the tear via each of these windows.
OPERATIVE PROCEDURE In all cases, a diagnostic arthroscopy is performed in conjunction with any rotator cuff surgery. At our institution, we prefer to perform this with the patient in the lateral decubitus position. An axillary roll is used, as well as a beanbag, to maintain positioning of the patient during the procedure. The operative arm is suspended using 15 pounds of arm traction. Preoperative intravenous antibiotics are administered to the patient. The procedure is carried out with general anesthesia but may be augmented with an interscalene block for postoperative pain. The shoulder, axilla, and hemithorax are prepared in the usual
An alternative to this technique involves a standard open rotator cuff repair. This involves an anterior deltopectoral incision performed with the patient in the modified beach 159
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Figure 14-1. Mini-open repair. The rotator cuff tear is identified, mobilized as necessary, and then multiple modified Mason-Allen sutures are placed through the cuff tear.
Figure 14-3. Sutures from anchors brought through cuff medially to Mason-Allen sutures previously placed.
chair position. The incision is made in line with the deltoid fibers using self-retaining retractors for exposure. Once the deltoid muscle attachment to the acromion is encountered, the anterior deltoid is detached from the acromioclavicular joint to the lateral border of the acromion using electrocautery. Classically, a suture is placed in this split to avoid further detachment. An alternate approach involves splitting the deltoid longitudinally and preserving its attachment on the acromion. If the deltoid muscle is detached, it is retracted from the anterior acromion and the rotator cuff tear is identified. The tear is then mobilized and repair is initiated as described for the mini-open repair, using medial suture anchors and lateral bone tunnels. If mobilization of the cuff tear is necessary, release of the coracohumeral ligament will aid in this endeavor.
On completion, the repair should be watertight and checked to ensure that it is secure. The repair may be performed with the patient’s arm in the abducted position secondary to excessive tension on the cuff. The point at which the cuff comes under excessive tension should be noted for postoperative positioning and rehabilitation. The repair should be performed without tension, with the arm positioned down at the side. After the wound is thoroughly irrigated, the detached deltoid muscle is re-approximated to the remaining cuff of tissue on the anterior acromion. If a secure repair cannot be achieved, the deltoid muscle can be re-approximated to the acromion using several small drill holes through the acromion and horizontal mattress sutures (Fig. 14-6).
Roughened area of bone
Figure 14-2. Rotator cuff footprint is roughened; anchors are placed within the medial aspect of the footprint.
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161
used for small to medium-sized tears without significant tension, but a large pillow and brace are used for more retracted larger tears with tension.
REHABILITATION Rehabilitation for open rotator cuff repairs is conservative in nature in comparison with mini-open and arthroscopic repairs. Rehabilitation consists of passive assisted motion until the repair is secure. After 6 to 8 weeks, active motion is again allowed. Once active motion is instituted, terminal stretching is required, but resisted motion is delayed until appropriate active motion has been achieved, usually during the third month. It is important to remind patients that rehabilitation after rotator cuff surgery takes many months; often, 6 months elapse before patients can elevate their arms above the horizontal position with comfort and efficiency4,5 (Appendix 14-1). Initial rehabilitation consists of assisted elevation and external rotation, followed by pendulum exercises, extension, and internal rotation. Active motion then begins, depending on the size of the tear and whether the repair is secure. Prolonged rehabilitation, emphasizing range-ofmotion and strengthening exercises, is continued for a minimum of 2 years. Although an open rotator cuff repair is not typically performed in overhead athletes, those who are involved in repetitive overhead sports, such as baseball pitchers, often undergo a prolonged and intense rehabilitation program for 1 to 2 years before return to the competitive arena. Throwing athletes are not permitted to
Figure 14-4. Air-driven device helps create standard transosseous tunnels.
With a mini-open deltoid splitting technique, the deltoid can be closed side to side without re-attachment to the anterior acromion. The subcutaneous layer is closed with 2-0 absorbable sutures, and the skin is re-approximated with running subcuticular 3-0 absorbable sutures. A nonadherent dressing is placed on the shoulder, and the arm is placed in a sling. A small abduction sling and pillow are
A
B
Figure 14-5. Sutures within transosseous tunnels are tied to themselves (A) and medial anchor sutures are secured (B).
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Hawkins6 have reported good results with this technique using a rotator cuff repair secured to a trough in the bone. Subacromial decompression is considered to be an important component of rotator cuff repairs, to allow space for tissue edema and healing postoperatively. Rotator cuff pathology caused by anterior instability may necessitate anterior capsulolabral reconstruction concomitant with rotator cuff repair. The goals in rotator cuff surgery are to relieve pain and then to improve function. Appropriate patient selection and meticulous surgical repair, coupled with an intense rehabilitation program, are the keys to success in open repair of the rotator cuff. Communication between the surgeon and rehabilitation team is critical.
References
Figure 14-6. Re-approximation of deltoid fascia to anterior acromion through vertical drill holes.
throw for a minimum of 6 months and are taken through a specific rehabilitation program that emphasizes mobility and strength, followed by a progressive throwing program. Preoperative consultation involving time parameters is helpful for patient cooperation and understanding. Open communication among the surgeon, physical therapist, and athletic trainer is important to plan the patient’s appropriate return to activities based on individual tear anatomy and repair strength.
SUMMARY The technique of open rotator cuff repair6-8 is well accepted for rotator cuff repair. This technique provides secure fixation of the ruptured ends of the rotator cuff with a watertight closure. Neer and colleagues9 and Kunkel and
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1. Gumina S, Di Giorgio G, Perugia D, Postacchini F: Deltoid detachment consequent to open surgical repair of massive rotator cuff tears. Int Orthop 32:81-84, 2008. 2. Sher JS, Iannotti JP, Warner JJ, et al: Surgical treatment of post-operative deltoid origin disruption. Clin Orthop Relat Res (343):93-98, 1997. 3. Hata Y, Saitoh S, Murakami N, et al: Atrophy of the deltoid muscle following rotator cuff surgery. J Bone Surg Am 86:1414-1419, 2004. 4. Hawkins RJ: The rotator cuff and biceps tendon. In Evarts CM (ed): Surgery of the Musculoskeletal System, 2nd ed. New York, Churchill Livingstone, 1990, pp 1393. 5. Hawkins RJ: Surgical management of rotator cuff tears. In Bateman JE, Welsh RP (eds): Surgery of the Shoulder. Philadelphia, BC Decker, 1984, pp 161. 6. Kunkel SS, Hawkins RJ: Rotator-cuff repair utilizing a trough in bone. Tech Orthop 3:51, 1989. 7. McLaughlin HL, Asherman EG: Lesions in the musculotendinous cuff of the shoulder: IV. Some observation based on the results of surgical repair. J Bone Joint Surg 33A:76, 1951 8. Yel M, Shankwiler JA, Noonan JE, Burkhead WZ. Am J Orthop 2001 Apr;30(4):347-52. Results of decompression and rotator cuff repair in patients 65 years old and older: 6- to 14-year follow-up. 9. Neer CS II, Flatow EL, Lech O: Tears of the rotator cuff: long term results of anterior acromioplasty and repair. Paper read at the 55th Annual Meeting of the American Academy of Orthopaedic Surgeons, Atlanta, GA, February 5, 1988.
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APPENDIX 14-1 Shoulder Conditioning and Therapy Checklist:
Phases I, II, and III
Postoperative Program: Rotator Cuff Repair Ice Days/week ______ “on” 15-20 minutes Phases I, II, and III Time/day ______ “off”
Phase III (week 10 or 12, depending on size of tear) Days/week ______ Times/day ______
60 minutes Active Motion (With Terminal Stretch)
Phase I (0-6 weeks or 8 weeks, depending on size of tear) Small: 6 weeks Large: 8 weeks Days/week ______ Times/day ______
Passive Motion
Sets
Reps
Pendulum exercises
1-2
20-30
External rotation
1-2
10-15
Internal rotation
1-2
10-15
Overhead elbow lift
1-2
5-10
Phase II (week 6 or 8, depending on size of tear) Days/week ______ Times/day ______
Active Motion (With Terminal Stretch)
Sets
Reps
Pendulum exercises
1-2
20-30
External rotation
1-2
10-15
Internal rotation
1-2
10-15
Overhead elbow lift
1-2
5-10
Sets
Reps
Pendulum exercises
1-2
20-30
External rotation
1-2
10-15
Internal rotation
1-2
10-15
Overhead elbow lift
1-2
5-10
Sport Cord Strengthening
Sets
Reps
External rotation
1-2
10-15
Internal rotation
1-2
10-15
Forward punch
1-2
10-15
Overhead punch press
1-2
10-15
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CHAPTER 15 Mini-Open Rotator
Cuff Repair Robert Afra, Ilya Voloshin, and Anthony Schepsis
Rotator cuff repair was described in the literature almost 100 years ago.1 Over the years, the technique for rotator cuff repair has undergone significant modifications. The major procedures addressing the rotator cuff tears are open, mini-open, and arthroscopic repairs. Although these can be viewed as three distinct techniques, we believe that they are better understood in a timeline as an evolution, from open to mini-open to an all-arthroscopic process. There are some indications for which a formal open rotator cuff repair is to be used, but we think that the mini-open technique remains a mainstay in the contemporary shoulder surgeon’s armamentarium. This would be especially true for patients in whom an all-arthroscopic technique using suture anchors would not provide adequate fixation of the rotator cuff tissue in primary or revision situations because of poor bone quality, inadequate bone stock, or large tear. The relevant anatomy, patient history, physical examination, and indications for rotator cuff repair are all important in the appropriate patient selection for surgical treatment. See elsewhere in this text for further discussion of these topics.
Advantages of Mini-Open Over Open Technique The mini-open technique has several advantages over the open technique. To perform an anterior acromioplasty in the open technique, it is necessary to detach the deltoid from the acromion. Because the deltoid muscle origin is preserved in the mini-open technique, the rehabilitation of the postoperative shoulder is less restricted—it is unnecessary to await deltoid attachment healing—and the rare and dreadful complication of postoperative deltoid detachment is avoided.3-6 Hata and colleagues7 have reported an increased incidence of postoperative deltoid atrophy after the open repair. They found that the thickness of the anterior deltoid fibers does not change significantly after surgery in the mini-open repair group, whereas it is significantly decreased in the open repair group at 6 and 12 months postoperatively (P ⬍ .05). It has been shown that a concomitant arthroscopic intra-articular glenohumeral evaluation and treatment of pathology during miniopen rotator cuff repair affect outcome.8,9
Advantages of Mini-Open Over Arthroscopic Approach
COMPARISON OF MINI-OPEN, ALL-ARTHROSCOPIC, AND OPEN ARTHROSCOPIC PROCEDURES
Major advantages of the mini-open technique over the arthroscopic approach include the ability to perform transosseous fixation, which possibly leads to better footprint restoration, and to place modified Mason-Allen sutures, which potentially leads to stronger suture gripping properties.
The meaning of the term arthroscopically assisted miniopen rotator cuff repair has become nebulous. There is no clearly defined cutoff point at which to convert an arthroscopic procedure into a mini-open repair. Yamaguchi2 has described two intermediary surgeries that lie somewhere in between an all–mini-open technique and an all-arthroscopic technique. The two intermediary surgeries simply vary in how much of the procedure is done arthroscopically. The first, arthroscopically assisted open repair, is arthroscopic subacromial decompression followed by open repair of the rotator cuff through a lateral deltoid-splitting approach. The mini-open arthroscopically assisted repair is arthroscopic subacromial decompression, release of adhesions, placement of tagging sutures, and débridement of the tendon edges, followed by a mini-open deltoid splitting approach that results in suture management and bone tendon fixation.
There are currently two generally acceptable methods to obtain cuff fixation to bone: suture anchors and transosseous tunnels. The literature must be searched carefully if any meaningful conclusions are to be drawn when comparing transosseous tunnels with suture anchors, especially because suturing techniques vary from one study to another in mini-open surgical procedures. Early suture anchors appear to have obtained less fixation strength than transosseous tunnels.10,11 With improved suture anchor designs, other studies have demonstrated that suture anchor constructs are stronger than transosseous tunnels.12-14 Interestingly, the anterior two thirds of the greater tuberosity have higher loads to failure for anchor fixation than the posterior one third (P ⬍ .01).15 Bynum 165
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and associates16 have determined that anchors placed at a standard depth level of the laser markings or with the eyelet proud have a higher cyclic load to failure than anchors placed at a deeper level. Chhabra and coworkers17 have shown in a biomechanical model that double-loaded suture anchors have a higher resistance to failure with cyclic loading than transosseous sutures (P ⫽ .009) or single-loaded suture anchors (P ⫽ .02). Based on biomechanical data, the weak link in the suture anchor fixation construct is the tendon-gripping strength of the suture material. Gerber and colleagues18 have shown that a modified Mason-Allen stitch has nearly twice the ultimate load to failure than a simple stitch. In a similar study, Gerber and associates19 have used a sheep model to show that a simple stitch fails 100% of the time by pulling out of the tissue; however, when using a modified Mason-Allen stitch, the strength of the suture material is the limiting factor. The fact that a modified Mason-Allen stitch can be used with the mini-open rotator cuff repair technique is a real advantage. Scheibel and Habermayer20 have described an all-arthroscopic cruciate stitch using suture anchors, but they offer no biomechanical evidence of its strength. However, MacGillivray and associates21 have described the Mac stitch, which is conceptually similar to the cruciate stitch, and they performed biomechanical testing. They used a sheep model to test the cyclic loading of four stitch configurations—simple, horizontal, Mac, and modified Mason-Allen. Ultimate tensile load was significantly higher (P ⬍ .05) for the massive cuff stitch (Mac; 233 ± 40 N) and the modified Mason-Allen stitch (246 ± 40 N) than for the simple stitch (72 ± 18 N) or horizontal stitch (77 ± 15 N). There was no significant difference in the ultimate load between the Mac and modified Mason-Allen stitches. The simple and horizontal stitches failed by tissue pull-out, whereas the Mac and Mason-Allen stitches failed by a mixture of suture breakage and pull-out. In addition to the soft tissue stitch, De Carli and coworkers23 have found that the suture material affects the fixation construct. They compared FiberWire (Arthrex, Naples, Fla) with Ethibond and found Ethibond to be much less resilient, making it more prone to breakage. FiberWire seems to increase the strength of metallic and bioabsorbable fixation devices under cyclic loading. Burkhart and colleagues,24 in a human cadaveric study, compared a transosseous construct with a simple suture technique and a transosseous construct with a horizontal mattress suture technique. They tested cadaveric shoulders for ultimate load to failure and found that the simple suture construct fails at an average of 189 N, whereas the horizontal mattress construct fails at an average of 136 N (P ⬍ .007). It must be noted that the suture was tied over the greater tuberosity in the simple suture construct, but was tied over a cortical bone bridge in the horizontal mattress construct. It is by analyzing the modes of failure in these studies that interesting conclusions can be reached. The suture used for
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the construct was a no. 2 braided polyethylene. The most common mode of failure in both groups was by suture breakage. The second most common mode of failure varied with the group. Although the simple suture construct group had more tendon failures (suture pulling through the cuff tissue), the horizontal mattress group had more bone failures (the bone bridge collapsed). Therefore, it follows that if a surgeon uses a newer “supersuture” and one of the cruciate-type stitches, a construct that ties the knot over a bone bridge that uses the greater tuberosity would be stronger than a construct that ties the knot over a bone bridge that uses the lateral humeral cortex. In a follow-up biomechanical study, Burkhart and associates25 have further evaluated the mode of failure in transosseous cuff repairs using cadaveric shoulders. The 15 specimens had almost an equal distribution of failure by suture pulling through the tendon substance versus failure by the transosseous sutures cutting through the bone bridge. However, when the specimens were stratified based on the location of the distal/lateral bone tunnel exit site, interesting findings were revealed. Of 7 specimens with the distal bone tunnel exit in cortical bone, 6 showed primarily cuff tissue failure. In contrast, of 9 specimens with the distal bone tunnel exit in metaphyseal bone, 6 showed primarily bone failure. Thus, the surgeon should try to use a newer supersuture with a cruciate-type stitch, tie the suture over the greater tuberosity, and have the bone tunnel exit in the cortex. Apreleva and coworkers26 have compared various fixation and suture methods in their efforts to reproduce the supraspinatus footprint. Transosseous simple sutures, transosseous mattress sutures, suture anchors with simple sutures, and suture anchors with mattress sutures were compared. The transosseous simple suture most approximated the native supraspinatus footprint by restoring 80% of the native footprint surface area. The other three methods covered less area, 67% of the native footprint. Park and colleagues27 have confirmed these findings of greater surface area contact with transosseous tunnels. Additionally, they found greater overall pressure distribution with bone tunnel constructs in comparison with suture anchors with simple or mattress stitches. To replicate the native footprint better, many surgeons use a double-row anchor fixation. In their study, Mazzocca and colleagues28 have demonstrated that a significantly greater supraspinatus footprint width is seen with a double-row technique compared with single-row repair. The size of the double-row suture anchor footprint obtained arthroscopically is believed to equal that obtained by mini-open techniques. Although a larger footprint has not been shown to result in larger loads to failure, the larger footprint arguably results in improved biologic quality of repair. Kim and associates,29 in a biomechanical model, have compared single-row with double-row fixation using suture anchors.
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They demonstrated an increase in strength and decrease in gapping with the double-row suture anchor fixation compared with the single-row repair (P ⬍ .05). They did not control for the number of sutures or suture anchors used, which likely explains the differences in their results and those of Mazzocca and coworkers.28 Presumably, like tendon repair, an increase in the number of sutures across the repair and the number of suture anchors augments the repair strength. The only conclusion that can be drawn is that the use of more sutures and more anchors results in more strength of repair fixation. An increase in footprint size has not been shown to improve healing potential; this has only been theorized. Burkhart and colleagues25 have compared the cyclic loading to failure of rotator cuff repair constructs using transosseous tunnels with constructs using suture anchors.14 Each construct used three simple sutures, either three transosseous tunnels or three suture anchors. They applied 180 N of tension cyclically until the cuff developed a 5- and 10-mm gap from the bone bed to which it was fixed. A 5-mm gap developed in the suture anchor construct at an average of 61 cycles, but developed in the transosseous construct after an average of 25 cycles. Similarly, although a 10-mm gap developed in the suture anchor construct at an average of 285 cycles, it developed in the transosseous construct after an average of 188 cycles. These results were described in two different articles; the number of sutures and cyclic loading method were similar, but the suture material used differed. The transosseous construct used no. 2 braided polyethylene; in contrast, the suture anchor construct used no. 2 braided polyester (Ethibond, Johnson & Johnson, New Brunswick, NJ).
Disadvantages of Mini-Open Over Arthroscopic Procedures It is important to keep in mind three potential drawbacks of mini-open over a fully arthroscopic technique. This will help the surgeon minimize the risks of complications and poor results. First, some studies have reported an increased incidence of stiffness, from 11% to 20%, following mini-open surgery versus a fully arthroscopic technique,30-32 It is postulated that this is secondary to damage to the deltoid muscle.33 Stiffness is even more common (36%) in patients with insulin-dependent diabetes mellitus for longer than 5 years who undergo open cuff repairs.34 This factor may be significant in that some of these patients required manipulation or release. Proponents of an arthroscopically assisted mini-open technique have argued that the stiffness can be avoided by performing the cuff releases arthroscopically during the index procedure, thus placing less stretch on the deltoid tissue.
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Second, shoulders undergoing an all-arthroscopic cuff repair technique seem to progress through rehabilitation more easily, in that there is less postoperative pain and better range of motion.31,35,36 Again, this is likely secondary to deltoid trauma, with manipulation and stretching of the muscle tissue. Third, the open and mini-open rotator cuff repairs are associated with an increased risk of infection.37,38 Herrera and colleagues37 have described a 2% incidence of infection in 360 arthroscopically assisted mini-open rotator cuff repairs. Six of seven (89%) patients had cultures grow Propionibacterium acnes. In addition to an average of two serial irrigation and débridement procedures and 6 weeks of antibiotics, four patients required revision rotator cuff repair. In the subsequent 300 cases, gloves were changed and the skin was re-prepared before transitioning to a mini-open procedure; there were no subsequent infections. However, there is a potential bias in this study. The patients who had a Propionibacterium infection all underwent a shoulder arthroscopy and, at the same sitting, subsequently underwent a mini-open rotator cuff repair. Thus, the infection might have been caused by the arthroscopic portals “affecting” the mini-open incision. The drop in the infection rate with re-preparation of the skin before converting to a mini-open surgery corroborates this theory.
MINI-OPEN SURGICAL TECHNIQUE The rotator cuff mini-open repair technique can be logically divided into five distinct steps—diagnostic arthroscopy, decompression, tissue mobilization, deltoid split, and re-creation of the footprint and fixation. We think it is important to perform a full arthroscopic examination to assess the architecture of partial or complete tears, tissue quality, bone quality, and concomitant intra-articular pathology adequately. We routinely perform a preoperative interscalene brachial plexus block. Patient positioning depends on the surgeon’s preference. The patient can be in the beach chair or lateral decubitus position. Both allow an arthroscopic or miniopen rotator cuff repair to be performed. Appropriate perioperative antibiotics are administered. Before skin preparation, local anesthetic with epinephrine is injected into the subacromial space to minimize bleeding. The skin is prepared and osseous landmarks are outlined—acromion, clavicle, acromioclavicular joint, coracoid, and scapular spine. Glenohumeral arthroscopy is then performed in the usual fashion. After the arthroscope is inserted through a standard posterior portal, an anterior portal is established in the rotator interval. If a full-thickness rotator cuff tear is
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not readily obvious, the surgeon who suspects a tear must be meticulous in evaluation of the tendon. We have made the clinical observation that if the rotator cuff rests on the biceps tendon, so that there is no space between them, there likely exists a tear. An 18-gauge spinal needle is placed percutaneously through the rotator cuff where an articular surface tear exists; alternatively, a 2-0 polydioxanone suture (PDS) suture can be passed and the needle withdrawn (Fig. 15-1). We use the technique described here to create “a room with a view” before creating the lateral portal, so that the lateral portal can be centered over the tear. The arthroscope in the posterior portal is re-directed into the subacromial space. The arthroscope trocar is placed into the subacromial space. The sheath-trocar is then pushed out the previously created anterior portal used during the diagnostic intra-articular arthroscopy. The cannulated metal handle with overriding cannula is positioned into the anterior part of the subacromial space. As the surgeon holds the sheath and cannula steady, the assistant replaces the trocar with the arthroscope and the metal cannulated handle with a 4.5-mm full-radius or incisor shaver. The advantage of this technique is that the shaver position is readily evident. The bursa in the anterior, posterior, and lateral subacromial space is sequentially débrided, always taking care to avoid injury to the cuff tissue. An acromioplasty for a type II or III acromion, as described by Izquierdo and Bigliani,39 can be addressed at this point or just before converting to a mini-open procedure. By delaying the blind placement of the lateral portal, one is allowed to position it strategically at the center of the rotator cuff tear under direct visualization.
Figure 15-1. Assessing for tears. An 18-gauge spinal needle is used to mark the location of an articular-sided cuff tear. The bursal side of the cuff is checked for a full-thickness tear.
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The advantage of performing the acromioplasty now is that it provides more subacromial space within which to work; the disadvantage is that the bone bleeds, obscuring visualization. We prefer to do acromioplasty just after the cuff has been mobilized, before making a mini-open incision. Once a tear is confirmed, a midlateral portal is obtained approximately 2 cm distal to the lateral acromial edge and in line with the center of the tear. Arthroscopic determination of the midlateral portal placed at the center of the tear is an essential step that effectively allows for the smallest possible deltoid muscle split, thereby limiting detachment and dissection.40 An 18-gauge needle can be used to localize the ideal position. An arthroscopic portal is made after a switching stick is used to penetrate laterally into the subacromial space in line with the spinal needle. A cannula, such as a 8.25-mm cannula, is passed with a cannulated metal handle over the switching stick if one plans on passing sutures through cuff tissue arthroscopically. Otherwise, a cannula is not necessary to perform the subacromial decompression. Characterization of the rotator cuff tear, as described by Klein and Burkhart,41 is essential to facilitate an appropriate approach. It is important to define the anterior and posterior extents of the tear and to determine the shape (L versus U). From the lateral portal, the shaver is used to débride the remaining overlying bursal tissue and an acromioplasty is done by the surgeon’s preferred method. The subacromial decompression plays two roles—it provides visualization and room within which to work and removes the source of external impingement. A radiofrequency device is used to obtain hemostasis and ablate tissue. A grasper is used to determine the excursion of the cuff. If mobilization is necessary, two traction sutures are passed using no. 2 nonabsorbable sutures through the cuff, anterior and posterior, by the surgeon’s preferred method. They can be passed through the cuff tissue using retrograde suture-passing instruments (e.g., suture lasso), antegrade suture-passing instruments (e.g., penetrator, bird’s beak), or antegrade needled instruments (e.g., Expressew, DePuy Mitek, Raynham, Mass). The traction sutures are stored outside the lateral cannula so that instruments can be passed via the lateral cannula unencumbered. An arthroscopic elevator is used on the bursal surface of the cuff anteriorly and posteriorly. The articular surface of the cuff is separated from the superior labrum (Fig. 15-2). The elevator should penetrate no deeper than 2 cm because of risk of injury to the suprascapular nerve.42 Typically, we stop the bursal surface release once we have visualized fatty tissue medially around the spinoglenoid notch. The cuff excursion is again checked. The release of the articular surface is limited to 1 cm or less medial to the superior glenoid. Further mobilization can be obtained by release of the rotator interval tissue. This release may be indicated for massive, contracted, immobile rotator cuff tears. Lo and Burkhart43 have popularized the term anterior interval slide.
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Capsule
Labrum
Biceps tendon
Glenoid
A
B
This release separates the supraspinatus tendon from the rotator interval tissue. As a result, the scarred coracohumeral ligament is released.44 This procedure is most easily performed using a cutting instrument or radiofrequency ablater from the lateral portal aimed at the coracoid base. If further release is necessary, a posterior interval slide is performed. This release separates the supraspinatus from the infraspinatus, resulting in an additional 2- to 2.5-cm excursion. Up to this point, an arthroscopic approach has clear advantages over an open technique because the deltoid tissue is left intact and over the mini-open technique because of visualization during tissue mobilization of the cuff, without overstretching of the deltoid. From this point, at any step along the way, one may transition from an arthroscopic technique to a mini-open procedure. Once the cuff tissue is mobilized, the decision to proceed to a mini-open technique is based on the bone quality of the greater tuberosity, ability to re-create the footprint, need for graft augmentation, and surgeon’s preference. The lateral portal is extended. Whether a transverse or longitudinal skin incision is made, the deltoid split occurs in the same spot along the muscle fibers. We prefer to make a transverse skin incision along Langer’s lines, incorporating the lateral portal (Fig. 15-3). For ease of repair, however, it is essential that the deltoid split be centered over the rotator cuff tear while the arm is in neutral rotation. This makes the following steps much less cumbersome. The dissection is carried out through the subcutaneous tissue. The tissue is elevated from the deltoid fascia in all four directions. The fascia and deltoid muscle are incised from the acromial edge distally for 3 to 4 cm. Particular attention must be paid not to extend the deltoid split beyond 5 cm, because it will put the axillary nerve at risk (Fig. 15-4).45 The fascial split is sutured with Vicryl to prevent distal propagation.
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Figure 15-2. An elevator is used to separate the labrum from the cuff for increased excursion. Do not penetrate deeper than 2 cm to avoid suprascapular nerve injury. A, The dotted line indicates the site of capsular release peripheral to the glenoid labrum. B, A blunt elevator is used to separate the capsule and rotator cuff tendons from the labrum. (Adapted from Warner JJ, Iannotti JP, Gerber C [eds]: Complex and Revision Problems in Shoulder Surgery. Philadelphia, Lippincott-Raven, 1997, pp 177-202.)
At this point in the procedure, the first four steps— diagnostic arthroscopy, decompression, tissue mobilization, and deltoid split—have been achieved. As noted, the acromioplasty can be performed at any stage in the operation before conversion to the mini-open technique. We typically defer this to the final steps of the arthroscopic portion of the surgery to minimize bleeding. The two remaining steps involve the method and type of fixation and the type of stitch to be used. There are currently two acceptable methods by which to obtain cuff fixation to bone: suture anchors and transosseous
Figure 15-3. Skin incision.
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A variation of this construct is to place a simple transosseous suture. A simple suture is placed into the cuff tissue; the caudad suture tail is passed through a bone tunnel, and the cephalad suture tail is then tied over the cuff to the caudad tail on the lateral aspect of the greater tuberosity. Various suture configurations can be used for maximal tissue-grasping strength: modified MasonAllen, cruciate, Bunnell, SCOI (Southern California Orthopaedic Institute), or simple. We prefer to use a modified Mason-Allen suture (Fig. 15-6).
Figure 15-4. Prevention of axillary nerve injury. To prevent risk of axillary nerve injury, a stitch at the distal aspect of the deltoid fascial split can be used to prevent further tearing of the fascia.
tunnels. There are several variations for the repair; these include a bone trough and transosseous tunnels, doublerow anchors, single-row anchors, and a single medial row of anchors and lateral trough with transosseous tunnels. We often use a medial row of anchors in addition to laterally placed transosseous tunnels with a trough (Fig. 15-5). The medial row sutures from the anchor are placed in a horizontal mattress stitch format. The lateral row fixation is performed with a modified Mason-Allen suture, with both ends passed through separate bone tunnels and tied over a bony bridge.
A rongeur is used to débride the lateral aspect of the greater tuberosity of tissue. Care is taken to avoid decorticating the bony bed. Excursion is checked to confirm that the cuff has been adequately mobilized and to determine the sites of anchor and bone tunnel placement (Fig. 15-7). The number of anchors is determined by the size of the tear. Ideally, the anchors are placed 1 cm apart. A punch is used to determine the bone quality. Depending on bone porosity, a 5.0-, 5.5-, or 6.5-mm anchor can be used; these can be of metal or bioabsorbable material. Although there is a correlation between cortical bone density and metal anchor pull-out strength (P ⬍ .01), this is not seen with bioabsorbable anchors.46 There are conflicting results when comparing bioabsorbable with metal anchors. Several studies in porcine models have demonstrated that metal anchors have twice the pull-out strength of bioabsorbable anchors, with a range of 185 to 570 N (P ⬍ .05).47,48 However, DeCarli and associates have compared the ultimate failure load of 5.0-mm bioabsorbable, 6.5-mm bioabsorbable, and metallic 5.0-mm anchors in a biomechanical study. They found similar ultimate failure loads, but the mode of failure varied. Whereas the metal anchors failed by anchor slippage, the bioabsorbable anchors underwent eyelet failure. Additionally, bioabsorbable anchors have been found to result in foreign body reactions and extensive osteolysis.49,50 While pulling on the traction sutures, a free needle with a tight radius of curvature is used to place the no. 2 suture from the anchor in a horizontal mattress fashion approximately 1.5 cm to 1.75 cm medial to the cuff edge. The sutures are left untied and are tagged.
Figure 15-5. Hybrid rotator cuff repair. This is comprised of a medial row of suture anchors and a lateral row of transosseous tunnels with a trough.
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A Concept rotator cuff repair system kit (ConMed Linvatec, Largo, Fla) is used to create the bone tunnels laterally (Fig. 15-8). The tunnels are placed approximately 1 cm apart so that there is an adequate bony bridge. Usually, three tunnels are placed. According to Caldwell and coworkers,51 the strength of fixation with the transosseous technique is directly proportional to the distance that the lateral tunnels exit in relation to the greater tuberosity tip. They recommend more than 10 mm.51 A no. 2 nonabsorbable suture, preferably one of the newer supersutures (e.g., FiberWire, Arthrex, Naples, Fla), on a tight curved free needle is used to place a modified Mason-Allen stitch
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A
B
171
C
Figure 15-6. Tissue-grasping suture configurations (modified Mason-Allen). A, Arrows indicate how to appropriately form stitch. B, Note that this limb passes anterior to the upper limb from image A. C, Note that this limb passes posterior to the lower limb from image A.
approximately 1 cm apart52; two are typically placed, anteriorly and posteriorly. The Mason-Allen suture is lateral to the previously placed horizontal mattress sutures from the suture anchor. The most anterior limb of the anterior Mason-Allen stitch is passed through the anterior tunnel. The most posterior suture limb of the posterior MasonAllen stitch is passed through the posterior tunnel. The two remaining limbs are passed through the middle bone tunnel (Fig. 15-9).
Figure 15-7. Simple stitch placed into the leading edge of cuff tissue can aid in traction. This helps the surgeon localize the site of anchor and bone tunnel placement and also is helpful when placing a complex cruciate stitch (e.g., modified Mason-Allen).
While the assistant pulls on the traction sutures, the surgeon ties the Mason-Allen sutures passed through the bone tunnels. Subsequently, the horizontal mattress sutures are tied. The wound is irrigated. Running 2-0 Vicryl is used to re-approximate the deltoid fascia; 0 Vicryl, 2-0 Vicryl, and 4-0 Monocryl sutures are used to close the subcutaneous tissue. We routinely use cryotherapy for additional pain control53 and to minimize swelling. We avoid the postoperative use of nonsteroidal anti-inflammatories, because they have been shown to be detrimental to rotator cuff healing.54
POSTOPERATIVE REHABILITATION
Figure 15-8. Concept rotator cuff repair system kit. (Courtesy of ConMed Linvatec, Largo, Fla.)
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The protocol described is based on a medium-sized tear (1 to 3 cm). Smaller or larger tears should have the rehabilitation protocol modified as appropriate. The arm is supported using a sling with an abduction pillow for 3 weeks. Pendulum exercises are initiated postoperative day 1 after surgery. The patient is encouraged to begin range-of-motion (ROM) exercises for the elbow, wrist, and cervical spine during this interval. The pace and vigor of therapy are dictated by the size of the tear and the amount of tension on the repair, as determined by the surgeon. Passive ROM exercises are started during the first week—external rotation and internal rotation motion in the scapular plane and flexion to tolerance. There is controversy as to when to start ROM
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A
B
exercises after rotator cuff repair. With the mini-open approach, we think that passive ROM exercises should be started relatively early. However formal active-assisted ROM exercises with a therapist are begun at 3 to 6 weeks, and active ROM should be delayed to 6 to 8 weeks. Active strengthening exercises are initiated at 3 months.
Results Of Mini-Open Repairs Eight studies55-62 of 339 patients were published from 1994 to 2002 with more than 2 years of follow-up after mini-open rotator cuff repair. The average follow-up was 4 years. An average of 90% of patients reported excellent or good results and an average of 94% of patients were satisfied. Posada and colleagues61 followed 60 patients for 6 years postoperatively who had a mini-open cuff repair with 7 small (less than 1 cm), 16 medium (1 to 3 cm), 19 large (3 to 5 cm), and 18 massive (more than 5 cm) tears. They compared results at 2 and 6 years and found that the improvement in outcome with the mini-open repair does not deteriorate with time. The improvements in pain, function, active forward flexion motion, and forward flexion strength that were seen at 2 years endured through the 6-year follow-up. Even when stratified by tear size, there was no diminution in outcomes for the large and massive tears. Interestingly, they found that patients who were undergoing revision surgery, even if the index procedure consisted solely of a subacromial decompression, were unsatisfied with their revision results. The positive results endured over time.
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Figure 15-9. Sutures passed through osseous tunnels and tied laterally. A, We prefer to pass the sutures through three cortical holes. B, With two sutures in place, the middle hole receives one end of each suture and the two outside holes each receive one suture end.
Although more recent articles tend to report on shorter follow-up times, many use statistical measures that were not previously reported. For example, Hersch and associates45 have reported results on mini-open rotator cuff repair with a 3-year average postoperative period in 22 patients, showing statistically significant improvement in pain and motion. They had 12 medium (1 to 3 cm), 5 large (3 to 5 cm), and 5 massive (more than 5 cm) tears. Symptoms improved in 95% of patients. There was a statistically significant improvement in pain (P ⫽ .0001); whereas 86% had constant pain preoperatively, only 9% had constant pain postoperatively. Also, 64% had no or slight pain postoperatively. There was a statistically significant improvement in active range of ROM postoperatively. Active elevation in the scapular plane improved from 130 degrees preoperatively to 164 degrees postoperatively (P ⫽ .0034). Postoperative strength was restored to 95% to 99% of that of the contralateral side. More importantly, Hersch and coworkers45 have determined several predictors of outcome: (1) a shorter duration of symptoms is significantly associated with a better outcome; (2) larger tears are associated with a worse UCLA shoulder score; (3) greater forward elevation strength is significantly associated with a better ConstantMurley outcome score; and (4) greater external rotation strength is significantly associated with a better American Shoulder and Elbow Surgeons (ASES) shoulder index. Other studies have reported on the outcomes of doublerow fixation. Fealy and colleagues63 have described followup results of patients undergoing a mini-open repair using
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double-row fixation—horizontal mattress stitch medially and a modified Mason-Allen stitch with anchor or bone tunnel laterally. The patients had 10 small (smaller than 1 cm), 35 medium (1 to 3 cm), and 30 large (3 to 5 cm) rotator cuff tears. Although this study did not address re-creation of the footprint, it was reported that 83% of patients returned to their preinjury level of activity.
Comparison Of Arthroscopic and Mini-Open Repair Results The reported results of studies using the mini-open technique are similar to those reported using an all-arthroscopic technique.31,64-70 Tears grouped according to size and compared with a mini-open technique and an allarthroscopic technique were found to have no difference in UCLA or ASES scores for tears of similar size. Kim and associates65 have reported that at 2 to 6 years of follow-up, results of mini-open and all-arthroscopic techniques are similar with respect to pain relief, improved function, and improved active ROM. It is important to point out that they attempted to perform all these procedures arthroscopically and used the mini-open technique as a bail-out procedure. As such, there is a selection bias in the cohort. In a long-term follow-up study, Weber71 has reported the outcomes of almost 300 patients who underwent a mini-open or an all-arthroscopic rotator cuff repair. The follow-up was approximately 6 years. Final outcomes, as measured by ASES, UCLA, and simple shoulder test scores, were not statistically different between the two groups. However, the mini-open group had several complications; two frozen shoulders required manipulation and three failed rotator cuff repairs required revision surgery. Buess and coworkers72 have also reported improved results with an arthroscopic technique over the open repair with respect to pain relief, functional mobility, and satisfaction. Two thirds of the procedures were performed using the mini-open technique. Despite good clinical outcomes, two studies73,74 have subsequently re-imaged or surgically evaluated the cuff and found a significant incidence of incomplete healing. Specifically, it appears that larger tears are more prone to re-tears or nonhealing. The figures cited, with all cuff tear sizes included, are no different among the all-arthroscopic, mini-open, and open repairs. Using an all-arthroscopic single-row rotator cuff repair technique, Boileau and colleagues75 have reported an incidence of 71% (46 of 65 shoulders) healed cuffs, as determined by computed tomography (CT) arthrography and magnetic resonance imaging (MRI). Liu and associates76 have reported a 66% overall intact rate as determined by arthrography following a mini-open repair. Similarly, Harryman and coworkers77 have reported that 65% of rotator cuff repairs remain intact, as determined by ultrasound following open reconstruction. Again, Gerber
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and associates78 have found 66% of their cuffs to be intact by MRI after open reconstruction for massive tears. Klepps and coworkers74 have prospectively evaluated postoperative rotator cuff integrity in patients undergoing open and mini-open rotator cuff repairs. As determined by MRI 1 year postoperatively, they found an overall re-tear rate of 31% (i.e., 69% of cuffs remained intact). There was no difference in age between those with an intact cuff and those with a re-torn cuff postoperatively in this study. However, those cuffs that became torn again tended to have larger initial tears (3.4 versus 2.4 cm), but the difference was not statistically significant (P ⫽ .10). Patients with small or medium tears (smaller than 3 cm) had a re-tear rate of 26%, whereas patients with large or massive tears (larger than 3 cm) had a re-tear rate of 38%, but this difference was not statistically different. Those whose repairs had failed still had a significant improvement in all areas assessed, regardless of the lack of structural integrity of the cuff. Although there was a statistically significant improvement in functional outcome measures comparing preoperative and postoperative function, as indicated by ASES, UCLA, and Constant-Murley scores, the difference between those with intact cuffs versus those with re-tears was not significant. In addition, although there was a statistically significant improvement in strength with forward flexion and external rotation—preoperative versus postoperative strength—the difference between those patients with intact cuffs versus those with re-tears was not significant in this study. Bishop and colleagues79 have corroborated the findings of the report by Klepps and associates.74 They found a similar incidence of cuff re-tears and similar results of statistically significant improvement in strength postoperatively in the patients undergoing arthroscopic rotator cuff repair. They compared patients with open rotator cuff repairs with those treated arthroscopically. Overall, 69% of the open repairs were intact by MRI at 1 year versus 53% of those fixed arthroscopically, but the difference was not statistically significant. These results were stratified by the size of the cuff tear. In tears smaller than 3 cm, 74% were intact in the open repairs and 84% in the arthroscopic group. In tears larger than 3 cm, 62% were intact in the open repairs and 24% in the arthroscopic group (this difference was not significant, but the exact figure was not reported). The patients with arthroscopic cuff repairs that remained intact at 1 year had significantly greater strength (P ⬍ .02) in forward flexion and external rotation in comparison with those with re-tears or failure of the cuff to heal at 1 year. Boileau and associates75 have reported that the improvement in strength is significantly higher than preoperative values when comparing patients with healed cuffs with those with unhealed cuffs (P ⫽ .01). Additionally, they identified several factors associated with a decreased healing rate. Patients younger than 65 years had a significantly improved rate of healing (P ⬍ .001); patients older than
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65 years had a 43% incidence of tendon healing. Tears extending into the infraspinatus or subscapularis had a much lower incidence of healing (P ⫽ .02). Interestingly, it was noted that as long as the tear is not retracted beyond the glenoid rim, the size of the tear from medial to lateral is not significant (P ⫽ .07). However, no association was shown among tendon healing and duration of symptoms, gender, or prior steroid injections. In contrast, Lam and coworkers80 have reported that with traditional open repairs, duration of symptoms beyond 34 months (P ⬍ .01), female gender (P ⬍ .05), and a high-anesthesia American Society of Anesthesiologists (ASA) grade is associated with a lower Constant-Murley score (P ⬍ 005).
SUMMARY Mini-open rotator cuff repair is a well-accepted technique, leading to successful results. The arthroscopic portion of the procedure entails a diagnostic arthroscopy, decompression, and tissue mobilization. Goals of the rotator cuff repair include minimizing tension on the repair, maximizing the strength of fixation, re-creating the tendon footprint, and instituting an efficacious rehabilitation protocol.
References 1. Codman E: Complete rupture of the supraspinatus tendon: Operative treatment with report of two successful cases. Boston Med Surg J 164:708-710, 1911. 2. Yamaguchi K: Transitioning to arthroscopic rotator cuff repair: The pros and cons. Instr Course Lect 52:81-92, 2003. 3. Bigliani LU, Cordasco FA, McIlveen SJ, Musso ES: Operative treatment of failed repairs of the rotator cuff. J Bone Joint Surg Am 74:1505-1515, 1992. 4. DeOrio JK, Cofield RH; Results of a second attempt at surgical repair of a failed initial rotator cuff repair. J Bone Joint Surg Am 66:563-567, 1984. 5. Neer CS 2nd, Marberry TA; On the disadvantages of radical acromionectomy. J Bone Joint Surg Am 63:416-419, 1981. 6. Neviaser R: Ruptures of the rotator cuff. Orthop Clin North Am 18:433-438, 1987. 7. Hata Y, Saitoh S, Murakami N, et al: Atrophy of the deltoid muscle following rotator cuff surgery. J Bone Joint Surg Am 86:1414-1419, 2004. 8. Miller C, Savoie FH: Glenohumeral abnormalities associated with full-thickness tears of the rotator cuff. Orthop Rev 23:159-162, 1994. 9. Gartsman GM, Khan M, Hammerman SM: Arthroscopic repair of full-thickness tears of the rotator cuff. J Bone Joint Surg Am 80:832-840, 1998. 10. Carpenter JE, Fish DN, Huston LJ, Goldstein SA: Pull-out strength of five suture anchors. Arthroscopy 9:109-113, 1993. 11. Barber FA, Cawley P, Prudich JF: Suture anchor failure strength—an in vivo study. Arthroscopy 9:647-652, 1993. 12. Hecker AT, Shea M, Hayhurst JO, et al: Pull-out strength of suture anchors for rotator cuff and Bankart lesion repairs. Am J Sports Med 21:874-879, 1993.
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13. Reed SC, Glossop N, Ogilvie-Harris DJ: Full-thickness rotator cuff tears: A biomechanical comparison of suture versus bone anchor techniques. Am J Sports Med 24:46-48, 1996. 14. Burkhart SS, Diaz Pagàn JL, Wirth MA, Athanasiou KA: Cyclic loading of anchor-based rotator cuff repairs: Confirmation of the tension overload phenomenon and comparison of suture anchor fixation with transosseous fixation. Arthroscopy 13:720-724, 1997. 15. Tingart MJ, Apreleva M, Lehtinen J, et al: Anchor design and bone mineral density affect the pull-out strength of suture anchors in rotator cuff repair: Which anchors are best to use in patients with low bone quality? Am J Sports Med 32:1466-1473, 2004. 16. Bynum CK, Lee S, Mahar A, et al: Failure mode of suture anchors as a function of insertion depth. Am J Sports Med 33:1030-1034, 2005. 17. Chhabra A, Goradia VK, Francke EI: In vitro analysis of rotator cuff repairs: A comparison of arthroscopically inserted tacks or anchors with open transosseous repairs. Arthroscopy 21:323-327, 2005. 18. Gerber C, Schneeberger AG, Beck M, Schlegel U: Mechanical strength of repairs of the rotator cuff. J Bone Joint Surg Br 76:371-380, 1994. 19. Gerber C, Schneeberger AG, Perren SM, Nyffeler RW: Experimental rotator cuff repair: A preliminary study. J Bone Joint Surg Am 81:1281-1290, 1999. 20. Scheibel MT, Habermeyer P: A modified Mason-Allen technique for rotator cuff repair using suture anchors. Arthroscopy 19:330-333, 2003. 21. MacGillivray, J, Ma CB: An arthroscopic stitch for massive rotator cuff tears: The Mac stitch. Arthroscopy 20:669-671, 2004. 22. Ma CB, MacGillivray JD, Clabeaux J, et al: Biomechanical evaluation of arthroscopic rotator cuff stitches. J Bone Joint Surg Am 86:1211-1216, 2004. 23. De Carli A, Vadalà A, Monaco E, et al: Effect of cyclic loading on new polyblend suture coupled with different anchors. Am J Sports Med 33:214-219, 2005. 24. Burkhart SS, Fischer SP, Nottage WM, et al: Tissue fixation security in transosseous rotator cuff repairs: A mechanical comparison of simple versus mattress sutures. Arthroscopy 12:704-708, 1996. 25. Burkhart S, Johnson TC, Wirth MA, Athanasiou KA: Cyclic loading of transosseous rotator cuff repairs: Tension overload as a possible cause of failure. Arthroscopy 13:172-176, 1997. 26. Apreleva, M, Ozbaydar M, Fitzgibbons PG, Warner JJ: Rotator cuff tears: The effect of the reconstruction method on threedimensional repair site area. Arthroscopy 18:519-526, 2002. 27. Park MC, Cadet ER, Levine WN, et al: Tendon-to-bone pressure distribution at a repaired rotator cuff footprint using transossesous suture and suture anchor fixation techniques. Am J Sports Med 33:1154-1159, 2005. 28. Mazzocca AD, Millett PJ, Guanche CA, et al: Arthroscopic single-row versus double-row suture anchor rotator cuff repair. Am J Sports Med 33:1861-1868, 2005. 29. Kim DH, Elattrache NS, Tibone JE, et al: Biomechanical comparison of a single-row versus double-row suture anchor technique for rotator cuff repair. Am J Sports Med 34:407-414, 2006. 30. Williams G, Iannotti J, Luchetti W: Mini versus open repair of isolated supraspinatus tears. J Shoulder Elbow Surg 7:310, 1998.
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31. Nottage WM: A comparison of all-arthroscopic versus miniopen rotator cuff repair: Results at 45 months. Presented at the 2001 Annual Meeting of the American Academy of Orthopaedic Surgeons, San Francisco, February 2001. 32. Yamaguchi K, Ball CM, Galatz LM: Arthroscopic rotator cuff repair: Transitioning from mini-open to all-arthroscopic. Clin Orthop Relat Res 390:83-94, 2001. 33. Nicholson G: Mini-open rotator cuff repair for supraspinatus tears. Presented at the Second Biennial Shoulder and Elbow Meeting, Miami, May 2000. 34. Chen AL, Shapiro JA, Ahn AK, et al: Rotator cuff repair in patients with type 1 diabetes mellitus. J Shoulder Elbow Surg 12:416-421, 2003. 35. Weber S: Comparison of all-arthroscopic and mini-open rotator cuff repairs. Presented at the 2001 Annual Meeting of the Arthroscopy Association of North America, Seattle, February 2001. 36. Severud E, Ruotolo C, Abbott DD, Nottage WM: Allarthroscopic versus mini-open rotator cuff repair: a long term retrospective outcome comparison. Arthroscopy 19:234-238, 2003. 37. Herrera MF, Bauer G, Reynolds F, et al: Infection after miniopen rotator cuff repair. J Shoulder Elbow Surg 11:605-608, 2002. 38. Settecerri JJ, Pitner MA, Rock MG, et al: Infection after rotator cuff repair. J Shoulder Elbow Surg 8:1-5, 1999. 39. Izquierdo R, Bigliani LU: Arthroscopic acromioplasty: History, rationale, and technique. Instr Course Lect 53:13-20, 2004. 40. Snyder SJ: Evaluation and treatment of the rotator cuff. Orthop Clin North Am 24:173-192, 1993. 41. Klein JR, Burkhart SS: Identification of essential anatomic landmarks in performing arthroscopic single- and doubleinterval slides. Arthroscopy 20:765-70, 2004. 42. Warner JJ, Higgins L, Parsons IM 4th, Dowdy P: Diagnosis and treatment of anterosuperior rotator cuff tears. J Shoulder Elbow Surg 10:37-46, 2001. 43. Lo IK, Burkhart SS: Spotlight on surgical techniques. Current concepts in arthroscopic rotator cuff repair. Am J Sports Med 31:308-324, 2003. 44. Clark JM, Harryman DT 2nd: Tendons, ligaments, and capsule of the rotator cuff. Gross and microscopic anatomy. J Bone Joint Surg Am 74:713-725, 1992. 45. Hersch JC, Sgaglione NA: Arthroscopically assisted miniopen rotator cuff repairs. Functional outcome at 2- to 7-year follow-up. Am J Sports Med 28:301-311, 2000. 46. Tingart MJ, Apreleva M, Zurakowski D, Warner JJ: Pull-out strength of suture anchors used in rotator cuff repairs. J Bone Joint Surg Am 85:2190-2198, 2003. 47. Barber, FA, Herbert MA: Suture anchors: Update 1999. Arthroscopy 15:719-725. 1999. 48. Barber, FA, Herbert MA, Click JN: Internal fixation strength of suture anchors: Update 1997. Arthroscopy 13:355-362. 1997. 49. Böstman OM, Pihlajamäki HK: Adverse tissue reactions to bioabsorbable fixation devices. Clin Orthop Relat Res (371):216-227. 2000. 50. Glueck D, Wilson TC, Johnson DL: Extensive osteolysis after rotator cuff repair with a bioabsorbable suture anchor. Am J Sports Med 33:742-744, 2005. 51. Caldwell GL, Warner JP, Miller MD, et al: Strength of fixation with transosseous sutures in rotator cuff repair. J Bone Joint Surg Am 79:1064-1069, 1997.
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52. Gerber C, Schneeberger AG, Beck M, Schlegel U: Mechanical strength of repairs of the rotator cuff. J Bone Joint Surg Br 76:371-380, 1994. 53. Singh H, Osbahr DC, Holovacs TF, et al: The efficacy of continuous cryotherapy on the postoperative shoulder: A prospective, randomized investigation. J Shoulder Elbow Surg 10:522-525, 2001. 54. Cohen DB, Kawamura S, Ehteshami JR, Rodeo SA: Indomethacin and celecoxib impair rotator cuff tendon to bone healing. Am J Sports Med 34:362-369, 2006. 55. Levy HJ, Uribe JW, Delaney LG: Arthroscopic assisted rotator cuff repair: Preliminary results. Arthroscopy 6:55-60, 1990. 56. Paulos LE, Kody MH: Arthroscopically enhanced “miniapproach” to rotator cuff repair. Am J Sports Med 22:19-25, 1994. 57. Liu SH: Arthroscopically-assisted rotator cuff repair. J Bone Joint Surg Br 76:592-595, 1994. 58. Blevins FT, Warren RF, Cavo C, et al: Arthroscopic assisted rotator cuff repair: Results using a mini-open deltoid splitting approach. Arthroscopy 12:50-59, 1996. 59. Weber SC: Arthroscopic debridement and acromioplasty versus mini-open repair in the treatment of significant partial-thickness rotator cuff tears. Arthroscopy 15:126-131, 1999. 60. Park JY, Levine WN, Marra G, et al: Portal-extension approach for the repair of small and medium rotator cuff tears. Am J Sports Med 28:312-316, 2000. 61. Posada A, Uribe JW, Hechtman KS, et al: Mini-deltoid splitting rotator cuff repair: Do results deteriorate with time? Arthroscopy 16:137-141, 2000. 62. Shinners TJ, Noordsij PG, Orwin JF: Arthroscopically assisted mini-open rotator cuff repair. Arthroscopy 18:21-26, 2002. 63. Fealy S, Kingham TP, Altchek DW: Mini-open rotator cuff repair using a two-row fixation technique: Outcomes analysis in patients with small, moderate, and large rotator cuff tears. Arthroscopy 18:665-670, 2002. 64. Warner JJ, Tétreault P, Lehtinen J, Zurakowski D: Arthroscopic versus mini-open rotator cuff repair: A cohort comparison study. Arthroscopy 21:328-332, 2005. 65. Kim SH, Ha KI, Park JH, et al: Arthroscopic versus mini-open salvage repair of the rotator cuff tear: Outcome analysis at 2 to 6 years’ follow-up. Arthroscopy 19:746-754, 2003. 66. Gartsman GM, Khan M, Hammerman SM: Arthroscopic repair of full-thickness tears of the rotator cuff. J Bone Joint Surg Am 80:832-840, 1998. 67. Burkhart SS: Arthroscopic repair of massive rotator cuff tears: Concept of margin convergence. Tech Shoulder Elbow Surg 1:232-239, 2000. 68. Hoffmann F, Schiller M, Reif G: Arthroscopic rotator cuff reconstruction. Orthopade 29:888-894, 2000. 69. Tauro JC: Arthroscopic rotator cuff repair: Analysis of technique and results at 2- and 3-year follow-up. Arthroscopy 14:45-51, 1998. 70. Stollsteimer GT, Savoie FH 3rd: Arthroscopic rotator cuff repair: Current indications, limitations, techniques, and results. Instr Course Lect 47:59-65, 1998. 71. Weber SS: All-arthroscopic versus mini-open rotator cuff repair: Long-term follow-up. Presented at the 2005 American Academy of Orthopaedic Surgeons Conference, Washington DC, February 2005. 72. Buess E, Steuber KU, Waibl B: Open versus arthroscopic rotator cuff repair: A comparative view of 96 cases. Arthroscopy 21:597-604, 2005.
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73. Galatz LM, Ball CM, Teefey S, et al: Complete Arthroscopic Repair of Large and Massive Rotator Cuff Tears: Correlation of Functional Outcome with Repair Integrity. Presented at the 2002 Annual Meeting of the American Academy of Orthopaedic Surgeons, Dallas, February 2002. 74. Klepps S, Bishop J, Lin J, et al: Prospective evaluation of the effect of rotator cuff integrity on the outcome of open rotator cuff repairs. Am J Sports Med 32:1716-1722, 2004. 75. Boileau P, Brassart N, Watkinson DJ, et al: Arthroscopic repair of full-thickness tears of the supraspinatus: Does the tendon really heal? J Bone Joint Surg Am 87:1229-1240, 2005. 76. Liu SH, Baker CL: Arthroscopically assisted rotator cuff repair: Correlation of functional results with integrity of the cuff. Arthroscopy 10:54-60, 1994.
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77. Harryman DT 2nd, Mack LA, Wang KY, et al: Repairs of the rotator cuff: Correlation of functional results with integrity of the cuff. J Bone Joint Surg Am 73:982-989, 1991. 78. Gerber C, Fuchs B, Hodler J: The results of repair of massive tears of the rotator cuff. J Bone Joint Surg Am 82:505-515, 2000. 79. Bishop J: Cuff integrity following arthroscopic versus open rotator cuff repair: A prospective study. Presented at the 2004 Annual Meeting of the Arthroscopy Association of North America, Palm Springs, Fall 2004. 80. Lam F, Mok D: Open repair of massive rotator cuff tears in patients aged sixty-five years and over: Is it worthwhile? J Shoulder Elbow Surg 13:517-521, 2004.
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CHAPTER 16 Arthroscopic Rotator Cuff Repair Ammar Anbari, Nikhil N. Verma, Brian S. Cohen, and Anthony A. Romeo
With recent advances in shoulder arthroscopy, techniques for performing a successful rotator cuff repair have evolved from full open procedures to arthroscopically assisted miniopen techniques and, more recently, to all-arthroscopic techniques. Advantages of all-arthroscopic techniques include preservation of the deltoid attachment, less postoperative pain, and decreased postoperative morbidity, with earlier return of motion. However, arthroscopic repair is a technically demanding procedure that requires special instrumentation and techniques to achieve successful outcomes.
Massive, Contracted, and Immobile Tears. This pattern is more commonly seen in older patients and is exceedingly rare in young athletes. It occurs when the tendon retracts significantly. Its mobilization is impossible without performing soft tissue releases anteriorly or posteriorly, or both. Millstein and Snyder2 have introduced the SCOI (Southern California Orthopaedic Institute) rotator cuff classification. It is a descriptive classification that uses letters and numbers to describe the pathologic condition of the cuff tendon. This type of classification may be more useful for athletes because it takes into account partial tears. The location of the tear is termed A for articular-sided tears, B for bursalsided tears, and C for complete tears. For partial-thickness tears, the degree of tendon damage is given a grade between 0 and 4. Grade 0 refers to a normal cuff, with smooth covering of the synovium and bursa. Grade 1 refers to a small tear (smaller than 1 cm), with superficial bursal or synovial irritation. Grade 2 is usually smaller than 2 cm and involves actual fraying and failure of some rotator cuff fibers. Grade 3 is smaller than 3 cm, including fraying and fragmentation of tendon fibers. Grade 4 is the most severe partial cuff tear and includes a flap tear, which encompasses more than one tendon.
CLASSIFICATION With the advancement of arthroscopic techniques for rotator cuff repair has come a better understanding of tear patterns, because of the ability to visualize the tear from a number of different directions and angles. This improved visualization has led to improved classification of tear patterns (Fig. 16-1). Recognition of tear patterns is an important first step to achieving an anatomic tension-free repair. Rotator cuff tears can be classified by tear pattern, tear size, and tear location. Lo and Burkhart1 have described four main types of tears. Crescent-Shaped Tears. These tears are the simplest to repair and recognize. Tears can be large but demonstrate minimal medial retraction. Therefore, the tears can be easily mobilized laterally and secured to the greater tuberosity without excessive tension.
Complete, or C, tears are full-thickness tears and are also classified into four categories. Grade C1 is a small complete tear, such as a puncture tear. Grade C2 is a complete tear smaller than 2 cm and involving one tendon with no retraction. Grade C3 is a large complete tear involving the entire tendon and measuring 3 to 4 cm. Minimal retraction may be seen. Grade C4 is a massive rotator cuff tear, which can involve more than one tendon and is usually retracted.
U-Shaped Tears. These tears resemble crescent-shaped tears but with significant medial retraction, often to the level of the glenoid rim. Therefore, the tendon cannot be simply pulled laterally to the greater tuberosity because it will place a significant amount of tension on the repair. Special techniques such as margin convergence can be used to help mobilize these tears before repair.
Although no single classification system is universally adopted, we use a simple classification based on tendon involvement and the amount of retraction. Type I is a single-tendon tear, type II is a two-tendon tear, and type III is a three-tendon tear. Type A is a minimally displaced tendon tear. Type B is a tendon tear retracted to the humerus. Type C is a tear retracted to the glenoid. In addition, it is important to inspect the magnetic resonance imaging (MRI) scan closely to determine the degree of muscle wasting and fatty infiltration. These factors play a paramount role in predicting the outcome of a cuff repair.
L-Shaped and Reverse L-Shaped Tears. These tears initially resemble U-shaped tears. We think that U-shaped tears are L-shaped until proved otherwise. The tears involve a tendon tear from bone, with an additional longitudinal split posteriorly or, more commonly, anteriorly, resulting in the posterior leaflet retracting posteriorly and medially. Care must be taken to reduce the corners of these tears anatomically. 177
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IS
IS
SS SS
A A IS A'
RI Sub CHL
SS
IS
RI Sub
IS
RI Sub CHL
CHL SS
SS
B
RI
RI Sub IS
Sub IS
CHL SS
CHL SS
RI Sub
RI Sub IS SS
CHL
IS
CHL
SS
C Figure 16-1. Tear classification and repair strategies. These include the crescent-shaped tear (A), U-shaped tear (B), and L-shaped tear (C).
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BIOMECHANICS Several factors play a role in the success or failure of an arthroscopic rotator cuff repair. These factors include the tear pattern and size, anchor placement, suture used, and knots placed to secure the repair.
Tear Pattern and Size The larger the tear, and the more retracted it is, the less likely full function will be restored to the patient. Simple crescent and minimally retracted U-shaped tears have more successful results than larger L-shaped and massively retracted tears. We believe strongly that correct pattern identification and anatomic repair are critical to minimize stress on the repair and maximize the chance of tendon healing and functional outcome.
Anchor Placement Suture anchors are the primary choice of fixation in arthroscopic repairs. When compared with bone tunnels, suture anchors behave favorably in rotator cuff repairs. Under cyclic loading, transosseous tunnels fail at low cycles by cutting of the suture through bone. In contrast, suture anchors fail by cutting of sutures through the tendon. These failures occur at higher cycles than transosseous tunnels.3 To maximize pull-out strength, the suture anchors should be placed at a 45-degree angle to the bone, also known as dead man’s angle (Fig. 16-2).4
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Suture Type Nonabsorbable sutures are currently used for the arthroscopic treatment of rotator cuff tears. Sutures made with no. 2 Ethibond (Ethicon, Johnson & Johnson, Norwood, Mass) are strong enough for maximum physiologic loading conditions. Recently, stronger suture material such as FiberWire (Arthrex, Naples, Fla) has been introduced and incorporated into suture anchors. These no. 2 sutures are equivalent in strength to no. 5 Ethibond sutures and result in easier knot tying with less chance of suture breakage. A number of stitch configurations have been described in arthroscopic repair techniques. Most commonly, simple or mattress sutures are used. In a biomechanical comparison, Burkhart and colleagues5 have concluded that simple sutures have a 39.7% greater ultimate load compared with mattress sutures. Recently, there has been increased interest in a doublerow repair technique to improve healing rates associated with rotator cuff repair. Studies have demonstrated that double-row fixation results in an increased area of contact between the repair footprint and the greater tuberosity.5 Furthermore, biomechanical data in a cadaveric model have demonstrated that double-row fixation results in increased ultimate failure strength and decreased gap formation with cyclic loading. However, limited clinical data are available. Although increased fixation strength would seem likely to improve healing rates, it does not change the biologic issues related to poor vascularity and tissue quality. Therefore, further clinical studies are necessary to justify the increased complexity and cost associated with double-row repairs.
Knot Placement Arthroscopic knot placement has been the subject of debate for years. There are two general types of knots, sliding and nonsliding. Sliding knots such as the Duncan loop, Tennessee slider, and Revo knot require the suture to slide through the soft tissue and the anchor itself. Alternatively, nonsliding knots or half-hitch knots do not require the suture to move through the tissue or the anchor.
Figure 16-2. Anchor insertion. The anchor is inserted at a dead man’s angle with regard to the greater tuberosity to minimize the risk of anchor pull-out.
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Two factors play a role in the placement of a knot: loop security and knot security. Loop security is the ability to keep a suture loop tight while the knot is tied. Knot security refers to the effectiveness of the knot in resisting slippage when a load is applied. In a biomechanical study aimed at comparing the different sliding and nonsliding knots, Lo and associates6 have concluded that a static nonsliding knot provides the best balance of loop security and knot security. This knot is performed by placing two half-hitches in the same direction on the same post followed by three alternating half-hitches on alternating posts. If a sliding knot is chosen, it is recommended that three alternating half-hitches be placed behind it to
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improve its knot security. Moreover, the knots placed with a no. 2 FiberWire have a better knot security compared with the same knot placed with a no. 2 Ethibond suture. Therefore, for most of our applications, we use a nonsliding knot using no. 2 FiberWire.
SURGICAL INDICATIONS AND CONTRAINDICATIONS The indications for arthroscopic rotator cuff repair are similar to those established for open and mini-open repairs. The primary indications for a repair are pain followed by weakness and poor function, with a failure of conservative management. However, in young patients and athletes with symptomatic full-thickness tears, we do not believe that there is a significant role for nonoperative management. In these cases, we believe that re-establishing tendon continuity is paramount for maximizing strength and function. Furthermore, as tears become more chronic, associated muscle changes such as atrophy and fatty infiltration, as well as tear progression, may occur and lead to compromised outcomes, with subsequent surgery. Absolute contraindications include acute or chronic infections and significant medical illnesses precluding anesthesia. Relative contraindications include advanced glenohumeral arthritis or significant retraction and fatty infiltration of the tendon, along with a fixed superior migration of the humeral head.
PREOPERATIVE CONSIDERATIONS A combination of interscalene block and general anesthesia is ideal for most patients. Advantages of regional anesthesia include decreased perioperative pain and nausea. Successful results with regional anesthesia alone have been reported, although our preference is to combine it with a general anesthetic.
hypotension. In these cases, we advise lowering the back of the table down or placing the patient in a lateral decubitus position.
Patient Positioning and Draping Beach Chair Position This is our preferred position for all arthroscopic procedures with primarily subacromial pathology (Fig. 16-3). The beach chair position has a number of advantages. The anatomy is in a familiar position and is easy to reference the instruments with respect to the body and floor. This position also allows easy conversion to an open procedure. Draping The patient is aligned on the edge of the table so that the affected shoulder and scapula are exposed. We place two folded towels on the medial edge of the scapula to retract it further laterally. The back of the table is elevated completely to position the acromion parallel to the floor. The head is secured to the operating table with tape or an optional head rest may be used if the table allows it. Care should be taken to prevent excessive flexion or extension in the neck.
Examination Under Anesthesia Examination under anesthesia should be performed in all cases and is of particular importance in the athlete in whom coexisting conditions such as instability may be present. The shoulder is checked to verify normal range of motion and exclude significant stiffness or internal rotation deficit. Stability testing should be performed in anterior, posterior, and inferior directions.
Portal Placement Consistent portal placement can help surgeons achieve reproducible results (Fig. 16-4). We begin every case by outlining the bony landmarks on the skin with a marking
Maintenance of a mean arterial pressure of 70 to 90 mm Hg or a systolic pressure near 100 mm Hg allows maximal visualization and minimizes bleeding in the subacromial space. We have also used epinephrine in the arthroscopic solution to help control bleeding and maximize visualization. Obesity is a factor in both placing the portals in the correct position and in controlling blood pressure. Most surgeons tend to place portals laterally in obese patients because it may be difficult to palpate the bony landmarks. In such cases, it is advisable to use an 18-gauge spinal needle to verify the accuracy of the portals before making incisions. Moreover, an obese patient placed in the beach chair position may run the risk of developing superior vena cava compression, leading to decreased venous return to the heart and uncontrollable
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Figure 16-3. Patient positioning. The patient is placed in a beach chair position for arthroscopic rotator cuff repair.
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long head of the biceps. Although this portal can be easily established with an outside-in technique using a spinal needle, we prefer to establish it through an inside-out technique. This involves driving the arthroscope anteriorly toward the triangle and gently pushing against the anterior capsule. The arthroscope is removed and a Wissinger rod is pushed through the scope cannula to create a puncture hole in the rotator interval. The skin is tented anteriorly and a no. 11 knife blade is used to create the skin incision. Ideally, the location of the portal is just lateral to the tip of the coracoid. The rod is pushed through the skin incision and a clear cannula is placed over the rod into the joint. The Wissinger rod is withdrawn and the arthroscope is reintroduced.
Figure 16-4. Surgical landmarks placed on skin. Standard portals include posterior, direct lateral, accessory anterolateral, and anteriorsuperior portals.
pen. Some bony landmarks should be palpable in most patients. The posterior and anterior corners of the acromion, as well as the soft spot between the posterior clavicle and anterior scapular spine, should be marked first. A line is drawn between the two corners of the acromion. The anterior and posterior edges of the clavicle are marked next, along with the scapular spine. The acromioclavicular (AC) joint is palpated and marked. Finally, a circle is drawn over the prominence of the coracoid.
Lateral Portal This is the viewing portal for arthroscopic cuff repairs and for the second stage of a subacromial decompression. It is only used for subacromial work. The ideal location of this portal is in the midaspect of the acromion. This portal is established by palpating the soft interval between the posterior edge of the clavicle and anterior edge of the scapular spine. A line is drawn from this point laterally past the acromial edge by 2 to 3 cm. A spinal needle is used to verify the appropriateness of the portal before making a skin incision. Accessory Superolateral Portal This portal is used for placement of suture anchors and for tying knots and suture shuttling. It is placed just lateral to the anterior corner of the acromial edge. A spinal needle is used to localize the portal (Fig. 16-5). It is important that this portal allow for the appropriate dead man’s angle for suture anchor placement within the greater tuberosity.
Posterior Portal This is the first portal to be created in most arthroscopic cases. Although precise measurements have been described to locate the posterior portal, we recommend relying on palpation of the landmarks instead. Using the Romeo three-finger shuck, the index finger of the same hand as the shoulder being operated on is placed in the soft spot between the clavicle and scapular spine. The middle finger is placed on the coracoid, and the thumb feels the interval between the infraspinatus and teres minor. This helps the surgeon find the best and softest location of the posterior portal. If the posterior portal is to be used primarily as a viewing portal, using direct suture-passing methods from the lateral portal, the surgeon may choose to place this portal superiorly and laterally to allow improved visualization during cuff repair. Anterior Portal The anterior portal is generally placed in the triangular space in the rotator interval formed by the humeral head, subscapularis muscle, and intra-articular portion of the
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Figure 16-5. Proper positioning for anchor placement. A spinal needle is used to localize the current position for placement of the superolateral accessory portal to allow the proper position for anchor placement.
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SURGICAL TECHNIQUES Diagnostic Arthroscopy In all cases, diagnostic glenohumeral arthroscopy is initially performed, and any intra-articular pathology is addressed. The rotator cuff can then be visualized to confirm the presence of a full-thickness tear and to provide an initial estimation of the size and configuration of the tear.
Subacromial Inspection and Decompression Once the glenohumeral inspection is complete, the arthroscope is placed in the subacromial space. This is achieved by angling the trocar superiorly until it passes just under the posterior acromion. The trocar is then angled anteriorly and laterally to enter the subacromial bursa. The arthroscope is reintroduced to verify the location of the trocar. A “room with a view” is achieved when the arthroscope is inside the bursal sac. If the view is not seen, the arthroscope may be too anterior or medial, and this procedure should be repeated if necessary.
adequate visualization of the posterior tear margins. At this point, a standard arthroscopic acromioplasty is completed using the cutting block technique.
Preparation of Tuberosity Insertion Site To enhance healing of the torn tendon to the bone insertion site, the bone should be prepared with gentle débridement to achieve a bleeding bony surface (Fig. 16-6). This can be accomplished while viewing through the posterior portal, using a burr or bone-resecting shaver through the lateral portal. Bone preparation should begin just off the articular margin and proceed laterally to re-create the normal 10- to 15-mm footprint for rotator cuff insertion. Care must be taken to avoid decortication because this could compromise fixation strength of the suture anchors.
Determination of Tear Configuration and Repair
Working from the lateral portal, a thorough débridement of bursal tissue is performed using a standard 5.0-mm shaver to allow visualization of the tear. Care must be taken to débride all bursal tissue thoroughly anteriorly, posteriorly, and within the lateral gutter, because soft tissue remnants may swell during the remainder of the procedure and can impede visualization.
At this point, the arthroscope is placed into the lateral portal to allow direct visualization of the tear and determine tear configuration. Accurate identification of tear patterns is extremely important to achieve anatomic repair of the rotator cuff. Anatomic repair minimizes stress on the repair during the postoperative period and maximizes the chance of tendon healing. Finally, the technique used to repair each type of tear varies slightly, and accurate tear pattern recognition is imperative so that the most appropriate repair configuration can be selected.
Once débridement is completed from the lateral portal, we prefer to switch the arthroscope to the lateral portal. Next, working from the posterior portal using the shaver, care is taken to remove any remaining posterior bursa to allow
Crescenteric Tears For small single-tendon tears, the crescenteric pattern is most commonly encountered. This pattern represents detachment of the cuff from the tuberosity with minimal
A
B
Figure 16-6. Bone preparation. A, A high-speed burr or bone-cutting shaver is used to decorticate the tuberosity repair site lightly to create bleeding bone for tendon healing. Care must be taken to avoid significant bone resection, which could compromise anchor fixation. B, Completed bone bed can be checked for adequate bleeding by decreasing the pump pressure and visualizing an adequate bleeding bony surface.
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retraction (Fig. 16-7A). The tear is easily reduced to the greater tuberosity with little tension and can be directly repaired to bone. Repair of crescenteric tears begins with appropriate placement of the accessory anterolateral portal using spinal needle localization, as described earlier. Next, the first suture anchor is placed at the most posterior aspect of the tear. Suture anchor placement may be facilitated by humeral rotation and abduction. Anchors should be placed 5 to 10 mm lateral to the articular surface and should be separated by 5 to 8 mm. Anchors are sequentially placed in a posterior to anterior direction. Once the anchor has been placed, a penetrator is placed through the posterior portal (Fig. 16-8). The device is used to penetrate the cuff tissue a minimum of 5 mm medially to the tear edge. The penetrator is then used to grasp one limb of the posterior suture and pass it through the torn cuff and out of the posterior portal. This step is repeated
A
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for one limb of the second suture. The free ends of the sutures are then retrieved out through the posterior portal using a crochet hook. At this point, sutures can be stored on a hemostat and tied after all anchors are placed, or they can be tied immediately. The advantage of delaying suture tying until all sutures are passed is that the tendon remains mobile, which allows easier passage of subsequent sutures. However, multiple sutures in the space can cause confusion and difficulties with suture tangling. At this point, additional anchors are placed anteriorly as needed, and sutures are passed using a similar technique. However, the most anterior portion of the tear is usually not reachable using a penetrator from the posterior portal. In this case, a curved spectrum from the posterior portal or a straight spectrum from the anterior portal can be used (Fig. 16-9). When shuttling sutures using a spectrum-type device, three of the four sutures from the anchor are brought out through the anterior or posterior portal, whichever one is not being used for the spectrum. Only one suture now
B
C Figure 16-7. Arthroscopic views from the lateral portal. A, Crescenteric-type tear. B, U-shaped tear. C, L-shaped rotator cuff tear.
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a complete repair that is stable throughout the normal range of motion (Fig. 16-10).
Figure 16-8. Suture penetrator-type device. This device can be used from the posterior portal to penetrate the torn tendon and retrieve one limb of the suture from the anchor.
remains in the accessory anterolateral portal. A curved spectrum through the posterior portal or straight spectrum through the anterior portal is then used to pierce the anterior portion of the torn cuff. A monofilament suture is then passed and retrieved out through the anterolateral portal. The monofilament suture is tied around the anchor suture and then used to shuttle the anchor suture through the torn cuff. This process is repeated for the second anchor suture. At this point, all sutures are tied, working from a posterior to anterior direction. The tear is then inspected and the arm taken through internal and external rotation to ensure
Figure 16-9. A curved spectrum from the posterior portal can be used to shuttle sutures through the anterior aspect of the tear. (Courtesy of ConMed Linvatec, Largo, Fla.)
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An alternate technique for suture passage involves direct suture-passing devices, such as the EXPRESSEW (DePuy Mitek, Raynham, Mass) or Scorpion (Arthrex, Naples, Fla). When using these devices, the scope is placed in the posterior or an accessory posterolateral portal for viewing because the lateral portal is required for suture management. A 6- or 8.25-mm cannula is placed in the direct lateral portal and suture anchors are placed percutaneously through an accessory superolateral portal. Using this technique, anchors are placed from anterior to posterior. After anchors are placed, the most medial and anterior limb of the first suture is brought out through the lateral portal and loaded into the suture passer. The tissue is then grasped and the suture directly passed using the device (Fig. 16-11). The suture is then brought out through the anterior portal using a grasper and the process is repeated for the second suture. Finally, the free limbs of the suture are transferred from the anterolateral portal to the anterior portal, where all four strands of suture from a single anchor are placed on a hemostat. When using this technique, suture tying must be delayed until all sutures are passed because tying sutures early impedes the ability to pass the device under the torn edge of the rotator cuff to pass subsequent sutures. Multiple anchors can be placed by repeating the same technique. Finally, sutures are tied in a posterior to anterior direction through the lateral portal to minimize suture tangling. U-Shaped Tears U-shaped tears occur as tears become larger and retract further medially (see Fig. 16-7B). The hallmark of a U-shaped tear is the inability to reduce these tears to
Figure 16-10. Completed repair of a crescenteric-type tear when viewed from the lateral portal.
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Side-to-side sutures can be placed using direct antegrade passing or a hand-off technique. In direct antegrade passing, a penetrator device is loaded with a suitable nonabsorbable suture. While viewing from the lateral portal, the penetrator is placed through the posterior portal and penetrates the posterior leaf of the tear, followed by the anterior leaf of the tear. A suture retriever is then used through the accessory anterolateral portal to retrieve the suture from the anterior leaf. The penetrator is removed and the suture retriever is again used from the anterolateral portal to retrieve the suture from the posterior leaf. The suture can then be tied from the anterolateral portal, reducing the anterior and posterior leaves of the tear. Additional sutures can be placed laterally as needed.
Figure 16-11. Direct suture-passing device used to pass a loop of suture in an antegrade fashion from the direct lateral portal. A grasper seen in the background is then used to retrieve the loop through the anterior portal.
the tuberosity without undue tension on the repair. Anterior to posterior mobility in these tears is commonly maintained. These tears are initially managed with a margin convergence technique using side-to-side sutures (Fig. 16-12). Placement of these sutures causes the free margin of the torn cuff to converge laterally toward the tuberosity insertion site, allowing eventual repair of the tendon to bone while minimizing tension on the repair site (Fig. 16-13).
Using the hand-off technique, the scope is again placed in the direct lateral portal. A penetrator is loaded with suture and placed through the posterior portal and then through the posterior leaf of the tear. A second free penetrator is then placed through the anterior portal and pierces the anterior leaf of the tear. The suture is handed off from the posterior to the anterior penetrator and brought out through the anterior portal. A suture retriever is used to retrieve the posterior and anterior ends of the suture out through the anterolateral portal, where it can be tied. Once all side-to-side sutures have been placed, the tear can be repaired primarily using the technique described for crescenteric tears. It may be helpful to place the sutures from the anchors medially to the side-to-side
Method 3 Method 2
3A
2A
Method 4 4A
2B
3B 4B
Method 1 1A C 1B D E
Figure 16-12. Diagrammatic representation of techniques used to place margin convergence sutures during repair of U-shaped tears.
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A
B
Figure 16-13. Repairing U-shaped tears. A, View from lateral portal of side-to-side suture placed through the anterior and posterior leaves of the tear. B, After tying, the anterior and posterior leaves are reduced and the tear edge is moved laterally.
sutures. This results in a Mac stitch configuration, which has been shown to improve strength at the suture-tissue interface.7 L-Shaped Tears L-shaped tears occur when the rotator cuff tears off the tuberosity with extension of the tear along the anterior rotator interval (see Fig. 16-7C). Less commonly, the tear may have an extension posteriorly in the interval between the supraspinatus and infraspinatus. Tears with anterior extension result in retraction of the torn tendon in a posterior and medial direction. The important step in repairing these tears is to reduce the corner of the tear initially, bringing it anteriorly and laterally so that the anterior and posterior leaves of the tear are aligned. Once this has been completed, the intertendinous split can be repaired in a side-to-side fashion, converting the tear into a crescenteric pattern, which can be repaired to the tuberosity as described earlier. As these tears become chronic, they assume a more U-shaped configuration. In these cases, it is important to identify the tears as an L-shaped pattern by identifying which leaf, anterior or posterior, is more mobile and easily reduced. The first step in the repair of these tears is to reduce the more mobile leaf of the tear to the opposite side, thus reducing the tendon and creating a crescenteric tear. This can be done by placing a suture anchor and reducing the corner of the tear, or by placing side-to-side sutures along the longitudinal split. Our preference is to place the initial anchor at the corner of the L portion of the tear to reduce the tendon anatomically. Once this anchor has been placed, we use penetrators through the anterior and posterior portals to place one limb of each suture through one
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leaf of the tear, and then the second limb through the opposite leaf of the tear. This creates a horizontal mattress to secure the tendon to bone and reduce the anterior and posterior leaves together. These sutures may be tied immediately, although this may complicate subsequent suture passage. If this is done, sutures or a stay stitch may be used for provisional reduction while the remaining sutures are passed to ensure that anchor sutures are passed through the appropriate location in the tendon. Next, additional side-to-side sutures are placed along the longitudinal split as necessary to complete this portion of the repair. Once completed, the tear now assumes a crescenteric pattern. Additional sutures anchors are then used in the greater tuberosity to complete the repair in standard fashion.
POSTOPERATIVE REHABILITATION In general, rehabilitation after arthroscopic rotator cuff repair can be divided into three phases focusing on restoration of passive motion, restoration of active motion and, finally, strengthening of the shoulder (Appendix 16-1). However, the rehabilitation program for a rotator cuff tear should not be a standard protocol, but should be customized based on factors such as patient age, tear size, tissue quality, and security of repair. Any concomitant procedures performed may also need to be considered. In the initial phase, restoration of passive motion and prevention of stiffness constitute the primary goals. Although it has been documented that early active range of motion will help restore normal shoulder kinematics, it is
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important to take the risk of compromising the surgical repair into consideration. The patient is maintained immobilized in a sling with a small abduction pillow for the initial 6 weeks. Passive motion is initiated after the first postoperative visit; this includes Codman’s exercises, external rotation at the side, and forward elevation in the scapular plane. These exercises should be performed with the patient supine, the arm at the side, and the elbow bent. This reduces the forces across the shoulder and decreases the effect of gravity by shortening the lever arm of the upper extremity.
between open and arthroscopic repairs of the rotator cuff is the amount of discomfort experienced early by the arthroscopic patients. Less pain early enables patients to tolerate their range-of-motion exercises more readily. However, it is important not to accelerate the rehabilitation of arthroscopic patients because of their comfort levels. In all cases, the biology of repair has to be given time to work.
Pain is one of the key elements in deterring the restoration of motion. Therefore, it is important to provide pain relief during the rehabilitation phase of treatment. This can include rest, medications, avoidance of painful movements, cryotherapy, ultrasound, and galvanic stimulation.8 Once the pain and discomfort are controlled, motion exercises can be initiated.
When evaluating the results of arthroscopic rotator cuff repairs, important factors include pain relief and clinically based scoring scales, recovery of objective strength measures, and radiographic evaluation of tendon healing. Although many studies have reported excellent clinical results, there are only limited data on objective tendon healing, which we think is the most important factor in predicting strength recovery. Finally, most series involve primarily older patients. We are not aware of any specific studies on the outcome of rotator cuff repair in competitive athletes.
At 6 weeks postoperatively, immobilization is discontinued and active range of motion is allowed. During this phase, the emphasis is on restoring symmetrical passive range of motion and progressing to normal active range of motion. Significant strengthening is avoided until 12 weeks postoperatively. Light rotator cuff, deltoid, and scapular isometrics can be initiated at 8 weeks postoperatively. Furthermore, it is important to initiate the strengthening of scapular stabilizers and other endurance exercises for the entire body early. With progressive recovery, more aggressive measures can be taken for strengthening the injured shoulder. At 12 weeks after surgery, we initiate aggressive strengthening of the shoulder, beginning with isometrics and progressing to Thera-Bands (Hygenic Corporation, Akron, Ohio), and finally light weights. Strength training should be restricted to three times weekly to minimize pain and aggravation of the repair site. Internal and external rotation exercises should be performed in the scapular plane because they put minimal stress on the joint capsule. The most functional open-chain exercises are plyometrics activities. They help the muscle recover its strength and power. The muscle is initially stretched eccentrically and then slowly loaded. Examples of plyometrics exercises include the use of Thera-Bands, medicine balls, and free weights. Sports-related rehabilitation is initiated at 5 months postoperatively. Throwing is delayed until 6 months postoperatively, with throwing from a mound delayed until about 9 months. We allow a return to contact sports at 9 months. Patients should expect maximal improvement to occur at about 12 months postoperatively. It is important to stress that the biology of repair of rotator cuff muscles is the same regardless of the method used (open versus arthroscopic). The most noticeable difference
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RESULTS AND OUTCOMES
Several studies have reported favorable clinical results after arthroscopic rotator cuff repairs. Bennett9 has reported the results of arthroscopic repairs of 24 small to medium-sized tears. Overall, 100% of patients were satisfied with their outcome and all had significant improvements in terms of pain relief and function. Burkhart and associates10 have reported the results of 59 rotator cuff tears repaired arthroscopically. The patients had 95% good to excellent results, and results were independent of the size of the tear and whether margin convergence sutures were used. Moreover, the delay from injury to surgery did not adversely affect surgical outcome. A large retrospective study by Wolf and coworkers11 has reviewed the results of 96 rotator cuff arthroscopic repairs after 4 to 10 years. Of the patients available for re-evaluation, 94% had good to excellent results using the UCLA shoulder rating scale. Gartsman and colleagues12 have followed 73 patients for a minimum of 2 years who were treated arthroscopically for full-thickness rotator cuff tears. Of their patients, 84% rated their results as good or excellent. Significant improvement was seen in range of motion, strength, and in the results of the SF-36 shortform health survey. These studies involved the general population. Because rotator cuff tears are rarely seen in younger athletes, few studies have focused on this population and the ability of those patients to return to their sporting activities. SonneryCottet and colleagues13 followed 51 middle-aged tennis players with rotator cuff tears for 57 months, with the following results: 42 patients underwent open repair and 9 patients underwent arthroscopic débridement, and 80% of patients were able to return to playing tennis with no difference between the open and arthroscopic groups.
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More recently, some studies have reported the extent of tendon healing after arthroscopic rotator cuff repairs. Boileau and associates14 followed 65 patients with fullthickness rotator cuff tears treated arthroscopically for an average of 29 months. Computed tomography (CT) arthrography and magnetic resonance imaging (MRI) were used to assess the extent of tendon healing. Of these patients, 71% completely healed radiographically and the remainder did not, but showed a smaller defect size. Overall, 93% of patients were satisfied with their surgery, regardless of their tendon healing. However, those patients who had radiographic evidence of healing had better forward elevation strength. Another unpublished study by Verma and coworkers used ultrasound to check the integrity of arthroscopic and mini-open rotator cuff repairs (personal communication). The patients were followed for a minimum of 2 years. Using ultrasound, the failure rate of the mini-open group was 24% and that of the arthroscopic group was 25%. Smaller tears had a lower rate of failure, 17% in the mini-open and 19% in the arthroscopic group. Wilson and associates15 used second-look arthroscopy to evaluate the healing of 33 patients with rotator cuff repairs. The rotator cuff healed completely in 67% of patients. Future directions of arthroscopic rotator cuff repair are focused on improving the rates of tendon healing. Promising techniques include double-row fixation, which can increase the repair footprint and may improve the chances of healing.16 In most cases, however, failure of healing is likely the result of a biologic failure rather than failure of fixation. Therefore, the application of select biologic stimulators of soft tissue healing, such as growth factors, will likely play an important role in the future of rotator cuff repair surgery.
7. MacGillivray JD, Ma CB: An arthroscopic stitch for massive rotator cuff tears: The Mac stitch. Arthroscopy 20:669-671, 2004. 8. Kibler WB, Livingston B, Chandler TJ: Current concepts in shoulder rehabilitation. Adv Oper Orthop 3:249-301, 1996. 9. Bennett WF: Arthroscopic repair of full-thickness supraspinatus tears (small to medium): A prospective study with 2- to 4- year follow-up. Athroscopy 19:249-256, 2003. 10. Burkhart SS, Danaceau SM, Pearce CR Jr: Arthroscopic rotator cuff repair: Analysis of results by tear size and by repair technique—margin convergence versus direct tendon-to-bone repair. Arthroscopy 17:905-912, 2001. 11. Wolf EM, Pennington WT, Agrawal V: Arthroscopic rotator cuff repair: 4- to 10-year results. Arthroscopy 20:5-12, 2004. 12. Gartsman GM, Khan M, Hammerman SM: Arthroscopic repair of full-thickness tears of the rotator cuff. J Bone Joint Surg Am 80:832-840, 1998. 13. Sonnery-Cottet B, Edwards TB, Noel E, Walch G: Rotator cuff tears in middle-aged tennis players: Results of surgical treatment. Am J Sports Med 30:558-564, 2002. 14. Boileau P, Brassart N, Watkinson DJ, et al: Arthroscopic repairs of full-thickness tears of the supraspinatus: Does the tendon really heal? J Bone Joint Surg Am Am 87:1229-1240 2005. 15. Wilson F, Hinov V, Adams G: Arthroscopic repair of fullthickness tears of the rotator cuff: 2- to 14- year follow-up. Arthroscopy 18:136-144, 2002. 16. Kim DH, Elattrache NS, Tibone JE, et al: Biomechanical comparison of a single-row versus double-row suture anchor technique for rotator cuff repair. Am J Sports Med 34:407-414, 2006.
References 1. Lo IKY, Burkhart SS: Current concepts in arthroscopic rotator cuff repair. Am J Sports Med 31:308-324, 2003. 2. Millstein ES, Snyder SJ: Arthroscopic management of partial, full-thickness and complex rotator cuff tears: Indications, techniques and complications. Arthroscopy 19:189-199, 2003 3. Burkhart SS, Diaz Pagan JL, Wirth MA, Athanasiou KA: Cyclic loading of anchor-based rotator cuff repairs: Confirmation of the tension overload phenomenon and comparison of suture anchor fixation with transosseous fixation. Arthroscopy 13:720-724, 1997. 4. Burkhart SS: Technical note: The dead man theory of suture anchor: Observation along a south Texas fence line. Arthroscopy 11:119-123, 1995. 5. Burkhart SS, Fischer SP, Nottage WM, et al: Tissue fixation security in transosseous rotator cuff repairs: A mechanical comparison of simple versus mattress sutures. Arthroscopy 12:704-708, 1996. 6. Lo IKY, Burkhart SS, Chan KC, Athanasiou KA: Arthroscopic knots: Determining the optimal balance of loop security and knot security. Arthroscopy 20:489-502, 2004.
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APPENDIX 16-1 Rehabilitation After Arthroscopic
Rotator Cuff Repair
4. Motion—shoulder a. Passive only i. 140 degrees of forward flexion ii. 40 degrees of external rotation iii. 60 degrees of abduction b. Codman’s pendulum exercises to promote early motion 5. Motion—elbow a. Passive and active flexion and extension b. Passive and active supination and pronation 6. Muscle strengthening a. Grip strengthening only 7. Progress to phase II if: a. 6 weeks of recovery b. Painless passive range of motion to: i. 140 degrees of forward flexion ii. 40 degrees of external rotation iii. 60 degrees of abduction
Phase I (weeks 0-6) 1. Restrictions a. No active or active-assisted range of motion i. Small tears (0-1 cm): No active forward flexion for 6 weeks ii. Medium tears (1-3 cm): No active range of motion for 6 weeks iii. Large tears (3-5 cm): No active range of motion for 8 weeks iv. Massive tears (⬎5 cm): No active range of motion for 12 weeks b. Passive range-of-motion exercises allowed i. 140 degrees of forward flexion ii. 40 degrees of external rotation iii. 60 degrees of abduction c. No strengthening until 12 weeks after surgery i. In young healthy patients with small acute tears, isometric exercises can be initiated at 8 weeks. 2. Immobilization a. Amount of abduction depends on tear and what is required to keep tension on repair at a minimum i. Sling only (if there is minimal tension on repair) 1. Small tears: 1-3 weeks 2. Medium tears: 3-6 weeks 3. Large or massive tears: 6-8 weeks ii. Abduction pillow (tension minimized with arm at 20-40 degrees of abduction) 1. Small tears: 6 weeks 2. Medium tears: 6 weeks 3. Large tears: 8 weeks 3. Pain control a. Medications i. Narcotics for 7-10 days after surgery ii. Nonsteroidal anti-inflammatory drugs (NSAIDs) for patients with discomfort beyond first 10 days b. Therapeutic modalities i. Moist heat before therapy, ice after therapy ii. Ultrasound iii. Galvanic stimulation
Phase II (weeks 6-12) 1. Restrictions a. No strengthening or resisted range of motion until 12 weeks after surgery b. No active range of motion for massive tears 2. Immobilization a. Discontinue sling or abduction pillow b. Use for comfort only 3. Pain control a. NSAIDs b. Therapeutic modalities 4. Motion—shoulder a. Goals i. 140-160 degrees of forward flexion ii. 40-60 degrees of external rotation iii. 60-90 degrees of abduction b. Exercises i. Continue with passive range of motion ii. Begin active-assisted range of motion iii. Progress to active range of motion iv. Light passive stretching at the end ranges of motion 5. Muscle strengthening a. Only for small nondisplaced tears i. Can advance to light Thera-Band for internal and external rotation ii. Can begin scapular stabilizers 189
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6. Progress to phase III if: a. Painless active range of motion b. No shoulder pain Phase III (months 3-6) 1. Goals a. Improve shoulder strength, power, and endurance b. Improve shoulder proprioception c. Establish a home maintenance program performed three times/week d. Stretching exercises daily 2. Motion a. Achieve motion equal to contralateral side b. Passive capsular stretching at end ranges of motion, including cross-body adduction and internal rotation to stretch posterior capsule 3. Strengthening a. Begin with closed-chain isometric exercises i. Internal rotation ii. External rotation iii. Abduction iv. Forward flexion v. Extension b. Progress to open-chain exercises with Thera-Bands i. Exercises with elbow bent to 90 degrees ii. Start with shoulder at 0 degrees of forward flexion, abduction, and external rotation iii. Arc of 45 degrees in each of five planes of motion
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iv. Progress through six color-coded bands v. Progression to next level band occurs at 2- to 3-week intervals vi. Thera-Bands permit isotonic eccentric and concentric shoulder strengthening vii. Progress to isotonic dumbbell exercises in all five planes c. Strengthening of deltoid (especially anterior) d. Strengthening of scapular stabilizers i. Closed-chain 1. Scapular retraction (rhomboids, middle trapezius) 2. Scapular protraction (serratus anterior) 3. Scapular depression (latissimus dorsi, trapezius, serratus) 4. Shoulder shrugs (trapezius, levator scapulae) ii. Progress to open-chain 4. Functional strengthening a. Begin after 70% of strength recovered b. Plyometrics 5. Return to sport a. Sport-specific exercises (e.g., throwing, golfing, tennis) 6. Maximum improvement a. Small tears (4-6 months) b. Medium tears (6-8 months) c. Large tears (8-12 months) d. Patients will continue to show improvements in function for at least 1 year.
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CHAPTER 17 Anterior Instability
of the Shoulder Samuel A. Taylor, Mark C. Drakos, and Stephen J. O’Brien
wrestling and 332,000 in soccer.3 Anterior shoulder dislocation is a common affliction of young active patients, often precipitated by a sports-related injury. Given the number of high school students alone participating in such sports and the traumatic nature of anterior glenohumeral dislocation, it is not surprising that the average age of patients seen for evaluation of anterior shoulder instability is younger than 28 years.4-9
Joint laxity does not indicate shoulder instability; rather, there are varying degrees of laxity in the normal shoulder.1,2 When a patient presents with glenohumeral instability, it is important to differentiate normal laxity from instability clinically and to establish the primary direction of instability. Patients should be separated clinically into two groups, those suffering from symptomatic laxity and those demonstrating overt instability of the glenohumeral joint. Furthermore, determining the positions and activity in which clinical instability occurs also provides useful information during the evaluation.
Young active patients presenting with an acute anterior dislocation of the glenohumeral joint who are treated nonoperatively re-dislocate at rates as high as 80% to 90%.7,10,11 It is our belief that young athletes who desire to return to their sport and present with acute anterior shoulder dislocation should be treated surgically.
Athletes experiencing symptomatic laxity may present with problems stemming from repetitive edge loading, traction on the glenoid labrum or biceps labral complex, rotator cuff tendinitis, or dead arm symptoms resulting from traction on the brachial plexus as the lax shoulder subluxes inferiorly or anteroinferiorly. A typical example of symptomatic laxity is the football lineman who develops posterior pain and labral injuries that result from blocking with the arms forward-flexed and elbows locked in extension. Additionally, baseball pitchers are particularly susceptible to exacerbations of internal impingement from symptomatic laxity. This is caused by tremendous forces incurred by the soft tissue structures surrounding the glenohumeral joint during the production of the throwing arc with the humerus abducted and externally rotated. Repetitive motions such as these stress the surrounding soft tissue structures, including the glenohumeral ligaments and supraspinatus rotator cuff tendon. The resulting microtrauma and tension can lead to refractory tendinitis and potentially to labral injuries caused by the supraspinatus tendon becoming impinged between the humerus and glenoid. Effectively, a pathologic cycle develops in which repetitive stress magnifies the glenohumeral laxity; this in turn contributes to internal impingement.
As our surgical technique and collective acumen continue to advance treatment options and prognoses for patients with anterior glenohumeral instability, a fundamental understanding of the anatomy and pathoanatomy of the glenohumeral joint is absolutely critical to the diagnosis and surgical treatment of overt anterior shoulder instability in the athlete. This point is emphasized by the field’s departure from nonanatomic techniques of stabilization, such as the Bristow, Putti-Platt, and Magnuson-Stack procedures. We believe that the most effective stabilization techniques focus on restoration of normal glenohumeral anatomy, particularly through repair and proper tensioning of the inferior glenohumeral ligament complex. Such intervention allows not only for stability, but some tailoring can be done to allow for the recovery of desired function in the throwing and nonthrowing athlete.
ANATOMY OF THE STABLE AND UNSTABLE SHOULDER The human shoulder joint (Fig. 17-1) is formed by the humeral head and glenoid surface of the scapula. As humans developed an orthograde posture, the glenohumeral joint evolved so that the head of the humerus abuts the glenoid fossa, as opposed to articulating within. Whereas this anatomic relation affords the glenohumeral joint tremendous flexibility and range of motion, it does so at the cost of biomechanical stability.12 Unlike other joints, the articulating surface area of the shoulder is limited. The biomechanical stability of the shoulder is reliant on two types of anatomic restraints, dynamic
In contrast to symptomatic laxity, overt instability refers to problems in which the athlete is unable to contain the humeral head within the glenoid fossa and it clearly dislocates, leaving the athlete in a fully compromised position, vulnerable to more serious nerve, bone, or joint injuries, until the shoulder is reduced. The focus of this chapter will be on those individuals who demonstrate overt anterior or anteroinferior instability. In 2001, it was reported that over 1 million U.S. high school students participated in football, almost 250,000 in 191
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Figure 17-1. Sagittal view of the glenohumeral joint.
and static, which work cooperatively to maintain glenohumeral stability by generating joint compressive forces and directing the net force through the humeral head into the glenoid fossa.13 Static stabilizers are unable to generate force and include the bony structures of the humeral head and glenoid fossa, the fibrous glenoid labrum, and several capsuloligamentous structures.14-16 Static mechanisms of stabilization provide the greatest contribution to glenohumeral stability at the extreme ranges of motion, because they remain lax through the midrange of motions13 and become taut as the shoulder approaches its normal limits of motion.17 Dynamic stabilizers include the muscles of the rotator cuff, the deltoid group, pectoralis major, and latissimus dorsi, and are therefore a critical component to glenohumeral stability. Concavity compression is a force that acts to contain the humeral head in the glenoid fossa and is a function of the depth of the articulating fossa (provided by the glenoid and the labrum) and forces generated by the surrounding musculature that direct the humeral head into the glenoid. In addition to generating compressive forces, dynamic stabilizers also initiate movement that leads to tightening of capsuloligamentous structures.14,18-20 The glenoid fossa is shaped like an inverted comma, with average measurements of 35 mm vertically and 25 mm transversely.21,22 Saha’s studies21-23 also noted an average of 7.4 degrees of glenoid retroversion in 75% of shoulders and 2 to 10 degrees of anteroversion in the remaining 25% of shoulders. The hemispherical surface of the humeral head—radii of curvature, 25 mm vertically and 22 mm transversely12—is designed to interact with the shallow concave surface of the glenoid (2.5 mm anteroposteriorly and 9 mm superoinferiorly)24 so that the contact surface area is maximized. Articular interaction is enhanced by the inclination of the humeral head with respect to the shaft and the retrotorsion.25 Saha22 has separated glenohumeral
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joints into three groups based on the radius of curvature of the glenoid fossa and radius of the humeral head. Type A articulation is defined by a humeral head radius smaller than that of the glenoid, Type B joints exhibit similar radii for the two surfaces, and type C articulation has a larger humeral head radius than glenoid radius. Interactions between a humeral head and glenoid fossa with differences in radii approaching zero (type B) are inherently the most stable because the contact surface area is maximized. However, Soslowsky and colleagues26 have claimed that in 88% of cases, the glenoid and humeral head exhibit less than a 2-mm difference in radii, suggesting that most glenohumeral joints could be considered type B; thus, inequality in radii of curvature fails to explain most anterior instability cases. The anatomic neck of the humerus also plays a crucial role in glenohumeral stability because it serves as an attachment site for the glenohumeral capsule and the glenohumeral ligaments (see later). The concept of osseous adaptation has been explored and documented in professional baseball pitchers27 and professional European handball players28; it was found that the dominant arm develops significant glenoid retroversion in the dominant arm. During the act of throwing, with the humerus in 90 degrees abduction and external rotation, tremendous forces are applied to the static and dynamic stabilizers of the shoulder. Osseous adaptation is the concept that the glenoid fossa adopts a modified bony conformation to accommodate the repetitive stress of the throwing motion. Thus, anterior stability of the shoulder is enhanced through the increased articular surface area present throughout the throwing arc. The glenoid labrum is dense fibrous tissue with a triangular shape that encircles the glenoid rim and attaches directly to the long head of the biceps tendon at the supraglenoid tubercle (Fig. 17-2). The labrum contributes greatly to glenohumeral stability by deepening the glenoid fossa,29 without changing the curvature of the glenoid.30 Lippitt and associates31 have demonstrated the labrum’s contribution to stability by showing that its resection leads to a 20% decrease in resistance to translation. Furthermore, the labrum increases the surface area in contact with the humeral head, and serves as an attachment point for the glenohumeral capsule and ligaments. The contribution of the shoulder capsule to stability depends on collagen integrity, attachment sites on the glenoid and humeral head, and position of the arm. The glenohumeral capsule consists of three layers,15 is less than 5 mm thick,32 and shows significant individual variation. The anterior capsule is more substantial than the thin posterior capsule; it is composed of loose areolar connective tissue33 and predominantly type I collagen.34 The primary role of the capsule in glenohumeral stabilization is to maintain negative intra-articular pressure. A capsular or
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ANTERIOR INSTABILITY OF THE SHOULDER
193
L
G hh Figure 17-2. Glenoid labrum (L). This is a triangularly shaped rim of dense fibrous tissue that acts mechanically to deepen the glenoid fossa and increase the surface area of the articulating glenoid (G) and humeral head (hh).
labral defect, such as is the case in a Bankart lesion (see later) results in a loss of the negative intra-articular pressure35 critical to the maintenance of shoulder stability through the midranges of motion. The glenohumeral ligaments are discrete thickenings of the glenohumeral capsule, identifiable grossly and histologically (Fig. 17-3). The most common cause of anterior shoulder instability is insufficiency of these capsuloligamentous structures. A thorough understanding of the anatomy, histology, and biomechanics of these structures is crucial to understanding and treating anterior shoulder instability. Turkel and coworkers36 have laid the groundwork for the study of these static contributions, by showing that in 0 degrees of abduction, anterior stability is maintained by the subscapularis tendon, in 45 degrees abduction the shoulder is stabilized by the subscapularis tendon, middle glenohumeral ligament, and anterior fibers of the inferior glenohumeral ligament, and in 90 degrees abduction and external rotation the inferior glenohumeral ligament provides stabilization. The superior glenohumeral ligament has been identified in 90% to 97% of specimens investigated.15,37,38 It takes its origin at the supraglenoid tubercle, just anterior to the insertion of the long head of the biceps tendon, and inserts into the anatomic neck to the humerus slightly superior to the lesser tuberosity. The superior glenohumeral ligament is also a component of the rotator interval39 (see later). The ligament’s size and integrity vary from person to person and are not easily visualized arthroscopically. The superior glenohumeral ligament contributes little to anteroposterior stability of the shoulder;40 however, it acts in concert
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Figure 17-3. Glenohumeral ligaments. This sagittal view represents an anatomic illustration of the glenohumeral ligaments and inferior glenohumeral ligament complex. A, anterior; AB, anterior band; AP, axillary pouch; B, long head biceps tendon; IGHLC, inferior glenohumeral ligament complex; MGHL, middle glenohumeral ligament; P, posterior; PB, posterior band; PC, posterior capsule; SGHL, superior glenohumeral ligament. (From Rockwood CA, Matsen FA III [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 26.)
with the coracohumeral ligament to limit inferior glenohumeral translation41 with the arm adducted or in the neutral position. The coracohumeral ligament is an extracapsular structure that courses from the lateral surface of the coracoid process to the greater and lesser tuberosities straddling the bicipital groove. The coracohumeral ligament aids the superior glenohumeral ligament in limiting inferior glenohumeral translation. Together, these two ligaments contribute greatest to stability when the arm is adducted or in 0 degrees abduction.16 As the arm is abducted to 90 degrees, the mechanical contribution of these ligaments to stability decreases progressively to zero, at which point the ligaments are slack. The middle glenohumeral ligament demonstrates even greater variability in its attachment, size, and integrity than the superior glenohumeral ligament. When the ligament is present, it typically originates just inferior to the superior glenohumeral ligament at the supraglenoid tubercle or at the same level from the glenoid neck and inserts into the humerus just medial to the lesser tuberosity.25 The thickness of the middle glenohumeral ligament has been found to vary tremendously, from a thick well-defined structure to a gossamer thickening of the anterior capsule.42 Additionally,
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this glenohumeral ligament has been shown to be absent in 27% of shoulders.15 Although the middle glenohumeral ligament’s contribution to glenohumeral stability varies in accordance with its size and integrity, studies have found that its primary function is to restrain inferior translation when the arm is adducted and externally rotated.16 It also works as an accessory stabilizer to anterior translation following damage to the anterior band of the inferior glenohumeral ligament complex when the arm is abducted to 90 degrees.40 The inferior glenohumeral ligament complex is perhaps the most critical for the prevention of dislocation in an abducted shoulder40,43 and surgical intervention for anterior glenohumeral instability (Fig. 17-4). Selective sectioning experiments15,29,36,44 have helped elucidate the inferior glenohumeral ligament’s role as the most important static stabilizer of the glenohumeral joint anteriorly. As O’Brien and colleagues15 have delineated, the inferior glenohumeral ligament complex consists of three distinct components—the anterior band, axillary pouch, and posterior band. Together, these three components make up what has been referred to as a hammock-like structure that offers anterior, posterior, and inferior stability to the abducted glenohumeral joint. Anatomically, the anterior band takes its origin from between the 2- and 4-o’clock positions on the face of the glenoid (Fig. 17-5).15 Histologic examination has revealed that the anterior band of the inferior glenohumeral ligament’s attachment to the glenoid is facilitated by direct attachment of collagen fibers to the labrum and by collagen fibers that interact directly with the bone.45 Meanwhile, the posterior band of the inferior glenohumeral ligament complex takes its origin from between the 7- and 9-o’clock
Posterior
Anterior
Figure 17-4. View of the attachment sites for the anterior and posterior bands of the inferior glenohumeral ligament complex of the glenoid. Note that the anterior band attaches higher up on the comma-like glenoid than the posterior band and that their attachment sites define the hammock-like structure of the complex.
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positions along the face of the glenoid and has been shown to be less consistent than either the anterior band or the axillary pouch in its structure and function.46 Histologically, the inferior glenohumeral ligament complex consists of three layers, similar to the structure of the shoulder capsule described earlier. However, the perpendicularly oriented fiber pattern within the three layers of the inferior glenohumeral ligaments makes it easy to differentiate it from the capsule. Both the anterior and posterior bands consist of easily distinguishable, abrupt, and well-organized collagen bundles visualized as thickenings of the innermost layer. In between the anterior and posterior bands lies the thickest section, the axillary pouch, which similarly runs from the glenoid to the humerus and is continuous with the other two elements of the inferior glenohumeral ligament complex anteroposteriorly. Histologically, however, the axillary pouch differs from the anterior and posterior bands in the orientation of its collagen fibers. O’Brien and associates15 noted in their landmark paper that the collagen fibers of the axillary pouch are not synchronously aligned, but rather are less well organized and exhibit mixing of fibers from the inner and middle layers of the capsule, making differentiation difficult. More recently, however, others have described the collagen fiber pattern of the axillary pouch to be more organized than originally proposed, to have a radial pattern in the ligament’s midsubstance,47 and to have a multiaxial fiber orientation that is somewhat similar to that seen in the anterior and posterior bands.48 Bigliani and coworkers19 have determined that the tensile strength of each of the three components of the inferior glenohumeral ligament is comparable when corrected for thickness and surface area, supporting the notion that the axillary pouch consists of equally organized collagen fibers. The anterior band, axillary pouch, and posterior band have been shown to be thicker toward their glenoid origin than laterally at their humeral insertions.46 Furthermore, the three components of the inferior glenohumeral ligament complex exhibit similar length, about 43 mm, despite the differences in their thickness, structure, and sites of origin and insertion. The inferior glenohumeral ligament complex, which originates between 2 and 9 o’clock on the face of the glenoid, follows two separate insertion patterns on the humerus: (1) a collar-like attachment in which the entire complex inserts along the same circumferential ring, slightly inferior to the articular margin of the humeral head; and (2) a V-shaped attachment, which gleans its name from the shape that results when the anterior and posterior bands attach just inferior to the articular margin, and the axillary pouch attaches further inferiorly (Fig. 17-6).15 As mentioned earlier, the three components of the inferior glenohumeral ligament complex act in concert as the primary stabilizer of the abducted shoulder through their hammock-like action around the axis of rotation (Fig. 17-7).
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195
B
A
C Depending on the position of the arm, the inferior glenohumeral ligament complex can stabilize against anterior, posterior, and inferior translation. As the arm is abducted to 90 degrees, the inferior glenohumeral ligament complex tightens beneath the humeral head and acts as the main stabilizer against inferior translation, because the nature of
A B C
Figure 17-6. Attachment sites of the glenohumeral ligaments. Left, the superior glenohumeral ligament inserts into the fovea capitis line just superior to the lesser tuberosity (A). The middle glenohumeral ligament inserts into the humerus just medial to the lesser tuberosity (B). The inferior glenohumeral ligament complex has two common attachment mechanisms (C). It may attach in a collar-like fashion, or it may have a V-shaped attachment to the articular edge (right). (From Rockwood CA, Matsen FA III [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 18.)
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Figure 17-5. Anterior band of the inferior glenohumeral ligament. A, Example of a collar-like attachment of the inferior glenohumeral ligament complex just inferior to the articular edge and closer to the articular edge than the remainder of the capsule. B, V-shaped attachment of the inferior glenohumeral ligament complex of the humerus, with the axillary pouch attaching to the humerus at the apex of the V farther from the articular edge. C, Inferior glenohumeral ligament complex (IGHLC). This is thicker than the anterior capsule (AC) and posterior capsule (PC). (From Rockwood CA, Matsen FA III [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 21.)
the superior glenohumeral ligament renders it slack and ineffective at this degree of abduction. O’Brien and colleagues40 have demonstrated anteroposterior translation of the glenohumeral joint to be greatest when the abducted arm is at 0 degrees of extension. Furthermore, they have shown that the anterior band of the glenohumeral ligament complex is the primary mechanism for resisting anteriorposterior translation with the abducted arm in the neutral position or in 30 degrees of extension as the anterior band becomes taut. However, when the 90-degree abducted arm is moved into 30 degrees of forward flexion, the anterior band becomes slack, allowing the now taut posterior band to bear the burden of stabilizing the glenohumeral joint against anterior-posterior translation. Similarly, the hammock-like action of the inferior glenohumeral ligament complex (Fig. 17-8) acts to stabilize this diarthrodial joint further when the abducted humerus is externally rotated. In such a position, the anterior band and axillary pouch fan out anteriorly to provide support to the humeral head and stabilize the joint against anterior translation.49 Conversely, the same is true of the posterior band and axillary pouch, which provide posterior support to the internally rotated abducted arm as fibers of the posterior band and axillary pouch fan out posteriorly to cradle the humeral head and resist posterior instability. Although of a variable thickness,15,19,50 the inferior glenohumeral ligament complex is continuous with the remainder of the shoulder capsule anteriorly and posteriorly.
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II 90˚ Abd.
M
amm
k oc
C
A
c
H
M
am
ck
A
H
C
H
H
a
K
K
d
mo
O
M
O
M
B
A
A
E.R. I.R.
C
D
Figure 17-7. Hammock-like action of the inferior glenohumeral ligament complex. A, The inferior glenohumeral ligament complex is tightened during abduction (Abd.). B, During abduction and internal (c) or external rotation (d), different parts of the band are tightened (a, c, d). C, With internal rotation (I.R.), the posterior band fans out to support the head and the anterior band becomes cordlike or relaxed, depending on the degree of horizontal flexion or extension. D, With abduction and external rotation (E.R.), the anterior band fans out to support the head and the posterior band becomes cordlike or relaxed, depending on the degree of horizontal flexion or extension. (From Rockwood CA, Matsen FA III [eds]: The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, p 20.)
Continuity of this hammock-like structure with the rest of the shoulder capsule is tremendously important because it allows us to consider the inferior glenohumeral ligament complex as a hammock within a hammock (see Fig. 17-8). That is, action can be taken surgically at various places in the shoulder capsule that will affect (tightening or loosening) the hammock-like action of the inferior glenohumeral ligament complex. This surgical approach, particularly through manipulation of the rotator interval, allows the surgeon to exploit the hammock within a hammock concept in a way that restores anterior stability to the ailing patient. (See later,“Surgical Techniques To Correct Anterior Instability,” for further discussion of this topic.) The final anatomic component that demands attention is the rotator interval. The rotator interval (Fig. 17-9) is a term first used by Neer51 to describe a triangular area defined medially by the coracoid process, superiorly by the anterior border of the supraspinatus tendon, and inferiorly by the superior aspect of the subscapularis tendon.52 The contents of this triangular space include the coracohumeral
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C
B
Figure 17-8. Schematic illustration of the thickened portion of the inferior glenohumeral ligament complex (IGHLC) as it exists in continuum with the remainder of the shoulder capsule. The anatomic relation leads to the concept of a hammock within a hammock, which maintains that actions taken on the glenohumeral capsule outside the IGHLC, such as surgical closure of the rotator interval, and will have a secondary effect of tightening of the IGHLC as it relates to stability. A, The glenoid fossa with its surrounding muscular and ligamentous attachments are seen in the sagittal view, demonstrating that the IGHLC (hammock) sits within the greater glenohumeral capsule (HAMMOCK). B, Sutures can be placed to close the rotator interval, which in turn tightens the capsule (HAMMOCK) and IGHLC (hammock). C, Closure of the rotator interval has the effect of raising and tightening the IGHLC (hammock).
SS
g
CP
hh
ST
Figure 17-9. Rotator interval. The rotator interval is seen here in an extra-articular anterior-posterior view through subdeltoid arthroscopy. The triangular space is anatomically defined superiorly by the supraspinatus tendon (SS), medially by the coracoid process (CP), and inferiorly by the subscapularis tendon (ST). The humeral head (hh) is seen as it articulates within the glenoid fossa (g).
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an r io
rb
d an rb rio te An d
Axillary pouch
an
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te Po s
Posterior translation
rb
Before discussing these pathologic lesions and their surgical treatment in detail, it is first important to understand the extent of the damage caused by an anterior dislocation of the shoulder. It is best to think of the capsuloligamentous structures spanning the glenoid and humeral head as being continuous, similar to a circle, just like the previously described hammock within a hammock concept. In such a model, damage to anterior and posterior structures is present, even though anterior instability predominates clinically (Fig. 17-10). Anterior dislocation, therefore, results in two traumas: (1) anterior damage typically manifested as a Bankart lesion; and (2) reciprocal posterior capsuloligamentous laxity from damage to the hammock. Therefore, it is common for cases of anterior
Axillary pouch
r io
A number of pathologic lesions have been identified that result in or contribute to anterior shoulder instability. Subfailure strain on the inferior glenohumeral ligament complex and the resulting microtrauma, anteroinferior labral lesions (Bankart lesions), rupture injury to the inferior glenohumeral ligament complex, and bone defects are all common pathologic consequences of the violent forces imposed on the joint during athletic activities.
ri
te
An
te
PATHOLOGIC LESIONS AND ANTERIOR INSTABILITY
d
an
b or
s Po
ligament, superior glenohumeral ligament, middle glenohumeral ligament, and long head of the biceps tendon, which runs through the intertubercular groove.53 Jost and associates39 have further elucidated the layers of the rotator interval through a series of dissections. They determined that the rotator interval space is actually two parts differentiated by the number of tissue layers. One part is defined as lateral to the cartilage bone transition and consists of four layers—superficial fibers of the coracohumeral ligament, fibers of the supraspinatus tendon and subscapularis tendon, deep fibers of the coracohumeral ligament, and fibers of the superior glenohumeral ligament and joint capsule. The other more medial part of the rotator interval covers the cartilaginous humeral head and consists of only two layers, the coracohumeral ligament and the superior glenohumeral ligament and joint capsule. Operative experience has revealed that the thickness and composition of the rotator interval are highly variable and can be visualized arthroscopically, ranging from a thick strong barrier to an almost translucent wispy structure invariably unable to offer structural support beyond maintenance of negative intra-articular pressure. Such anatomic variability was demonstrated by Cole and coworkers53 in 2001 when they evaluated the rotator interval regions from 37 fetuses and 10 fresh-frozen cadavers, demonstrating that the inner capsular layer of 75% of the rotator intervals studied lacks a continuous link of loosely associated collagenous connective tissue; instead, it is covered only by a thin synovial membrane.
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d
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Axillary pouch Anterior translation
Figure 17-10. Circle concept. This can be regarded as a means to understanding the role of the shoulder capsule in shoulder stability. Damage to both sides of the capsule is required to produce dislocation in one direction.
shoulder instability to manifest clinically with some degree of posterior laxity. Similarly, anterior laxity will accompany posterior dislocation. This concept has been reinforced by studies that have revealed anterior and posterior injury of the capsule resulting from a unidirectional trauma in the cadaveric shoulder.54-56 Speer and colleagues57 have demonstrated with a cadaveric model that anteroinferior labral injury increases the amount of anterior glenohumeral translation by a mean of 3.4 mm. They deemed this degree of translation minimal, unable to account for anterior dislocation of the joint on its own, and suggested that other anatomic abnormalities, especially capsular stretching, must be present to permit the humeral head to dislocate anteriorly. A Bankart lesion typically occurs as a result of anterior humeral head dislocation. It is defined as a detachment of the anteroinferior glenoid labrum, with its attached anterior band of the inferior glenohumeral ligament complex. A Bankart lesion causes a decrease in the tension of the anterior band and thus reduces the ligament’s ability to retain the humeral head in the glenoid fossa, especially with the arm in positions of glenohumeral vulnerability. It is important to reiterate that as the shoulder reaches 90 degrees of abduction with external rotation, the primary restraints to anterior translation are the anterior band and axillary pouch of the inferior glenohumeral ligament complex, which fan anteriorly.40 In 90 degrees of abduction and forward flexion, the anterior band becomes slack, whereas the posterior band tightens and acts to prevent anterior translation. Therefore, to restore stability to the glenohumeral joint, even in the case of anteroinferior avulsion of the glenoid labrum, competency and proper tensioning of all three components of the inferior glenohumeral ligament complex must be re-established. Two other types of injury to the inferior glenohumeral ligament complex can occur in the athlete’s shoulder, rupture
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of the ligament and subfailure injury resulting in elongation stretching of capsuloligamentous tissues. There are three potential sites of failure for the inferior glenohumeral complex: (1) at the glenoid insertion; (2) in the ligament’s midsubstance; and (3) at the humeral insertion point. During unidirectional testing, studies have indicated that 40% of specimens rupture at their glenoid origin (Bankart lesion), 35% fail in the midsubstance, and 25% fail at the humeral insertion.19 Wolf and colleagues58 have looked arthroscopically at 64 shoulders with diagnosed anterior instability and found that just 9.3% of patients present with a humeral avulsion of the inferior glenohumeral ligament complex anteriorly, 17.2% of patients demonstrate generalized capsular laxity, and the overwhelming majority of patients, 73.5%, present with a primary Bankart lesion. Malicky and associates58 have demonstrated through a new technique that stress on the anteroinferior capsule yields variable force vectors with a multiaxial representation. Furthermore, their biomechanical analysis showed that the highest levels of strain on the anteroinferior capsule are near the ligament’s glenoid insertion as opposed to near the humeral insertion. Although the most common pathology seen in anterior instability is certainly a primary Bankart lesion, it is important to rule out humeral insertion failures58 through arthroscopic visualization or radiographic imaging. Variable subfailure stresses encountered by the glenohumeral joint have been implicated in stretching of the associated capsuloligamentous structures. Bigliani and coworkers19 have in fact noted significant elongation of the inferior glenohumeral ligament complex. Pollock and colleagues61 have determined, through exposure of the inferior glenohumeral ligament to several different levels of subfailure stress, that repetitive loads similar to those experienced by athletes result in ligament elongation and joint laxity. Moreover, they speculated that this unrecoverable ligamentous elongation might be the end product of accumulated microdamage to the ligament tissues. This concept was used by Remia and associates62 to stretch the capsuloligamentous structures of the shoulder to 20% beyond their original length to create a model of generalized glenohumeral laxity with increased rotation and translation for analysis of various surgical techniques. Bone pathology associated with anterior instability is not uncommon. The Hill-Sachs lesion occurs on the posterior aspect of the humeral head as a result of the violent collision between the posterior humeral head and anterior glenoid rim during anterior dislocation. A Hill-Sachs lesion that interacts with the anterior glenoid rim when the arm is in 90 degrees abduction and external rotation has been termed an engaging Hill-Sachs lesion by Burkhart and De Beer63 and noted to be a contraindication for arthroscopic stabilization. They also described a glenoid in which the bone has been ground down anteroinferiorly as an inverted pear glenoid and noted this as another contraindication to arthroscopic
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repair. Sugaya and associates64 have used three-dimensional reconstructed computed tomography (CT) to evaluate 100 shoulders of patients with recurrent anterior glenohumeral instability. They found that osseous Bankart lesions are present in 50% of cases. Additionally, 40% of patients had scans consistent with erosion or compression of the anterior glenoid rim.
SURGICAL TECHNIQUES TO CORRECT ANTERIOR INSTABILITY Historically, the methods for the surgical correction of anterior glenohumeral shoulder instability have fallen into one of two distinct genres—anatomic reconstruction or nonanatomic reconstruction. Anatomic reconstruction focuses on restoring normal anatomy to the shoulder joint by addressing pathology associated with dislocation. To be effective, anatomic reconstruction must pay particular attention to the hammock-like inferior glenohumeral ligament complex. Conversely, the emphasis of nonanatomic approaches is to construct new structures to contain the humeral head and thus prevent anterior dislocation. Effective primary surgical treatment of anterior shoulder instability lies in anatomic reconstruction, particularly when addressing any pathoanatomy associated with the inferior glenohumeral ligament complex.
Open Repair Techniques A Bankart lesion is the most common surgical finding in patients with anterior instability. As such, the open Bankart repair is traditionally considered to be the gold standard for the surgical treatment of anterior shoulder instability. In the classic study by Rowe and colleagues,65 a long-term review of 145 patients treated with open Bankart repairs was conducted; results indicated only a 3.5% recurrence rate, with 69% of patients able to achieve full range of motion. The hallmark of the Bankart repair is restoration of tension to the anteroinferior capsule and inferior glenohumeral ligament complex. To address these structures, the surgeon must enter the capsule vertically and medially to the inferior rim of the glenoid. Removal of soft tissue attachments to the glenoid precedes the drilling of three holes in the glenoid, through which sutures are passed to facilitate the superomedial advancement of the inferior capsule and anterior band of the inferior glenohumeral ligament complex. Such superomedial advancement of these structures restores tension to the hammock-like complex. This technique, however, is often ineffective for treating anteriorly dislocating patients with excessive capsular laxity or for treating multidirectional instability patients who primarily dislocate anteriorly. Treating these patients requires a form of capsular shift (Fig. 17-11). Neer and Foster66 have described an inferior capsular shift in which
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stabilization, anchor fixation, and thermal capsulorrhaphy. Failure rates of these procedures vary among studies, and the relative indications for arthroscopic stabilization versus open stabilization will be discussed elsewhere in this text (Chapter 21).
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Figure 17-11. Neer capsular shift. A, Lateral and vertical incisions are made in the lax capsule. B, The lax capsule is then imbricated, improving tension and removing capsular redundancy.
lax capsular tissue is addressed via lateral and vertical incisions through the capsule (see Fig. 17-11A) at the humeral neck and advanced laterally and superiorly (see Fig. 17-11B), thus removing capsular redundancy. Recommended Open Technique T-plasty modification of the Bankart repair has been described by Altchek and associates67 as a method to correct multidirectional instability (Fig. 17-12). In this technique, both a transverse incision in the capsular midsubstance and a vertical incision along the glenoid margin are used (see Fig. 17-12A). The latter incision is used first to inspect the joint for a Bankart lesion and then to repair that lesion, if present (see Fig. 17-12B). The transverse incision affords the ability to advance the inferior flap superiorly and the superior flap inferiorly to imbricate the capsule, thereby reducing joint laxity.
Arthroscopic Repair Tremendous advancements have been made in the arthroscopic treatment of anterior shoulder instability since Johnson and Bayley68 introduced the arthroscopic application of metal staples as a method for repairing a Bankart lesion. Today, many arthroscopic methods have been described in the literature, including transglenoid arthroscopic
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B
Before beginning any arthroscopic procedure, a complete examination under anesthesia should be performed comparing the injured shoulder with the contralateral shoulder, because such an assessment is often difficult to perform on the awake patient. Once the arthroscope is introduced into the injured shoulder, a thorough arthroscopic evaluation of the status of the inferior glenohumeral ligament complex, labrum, rotator cuff, and any bony lesions that may be present should be performed. In addition to these two procedures, the arthroscopic drivethrough sign69-71 is often a valuable intraoperative tool for assessment of glenohumeral laxity. The arthroscopic drivethrough sign is the ability to maneuver the arthroscope in between the humeral head and the glenoid fossa at the level of the anterior band of the inferior glenohumeral ligament complex. McFarland and coworkers72 have evaluated the clinical significance of the drive-through sign and its pertinence to the diagnoses of various shoulder abnormalities. They examined 234 shoulders arthroscopically and found that the drive-through sign has a high sensitivity (92%) and negative predictive value (94.2%), but low specificity (37.6%) for glenohumeral instability. Their results indicate that a positive drive-through sign should be used in conjunction with other diagnostic criteria in determining shoulder instability, because it is not in itself specific to the pathology. Although the diagnosis of anterior shoulder instability may not accurately be made using this sign, it is our clinical experience that elimination of a positive arthroscopic drive-through sign intraoperatively is a good predictor of proper tensioning of the hammock-like inferior glenohumeral ligament complex (Fig. 17-13). Arthroscopic staple capsulorrhaphy, in which a metal staple is used to repair a Bankart lesion, described in 1982 by
Figure 17-12. T-plasty modification of Bankart repair. A, The transverse and vertical incisions allow access to the joint for a Bankart repair. B, The capsule can then be imbricated to reduce joint laxity.
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g
hh
g hh
A
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Figure 17-13. Positive arthroscopic drive-through sign. A, Viewed from the standard posterior portal. The drive-through sign can be seen when the surgeon can maneuver the arthroscope between the glenoid (g) and the humeral head (hh). B, Removal of the arthroscopic drive-through sign after surgical intervention may help estimate proper correction of anterior shoulder instability.
Johnson and Bayley, was the first in a series of arthroscopic techniques developed to address pathology associated with anterior dislocation of the glenohumeral joint. Reported rates of recurrent dislocation and subluxation in the literature are high. Johnson and Bayley, in fact, have reported a recurrence rate of 21%.68 Lang and colleagues73 have evaluated 54 shoulders at an average of 39 months, describing a 33% occurrence of postoperative instability, loose staples in 15% of patients, and less than 50% of treated athletes able to return to overhead sporting activities. Furthermore, Coughlin and associates74 have described a 25% failure rate among the 47 patients they followed at 4 years postoperatively. Because of the substantial failure rates and the occurrence of some articular injuries associated with loose hardware, staple capsulorrhaphy has been essentially abandoned in favor of newer techniques that attempt to ameliorate these pitfalls.
is freed to the 6-o’clock position, followed by reattachment of the Bankart lesion,78 with proper reattachment and tensioning of the inferior glenohumeral ligament complex. Arciero and coworkers79 have reported on 19 military cadets followed at a mean of 19 months, all of whom were treated with bioabsorbable anchor fixation, and there was only one recurrence of subluxation (5%). In this study, all athletes were able to return to preinjury levels of performance and 94.7% indicated a Rowe score of good or excellent. Other studies in the literature have reported failure rates of 10%,7 15%,80 and 3.2%.81 Although their results are promising, Cole and colleagues82 have emphasized the importance of patient selection for bioabsorbable anchor fixation, with the prime candidate being an individual with a relatively healthy capsule and only a Bankart lesion resulting from traumatic anterior dislocation.
The evaluation of arthroscopic stabilization has included numerous other techniques, such as thermal capsulorrhaphy and anchor fixation. Thermal capsulorrhaphy uses the application of thermal energy75,76 to “shrink” the capsule by altering the capsular collagen architecture. Although this technique was widely embraced by orthopedic surgeons in the late 1990s because it appeared to offer a quick and effective intervention for management of the unstable shoulder, it has since fallen out of favor specifically because of the variability of the host reaction and its failure to address the primary pathologic process, the Bankart lesion. We believe that thermal capsulorrhaphy is not indicated for the treatment of anterior shoulder instability and that the issues of capsular redundancy are more effectively addressed through closure of the rotator interval.
Recommended Arthroscopic Technique Suture anchors are the preferred method for arthroscopic repair of anterior glenohumeral instability, because this technique offers the safest and most accurate method for repairing a Bankart lesion. As with any arthroscopic procedure for shoulder instability, examination under anesthesia should be performed to compare the injured shoulder with the contralateral shoulder to determine the direction and extent of humeral translation. Furthermore, diagnostic arthroscopy is a useful tool for evaluation of the inferior glenohumeral ligament, labrum, rotator cuff, and any bony lesions that may be present.
Anchor fixation stabilization is an arthroscopic technique that uses a cannulated spike to repair Bankart lesions. Both bioabsorbable and fixed anchors have been used to this end, each with their own pull-out specifics that must be taken into account.77 The surgical technique requires an initial stripping of the glenoid neck so that the labrum
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With the patient in the beach chair position (Fig. 17-14), the glenoid neck is first stripped so that the labrum is mobilized to the 6-o’clock position. Once this has been accomplished, anchors are screwed into the glenoid rim and sutures are passed at the 5-, 4-, and 3-o’clock positions. The capsuloligamentous tissue is then secured to the anchors via sutures that are tied sequentially, so that proper tension is restored to the inferior glenohumeral ligament complex.83
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Figure 17-14. Beach chair position. This position allows for easy access to the structures that need to be addressed during arthroscopic correction of anterior shoulder instability, including access to the subdeltoid space.
Although suture anchors offer an accurate means of addressing the pathologies of anterior instability, they are not without risk. Eight cases of suture anchor migration were reported by Kaar and associates84 in 2001, reaffirming the importance of anchor placement and indicating the potential risks associated with implantation of this type of hardware. Rotator interval closure is frequently an integral component of the surgical correction of anterior shoulder instability (Fig. 17-15). As noted, the rotator interval is a triangular space bordered medially by the coracoid process, inferiorly by the subscapularis tendon, and superiorly by the supraspinatus tendon. Field and coworkers85 have selectively closed the rotator interval in patients with isolated rotator interval lesions and associated inferior instability and noted
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good or excellent results in all patients. Manipulation of the rotator interval, in addition to an arthroscopic Bankart repair, can be a powerful tool, allowing the surgeon to remove capsular redundancy, especially in patients with an inferior component to their instability. The inferior glenohumeral ligament complex functions as a hammock-like structure that supports the humeral head throughout a wide range of glenohumeral motion. The inferior glenohumeral ligament complex sits within and is continuous with the remainder of the joint capsule—hence, the hammock within a hammock concept. Thus, closure of the rotator interval indirectly tightens the inferior glenohumeral ligament complex. Suture anchor Bankart repair, in conjunction with rotator interval closure, allows the surgeon to address the instability and, more importantly, preserve a patient’s functional needs.
Nonanatomic Reconstructions Several nonanatomic surgical repairs of anterior glenohumeral instability have been described over the years. The general goal of nonanatomic methods of repair is to stabilize the glenohumeral joint by creating physical obstacles to humeral translation. Nonanatomic repairs come in three different forms: (1) subscapularis muscle alteration procedures; (2) suspensory procedures; and (3) bone block procedures. Although some of these nonanatomic techniques have been reported to have positive results in terms of prevention of further shoulder dislocations and patient satisfaction,86,87 many associated complications have been associated with these types of repairs, such as recurrent anterior dislocations, restricted motion, and premature osteoarthritis.86-92 Moreover, nonanatomic procedures leave the shoulder’s anatomy altered, leading to increased difficulty for the surgeon in addressing the joint if future revision surgeries become
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D
Figure 17-15. Rotator interval closure. The exposed rotator interval (A) is viewed in an anterior to posterior direction through the subdeltoid space. Sutures are passed arthroscopically (B, C) to oppose the edges of the supraspinatus and subscapularis tendons, resulting in surgical closure (D) of the rotator interval. A subdeltoid approach to such a closure allows for extra-articular knot placement, as seen here.
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necessary.93,94 It is our experience, therefore, that the surgical complications mentioned, along with the failure to address the inferior glenohumeral ligament complex, render nonanatomic approaches ineffective and an inappropriate first line of defense against glenohumeral instability. However, for historical purposes, we will briefly outline some of these nonanatomic procedures. Two procedures have been used by orthopedists that involve alteration of the subscapularis muscle. The PuttiPlatt procedure (Fig. 17-16) involves both—shortening the subscapularis muscle through its division and subsequent reattachment and reinforcement of the anterior joint through a reattachment that creates overlap of the muscle’s divided ends.95 Similarly, the Magnuson-Stack procedure attempts to produce stability by advancing the subscapularis tendon laterally, reattaching it to a point on the humerus just lateral to the bicipital groove.96
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Two suspensory procedures, the Nicola97,98 and Gallie99 procedures, are noteworthy. The former uses the long head of the biceps tendon as a suspensory ligament and the latter uses a graft of fascia lata to suspend the humeral head. Finally, two bone block procedures have been described. The Bristow-Latarjet procedure uses a transfer of the distal end of the coracoid process, including the insertion of the conjoint tendon, to the inferior portion of the glenoid rim, thus preventing anterior humeral translation.100,101 The Eden-Hybbinette102,103 procedure functions via much the same concept—namely, blocking anterior translation of the humerus using a bone block. Both procedures can result in early osteoarthritis and restrictions in range of motion, have been linked to complications arising from the implanted hardware,104,105 and can further complicate revision surgery because of significant scarring.93
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Ongoing Debate: Open Versus Arthroscopic Stabilization Despite the data that exist regarding recurrence rates, postoperative morbidities, and a narrowing of the gap between open and arthroscopic stabilization failure rates,106 the decision to pursue one of these two types of stabilization procedures must ultimately be based on what is best for a particular patient. In their 2000 studies, Cole and colleagues107,108 concluded that the outcome differences between open and arthroscopic repair are negligible in the surgical management of traumatic instability of the shoulder if patients are selected appropriately, based on observed intraoperative pathoanatomy. Ultimately, a physician who begins an arthroscopic stabilization should never fear conversion to an open repair because “a good open procedure will always outperform a bad arthroscopic one.”94 Green and Christensen’s 1993 study109 evaluated common surgical morbidities in 38 patients who had Bankart repairs
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C Figure 17-16. Putti-Platt procedure. Subscapularis tendon is divided (A), reattached in overlapping fashion (B), and imbricated (C) at the anterior joint to reinforce the joint and improve anterior glenohumeral stability. (From Osmond-Clark H: Habitual dislocation of the shoulder: The Putti-Platt operation. J Bone Joint Surg 30B:19-25, 1948.)
(20 arthroscopic, 18 open). They found significant decreases in operative time, blood loss, postoperative narcotic use, hospital stay, postoperative fevers, and time lost from work as compared with patients who underwent an open Bankart repair. Today, most arthroscopic stabilization patients are ambulatory. Moreover, as arthroscopic techniques and collective surgical acumen continue to evolve, these morbidities are certain to show continued improvements.
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The open Bankart repair is the gold standard for anterior instability treatment and has typically had low failure rates.65 Pagnani and Dome110 have followed 58 American football players at an average time point of 37 months post–open Bankart repair and found that only 3.4% of patients experienced a recurrent subluxation, 94.8% were rated as excellent or good, and 89.6% were able to return to playing their sport for at least 1 year. However, other studies have generated contradictory data. Uhorchak and associates111 have reported on 66 patients followed up at an average of 47 months; 23% experienced recurrent dislocation (3%), fewer than three postoperative subluxations (12%), or multiple recurrent subluxations (8%). Magnusson and coworkers112 have reported similarly high failure rates for open repair. Mohtadi and colleagues,113 however, came to the conclusion, through their metaanalysis, that “open repair has a more favorable outcome with respect to recurrence and return to activity.” The question must be asked as to whether an open Bankart repair is still the gold standard for treatment of anterior shoulder instability. Arthroscopic stabilization techniques have matured over the past 2 decades, as evidenced by reports of low failure rates and patient satisfaction. In a comprehensive study of the early evolution of arthroscopic shoulder stabilization, DeBarardino and associates7 have conducted an extensive study of 127 West Point cadets who experienced acute glenohumeral dislocations; 72 patients were treated with arthroscopic stabilization and evaluated by the authors in three cohorts determined by the time period in which the surgery was performed. They found that the first group of 9 cadets, treated with staple capsulorrhaphy between 1986 and 1988, showed a failure rate of 22.2%. The second group of 21 cadets, treated using transglenoid sutures between 1988 and 1991, demonstrated a failure rate of 14%. The final group of 42 cadets yielded a failure rate of only 10% and were treated with bioabsorbable tack fixation. This study is of particular note because it demonstrates the evolution from staple capsulorrhaphy to bioabsorbable anchor fixation and its associated decrease in failure rates, and because the cohorts were made up of young men (average age, 19.5 years) leading active lives. Not all reports have shown failure rates as low as 10%. In fact, other studies have reported highly variable failure rates, ranging from 0% to almost 50%.4-6,8,69,114-116 More recently, however, reports have indicated recurrence rates in arthroscopically treated patients that rival those seen in patients treated with the more traditional open Bankart repairs.106,117,118 Kim and coworkers117 have reported a recurrence rate of only 4% in 167 patients followed up at a mean of 44 months who had a suture anchor fixation. They cited Rowe scores of excellent or good in 95% of patients, with 91% of patients able to return to a preinjury levels of activity, and an average loss of only 2 degrees of external rotation.
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Contact athletes who present with anterior shoulder instability represent a very controversial subset of patients. Deciding whether these high demand patients should be managed with open surgical repair instead of arthroscopic repair remains a crux and is debated substantially in the literature. Hubbell and colleagues119 have reported on differences in arthroscopic and open repairs in collision athletes and found that 6 of 9 such athletes treated arthroscopically experienced “repeat instability,” whereas no such patients treated with an open repair developed a recurrence. Although patients treated with an open repair showed a lower rate of recurrence, the patients demonstrated restrictions in their range of motion, particularly that of external rotation. Based on their findings, it was recommended that collision athletes suffering from anterior shoulder instability should undergo an open repair, whereas athletes whose sport demands a more extensive range of motion, such as swimmers and throwers, should undergo arthroscopic repair. In contrast to the results of this study, other reports have suggested that arthroscopic repair of the unstable glenohumeral joint in collision and contact athletes is an acceptable means of intervention.120,121 Burkhart and DeBeer63 have described their results for 101 contact athletes who underwent arthroscopic Bankart repairs. Initial review of the results seems to be incomplete, because recurrence rates appear high. However, when the patients are segregated into two cohorts based on anatomic findings—(1) those who demonstrate an engaging Hill-Sachs lesion or an inverted pear glenoid, and (2) those not in the first group—the results are striking. The stratified results showed an 87% recurrence rate in group 1 and only a 6.5% recurrence rate for those in group 2. Burkhart and DeBeer’s study63 has demonstrated the importance of intraoperative decision making that best suits the patient. Although it is not our practice to exclude arthroscopic stabilization before entering the operating room, some have suggested contraindications to this procedure, which include an inverted pear glenoid or an engaging Hill-Sachs lesion,63 capsular defects, previously failed open or arthroscopic stabilizations, or previously failed thermal capsulorrhaphy.94,122 Ultimately, we believe that we can address anterior instability arthroscopically with equal or greater efficacy than through the use of an open technique for most patients. However, when unable to accomplish a satisfactory stabilization arthroscopically because of any of the aforementioned contraindications, we do not hesitate to convert to an open procedure. If a patient has an isolated Bankart lesion with unidirectional instability, arthroscopic failure rates today almost match those of open repairs. Failure rates, however, do not match in patients with multidirectional instability. Also, as discussed earlier, closure of the rotator interval is an important and useful method for reducing or eliminating capsular redundancy, especially when the patient has an inferior component to their instability.85
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Millet and colleagues94 have also prescribed humeral avulsion of the inferior glenohumeral ligament complex as a potential contraindication to arthroscopic stabilization because of difficulty in accessing the space adequately with current arthroscopic techniques. Pagnani and Dome110 have cited advantages to the open technique, including (1) being able to leave the arm in a position that facilitates surgery without having to worry about losing proper visibility, and (2) better extracapsular visualization of the rotator interval, with easier access for closure of this space, if necessary. Open technique offers access to and visualization of what current arthroscopic techniques cannot encompass, but what future techniques may allow.
Subdeltoid Arthroscopic Stabilization Subdeltoid arthroscopy was developed by Stephen J. O’Brien as a means of arthroscopically transferring the long head of the biceps tendon from its intra-articular origin at the supraglenoid tubercle to the extracapsular conjoint tendon on the coracoid process (Fig. 17-17).123 Subdeltoid arthroscopy allows for visualization of many anatomic structures that were once unviewable arthroscopically in a clear, welldistended field that can be easily maintained through saline insufflation for over 2 hours if necessary (Fig. 17-18). Verma and asssociates123 have briefly described reaching the subdeltoid space using careful dissection with a mechanical shaver and a radiofrequency device from the posterior
Figure 17-18. Subdeltoid space. This can be visualized through clearing of the fascial plane with a radiofrequency device while insufflating with normal saline.
portal after first moving anteriorly through the subacromial space. Within the fascial plane, the subdeltoid space is readily cleared with the same devices (Fig. 17-19). The resulting space, now distended with saline, allows direct visualization of many anatomic structures of the anterior shoulder and chest, previously seen only during open procedures, including the coracoid process, conjoint tendon, pectoralis major and minor, anterior capsule subscapularis tendon,
d
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Figure 17-17. Subdeltoid arthroscopy. The normal anatomy exposed by subdeltoid arthroscopy includes the anterior glenohumeral capsule, pectoralis major tendon, long head of the biceps tendon, conjoint tendon, coracoid process, coracohumeral ligament, supraspinatus tendon, and subscapularis tendon.
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Figure 17-19. Arthroscopic exposure of the subdeltoid space. This reveals a “room with a view” and allows the surgeon to view the coracoid process (cp), conjoint tendon (ct), deltoid muscle (d), pectoralis major muscle and tendon (pm), anteroinferior glenohumeral capsule (gc), and humerus (h) clearly. The anatomy is clearly defined from a posterior portal looking anteriorly in this right shoulder.
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supraspinatus tendon, and the rotator interval. In addition to reducing the bleeding, scarring, pain, and soft tissue damage associated with open procedures, we believe that when the subdeltoid space is distended with saline, visibility is actually greater than what can be achieved with an open technique because the surgeon can see more normal anatomic relationships. Furthermore, subdeltoid arthroscopy allows the surgeon to perform essentially the same gold standard operation as an open procedure. To date, Dr. O’Brien has performed several virgin and revision arthroscopic stabilizations using the subdeltoid space. These are exciting advances; subdeltoid arthroscopy will provide shoulder surgeons with another tool to address anterior shoulder pathology through less invasive means and obviate the need for open shoulder procedures.
REHABILITATION FOLLOWING ANTERIOR STABILIZATION Postoperatively, patients should be given limitations in range of motion for at least 3 weeks according to the goals set at the time of surgery. Because a baseball pitcher needs greater flexibility of the shoulder than a football linebacker, these two athletes’ recoveries should be tailored according to performance needs. The rehabilitative process begins with passive range-of-motion exercises, with progression to active assisted and finally to active range-of-motion and strengthening exercises. Successful rehabilitation often demands the involvement of a physical therapist who is knowledgeable and experienced in handling patients who have had recent anterior stabilization procedures. References 1. McFarland EG, Campbell G, McDowell J: Posterior shoulder laxity in asymptomatic athletes. Am J Sports Med 24: 468-471, 1996. 2. Harryman DT 2nd, Sidles JA, Harris SL, et al: Laxity of the normal glenohumeral joint: A quantitative in vivo assessment. J Shoulder Elbow Surg 1:66-76, 1992. 3. National Federation of State High School Associations: 2001 Athletic Participation Summary. Indianapolis, National Federation of State High School Associations, 2002. 4. Arciero RA, Taylor DC, Snyder RJ, Uhorchak JM: Arthroscopic bioabsorbable tack stabilization of initial anterior shoulder dislocations: A preliminary report. Arthroscopy 11:410-417, 1995. 5. Grana WA, Buckley PD, Yates CK: Arthroscopic Bankart suture repair. Am J Sports Med 21:348-353, 1993. 6. Youssef JA, Carr CF, Walther CE, Murphy JM: Arthroscopic Bankart suture repair for recurrent traumatic unidirectional anterior shoulder dislocations. Arthroscopy 11:561-563, 1995. 7. DeBerardino TM, Arciero RA, Taylor DC: Arthroscopic stabilization of acute initial anterior shoulder dislocation: the West Point experience. J South Orthop Assoc 5:263-271, 1996.
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8. Speer KP, Warren RF, Pagnani M, Warner JJ: An arthroscopic technique for anterior stabilization of the shoulder with a bioabsorbable tack. J Bone Joint Surg Am 78:1801-1807, 1996. 9. Kim SH, Ha KI, Cho YB, et al: Arthroscopic anterior stabilization of the shoulder: Two- to six-year follow-up. J Bone Joint Surg Am 85:1511-1518, 2003. 10. Henry JH, Genung JA: Natural history of glenohumeral dislocation—revisited. Am J Sports Med 10:135-137, 1982. 11. Arciero RA, Wheeler JH, Ryan JB, McBride JT: Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am J Sports Med 22:589-594, 1994. 12. O’Brien S, Fealy S, Drakos M, Botts J: Developmental anatomy of the shoulder and anatomy of the glenohumeral joint. In Rockwood CA Jr., Matsen FA III, Wirth MA, Lippitt SB (eds): The Shoulder, 3rd ed. Philadelphia, WB Saunders, 2004, pp 1-31. 13. Lippitt S, Matsen F: Mechanisms of glenohumeral joint stability. Clin Orthop Relat Res (291):20-28, 1993. 14. Ferrari DA: Capsular ligaments of the shoulder. Anatomical and functional study of the anterior superior capsule. Am J Sports Med 18:20-24, 1990. 15. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 16. Warner JJ, Deng XH, Warren RF, Torzilli PA: Static capsuloligamentous restraints to superior-inferior translation of the glenohumeral joint. Am J Sports Med 20:675-685, 1992. 17. Bigliani LU, Kelkar R, Flatow EL, et al: Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res (330):13-30, 1996. 18. Bach BR, Warren RF, Fronek J: Disruption of the lateral capsule of the shoulder. A cause of recurrent dislocation. J Bone Joint Surg Br 70:274-276, 1988. 19. Bigliani LU, Pollock RG, Soslowsky LJ, et al: Tensile properties of the inferior glenohumeral ligament. J Orthop Res 10:187-197, 1992. 20. Blasier RB, Guldberg RE, Rothman ED: Anterior shoulder stability: Contribution of rotator cuff forcesand the capsular ligaments in a cadaver model. J Shoulder Elbow Surg 1: 140-50, 1992. 21. Saha AK: The classic. Mechanism of shoulder movements and a plea for the recognition of “zero position” of glenohumeral joint. Clin Orthop Relat Res (173):3-10, 1983. 22. Saha AK: Theory of Shoulder Mechanism: Descriptive and Applied. Springfield, Ill, Charles C Thomas, 1961. 23. Saha AK: Dynamic stability of the glenohumeral joint. Acta Orthop Scand 42:491-505, 1971. 24. Howell SM, Galinat BJ: The containment mechanism: The primary stabilizer of the glenohumeral joint. Presented at the Annual Meeting of The American Academy of Orthopedic Surgeons. San Francisco, January 23, 1987. 25. Dugas JR, Cooper DE, O’Brien SJ: Gross and microscopic anatomy of the shoulder. In Warren RF, Craig EV, Altchek DW (eds): The Unstable Shoulder. Philadelphia, Lippincott-Raven, 1999, pp 27-50. 26. Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC: Articular geometry of the glenohumeral joint. Clin Orthop Relat Res (285):181-190, 1992. 27. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 30:20-26, 2002.
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28. Pieper HG: Humeral torsion in the throwing arm of handball players. Am J Sports Med 26:247-253, 1998. 29. Howell SM, Galinat BJ, Renzi AJ, Marone PJ: Normal and abnormal mechanics of the glenohumeral joint in the horizontal plane. J Bone Joint Surg Am 70:227-232, 1988. 30. Cooper DE, Arnoczky SP, O’Brien SJ, et al: Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am 74:46-52, 1992. 31. Lippitt SB, Vanderhooft JE, Harris SL, et al: Glenohumeral stability from concavity-compression: A quantitative analysis. J Shoulder Elbow Surg 2:27-35, 1993. 32. Ciccone WJ 2nd, Hunt TJ, Lieber R, et al: Multiquadrant digital analysis of shoulder capsular thickness. Arthroscopy 16:457-641, 2000. 33. Yamazaki S: Fibrous structure of the joint capsule in the human shoulder. Okajimas Folia Anat Jpn 67:127-139, 1990. 34. Rodeo SA, Suzuki K, Yamauchi M, et al: Analysis of collagen and elastic fibers in shoulder capsule in patients with shoulder instability. Am J Sports Med 26:634-643,1998. 35. Habermeyer P, Schuller U, Wiedemann E: The intra-articular pressure of the shoulder: An experimental study on the role of the glenoid labrum in stabilizing the joint. Arthroscopy 8:166-172, 1992. 36. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 37. Steinbeck J, Liljenqvist U, Jerosch J: The anatomy of the glenohumeral ligamentous complex and its contribution to anterior shoulder stability. J Shoulder Elbow Surg 7: 122-126, 1998. 38. DePalma AF, Callery G, Bennett GA: Variational anatomy and degenerative lesions of the shoulder joint. AAOS Instr Course Lect 6:255-281, 1949. 39. Jost B, Koch PP, Gerber C: Anatomy and functional aspects of the rotator interval. J Shoulder Elbow Surg 9:336-341, 2000. 40. O’Brien SJ, Schwartz RS, Warren RF, Torzilli PA: Capsular restraints to anterior-posterior motion of the abducted shoulder: A biomechanical study. J Shoulder Elbow Surg 4:298-308, 1995. 41. Levine WN, Flatow EL: The pathophysiology of shoulder instability. Am J Sports Med 28:910-917, 2000. 42. DeLorme D: Die Hemmungs bander des Schultergelenks and ihre Deductung fur die Schulter Luxationen. Arch Klin Chir (92):79, 1910. 43. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 44. Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53-66, 1992 . 45. McMahon PJ, Dettling J, Sandusky MD, et al: The anterior band of the inferior glenohumeral ligament. Assessment of its permanent deformation and the anatomy of its glenoid attachment. J Bone Joint Surg Br 81:406-413, 1999. 46. Ticker JB, Bigliani LU, Soslowsky LJ, et al: Inferior glenohumeral ligament: Geometric and strain-rate dependent properties. J Shoulder Elbow Surg 5:269-279, 1996. 47. Gohlke F, Essigkrug B, Schmitz F: The pattern of the collagen fiber bundles of the capsule of the glenohumeral joint. J Shoulder Elbow Surg 3:111-128, 1994.
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48. Debski RE, Moore SM, Mercer JL, et al: The collagen fibers of the anteroinferior capsulolabrum have multiaxial orientation to resist shoulder dislocation. J Shoulder Elbow Surg 12:247-252, 2003. 49. Soslowsky LJ, Malicky DM, Blasier RB: Active and passive factors in inferior glenohumeral stabilization: A biomechanical model. J Shoulder Elbow Surg 6:371-379, 1997. 50. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 18:579-584, 1990. 51. Neer CS 2nd: Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am 52:1077-1089, 1970. 52. Bennett WF: Visualization of the anatomy of the rotator interval and bicipital sheath. Arthroscopy 17:107-111, 2001. 53. Cole BJ, Rodeo SA, O’Brien SJ, et al: The anatomy and histology of the rotator interval capsule of the shoulder. Clin Orthop Relat Res (390):129-137, 2001. 54. Curl LA, Warren RF: Glenohumeral joint stability. Selective cutting studies on the static capsular restraints. Clin Orthop Relat Res (330):54-65, 1996 . 55. Pagnani MJ, Warren RF: Stabilizers of the glenohumeral joint. J Shoulder Elbow Surg 3:173-190, 1994. 56. Warren RF, Kornblatt IB, Marchand R: Static factors affecting posterior shoulder stability. Orthop Trans 8:89, 1984. 57. Speer KP, Deng X, Borrero S, et al: Biomechanical evaluation of a simulated Bankart lesion. J Bone Joint Surg Am 76:1819-1826, 1994. 58. Wolf EM, Cheng JC, Dickson K: Humeral avulsion of glenohumeral ligaments as a cause of anterior shoulder instability. Arthroscopy 11:600-607, 1995. 59. Malicky DM, Kuhn JE, Frisancho JC, et al: Neer Award 2001. Nonrecoverable strain fields of the anteroinferior glenohumeral capsule under subluxation. J Shoulder Elbow Surg 11:529-540, 2002. 60. Malicky DM, Soslowsky LJ, Kuhn JE, et al: Total strain fields of the antero-inferior shoulder capsule under subluxation: A stereoradiogrammetric study. J Biomech Eng 123:425-431, 2001. 61. Pollock RG, Wang VM, Bucchieri JS, et al: Effects of repetitive subfailure strains on the mechanical behavior of the inferior glenohumeral ligament. J Shoulder Elbow Surg 9: 427-435, 2000. 62. Remia LF, Ravalin RV, Lemly KS, et al: Biomechanical evaluation of multidirectional glenohumeral instability and repair. Clin Orthop Relat Res (416):225-236, 2003. 63. Burkhart SS, De Beer JF: Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: Significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 16:677694, 2000. 64. Sugaya H, Moriishi J, Dohi M, et al: Glenoid rim morphology in recurrent anterior glenohumeral instability. J Bone Joint Surg Am 85:878-884, 2003. 65. Rowe CR, Patel D, Southmayd WW: The Bankart procedure: A long-term end-result study. J Bone Joint Surg Am 60: 1-16, 1978. 66. Neer CS 2nd, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am 62:897-908, 1980.
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67. Altchek DW, Warren RF, Skyhar MJ, Ortiz G: T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone Joint Surg Am 73:105-112, 1991. 68. Johnson JR, Bayley JI: Early complications of acute anterior dislocation of the shoulder in the middle-aged and elderly patient. Injury 13:431-434, 1982. 69. Pagnani MJ, Warren RF, Altchek DW, et al: Arthroscopic shoulder stabilization using transglenoid sutures. A four-year minimum follow-up. Am J Sports Med 24:459-467, 1996. 70. Peterson CA, Altchek DW, Warren RF: Operative arthroscopy. In Rockwood CA, Matsen FA (eds): The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 290-335. 71. Pagnani MJ, Warren RF: Arthroscopic shoulder stabilization. Oper Tech Sports Med 1:276-284, 1993. 72. McFarland EG, Neira CA, Gutierrez MI, et al: Clinical significance of the arthroscopic drive-through sign in shoulder surgery. Arthroscopy 17:38-43, 2001. 73. Lane JG, Sachs RA, Riehl B: Arthroscopic staple capsulorrhaphy: A long-term follow-up. Arthroscopy 9:190-194, 1993. 74. Coughlin L, Rubinovich M, Johansson J, et al: Arthroscopic staple capsulorrhaphy for anterior shoulder instability. Am J Sports Med 20:253-256, 1992. 75. Arnoczky SP, Aksan A: Thermal modification of connective tissues: Basic science considerations and clinical implications. Instr Course Lect 50:3-11, 2001. 76. Arnoczky SP, Aksan A: Thermal modification of connective tissues: Basic science considerations and clinical implications. J Am Acad Orthop Surg 8:305-313, 2000. 77. Fealy S, Drakos MC, Allen AA, Warren RF: Arthroscopic bankart repair: Experience with an absorbable, transfixing implant. Clin Orthop Relat Res (390):31-41, 2001. 78. Flik KR, Lopez V, Allen AA: Single-point fixation for shoulder instability. In Miller MD, Cole BJ (eds): Textbook of Arthroscopy. Philadelphia, Elsevier; 2004, pp 94-104. 79. Arciero RA, Taylor DC, Snyder RJ, Uhorchak JM: Arthroscopic bioabsorbable tack stabilization of initial anterior shoulder dislocations: A preliminary report. Arthroscopy 11:410-417, 1995. 80. Karlsson J, Magnusson L, Ejerhed L, et al: Comparison of open and arthroscopic stabilization for recurrent shoulder dislocation in patients with a Bankart lesion. Am J Sports Med 29:538-542, 2001. 81. Segmuller HE, Hayes MG, Saies AD: Arthroscopic repair of glenolabral injuries with an absorbable fixation device. J Shoulder Elbow Surg 6:383-392, 1997. 82. Cole BJ, Romeo AA, Warner JJ: Arthroscopic Bankart repair with the Suretac device for traumatic anterior shoulder instability in athletes. Orthop Clin North Am 32:411-421, 2001. 83. Moskal MJ, Pearl ML: Suture anchor fixation for shoulder instability. In Miller MD, Cole BJ (eds): Textbook of Arthroscopy. Philadelphia, Elsevier, 2004, pp 105-112. 84. Kaar TK, Schenck RC Jr, Wirth MA, Rockwood CA Jr: Complications of metallic suture anchors in shoulder surgery: A report of 8 cases. Arthroscopy 7:31-37, 2001. 85. Field LD, Warren RF, O’Brien SJ, et al: Isolated closure of rotator interval defects for shoulder instability. Am J Sports Med 23:557-563, 1995. 86. Hill JA, Lombardo SJ, Kerlan RK, et al: The modification of the Bristow-Helfet procedure for recurrent anterior shoulder subluxations and dislocations. Am J Sports Med 9:283-287, 1981.
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87. Hovelius L, Sandstrom B, Sundgren K, Saebo M: One hundred eighteen Bristow-Latarjet repairs for recurrent anterior dislocation of the shoulder prospectively followed for fifteen years: Study I—clinical results. J Shoulder Elbow Surg 13:509-516, 2004. 88. Rowe CR, Zarins B, Ciullo JV: Recurrent anterior dislocation of the shoulder after surgical repair. Apparent causes of failure and treatment. J Bone Joint Surg Am 66:159-168, 1984. 89. Hovelius L, Thorling J, Fredin H: Recurrent anterior dislocation of the shoulder. Results after the Bankart and PuttiPlatt operations. J Bone Joint Surg Am 61:566-569, 1979. 90. Fredriksson AS, Tegner Y: Results of the Putti-Platt operation for recurrent anterior dislocation of the shoulder. Int Orthop 15:185-188, 1991. 91. van der Zwaag HM, Brand R, Obermann WR, Rozing PM: Glenohumeral osteoarthrosis after Putti-Platt repair. J Shoulder Elbow Surg 8:252-258, 1999. 92. Rachbauer F, Ogon M, Wimmer C, et al: Gleohumeral osteoarthrosis after the Eden-Hybbinette procedure. Clin Orthop Relat Res (373):135-140, 2000. 93. Young DC, Rockwood CA Jr: Complications of a failed Bristow procedure and their management. J Bone Joint Surg Am 73:969-981, 1991. 94. Millett PJ, Clavert P, Warner JJ: Open operative treatment for anterior shoulder instability: When and why? J Bone Joint Surg Am 87:419-432, 2005. 95. Osmond-Clarke H: Habitual dislocation of the shoulder: The Putti-Platt operation. J Bone Joint Surg Br 30:19-25, 1948. 96. Magnuson PB, Stack JK: Recurrent dislocation of the shoulder. JAMA 123:889-892, 1943. 97. Nicola T: Recurrent dislocation of the shoulder: Its treatment by transplantation of the long head of the biceps. Am J Surg 6:815, 1929. 98. Nicola T: Recurrent dislocation of the shoulder. Am J Surg 86:85-91, 1953. 99. Gallie WE, Le Mesurier AB: An operation for the relief of recurring dislocation of the shoulder. Trans Am Surg Assoc 45:392-398, 1927. 100. Helfet AJ: Coracoid transplantation for recurring dislocation of the shoulder. J Bone Joint Surg Br 40:198-202, 1958. 101. Latarjet M: Technic of coracoid preglenoid arthroereisis in the treatment of recurrent dislocation of the shoulder. Lyon Chir 54:604-607, 1958. 102. Eden R: Zur operativen Behandlung der habituellen Schulterluxation unter mitteilung, eines neuen Verfahrens bei abriss am inneren Pfannenrande. Deutsche Z Chir 144:269, 1918. 103. Hybbinette S: De la transplantation d’un fragment osseux pour remedier aux luxations recidivantes de l’epaule; constatations et resultats operatiores. Acta Chir Scand 71: 411-445, 1932. 104. Zuckerman JD, Matsen FA 3rd: Complications about the glenohumeral joint related to the use of screws and staples. J Bone Joint Surg Am 66:175-180, 1984. 105. Bach BR Jr, O’Brien SJ, Warren RF, Leighton M: An unusual neurological complication of the Bristow procedure. A case report. J Bone Joint Surg Am 70:458-460, 1988. 106. Kim SH, Ha KI, Kim SH: Bankart repair in traumatic anterior shoulder instability: Open versus arthroscopic technique. Arthroscopy 18:755-763, 2002.
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107. Cole BJ, L’Insalata J, Irrgang J, Warner JJ: Comparison of arthroscopic and open anterior shoulder stabilization. A two- to six-year follow-up study. J Bone Joint Surg Am 82:1108-1114, 2000. 108. Cole BJ, Warner JJ: Arthroscopic versus open Bankart repair for traumatic anterior shoulder instability. Clin Sports Med 19:19-48, 2000. 109. Green MR, Christensen KP: Arthroscopic versus open Bankart procedures: A comparison of early morbidity and complications. Arthroscopy 9:371-374, 1993. 110. Pagnani MJ, Dome DC: Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg Am 84:711-715, 2002. 111. Uhorchak JM, Arciero RA, Huggard D, Taylor DC: Recurrent shoulder instability after open reconstruction in athletes involved in collision and contact sports. Am J Sports Med 28:794-799, 2000. 112. Magnusson L, Kartus J, Ejerhed L, et al: Revisiting the open Bankart experience: A four- to nine-year follow-up. Am J Sports Med 30:778-782, 2002. 113. Mohtadi NG, Bitar IJ, Sasyniuk TM, et al: Arthroscopic versus open repair for traumatic anterior shoulder instability: A meta-analysis. Arthroscopy 21:652-658, 2005. 114. Walch G, Boileau P, Levigne C, et al: Arthroscopic stabilization for recurrent anterior shoulder dislocation: Results of 59 cases. Arthroscopy 11:173-179, 1995. 115. Mologne TS, Lapoint JM, Morin WD, et al: Arthroscopic anterior labral reconstruction using a transglenoid suture technique. Results in active-duty military patients. Am J Sports Med 24:268-274, 1996.
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116. Morgan CD, Bodenstab AB: Arthroscopic Bankart suture repair: Technique and early results. Arthroscopy 3:111-122, 1987. 117. Kim SH, Ha KI, Cho YB, et al: Arthroscopic anterior stabilization of the shoulder: Two- to six-year follow-up. J Bone Joint Surg Am 85:1511-1518, 2003. 118. Potzl W, Witt KA, Hackenberg L, et al: Results of suture anchor repair of anteroinferior shoulder instability: A prospective clinical study of 85 shoulders. J Shoulder Elbow Surg 12:322-326, 2003. 119. Hubbell JD, Ahmad S, Bezenoff LS, et al: Comparison of shoulder stabilization using arthroscopic transglenoid sutures versus open capsulolabral repairs: A 5-year minimum follow-up. Am J Sports Med 32:650-654, 2004. 120. Mazzocca AD, Brown FM,Jr, Carreira DS, et al: Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med 33:52-60, 2005. 121. O’Neill DB: Arthroscopic Bankart repair of anterior detachments of the glenoid labrum. A prospective study. J Bone Joint Surg Am 81:1357-1366, 1999. 122. Stein DA, Jazrawi L, Bartolozzi AR: Arthroscopic stabilization of anterior shoulder instability: A review of the literature. Arthroscopy 18:912-924, 2002. 123. Verma NN, Drakos M, O’Brien SJ: Arthroscopic transfer of the long head biceps to the conjoint tendon. Arthroscopy 21:764, 2005.
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CHAPTER 18 Posterior Shoulder Instability John C. Austin, Samer S. Hasan, Timothy P. Heckmann, and Thomas N. Lindenfeld
Posterior instability of the shoulder is less commonly diagnosed than anterior instability of the shoulder. The prevalence of posterior instability is unknown because of a lack of specific diagnostic criteria, but it may affect 5% or more of all patients with glenohumeral instability.1,2 The cause of posterior shoulder instability can be traumatic or atraumatic, or it can arise as a component of multidirectional instability. Patients are most commonly young men between the ages of 15 and 30 years who are frequently involved in overhead or contact sports. Partly because of the difficulty in accurate diagnosis, treatment strategies have varied widely and many open and arthroscopic surgical techniques have been described in the literature.3-7
a primary cause of posterior shoulder instability, although it may be a contributory factor.9,10 In this chapter, the pathoanatomy, description of affected athletes, physical examination, imaging studies, nonoperative management, operative management, and treatment results for posterior shoulder instability will be reviewed.
ANATOMY, BIOMECHANICS, AND PATHOMECHANICS OF POSTERIOR INSTABILITY There are static and dynamic determinants that function to achieve glenohumeral joint stability. Static determinants include glenohumeral joint morphology, the labrum, and capsuloligamentous constraints.
Traumatic posterior shoulder instability frequently involves contact sports such as football or rugby. Other traumatic causes include accidents involving automobiles, all-terrain vehicles, and motocross racing and violent military or labor injuries that often involve catching a heavy load from overhead. The mechanism of injury is frequently an acute posterior force on the glenohumeral joint in a flexed, adducted, and internally rotated position. As a result of the injury, the shoulder may dislocate. The direction of dislocation is typically posteroinferior, in the same manner as the more common anteroinferior dislocation. Traumatic injuries are often associated with a posterior Bankart lesion, with detachment of the posterior capsule and labrum below the glenoid equator, and a stretch injury to the posteroinferior capsule with injury to the posterior band of the inferior glenohumeral ligament. These injuries can be associated with a bony posterior glenoid rim fracture and a reverse Hill-Sachs lesion (Fig. 18-1), which is an anterosuperior humeral head impaction fracture or defect resulting from a posterior dislocation.
The concave shape of the glenoid provides some inherent stability as it articulates with the convex surface of the humeral head. This depth is increased by the glenoid labrum. Concavity compression is an important stabilizing mechanism in which compression of the convex humeral head into the concave glenoid fossa resists humeral head translation. Glenoid version influences glenohumeral stability and varies in the normal population.11,12 Excessive retroversion of the glenoid and loss of concavity of the inferior aspect of the glenoid have been associated with atraumatic posterior shoulder instability.12,13 Glenoid retroversion is infrequently a primary cause of instability,2 but it should be considered as a contributory factor. Kim and colleagues12 have assessed glenoid osseous and chondrolabral retroversion using magnetic resonance arthrography. Osseous and chondrolabral retroversion varies between the superior, middle, and inferior aspects of the glenoid. Furthermore, patients with posteroinferior glenohumeral instability had 4 degrees of increased chondrolabral retroversion in the middle and inferior planes compared with normal controls. Normal chondrolabral glenoid retroversion ranged from 1 to 8 degrees in patients without glenohumeral instability and from 5 to 9 degrees in patients with posteroinferior instability.
Atraumatic posterior shoulder instability can be associated with repetitive microtrauma such as repetitive heavy weightlifting during bench press activities, cumulative injury from push-ups, and sports that demand wide arcs of glenohumeral motion, such as swimming and golf. The follow-through phases of golf and swimming can place significant stress on the posterior shoulder capsule. Atraumatic posterior instability may occur theoretically from excessive humeral head retroversion, posterior glenoid dysplasia, or increased glenoid retroversion. Glenoid dysplasia is rare and is often associated with brachial plexus birth palsy.8 Increased glenoid retroversion is infrequently
Soft tissue structures such as the glenohumeral ligaments and shoulder capsule also contribute to glenohumeral stability. Just as the anterior band of the inferior glenohumeral ligament is an important restraint to anterior humeral head translation in abduction and external rotation, 209
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Figure 18-1. Reverse Hill-Sachs lesion. Note the increased signal on this magnetic resonance imaging scan along the anterosuperior humeral head.
the posterior band of the inferior glenohumeral ligament similarly restricts posterior translation of the humeral head in internal rotation.14 Tears involving the posteroinferior capsulolabral complex, termed a reverse Bankart lesion, often involve the posterior band of the inferior glenohumeral ligament and are frequently associated with a traumatic shoulder injury. Posterior capsulolabral deficiency can also be degenerative in origin, related to repetitive microtrauma or recurrent subluxations.4,6,7 Biomechanical studies have increased our understanding of the pathology associated with posterior shoulder dislocation and subluxation. Recurrent subluxation can create plastic deformation of the posteroinferior capsule, leading to increased joint volume.2 The presence of synovial fluid within a finite volume contributes to articular adhesioncohesion forces and, with negative intra-articular pressure, helps stabilize the glenohumeral joint further.15 These passive restraints become less effective in the presence of increased capsular volume. Other studies have examined capsuloligamentous injury following posterior shoulder dislocation using cadaver models. Warren and associates16 have reported increased posterior translation of the humeral head relative to the glenoid in adduction and internal rotation with sectioning of the posterior band of the inferior glenohumeral ligament and posterior capsule. The rotator interval is the region of the anterosuperior capsule between the superior border of the subscapularis tendon and anterior border of the supraspinatus tendon (anterosuperior capsule from the 12- to 3-o’clock position for a right shoulder). It helps to prevent instability in patients
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with excessive posterior or inferior translation, especially with the arm adducted.17 Warren and coworkers16 have found that the rotator interval has to be sectioned for complete posterior shoulder dislocation to occur. Ovesen and colleagues18,19 have reported that posterior glenohumeral dislocation in a position of adduction and internal rotation creates a posterior capsule injury, along with complete rupture of the teres minor and partial injury of the infraspinatus. There is also injury to the anterior capsule, most notably at the rotator interval. Weber and Caspari20 have studied posterior dislocations in cadavers with the shoulder in forward flexion and internal rotation. Posterior capsulolabral avulsions were found in all specimens tested; it was concluded that injury to the posterior band of the inferior glenohumeral ligament and posterior capsule leads to posterior instability. Collectively, these studies have contributed to the development of the circle concept of shoulder instability, in which increased translation and subluxation are possible with ligament injuries to one side of the joint, whereas complete dislocation requires capsuloligamentous injury on both sides. This has led to the concept of repair of the rotator interval in the treatment of marked posteroinferior glenohumeral instability. Other cadaver studies have examined the material properties of the posterior capsule and the effect of capsulorrhaphy on glenohumeral range of motion. Bey and associates21 have examined the mechanical properties of the posterior glenohumeral capsule and found no significant differences in failure strains or material properties among the superior, middle, and inferior portions of the posterior capsule and the anterior band of the inferior glenohumeral ligament. Mechanical testing has demonstrated that 75% of specimens fail near the glenoid insertion. The posterior strains are highest near the glenoid, which explains why the glenoid labrum and capsule near the glenoid fail more commonly than off the humeral attachment or in the midcapsular region. Gerber and coworkers22 have performed a cadaver study examining the effects of selective capsulorrhaphy on glenohumeral joint passive range of motion. One-centimeter selective capsular plications were performed on eight human cadaver shoulders, with subsequent analysis of shoulder range of motion. Anterosuperior capsular plication (rotator interval closure) decreases external rotation of the adducted arm by 30 degrees. Total posterior capsular plication limits internal rotation by more than 20 degrees. Total inferior capsular plication restricts abduction by a mean of 28 degrees. Another cadaver study23 has examined the effects of arthroscopic thermal capsulorrhaphy of the posterior glenohumeral capsule with a radiofrequency probe. There was no significant decrease in posterior or anterior glenohumeral translation following thermal capsulorrhaphy. It was proposed that the paucity of collagen in the thin posterior capsule explains the ineffectiveness of thermal capsulorrhaphy in this region. Lesions associated with posterior shoulder instability include injuries to the posterior capsule and ligaments,
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labral lesions, chondrolabral lesions, and glenoid defects. Posterior capsuloligamentous disruption can occur at its glenoid or humeral attachment sites, as well as in the midportion of the posterior capsule. Posterior capsuloligamentous disruption at the glenoid attachment site is the most common.6,21,24 Avulsion of the humeral attachment of the posterior capsule and posterior band of the inferior glenohumeral ligament is called a reverse humeral avulsion of the glenohumeral ligament (reverse HAGHL) and is relatively uncommon (Fig.18-2).25-27 There have been case reports of reverse HAGHL lesions caused by sports contact injury and trauma. Posterior midcapsular disruption allows for arthroscopic visualization of the infraspinatus and teres minor and is less common than avulsion from the posterior labrum.28 Rotator interval insufficiency can be associated with injuries to the coracohumeral, superior, and middle glenohumeral ligaments, and may contribute to bidirectional (posterior and inferior) instability.2 Four types of labral lesions have been described— nondisplaced tear, marginal crack (Kim lesion), chondrolabral erosion, or flap tear. The Kim lesion is a superficial crack between the posteroinferior labrum and glenoid articular cartilage.29 This subtle surface change often belies more extensive deep capsuloligamentous stripping. Posterior labral and chondrolabral lesions include posterior chondrolabral defect of the glenoid rim and posterior labrocapsular periosteal sleeve avulsion (reverse anterior labroligamentous periosteal sleeve avulsion [reverse ALPSA] lesion).30 Posterior chondrolabral defects of the glenoid rim are caused by posterior subluxation or dislocation of the humeral head.5,6 A posterior labrocapsular periosteal sleeve avulsion occurs when the posterior labrum is avulsed along
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with a sleeve of adjacent periosteum of the posterior glenoid neck, with subsequent healing of the posterior labrum to the glenoid neck. An osseous defect of the posterior glenoid rim (reverse osseous Bankart lesion) can be associated with posterior shoulder instability.7 One study has found an association between recurrent posteroinferior glenohumeral instability and an osseous defect of the posteroinferior glenoid rim longer than 12 mm.10 Lippitt and Matsen31 have reported a study of ten cadaver shoulders in which all soft tissue had been resected, leaving only the glenoid bone, labrum, and humeral head to provide stability. With a 50-N compressive load, the maximum posterior translation force that can be maintained without posterior humeral head dislocation is 17 N. With 100 N of compression, the maximum posterior translation force is 30 N. This can be expressed as a posterior glenohumeral stability ratio, which is a measure of posterior translation force that can be stabilized under a given compressive load of 30%. The stability ratio following labral excision was reduced by approximately 20%; however, because the study involved older cadavers with relatively atrophic labra, the labrum may provide even greater stability in younger individuals. Concavity compression is hypothesized to be particularly important in the midrange of glenohumeral motion because the capsuloligamentous structures are lax in this position.32
ATHLETE AND PATIENT PRESENTATION Athletes who develop posterior shoulder instability are frequently involved in sports involving strenuous or repetitive upper extremity use, such as football, baseball, swimming, gymnastics, and golf. Athletes may present with a chief complaint of pain, instability, or both. They often present with posterior shoulder pain and may also report involuntary subluxation that affects their athletic performance. This group of patients often has symptoms in only one shoulder.2 Some patients can voluntarily subluxate or dislocate their shoulder in certain positions or have subluxation that is present during the physical examination. Pain or a sensation of instability or subluxation is usually present during axial loading of the humerus in flexion, adduction, and internal rotation.
Figure 18-2. Reverse humeral avulsion of the glenohumeral ligament (reverse HAGHL) lesion. The posterior capsuloligamentous structures have avulsed off of their humeral attachment in this T2-weighted magnetic resonance imaging scan.
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Posterior shoulder instability may be traumatic, atraumatic, or voluntary. Traumatic posterior shoulder instability includes dislocation and subluxation. Recurrent posterior shoulder instability can develop following a posterior shoulder dislocation,3 although this is less common than recurrent anterior instability following an anterior dislocation. Posterior shoulder subluxation often occurs in patients who report a significant injury (“macrotrauma”), such as an
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axial loading injury in internal rotation or a suddenly applied posterior force to the front of the shoulder.6,24,25 Posterior shoulder subluxation, which commonly manifests as pain rather than instability, is common in contact athletes, such as football, lacrosse, and rugby players.33 Although not common in the athletic population, a locked posterior shoulder dislocation (Fig. 18-3) can occur. Patients frequently present with the affected arm in an adducted and internally rotated posture. Posterior shoulder dislocations are associated with seizures (epilepsy), electrocution, and falls sustained by older patients with dementia. A locked posterior shoulder dislocation can be associated with large, engaging reverse Hill-Sachs lesions and reverse Bankart lesions in addition to disruption of the posterior capsulolabral restraints. These injuries can be missed in the emergency room because, unlike an anterior shoulder dislocation, the findings on anteroposterior
radiographs may be subtle. An axillary lateral radiograph will clearly reveal the posterior dislocation (see Fig. 18-3), although obtaining this can be challenging because of patient discomfort. Atraumatic posterior shoulder instability includes patients who develop symptoms insidiously after repetitive minor trauma characterized by a posteriorly directed force applied to the shoulder in a flexed, internally rotated position. Repetitive microtrauma is commonly seen in athletes such as football linebackers and linemen involved in tackling and blocking, bench pressing with heavy weights, and repetitive overhead activities, such as swimming, golf, baseball, tennis, and gymnastics. Hovis and associates34 have described a group of elite golfers who developed posterior instability of the shoulder of the lead arm, which is in the provocative position of adduction and flexion at the top of the back swing. The third group consists of patients who can voluntarily demonstrate posterior shoulder instability in certain provocative positions. Patients with psychological problems may be able to demonstrate voluntary subluxation or dislocation. They often develop instability during adolescence for secondary gain or attention seeking. Some patients can subluxate their shoulder when it is positioned in flexion, adduction, and internal rotation. The shoulder relocates as it is moved into abduction from this position. Positional shoulder subluxation is not usually associated with psychological abnormalities, and these patients generally present with instability rather than pain.
PHYSICAL EXAMINATION A
B Figure 18-3. Locked posterior shoulder dislocation radiographs. A, Anteroposterior view. B, Lateral view. These images reveal humeral head impaction on the posterior glenoid rim. The axillary radiograph clearly reveals the posterior position of the humeral head relative to the glenoid.
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Physical examination begins with a thorough evaluation of all aspects of the shoulder. It is important to establish whether the instability is unidirectional, bidirectional, or multidirectional. The signs of instability are often subtle and nonspecific, and other pathology such as impingement or muscular weakness may also be present. Comparison testing of the affected shoulder with the opposite shoulder is also important. Posterior humeral head translation on the glenoid up to the posterior glenoid rim is common in athletes and may not be pathologic. There is a wide spectrum of symmetrical glenohumeral joint laxity in recreational athletes, and increased shoulder passive range of motion has not been found to correlate with increased glenohumeral joint laxity.35 Provocative testing may help establish the diagnosis by demonstrating asymmetrical and excessive posterior humeral head translation as well as pain, discomfort, or apprehension during testing. Tests include the load and shift test,36 sulcus sign,37 posterior drawer test,38 jerk test,39 and Kim test39 (see Chapter 4). We briefly review a few select tests that we use for patients with posterior instability.
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Gerber and Ganz38 first described the posterior drawer test (Fig. 18-4). The patient is supine with the examiner standing in front of the patient. For examination of the left shoulder, the examiner grasps the proximal forearm with his or her left hand, positions the elbow in 120 degrees of flexion, and positions the shoulder in 80 to 120 degrees of abduction and 20 to 30 degrees of forward flexion. The examiner holds the scapula with her or his right hand, with the index and middle fingers on the scapular spine and thumb immediately lateral to the coracoid process. The examiner then slightly rotates the patient’s upper arm medially and flexes it to about 60 to 80 degrees with the left hand while the examiner’s right hand thumb applies a posterior force to the humeral head. The degree of posterior displacement of the humeral head can be appreciated as the thumb slides along the lateral aspect of the coracoid process while the humeral head contacts the ring finger of the examiner’s right hand posteriorly. Apprehension
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during the application of posterior force is considered to be a positive test for posterior instability. The jerk and Kim tests have been used to assess posteroinferior instability of the shoulder. The jerk test (Fig. 18-5) is performed with the patient sitting. The examiner holds the scapula with one hand, and the patient’s arm is flexed 90 degrees and internally rotated 90 degrees. The elbow is flexed to 90 degrees and a posterior force is then applied with the examiner’s other hand by pushing on the patient’s flexed elbow. The shoulder is then brought into extension beyond the scapular plane. A palpable and often painful audible shift occurs in a positive test as the humeral head
A
A
B B Figure 18-4. Posterior drawer test. A, Starting position. B, Completed position.
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Figure 18-5. Jerk test. A, A posterior force is applied to a flexed, internally rotated shoulder. B, The shoulder is then extended beyond the scapular plane. Anterior humeral head translation and pain during the maneuver is a positive test.
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reduces over the glenoid rim and into the glenoid fossa from a subluxed position.40,41 Pain may or may not be associated with posterior clunking during the jerk test. One study42 has divided patients with posteroinferior shoulder instability into two groups, patients with a painless jerk test and those with a painful jerk test. The group with a painful jerk test had a significantly higher failure rate with 6 months of nonoperative treatment (84% versus 7% failure for the group with a painless jerk test). It was concluded that shoulders with symptomatic posteroinferior instability coupled with a painful jerk test have a high likelihood of a posteroinferior labral lesion requiring arthroscopic repair. The Kim test is performed with the patient sitting with the arm in 90 degrees of abduction. The examiner holds the patient’s elbow and lateral aspect of the proximal arm, and an axial loading force, and 45 degrees of upward diagonal elevation are applied simultaneously. The onset of posterior shoulder pain is defined as a positive test result, regardless of the accompanying clunk of the humeral head. A countersupport, such as the back of a chair or an assistant providing scapular stabilization, is important to allow for application of firm axial compression to the humeral head against a fixed glenoid surface. Kim and coworkers39 have reported that the Kim test is more sensitive in detecting an inferior labral lesion, whereas the jerk test is more sensitive in detecting a posterior labral lesion. One specific type of traumatic posterior instability is the locked posterior dislocation. Patients with a locked posterior shoulder dislocation often present with the shoulder in an adducted, internally rotated position, with loss of external rotation. The coracoid process may be prominent with posterior shoulder fullness.
posterior dislocation (see Fig. 18-3). The anteroposterior radiograph is less reliable for the identification of a posterior dislocation, although it may demonstrate overlap of the medial aspect of the humeral head with the lateral aspect of the glenoid or an incongruent glenohumeral joint space. Computed tomography (CT) is useful for assessment of osseous structures, such as glenoid retroversion and associated glenoid fractures and insufficiency. Humeral head retroversion and reverse Hill-Sachs lesions are also clearly visualized. CT arthrography can assess the glenoid labrum in cases in which magnetic resonance imaging (MRI) cannot be performed for medical reasons (e.g., pacemaker implantation), although CT arthrography now has largely been supplanted by magnetic resonance arthrography. Ultrasound has not been used routinely for the assessment of posterior glenohumeral instability. Borsa and colleagues45 have compared dynamic ultrasound with stress radiographs and found that ultrasound can be a valid and reproducible method for assessing glenohumeral laxity in a clinical setting. Ultrasound, which is cost effective and uses nonionizing radiation, may become a useful tool for evaluating glenohumeral stability in the future. MRI (Fig. 18-6) is the most common method used for shoulder imaging; it is especially useful for imaging soft tissues such as muscle, tendon, labrum, and capsule. MRI also clearly illustrates associated bone marrow edema on T2-weighted imaging. Magnetic resonance arthrography (MRA) involves injection of a contrast agent into the shoulder joint before MRI (Fig.18-7). This is an invasive procedure, but it allows for
IMAGING STUDIES Standard shoulder radiographs are often normal in patients with posterior shoulder instability,24 especially when the cause is atraumatic. Nonetheless, radiographs should be obtained, including true anteroposterior (Grashey view, 30 degrees from the horizontal axis of the body), axillary lateral, and supraspinatus outlet views. Radiographs may demonstrate bony defects of the glenoid and humeral head, especially following acute trauma. The anteroposterior view in external rotation may allow for identification of a reverse Hill-Sachs lesion of the anterosuperior humeral head. The axillary lateral radiograph may demonstrate a reverse bony Bankart lesion. The axillary lateral may also demonstrate calcification along the posterior aspect of the capsule and glenoid labrum. This calcification or exostosis is termed the Bennett lesion43 and is a sign of the presence of posterior instability.44 As shown earlier, the axillary lateral is also useful to rule out a locked
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Figure 18-6. Magnetic resonance imaging scan of posterior labral tear. A gap is clearly visualized between the posterior glenoid and the labrum. Note the slight posterior subluxation of the humeral head.
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Stages of Conservative Rehabilitation Conservative management can be broken up into four phases: (1) acute phase, (2) intermediate phase, (3) advanced strengthening phase, and (4) return to activity. These phases do not have specific timetables, and typically there are no clear-cut demarcations when moving from one phase to the next. The goal of nonoperative rehabilitation is to allow the patient to return to full activity with minimal risk for reinjury. Again, it is important to keep in mind that the program progression is not time based but is based on achieving evaluation goals.
Figure 18-7. Magnetic resonance arthrography scan of posterior capsular laxity. Note the redundant posterior capsule in a patient with posterior glenohumeral subluxation.
superior evaluation of subtle labral tears and joint volume. MRA is currently the best method for imaging capsulolabral disruption46-49; it can visualize posterior labral tears and rotator interval lesions effectively in addition to assessing posterior capsular volume.24 Volpi and associates50 have compared MRI with MRA in 58 patients with glenohumeral joint instability; 11 of 52 labral tears were not recognized before gadolinium contrast injection. Osseous deficiencies can also be visualized, although not as well as with CT.
Phase 1—Acute Phase. Initiation of conservative treatment begins with immobilization after an acute traumatic dislocation. Immobilization begins with the use of an UltraSling (DonJoy, Vista, Calif) positioning the arm in slight abduction and neutral to slight external rotation (Fig. 18-8). The sling is for short-term use to control pain and allow return of active muscle control. Cryotherapy and therapeutic physical therapy modalities are used for pain and swelling management. Pain control is important to allow for early return of muscle function. Passive ROM is initiated, followed by a progression to active ROM as tolerated. Early avoidance of abduction, horizontal adduction, and internal rotation is necessary to protect the posterior structures. ROM exercises include the use of Codman’s exercises, pendulum, pulleys, wand, and gentle external rotation stretching. Progression to strength exercises are also initiated during this phase. These exercises include co-contraction upper extremity shrugs and isometrics for flexion, abduction,
TREATMENT OF POSTERIOR INSTABILITY Nonoperative Management Conservative management for posterior instability is typically the initial treatment of choice. The key to success for this type of treatment lies in the initial accurate diagnosis of the primary injury (e.g., instability) and potential secondary problems (e.g., rotator cuff impingement, scapular dyskinesia). In many cases, glenoid labrum tears are associated with posterior instability. As noted, the skills of the clinician for differential diagnosis are critical. Conservative management requires close communication between the physician and rehabilitation staff. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be necessary to control pain and subacromial swelling. Physical therapy modalities should be used when appropriate. Emphasis on restoring normal function through range-of-motion (ROM) and strength exercises is important. Neuromuscular control by balancing the rotator cuff and the periscapular muscles will assist in controlling overuse injuries. Patient education is important for limiting voluntary subluxation episodes to control joint surface damage.2
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Figure 18-8. Immobilization after acute traumatic dislocation. The arm is positioned in slight abduction and neutral to slight external rotation.
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extension, and external rotation. During this phase, monitoring the return of normal scapulohumeral rhythm can be initiated. Isometric and gentle isotonic scapular retraction exercises can be included. The goals of phase 1 treatment emphasize decreasing pain and inflammation, restoring full, nonpainful ROM, and maintaining active muscle control. Therefore, any activity that reproduces symptoms should be avoided. Phase 2—Intermediate Phase. Progression to this phase occurs when the patient has complete or almost complete ROM, and minimal to no pain. Emphasis shifts to allow for continuing stretching and ROM exercises to restore any ROM not regained with the initial phase of treatment (Fig. 18-9). ROM activity in the elevation planes should be completed in the plane of the scapula. Cryotherapy and other modalities may be used as needed. Strength exercises progress to isotonic exercises with a Thera-Band (Hygenic, Akron, Ohio,) or dumbbell weights. Although dumbbells might be preferred, it may be necessary to use a Thera-Band for the home exercise program. One of the advantages of using dumbbells is the ability to progress the resistance in small, objective increments. Directions of exercise should emphasize flexion, abduction, internal rotation, external rotation (Fig. 18-10), and extension and scapular retraction, protraction, elevation, and depression. However, care is needed to ensure that there is sufficient rotator cuff strength before initiating elevation exercises to avoid impingement. This must be achieved by emphasizing muscular control for the posterior rotator cuff and serratus anterior, which is important because many patients with nontraumatic posterior instability have poor scapular protraction control with elevation. During this phase, eccentric control is emphasized with the use of a Thera-Band for external rotation from neutral rotation to external rotation and return to start position. Neuromuscular control should be initiated with various proprioceptive neuromuscular facilitation (PNF)
Figure 18-10. Thera-Band exercise. This exercise emphasizes external rotation.
Figure 18-9. Stretching and range-of-motion exercises. These exercises are used to restore any range of motion not regained during the initial phase of treatment.
Figure 18-11. Enhancement of the dynamic stability of the glenohumeral joint with the use of proprioceptive neuromuscular facilitation techniques.
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techniques.51 These are designed to enhance the dynamic stability of the glenohumeral joint as the patient is progressed into the later stages of rehabilitation (Fig. 18-11). Diagonal patterns for strengthening using a Thera-Band represent an excellent method for control during the home exercise program. Goals of this phase allow for regaining and improving muscular strength and improving neuromuscular control. Rotator cuff control dictates this progression. Dumbbell progression goals for side-lying external rotation and internal rotation (Table 18-1) are 10 and 15 pounds, respectively, and 15 to 25 pounds for shoulder shrugs.
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TABLE 18-1 Dumbbell Progression Goals Athlete External Rotation (lb)
Internal Rotation (lb)
Female
7-8
10-12
Male
8-10
12-15
Phase 3—Advanced Strengthening Phase. Isotonic exercise is continued, with an emphasis on rotator cuff and scapular muscle strengthening. Emphasis should be placed on proper technique and on sufficient sets and repetitions to allow for achieving muscle fatigue. When dealing with an athletic population, isokinetic exercise programs can be used. A velocity spectrum program at moderate to high speeds (180 to 300 deg/sec) can be used to allow for accommodating resistance programs. Seated external and modified internal rotation in the scapular plane with the arm at the side is the initial position for strength training. Plyometric exercises are used to allow for functional progression in an attempt to return an athlete to his or her sport. Initially, the TheraBand is used and then progressed to include medicine balls, wall push-ups (Fig. 18-12), and reverse wall push-ups. Care must be taken regarding strenuous exercises that could stress the posterior capsule. For example, this would relate to using the wall push-up to strengthen the serratus anterior while potentially stressing the posterior aspect of the shoulder (Fig. 18-13). Goals of this program include increasing strength, power, and endurance to within normal limits and preparing the athlete for return to activity. Phase 4—Return to Activity. Transition into this phase requires continuation of the prior exercise program to allow full return of strength. Evaluation must be a key to
Figure 18-13. Use of the wall push-up to strengthen the serratus anterior while stressing the posterior aspect of the shoulder.
this transition. Pain, ROM, strength, and tolerance for activities of daily living (ADLs) should all be considered. Typically, this is the preparation phase for resuming full activity. Strength and plyometric exercises attempt replication of functional sports movement. In addition, performing sport-specific tasks are included. If overhead throwers are used as an example, an interval throwing program would be initiated during this phase. Progression of throwing uses a warm-up, short toss–long toss; pitchers throw from the level surface and advance to the mound, and eventually progress to game simulation. This progression is predicated on using evaluation as the basis for program advancement. Because of the posterior instability, care should be observed during the pullthrough phases of swimming and rowing, swinging a bat, and overhead sports. Goals of this program allow for full return to sports or activity.
Operative Management
Figure 18-12. Plyometric exercise, such as wall push-ups, are used to allow for functional progression back into sports.
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Many have suggested that surgical treatment of posterior shoulder instability may be considered after failure of conservative treatment that has consisted of an initial trial of physical therapy for 6 months.1,4,6 The senior author (TNL) does not set arbitrary limits on time before recommending surgical intervention. If, by isokinetic testing, the patient can objectively demonstrate full rehabilitation of the rotator cuff, no further improvement in symptoms are likely to be achieved with continued physical therapy. Surgery may be indicated at this time. Furthermore, if the patient
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appears genuinely motivated to participate fully in a physical therapy program, but these efforts cannot continue because of pain or repeated episodes of instability, a decision to proceed with surgery may be reasonable. Operative treatment aimed at repairing structural damage may be offered at an earlier stage to select patients, such as collision athletes with traumatic posterior instability and a posterior labral tear.2 Factors favoring acute repair include age younger than 30 years, trauma with significant force in a patient without a history of shoulder subluxations, dominant arm, high present activity level with a desire to continue a high level of activities, or a sensation of instability while the arm is in the sling or with minimal arm movement.52 Timing of surgery for athletes should correspond to the patient’s specific situation. Surgery should be coordinated to minimize the risk of further injury while optimizing the patient’s participation in future athletic endeavors. Most lesions associated with posterior instability can be treated arthroscopically, although some situations may demand open intervention. In all cases, surgery begins with an examination under anesthesia and careful, systematic diagnostic arthroscopy. Examination under anesthesia allows for comparison of findings present during physical examination in the awake patient and provides a final confirmation of the pathology before surgical treatment. Both shoulders should be examined for side-to-side comparison. The patient can be positioned in the beach chair or lateral decubitus position. The lateral decubitus position may allow for better exposure to the inferior capsule and inferior labrum because of the enhanced ability to distract the glenohumeral joint. Diagnostic arthroscopy can be performed to confirm findings seen on MRI or MRA, assess for additional pathology that may be contributing to the instability, and verify the appropriateness of arthroscopic versus open repair. Following the examination under anesthesia, the patient is turned into the lateral decubitus position (Fig. 18-14). The arm is placed in approximately 30 degrees of abduction and 20 degrees of flexion with a pulley system with approximately 10 pounds of weight used to suspend the arm. The amount of weight used is adjusted appropriately according to the patient’s size. The arthroscope is inserted into the posterior portal first and the articular surfaces of the glenoid and humeral head are assessed, as well as the attachment of the rotator cuff tendons. The biceps anchor and superior labrum are visualized, followed by the anterior labrum, anterior capsuloligamentous structures, and axillary pouch. An anterior superior portal is created with a spinal needle entering through the rotator interval. The arthroscope is then moved using a switching stick from the posterior to the anterior portal and the entire posterior and inferior labrum and capsule are carefully inspected and probed. A diagnostic arthroscopy before repair of the injured structures allows for verification of suspected pathology and for assessment of additional pathologic lesions.53
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Figure 18-14. Lateral decubitus position. Note that the arm is in a position of abduction, with slight forward flexion, with the pulley system attached to the contralateral side of the operating table.
Excessive posterior inferior capsular laxity is often observed arthroscopically in patients with posterior shoulder instability. The posterior capsule forms a large pouch in the posterior aspect of the joint, and the entire posterior glenoid rim and labrum can often be viewed from the posterior portal when the tip of the arthroscope is pulled back to the capsule. This unusual view has been termed the skybox view1 (Fig. 18-15). Open Management Posterior capsulolabral plication can be successfully performed arthroscopically, but there are indications for open repair. These include cases of significant posterior glenoid bone loss or a large, engaging reverse Hill-Sachs lesion such as that which might occur with a locked posterior dislocation. Revision surgery for capsuloligamentous
Figure 18-15. Skybox view. The arthroscope is in the posterior portal, demonstrating a patulous posterior capsule with visualization of the posterior labrum.
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deficiency caused by thermal necrosis from prior thermal capsulorrhaphy may require an open approach for reconstruction of the capsuloligamentous structures with allograft or autograft. Open treatment is typically performed via a posterior approach (Fig. 18-16). The patient can be placed in the lateral decubitus or beach chair position as long as a positioner is used that allows for adequate exposure of the posterior shoulder. The skin incision begins 2 cm medially to the posterolateral corner of the acromion and extends 8 cm
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inferiorly toward the posterior axillary crease. The deltoid muscle is then split along its raphe between the middle and posterior thirds. If adequate exposure is not obtained through the deltoid split, the deltoid can be partially detached from the scapular spine and posterior acromion to improve visualization of the posterior aspect of the rotator cuff. There are two approaches through the posterior aspect of the rotator cuff. First, the transverse interval between the infraspinatus and teres minor is developed. Note that this interval is more easily appreciated with medial dissection and identification of the separate muscle bellies because the infraspinatus and teres minor tendons merge together at their lateral insertion on the humerus. Care is taken to protect the suprascapular nerve with medial dissection. Alternately, the infraspinatus tendon is split horizontally in line with its muscle fibers. The infraspinatus muscle is bipennate and inserts onto a broad facet along the posterior aspect of the greater tuberosity, which helps differentiate it from the teres minor. The infraspinatus tendon may be incised vertically at its humeral insertion if additional exposure of the posterior shoulder capsule is required. Care is taken to separate the interval between the rotator cuff tendons and posterior capsule. The infraspinatus tendon is retracted superiorly and the teres minor tendon is retracted inferiorly.
A
B Figure 18-16. Open posterior approach to the glenohumeral joint. A, The deltoid is split along its raphe between the middle and posterior thirds. It can be partially detached along the scapular spine for 1 to 2 cm if improved visualization is required. B, The interval between the infraspinatus and teres minor is developed, and the posterior capsule is exposed. Care is taken to protect the axillary nerve inferior to the teres minor and the suprascapular nerve medially. (From Miller S, Flatow EL: Posterior and Multidirectional Instability: Open Solutions. In Warner JP, Iannotti JP, Flatow EL (eds): Complex and Revision Problems in Shoulder Surgery, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2005, pp 80-81.)
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The capsule is then incised in a craniocaudal direction 1 cm medially to its insertion on the humerus, starting superiorly and carefully proceeding inferiorly. The capsule is split in a T fashion transversely from the middle of the glenoid to the middle of the humeral head articular surface. The plane between the capsule and the teres minor is bluntly developed, and the axillary nerve is identified and protected. The axillary nerve and posterior circumflex humeral artery reside in the quadrangular space just inferior to the teres minor. The borders of the quadrangular space are the teres minor superiorly, teres major inferiorly, long head of the triceps medially, and humeral shaft laterally. The capsule is dissected off the humeral neck as far inferiorly as is necessary to allow for adequate capsulorrhaphy of the posterior or posteroinferior capsule. The surgeon places an index finger into the axillary pouch to determine the appropriate amount of capsular mobility. Adequate mobilization has been achieved when the surgeon’s finger is extruded by pulling superiorly on capsular traction sutures. The posterior labrum is inspected and repaired, if necessary. When there is a large redundant capsule, the superior capsular flap is shifted inferiorly and secured with nonabsorbable braided sutures; the inferior capsular flap is shifted superiorly in a similar manner. The arm is positioned in 10 degrees of external rotation, 15 degrees of abduction, and 0 degrees of flexion while the capsular flaps are secured. The infraspinatus tendon is repaired (if necessary) with no. 2 braided nonabsorbable suture anchors, and the split in the posterolateral deltoid raphe is repaired. The skin incision is closed with an absorbable subcuticular suture.5
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Correction of osseous anatomy in posterior shoulder instability is infrequently performed. Excessive glenoid retroversion has been treated with posterior glenoplasty, consisting of a posterior opening wedge osteotomy of the glenoid neck with bone graft interposition.9 Posterior bone block glenoid augmentation has been described as primary treatment for patients with deficiency of the posterior lip of the glenoid.54 This is also used in the revision setting in the presence of distorted osseous anatomy. Metcalf and colleagues55 have described the surgical technique for posteroinferior glenoplasty. The glenoid osteotomy is performed 1 cm medial to the posteroinferior glenoid rim. A 2.5-cm osteotome is inserted starting posteroinferiorly and aiming anterosuperiorly for a distance of one half the anteroposterior diameter of the glenoid. The osteotome is carefully wedged open, and a bone graft wedge with a 5-mm base taken from the posterior acromion is carefully impacted into the osteotomy site. It has been demonstrated that posteroinferior glenoplasty increases the tangential force necessary to produce a posteroinferior glenohumeral dislocation under a 50-N compressive load by 70%. These procedures are challenging and should not be performed by the inexperienced shoulder surgeon. The techniques should be practiced first on a cadaver to understand better the three-dimensional glenoid anatomy, especially when approached posteriorly. Arthroscopic Management Arthroscopic treatment of posterior shoulder instability has the advantages of smaller incisions, decreased postoperative pain, and better visualization of capsular and intraarticular anatomy and associated pathology compared with the open approach. Concomitant impingement, acromioclavicular arthrosis, rotator cuff tears, biceps tendon injury, anterior labral tears, and superior labral anteriorposterior (SLAP) tears can be addressed arthroscopically with subacromial decompression, distal clavicle excision, rotator cuff repair, biceps tenodesis or tenotomy, anterior labral repair, or SLAP repair, respectively. Posterior stabilization can be technically challenging because posterior instability is less common than its anterior counterpart. Patients with unidirectional posterior instability and associated capsulolabral lesions have been effectively treated arthroscopically.6,24,56 First, an examination under anesthesia is performed by maintaining scapular stability with one hand and performing humeral head translation with the other hand. The patient is then placed in the lateral decubitus position on the beanbag, as described earlier. Exposure can be enhanced by applying an overhead traction sleeve for abduction, but this may only be needed during the repair process and does not need to be applied during diagnostic arthroscopy or during lesion preparation before repair. A diagnostic shoulder arthroscopy is carried out with the arthroscope in the posterior portal. The skybox view1 is usually noted because of the enlarged posterior capsule
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(see Fig. 18-15). The arthroscope is then transferred to the anterior portal via switching sticks, and the posterior labrum and capsuloligamentous structures are carefully assessed. When a labral detachment is identified, a capsulolabral repair is carried out, whereby a glenoid-based capsular shift is included in the labral reattachment. If the labrum is still attached to the glenoid, a capsular plication is carried out using suture anchors, sutures passed through the intact labrum, or some combination of both. When a posteroinferior labral tear is identified, it is freed from the scapular neck using an arthroscopic elevator. The underlying bone is abraded with a mechanical shaver or small burr, and the capsule and posterior band of the inferior glenohumeral ligament are abraded with an arthroscopic rasp or mechanical shaver, such as a whisker shaver. An accessory posterolateral portal is created about 2 cm inferior and 1 cm lateral to the posterolateral corner of the acromion to assist with suture anchor placement (7-o’clock portal). An inside-out or outside-in technique may be used for placement of the accessory portal. In the inside-out technique, a switching stick or Wissinger rod is placed in the anterosuperior portal and out the posteroinferior capsule. This portal can then be enlarged using dilators. A spinal needle can identify the ideal angle of entry to optimize placement of the accessory posterolateral portal when using the outside-in technique. Care must be taken to avoid placement of the low portal more than 3 cm distal to the acromion to protect the axillary nerve. Other options for portals include using two anterior portals so that the accessory anterior portal is used instead of a second posterior portal for suture management. However, using one posterior portal requires that this portal have an adequate trajectory for appropriate anchor placement and suture passage. Bioabsorbable suture anchors loaded with no. 2 braided nonabsorbable sutures are then placed (Fig. 18-17) and the labrum is repaired (Fig. 18-18) to its anatomic location along the posterior edge of the glenoid rim articular surface. The suture anchors should be on the glenoid face and not medially along the glenoid neck. An appropriate angle of insertion is necessary to avoid damage to the more central aspect of the glenoid articular cartilage as the anchor is inserted. If the posterior capsule is redundant, a capsular plication (Fig. 18-19) may be performed using a Bird Beak suture retriever (Arthrex, Naples, Fla) or a shuttle technique to pass labral sutures. The posteroinferior capsule is shifted superiorly, plicated, and included in the labral repair. A 45-degree curved suture hook, such as the Linvatec Spectrum (ConMed Linvatec, Largo, Fla), is used to pass a no. 1 monofilament suture such as a polydioxanone suture (PDS) through the capsule and then the labrum. The amount of capsule incorporated is proportional to the amount of excess capsular volume. The capsule is first
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Figure 18-17. Suture anchor placement for labral repair. Note that the cannula is kept close to the suture anchor to avoid entangling the sutures in the adjacent soft tissues.
221
Figure 18-19. Posteroinferior capsular plication. A curved shuttle device loaded with monofilament suture is used to capture the posterior capsule inferior to the entrance point in the posterior labrum.
through the suture anchor eyelet. Sliding locking knots are attractive but less forgiving. All knot tying needs to be mastered outside the operating room. Suture anchors and capsular plication proceed in a posteroinferior to posterosuperior direction.
punctured with the curved suture hook inferior to the suture anchor and the second puncture, which includes the labrum, is made more superiorly near the suture anchor. This creates a superior capsular shift along with posterior capsular tightening and advances the posterior band of the inferior glenohumeral ligament. The nonabsorbable suture attached to the anchors is then shuttled through the capsular tissue via the monofilament suture.
The rotator interval capsule should be assessed between the superior aspect of the subscapularis and anterior aspect of the supraspinatus. The rotator interval, which includes the superior and middle glenohumeral ligaments, may be stretched or injured in patients with multidirectional instability.2 If persistent posteroinferior laxity or excessive external rotation, or both, is still present following posterior capsulolabral plication, rotator interval closure (Fig. 18-20) may be performed. Rotator interval closure has been shown to reduce posteroinferior humeral head translation in the adducted position,17 and can be accomplished with the placement of one suture adjacent to the glenoid rim. Additional sutures placed in the rotator interval can lead to overtightening and loss of external rotation.57 The rotator interval capsule tissue is plicated with the patient’s arm in 30 degrees of external rotation; the supraspinatus and subscapularis tendons should not be included in the repair.53 Rotator interval closure may be performed via the anterior cannula with an inside-out technique. With the arm held in 30 degrees of external rotation, the suture is tied over the anterior capsule, with the anterior cannula partially retracted. This can be accomplished without direct visualization or by direct visualization within the subacromial space.
Sutures that slide freely through the anchor eyelet are then tied with a sliding knot, followed by three alternating halfhitches. Surgeons performing arthroscopic repairs should be familiar with sliding and nonsliding knots. Nonsliding knots are required when the suture does not slide freely
Patients with a Kim lesion, an incomplete and concealed avulsion of the posteroinferior labrum (Fig. 18-21), are treated by completing the partial tear with subsequent labral repair, along with repair of the posterior band of the inferior glenohumeral ligament via suture anchors.29
Figure 18-18. Labral repair with suture anchors. The imbricated capsular tissue forms a bumper adjacent to the posterior labrum.
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A Figure 18-21. Kim lesion of posteroinferior labrum.
POSTOPERATIVE REHABILITATION
B Figure 18-20. Rotator interval closure. A single suture is tied in the rotator interval superior to the subscapularis and anterior to the supraspinatus tendons. A, Prerepair. The subscapularis tendon is running in a vertical direction with the widened rotator interval located superiorly (to the right of the subscapularis in the picture). B, Postrepair. Note the decreased space superior to the subscapularis tendon.
Patients with Kim lesions are repaired in the same fashion as those with complete posterior labral tears. The key is to recognize the Kim lesion as a posterior labral tear. This lesion must be fully released from its partially healed position so that the posterior labrum may be advanced and secured to its anatomic location. In patients without labral tears but with posterior capsuloligamentous deficiency, the 45-degree suture hook with monofilament suture is again used to plicate the posterior capsule and repair the posterior band of the inferior glenohumeral ligament to the intact labrum following abrasion of the soft tissues with an arthroscopic rasp. Nonabsorbable sutures are shuttled in a similar fashion via the monofilament suture and are subsequently tied.
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Postoperative rehabilitation is critical to the success of the surgical procedure. Rehabilitation is initiated within the first 2 days postoperatively and is progressed based on the healing principles of the tissues involved, as well as constant re-evaluation of the patient to determine his or her symptomatic progression related to pain, ROM, and strength. It is anticipated that the rehabilitation period will last approximately 6 months, with ROM goals being achieved by approximately 2 to 3 months postoperatively and strength goals by 4 to 5 months. Soft tissue strength may take 6 months or longer to achieve. This is related to the level of postoperative activity the patient desires, as well as any potential postoperative complications.
Acute Phase of Physical Therapy Postoperative immobilization is used to protect the repair. A sling with an abduction pillow is measured and fit to the patient with the arm slightly abducted by the sling’s pillow, and maintained in approximately 15 degrees of external rotation. The sling is removed to permit exercise, icing, and showering. Otherwise, the sling is used for the first 4 to 6 weeks postoperatively. The patient is also encouraged to avoid active internal rotation and horizontal adduction for the initial 4-week postoperative period.59 Within the first 2 days after surgery, active-assisted ROM for the hand, elbow, and neck are initiated. By the end of the first week, active-assisted abduction and external rotation are initiated. Early muscle activation is permitted through submaximal isometric contraction for abduction, adduction, flexion, and extension during the first 1 to 2 weeks. Care must be taken to use pain as a guideline, especially with the elevation planes of movement. ROM goals by the end of the first
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4 weeks are 90 degrees of abduction and 90 degrees of external rotation.59 The sling is normally discontinued after 4 to 6 weeks. Cryotherapy and other physical therapy modalities such as electrical stimulation are encouraged to help control the postoperative pain and inflammation. Arthroscopic intervention may create some slight modifications to the postoperative rehabilitation program. Studies have recommended the use of sling immobilization for approximately 3 to 4 weeks; ROM activities begin at this time. This program uses passive- and active-assisted ROM exercises, such as Codman’s, pendulum, scapular control, and elbow and wrist exercises.6,7,34
Intermediate Phase of Physical Therapy ROM and strengthening are advanced as protective range limitations are slowly lifted. Overhead pulleys are started for forward flexion and abduction. The L bar is also permitted for overhead elevation and external rotation.59 External rotation motion is advanced to include the 0-degree abducted position in the plane of the scapula as well as the 45- and 90-degree abducted positions. Active internal rotation begins with the arm at the side, resting on a towel roll in the gravity neutral position, and is gradually progressed to the antigravity position. At this stage, internal rotation should be attained to approximately 80% of that of the contralateral side.27 Progressive resisted exercises (PREs) are initiated for external rotation, flexion, and abduction.59 In open repairs where the infraspinatus muscle has been detached, external rotation PREs must progress cautiously. Scapular control is also emphasized for protraction, retraction, elevation, and depression. Posterior rotator cuff and scapular control must be emphasized before deltoid control to prevent early overuse injuries. During this phase of rehabilitation, early dynamic control can be enhanced through various PNF procedures. Manual techniques, such as rhythmic stabilization, and equipment techniques, such as the Bodyblade (Hymanson, Playa del Ray, Calif; Fig. 18-22) and Therabar (Hygenic, Akron, Ohio), are designed to produce coordinated muscle effort. Cryotherapy is encouraged after exercising, and modalities are used as needed. This phase of rehabilitation after arthroscopic intervention has a primary focus of initiating a full ROM program to achieve full functional mobility. It includes early work on internal rotation and horizontal adduction. A progressive strength program uses a Thera-Band and PREs. Strength exercises emphasize rotator cuff and scapular stabilizing muscles.6,7,34
Advanced Strengthening Phase During this phase, ROM should be returning to full. Emphasis is placed on progressing muscle strength and dynamic control. Attempts to control the force couples
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Figure 18-22. Demonstration of rhythmic stabilization using the Bodyblade.
between the rotator cuff and scapular stabilizing muscles are initiated. A Thera-Band can be used for early muscle control but, as strength is progressed, a shift in emphasis is placed on dumbbells and free weights. This provides the potential for an objective approach to increasing muscle strength. External rotation at 0 (Fig. 18-23A) and 90 degrees (see Fig 18-23B), internal rotation, scapular retraction, scapular elevation, scapular protraction, horizontal abduction (Fig.18-24), and shoulder extension provide the early key planes for strength. Surgical tubing and a TheraBand are used for eccentric control for external rotation59 (Fig. 18-25). By 12 to 16 weeks postoperatively, it is generally safe to add light horizontal adduction stretching (Fig.18-26) to the program. As long as the program is supervised, a full free weight program can be undertaken. Focus is placed on maximal muscle strengthening and dynamic control. Goals of this phase include asymptomatic ADL activity, full return of muscle strength, and initiating early functional activity for returns to sports or work. By this time after surgery, there is little difference between open and arthroscopic postoperative rehabilitation. The primary focus is on muscle strengthening and controlled sport-specific training. Aggressive strength training may begin if manual muscle testing reaches grade 4⫹ to 5. For activities such as golf, permission for putting and chipping may be given.34 However, protection for overhead and contact activity is still important.6
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A
Figure 18-25. Demonstration of Thera-Band exercise for eccentric control for external rotation.
B Figure 18-23. External rotation. A, Demonstrated at 0 degrees. B, Demonstrated at 90 degrees.
Figure 18-26. Light horizontal adduction stretching.
Figure 18-24. Horizontal abduction. This exercise is an early key plane for strength.
Return to Activity Phase In an athletic population, isokinetic testing would be initiated at approximately 16 weeks postoperatively. The results of the test will dictate the rate of return to activity progression. The patient’s progression from weight training to
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plyometric training using the Plyoback (Exertools, Novato, Calif) and medicine balls (Fig. 18-27) permits advanced strength and function training.59 Isokinetic testing would be used at approximately 4-week intervals to allow for a continued progression of the exercise program. After achieving approximately 80% on bilateral comparisons of the isokinetic data, the patient is permitted to begin the sport-specific training. This level of training typically will occur during postoperative months 4 to 6. Exercise programs at an advanced level continue until the goals for strength and return to the desired activity are achieved. Most patients return to full activity between 6 and 12 months postoperatively.27,58,59
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225
OUTCOMES Open Procedures
A
There have been several studies reporting on the outcomes following open and arthroscopic posterior capsulolabral repair. Studies frequently report on different and often heterogeneous populations, such as patients with traumatic, atraumatic, and volitional causes; many include patients who underwent additional procedures, such as anterior capsulolabral and SLAP repair. Posterior shoulder instability can be difficult to diagnose because of a continuum of pathology, ranging from unidirectional posterior shoulder instability to multidirectional instability with a primary posterior component. The importance of distinguishing patients with acute, traumatic posterior shoulder dislocations from those with recurrent, atraumatic instability has been pointed out.2,24,60 As noted, the former condition results from an isolated traumatic event, whereas the latter condition is related to repetitive microtrauma— repetitive stress to the posterior capsule over time.
Open Treatment
B
C Figure 18-27. Advanced strength and function training using the Plyoback and medicine balls. The rotator cuff and periscapular muscles must work in concert to throw (A, C) and catch (B) at varying trajectories and velocities.
Isokinetic testing following arthroscopic reconstruction begins at approximately 4 months after surgery. This testing represents an important component for activity progression. Goals for return to activity are at 4 to 6 months postoperatively,6 with contact activity protected for a minimum of 6 months.7 Precautions for return to overhead activity require a good maintenance exercise program to control the risk for overuse injuries.
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Hawkins and associates60 first reported on open treatment of posterior shoulder subluxations. Their study reported a high failure and complication rate in 26 shoulders treated with three different surgical techniques—17 glenoid osteotomies, 6 reverse Putti-Platt capsular plications, and 3 biceps tendon transfers. The overall recurrence rate was 50%. Bigliani and coworkers61 have evaluated 35 shoulders in 34 patients treated with open posteroinferior capsular shift; 11 shoulders had prior operations. The patient population was mixed, with 6 shoulders with posterior instability, 7 shoulders with posteroinferior instability, and 22 shoulders with multidirectional instability, posterior and inferior dislocation along with anterior subluxation. Capsular redundancy was found intraoperatively, with only 4 shoulders with complete posterior labral detachment. Subjective patient assessment at a mean 5-year follow-up revealed 80% excellent or good results. Of the fair or poor results, 6 of 7 were in revision cases. Fuchs and colleagues58 have reported on 26 shoulders that underwent open posteroinferior capsular shift; these patients had recurrent, voluntary posterior shoulder subluxation. The mean follow-up period was 7.5 years. All patients failed at least 3 months of physical therapy before operative treatment. Posterior labral repairs were performed in 7 shoulders, 1 shoulder underwent a posterior bone block, and 3 shoulders had a posterior glenoid osteotomy for excessive glenoid retroversion. Recurrent instability developed in 6 of 26 patients (23%); three of these were primary procedures and three were revisions. The clinicians concluded that their intermediate-term results were satisfactory. Recurrence was associated with a prior operation on the
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posterior shoulder or a new traumatic injury. Prevalence of recurrent posterior shoulder instability did not increase over time.
Arthroscopic Procedures Wolf and Eakin1 have studied 14 patients with recurrent posterior shoulder instability treated arthroscopically with a minimum 2-year follow-up. Posterior capsule laxity was present in all cases, and labral pathology was present in 12 patients (86%). Reverse Bankart lesions were seen in 8 of 14 patients (57%). Subjective patient evaluation revealed 12 excellent and 2 fair results; 9 of 10 patients reported full return to preinjury level of function in their respective sport. There was one recurrence, which was treated with a second arthroscopic capsular plication. Antonio and associates4 have evaluated 41 patients with posteroinferior shoulder instability treated with arthroscopic posteroinferior capsular shift, with a mean follow-up of longer than 2 years. Of these patients, 78% reported a traumatic injury; 32 patients had a primary procedure and 9 patients underwent a revision procedure. The patient population consisted of athletes and laborers. No postoperative instability was reported by 59% of patients; 85% of patients noted improved shoulder stability postoperatively based on self-assessment of shoulder function and general health status. Only 2 of the 9 patients who underwent a revision procedure noted no postoperative instability; 19 patients were receiving workers’ compensation, and they showed no statistically significant improvement. Abrams and coworkers53 have studied 48 patients with posterior and posteroinferior instability treated with arthroscopic repair. Posterior labral lesions were noted in 26 patients; 13 patients had anterior labral tears and 4 had SLAP lesions. The series included 26 athletes and 7 workers’ compensation patients. At a mean follow-up of 2 years, they reported a 4% rate of recurrent instability (2 of 48 patients). Four patients had a stable shoulder with residual pain, and 2 patients developed postoperative stiffness that resolved over 6 months. The rate of return to competitive athletics was 85% (22 of 26 athletes). Williams and colleagues7 have conducted a retrospective review of 27 shoulders (26 patients) who underwent arthroscopic posterior Bankart repair, with an average 5-year follow-up. There were no patients with ROM deficits, and 92% of patients were stable at follow-up. Kim and associates6 have reported on 27 patients with traumatic unidirectional recurrent posterior subluxation treated with arthroscopic labral repair along with posterior capsular shift. Patients were evaluated at more than 3 years postoperatively. All patients had a posteroinferior labral lesion, 96% of the shoulders were stable postoperatively, and there were no operative complications. The clinicians concluded that arthroscopic posterior labral repair with
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posterior capsulorrhaphy is an effective treatment for traumatic unidirectional recurrent posterior subluxation, providing stability, pain relief, and functional restoration. Bottoni and coworkers62 have reported on 31 shoulders in 30 patients, with 40-month follow-up, who underwent arthroscopic or open treatment of posterior shoulder instability; 19 patients were treated arthroscopically and 12 were treated via an open posterior approach. Superior outcomes were noted following arthroscopic repair using both the Western Ontario shoulder stability index and the Rowe score. Provencher and colleagues24 have studied 33 patients with posterior shoulder instability who underwent arthroscopic treatment, with a mean follow-up of more than 3 years. Labral repairs were performed in 17 patients, and capsular plication alone was performed in another 16 patients. The rotator interval was closed in 2 of the 33 patients. Thirty patients recalled a traumatic event, and 3 others sustained repetitive microtrauma. Stability was successfully restored in 88% of patients; 7 patients were defined as failures, 4 for recurrent instability and 3 for persistent pain. Patients with voluntary instability and those with prior shoulder surgery demonstrated worse outcomes; 3 of 4 patients who underwent prior thermal capsulorrhaphy were failures. Chhabra and associates56 have recently reported on the largest series of patients undergoing operative posterior shoulder stabilization. They studied 100 overhead and contact athletes with posterior inferior instability who underwent posteroinferior capsulolabral repair using suture anchors without rotator interval closure. Of these athletes, 95% had stable shoulders at a mean follow-up of 2 years postoperatively, and 83% returned to the same level of sport. Other studies have incorporated methods aimed at improving arthroscopic management of posterior shoulder instability. These include various techniques for capsulolabral repair, rotator interval closure, placement of accessory posterior portals, and closure of the capsule defect created by the posterior portal. Different arthroscopic techniques have been described to improve repair of the inferior glenohumeral ligament with capsulolabral plication.63,64 Appropriate placement of accessory posterior portals may allow for improved posteroinferior capsulolabral repair.24,65 Arthroscopic posterior portal closure has been described,66 although it is not done routinely. The significance of holes created by cannulas in the posterior capsule is currently unknown.
SUMMARY Posterior shoulder instability is becoming a more common clinical entity as diagnosis and recognition improve. Most patients with recurrent posterior shoulder instability experience a decrease or resolution of their symptoms following
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physical therapy, which is the initial treatment of choice. Operative intervention is indicated only for certain cases of traumatic instability and when symptomatic involuntary instability or pain persists despite appropriate physical therapy, such as strengthening and neuromuscular conditioning. Operative results of treatment of posterior shoulder instability are initially less favorable than results for anterior shoulder instability. More recently, appropriate recognition and subsequent treatment of specific lesions leading to correction of all components of posterior instability have improved results. Outcomes following arthroscopic treatment are improving over time as techniques evolve. Lesions associated with posterior instability that can be surgically addressed include labral tears, increased posterior capsular volume, a widened rotator interval, and osseous deformity (reverse bony Bankart or large reverse Hill Sachs defect). The best outcomes to date following an open or arthroscopic soft tissue repair have consisted of anatomic restoration of appropriate posteroinferior capsulolabral tension, along with repair of posterior labral pathology. Complex posteroinferior or multidirectional instability patterns may also require plication of the anterior and inferior parts of the capsule and rotator interval closure. Osseous reconstructive procedures are reserved for the rare unstable shoulder with marked glenoid erosion or glenoid retroversion.
References 1. Wolf EM, Eakin CL: Arthroscopic capsular plication for posterior shoulder instability. Arthroscopy 14:153-163, 1998. 2. Robinson CM, Aderinto J: Recurrent posterior shoulder instability. J Bone Joint Surg Am 87:883-892, 2005. 3. McIntyre LF, Caspari RB, Savoie FH 3rd: The arthroscopic treatment of posterior shoulder instability: Two-year results of a multiple suture technique. Arthroscopy 13:426-432, 1997. 4. Antoniou J, Duckworth DT, Harryman DT 2nd: Capsulolabral augmentation for the management of posteroinferior instability of the shoulder. J Bone Joint Surg Am 82:1220-1230, 2000. 5. Pollock RG, Owens JM, Flatow EL, Bigliani LU: Operative results of the inferior capsular shift procedure for multidirectional instability of the shoulder. J Bone Joint Surg Am 82:919-928, 2000. 6. Kim SH, Ha KI, Park JH, et al: Arthroscopic posterior labral repair and capsular shift for traumatic unidirectional recurrent posterior subluxation of the shoulder. J Bone Joint Surg Am 85:1479-1587, 2003. 7. Williams RJ 3rd, Strickland S, Cohen M, et al: Arthroscopic repair for traumatic posterior shoulder instability. Am J Sports Med 31:203-209, 2003. 8. Waters PM, Bae DS: Effect of tendon transfers and extraarticular soft-tissue balancing on glenohumeral development in brachial plexus birth palsy. J Bone Joint Surg Am 87:320-325, 2005. 9. Wirth MA, Seltzer DG, Rockwood CA Jr: Recurrent posterior glenohumeral dislocation associated with increased retroversion of the glenoid. A case report. Clin Orthop Relat Res (308):98-101, 1994. 10. Weishaupt D, Zanetti M, Nyffeler RW, et al: Posterior glenoid rim deficiency in recurrent (atraumatic) posterior shoulder instability. Skeletal Radiol 29:204-210, 2000.
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11. Churchill RS, Brems JJ, Kotschi H: Glenoid size, inclination, and version: An anatomic study. J Shoulder Elbow Surg 10:327-332, 2001. 12. Kim SH, Noh KC, Park JS, et al: Loss of chondrolabral containment of the glenohumeral joint in atraumatic posteroinferior multidirectional instability. J Bone Joint Surg Am 87:92-98, 2005. 13. Inui H, Sugamoto K, Miyamoto T, et al: Glenoid shape in atraumatic posterior instability of the shoulder. Clin Orthop Relat Res (403):87-92, 2002. 14. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 15. Matsen FA 3rd, Lippitt SB, Sidles JA, Harryman DT 2nd (eds): Practical Evaluation and Management of the Shoulder. Philadelphia, WB Saunders, 1994. 16. Warren RF, Kornblatt IF, et al: Static factors affecting posterior shoulder stability. Orthop Trans 8:89, 1984. 17. Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53-66, 1992. 18. Ovesen J, Nielsen S: Anterior and posterior shoulder instability. A cadaver study. Acta Orthop Scand 57:324-327, 1986. 19. Ovesen J, Sojbjerg JO: Posterior shoulder dislocation. Muscle and capsular lesions in cadaver experiments. Acta Orthop Scand 57:535-536, 1986. 20. Weber SC, Caspari RB: A biomechanical evaluation of the restraints to posterior shoulder dislocation. Arthroscopy 5:115-121, 1989. 21. Bey MJ, Hunter SA, Kilambi N, et al: Structural and mechanical properties of the glenohumeral joint posterior capsule. J Shoulder Elbow Surg 14:201-206, 2005. 22. Gerber C, Werner CM, Macy JC, et al: Effect of selective capsulorrhaphy on the passive range of motion of the glenohumeral joint. J Bone Joint Surg Am 85:48-55, 2003. 23. Selecky MT, Tibone JE, Yang BY, et al: Glenohumeral joint translation after arthroscopic thermal capsuloplasty of the posterior capsule. J Shoulder Elbow Surg 12:242-246, 2003. 24. Provencher MT, Bell SJ, Menzel KA, Mologne TS: Arthroscopic treatment of posterior shoulder instability: results in 33 patients. Am J Sports Med 33:1463-1471, 2005. 25. Weinberg J, McFarland EG: Posterior capsular avulsion in a college football player. Am J Sports Med 27:235-237, 1999. 26. Chhabra A, Diduch DR, Anderson M: Arthroscopic repair of a posterior humeral avulsion of the inferior glenohumeral ligament (HAGL) lesion. Arthroscopy 20(Suppl 2):73-76, 2004. 27. Safran O, Defranco MJ, Hatem S, Iannotti JP: Posterior humeral avulsion of the glenohumeral ligament as a cause of posterior shoulder instability. A case report. J Bone Joint Surg Am 86:2732-2736, 2004. 28. Hottya GA, Tirman PF, Bost FW, et al: Tear of the posterior shoulder stabilizers after posterior dislocation: MR imaging and MR arthrographic findings with arthroscopic correlation. Am J Roentgenol 171:763-768, 1998. 29. Kim SH, Ha KI, Yoo JC, Noh KC: Kim’s lesion: An incomplete and concealed avulsion of the posteroinferior labrum in posterior or multidirectional posteroinferior instability of the shoulder. Arthroscopy 20:712-720, 2004. 30. Yu JS, Ashman CJ, Jones G: The POLPSA lesion: MR imaging findings with arthroscopic correlation in patients with posterior instability. Skeletal Radiol 31:396-399, 2002.
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31. Lippitt S, Matsen F: Mechanisms of glenohumeral joint stability. Clin Orthop Relat Res (291):20-28, 1993. 32. Lippitt SB, Vanderhooft JE, Harris SL, et al: Glenohumeral stability from concavity-compression: A quantitative analysis. J Shoulder Elbow Surg 2:27-35, 1993. 33. Tibone JE, Bradley JP: The treatment of posterior subluxation in athletes. Clin Orthop Relat Res (291):124-137, 1993. 34. Hovis WD, Dean MT, Mallon WJ, Hawkins RJ: Posterior instability of the shoulder with secondary impingement in elite golfers. Am J Sports Med 30:886-890, 2002. 35. Sauers EL, Borsa PA, Herling DE, Stanley RD: Instrumented measurement of glenohumeral joint laxity and its relationship to passive range of motion and generalized joint laxity. Am J Sports Med 29:143-150, 2001. 36. Silliman JF, Hawkins RJ: Classification and physical diagnosis of instability of the shoulder. Clin Orthop Relat Res (291):7-19, 1993. 37. Tennent TD, Beach WR, Meyers JF: A review of the special tests associated with shoulder examination. Part II: Laxity, instability, and superior labral anterior and posterior (SLAP) lesions. Am J Sports Med 31:301-307, 2003. 38. Gerber C, Ganz G: Clinical assessment of instability of the shoulder. With special reference to anterior and posterior drawer tests. J Bone Joint Surg Br 66:551-556, 1984. 39. Kim SH, Park JS, Jeong WK, Shin SK: The Kim test: A novel test for posteroinferior labral lesion of the shoulder—a comparison to the jerk test. Am J Sports Med 33:1188-1192, 2005. 40. Warren RF, Craig EV, Altchek DW (eds): The Unstable Shoulder. Philadelphia, Lippincott Williams & Wilkins, 1999. 41. Cuéllar R, González J, de la Herrán G, Usabiaga J: Exploration of glenohumeral instability under anesthesia: The shoulder jerk test. Arthroscopy 21:672-679, 2005. 42. Kim SH, Park JC, Park JS, Oh I: Painful jerk test: A predictor of success in nonoperative treatment of posteroinferior instability of the shoulder. Am J Sports Med 32:1849-1855, 2004. 43. Nakagawa S, Yoneda M, Hayashida K, et al: Posterior shoulder pain in throwing athletes with a Bennett lesion: Factors that influence throwing pain. J Shoulder Elbow Surg 15: 72-77, 2006. 44. Schwartz E, Warren RF, O’Brien SJ, Fronek J: Posterior shoulder instability. Orthop Clin North Am 18:409-419, 1987. 45. Borsa PA, Jacobson JA, Scibek JS, Dover GC: Comparison of dynamic sonography to stress radiography for assessing glenohumeral laxity in asymptomatic shoulders. Am J Sports Med 33:734-741, 2005. 46. Beltran J, Rosenberg ZS, Chandnani VP, et al: Glenohumeral instability: Evaluation with MR arthrography. Radiographics 17:657-673, 1997. 47. Tung GA, Hou DD: MR arthrography of the posterior labrocapsular complex: Relationship with glenohumeral joint alignment and clinical posterior instability. Am J Roentgenol 180:369-375, 2003. 48. Magee T, Williams D, Mani N: Shoulder MR arthrography: Which patient group benefits most? Am J Roentgenol 183:969-974, 2004.
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49. Tirman PF, Smith ED, Stoller DW, Fritz RC: Shoulder imaging in athletes. Semin Musculoskelet Radiol 8:29-40, 2004. 50. Volpi D, Olivetti L, Budassi P, Genovese E: Capsulo-labroligamentous lesions of the shoulder: Evaluation with MR arthrography. Radiol Med (Torino) 105:162-170, 2003. 51. Engle RP, Canner GC: Posterior shoulder instability: Approach to rehabilitation. J Orthop Sports Phys Ther 10: 488-494, 1989. 52. Gartsman GM: Shoulder Arthroscopy. Philadelphia, WB Saunders, 2003. 53. Abrams JS, Savoie FH 3rd, Tauro JC, Bradley JP: Recent advances in the evaluation and treatment of shoulder instability: Anterior, posterior, and multidirectional. Arthroscopy 18(Suppl 2):1-13, 2002. 54. Pearsall AW 4th, Jarrett CA: A salvage procedure for refractory shoulder instability. Clin Orthop Relat Res (431): 245-249, 2005. 55. Metcalf MH, Duckworth DG, Lee SB, et al: Posteroinferior glenoplasty can change glenoid shape and increase the mechanical stability of the shoulder. J Shoulder Elbow Surg 8:205-213, 1999. 56. Chhabra A, Bradley JP, Herzka A, et al: Arthroscopic capsulolabral reconstruction for posterior inferior instability of the shoulder: A prospective study of 100 athletes. Presented at the American Orthopaedic Society for Sports Medicine 2005 Annual Meeting, Keystone, Colo, July 2005. 57. Plancher KD, Johnston JC, Peterson RK, Hawkins RJ: The dimensions of the rotator interval. J Shoulder Elbow Surg 14:620-625, 2005. 58. Fuchs B, Jost B, Gerber C: Posterior-inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg Am 82:16-25, 2000. 59. Scarpinato DF, Andrews JR: Posterior instability of the shoulder. In Andrews JR, Wilk KE (eds): The Athlete’s Shoulder. New York, Churchill Livingstone, 1994, pp 205-214. 60. Hawkins RJ, Koppert G, Johnston G: Recurrent posterior instability (subluxation) of the shoulder. J Bone Joint Surg Am 66:169-174, 1984. 61. Bigliani LU, Pollock RG, McIlveen SJ, et al: Shift of the posteroinferior aspect of the capsule for recurrent posterior glenohumeral instability. J Bone Joint Surg Am 77: 1011-1020, 1995. 62. Bottoni CR, Franks BR, Moore JH, et al: Operative stabilization of posterior shoulder instability. Am J Sports Med 33:996-1002, 2005. 63. Nebelung W, Röpke M, Urbach D, Becker R: A new technique of arthroscopic capsular shift in anterior shoulder instability. Arthroscopy 17:426-429, 2001. 64. Boileau P, Ahrens P: The TOTS (temporary outside traction suture): A new technique to allow easy suture placement and improve capsular shift in arthroscopic bankart repair. Arthroscopy 19:672-677, 2003. 65. Goubier JN, Iserin A, Augereau B: The posterolateral portal: A new approach for shoulder arthroscopy. Arthroscopy 17:1000-1002, 2001. 66. Schneeberger AG, Yian EH: Arthroscopic posterior portal closure. Arthroscopy 20(Suppl 2):110-112, 2004.
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CHAPTER 19 Multidirectional Instability
of the Shoulder John Uribe, John Zvijac, Bashir Zikria, and Angie Botto-van Bemden
Multidirectional instability as a pathologic entity was first described by Carter Rowe in 1956.1,2 He was also the first to focus on the relative atraumatic nature of humeral instability in more than one direction. Today, we recognize multidirectional instability as a major cause of shoulder instability in the athletic population.
static and dynamic restraints help maintain stability while allowing the most motion of any joint in the body. Thorough descriptions of the anatomy and biomechanics of the shoulder in relation to shoulder instability may be found in Chapters 1 and 2. Table 19-1 lists anatomic factors that may affect the stability of the glenohumeral joint.
In 1971, Endo and colleagues3 reported on atraumatic inferior subluxation of the humeral head in relation to the glenoid, which they had observed on radiographs of loaded shoulders. Neer and Foster4 expanded on the concept of degrees of atraumatic multidirectional instability, ranging from mild subluxation to frank dislocation of the humeral head in more than one direction. In 1980, they reported on a series of 36 patients (40 shoulders) with atraumatic instability in multiple directions. All their patients were noted to have involuntary inferior subluxation or dislocation associated with anterior or posterior instability of the shoulder, or both. They defined multidirectional instability as excessive humeral translation in more than one direction. The current literature, however, is inconsistent in its definition of multidirectional instability. As a consequence, the prevalence of this condition remains controversial.
CLINICAL PRESENTATION Patients with multidirectional instability typically present with the shoulder reduced, but complain of pain, a feeling of instability, or both, without a history of significant trauma. The direction of the instability may be determined by the symptoms, even if they are vague. A patient with symptoms produced by carrying heavy objects indicates inferior instability. Symptoms produced while pushing heavy doors—the arm in forward elevation and internal rotation—suggest posterior instability. Traction parasthesias often accompany these symptoms of instability. Patients may also have a history of laxity in other joints, or a ligamentous laxity may be present in other members of the patient’s family. Dowdy and O’Driscoll15 have discovered a 24% probability of instability in family members of patients treated surgically for recurrent anterior shoulder instability. Additionally, collagen disorders such as Ehlers-Danlos syndrome and other biomechanical disorders may manifest with generalized joint laxity.
Accurate use of the term multidirectional is not only essential for proper diagnosis, but also for choosing the appropriate treatment.5 In this chapter, multidirectional instability is defined as symptomatic excessive translation of the humeral head with respect to the glenoid in more than one direction. It is important to distinguish pathologic instability from normal laxity. For example, the sulcus sign is a clinical sign of inferior laxity that may or may not be pathologic; moreover, patients with instability in one direction, who also have generalized ligamentous laxity, should not be classified as having multidirectional instability. Patients who meet the criteria for the definition of multidirectional instability represent diagnostic and therapeutic challenges to the physician and physical therapist.
The physical examination may demonstrate generalized ligamentous laxity in other joints. Multidirectional instability of the opposite shoulder may provide a clue to the origin of instability in the involved shoulder. It is important to assess the acromioclavicular and sternoclavicular joints for tenderness, because they may be a source of hypermobility of the shoulder. Eliciting the glenohumeral translations that reproduce symptoms may be informative. The sulcus sign is an inferior sag of the humerus with the arm in adduction, indicating inferior laxity. Additional tests for laxity include the anterior, inferior, and posterior apprehension signs, relocation tests, and clunk tests. Superior labral anterior-posterior (SLAP) lesions may be clinically diagnosed with the O’Brien or grind test. Table 19-2 lists common tests and their clinical significance for assessing shoulder instability.
ANATOMY AND BIOMECHANICS A thorough comprehension of glenohumeral anatomy and biomechanics is essential to understanding the complex nature of multidirectional instability.6-14 The glenohumeral articulation is an inherently unstable joint. Contributions of
Routine radiographs include an anteroposterior (AP), internal and external rotation views of the humerus, 229
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TABLE 19-1 Anatomic Factors Involved With Glenohumeral Joint Stability Factor
Function
Abnormality
Congruity of articular surface
Concavity-compression effect
Glenoid dysplasia, fracture, Hill-Sachs lesion, reverse Hill-Sachs lesion
Glenoid labrum
Increases depth of socket and surface area; anchoring point for ligaments and capsule
Bankart lesion
Negative intra-articular pressure
Vacuum effect
Capsular rupture, defect of rotator interval, capsular laxity, capsular injury
Coracohumeral ligament–superior glenohumeral ligament
Limits external rotation and inferior translation in adduction, posterior translation in flexion
Lesion of rotator interval
Middle glenohumeral ligament
Limits external rotation and inferior translation in adduction; anterior translation in midabduction
Bankart lesion and capsular injury
Inferior glenohumeral ligament complex
Limits anterior, posterior, and inferior translation in abduction
Bankart lesion and capsular injury
Posterior aspect of the capsule
Limits posterior translation in flexed, adducted, and internally rotated shoulder
Posterior capsular laxity and injury
Rotator cuff
Dynamic joint compression; steering effect
Overuse injury (fatigue) and rupture
Biceps (long head)
Dynamic restraint to anterior and superior Lesion of superior portion of labrum, translation anterior and posterior (SLAP lesion), rupture
Adapted from Warner JJP, Schulte KR, Imhoff AB: Current concepts in shoulder instability. Adv Oper Orthop 3:219, 1995.
scapular Y, and axillary lateral; however, they are often insignificant in a patient with multidirectional instability. They should still be evaluated for any presence of humeral defects, such as a Hill-Sachs lesion, which is best seen on the internal rotation view, or glenoid lesions, seen best on axillary views. Magnetic resonance imaging (MRI) allows visualization of the superficial and deep structures with multiplanar capabilities of the glenohumeral joint. It may be useful in assessing rotator cuff pathology, labral morphology, and osseous integrity. Furthermore, MRI is beneficial if instability results in an injury to the axillary or suprascapular nerves. Denervated muscle demonstrates edema in the acute phase and then atrophy and fatty replacement during the chronic phase. Computed tomography (CT) scans provide a reliable measure of the osseous structures of the shoulder, helping to assess the glenoid version and identify any bony defects that may be difficult to identify on plain radiographs. CT arthrography is an invasive procedure that can be used to define osseous structures as well as labral and capsular integrity. This method, confined predominantly to axial images, has limited planar capabilities when compared with MRI. Ultrasonography offers little visualization of the labrum and capsule. It has been advocated for rotator cuff pathology, but even then it is operator dependent.
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TREATMENT Nonoperative Treatment Multidirectional instability may be treated operatively or nonoperatively. Initially, all patients should attempt conservative management, including activity modification and physical therapy. The goal of nonoperative therapy is to strengthen the scapular stabilizers, rotator cuff, and deltoid muscles. Matsen and Zuckerman16 have studied athletes with loose or lax capsules and found that the stability of the shoulder is dependent on the scapular stabilizers. Additional studies have shown that patients with shoulder instability have imbalances in muscle coordination17 and deficits in proprioception.18 Along with strengthening the muscles, it is important to improve muscle coordination and increase the patient’s functional adaptation. Activity modification entails patients avoiding any movement that might reproduce symptoms of instability. Patients should be informed that subsequent subluxations, or dislocations, of their shoulder increase the probability of recurrence. Strengthening of the rotator cuff, deltoid, and scapula-stabilizing muscles can be accomplished with a series of exercises. Initially, patients are taught to use the shoulder in the most stable position, with the humerus
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TABLE 19-2 Clinical Tests for Instability and Laxity
Diagnostic Test
Provocation
Patient Positioning Arm Positioning
Technique
Outcome
Provocation and Relief Tests for Instability Relocation
Pain and apprehension
Supine
Abducted to 90º and externally rotated to 90º
Humeral head pressed posteriority while arm is externally rotated
Relieves pain and apprehension
Anterior release
Pain and apprehension
Supine
Abducted to 90º and externally rotated to 90º
Same as relocation test, then posterior pressure is suddenly released
Pain and/or apprehension
Apprehension
Pain and apprehension
Sitting or standing
90º abduction and full external rotation
Arm is externally rotated while pressure is applied anteriorly to humeral head
Pain and/or apprehension
Clunk
Clunk or grinding
Supine
Full abduction
Arm is rotated in full external rotation, caput human is pushed slightly in anterior direction
Clunk or grinding
Laxity Tests for Instability Load and shift anterior or posterior
Anterior or posterior laxity
Sitting, standing, or supine
Neutral position
Humeral head is fixed by clinician’s hand, clinician tries to shift humeral head in anterior (or posterior) direction
Does not evoke discomfort: degree of humeral head translation on the glenoid in different positions of the humerus is evaluated using the Hawkins grading scheme*
Sulcus sign
Inferior laxity
Sitting or standing
Neutral position
Arm is pulled vertically downward
Positive when sulcus becomes visible between acromion and humeral head
Provocation and Relief Tests for Labral Tears Biceps load I
Pain
Supine
Arm is 90º abducted, elbow is 90º flexed
Clinician applies flexion pressure as patient resists
Positive if pain occurs
Biceps load II
Pain
Supine
120º abduction
Clinician applies lateral force as patient resists
Positive if pain occurs
Mimori
Pain and apprehension
Sitting or standing
Arm is 90º abduction, elbow is 90º flexed, forearm is supined
Forearm is brought from maximum supination to maximum pronation
Positive if pain occurs
Zaslav
Compares strength Sitting or standing in internal rotation with that of external rotation, excluding impingement from labral tears
Arm is in 90º abduction and 80º external rotation, elbow is 90º flexed
Patient resists external rotation force applied by the clinician, followed by applied internal rotation force
Positive (labral tear present) when the patient has good strength against external rotation and apparent weakness against internal rotation
Continued
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TABLE 19-2 Clinical Tests for Instability and Laxity—cont’d
Diagnostic Test
Provocation
Patient Positioning Arm Positioning
Technique
Outcome Positive if pain elicited with first maneuver, is reduced or eliminated in the second
Active compression Pain and relief (O’Brien)
Sitting or standing
Arm is in 90º forward flexion and 10º-15º abduction and full internal rotation
Clinician stands in front of patient. Arm is pushed down as patient resists. Repeated with arm in external rotation
Compression rotation
Pain or clicking
Supine
Arm at 90º abduction, elbow in 90º flexion
Positive if pain or Axial load placed on clicking occurs shoulder while rotated and circumducted (note McMurray knee test)
SLAP-prehension
Pain or clicking
Sitting or standing
Arm at 90º forward flexion
Arm is rotated internally in 90º flexion of the humerus
Positive if pain or clicking occurs
Speed
Pain in the anterior shoulder
Sitting or standing
90º elevation
Downward force applied to forearm, full supination of forearm and elbow is fully extended
Positive if pain occurs
Tenderness of bicipital groove
Pain
Sitting
Neutral
Palpating the bicipital groove
Positive if pain occurs
Yergason
Pain in the biceps tendon
Sitting with elbow at 90º
Neutral
Patient supinates forearm against clinician’s resistance, who simultaneously palpates biceps tendon
Positive if pain occurs
SLAP, superior labral anterior-posterior. * Hawkins grading scheme: grade 0 denotes little to no movement: grade 1 denotes the humeral head moves onto the glenoid rim; grade 2 indicates the humeral head can be dislocated-but spontaneously relocates: and grade 3 indicates the humeral head does not relocate when the pressure is removed in the Hawkins scheme, grades 1 to 3 are seen as positive outcomes on a laxity test. From Luime JJ, Verhagen AP, Miedema HS, et al: Does this patient have an instability of the shoulder or a labrum lesion? JAMA 292:1989-1999, 2004.
positioned in the plane of the scapula. It is thought that performing strengthening exercises in the scapular plane enhances muscle force by optimizing the length-tension relationship of the deltoid and rotator cuff musculature. Furthermore, in this position, less stress is placed on the anterior and posterior capsule. As muscle strength and coordination improve, the shoulder is brought into less intrinsically stable positions. Strengthening exercises for the rotator cuff muscles are performed by maintaining the humerus in close proximity to the body while rotating it against resistance. Push-ups and shoulder shrugs also assist in strengthening the scapular stabilizers. Jobe and associates19 have further emphasized the benefits of including isometric exercises as part of the rehabilitation program. If isotonic exercises are performed, they should initially be performed in a limited range of motion to avoid irritating the joint capsule and ligaments. Neuromuscular patterns required for stability are learned again through smooth repetitive motions such as swimming. To prevent further irritation during
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rehabilitation, a brief course of nonsteroidal antiinflammatory drugs (NSAIDs) may be used. NSAIDs may also help if the instability causes a secondary bursitis or rotator cuff tendonitis. The outcomes of rehabilitation are much more promising in atraumatic instability as compared with traumatic instability. Burkhead and Rockwood20 have compared traumatic versus atraumatic instability in 140 shoulders. Only 12 of 74 shoulders (16%) with a traumatic instability had a good or excellent postexercise outcome. In patients with atraumatic instability, 53 of 66 shoulders (80%) had a good or excellent outcome with rehabilitation. They also reported that rehabilitation may even be successful in multidirectional instability secondary to congenital factors. Ide and coworkers21 have reported on shoulder-strengthening exercises with an orthosis on 73 shoulders with multidirectional instability at a mean follow-up of 7 years. Most patients demonstrated significant improvements in strength, with only 3 patients not responding to conservative management and requiring surgery.
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Not all studies reported positive patient outcomes following conservative management. Misamore and colleagues22 have recently reported poor results following conservative treatment in young athletic patients diagnosed with multidirectional instability. Poor outcomes were seen in 19 of 36 patients, with only 8 patients demonstrating freedom from pain and instability with nonsurgical management.
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Flatow23 have recommended the anterior approach for shoulders that dislocate anteriorly and posteriorly.
Open Surgical Procedures The gold standard procedure in the literature is the inferior capsular shift, as described by Neer and Foster in 1980.4 The inferior capsular shift reduces the capsular volume of the glenohumeral joint inferiorly, anteriorly, and posteriorly by equilibrating capsular tension on all sides and balancing the humeral head (Fig. 19-1). The approach for the capsular shift may be anterior or posterior; this may be determined by the patient’s history and a physical examination. The side with the greatest clinical instability should be addressed using the surgical approach. Yamaguchi and
Anterior Approach. The skin incision for the anterior approach is an axillary incision from the tip of the coracoid to the inferior border of the pectoralis major. The deltopectoral interval is identified and the cephalic vein taken laterally, because there are fewer branches laterally than medially.24 The pectoralis major is retracted medially and the deltoid is retracted laterally. The clavipectoral fascia is incised lateral to the strap muscles. The subscapularis muscle is identified with the arm in a slight degree of external rotation to assist in identifying the superior and inferior borders of the muscle. The subdeltoid bursa is excised and the insertion of the subscapularis tendon is identified on the lesser tuberosity. The anterior humeral circumflex vessels are cauterized on the inferior border of the subscapularis. The subscapularis tendon is taken down 1 cm medial to its insertion on the lesser tuberosity from the rotator interval to the lower border of the tendon. The subscapularis tendon is lifted off the capsule and retracted medially, with stay sutures placed in the tendon. Occasionally, one half of the tendon remains attached to the capsule in an effort to reinforce the anterior aspect of the capsule when the tissue is thin or weak. A T-shaped incision is made in the capsule. The vertical segment of the T is just medial to the capsular attachment on the humerus. The superior flap contains the superior and middle glenohumeral ligaments, whereas the inferior glenohumeral ligament is contained within the inferior flap. The inferior flap is then shifted superiorly to eliminate the inferior redundancy and tension on the posterior capsule. The superior flap is pulled downward and sutured to the soft tissue of the humerus. The capsule is repaired with the arm in external rotation and abduction. The amount of external rotation and abduction is modified and determined according to the patient. For example, the dominant arm in throwing athletes would require more abduction and external rotation. Altchek and associates25 have described a similar approach to the T-plasty, basing the capsular incision on the glenoid rim (Fig. 19-2). According to their study, this technique allows for simultaneous Bankart repair and capsular shift.
Figure 19-1. Inferior capsular shift. (From Neer CS 2nd, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897-908, 1980.)
Posterior Approach. In the posterior approach, a vertical incision is made midway between the lateral border of the acromion and the posterior axillary crease. The deltoid is split to expose the tendons of the infraspinatus and teres minor, developing an interval within the infraspinatus muscle without dividing its tendon. Caution is used to avoid dissecting below the infraspinatus, allowing the axillary nerve and posterior humeral circumflex vessels to remain intact. The posterior capsule is identified and a T-shaped capsular incision is made medially, near the glenoid (Fig. 19-3). The inferior limb is advanced medially and superiorly to eliminate the posterior inferior capsular redundancy. The capsule is reattached to the glenoid using suture anchors.
Generally, the standard of care involves a 6- to 12-month period of rehabilitation as initial treatment for multidirectional instability. If the patient fails conservative management—pain and instability persist—operative intervention may then be considered.
Operative Treatment The decision to operate on a patient with multidirectional instability should only be considered if pain and instability persist following an adequate rehabilitation program (minimum of 6 months’ duration). The patient’s symptoms, cause, and level of activity must also be carefully considered. Operative interventions for multidirectional instability include open and arthroscopic procedures. Because the primary pathology in multidirectional instability is the loose redundancy of the capsule, standard surgical procedures for unidirectional instability are inadequate because they fail to address this excessive redundancy. Operative intervention for multidirectional instability attempts to reduce the total capsular volume.
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The results of the inferior capsular shift have been promising for multidirectional instability. Neer and Foster4 have reported a successful outcome, with a failure of only 1 in 32 patients (3%). They later reported similar results on 100 additional capsular shifts. Altchek and associates25 have reported 90% patient satisfaction on 42 shoulders with the T-plasty procedure. Pollock and coworkers26 have reported successful outcomes on 52 shoulders with an inferior capsular shift, with a mean follow-up of 61 months. Their results demonstrated the efficacy and durability of the inferior capsular shift for multidirectional instability. Figure 19-2. T-plasty modification of Bankart procedure. (From Altchek DW, Warren RF, Skyhar MJ, Ortiz G: T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone and Joint Surg Am 73:105-112, 1991.)
Most surgeons prescribe immobilization in a sling for approximately 6 weeks postoperatively. Passive and active range-of-motion exercises begin between 6 to 12 weeks. At 3 months, the patient may begin strengthening exercises and, at 6 months, throwing. Patient participation in sports is only permitted once full range of motion and strength have returned.
B
A
Figure 19-3. Posterior inferior capsular shift. The teres minor musculotendinous unit is not detached. Dissection is performed between the infraspinatus tendon and capsule. The capsule is opened with a T-shaped incision, creating a superior flap (A) and an inferior flap (B). The superior flap is then shifted inferiorly and the inferior flap is shifted superiorly. (From Fuchs B, Jost B, Gerber C: Posterior-inferior capsular shift for the treatment of recurrent, voluntary posterior subluxation of the shoulder. J Bone Joint Surg Am 82:16-25, 2000.)
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The complication most often reported for inferior capsular shift for multidirectional instability is recurrent instability. Additional complications have included axillary nerve neuropraxia, brachial plexus injuries, and capsular contractures. Arthroscopic Surgical Procedures In recent years, arthroscopic suture capsulorrhaphy and thermal capsulorrhaphy have yielded a high percentage of patient satisfaction for multidirectional instability. Detrisac and Johnson27 pioneered the use of arthroscopic techniques for treating shoulder instability. In 1997, McIntyre, and colleagues28 described modified arthroscopic techniques to accomplish the same stabilizing vertical shift of the capsule as Neer had demonstrated with his open capsular shift. Hewitt and associates29 have continued modifying arthroscopic techniques, describing the use of anchors and sutures and developing an all-inside technique for the treatment of multidirectional instability. The indications for arthroscopic stabilization of multidirectional instability are similar to those for the open procedure. The arthroscopic technique should address the capsular laxity and also correct secondary changes from the continuing symptomatic subluxation and dislocation of the shoulder. For example, associated capsulolabral tears or avulsions should be repaired concomitantly. The potential to identify and treat concomitant pathologies is one of the major advantages of arthroscopic versus open repair. Additional advantages include lower morbidity, reduced pain, shorter surgical time, and improved cosmesis. The patient is placed in the lateral or beach chair position for the arthroscopic procedure. The standard posterior portal is made and the arthroscope introduced into the joint. Two anterior portals are made using an outside-in technique. It is imperative to have these utility portals in the proper position because they function for instrument passage, glenoid preparation, suture management, and knot tying. The anterior superior portal is made just underneath the biceps tendon and the anterior inferior portal is made just above the subscapularis tendon (Fig. 19-4). A diagnostic arthroscopy is performed from the posterior and anterior portals. Suture anchors are placed on the glenoid rim from inferior to superior. The first anchor is critical in establishing proper capsular tension. After mobilization of the capsulolabral periosteal sleeve, it is usually
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235
often have significant inferior laxity when the arm is in adduction and external rotation during the physical examination. This interval lies within the anterior and superior capsular region, between the anterior border of the supraspinatus tendon and superior border of the subscapularis tendon. The superior and middle glenohumeral ligaments are the major ligamentous components of the rotator interval. If the shoulder still demonstrates persistent inferior or inferoposterior translation after the arthroscopic capsular shift, the rotator interval should be closed. Wolf and colleagues.31 have demonstrated on cadaveric shoulders that closure of the rotator interval significantly decreases laxity in all planes of the glenohumeral joint. Specifically, closure of the rotator interval decreases anterior, posterior, and inferior translation by 17%, 15%, and 28%, respectively, when compared with untreated shoulders in their study.
Figure 19-4. Schematic of portal placement for arthroscopic stabilization. This illustration of portal placement shows the relation of the two anterior portals relative to the subscapularis and biceps tendons. (From Cohen B, Cole B, Romeo A: Thermal capsulorrhaphy of the shoulder. Oper Tech Orthop 11:38-45, 2001.)
placed in the 5-o’clock position. Appropriate suture management is imperative to prevent loosening of the suture from the anchor. There are many techniques and devices for passing sutures through the tissue. The device of the surgeon’s preference should be placed through the capsulolabral complex medial and inferior to the lowest anchor in order for the entire inferior glenohumeral ligament to shift superiorly and laterally onto the glenoid rim. A minimum of two or three anchors is often needed for an arthroscopic shift beginning from inferior to superior. Recently, Alberta and coworkers30 have reported on arthroscopic anterior-inferior suture plications in the cadaveric model. They described a glenoid-based anterior-inferior capsular plication in a direct medial to lateral direction, with no attempt to advance the capsule superiorly. The surgical technique consists of placing suture anchors just medial to the labrum at the 5-o’clock position and at the superior border of the anterior-inferior glenohumeral ligament. Arthroscopic knots are tied, beginning with the inferior anchor, to complete the capsulorrhaphy. The capsular plication effectively reduces anterior and posterior glenohumeral translation. Anterior translation is consistently reduced by more than 60%. The loss of external rotation is similar to that of open capsular shifts and is among the lowest reported in the literature. Insufficiency within the region of the capsule known as the rotator interval has received attention recently because of some failed arthroscopic techniques attributed to this disorder. Patients with rotator interval lesions
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The outcomes of arthroscopic surgery should be compared with the gold standard, inferior capsular shift. McIntyre and associates28 have reported on 19 patients with multidirectional instability; 14 of the 19 patients were athletes. One patient had recurrent instability; 13 of the 14 athletes returned to their previous level of performance. Treacy and coworkers32 have reported an average follow-up of 60 months for 25 patients who underwent arthroscopic capsular shifts. Of these patients, 88% were satisfied with the procedure, with only 3 of 25 (12%) reporting continued instability. Their results were similar to those reported for inferior capsular shift. The major complications reported with arthroscopic capsular shifts have been with recurrent instability. There is less risk of injuring the axillary nerve and reducing motion, by preserving the subscapularis tendon on the lesser tuberosity. Thermal Capsulorrhaphy. If capsular laxity persists after the capsulolabral repair translation, persistent laxity may be reduced using thermal capsulorrhaphy. Heat treatment for multidirectional instability was introduced during the past decade. Initial interest, however, has steadily declined because of inconsistent results. Thermal energy works on the type I collagen of ligaments and joint capsules. The heating of collagen breaks the intramolecular cross-links, denaturing the protein. The collagen undergoes a transition from a highly organized state to a random gelatinous state because of the cumulative effect of the unwinding riple helices and residual tension of the heat-resistant intermolecular bonds working in concert to shrink collagen. The initial degree of shrinkage is directly related to the rate and amount of heat applied. Studies have demonstrated that this shrinkage reduces the joint capsule volume. Early on, Hayashi and colleagues33 showed the potential benefits of heat treatment for shoulder instability. They reported a significant decrease in capsular laxity after heat treatments in rabbits. Karas and associates34 have reported reduced capsular volume by 34% alone and 41% when used in combination with capsular plication in the cadaver
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model. Conversely, Luke and coworkers35 have compared the difference in reduction of capsular joint volume of an open capsular shift with thermal capsulorrhaphy in the cadaveric model; the open capsular shift reduces capsular volume by 50% compared with a 30% reduction for thermal capsulorrhaphy. As noted, the capsular response is dependent on temperature and rate. The technique for thermal capsulorrhaphy begins with the speed at which the probe is moved across the tissue and the areas of application (Fig. 19-5). Areas with the highest amount of collagen density will respond the most, such as the inferior glenohumeral ligaments. It is of utmost importance not to leave the probe in one position to prevent significant injury to the capsule. Fanton36 has shown encouraging results for shoulder instability with thermal capsular shrinkage; the study of 54 patients had a success rate higher than 90%, with a minimum follow-up of 2 years. Levitz and colleagues34 have reported successful results of using thermal capsulorrhaphy in overhead athletes; 90% returned to their preinjury
level of competition. Two other studies by Fitzgerald38 and Noonan39 and their associates have reported approximately 80% success rates with thermal capsulorrhaphy, although both these studies had short-term follow- up. Conversely, the results of Levy and colleagues40 were not as promising. They reported a significant failure rate for thermal capsulorrhaphy in patients with multidirectional instability—a 36.1% failure rate with laser-assisted capsulorrhaphy over a 40-month follow-up. D’Alessandro and associates41 have reported on 84 shoulders with instability and found a high rate of unsatisfactory overall results (37%), with an average follow of 38 months. Finally, Miniaci and McBirnie42 have studied 19 patients with multidirectional instability and found that thermal capsular shrinkage has a substantial failure rate, with associated postoperative complications. Complications included recurrence of instability (9 patients), stiffness (5 patients), and neurologic symptoms (4 patients). Complications from thermal capsulorrhaphy include shoulder stiffness, cartilage damage, capsular necrosis, axillary nerve injury, and failure of the procedure itself. Park and coworkers43 have shown that in 14 patients with failed thermal capsulorrhaphy, capsular thinning or necrosis often occurs (43%). They were able to perform revision surgery with the remaining capsular tissue using an open subscapularis splitting technique. It was concluded that recurrent laxity after thermal capsulorrhaphy is common, but in most cases the capsule quality does not affect the revision procedure. Postoperative rehabilitation after arthroscopic repair is identical to that after open reconstruction. Sling immobilization generally is required for 4 to 6 weeks, depending on the methods used and the instability pattern treated. In roughly 6 to 12 weeks, patients begin passive and active range-of-motion exercises. The patient is generally allowed to return to sports participation in 18 to 36 weeks.
SUMMARY
Figure 19-5. Arthroscopic thermal capsulorrhaphy after anterior stabilization with suture anchors. A monopolar radiofrequency device (OraTec Interventions, Menlo Park, Calif) may be used to reduce capsular volume additionally after an arthroscopic Bankart repair. A grid technique is used to treat the capsule. Care is taken to avoid thermal treatment near the suture line to avoid weakening the surgical repair. Treatment of the capsule (gray shaded area) within the regions of the middle, inferior, and posterior glenohumeral ligaments may be required, depending on the degree of capsular laxity. Thermal treatment of the axillary pouch is avoided entirely. (From Cohen B, Cole B, Romeo A: Thermal capsulorrhaphy of the shoulder. Oper Tech Orthop 11:38-45, 2001.)
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Multidirectional instability is more prevalent than previously thought. It is imperative to have an accurate definition for multidirectional instability prior to diagnosis and appropriate treatment. The diagnosis may be derived on the basis of a careful history and physical examination. Radiographs, such as an MRI or CT scan, are helpful in identifying associated pathology with multidirectional instability. Most patients may be treated conservatively with an appropriate rehabilitation program of 6 months’ minimum duration. Surgery is only indicated for those patients who fail to respond to conservative treatment. The gold standard surgical procedure is Neer’s open inferior capsular shift. All other surgical procedures, such as arthroscopic capsular shifts, should be compared with the gold standard. In recent years, with the advance of arthroscopic techniques, the results of both procedures are similar.
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References 1. Rowe CR: Prognosis in dislocations of the shoulder. J Bone Joint Surg Am 38:957-977, 1956. 2. Rowe CR: Acute and recurrent dislocations of the shoulder. J Bone Joint Surg Am 44:998-1008, 1962. 3. Endo H, Takigawa H, Takata K, Miyoshi S: A method of diagnosis and treatment of the loose shoulder. Cent Jpn J Orthop Trav Surg 14:630, 1971. 4. Neer CS 2nd, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897-908, 1980. 5. McFarland EG, Kim TK, Park HB, et al: The effect of variation in definition on the diagnosis of multidirectional instability of the shoulder. J Bone Joint Surg Am 85:2138-2144, 2003. 6. Kondo T, Hashimoto J, Nobuhara K, Takakura Y: Radiographic analysis of the acromion in the loose shoulder. J Shoulder Elbow Surg 13:404-409, 2004. 7. Soslowsky LJ, Flatow EL, Bigliani LU, Mow VC: Articular geometry of the glenohumeral joint. Clin Orthop 285: 181-190, 1992. 8. Howell, SM, Galinat, BJ: The glenoid-labral socket. A constrained articular surface. Clin Orthop 243:122-125, 1989. 9. Inui H, Sugamoto K, Miyamoto T, et al: Glenoid shape in atraumatic posterior instability of the shoulder. Clin Orthop Relat Res (403):87-92, 2002. 10. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990. 11. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 18:579-584, 1990. 12. Terry GC, Hammon D, France P, Norwood LA: The stabilizing function of passive shoulder restraints. Am J Sports Med 19:26-34, 1991. 13. Pollock RG, Bucchieri JS, Wang VM, et al: Subfailure repetitive loading of the IGHL affects its mechanical properties. Trans Orthop Res Soc 22:164, 1997. 14. Boardman ND, Debski RE, Warner JJ, et al: Tensile properties of the superior glenohumeral and coracohumeral ligaments. J Shoulder Elbow Surg 5:249-254, 1996. 15. Dowdy PA, O’Driscoll SW: Shoulder instability. An analysis of family history. J Bone Joint Surg Br 75:782-784, 1993. 16. Matsen FA III, Zuckerman JD: Anterior glenohumeral instability. Clin Sports Med 2:319-338, 1983. 17. Kronberg M, Broström LÅ, Németh G: Differences in shoulder muscle activity between patients with generalized joint laxity and normal controls. Clin Orthop, 269:181-192, 1991. 18. Lephart SM, Warner JJP, Borsa PA, et al: Proprioception of the shoulder joint in healthy, unstable, and surgically repaired shoulders. J Shoulder Elbow Surg 3:371-380, 1994. 19. Jobe FW, Giangarra CE, Kvitne RS, Glousman RE: Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med 19:428-434, 1991. 20. Burkhead WZ Jr, Rockwood CA Jr: Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg Am 74:890-896, 1992. 21. Ide J, Maeda S, Yamaga M, et al: Shoulder-strengthening exercise with an orthosis for multidirectional shoulder instability: Quantitative evaluation of rotational shoulder strength before and after the exercise program. J Shoulder Elbow Surg 12:342-345, 2003.
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22. Misamore GW, Sallay PI, Didelot W: A longitudinal study of patients with multidirectional instability of the shoulder with seven- to ten-year follow-up. J Shoulder Elbow Surg 14:466-470, 2005. 23. Yamaguchi K, Flatow EL: Management of multidirectional instability. Clin Sports Med 14:885-902, 1995. 24. Radkowski CA, Richards RS, Pietrobon R, Moorman CT III: An anatomic study of the cephalic vein in the deltopectoral shoulder approach. Clin Orthop Relat Res 442:139-142, 2006. 25. Altchek DW, Warren RF, Skyhar MJ, Ortiz G: T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone and Joint Surg Am 73:105-112, 1991. 26. Pollock RG, Owens JM, Flatow EL, Bigliani LU: Operative results of the inferior capsular shift procedure for multidirectional instability of the shoulder. J Bone Joint Surg Am 82:919-928, 2000. 27. Detrisac DA, Johnson LL; Arthroscopic shoulder capsulorrhaphy using metal staples. Orthop Clin North Am 24: 71-88, 1993. 28. McIntyre LF, Caspari RB, Savoie FH III: The arthroscopic treatment of multidirectional shoulder instability: Two-year results of a multiple suture technique. Arthroscopy 13: 418-425, 1997. 29. Hewitt M, Getelman MH, Snyder SJ: Arthroscopic management of multidirectional instability: Pancapsular plication. Orthop Clin North Am 34:549-557, 2003. 30. Alberta FG, Elattrache NS, Mihata T, et al: Arthroscopic anteroinferior suture plication resulting in decreased glenohumeral translation and external rotation. Study of a cadaver model. J Bone Joint Surg Am 88:179-187, 2006. 31. Wolf RS, Zheng N, Iero J, Weichel D: The effects of thermal capsulorrhaphy and rotator interval closure on multidirectional laxity in the glenohumeral joint: A cadaveric biomechanical study. Arthroscopy 20:1044-1049, 2004. 32. Treacy SH, Savoie FH III, Field LD: Arthroscopic treatment of multidirectional instability. J Shoulder Elbow Surg 8: 345-350, 1999. 33. Hayashi K, Thabit G III, Vailas AC, et al: The effect of nonablative laser energy on joint capsular properties. An in vitro histologic and biochemical study using a rabbit model. Am J Sports Med 24:640-646, 1996. 34. Karas SG, Creighton RA, DeMorat GJ: Glenohumeral volume reduction in arthroscopic shoulder reconstruction: a cadaveric analysis of suture plication and thermal capsulorrhaphy. Arthroscopy 20:179-184, 2004. 35. Luke TA, Rovner AD, Karas SG, et al: Volumetric change in the shoulder capsule after open inferior capsular shift versus arthroscopic thermal capsular shrinkage: A cadaveric model. J Shoulder Elbow Surg 13:146-149, 2004. 36. Fanton GS: Arthroscopic electrothermal surgery of the shoulder. Oper Tech Sports Med 6:139-146, 1998. 37. Levitz CL, Dugas J, Andrews JR: The use of arthroscopic thermal capsulorrhaphy to treat internal impingement in baseball players. Arthroscopy 17:573-577, 2001. 38. Fitzgerald BT, Watson BT, Lapoint JM: The use of thermal capsulorrhaphy in the treatment of multidirectional instability. J Shoulder Elbow Surg 11:108-113, 2002. 39. Noonan TJ, Tokish JM, Briggs KK, Hawkins RJ: Laserassisted thermal capsulorrhaphy. Arthroscopy 19:815-819, 2003.
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40. Levy O, Wilson M, Williams H, et al: Thermal capsular shrinkage for shoulder instability. Mid-term longitudinal outcome study. J Bone Joint Surg Br 83:640-645, 2001. 41. D’Alessandro DF, Bradley JP, Fleischli JE, Connor PM: Prospective evaluation of thermal capsulorrhaphy for shoulder instability: Indications and results, two- to five-year follow-up. Am J Sports Med 32:21-33, 2004.
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42. Miniaci A, McBirnie J: Thermal capsular shrinkage for treatment of multidirectional instability of the shoulder. J Bone Joint Surg Am 85:2283-2287, 2003. 43. Park HB, Yokota A, Gill HS, et al: Revision surgery for failed thermal capsulorrhaphy. Am J Sports Med 33:1321-1326, 2005.
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CHAPTER 20 Management of the First-Time
Shoulder Dislocation in the Athlete Robert Y. Wang, Augustus D. Mazzocca, James Bicos, and Robert A. Arciero
Acute traumatic anterior shoulder dislocation is a relatively common occurrence, especially in the athletic population. There are various options available when advising patients about treatment. This chapter will discuss the classification, pathoanatomy, causes, epidemiology, diagnosis, and treatment considerations for the first-time anterior shoulder dislocation.
glenoid hypoplasia and disorders of collagen structure that result in excessive joint laxity. The active mechanisms involved with glenohumeral stability are primarily provided by the rotator cuff muscles. The type and severity of pathoanatomic lesions may be influenced by the patient’s age, mechanism of injury, and degree of trauma.
Bankart Lesion
CLASSIFICATION
The inferior glenohumeral ligament (IGHL) complex is the primary ligamentous restraint to anterior glenohumeral translation, specifically with the arm in an abducted and externally rotated position (Fig. 20-1).3 The specific anatomy of the IGHL has been described as having anterior and posterior bands, with an intervening axillary pouch. Detachment of the anterior-inferior labrum and capsule, comprising the anterior band of the IGHL as a capsulolabral complex, is considered one of the major pathoanatomic features of traumatic anterior shoulder instability.4 Up to 85% of traumatic anterior shoulder dislocations can be associated with detachment of the anterior-inferior labrum and capsule. Broca and Hartman first described the lesion in 1890, followed by Perthes in 1906 and Bankart in 1923. This lesion has subsequently been named the Perthes-Bankart lesion (Fig. 20-2).
Although we will focus on acute traumatic anterior dislocation, it is important to recognize the spectrum of presentation in shoulder instability. Traumatic anterior dislocation would therefore represent one extreme end of the spectrum, as described by Matsen.1 The patient with hyperlaxity, bidirectional instability, and little or no provocation for symptoms would represent the other end. The surgeon should recognize the great degree of crossover that can be observed between these two ends of the spectrum. For example, a hyperlax patient can present with a traumatic dislocation. Understanding the variability of presentation and the unique anatomic and individual characteristics in each patient will lead to optimum treatment. By definition, an acute anterior dislocation is one that requires a reduction; a traumatic instability event can also occur as a subluxation. Spontaneous reduction in this case is oftentimes reported by the athlete as a sensation of a definite clunk and relief of pain. Rowe described this phenomenon as the “dead arm” syndrome, as transient anterior subluxation results in a sudden sharp or “paralyzing” pain where the arm becomes weak or “goes dead.”20 Other classification systems include the direction of instability and timing (acute, recurrent, or chronic).
The mechanism of how the Bankart lesion leads to instability has been studied extensively. The detachment of the labrum from the anterior-inferior glenoid is the essential lesion leading to anterior instability. By displacing the anterior labrum, glenoid depth is decreased by up to 50% and passive restraints, such as the concavity-compression mechanism discussed earlier, are also lost.5,6 Lazarus6 has demonstrated that detachment of the anterior inferior labrum and capsule from the glenoid results in nearly doubling of glenohumeral anterior translation. A Bankart repair is then performed, repairing the anterior IGHL and labrum back to the glenoid, and restoring glenohumeral stability. In another cadaver study, Bigliani has demonstrated that the strain before failure for all boneligament-bone preparations of the shoulder capsule was 27%; the authors concluded that plastic deformation of the capsule is a fundamental component of anterior instability. This is an important concept for the treatment of anterior instability because, in addition to repair of the glenoid labrum, capsular redundancy may require plication, especially in the recurrent instability situation.
PATHOANATOMY The overall stability of the glenohumeral joint involves passive and active mechanisms. Passive or static factors include joint conformity, adhesion and cohesion, finite joint volume, and ligamentous restraints, including the labrum.1 The ligaments and capsule are aided by receptors that provide proprioceptive feedback. When capsuloligamentous structures are damaged, alterations in proprioception occur that are partially restored with operative repair.2 Static stabilizers are also affected by congenital factors; these include 239
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AILC
IGHL
Figure 20-1. Cadaveric images. Shown are the inferior glenoid humeral ligament (IGHL) and anterior inferior labral complex (AILC).
The incidence of a Bankart lesion in the athlete who sustains an anterior dislocation has been studied extensively. Its incidence in the initial dislocation has been reported to be 87% to 100%.8-11 Neviaser, in 1993, added a differentiation between the Bankart lesion and what he termed the anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion (Fig. 20-3).12 In this description of acute and chronic anterior dislocations, the capsule and labrum are not detached as in a Bankart lesion, but the anterior IGHL, labrum, and anterior scapular periosteum are stripped and displaced in a sleevetype fashion medially on the glenoid neck. This is an important diagnostic variant to recognize because in a chronic situation, a cursory inspection of the anterior inferior quadrant of the glenoid may not reveal evidence of trauma. However, closer inspection more medially will show a large, medially displaced labrum on the anterior portion of the glenoid neck.
Capsulolabral complex
Superior Labrum Extension An arthroscopic shoulder examination frequently leads to observations of additional lesions associated with anterior instability. Arciero and coworkers13 have described injuries that may also extend superiorly into the attachment of the biceps tendon, producing a concomitant superior labrum anterior-posterior (SLAP) lesion (Fig. 20-4). This lesion is generally observed when the dislocation involves an extreme type of trauma. In a variation of the anterior superior labrum lesion, the anterior supraspinatus can have partial or complete tears, resulting in varying amounts of instability. This has been called the SLAC lesion (superior labrum, anterior cuff)14; it can be observed in acute and chronic trauma.
Glenoid
Figure 20-2. Bankart lesion. This is an arthroscopic view of the left shoulder, viewed posteriorly, with the patient in a sitting position.
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Figure 20-3. Arthroscopic view of an anterior labrum periosteal sleeve avulsion (ALPSA) lesion. This is an anterior view of the left shoulder, with the lesion being mobilized.
Figure 20-4. Arthroscopic view of a superior labral anterior-posterior (SLAP) lesion, type IV.
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MANAGEMENT OF THE FIRST-TIME SHOULDER DISLOCATION IN THE ATHLETE
Humeral Avulsion of Glenohumeral Ligament Lesions A third type of lesion that can be observed is a lateral detachment of the IGHL from the humeral neck. This has been described by Nicola15 as a humeral avulsion of the glenohumeral ligament (HAGHL) lesion (Fig. 20-5); its proposed mechanism was also discussed. Richards and Burkhart16 have described an all-arthroscopic technique using suture anchors to repair HAGHL lesions, and noted that it is a difficult and demanding technique. Wolf17 has found an incidence of 9.3% in a series of patients presenting with recurrent anterior instability and also described an arthroscopic technique for repair of HAGHL lesions. In this procedure, a standard anterior inferior portal is made, and the bone at the anterior inferior aspect of the humeral neck is burred through this portal. An anterior lateral portal is created 2 cm lateral
A
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and 2 cm inferior to the coracoid process. A suture hook is used to place monofilament absorbable sutures through the capsule; these are tied through the anterior lateral portal over the subscapularis tendon. Bokor and associates18 have reported on 41 cases of HAGHL lesions in 547 shoulders, with an overall incidence of 7.5%. In 2002, Bui-Mansfield19 published a retrospective review of 307 patients with anterior instability; they identified six HAGHL lesions, an incidence of 2%. Although relatively rare, this lesion must be sought for during any anterior instability arthroscopic examination. Taylor and Arciero have also described HAGHL lesions after acute anterior dislocations.10
Traumatic Bone Lesions Traumatic glenoid and humeral head fractures can occur with an anterior shoulder dislocation. The anatomy of the glenoid and proximal humerus is consistent. The articular surface of the proximal humerus is similar to that of a sphere. It is composed of cartilage and subchondral and trabecular bone that is relatively soft, even in young athletes. The glenoid has a consistent morphology as well. It is pear-shaped, with the inferior portion approximating that of a true circle. Bone loss should not be overlooked in any anterior instability event. Even with transient anterior subluxation, Rowe found 15 of 32 breakout lesions involved avulsion of the anterior glenoid rim.20 Studies have shown the average superior-inferior glenoid diameter to be 30.4 to 42.6 mm in males and 29.4 to 37.0 mm in females. Bony lesions of the glenoid or humeral head place greater demand on the integrity of soft tissue repairs and have been shown to cause recurrent anterior instability of the shoulder.21
Humeral Head Lesions
B Figure 20-5. Humeral avulsion of the glenohumeral ligament (HAGHL) lesion. A, Arthroscopic view of HAGHL, sitting position, posterior left shoulder. The subscapularis muscle is seen as a shadowed area in the background. B, Open example of HAGHL lesion, right shoulder. The subscapularis is tagged with suture to the right. The HAGHL lesion is tagged with sutures inferiorly.
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The Hill-Sachs lesion is found on the humerus. This is an impression fracture caused by the humeral head being dislocated anteriorly and impacting on the anterior glenoid. It is generally located at the posterior-superior portion of the humeral head. Burkhart and De Beer21 have reported and defined what they describe as an engaging Hill-Sachs lesion, which catches and locks the humeral head in a functional position of abduction and external rotation. The long axis of the Hill-Sachs lesion is parallel to the glenoid and engages its anterior corner. The nonengaging Hill-Sachs lesion passes diagonally across the anterior glenoid with external rotation so that there is continual contact between the articular surfaces. These shoulders are reasonable candidates for arthroscopic Bankart repair. It is important to realize, however, that the Hill-Sachs lesion is created by the position of the arm when the dislocation occurs. A Hill-Sachs lesion that develops with the arm at the side with some extension of the shoulder will be located more vertically and superiorly
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than the lesion that occurs with the shoulder abducted and externally rotated. The Hill-Sachs lesion that develops with the arm at the side is generally a nonengaging lesion. Norlin9 has shown that in Hill-Sachs lesions, 25% of cases are down to subchondral bone and 75% are just chondral lesions. Taylor and Arciero10 have show that of 57 patients with Hill-Sachs lesions, 23 were chondral and 34 were osteochondral. None of these lesions was large and had no effect on stability, as demonstrated arthroscopically. In their series, Jakobsen11 has documented 19% Hill-Sachs lesions diagnosed on craniocaudal radiographs.
Glenoid Bone Lesions Two types of fractures occur involving the anterior inferior glenoid, the glenoid rim fracture and an avulsion fracture. The glenoid rim fracture is secondary to compression of the anterior inferior bony articulation of the glenoid by the humeral head (Fig. 20-6). Studies have shown an incidence of anterior glenoid rim fractures associated with an anterior dislocation ranging from 5.4% to 44%.22,23 However, we are unaware of any reports on the incidence of anterior glenoid rim fractures resulting from an initial first-time acute dislocation. Repeated episodes of instability create the inverted pear lesion as well as a typical bony Bankart lesion, and this is observed in the recurrent instability. Investigators in the past have recommended a coracoid transfer if the glenoid rim fracture comprises 25% of the anterior-posterior diameter of the glenoid. Lo24 commented on the containment of the humeral head by the glenoid as a result of two geometric variables. The first is the deepening effect of a wire glenoid caused by the longer arc of its concave surface; the second is the arc length of the glenoid itself. They cautioned that if the bony fragment is excised or if there is an inverted pear-shaped glenoid, arthroscopic techniques without a bone augmentation procedure may be predisposed to failure. The recognition and proper management of bone defects in the acute dislocation are important. In recurrent dislocations, increased failure rates with arthroscopic repair have been observed in the presence of bone loss.21,25,26
The pathoanatomy described pertains to the young athletic population. In athletes older than 50 years, Reeves27 has found capsular rupture, capsular detachment, and rotator cuff tear to be the predominant pathoanatomy after performing an arthrogram on postacute anterior dislocation patients. Most patients in Robinson’s study28 were middleaged. Of the seven isolated dislocations without a fracture, five had a massive rotator cuff tear; it was found that the presence of a rotator cuff tear is associated with a much higher risk of redislocation.
CAUSES AND EPIDEMIOLOGY For an anterior shoulder dislocation to occur, the mechanism of injury typically involves the position of abduction and external rotation, as seen in many contact sports. Studies have shown the incidence of traumatic shoulder instability in the general population to be approximately 1.7%. However, this can be doubled in those with high physical demands. In the United States Military Academy, the 1-year incidence was 2.8%, and 85% of instability events were caused by traumatic subluxation.29 After an anterior shoulder dislocation, the risk of recurrent shoulder instability is related primarily to the age at the time of dislocation. This is the single most important prognostic factor. There is a significantly higher rate of recurrent anterior shoulder instability in younger patients with acute traumatic anterior shoulder dislocations. Most recurrent instability episodes occur in the first 2 years after the primary incident. A study by McLaughlin and Cavallaro30 has found a 90% chance of recurrent instability in patients younger than 20 years, a 60% recurrence rate in patients 20 to 40 years of age, and a recurrence rate lower than 10% in patients older than 40 years. Hovelius31 published long-term rates of recurrent instability (at 10 years) and found a 66% risk of recurrent anterior instability for patients younger than 22 years, a 56% risk for patients aged 23 to 29 years, and a 20% risk for patients 30 to 40 years. More recently, at 2 years, Jakobsen11 found a 54% recurrence rate in patients treated conservatively after an initial anterior dislocation. There was a 3% recurrence in the group treated with open repair. Larrain32 reported a 5.1% recurrence in the acute instability group, with the events occurring during rugby. In the recurrent instability group, the recurrence rate was 8.3%. Postacchini33 reviewed patients 14 to 17 years of age and found that the recurrence rate after a primary traumatic dislocation is 92%; for adolescents with a Bankart lesion, they recommended prophylactic surgical stabilization at the time of initial injury.
Figure 20-6. Radiograph of a bony Bankart lesion.
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Activity level may also be an important factor when considering the risk of recurrence after an anterior dislocation. Arciero34 has shown that for first-time contact sport athletes, there is an 80% recurrence rate with conservative treatment and return to contact sports. Conversely, there is
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a 14% recurrence rate with arthroscopic treatment of the Bankart lesion and return to contact sports. In Hovelius’ series of Swedish hockey players, the redislocation rate was 90% in players older than 20 years, with a diminishing frequency with increasing age.35 Larrain36 found that most dislocations are in rugby players.
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conscious sedation or intra-articular local anesthetic. Miller39 reported the use of intra-articular lidocaine to facilitate reduction with the Stimson technique as a safe and effective method for treating acute shoulder dislocations in an emergency room. In this setting, it would be prudent first to obtain an x-ray (anteroposterior [AP], lateral, and axillary views) to confirm the direction of dislocation and to rule out associated fractures.
DIAGNOSIS Radiologic Features Evaluation and Physical Examination In the setting of an acute anterior shoulder dislocation in the athlete, the physician usually encounters the athlete on the field, in the training room, or in the emergency department (ED). Initial evaluation should focus on airway, breathing, and circulation to assess the overall stability of the patient. Once the patient is deemed stable, a detailed assessment of the injured extremity is conducted. If the physician is covering the game from the sidelines, he or she will witness the mechanism of the injury. The focused history should rule out associated injuries by asking about other symptomatic areas. In an acute first-time dislocation, the athlete will be in obvious discomfort and experiencing intense pain. The physical examination of the shoulder should follow a systematic approach to avoid missing concurrent pathology. It is important to perform pre- and postreduction neurovascular examinations. Nerve lesions include injury to the axillary nerve (most common), suprascapular nerve traction injury, and long thoracic nerve injury. Visser and colleagues38 have reported axillary nerve injury in 42% of anterior shoulder dislocations. Immediate recognition of an acute anterior dislocation is often possible because of the characteristic position of the athlete’s arm, which is held internally rotated against the body and supported by the contralateral arm. The athlete will resist any attempt to move the affected arm. Physical examination findings include the following: • Asymmetry of the deltoid contour. The affected side will demonstrate a sharp contour and a more prominent acromion when compared with the unaffected side. • The affected side may have a palpable fullness below the coracoid and toward the axilla. A closed reduction on the field or sideline or in training without first obtaining an x-ray is controversial. Many experienced physicians will perform a closed reduction on the field with the rationale that a reduction can be achieved before the onset of muscle spasms. This would allow a timely reduction, which would significantly reduce the level of pain without the need for conscious sedation. It is imperative that a repeat neurovascular examination be conducted postreduction. The other scenario is that the dislocation is not reduced on the field and the physician first sees the patient in the ED. By the time the patient arrives in the ED, a closed reduction is usually not possible without
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Radiographs should include a trauma series to document the direction of the dislocation and any associated fractures of structures such as the glenoid rim or greater tuberosity. A standard AP view of the arm in slight internal rotation is used to identify a fracture of the greater tuberosity. A true scapular AP radiograph permits evaluation of a glenoid fossa fracture, if present. In the office, after reduction, the West Point modified axillary view is used to assess bony avulsions of the attachment of the IGHL, bony Bankart lesions, or anterior-inferior glenoid deficiency.40 It is difficult to obtain this radiograph acutely because of guarding and pain but usually it can be obtained within several days. The Hill-Sachs lesion can be quantified and evaluated by examining the Stryker notch view. Computed Tomography A computed tomography (CT) scan can be an accurate means of determining glenoid version and overall glenoid morphology and, with three-dimensional reconstructions, provides an accurate assessment of any bone loss or size of rim fracture after an acute dislocation.41 Currently, the senior author uses CT to quantify the size of an anterior rim fracture after an acute dislocation (Fig. 20-7). Magnetic Resonance Imaging Magnetic resonance imaging (MRI) is used for the assessment of associated pathology. Contrast enhancement improves the diagnostic ability to detect labral tears (superior and anterior-inferior), rotator cuff tears (partialand full-thickness), and articular cartilage lesions. In the identification of HAGHL lesions, MRI scans in the midsagittal coronal oblique plane show the detachment of the inferior glenoid labrum (IGL) and reveal that the axillary pouch is converted from a fully distended U-shaped structure to a J-shaped structure as the IGL drops inferiorly (Fig. 20-8).42 This has been further defined in a follow-up study that describes the MRI appearance of a HAGHL lesion as an avulsion fracture from the neocortex in the humeral neck. The fluid-filled, distended, U-shaped axillary pouch is converted into a J-shaped structure by the extravasation of contrast material.19 Occasionally, with plain radiography, a thin, crescent-shaped calcific density is observed inferior to the anatomic neck of the humerus. The presence of this lesion may also be a relative contraindication to an arthroscopic shoulder stabilization procedure.
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and quality of life.36,37,43,44 On the contrary, Sachs found only half of his “high risk” contact or collision athletes requesting surgical stabilization during the follow-up period and concluded that early surgery should not be based on the presumption of future dislocations and disability.45 Patients 25 to 40 years have a much lower recurrence rate and rehabilitation after the dislocation is generally the best treatment. Patients older than 40 years who sustain an anterior dislocation have much lower recurrence rates in general (10% to 15%) but can have residual disability requiring priority treatment because of other soft tissue lesions, such as rotator cuff tear, nerve injury, and vascular injury.46
Nonoperative Treatment
Figure 20-7. Arthroscopic example of an inverted pear-shaped glenoid of the left shoulder, anterior-superior viewing portal, lateral posterior. Note the bony deficiencies of the anterior-inferior glenoid to the right.
TREATMENT Acute Anterior Instability Algorithm The decision for treatment in any patient after a dislocation should be individualized. In the case of a minor, it must involve the parent or legal guardian, and it must be remembered that choices always involve advantages and disadvantages. Once the diagnosis is made and the shoulder is reduced, the decision for subsequent treatment can be made. Age and activity levels are the most important factors guiding treatment. For the young athlete particularly involved in contact sports, 15 to 25 years, acute repair may be a viable option based on the high risk of recurrence, apprehension, and impact on sports participation
Traditional nonoperative treatment has included a period of immobilization with the arm in internal rotation. However, the length of immobilization, even up to 6 weeks, has not been found to reduce recurrence rates. In a long-term (10-year follow-up) study on immobilization outcomes after anterior shoulder dislocations by Hovelius,31 no effect on recurrence rates related to the length of immobilization was seen. Out of 247 primary anterior shoulder dislocators, 50% had a recurrent dislocation at 10 years. Of the recurrent dislocators, 50% had surgery and, of those with surgery, 50% were stable at 10-year follow-up. Interestingly, degenerative joint disease was found in surgical and nonsurgical candidates, with 11% of patients who underwent surgery having mild secondary degenerative joint disease at the 10-year follow-up.31 Recently, Itoi and colleagues47 have demonstrated with MRI better reapproximation of the Bankart lesion with the arm in 30 degrees of external rotation. A short-term clinical study has revealed decreased recurrence rates in patients immobilized in external rotation compared with those immobilized in internal rotation.47 Maintaining arm position in 30 degrees of external rotation for 3 to 4 weeks may make compliance with this treatment difficult for the young competitive athlete. The athlete who sustains a dislocation during a competitive season poses a unique clinical dilemma. Buss,48 in a review of athletes sustaining an anterior dislocation in season, has shown that a regimen of early range of motion and a shoulder brace restricting abduction and external rotation allowed 26 of 30 athletes to return and complete the season; 4 of 30 required in-season surgery. Many athletes coped with continued instability events during the season, and 16 additional athletes underwent surgical stabilization at the end of the season. Therefore, a total of 20 of 30 athletes underwent surgery within the first year after sustaining an acute anterior dislocation.
Figure 20-8. Magnetic resonance imaging (MRI) of lesions. MRI scan of humeral avulsion of the glenohumeral ligament (HAGHL) lesion.
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Although not proven, it can be hypothesized that with more dislocations or subluxations, more damage to the articular cartilage, bone, and capsule develops.49 It is our opinion that if an athlete has a second or third recurrence
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during the sport, then nonoperative management should be discontinued and surgical treatment options considered. Other at-risk periods for the athlete who sustains a firsttime dislocation are at the end of the season and spring training. The options are early mobilization, rehabilitation, and return to full activity. For the collision athlete, this is unpredictable. Another option is to immobilize the athlete in external rotation for 3 to 4 weeks, proceed with rehabilitation, and return to sports after 6 to 8 weeks. The experience of Itoi47 has suggested a reduced recurrence rate; however, further studies using this treatment regimen in young contact athletes are needed. In the young
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contact athlete, modern operative stabilization techniques (open and arthroscopic) reduce the recurrence rate from 80% to 90% to 3% to 15% and improve the quality of outcome.34,35,43,44 The algorithm presented in Figure 20-9 is a suggestion based on the literature and our experience. It should be used as a guide only.
Operative Treatment The rationale for acute repair is based on the following: (1) high recurrence rates in young athletic patients; (2) 87% to 100% incidence of acute capsulolabral avulsions
Primary traumatic anterior shoulder dislocation requiring reduction
Diagnostic workup: • X-rays • MRI arthrogram (to r/o HAGHL lesion)
In-season athlete Operative fixation Open/arthroscopic Bankart repair
Rehab
Immobilization Brace in external rotation
RTP in 6 months
RTP with brace (average 10 days); without brace when full strength and full ROM
RTP in 6 weeks
Recurrent anterior shoulder dislocations Doesn’t mind loss of time
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In-season athlete
Operative intervention
Conservative treatment Rehab and prophylactic brace: Sawa brace Duke Wyre brace
R/O bone lesion • X-ray: West Point, Stryker notch view • CT scan
Bone lesion
No bone lesion
Open Bankart repair PLUS capsulorraphy PLUS bone restoration procedure (e.g., Laterget, allograft, humeral head allograft)
Open or arthroscopic Bankart repair PLUS capsulorraphy
Figure 20-9. Decision-making algorithm for primary traumatic anterior shoulder dislocations. HAGHL, humeral avulsion of the glenohumeral ligament ; MRI, magnetic resonance imaging; ROM, range of motion; RTP, return to play.
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documented in clinical series that were amenable to repair; and (3) reversal of natural history and improved outcomes. In the operative repair of an acute dislocation, it is our preference to perform the repair within 2 weeks of the injury, taking advantage of the unique repair process and, in most cases, excellent capsulolabral tissue. The focus of the surgery is repair of the capsulolabral avulsion, usually with three suture anchors. With the introduction of high-strength suture material, retensioning of the inferior glenohumeral ligament is combined with repair of the Bankart lesion to address the stretch component of the ligament that occurs with the labral avulsion. Bigliani7 reported that with any type of capsular failure, there is a significant amount of elongation, suggesting that plastic deformation of the capsule has occurred. In the acute situation, an extensive capsular plication and routine closure of the rotator interval are not performed. Closure of the rotator interval is controversial and there are no clinical studies identifying the specific role of interval closure in the treatment of the shoulder instability. If the athlete has more than a 1⫹ sulcus sign with the arm in 30 degrees, or engages in a contact sport, we strongly consider rotator interval closure after acute repair of the capsulolabral lesion. Examination Under Anesthesia An examination under anesthesia (EUA) of both shoulders, in the supine position, is performed, documenting forward elevation, external and internal rotation with the arm at the side, and external and internal rotation with the arm abducted to 90 degrees. Anterior load and shift, posterior jerk, and sulcus tests are performed to assess instability. The EUA is used to confirm and add further information and assess for other pathology that may be present, not to make the diagnosis. When performing the load and shift test, care should be taken to compare both shoulders for the amount of humeral head translation. In addition, the amount of translation should be noted for each arm position with respect to the degree of humeral rotation and position of the arm in relation to the plane of the scapula. Arm rotation and position will influence the degree of translation because of their effects on changes in ligament length. Patient Position The lateral decubitus or beach chair position can be used for instability surgery. The beach chair position offers the advantage of being able to convert to an open procedure easily. When the beach chair position is used, a sterile arm holder is helpful for holding a desired arm position and for applying a distraction force to the arm. For the lateral decubitus position, a three-point distraction device (Arthrex, Naples, Fla) is used that allows longitudinal and vertical traction and enables the humeral head to
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be lifted reproducibly from the glenoid (Fig. 20-10A and B). A beanbag is used to stabilize the patient, with a hip holder also used just below the scapula posteriorly to stabilize the beanbag in case air is accidentally released. The patient is positioned in a 30-degree backward tilt, placing the glenoid in a parallel orientation to the floor. We frequently add a knee bump (see Fig. 20-10C) placed into the axilla, which provides improved exposure of the inferior aspect of the joint. In most cases, general endotracheal intubation is used for anesthesia, with an interscalene block for pain control. The beach chair position is amenable only to an interscalene block for the procedure; because of the uncomfortable nature of the lateral position, we advocate general anesthesia with or without regional block. Preoperative antibiotics are administered intravenously before skin incision. Portal Placement A standard posterior portal should be placed slightly more laterally than the joint line. If the portal is placed medially to the joint line, this will require the surgeon to lever the arthroscope against the glenoid, making the stabilization procedure difficult. An 8- to 10-mm incision is made, and the blunt arthroscope sheath and trocar are inserted atraumatically into the space between the glenoid rim and humeral head. The anterior portals are then made using spinal needles for localization. The first anterior portal made is superior in the rotator interval, as high in the anterior superior quadrant of the shoulder as possible, while still allowing the cannula to be placed anterior to the biceps tendon. On the outside of the shoulder, this portal is closer to the anterior acromion. Medial placement of the cannula will compromise access to the glenoid. In general, a 7- ⫻ 7-cm cannula, smooth or ridged, is placed for suture shuttling. The second portal is the anterior inferior portal.Because of the instruments used through this portal, it usually requires an 8.25- ⫻ 7-cm cannula. Two different anterior inferior portals can be placed. The primary anterior inferior portal is made at the superior rolled edge of the subscapularis and angled inferiorly. Once again, this is also made with spinal needle localization but avoids the trauma of going through the subscapularis tendon. In viewing the portal placement from the outside, the spinal needle is generally placed just lateral to the coracoid process. This portal is typically used to place anchors along the anteroinferior glenoid. In most cases, the anterosuperior and anteroinferior portals are sufficient to perform the repair. Occasionally, the anteroinferior portal is not adequately positioned to gain access to the anteroinferior glenoid rim for anchor placement. The solution for this is a trans-subscapular portal initially established by placing an 18-gauge spinal needle through
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the subscapularis muscle. This is usually slightly inferior to the traditional anteroinferior portal. A percutaneous incision is made, followed by blunt spreading using a hemostat to the joint level. A small-diameter trocar can be placed and permits drilling and anchor placement at the 5-o’clock position (Fig. 20-11).
A 30°
A
B
B
C Figure 20-10. Traction device. A, Lateral position traction device (Arthrex, Naples, Fla). B, Positioning of the patient with the lateral traction device and a 30-degree posterior tilt. C, Knee bump placed into the axilla.
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C Figure 20-11. Inferior anchor placement. A, Percutaneous 18-gauge needle used to set up trans-subscapular portal. B, Outside view of 3-mm trocar through subscapularis. C, Arthroscopic view of trocar for placement of drill at the 5-o’clock position on the glenoid rim.
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We recognize that there are many individual preferences to performing a repair with regard to portal placement and positioning of the arthroscope and instrumentation. Many surgeons prefer to keep the arthroscope posterior and work through the anterosuperior and anteroinferior portals. Some surgeons prefer visualization for most of the procedure, with the arthroscope in the anterosuperior portal and instrumentation from the anteroinferior and posterior portals. The surgeon should be comfortable with changing portals to improve access and adjust to any condition encountered, which improves the technical performance of the procedure. Fluid management is also important. Shoulder overdistention is compounded by improper portal development and a lengthy procedure. It is always important to establish accurate and small portals, use cannulas at all times to create a seal in the glenohumeral joint, and monitor the amount of fluid pressure to decrease the amount of fluid extravasation. An ideal pressure to perform arthroscopic stabilization has not been reported. However, analysis and evaluation of pressure and shoulder distention as the procedure progresses are critical. Bankart Repair With Suture Anchors Repair of the Bankart lesion is the critical step in this procedure. The suture anchor repair with arthroscopic knot tying is similar to the open repair technique and is extremely versatile and reproducible. Although arthroscopic repair has been performed with transglenoid suturing, bioabsorbable tacks, and knotless devices, we favor the suture anchor technique because it most closely resembles the open technique, which has a long history of satisfactory results. There are two variations of this technique, the suture-first and anchor-first methods. Clinically there have been no reported differences between any of these techniques in the literature and their use is based on surgeon preference. The anchors themselves can be metal or bioabsorbable. No differences have been reported clinically based on the material of the anchor. We recommend bioabsorbable anchors because most instability patients are young, and we attempt to avoid the theoretical possibility of migration. Proper anchor placement is the most critical step and no material can help an improperly placed anchor. Anchor-First Technique. The anchor first technique involves placing an anchor through the anterior inferior cannula first, and then shuttling the suture limb. At this time, it is important to note the position of the anterior inferior cannula and the position in which the anchor should be placed into the glenoid. Occasionally, the position of the cannula is appropriate for suture shuttling but not for placement of the anchor. In this case, a percutaneous approach can be used to insert an anchor into the glenoid at the 5-o’clock position. The advantage of this technique allows a more appropriate perpendicular
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placement of the anchor into the glenoid face at approximately 2 to 3 mm over the articular service without bubbling or causing articular injury. After the anchor has been successfully inserted, one of the suture limbs is passed out of the anterior superior cannula. This limb, if using a metal anchor or anchor with a fixed eyelet, is the limb on the tissue side of the suture. The eyelet should be perpendicular to the labrum. A tissue penetrator or suture-shuttling device is used to pass a suture into the tissue inferior to the anchor. The end of the suture is then grasped and pulled out through the anterior superior cannula. A small square knot is tied in the passing suture, serving as a dilating knot. This is followed by tying the nonabsorbable braided suture to the monofilament suture line further distally and pulling the passing stitch through the anterior inferior cannula—hence, shuttling the suture through the labrum, inferior-glenoid ligament, and scapular periosteal complex. On tightening this suture with proper arthroscopic knottying technique, a shift of tissue from inferior to superior should be observed. If the tissue bite was not placed inferior enough to the anchor, this step should be repeated before continuing the operation. To tie the knot, the knot pusher is placed on the suture limb that is on the tissue side. This will be the post. A sliding locking knot or a nonsliding knot (multiple half-hitches) can be tied at this time. It has been determined that after placement of a sliding knot or multiple half-hitches, three alternating half-hitches while switching the post is the most secure final fixation.50 The knot should end up on the tissue side so that the labrum can create a bumper effect. The next two or three anchors are then placed approximately 5 to 7 mm apart from each other in the same fashion as described. On completion of the procedure, a bumper should be observed at the anterior inferior glenoid between the 3- and 6-o’clock positions. Suture-First Technique. The suture first-technique, which is our preference, involves placing a suture-passing device initially to ensure adequate soft tissue shift, followed by placement of the anchor. A suture-passing device is initially placed through the anterior inferior cannula. The capsular tissue is pierced about 5 to 7 mm laterally to the labrum as close to the 6-o’clock position as possible and the labrum is pierced slightly more cephalad. The passing suture is passed through the tissue and shuttled through the posterior portal; the arthroscope is in the anterosuperior portal (Fig. 20-12). The shuttling suture or device is now in the anteroinferior and posterior portals. Tension is placed on this suture to observe the amount of shift that can be accomplished by placing the anchor at the appropriate position. If it is determined that this suture is not inferior enough, this suture can be used as a traction suture and a second suture can be placed more inferiorly.
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Figure 20-12. Arthroscopic view of the right shoulder viewed from anterosuperior portal. The shuttle suture is placed through the capsule and labrum near the 6-o’clock position.
When an appropriate amount of tissue tension is established, the anchor is placed through the anterior inferior portal and onto the glenoid rim slightly more cephalad than the passing suture. For example, for a right shoulder, the passing suture should be placed at the 5:30- or 6-o’clock position and the anchor at the 5-o’clock position (Fig. 20-13). As noted, once the anchor is placed, the two limbs of the suture are separated, one through the anterior superior cannula and the other shuttled through the tissue. Because of the cephalad positioning of the anchor relative to the shuttling suture, when the nonabsorbable suture is shuttled and then tied, the labrum is repaired and there is retensioning of the inferior glenohumeral ligament with each anchor (Fig. 20-14). The same steps are repeated two or three times, depending on the repair quality and amount of injury (Fig. 20-15).
Figure 20-13. Arthroscopic view of the right shoulder depicting shuttling suture inferior to anchor placed at about the 5-o’clock position.
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Figure 20-14. Knot tying. With this technique, the capsule and labrum can be retensioned in a cephalic position.
Rotator Interval Closure The rotator interval is an important anatomic region with respect to anterior shoulder stability. This anatomic region is defined as the articular capsule bounded superiorly by the anterior portion of the supraspinatus tendon, inferiorly by the superior portion of the subscapularis tendon, medially by the base of the coracoid process, and laterally by the long head of the biceps tendon. The capsular tissue is reinforced by the coracohumeral ligament (CHL) and superior glenohumeral ligament (SGHL). The rotator interval is of varying size and is present in the fetus as well as in the adult. Harryman51 demonstrated that sectioning the rotator interval in cadaveric specimens results in increased glenohumeral translation in all planes tested. Imbrication of rotator interval lesions results in
Figure 20-15. Completed repair.
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decreased posterior and inferior glenohumeral translation when compared with the intact state. Field52 reported good or excellent results in 15 patients who underwent surgical repair of isolated rotator interval defects. There is no consensus regarding the indications for rotator interval closure. In the acute, first-time dislocation, we are cautious of routine performance of this procedure because of concerns of postoperative stiffness. During operative stabilization after a primary dislocation, we currently use this adjunct for the collision athlete and the athlete with a 1⫹ sulcus that is not reduced with the arm in 30 degrees of external rotation Many surgeons have reported techniques for closing the rotator interval. One involves removing the anterior inferior cannula and placing all instrumentation through the anterior superior cannula. We prefer using an absorbable suture for the closure. The middle glenohumeral ligament (MGHL), a small portion of the subscapularis tendon, or both, is pierced with a spinal needle or sutureshuttling device and a monofilament suture is deployed (Fig. 20-16A). The SGHL-CHL complex is pierced with a penetrator and the monofilament suture is grasped (see Fig. 20-16B). This tissue then can be tied through a cannula internally or externally and cut with a guillotine knot cutter (see Fig. 20-16C). Special Pathoanatomic Variants Extension of Anterior Inferior Labrum Tear Into Superior Labrum. If the labral tear extends from the anterior inferior glenoid up into the superior labrum, the same anterior cannula can be used to continue placing suture anchors. We recommend two or three suture anchors for superior labrum tears, with one placed in front of the biceps tendon anchor and one or two placed behind the biceps tendon anchor, depending on the amount of biceps instability. The anchor is placed in front of the biceps tendon anchor and guided through the anterior superior cannula. The one or two anchors placed posteriorly to the biceps anchor can be placed percutaneously via the Port of Wilmington portal.53 This portal is 1 cm lateral and 1 cm anterior to the posterior lateral corner of the acromion, through the musculotendinous junction of the rotator cuff. Extension of Capsulolabral Injury Posteriorly. In some cases, the lesion may involve the posterior labrum, necessitating placement of anchors and repair along the posteroinferior glenoid. To have appropriate access to the posteroinferior glenoid and avoid iatrogenic injury to the articular surface, an accessory posteroinferior portal is required. This portal is made roughly 2 cm lateral and 1 cm inferior to the standard posterior portal. An 18-gauge spinal needle is used under direct visualization to assess the position and an 8.25- ⫻ 9-cm cannula is then placed. This portal results in accurate posteroinferior anchor insertion, because the arthroscope is kept in the anterosuperior portal and suture-shuttling devices are used in the posterior and anteroinferior portals (Fig. 20-17).
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A
B
C Figure 20-16. Closing the rotator interval. A, Suture-shuttling device through the middle glenohumeral ligament placing a monofilament suture into the joint. B, Tissue penetrator through the superior glenohumeral ligament and coracohumeral ligament retrieving a monofilament suture. C, Rotator interval is closed extra-articularly.
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Acute Osseous Bankart Lesions. Acute osseous Bankart lesions can be repaired according to Sugaya’s technique.54 An arthroscopic evaluation is first conducted. Viewing from the anterior portal helps confirm the osseous glenoid defect in the anteroinferior quadrant. Mobilization of the labroligamentous complex and the osseous fragment from the glenoid neck needs to be performed carefully, followed by repair of the inferior labrum adjacent to the osseous fragment. Bony fragment fixation can be achieved by different methods, such as passing the suture through or around the fragment. Suture anchors are then used to reconstruct the entire labroligamentous complex.
A
POSTOPERATIVE CARE The biologic healing response of the repaired and imbricated tissue must be respected. One observation that may have led to some of the earlier arthroscopic failures for anterior instability is that, because of the significant reduction in postoperative pain, these patients want to move their shoulders earlier, imparting more stress to the repair site. This early cyclic stress and motion eventually fatigue the plication stitches and cause a failure of the repair. The first goal to postoperative success is maintenance of anterior-inferior stability. The second goal is the restoration of adequate motion—specifically, external rotation. The third is a successful return to sports or physical activities of daily living in a reasonable amount of time.
B
C Figure 20-17. Creating an accessory posteroinferior portal. A, Outside image of an 18-gauge needle used to guide placement of posteroinferior anchor. B, Arthroscopic image of an 18-gauge needle in proper trajectory to drill into posteroinferior glenoid. C, Arthroscopic image of posteroinferior trocar.
Our protocol for anterior-inferior shoulder instability treated by arthroscopic means involves postoperative immobilization immediately in an abduction arthrosis. This allows the arm to be fixed in a slight amount of external rotation. Codman’s exercises, combined with pendulum exercises, are started immediately. Active-assisted rangeof-motion, external rotation (0 to 30 degrees), and forward elevation (0 to 90 degrees) exercises are also started at this time. This regimen is maintained for the first 6 weeks. The use of cold therapy devices has been successful in reducing postoperative pain. From weeks 6 to 12, activeassisted as well as active range-of-motion exercises are started, with the goal of establishing full range of motion. No strengthening exercises or any type of repetitive exercises are started until after full range of motion has been established. This protocol is based on tendon to bone healing in a dog model.55 Early resistance exercises with aggressive early postoperative rehabilitation do not appear to offer substantial advantages and could compromise the repair. Strengthening is begun once there is full, painless, active range of motion. Strengthening is begun at 12 weeks, with sports-specific exercises started at 16 to 20 weeks. Final
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contact athletic training is started between 20 and 24 weeks postoperatively. Pagnani and Dome56 have reported on open stabilization in American football players. Their postoperative program is similar to the one described here. At 0 to 4 weeks, the arm is immobilized with a sling and internal rotation and double range-of-motion and pendulum exercises are begun. From 4 to 8 weeks, passive- and active-assisted shoulder range-of-motion exercises with external rotation limited to 45 degrees are initiated. Rotator cuff strengthening and internal and external rotation strengthening with the arm at low abduction angles are begun when 140 degrees of active forward elevation has been achieved. From 8 to 12 weeks, deltoid isometric exercises with the arm in low abduction angles and body blade exercises are started. Abduction is slowly increased during rotator cuff and deltoid-strengthening exercises. In addition, scapular stabilizer strengthening and horizontal abduction exercises are also begun. From 12 to 16 weeks, restoration of terminal external rotation is achieved. Proprioceptive neuromuscular feedback patterns are used, and plyometric and sports-specific motion exercises using pulley, wand, or manual resistance, are begun. After 16 weeks, conventional weight training is started and rehabilitation is orientated toward return to sports, progressing from field drills to contact drills. An abduction harness can be used for select football positions, such as linemen. Full contact sports are instituted when abduction and external rotation strength are symmetrical on manual muscle testing, typically 4 to 5 months postoperatively.
TECHNICAL ERRORS For successful treatment of arthroscopic anterior-inferior instability, adequate visualization is imperative. The lateral decubitus position with a traction device can provide vertical distraction, enabling the humeral head to float superiorly, and horizontal distraction, pulling the humeral head inferiorly. Traction allows the surgical team to work unencumbered by not having to hold the arm. If adequate visualization of the anterior inferior glenoid and pathology cannot be established, an open procedure is recommended.
lateral position will force the arthroscope to be placed at an angle at which it has to look over the posterior glenoid, which makes the following procedures more difficult. If the surgeon finds that she or he has to look over the top of the glenoid, a new posterior-inferior portal should be established immediately. If the surgeon is worried about extravasation of fluid into the posterior compartment, or if the fluid dynamics is altered by making a second portal posteriorly, a nonfunctional cannula can be placed into the first portal. This will seal off potential extravasation of fluid. When establishing the anterior portals, two important concepts must be observed. The first is that the two cannulas should be separated as far from each other as possible, internally and externally. This allows for easier passage when shuttling sutures. The second is to ensure that the anteriorsuperior portal is not placed into the posterior aspect of the biceps. If this does occur, care must be taken not to lock the proximal biceps tendon in the suture loop.
Suture Anchors Suture anchor placement should be 2 to 3 mm from the articular margin. Visualization should be maintained as the anchor is inserted. Improper angle of anchor insertion can cause articular surface damage or inadequate bone placement, allowing anchor migration and possible articular cartilage damage (Fig. 20-18). Two types of anchors are available, metal or bioabsorbable. Each has its advantages and disadvantages. Metal anchors generally can be inserted without taping after drilling or punching, eliminating a potential step during insertion. Also, they are mechanically stronger, with infrequent physical anchor breakage. In long-term follow-up, the anchor or cartilage may subside and there may be erosion of the metal anchor on the articular surface.
Incorrect Portal Placement Portal placement is critical to adequate visualization and execution of an arthroscopic anterior inferior stabilization procedure using capsular plication and suture anchors. In the lateral position, to establish the posterior portal, it is important to err slightly more laterally than normal. A direct entrance from the posterior skin through the infraspinatus muscle and capsule is ideal but, if an error is going to be made or if the patient is large, the portal should be placed more laterally. Medial portal placement in the
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Figure 20-18. Improper anchor placement. Intra-articular metal is exposed and there is articular damage to the humeral head.
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Bioabsorbable anchors have the advantage of being incorporated into the body over time, but have the disadvantage of causing varying degrees of tissue reaction. They generally require tapping, which is an additional step. This can lead to anchor-hole mismatch, which may cause anchor fracture. The advantage of the bioabsorbable anchor at this point is that a second anchor then can be placed right on top of the first anchor by retapping or drilling the original hole should this be necessary. Bioabsorbable anchors, such as BioFastak and BioSutureTak (Arthrex, Naples, Fla), also have the advantage of having a suture loop placed inside them, in which a suture is embedded into the bioabsorbable anchor. This allows for consistent sliding of different types of sutures.
Suture Shuttling and Knot Tying Passing the suture through the tissue can be frustrating. It is important to ensure that the suture shuttled through the tissue is inferior to the anchor, allowing a superior shift of tissue. This can be done directly with a sharp penetrator, which pierces the tissue, grabs the sutures, and then pulls them out, or indirectly by a suture shuttle system, in which a suture-passing device passes a monofilament suture into the tissue. This is retrieved through a cannula and the suture to be shuttled through is then tied to this and brought back through the tissue. Tangling and confusion of the sutures can occur at this time, and it is important to be methodical. Unloading of the anchor can also occur during suture shuttling. To prevent this, the arthroscope should visualize the anchor directly. If both limbs of the suture are seen moving, then the anchor is being unloaded. This is satisfactory initially as the loop is pulled out through the cannula. However, once the loop is out of the cannula, special attention should be paid so that no further suture is removed from the anchor. Because it may be difficult to determine which limb will unload the anchor, look at the anchor and pull on one limb of the suture. If there is no further movement of the suture through the anchor, this is the free limb, which can be pulled through the cannula without further concern. For further safety, a hemostat can be placed on the limb that is not sutured, so that it cannot be pulled through the cannula. Although at times time-consuming and cumbersome, these small checks can prevent the unfortunate complication of unloading an anchor. If sutures do become tangled intraarticularly (Fig. 20-19), the suture should be withdrawn from the joint and untied, and the process started from the beginning. If there is not enough room or suture length, a second suture can be tied to the end of the tangled suture; this can be pulled through, allowing more length of the suture to be untied outside the cannula and then easily brought back in through the anchor. There are two classifications of knots that can be tied, sliding and nonsliding knots. We will not describe the different knots available here, but it is important to realize that this is a potential area of difficulty if the knot prematurely locks
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Figure 20-19. Example of suture tangled in the shoulder.
or there is neither knot nor loop security. After tying the initial throw, it is important to observe whether all excess suture has been taken out of the system and whether the knots and loops are indenting the tissue. If this has not been achieved, the knots should not be locked until this is observed. To avoid twisting of the sutures and loose knots, the knot pusher can be placed on one of the limbs. This is then slid down and, if there is a twist, can be untwisted at this time. Any other abnormalities in the suture can be observed. If a knot prematurely locks or if it is tied and is not securing the tissue adequately, a second anchor and suture must be placed as close to the original knot as possible. A loose knot will never get stronger over time.
Postoperative Glenohumeral Noise This is an inconsistent physical examination finding that occasionally plagues the postoperative course. Normally, there is synovialization of the sutures (Fig. 20-20). If this does not happen, a squeak can be detected that may necessitate removal of the knot after healing has been established.
OUTCOMES Many studies have reported improved outcomes following acute arthroscopic repair. In one prospective randomized trial,44 arthroscopic repair not only decreased recurrence rates, but also resulted in improved quality of life. Other surgeons have reported improved outcomes following acute arthroscopic repair, as measured by SF-36 and Rowe scores.36,43,57 Most recently, Jakobsen and associates11 have reported on the 10-year outcome of primary open repair versus nonoperative treatment for primary anterior dislocation. At 10 years, the surgical group had
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Figure 20-20. Example of arthroscopic labral repair 3 weeks post op. This shoulder underwent arthroscopy for squeak secondary to the prominent suture.
75% good or excellent results and the nonoperative group had 75% unsatisfactory results secondary to pain, apprehension, or recurrent instability. In addition, in the nonoperative group (even the patients who did not experience recurrent dislocation), 39% had limitation of activity and positive apprehension. Furthermore, this study has demonstrated that patients initially treated nonoperatively, who then required surgical stabilization, have inferior results compared with those stabilized primarily. Therefore, it can be concluded that acute arthroscopic repair for the athlete with a first-time traumatic anterior dislocation leads to improved outcomes. The decision needs to be made in conjunction with the patient and family. The timing of the season also needs to be considered. If the dislocation occurs during the season, consideration should be given to nonoperative management to help the athlete complete the season. A thorough discussion with the patient regarding surgical stabilization after the season should also be undertaken.
References 1. Matsen FA, Thomas SC, Rockwood CA, Wirth MA: Glenohumeral instability. In Rockwood CA, Matsen FA (eds): The Shoulder, 2nd ed, vol 2. Philadelphia, WB Saunders, 1998, pp 633-639. 2. Lephart SM, Warner JP, Borsa PA, Fu FH: Proprioception of the shoulder joint in healthy, unstable, and surgically repaired shoulder. J Shoulder Elbow Surg 3:371-379, 1994. 3. Turkel SJ, Panio MW, Marshall JL: Stabilizing mechanism preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 4. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990.
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5. Howell SM, Galinat BJ: The glenoid-labral socket. A constrained articular surface. Clin Orthop Relat Res (243): 122-125, 1989. 6. Lazarus MD, Sidles JA, Harryman DT 2nd, Matsen FA 3rd: Effect of a chondral-labral defect on glenoid concavity and glenohumeral stability. A cadaveric model. J Bone Joint Surg Am 78:94-102, 1996. 7. Bigliani LU, Pollock RG, Soslowsky U, et al: Tensile properties of the inferior glenohumeral ligament. J Orthop Res 10:187-197, 1992. 8. Baker CL, JW Uribe JW, Whitman C: Arthroscopic evaluation of acute initial anterior shoulder dislocations, Am J Sports Med 18:25-28, 1990. 9. Norlin R: Intraarticular pathology in acute, first-time anterior shoulder dislocation: An arthroscopic study. Arthroscopy 9:546-549, 1993. 10. Taylor DC, Arciero RA: Pathologic changes associated with shoulder dislocations. Arthroscopic and physical examination findings in first-time, traumatic anterior dislocations. Am J Sports Med 25:306-311, 1997. 11. Jakobsen BW, Johannsen HV, Suder P, Sojbjerg JO: Primary repair versus conservative treatment of first-time traumatic anterior dislocation of the shoulder: A randomized study with 10-year follow-up. Arthroscopy 23:118-123, 2007. 12. Neviaser TJ: The anterior labroligamentous periosteal sleeve avulsion lesion: A cause of anterior instability of the shoulder. Arthroscopy 9:17-21, 1993. 13. Arciero RA, Taylor DC, Snyder RJ, et al: Arthroscopic bioabsorbable tack stabilization of initial anterior shoulder dislocations: A preliminary report. Arthroscopy 11:410-417, 1995. 14. Savoie FH, Field LD, Atchinson S: Anterior superior instability with rotator cuff tearing: SLAC lesion. Oper Tech Sports Med 8:221-224, 2000. 15. Nicola T: Anterior dislocation of the shoulder. J Bone Joint Surg 26:619-616, 1941. 16. Richards DP, Burkhart SS: Arthroscopic humeral avulsion of the glenohumeral ligaments (HAGHL) repair. Arthroscopy 20(Suppl 2):134-141, 2004. 17. Wolf EM, Cheng JC, Dickson K: Humeral avulsion of glenohumeral ligaments as a cause of shoulder instability. Arthroscopy 11:600-607, 1995. 18. Bokor DC, Conboy VB, Olsen C: Anterior instability of the glenohumeral joint with humeral avulsion of the glenohumeral ligament: A review of 41 cases. J Bone Joint Surg Br 81:93-96, 1999. 19. Bui-Mansfield LT, Taylor DC, Uhorchak JM, Tenuta JJ: Humeral avulsions of the glenohumeral ligament: Imaging features and a review of the literature. AJR Am J Roentgenol 179:649-655, 2002. 20. Rowe CR, Zarins B: Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am 63:863-873, 1981. 21. Burkhart SS, De Beer JF: Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: Significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 16:677-694, 2000. 22. Scheibel M, Magosch P, Lichtenberg S, Habermeyer P: Open reconstruction of anterior glenoid rim fractures. Knee Surg Sports Traumatol Arthrosc 12:568-573, 2004. 23. Bigliani LU, Newton PM, Steinmann SP, et al: Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am J Sports Med 26:41-45, 1998.
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24. Lo IK, Parten PN, Burkhart SS: The inverted pear: An indicator of significant bone loss. Arthroscopy 20:169-174, 2004. 25. Tauber M, Resch H, Forstner R, et al: Reasons for failure after surgical repair of anterior shoulder instability. J Shoulder Elbow Surg 13:279-285, 2004. 26. Boileau P, Villalba M, Héry JY, et al: Risk factors for recurrence of shoulder instability after arthroscopic Bankart repair. J Bone Joint Surg Am 88:1755-1763, 2006. 27. Reeves B: Arthrography of the shoulder. J Bone Joint Surg Br 48:424-435, 1966. 28. Robinson CM, Kelly M, Wakefield AE: Redislocation of the shoulder during the first six weeks after a primary anterior dislocation: Risk factors and results of treatment. J Bone Joint Surg Am 84:1552-1559, 2002. 29. Owens BD, Duffey ML, Nelson BJ, et al: The incidence and characteristics of shoulder instability at the United States Military Academy. Am J Sports Med 35:1168-1173, 2007. 30. McLaughlin HL, Cavallaro WU: Primary anterior dislocation of the shoulder. Am J Surg 80:615-621, 1950. 31. Hovelius L, Augustini BG, Fredin H, et al: Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J Bone Joint Surg Am 78:1677-1684, 1996. 32. Larrain MV, Montenegro HJ, Mauas DM, et al: Arthroscopic management of traumatic anterior shoulder instability in collision athletes: Analysis of 204 cases with a 4- to 9-year follow-up and results with the suture anchor technique. Arthroscopy 22:1283-1289, 2006. 33. Postacchini F, Gumina S, Cinotti G: Anterior shoulder dislocation in adolescents. J Shoulder Elbow Surg 9:470-474, 2000. 34. Arciero RA, Wheeler JH, Ryan ID, et al: Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am J Sports Med 22: 589-594, 1994. 35. Hovelius L: Shoulder dislocation in Swedish ice hockey players. Am J Sports Med 6:373-377, 1978. 36. Larrain MV, Botto GJ, Montenegro HJ, Mauas DM: Arthroscopic repair of acute traumatic anterior shoulder dislocation in young athletes. Arthroscopy 17:373-377, 2001. 37. Law BK, Yung PS, Ho EP, et al: The surgical outcome of immediate arthroscopic Bankart repair for the first time anterior shoulder dislocation in young active patients. Knee Surg Sports Traumatol Arthrosc 16:188-193, 2008. 38. Visser CP, Coene LN, Brand R, Tavy DL: The incidence of nerve injury in anterior dislocation of the shoulder and its influence on functional recovery. A prospective clinical and EMG Study. J Bone Joint Surg Br 81:679-685, 1999. 39. Miller SL, Cleeman E, Auerbach J, Flatow EL: Comparison of intra-articular lidocaine and intravenous sedation for reduction of shoulder dislocations: A randomized, prospective study. J Bone Joint Surg Am 84:2135-2139, 2002. 40. Rokous JR, Feagin JA, Abbott HG: Modified axillary roentgenogram. A useful adjunct in the diagnosis of recurrent instability of the shoulder. Clin Orthop Relat Res 82:84-86, 1972. 41. Sugaya H, Moriishi J, Dohi M, et al: Glenoid rim morphology in recurrent anterior glenohumeral instability. J Bone Joint Surg Am 85:878-884, 2003. 42. Stoller DW: MR arthrography of the glenohumeral joint. Radiol Clin North Am 35:97-116, 1997.
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43. Bottoni CR, Wilckens JH, DeBerardino TM, et al: A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med 30:576-580, 2002. 44. Kirkley A, Werstine R, Ratjek A, Griffin S: Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: Long-term evaluation. Arthroscopy 21:55-63, 2005. 45. Sachs RA, Lin D, Stone ML, et al: Can the need for future surgery for acute traumatic anterior shoulder dislocation be predicted? J Bone Joint Surg Am 89:1665-1674, 2007. 46. Simank HG, Dauer G, Schneider S, Loew M: Incidence of rotator cuff tears in shoulder dislocations and results of therapy in older patients. Arch Orthop Trauma Surg 126:235-240, 2006. 47. Itoi E, Hatakeyama Y, Sato T, et al: Immobilization in external rotation after shoulder dislocation reduces the risk of recurrence. A randomized controlled trial. J Bone Joint Surg Am 89:2124-2131, 2007. 48. Buss DD, Lynch GP, Meyer CP, et al: Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med 32:1430-1433, 2004. 49. Buscayret F, Edwards TB, Szabo I, et al: Glenohumeral arthrosis in anterior instability before and after surgical treatment: Incidence and contributing factors. Am J Sports Med 32:1165-1172, 2004. 50. Lo IK, Burkhart SS: Biomechanical principles of arthroscopic repair of the rotator cuff. Operat Tech Orthop 12:152-153, 2002. 51. Harryman DT 2nd, Sidles JA, Harris SL, Matsen FA 3rd: The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74:53-66, 1992. 52. Field LD, Warren RF, O’Brien SJ, et al: Isolated closure of rotator interval defects for shoulder instability. Am J Sports Med 23:557-563, 1995. 53. Morgan CD, Burkhart SS, Palmeri M, Gillespie M: Type II SLAP lesions: Three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14:553-565, 1998. 54. Sugaya H, Moriishi J, Kanisawa I, Tsuchiya A: Arthroscopic osseous Bankart repair for chronic recurrent traumatic anterior glenohumeral instability. J Bone Joint Surg Am 87: 1752-1760, 2005. 55. Rodeo SA, Arroczhy SP, Tobilli PA, et al: Tendon healing in a bone tunnel: A biomechanical and histological study in the dog. J Bone Joint Surg Am 75:1795-1803, 1993. 56. Pagnani MJ, Dome DC: Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg Am 84:711-715, 2002. 57. DeBerardino TM, Arciero RA, Taylor DC, Uhorchak JM: Prospective evaluation of arthroscopic stabilization of acute, initial anterior shoulder dislocations in young athletes. Two- to five-year follow-up. Am J Sports Med 29:586-592, 2001.
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CHAPTER 21 Bankart Lesions: Diagnosis
and Treatment with Arthroscopic and Open Approaches J.R. Rudzki and David W. Altchek
As the instrumentation and techniques for arthroscopic stabilization and capsulolabral reconstructive procedures continue to improve, the debate over the optimal surgical approach for operative management of the Bankart lesion persists. First described in 1938, the Bankart lesion is a detachment of the anteroinferior labrum,1 which in conjunction with a concomitant capsular injury2 may result in anterior or anteroinferior glenohumeral instability (Fig. 21-1). Anatomic surgical reconstructions for this injury pattern include the classic Bankart repair described by Rowe and colleagues in 1978,3 with or without the capsular shift procedure described by Neer and associates in 1980.4 Several modifications of these open techniques were subsequently described,5-8 with a high rate of good to excellent results; this led some surgeons to declare open surgical treatment of the Bankart lesion the gold standard as the era of arthroscopic anterior stabilization began. The debate over optimal treatment of Bankart lesions and anterior instability continues today, at a time when arthroscopic techniques and instrumentation have rapidly and dramatically transformed these surgical procedures. Anterior and multidirectional instability is addressed in Chapters 17 and 19. This chapter will focus on the diagnosis and treatment of Bankart lesions with arthroscopic and open techniques through an examination of anatomy and pathophysiology, as well as the biomechanical and clinical outcomes data presented in the literature. Limitations of the available literature and opportunities for future research will be discussed in the context of clinical relevance.
tissue Bankart lesions, capsular injury and laxity, Hill-Sachs lesions, and concomitant injuries to the superior labral anterior-posterior (SLAP) and posterior aspects of the glenoid labrum. Less common but important injuries to recognize include superior rotator cuff and subscapularis injuries, glenoid fractures with bony compromise, humeral avulsion of the glenohumeral ligament (HAGHL) lesions, and glenoid dysplasia. Bankart lesions have been reported in 65% to 97% of patients who undergo surgical treatment for anterior instability.3,19-21 Fracture or injury to the glenoid rim has been reported in up to 73%, Hill-Sachs lesions have been reported in up to 90%, rotator cuff tears in up to 13%, and SLAP or posterior labral tears in 10% of cases.3,11,20 The Bankart lesion is an avulsion of the anteroinferior labrum (Fig. 21-2), which in conjunction with a concomitant capsular injury2 may result in anterior or anteroinferior glenohumeral instability. Bony Bankart lesions refer to those situations in which a portion of the adjacent anteroinferior aspect of the glenoid has fractured. These fragments typically remain attached to the avulsed labral and capsular tissue and may alter the normal geometry and surface area of the glenoid.22,23 This is clinically relevant because anterior glenoid rim fractures are a known cause of recurrent anterior shoulder instability.22,24-26 In discussing post-traumatic alterations of normal glenoid and humeral head osseous geometry, the concept of articular arc deficit as popularized by Burkhart and DeBeer23 is useful. Loss of bone from the anteroinferior aspect of the glenoid may result in what they have termed the inverted-pear glenoid, which has significant implications for choice of operative approach and long-term prognosis. In a study of 194 consecutive arthroscopic Bankart repairs, they reported a 4% recurrence rate in patients without significant bone defects (articular arc disruption) in comparison with a 67% recurrence rate for patients with significant bone defects and for contact athletes, and an increase in recurrence rate from 6.5% to 89% for patients without and with significant bone defects, respectively.
PATHOANATOMY A thorough understanding of the pathoanatomy involved in the diagnosis and treatment of Bankart lesions is essential for their treatment.9,10 The importance of this knowledge is emphasized by the literature, which supports the concept that there is no one essential lesion responsible for recurrent anterior shoulder instability.2,11-19 A recognition of the implications of common injury patterns and subtle findings help direct treatment intra-operatively in cases with multiple factors involved (e.g., symptomatic laxity versus instability). Typical pathoanatomy encountered in the treatment of anterior instability includes bony and soft
The Hill-Sachs lesion is an osteochondral impaction fracture involving the posterosuperior aspect of the humeral head (Fig. 21-3).27 It results from an impaction of the subchondral bone of the posterolateral aspect of the humeral 257
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Glenoid HH
Glenoid
C L C
L a b r u m
AIGHL Humeral head
A Figure 21-1. Bankart lesion in a left shoulder. This lesion is viewed from the posterior portal. CLC, capsulolabral complex; HH, humeral head.
head on the anterior aspect of the glenoid as the humeral head dislocates anteriorly. There are two types of Hill-Sachs lesions with which the surgeon must be familiar, the engaging and nonengaging forms. Just as a glenoid bone deficit may impair stability of the glenohumeral articular arc, the Hill-Sachs lesion may compromise glenohumeral stability and is an important potential cause of recurrent anterior shoulder instability. The presence of a large Hill-Sachs lesion has been reported in one study to double the recurrence rate of anterior instability after Bankart repair20 and has otherwise been reported to carry a statistically significant worse prognosis with regard to recurrent instability.28 The most common type of Hill-Sachs lesion is the nonengaging lesion, which does not mechanically interact with the anterior corner of the glenoid; therefore, by itself, it is not a significant threat for recurrent instability.
LITERATURE REVIEW Basic Science Familiarity with the clinical pathoanatomy encountered in the treatment of Bankart lesions is greatly enhanced through a knowledge of the relevant basic science data that support the clinical observations and associations reported in the literature. Several studies have improved our understanding of the multiple factors involved in recurrent instability and greatly assist the surgeon in patient and procedure selection for arthroscopic and open treatment of Bankart lesions. As noted, cadaveric studies have suggested that an isolated Bankart lesion may not be sufficient to cause abnormal glenohumeral translation or recurrent anterior
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HH
AIGHL G
B Figure 21-2. Bankart lesion. A, Bankart lesion in a right shoulder with identification of the AIGHL (anterior band of the inferior glenohumeral ligament). B, Arthroscopic image demonstrating attenuation of the AIGHL in a left shoulder.
instability.2,11,18,19 Bigliani and coworkers18 have determined that capsular injury is a significant factor in the development of anterior instability after finding that significant capsular stretching occurs before failure in their cadaveric model. Subsequently, Speer and associates2 reported on the results of a separate model, which demonstrated that Bankart lesions in isolation result in minimal anterior glenohumeral translations; they concluded that isolated Bankart lesions are not likely to be responsible for recurrent anterior shoulder instability. A cadaveric study of 16 scapulae by Itoi and colleagues22 in 2000 was used to investigate 10 separate fresh-frozen specimens in a custom multiaxial testing apparatus to determine that an osseous defect with a width at least
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instability in an attempt to elucidate which patients would benefit from conservative treatment or early aggressive surgical stabilization.
HH
Glenoid
Hill-Sachs lesion
Figure 21-3. Hill-Sachs lesion in a right shoulder. This is viewed from the posterior portal. HH, humeral head.
21% of the glenoid length (average width, 6.8 mm) may result in significant persistent instability and loss of functional ROM after Bankart repair. In addition, the clinicians noted that isolated Bankart repair in the setting of a large osseous defect may result in a dramatic loss of external rotation because the capsuloligamentous reconstruction overtensions the capsule to a glenoid that has lost concavity.22 This loss of external rotation is not only significant for short- and mid-term functional loss, but has been shown in other studies to produce unacceptable long-term results of early-onset glenohumeral arthrosis.29-32 These concerns become even more relevant when considering the results of a case-control study that demonstrated that the risk of developing severe arthrosis of the shoulder is from 10 to 20 times higher for individuals who have had a shoulder dislocation.33
Causative Factors and Natural History The lack of osseous constraint, combined with the broad ROM and translation of the glenohumeral joint, make it particularly susceptible to dislocation and recurrent instability. Chapters 17 and 19 present a thorough review of anterior and multidirectional instability. Our focus in this section are the aspects of anterior instability relevant to the diagnosis and treatment of Bankart lesions. The most common mechanism by which a Bankart lesion is sustained is through anterior dislocation of the shoulder, with the arm abducted and externally rotated. The abnormal translation of the humeral head that occurs in the process of dislocation results in a capsulolabral avulsion of the anterior or anteroinferior capsulolabral complex. Several studies have examined the risk factors for recurrent
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A classic study of conservative treatment for primary anterior shoulder dislocation was presented by Hovelius and associates28 in 1983. In this 10-year prospective multicenter Swedish study, 245 patients (247 shoulders) were assigned to one of three treatment groups as follows: (1) postreduction immobilization with arm secured to torso for 3 to 4 weeks; (2) postreduction use of a sling, which was discontinued after the patient became comfortable; and (3) postreduction immobilization for various durations. At the 10-year follow-up evaluation, 52% of shoulders had no subsequent dislocation, and recurrent instability requiring operative stabilization developed in 23%. Of the shoulders that developed recurrent instability requiring operative stabilization, there was a distinct difference in the percentage of recurrent instability relative to patient age—34% of patients 12 to 22 years, 28% of patients 23 to 29 years, and 9% of patients 30 to 40 years. This finding, that patients who are younger than 20 to 30 years are at a significantly increased risk of recurrent instability, is consistent with other studies in the literature that have reported recurrence rates of 83% to 95% for patients younger than 20 years, particularly in those who participate in athletics.34-36 Of additional interest, however, was the finding that 22% of the shoulders that sustained at least two recurrences during the initial 2- to 5-year follow-up period “stabilized spontaneously” at 10 years without surgical intervention.28 This latter finding is debatable and has been contested in the literature.37 Spontaneous stabilization of instability in this study has been proposed to be potentially related to age-related capsular changes and decreased physical demands in patients with increasing age.37 It must also be noted that less than 50% of patients in the study by Hovelius and coworkers28 sustained dislocations caused by a sports activity. It may therefore be inferred that their substantial but lower rate of recurrent instability requiring operative stabilization underestimates the risks of recurrent instability in young athletes (younger than 30 years) as reported in other studies. The natural history of recurrent instability for the athlete’s shoulder is a critical concept in determining operative indications and has not been definitively established in the literature. Patient-specific factors such as age, activity level, participation in contact or overhead athletics, and associated pathology play a critical role in patient counseling for the treatment of Bankart lesions. Simonet and Cofield36 have reported a recurrence rate of 82% after primary acute glenohumeral dislocation in athletes younger than 30 years. In a study of Swedish hockey players, Hovelius38 has reported a 90% rate of recurrence in patients younger than 20 and 65% in patients 20 to 25 years of age. Henry and Genung39 have reported a 95% rate of recurrence in a series of 100 patients, predominantly athletes, with almost
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75% requiring surgical stabilization to continue participation in athletics. Taylor and Arciero19 have reported a 90% recurrence rate in young athletes participating in collision sports. In a prospective randomized study of nonoperative treatment versus arthroscopic stabilization in patients with acute, traumatic, first-time shoulder dislocations, with 36-month average follow-up, Bottoni and colleagues have40 reported a 75% rate of recurrent instability in the nonoperative treatment group (4 weeks immobilization followed by a rehabilitation program). This is in contrast to an 11.1% recurrence rate for the group who underwent arthroscopic Bankart repair. Buss and associates41 have examined the results of nonoperative management for in-season athletes with anterior shoulder instability; they reported that 87% were able to return to sports for completion of the season without further injuries attributable to shoulder instability, despite 37% of patients experiencing at least one additional episode of instability during the season. In critically appraising the results of this study, it should be noted that 53% of patients in this study underwent subsequent surgical stabilization. A recent prospective, randomized, clinical trial by Kirkley and coworkers42 have compared the effectiveness of immediate arthroscopic stabilization with immobilization and rehabilitation for the treatment of primary traumatic anterior shoulder dislocation, with an average 75-month follow-up. They reported differences in the rate of redislocation for the two groups as well as for functional evaluation using the Western Ontario shoulder instability index questionnaire. No statistically significant difference was noted using the American Shoulder and Elbow Surgeons or disabilities of the arm, shoulder, and hand questionnaire. Based on these results, it was concluded that “immediate arthroscopic stabilization is the treatment of choice in a subset of patients who are younger than 30 years and are higher level athletes, and the timing for their surgery is good or their sport is risky.”42 Therefore, although it may be concluded that it is reasonable to consider a trial of conservative management after primary anterior glenohumeral dislocation in an athlete younger than 30 years, study results would support a substantial concern for recurrent instability in this population.
(e.g., Hill-Sachs, bony Bankart, glenoid and coracoid fractures). Specific views have been used to improve the sensitivity of detecting certain lesions, including the Stryker’s notch view for a Hill-Sachs lesion and West Point axillary view for a Bankart lesion. Magnetic resonance imaging (MRI), with or without gadolinium contrast injection, has become the primary imaging modality used for the assessment of shoulder instability. The acute MRI appearance of Bankart lesions typically shows a hemorrhagic effusion and elevation of the capsulolabral complex from the glenoid (Fig. 21-4). Usually, the scapular periosteum is also injured. If the capsulolabral injury extends medially and inferiorly, the lesion is referred to as an ALPSA (anterior labroligamentous periosteal sleeve avulsion).43 Takubo and colleagues44 have recently compared nonarthrographic MRI in abduction and external rotation with arthroscopic examination of the inferior glenohumeral ligament in 51 shoulders with traumatic anterior instability. They reported a 94% sensitivity and a 82% specificity for this MRI technique in assessing the inferior glenohumeral ligament. Limitations of traditional neutral positioning of the shoulder for routine MRI include the orientation of the anterior band of the inferior glenohumeral ligament (AIGHL) in a near-vertical orientation to the axial images, which supports the contention of several studies regarding the usefulness of abduction and external rotation when positioning the arm of the patient with anterior instability.44-46 In patients with bony deficiency resulting from a bony Bankart lesion, glenoid rim fracture, or large Hill-Sachs lesion, computed tomography (CT) with three-dimensional reconstructions is often useful for delineating the degree of bone loss and providing additional information about articular surface orientation and version.47
DIAGNOSIS AND ASSESSMENT OF BANKART LESIONS After a thorough history and physical examination documenting the neurovascular status of the involved extremity, the initial plain radiographic evaluation consists of anteroposterior (AP), true AP, axillary, scapular Y, and acromial outlet views. Although plain film imaging is an important initial modality in the workup of an anterior shoulder dislocation, its role is primarily to rule out associated fractures and identify frank osseous deformities
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Figure 21-4. Bankart lesion. This axial T1-weighted magnetic resonance imaging scan is of a right shoulder.
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In addition to the thorough physical examination performed in the office at the time of initial patient assessment, the examination under anesthesia is an imperative component of the workup and provides critical information for intraoperative decision making. Particular attention is given to ROM and degree of translation—anterior, posterior, and inferior. The distinction among asymptomatic, adaptive laxity, and pathologic instability, particularly in the overhead athlete’s shoulder, is not always clear. Thus, meticulous attention to detail when correlating the patient’s history, physical examination, diagnostic imaging, and examination under anesthesia provides the surgeon with the best chance for successful reconstruction and obtaining the maximal functional outcome.
OPERATIVE INDICATIONS The determination of operative indications for anterior shoulder stabilization in the setting of a Bankart lesion is predicated on patient age, activity level, history of shoulder pain or instability in the past, and desired future activity level. It is not unreasonable to consider a nonoperative approach for acute traumatic primary anterior dislocations in patients older than 40 years who do not desire to participate in recreational activities and have no evidence of gross instability or disruption of the normal osseous restraints to glenohumeral instability. After a brief period of immobilization (3 to 4 weeks), a functional rehabilitation program may allow for return to activities of daily living without further instability. If a patient develops recurrent instability, surgical stabilization would be indicated. A 3-year prospective observational cohort study of 538 patients by Robinson and associates48 has suggested that early operative stabilization is justified for patients with severe disruption of the soft tissue envelope caused by a large rotator cuff tear, disruption of the osseous restraints from a glenoid rim fracture, or combined glenoid rim fracture and greater tuberosity fracture with evidence of gross instability. The primary focus of our discussion here is the young athlete who desires to continue participation in sports after an acute, primary, traumatic, anterior shoulder dislocation.
BOX 21-1.
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This population, as noted, has a definitively increased risk for recurrent instability and several studies have supported early surgical stabilization.40,42,49 There is a spectrum of instability, however, and accordingly indications range from relative to absolute. Typical indications for surgical stabilization are listed in Box 21-1. The controversial issues regarding surgical stabilization with an arthroscopic or open approach will be discussed in detail.
ARTHROSCOPIC TECHNIQUES Procedural Approaches Several factors require thorough consideration when critically appraising the literature regarding arthroscopic Bankart repair. The debate over open and arthroscopic Bankart repair has unfolded during a period of rapid development of arthroscopic techniques and instrumentation for the treatment of anterior shoulder instability. Simultaneously, as noted, our understanding of the relevant basic science and biomechanical issues involved in shoulder instability has enabled us to develop and perform arthroscopic procedures that can achieve improved restoration of the capsulolabral complex and approximation of the native anatomy. Several issues become clear in reviewing the literature regarding arthroscopic Bankart repair. Initial results for arthroscopic Bankart repair with staple capsulorrhaphy have produced not only higher failure rates than open surgery, but an increased risk of complications.50 Subsequent techniques have included transglenoid suture and bioabsorbable tacks for Bankart repair. The former technique yielded varying results (0% to 49% failure rate) and had several limitations, including an inability to address capsular laxity adequately, medialization of the capsulolabral complex, the need to tie sutures over the posterior soft tissues, and the risk of suprascapular nerve injury.51 The technique of bioabsorbable tack fixation has produced somewhat lower failure rates, ranging from 9% to 23%, and represents a significant technical advance in the field of arthroscopy for labral repair and the treatment of instability.11,40,52-54 Disadvantages of this technique include its limited ability
Operative Indications for Anterior Shoulder Instability with a Bankart Lesion
Acute, primary, traumatic anterior dislocation in a young patient (⬍30 years) who participates in high-demand or high-risk athletics or activities with a propensity for recurrent instability (e.g., competitive overhead and contact athletes, construction workers, climbers) Acute, primary, traumatic anterior dislocation with a concomitant large rotator cuff tear or osseous compromise of the normal osseous restraints to glenohumeral instability Post-traumatic recurrent instability (subluxation or dislocation) limiting activities of daily living Pain related to persistent luxation after an acute, primary, traumatic anterior dislocation treated with an adequate nonoperative management program
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to address capsuloligamentous laxity and reports of a polyglycolic acid–induced synovitis.23,55 In 1996, Guanche and associates56 reported a 33% incidence of recurrent instability after arthroscopic Bankart repair with transglenoid sutures or a bioabsorbable tack; it was concluded that open stabilization is the procedure of choice. In retrospect, the critical technical flaw in the arthroscopic approach used in this study can be identified as a failure to mobilize and reconstruct the capsuloligamentous complex. A 2004 meta-analysis of six studies by Freedman and coworkers has concluded that arthroscopic Bankart repair with transglenoid sutures or bioabsorbable tacks results in a higher rate of recurrent instability (20.3% vs 10.3%; P ⫽ .01) and dislocation (12.6% vs 3.4%; P ⫽ .01) compared with open surgical techniques.51 In reviewing these data, one might conclude that arthroscopic Bankart repair produces inferior results compared with a traditional open surgical approach. However, in more recent studies, which used contemporary approaches to arthroscopic Bankart repair, addressed capsuloligamentous laxity, and used suture anchors, significantly improved results were obtained.42,49 In a 2003 prospective study of 167 patients with recurrent anterior shoulder instability treated with arthroscopic anterior stabilization that used suture anchors and a concomitant capsular shift, Kim and colleagues49 have reported a 4% failure rate, with an average follow-up of 44 months. Therefore, it becomes clear that it is imperative to consider more recent studies, which have used significantly improved techniques, when debating the strengths and limitations of arthroscopic and open surgery for anterior shoulder instability. In addition, it is clear that further prospective comparisons of contemporary arthroscopic techniques and open surgical approaches are needed, with adequate sample sizes, validated outcomes measures, and longer term follow-ups.
Theoretical Benefits of an Arthroscopic Approach There are several theoretical benefits of using an arthroscopic approach for the treatment of Bankart lesions, including selective tissue tensioning in restoring the capsuloligamentous anatomy, preservation of subscapularis integrity, improved postoperative ROM, and decreased postoperative pain. Suture anchors allow for precise restoration of the labrum at the glenoid face and concomitant capsulorrhaphy or capsular plication to reconstruct the anterior band of the inferior glenohumeral ligament. Some have suggested that assessment of capsular laxity and subscapularis deficiency in complex cases is best performed through an open approach.11,57 Others have proposed that these situations represent the cases for which arthroscopic assessment and treatment may be best suited. The magnification with which direct examination of the capsular tissue and subscapularis quality can be examined through the arthroscope may provide a more precise
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evaluation of structural integrity. Surgeon experience and technical skill clearly define the approach that is best suited for an individual case. However, current evidence in the literature would not support a statement claiming that open approaches categorically provide superior assessment.54
OPEN TECHNIQUES Open surgical treatment of Bankart lesions has been hailed in the literature as the gold standard. This approach has consistently provided reliable reproducible results, as reported in several studies.3,5,20,47
Anatomic Repairs The primary focus of our review will be on anatomic repairs, which are the most commonly performed procedures in North America. Nonanatomic repairs such as the Bristow, Latarjet, Magnuson-Stack, and Putti-Platt procedures are used with greater frequency in Europe—and occasional revision situations—and can yield low failure rates with regard to recurrent instability. Failure to address a Bankart lesion adequately with repair has been reported to be a major cause of failure when nonanatomic reconstructions are performed.58 In addition, the frequent complication of external rotation motion loss of up to 30 degrees has been associated with glenohumeral arthrosis.11,47 The Putti-Platt procedure was first described in 1948 by Osmond-Clarke. Familiarity with these procedures and their limitations and complications strengthens a shoulder surgeon’s ability to address complex revision situations with sound intraoperative decision making in cases for which capsular necrosis, poor soft tissue quality, and prior surgery limit options for reconstruction. In North America, the current standard for open Bankart repair and anterior shoulder stabilization is an anatomic repair that seeks to restore normal glenohumeral stability within the broadest arc of motion possible. This can be accomplished by addressing all pertinent labral and capsuloligamentous pathology without overconstraining the joint. Typically performed through a modified deltopectoral approach, which more closely parallels the anterior axillary fold, the subscapularis is divided with a vertical incision according to surgeon preference to provide maximal exposure of the glenohumeral joint and capsule, with minimal excess dissection and soft tissue trauma. Some have proposed a subscapularis-splitting horizontal approach to minimize the risk of postoperative rupture.59,60 The subscapularis is then meticulously dissected free from the anterior capsule and a capsulotomy is made medially, laterally, or in a T configuration for exposure of the glenohumeral joint. For open Bankart repair and anterior stabilization, we prefer the T-plasty modification of the Bankart procedure, as described in a 1991 study.5 With this technique, a vertical medial capsulotomy is made with a horizontal extension of the
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incision in a T configuration; this allows for tensioning of the superior and inferior flaps at the completion of the case before repair of the subscapularis. Bankart repair is most commonly performed through reattachment of the capsulolabral complex to the anterior glenoid rim with suture anchors. Suture anchors are lowprofile devices capable of providing stable fixation, with minimal articular surface compromise.61 With the use of suture anchors, the surgeon can specifically select the amount of tissue to incorporate at each level of the capsulolabral reconstruction and tension it accordingly by tying arthroscopic knots on the extra-articular side of the labrum. This technique allows not only for restoration of the labral bumper as a restraint to humeral head translation, but for restoration of the capsuloligamentous complex at an appropriate tension to restrain pathologic glenohumeral motion without excessive constraint.
Recommended Technique Our preferred technique is a follows. After induction of anesthesia, the patient is placed in the beach chair position on a beanbag with careful attention to padding all bony prominences and maintenance of a neutral cervical spine position. The beanbag is translated with the patient to the edge of the table and the entire scapula is exposed, with a medial bean buttress to stabilize it. A preoperative examination under anesthesia is performed to assess ROM and anterior, posterior and inferior translation, which are graded and documented. The patient is then prepared and draped in the usual sterile fashion and a marking pen is used to identify pertinent surface anatomic landmarks; these include the scapular spine, acromion, clavicle, and coracoid process. Arthroscopy is initiated from a standard posterolateral portal. For the performance of a Bankart repair and anterior stabilization, a far-lateral rotator interval portal is established just lateral to the biceps tendon and anterior to the leading edge of the supraspinatus. A second rotator interval portal is established more medially and inferiorly, just above the superior aspect of the subscapularis tendon. Cannula choice is predicated on patient size and anticipated repair location. We prefer to use a partially threaded 7-mm (inner diameter) cannula (Arthrex, Naples, Fla) for the more medial and inferior portal and a smaller Wolf cannula (ConMed Linvatec, Largo, Fla) for the accessory anterolateral portal. A curved spectrum instrument preloaded with polydioxanone suture (PDS) is shuttled through the anterior band of the inferior glenohumeral ligament and the capsulolabral complex inferiorly to shift this tissue superiorly and back up to the face of the glenoid (Fig. 21-5). After placement of the PDS, a pilot hole for a 3.0-mm BioSutureTak (Arthrex) is drilled at the peripheral margin of the glenoid face and the anchor is tapped into place. For revision situations and patients whose bone stock provides a suboptimal anchor purchase, a 3.7-mm BioSutureTak is available. This anchor is preloaded with a single no. 2 FiberWire (Arthrex) suture
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and is also available as a double-loaded anchor. The PDS is then securely attached to the extra-articular limb of the FiberWire suture and shuttled through the soft tissue. The extra-articular limb of the FiberWire suture then serves as the post for an arthroscopic knot to be tied under direct arthroscopic visualization to confirm optimal tensioning of the capsulolabral complex. This last step may be facilitated by switching the arthroscope from the posterior portal to the superolateral accessory portal, which provides a more direct view of the knot being tied through the more medial and inferior rotator interval portal. This process is performed at two or three points along the anterior inferior aspect of the glenoid sequentially, from inferior to superior. The portals are then closed in standard fashion and the extremity is placed in a sling.
REHABILITATION PRINCIPLES Selection of parameters for the postoperative rehabilitation protocol is critical to achieve a successful outcome after open or arthroscopic Bankart repair and anterior stabilization. We typically follow a six-phase program, as follows. Phase I. This consists of the first 3 weeks after surgery, during which the patient is immobilized in a sling with gradual incorporation of pendulum exercises and wrist and elbow ROM exercises. During this phase, active-assisted supine forward elevation to 90 degrees is allowed in addition to passive external rotation to neutral and shoulder abduction to 30 degrees. Scapula-tightening exercises and modalities are incorporated through participation in physical therapy. Phase II. This occurs during weeks 4 to 6 after surgery and begins with gradual discontinuation of the sling. Pulley exercises are then incorporated to encourage the development of full forward elevation, and active-assisted external rotation exercises are allowed to increase ROM from 0 to 30 degrees. Therapist-assisted, side-lying manual scapular stabilization exercises are initiated and pain-free internal and external rotation isometric exercises are performed in a neutral position. Phase III. This takes place during weeks 6 to 8 after surgery and involves the incorporation of biceps and triceps strengthening, progressive scapular strengthening within a protective arc (emphasizing closed-chain activities), and a further emphasis on increasing forward elevation and external rotation through active-assisted ROM exercises. Latissimus strengthening and the use of an upper body ergometer are initiated below 90 degrees of elevation and patients begin humeral head stabilization exercises when strength and ROM permit. Phase IV. This takes place during weeks 8 to 10 and focuses on aggressive periscapular muscle strengthening, as well as
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G
CLC
G
AID
CLC
HH HH 0
4
A
B
G
CLC
HH
C
8
D Figure 21-5. Bankart repair and anterior stabilization. A, Spectrum suture passer placing a polydioxanone suture (PDS) through the capsular tissue and underneath the anteroinferior labrum. B, Anchor insertion for Bankart repair. C, Suture shuttling (monofilament suture, PDS; braided suture, FiberWire (Arthrex, Naples, Fla). D, Bankart repair completed, with anatomic restoration of the capsulolabral complex. AID, anchor insertion device; CLC, capsulolabral complex; G, glenoid; HH, humeral head.
on deltoid, biceps, triceps, and latissimus strengthening as tolerated. Humeral head stabilization exercises receive a greater emphasis and proprioceptive neuromuscular facilitation pattern exercises are initiated. When patients are pain-free and have regained adequate strength, internal and external rotation exercises are incorporated with the arm in an elevated position. Phases V and VI. These final phases take place during weeks 10 to 24 after surgery. They focus more on upper extremity strengthening with eccentric exercises,
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development of coordinated scapulohumeral mechanics, endurance training, and sport-specific interval program.
COMPLICATIONS The primary complications of Bankart repair may be subdivided into perioperative and postoperative. Perioperative complications consist primarily of anchor failure, suture failure, glenoid rim fracture, musculocutaneous and axillary nerve injury, hematoma formation, and infection.
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Meticulous attention to detail during anchor placement (e.g., pilot hole placement and eyelet orientation) and to suture management will reduce the incidence of these complications. Glenoid rim fracture has been associated with the establishment of transosseous tunnels for Bankart repair; this has become less prevalent because the use of suture anchors has largely replaced this technique. Iatrogenic nerve injury may be avoided through a detailed knowledge of the regional anatomy and careful attention to retractor placement and arm positioning during open surgery.
surgeon considers the patient’s history, clinical examination, diagnostic imaging studies, future goals for functional outcome, and procedure that he or she thinks will most predictably and reliably yield an optimal outcome. Further prospective analysis of arthroscopic treatment of Bankart lesions in randomized controlled studies is needed to compare its success with that of open procedures and to identify the limitations of current techniques so that they may be improved.
Postoperative complications include recurrence of instability, subscapularis rupture (with open surgery), loss of motion (most commonly external rotation), implant failure and migration, premature arthrosis, and infection. As noted, a wide variation in recurrence rates has been reported in the literature for open and arthroscopic repairs. Pertinent issues to consider in evaluating the literature for recurrence rates include the criteria used by the authors (e.g., subluxation or dislocation and single or multiple episodes).42 Causes of recurrence have been described in detail earlier; these primarily include articular-arc compromise (bony Bankart and large, engaging Hill-Sachs lesions) and failure to address capsuloligamentous compromise.2,11,18,19,23 Subscapularis rupture has been described as a complication of open surgical reconstruction.62 Prompt recognition of this complication is critical to minimize the chance of a poor outcome and, as described by Neviaser and coworkers,63 should be suspected in all patients with recurrent instability and older patients after an anterior shoulder dislocation.47 Loss of external rotation may occur after Bankart repair and anterior stabilization,64 with the short-term consequence of failure to return to the desired preinjury level of activity and the long-term potential consequence of glenohumeral arthrosis caused by overconstraint of the glenohumeral joint.47 With careful attention to arm position during the performance of a selective capsular shift (open or arthroscopic), several studies have reported good results, with minimal loss of external rotation.49,65
1. Bankart ASB: The pathology and treatment of recurrent dislocation of the shoulder joint. Br J Surg 26:23-29, 1938. 2. Speer KP, Deng X, Borrero S, et al: Biomechanical evaluation of a simulated Bankart lesion. J Bone Joint Surg Am 76: 1819-1826,1994. 3. Rowe CR, Patel D, Southmayd WW: The Bankart procedure. A long-term end-result study. J Bone Joint Surg Am 60: 1-16, 1978. 4. Neer CS 2nd: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am 62:897-908, 1980. 5. Altchek DW, Warren RF, Skyhar MJ, et al: T-plasty modification of the Bankart procedure for multidirectional instability of the anterior and inferior types. J Bone Joint Surg Am73:105-112, 1991. 6. Bigliani LU, Kurzweil PR, Schwartzbach CC, et al: Inferior capsular shift procedure for anteroinferior shoulder instability in athletes. Am J Sports Med 22:578-584, 1994. 7. Warner JJP, Johnson D, Miller M, et al: Technique for selecting capsular tightness in repair of anterior-inferior shoulder instability. J Shoulder Elbow Surg 4:352-364, 1995. 8. Wirth MA, Blatter G, Rockwood CA Jr. The capsular imbrication procedure for recurrent anterior instability of the shoulder. J Bone Joint Surg Am78:246-259, 1996. 9. Howell SM, Galinat BJ: The glenoid-labral socket: A constrained articular surface. Clin Orthop 243:122-125, 1989. 10. Iannotti JP, Gabriel JP, Schneck SL, et al: The normal glenohumeral relationships. An anatomical study of one hundred and forty shoulders. J Bone Joint Surg Am 74:491-500, 1992. 11. Gill TJ, Zarins B: Open repairs for the treatment of anterior shoulder instability. Am J Sports Med 31:142-153, 2003. 12. Cooper DE, Arnoczky SP, O’Brien SJ, et al: Anatomy, histology, and vascularity of the glenoid labrum. J Bone Joint Surg Am 74:46-52, 1992. 13. Lazarus MD, Harryman DT II: Complications of open anterior stabilization of the shoulder. J Am Acad Orthop Surg 8:122-132, 2000. 14. Fehringer EV, Schmidt GR, Boorman RS, et al: The anteroinferior labrum helps center the humeral head on the glenoid. J Shoulder Elbow Surg 12:53-58, 2003. 15. Warner JJP, Caborn DNM, Berger R, et al: Dynamic capsuloligamentous anatomy of the glenohumeral joint. J Shoulder Elbow Surg 2:115-133, 1993. 16. Turkel SJ, Panio MW, Marshall JL, et al: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 63:1208-1217, 1981. 17. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990.
CONCLUSION The debate continues in regard to the optimal treatment of Bankart lesions and anterior instability. The excellent results obtained with open surgical reconstruction in the past are now being reported with state-of-the-art arthroscopic approaches. It is critical to consider what techniques are being used when critically appraising the literature. Although open treatment was once the gold standard, we hesitate to use this term, because it implies that other procedures are suboptimal. Its use is therefore inappropriate when considering the dramatic technical advances in arthroscopic anterior stabilization that have been reported in recent studies. In the final analysis, the decision for which surgical approach to use is best made when the treating
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18. Bigliani LU, Pollock RG, Soslowsky LJ, et al: Tensile properties of the inferior glenohumeral ligament. J Orthop Res 10:187-197, 1992. 19. Taylor DC, Arciero RA: Pathologic changes associated with shoulder dislocations: Arthroscopic and physical examination findings in first time anterior dislocations. Am J Sports Med 25:306-311, 1997. 20. Gill TJ, Micheli LJ, Gebhard F, et al: Bankart repair for anterior instability of the shoulder. Long-term outcome. J Bone Joint Surg Am 79:850-857, 1997. 21. Mosely HF, Overgaard B: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br 44:913, 1962. 22. Itoi E, Lee SB, Berglund LJ, et al: The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: A cadaveric study. J Bone Joint Surg Am 82:35-46, 2000. 23. Burkhart SS, DeBeer JF: Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: Significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 16:677-694, 2000. 24. Bigliani LU, Newton PM, Steinmann SP, et al: Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am J Sports Med 26:41-45, 1998. 25. Saito H, Itoi E, Sugaya H, et al: Location of the glenoid defect in shoulders with recurrent anterior dislocation. Am J Sports Med 33:889-893, 2005. 26. Montgomery WH, Jr., Wahl M, Hettrich C, et al: Anteroinferior bone-grafting can restore stability in osseous glenoid defects. J Bone Joint Surg Am 87:1972-1977, 2005. 27. Hill HA, Sachs MD: The grooved defect of the humeral head. A frequently unrecognized complication of dislocations of the shoulder joint. Radiology 35:690-700, 1940. 28. Hovelius L, Eriksson K, Fredin H, et al: Recurrences after initial dislocation of the shoulder. Results of a prospective study of treatment. J Bone Joint Surg Am 65:343 -349, 1983. 29. Hawkins RJ, Angelo RL: Glenohumeral osteoarthrosis: A late complication of the Putti-Platt repair. J Bone Joint Surg Am 72:1193-1197, 1990. 30. Rosenberg BN, Richmond JC, Levine WN: Long-term followup of Bankart reconstruction: Incidence of late degenerative glenohumeral arthrosis. Am J Sports Med 23:538-544, 1995. 31. Matsen FA, Rockwood CA, Wirth MA, et al. Gleno-humeral arthritis and its management. In Rockwood CA, Matsen FA (eds): The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 870-872. 32. Buscayret F, Edwards TB, Szabo I, et al: Glenohumeral arthrosis in anterior instability before and after surgical treatment: Incidence and contributing factors. Am J Sports Med 32:1165-1172, 2004. 33. Marx RG, McCarty EC, Montemurno TD, et al: Development of arthrosis following dislocation of the shoulder: A casecontrol study. J Shoulder Elbow Surg 11:1-5, 2002. 34. Rowe CR: Prognosis in dislocations of the shoulder. J Bone and Joint Surg Am 38:957-977, 1956. 35. McLaughlin HL, MacLellan DI: Recurrent anterior dislocation of the shoulder: A comparative study. J Trauma 7:191-201, 1967. 36. Simonet WT, Cofield RH: Prognosis in anterior shoulder dislocation. Am J Sports Med 12:19-24, 1984.
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37. Arciero RA, Taylor DC, Hovelius L, et al: Correspondence. J Bone Joint Surg Am 80:299-300, 1998. 38. Hovelius L: Shoulder dislocation in Swedish ice hockey players. Am J Sports Med 6:373-377, 1978. 39. Henry JH, Genung JA: Natural history of glenohumeral dislocation-revisited. Am J Sports Med 10:135-137, 1982. 40. Bottoni CR, Wilckens JH, DeBerardino TM, et al: A prospective, randomized evaluation of arthroscopic stabilization versus nonoperative treatment in patients with acute, traumatic, first-time shoulder dislocations. Am J Sports Med 30:576-580, 2002. 41. Buss DD, Lynch GP, Meyer CP, et al: Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med 32:1430-1433, 2004. 42. Kirkley A, Werstine R, Ratjek A, et al: Prospective randomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: Long-term evaluation. Arthroscopy 21:55-63, 2005. 43. Neviaser TJ: The anterior labroligamentous periosteal sleeve avulsion lesion: A cause of anterior instability of the shoulder. Arthroscopy 9:17-21, 1993. 44. Takubo Y, Horii M, Kurokawa M, et al: Magnetic resonance imaging evaluation of the inferior glenohumeral ligament: Non-arthrographic imaging in abduction and external rotation. J Shoulder Elbow Surg 14:511-515, 2005. 45. Neumann CH, Tirman PFJ, Steinbach LS, et al: Normal anatomy. In Steinbach LS, Tirman PFJ, Peterty CG, et al (eds): Shoulder Magnetic Resonance Imaging. Philadelphia, Lippincott-Raven, 1998, pp 1-36. 46. Kwak SM, Brown RR, Trudell D, et al: Glenohumeral joint: Comparison of shoulder positions at MR arthrography. Radiology 208:375-380, 1998. 47. Millett PJ, Clavert P, Warner JJP: Open operative treatment for anterior shoulder instability: When and why? J Bone Joint Surg Am 87:419-32, 2005. 48. Robinson CM, Kelly M, Wakefield AE: Redislocation of the shoulder during the first six weeks after a primary anterior dislocation: Risk factors and results of treatment. J Bone Joint Surg Am 84:1552-1559, 2002. 49. Kim SH, Ha KI, Cho YB, et al: Arthroscopic anterior stabilization of the shoulder: Two to six-year follow-up. J Bone Joint Surg Am 85:1511-1518, 2003. 50. Coughlin L, Rubinovich M, Johansson J, et al: Arthroscopic staple capsulorrhaphy for anterior shoulder instability. Am J Sports Med 20:253-256, 1992. 51. Freedman KB, Smith AP, Romeo AA, et al: Open Bankart repair versus arthroscopic repair with transglenoid sutures or bioabsorbable tacks for recurrent anterior instability of the shoulder: A meta-analysis. Am J Sports Med 32: 1520-1527, 2004. 52. Laurencin CT, Stephens S, Warren RF, et al: Arthroscopic Bankart repair using a degradable tack. Clin Orthop 332:132-137, 1996. 53. Dora C, Gerber C: Shoulder function after arthroscopic anterior stabilization of the glenohumeral joint using an absorbable tack. J Shoulder Elbow Surg 9: 294-298, 2000. 54. Karlsson J, Magnusson L, Ejerhed L, et al: Comparison of open and arthroscopic stabilization for recurrent shoulder dislocation in patients with a Bankart lesion. Am J Sports Med 29:538-542, 2001.
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55. Edwards DJ, Hoy G, Saies AD, et al: Adverse reaction to an absorbable shoulder fixation device. J Shoulder Elbow Surg 3:230-233, 1994. 56. Guanche CA, Quick DC, Sodergren KM, et al: Arthroscopic versus open reconstruction of the shoulder in patients with isolated Bankart lesions. Am J Sports Med 24:144-148, 1996. 57. Geiger DF, Hurley JA, Tovey JA, et al: Results of arthroscopic versus open Bankart suture repair. Clin Orthop 337:1 11-117, 1997. 58. Rowe C, Zarins B, Ciullo J: Recurrent anterior dislocation of the shoulder after surgical repair. Apparent causes of failure and treatment. J Bone Joint Surg Am 66:159-168, 1984. 59. Jobe FW, Giangarra CE, Kvitne RS, et al: Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med 19:428-434, 1991. 60. Andrews JR, Satterwhite YE: Anatomic capsular shift. J Orthop Tech 1:151-160, 1993.
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61. Rudzki JR, Purcell DB, Wright RW: Options for glenoid labral suture anchor fixation. Oper Tech Sports Med 12: 225-231, 2004. 62. Lazarus MD, Sidles JA, Harryman DT, et al: Effect of a chondral-labral defect on glenoid concavity and glenohumeral stability: A cadaveric model. J Bone Joint Surg Am 78:94-102, 1996. 63. Neviaser RJ, Neviaser TJ, Neviaser JS: Concurrent rupture of the rotator cuff and anterior dislocation of the shoulder in the older patient. J Bone Joint Surg Am 70:1308-1311, 1988. 64. Lusardi DA, Wirth MA, Wurtz D, et al: Loss of external rotation following anterior capsulorraphy of the shoulder. J Bone Joint Surg Am 75:1185-1192, 1993. 65. Cohen SB, Altchek DW, Warren RF: Selective capsular shift approach for treatment of anterior and multidirectional shoulder instability. Tech Shoulder Elbow Surgery 2: 225-233, 2001.
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CHAPTER 22 Superior Labral Anterior-Posterior
Lesions of the Shoulder David A. Cortese and Stephen J. Snyder
Since the advent of arthroscopic techniques of evaluating and treating shoulder injuries in the 1980s, much has been learned about the insertion of the long head of the biceps tendon. The 20-power magnification provided by the arthroscope has led to the identification of lesions previously undetected by open surgical techniques. Over the ensuing years, various arthroscopic techniques have been developed to treat these lesions. Surgeons treating patients with shoulder injuries must have a good understanding of the normal anatomy, normal anatomic variants, and pathologic findings associated with this region, and must be adept in the arthroscopic skills developed to treat these lesions.
Typically, the inner edge of the labrum is firmly attached to and continuous with the hyaline cartilage of the glenoid surface. Superiorly, the labrum may occasionally have a more meniscal appearance, with the inner edge attached only loosely to the glenoid, a variation seen in approximately 15% of patients (Fig. 22-1). The anterosuperior labrum is the area from the anterior insertion of the biceps tendon to the anterior midglenoid notch, and is the area where anatomic variants are most common. In the usual situation (in approximately 80% of patients), the anterosuperior labrum is firmly and smoothly attached to the glenoid articular cartilage. The middle glenohumeral ligament appears as a thickening of the anterior capsule that crosses over the subscapularis tendon at an angle of about 45 degrees and inserts onto the anterosuperior glenoid neck just medial to the labrum (Fig. 22-2).
BACKGROUND The first description of labral tears involving the superior aspect of the glenoid labrum was made in 1984 by Andrews and colleagues1 in a report on 73 overhead athletes. They hypothesized that the lesion is a traction injury caused by the biceps tendon pulling off the labrum. In 1990, Snyder and associates2 reported on 27 patients with a specific injury pattern involving the superior aspect of the labrum identified as part of a retrospective review of 700 shoulder arthroscopies. They found that the lesion extends anteriorly and posteriorly from the insertion of the biceps tendon, and coined the term SLAP (superior labral anterior-posterior) lesion. Although not common and difficult to diagnose clinically, SLAP lesions can be a significant cause of disability, particularly in the overhead athlete.
It is important to recognize two normal variants for anterosuperior labral anatomy to diagnose labral abnormalities accurately. One variant involves an opening beneath the labral attachment of the anterosuperior labrum, termed a sublabral foramen. This foramen may be as small as 1 or 2 mm or extend along the entire anterosuperior quadrant (Fig. 22-3). As long as the opening is superior to the midglenoid notch and inferior to the anterior insertion of the biceps tendon, it is likely a normal variant. The second situation is the so-called Buford complex.3 This anatomic variant, described in 1994, consists of a cordlike middle glenohumeral ligament that attaches directly to the superior labrum at the anterior insertion of the biceps tendon. The anterosuperior labrum is completely absent and the thickened, cordlike, middle glenohumeral ligament crosses over the subscapularis tendon (Fig. 22-4). The anteroinferior labrum has a normal appearance below the mid glenoid notch. This anatomic variant is often incorrectly identified as a labral tear. If the thickened ligament is attached to the glenoid in an attempted repair, it will severely limit external rotation.
ANATOMY The glenoid labrum is a fibrocartilaginous structure that surrounds the glenoid and aids in shoulder stability by deepening the concavity of the glenoid. The vascular supply to the labrum arises from branches of the suprascapular, circumflex scapular, and posterior circumflex humeral arteries. Similar to the menisci of the knee, the labrum receives its blood supply from capsular and periosteal vessels through the periphery rather than the underlying bone, and the inner edge is relatively avascular.
CLASSIFICATION The original classification of SLAP lesions was proposed in Snyder’s 1990 article2 and consists of four types:
The supraglenoid tubercle is approximately 5 mm medial to the articular surface of the glenoid at the 12-o’clock position. The long head of the biceps tendon originates from the superior labrum and the supraglenoid tubercle.
Type I lesions involve degenerative fraying of the free edge of the superior labrum, similar to a degenerative meniscus in 269
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Sublabral hole
A Figure 22-1. Arthroscopic image showing normal variant of superior labrum with meniscoid appearance.
the knee; however, the attachment of the peripheral labrum and biceps tendon to the glenoid remains intact (Fig. 22-5). These lesions were found to comprise 21% of cases in a study of 140 SLAP lesions.4 Type I SLAP lesions are usually found in middle-aged and older patients and are not considered to be a common source of clinical symptoms. Type II SLAP lesions are the most common, occurring in 55% of patients in the same study.4 This lesion may be
B Figure 22-3. Arthroscopic image (A) and diagrammatic representation (B) of a sublabral foramen (arrow), a normal anatomic variant.
associated with variable fraying of the edge of the labrum, as in type I lesions; however, it also involves significant detachment of the superior labrum and biceps anchor from the superior glenoid (Fig. 22-6). Traction on the biceps tendon causes the biceps anchor–superior labral complex to arch away from the glenoid neck. Depending on the extent of the detachment, a type II SLAP lesion may undermine the labral insertions of the superior and middle glenohumeral ligaments and result in some degree of anterior instability.
Figure 22-2. Arthroscopic image showing normal appearance of anterosuperior quadrant.
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Type III SLAP lesions are less common, occurring in only 9% of patients. This lesion involves a split of a meniscoid superior labrum, forming a mobile, bucket-handle labral fragment (Fig. 22-7). The biceps tendon and peripheral labral attachment to the superior glenoid are intact. Symptoms develop as a result of catching of the mobile labral
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(1) Biceps tendon (2) Cordlike MGHL
(3) Absent anterior-superior labrum
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Figure 22-4. Arthroscopic image (A) and diagrammatic representation (B) of a Buford complex, a normal anatomic variant.
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Figure 22-5. Diagrammatic representation (A) and arthroscopic image (B) of a type I superior labral anterior-posterior (SLAP) lesion.
fragment within the joint. Occasionally, the middle glenohumeral ligament may be attached to the torn fragment and thus be rendered unstable.
involve bucket-handle tears of the labrum associated with an unstable labrum and anchor, and are thus classified as complex SLAP types II and III or types II and IV lesions.
Type IV SLAP lesions are also relatively uncommon, seen in only 10% of patients. Like the type III SLAP lesion, this lesion involves a bucket-handle tear of a meniscoid superior labrum but, in this case, the tear extends into the biceps tendon (Fig. 22-8). The biceps tendon fragment may displace into the joint with the labral fragment, causing clinical symptoms.
Since Snyder’s original description, others have expanded the classification. Morgan and coworkers5 have subclassified type II SLAP lesions into anterior, posterior, and combined anterior-posterior lesions. Maffet and colleagues6 have described three additional types: (1) anteroinferior labral separation extending superiorly to undermine the biceps anchor; (2) biceps tendon separation with an unstable flap tear of the labrum; and (3) extension of the superior labrum–biceps tendon separation anteriorly to undermine the middle glenohumeral ligament.
Complex SLAP lesions, which are combinations of the four basic types, have also been observed. Most commonly, these
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Figure 22-6. Diagrammatic representation (A) and arthroscopic image (B) of a type II superior labral anterior-posterior (SLAP) lesion.
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Figure 22-7. Diagrammatic representation (A) and arthroscopic image (B) of a type III superior labral anteriorposterior (SLAP) lesion.
DIAGNOSIS The clinical diagnosis of a SLAP lesion is difficult and requires a high index of suspicion on the part of the treating physician. This is in part a result of the association of SLAP lesions with other shoulder maladies. In a study of 140 patients with injuries to the superior labrum, Snyder and associates4 found that only 28% of the SLAP lesions are isolated injuries. Conditions associated with SLAP lesions include partial and complete rotator cuff tears, Bankart lesions, impingement, acromioclavicular arthrosis, and supraglenoid ganglion cysts.
trauma, such as a fall or motor vehicle accident, or of chronic overuse, such as throwing or striking a ball. Patients may complain of a vague pain or discomfort that limits athletic performance and is located deep in the joint or in the posterior aspect of the shoulder. The pain is usually aggravated by overhead activity, particularly with the cocking phase of throwing. Mechanical symptoms of catching or popping are also common. Complaints of night pain, weakness, or instability are not uncommon and may be caused by associated pathology, as described earlier.
SLAP lesions typically occur in young and active male patients. The onset of symptoms may be the result of acute
In the acute injury, the mechanism is believed to be a compressive force between the humeral head and glenoid. The
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Figure 22-8. Diagrammatic representation (A) and arthroscopic image (B) of a type IV superior labral anterior-posterior (SLAP) lesion.
cause is often a fall onto a slightly abducted and flexed shoulder, which drives the head superiorly against the labrum and biceps anchor and results in increased tension in the biceps tendon as it courses over the humeral head. In the chronic overuse injury, the patient reports insidiously progressive symptoms that limit performance in overhead sports. Burkhart and coworkers have proposed a peel-back mechanism, in which abduction and external rotation cause a twisting at the base of the biceps tendon and result in a tear that begins anteriorly and extends posteriorly with time. In addition to the history, a thorough physical examination is essential for making a clinical diagnosis. However, because of the presence of associated pathology, the physical examination may be nonspecific or confusing. Various specific tests have been described to help in the clinical diagnosis of a SLAP lesion. Biceps tension tests, such as the Speed’s test and O’Brien’s test, are typically positive in patients with type II lesions because of the instability of the biceps anchor. Speed’s test is performed by positioning the patient’s arm in 90 degrees of forward flexion at the shoulder, with the elbow extended and the forearm supinated, while the patient resists a downward force applied to the patient’s wrist. O’Brien’s test is similar, with the arm positioned in 90 degrees forward flexion and 20 degrees adduction at the shoulder (Fig. 22-9). A downward force applied at the wrist is resisted with the forearm in a supinated and then a pronated position, comparing the two results. A positive test result is when the pain is worse in the pronated position. Other useful tests involve a compressive load applied to the labrum that elicits pain or mechanical symptoms. The compression rotation test is similar to the McMurray test for meniscal pathology in the knee. This test is
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performed by positioning the patient’s arm with the shoulder abducted 90 degrees, applying a compressive load, and internally and externally rotating the humerus on the glenoid (Fig. 22-10). The crank test, as described by Liu and colleagues8 in 1996 is similar, except that the arm is in extreme elevation (to 160 degrees) in the scapular plane while the shoulder is compressed and rotated. The anterior slide test was described by Kibler in 1995.9 The patient positions his or her arm with the hand on the hip, with the thumb facing posteriorly. The examiner stabilizes the scapula with one hand while the patient resists a superiorly and anteriorly directed force applied to the glenoid through the elbow and upper arm. The ability of these tests to predict SLAP lesions conclusively and reliably has been debated. In each study describing a new diagnostic test, the sensitivity and specificity of the test are reportedly high, typically 90% or higher. However, these results have not been obtained in studies by other clinicians, including ourselves. Several studies comparing the clinical value of various tests have
Figure 22-9. O’Brien’s test performed with shoulder flexed 90 degrees and adducted 20 degrees, elbow extended, and forearm pronated.
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Figure 22-10. Compression-rotation test.
Figure 22-11. Arthroscopic image of superior labral anterior-posterior (SLAP) fracture of the superior humeral head.
shown that no single test or combination of tests can conclusively or reliably predict a SLAP lesion.10-12 Radiographic imaging studies can aid in the diagnosis when the clinical examination is suggestive of labral injury. Conventional radiographs may reveal characteristic findings for associated shoulder anomalies, such as subacromial impingement, degenerative arthritis, and instability. Occasionally, a SLAP fracture may be seen on plain radiographs, but typically they are of little value in diagnosing SLAP lesions (Fig. 22-11). Ultrasound imaging has not proved useful in identifying labral injuries. Computed tomography (CT) arthrography has improved the detection of labral pathology, but it is better at defining abnormalities of bone than of soft tissue. Magnetic resonance imaging (MRI) has proved useful for evaluating soft tissue pathology about the shoulder, particularly for injuries of the rotator cuff, biceps tendon, and capsule. MRI has been shown to have good sensitivity and specificity for identifying injuries of the anterior and inferior labrum, and the presence of a supraglenoid cyst on an MRI scan is suggestive of a superior labral tear (Fig. 22-12). However, conventional MRI techniques are somewhat limited for evaluating injuries to the superior labrum. In an effort to increase the accuracy of MRI for evaluating labral injuries, MR arthrography using intra-articular injection of dilute gadolinium has gained widespread use. The SLAP lesion is best appreciated on coronal oblique images as a distinct cleft extending medially beneath the biceps anchor between the superior labrum and cortical surface of the glenoid. The contrast often diffuses into the labral fragment, causing it to have a ragged, indistinct appearance (Fig. 22-13). In a study
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Figure 22-12. Magnetic resonance imaging scan of a supraglenoid cyst (arrow) suggestive of a superior labral tear.
comparing results of MR arthrography with those of diagnostic arthroscopy, Waldt and associates13 have found that MR arthrography shows a sensitivity of 82% and specificity of 98% for the detection of SLAP lesions, but that the technique has limited ability in classifying the type of SLAP lesion.
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Figure 22-13. Magnetic resonance arthrogram of a superior labral anterior-posterior (SLAP) lesion.
Because of the limitations of the history, physical examination, and imaging studies to diagnose SLAP lesions definitively, a high index of suspicion should be maintained by the treating physician. In the young athletic male patient with persistent shoulder pain, whose symptoms and clinical findings are not consistent with those of other diagnostic entities, labral pathology should be considered. Ultimately, the diagnosis of SLAP lesions is often only made by performing an accurate diagnostic shoulder arthroscopy. A complete diagnostic arthroscopic examination should be performed, with particular attention paid to the anterosuperior quadrant. Findings consistent with SLAP lesions include hemorrhage or granulation tissue beneath the biceps anchor and superior labrum, the presence of a space between the peripheral articular cartilage margin of the glenoid and attachment of the labrum and biceps anchor, and displacement of the superior labrum and biceps anchor more than 3 or 4 mm away from the glenoid when traction is applied to the biceps tendon (Fig. 22-14).
TREATMENT Treatment of SLAP lesions is based on lesion type. Because type I SLAP lesions are degenerative and by definition do not involve instability of the labrum or biceps anchor, they are treated with débridement of the frayed labrum to address pain and mechanical symptoms. A 4.0-mm full-radius shaver is used to remove only the damaged labral tissue, being careful to preserve the anterosuperior labral attachment, biceps anchor, and insertion of the middle glenohumeral ligament.
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Figure 22-14. Arthroscopic image of a type II superior labral anterior-posterior (SLAP) lesion that displaces when traction is applied to the bicep tendon (arrow).
Type II SLAP lesions are repaired using a single-anchor, double-suture technique (see later,“Single-Anchor DoubleSuture SADS Repair for Type II SLAP Lesions”). A 4-mm Big Eye Revo anchor (ConMed Linvatec, Largo, Fla) or similar suture anchor is loaded with two strands of strong braided suture and inserted into the superior glenoid just below the biceps tendon. The sutures are placed through the labrum and one is then directed anteriorly and one posteriorly around the biceps, forming a sling around the anchor and providing secure fixation of the labrum for healing. Type III SLAP lesions are treated with resection of the bucket-handle labral fragment, followed by close inspection of the remaining labrum for stability. A basket punch is first used to divide the posterior attachment of the bucket handle and then a shaver is used to remove the labral fragment. Careful attention is made to ensure that the attachment of the middle glenohumeral ligament (MGHL) is not compromised before completing the resection. If a cordlike MGHL is attached to the anterior fragment of the torn labrum, a robust anterior tag is left to preserve the attachment. This tag should be reattached to the glenoid with a suture anchor if traction on the ligament reveals instability of the MGHL. Type IV lesions are treated based on the severity of biceps tendon involvement. In patients with minimal involvement of the tendon, the involved tendon is excised along with the labral fragment, as in type III lesions. If more than 30% of the tendon is involved with the displaced labral tear, repair of the tendon should be considered to release it and repair the labrum, as in type II lesions, or to tenodese the end of the tendon to bone. The treatment choice
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depends on the age and activity level of the patient and condition of the remaining portion of the tendon. In most cases, the labral fragment and involved portion of the biceps tendon are excised. If the remaining tendon appears degenerative and frayed, or the anchor site is unstable, the tendon should be released and often tenodesed, especially in the young active patient. When encountered, complex types II and III or complex types II and IV lesions can be treated using the principles described earlier. Torn segments of the labrum and biceps tendon can be débrided and, if the remaining portion of the biceps anchor is substantial and unstable, it can be repaired back to the glenoid using the technique described later for repair of type II SLAP lesions. Because SLAP lesions usually occur with concomitant shoulder abnormalities, it has been difficult to interpret results of suture anchor repair techniques. Stetson and colleagues14 have evaluated a subset of 23 patients with isolated SLAP lesions, with average follow-up of 3.8 years (range, 14 months to 8 years). Of the 23 SLAP lesions studied, 1 type I lesion was treated with débridement, 6 type II lesions were treated with débridement and abrasion, 12 type II lesions were treated with fixation using one of three suture anchors, 1 type III lesion was treated with débridement, 2 type IV lesions were treated with débridement, and 1 complex types II and III lesion was treated with a combination of débridement and fixation with an absorbable anchor. Based on the Rowe scoring system at final follow-up, 82% of patients had good or excellent results, 9% had fair results, and 9% had poor results. Of the two patients with poor results, one had a type II SLAP lesion that was treated with débridement alone and ultimately required open anterior shoulder stabilization. The other patient had a type IV SLAP lesion treated with
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débridement that was clinically unstable on follow-up. Of the two patients with fair results, one had a complex types II and III lesion that had cracking in the joint and ultimately required removal of the absorbable tack fragments. The second patient had a type III SLAP lesion that was treated with débridement. Notably, all three patients whose type II SLAP lesion was treated with a screw-type suture anchor were able to return to their previous level of sports competition. Kim and associates15 have also reported their results of 34 patients with isolated SLAP lesions who underwent arthroscopic repair with suture anchors, with a mean follow-up of 33 months. Based on the UCLA shoulder score at final follow-up, 32 patients (94%) had a satisfactory result, and 2 patients had an unsatisfactory result. Of 34 patients, 31 (91%) regained their preinjury level of shoulder function. However, they reported inferior results in overhead throwing athletes compared with patients not involved in overhead sports.
Single-Anchor Double-Suture SADS Repair for Type II SLAP Lesions The single-anchor double-suture (SADS) SLAP repair can be performed with the following steps: 1. Begin with the arthroscope in the standard posterior superior portal (PSP). Create an anterior superior portal (ASP) using an outside-in technique with a spinal needle. The proper placement of the portal is in the superior aspect of the rotator interval, anterior and slightly superior to the biceps tendon (Fig. 22-15). The needle is inserted at a point approximately 2 cm from the anterolateral corner of the acromion, and the path of the needle must approach the superior tubercle of the
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Figure 22-15. Diagrammatic representation (A) and arthroscopic image (B) illustrating creation of an anterior-superior portal using the outside-in technique with spinal needle.
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glenoid at an angle of 45 degrees, just posterior to the biceps tendon. Once the needle is properly positioned, the portal is created using a smoothwalled crystal cannula (Arthrex, Naples, Fla). 2. Create an anterior midglenoid portal (AMGP) using an outside-in technique by placing a spinal needle just superior to the subscapularis tendon at a position midway between the glenoid surface and tuberosity. A second smooth cannula is placed through this portal. 3. Débride the fibrous tissue down to cancellous bone from the superior glenoid below the detached labrum and biceps anchor using a 4-mm full-radius shaver (Fig. 22-16). It is often useful to débride the posterior aspect of the superior glenoid
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with the shaver in the PSP and arthroscope in the AGMP. Conversely, the anterior aspect of the superior glenoid is more easily débrided with the shaver in the AGMP and the arthroscope in the PSP. 4. Create a pilot hole for a suture anchor in the superior tubercle of the glenoid by placing a Revo punch through the cannula in the ASP, posteriorly around the biceps tendon. The tip of the punch should be directly below the biceps tendon, at the midpoint of the biceps anchor anteriorly and posteriorly, and 2 to 3 mm medial to the articular cartilage (Fig. 22-17). Carefully observe the insertion of the punch to ensure that it does not skive off the bone into the articular cartilage or down the neck of the glenoid. The handle of the punch
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Figure 22-16. Diagrammatic representation (A) and arthroscopic image (B) illustrating preparation of a superior glenoid by débridement of fibrous tissue with 4-mm shaver.
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Figure 22-17. Diagrammatic representation (A) and arthroscopic image (B) illustrating creation of a pilot hole for suture a anchor placement using an anchor punch with tip seated 3 mm medially to the articular surface of glenoid.
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should be maneuvered laterally and posteriorly to direct the tip into the bone (Fig. 22-18). Prepare a 4-mm Big Eye Revo or 5-mm SuperRevo anchor (ConMed Linvatec, Largo, Fla) by loading it with two no. 2 nonabsorbable, braided sutures. To facilitate suture management, one suture should be white and one green. One half of each suture is colored purple so that there are four differently colored suture limbs for easier suture management, with the purple-colored limbs exiting on the same side of the anchor eyelet (Fig. 22-19). Place the anchor through the cannula in the ASP, posterior to the biceps tendon and into the pilot hole. Seat the anchor to the appropriate depth and align it so that the purple-colored suture limbs are oriented toward the biceps tendon (Fig. 22-20). Test the anchor security by gently pulling on the sutures. Retrieve both the all-white and all-green suture limbs out through the cannula in the AMGP with a crochet hook (Fig. 22-21). Store the suture limbs outside the cannula by inserting a switching stick, removing the cannula, and then replacing the cannula with both suture limbs outside the cannula. Retrieve both the white-purple and green-purple sutures out through the cannula in the AMGP with a crochet hook (Fig. 22-22). These sutures will be passed through the labrum together to form the stitch of Burns. Insert a medium Spectrum Crescent hook loaded with a Shuttle Relay Suture Passer (both from ConMed Linvatec, Largo, Fla) through the cannula into the ASP. Pierce the biceps tendon at the midpoint of the biceps anchor, and angle the tip to exit just below the labrum and above the suture anchor. Insert a grasper through the cannula in the AMGP following the path of the whitepurple and green-purple suture limbs. Pass 3 cm
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Figure 22-18. Direction of insertion of anchor punch with handle pushed laterally and posteriorly (arrow).
Figure 22-19. Four-mm Revo anchor with suture ends prepared for insertion and simplifying suture management.
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Figure 22-20. Diagrammatic representation (A) and arthroscopic image (B) illustrating insertion of a suture anchor (A, inset) through an anterior-superior portal into pilot hole.
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Figure 22-21. Diagrammatic representation (A) and arthroscopic image (B) illustrating retrieval of different-colored sutures out through the cannula in the anterior midglenoid portal.
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Figure 22-22. Diagrammatic representation (A) and arthroscopic image (B) illustrating retrieval of different-colored sutures out through the anterior midglenoid portal.
of the Shuttle Relay Suture Passer into the joint, secure it with the grasper, and retrieve it into the cannula in the AMGP (Fig. 22-23). 9. Load the Shuttle Relay Suture Passer with both purple-colored suture limbs and draw them back through the labrum and out through the cannula in the ASP, being careful to ensure that they are not twisted around the other suture limbs (Fig. 22-24). 10. Retrieve the white-purple suture limb back into the AMGP. Retrieve the all-green suture limb into the cannula in the ASP using a crochet hook. This suture limb needs to be directed posterior to the biceps tendon (Fig. 22-25). Shorten the greenpurple suture limb to act as a post, and tie a sliding-locking knot to secure the posterior aspect of the superior labrum to the anchor (Fig. 22-26).
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11. Retrieve both the all-white and the white-purple suture limbs into the cannula in the ASP anterior to the biceps tendon using a crochet hook (Fig. 22-27). Shorten the white-purple limb to act as a post. Tie a sliding-locking knot to secure the anterior aspect of the superior labrum to the anchor. 12. Test the repair by pulling on the biceps tendon with a probe through the AMGP (Fig. 22-28). The labrum should be firmly secured and there should be no gap when tension is applied.
POSTOPERATIVE CARE Postoperatively, the operative extremity is placed into a 15-degree external rotation shoulder sling for 4 weeks. The patient is encouraged to perform gentle range-of-motion
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Figure 22-23. The Spectrum Crescent Hook is passed through the middle of the biceps anchor and the Shuttle Relay Suture Passer is retrieved through the anterior midglenoid portal.
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Figure 22-24. Diagrammatic representation (A) and arthroscopic image (B) illustrating passage of different-colored sutures through the biceps anchor and out through the anterior superior portal.
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Figure 22-25. Diagrammatic representation (A) and arthroscopic image (B) illustrating retrieval (A, inset) of different-colored sutures out through the anterior superior portal.
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Figure 22-26. Diagrammatic representation (A) and arthroscopic image (B) illustrating a sliding knot being tied posterior to a biceps tendon to secure posterosuperior labrum to glenoid rim.
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Figure 22-27. Diagrammatic representation (A) and arthroscopic image (B) illustrating retrieval (A, inset) of different-colored sutures out through the anterior superior portal.
(ROM) exercises of the elbow, wrist, and hand in the immediate postoperative period. Pendulum and passive ROM exercises begin 1 week after surgery. It is important to protect the shoulder from excessive stress on the biceps tendon for 6 weeks, so the patient is instructed to avoid any lifting with the operative extremity. Progressive resistance exercises begin at 6 weeks after surgery, with vigorous throwing and heavy lifting activities delayed until 3 months, provided that painless motion has returned to normal.
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SUMMARY A wide variety of pathology may affect the superior aspect of the labrum. Clinical examination is often difficult because of the numerous injury mechanisms and variable extent of labral pathology. Proper identification of the exact mechanism and specific severity of pathology is vital to diagnose and manage these injuries accurately. Surgical procedures to address SLAP lesions vary from minimal débridement to extensive labral repair. Postoperative
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Figure 22-28. Diagrammatic representation (A) and arthroscopic image (B) showing appearance of final repair with one knot tied anterior and one knot tied posterior to biceps tendon.
rehabilitation must be based on the specific injury and surgical procedure performed, as well as on an understanding of the basic science related to injury and tissue healing. References 1. Andrews JR, Carson WG, McLeod WD: The arthroscopic treatment of glenoid labrum tears—the throwing athlete. Orthop Trans 8:44, 1984. 2. Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274-279, 1990. 3. Williams MM, Snyder SJ, Buford D Jr: The Buford complex— the “cord-like” middle glenohumeral ligament and absent anterosuperior labrum complex: A normal anatomic capsulolabral variant. Arthroscopy 10:241-247, 1994. 4. Snyder SJ, Banas MP, Karzel RP: An analysis of 140 injuries to the superior glenoid labrum. J Shoulder Elbow Surg 4: 243-248, 1995. 5. Morgan CD, Burkhart SS, Palmeri M, Gillespie M: Type II SLAP lesions: Three subtypes and their relationship to superior instability and rotator cuff tears. Arthroscopy 14:553-565, 1998. 6. Maffet MW, Gartsman GM, Mosley B: Superior labrumbiceps tendon complex lesion of the shoulder. Am J Sports Med 23:93-98, 1995. 7. Burkhart SS, Morgan CD: The peel-back mechanism: Its role in producing and extending posterior type II SLAP lesions
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and its effect on SLAP repair rehabilitation. Arthroscopy 14:637-640, 1998. 8. Liu SH, Henry MH, Nuccion SL: A prospective evaluation of a new physical examination in predicting glenoid labral tears. Am J Sports Med 24:721-725, 1996. 9. Kibler WB: Specificity and sensitivity of the anterior slide test in throwing athletes with superior glenoid labral tears. Arthroscopy 11:296-300, 1995. 10. Guanche CA, Jones DC: Clinical testing for tears of the glenoid labrum. Arthroscopy 19:517-523, 2003. 11. Holtby R, Razmjou B: Accuracy of the Speed’s and Yergason’s tests in detecting biceps pathology and SLAP lesions: Comparison with arthroscopic findings. Arthroscopy. 20:231-236, 2004. 12. McFarland EG, Kim TK, Savino RM: Clinical assessment of three common tests for superior labral anterior-posterior lesions. Am J Sports Med 30:810-815, 2002. 13. Waldt S, Burkart A, Lange P, et al: Diagnostic performance of MR arthrography in the assessment of superior labral anteroposterior lesions of the shoulder. AJR Am J Roentgenol 182:1271-1278, 2004. 14. Stetson WB, Snyder SJ, Karzel RP: Long-term clinical followup of isolated SLAP lesions of the shoulder. Presented at the 65th Annual Meeting of the American Academy of Orthopedic Surgeons, New Orleans, March 1998. 15. Kim SH, Ha KI, Kim SH, Choi HJ: Results of arthroscopic treatment of superior labral lesions. J Bone Joint Surg Am 84:981-985, 2002.
9/19/08 7:09:43 PM
CHAPTER 23 Soft Tissue Injuries
of the Shoulder Judson W. Ott, William G. Clancy, Jr., and Kevin E. Wilk
There are a multitude of painful soft tissue injuries about the shoulder. Most of these injuries are a result of primary injury to the tendon sheath or primary fatigue failure within the tendon. Additional injuries may result from complete or partial rupture of a tendon or the muscle tendon complex, whereas other painful conditions are caused by acute or chronic bursitis or bony impingement.
only the tendon sheath in those with acute tendinitis. Biopsies of patients with chronic tendinitis, as reported by Clancy5 and Nirschl,7,8 have indicated a complete absence of inflammatory cells in the tendinous tissue itself, particularly in areas of tendon degeneration; it was noted that inflammatory cells are found only in those patients with gross partial ruptures. This lack of inflammatory cells has been noted by Becker and Cofield9 on histologic examination of the biceps tendon. These areas are characteristic in that there is a loss of the normal collagen architecture and a paucity of tenocytes. Degenerative changes within a tendon in patients who were asymptomatic and histologic examination showed no signs of inflammation; this was described by Puddu and colleagues10 as representing a condition termed tendinosis. More appropriately, Clancy5 has used the term paratenonitis with tendinosis to describe more accurately the clinical and histologic findings in those patients with classic symptomatic tendinitis.
TENDINITIS, BURSITIS, AND THE INFLAMMATORY RESPONSE Most soft tissue injuries about the shoulder occur as a result of primary failure within a tendon, with pain emanating from the inflammatory repair response within the tendon sheath. Inflammation can be thought of as a series of steplike processes, beginning with vasal dilation mediated by histamine, serotonin, and kinins, followed by the appearance of gaps in the endothelial cells, resulting in increased vascular permeability and subsequent local tissue inflammation. Inflammatory cells, such as leukocytes, are drawn to a specified area by a process known as chemotaxis.1,2 Acute inflammation typically lasts hours to days. If the initiating stimuli continues, the inflammatory response will produce a thickened, chronically inflamed tendon sheath. The process of inflammation is perceived as pain through the detection of noxious stimuli by afferent nerve fibers.3 These consist primarily of two fiber types—the unmyelinated, slow-conducting C fibers, which are responsible for dull, aching, or burning-type pain, and the finely myelinated, fast-conducting A gamma fibers, which are important in the perception of joint pain.3 These nerve endings become sensitized to the release of tissue mediators and prostaglandins; inflammatory mediators may moderate the release of neural peptides, all of which are ultimately perceived through peripheral nerves, transported to the central nervous system, and perceived as pain.
Bursitis is an inflammation of the synovial sac, which is generally present at any site at which increased friction may develop. The olecranon, greater trochanter, and patella are three of the common areas in which bursal inflammation may occur. A bursa is located between the superomedial angle of the scapula and the underlying rib cage and may become inflamed as a result of mechanical irritation. Even though bursal tissue is usually located in areas of friction, a bursa may also act as a tendon sheath in some locations. The subacromial and subdeltoid bursa represents the tendon sheath of the rotator cuff and, as such, may be primarily inflamed because of mechanical irritation by the coracoacromial ligament or by anterolateral impingement of the acromion. It may be secondarily inflamed when there is failure within the tendon, manifested as a partial or complete rupture of any of the cuff tendons. It is almost impossible to differentiate clinically rotator cuff bursitis as primary or secondary unless there is adequate biopsy material from the rotator cuff tendon. We think that in the young throwing athlete, the primary entity is a bursitis caused by mechanical impingement from the coracoacromial ligament, without rotator cuff pathology.
Tendinitis, as described by Clancy4,5 and Clement and colleagues,6 is believed to represent devitalization and disruption of tendon fascicles caused by repetitive microtrauma. Some unknown mechanism stimulates an inflammatory response within the tendon sheath; however, no observable inflammatory response appears to be initiated within the tendon. To our knowledge, there have been no biopsy reports of any tendon in patients with a first episode of acute tendinitis. All published pathologic studies have dealt with biopsies of those with chronic tendinitis or biopsies of
BICEPS TENDON Lesions of the biceps tendon are not infrequent about the shoulder, whether related to a single traumatic incident, repetitive microtrauma, or impingement. These lesions can 283
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be divided into three main categories—bicipital tendinitis, primary or secondary, instability of the biceps tendon (subluxation or dislocation), and biceps tendon rupture. DePalma and Callery11 have reported biceps tenosynovitis as the most common cause of shoulder pain and found that it usually coexists with frozen shoulder. Barnes and Tullos12 have reported five cases of bicipital tendinitis and three cases of subluxation of the biceps long head tendon in 56 painful shoulders in baseball players, reiterating its common cause of the painful shoulder. Occasionally, patients with superior labral anterior-posterior (SLAP) lesions, partial- to full-thickness rotator cuff tears, or both, present with biceps tendon pain.
Functional Anatomy of the Biceps The long head of the biceps tendon arises from the supraglenoid tubercle of the scapula and from the superior glenoid labrum of the shoulder joint. The tendon traverses the glenohumeral joint through a synovial extension of the shoulder and leaves the joint in the intertubercular groove deep to the transverse humeral ligament. The muscle then joins the short head arising from the coracoid process and extends down the humerus before reaching a common insertion on the bicipital tuberosity of the radius.13,14 The nerve supply emanates from the musculocutaneous nerve derived from a coalescence of the fifth and sixth cervical nerve roots. The long head appears to assist in depression of the humeral head and further aids in the stabilization of the humeral head in the glenoid. The biceps muscle is important in flexion and supination of the forearm, performing maximally with the elbow flexed at 90 degrees. Cadaveric studies15 have shown that the long head is important in preventing upward migration of the humeral head when the short head is contracted. Kumar and associates15 have noted that an absent long head tendon would allow upward migration of the humeral head when the short head is stimulated; this is believed to be important in fine positioning of the head in the glenoid to improve elbow flexion and supination power. Studies by Rodosky and coworkers16 have noted that the biceps contributes to shoulder stability by resisting external rotation forces that occur in the abducted, externally rotated position, as occurs during the late cocking phase of throwing. Electromyographic studies by Jobe and colleagues17,18 in throwers have noted modest intensity during the cocking phase, with a lessening of activity until ball release, and peak activity occurring during the follow-through phase. The activity is believed to be closely associated with elbow motion (deceleration and forearm pronation) during follow-through and to be important in preventing hyperextension of the elbow.17-20
Biceps Tendinitis Although biceps tendinitis is not uncommon, it is not known whether this is an isolated entity or whether it exists secondary to some other shoulder pathology. DePalma
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and Callery11 have reported biceps tendinitis as the most common cause of shoulder pain, and early literature is replete with articles on the diagnosis and treatment of the primary entity. Neer21-23 has noted the potential for biceps tendinitis in those with impingement and has indicated that biceps tendinitis may be an early sign of impingement. It is our experience that both conditions exist, and we concur with Post and Benca24 that primary biceps tendinitis represents about 5% of all clinical cases. In most cases, the biceps tendinitis appears secondary to mechanical or chemical irritation. Clinical Presentation Typically, the patient will complain of anterior shoulder pain, usually with activity. This may be insidious in onset, follow a single traumatic incident or, as usually occurs in the athletic population, frequently occurs as an overuse phenomenon as a consequence of repetitive microtrauma or secondary to impingement. It may occur as an isolated entity but usually is secondary to some other pathologic process. It is important to note the presence of other shoulder pathologies, particularly rotator cuff pathology, glenohumeral instability,25 impingement, or generalized inflammatory conditions of the shoulder as the cause. We believe that in those patients with chronic rotator cuff tendinitis, the long head of the biceps acts in a prolonged fashion to depress and steer the humeral head and provide more room for the inflamed bursa and cuff. Thus, these patients will be more susceptible to the development of a painful tendinitis-type syndrome. The most common physical examination finding is tenderness to palpation over the bicipital groove.11,24,26,27 Speed’s test26,28 is performed by flexing the shoulder against resistance while the elbow is extended and forearm supinated. A positive test localizes pain to the bicipital groove. Yergason’s sign28,29 is positive when biceps pain results from supination against resistance with the elbow flexed. Both tests can be helpful but are often nonspecific.23 The relation of bicipital tendinitis and frozen shoulder has been described11,26 and must be taken into account during the examination. Also, the possibility of cervical pathology in the patient with shoulder pain and a paucity of physical examination findings must be remembered. Radiographic Evaluations Although radiographs are believed to be of little value,24 several abnormalities have been reported to be associated with biceps tendinitis, including the presence of a supratubercular ridge and shallow bicipital grooves27,30 and any osteophyte or spur formation in or near the groove.11,29 Ahovuo and associates31 have noted that plain radiographs reveal degenerative changes in the walls of the grooves in 50% of patients with bicipital tendinitis. They also indicated that arthrography is helpful for those with dislocated biceps tendons, but that there is no difference in filling of the tendon sheath in patients with surgically verified
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tendinitis compared with those with normal tendons. They also reported on the accuracy of sinography in discerning biceps tendon position and noted that this is a useful technique when the sheath is not visualized by arthrography.32 Magnetic resonance imaging (MRI) has proved useful in delineating the different pathologic entities that may be present in patients with rotator cuff symptoms.33,34 It has proved as accurate as ultrasound for evaluating rotator cuff tendinitis and tendon disruption but is more accurate for diagnosing biceps tendon dislocation.35 Pathology DePalma and Callery11 have reported on gross and microscopic pathologic findings in 86 symptomatic shoulders, noting isolated biceps tendon involvement in 62%; in 38%, this was found to be secondary to a more generalized inflammatory process. The essential pathology is of varying intensity and involves the tendon sheath complex. Grossly, the outer synovial sheath is hemorrhagic and constricted on either side of the transverse humeral ligament. Microscopically, edema, collagen degeneration, increased vascularity, and round cell infiltration are noted. In an operative procedure for refractory bicipital tenosynovitis, Michele29 has noted that an adhesive inflammatory process may actually attach the tendon to the groove, diminishing the effect of the gliding mechanism. In patients diagnosed with bicipital tenosynovitis, Crenshaw and Kilgore26 have noted capillary dilation, edema, and cellular infiltration in acute cases, with tendon fraying, narrowing, and fibrosis in chronic cases. In general, pathologic processes are believed to parallel the duration and severity of clinical symptoms.11,29 In 13 inflammatory tendons in which tenodesis was performed, Dines and coworkers36 have noted varying degrees of inflammation; adhesions and synovitis were found in all patients, with only one grossly irregular groove. In patients with chronic tendinitis, Becker and Cofield9 have noted gross tendon abnormalities in 32 of 38 tendons; however, in contrast to other histologic studies, most tendons were normal, and only one had evidence of tendon inflammation. Biceps Tendon Subluxation and Dislocation Biceps tendon dislocation typically occurs medially, as originally described by Meyer.30 It may occur after a specific traumatic incident, such as a tuberosity fracture, or on a chronic basis associated with rotator cuff pathology. Neer23 has noted that this is unusual in patients younger than 40 years unless in association with a fracture. Clinically, there is no pathognomonic sign,37 but the test of Abbott and Saunders38 may help differentiate biceps tendon dislocation from tendinitis. The test is performed by placing the patient’s arm in full abduction and external rotation, and then slowly brought down to the side. A palpable, audible, or painful click may be felt or heard, which strongly suggests the diagnosis. Frequently, however, the patient will complain of pain and a feeling of snapping in the anterior shoulder. The definitive diagnosis of a subluxating biceps tendon is difficult to make based on examination findings
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but arthrography, ultrasound, and MRI are all helpful in identifying the chronically dislocated tendon. DePalma and Callery11 have reported seven cases of subluxation and dislocation. They discerned the tendon slipping in and out of the groove with abduction and external rotation. Dines and colleagues36 have also reported seven cases diagnosed at the time of biceps tenodesis for localized anterior shoulder pain over the bicipital groove. In cadaveric studies, Slatis and Aalto37 have found that the most important ligament for stabilization is not the transverse humeral ligament but the medial portion of the coracohumeral ligament. Transection of the transverse humeral ligament does not affect stability of the biceps tendon. They also reported five cases of medial dislocation and four cases of subluxation in live patients. In the dislocation patients, the biceps tendon was found displaced medially, lying on the superficial aspect of the subscapularis; they were noted to have associated supraspinatus tears, with involvement of the coracohumeral ligament. The tendon was located in a fascial sling on the ventral aspect of the subscapularis tendon. The four patients with subluxating tendons had limited cuff lesions, and these tendons were located in the groove. Good results were obtained in eight of nine patients when treated by tenodesis and rotator cuff repair when indicated. Petersson39 has reported an incidence of medial dislocation of 6.5% in 77 autopsy dissections. Dislocation was always found to be associated with full-thickness supraspinatus tendon ruptures and with partial- or full-thickness subscapularis tears, allowing the tendon to dislocate deep to the subscapularis muscle. Paulos and associates40 have reported on three unstable tendons after shoulder injuries that usually consisted of a combined distal arm traction and biceps contraction, or a forceful biceps contraction alone, in athletic activity. Two were dislocated superficial to an intact subscapularis and one deep to a partially ruptured subscapularis. Two main mechanisms of dislocation have been described; they generally occur in concert with rotator cuff pathology. The tendon dislocates medially and lies superficial to the subscapularis after coracohumeral ligament rupture, or dislocates after undersurface subscapularis rupture in which the superficial fibers stay attached to the transverse humeral ligament, allowing the tendon to dislocate medially and deep to the subscapularis muscle. Tenodesis is believed to be the treatment of choice, combined with rotator cuff reconstruction when indicated. Nonoperative Rehabilitation Approach The nonoperative treatment of biceps pain is based on the recognition and classification of the pathology. Thus, a differential diagnosis is critical to a successful outcome. We have found biceps pain to have several different causes (Box 23-1).
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BOX 23-1.
• • • • • • •
Potential Causes of Biceps Pain
Biceps tendon instability Peritendinitis (tendinitis) Tendinosis Glenohumeral joint hypermobility Capsular inflammation SLAP lesions Rotator cuff failure
SLAP, superior labral anterior-posterior.
The most common cause of this pain response is tendinosis or tendinitis of the biceps brachii long head tendon. The differential diagnosis is based on the patient’s history (e.g., chronicity of pathology, number of episodes), nature of the pain, elasticity and flexibility of the tendon, and MRI findings. Patients with peritendinitis present with acute onset, no or minimal previous history of symptoms, mild stiffness, and MRI findings that indicate inflammation of the paratenon.5 The treatment of paratendinitis is cryotherapy,41 nonsteroidal anti-inflammatory drugs (NSAIDs), iontophoresis with dexamethasone,42-45 and moderateintensity exercise. The patient is encouraged to restore flexibility and perform light strengthening exercises. The goal of the program is to reduce inflammation, so aggressive exercise is contraindicated. We use the disposable iontophoresis patch (Empi Medical, St. Paul, Minn) for the treatment of biceps paratendinitis (Fig. 23-1). Conversely, the treatment for biceps tendinosis is dramatically different. Its goal is to produce a healing response to the degenerative tendon by increasing circulation to the tendon. Treatment measures include heat, ultrasound, transverse massage, cross-friction massage, eccentric muscle training, flexibility exercises, and a progressive loading program to allow the tendon to respond to the stress. The purpose of the eccentric training is to load the tendinous and musculotendinous junction rather than the muscle belly. The exercise should be progressive in nature, with the goal of loading the tendon to produce collagen synthesis and organization.46 Another cause of biceps tendon pain is capsular inflammation, synovitis, or both. This can be seen in the early stages (I and II) of adhesive capsulitis (see Chapter 24). As noted earlier, with adhesive capsulitis, the biceps tendon sheath often becomes involved, resulting in biceps tenosynovitis.11,29,36 We recommend treating these patients for inflammation with NSAIDs, cryotherapy, iontophoresis, and gentle exercise. During the synovitisinflammatory stage, we encourage frequent bouts of light range-of-motion (ROM), stretching, and flexibility exercises (see Chapter 24 for specific details.)
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Figure 23-1. Disposable iontophoresis patch (Empi Medical, St. Paul, Minn). This patch is used for the treatment of biceps paratendinitis.
Other types of glenohumeral joint lesions that can cause biceps pain include rotator cuff pathologies (e.g., impingement, tendinitis, failure), glenohumeral joint hypermobility, and SLAP lesions. The clinician is encouraged to treat each pathology specifically based on the differential diagnosis.
Long Head Tendon Ruptures Petersson39 has reported 6 cases of long head tendon rupture in 153 cadaver shoulders. In most cases, this is believed to occur in patients older than 40 years23 with a history of shoulder pain suggesting a preexisting rotator cuff lesion. Carroll and Hamilton47 have reported an average age of 51 years in their series of 54 long head ruptures. Rarely does a long head rupture occur in an individual before the fourth decade. If it does, it is frequently the result of a single traumatic incident and may occur at the musculotendinous junction.25 A mechanism of traumatic injury has been described as a forceful biceps contraction during athletic maneuvers with biceps contraction combined with arm traction (gymnastics),40 or the result of a sudden biceps contraction with the arm in external rotation abduction. Neer23 has described three types of biceps long head ruptures that usually occur at the cephalad aspect of the groove. These include rupture with retraction,
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in which the diagnosis is often easily made based on swelling, pain, and the sudden appearance of a “Popeye” muscle. Rupture may also occur with partial recession or self-attachment to the groove or transverse ligament, which makes the diagnosis more difficult because of lack of deformity. We have noted an occasional patient with chronic rotator cuff tendinitis in whom the symptoms are relieved, at least initially, after rupture of the long head. Isokinetic strength testing at 2 years after rupture in 10 patients has revealed no significant loss of elbow flexion strength and only a 10% decrease in elbow supination strength.25 Sturzeneggar and colleagues48 have used isokinetic testing to compare strength in the conservatively treated long head biceps tendon rupture with that in the surgically treated (tenodesis) group; they found that strength decreases by 16% in elbow flexion in the nonoperative group versus 8% in the surgical group. Comparing supination, strength was decreased 11% in the conservative group and 7% in the surgical group. Interestingly, a slight strength loss (4%) of shoulder abduction was noted in the surgical group. There have been reports of rotator cuff tears coexisting with biceps ruptures.22,25 Usually the supraspinatus tear precedes the biceps rupture. As noted, treatment is based on several factors, the most important of which is the presence of preexisting shoulder pain. If pain is present prerupture, an arthrogram is indicated to rule out associated rotator cuff tear. If the arthrogram reveals a tear and pain persists, cuff repair, acromioplasty, and biceps tenodesis are performed. If the arthrogram is negative and the patient accepts the Popeye muscle, nonoperative treatment is indicated. If the patient does not like the cosmetic deformity, tenodesis, acromioplasty, and exploration of the rotator cuff are indicated. Early tenodesis is usually considered for the young athlete only after an acute traumatic incident. Burkhart and Fox49 have reported two cases of long head tendon rupture in young patients associated with significant intra-articular pathology, including labral tears. A loose body and retained biceps tendon stump, resulting in grade IV chondromalacia of the glenoid, were noted in one. Arthroscopy was recommended after acute rupture when surgical tenodesis is chosen or for those patients with persistent symptoms after nonoperative management to rule out significant intra-articular pathology. Recommended Treatment It is our contention that actual cases of primary bicipital tendinitis are rare and that most cases are secondary to underlying shoulder pathology, such as chronic rotator cuff tendinitis, SLAP lesions, or instability. Although biceps tendinitis may be the most prominent symptom at any time during the disease course, careful evaluation of the rotator cuff is mandatory. Conservative treatment consists of a comprehensive exercise program and a short course of oral NSAIDs. Selective injections with a 1% lidocaine and dexamethasone (Decadron) mixture are helpful
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therapeutically and diagnostically. These may be delivered into the subacromial space or biceps tendon sheath or groove, avoiding direct injection of the tendon. Rehabilitation programs to treat the rotator cuff pathologies may be beneficial. Modalities such as iontophoresis42 and cryotherapy have been successful. Performing isolated biceps tenodesis is rarely indicated, with the exception of the previously operated shoulder in which the patient has failed an adequate decompression and continues to have pure shoulder pain consistent with biceps tendinitis. Kelly and associates50 have reported excellent results in 77% of patients who exhibited biceps pain with a biceps tenotomy. The other side effects noted were cosmesis and elbow flexor cramping with exertion. It may be indicated to perform a biceps tenodesis or to make several longitudinal incisions in the long head tendon. These may be carried out in the hope of stimulating a healing response in those with persistent symptoms suggestive of biceps tendinitis, despite being adequately treated for rotator cuff tendinitis with a nonoperative regimen, or in those undergoing arthroscopic decompression. Subluxating or dislocating long head biceps tendons are not common clinically, particularly in the young, active athletic population. This usually occurs in combination with rotator cuff tears and, if tenodesis becomes necessary, it is usually combined with decompression and rotator cuff reconstruction. Although long head ruptures are also rare in the young athlete, an aggressive surgical approach is indicated for some of these patients. In the older athlete, long head ruptures are usually treated early with oral NSAIDs and an aggressive functional rehabilitation program. However, in patients with persistent shoulder pain or weakness, an arthrogram or MRI scan should be obtained; if a partial- or full-thickness rotator cuff tear exists, an arthroscopic evaluation, rotator cuff repair, tenodesis, and acromioplasty should be considered.
PECTORALIS MAJOR RUPTURES Anatomy and Function The pectoralis major originates from the clavicle and sternum, courses laterally, and is invested by the pectoral fascia as it forms the anterior axillary fold. It has clavicular, sternocostal, and abdominal portions; the sternocostal is the largest. The fibers converge to insert on the crest of the greater tuberosity of the proximal humerus.13,14 The muscle functions in flexion and adduction and assists in internal rotation of the humerus and, to a lesser extent, elevation and depression of the shoulder. Marmor and colleagues51 have studied strength differences between arms in a patient with a congenital absence of the pectoralis major, noting the primary strength loss in adduction and internal rotation of the humerus. Innervation is by the lateral and
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medial pectoral nerves. Electromyographic studies of the throwing shoulder17,18,52 report that the pectoralis major becomes active in the late cocking phase, when external rotation reaches its maximum. Activity continues in the muscle in concert with the latissimus dorsi during the acceleration phase (internal rotation and adduction); activity decreases during follow-through. The pectoralis major is of primary importance in producing ball velocity.52
Causative Factors Marmor and associates51 have noted that pectoralis major ruptures are rare. They postulated that because of its unique anatomy, rupture must be a result of trauma to a normal tendon. They studied load velocity curves in healthy muscles and found that muscle can hold four times as much as it can lift. They postulated that rupture in a healthy athlete is caused by application of excessive weight when the muscle is already holding at its maximum power. As reported by McMaster,53 under heavy loads, rupture would occur at the tendon insertion or musculotendinous junction and not through a healthy tendon. The age range reported is from infancy to 72 years54; The median age, excluding infants, is 30 years, with a peak age between 20 and 30 years. The most common cause of rupture is improper muscle coordination during heavy lifting, as occurs during violent involuntary contractions caused by excessive muscle tension; in two studies, all patients were male.54-56 Complete ruptures usually occur at the tendinous insertion. Partial ruptures may occur at the musculotendinous junction or within the muscle belly itself.49 Tendinitis of the pectoralis major insertion is no doubt more common than rupture but, because of the benign nature of the injury and excellent response to nonoperative treatment, few studies have been done.
present. Effort to contract against resistance is painful and accentuates the defect. A visible palpable defect in the lower fibers of the pectoralis muscle adjacent to the deltopectoral interval may be present, but this is not believed to be a reliable sign, because a fascial covering may remain intact and feel remarkably similar to an intact tendon.56 The most reliable clinical test is to have the patient place both hands on his or her lateral iliac crest and then push inward (Fig. 23-3). One can then readily palpate the combined tendon of the sternal and clavicular portions and compare it with the opposite noninjured side. Partial ruptures, although not common, appear in our experience to be equal to complete ruptures in incidence (Fig. 23-4). This latter entity is often missed or misdiagnosed but, with the clinical tests described earlier, is more easily discovered. Chest x-ray may show a loss of the normal axillary tendon shadow.51,54,56 MRI may prove to be the best available diagnostic test in the future.
Figure 23-2. Patient referred with a presumed diagnosis of proximal long head of biceps rupture based on location of the ecchymosis. This location is commonly seen in pectoralis major ruptures.
Chadwick57 has reported two cases of insertional tendinitis manifesting as a suspicious humeral lesion at the insertion site, necessitating biopsy. Pathology was consistent with benign inflammation and tendon degeneration, indicating that the diagnosis does exist. Whether insertional tendinitis or tendinosis is a common precursor to rupture is a matter of conjecture.
Presentation The typical presenting complaint is a sudden sharp pain in the upper arm or shoulder53 during an exertional athletic maneuver or a fall. An audible snap or pop may be heard.55 On examination, ecchymosis is common over the lateral chest wall, axilla, or proximal humerus (Fig. 23-2). Hemorrhage may occur almost entirely over the area of the biceps muscle, suggesting a possible proximal biceps rupture, particularly when the individual has pain with resisted arm flexion. A bulge of the anterior chest wall on flexion and pain and weakness on adduction internal rotation are
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Figure 23-3. Asymmetrical pectoralis major muscles consistent with partial rupture. A complete rupture usually shows a more dramatic asymmetry.
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289
SNAPPING SCAPULA SYNDROME
Figure 23-4. Palpation of the pectoralis major tendon. This is key to a successful examination.
Treatment Although satisfactory results can be obtained in the non– high-profile, non–weight-lifting athlete with nonoperative treatment, surgical repair is otherwise necessary and has been proved successful.54-56 The chosen method of treatment depends not only on the activity level and age of the patient, but on the location of the tear and the ability of the patient to accept a cosmetic defect. Proximal injuries at the muscle tendon junction—probably rare—respond favorably to nonoperative treatment, but distal lesions are best treated surgically.56 Zeman and coworkers56 have reported on nine ruptures. The average patient age was 30 years. Seven were believed to be caused by excessive muscle tension. The five patients treated nonoperatively could not return to their previous athletic activity levels, but the four patients treated surgically had excellent results and all were able to return to their prior activity levels. Kretzler and Richardson58 have reported operative treatment of 16 ruptures treated up to 5.5 years postinjury. All 16 had good pain relief; 13 reported full, subjective strength return. Recommended Treatment Our experience is consistent with that of others in that most ruptures occur during violent muscle contraction, such as bench pressing or lifting heavy objects. The diagnosis can usually be made on the basis of a typical history and physical examination findings, although MRI may prove helpful in difficult cases. We are aggressive in recommending repair for the young athletic population. Most tears occur at the tendinous insertion and are readily repaired to the original insertion sites through a bony trough, with consistently good results. Bone-implanted suture devices can facilitate the repair process.
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This uncommon but significant disorder affecting the shoulder region is frequently confused with myofascitis and seldom recognized. The scapula is the site of origin of rotator cuff musculature, and the scapulothoracic joint is an important contributor to shoulder motion. As noted by Milch,59 the snapping scapula is not uncommon but is usually neglected; patients are often described as neurotic and are rarely referred to an orthopedist for evaluation. Causes of the snapping scapula are believed to include an abnormal superior scapular angle, tumorous conditions, particularly osteochondromas, and changes consistent with interstitial fibrosis in the surrounding musculature.32 A series of five cases resulting from subscapular exostoses has been reported.60 Four cases caused by scapulothoracic bursitis at the inframedial scapular border in professional baseball pitchers have been reported.61 Three subsequent cases at the superior medial angle have been described in manual laborers, citing repetitive trauma as a possible cause.62 It has been our experience that the undersurface of the superior medial angle may be more rounded and somewhat thicker than normal, subsequently rubbing over the posterior upper thoracic ribs to produce a painful bursitis, and perhaps a periostitis.
Clinical Presentation The patient usually presents with neck pain but, on questioning, can pinpoint the pain to the general area of the insertion of the trapezius and rhomboid muscles at or near the superior angle of the scapula. Often, the patient may also complain of a painful snapping or grating over the superior medial scapular angle. These symptoms are made worse with overhead rotation of the arm, which produces scapular compression over the posterior ribs. On physical examination, the painful area can usually be localized to this area, and often a palpable audible snapping or popping sensation can be elicited, particularly when the examiner applies compression to the superior scapula during the overhead motion. This frequently will produce a grating sound, which may be caused by compression of the bursa or by the scapula grating over the ribs. This can usually be differentiated from myofascitis (trigger point) in that the maximal area of tenderness is not at the scapular angle but is localized to a small area in the trapezius muscle in the case of myofascitis. A local injection of xylocaine or bupivacaine (Marcaine) under the superior medial edge of the scapula should render the area almost completely asymptomatic, even with overhead motion and compression applied to the superior medial angle of the scapula. Plain radiographs are usually normal.61 The importance of obtaining oblique views60 and a computed tomography (CT) scan62 have been reported; CT scanning is now the procedure of choice, particularly when bony lesions are suspected.
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Treatment This syndrome is occasionally seen in pitchers, throwers, and golfers acutely or subacutely. Initial treatment consists of differentiating it from the more commonly occurring muscle strain and myofascitis. If the diagnosis is consistent with snapping scapula, the primary entity is probably a bursitis, and treatment consists of active rest, combined with oral NSAIDs and occasional injections. In resistant pain, particularly if the problem is secondary to an exostosis, surgical treatment can be offered. Milch59 has reported that simple removal of small parts of the scapula will predictably result in a cure. Surgical Therapy Parsons60 has reported four cases resulting from exostoses that were successfully treated surgically. Sisto and Jobe61 have reported four bursal excisions at the inferomedial angle, allowing four professional pitchers to return to their prior levels of competition. Richards and McKee62 have reported three successful outcomes after resection of the superior medial angle of the scapula in laborers, and Arntz and Matsen63 have reported satisfactory outcomes in 12 of 14 patients after superior medial angle resection. Nonoperative Treatment The nonoperative treatment of snapping scapula is focused on correcting the patient’s postural adaptations after patients exhibit anterior tilting and retracted posture. Stretching and strengthening exercises are encouraged. The purpose of this program is to reduce the inflammation of the bursa and restore mobility of the scapulothoracic joint through soft tissue and joint mobilization techniques. The patient is encouraged to restore proper posture with an emphasis on scapular refraction, posterior tilting, and external rotation. Stretching of the pectoralis minor and major is performed with scapular refraction and posterior tilting exercises. Physiotaping, bracing, or both may be beneficial. The patient is encouraged to perform rotator cuff and shoulder strengthening exercises. The patient is instructed to restore shoulder motion but not perform repetitive work or sport movement over the head, allowing the inflammation to reduce. Recommended Treatment We have seen several cases, usually of a chronic nature, within the past several years. None of these patients had an exostosis or osteochondroma. Initial treatment consists of rest, oral anti-NSAIDs, and injections. Proper injection technique is important because of the proximity to the posterior thoracic wall and pleural cavity. After applying a sterile preparation, a 22-gauge 1.5-inch needle with 1% lidocaine and dexamethasone is introduced, angling from cephalad to caudad at a 45-degree angle just off the superior medial tip of the scapula, because the bursa is usually approximately 2 cm lateral to the superior medial angle.
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Conservative treatment consists of gentle active assisted ROM exercises and isometric shoulder and scapular strengthening, progressing to isotonic strengthening. Once the patient has accomplished full nonpainful motion and strength equal to those of the opposite side, a return to sport is allowed. If conservative treatment fails, surgery is indicated if so desired by the patient. The technique62 consists of making a curved 4-cm incision over the superior medial angle. The fascia is divided longitudinally and the trapezius is split in line with its fibers. The levator and subscapularis attachments are elevated subperiosteally off the angle. A large malleable retractor is placed beneath the tip to protect the posterior chest wall. A 1-inch osteotome is used to remove the tip, which consists of a 3- ⫻ 1.5-cm area of bone. The edges are trimmed with a rongeur and the bursal tissue is excised. The wound is closed in routine fashion. The results are predictably good in our limited experience. Early functional rehabilitation is begun immediately postsurgery, and it is essentially similar to that used for an arthroscopic shoulder decompression.
QUADRILATERAL SPACE SYNDROME The quadrilateral space is defined as the area bounded medially by the long head of the triceps, laterally by the humerus, superiorly by the teres minor, and inferiorly the teres major, through which pass the axillary nerve and posterior circumflex humeral artery.14 Quadrilateral space syndrome was originally described by Cahill and Palmer64 in 1983. The syndrome typically occurs in young active adults between the ages of 22 and 35 years. It usually is not associated with any history of shoulder trauma. A patient complains of insidious onset of pain and nondermatomal, nonradiating paresthesias in the involved shoulder. A throwing athlete may complain of early fatigue, weak abduction, a numb shoulder, or dead arm– type syndrome.64 Physical examination reveals tenderness consistently over the involved quadrilateral space, and symptoms may be reproduced with abduction and external rotation of the arm. The cause is believed to be tethering of the neurovascular structures by obliquely oriented fiber bands in the quadrilateral space. Electromyographic and nerve conduction velocity studies are not helpful in making the diagnosis and are usually normal. Arteriographic evidence of posterior circumflex arterial occlusion and the associated axillary nerve compression, combined with a typical history and physical examination findings, are believed to be diagnostic. The importance of proper angiographic technique to visualize the posterior circumflex humeral artery with the arm at the side and in the abduction–external rotation position has been stressed.65 As noted by Cahill and
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Palmer,64 70% of patients in their series had symptoms that did not warrant surgery, and alteration of pitching mechanics may prove beneficial in symptom relief. In those resistant to nonoperative treatment methods, 18 patients were treated surgically; 16 of 18 improved with surgical decompression.
SUMMARY There are numerous soft tissue lesions about the shoulder that can cause the patient to experience significant shoulder pain. Most of these lesions can be successfully treated with nonoperative treatment regimens. The team approach—the team is comprised of the physician, physical therapist, and athletic trainer—is critical for successful treatment. The differential diagnosis must be communicated to the treatment team; a specific and differential diagnosis is vital to successful treatment. Based on the differential diagnosis and identification of all involved tissues, a well-designed rehabilitation program must be established. If the nonoperative approach fails and does not meet the functional demands of the patients, surgical intervention may be indicated. Nonoperative and operative treatment modalities have been discussed in this chapter.
References 1. Ryan GB: Inflammation.. Kalamazoo, Mich, Upjohn, 1977. 2. Schurman DJ, Goodman SB, Smith RL: Inflammation and tissue repair. In Leadbetter WB, Buckwalter JA, Gordon SL (eds): Sports-Induced Inflammation. Chicago, American Academy of Orthopaedic Surgeons, 1990, pp 277. 3. Hargreaves KM: Mechanisms of pain sensation resulting from inflammation. In Leadbetter WB, Buckwalter JA, Gordon SL (eds): Sports-Induced Inflammation. Chicago, American Academy of Orthopaedic Surgeons, 1990, pp 383. 4. Clancy WG Jr: Specific rehabilitation for the injured recreational runner. Instr Course Lect 38:483, 1989. 5. Clancy WG Jr: Tendon trauma and overuse injuries. In Leadbetter WB, Buckwalter JA, Gordon SL (eds): SportsInduced Inflammation. American Academy of Orthopaedic Surgeons, Chicago, 1990, pp 609. 6. Clement DB, Taunton JE, Smart GW: Achilles tendinitis and peritendinitis: Cause and treatment. Am J Sports Med 12:179, 1984. 7. Nirschl RP: Patterns of failed healing in tendon injury. In Leadbetter WB, Buckwalter JA, Gordon SL (eds): SportsInduced Inflammation. Chicago, American Academy of Orthopaedic Surgeons, 1990. 8. Nirschl RP: Rotator cuff tendinitis: basic concepts of pathocause. Instr Course Lect 38:439, 1989. 9. Becker DA, Cofield RH: Tenodesis of the long head of the biceps brachii for chronic bicipital tendinitis. J Bone Joint Surg Am 71:376, 1989. 10. Puddu G, Ippolito E, Postacchini F: A classification of achilles tendon disease. Am J Sports Med 4:145, 1976.
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11. DePalma AF, Callery GE: Bicipital tenosynovitis. Clin Orthop 3:69, 1954. 12. Barnes DA, Tullos HS: An analysis of 100 symptomatic baseball players. Am J Sports Med 6:62, 1978. 13. Netter F: The Ciba Collection of Medical Illustrations, vol 8, part 1. Anatomy of the Musculoskeletal System. West Caldwell, NJ, Ciba-Geigy, 1987. 14. Romanes GJ: Cunningham’s Textbook of Anatomy. New York, Oxford University Press, 1981. 15. Kumar VP, Satku K, Balasubramaniam P: The role of the long head of biceps brachii in the stabilization of the head of the humerus. Clin Orthop 244:172, 1989. 16. Rodosky MW, Harner CD, Rudert MJ, et al: The role of the biceps-superior glenoid labrum complex in anterior stability of the shoulder. Orthop Trans 15:58, 1991. 17. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the shoulder in throwing and pitching. Am J Sports Med 11:3, 1983. 18. Jobe FW, Moynes DR, Tibone JE, Perry J: An EMG analysis of the shoulder in pitching—a second report. Am J Sports Med 12:218, 1984. 19. Abrams JS: Special shoulder problems in the throwing athlete: Pathology, diagnosis, and nonoperative management. Clin Sports Med 10:839, 1991. 20. Andrews JR, Carson WG Jr, McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337, 1985. 21. Neer CS II: Anterior acromioplasty for the chronic impingement syndrome in the shoulder. J Bone Joint Surg Am 54:41, 1972. 22. Neer CS II: Impingement lesions. Clin Orthop 173:70, 1983. 23. Neer CS II: Cuff tears, biceps lesions, and impingement. In Neer CS II (ed): Shoulder Reconstruction. WB Saunders, Philadelphia, 1990, pp 62-__. 24. Post M, Benca P: Primary tendinitis of the long head of the biceps. Clin Orthop 246:117, 1989. 25. Warren RF: Lesions of the long head of the biceps tendon. Instr Course Lect 34:204, 1985. 26. Crenshaw AH, Kilgore WE: Surgical treatment of bicipital tenosynovitis. J Bone Joint Surg Am 48:1496, 1966. 27. Hitchcock HH, Bechtol CO: Painful shoulder—observations on the role of the tendon of the long head of the biceps brachii in its causation. J Bone Joint Surg Am 30:263, 1948. 28. Simon WH: Soft tissue disorders of the shoulder—frozen shoulder, calcific tendinitis, and bicipital tendinitis. Orthop Clin North Am 6:521, 1975. 29. Michele AA: Bicipital tenosynovitis. Clin Orthop 18:261, 1960. 30. Meyer AW: Spontaneous dislocation of the tendon of the long head of the biceps brachii. Arch Surg 13:109, 1926. 31. Ahovuo J, Paavolainen P, Slatis P: Radiographic diagnosis of biceps tendinitis. Acta Orthop Scand 56:75, 1985. 32. Ahovuo J, Paavolainen P, Slatis P: Diagnostic value of sonography in lesions of the biceps tendon. Clin Orthop 202:184, 1986. 33. Iannotti JP, Zlatkin MB, Esterhai JL, et al: Magnetic resonance imaging of the shoulder. J Bone Joint Surg Am 73:17, 1991. 34. Nelson MC, Leather GP, Nirschl RP, et al: Evaluation of the painful shoulder. J Bone Joint Surg Am 73:707, 1991. 35. Vellet AD, Munk PL, Marks P: Imaging techniques of the shoulder: Present perspectives. Clin Sports Med 10:721, 1991.
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36. Dines D, Warren RF, Inglis AE: Surgical treatment of lesions of the long head of the biceps. Clin Orthop 164:165, 1982. 37. Slatis P, Aalto K: Medial dislocation of the tendon of the long head of the biceps brachii. Acta Orthop Scand 50: 73, 1979. 38. Abbott LC, Saunders JB: Acute traumatic dislocation of the tendon of the long head of the biceps brachii. A report of six cases with operative findings. Surgery 6:817, 1939. 39. Petersson CJ: Spontaneous medial dislocation of the tendon of the long biceps brachii—an anatomic study of prevalence and pathomechanics. Clin Orthop 211:224, 1986. 40. Paulos LE, Grauer JD, Smutz WP: Traumatic lesions of the biceps tendon, rotator cuff interval, and superior labrum. Orthop Trans 15:85, 1991. 41. Knight KL: Cryotherapy: Theory, Technique, and Physiology. Chattanooga, Tenn, Chattanooga Corporation, 1985. 42. Nowicki KD, Hummer CD, Heidt RS, Colosimo AJ: Effects of iontophoretic versus injection administration of dexamethasone. Med Sci Sports Exerc 34:1294, 2002. 43. Bertolucci LE: Introduction of anti-inflammatory drugs by iontophoresis: Double-blind study. J Orthop Sports Phys Ther 4:103, 1982. 44. Delacerda FG: A comparative study of three methods of treatment for shoulder girdle myofascial syndrome. J Orthop Sports Phys Ther 4:52, 1982. 45. Harris PR: Iontophoresis: Clinical research in musculoskeletal inflammatory conditions. J Orthop Sports Phys Ther 4:109, 1982. 46. Langberg H, Ellingsgaard T, Madsen J, et al: Eccentric rehabilitation exercise increases peritendinous type I collagen synthesis in humans with Achilles tendinosis. Scand J Med Sci Sports 17:61-66, 2007. 47. Carroll RE, Hamilton LR: Rupture of biceps brachii—a conservative method of treatment. J Bone Joint Surg Am 49:1016, 1967. 48. Sturzeneggar M, Beguin D, Grunig B, Jakob RP: Muscular strength after rupture of the long head of the biceps. Arch Orthop Trauma Surg 105:18, 1986. 49. Burkhart SS, Fox DL: SLAP lesions in association with complete tears of the long head of the biceps tendon: A report of two cases. J Arthrosc Relat Surg 8:31, 1992.
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50. Kelly AM, Drakos MC, Fealy S, et al: Arthroscopic release of the long head of the biceps tendon: Functional outcome and clinical results. Am J Sports Med 33:208, 2005. 51. Marmor L, Bechtol CO, Hall CR: Pectoralis major muscle— function of sternal portion and mechanism of rupture of normal muscles: Case reports. J Bone Joint Surg Am 43: 81, 1961. 52. Bradley JP, Tibone JE: Electromyographic analysis of muscle action about the shoulder. Clin Sports Med 10:789, 1991. 53. McMaster PE: Tendon and muscle ruptures. Clinical and experimental studies on the causes and location of subcutaneous ruptures. J Bone Joint Surg 15:705, 1933. 54. Park JY, Espiniella JL: Rupture of pectoralis major muscle— a case report and review of literature. J Bone Joint Surg Am 52:577, 1970. 55. McEntire JE, Hess WE, Coleman SS: Rupture of the pectoralis major muscle—a report of eleven injuries and review of fifty-six. J Bone Joint Surg Am 54:1040, 1972. 56. Zeman SC, Rosenfeld RT, Lipscomb PR: Tears of the pectoralis major muscle. Am J Sports Med 7:343, 1979. 57. Chadwick CJ: Tendinitis of the pectoralis major insertion with humeral lesions—a report of two cases. J Bone Joint Surg Br 71:816, 1989. 58. Kretzler HH Jr, Richardson AB: Rupture of the pectoralis major muscle. Am J Sports Med 17:453, 1989. 59. Milch H: Partial scapulectomy for snapping of the scapula. J Bone Joint Surg Am 32:561, 1950. 60. Parsons TA: The snapping scapula and subscapular exostoses. J Bone Joint Surg Br 55:345, 1973. 61. Sisto DJ, Jobe FW: The operative treatment of scapulothoracic bursitis in professional pitchers. Am J Sports Med 14:192, 1986. 62. Richards RR, McKee MD: Treatment of painful scapulothoracic crepitus by resection of the superomedial angle of the scapula—a report of three cases. Clin Orthop 247:111, 1989. 63. Arntz CT, Matsen FA: Partial scapulectomy for disabling scapulo-thoracic snapping. Orthop Trans 14:552, 1990. 64. Cahill BR, Palmer RE: Quadrilateral space syndrome. J Hand Surg 8:65, 1983. 65. Redler MR, Ruland LJ III, McCue FC III: Quadrilateral space syndrome in a throwing athlete. Am J Sports Med 14:511, 1986.
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CHAPTER 24 Adhesive Capsulitis
of the Shoulder E. Lyle Cain, Stephen M. Kocaj, and Kevin E. Wilk
Adhesive capsulitis is a condition of global shoulder motion loss that has been referred to by several names, including periarthritis, pericapsulitis, obliterative subdeltoid bursitis, humeroscapular periarthritis, adhesive capsulitis, bicipital tenosynovitis, and “check rein” shoulder. In 1934, Codman described frozen shoulder as a“pattern of glenohumeral stiffness difficult to define, difficult to treat, and difficult to explain from the point of view of pathology.”1 Nevasier later defined adhesive capsulitis as a “chronic inflammatory process involving the capsule, causing a thickening and contracture, which secondarily becomes adherent to the humeral head.”2 The Shoulder and Elbow Society Consensus in 1992 defined frozen shoulder syndrome as a “condition of uncertain etiology characterized by significant restriction of both active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder.” Shoulder rangeof-motion deficit may be seen after injury, trauma, or postsurgical conditions; however, the post-traumatic or postsurgical stiff shoulder differs from adhesive capsulitis, which is usually idiopathic in onset. Adhesive capsulitis is global limitation of active and passive glenohumeral motion resulting from contracture and loss of compliance of the glenohumeral joint capsule. It is caused by intra-articular pathology (capsular contracture), whereas post-traumatic or postsurgical motion deficit is generally caused by extra-articular adhesions or pathology and intra-articular adhesions, rather than solely intraarticular capsular thickening as seen in adhesive capsulitis.
typical age at onset is between 40 and 70 years (mean, 56). It occurs in women more often than men and there is a questionable increased occurrence in the nondominant upper extremity. Patient who have sedentary occupations tend to be more at risk than manual laborers. Interestingly, the diabetic population is more frequently afflicted by this condition than their nondiabetic counterparts. It has been suggested that from 10% to 35% of diabetics will experience adhesive capsulitis during their lifetime.7,8 In addition, bilateral disease is also more common in the diabetic population (30%), especially if the patient has been insulin-dependent for longer than 10 years. Adhesive capsulitis syndrome may antedate the onset of diabetic disease in what has been termed limited joint motion syndrome. The age at onset in this population is often earlier than that of the standard population, and it has been commonly associated with the early skin changes pathognomonic of the diabetic process. The pathophysiology of adhesive capsulitis has been described by Rodeo and colleagues9 as being cytokinemediated. In their study, it was found that cytokines such as transforming growth factor  (TGF-) and plateletderived growth factor (PDGF) may play a role. However, it was concluded that “although the etiology of the stiffness that results in capsular fibrosis remains elusive, our understanding of its pathogenesis is increasing.”9
The mainstay of adhesive capsulitis is nonoperative rehabilitation, with a focus on physical therapy. The rehabilitation approach should vary based on the stage of adhesive capsulitis presented by the patients. In this chapter, we will discuss pathogenesis, differential diagnosis, and various treatment options.
In 1995, Bunker and associates10 described the pathology of the adhesive capsulitis as being similar to that found in Dupuytren’s disease. They compared the histologic findings of 12 patients who underwent open capsular release for adhesive capsulitis with those of 6 patients who underwent surgery for Dupuytren’s contracture in the hand. The histologic and immunocytochemical findings showed that the pathologic process is active fibroblastic proliferation, accompanied by some transformation to a smooth muscle phenotype (myofibroblasts). No inflammation and no synovial involvement were found.
CAUSATIVE FACTORS AND PATHOGENESIS The cause of adhesive capsulitis syndrome still remains unclear. Several proposed mechanisms include autoimmune, inflammatory, fibrogenic, and psychogenic origins.2-6 Diseases associated with adhesive capsulitis include diabetes, thyroid disease, rheumatoid arthritis, scleroderma, cardiovascular disease, and regional sympathetic dystrophy.
DIAGNOSIS The diagnosis of adhesive capsulitis syndrome is made clinically. Diagnostic criteria include a history of restricted shoulder motion without a previous major injury or reconstructive surgery and an examination that demonstrates
Adhesive capsulitis syndrome has been reported to have an incidence of 2% to 5% in the general population. The 293
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global shoulder stiffness. Radiologic examination demonstrates normal cartilaginous and periarticular surfaces. Adhesive capsulitis syndrome involves a spectrum of disease that has been characterized by four stages. Stage I, or the painful stage, occurs at the onset and can last up to 3 months. There is pain in the involved extremity with active and passive motion, with normal motion early followed by mild limitation in global motion, including flexion, abduction, and rotation. Examination under anesthesia is normal or shows minimal loss of range of motion. Arthroscopic evaluation shows diffuse synovitis and capsular erythema, with pathology demonstrating hypertrophic and hypervascular synovitis. The main presentation of this stage is synovitis and no capsular tightness; motion loss is caused by pain. Stage I is often misdiagnosed as some other shoulder pathology, most commonly subacromial impingement syndrome. However, surgical treatment with subacromial decompression does not resolve the pain, the patient often loses more motion, and pain worsens postoperatively. Stage II is the adhesion stage and occurs between 3 and 6 months. There is severe pain with active and passive motion. During this phase, pain is present both from synovitis and from the capsule beginning to become adherent to the humerus. Global motion is limited, often with progressive severe loss in all planes. Examination under anesthesia shows limited passive range of motion equal to awake passive and active motion, with a tight capsular end feel and difficulty with attempts to improve the motion passively. Arthroscopy shows diffuse, thick synovitis. Pathology demonstrates hypertrophic and hypervascular synovitis. Stage III is the frozen stage, and occurs between 6 and 12 months. Patients experience pain at the extremes of motion, but have generally recovered from the severe pain of the painful and freezing stages. There is a marked limitation in global motion, with a rigid end point. Examination under anesthesia shows range of motion equal to awake values, with a rigid capsular end feel. Arthroscopy demonstrates fibrotic synovium and pathology demonstrates burned out synovitis and dense scar. Additionally, during this phase, the inferior capsule has loosened it adhesion. Stage IV is the chronic or thawing stage, which occurs between 15 and 24 months. There is a gradual increase in range of motion, with a concomitant decrease in pain. Pathology continues to show a burned out synovitis and dense scar. Because many disorders may manifest with shoulder pain, a thorough physical and shoulder examination will aid in the diagnosis of adhesive capsulitis syndrome. The most important aspect of the physical examination while evaluating a patient for a frozen shoulder is determination of active and passive range of motion of the glenohumeral joint while stabilizing the scapula to prevent scapulothoracic motion.
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During the third stage, active and passive range of motion will be the same, with a rigid end point, whereas many other pathologic shoulder conditions manifest with limited active motion and normal passive motion. It is important to perform a thorough examination of the cervical spine to rule out a source of referred pain that may be manifest in the shoulder. Strength of the rotator cuff and shoulder girdle muscles is generally not affected. However, patients may appear to have weakness at the extremes of motion because of pain. Imaging studies can be an important tool for the diagnosis of adhesive capsulitis syndrome by ruling out other possible causes of shoulder pain. Standard shoulder radiographs can determine the presence of arthritis or prior trauma, which can be a source of pain that leads to decreased joint motion. In addition, cervical spine radiographs are useful for determining a cervical origin of shoulder pain, such as stenosis, degenerative disc disease, arthritis, and fracture. Magnetic resonance imaging (MRI) studies are generally not helpful for demonstrating primary frozen shoulder, but can assist in determining the presence of a rotator cuff tear that may lead to decreased shoulder motion and a secondary frozen shoulder. Later in the process of adhesive capsulitis (stage II or III), MRI may demonstrate global loss of shoulder volume and obliteration of the axillary recess.11
TREATMENT The natural history of adhesive capsulitis syndrome is generally reported to be gradual resolution, with a return of range of motion and a decrease in pain in the involved shoulder. However, several studies have shown that persistent deficits are often seen at long-term follow-up.12,13 Shaffer and coworkers13 have evaluated patients who experienced adhesive capsulitis syndrome at long-term follow-up. They examined 97 patients with primary (idiopathic) frozen shoulders at 7 years’ follow-up. Only 62 patients were available for examination; 60% of them continued to have some restricted range of motion at long-term follow-up, and most of this occurred with external rotation. Mild functional limitations were reported by 11%; none reported limitations greater than mild. Pain resolved at an average of 6 months. The time from onset of symptoms to resolution of pain and stiffness averaged 12 months. Treatment for adhesive capsulitis syndrome should always begin with conservative measures. Clinical decision making plays an important role, because many patients with a frozen shoulder present to their physician with other diagnoses. Patients often have had partial treatment elsewhere and it is sometimes difficult to decide where in the treatment algorithm patient care should begin. A regimen of physical therapy and nonsteroidal anti-inflammatory drugs (NSAIDs) is initiated primarily. The exact physical therapy regimen is discussed later.
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The use of intra-articular steroid injections may be warranted. Reports vary on the results of steroid injections for the treatment of adhesive capsulitis syndrome, but these may be useful for select patients for temporary benefit to allow participation in a stretching program. Steroid injection in diabetics must be used carefully because it can elevate blood glucose levels.
Physical Therapy Rehabilitation The mainstay of treatment of adhesive capsulitis is physical therapy and nonoperative rehabilitation. The treatment of this pathology is based on the accurate identification of the disorder and classification of the stage of adhesive capsulitis. The differential diagnosis of adhesive capsulitis is based on several typical clinical signs and symptoms. Most patients present with a capsular pattern—external rotation is not limited, followed by a limit in abduction, with internal rotation being the least limited.14 Second, patients exhibit a restriction in inferior accessory glenohumeral gliding, followed by an anterior restriction. The patient’s end feel pain and resistance from end feel are also important to determine the stage of adhesive capsulitis.14 Finally, the gold standard, as discussed by Neviaser,4 is an arthrogram. If the inferior capsule is drawn up and adhering to the anatomic neck of the humerus, the differential diagnosis of adhesive capsulitis is made. The approach to treatment for adhesive capsulitis is different than that for a patient who exhibits a stiff and painful shoulder. The nonoperative rehabilitation program is based on the stage of the lesion and characteristics of each stage (Boxes 24-1 and 24-2). Stage I, adhesive capsulitis, is typically identified by the patient exhibiting moderate pain
BOX 24-1. Treatment Based on Stage of Adhesive Capsulitis
Stage I: Preadhesive stage (synovial inflammation, minimal or no limitation of motion) • Easy frequent light motion Stage II: Acute adhesive capsulitis (synovitis, early adhesions) • Sustained stretching—prolonged stretches (light) Stage III: Maturation stage (loss of axillary fold, decreased synovitis) • Inferior capsular stretches, LLLD stretches Stage IV: Chronic stage (mature adhesions, restrictions) • Prolonged LLLD stretching
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BOX 24-2. Specific Treatment Techniques Based on Adhesive Capsulitis Stages
Stage I: Painful Inflammatory Stage • • • • • • • • •
Moist hot packs AAROM with L bar Pendulum exercises Single-plane mobilization (I-III) Soft tissue mobilization Postural exercises, stretching, corrections Stretching techniques (physiologic, CR, HR) Midrange submaximal isometrics Home program (10-12 times daily) • Motion frequently during the day • Light motion
Stage II: Acute Adhesion with Synovitis Stage • • • • • • • • •
Active warm-up AAROM exercises Single-plane, end-range mobilizations (III, IV) Stretching (physiologic, CR, HR) End-range stretching End-range submaximal isometrics Self-capsular stretching Postural corrections and soft stretching Home program (8-10 times daily) • Frequent stretching and ROM exercises • Sustained stretch at end range
Stage III: Maturation Adhesion Stage • • • • • • • • • • •
Heat Active warm-up (AAROM, UBE) LLLD stretch with concomitant superficial heat Aggressive joint mobilization Single multiplanar glides and combined glides Joint mobilization—emphasize inferior glides CR, HR stretching Self-joint mobilization at home Sustained stretching at home (TERT principle) Strengthening (PNF) exercises Home program (4-6 times daily) Keep it moving
Stage IV: Chronic Adhesion Stage • Continue all treatments listed (see above) • During this phase, emphasize • Oblique and multiplanar mobilizations • Sustained LLLD stretching • Use of home LLLD device for 15-min sessions (4 times daily) • Inferior mobilizations • Postural exercises and stretching
AAROM, active-assisted range of motion; CR, contract relax; HR, hold relax; LLLD, low-load, long-duration; PNF, proprioceptive neuromuscular fasciculation; TERT, total end-range time; UBE, upper body ergometer.
LLLD, low-load, long-duration.
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caused by synovitis and a loss of motion because of pain. No mechanical tightness is present. During this stage, the physical therapy treatment plan is focused on reducing inflammation and encouraging the patient to perform light motion of the shoulder frequently during the day. The patient is often placed on NSAIDs and other modalities for pain and inflammation. The patient is instructed to move the shoulder in a light and easy manner to maintain motion, and is encouraged to perform these exercises for 5 to 10 minutes, at least 8 to 10 times daily. Aggressive stretching and exercise are not encouraged because of the synovitis present. Pool, rope and pulley, pendulum, active-assisted range of motion, grades I and II joint mobilization, and passive range-of-motion (ROM) exercises are encouraged. In stage II, adhesive capsulitis, the patient exhibits a restriction of motion secondary to capsular scarring and thickening, and synovitis is still present. During this stage, the program is slightly more aggressive in restoring motion than in stage I; the physical therapist may treat with grades III and IV mobilization to stretch the capsule, slightly more aggressive stretching is performed, and sustained stretching is done at end range (Fig. 24-1). Additionally, the patient may perform all the other exercises listed for stage I. Stage III is characterized by the patient exhibiting a mechanical restriction in motion. The patient’s end feel is often firm and painful. In this phase, the capsule is tightened and adherent to the humerus, and there is a loss of the axillary fold. During this phase, the focus of treatment is to create a stretch that covers a mechanical deformation of the scarred, thickened, and tightened capsule. In this phase, we recommend the use of low-load, long-duration (LLLD) stretches. The characteristics of this type of stretch is to impart a low-intensity stretch for a longer period of time to create deformation of the collagen tissue. Numerous studies
have documented the efficacy of this type of stretch on adhesions.15-19 We perform this stretch with a Thera-Band (Hygenic, Akron, Ohio) or similar device (Fig. 24-2). The patient is instructed to perform this stretch for 12 to 15 minutes, at least four times daily. This uses the TERT principle, total end-range time, whereas McClure has documented that to improve ROM, the patient must spend 60 minutes per day at end range to ensure plastic deformation of collagen.20 LLLD stretches are performed with superficial heat to help promote relaxation.21 Furthermore, the use of multiplanar joint mobilization glides and oblique plane glides is recommended. The focus and purpose of multiplanar glides is to use joint mobilization techniques that combine rotational stress with concomitant translation; thus, collagen is being stretched in more than one plane simultaneously. An example of a multiplanar glide to improve external rotation would be to apply a distraction force and rotate the humeral head into external rotation while gliding anteriorly, with the arm in abduction and external rotation (Fig. 24-3). The joint mobilization techniques are usually described as anterior, posterior, and inferior. The oblique mobilization technique divides the capsule into quadrants (Fig. 24-4A)—anteroinferior, posteroinferior, anterosuperior, and posterosuperior capsular regions. The specific oblique joint mobilization technique to improve external rotation would be to impart a distraction force and glide the humeral head anteroinferiorly, with the arm in external rotation. These techniques have been extremely beneficial for patients with gross restrictions in motion (see Fig. 24-4B). During all phases of treatment for adhesive capsulitis, the patient is encouraged to perform stretches for postural restoration, scapular positioning, and soft tissue mobility. Scapular mobilization, soft tissue mobilization, and stretching exercises are performed. Patients are also instructed to perform low-level strengthening in all phases of treatment. They should perform exercises for both shoulders and, if the contralateral shoulder exhibits tightening during treatment or later, the patient should aggressively attempt to restore mobility to prevent bilateral involvement. Once the adhesive capsulitis condition has been successfully treated, the patient is encouraged to continue a light exercise program for the entire upper extremity, with a focus on ROM, flexibility, posture, and light strengthening exercises.
Manipulation Under Anesthesia When physical therapy alone fails to produce desired results, manipulation under anesthesia (MUA) can be used. It should be considered for patients who are not responding to a stretching program or who are worsening. It is generally performed under interscalene anesthesia. Figure 24-1. Sustained stretch at end range to improve external rotation motion.
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Loew and colleagues22 have reported on 30 patients who underwent MUA; all 30 exhibited acute capsular rupture
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A
C
B
Figure 24-2. Low-load, long duration (LLLD) stretches. A, LLLD stretches with Thera-Band (Hygenic, Akron, Ohio) to improve external rotation. B, LLLD stretches with Thera-Band and superficial heat to improve external rotation. C, LLLD stretches to improve shoulder external rotation using the Joint Active System (JAS, Atlanta).
postmanipulation. The most common area of rupture was the anteroinferior and posterosuperior capsules. Anderson and associates23 have described their findings associated with MUA and reported on 24 patients who underwent premanipulation arthroscopy of the involved frozen shoulder. Diffuse synovitis and dense scarring were noted. The arthroscope was then removed, MUA was performed, and a palpable release was noted. The arthroscope was then reintroduced into the glenohumeral joint and the
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postmanipulation findings were recorded. All patients were noted to have diffuse synovitis; 79% had a rupture at the anteroinferior capsule that had not been ruptured on initial premanipulation arthroscopy. If the adhesive capsulitis being treated occurred after a rotator cuff repair, the amount of rotator cuff healing at the repair site is considered carefully. Motion loss following rotator cuff repair is often caused by intra-articular and
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B
P
S GH L M G H L
PC
A
PB
A
B
AP Figure 24-3. Multiplanar joint mobilization glide for external rotation.
extra-articular (subacromial) adhesions, which differs in cause and treatment from idiopathic adhesive capsulitis. Generally, forward elevation and external rotation in midelevation theoretically relax tension on the repair.
IG
H
L C
A
Contraindications to MUA include no improvement or a worsening ROM after a previous manipulation and significant osteopenia, which represents an increased fracture risk. In addition, long-term insulin-dependent diabetics have demonstrated a decreased benefit from manipulation alone. The patient and surgeon should discuss preoperatively whether to proceed with surgical intervention; the patient must be made aware of the potential for complications, especially fracture of the humerus, and failure to maintain complete motion. The sequence of manipulation in cases of adhesive capsulitis is variable. Generally, we prefer manipulation in forward elevation before rotation (Fig. 24-5). Manipulation should be performed with the surgeon’s hand close to the patient’s shoulder to decrease the moment arm. With constant firm pressure, a palpable and audible release is often appreciated. If crepitant motion does not occur, manipulation is discontinued. After full forward flexion is obtained, gentle external rotation followed by internal rotation is performed. Again, the surgeon’s hands should be close to the glenohumeral joint to minimize the lever arm and risk of humeral fracture (Fig. 24-6). Overly aggressive manipulation can result in soft tissue (rotator cuff tear) or bony (humeral shaft fracture) iatrogenic injury. Complications of MUA include rotator cuff tear, fracture or dislocation of the shoulder, and brachial plexus injury. After a successful manipulation, continuous passive range of motion (CPROM) may be used to maintain motion. Physical therapy is pursued on a daily basis for the first 1 to 2 weeks and home devices can be used to maintain and improve motion. If MUA is initially successful but
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B Figure 24-4. Glenohumeral joint capsule. A, The glenohumeral joint capsule is divided into quadrants. B, An oblique glenohumeral joint glide to improve shoulder external rotation.
motion is lost over the first 3 to 4 weeks, a repeat manipulation is often effective.
Arthroscopic Capsular Release In the setting of a failed MUA or when MUA is contraindicated, arthroscopic release of the shoulder capsule can be performed. We have recently become more aggressive in performing surgical capsular release instead of manipulation alone. The extent of capsule release can be modified and controlled more easily using arthroscopic techniques, depending on preoperative motion loss and capsular tightness. In idiopathic (primary) adhesive capsulitis, motion loss is generally global and release of the anterior, posterior, and inferior capsule is performed.
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A
299
A
B Figure 24-5. Manipulation initiated in forward elevation before rotation. A, Manipulation should be performed with the surgeon’s hand close to the patient’s shoulder to decrease the moment arm. B, Gentle release of the tight capsule with crepitation results in return of passive forward flexion.
Before beginning arthroscopy, a gentle manipulation is performed following the same guidelines as for MUA. A posterior portal is placed and the arthroscope is introduced into the glenohumeral joint. An anterior portal is placed under direct visualization through the rotator interval. Routine glenohumeral arthroscopy is performed. Partial synovectomy is performed at the rotator interval and in the glenohumeral joint for synovitis. The entire soft tissue structure making up the rotator interval is then excised, including the superior glenohumeral ligament and capsule (Fig. 24-7). The postmanipulation arthroscopic findings are noted, as is the partial inferior capsular rupture that often accompanies MUA. This information will guide the surgeon in deciding which additional structures need to be released. The posterior capsule is then released (Fig. 24-8). A combination of arthroscopic punches and electrocautery may be used. The release is performed approximately 1 cm peripheral to the labrum. The anterior capsule is cut from the rotator interval to the inferior axillary pouch, sequentially releasing the middle and inferior (anterior band)
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B
C Figure 24-6. After full forward flexion is obtained, gentle external rotation is performed. A, The surgeon’s hands should be close to the glenohumeral joint to minimize the lever arm and risk of humeral fracture. Release allows full external rotation (B) and internal rotation (C).
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Figure 24-7. Arthroscopic view of a left shoulder from the posterior portal. The soft tissue structures of the rotator interval are excised, including the superior glenohumeral ligament and capsule. Note the biceps tendon running vertically along the right edge of the image.
Figure 24-9. Arthroscopic view of a left shoulder from the posterior portal toward the inferior axillary pouch. Inferior capsular release proceeds with care to avoid injury to the axillary nerve.
evaluation is performed, although only patients with preoperative impingement symptoms undergo decompression and bursectomy. Pearsall and associates24 have evaluated 46 patients who failed an average of 12 months of nonoperative management of adhesive capsulitis syndrome. They were treated with arthroscopic release of the involved shoulder. Release included the anteroinferior capsule, intra-articular portion of the subscapularis, middle glenohumeral ligament (MGHL), superior glenohumeral ligament (SGHL), and the coracohumeral ligaments. All 46 patients showed substantial gains in ROM and decreased pain.
Figure 24-8. Arthroscopic view of a left shoulder from the anterior portal. The posterior capsule is released using a combination of arthroscopic punches and electrocautery. The release is performed approximately 1 cm peripheral to the labrum. The infraspinatus and teres minor muscles are visible after capsular release.
glenohumeral ligaments. Inferior capsule release proceeds in the same fashion, with care taken inferiorly to avoid injury to the axillary nerve (Fig. 24-9). We prefer careful use of arthroscopic meniscal punches to complete the inferior release. Following release, a routine subacromial
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Postoperative care involves ROM exercises in a continuous passive ROM machine and passive- and active-assisted motion with a physical therapist. The interscalene catheter used during the surgical procedure is left in place postoperatively and the patient may be manipulated at the bedside the evening after surgery. We have found it helpful for the patient to visualize the motion gains early in the postoperative course while the regional anesthetic catheter is effective. A patient can be expected to remain hospitalized for 1 to 2 days. Physical therapy is done daily for the first 2 weeks after surgery.
Open Surgical Release Open surgical release has yielded mixed results and is not generally used as a treatment option for primary frozen shoulder. Morbidity is consistently higher in these patients when compared with those who have undergone
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arthroscopic releases. It is still indicated for some extraarticular causes for shoulder stiffness, such as malunion of the proximal humerus or glenoid. It does have the advantage of access to the entire humeroscapular motion interface and allows excision of heterotopic ossification and bone spurs, as necessary. For a contracted subscapularis muscle or tendon unit, open shoulder release allows the option of subscapularis musculotendinous lengthening. Ogilvie-Harris and colleagues25 have compared the results of arthroscopic capsular release with those of open surgical release for the treatment of frozen shoulder. Twenty patients were included in each group. At 2- to 5-year follow-up, both groups had similar shoulder motion. However, the arthroscopic release group had better functional recovery and less pain. At the first follow-up visit after surgical intervention, glenohumeral motion must be measured accurately. If the patient is unable to comply with the examination because of pain, an intra-articular xylocaine injection may be administered. Physical therapy is generally continued over the next 3 months. As the patient improves, a self-directed home stretching program is continued. If the patient experiences increased global stiffness, with no improvement in ROM, repeat MUA, arthroscopic release, or both is considered.
SUMMARY Adhesive capsulitis is a condition of global shoulder motion loss with limitation of active and passive glenohumeral motion resulting from contracture and loss of compliance of the glenohumeral joint capsule. Treatment depends on the stage of the disease process and functional demands of the patient with a ROM deficit. Early physical therapy and NSAIDs are helpful for relieving pain and increasing motion; however, resistant cases may require more aggressive treatment with manipulation under anesthesia or capsular release. A proper and well-designed rehabilitation program based on the stage of the patient is vital to a successful outcome. When physical therapy does not improve the patient’s condition, surgical intervention may be indicated. When appropriate, a controlled release may be obtained by manual manipulation or arthroscopic techniques; arthroscopic capsular release is now used as a primary modality for certain patients with resistant adhesive capsulitis. References 1. Codman EA: The Shoulder: Rupture of the Supraspinatus Tendon and Other Lesions in or About the Subacromial Bursa: Boston, Thomas Todd, 1934. 2. Neviaser JS: Adhesive capsulitis of the shoulder. J Bone Joint Surg 27: 211-222, 1945. 3. McKeever DC: Thawing the frozen shoulder: Clin Orthop 11:168-176, 1958.
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4. Neviaser JS: Adhesive capsulitis and the stiff and painful shoulder. Orthop Clin North Am 11:327-331, 1980. 5. Sheridan MA, Hannafin JA. Upper extremity: Emphasis on frozen shoulder: Orthop Clin North Am 37:531-539, 2006. 6. Smith SP, Devaraj VS, Bunker TD: The association between frozen shoulder and Dupuytren’s disease. J Shoulder Elbow Surg 10:149-151, 2001. 7. Massoud SN, Pearse EO, Levy O, Copeland SA: Operative management of the frozen shoulder in patients with diabetes. J Shoulder Elbow Surg 11:609-613, 2002. 8. Ogilvie-Harris DJ, Myerthall S: The diabetic frozen shoulder: Arthroscopic release. Arthroscopy 13:1-8, 1997. 9. Rodeo SA, Hannafin JA, Tom J, et al: Immunolocalization of cytokines and their receptors in adhesive capsulitis of the shoulder. J Orthop Res 15:427-436, 1997. 10. Bunker TD, Anthony PP: The pathology of frozen shoulder. A Dupuytren-like disease. J Bone Joint Surg Br 77:677-683, 1995. 11. Mengiardi B, Pfirrmann CW, Gerber C, et al: Frozen shoulder: MR arthrographic findings. Radiology 233:486-492, 2004. 12. Farrell CM, Sperling JW, Cofield RH: Manipulation for frozen shoulder: Long-term results. J Shoulder Elbow Surg 14:480-484, 2005. 13. Shaffer B, Tibone JE, Kerlan RK: Frozen shoulder. A long-term follow-up. J Bone Joint Surg Am 74:738-746, 1992. 14. Cyriax J: Textbook of Orthopaedic Medicine, vol 1. Diagnosis of Soft Tissue Lesions. 6th ed. London, Balliere Tindall, 1975, pp 76-77. 15. Light LE, Nuzik S, Personius W, et al: A low-load prolonged stretch vs high load in treating knee contractures. Phys Ther 64:330-334, 1984. 16. Warren CG, Lehmann JF, Kablanski JN: Elongation of rat tail tendon: Effect of load and temperature. Arch Phys Med Rehabil 52:465-474, 1971. 17. Warren CG, Lehmann JF, Kablanski JN: Heat and stretch procedures: An evaluation using rat tail tendon. Arch Phys Med Rehabil 57:122-126, 1976. 18. Tabarg JC, Tabarg C, Tardiev C: Physiological and structural changes in the cat’s soleus muscle caused by immobilization at different lengths by plaster casts. J Physiol 224:231-234, 1972. 19. Arem AJ, Madden JW: Effects of stress on healing wounds: Intermittent non-cyclical tension. J Surg Res 20:93-98, 1976. 20. McClure PW, Blackburn LG, Dusold C: The use of splints in the treatment of joint stiffness: Biologic rationale and an algorithm for making clinical decisions. Phys Ther 74: 1101-1107, 1994. 21. Lentell G, Hetherington T, Eagan J, et al: The use of thermal agents to influence the effectiveness of a low load prolonged stretch. J Orthop Sports Phys Ther 5:200-204, 1992. 22. Loew M, Heichel TO, Lehner B: Intra-articular lesions in primary frozen shoulder after manipulation under general anesthesia. J Shoulder Elbow Surg 14:16-21, 2005. 23. Andersen NH, Sojbjerg JO, Johannsen HV, Sneppen O: Frozen shoulder: Arthroscopy and manipulation under general anesthesia and early passive motion: J Shoulder Elbow Surg 7:218-222, 1998. 24. Pearsall AW 4th, Osbahr DC, Speer KP: An arthroscopic technique for treating patients with frozen shoulder. Arthroscopy 15:2-11, 1999. 25. Ogilvie-Harris DJ, Biggs DJ, Fitsialos DP, MacKay M: The resistant frozen shoulder. Manipulation versus arthroscopic release. Clin Orthop Relat Res (319):238-248, 1995.
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CHAPTER 25 Acromioclavicular
Joint Injuries Albert Tom, Augustus D. Mazzocca, and Christ J. Pavlatos
Acromioclavicular joint separation represents one of the most common shoulder injuries seen in general orthopedic practice. The most common mechanism of this injury is a fall with a direct force to the lateral aspect of the shoulder with the arm in an abducted position. Depending on the magnitude of injury to the acromioclavicular joint capsule and ligaments, as well as the coracoclavicular ligaments, these injuries can be classified with increasing severity as types I through VI. Typically, first- and second-degree sprains of the acromioclavicular joint, otherwise known as types I and II injuries, are treated conservatively, with the vast majority returning to preinjury status. Although the treatment of type III dislocations remain controversial, high-grade injuries, usually types IV to VI, with more than 100% in a posterior or inferior direction, or both, are typically treated surgically. This chapter will review the relevant anatomy, pathomechanics, examination, and treatment options for acromioclavicular joint injuries.
on the posteromedial side of the clavicle. The trapezoid ligament arises anteriorly and laterally to the conoid ligament on the coracoid process and extends to the undersurface of the clavicle, anterior and lateral to the conoid tubercle. The coracoclavicular ligaments play an important role in vertical stability. Studies by Fukuda and colleagues3 have shown that at large displacement, the conoid ligament provides the primary restraint to superior displacement. The trapezoid ligament is the primary restraint to acromioclavicular joint compression at small and large displacements.
ANATOMY
MECHANISMS OF INJURY
The acromioclavicular joint is classified as a diarthrodial joint and the articular surfaces are covered with fibrocartilage. There may be two types of fibrocartilaginous interarticular discs, complete and partial (meniscoid). There are great variations in size and shape. DePalma1 has shown that with age, the meniscus undergoes rapid degeneration until it is essentially no longer functional by the fourth decade. Nerve supply is from the branches of the axillary, suprascapular, and lateral pectoral nerves.
Most acromioclavicular injuries are caused by a direct fall on the point of the shoulder, with the arm at the side in the adducted position (Fig. 25-2). The downward force on the acromion results in a fracture of the clavicle. If no fracture occurs, the acromioclavicular ligaments are first stretched (mild sprain); then, as the force continues, the acromioclavicular ligaments tear and the coracoclavicular ligaments are stressed (moderate sprain). As the downward force continues, the coracoclavicular ligaments tear, along with the muscle attachments of the deltoid and trapezius muscles, resulting in a severe acromioclavicular sprain (complete dislocation).
According to Inman and associates,5 the clavicle rotates as the arm is elevated. There is a total range of motion of the acromioclavicular joint of 20 degrees, which occurs early (in the first 30 degrees of abduction) and late (after 135 degrees of elevation of the arm). During full elevation of the arm, the clavicle rotates about 40 degrees.
The acromioclavicular joint is inherently an unstable joint. It is stabilized by a set of ligaments and two muscles (Fig. 25-1). The first set are the acromioclavicular ligaments, which envelop the joint and are thick on the superior aspect and thin on the inferior aspect. Horizontal stability is controlled by the acromioclavicular ligaments.2 At small displacement, the acromioclavicular ligaments are the primary restraint to posterior and superior translation of the clavicle.3
CLASSIFICATION AND INCIDENCE Injuries to the acromioclavicular joint are best classified according to the amount of damage created by a given force. Allman categorized injuries to the acromioclavicular joint into grades I, II, and III.1 Rockwood and Young2 have identified six types, the first three of which are the same as Allman’s grades. Their additional types IV, V, and VI are Allman’s grade III injuries, varying only in the degree of direction of displacement of the distal part of the clavicle; the modified classification6 is as follows (Fig. 25-3).
The second set are the strong and heavy coracoclavicular ligaments, with fibers that run from the outer inferior surface of the clavicle to the base of the coracoid process of the scapula. These ligaments are divided into two parts.4 The conoid ligament is cone shaped, running from the posterior medial side of the coracoid to the conoid tubercle 303
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Lesser tuberosity
Type II Acromioclavicular joint disrupted, with tearing of acromioclavicular ligament Coracoclavicular ligament sprained Deltoid and trapezius muscles intact
Coracoid process
Bicipital groove
Figure 25-1. Normal anatomy of the acromioclavicular joint. (From Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, p 860.)
Type III Acromioclavicular ligament disrupted Acromioclavicular joint displaced; shoulder complex displaced inferiorly Coracoclavicular ligament disrupted, with coracoclavicular interspace 25% to 100% larger than normal shoulder Deltoid and trapezius muscles usually detach from distal end of clavicle
Type IV Acromioclavicular ligaments disrupted, acromioclavicular joint displaced, clavicle anatomically displaced posteriorly through trapezius muscle Coracoclavicular ligaments disrupted, with wider interspace Deltoid and trapezius muscles detached
Type V Acromioclavicular and coracoclavicular ligaments disrupted Acromioclavicular joint dislocated; gross displacement between clavicle and scapula (100% to 300% more than normal shoulder) Deltoid and trapezius muscles detached from distal end of clavicle
Type VI Acromioclavicular and coracoclavicular ligaments disrupted Distal clavicle inferior to acromion or coracoid process Deltoid and trapezius muscles detached from distal end of clavicle Figure 25-2. The most common mechanism of injury is a direct force that occurs from a fall on the point of the shoulder. (From Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, p 860.)
Type I Sprain of acromioclavicular ligament Acromioclavicular ligament intact Coracoclavicular ligament, deltoid and trapezius muscles intact
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Acromioclavicular (AC) dislocations account for 12% of all dislocations about the shoulder.2 Injuries are more common in male than female patients, with a ratio of 5:1 to 10:1. Incomplete injuries to the acromioclavicular joint are twice as common as complete dislocations.
DIAGNOSIS The pain associated with AC injury may be difficult to localize because of the complex sensory innervation of the joint. A history revealing an acute injury, as described earlier, is
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Normal
Type I
Type IV
Type II
Type V
Conjoined tendon of biceps and coracobrachialis Type III
Type VI
an important starting point in the diagnosis. The lack of a discrete injury with AC joint pain and joint separation is instead consistent with a degenerative condition. Given an acute injury, it is important to determine the level of perceived pain and its location, as well as any history of previous shoulder injuries. During examination, the patient should be upright so that the weight of the arm will help exaggerate any deformities.
Figure 25-3. Schematic representations of the classification of ligamentous injuries that can occur to the acromioclavicular ligament. Type I, A mild force applied to the point of the shoulder does not disrupt the acromioclavicular or coracoclavicular ligaments. Type II, A moderate to heavy force applied to the point of the shoulder will disrupt the acromioclavicular ligaments, but the coracoclavicular ligaments remain intact. Type III, When a severe force is applied to the point of the shoulder, the acromioclavicular and coracoclavicular ligaments are disrupted. Type IV, In this major injury, not only are the acromioclavicular and coracoclavicular ligaments disrupted, but the distal end of the clavicle is displaced posteriorly into or through the trapezius muscle. Type V, A violent force has been applied to the point of the shoulder that not only ruptures the acromioclavicular and coracoclavicular ligaments but also disrupts the deltoid and trapezius muscle attachments and creates a major separation between the clavicle and acromion. Type VI, Another major injury is an inferior dislocation of the distal end of the clavicle to the subcoracoid position. The acromioclavicular and coracoclavicular ligaments are disrupted. (From Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, p 860.)
extremity is depressed when compared with the normal shoulder. Patients with type IV dislocations often present with significant pain, with a prominence noted on the posterior aspect of the shoulder. When viewed from above and
Pain and swelling are the most common symptoms seen in injuries to the AC joints. Mild to moderate pain is noted in types I and II AC joint injuries, respectively. Swelling, although minimal in type I AC joint sprains, is more prominent in type II AC joint injuries, making palpation of the slightly prominent clavicle difficult. In type III AC joint injuries, significant pain and swelling are noted, with a noticeable prominence of the distal clavicle. Gross displacement of the distal end of the clavicle and tenting of the skin are seen in type V AC joint injuries (Fig. 25-4). The patient characteristically presents with the upper extremity adducted close to the body and held upward by the other arm to relieve the discomfort in the affected joint. The entire upper
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A
B
Figure 25-4. Type V acromioclavicular dislocations. A, The clavicle is quite prominent, secondary to the downward displacement of the right upper extremity. B, Severe prominence of the right clavicle. (From Rockwood CA, Matsen FA III [eds]: The Shoulder, vol 1. Philadelphia, WB Saunders, 1990, p 427.)
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behind the patient, the distal end of the clavicle may be seen displaced through the fibers of the trapezius muscle.
RADIOGRAPHIC EVALUATION Radiographic evaluation of the AC joint will clearly demonstrate any displacement of the distal clavicle. Standard radiographs should include anteroposterior and lateral views of the AC joint.2 Standard anteroposterior views (Fig. 25-5) are taken with a 10- to 15-degree cephalic tilt (Fig. 25-6) to avoid superimposition of the AC joint on the spine of the scapula.7 Upward displacement of the clavicle, as well as increased distance between the undersurface of the clavicle and the coracoid process, will confirm AC dislocations. Posterior dislocations may be missed on standard anteroposterior views. A scapular lateral view, as described by Alexander,8 will help identify posterior dislocations. Patients in whom it is difficult to differentiate type II from type III AC joint injuries may require stress films of both shoulders. These stress films will test the integrity of the coracoclavicular ligaments and assist in evaluating the degree of displacement of the distal end of the clavicle. These films are taken with the patient sitting or standing and 10 to 15 pounds of weight suspended from each wrist. Anteroposterior views of both shoulders are taken. A difference of 25% in the distance from the coracoid process to the clavicle in the injured and normal shoulders will confirm a complete AC dislocation.
A
B
TREATMENT The management of injuries to the AC joint may range from benign neglect to the use of slings,9 braces,10 harnesses,11 or several surgical procedures, as described in the literature.12-20 Most clinicians agree on conservative or nonoperative management of acute types I and II AC sprains. The treatment of acute type III AC joint dislocations is controversial. There are three basic and fundamental different views concerning the management of acute type III AC joint dislocations: 1. Nonoperative or conservative approach 2. Surgical repair recommended for all patients 3. Surgical repair recommended for select patients
C Figure 25-5. Why the acromioclavicular joint is poorly visualized on routine shoulder radiographs. A, This routine anteroposterior view of the shoulder shows the glenohumeral joint well. However, the acromioclavicular joint is too dark to interpret, because that area of the anatomy has been overpenetrated by the x-ray technique. B, When the exposure usually used to take the shoulder films is decreased by two thirds, the acromioclavicular joint is well visualized. However, the inferior corner of the acromioclavicular joint is superimposed on the acromion process. C, Tilting the tube 15 degrees upward provides a clear view of the acromioclavicular joint. (From Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP [eds]: Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, p 860.)
Management of Specific Injuries Type I The type I injury involves a mild sprain of the AC ligaments, with the AC and coracoclavicular ligaments intact. Treatment consists of application of ice bags to relieve discomfort and a sling to support the extremity for several days. Active-assisted range of motion is initiated immediately, followed by isometric strengthening. Once full
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motion and strength have returned, the patient may return to normal activities. Type II The type II injury involves disruption of the AC ligament, with the coracoclavicular ligament intact. Most clinicians agree that nonsurgical measures are indicated to treat this
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X-ray
10°
Figure 25-8. Plaster cast device for acromioclavicular separations (older method used in 1952). (From Rowe CR: Acromioclavicular and sternoclavicular joints. In Rowe CR (ed): The Shoulder. New York, Churchill Livingstone, 1988, p 293.)
Figure 25-6. Position of the patient for Zanca view using 10- to 15-degree cephalic tilt of the standard view for the acromioclavicular joint. (From Rockwood CA, Matsen FA III [eds]: The Shoulder, vol 1. Philadelphia, WB Saunders, 1990, p 427.)
injury. However, there are differences of opinion as to which conservative measure is indicated. Many use a sling9 for 7 to 14 days to rest the shoulder, followed by a gradual rehabilitation program. Others have recommended the use of adhesive tape strappings,21 harnesses,10 and a plaster cast.22 Allman23 has recommended the use of a sling harness immobilizing device, the Kenny-Howard sling (Fig. 25-7), for 3 weeks. Some have recommended a plaster cast device (Fig. 25-8), as described by Urist,22 with a strap over the top of the clavicle in an effort to depress the clav-
Figure 25-7. Kenny-Howard shoulder halter for acromioclavicular separations. (From Rowe CR: Acromioclavicular and sternoclavicular joints. In Rowe CR (ed): The Shoulder. New York, Churchill Livingstone, 1988, p 293.)
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icle down to the acromion. However, the problem is a depressed upper extremity and not an elevated clavicle. These harnesses and devices can be used for 3 to 6 weeks to prevent another injury from converting a type II subluxation to a type III dislocation. Heavy lifting and contact sports should be avoided for approximately 8 to 12 weeks, until the ligaments have completely healed. Although conservative management has been recommended for types I and II injuries, reports from Bergfeld and coworkers24 and Cox25 have suggested that these injuries may cause more problems than previously recognized. In type I injuries, 36% of patients have residual symptoms, with radiographic changes in 70%. In type II injuries, 48% to 65% of patients have symptoms, with radiographic changes in 75%. These injuries may require excision of the outer 2 cm of the clavicle, as described by Mumford.26 This can be performed via an open or arthroscopic technique with gratifying results. In athletes, the Mumford procedure has produced successful results, as reported by Cook and Tibone.27 Twenty-three athletes were followed for an average of 3.7 years after a Mumford procedure for type I or II AC joint injuries. Most of the athletes achieved preinjury performance levels after the procedure, with little weakness noted with slow-speed and no weakness noted with high-speed isokinetic testing. Type III The management of type III AC injuries has created much controversy in the orthopedic literature. Many have recommended the nonoperative approach.9,28-36 Most agree that a simple sling is adequate for rest and comfort. As in type II injuries, a gradual rehabilitation program begins as symptoms subside over a 7- to 14-day period. The use of a harness to reduce the dislocation has not been as rewarding. The harness must be worn continuously for 6 weeks to maintain a reduction, but few patients can comply with this form of management.
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This conservative approach has become more popular during the past 10 years, because the patient loses little time from work or athletics and does not have to be hospitalized. Cox25 has reported improved results with no support to the arm in 62% of patients, whereas with immobilization and a sling only 25% improved at 3 to 6 weeks. Further studies have also recommended conservative treatment of type III AC injuries. Glick and associates32 have reported on 35 unreduced type III AC dislocations in athletes. They concluded that a complete reduction is unnecessary and that none of the athletes were disabled at follow-up. Bjerneld,29 Dias,30 and Sleeswijk and colleagues,36 and Schwarz and Leixnering,35 have also reported on a series of patients with type III AC injuries treated nonoperatively, with 90% to 100% satisfying results and with follow-ups averaging 5 to 7 years. Studies comparing operative and nonoperative treatments of type III have also supported conservative measures. In their comparative studies, Hawkins9 and Bannister,28 Galpin,31 Imatani,33 Larsen34 and associates have concluded that nonoperative treatment yields good, if not better, results than surgical treatment. Operative management of complete type III AC dislocations may be indicated for patient populations such as laborers, throwers, or other athletes. Types IV, V, and VI Because of the severe posterior displacement in type IV injuries and gross displacement in type V injuries, most clinicians have recommended a surgical repair.37-41 Few type VI injuries have been described in the literature42-45; all were treated with surgery. Attempts at closed reduction are usually unsuccessful. Gerber and Rockwood42 have reported using the extra-articular technique with a coracoclavicular lag screw, repair of the ligaments, and imbrication of the deltoid trapezius fascia over the top of the clavicle, with successful results. The rehabilitation following surgery to correct a type IV, V, or VI sprain tends to be somewhat slower because of the severity of the initial injury. The program is similar to those discussed and matches the exact surgical procedure and specific patient demands and desires.
Recommended Technique The literature is replete with surgical techniques to address complete AC dislocations, including primary repair of the coracoclavicular ligaments, augmentation with autogenous tissue (coracoacromial ligament), augmentation with absorbable and nonabsorbable sutures and prosthetic material, including coracoclavicular stabilization with metallic screws.37-41,46-75 The Weaver-Dunn technique using transfer of the coracoacromial ligament has been the most popular procedure for acute and chronic injuries. Several
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more recent reports have described good results with modifications of the Weaver-Dunn technique. Anatomic Coracoclavicular Reconstruction From a biomechanical perspective, the importance of the coracoclavicular and AC ligaments in controlling superior and horizontal translations has been elucidated. Failure to reproduce conoid, trapezoid, and AC ligament function surgically with current techniques may explain the observed incidence of recurrent instability and pain. We advocate using a separate, more robust graft source to improve surgical results. The use of a free autogenous or allograft tendons have been further supported in the biomechanics laboratory. Box 25-1 lists some recommendations when performing procedures. BOX 25-1.
Surgical Pearls
• Include the entire clavicle to the SC joint in the operative field for draping to allow for wide exposure. • Place a small towel bump under the medial scapular edge. • Bullet the semitendinosus ends to allow for easy graft passage. • Make sure that the head of the patient can be repositioned to the side to allow room for conoid tunnel drilling. • Instead of repositioning the patient’s head, an alternative is to displace the clavicle anteriorly with a towel clip to allow access for conoid tunnel drilling. • Make a skin incision over the coracoid process, more medially than usual (not over the AC joint). • Make a medial skin incision to allow direct visualization of the coracoclavicular ligament and coracoid. • Tag the deltoid and trapezial fascia for good repair. • Pass sutures under the coracoid from medial to lateral or lateral to medial. • If passing lateral to medial, make sure that the medial coracoid base is exposed and insert a Darrach retractor on the medial base to catch the suture-passing device. • Do not spin the reamer out to avoid tunnel widening. • Over-reduce the AC joint if the distal clavicle is resected; abut the clavicle to the coracoid process. • Do not over-reduce the clavicle if the distal clavicle is to be preserved. • Insert 5.5- ⫻ 8-mm Peek screws into the 5.5-mm bone tunnel (line to line). • Drill up to 1⁄2 mm if the graft is too big for screw fixation. • Insert the Peek screw anterior to the graft to re-create the posterior coracoclavicular ligaments equally.
SC, sternoclavicular.
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Procedure Anesthesia and Positioning. The patient is placed in the beach chair position after induction of general anesthesia. Ensure that the head is mobile for possible repositioning. A small bump is placed on the medial scapular edge to elevate the coracoid anteriorly. Drape wide to expose the sternoclavicular (SC) joint and posterior clavicle. The arm is free-draped. Exposure. A no. 10 scalpel is used to make a 6-cm longitudinal incision, centered over or slightly medial to the coracoid. Medial and lateral skin flaps are elevated with a needle-tipped bougie. Gelpi retractors are used to assist with exposure. A transverse incision is made along the midaxis of the clavicle, extending into the AC joint. Full-thickness flaps of the superior AC joint capsule are elevated superiorly and inferiorly with a needle-tipped bougie. The anterior and posterior portion of the distal clavicle is completely exposed (Fig. 25-9). Five mm of distal clavicle is resected if AC joint arthrosis is present. The medial and lateral coracoid base is exposed with a Cobb elevator. A headlight may be useful for this portion of the procedure. Care is taken to avoid excessive medial dissection to prevent musculocutaneus nerve injury.
Figure 25-10. Distal clavicle resection.
The standard of care is to perform a distal clavicle resection (Figs. 25-10 and 25-11). However, there is tremendous variability in the AC joint and there seems to be tremendous stability from an intact AC joint. Therefore, we believe that it may be advantageous to preserve the distal clavicle and we have done this in select patients. Passing Under the Coracoid. A specially designed cannulated suture-passing device (Arthrex, Naples, Fla) is passed medially to laterally around the coracoid. A FiberWire or FiberStick (Arthrex) is then shuttled through the cannulated handle and retrieved laterally at the tip. This passing stitch is later used for graft passage around the coracoid (Figs. 25-12 and 25-13).
Figure 25-11. Beveling posterior edge of distal clavicle.
An alternate means of coracoid graft fixation is biotenodesis screw fixation of the looped end of the semitendinosus
Figure 25-12. FiberWire placed around coracoid.
graft in a coracoid base bone tunnel. This is best achieved by positioning the 7-mm offset AC ligament guide on the medial coracoid base and reaming an 8- to 9-mm bone tunnel.
Figure 25-9. Initial surgical exposure.
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Clavicular Tunnels. The conoid ligament tunnel is established with a guide pin drilled 4.5 cm medially from the
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Figure 25-13. Close-up of FiberWire around coracoid.
Figure 25-15. Placing guide pins in tunnels.
intact lateral distal clavicle edge. This is positioned along the posterosuperior cortex and marked before distal clavicle resection. The pin is directed 30 degrees anteriorly, aiming toward the coracoid. A second guide pin from the Arthrex biotenodesis set is drilled in the center of the clavicular anteroposterior (AP) dimension, 1.5 cm lateral to the medial pin. This tunnel will be used to reconstruct the trapezoid ligament and is again directed 30 degrees anteriorly toward the coracoid (Figs. 25-14, 25-15, and 25-16). A 5.5-mm reamer is used to ream both tunnels (Figs. 25-17 and 25-18). The reamer is removed by hand twisting after penetrating the far cortex to avoid tunnel widening. Graft Preparation. An allograft semitendinosus graft is contoured to fit through a 5.5-mm tunnel. A no. 2 FiberWire is used to place baseball stitches at each end of the graft (Fig. 25-19).
Figure 25-16. Measuring guide pins.
Graft Passage. The initially passed FiberWire or FiberStick is used to shuttle the prepared semitendinosus graft along with an additional no. 2 FiberWire around the coracoid process. The accessory FiberWire will provide secondary fixation. The free ends of the semitendinosus graft along
Figure 25-17. Reaming conoid tunnel.
with the free no. 2 FiberWire is shuttled into the respective clavicular bone tunnels using a Hewson suture passer (Fig. 25-20).
Figure 25-14. Marking clavicular tunnels.
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Biotenodesis Fixation. A 5.5- ⫻ 8-mm PEEK tenodesis screw is then loaded onto the Bio-Tenodesis screwdriver
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will also help reduce the clavicle. If the distal clavicle is preserved, we avoid over-reducing the AC joint. A second PEEK tenodesis screw is inserted into the second clavicular tunnel through the FiberWire suture. The graft is tensioned as the screw is inserted. The actual order of tunnel fixation is unimportant. The FiberWire is then tensioned and tied with surgeon knots. The graft ends are then sutured to one another and the excess graft is excised.
Figure 25-18. Reaming trapezoid tunnel.
Superior Acromioclavicular Joint Capsular Ligament Repair. No. 2 FiberWire stitches are used to imbricate the superior AC joint capsular ligaments in a pants-over-vest configuration. This will offer additional AP stability to the reconstruction. The deltoid trapezius fascia is also repaired in this step as full thickness flaps of fascia and AC joint capsular ligaments are elevated in a single layer. Closure. After copious wound irrigation, 2-0 Vicryl sutures are used to close the subcutaneous tissues. A 3-0 Monocryl suture is used to perform a subcutaneous skin closure. The wound is injected with bupivacaine (Marcaine). Follow-up. Sutures are removed after approximately the first 7 days. Patients are typically seen at 1, 2, 3, and 6 months and then annually (Fig. 25-21) for examination. During these visits, postoperative x-rays include bilateral Zanca views to measure the coracoid’s clavicular distances.
Figure 25-19. Preparing graft.
REHABILITATION The patient is instructed to wear a sling for the first 8 weeks. Postoperative rehabilitation begins with gentle exercises for the patient, including immediate pendulum exercises and passive external rotation to 30 degrees.
Figure 25-20. Graft passage.
(Arthrex). The nitinol loop retriever is used to pass the FiberWire through the cannulated screwdriver system. With countertension on the opposite graft end, the PEEK screw is inserted flush to the cortical surface. The clavicle is then over-reduced with downward pressure from a Cobb elevator. A superiorly directed force on the humerus
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Figure 25-21. Postoperative x-ray obtained during re-examination of patient.
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These exercises are progressed to include active range of motion at week 8 and isotonic strengthening at 12 to 16 weeks. Sports-specific activities and return to full athletics usually occur between weeks 16 and 24. Heavy laborers may return to work activities at approximately 6 months postoperatively.
SUMMARY On review of the literature, types I and II acromioclavicular joint injuries are best treated conservatively, with good results seen in most patients. A certain percentage of these patients may have residual pain and stiffness as a result of degenerative changes, which may necessitate excision of the distal clavicle in some patients. In both types of injury, immediate motion and strengthening appear to yield better success. Results of treatment of type III acromioclavicular joint injuries have been successful in nonoperative and operative groups. Based on these findings, a nonoperative approach to this injury would be appropriate for most patients. If pain is noted on follow-up, an operative procedure may be performed. Types IV, V, and VI injuries are best treated with open reduction and surgical stabilization of the acromioclavicular joint.
References 1. DePalma AF: The role of the disks of the sternoclavicular and acromioclavicular joints. Clin Orthop 13:7, 1959. 2. Rockwood CA, Young DC: Disorders of the acromioclavicular joint. In Rockwood CA, Matsen FA III (eds): The Shoulder. Philadelphia, WB Saunders, 1990, pp 413. 3. Fukuda K, Craig EV, An K-N et al: Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg Am 68:434, 1986. 4. Johnston TB, Davies DV, Davies F (eds): Gray’s Anatomy, 32nd ed. London, Longmans, Green, 1958. 5. Inman VT, Saunders JB, Abbott LC: Observations on the function of the shoulder joint. J Bone Joint Surg Am 26:1, 1944. 6. Rockwood CA Jr: Injuries to the acromioclavicular joint. In Rockwood CA Jr, Green DP (eds): Fractures in Adults, vol 1, 2nd ed. Philadelphia, JB Lippincott, 1984, pp 860. 7. Zanca P: Shoulder pain: Involvement of the acromioclavicular joint: Analysis of 1,000 cases. AJR Am J Roentgenol 112:493, 1971. 8. Alexander OM: Dislocation of the acromio-clavicular joint. Radiography 15:260, 1949. 9. Hawkins RJ: The acromioclavicular joint. Presented at the American Academy of Orthopaedic Surgeons Summer Institute, Chicago, July 10-11, 1980. 10. Giannestras NJ: A method of immobilization of acute acromioclavicular separation. J Bone Joint Surg Am 26:597, 1944. 11. Warner AH: A harness for use in the treatment of acromioclavicular separation. J Bone Joint Surg Am 19:1132, 1937.
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12. Augereau B, Robert H, Apoil A: Treatment of severe acromioclavicular dislocation: A coracoclavicular ligamentoplasty technique derived from Cadenat’s procedure. Ann Chir 35:720, 1981. 13. Bateman JE: Athletic injuries about the shoulder in throwing and body-contact sports. Clin Orthop 23:75, 1962. 14. Bearden JM, Hughston JC, Whatley GS: Acromioclavicular dislocation: Method of treatment. J Sports Med 1:5, 1973. 15. Bosworth BM: Acromioclavicular separation: New method of repair. Surg Gynecol Obstet 73:866, 1941. 16. Bundens WD Jr, Cook JI: Repair of acromioclavicular separations by deltoid-trapezius imbrication. Clin Orthop 20:109, 1961. 17. Dewar FP, Barrington TW: The treatment of chronic acromioclavicular dislocation. J Bone Joint Surg Br 47:32, 1965. 18. Sage FP, Salvatore JE: Injuries of acromioclavicular joint: Study of results in 96 patients. South Med J 56:486, 1963. 19. Weaver JK, Dunn HK: Treatment of acromioclavicular injuries, especially complete acromioclavicular separation. J Bone Joint Surg Am 54:1187, 1972. 20. Weitzman G: Treatment of acute acromioclavicular joint dislocation by a modified Bosworth method: Report on twenty-four cases. J Bone Joint Surg Am 49:1167, 1967. 21. Rawlings G: Acromioclavicular dislocations and fractures of the clavicle. A simple method of support. Lancet 2:789, 1939. 22. Urist MR: Complete dislocation of the acromioclavicular joint: The nature of the traumatic lesion and effective methods of treatment with an analysis of 41 cases. J Bone Joint Surg Am 28:813, 1946. 23. Allman FL Jr: Fractures and ligamentous injuries of the clavicle and its articulation. J Bone Joint Surg Am 49:774, 1967. 24. Bergfeld JA, Andrish JT, Clancy WG: Evaluation of the acromioclavicular joint following first- and second-degree sprains. Am J Sports Med 6:153, 1978. 25. Cox JS: The fate of the acromioclavicular joint in athletic injuries. Am J Sports Med 9:50, 1981. 26. Mumford E: Acromioclavicular dislocation. J Bone Joint Surg Am 23:799, 1941. 27. Cook FF, Tibone JE: The Mumford procedure in athletes: An objective analysis of function. Am J Sports Med 16:97, 1988. 28. Bannister GC, Wallace WA, Stableforth PG, Hutson M: The management of acute acromioclavicular dislocation. J Bone Joint Surg Br 71:848, 1989. 29. Bjerneld H, Hovelius L, Thorling J: Acromio-clavicular separations treated conservatively: A 5-year follow-up study. Acta Orthop Scand 54:743, 1983 30. Dias JJ, Steingold RA, Richardson RA et al: The conservative treatment of acromioclavicular dislocation: Review after five years. J Bone Joint Surg Br 69:719, 1987. 31. Galpin RD, Hawkins RJ, Grainger RW: A comparative analysis of operative versus nonoperative treatment of grade III acromioclavicular separations. Clin Orthop 193:150, 1985. 32. Glick JM, Milburn LJ, Haggerty JF, Nishimoto D: Disclocated acromioclavicular joint: Follow-up study of 35 unreduced acromioclavicular dislocations. Am J Sports Med 5:264, 1977. 33. Imatani RJ, Hanlon JJ, Cady GW: Acute complete acromioclavicular separation. J Bone Joint Surg Am 57:328, 1975. 34. Larsen E, Bjerg-Neilsen A, Christensen P: Conservative or surgical treatment of acromioclavicular dislocation: A prospective, controlled, randomized study. J Bone Joint Surg Am 68:552, 1986.
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35. Schwarz N, Leixnering M: Results of nonreduced acromioclavicular Tossy III separations. Unfallchirurg 89:248, 1986. 36. Sleeswijk-Visser SV, Haarsma SM, Speeckaert MT Conservative treatment of acromioclavicular dislocation: Jones strap versus mitella [abstract]. Acta Orthop Scand 55:483, 1984. 37. Barber F: Complete posterior acromioclavicular dislocation: A case report. Orthopedics 10:493, 1987. 38. Hastings DE, Horne JG: Anterior dislocation of the acromioclavicular joint. Injury 10:285, 1978. 39. Malcapi C, Grassi G, Oretti D: Posterior dislocation of the acromioclavicular joint: A rare or an easily overlooked lesion? Ital J Orthop Traumatol 4:79, 1978. 40. Nieminen S, Aho AJ: Anterior dislocation of the acromioclavicular joint. Ann Chir Gynaecol 73:21, 1984. 41. Sondergard-Petersen P, Mikkelsen P: Posterior acromioclavicular dislocation. J Bone Joint Surg Br 64:52, 1982. 42. Gerber C, Rockwood CA Jr: Subcoracoid dislocation of the lateral end of the clavicle: A report of three cases. J Bone Joint Surg Am 69:924, 1987. 43. McPhee I: Inferior dislocation of the outer end of the clavicle. J Trauma 20:709, 1980. 44. Patterson WR: Inferior dislocation of the distal end of the clavicle. J Bone Joint Surg Am 49:1184, 1967. 45. Sage J: Recurrent inferior dislocation of the clavicle at the acromioclavicular joint. Am J Sports Med 10:145, 1982. 46. Grauthoff VH, Klammer HL: Complications because of migration of a Kirschner wire from the clavicle. Fortschr Rontgenstr 128:591, 1978. 47. Mazet RJ: Migration of a Kirschner wire from the shoulder region into the lung: Report of two cases. J Bone Joint Surg Am 25:477, 1943. 48. Norrell H, Llewellyn RC: Migration of a threaded Steinmann pin from an acromioclavicular joint into the spinal canal: A case report. J Bone Joint Surg Am 47:1024, 1965. 49. Rockwood CA Jr, Green DP (eds): Fractures in Adults, 2nd ed. Philadelphia, JB Lippincott, 1984. 50. Kennedy JC, Cameron H: Complete dislocation of the acromioclavicular joint. J Bone Joint Surg Br 36:202, 1954. 51. Kennedy JC: Complete dislocation of the acromioclavicular joint: 14 years later. J Trauma 8:311, 1968. 52. Lowe GP, Fogarty MJP: Acute acromioclavicular joint dislocation: Results of operative treatment with the Bosworth screw. Aust N Z J Surg 47:664, 1977. 53. Alldredge RH: Surgical treatment of acromioclavicular dislocation. Clin Orthop 63:262, 1969. 54. Kappakas GS, McMaster JH: Repair of acromioclavicular separation using a Dacron prosthesis graft. Clin Orthop 131:247, 1978. 55. Park JP, Arnold JA, Coker TP, et al: Treatment of acromioclavicular separations: A retrospective study. Am J Sports Med 8:251, 1980. 56. Tagliabue D, Riva: Current approaches to the treatment of acromioclavicular joint separation in athletes. Ital J Sports Traumatol 3:15, 1981. 57. Dahl E: Velour prosthesis in fractures and dislocations in the clavicular region. Chirurgerie 53:120, 1982.
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58. Bargren JH, Erlanger S, Dick HM: Biomechanics and comparison of two operative methods of treatment of complete acromioclavicular separation. Clin Orthop 130:267, 1962. 59. Kiefer H, Claes L, Burri C, Holzworth J: The stabilizing effect of various implants on the torn acromioclavicular joint: A biomechanical study. Arch Orthop Trauma Surg 106:42, 1986. 60. Lancaster S, Horowitz M, Alonso J: Complete acromioclavicular separations: A comparison of operative methods. Clin Orthop 216:80, 1987. 61. Taft TN, Wilson FC, Oglesby JW: Dislocation of the acromioclavicular joint: An end-result study. J Bone Joint Surg Am 69:1045, 1987. 62. Rauschning W, Nordesjo LO, Nordgren B et al: Resection arthroplasty for repair of complete acromioclavicular separations. Arch Orthop Traumatol Surg 97:161, 1980. 63. Smith DW: Coracoid fracture associated with acromioclavicular dislocation. Clin Orthop 108:165, 1975. 64. Smith MJ, Stewart MJ: Acute acromioclavicular separations. Am J Sport Med 7:62, 1979. 65. Bailey RW, O’Connor GA, Tilus PD, Baril JD: A dynamic repair for acute and chronic injuries of the acromioclavicular area [abstract]. J Bone Joint Surg Am 54:1802, 1972. 66. Bailey RW: A dynamic repair for complete acromioclavicular joint dislocation [abstract]. J Bone Joint Surg Am 47:858, 1965. 67. Berson BL, Gilbert MS, Green S: Acromioclavicular dislocations: Treatment by transfer of the conjoined tendon and distal end of the coracoid process to the clavicle. Clin Orthop 135:157, 1978. 68. Caspi I, Ezra E, Neurbay J, Horoszovski H: Musculocutaneous nerve injury following dynamic fixature of distal clavicle. Clin Orthop 1985. 69. Costic RS, Labriola JE, Rodosky ME, Debski RE: Biomechanical rationale for development of anatomical reconstruction of coracoclavicular ligaments after complete acromioclavicular joint dislocations. Am J Sports Med 32:1929, 2004. 70. Lee SJ, Nicholas SJ, Akizuki KH, et al: Reconstruction of the coracoclavicular ligaments with tendon grafts. Am J Sports Med 31:648, 2003. 71. Grutter PW, Petersen S: Anatomical acromioclavicular ligament reconstruction. Am J Sports Med 31:1, 2005. 72. Mazzocca AD, Santangelo SA, Johnson ST, et al: A biomechanical evaluation of an anatomical coracoclavicular ligament reconstruction. Am J Sports Med 34:236, 2006. 73. Jari R, Costic RS, Rodosky MW, Debski RE: Biomechanical function of surgical procedures for acromioclavicular joint dislocations. Arthroscopy 20:237, 2004. 74. Jones HP, Lemos MJ, Schepsis A: Salvage of failed acromioclavicular joint reconstruction using autogenous semitendinosus tendon from the knee. Am J Sports Med 29:234,2001. 75. Debski RE, Parson IM, Woo S, Fu FH: Effect of capsular injury on acromioclavicular joint mechanics. J Bone Joint Surg Am 83:1344, 2001.
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CHAPTER 26 Shoulder Arthroplasty
in the Athletic Shoulder Todd S. Ellenbecker and David S. Bailie
The most common reasons and diagnostic classifications for which shoulder arthroplasty is performed are degenerative osteoarthritis, secondary degenerative osteoarthritis, capsulorrhaphy arthropathy, and rheumatoid arthritis.1 Although all four of these can be found in the athletic shoulder, degenerative osteoarthritis occurring solely from repetitive overuse and wear or secondary to athletic trauma, as well as capsulorrhaphy arthropathy, are particularly common indications in the athlete. A brief overview of each diagnostic classification has implications for the role of shoulder arthroplasty in the treatment of arthritis in the athletic shoulder.
Characteristic wear of the subchondral bone and glenoid cartilage in the shoulder with degenerative osteoarthritis occurs posteriorly, often leaving an area of intact cartilage anteriorly.5 The cartilage of the humeral head is typically eroded in a pattern of central baldness, the so-called Friar Tuck pattern (Fig. 26-1). This differs from the pattern of humeral head wear in cuff tear arthropathy, in which a chronic large rotator cuff defect subjects the uncovered humeral head to abrasion against the acromion and coracoacromial arch, resulting in superior rather than central wear patterns. Recent research by Mochizuki and colleagues6 has identified specific patterns of glenoid load distribution in the throwing shoulder at the anterior, anteroinferior, posterior, and posteroinferior aspects of the dominant glenoid. These were compared with more central glenoid load patterns in the contralateral shoulder and in the shoulder of nonthrowing subjects. The repetitive loading of the athletic shoulder is further compromised in cases of glenohumeral instability.6,7
DEGENERATIVE GLENOHUMERAL OSTEOARTHRITIS Degenerative osteoarthritis of the glenohumeral joint is less common than in the weight-bearing joints (e.g.,. hip, knee) of the lower extremity, accounting for only 3% of all osteoarthritis lesions.2 Osteoarthritis of the glenohumeral joint (GHOA) can be classified as primary or secondary. Primary GHOA usually manifests with no apparent antecedent cause, whereas secondary GHOA results from a preexisting problem, such as a previous fracture, avascular necrosis, burned out rheumatoid arthritis, or crystalline arthropathy.
Another important diagnosis for which shoulder arthroplasty is performed is capsulorrhaphy arthropathy.1 In 1982, Neer and associates8 initially reported glenohumeral arthritis after anterior shoulder instability in an initial series of 26 patients with prior anterior or posterior instability who underwent shoulder arthroplasty. Many patients in this series had prior stabilization surgery. Samilson and Prieto9 later suggested the term dislocation arthropathy in their study of 74 patients with glenohumeral arthritis with prior anterior and posterior instability.
Athletes at risk include weightlifters, throwing athletes (baseball players, softball players) and those engaged in racquet sports (tennis, racquetball, squash).3 This degenerative osteoarthritis seems to be the end result of trauma, whether from pure instability, repetitive loading, fracture, rotator cuff arthropathy, or postsurgery. At the macroscopic level of osteoarthritis (OA), cartilage is noted to have irregularity, with delamination of the cartilage surface and eventually frank cartilage loss, resulting in bone on bone contact in the joint. Early in the degenerative process, inflammatory cells are seen, but this effect is transient and inflammation is not considered to play a major long-term role. Biochemically, OA is associated with a decrease in glycosaminoglycan (GAG) levels, including chondroitin sulfate and hyaluronic acid, increased water content because of increased permeability of water diffusing into the cartilage as GAGs are lost, and increased enzymatic activity from metalloproteinases (MMPs). MMPs play an important role in degeneration of the extracellular matrix of cartilage.4
Neer10 has further reported on the association of osteoarthritis and glenohumeral instability by finding subluxation of the humerus in the direction opposite that of the initial instability caused by excessive tightening at the time of initial stabilization surgery. Matsen and coworkers11 have coined the term capsulorrhaphy arthropathy for patients who develop OA as a consequence of overly tightened soft tissue structures in the treatment of glenohumeral joint instability. Buscayret and colleagues12 have reported the incidence of glenohumeral osteoarthritis to range between 12% and 62% following operative treatment of shoulder instability. Factors specific to stabilization procedures that may contribute to the development of glenohumeral arthritis include encroachment on the articular cartilage by hardware, laterally placed bone block in a Bristow or Latarjet procedure, and excessive soft tissue tensioning resulting from a Putti-Platt procedure.13
Wear patterns in the human shoulder vary based on the types of underlying arthritic condition and causative factors. 315
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Tight anterior capsule
P
External rotation
Obligate posterior translation Figure 26-1. Central pattern of humeral head cartilage wear (Friar Tuck pattern).
Figure 26-2. Concept of obligate translation. P, posterior directed translation.
CONCEPT OF OBLIGATE TRANSLATION
rotator cuff tissue, stability, activity level and desire, and age. Hettrich and coworkers18 have studied preoperative factors in 71 shoulders from 68 patients who underwent shoulder hemiarthroplasty to determine which factors contributed to greater postoperative success. Patients with a preoperative absence of glenoid erosion, no previous surgery, and intact rotator cuff showed significantly greater improvement in active range of motion, more postoperative comfort, and ability to lift weight above shoulder level than patients with glenoid erosion, prior surgery, or rotator cuff tears.
The concept of obligate translation has been applied extensively in orthopedic and sports physical therapy, and in orthopedics in general, since the publication of the study by Harryman and colleagues.14 They identified increases in anterior humeral head translation and shear following a controlled posterior capsular placation in cadaveric specimens. Obligate translation, defined as the translation of the humeral head in the direction opposite that of the tight capsule and soft tissue structures, has been a paramount concept applied in the treatment of the overhead athlete with subtle anterior glenohumeral joint instability secondary to adaptive posterior rotator cuff and posterior capsule tightness.15,16 Harryman and associates17 have also reported the presence of obligate translation in flexion, internal and external rotation, and maximal elevation with shoulder arthroplasty following insertion of an oversized humeral head prosthesis. Shoulder arthroplasty can tend to cause global capsular restriction because of the substitution of a humeral head prosthesis for a degenerative and collapsed humeral head. This overstuffing can prohibit return of optimal range of motion unless the patient undergoes adequate capsular release and early postoperative physical therapy to address capsular tightness.5 Figure 26-2 demonstrates the concept of obligate translation.
INDICATIONS Patients who do not respond to nonoperative therapy and have a progressive loss of range of motion and strength are candidates for shoulder arthroplasty. Shoulder arthroplasty and hemiarthroplasty can provide symptomatic relief and restoration of function in individuals with glenohumeral arthritis. The type of surgical procedure chosen is dependent on overall shoulder function, anatomy, condition of bone and
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Indications for humeral hemiarthroplasty are primary glenohumeral osteoarthritis, secondary degenerative joint disease, osteonecrosis of the humeral head, and combined loss of glenohumeral joint surface and rotator cuff.18 Hemiarthroplasty remains an attractive option for younger patients because of concerns about the longevity of the glenoid prosthesis. Additionally, cementless surface replacement arthroplasty replaces only the damaged portion of the joint-bearing surface, with the advantages of minimal bone resection and restoration of normal anatomy, including humeral head version, inclination, and offset without a humeral stem.19
Surgical Considerations Athletes represent a unique subset of patients with shoulder arthritis that may require arthroplasty. The goals must be to restore full motion and strength and preserve the anatomy for potential revision in the future. One must also consider the types of sports involved (collision versus noncollision) and dominance of the extremity. Conservative measures, such as nonsteroidal antiinflammatory drugs (NSAIDs), steroid injections (occasional), hyaluronic acid preparations (e.g., viscosupplementation), physical therapy to increase motion and restore strength, and arthroscopic débridement, must have failed before considering arthroplasty in the athletic population.
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Optimizing rotator cuff status with arthroscopic subacromial decompression, repair of rotator cuff tears, or both may precede the arthroplasty or be done concurrently. The selected implant should provide immediate stability to limit micromotion with therapy and sports and be durable, revisable, and allow for anatomic reconstruction. The need to replace the glenoid may dictate overall postoperative ability to participation in sports, because this is still the weak link in shoulder arthroplasty. Placement of a glenoid component entails the risk of early loosening with more physical activities. Performing a more anatomic reconstruction theoretically may reduce the incidence of radiographic and real glenoid loosening by limiting eccentric loading of the component. Restoring the anatomy will also ensure optimal kinematics to maximize motion, strength, and recovery potential. In general, surgical considerations must first include anatomic joint reconstruction with a well-fixed stable implant. This is done with a humeral head resurfacing implant or a third- or fourth-generation stemmed implant. The ultimate goal is to match the native humeral version, inclination, offset, and height. The glenoid can then be resurfaced with a prosthesis or managed with a number of nonimplant resurfacing techniques. Finally, the soft tissues must be released, balanced, and repaired to allow for adequate restoration of long-term function. Although every surgeon may have a preference, we use resurfacing primarily for those patients who desire to return to high-demand activities, such as strength training, collision sports (e.g., skiing, football, mountain biking), tennis, basketball, and martial arts.20 We also have chosen to avoid placing a glenoid component in these individuals to avoid the potential pitfalls of loosening and revision. Other alternatives we have used include microfracture, reaming the glenoid to restore version, and bone grafting cysts and defects with biologic covering of the glenoid surface with autograft or allograft tissue. Key to the success of arthroplasty in any patient, but especially in those who desire to return to more demanding sports, is restoration of soft tissue tension. Specifically, a complete 360-degree subscapularis release is needed to increase excursion and restore external rotation. Lengthening the tendon is not needed and will ultimately weaken this structure, with the potential for delayed rupture. This release will allow the humeral head to return to the center of the glenoid and permit the normal obligate translation that occurs with rotational motion. This in turn helps restore the normal forces across the glenohumeral joint and leads to decreased pain, improved strength, and function (Figs. 26-3, 26-4, and 26-5). Rehabilitation considerations must take into account the amount of motion obtained under anesthesia after subscapularis closure. This should be communicated to the patient and therapist. The goal is to obtain normal motion, which can be achieved in almost all cases. The subscapularis
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Figure 26-3. Shoulder arthroplasty. Intra-operative photo of a severely arthritic humeral head in a young patient, resulting in poor function and pain.
Figure 26-4. Shoulder arthroplasty. Subscapularis closure after shoulder arthroplasty. The repair must be protected post-operatively, while attempting to regain motion of the shoulder in rehabilitation.
repair must be sound and protected for the first 6 weeks; external rotation is limited to 30 to 45 degrees. If a larger rotator cuff repair is performed, these precautions should also be instituted according to the surgeon’s confidence in the repair. Full passive range of motion (ROM) can be obtained immediately, with rapid progression to activeassisted and active ROM during the initial 6 weeks. Communication with the therapist is critical; we encourage preoperative evaluation to meet the specific needs and desires of the patient after surgery.
REHABILITATION The surgical exposure used during shoulder arthroplasty has significant ramifications for the immediate postoperative management of these patients. Two approaches are typically used—the deltopectoral approach and anterosuperior or
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TABLE 26-1 Factors Affecting Progression of Rehabilitation Following Arthroplasty
Figure 26-5. X-ray of shoulder arthroplasty. Radiograph of a cementless humeral resurfacing arthroplasty in a young patient with a history of glenohumeral arthrosis.
Mackenzie approach.21 The skin incision for the anterosuperior approach extends distally in a straight line from the acromioclavicular (AC) joint for a distance of 9 cm. The anterior deltoid fibers are split for a distance of not more than 6 cm to protect the axillary nerve. The acromial attachment of the deltoid is detached to expose the anterior aspect of the acromion. The subscapularis is completely released and held by stay sutures and detached. The long head of the biceps can be dislocated posteriorly over the humeral head as the humeral head is dislocated anteriorly.19,21 The complete release and detachment of the subscapularis with this approach are required to gain exposure for preparation of the humeral head during hemiarthroplasty, as well as during total shoulder arthroplasty (Table 26-1).
Subscapularis Precautions For the first 6 weeks, specific subscapularis precautions must be followed to protect this important structure postoperatively. This entails limitation of passive or active external rotation ROM and no active resistive exercise for internal rotation. Although gentle attempts at passive external rotation can occur to as far as 30 to 45 degrees of external rotation beyond neutral, techniques that place increased or undue tension on the anterior capsule and subscapularis are avoided for the first 6 weeks following surgery. Additional precautions may be needed, depending on the repair of additional rotator cuff tendons at the time of surgery, as well as whether bicep tenolysis, tenodesis, or tenotomy has been performed. Specifically,
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Factor
Indication
Subscapularis release and repair—exercise in first 6 weeks postoperatively
Limitation of external rotation ROM and resistive internal rotation
Supraspinatus tear and repair—elevation, delayed active abduction range of motion (ROM)
Delayed reattainment of antigravity
Biceps tenolysis and tenodesis—6 weeks postoperatively
No resistive elbow flexion exercise in initial 6 weeks postoperatively
Age, tissue quality
Delayed return of active ROM
resistive exercise for the biceps brachii is not performed for the first 6 weeks postoperatively if a release of the biceps long head or tenodesis has been performed to minimize the chance of rerupture and reappearance of a Popeye deformity. It is beyond the scope of this chapter to discuss the entire rehabilitation process following shoulder arthroplasty; a detailed summary of our postoperative protocol is presented in Box 26-1.
Range of Motion and Optimization of Capsular Relationships Concomitant with therapy during the initial stages of postoperative rehabilitation are the use of mobilization and passive stretching to decrease abnormal glenohumeral joint shear forces14,15 and improve gross glenohumeral joint ROM. Typical patterns of ROM loss following shoulder injury adhere to the predictable pattern described by Cyriax and Cyriax,22 which states that external rotation, abduction, and internal rotation are most limited, followed by forward flexion, which is least limited.22 To address selective capsular tightness, posterior glides of the humeral head relative to the glenoid, with varying degrees of internal rotation of the glenohumeral joint, are used to mobilize the posterior capsule and address limitations in internal glenohumeral joint rotation. Anterior glides of the humeral head are often used later in the rehabilitation process once initial subscapularis healing has occurred to address limitations in external rotation, if indicated. Optimization of capsular length between the anterior and posterior capsule is theoretically purported to minimize humeral head shear within the glenoid with glenohumeral joint movement.14,15 In addition to the use of glenohumeral joint mobilization, application of passive stretching using the low-load, long-duration stretching concept is also recommended.23
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BOX 26-1.
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Rehabilitation Following Glenohumeral Joint Arthroplasty
General Guidelines
glenohumeral joint in scapular plane and 10-20 degrees of abduction (towel roll or pillow under axilla)
• Sling use and duration as directed by surgeon in postoperative instructions • Immediate postoperative passive and active-assisted range of motion (ROM) consisting of stomach rubs, sawing movements, and elbow range of motion as instructed following hospital discharge
Postoperative Weeks 6-8
Postoperative Weeks 1-4
2. Initiation of internal rotation submaximal resistive exercise progression
1. Modalities to decrease pain and inflammation 2. Passive range of motion initiated, with no limitation in flexion, abduction, or internal rotation; no external rotation stretching or anterior capsular mobilization in this rehabilitation phase to protect subscapularis repair; movement-ROM into 30-40 degrees external rotation with 30-45 degrees abduction allowed by therapist, provided it is not against tension 3. Elbow, wrist, and forearm ROM and stretching 4. Manually applied scapular resistive exercise for protraction and retraction, submaximal biceps and triceps manual resistance with shoulder in supported position supine 5. Ball approximation (closed-chain Codman’s exercise) using Swiss ball or tabletop
Postoperative Weeks 2-4
1. Initiation of passive external rotation ROM and stretching beyond neutral rotation position
3. Traditional rotator cuff isotonic exercise program a. Side-lying external rotation b. Prone extension c. Prone horizontal abduction—limited from neutral to scapular plane position initially, with progression to coronal plane as ROM improves 4. Biceps and triceps curls in standing position, with glenohumeral joint in neutral resting position 5. Oscillation exercise with resistance bar or Bodyblade (Hymanson, Marina Del Rey, Calif) 6. Rhythmic stabilization in open and closed kinetic chain environments
Postoperative Weeks 8-12 1. Continuation of resistive exercise and ROM progressions
1. Initiation of active-assisted ROM using pulley for sagittal plane flexion and scapular plane elevation
2. Addition of ball dribbling and upper body plyometrics with small Swiss ball
Postoperative Weeks 4-6
Postoperative Weeks 12-24
1. Continuation of above program
1. Continuation of rehabilitation
2. Initiation of submaximal multiple-angle isometrics and manual resistive exercises for shoulder external rotation, abduction and adduction, flexion and extension
2. Isometric internal and external rotation strength testing and assessment in neutral scapular plane position
3. Upper body ergometer (UBE)
3. Subjective rating scale completion
4. External rotation isotonic exercises using pulley, weights, or tubing, with elbow supported and
4. ROM assessment
Strengthening Early strengthening following glenohumeral arthroplasty focuses on the scapular stabilizers and safe, submaximal rotator cuff activation.16,24 Techniques described in Chapter 50 show manual scapular stabilization for retraction and protraction. This allows for early contraction of the lower trapezius and serratus anterior force couple components without stressing the glenohumeral joint. Multiple sets to induce muscular fatigue of these important muscles are indicated.16 In addition to the scapular stabilization exercise, early application of external rotation exercise is initiated. As noted,
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internal rotation strengthening cannot commence before 6 weeks postoperatively to protect the subscapularis muscle tendon unit. Progression of rotator cuff strengthening follows patterns outlined in the literature, with documented high levels of activation of the posterior rotator cuff to enhance recruitment and improve local muscular endurance with multiple sets of 15 to 20 repetitions.25-28 Additional application of resistive exercise and proprioceptive training occurs in the supine position; the patient places the shoulder in 90 degrees of shoulder flexion with assistance from the therapist. This position is termed the balance point position because patients can balance the extremity in this position despite being unable to elevate the shoulder to 90 degrees
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independently. From this position, the therapist can progressively apply manual contacts or modified rhythmic stabilization while the patient provides cocontraction to maintain this position. Additionally, in this early stage, external rotation isometrics with elastic resistance using a TheraBand (Hygenic, Akron, Ohio) are performed (Fig. 26-6). The neutral position is used, with a towel roll placed under the axilla. This is maintained during the exercise and the patient steps laterally away from the attachment point of the tubing. After a several-second pause at the point of increased tension, the patient is directed to step back toward the attachment point of the tubing again. Actual motion at the glenohumeral joint does not occur but variable loading during this isometric exercise is transmitted to the glenohumeral and scapulothoracic muscles. This exercise is well tolerated and safe, and can be used as a home exercise program to facilitate development of the posterior rotator cuff and scapular stabilizers.
Rotator Cuff and Scapular Exercise Progression Gradual progressions in rotator cuff and scapular strengthening occur with increased intensity and variety following 5 to 6 weeks postoperatively. The important role of the
rotator cuff musculotendinous units in controlling and centering the humeral head, especially during midrange movement patterns, cannot be underestimated.29 Submaximal strengthening methods to recruit the rotator cuff musculature selectively, using exercise patterns that place the shoulder in neutral nonimpinging positions, forms the basis for in-clinic and home-based rehabilitative exercise programs. Exercises such as side-lying external rotation, prone extension, and prone horizontal abduction are used and recommended, based on electromyographic research studies that documented high levels of posterior rotator cuff activation.25-28 As a general rule, shoulder exercises that keep the shoulder below 90 degrees of elevation and the arm slightly anterior to and in the scapular plane are recommended.16 Progressive advances in exercise for the muscles that stabilize the scapula are also indicated. Exercises that strengthen the serratus anterior and lower trapezius are particularly recommended to improve scapular upward rotation during elevation.30 Resistance patterns with light weights, medicine balls, or a Thera-Band can be used to perform shoulder punches, with emphasis on the position of maximal scapular protraction (termed the plus position) to recruit the serratus anterior.31,32 Scapular retraction exercises, such as rowing with multiple positions of arm abduction, are also indicated. Lower resistance levels allow rotator cuff activation, with less compensation and shoulder girdle elevation that often accompany independent exercise programs with higher resistance levels and movement patterns characterized by full, end-range, overhead elevation. Care must be taken to ensure that resistive exercise does not elevate pain levels, which lead to muscular inhibition and compensation. The restoration of optimal muscle balance is imperative during the rehabilitation of all shoulder injuries and pathologies, but it is particularly important following shoulder arthroplasty. Figures 26-7 and 26-8 illustrate the effect of unbalanced muscular forces during shoulder muscular contraction and volitional movement. Unbalanced internal rotation strength or dominant anterior muscular strength development can lead to anterior translation of the humeral head relative to the glenoid.29 Similarly, excessive posterior development can accentuate posterior subluxation from an eroded posterior glenoid and overly tight anterior structures (obligate translation) and produce posterior instability.
Figure 26-6. Dynamic isometric step-outs. This exercise uses elastic resistance, with the patient holding the arm in neutral rotation with a towel roll or bolster under the involved arm. Holding the arm in this position, the subject repeatedly takes a large step away from the attachment site of the tubing while holding the extremity stationary. A step back to the starting position completes one repetition of this exercise.
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Optimal muscle balance between the external and internal rotators has been reported and recommended in the range from 66% to 75% external rotation (ER) to internal rotation (IR).33,34 This can be assessed with a hand-held dynamometer or isometric function of an isokinetic dynamometer system to ensure proper restoration of this optimal muscle balance.33,35 Patients frequently present with overly dominant anterior muscular strength, which can
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321
Unbalanced net force Applied force
Balanced net force Applied force
Figure 26-7. Diagrammatic representation of unbalanced muscular force.
jeopardize glenohumeral mechanics and lead to complications and functional impairment. The rocking horse phenomenon (see Fig. 26-8) can lead to implant loosening, one of the most frequently encountered complications following total shoulder arthroplasty.5,11 Restoration of proper muscular balance via monitoring and addressing the ER/IR strength ratio, as well as application of ROM, physiologic stretching, and accessory mobilization techniques during postoperative rehabilitation, ensure proper capsular excursion and minimize the effects of obligate translation. Research studies14,15,36 have shown the effects of capsular tightness on glenohumeral kinematics. Progression to elevated positions of rotator cuff and scapular stabilization is indicated to assist patients with the return of shoulder elevation against gravity following these extensive surgical procedures. Figure 26-9 shows an exercise position using the scapular plane, 80 to 90 degrees of elevation, and an exercise ball. The patient is asked to maintain his or her position on the ball while the therapist provides challenges or perturbations to the extremity in all
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Figure 26-8. Rocking horse phenomenon. Loosening of the glenoid component results when translation of the head on the glenoid produces eccentric forces on the glenoid component. (From Matsen FA III, Lippitt SB, Sidles JA, and Harryman DT II. Practical evaluation and management of the shoulder. Philadelphia, WB Saunders, 1994.)
directions to elicit muscular activation in this functional position. As with all shoulder elevation exercises, great care is taken to avoid the presence of excessive scapular elevation, which results in the shoulder hiking during exercise.37 This compensatory pattern leads to the development of inappropriate motor patterns and produces long-term scapular pathology with arm elevation. The exercises listed in this chapter minimize positions and movement patterns that increase glenohumeral contact forces and compressive loading.38 The use of closed kinetic chain exercise in the
Figure 26-9. Closed-chain scapular plane exercise using exercise ball on the wall (exercise ball from Hygenic, Akron, Ohio.)
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form of weightbearing is minimized in the initial postoperative rehabilitation exercise progression.38,39
OUTCOMES Following arthroplasty, careful monitoring of the patient for ROM and muscular strength enables the progression of mobilization and stretching using objectively based guidelines to be monitored. We have determined ROM, strength, and functional rating scores 12 weeks following total arthroplasty (PROMOS stemmed implant, Promos Shoulder System, Smith-Nephew Orthopaedics, Memphis, TN) and hemiarthroplasty (Copeland shoulder, Biomet, Warsaw, Ind) when the patient is still typically under the care of a physical therapist in a supervised rehabilitation program.38 Our results show average antigravity flexion and abduction ROM to be approximately 135 degrees, 70 degrees of external rotation with 90 degrees of abduction, and 35 degrees of internal rotation with 90 degrees of glenohumeral joint abduction. Muscular strength measured isometrically using a dynamometer revealed a 47% deficit in external rotation strength compared with the contralateral extremity and a 35% deficit in internal rotation strength. The self-report section of the Modified ASES rating scale produced values of 31 of 45 points in these patients following total and hemiarthroplasty, with comparable values of 38 of 45 points in patients following mini-open rotator cuff repair in the same 12-week postoperative time frame. Longer term follow-up has been done following hemiarthroplasty and total shoulder arthroplasty, although limited data are available on younger, more athletic patient populations at present. Levy and Copeland19 have reported on long-term results (more than 2 years; mean, 7.6 years) following Copeland cementless humeral resurfacing (Biomet, Warsaw, Ind) in 42 elderly patients. Constant scores improved from 20 points preoperatively to 61.9 points postoperatively at final follow-up. Of particular importance was the improvement of active elevation from a mean of only 59.9 degrees preoperatively to 128 degrees postoperatively for those undergoing total shoulder replacement and 124 degrees postoperatively for those undergoing hemiarthroplasty. Of these patients, 89.9% considered their shoulder much better or better following the procedure.
final follow-up. Similar increases in active external rotation were reported, ranging from 4 to 38 degrees. Results were reported as good or excellent in 50 of 55 patients. Further research is clearly needed to establish the short- and longterm outcomes of patients following hemiarthroplasty and total shoulder arthroplasty, particularly in the younger, active athletic patient. The American Shoulder and Elbow Surgeons Society has recommended guidelines for return to sports activity following shoulder arthroplasty (Table 26-2). Current research continues to identify osteoarthritic changes in the overhead athlete.40,41 Maquirrain and associates41 have reported a 33% incidence of osteoarthritic changes in older tennis players (mean age, 57.2 years). The incidence of glenohumeral arthritic changes was higher in this study than in age-matched sedentary control subjects. Additional research on specific populations of overhead athletes will likely identify early degenerative changes in the shoulder that may ultimately require shoulder arthroplasty.
SUMMARY The combination of high-load activity and repetitive overuse can lead to osteoarthritic changes in the athletic shoulder. Early recognition and treatment of the arthritic shoulder in the athlete, coupled with advances in humeral and glenoid components, have allowed patients to return to higher levels of function following shoulder arthroplasty. TABLE 26-2 Activity Recommendations After Total Shoulder Arthroplasty
Recommended
Allowed With Experience Not Recommended
Bicycling
Golf
Football
Swimming
Ice skating
Hockey
Cross-country skiing Shooting
Gymnastics
Speed walking
Rock climbing
Downhill skiing
Jogging Doubles tennis Low-impact aerobics Bowling
Matsoukis and colleagues13 have evaluated 55 patients who had suffered a prior dislocation 45 months following shoulder arthroplasty. The mean delay between the instability event and arthroplasty was 24.2 years, with an average age of 55.9 years; 24 patients had undergone a prior stabilization procedure to address their instability, including coracoid transfers and Putti-Platt–type soft tissue transfer procedures. Constant scores improved from 30.8 preoperatively to a mean of 65.8 at follow-up. Active forward elevation improved from 82 degrees preoperatively to 138 degrees at
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Canoeing Croquet Shuffleboard Horseshoes Ballroom dancing *Based on 1999 American Shoulder and Elbow Surgeons Society recommendations. From Healy WL, Iorio R, Lemos MJ: Athletic activity after joint replacement. Am J Sports Med 29:377-388, 2001.
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The rehabilitation guidelines discussed have included the protection of anterior structures during initial range-ofmotion and progressive resistive exercises for the return of rotator cuff and scapular strength. These are keys for successful rehabilitation programs for these patients. Further advances in orthopedic technology and research, including biologic resurfacing42 and microfracture, may lead to additional options for the younger active patient with glenohumeral arthritis. More basic science and patient outcomes research studies are needed to develop optimal patient management techniques for glenohumeral arthritis in the athletic shoulder. References 1. Parsons M, Campbell B, Titelman RM, et al: Characterizing the effect of diagnosis on presenting deficits and outcomes after total shoulder arthroplasty. J Shoulder Elbow Surg 14:575-584, 2005. 2. Badet R, Boileau P, Noel E, Walch G: Arthrography and computed arthrotomography study of seventy patients with primary glenohumeral osteoarthritis. Rev Rhum Engl Ed 62:555-562, 1995. 3. Andrews J: Arthroscopic débridement for glenohumeral arthritis. Presented at the Symposium of the American Orthopaedic Society for Sports Medicine (AOSSM): Arthritis of the Glenohumeral Joint in the Young Patient. March 2000. 4. Carfagno DC, Ellenbecker TS: Osteoarthritis of the glenohumeral joint: Nonsurgical treatment options. Physician Sports Med 30:19-32, 2002. 5. Rockwood CA, Wirth MA, Lippitt SB: Glenohumeral arthritis and its management. In Rockwood CA, Matsen FA III (eds): The Shoulder. Philadephia, WB Saunders, 1998, pp 840-964. 6. Mochizuki Y, Natsu K, Kashiwagi K, et al: Changes of the mineralization pattern in the subchondral bone plate of the glenoid cavity in the shoulder joints of the throwing athletes. J Shoulder Elbow Surg 14:616-619, 2005. 7. Schultz CU, Anetzberger H, Pfahler M, et al: Anterior shoulder instability modifies glenoid subchondral bone density. Clin Orthop Relat Res (423):259-263, 2004. 8. Neer CS, Watson KC, Stanton FJ: Recent experience in total shoulder replacement. J Bone Joint Surgery Am 64:319-337, 1982. 9. Samilson RL, Prieto V: Dislocation arthropathy of the shoulder. J Bone Joint SurgeryAm 65:456-460, 1995. 10. Neer CS: Shoulder Reconstruction. Philadelphia, WB Saunders, 1990, pp 208-212 . 11. Matsen FA, Rockwood CA, Wirth MA, Lippitt SB: Glenohumeral arthritis and its management. In Rockwood CA, Matsen FA III (eds): The Shoulder, 3rd ed. Philadelphia, WB Saunders, 1998, pp 879-888. 12. Buscayret F, Edwards TB, Szabo I, et al: Glenohumeral arthrosis in anterior instability before and after surgical treatment. Am J Sports Med 32:1165-1172, 2004. 13. Matsoukis J, Tabib W, Guiffault P, et al: Shoulder arthroplasty in patients with a prior anterior shoulder dislocation. J Bone Joint Surgery Am 85:1417-1423, 2003. 14. Harryman DT, Sidles JA, Clark JM, et al: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334-1343, 1990.
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15. Grossman MG, Tibone JE, McGarry MH, et al: A cadaveric model of the throwing shoulder: A possible etiology of superior labrum anterior-to-posterior lesions. J Bone Joint Surg Am 87:824-831, 2005. 16. Ellenbecker TS: Nonoperative Treatment of the Shoulder. New York, Thieme, 2006. 17. Harryman DT, Sidles JA, Harris SL, et al: The effect of articular conformity and the size of the humeral head component on laxity and motion after glenohumeral arthroplasty. A study in cadavera. J Bone Joint Surg Am 77:555-563, 1995. 18. Hettrich CM, Weldon E, Boorman RS, et al: Preoperative factors associated with improvements in shoulder function after humeral hemiarthroplasty. J Bone Joint Surgery Am 86:1446-1451, 2004. 19. Levy O, Copeland SA: Cementless surface replacement arthroplasty (Copeland CSRA) for osteoarthritis of the shoulder. J Shoulder Elbow Surgery 13:266-270, 2004. 20. Bailie DS, Ellenbecker TS: Shoulder arthroplasty in patients under 55 years of age. Abstract AAOS-2006. 21. Levy O, Funk L, Sforza G, Copeland SA: Copeland surface replacement arthroplasty of the shoulder in rheumatoid arthritis. J Bone Joint Surgery Am 86:512-518, 2004. 22. Cyriax, JH, Cyriax PJ: Illustrated Manual of Orthopaedic Medicine. London, Butterworths, 1983. 23. Bonutti PM, Windau JE, Ables BA, Miller BG: Static progressive stretch to reestablish elbow range of motion. Clin Orthop Relat Res (303):128-134, 1994. 24. Wilcox RB, Arslanian LE, Millett P: Rehabilitation following total shoulder arthroplasty. J Orthop Sports Phys Ther 35:821-836, 2005. 25. Ballantyne BT, O’Hare SJ, Paschall JL, et al: Electromyographic activity of selected shoulder muscles in commonly used therapeutic exercises. Phys Ther 73:668-677, 1993. 26. Blackburn TA, McLeod WD, White B, Wofford L: EMG analysis of posterior rotator cuff exercises. Athletic Training 25:40-45, 1990. 27. Reinhold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34:385-394, 2004. 28. Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19:264-272, 1991. 29. Lee SB, An KN: Dynamic glenohumeral stability provided by three heads of the deltoid muscle. Clin Orthop Rel Research (400):40-47, 2002. 30. Kilber WB: The role of the scapula in athletic shoulder function. Am J Sports Med 26:325-337, 1998. 31. Mosely JB, Jobe FW, Pink M: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. 32. Decker MJ, Hintermeister RA, Faber KJ, Hawkins RJ: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27:784-791, 1999. 33. Davies GJ: A Compendium of Isokinetics in Clinical Usage. LaCrosse, Wisc, S & S Publishing, 1984. 34. Ivey FM, Calhoun JH, Rusche K, Bierschenk J: Isokinetic testing of shoulder strength: Normal values. Arch Phys Med Rehabil 66:384-386, 1985. 35. Ellenbecker TS, Davies GJ: The application of isokinetics in testing and rehabilitation of the shoulder complex. J Athletic Training 35:338-350, 2000.
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36. Koffler KM, Bader D, Eager M, et al: The effect of posterior capsular tightness on glenohumeral translation in the late-cocking phase of pitching: A cadaveric study [abstract SS-15]. Presented at the Arthroscopy Association of North America Annual Meeting, Washington, DC, April 2001. 37. Kibler WB, Uhl TL, Maddux JWQ, et al: Qualitative clinical evaluation of scapular dysfunction: A reliability study. J Shoulder Elbow Surgery 11:550-556, 2002. 38. Conzen A, Eckstein F: Quantitative determination of articular pressure in the human shoulder joint. J Shoulder Elbow Surgery 9:196-204, 2000. 39. Ellenbecker TS, Davies GD: Closed Kinetic Chain Exercise: A Comprehensive Guide to Multiple-Joint Exercise. Champaign, Ill, Human Kinetics, 2001.
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40. Ellenbecker TS, Sum J, Bailie DS: Glenohumeral joint range of motion, rotational muscle strength and functional self-report following shoulder arthroplasty. J Orthop Sports Phys Ther 36:28, 2006. 41. Maquirrain J, Ghisi P, Amato, S: Is tennis a predisposing factor for degenerative shoulder disease? A controlled study in former elite players. Br J Sports Med 40:447-450, 2006. 42. Krishnan, SG, Burkhead, WZ, Nowinski RJ: Humeral hemiarthroplasty with biologic resurfacing of the glenoid and acromion for rotator cuff tear arthropathy. Tech Shoulder Elbow Surg 5:51-59, 2004.
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CHAPTER 27 Neurovascular Compression
Syndromes of the Shoulder Champ L. Baker, Jr. and Champ L. Baker III
During athletic activities, tremendous shear and compressive loads are placed on the glenohumeral joint and supporting structures. Repetitive overhead activities place the athlete’s shoulder at risk. Common problems caused by these activities in the overhead athlete include labral injury, joint instability, impingement, and rotator cuff failure. However, neurovascular compression syndromes, such as thoracic outlet syndrome, axillary artery occlusion, effort thrombosis, and quadrilateral space syndrome, should be considered in the differential diagnosis. Although they are less common, these entities should be considered during the examination of the injured athlete. The signs and symptoms of neurovascular compression are often vague and can be frequently overlooked. Diagnosis and treatment are commonly delayed. Failure of prompt recognition and treatment of neurovascular compression syndromes of the shoulder can lead to progressive dysfunction and disability.
occluded by external pressure exerted by the pectoralis minor muscle when the arm is brought overhead. Peet and associates,15 in 1956, were the first to use the term thoracic outlet syndrome. Brantigan and Roos16 have defined the syndrome as upper extremity neurovascular symptoms presumably caused by narrowing of the thoracic outlet through which the major vessels and nerves pass.
NEUROVASCULAR COMPRESSION SYNDROMES Thoracic Outlet Syndrome Thoracic outlet syndrome is an ill-defined term that encompasses the signs and symptoms attributed to compression of the neurovascular structures as they traverse the space from the neck to the axilla. Because of the intimate proximity of the nerves and vessels to each other in this space, varying degrees of compression of the brachial plexus and subclavian vessels can exist. Thus, the clinical presentation of this syndrome can be highly variable. Although Wood and coworkers17 have stated that this complex syndrome is “incompletely understood, difficult to diagnose, and often poorly managed,” a thorough understanding of the anatomy is essential for the clinician treating an athlete with this disorder.
HISTORY The earliest reports of neurovascular compression in the shoulder focused on thoracic outlet syndromes. In 1743, Hunald (cited by Tyson and Kaplan1) was the first to describe cervical ribs as an anatomic anomaly causing thoracic outlet compression. Coote,2 in 1861, performed a successful decompression of the thoracic outlet by surgically removing the offending cervical rib. Similarly, Murphy3 in 1905 and Keen4 in 1907 reported the symptoms of neurovascular compression and the role of the cervical rib. Stopford and Telford5 in 1919 and Wheeler6 in 1920 showed that thoracic outlet structures could be compressed by the first thoracic rib and that surgical removal of the rib alleviated associated symptoms. Brickner and Milch,7 in 1925, suggested strengthening the shoulder girdle suspensory muscles in patients with thoracic outlet compression but without a cervical rib. Adson and Coffey8 were the first to describe successful relief of thoracic outlet compression by sectioning the scalenus anticus muscle in their 1927 report. Their results were confirmed in similar reports by Ochsner and colleagues9 in 1935 and Naffziger and Grant10 in 1938. Costoclavicular level neurovascular compression secondary to hyperabduction of the arm was first described by Lewis and Pickering11 in 1934 and later by Eden in 1939.12 Vascular compression in this region was defined as costoclavicular syndrome by Falconer and Weddel13 in 1943. Wright,14 in 1945, reported on a hyperabduction syndrome in which the second part of the axillary artery is
The thoracic outlet is the space extending from the supraclavicular fossa to the axilla; it includes the costoclavicular space, which is the interval between the clavicle and first rib. The anterior primary rami of the C5-T1 nerves exit their respective intervertebral foramen to form the brachial plexus as they pass through the anterior and middle scalene muscles (Fig. 27-1). The anterior scalene muscle originates from the transverse processes of the third through sixth cervical vertebrae and inserts posterior to the subclavian vein onto the first rib. The middle scalene muscle originates from the transverse processes of the second through seventh cervical vertebrae and inserts behind the subclavian artery into the first rib. The subclavian artery joins the trunks of the brachial plexus lying on the anterior aspect of the middle scalene muscle. Thus, the brachial plexus and subclavian artery travel through a triangle bordered by the middle scalene muscle laterally and the anterior scalene muscle medially, with the first rib as the base.18 The subclavian vein courses anterior to the anterior scalene muscle as it passes over the first rib, before joining the subclavian artery and brachial 325
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C3 C4
C6 Cervical rib C7
Anterior scalene muscle Middle scalene muscle Posterior scalene muscle Brachial plexus
C5
C6
Fibrous bands
T1
Subclavian artery C7 T1
Figure 27-2. Fibrous bands originating from a cervical rib. Figure 27-1. Thoracic outlet anatomy.
plexus as they pass through the costoclavicular space and continue beneath the coracoid process, posterior to the pectoralis minor muscle. Although there is considerable controversy regarding the exact pathophysiology of thoracic outlet syndrome, there are several basic concepts. Symptomatic compression of the neurovascular structures results from a mechanical space problem of the thoracic outlet. One theory states that afflicted patients have one or more congenital anomalies that predispose them to developing symptoms. Any superimposed trauma or insult can narrow the available space further and cause compression from muscle swelling, hemorrhage, or fibrosis.19 Such congenital anomalies include cervical ribs, fibrous bands, and scalene muscle abnormalities (Fig. 27-2). A well-developed cervical rib is the most common bony abnormality associated with thoracic outlet syndrome.20 It has been found in approximately 0.5% to 1% of the general population, with approximately 50% of patients demonstrating bilaterality.21 Several clinicians have noted compression in patients in the absence of cervical ribs and have determined the presence of congenital fibrous bands connecting an elongated cervical transverse process or adventitial rib to the first rib as an important causative factor.22-25 Compression of the brachial plexus can result from abnormalities of the first rib. Roos22 has described nine different types of congenital bands that could produce compression in the thoracic outlet. Swank and Simon23 have described variations in the insertion of the scalene muscles on the first rib, and others have targeted the anterior scalene muscle as the ultimate culprit.24,25 Another theory in the pathogenesis of thoracic outlet syndrome proposes that conditions that increase the
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descent of the scapula further bring the neurovascular structures downward and can result in compression.18 Injury to the neck or trapezius and other supporting structures, with later weakness or disuse atrophy, could increase the descent of the scapula and result in symptoms.26,27 Other aggravating factors include obesity and poor posture. Lastly, the costoclavicular space can be narrowed from exuberant callus formation from a clavicular nonunion or malunion,28,29 an anomalous subclavius muscle,30 or pulling the shoulders down and back as if in a military brace position. The clinical presentation of thoracic outlet syndrome is highly variable, depending on which neurovascular structures at risk are compressed—neurologic, arterial, or venous. Thus, there are no pathognomonic signs or symptoms to confirm this syndrome, and it is often a diagnosis of exclusion.31 The disorder is most commonly found in women. Thoracic outlet syndrome has been reported in baseball players, rowers,32 swimmers,33,34 wrestlers,35 football players,36 and long distance runners.37 Many patients report an episode of trauma preceding the onset of symptoms.19,31,38,39 Although the subjective complaints can vary secondary to the compromised thoracic outlet structures, up to 98% of patients report some neurologic symptoms.19 In a study of 236 patients with a diagnosis of thoracic outlet syndrome who later underwent transaxillary first rib resection, paresthesia of the hand was the most common complaint, present in 90% of patients, with the little finger affected four times as often as the thumb.38 Most patients identify symptoms in the ulnar nerve or lower trunk distribution. Pain can be present in the hand, forearm, arm, neck, chest, and head. Because of intrinsic muscle involvement, weakness of grip strength and loss of manual dexterity may be noticeable. An athlete may
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also complain of fatigue, weakness, or heaviness of the upper extremity. Significant vascular compression can result in swelling, cyanosis, coldness, pallor, and fatigue or claudication-type symptoms with exercise. Leffert and Perlmutter,38 in 1999, reported overhead activities as being provocative in 89% of patients, and symptoms could usually be reproduced with specific athletic activities and relieved with rest.
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rotation while the examiner palpates the ipsilateral radial pulse (Fig. 27-4). Again, elimination or diminution of the pulse with reproduction of symptoms is considered a positive test result. As originally described, the Wright maneuver was believed to reproduce compression of the axillary artery in the subcoracoid region under the pectoralis minor muscle. In the Roos stress test,22 both shoulders are placed in 90 degrees of abduction and external rotation and the patient is asked to open and close the hands for several minutes. Reproduction of symptoms with pain, paresthesia, or a sense of heaviness is considered a positive test result. In the costoclavicular maneuver, the patient thrusts both shoulders downward and backward, similar to a military brace position (Fig. 27-5). This maneuver decreases the space between the first rib and clavicle, with reproduction of symptoms in a positive test.
A careful neurovascular examination of the neck, shoulder girdle, and upper extremity should be performed. Subtle findings on inspection may include scapular ptosis, trapezial atrophy, and a more horizontally oriented clavicle. The supraclavicular fossa can demonstrate tenderness to palpation, and Tinel’s sign over the brachial plexus can sometimes be elicited. Detailed manual muscle testing may reveal weakness of the interossei and hypothenar musculature. Most patients have no sensory deficits, although sometimes hypesthesia and hypalgesia are found in the little finger, hypothenar eminence, and medial aspect of the forearm.38 Some classic but nonspecific tests for thoracic syndrome are the Adson test,24 the Wright maneuver,14 the Roos, or overhead stress test,22 and the costoclavicular maneuver. During the Adson test,24 the patient extends the neck, turns the head toward the affected shoulder, and inhales deeply (Fig. 27-3). The examiner palpates the ipsilateral radial pulse with the patient’s arm lying at his or her side. Elimination or diminution of the pulse while simultaneously reproducing the patient’s symptoms constitutes a positive test result. This test was originally believed to be pathognomonic for scalenus anticus syndrome. In the Wright maneuver,14 the affected arm is brought into progressive hyperabduction and external
Although these classic provocative maneuvers are often performed during the examination of the patient with suspected thoracic outlet syndrome, they are not specific. Studies have demonstrated obliteration of the radial pulse in asymptomatic subjects during the Adson, Wright, and costoclavicular maneuvers.40,41 Rayan and Jensen41 have performed provocative maneuvers in 200 extremities in 100 asymptomatic volunteers and found a vascular response present in 27 extremities during the Adson maneuver (13.5%), 114 extremities for the Wright maneuver (57%), and 94 extremities for the costoclavicular maneuver (47%). The neurologic response was present in 4 extremities for the Adson maneuver (2%), 33 extremities for the Wright maneuver (16.5%), and 20 extremities for the costoclavicular maneuver (10%). Thus, each test result should only be considered positive if it reproduces the patient’s symptoms.
Figure 27-3. The Adson test.
Figure 27-4. The Wright, or hyperabduction, maneuver.
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Figure 27-5. The costoclavicular maneuver.
The diagnosis of thoracic outlet syndrome remains clinical, although ancillary studies can provide additional information. Cervical spine radiographs should be obtained in all patients to evaluate for cervical spondylolysis, because cervical radiculopathy can mimic symptoms of thoracic outlet syndrome. Radiographs should also be inspected for the presence of cervical ribs (Fig. 27-6), elongated C7 transverse processes, and irregularities of the clavicle or first rib. A chest radiograph may reveal evidence of a Pancoast tumor that is causing referred shoulder pain. Magnetic resonance imaging (MRI) of the cervical spine is warranted if symptoms are primarily consistent with cervical nerve root compression. MRI of the thoracic outlet has recently been described to evaluate for evidence of brachial plexus compression or structural pathology,42-44 although some clinicians have not found MRI to be helpful in the diagnosis.45 Electrodiagnostic studies, including somatosensory evoked potentials, electromyography (EMG), and nerve conduction velocities have also been used to help determine the diagnosis. Brachial plexus compression is often intermittent and positional; thus, there are usually no fixed neurologic deficits that can be identified.46 Electrodiagnostic studies are helpful in the examination of a patient with a suspected concurrent or isolated lesion of a peripheral nerve.47 Vascular evaluation with arterial angiography or venography should be limited to cases with strong evidence of serious vascular pathology, such as acute subclavian or axillary artery occlusion or effort thrombosis. Ancillary tests, in conjunction with the clinical presentation and physical examination, are useful for narrowing the differential diagnosis, which includes cervical
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Figure 27-6. Radiographic demonstration of a cervical rib.
spine pathology, ulnar neuropathy, carpal tunnel syndrome, brachial neuritis, supraclavicular fossa or lung pathology, reflex sympathetic dystrophy, cardiac disease, and glenohumeral instability.18,38 The initial treatment for thoracic outlet syndrome is almost always nonoperative as long as there is no severe limb-threatening vascular compromise. An exercise program focused on correction of postural abnormalities and strengthening of the shoulder girdle and scapular musculature is essential. It is important that exercises involving shoulder bracing and overhead activity be avoided because they may aggravate symptoms.15,18,20,48 Other principles of nonoperative management include relative rest, nonsteroidal anti-inflammatory drugs (NSAIDs), weight reduction, if indicated, and avoidance of precipitating activities. In the first report of thoracic outlet compression in athletes, Strukel and Garrick in 1978 successfully treated four athletes conservatively to allow safe return to competition.32 Most cases of thoracic outlet syndrome may be successfully treated conservatively; however, there are certain cases that do require surgical intervention for optimal treatment. The most common indication for surgical management of thoracic outlet syndrome is failure of a carefully supervised postural re-education and exercise program. Other
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indications include impending vascular compromise of the extremity, intractable pain after exhaustion of every measure of conservative treatment, and the presence of a significant neurologic deficit, such as severe intrinsic wasting of the hand.38 Many different surgical procedures have been described, including scalenotomy, pectoralis minor tenotomy, claviculectomy, first rib resection, resection of cervical ribs or fibromuscular bands, or combinations of these procedures. Although there is controversy regarding the optimal surgical procedure and approach, the most commonly performed operation is a transaxillary first rib resection, with decompression of the thoracic outlet. Because of the many procedures and approaches described, lack of a standardized evaluation, and reports of mixed patient populations, it is difficult to determine the true outcomes of thoracic outlet surgery, especially in athletes.31 Most surgeons report good to excellent results, with emphasis on proper diagnosis and patient selection.
Axillary Artery Occlusion and Aneurysm The axillary artery is the main artery of the upper extremity and originates as a continuation of the subclavian artery at the lateral margin of the first rib. The artery has six primary branches and is divided into three parts based on its relation to the pectoralis minor muscle (Fig. 27-7). The first part is proximal to the muscle; this includes the superior thoracic artery. The second part is posterior to the muscle and has the thoracoacromial and lateral thoracic artery
1 2 3
Axillary artery Pectoralis minor muscle
Figure 27-7. Anatomy of the axillary artery. The first part is proximal to the pectoralis minor muscle (1), the second part is posterior to the muscle (2), and the third part is located distal to the muscle (3).
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branches. The third part is located distally to the pectoralis minor; this includes the anterior and posterior humeral circumflex and subscapular arteries. In 1945, Wright described a “hyperabduction syndrome,” in which the second part of the axillary artery was occluded by the overlying pectoralis minor muscle when the arm was brought overhead.14 Tullos and associates,49 in 1972, were the first to report on a major league pitcher with axillary artery occlusion. They postulated that in the cocking phase of pitching, the arm is brought into abduction, extension, and extreme external rotation, with resultant transient occlusion of the axillary artery by a stretched pectoralis minor muscle. Over time, with the repetitive trauma of pitching, enough injury was inflicted to produce intimal damage and subsequent thrombosis. The pectoralis minor and humeral head have been shown to be hypertrophied in pitchers.50,51 Such structures might be more prone to compress adjacent neurovascular structures. McCarthy and coworkers,52 in their report on 11 athletes with thoracic outlet compression, have noted compression of the subclavian and axillary arteries and their branches by hypertrophied anterior scalene and pectoralis minor muscles; the 6 baseball pitchers treated with anterior scalene or pectoralis minor resection all returned to competition. Other clinicians have documented compression of the third part of the axillary artery by the humeral head. Using duplex Doppler scanning, Rohrer and colleagues53 have demonstrated that with the arm in the throwing position, the axillary artery is compressed by the humeral head in 83% of the 92 arms examined; however, there is more than 50% stenosis in only 7.6% of arms. It was concluded that this intermittent compression of the axillary artery by the humeral head predisposes the throwing athlete to axillary artery thrombosis. In conjunction with thrombosis of the axillary artery, there have been many reports describing aneurysms of the axillary artery and its branches in overhead athletes.49,52-59 The humeral circumflex arteries encircle the surgical neck of the humerus and tether the axillary artery in a fixed position relative to the humerus. In the throwing motion, with downward displacement of the humeral head during abduction and external rotation, the axillary artery can become compressed proximally or stretched at its junction with the humeral circumflex arteries. Repeated compression can lead to intimal damage and thrombosis, and such repetitive stretching can lead to aneurysmal formation.54,60,61 Affected patients may complain of nonspecific symptoms of pain, intermittent paresthesia, digital pain, arm heaviness, and cold intolerance. The well-conditioned athlete may present initially with easy fatigability, loss of pitching velocity, loss of arm control, and the dead arm syndrome. On physical examination, the clinician may note signs of digital ischemia, such as ulcers, sluggish capillary refill of the digits, coolness to the affected extremity, and tenderness about the
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pectoralis minor. The physician should attempt to palpate pulses and auscultate for bruits in the patient’s arm in the neutral and functional positions. Placing the arm in abduction and external rotation can sometimes reproduce symptoms. In addition to a detailed history and physical examination, the diagnosis requires a high index of suspicion and other ancillary studies. Noninvasive tests for vascular pathology include duplex Doppler scanning, pulse volume recording, and digital photoplethysmography.61 The definitive test is positional angiography to define the arterial anatomy clearly, identify areas of compression, occlusion, and aneurysm formation, and evaluate the distal arterial architecture for sites of embolization. Nonoperative treatment is generally not effective for axillary artery compression and aneurysm. Anticoagulation has been used primarily as an adjunct to surgical intervention but has sometimes been used as the sole therapy. Rohrer and associates53 have treated a major league pitcher with axillary artery thrombosis with an intra-arterial urokinase infusion, followed by aspirin and dipyridamole. Recurrent occlusion was treated with a similar course of urokinase followed by warfarin (Coumadin). Maintenance therapy with subcutaneous heparin injections after pitching outings allowed resumption of his career, with no further episodes. Common surgical options include sympathectomy, decompression with muscle resection, and various vascular reconstructive procedures.49,52,57,61,62 Tullos and coworkers49 initially performed a transthoracic cervical sympathectomy on a major league pitcher with complete occlusion of the axillary artery. He was able to pitch effectively for almost 2 years until recurrence of symptoms required a subclavian to brachial artery bypass graft. In the vascular and orthopedic literature, McCarthy52 and Nuber57 and colleagues have reported on a group of athletes with symptomatic compression or occlusion of the subclavian or axillary arteries and their branches. Patients with subclavian aneurysms were treated with a saphenous vein bypass graft and cervical rib resection. The athletes with muscular compression were treated with resection of the anterior scalene, pectoralis minor muscles, or both. Specific arterial branch compressions were freed with dissection. All pitchers except one were able to return to their previous levels of competition. In the presence of an aneurysm, surgical options include bypass grafting and segmental resection with patching or primary anastomosis. Todd and associates60 have reported on two major league pitchers with symptomatic aneurysms of the axillary artery at the origin of the circumflex humeral arteries who were successfully treated with resection and reversed saphenous vein interposition graft. Arko and coworkers63 published their results of treatment of vascular complications in high-performance athletes. Seven patients, including five pitchers, one volleyball player, and one cyclist had aneurysms of the proximal upper extremity arteries. The five athletes with arteriographic evidence of significant distal
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embolization underwent preoperative lytic therapy. Six patients underwent operative intervention with resection— lateral arterial repair with vein patch angioplasty in four patients, and resection and reversed saphenous vein interposition graft in the remaining two patients. All six arterial reconstructions remained patent at a mean follow-up of 42.2 months, with each patient returning to competition without recurrent symptoms. Case reports of major league pitchers with aneurysms of axillary artery branches, who presented with digital ischemia of their pitching hands as a result of embolic phenomenon, have documented successful return to competition after resection and arterial repair.55,61 Ishitobi and colleagues62 have performed extra-anatomic bypass grafting with a reversed saphenous vein graft anterior to the pectoralis minor muscle and posterior to the pectoralis major muscle in four Japanese baseball pitchers with axillary artery occlusion. All pitchers were able to continue pitching for 3 to 9 more years of competition. Long-term evaluation demonstrated normally functioning bypass grafts. Pitchers and other overhead athletes with complaints of early fatigue, claudication-type symptoms, or evidence of emboli require an early complete examination for axillary artery injury and prompt institution of appropriate therapy. Failure to recognize this disorder can lead to disastrous and catastrophic consequences. Fields and associates64 have reported on a major league pitcher who sustained a stroke, likely from retrograde propagation of a thrombus, with resultant complete occlusion of the innominate artery.
Effort Thrombosis The axillary vein originates at the lower border of the teres major muscle as a continuation of the basilic vein and becomes the subclavian vein at the lateral margin of the first rib. The axillosubclavian vein courses through a tunnel formed by the first rib posteroinferiorly, the clavicle and subclavius muscle anteriorly, the scalenus anticus muscle laterally, and the costoclavicular ligament medially.65 Compression of the axillosubclavian vein can occur at a number of locations along its anatomic course. The most commonly proposed site of compression is the costoclavicular space between the first rib and either the scalenus anticus muscle, clavicle, or costoclavicular ligament (Fig. 27-8).66 The costoclavicular space can be further narrowed by shoulder depression and especially by humeral abduction and external rotation. Described in separate publications by Paget in 187567 in London and Von Schroetter in 188468 in Vienna, primary or spontaneous thrombosis of the axillosubclavian vein typically affects young, healthy, athletic individuals. PagetSchroetter syndrome has also been called effort thrombosis because of its common association with repetitive or strenuous upper extremity activities.69-72 It has been theorized that chronic intermittent compression of the affected portion of the vein leads to intimal damage and subsequent inflammation and thrombosis.73 Effort thrombosis
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Costoclavicular compression area
Subclavian vein
Clavicle
1st rib
Axillary vein Figure 27-8. Anatomy of the axillosubclavian vein.
has been reported in many athletes, including football players,63 swimmers,74 hockey players,75 wrestlers,76 weightlifters,73 volleyball players,77 and elite pitchers in baseball.78 Although axillary vein thrombosis represents only 2% of all deep venous thrombosis cases, effort thrombosis is probably the most common vascular problem in athletes.79 Affected patients typically will give a history of strenuous or repetitive overhead activity before the onset of symptoms. Patients will complain of a feeling of arm heaviness or tiredness, dull aching pain, paresthesia, and easy fatigability during activities involving the extremity. On physical examination, the clinician may note swelling of the entire upper extremity with mottled, cool skin and dilated, prominent superficial veins (Fig. 27-9). Pulses are usually normal and symmetrical, although they may become diminished with the costoclavicular, Adson,24 and Wright14 maneuvers. The neurologic examination is normal, although nondermatomal hyperesthesia may be documented. Occasionally, tender cords may be palpated in the axilla. These physical signs may become even more
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pronounced when the patient is instructed to perform exercise tests or overhead activities. 20,77,78,80 The diagnosis of effort thrombosis is often made with a complete history and physical examination; it is confirmed with venography demonstrating occlusion or substantial narrowing of the axillosubclavian vein in the area of the clavicle and first rib (Fig. 27-10). Venography must be considered the gold standard test for diagnosis.81 Treat and coworkers77 have discussed the role of Doppler ultrasound versus venography and determined that Doppler studies have limited use in the evaluation of patients with effort thrombosis. Additionally, some physicians have advocated serologic screening for a possible hypercoagulable state.78 The goals in treatment of Paget-Schroetter syndrome of the athlete include immediate relief of the venous obstruction, correction of any predisposing anatomic abnormalities, prevention of recurrent thrombosis, and a safe return to competition.82 Historically, patients with effort thrombosis were treated nonoperatively with bed rest, arm elevation, and anticoagulation with heparin and warfarin.69,70,78,83-85 However, many reports have documented a high rate of disabling residual symptoms with this treatment. Adams and DeWeese,84 in 1971, noted late residual symptoms of swelling, pain, and superficial thrombophlebitis in 68% of patients and a troubling 12% incidence of pulmonary embolism. The presence of these persistent symptoms has led to more aggressive treatment. Currently, management of effort thrombosis includes a multidisciplinary approach with venography, followed by thrombolytic therapy and surgical decompression of the thoracic outlet. Many reports have documented the efficacy of early thrombolytic therapy with streptokinase or urokinase.65,69,73,78,81,83,86-89 Through venography and thrombolysis, it was discovered that most patients had compression of the axillosubclavian vein in the costoclavicular space, which was accentuated with humeral abduction and external rotation.70,73,87 Whereas venous thrombosis occurs
B
A
Figure 27-9. Vein dilation. A, Shoulder. B, Arm.
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Figure 27-10. Venogram showing effort thrombosis.
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in 1.5% to 12% of patients with thoracic outlet syndrome, approximately 80% of patients with Paget-Schroetter syndrome have thoracic outlet compression.90 Surgical decompression of the thoracic outlet has been recommended for these patients. The risk for subsequent thrombosis is increased from recurrent compression on the vein causing repeated intimal injury, venous stasis, and a transient hypercoagulable state.89 Controversy exists about the optimal approach and timing of surgical decompression for these patients. Some clinicians have advocated a transaxillary approach with first rib resection and division of the scalenus anticus muscle,65,82,89 whereas others have advocated a supraclavicular approach.63,70 Early surgery is recommended by some who believe that thrombolysis, followed by prompt surgical decompression, should be considered the standard of care in the management of effort thrombosis.65,70,82 Others prefer the traditional staged approach of thrombolysis, followed by an intervening period of anticoagulation before surgical decompression.89 It is critical that thrombolysis therapy be instituted promptly. Numerous reports have demonstrated the efficacy of acute intervention and treatment with superior results compared with delayed intervention.65,91,92 Patients with Paget-Schroetter syndrome can expect excellent clinical results with a low rate of residual symptoms with an early diagnosis, thrombolysis and, if indicated, thoracic outlet decompression.89 Even though the syndrome is rare, athletes who perform repetitive and vigorous upper extremity activities are at risk for developing effort thrombosis. Physicians should be familiar with the signs and symptoms associated with this condition so that appropriate therapy may be instituted early.
Quadrilateral Space Syndrome The quadrilateral, or quadrangular space, is located over the posterior scapular and subdeltoid regions. The boundaries include the teres minor superiorly, the long head of the triceps medially, the teres major inferiorly, and the surgical neck of the humerus laterally (Fig. 27-11). The neurovascular bundle, consisting of the axillary nerve and posterior humeral circumflex artery, passes through the space. In a critical review of the results of thoracic outlet syndrome surgery, many failures were noted that seem to have the common denominator of occlusion of the posterior humeral circumflex artery in the position of abduction and external rotation.93,94 Further investigations have led to the description of quadrilateral space syndrome. This syndrome is an uncommon neurovascular compression syndrome, primarily affecting young active adults.95 Patients usually present with complaints of intermittent, poorly localized anterior shoulder pain. Concurrent paresthesia typically radiates in a nondermatomal distribution. Symptoms are aggravated with forward flexion, abduction, and external rotation. There is usually no
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Surgical neck of humerus
Teres minor m. Teres major m.
Axillary nerve
Posterior humeral circumflex artery Quadrilateral space Long head of triceps m. Figure 27-11. Anatomy of the quadrilateral space.
history of a specific injury, although the syndrome may be associated with chronic repetitive stress to the shoulder.95,96 On physical examination, discrete point tenderness is found posteriorly over the quadrilateral space.94 Symptoms are usually reproduced with the patient’s arm held flexed, abducted, and externally rotated for 1 minute. The neurologic examination and electrodiagnostic study results are usually normal, although sometimes deltoid atrophy may be seen.97 The definitive diagnosis is made with a subclavian arteriogram. The arteriogram is obtained with the arm held at the patient’s side and in an abducted, externally rotated position. In affected patients, the arteriogram will show a patent posterior humeral circumflex artery with the humerus at the side, but reveals occlusion of the artery when the humerus is abducted and externally rotated (Fig. 27-12). Magnetic resonance angiography has not been shown to have value in the diagnosis of quadrilateral space syndrome,98 and MRI findings demonstrating selective atrophy of the teres minor are only suggestive of the diagnosis in the appropriate clinical setting.99 There have been case reports of quadrilateral space syndrome caused by a paralabral cyst or ganglion as seen on MRI scans.100,101 Once the definitive diagnosis has been made, the initial treatment is nonoperative and includes rest, reassurance, symptomatic care, and physical therapy. Gentle internal rotation stretching of the glenohumeral joint, horizontal stretching into adduction, and posterior rotator cuff strengthening may help alleviate symptoms.80 Redler and associates102 have reported on a baseball pitcher who experienced symptomatic relief and continued pitching after changing
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A
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B
Figure 27-12. Arteriograms showing compression of posterior humeral circumflex artery. A, Patient’s arm at side. B, Patient’s arm abducted.
his delivery from an overhead to a three-quarters overhead pitching motion. On average, 30% of patients will have continued symptoms, despite appropriate conservative treatment, that warrant surgical management.94,95 Reports of operative treatment have consisted largely of small patient series.94-96,103 In the largest report to date, Cahill and Palmer94 have described 18 patients whom they treated operatively with decompression of the quadrilateral space through a posterior approach. At surgery, they discovered obliquely oriented fibrous bands filling the space and tethering the neurovascular bundle. After the fibrous bands were released, decompression was deemed to be adequate when the posterior humeral circumflex artery pulse remained palpable in the position of abduction and external rotation. Of these 18 patients, 16 had partial or complete resolution of symptoms. Symptoms were believed to arise from compression of the axillary nerve and its afferent fibers by the fibrous bands. The origin of these fibrous bands remains unknown, and Cahill and Palmer were unable to identify these bands in cadavers. It has been theorized that normal structures in the quadrilateral space may fibrose and scar after chronic repetitive overhead activity, resulting in pathologic anatomy and compression.20,95
SUMMARY Although relatively rare, neurovascular compression syndromes of the shoulder can be a significant cause of disability and can prevent an athlete from performing at his or her highest level. Early diagnosis and institution of therapy require a detailed history and physical examination, a high index of suspicion, and selective use of ancillary studies. With appropriate treatment, most athletes are able to return to sports successfully.
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References 1. Tyson RR, Kaplan GF: Modern concepts of diagnosis and treatment of the thoracic outlet syndrome. Orthop Clin North Am 6:507-519, 1975. 2. Coote H: Pressure on the axillary vessels and nerve by an exostosis from a cervical rib: Interference with the circulation of the arm, removal of the rib and exostosis; recovery. Med Times Gazette 2:108, 1861. 3. Murphy JB: A case of cervical rib with symptoms resembling subclavian aneurysm. Ann Surg 41:398-406, 1905. 4. Keen W: The symptomatology, diagnosis, and surgical treatment of cervical ribs. Am J Med Sci 133:173, 1907. 5. Stopford JSB, Telford ED: Compression of the lower trunk of the brachial plexus by a first dorsal rib with a note on the surgical treatment. Br J Surg 7:168, 1919. 6. Wheeler WI: Compression neuritis due to the normal first dorsal rib. Practitioner 104:409, 1920. 7. Brickner WM, Milch H: First dorsal simulating cervical rib by maldevelopment or by pressure symptoms. Surg Gynecol Obstet 40:38, 1925. 8. Adson AW, Coffey JR: Cervical rib: A method of anterior approach for relief of symptoms by division of the scalenus anticus. Ann Surg 85:839-857, 1927. 9. Ochsner A, Gage M, DeBakey M: Scalenus anticus (Naffziger) syndrome. Am J Surg 28:696-699, 1935. 10. Naffziger FC, Grant WT: Neuritis of the brachial plexus, mechanical in origin: The scalenus syndrome. Surg Gynecol Obstet 67:722, 1938. 11. Lewis T, Pickering G: Observations upon maladies in which the blood supply to the digits ceases intermittently or permanently. Clin Sci 1:327, 1934. 12. Eden JC: Vascular complications of cervical ribs and first thoracic rib abnormalities. Br J Surg 27:105, 1939. 13. Falconer MA, Weddel G: Costoclavicular compression of the subclavian artery and vein. Relation to the scalenus anticus syndrome. Lancet 2:539, 1943. 14. Wright IS: The neurovascular syndrome produced by hyperabduction of the arms. Am Heart J 29:1-19, 1945.
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15. Peet RM, Hendirksen JD, Anderson TD, et al: Thoracic outlet syndrome: Evaluation of a therapeutic exercise program. Mayo Clin Proc 31:281-287, 1956. 16. Brantigan CO, Roos DB: Etiology of neurogenic thoracic outlet syndrome. Hand Clin 20:17-22, 2004. 17. Wood VE, Twito R, Versake JM: Thoracic outlet syndrome: The results of first rib resection in 100 patients. Orthop Clin North Am 19:131-146, 1988. 18. Leffert RD: Thoracic outlet syndrome. J Am Acad Orthop Surg 2:317-325, 1994. 19. Brantigan CO, Roos DB: Diagnosing thoracic outlet syndrome. Hand Clin 20:27-36, 2004. 20. Kaminsky SB, Baker CL Jr: Neurovascular injuries in the athlete’s shoulder. Sports Med Arthrosc Rev 8:170-181, 2000. 21. Pollack EW: Surgical anatomy of the thoracic outlet syndrome. Surg Gynecol Obstet 150:97-103, 1980. 22. Roos DB: Congenital anomalies associated with thoracic outlet syndrome. Anatomy, symptoms, diagnosis, and treatment. Am J Surg 132:771-778, 1976. 23. Swank RL, Simon FA: The scalenus anticus syndrome: Types, their characterization, diagnosis and treatment. Arch Neurol Psych 51:432-445, 1944. 24. Adson AW: Surgical treatment for symptoms produced by cervical ribs and the scalenus anticus muscle. Surg Gynecol Obstet 85:687-700, 1947. 25. Adson AW: Cervical ribs: Symptoms, differential diagnosis and indications for section of the insertion of the scalenus anticus muscle. J Int Coll Surg 16:546-559, 1951. 26. Capistrant TD: Thoracic outlet syndrome in whiplash injury. Ann Surg 185:175-178, 1977. 27. Mulder DS, Greenwood FAH, Brooks CE: Posttraumatic thoracic outlet syndrome. J Trauma 13:706-715, 1973. 28. Jupiter JB, Leffert RD: Non-union of the clavicle. Associated complications and surgical management. J Bone Joint Surg Am 69:753-760, 1987. 29. Fujita K, Matsuda K, Sakai Y, et al: Late thoracic outlet syndrome secondary to malunion of the fractured clavicle: Case report and review of the literature. J Trauma 50:332-335, 2001. 30. Hasan SS, Romeo AA: Thoracic outlet syndrome secondary to an anomalous subclavius muscle. Orthopedics 24: 793-794, 2001. 31. Safran MR: Nerve injury about the shoulder in athletes, part 2. Long thoracic nerve, spinal accessory nerve, burners/ stingers, thoracic outlet syndrome. Am J Sports Med 32:1063-1076, 2004. 32. Strukel RJ, Garrick JG: Thoracic outlet compression in athletes: A report of four cases. Am J Sports Med 6:35-39, 1978. 33. Katirji B, Hardy RW Jr: Classic neurogenic thoracic outlet syndrome in a competitive swimmer: a true scalenus anticus syndrome. Muscle Nerve 18:229-233, 1995. 34. Richardson AB: Thoracic outlet syndrome in aquatic athletes. Clin Sports Med 18:361-378, 1999. 35. Karageanes SJ, Jacobs AW: Anomalous first rib in a high school wrestler. Clin J Sports Med 8:240-242, 1998. 36. Tucker AM: Shoulder pain in a football player. Med Sci Sports Exerc 26:281-284, 1994. 37. Leung YF, Chung OM, Ip IS, et al: An unusual case of thoracic outlet syndrome associated with long distance running. Br J Sports Med 33:279-281, 1999. 38. Leffert RD, Perlmutter GS: Thoracic outlet syndrome: Results of 282 transaxillary first rib resections. Clin Orthop Relat Res 368:66-79, 1999.
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39. Sanders RJ, Hammond SL: Etiology and pathology. Hand Clin 20:23-26, 2004. 40. Eklof B: Vascular compression syndromes of the upper extremitiy. Acta Chir Scand 465:74-77, 1976. 41. Rayan GM, Jensen C: Thoracic outlet syndrome: Provocative examination maneuvers in a typical population. J Shoulder Elbow Surg 4:113-117, 1995. 42. Panegyres PK, Moore N, Gibson R, et al: Thoracic outlet syndromes and magnetic resonance imaging. Brain 116:823-841, 1993. 43. Collins JD, Disher AC, Miller TQ: The anatomy of the brachial plexus as displayed by magnetic resonance imaging: Technique and application. J Natl Med Assoc 87:489-498, 1995. 44. Espositio MD, Arrington JA, Blackshear MN, et al: Thoracic outlet syndrome in a throwing athlete diagnosed with MRI and MRA. J Magn Reson Imaging 7:598-599, 1997. 45. Poole GV, Thomas KR: Thoracic outlet syndrome reconsidered. Am Surg 62:287-291, 1996. 46. Leiberman JL, Taylor RG: Electrodiagnosis in upper extremity nerve compression. In Szabo RM (ed): Nerve Compression Syndromes: Diagnosis and Treatment. Winsdale, Ontario, Canada, Slack, 1989, pp 67-88. 47. Wood VE, Biondi J: Double-crush nerve compression in thoracic outlet syndrome. J Bone Joint Surg Am 72:85-87, 1990. 48. Britt LP: Nonoperative treatment of the thoracic outlet syndrome symptoms. Clin Orthop Relat Res 51:45-48, 1967. 49. Tullos HS, Erwin WD, Woods GW, et al: Unusual lesions of the pitching arm. Clin Orthop Relat Res 88:169-182, 1972. 50. Jones HH, Priest JD, Hayes WC, et al: Humeral hypertrophy in response to exercise. J Bone Joint Surg Am 59:204-208, 1977. 51. King JW, Brelsford HJ, Tullos HS: Analysis of the pitching arm of the professional baseball pitcher. Clin Orthop Relat Res 67:116-123, 1969. 52. McCarthy WJ, Yao JS, Schafer MF, et al: Upper extremity arterial injury in athletes. J Vasc Surg 9:317-327, 1989. 53. Rohrer MJ, Cardullo PA, Pappas AM, et al: Axillary artery compression and thrombosis in throwing athletes. J Vasc Surg 11:761-769, 1990. 54. Durham JR, Yao JS, Pearce WH, et al: Arterial injuries in the thoracic outlet syndrome. J Vasc Surg 21:57-70, 1995. 55. Kee ST, Dake MD, Wolfe-Johnson B, et al: Ischemia of the throwing hand in major league baseball pitchers: Embolic occlusion from aneurysms of axillary artery branches. J Vasc Interv Radiol 6:979-982, 1995. 56. Lee AW, Hopkins SF, Griffen WO Jr: Axillary artery aneurysm as an occult source of emboli to the upper extremity. Am Surg 53:485-486, 1987. 57. Nuber GW, McCarthy WJ, Yao JS, et al: Arterial abnormalities of the shoulder in athletes. Am J Sports Med 18: 514-519, 1990. 58. Reekers JA, den Hartog BM, Kuyper CF, et al: Traumatic aneurysm of the posterior humeral circumflex artery: A volleyball player’s disease? J Vasc Interv Radiol 4:405-408, 1993. 59. Rosi G, Pichot O, Bosson JL, et al: Echographic and Doppler screening of the forearm arteries in professional volleyball players. Am J Sports Med 20:604-606, 1992. 60. Todd GJ, Benvenisty AI, Hershon S, Bigliani LU: Aneurysms of the mid-axillary artery in major league baseball pitchers: A report of two cases. J Vasc Surg 28:702-707, 1998. 61. Schneider K, Kasparyan NG, Altchek DW, et al: An aneurysm involving the axillary artery and its branch vessels in a
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major league baseball pitcher: A case report and review of the literature. Am J Sports Med 27:370-375, 1999. Ishitobi K, Moteki K, Nara S, et al: Extra-anatomic bypass graft for management of axillary artery occlusion in pitchers. J Vasc Surg 33:797-801, 2001. Arko FR, Harris EJ, Zarins CK, Olcott C IV:Vascular complications in high-performance athletes. J Vasc Surg 33: 935-942, 2001. Fields WS, Lemak NA, Ben-Menachem Y: Thoracic outlet syndrome: Review and reference to stroke in a major league pitcher. Am J Neuroradiol 7:73-78, 1986. Urschel HC Jr, Razzuk MA: Paget-Schroetter syndrome: What is the best management? Ann Thor Surg 69: 1663-1669, 2000. Sanders RJ, Haug C: Subclavian vein obstruction and thoracic outlet syndrome: A review of the etiology and management. Ann Vasc Surg 4:397-410, 1990. Paget J: Clinical Lectures and Essays. London, Longmans Green, 1875. Von Schroetter L: Erkrandungen der gefossl. In Nathnogel Handbuch der Pathologie und Therapie. Vienna, Holder, 1884. AbuRahma AF, Sadler D, Stuart P, et al: Conventional versus thrombolytic therapy in spontaneous (effort) axillarysubclavian vein thrombosis. Am J Surg 161:459-465, 1991. Azakie A, McElhinney DB, Thompson RW, et al: Surgical management of subclavian vein effort thrombosis as a result of thoracic outlet compression. J Vasc Surg 28:777-786, 1998. Cohen GS, Braunstein L, Ball DS, et al: Effort thrombosis: Effective treatment with a vascular stent after unrelieved venous stenosis following a surgical release procedure. Cardiovasc Intervent Radiol 19:37-39, 1996. Dunant JH: “Effort” thrombosis, a complication of thoracic outlet syndrome. Vasa 10:322-324, 1981. Sheeran SR, Hallisey MJ, Murphy TP, et al: Local thrombolytic therapy as part of a multidisciplinary approach to acute axillosubclavian vein thrombosis (Paget-Schroetter syndrome). J Vasc Interv Radiol 8:253-260, 1997. Vogel CM, Jensen JE: “Effort” thrombosis of the subclavian vein in a competitive swimmer. Am J Sports Med 13: 269-272, 1985. Butsch JL: Subclavian thrombosis following hockey injuries. Am J Sports Med 11:448-450, 1983. Medler RG, McQueen DA: Effort thrombosis in a young wrestler. A case report. J Bone Joint Surg Am 75:1071-1073, 1993. Treat SD, Smith PA, Wen DY, Kinderknecht JJ: Deep vein thrombosis of the subclavian vein in a college volleyball player. Am J Sports Med 32:529-532, 2004. DiFelice GS, Paletta GA, Phillips BB, Wright RW: Effort thrombosis in the elite throwing athlete. Am J Sports Med 30:708-712, 2002. Sotta RP: Vascular problems in the proximal upper extremity. Clin Sports Med 9:379-388, 1990. Baker CL Jr, Liu SH: Neurovascular injuries to the shoulder. J Orthop Sports Phys Ther 18:360-364, 1993. Machleder HI: Evaluation of a new treatment strategy for Paget-Schroetter syndrome: Spontaneous thrombosis of the axillary-subclavian vein. J Vasc Surg 17:305-317, 1993. Angle N, Gelabert HA, Farooq MM, et al: Safety and efficacy of early surgical decompression of the thoracic outlet for Paget-Schroetter syndrome. Ann Vasc Surg 15:37-42, 2001.
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83. Urschel HC Jr, Razzuk MA: Neurovascular compression in the thoracic outlet: Changing management over 50 years. Ann Surg 228:609-617, v. 84. Adams JT, DeWeese JA: “Effort” thrombosis of the axillary and subclavian veins. J Trauma 11:923-930, 1971. 85. Hughes ESR: Venous obstruction in the upper extremity. Br J Surg 36:155-163, 1949. 86. Becker GJ, Holden RW, Rabe FE, et al: Local thrombolytic therapy for subclavian and axillary thrombosis. Radiology 149:419-423, 1983. 87. Kunkel JM, Machleder HI: Treatment of Paget-Schroetter syndrome: A staged, multidisciplinary approach. Arch Surg 124:1153-1158, 1989. 88. Druy EM, Trout HH III, Giordano JM: Lytic therapy in the treatment of axillary and subclavian vein thrombosis. J Vasc Surg 2:821-827, 1985. 89. Adelman MA, Stone DH, Riles TS, et al: A multidisciplinary approach to the treatment of Paget-Schroetter syndrome. Ann Vasc Surg 11:149-154, 1997. 90. Machleder HI: Thrombolytic therapy for acute primary axillosubclavian vein thrombosis. In Comerota A (ed): Thrombolytic therapy for peripheral vascular disease. Philadelphia, JB Lippincott, 1995, pp 197-207. 91. Molina JE: Need for emergency treatment in subclavian vein effort thrombosis. J Am Coll Surg 181:414-420, 1995. 92. Molina JE: Surgery for effort thrombosis of the subclavian vein. J Thorac Cardiovasc Surg 103:341-346, 1992. 93. Cahill BR: Quadrilateral space syndrome. In Omer GE, Spinner M (eds): Management of Peripheral Nerve Problems. Philadelphia, WB Saunders, 1980, pp 602-606. 94. Cahill BR, Palmer RE: Quadrilateral space syndrome. J Hand Surg 8:65-69, 1983. 95. Lester B, Jeong GK, Weiland AJ, Wickiewicz TL: Quadrilateral space syndrome: Diagnosis, pathology, and treatment. Am J Orthop 28:718-722,725, 1999. 96. Francel TJ, Dellon AL, Campbell JN: Quadrilateral space syndrome: Diagnosis and operative decompression technique. Plast Reconstr Surg 87:911-916, 1991. 97. Chautems RC, Glauser T, Waeber-Fey MC, et al: Quadrilateral space syndrome: Case report and review of the literature. Ann Vasc Surg 14:673-676, 2000. 98. Mochizuki T, Isoda H, Masui T, et al: Occlusion of the posterior humeral circumflex artery: Detection with MR angiography in healthy volunteers and in a patient with quadrilateral space syndrome. Am J Roentgenol 163:625-627, 1994. 99. Linker CS, Helms CA, Fritz RC: Quadrilateral space syndrome: Findings at MR imaging. Radiology 188:675-676, 1993. 100. Sanders TG, Tirman PF: Paralabral cyst: An unusual cause of quadrilateral space syndrome. Arthroscopy 15:632-637, 1999. 101. Ishima T, Usui M, Satah E, et al: Quadrilateral space syndrome caused by a ganglion. J Shoulder Elbow Surg 7:80-82, 1998. 102. Redler MR, Ruland LJ 3rd, McCue FC 3rd: Quadrilateral space syndrome in a throwing athlete. Am J Sports Med 14:511-513, 1986. 103. McKowen HC, Voorhies RM: Axillary nerve entrapment in the quadrilateral space: Case report. J Neurosurg 66: 932-934, 1987.
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CHAPTER 28 Brachial Plexus Injuries Tandy R. Freeman and William G. Clancy, Jr.
Athletic injuries to the brachial plexus and peripheral nerves about the shoulder are most commonly seen in contact sports, such as American football. Hirasawa and Sakakida1 have reported that among 1176 cases of peripheral nerve and brachial plexus injuries treated over an 18-year period, only 66 were related to sports. Of these, 16 were compression injuries to the brachial plexus. They also noted a report by Takazawa and colleagues2 of only 28 peripheral nerve injuries among 9550 sports injuries seen over 5 years. In contrast to these Japanese studies, Clarke3 has reported the incidence of brachial plexus injury in U.S. high school and college football players over a 4-year period to be 2.2 injuries per 100 players per year. Clancy and associates4 have noted a 30% to 50% incidence of transitory brachial plexus injuries over the course of high school or college career. Peripheral nerve injuries, although rare, tend to be more prevalent than brachial plexus injuries in sports other than football and wrestling, especially in noncontact sports.1 Prompt recognition, appropriate assessment, and proper treatment are essential for the safe and timely return of the injured athlete to participation.
Neurotmesis is an injury in which not only is the axon disrupted, but there is also loss of the integrity of the supporting stroma of the nerve, including the endoneurium. Nonoperative recovery is unlikely because of loss of continuity of the neural tube and, even with surgical repair or reconstruction, complete return of function is unlikely. Electromyographic studies have shown denervation patterns at 3 weeks and at 1 year or later.
ANATOMY An understanding of the anatomy of the brachial plexus is essential for establishing an accurate diagnosis and prognosis in brachial plexus injuries. The brachial plexus is formed in the neck from the ventral rami of cervical nerve roots V through VIII and the first thoracic nerve root and lies between the anterior and middle scalene muscles. It passes over the first rib and deep to the sternocleidomastoid and clavicle in its course. It may receive contributions from C4 (prefixed plexus) or T2 (postfixed plexus). The ventral (motor) and dorsal (sensory) roots at each level unite near or within the vertebral foramen to form the nerve roots (Fig. 28-2). The cell bodies of the sensory nerves in the dorsal root are located in the dorsal root ganglia, situated just proximal to the confluence of the ventral and dorsal roots and outside the spinal cord. Injury proximal to the dorsal ganglion—preganglionic lesion or root avulsion—is, at this time, irreparable and has a hopeless prognosis. Injury distal to the dorsal ganglion, postganglionic lesion, represents a peripheral nerve injury with the potential for recovery spontaneously or with surgical repair or reconstruction.
CLASSIFICATION OF NERVE INJURIES Seddon5 has classified peripheral nerve injuries based on the degree of injury, correlating histologic and clinical findings with prognosis. Injury may result in varying amounts of damage to neural fibers within a given nerve, producing a mixed clinical picture based on this classification system. Neurapraxia represents a physiologic interruption of nerve function without anatomic axonal disruption. Demyelination may occur,6-8 but repair is rapid. Function returns from within minutes to 3 weeks of injury, and neurophysiologic studies are normal at that time. Axonotmesis is an injury resulting in axonal disruption without significant injury to the supporting stroma, including the endoneurium, perineurium, and epineurium (Fig. 28-1). Wallerian degeneration of the axon occurs distally and, to some extent, proximally to the level of injury, but the neural tube remains intact. Return of function requires complete regeneration of the axon, which is facilitated by intact fascicles. Electromyographic studies at 3 weeks have revealed fibrillations and positive sharp waves, with loss of motor unit potentials in the denervated muscles. After recovery, the electromyogram (EMG) may show large motor unit potentials.
Just distal to the confluence of the ventral and dorsal roots, and as the nerve root exits the vertebral foramen, the root divides into ventral and dorsal rami. The ventral rami are larger and form the brachial plexus. The smaller dorsal rami innervate the paraspinal musculature and provide sensation dorsally. The ventral rami unite just above the clavicle to form the three trunks—upper (C5 to C6), middle (C7), and lower (C8 to T1; Fig. 28-3). The site of confluence of C5 and C6 is known as Erb’s point. Between the takeoff of the dorsal rami and Erb’s point, the long thoracic nerve (serratus anterior) arises from C5 through C7, and the dorsal scapular 337
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Vessel Epineurium Perineurium
medial brachial cutaneous, and medial antebrachial cutaneous nerves arise from the cords. The cords terminate in the five terminal branches—the musculocutaneous, axillary, radial, ulnar, and median nerves.
Endoneurium
Fascicle
Nerve fiber
High-Velocity Injuries
Endoneurium Perineurium
Group of fascicles
Epineurium
Figure 28-1. Cross-sectional anatomy of a peripheral nerve. (From Wilgis EFS, Brushart TM: Nerve repair and grafting. In Green DP [ed]: Operative Hand Surgery, 3rd ed. Churchill Livingstone, New York, 1993, p 1315.)
nerve (rhomboids) arises from C5. The suprascapular nerve (supraspinatus, infraspinatus) arises distal to Erb’s point from the upper trunk. Postganglionic injury of C5 to C6 proximal to Erb’s point represents a peripheral nerve root injury, with loss of C5 to C6 paraspinous, serratus anterior, and rhomboid function. This distinguishes nerve root injuries from upper trunk injuries, which leave dorsal rami, long thoracic, and dorsal scapular nerve functions intact. Below the clavicle, the trunks divide into anterior and posterior divisions, which then form the lateral (C5 to C7), posterior (C5 to T1), and medial (C8 to T1) cords, named for their relations to the axillary artery. The upper and lower subscapular, medial and lateral pectoral, thoracodorsal,
Sympathetic ganglion Vertebral artery
Costal process Grey ramus communicans
Ventral nerve root Ventral ramus of spinal nerve Transverse process
Spinal cord
Spinal ganglion Articular process Dorsal ramus of spinal nerve Dura mater
Dorsal nerve root Figure 28-2. Relation of a cervical nerve and its ganglion to a cervical vertebra. (From Williams PL, Warwick R, Dyson M, Bannister LH: Gray’s Anatomy, 37th ed. Edinburgh, Churchill Livingstone, 1989.)
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TYPES OF INJURIES High-velocity injuries are rare in sports, typically occurring as a result of motorcycle or motor vehicle accidents or fall from a height. These injuries are the result of severe traction on the plexus caused by forcible displacement of the head and shoulder away from one another. High-velocity traction injuries are usually root avulsions, with the involved levels determined by the position of the upper extremity at the time of impact. Adduction results in injury to the upper roots. Abduction and extension result in injury to the entire plexus, and overhead abduction results in lower root injury. Clinically, root avulsions are often accompanied by other significant injuries, including head injuries. Examination reveals motor and sensory deficits attributable to the involved roots. Cervical spine films may show transverse process fractures. Myelography and magnetic resonance imaging (MRI) may be used to show evidence of root avulsion, such as traumatic meningoceles. Histamine skin testing produces a normal three-phase response. The injection of a 1% solution of histamine acid phosphate intradermally results in local vasodilation, whealing, and flare formation in the normal state. The vasodilation and whealing are caused by local effects of the histamine. The flare reaction is caused by vasodilation mediated through the sensory root ganglion and its distal afferent axons. Postganglionic injury disrupts the distal afferent axons, and the flare response is blocked. In preganglionic lesions, the distal afferent axons are intact, and the flare response is present. A normal three-phase response resulting from identification of a preganglionic lesion suggests a poor prognosis. This test is seldom used clinically. Sensory nerve conduction velocities and sensory nerve action potentials to the anesthetic regions are normal in these preganglionic lesions because the dorsal root ganglion and distal afferent axons are intact. The EMG of the posterior cervical muscles, as well as serratus anterior and rhomboids, will reveal denervation patterns. Recovery of function does not occur in root avulsions. Current surgical treatment consists primarily of muscle transfers with or without arthrodesis, although attempts at microsurgical repair may prove beneficial in the future. Associated postganglionic injury, which may heal and reduce the extent of reconstruction required to obtain optimal
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339
Figure 28-3. Brachial plexus. Site of upper trunk plexus injury and distribution. (From Patten JP: Neurological Differential Diagnosis. New York, Springer-Verlag, 1977.)
function, is the primary reason for delaying reconstruction. Early aggressive rehabilitation to maintain joint motion is important for achieving optimal results.
Burners and Stingers Burners, often referred to as stingers or cervical nerve pinch injuries, and upper trunk brachial plexus injuries are among the most common injuries in American football and are seen, to a lesser degree, in wrestling and other contact sports. Clarke3 has reported an incidence of 2.2 brachial plexus injuries per 100 players per year between 1975 and 1978. Clancy and colleagues4 have reported that at the collegiate level, approximately 50% of football players have sustained a burner at some time during their career. Of these, approximately 30% sustain their first injury in high school. It has been theorized that athletes at a younger age may not be instructed on proper tackling procedures. Warren9 has noted a similar incidence in professionals on one team. Injury most commonly occurs while tackling; thus, it usually affects defensive and specialty team players. The mechanism of injury initially is a downward or backward blow to the ipsilateral shoulder, with the neck flexed laterally away from the side of injury. This results in an increase in the acromiomastoid distance, stretching of the
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brachial plexus, and damage to the plexus, the degree of which depends on the force applied.10 The mechanism of initial injury is similar to that producing acromioclavicular sprain, with the difference being the site of application of force—the acromion in acromioclavicular joint injuries and the clavicle in brachial plexus injuries.11 Concomitant burners and acromioclavicular joint injuries are therefore rare. Subsequent injury may occur with the neck laterally flexed toward the side of injury or hyperextended. This may be the result of scarring and fixation of the plexus to the scalene muscles12 or foraminal narrowing.13 Cadaver studies,4 however, have shown that tension in the upper trunk of the brachial plexus can be increased with a posterior force on the shoulder girdle while the neck is ipsilaterally flexed or ipsilaterally rotated and hyperextended. In a previously injured brachial plexus, this mechanism may produce enough tension to cause reinjury without the presence of scarring or foraminal narrowing. When the injury occurs, the athlete feels a sharp burning or stinging pain (hence, the common names burner or stinger) radiating from the supraclavicular area down the arm to the hand. This is accompanied by numbness or tingling of the upper extremity. The pain and paresthesia are not dermatomal in distribution and usually resolve within 1 to 2 minutes. The athlete will usually try to shake off the injury
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to restore feeling. True neck pain is not associated with brachial plexus injury and, when present, should raise concern about a possible cervical spine injury. Weakness may be present at the time of injury, with the athlete supporting the slightly dangling extremity with the uninjured hand while leaving the field. Weakness present at the time of injury usually resolves within minutes. Conversely, weakness may not develop for hours or several days after the injury, necessitating repeated neurologic examinations postinjury. Weakness involves the deltoid, supraspinatus, infraspinatus, biceps and, on rare occasions, the supinator, brachioradialis, and/or pronator teres. Tenderness over the trapezius in the supraclavicular region may be found on examination up to several days after injury. Chrisman and associates14 have reported a 9% decrease in lateral neck flexion. This is probably related to the trapezial tenderness and muscle spasm and is frequently too small to detect clinically. The site of injury has varyingly been postulated as the upper trunk4,14-19 or upper nerve roots.14,18-21 Based on clinical evidence and electrophysiologic studies showing involvement of muscles in the distribution of the upper trunk, but no involvement of the cervical paraspinal muscles, serratus anterior, or rhomboids, which received their innervation from proximal to Erb’s point, Clancy and coworkers4 have identified the upper trunk as the site of injury. Subsequent studies16,17 have confirmed these findings. Others18,19,21 have identified some athletes with involvement of posterior cervical musculature, indicating injury at the root level; however, included in these studies are athletes with abnormal spine films, which are not associated with burners. These root injuries appear to be more severe in terms of duration of symptoms and disability. Clancy22 has classified brachial plexus injuries based on the duration of motor weakness and, roughly, paralleling Sunderland’s classification of nerve injury.23 Grade I injuries are the most common brachial plexus injuries with a transitory loss of motor and nerve function, lasting from minutes to hours and completely resolving within 2 weeks. This represents a neurapraxia or physiologic interruption of nerve function. It may be caused by edema or demyelination of the axon without intrinsic axonal disruption, leading to a conduction block at the site of injury. Function returns as the edema resolves or when remyelination is completed, usually within 2 to 3 weeks of injury. There is complete return of strength. Electromyographic studies at 2 to 3 weeks do not show any findings. Grade II injuries exhibit motor weakness lasting longer than 2 weeks but with eventual full clinical recovery. Some have significant weakness from the time of injury, whereas others may not exhibit weakness for several days. This is consistent with the work of Denny-Brown and Brenner.6,7 There appears to be a two-phase recovery, with the return
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of 80% to 90% of strength and endurance in 6 weeks and full recovery by 6 months. The pattern of injury suggests a combined neurapraxia and axonotmesis. Wallerian degeneration of the distal axon is responsible for the delay in complete recovery, because axon regeneration requires as long as 6 months in this region. Electromyographic changes at 3 weeks postinjury reveal classic evidence of muscle denervation, with decreased motor unit potentials, fibrillations, and sharp positive waves. After complete clinical recovery, there may continue to be electromyographic changes, most commonly large motor unit potentials. Grade III injuries occur rarely. Affected athletes continue to exhibit motor and sensory loss at 1 year, without clinical improvement. This represents a neurotmesis with axonal regeneration frequently impossible because of the extent of injury. EMGs show evidence of denervation at 3 weeks and, subsequently, at 3 months, without evidence of recovery. Differentiation of axonotmesis from neurotmesis is important for determining the prognosis of the injury and course of treatment. A grade III injury may benefit from operative intervention at or before 3 months. Management of the athlete with brachial plexus injury is based on clinical presentation. On the field, evaluation includes motor and sensory examination. Weakness and anesthesia will persist while the pain is present but will usually resolve rapidly after the pain subsides. The supraspinatus, infraspinatus, deltoid, and biceps muscles are most often involved. Elbow flexion and shoulder flexion usually return first, followed by shoulder external rotation and abduction. Sensory deficits are usually patchy and are most often present over the lateral shoulder. Persistent anesthesia is uncommon. Also uncommon in brachial plexus injuries are neck pain and loss of neck motion, and the presence of either should raise concern about a cervical spine injury, with the athlete appropriately managed. Bilateral upper extremity burning dysesthesias may also represent a significant cervical spine injury.24 On the field, if the athlete has no evidence of neck injury, testing the shoulder rotators, deltoid, biceps, and triceps against resistance is performed. If the athlete’s pain and subjective weakness have resolved and if no weakness is shown on examination, he or she may return to play. The athlete must be examined again after the game and during the following week, because weakness may appear on a delayed basis. Routine cervical spine films are recommended for athletes sustaining their first brachial plexus injury. Athletes with persistent pain or weakness beyond 2 weeks (grade II injury) should have routine cervical spine films taken and an EMG obtained at 3 weeks to identify the site of the lesion. Evidence of nerve root injuries should prompt further study to rule out a disc herniation. Treatment of grades I and II injuries involves removal of the athlete from participation as long as symptoms or
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weakness to manual testing persist. The athlete is placed on a program of neck and shoulder strengthening as soon as tolerated. Return to contact sports is based on a return of strength and endurance of the shoulder muscles to normal as compared with those of the opposite side. Electromyographic studies in grade II injuries may show persistent changes, even after return of strength, and are not useful for determining return to sport.17-19,25 With return to football, a neck roll to prevent lateral flexion and posterior extension and built-up shoulder pads may reduce the incidence of recurrence of burners.9,13,16,18 Athletes with multiple burners may continue to participate as long as there is no loss of strength. Weakness should preclude participation until strength returns to normal. Neck and shoulder strengthening and the use of neck rolls and builtup shoulder pads may reduce the frequency of burners. Stopping contact sports will eliminate further burners but return to the sport, even after a prolonged period of nonparticipation, is frequently associated with recurrence. Treatment of grade III injuries parallels early treatment of lesser injuries. Return to contact sports is prohibited because of the continued weakness.
Pack Palsy (Backpack Paralysis) Pack palsy, or backpack paralysis, represents an injury to the brachial plexus or its branches and is generally believed to be caused by extrinsic compression of the plexus. The shoulder straps on a heavy pack create a compressive force on the plexus against the clavicle or first rib. The backward pull of a heavy pack on the shoulder girdle, placing traction on the plexus, has also been postulated as a contributing factor. Either mechanism is consistent with the studies of Denny-Brown and colleagues,6-8 which have shown that prolonged compression or low-grade traction can disrupt nerve function, which can subsequently be recovered. Pack palsy typically results in weakness involving a significant portion of the brachial plexus but may be restricted to the axillary or radial nerves. The clinical picture is one of profound weakness in the muscle groups involved. The condition is rarely painful, and sensory changes are not prominent. Treatment of pack palsy is nonoperative with an excellent prognosis. Hirasawa and Sakakida1 have described the complete recovery of all 19 patients in their review, with good results using range-of-motion (ROM) and strengthening exercises. Fractures of the clavicle may injure the brachial plexus by compression from a displaced fragment acutely or from excessive callous formation or hypertrophic nonunion in a delayed fashion. Treatment of an acute clavicle fracture with a figure-eight bandage may also result in compression of the brachial plexus.
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Hypertrophic nonunions producing brachial plexus symptoms generally involve the middle third of the clavicle compressing the plexus between the clavicle and first and second ribs. The medial cord is usually involved, producing ulnar nerve symptoms. Treatment consists of open reduction and internal fixation, with bone grafting or partial excision of the clavicle. Exuberant callous formation may result in brachial plexus compression, with gradual onset of symptoms at about the third week. Treatment is resection of the excessive callous. Cervical ribs have also been implicated in brachial plexus compression.
Acute Brachial Neuropathy Acute brachial neuropathy is a clinical entity of unknown cause that must be considered in the differential diagnosis of shoulder pain in the athlete. Acute brachial neuropathy has been described in the literature as serum brachial neuritis, multiple neuritis, localized neuritis of the shoulder girdle, acute brachial radiculitis, neuralgic amyotrophy, shoulder girdle syndrome, paralytic brachial neuritis, Parsonage-Turner syndrome, and brachial plexus neuropathy. Acute brachial neuropathy can be related to trauma, exercise, surgery, infection, immunization, and genetics. It is characterized by constant, severe shoulder pain that is present at rest and responds poorly to analgesics. The onset of pain is sudden, frequently waking the patient; it may occur acutely or subacutely in association with sports and is typically not related to a specific traumatic event. The pain may last for several hours to weeks. Shoulder and elbow motion aggravate the pain. Shoulder adduction with elbow flexion is the most comfortable resting posture. Radiation of pain below the elbow suggests diffuse involvement of the brachial plexus or involvement of the lower plexus. Weakness or paralysis usually appear within 2 weeks of pain onset. This may accompany the onset of pain but is more commonly noted as the pain is resolving and may become apparent during athletic activity. Weakness or paralysis is characteristically patchy in distribution and involves lower motor neurons without a precise motor nerve, radicular, or nerve trunk pattern. The most commonly affected muscle is the deltoid, followed by the supraspinatus and infraspinatus, serratus anterior, biceps, triceps, and wrist and finger extensors. Sensory deficits are minimal, usually limited to a small area over the lateral shoulder or radial surface of the forearm; these do not parallel the motor changes. Changes in deep tendon reflexes depend on the severity of muscle weakness, and decreased biceps and triceps reflexes are most common. Bilateral involvement is common and is usually asymmetrical, with subclinical involvement of one side, requiring electromyographic evaluation for diagnosis. The EMG yields variable data with involvement of a single muscle to diffuse involvement of the brachial plexus. Electromyographic findings are primarily fibrillation potentials in affected muscles, and nerve conduction changes consist
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of decreases in amplitudes of motor and sensory nerve conduction in involved nerves. Nerve conduction velocities and motor distal latencies are not affected to any significant degree. The principal findings in electromyographic studies in acute brachial neuropathy that differ from those of traumatic upper trunk injuries include the following: involvement of muscles not innervated by the upper trunk (trapezius, serratus anterior, diaphragm); involvement of muscles enervated by one or two peripheral nerves; involvement of a single muscle or sparing of other muscles enervated by the same portion of the trunk or plexus; severe motor involvement with sparing of sensory functions in the same portion of the plexus; and unequal involvement of sensory nerves in the same portion of the plexus. These findings have led some to consider acute brachial neuropathy to be a multiple-axon loss mononeuropathy multiplex rather than a brachial plexopathy. The treatment of acute brachial neuropathy is divided into two phases. Phase 1 is from onset to resolution of pain, with treatment consisting of rest, support with a sling, and analgesia. Activity may exacerbate the pain but, if tolerated, general ROM exercises are performed to maintain joint motion. The second phase begins after the resolution of pain and consists of bilateral complete upper body strengthening, including scapular rotators. This total upper extremity approach is important because of the frequent subclinical involvement of muscles. Return to normal function occurs in 75% of patients within 2 years and 90% of patients within 3 years. Recovery usually begins within 1 to 2 months, with upper trunk, unilateral, and incomplete lesions progressing more rapidly than lower trunk, bilateral, or complete lesions. Mild residual deficits are relatively frequent and scapular winging, when present initially, is likely to persist. Return to sport is considered when strength has reached a plateau that is adequate for safe participation. This requires individual consideration of each case. Recurrences are rare and are characterized by less severe symptoms that are of shorter duration.
SUMMARY Brachial plexus injuries, although rare in noncontact sports, are common in American football and wrestling. Although severe permanent disability may result, complete clinical recovery from sports-related brachial plexus injuries is the rule. During the recovery period, protection from further injury by avoidance of contact sport and rehabilitation through ROM and strengthening exercises are the cornerstones of treatment. Safe return to sports may be allowed when clinical recovery—normal sensation and strength parity—is achieved, despite mild changes in neurophysiologic studies.
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References 1. Hirasawa Y, Sakakida K: Sports and peripheral nerve injury. Am J Sports Med 11:420, 1983. 2. Takazawa H, Sudon, Aoki K, et al: Statistical observation of nerve injuries in athletics [in Japanese]. Brain Nerve Injuries 3:11, 1971. 3. Clarke K: An epidemiologic view. In Torq JS (ed): Athletic Injuries to the Head, Neck, and Face. 2nd ed. St. Louis, Mosby Year Book, 1991. 4. Clancy W, Brand R, Bergfeld J: Upper trunk brachial plexus injuries in contact sports. Am J Sports Med 5:209, 1977. 5. Seddon H: Surgical Disorders of the Peripheral Nerves. Edinburgh, Churchill Livingstone, 1972. 6. Denny-Brown D, Brenner C: Paralysis of nerve induced by direct pressure and by tourniquet. Arch Neurol Physiol 51:1, 1944. 7. Denny-Brown D, Brenner C: Lesion in peripheral nerve resulting from compression by spring clip. Arch Neurol Physiol 52:1, 1944. 8. Denny-Brown D, Doherty M: Effects of transient stretching of the peripheral nerve. Arch Neurol Psychiatry 54:116, 1945. 9. Warren R: Neurologic injuries in football. In Jordan BD, Tsairis P, Warren RF (eds): Sports Neurology. Rockville, Md, Aspen, 1989. 10. Barnes R: Traction injuries of the brachial plexus in adults. J Bone Joint Surg Br 31:10, 1949. 11. Bergfeld J: Brachial plexus injuries. Presented at the American Association of Orthopaedic Surgeons Winter Sports Injuries Course, Steamboat Springs, Colo, March 27, 1987. 12. Rockett F: Observations on the “burner:” Traumatic cervical radiculopathy. Clin Orthop 164:18, 1982. 13. Marshall T: Nerve pinch injuries in football. J Ky Med Assoc 68:648, 1970. 14. Chrisman O, Snook G, Stanitis J, et al: Lateral-flexion neck injuries in athletic competition. JAMA 192:117, 1965. 15. Archambault J: Brachial plexus stretch injury. J Am Coll Health 31:256, 1983. 16. DiBenedetto M, Markey K: Electrodiagnostic localization of traumatic upper trunk brachial plexopathy. Arch Phys Med Rehabil 65:15, 1984. 17. Robertson W, Eichman P, Clancy W: Upper trunk brachial plexopathy in football players. JAMA 241:1480, 1979. 18. Speer K, Bassett F: The prolonged burner syndrome. Am J Sports Med 18:591, 1990. 19. Wilbourn A, Hershman E, Bergfeld J: Brachial plexopathies in athletes: The EMG findings. Muscle Nerve 9:254, 1986. 20. Albright J, Moses J, Feldick H, et al: Nonfatal cervical spine injuries in interscholastic football. JAMA 236:1243, 1976. 21. Poindexter D, Johnson E: Football shoulder and neck injury: A study of the “stinger.”Arch Phys Med Rehabil 65:601, 1984. 22. Clancy W: Brachial plexus and upper extremity peripheral nerve injuries. In Torq JS (ed): Athletic Injuries to the Head, Neck, and Face. Philadelphia, Lea & Febiger, 1982. 23. Sunderland S: Nerve and Nerve Injuries, 2nd ed. Edinburgh, Churchill Livingstone, 1978. 24. Maroon J: “Burning hands” in football spinal cord injuries. JAMA 238:2049, 1977. 25. Bergfeld J, Hershman E, Wilbourn A: Brachial plexus injury in sports: A five-year follow-up. Orthop Trans 12:743, 1988.
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CHAPTER 29 Suprascapular Nerve
Entrapment Gregory Gebauer and Andrew J. Cosgarea
Suprascapular nerve entrapment is an uncommon cause of shoulder pain and weakness but, because of its infrequent occurrence, it is often overlooked. Suprascapular nerve dysfunction can result from trauma, compression of the nerve by ganglion cysts, or traction from repetitive motion, particularly in athletes involved in sports that require overhead movement of the arm (overhead activities). The suprascapular nerve is particularly prone to injury at the suprascapular and spinoglenoid notches. Although Thomas1 first described entrapment of the suprascapular nerve in France in 1936, Thompson and Kopell2 were the first to describe it in the English literature in 1959. Compression at the spinoglenoid notch was first described by Aiello and colleagues3 in 1982.
coracohumeral ligaments, acromioclavicular joint, and subacromial bursa originate at or just before the suprascapular notch. After passing through the suprascapular notch, the nerve proceeds toward the spinoglenoid notch, which is located 1.8 to 2.1 cm from the posterior glenoid rim.14 Passing over the notch is the spinoglenoid ligament. This ligament, when present, originates at the scapular spine and can insert at the superior aspect of the glenoid neck or at the posterior glenohumeral joint. Just before entering the notch, the nerve gives off a sensory branch to the posterior aspect of the glenohumeral joint. In approximately 15% of the population, there is also a cutaneous branch of the suprascapular nerve that innervates skin over the deltoid muscle in the area normally innervated by the axillary nerve.12,15 After the nerve passes through the spinoglenoid notch, two, three, or four branches separate and innervate the infraspinatus muscle.
In 1% to 2% of patients in the general population presenting with shoulder pain, suprascapular neuropathy has been identified as the cause of that pain.4 The incidence in overhead athletes, especially volleyball players, is believed to be higher. It is more common in men than in women and typically manifests between the ages of 20 and 50 years. Athletic activities associated with nerve injury include softball, baseball, volleyball, tennis, dancing, and weightlifting.5,6 Baseball pitchers and volleyball players are at particularly high risk.7-11 Entrapment has been reported in 25% to 45% of high-level volleyball players.
PATHOPHYSIOLOGY Several mechanisms have been described as causes of supraspinatus neuropathy, including trauma, repetitive motion, compression, and iatrogenic causes. Traumatic causes include fractures of the clavicle and scapula, shoulder dislocations, penetrating trauma, and sudden forceful depression of the scapula.16-19 Depression of the scapula may occur as an isolated traumatic event (such as a fall) or may be the result of repeated episodes, such as those experienced by football linemen and linebackers. The proximity of the nerve to the middle and distal thirds of the clavicle leaves it particularly susceptible to injury, with fractures occurring at these locations. Injury to the nerve has been reported during clavicle resection.20 Rare cases of suprascapular nerve injury also have been reported after rotator cuff surgery.21
ANATOMY The suprascapular nerve is a mixed motor and sensory peripheral nerve (Fig. 29-1). It originates from the superior trunk of the brachial plexus just distal to Erb’s point, the meeting point of the C5 and C6 nerve roots. The suprascapular nerve has contributions from these two nerve roots and a variable contribution from C4.12 From its origin, the nerve passes through the posterior triangle of the neck and then proceeds laterally toward the suprascapular notch, deep to the trapezius and close to the middle and distal thirds of the clavicle. The suprascapular notch is located on average 1.3 ⫾ 0.3 cm posterior to the clavicle and 2.9 ⫾ 0.8 cm medial to the acromioclavicular joint.13 The nerve passes through the notch, under the superior transverse scapular ligament. The suprascapular artery and vein pass above the ligament. After the nerve passes through the suprascapular notch, the nerve sends out one or two branches that innervate the supraspinatus muscle. Sensory branches to the coracoclavicular and
The nerve is anatomically constrained at several points along its course. Its origin at Erb’s point is relatively fixed and immobile, as are its muscular insertions. Two other points, the suprascapular and spinoglenoid notches, are also relatively fixed and are believed to be potential sites of entrapment. Rengachary and associates22 have described six different shapes of the notch—the U shape is the most common of these. They have theorized that the rarer, shallow V-shaped notch may contribute to compression; however, 343
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They found that the presence of the coracoscapular ligament decreases the height of the notch on average from 5.6 ⫾ 0.3 mm to 2.3 ⫾ 0.4 mm and theorized that this decreased height could lead to a higher incidence of compression.
A
Particular movements may put the nerve at risk. At the suprascapular notch, the nerve is vulnerable as it crosses below the underside of the transverse scapular ligament during retraction and depression or hyperabduction of the shoulder. Lateral protraction of the scapula may lead to traction injury because the nerve is stretched between its fixed attachments at Erb’s point and the suprascapular notch. These traction forces and extremes of ranges of motion may be seen during overhead activities, particularly baseball pitching and volleyball serving and spiking. Injury to the vaso nervorum of the suprascapular nerve can be a cause of suprascapular nerve injury.9 Traction or friction at the level of the suprascapular notch may cause intimal damage to the axillary or suprascapular artery. This damage, in turn, may cause the formation of microemboli that travel distally, resulting in ischemic injury to the nerve.
B Figure 29-1. Suprascapular nerve anatomy. A, The arrow shows the suprascapular nerve as it branches from the superior trunk of the brachial plexus and passes posterior to the clavicle. B, Here the arrow shows the suprascapular nerve as it passes below the suprascapular notch and around the spinoglenoid notch, terminating in the infraspinatus. (From Cummins CA, Messer TM, Nuber GW: Suprascapular nerve entrapment. J Bone Joint Surg Am 82:415-424, 2000.)
this theory has not been supported clinically. Additionally, partial and complete bony bridging of the notch were described which may contribute to compression. Variations in the morphology of the transverse scapular ligament are believed to contribute to the suprascapular nerve compression. Bayramoglu and coworkers23 have described bifid and trifid ligaments, as well as hypertrophy of the ligament. Avery and colleagues24 have described finding an anterior coracoscapular ligament, which passes through the notch anterior and inferior to the transverse scapular ligament. This ligament was present in 16 of 27 cadavers and was found bilaterally in 11 of those 16.
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Another point of potential entrapment is the spinoglenoid notch, because the inferior transverse scapular ligament passes over the nerve and across the notch. The prevalence and morphology of this ligament have been disputed in the literature. Cummins and associates7 have found the ligament to be present in 80% of 112 cadavers. Of these, 75% had what they described as a thin ligament, and the remainder had a thick ligament. Demirkan25 and Plancher26 and coworkers have found it to be present in all cadavers studied. However, Bektas and colleagues27 have reported that only 16% of their cadaveric specimens have the ligament. Instead, they found what they described as a thick fibrous septum between the infraspinatus and supraspinatus muscles. Ide and associates28 have reported finding what they describe as a thick ligament-type structure in 21.7% of 115 cadaver specimens and a thin membranetype structure in 60% of the specimens; no ligament-like structure was found in 18.3% of the specimens. It has been theorized that the thicker ligaments may contribute to constriction at this point. Additionally, the ligament has been found to become taut with shoulder adduction and internal rotation, which may contribute to nerve compression at this location.29 Additionally, enlargement of the veins crossing over the nerve at the spinoglenoid notch has been described as a possible cause of compression.30 Compression of the nerve also can occur between the scapular spine and medial musculotendinous junction of the infrascapular and suprascapular muscles. Injury to the nerve at the level of the spinoglenoid notch results in selective impairment of the infraspinatus muscle, because the branches innervating the supraspinatus separate from the main nerve before the nerve entering the notch.
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In a study of high-level volleyball players, Witvrouw and coworkers11 have reported that electromyography reveals suprascapular nerve dysfunction in 4 of 16 players. Interestingly, those 4 players were asymptomatic but had increased external rotation, forward flexion, and isokinetic strength of the affected arm compared with the contralateral arm. It was theorized that traction on the nerve might have caused this dysfunction and that the stronger, bulkier muscle might contribute to compression of the nerve against the scapula. It is unclear why some patients are asymptomatic and others experience pain. Supraspinatus neuropathy also can be caused by compression from mass lesions, most often a ganglion cyst.31,32 These cysts are believed to result from glenohumeral joint capsular injury, particularly labral injuries. Perilabral cysts are believed to be caused by a one-way, valve-type mechanism that allows fluid from the joint to pass through and become entrapped in the cyst. This phenomenon is similar to the formation of meniscal cysts in the knee. The expansion of the cyst causes compression of the nerve against the scapula, often at the level of the spinoglenoid notch. Piatt and associates33 have reported that 53 of 63 patients with ganglion cysts also have labral tears on magnetic resonance imaging (MRI). Higher incidences of associated cysts and labral injuries have been reported when the diagnosis is made by arthroscopy.34 Compression also has been reported secondary to the mass effect of tumors, such as metastatic renal cell carcinoma, Ewing’s tumor, chondrosarcoma, synovial cell sarcoma, lipoma, lymphoma, and schwannoma.35-39 The nature of the pathology causing the suprascapular nerve dysfunction has a direct effect on the patient’s presenting symptoms. In a meta-analysis, Zehetgruber and coworkers40 have found that of patients with suprascapular neuropathy who were later found to have a perilabral cyst, 83% have isolated atrophy of the infraspinatus and only 13% have atrophy of both the supraspinatus and infraspinatus. They also noted that in patients without a perilabral cyst, 48% have atrophy of both muscles, 8% have isolated infraspinatus atrophy, and 35% have no atrophy.
CLINICAL EVALUATION History Athletes with suprascapular nerve entrapment generally present with weakness, shoulder pain, or both. The pain is described as burning, aching, or crushing; it is often deep and diffuse and can be referred to the neck, lateral arm, or anterior chest wall. The onset most commonly is insidious but may be acute after a direct blow or fall. Symptoms may be exacerbated by overhead activities. The athlete may report weakness of the shoulder, particularly with overhead activities. Athletes with proximal lesions are more likely to
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complain of pain, whereas patients with distal lesions may present with weakness and no pain.40 Because of the high functional demand of sports, an athlete may be more likely to present with painless weakness than the average nonathlete patient.
Physical Examination Clinical evaluation should begin with a complete examination of the shoulder and neck and a thorough neurologic examination. Other causes of shoulder pain, including rotator cuff injury, intra-articular glenohumeral pathology, cervical spine disease, and diffuse peripheral neuropathy, must be excluded. The supraspinatus and infraspinatus fossae should be visualized and palpated during resisted abduction and external rotation to assess atrophy and muscle contraction. Atrophy of the supraspinatus may be difficult to appreciate because of the overlying trapezius. In addition, the presence of atrophy depends on the site of the lesion. Distal compression at the spinoglenoid notch is likely to produce isolated atrophy of the infraspinatus, because the branches innervating the supraspinatus are given off before entering the notch. Additional findings may include tenderness to palpation at the spinoglenoid notch for distal lesions or in the triangle bordered by the clavicle and scapular spine for proximal lesions. Adduction of the arm across the body may cause pain as the nerve is stretched across the scapular notch. Weakness of the supraspinatus, infraspinatus, or both may be present. Compensation by the teres minor may hide some of the patient’s weakness in external rotation. Patients generally have normal range of motion. A diagnostic nerve block (injection of an anesthetic agent into the suprascapular notch) can be performed to help confirm the diagnosis. Relief of pain supports the diagnosis of entrapment,3 but a negative test does not exclude the diagnosis because of the technical difficulty associated with localizing the notch and the inability to assess whether the nerve has been paralyzed.
Imaging Studies Imagining studies should be part of the workup for any suspected suprascapular neuropathy. Initial studies should include plain radiographs of the shoulder and cervical spine. A Stryker notch view or an anteroposterior view tilted 15 to 30 degrees caudally may provide better visualization of the scapular notch. Radiographs may show acute fractures in patients with a recent history of trauma or fracture callus in patients with an older injury. Computed tomography (CT) scans are of limited value but may be helpful in identifying occult fractures. Ultrasound, which can be used to identify and localize mass lesions that may be compressing nerves, has the advantage of being relatively inexpensive and noninvasive compared with
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other imaging modalities. However, the quality of the study depends to a large extent on the technician performing the study, and it lacks the ability to identify other pathology that may be causing or contributing to the patient’s symptoms. With ultrasound, ganglion cysts appear as well-defined hypoechoic, homogenous lesions. MRI is the mainstay for visualizing the soft tissue around the shoulder; it can help rule out other pathologies and identify causes of nerve compression. A ganglion cyst appears as a well-defined mass with smooth margins with a low signal on T1-weighted images and a high signal on T2-weighted images (Fig. 29-2). MRI also may show abnormalities associated with cyst formation, including capsular and labral injuries. Magnetic resonance arthrography has been shown to be the best study for the identification of labral pathology, with a sensitivity of 92% for type II superior labrum anterior and posterior tears.41 The absence of a labral tear on a MRI scan does not exclude its presence; there have been cases of tears being identified
only during arthroscopic visualization.34,42 MRI also can show evidence of atrophy in the supraspinatus and infraspinatus, including decreased muscle bulk and increased fatty infiltration.43
Electromyography and Nerve Conduction Studies Electromyographic and nerve conduction studies can help confirm the diagnosis and aid in localizing the site of the pathology (Fig. 29-3). In a healthy patient, the mean latency from Erb’s point to the supraspinatus muscle is 2.7 ± 0.5 msec and the mean latency to the infraspinatus is
A
A
B B Figure 29-2. Magnetic resonance imaging scans of a perilabral cyst. A, Origin near the superior rim of the glenoid. B, Extension down the neck of the glenoid. Note the high signal strength of the cyst on the T2-weighted images.
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Figure 29-3. Intraoperative views of a perilabral cyst being decompressed during a shoulder arthroscopy. Note the rasp being passed underneath the superior labrum (A) and then into the neck of the cyst (B). The labral defect was subsequently repaired with an arthroscopic suture anchor technique.
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3.3 ± 0.5 msec.44 The results of electromyographic and nerve conduction studies of the affected shoulder should be compared with those of the asymptomatic extremity. Entrapment of the suprascapular notch results in increased latency of the supraspinatus and infraspinatus, but lesions of the spinoglenoid notch result in delayed conduction only of the infraspinatus. Electromyographic studies may show increased spontaneous activity, fibrillations, and positive sharp waves. In cases of an initiating traumatic event, changes usually are apparent at 3 to 4 weeks.7
TREATMENT Treatment depends on the nature of the pathology causing the problem. For neuropathy without an identifiable mass lesion, nonoperative treatment is the mainstay. Patients should avoid exacerbating activities, including any sportsrelated activities that produce pain. A rehabilitation program should focus on increasing flexibility and gradual strengthening. Specific attention should be paid to the rotator cuff muscles, deltoid, and scapula-stabilizing muscles, including the rhomboids, serratus anterior, and trapezius. In a series of 15 patients treated nonoperatively, Martin and colleagues45 have reported excellent results in 5 and good results in 7 patients; nonoperative treatment failed for 3 patients, who subsequently underwent surgery. Symptoms may take more than 1 year to resolve completely. Operative treatment should be considered when nonoperative options have failed, but opinions differ on the length of time that should be allotted for a trial of nonoperative treatment before surgical intervention is advised. Most authors recommend 6 months of nonoperative treatment,46 but some advocate earlier intervention. Post47 and Post and Mayer48 have recommended immediate decompression of the nerve without a trial of nonoperative treatment. Fabre and associates49 have reported better outcomes in patients who undergo operative decompression before 6 months compared with patients whose surgery is delayed for more than 6 months. Lesions localized to the suprascapular notch can be treated with surgical decompression of the notch. Post47 has described a posterior approach. The skin is incised in line with the scapular spine, the trapezius is sharply elevated, and the supraspinatus can be retracted inferiorly to expose the suprascapular notch. The superior transverse scapular ligament then is visualized directly and released. Care is taken to avoid the suprascapular artery and vein, which pass over the ligament. A notchplasty has been advocated by some authors.45,50 Most patients report complete resolution of their symptoms after release of the transverse suprascapular ligament. Fabre and coworkers49 have reported an increase in the Constant score,51 from 47 before surgery to 77 postoperatively. Another study47 has reported excellent results in 27 of 39 patients. Greater return of strength and
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function in the supraspinatus muscle has been reported more often than in the infraspinatus muscle.52,53 Lesions localized to the spinoglenoid notch and without evidence of mass can be decompressed by the method described by Sandow and Ilic.10 The notch is approached from above and below the scapular spine. Superiorly, the supraspinatus is reflected. To approach the notch inferiorly, the deltoid is split or partially dissected off of the scapular spine. The spinoglenoid ligament then can be released and, if necessary, the notch can be deepened with a burr. To avoid the risk of fracture of the acromion, the notch should not be deepened more than 1 cm. In general, good results can be expected with regard to pain relief; however, return of muscle strength is more variable. Sandow and Ilic10 have reported operating on five professional volleyball players, all of whom returned to the same level of function (or improved) at 8 months. Patients with ganglion cysts or other mass lesions compressing the nerve can expect better results with surgical than with nonoperative intervention. Piatt and colleagues33 have reported only a 53% satisfaction rate in 19 patients with perilabral cysts treated nonoperatively with physical therapy and nonsteroidal anti-inflammatory drugs (NSAIDs). Percutaneous decompression of the cyst can be performed with CT or ultrasound guidance. Initially, CT-guided decompression has an 86% success rate for decompressing the cyst and providing pain relief54; however, there is a high recurrence and only a 64% satisfaction rate with the procedure.33,54 The high failure rate is likely the result of the inability to address any causative intra-articular pathology. Nevertheless, percutaneous decompression is a relatively noninvasive option and may be viable for patients who are not good surgical candidates. Symptomatic ganglion cysts can be treated arthroscopically. Because perilabral cysts often are associated with superior labral tears that may not always be apparent on an MRI scan, they are often diagnosed only with direct visualization during arthroscopy. A probe can be placed underneath the torn labrum to identify the passage to the cyst cavity (see Fig. 29-3). In patients with an MRI-identified cyst but for whom no intra-articular communication is identified, a capsulotomy can be performed to drain the cyst by making an incision into the peripheral portion of the labrum at the spinoglenoid notch. The cyst wall can be débrided with a shaver, but care should be taken to avoid injury to the suprascapular nerve and vein. The shaver should not be inserted deeper than 1 cm past the posterior attachment of the capsule, and care should be used when adjusting the amount of suction.55 If a capsulotomy is performed, the incision is left open. Any labral pathology should be repaired or débrided, as indicated. Several authors have reported excellent results with arthroscopy and open decompression. Moore and associates34
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have reported a series of 16 patients treated with this regimen; of these, 10 had complete resolution of symptoms, 5 had partial resolution, and 1 was noted to have a superior labrum anterior and posterior lesion that was missed during the initial procedure. Piatt and coworkers33 have reported a 96% patient satisfaction rate in 27 patients treated with arthroscopy and arthroscopic or open decompression. In a series of cysts treated only with arthroscopic decompression, Lichtenberg and colleagues56 have reported an average postoperative Constant score of 93, an increase from 70 before surgery. They reported only one case of MRI-identified recurrence, but that patient developed no recurrence of symptoms. Treating ganglions with repair of the intraarticular pathology alone and no decompression of the cysts has been suggested, but Piatt and associates33 have reported only a 67% satisfaction rate with this procedure.
SUMMARY Suprascapular nerve entrapment should be considered in the differential diagnosis for patients experiencing shoulder pain. Athletes may or may not present with a precipitating traumatic event; however, if trauma is present, the pathology is more likely to be localized at the level of the suprascapular notch than elsewhere along the course of the nerve. Careful attention should be paid to at-risk athletes, especially volleyball players and baseball pitchers. Initial evaluation should include a detailed physical examination and imaging studies, particularly plain radiography and MRI. Electromyographic and nerve conduction studies are useful for confirming the diagnosis, localizing the abnormality, and tracking recovery. Treatment is based on the cause of the neuropathy. When no mass lesion is present, initial management should be nonoperative and consist of relative rest, anti-inflammatory medications, and physical therapy. It may be several months before a patient begins to show relief of symptoms. If nonoperative therapy fails, operative decompression of the nerve can be considered. Difficulty in determining the cause of an athlete’s abnormality may arise when both cysts and labral tears are present. Treatment should address any intra-articular pathology with an attempt at decompression of the cyst. It should be noted that labral injuries are often present, even when not visualized on MRI. Excellent pain relief can be expected from operative treatment, but return of muscle strength is more variable.
References 1. Thomas A: La paralysie du muscl sous-epineux. Presse Med 64:1283-1284, 1936. 2. Thompson WA, Kopell HP: Peripheral entrapment neuropathies of the upper extremity. N Engl J Med 260:1261-1265, 1959.
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3. Aiello I, Serra G, Traina GC, Tugnoli V: Entrapment of the suprascapular nerve at the spinoglenoid notch. Ann Neurol 12:314-316, 1982. 4. Vastamaki M, Goransson H: Suprascapular nerve entrapment. Clin Orthop Relat Res (297):135-143, 1993. 5. Kukowski B: Suprascapular nerve lesion as an occupational neuropathy in a semiprofessional dancer. Arch Phys Med Rehabil 74:768-769, 1993. 6. Zeiss J, Woldenberg LS, Saddemi SR, Ebraheim NA: MRI of suprascapular neuropathy in a weight lifter. J Comput Assist Tomogr 17:303-308, 1993. 7. Cummins CA, Bowen M, Anderson K, Messer T: Suprascapular nerve entrapment at the spinoglenoid notch in a professional baseball pitcher. Am J Sports Med 27:810-812, 1999. 8. Dramis A, Pimpalnerkar A: Suprascapular neuropathy in volleyball players. Acta Orthop Belg 71:269-272, 2005. 9. Ringel SP, Treihaft M, Carry M, et al: Suprascapular neuropathy in pitchers. Am J Sports Med 18:80-86, 1990. 10. Sandow MJ, Ilic J: Suprascapular nerve rotator cuff compression syndrome in volleyball players. J Shoulder Elbow Surg 7:516-521, 1998. 11. Witvrouw E, Cools A, Lysens R, et al: Suprascapular neuropathy in volleyball players. Br J Sports Med 34:174-180, 2000. 12. Ajmani ML: The cutaneous branch of the human suprascapular nerve. J Anat 185(Pt 2):439-442, 1994. 13. Weinfeld AB, Cheng J, Nath RK, et al: Topographic mapping of the superior transverse scapular ligament: a cadaver study to facilitate suprascapular nerve decompression. Plast Reconstr Surg 110:774-779, 2002. 14. Bigliani LU, Dalsey RM, McCann PD, April EW: An anatomical study of the suprascapular nerve. Arthroscopy 6:301-305, 1990. 15. Harbaugh KS, Swenson R, Saunders RL: Shoulder numbness in a patient with suprascapular nerve entrapment syndrome: Cutaneous branch of the suprascapular nerve: case report. Neurosurgery 47(6):1452-1455, 2000. 16. de Laat EAT, Visser CPJ, Coene LN, et al: Nerve lesions in primary shoulder dislocations and humeral neck fractures. A prospective clinical and EMG study. J Bone Joint Surg Br 76:381-383, 1994. 17. Edeland HG, Zachrisson BE: Fracture of the scapular notch associated with lesion of the suprascapular nerve. Acta Orthop Scand 46:758-763, 1975. 18. Huang KC, Tu YK, Huang TJ, Hsu RWW: Suprascapular neuropathy complicating a Neer type I distal clavicular fracture. A case report. J Orthop Trauma 19:343-345, 2005. 19. Zoltan JD: Injury to the suprascapular nerve associated with anterior dislocation of the shoulder: Case report and review of the literature. J Trauma 19:203-206, 1979. 20. Mallon WJ, Bronec PR, Spinner RJ, Levin LS: Suprascapular neuropathy after distal clavicle excision. Clin Orthop Relat Res (329):207-211, 1996. 21. Zanotti RM, Carpenter JE, Blasier RB, et al: The low incidence of suprascapular nerve injury after primary repair of massive rotator cuff tears. J Shoulder Elbow Surg 6:258-264, 1997. 22. Rengachary SS, Burr D, Lucas S, et al: Suprascapular entrapment neuropathy: a clinical, anatomical, and comparative study. Part 2: Anatomical study. Neurosurgery 5:447-451, 1979. 23. Bayramoglu A, Demiryurek D, Tuccar E, et al: Variations in anatomy at the suprascapular notch possibly causing
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suprascapular nerve entrapment: An anatomical study. Knee Surg Sports Traumatol Arthrosc 11:393-398, 2003. Avery BW, Pilon FM, Barclay JK: Anterior coracoscapular ligament and suprascapular nerve entrapment. Clin Anat 15:383-386, 2002. Demirkan AF, Sargon MF, Erkula G, Kiter E: The spinoglenoid ligament: An anatomic study. Clin Anat 16:511-513, 2003. Plancher KD, Peterson RK, Johnston JC, Luke TA: The spinoglenoid ligament. Anatomy, morphology, and histological findings. J Bone Joint Surg Am 87:361-365, 2005. Bektas U, Ay S, Yilmaz C, et al: Spinoglenoid septum: A new anatomic finding. J Shoulder Elbow Surg 12:491-492, 2003. Ide J, Maeda S, Takagi K: Does the inferior transverse scapular ligament cause distal suprascapular nerve entrapment? An anatomic and morphologic study. J Shoulder Elbow Surg 12:253-255, 2003. Demirhan M, Imhoff AB, Debski RE, et al: The spinoglenoid ligament and its relationship to the suprascapular nerve. J Shoulder Elbow Surg 7:238-243, 1998. Carroll KW, Helms CA, Otte MT, et al: Enlarged spinoglenoid notch veins causing suprascapular nerve compression. Skeletal Radiol 32:72-77, 2003. Sjoden GO, Movin T, Guntner P, Ingelman-Sundberg H: Spinoglenoid bone cyst causing suprascapular nerve compression. J Shoulder Elbow Surg 5(Pt 1):147-149, 1996. Tung GA, Entzian D, Stern JB, Green A: MR imaging and MR arthrography of paraglenoid labral cysts. AJR Am J Roentgenol 174:1707-1715, 2000. Piatt BE, Hawkins RJ, Fritz RC, et al: Clinical evaluation and treatment of spinoglenoid notch ganglion cysts. J Shoulder Elbow Surg 11:600-604, 2002. Moore TP, Fritts HM, Quick DC, Buss DD: Suprascapular nerve entrapment caused by supraglenoid cyst compression. J Shoulder Elbow Surg 6:455-462, 1997. Faridah Y, Abdullah BJJ: Non-Hodgkin’s lymphoma with left suprascapular neuropathy on magnetic resonance imaging. Hong Kong Med J 9:134-136, 2003. Fritz RC, Helms CA, Steinbach LS, Genant HK: Suprascapular nerve entrapment: Evaluation with MR imaging. Radiology 182(2):437-444, 1992. Hazrati Y, Miller S, Moore S, et al: Suprascapular nerve entrapment secondary to a lipoma. Clin Orthop Relat Res (411):124-128, 2003. Sharma RR, Pawar SJ, Netalkar AS: Schwannoma of the suprascapular nerve presenting with atypical neuralgia: Case report and review of the literature. J Clin Neurosci 8:60-63, 2001. Zvijac JE, Sheldon DA, Schurhoff MR: Extensive lipoma causing suprascapular nerve entrapment. Am J Orthop 32:141-143, 2003. Zehetgruber H, Noske H, Lang T, Wurnig C: Suprascapular nerve entrapment. A meta-analysis. Int Orthop 26:339-343, 2002.
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41. Jee WH, McCauley TR, Katz LD, et al: Superior labral anterior posterior (SLAP) lesions of the glenoid labrum: reliability and accuracy of MR arthrography for diagnosis. Radiology 218:127-132, 2001. 42. Ferrick MR, Marzo JM: Ganglion cyst of the shoulder associated with a glenoid labral tear and symptomatic glenohumeral instability. A case report. Am J Sports Med 25: 717-719, 1997. 43. Bredella MA, Tirman PFJ, Fritz RC, et al: Denervation syndromes of the shoulder girdle: MR imaging with electrophysiologic correlation. Skeletal Radiol 28:567-572, 1999. 44. Kraft GH: Axillary, musculocutaneous and suprascapular nerve latency studies. Arch Phys Med Rehabil 53:383-387, 1972. 45. Martin SD, Warren RF, Martin TL, et al: Suprascapular neuropathy. Results of non-operative treatment. J Bone Joint Surg Am 79:1159-1165, 1997. 46. Drez D, Jr.: Suprascapular neuropathy in the differential diagnosis of rotator cuff injuries. Am J Sports Med 4:43-45, 1976. 47. Post M: Diagnosis and treatment of suprascapular nerve entrapment. Clin Orthop Relat Res (368):92-100, 1999. 48. Post M, Mayer J: Suprascapular nerve entrapment. Diagnosis and treatment. Clin Orthop Relat Res (223): 126-136, 1987. 49. Fabre T, Piton C, Leclouerec G, et al: Entrapment of the suprascapular nerve. J Bone Joint Surg Br 81:414-419, 1999. 50. Callahan JD, Scully TB, Shapiro SA, Worth RM: Suprascapular nerve entrapment. A series of 27 cases. J Neurosurg 74:893-896, 1991. 51. Constant CR, Murley AHG: A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res (214):160-164, 1987. 52. Kim DH, Murovic JA, Tiel RL, Kline DG: Management and outcomes of 42 surgical suprascapular nerve injuries and entrapments. Neurosurgery 57:120-126, 2005. 53. Antoniadis G, Richter HP, Rath S, et al: Suprascapular nerve entrapment: Experience with 28 cases. J Neurosurg 85(6):1020-1025, 1996. 54. Chiou HJ, Chou YH, Wu JJ, et al: Alternative and effective treatment of shoulder ganglion cyst: Ultrasonographically guided aspiration. J Ultrasound Med 18:531-535, 1999. 55. Westerheide KJ, Karzel RP: Ganglion cysts of the shoulder: Technique of arthroscopic decompression and fixation of associated type II superior labral anterior to posterior lesions. Orthop Clin North Am 34:521-528, 2003. 56. Lichtenberg S, Magosch P, Habermeyer P: Compression of the suprascapular nerve by a ganglion cyst of the spinoglenoid notch: The arthroscopic solution. Knee Surg Sports Traumatol Arthrosc 12:72-79, 2004.
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CHAPTER 30 Cervicogenic Shoulder Pain Michael B. Fox, Benjamin Gelfand, and Stanley Rutkowski
Close interaction between the cervical spine and upper extremities is imperative for optimal joint function during athletic activities. Because of this close interaction, cervicogenic shoulder pain is often observed. This chapter will discuss the causes and treatment of cervicogenic shoulder pain in athletes.
Each intervertebral segment consists of an intervertebral joint and two facet joints. The facet joints are synovial joints surrounded by a thin, loose articular capsule attached to the margins of the articular facets of the adjacent vertebrae. The alignment of the facet joints permits gliding movement and determines the type of movement possible. These joints are innervated by branches arising from the medial branches of the posterior primary rami of the spinal nerves. The articulation between these joints forms the intervertebral foramen, where the nerve roots exit and create the brachial plexus.1-3
FUNCTIONAL ANATOMY The cervical spine consists of seven vertebrae that support the head and allow for movement of the head and neck in three planes. This region also houses the spinal cord as it exits the skull. The brachial plexus contributes all the nerves of the shoulder and upper extremities. There is a complex system of muscles, tendons, and ligaments that restrict or facilitate motion of the head and neck.1-3 Because of its anatomy, the cervical spine has an intimate relation to the shoulder girdle complex and upper extremity function. The first two vertebrae, C1 and C2, are atypical and the rest, C3 through C7, are typical. The C1 vertebra, also known as the atlas, has no spinous process and consists of two lateral masses connected by the anterior and posterior arches. It carries the cranium and rotates on the second vertebra’s relatively flat articular facets. The C2 vertebra, also known as the axis, is the strongest of the cervical vertebrae and has a unique structure called the dens, which projects superiorly from its body. There is no intervertebral disc between the C1 and C2 vertebrae. The discs between C2 and C7 allow for shock absorption and contribute to movement of the region.
Joint Movement The primary role of the cervical spine is to maintain and position the sense organs located in the head while it goes through different ranges of motion. This is accomplished through flexibility of the cervical spinal column as well as endurance of the surrounding musculature.4,5 The cervical motion segment has three degrees of freedom. These movements include flexion, extension, lateral deviation, and rotation. Ligaments of the vertebral column act as a checkrein against excessive motion in all three planes. Some of these ligaments attach from one individual vertebra to its adjacent one. Other ligaments are continuous throughout the entire segment. The muscles of the vertebral column are divided into three layers—deep, intermediate, and superficial. The muscles include the intrinsic back muscles and transversospinal muscles, as well as the splenius capitis and splenius cervicis. These muscles control movement and posture. The intermediate and superficial muscle layers of the vertebral column are involved with respiration and limb movements. These muscle groups include the trapezius, latissimus dorsi, levator scapulae, and rhomboids; they connect the upper limb to the trunk and control limb movements via the shoulder girdle. Nerves coming from the anterior rami of the cervical region and cranial nerves innervate the muscles.
The discs consist of two parts—the outer layer, the annulus fibrosis, and the inner layer, the nucleus pulposus. The annulus fibrosis is innervated by a branch off of the anterior primary ramus. Its blood supply comes from the vertebral and ascending arteries of the neck. The annulus fibrosis is a ring consisting of concentric lamellae of fibrocartilage that form the circumference of the intervertebral disc. It inserts on the epiphysial rings on the articular surface of the vertebral body. The nucleus pulposus is the core of the disc. It has high water content, but this decreases with age. It functions as a shock absorber for axial loads and contributes to the motions of flexion, extension, rotation, and lateral bend. This part of the disc is avascular and receives its nutrition by diffusion from blood vessels at the periphery of the annulus fibrosis and vertebral body.1,2
Interaction Between the Cervical Spine and Shoulder Girdle Interactions between the vertebral column and shoulder girdle dictate upper extremity movement. Vascular and neurologic structures originating from the cervical region must pass through the shoulder girdle on their way to supplying the structures of the upper extremity. 351
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The compression of the neurovascular structures can occur as the spinal nerves exit through the forearm—in particular, the dorsal root ganglion can be compressed by disc herniation or spondylitic spurring. Compression can also occur as the nerves pass through the scalene muscles. The lower trunk of the brachial plexus, along with the subclavian artery, are closely applied to and may be compressed against the first rib.6 The brachial plexus has gross structures, trunks, divisions, and cords, that separate and re-combine throughout its path. Its smaller structures, called fascicles, also separate and recombine and may be the source of compression and shoulder pain. Normal posture can be held for extended periods without fatigue or pain. This is accomplished via a combination of anatomic, physiologic, and biomechanical factors. As the spine ages, these factors change and the range of motion of the cervical spine decreases.7,8 The degenerative processes that lead to cervical spondylosis most likely begin with a series of changes at the cervical disc level. Other degenerative findings in the aging cervical spine are loss of disc height, osteophyte formation, facet and uncovertebral joint arthrosis, and foraminal stenosis. These changes seem to be a natural consequence of aging, but may result in a decrease in the dimensions of the spinal canal and vertebral foramen that will ultimately reduce the space available for the spinal cord and nerve roots.4 The dorsal root ganglion contains peripheral nociceptors that are mechanoreceptors or chemoreceptors. The mechanoreceptors are pain corpuscles sensitive to the mechanical stimuli of injured tissue. The impulses are carried by unmyelinated C fibers as well as A delta fibers. Chemoreceptors are free nerve endings of the tissues that respond to accumulation of the chemical mediators of pain tissue metabolites. This mechanical pressure on the nerve may lead to symptoms of motor weakness, sensory deficits, and pain. The pain generated as a result of a radiculopathy has several components—a mechanical component caused by joint space narrowing (e.g., disc herniation, foraminal stenosis), an inflammatory component (e.g., ParsonageTurner syndrome, diabetes), and a vascular component (e.g., venous ischemia). These factors may manifest together or separately. The facet joints in the cervical vertebrae have an abundance of small C-type pain fibers. These joints contain an abundance of protein gene product 9.5 reactive nerve fibers, as well as substance P and calcitonin gene-related peptide-reactive nerve fibers. These regional neuropeptides serve various functions and contribute to nociception, inflammation, vasoactivity, and tissue repair.9 The inflammatory process contributing to radiculopathy is not well understood. Herniated discs seem to produce matrix metalloproteinases, nitric oxides, prostaglandins, and interleukins. The nucleus pulposus
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contains a cytokinin tumor necrosis factor ␣, which has been suggested to cause axonal and myelin injury.10 These substances may leak from the injured disc to the nerve root, resulting in a chemical radiculitis. In cervical radiculopathy, neck pain often precedes and then accompanies pain radiating down a dermatomal pattern. Radiculopathy occurring at the level of C4 and below may cause pain, numbness, and paresthesias of the neck and the upper extremity. These symptoms are usually exacerbated by extension and lateral rotation to the side of pain (Spurling’s maneuver).11-13 The patient’s symptoms may be relieved by bringing the shoulder abducted over the head (SAD sign) or creating manual traction that relieves the nerve compression by holding the head in the hand. Referred pain refers to pain generated from a peripheral nerve that does not follow a dermatomal pattern. It may have myofascial origins, such as trigger points, muscle strain, or pain, as well as possible disc involvement. Movement of the neck in all ranges of motion can produce pain.4 The relation between the cervical vertebrae, shoulder, and upper extremity can be the source of pain and disability.
DIFFERENTIAL DIAGNOSIS The differential diagnosis of primary shoulder disease from cervical spine disease can be difficult because of the close anatomic proximity of the neck and shoulder and similar presentation. Athletes may also present with coexisting shoulder and cervical pathologies. It is therefore critical to determine the correct diagnosis to provide the most appropriate treatment. Cervical spine disease includes conditions that can be acute, such as cervical disc herniations, or chronic, as in cervical spondylosis and stenosis.14 Degenerative changes of the cervical spine are inevitable as the athlete ages. Almost all persons older than 40 years have evidence of cervical disc degeneration.15 The initial event in this process seems to be dehydration of the intervertebral disc,16 which leads to loss of elasticity and joint space, with increased stresses on the vertebral end plates. Osteophyte formation may extend from the lateral aspect of the disc and from the facet and uncovertebral joints; it can cause encroachment of the exiting nerve roots in the intervertebral foramen.17 It is well known that cervical radiculopathy can cause shoulder pain.18 There has been much debate with respect to cervicogenic shoulder pain and its causes. Brain and Wilkerson19 have maintained that disc degeneration is frequently observed in the lower cervical spine of patients with a stiff and painful shoulder. Gorski and colleagues20 have concluded that chronic neck pain located in the upper back might be referred from shoulder impingement syndrome in those presenting with neck pain rather than with the typical shoulder pain. “Common innervation or
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overlapping of nerve fibers from different dermatomes supplying the neck, upper back, and shoulder may be the cause of the referred pain.”20 Patients with shoulder disorders can present with pain over the shoulder, with radiation proximally into the region of the neck and distally into the arm.14 Neck and shoulder pain (NSP) is a common occurrence in adolescents. In young populations, 15% to 30% suffer from weekly NSP, with the symptoms and prevalence increasing with age.21,22 Siivola and associates23 have also concluded that physical activities that dynamically load the upper extremities are the only sports associated with a low prevalence of NSP, whereas other sports are associated with a higher prevalence. These results support those of Dimberg and coworkers,24 which showed that the prevalence of NSP in industrial workers is lower in those who played racquet sports than those with other hobbies. In the athlete, it is imperative to differentiate between those with cervical pathologies, including peripheral nerve injuries, and those with shoulder disorders. This is challenging for any clinician but the use of ancillary tests is helpful. History and physical examination influence the diagnostic procedure to be used. The reliability of clinical tests to appropriately diagnose patients with shoulder or neck pain, or both, has been studied.25-27 Bertilson and colleagues25 have concluded that measurements of cervical range of motion and strength testing of the neck and upper extremity show poor or fair reliability. The Spurling test has the patient laterally flex and extend the neck, after which the examiner applies axial pressure on the spine. The test is positive for nerve root compression if pain or tingling is present that starts in the shoulder and radiates distally. Tong27 and Viikari-Juntura28 and associates have concluded that the test is not very sensitive but is very specific for cervical radiculopathy diagnosed by electromyography. Shah and coworkers29 have determined that the Spurling test has high sensitivity and specificity for predicting the diagnosis of soft lateral cervical disc prolapse. The upper limb tension test (ULTT) is performed with the patient in the supine position. The examiner sequentially introduces the following movements to the symptomatic upper extremity: (1) scapular depression; (2) shoulder abduction; (3) forearm supination, wrist and finger extension; (4) shoulder lateral rotation; (5) elbow extension; and (6) contralateral and then ipsilateral cervical side bending. Wainner and colleagues26 have reported excellent reliability in the diagnosis of cervical radiculopathy with the ULTT. This was contrary to the results of Viikari-Juntura and associates,28 who reported poor reliability. The distraction test is performed with the patient in the supine position. The examiner grasps under the chin and
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occiput, flexes the patient’s neck to a position of comfort, and gradually applies a distraction force. A positive test result is relief of radicular symptoms. Using the distraction test, Wainner and coworkers26 have reported excellent reliability in the diagnosis of cervical radiculopathy but Viikari-Juntura and colleagues28 have reported only fair results.
Imaging Studies The diagnostic evaluation of the athlete with neck or shoulder pain, or both, includes plain radiographs of the spine and shoulder. Anteroposterior, oblique, and lateral views of the spine and anteroposterior, lateral, and axillary radiographs of the shoulder will be obtained. These can reveal osteophytes encroaching into the intervertebral foramen, any underlying deformity or instability, spurs, or joint space narrowing. Interpretation of these radiographs must be correlated with the patient’s symptoms because some of these spondylotic changes normally accompany aging and are often seen in asymptomatic patients.15 Advanced imaging modalities are needed to visualize soft tissue structures and neural elements. Magnetic resonance imaging (MRI) is arguably the single best test to distinguish among the various clinical diagnoses that may cause neck pain.30 Care must be taken not to overinterpret the results, because rotator cuff tears and disc degeneration can be present in asymptomatic patients.15 MRI of the cervical spine is indicated in the athlete with progressive neurologic deficit, disabling weakness, or long tract signs.31 It is also indicated for those who have cervical radiculopathy who fail to improve after a 6-week trial of conservative therapy.32 Computed tomography (CT) provides excellent detail and differentiation of lesions of bone from soft tissue. CT is the study of choice in the presence of severe degenerative changes and significant end-plate osteophytes in the cervical spine. Disadvantages include exposure to radiation and the invasive nature of administering intrathecal contrast in CT myelography.32
Electromyelography Peripheral nerve injuries about the shoulder in athletes are best diagnosed and managed by obtaining an electromyelogram (EMG).33 Electromyography consists of needle electrode examination and a nerve conduction velocity study. The needle electrode examination records electrical potentials produced by muscle fibers. The nerve conduction velocity study records conduction velocity of nerve fiber action potentials by myelinated fibers and is useful for localizing the site of nerve compression. In the athletic setting, the EMG has certain limitations, however. Characteristic degeneration of the muscle surface membrane does not occur immediately after nerve injury and cannot
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be detected by needle electrode examination for approximately 2 to 3 weeks. Also, an EMG cannot differentiate between second- and third-degree nerve injuries. Regardless of these limitations, the EMG is a valuable tool for the diagnosis and management of athletes sustaining nerve injuries about the shoulder.34
also from traction in weightlifting.34,37 Athletes often complain of disabling pain, weakness, and deformity. A heavy feeling about the shoulder or dull ache may also be present. Loss of function of the trapezius muscle results in scapular winging and weakness in abduction, leading to significant impairment in the overhead athlete. Recovery in athletes is generally 12 months.36
SPECIFIC CERVICOGENIC INJURIES
Injury to the musculocutaneous nerve is rare and manifests with wasting of the biceps and brachialis muscles, weakness of elbow flexion, and loss of sensation along the lateral aspect of the forearm but no significant pain.34 The prognosis for athletes with a musculocutaneous injury is generally good.
Athletic injuries to the shoulder are common and often involve the rotator cuff, glenohumeral joint, and acromioclavicular joint. Peripheral nerve injuries about the shoulder may be difficult to diagnose because the mechanism of injury can be subtle, with overlapping symptoms. Contact sports such as football and wrestling contribute to most of these injuries, although peripheral nerve injuries to the shoulder have been reported in almost every sport, including bowling, golf, backpacking, and rope skipping.34 Specific clinical syndromes about the shoulder occur from injuries to the suprascapular, long thoracic, axillary, spinal accessory, and musculocutaneous nerves.35,36 Early diagnosis of these injuries is important for prompt treatment and return to sport. Nerve injuries can be seen after a forceful traumatic injury or as the result of chronic repetitive stress.33 The severity of nerve injuries increases from neurapraxia to axonotmesis to neurotmesis. Most peripheral nerve injuries about the shoulder in sports are neurapraxias, or firstdegree injuries, consisting of a conduction block in the presence of intact neural elements. Recovery in these athletes is excellent. The differential diagnosis in the evaluation of peripheral nerve injuries affecting the shoulder must always include injuries to the cervical roots and brachial plexus. On the field, when nerve injuries are identified, one must maintain a high degree of suspicion for cervical spine injuries. Precautions must be maintained at the cervical spine until injury is ruled out. Peripheral nerve injuries about the shoulder are more common than cervical spinal cord injuries.37 Axillary nerve injury can be caused by direct contusion, traction associated with a dislocation or fracture, or quadrilateral space syndrome.35 Quadrilateral space syndrome is a compression of the axillary nerve in throwing athletes. The axillary nerve is compressed in the quadrilateral space when the arm is placed in the abducted, externally rotated, or throwing position. Athletes may present with weakness in abduction and decreased sensation in the lateral shoulder; symptoms are exacerbated in the throwing position.38 Treatment consists of conservative management with observation and physical therapy. The short length of the axillary nerve allows for a good prognosis because of the short distance between the site of injury and muscle end plates. Spinal accessory nerve injury is rare in sports but has been reported from a blow from a hockey or lacrosse stick and
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Contact Sports Injuries In contact sports such as football, rugby, and wrestling, degenerative cervical spine changes have been noted to occur more frequently than in the general population.39,40 Burners are an injury to the cervical nerve root–spinal nerve complex or brachial plexus; these manifest as immediate and usually short-lived burning sensations into the extremity and weakness in the arm. The anterior motor nerve is more vulnerable than the dorsal root to injury; thus, motor weakness usually lasts longer.41 In younger athletes, traction to the nerve complex via contralateral side bending of the neck, ipsilateral shoulder depression, or both is likely the mechanism of injury because of the inherent flexibility and lack of muscular development of the neck in those in this age group. Poor tackling technique has been implicated, and proper coaching is indicated to prevent burners in young football and rugby players. In older and more mature athletes, compression at the nerve root is generally the cause of injury and has been associated with degenerative changes and stenosis at the spinal canal and neural foramen. The mechanism replicates Spurling’s maneuver, compression with ipsilateral side bending and rotation of the cervical spine. Kelley and colleagues39 have shown that young athletes who have a history of at least one burner compared with age-matched controls have a significantly smaller neuroforamen (foramen–vertebral body ratio) and central canal (Pavlov’s ratio). Pavlov’s ratio is determined from the lateral radiograph; it is a measure of central canal sagittal diameter relative to the vertebral body sagittal diameter. A value of 0.8 or larger is considered normal. Treatment should consist of strengthening the cervical spine, especially in younger and more flexible athletes, and strengthening the muscles of the C5, C6, and C7 myotomes. Equipment modification, such as cervical rolls, can be added to a football player’s shoulder pads to prevent full cervical side bending. Cervical cord neurapraxia (CCN) is also seen in athletes engaged in contact sports and can be distinguished from a nerve root injury by the number of limbs involved. CCN is a sensory and motor disturbance that can involve both upper
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and both lower extremities. Symptoms usually resolve in 10 minutes but may continue for as long as 24 hours. There is up to a 50% chance of recurrence if the athlete continues in the contact sport, but it is unknown whether there is an increased likelihood of permanent neurologic injury.42 High school, college, and professional football players sustaining CCN have been to shown to have significantly smaller Pavlov ratios than controls.43 It is believed that central stenosis makes them vulnerable to recurrence. Boockvar and associates have reported on children (mean age, 11.5) years who sustained CCN from sports and found normal central canal parameters. They concluded that the inherent mobility of the pediatric spine is responsible for the injury.44 Significant degenerative changes have been reported in the cervical spine of contact athletes. Albright and coworkers45 have reported an increase in x-ray changes of the cervical spine, especially in defensive linebackers and halfbacks. The incidence increased with years playing experience, reaching 32% in older players; of those who reported a history of neck injury, x-ray changes were found in 50% of players. Berge and colleagues40 have reported on agerelated MRI changes in the cervical spine in asymptomatic front-line rugby players who experience frequent head and shoulder impact. The changes in older players, when compared with those of age-matched controls, were as follows: advanced osteosclerosis and loss of vertebral body bone marrow, degeneration of the vertebral end plate, facet joint hypertrophy, disc degeneration with loss of disc height, herniated nucleus pulposus, disc protrusions, and central canal stenosis. These documented changes are important to note when evaluating shoulder injuries. Degenerative changes leading to foraminal and central canal stenosis can cause myotomal weakness mimicking rotator cuff pathology or pain into the shoulder and arm. In older athletes, the complaints of pain or weakness, or both, in the upper extremity caused by cervical spine pathology are generally accompanied by limited and painful cervical motion and possibly by positive clinical findings on examination, such as Spurling’s maneuver. However, in contact athletes of high school age and younger, a study by Albright and associates45 has indicated that suspicion may need to be higher for potential cervical involvement because the pre-season physical examination has shown poor correlation with cervical spine x-ray abnormalities found in these athletes (Figs. 30-1 and 30-2).
355
S
A
P
I
Figure 30-1. Acute disc herniation at C6-C7.
side flexion. This places increased load on the articular cartilage of the facet joints, which can lead to premature degeneration and encroachment on the spinal nerves as they exit the foramen. If there is degeneration at the level of the cervical spine, the extension and side bending required to continue pitching and serving may inflame the respective nerve root(s) and result in weakness of the upper extremity muscles—most
A
P
Injuries in the Overhead Athlete The overhead athlete is more prone to shoulder injuries than other athletes. Because it is so common to treat these athletes for shoulder injuries, concomitant cervical spine pathology can be missed. Lee46 has studied the relation between the cervical spine and overhead pitching and tennis serving and noted that especially in tennis, the neck is vulnerable to rotational forces while in positions of extension and
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I Figure 30-2. Chronic degenerative disc changes seen in older contact athletes, with loss of disc space and diminished spinal canal dimension.
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importantly, those of the rotator cuff, which are vital to the normal mechanics of the glenohumeral joint in overhead activities. Young and coworkers47 have hypothesized that lack of full cervical motion during throwing and serving leads to altered compensatory mechanics at the shoulder. In pitching, the result is an inability to load the arm fully, which results in the slow arm phenomenon. Inability to site the ball accurately throughout the serving motion leads to heightened shear and tensile loads about the shoulder. In another study, college (division 1) pitchers showed a 40% loss in accuracy and a 3 to 4 miles per hour loss of velocity when pitching while wearing a soft cervical collar, supporting the notion that loss of cervical range of motion leads to opening up too soon in the late cocking phase of throwing.47 The follow-through phase of both motions places high amounts of stress on the posterior muscles of the shoulder complex as well as on those muscles that attach the scapula to the cervical and thoracic spine. These eccentric contractions load the articular cartilage in the facet joints as the cervical spine once again moves into extension and side bending and the athlete strives to keep his or her eyes toward home plate or the opponent.46 The relation between cervical spine pathology and the shoulder is especially important in tennis, because tennis players tend to play well beyond their youth. As athletes age, weakness associated with cervical pathology, combined with the loss of motion associated with fixed postural dysfunctions, make the shoulder more prone to injury, especially rotator cuff impingement. Thoracic extension decreases by as much as 35% as people age.48 This can lead to decreased scapulothoracic contribution to the overhead motion required to serve the ball. As a result, the glenohumeral joint may be subject to increased external rotation motion and extra stress on the anterior capsule.
Relation of Posture to Shoulder Dysfunction The relation of posture to shoulder dysfunction is important to note. In their series, which included 60 patients with impingement, Lewis and colleagues49 failed to show a relation between cervicothoracic postural dysfunction and subacromial impingement syndrome. However, there is ample evidence in the literature to support evaluation and treatment of postural dysfunction when addressing shoulder pathology. Typical postural dysfunction includes increased lumbar lordosis, increased thoracic kyphosis, and forward flexion of the lower and middle cervical segments, with hyperextension at the suboccipital segments. Chronically, this results in shortened upper trapezius, latissimus dorsi and serratus anterior muscles and lengthened muscles, including the middle and lower trapezius and anterior muscles of the cervical spine. Sahrmann50 has stated that shortened muscles are favored over lengthened muscles that become weakened. Kebaetse and associates48 have found that shoulder abduction range of motion is
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decreased by 23 degrees, scapula dynamics are altered, and abduction strength is decreased by 16% when the thoracic spine is slouched. This is likely the result of altered length-tension relation in muscles such as the deltoid and supraspinatus as the scapula tilts anteriorly and downward. Lukasiewicz and coworkers51 have found a correlation between the anterior tilted scapula position and impingement syndrome. It is important to note that correction of postural dysfunction at the cervical spine should include attention to the abdominal muscles’ ability to control hyperlordosis at the lumbar spine and range of motion of the latissimus dorsi, which influences the lumbar and thoracic spine, and pectoral and levator scapulae muscles. Specific exercises to address these issues are discussed later in this chapter.
TREATMENT Exercises to increase strength and endurance of the muscles of the cervical spine, especially the flexors, and shoulder muscles have been shown to improve pain and function of the neck and shoulder. Studies have consistently shown significant strength gains of up to 60% in women who were put in progressive cervical strength-training programs.52-56 Electromyographic studies of the cervical flexors in subjects with neck pain have shown mean frequency changes consistent with improved endurance and a shift in recruitment from predominantly type II to type I fibers after a 6-week strengthtraining program.52 Conley and colleagues56 have shown an increase in cross-sectional area of the cervical muscles of 13% after a 12-week strength-training program. Manipulation and manual therapy alone have questionable long-term benefits but, when combined with exercise to strengthen the muscles of the neck, have been shown to improve pain and function. Mechanical traction for the cervical spine may be of some benefit. A recent literature review has found evidence of benefit for intermittent mechanical traction, but not for continuous traction (Fig. 30-3).58 Careful evaluation of the coordination of movements between the upper extremity and trunk is essential, especially for athletes with neck injuries. Neck trauma in the form of whiplash disorders has been shown to result in proprioceptive deficits in the upper extremity.59 Inflammation as a result of trauma to the facet joints and muscle spindles that relay sensory information may be responsible for the loss of position sense in the upper extremity. We use manual therapy to normalize cervical and thoracic ranges of motion and manual resistive strengthening exercises specific to the cervical flexors and rotators to improve muscular control of the cervical spine as the core of their treatment (Figs. 30-4, 30-5, and 30-6). Proprioceptive and functional training of the upper extremities can be built onto this foundation. We use resistance training with a cable column or surgical tubing for endurance and neuromuscular coordination between the muscles of the trunk and upper extremity (Figs. 30-7 and 30-8).
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Figure 30-3. Mechanical traction.
357
Figure 30-6. Cervical flexion strength training on cervical eight-way strengthening machine.
REHABILITATION PROGRESSION Athletes found on evaluation to have a positive finding with Spurling’s maneuver, compression testing, and/or upper limb nerve tension testing should be progressed with caution because inflammation of the nerve root is likely present (Figs. 30-9, 30-10, and 30-11). This is usually a result of the nerve root being in contact with herniated nuclear material but could also occur because of stenotic
Figure 30-4. Manual therapy to improve cervical and upper thoracic range of motion, specifically rotation and side bending left.
Figure 30-5. Manual resisted cervical rotation strength and proprioceptive training.
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Figure 30-7. Training of trunk flexors in coordination with anterior shoulder muscles performed to protect the anterior shoulder capsule and labrum.
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Figure 30-10. Compression test. Figure 30-8. Training of trunk extensors in coordination with posterior rotator cuff muscles.
compression or prior traumatic traction injury. In our experience, these athletes have exacerbations when returning to running too early after initial onset of symptoms, probably because of the forces of impact at heel strike. Phase one of conditioning and progression to running starts with recumbent cycling in an upright posture to
Figure 30-11. Nerve tension test, median nerve bias.
Figure 30-9. Spurling’s test.
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avoid excess cervical extension positioning; an elliptical machine is then used, with the hands holding the stationary hand-holds to avoid neck strain caused by the alternating pushing and pulling on the moving hand-holds. In phase two, progression to using the mobile hand-holds on the elliptical machine and treadmill walking with an uphill grade is implemented. When these phase two activities
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359
can be performed symptom free for 1 week, light jogging on a treadmill for up to 20 minutes can be added; this is the beginning of phase three. If neck or radicular pain is present at any phase, the athlete takes 1 day off and then returns to the previous phase until symptom free. The first 2 to 3 weeks of running progression of phase three are performed on a treadmill because impact is reduced at heel strike compared with pavement and the ability to control speed and incline parameters easily. After speed and endurance parameters have been progressed on the treadmill, running outdoors can be performed and progressed if the athlete is symptom free.
muscles to resist fatigue. Any athlete who reports a history of cervical radiculopathy, regardless of how long ago it occurred, should have the muscles of their upper extremity tested for endurance using the uninvolved upper extremity for comparison. In our experience, acute onset of upper extremity myotomal weakness can improve to 85% of normal strength compared with the uninvolved side in as little as 6 weeks, but can take 1 year or longer, especially in older athletes with chronic presentation and degenerative findings. Regular follow-up with the spine surgeon is critical for these patients to prevent permanent deficit.
Return to throwing can follow an interval throwing program progression designed for shoulder injuries and is progressed through the phases based on reproduction of symptoms. It has been shown in sheep models that lumbar discs display 75% return of strength 6 weeks after injury with pressure volume testing.60 Annular healing after a disc herniation needs to occur to prevent further herniation. Light throwing is allowed in the first 6 to 8 weeks after onset of radicular symptoms if it does not increase symptoms. Once radicular pain is minimal, neck muscular strength is normal, and myotomal weakness and endurance are improved to 85% of the uninvolved side, an aggressive throwing program can be progressed, but only if it does not reproduce radicular symptoms or signs.
SUMMARY
Any myotomal weakness is monitored weekly. We use hand-held dynamometers for grip strength and a handheld manual muscle tester to test triceps (Fig. 30-12), pectoralis, and biceps weakness. Rotator cuff strength is best tested with an isokinetic unit, but can also be tested with a hand-held dynamometer. The advantage of the isokinetic unit is that it can detect endurance deficits that often remain a problem after gross maximal strength returns to normal. In the overhead athlete, it is important to detect these endurance limitations and train the specific
Figure 30-12. Hand-held dynamometer used for strength testing of triceps.
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Athletes, especially those with a history of trauma presenting with shoulder and upper extremity symptoms, should be examined to rule out cervical spine pathology. All segments of the spine and pelvis should be evaluated for deficits in strength, ROM, and proprioception when developing treatment plans for athletes with complaints of shoulder pain. Any deficits in these areas can lead to excessive stress on the shoulder, especially in overhead athletes. This comprehensive approach best enables the athlete to return to his or her particular sport quickly and safely.
References 1. Moore KL: Clinically Oriented Anatomy, 3rd ed. Baltimore, Williams & Wilkins, 1992, pp 333-365. 2. Moore KL, Agur AMR: Essentials of Clinical Anatomy, 2nd ed. Baltimore, Lippincott Williams and Wilkins, 2002 pp 276-302. 3. Anderson JE: Grant’s Atlas of Anatomy, 7th ed. Baltimore, Williams & Wilkins, 1976, pp 5.1-5.23. 4. Rao R: Neck pain, cervical radiculopathy, and cervical myelopathy: Pathophysiology, natural history, and clinical evaluation. J Bone Joint Surg Am 84:1872-1881, 2002. 5. Harrison DD, Janik TJ, Troyanovich SJ, Holland B: Comparisons of lordotic cervical spine curvature to a theoretical ideal model of the static sagittal cervical spine. Spine 21:667-675, 1996. 6. McGillicuddy J: Cervical radiculopathy, entrapment neuropathy, and thoracic outlet syndrome: how to differentiate? Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine 1:179-187, 2004. 7. Trott P, Pearcy M, Rushton S, et al: Three-dimensional analysis of active cervical motion: The effect of age and gender. Clin Biomech (Bristol, Avon) 11:201-206, 1996. 8. Boyle JJ, Milne JJ, Singer KP: Influence of age on cervicothoracic spinal curvature: An ex vivo radiographic survey. Clin Biomech (Bristol, Avon) 17:361-367, 2002. 9. Kim KH, Choi SH, Kim TK, et al: Cervical facet joint injections in the neck and shoulder pain. J Korean Med Sci 20:659-662, 2005. 10. Urban JP, Roberts S: Degeneration of the intervertebral disc. Arthritis Res Ther 5:120-130, 2003.
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11. Guyer RD, Burton DC: Differential diagnosis of spinal disorders. In Fardon DF, Garfin SR (eds): Orthopaedic Knowledge Update: Spine 2. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 2002, pp 88-89. 12. Rao R: Epidemiology, pathophysiology, and clinical evaluation of neck pain. In Fischgrund JS (ed): Neck Pain. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 2004, pp 1-10. 13. Kang JD, Georgescu HI, McIntyre-Larkin L, et al: Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 21:271-277, 1996. 14. Manifold SG, McCann PD: Cervical radiculitis and shoulder disorders. Clin Orthop Relat Res (368):105-113, 1999. 15. 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 72:1178-1184, 1990. 16. Garvey TA, Eismont FJ: Diagnosis and treatment of cervical radiculopathy and myelopathy. Orthop Rev 20:595-603, 1991. 17. Bernhardt M, Hynes RA, Blume HW, et al: Cervical spondylotic myelopathy. J Bone Joint Surg Am 75:119-128, 1993. 18. Coventry MB: Problem of painful shoulder. JAMA 151: 177-185, 1953. 19. Brain WR, Wilkinson M: Cervical Spondylosis. London, Heinemann, 1967. 20. Gorski JM, Schwartz LH: Shoulder impingement presenting as neck pain. J Bone Joint Surg Am,. 85:635-638, 2003. 21. Vikat A, Rimpela M, Salminen JJ, et al: Neck or shoulder pain and low back pain in Finnish adolescents. Scand J Public Health 28:164-173, 2000. 22. Niemi S, Levoska S, Kemila J, et al: Neck and shoulder symptoms and leisure time activities in high school students. J Orthop Sports Phys Ther 24:25-29, 1996. 23. Siivola SM, Levoska S, Latvala K, et al: Predictive factors for neck and shoulder pain: A longitudinal study in young adults. Spine 29:1662-1669, 2004. 24. Dimberg L, Olafsson A, Stefansson E, et al: The correlation between work environment and the occurrence of cervicobrachial symptoms. J Occup Med 31:447-453, 1989. 25. Bertilson BC, Grunnesjo M, Strender LE: Reliability of clinical tests in the assessment of patients with neck/ shoulder problems—impact of history. Spine 28: 2222-2231, 2003. 26. Wainner RS, Fritz JM, Irrgang JJ, et al: Reliability and diagnostic accuracy of the clinical examination and patient self-report measures for cervical radiculopathy. Spine 28: 52-62, 2003. 27. Tong HC, Haig AJ, Yamakawa K: The Spurling test and cervical radiculopathy. Spine 27:156-159, 2002. 28. Viikari-Juntura E, Porras M, Laasonen EM: Validity of clinical tests in the diagnosis of root compression in cervical disc disease. Spine 14:253-257, 1989. 29. Shah KC, Rajshekhar V: Reliability of diagnosis of soft cervical disc prolapse using Spurling’s test. Br J Neurosurg 18:480-483, 2004. 30. Boutin RD, Steinbach LS, Finnesey K: MR imaging of degenerative diseases in the cervical spine. Magn Reson Imaging Clin North Am 8:471-490, 2000. 31. Levine MJ, Albert TJ, Smith MD: Cervical radiculopathy: Diagnosis and nonoperative management. J Am Acad Orthop Surg 4:305-316, 1996.
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32. Boyce RH, Wang JC: Evaluation of neck pain, radiculopathy, and myelopathy: Imaging, conservative treatment, and surgical indications. Instr Course Lect 52;489-495, 2003. 33. Sicuranza MJ, McCue FC 3rd: Compressive neuropathies in the upper extremity of athletes. Hand Clin 8:263-273, 1992. 34. Duralde XA: Neurologic injuries in the athlete’s shoulder. J Athl Train 35:316-328, 2000. 35. Safran MR: Nerve injury about the shoulder in athletes, part 1: Suprascapular nerve and axillary nerve. Am J Sports Med 32:803-819, 2004. 36. Safran MR: Nerve injury about the shoulder in athletes, part 2: Long thoracic nerve, spinal accessory nerve, burners/ stingers, thoracic outlet syndrome. Am J Sports Med 32:1063-1076, 2004. 37. Bateman JE: Nerve injuries about the shoulder in sports. J Bone Joint Surg Am 49:785-792, 1967. 38. Redler MR, Ruland LJ 3rd, McCue FC 3rd: Quadrilateral space syndrome in a throwing athlete. Am J Sports Med 14:511-513, 1986. 39. Kelly JD, Aliquo D, Sitler MR, et al: Association of burners with cervical canal and foraminal stenosis. Am J Sports Med 28:214-217, 2000. 40. Berge J, Marque B, Vital JM, et al: Age-related changes in the cervical spines of front-line rugby players. Am J Sports Med 27:422-429, 1999. 41. Weinstein SM, Herring, SA: The spine in sports. In Fardon DF, Garfin SR (eds): Orthopaedic Knowledge Update: Spine 2. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 2002, pp 97-106. 42. Torg JS, Corcoran TA, Thibault LE, et al: Cervical chord neurapraxia: Classification, pathomechanics, morbidity and management guidelines. J Neurosurg 87:843-850, 1997. 43. Torg JS, Naranja RJ, Pavlov H, et al: The relationship of developmental narrowing of the cervical spinal canal to reversible and irreversible injury of the cervical spinal cord in football players. An epidemiological study. J Bone Joint Surg Am 78:1308-14, 1996. 44. Boockvar JA, Durham SR, Sun PP: Cervical spinal stenosis and sports-related cervical cord neurapraxia in children. Spine 26:2709-2712, 2001. 45. Albright JP, Moses JM, Feldick HG, et al: Nonfatal cervical spine injuries in interscholastic football. JAMA 236:12431245, 1976. 46. Lee HWM: Mechanisms of neck and shoulder injuries in tennis players. J Orthop Sports Phys Ther 21:28-37, 1995. 47. Young JL, Casazza BA, Press JM, et al: Biomechanical aspects of the spine in pitching. In Andrews JR, Zarins B, Wilk KE (eds): Injuries in Baseball. Philadelphia, LippincottRaven, 1998, pp 23- 35. 48. Kebaetse M, McClure P, Pratt N: Thoracic position effect on shoulder range of motion, strength and three-dimensional scapular kinematics. Arch Phys Med Rehabil 80:945-950, 1999. 49. Lewis JS, Green A, Wright C: Subacromial impingement syndrome: The role of posture and muscle imbalance. J Shoulder Elbow Surg 14:385-392, 2005. 50. Sahrmann S: The movement system balance theory: Relationship to musculoskeletal pain syndrome. Course notes (unpublished), 1990.
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51. Lukasiewicz AC, Michener LA, Pratt N, et al: Comparison of 3-dimensional scapular position and orientation between subjects with and without shoulder impingement. J Orthop Sports Phys Ther 29:574-586,1999. 52. Falla D, Jull G, Hodges P, et al: An endurance-strength training regime is effective in reducing myoelectric manifestations of cervical flexor muscle fatigue in females with chronic neck pain. Clin Neurophys 117:828-837, 2006. 53. Portero P, Bigard A, Gamet D, et al: Effects of resistance training in humans on neck muscle performance, and electromyogram power spectrum changes. Eur J Appl Physiol 84:540-546, 2001. 54. Ylinen JJ, Hakkinen AH, Takala EP, et al: Effects of neck muscle training in women with chronic neck pain: One-year follow-up study. J Strength Cond Res 20:6-13, 2006. 55. Randlov A, Ostergaard M, Manniche C, et al: Intensive dynamic training for females with chronic neck/shoulder pain. A randomized controlled trial. Clin Rehabil 12: 200-210, 1998.
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56. Conley MS, Stone MH, Nimmons M, et al: Specificity of resistance training responses in neck muscle size and strength. Eur J Appl Physiol 75:443-448, 1997. 57. Gross AR, Kay T, Hondras M, et al: Manual therapy for mechanical neck disorders: A systematic review. Man Ther 7:131-149, 2002. 58. Graham N, Gross AR, Goldsmith C: Mechanical traction for mechanical neck disorders: A systematic review. J Rehabil Med 38:145-152, 2006. 59. Sandlund J, Djupsjobacka M, Ryhed B, et al: Predictive and discriminative value of shoulder proprioception tests for patients with whiplash-associated disorders. J Rehabil Med 38:44-49, 2006. 60. Ahlgren BD, Lui W, Herkowitz HN: Effect of annular repair on the healing strength of the intervertebral disc: A sheep model. Spine 25:2165-2170, 2000.
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CHAPTER 31 Biomechanics of the Shoulder
During Sports Glenn S. Fleisig, Shouchen Dun, and David Kingsley
Before studying prevention and treatment of shoulder injuries, it is vital to understand the anatomy of the shoulder complex and shoulder biomechanics during various athletic motions. Shoulder biomechanics are particularly important for chronic and overuse injuries, because the cumulative effect of repetitive motions and forces may be paramount in the pathology. The vast majority of overuse shoulder injuries treated in sports medicine result from overhead throwing or striking. An especially large portion of the patient population comes from baseball pitchers.
preparation for raising the lead leg (Fig. 31-1A). The lead leg is lifted by concentric contractions of the hip flexors (rectus femoris, iliopsoas, sartorius, pectineus).5 When the knee has reached its maximum height, the pitcher should be in a balanced position with the lead side (left side for right-handed pitcher) facing toward home plate and the left knee and both hands anterior to the chest (see Fig. 31-1B). The stance leg bends, slightly controlled by eccentric contractions from the quadriceps muscle, and remains in a fairly fixed position due to isometric contractions of the quadriceps until a balanced position is achieved.5 The hip abductors (gluteus medius, gluteus minimis, and tensor fascia latae) of the stance leg must also contract isometrically to prevent a downward tilting of the opposite side pelvis, and the hip extensors of the stance leg contract both eccentrically and isometrically to control and stabilize hip flexion.5
In this chapter, the biomechanics of overhand throwing and striking will be explained. The rapid, forceful biomechanics of baseball pitching are described first and serve as a basis for the general understanding of all overhand throws. Specific characteristics of other types of overhand throws are then described, followed by the biomechanics of various striking and swinging motions in sports. The overall biomechanics of these activities are quantified and described, but shoulder biomechanics are emphasized. For the sake of brevity, approximate values for the kinematic and kinetic parameters are often included in this text without standard deviation or ranges.
The shoulders are partially flexed and abducted, and they are held in this position by the anterior and medial deltoids, supraspinatus, and the clavicular portion of the pectoralis major.6,7 In addition, elbow flexion is maintained by isometric contraction8 of the elbow flexors (biceps brachii, brachialis, and brachioradialis).7,8 Wind-up ends with the pitcher in a good balanced position. Except for the potential energy from lifting the lead leg, very little energy is generated in the wind-up phase. Electromyographic (EMG) studies have shown that upper extremity muscle activity during this phase is minimal.6-12
BASEBALL PITCHING Normal Biomechanics Of all sports motions, the greatest shoulder angular velocity and greatest incidence of shoulder injuries occur during baseball pitching. Even though a baseball pitch is a continuous motion, it can be divided into different phases to help understand the mechanics involved.1-4 A summary of shoulder kinematics (motions) and shoulder kinetics (forces and torques) during these phases is presented in Table 31-1 and in the text. A pitch is broken into six phases: 1. Wind-up 2. Stride 3. Arm cocking 4. Arm acceleration 5. Arm deceleration 6. Follow-through
Stride The stride phase begins at the end of the wind-up, when the lead leg begins to fall and move toward the target and the hands separate. The stride ends when the lead foot first contacts the ground (see Fig. 31-1C to F). Eccentric contraction of the hip flexors controls the lowering of the lead leg, and concentric contraction from the hip abductors of the stance leg help lengthen the stride.5 In pitching, the forward movement is probably initiated to some degree by hip abduction, followed by knee and hip extension from the stance leg. As the lead leg falls downward and forward, the lead hip begins to externally rotate, while the stance hip begins to internally rotate.3 The stance hip also extends due to concentric contractions from the hip extensors.13 Throughout the stride phase the trunk is tilted slightly sideways, away from the target.
Wind-up The purpose of the wind-up phase is to put the athlete in a good starting position to pitch. The wind-up begins as the pitcher plants the back foot against the rubber in 365
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TABLE 31-1 Shoulder Biomechanics During Baseball Pitching Parameter
Fleisig et al1 Dillman et al2 Werner et al3 Feltner and Dapena4 Pappas et al5
Subject Sample size
26
29
7
8
15
Trials analyzed per subject
3
3
1
1
10
38 ± 1
38 ± 1
36
34
—
Pitch speed (m/sec) Arm Cocking Max anterior shear force (N)
380 ± 90
—
—
—
—
Max proximal force (N)
660 ± 110
—
—
—
—
Max horizontal adduction torque (N•m)
100 ± 20
—
—
110 ± 20
—
Max internal rotation torque (N•m)
67 ± 11
—
—
90 ± 20
—
173 ± 10*
178
185
170
160
20 ± 8*
14
—
—
—
Abduction at ball release (deg)
—
95
—
—
—
Max internal rotation velocity (deg/sec)
7430 ± 1270*
6940
—
6100 ± 1700
6180
Max posterior shear force (N)
400 ± 90
—
—
390 ± 240
—
Max inferior shear force (N)
310 ± 80
—
—
—
—
Max external rotation (deg) Max horizontal adduction (deg) Arm Acceleration
Arm Deceleration
Max proximal force (N)
1090 ± 110
—
—
860 ± 120
—
Max adduction torque (N•m)
83 ± 26
—
—
—
—
Max horizontal adduction torque (N•m)
97 ± 25
—
—
—
—
Max, maximum. 1 Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 18:402-408, 1993. 2 Fleisig GS, Andrews JR, Dillman CJ, et al: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233-239, 1995. 3 Werner SL, Fleisig GS, Dillman CJ, et al: Biomechanics of the elbow during baseball pitching. J Orthop Sports Phys Ther 17:274-278, 1993. 4 Feltner M, Dapena J: Dynamics of the shoulder and elbow joints of the throwing arm during a baseball pitch. Int J Sport Biomech 2:235-259, 1986. 5 Pappas AM, Zawacki RM, Sullivan TJ: Biomechanics of baseball pitching. A preliminary report. Am J Sports Med 13:216-222, 1985.
These motions cause the upper and lower body to stretch out, creating elastic energy to be used to drive the upper body forward. The stride of the body from the high leg position toward the plate also creates kinetic energy. The lead foot lands almost directly in front of the stance foot or a few centimeters closer. The stride length from the rubber to the lead foot should be slightly less than the pitcher’s height. At foot contact, the pitching arm abducts 91 ± 11 degrees, externally rotates 58 ± 25 degrees, and horizontally abducts 22 ± 10 degrees behind the trunk. Arm Cocking The arm cocking phase begins at foot contact and ends at maximum shoulder external rotation. During the stride and arm cocking phases, the pelvis rotates open to face home plate. Shortly after the pelvis begins to rotate, the torso begins transverse rotation about the spinal column. As the trunk rotates toward the target, the forearm and
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hand segments lag behind the rapidly rotating trunk and shoulder, producing a maximum external rotation (MER) of 165 to 180 degrees.2,4,5,14-16 The pitching shoulder horizontally adducts, moving from a position of horizontal abduction at foot contact to a position of 15 to 20 degrees of horizontal adduction at MER.2 A maximum shoulder horizontal adduction velocity of 581 deg/sec is reached during this period.5 The shoulder remains abducted 80 to 100 degrees throughout the arm cocking phase.5 Great amounts of shoulder forces and torques are generated throughout arm cocking (Figs. 31-2 and 31-3). As the pelvis and upper torso rapidly rotate, a centrifugal force is created to distract the shoulder. To balance these actions, a peak force of 550 to 770 N is generated at the shoulder mainly by the rotator cuff muscles.14,15 Furthermore, the internal rotator muscles are eccentrically loaded and elastically stretched to decelerate shoulder external rotation.
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A
B
C
F
I
D
E
G
J
H
K
An 80-N•m shoulder internal rotation torque is generated just before MER. A maximum shoulder anterior shear force of 380 ± 90 N and a shoulder horizontal adduction torque of 100 ± 20 N•m are produced to resist posterior translation of the arm and keep the arm moving forward with the trunk.14,15 High forces and torques are also generated at the elbow joint throughout the arm cocking phase (see Table 31-1).4,14,15 Arm Acceleration The arm acceleration phase begins at MER and ends at ball release. As the arm reaches the point of MER, the elbow begins to extend. Elbow extension is followed immediately by the onset of shoulder internal rotation. There is a short delay between the onset of elbow extension and shoulder internal rotation. This crucial delay allows the thrower to reduce the arm’s rotational resistance about its longitudinal axis, thereby allowing greater internal rotation velocity to be generated. The shoulder internal rotators contract concentrically to help produce a peak maximal internal rotation velocity of 6000 to 8000 deg/sec near ball release.2,14,16,17 The pitching shoulder is abducted approximately 80 to 100 degrees throughout the arm acceleration phase.2
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Figure 31-1. The six phases of pitching. A to C, Wind-up. C to F, Stride. F to H, Arm cocking. H to I, Arm acceleration. I to J, Arm deceleration. J to K, Follow-through. (From Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 18:402, 1993. Reprinted with permission of the Orthopaedic and Sports Physical Therapy Sections of the American Physical Therapy Association.)
Biomechanical analysis suggests that approximately 90 degrees of abduction is the strongest angle for the shoulder during a throw, as well as the angle with minimum chance of impingement or other shoulder injury.2,18 A peak shoulder horizontal adduction of 18 ± 6 degrees is reached at the time of MER, positioning the elbow slightly in front of the trunk. As the shoulder internally rotates, the hand moves forward and the elbow moves backward. Shoulder horizontal adduction at ball release is reduced to 9 ± 7 degrees. Arm Deceleration The arm deceleration phase begins at ball release and ends at maximum shoulder internal rotation (MIR) (see Fig. 31-1I to J). At the end of arm deceleration, the shoulder rotation is approximately neutral (0 degrees of internal rotation).5 Large eccentric loads are needed at both the shoulder and elbow joints to decelerate the arm. Interestingly, some studies showed minimal external rotation torque generated about the shoulder after ball release.14,15 The reason is that after ball release the arm is extended at the elbow, abducted at the shoulder, and directed toward home plate. In this position, the rotator cuff and related musculature decelerate the arm primarily by resisting distraction. A maximum proximal force of approximately
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500
100
Anterior
Abduction
P A
0
AB
Posterior
0 AD Torque (in Newtons-meters)
Force (in Newtons)
Adduction 500 500
Superior
S 0 Inferior I 500 1000
100 100
Hor Adduction
HOR ABD 0 HOR ADD
Proximal
C
Hor Abduction
500
100 100
0 FC
MER REL
Internal Rotation
MIR
Time Figure 31-2. Forces generated at the shoulder in pitching: anterior to posterior (top), superior to inferior (middle), and proximal to distal (bottom). FC, front foot contact; MER, maximum external rotation; MIR, maximum internal rotation; REL, ball release. (From Fleisig GS, Dillman CJ, Escamilla RF, Andrews JR: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233, 1995. Reprinted with permission.)
body weight (1000-1200 N) is generated at the shoulder during arm deceleration.14,15 The posterior muscles of the shoulder have been identified as having a paramount role in resisting shoulder distraction force and anterior subluxation force.2,6,9 A maximum shoulder posterior force of 400 ± 90 N and a maximum shoulder horizontal abduction torque of 97 ± 25 N•m are applied to the arm in order to decelerate shoulder horizontal adduction and resist anterior humeral head translation, respectively.15 Moreover, a maximum shoulder inferior force of 310 ± 80 N and a maximum shoulder adduction torque of 83 ± 26 N•m are produced to resist shoulder abduction and superior humeral head translation, respectively.15 Follow-Through A good follow-through is critical in minimizing the risk of injury. Most overuse injuries to the posterior side of the arm or trunk occur during arm deceleration and follow-through. This is because all of the energy generated in the body to accelerate the ball forward must be dissipated after ball release. The key to a good follow-through is to let the larger body parts help dissipate the energy in the pitching arm.
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IR 0 FC
MER REL
MIR
Time Figure 31-3. Torques experienced by the shoulder in pitching: abduction (AB) and adduction (AD) (top), horizontal adduction (HOR ADD) and horizontal abduction (HOR ABD) (middle), and internal rotation (IR) (bottom). FC, front foot contact; MER, maximum external rotation; MIR, maximum internal rotation; REL, ball release. (From Fleisig GS, Dillman CJ, Escamilla RF, Andrews JR: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233, 1995. Reprinted with permission.)
The trunk should flex forward and the upper trunk should continue to rotate (see Fig. 31-1K). As in the arm deceleration phase, the posterior shoulder muscles continue to be eccentrically active throughout the follow-through, thus continuing to decelerate the horizontally adducting shoulder. Shoulder joint forces and torques generated during the follow-through are generally lower than those generated during the arm deceleration phase.5
Biomechanical Comparison Among Various Levels of Development Although pitching biomechanics of adult pitchers have been extensively studied, information on younger pitchers and the difference between adult and younger pitchers is limited. Cosgarea and colleagues19 compared pitching kinematics
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among levels of competition (9-12 years, 13-16 years, collegiate, and professional). They showed that a younger pitcher generated significantly less shoulder internal rotation velocity. Fleisig and colleagues17 also compared youth, high school, college, and professional baseball pitchers, measuring both the kinematics and kinetics. They found that no position and temporal shoulder parameters showed
significant differences among the four competition levels, whereas all the velocity and kinetic shoulder parameters displayed significant differences (Table 31-2). In an earlier study where pitching kinetics were compared between 10 youth and 10 professional pitchers,20 the researchers found that the adult pitcher produced greater shoulder anterior force and shoulder internal rotation torque during the
TABLE 31-2 Shoulder Biomechanics Among Various Levels of Development
Parameter
Youth High School College Professional (n23) (n33) (n115) (n60) Mean ± SD Mean ± SD Mean ± SD Mean ± SD Statistical Significance
Kinematic Parameters External rotation at foot contact (deg)
67 ± 28
64 ± 25
55 ± 29
58 ± 26
Max horizontal adduction during arm cocking phase (deg)
21 ± 8
20 ± 9
20 ± 8
17 ± 9
Max external rotation during arm cocking phase (deg)
177 ± 12
174 ± 9
173 ± 10
175 ± 11
Max internal rotation velocity during arm acceleration phase (deg/s)
6900 ± 1050
6820 ± 1380
7430 ± 1270
7240 ± 1090
Horizontal adduction at ball release (deg)
11 ± 9
10 ± 8
9±9
9 ± 10
Max external rotation (% pitch)
80 ± 6
81 ± 5
81 ± 5
81 ± 5
Max internal rotation angular velocity (% pitch)
103 ± 2
102 ± 3
102 ± 5
102 ± 4
Internal rotation torque during arm cocking phase (N•m)
30 ± 7
51 ± 13
58 ± 12
68 ± 15
P ⬍ 0.01 among 4 levels P ⬍ 0.05 between Y and HS, Y and C, Y and P, HS and C, HS and P, C and P
Anterior force during arm cocking phase (N)
210 ± 60
290 ± 70
350 ± 70
390 ± 90
P ⬍ 0.01 among 4 levels P ⬍ 0.05 between Y and HS, Y and C, Y and P, HS and C, HS and P, C and P
Proximal force during arm deceleration phase (N)
480 ± 100
750 ± 170
910 ± 130
1070 ± 190
P ⬍ 0.01 among 4 levels P ⬍ 0.05 between Y and HS, Y and C, Y and P, HS and C, HS and P, C and P
Posterior force during arm deceleration phase (N)
160 ± 70
280 ± 100
350 ± 160
390 ± 240
P ⬍ 0.01 among 4 levels P ⬍ 0.05 between Y and HS, Y and C, Y and P, HS and C, HS and P, C and P
Horizontal abduction torque during arm deceleration phase (N)
40 ± 14
69 ± 25
89 ± 49
109 ± 85
P ⬍ 0.01 among 4 levels P ⬍ 0.05 between Y and HS, Y and C, Y and P, HS and C, HS and P, C and P
P ⬍ 0.05 HS and C
Temporal Parameters
Kinetic Parameters
C, college; HS, high school; max, maximum; P, professional; Y, youth. Data from Fleisig GS, Barrentine SW, Zheng N, et al: Kinematic and kinetic comparison of baseball pitching among various levels of development. J Biomech 32:1371-1375, 1999.
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arm cocking phase. The adult pitcher also generated greater shoulder posterior force during the follow-through. The kinematic data from these studies suggest that pitching mechanics did not change significantly with level. They also supported the common coaching philosophy that a child should be taught proper pitching mechanics that could be used throughout a career. The increases of shoulder joint forces and torques with competition levels were most likely due to greater muscle strength at higher levels. The greater shoulder angular velocities produced by higher-level pitchers were most likely due to the greater joint forces and torques generated during the arm cocking and arm acceleration phases (see Table 31-2). In another study by the American Sports Medicine Institute (ASMI), Dun’s group21 compared the baseball pitching kinematics between a group of younger professional pitchers (mean age, 19.7 years) and a group of older professional pitchers (mean age, 29.5 years). They showed that the older group produced less shoulder external rotation during the arm cocking phase. However, this difference was not
associated with ball velocity. Their results implied that both biologic changes and technique adaptations occur during the career of a professional baseball pitcher.
Biomechanical Comparison Among Pitch Types Fleisig and colleagues conducted two studies to compare the biomechanics of four common pitch types—fastball, change-up, curveball, and slider—in collegiate pitchers.22,23 Compared with fastball kinematics, the kinematics of the slider were similar, whereas the change-up and curveball demonstrated decreased range of motion and decreased joint velocities.22 Shoulder internal rotation torque, horizontal adduction torque, abduction torque, and proximal force were significantly less in the change-up than in the other three pitch types.23 Shoulder horizontal adduction torque was greater in the fastball than in the curveball and slider. Shoulder proximal force was greater in the slider than in the curveball (Table 31-3). Both studies showed that the curveball and change-up displayed kinematic differences from the fastball (Table 31-4). Therefore, there were significant (but few) kinematic differences between
TABLE 31-3 Differences in Shoulder Kinetics Among the Different Pitches
Study
Fastball (N 18)
Curveball (N 17)
Change-up (N 17)
Slider (N 9)
45 ± 26
41 ± 27
Statistical Significance (P ⬍ 0.01)
External Rotation at Lead Foot Contact (deg) Fleisig et al
46 ± 25
45 ± 29
Max Horizontal Adduction During Arm Cocking Phase (Deg) Dillman et al
20 ± 6
22 ± 6
24 ± 6
20 ± 5
CH and FA, CH and SL
Fleisig et al
18 ± 6
19 ± 6
21 ± 6
16 ± 6
CH and FA, CH and SL CH and CU, CH and SL
Max External Rotation During Arm Cocking Phase (Deg) Dillman et al
170 ± 6
172 ± 6
168 ± 8
172 ± 7
Fleisig et al
178 ± 7
180 ± 6
177 ± 8
183 ± 10
Max Internal Rotation Ang. Velocity During Arm Acceleration Phase (Deg/Sec) Dillman et al
7465 ± 1070
6985 ± 1143
6535 ± 1091
7924 ± 1490
CH and FA, CH and SL, CU and SL
Fleisig et al
6518 ± 946
6484 ± 857
5799 ± 778
6356 ± 721
CH and CU, CH and FA, CH and SL
94 ± 8
94 ± 9
CH and FA, CH and SL, CU and FA, CU and SL
Average Abduction During Arm Acceleration Phase (Deg) Dillman et al
98 ± 10
97 ± 8
Horizontal Adduction at Ball Release (Deg) Dillman et al
15 ± 7
11 ± 8
9±8
10 ± 7
CH and CU, CH and FA, CH and SL
Fleisig et al
12 ± 8
14 ± 7
16 ± 7
11 ± 10
CH and CU, CH and FA, CH and SL
98 ± 10
99 ± 10
94 ± 9
CH and FA, CH and SL, CU and SL
Abduction at Ball Release (Deg) Fleisig et al
96 ± 9
CH, change-up; CU, curveball; FA, fastball; SL, slider. Dillman CJ, Fleisig GS, Werner SL, et al: Biomechanics of the shoulder in sports: Throwing activities. In Prentice W, Hooker DN (eds): Postgraduate Studies in Sports Physical Therapy. Berryville, Va, Forum Medicum,1991, pp 1-9. Fleisig GS, Kingsley DS, Loftice JW, et al: Kinetic comparison among the fastball, curveball, change-up, and slider in collegiate baseball pitchers. Am J Sports Med 34(3):423-430, 2006.
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371
TABLE 31-4 Differences of Shoulder Kinematics Among the Different Pitches CU (n 17)
CH (n 17)
FA (n 18)
SL (n 9)
Internal rotation torque during arm cocking phase (N•m)
81 ± 14
73 ± 13
84 ± 13
84 ± 6
Horizontal adduction torque during arm acceleration phase (N•m)
109 ± 20
98 ± 20
111 ± 29
130 ± 35
Proximal force during arm acceleration phase (N)
998 ± 155
910 ± 169
Adduction torque during arm deceleration phase (N•m)
116 ± 34
100 ± 23
Parameter
Statistical Significance CH and CU, CH and FA, CH and SL CH and CU, CH and FA, CH and SL, CU and SL, FA and SL
1056 ± 157 1145 ± 113 CH and CU, CH and FA, CH and SL, CU and SL 110 ± 27
127 ± 33
CH and CU, CH and FA, CH and SL
CH, change-up; CU, curveball; FA, fastball; SL, slider. Data from Fleisig GS, Kingsley DS, Loftice JW, et al: Kinetic comparison among the fastball, curveball, change-up, and slider in collegiate baseball pitchers. Am J Sports Med 34(3):423-430, 2006.; Escamilla R, Fleisig GS, Barrentine, et al: Kinematic comparisons of throwing different types of baseball pitches. J Appl Biomech 14:1-23, 1998.
the fastball and curveball. The change-up had lower joint kinetics, lower angular velocities, and different body positions than the other three pitch types. The low kinetics in the change-up suggests that it is the safest pitch for college-level pitchers. Because the resultant joint loads were similar among the fastball, curveball, and slider, this study did not imply that any of these pitches was most dangerous for the collegiate pitcher. Future studies comparing pitches at different levels, especially younger levels, are needed.
Flat Ground Throwing Flat ground throwing is used in training and rehabilitation for baseball pitchers. The Interval Throwing Program was developed to assist in the rehabilitation of baseball athletes. In the Interval Throwing Program, a pitcher is instructed to throw from flat ground with a crow-hop and with normal pitching mechanics. The pitcher throws to a prescribed distance anywhere from 45 to 180 feet away. The idea is that throwing from flat ground is less harmful to the shoulder than throwing from the mound. By gradually increasing applied loads to the shoulder, the pitcher can return to full strength without putting the shoulder at risk too soon.24 To determine differences between pitching from a mound and throwing from flat ground, Fleisig and colleagues25 tested 27 college pitchers. Each subject threw in different conditions that included pitching with full effort from a standard mound and three flat ground throws: 180-foot crow-hop throw, 120-foot crow-hop throw, and 60-foot crow-hop throw. Reflective markers were placed on anatomic landmarks, and their motion was analyzed using an automatic digitizing system. The analysis revealed that there were some significant differences between flat ground throwing and pitching from a mound. Stride length was 71% ± 4% of the body height
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when throwing from the mound and about 66% of the body height when throwing from flat ground. With the shorter stride, a pitcher achieves less external rotation at foot contact when throwing from flat ground (about 28 degrees) than when pitching from the mound (42 ± 26 degrees). However, maximum external rotation was approximately 170 degrees for all of the throws. There was no significant difference in shoulder internal rotation torque, shoulder anterior force, or shoulder internal rotation velocity produced to accelerate the ball between pitching from the mound and throwing from flat ground.25 One key variable that might be related to overuse injuries in pitchers is shoulder proximal force. Shoulder proximal force was 910 ± 110 N when pitching from the mound and approximately 850 N when throwing from flat ground for the three throwing-distance conditions.25 Less force required to resist distraction in flat ground throws may be related to the low injury rate during throwing for nonpitchers.
Pathomechanics With improper mechanics, force in shoulder muscles may be unusually large. It has been demonstrated that muscle activity of the infraspinatus, teres minor, supraspinatus, and biceps was two to three times higher in amateur pitchers than in professional pitchers.12 These findings imply that professional pitchers better coordinate the movements of their body segments to increase pitching efficiency. During the wind-up phase of a pitching motion, the tendency of many pitchers, especially young pitchers, is to rush their motion by moving their lead leg toward home plate as it is lifted. By rushing, a pitcher does not have the proper coordination between the arms and lower body, which can limit the amount of energy passed from the legs to the arm. A pitcher who rushes can therefore place too great a demand on the pitching arm and increase the chance of shoulder injury.
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Because of the large magnitudes and rapid changes of the forces experienced by the shoulder during baseball pitching, maintaining a stable shoulder joint may be difficult. Forces in the shoulder during pitching that shift the humeral head to the rim of the glenoid fossa, coupled with glenohumeral distraction, cause the humeral head to be reseated off-center and place the labrum in jeopardy for injury.26 Specifically, translation and subluxation of the humeral head in the anterior or posterior direction can cause forceful entrapment of the labrum between the humeral head and the glenoid rim, resulting in labral tearing.27 Capsular laxity, as well as muscle weakness or fatigue, makes maintaining shoulder stability even more difficult, further increasing the chance of injury.
the inferior surface of the acromion or coracoacromial ligament.
Rotator Cuff Injuries Most rotator cuff tears in throwers are located from the mid supraspinatus posterior to the mid infraspinatus area.28 These tears are presumably caused by tensile failure, as the rotator cuff muscles tried to resist distraction, horizontal adduction, and internal rotation at the shoulder during arm deceleration. Proximal force and horizontal adduction torque are produced and the posterior shoulder muscles are very active during the arm deceleration phase10; this supports the belief that the posterior shoulder muscles are susceptible to injury during arm deceleration.
The primary function of the biceps brachii is to supply elbow flexion torque. Eccentric flexion torque, found during the arm acceleration and the arm deceleration phases, reaches a maximum value of 61 N•m right before ball release. Because the long head of the biceps brachii originates on the anterosuperior aspect of the glenoid labrum, contraction of the muscle produces tension on the biceps tendon–labrum complex. Another important function of the biceps brachii is to resist humeral distraction. Contraction of the biceps is particularly efficient in applying a proximal force to the arm at the instant of maximum proximal force, because reduced external rotation at this time allows the long head of the biceps to be closely aligned with the proximal direction. Total force generated by the biceps is a combination of its contribution to elbow flexion torque and shoulder proximal force.
Baseball pitchers at the professional level,29-32 college level,33,34 and youth level35 have all been found to demonstrate significantly greater shoulder external rotation in the dominant arm. Similar results have been found in position players, too.30 In maximum external rotation at the end of the arm cocking phase, the posterior rotator cuff can become impinged between the glenoid labrum and the humeral head.36 This over-rotation injury can lead to degeneration of the superior labrum and the rotator cuff.36 Shoulder-Grinding Factor The shoulder-grinding factor proposed by McLeod and Andrews states that if the humeral head translates anteriorly or posteriorly, rapid internal rotation and proximal force can cause the humerus to grind on the labrum.26 The shoulder-grinding factor can increase the degeneration of the labrum resulting from humeral translation. Subacromial Impingement Subacromial impingement is another shoulder injury associated with baseball pitching.28 It can cause inflammation of the supraspinatus, infraspinatus, or bicipital tendon, and it can cause abrasion wears. During the arm deceleration phase, 310 N of inferior force is required to keep the humerus in a balanced position (Fig. 31-2). The inability to generate this amount of force could result in superior translation of the humerus. Because the arm is abducted, horizontally adducted, and internally rotated, the superior translation of the humerus can cause impingement of the greater tuberosity, rotator cuff muscles, or biceps against
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SLAP Lesions A SLAP lesion is a tear to the superior labrum, anterior and posterior.37 Andrews and colleagues reported a tear to the anterosuperior labrum in a series of 73 baseball pitchers and other throwing athletes.38 The injury was believed to result from repetitive overuse throwing, because a traumatic episode was not present for most of these patients. It was proposed that the injuries were caused by forces imparted by the long head of the biceps brachii, particularly during arm deceleration, which peel the labrum away from the glenoid.37,38
With proper pitching mechanics, maximum elbow flexion torque occurs before maximum shoulder proximal force. With improper timing between these two loads or other mechanical faults, greater total force by the biceps may be required. Laxity in the shoulder joint can also result in increased shoulder proximal force needed, further increasing the demand on the biceps tendon–labrum complex. This is supported by the findings that the EMG activity level in the biceps is larger in shoulders with chronic anterior instability.11 Bey and colleagues39 showed that a SLAP lesion could be reliably produced with traction on the long head of the biceps tendon with the shoulder inferiorly subluxated. This study supports the belief that SLAP lesions can occur at or shortly after the instant of ball release. Morgan and colleagues40 and Burkhart and Morgan41 proposed a peel-back mechanism. During the arm cocking phase of pitching, the abduction and external rotation of the pitching arm cause the biceps tendon to assume a more vertical and posterior angle. The dynamic angle change produces a twist at the base of the biceps, transmitting a torsional force to the posterosuperior labrum. This torsion force causes the posterosuperior labrum and biceps anchor to rotate medially over the corner of the glenoid onto the scapular neck, which can eventually result in a SLAP lesion.
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To determine if SLAP lesions are more likely to occur with the in-line mechanism (McLeod and Andrews theory) or the peel-back mechanism (Morgan and Burkhart theory), it would be helpful to compare the force on the biceps tendon during pitching with the force the biceps can handle without tearing. Near the time of ball release, the long head of the biceps tendon is aligned approximately in the distal direction of the glenoid as the arm is abducted about 90 degrees and internally rotates from a cockedback position to a neutral position. At this time, the biceps contributes to the roughly 1000-N shoulder proximal force shown in Table 31-1. The force contribution of the biceps has not been quantified. When the arm is cocked back into external rotation, force in the biceps contributes toward the 380-N anterior shear force and 67-N•m internal rotation torque shown in Table 31-1. Again, the force contribution of the biceps has not been quantified. A cadaver study,42 found that the biceps anchor demonstrated significantly greater ultimate strength with in-line loading (group A, 508 N) as opposed to peel-back posterior loading (group B, 262 N). All group B specimens failed at the biceps anchor, resulting in a type II SLAP lesion. If biceps tendon forces during pitching could be calculated, then these strengths during cadaveric testing could be compared. It is likely that SLAP lesions actually occur from a combination of the proposed in-line and peel-back mechanisms. A weed-pull theory has been proposed as the cause of SLAP lesions in the overhead athlete.43 This theory states that repetition of the rapid, forceful motion from the peelback position to the in-line position pulls the biceps tendon away from the glenoid rim. Humeral Retroversion During a baseball pitching motion, a torque about the long axis of the humerus reaches a peak value of 67 ± 11 N•m for adult pitchers15 right before maximum shoulder external rotation. The direction of this torque tends to rotate the distal end of the humerus externally relative to the proximal end. This high torque could lead to deformation of the weak proximal humeral epiphyseal cartilage, causing humeral retroversion over time.44 Humeral retroversion has been found in professional pitchers,31 college pitchers,31,34 and youth baseball pitchers.45 Greater retroversion has been demonstrated to be significantly associated with an increased maximum shoulder external rotation.34,46,47 It is believed that humeral retroversion may be beneficial for baseball pitchers in two respects. First, with greater retroversion of the humerus there is the potential for increased shoulder external rotation, which increases the range of shoulder motion to generate energy and therefore greater ball velocity. Secondly, the shoulder may be more stable to resist anterior force with greater humeral retroversion. This is because the anterior soft tissue structures would have to stretch less for a given amount of external rotation. If the soft tissues are able
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to stay within their elastic range, they will be better shoulder stabilizers.47 On the other hand, proximal humeral epiphysiolysis is a pathologic response to the shear stress arising from the high torque that causes humeral retroversion.44
FOOTBALL THROWING An understanding of shoulder biomechanics in baseball pitching serves as a foundation for understanding, preventing, and treating shoulder injuries in other throwing motions. Fleisig and colleagues48 compared throwing kinematics and kinetics between 26 baseball pitchers and 26 football quarterbacks from high schools and colleges. Reflective markers were placed on bony landmarks of subjects, and their motion was analyzed using a three-dimensional automatic digitizing system. Seven of the eight shoulder kinematic variables that were analyzed showed significant differences (Table 31-5). Compared with pitchers, quarterbacks had greater external rotation at the instant of foot contact. Quarterbacks externally rotated the shoulder 90 ± 33 degrees at foot contact to reach a maximum of 164 ± 12 degrees through the passing motion. Quarterbacks also exhibited a greater degree of shoulder horizontal adduction through ball release than pitchers. Shoulder horizontal adduction of quarterbacks was approximately 7 ± 15 degrees at foot contact, reached a maximum of 32 ± 9 degrees during the arm cocking phase, and decreased to 26 ± 9 degrees at ball release. Quarterbacks also exhibited 96 ± 13 degrees of shoulder abduction at foot contact and reached a maximum of 108 ± 8 degrees during the arm acceleration phase.48 Although quarterbacks had greater shoulder external rotation than pitchers at the time of front foot contact, pitchers had greater maximum shoulder external rotation and greater maximum shoulder internal rotation angular velocity. The maximum shoulder internal rotation angular velocity of quarterbacks was 4950 ± 1080 deg/sec compared with 7550 ± 1360 deg/sec for pitchers. The lack of higher angular velocities might be due to the weight of the football, which is three times more than a baseball (0.42 kg and 0.14 kg, respectively). This is also perhaps why quarterbacks rotate their shoulders sooner and farther back, to give them more time to accelerate the arm.48 Of seven shoulder kinetic variables compared between baseball pitching and football passing, only two showed significant differences (Table 31-6). McLeod and Andrews26 proposed that forces about the shoulder could shift the humerus to the rim of the glenoid fossa, causing injury to the anterior glenoid labrum in pitchers. However, no difference in shoulder anterior force between quarterbacks and pitchers was discovered in the current study. The low incidence of anterior glenoid labrum injuries in quarterbacks might be due to their greater horizontal abduction, which
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TABLE 31-5 Differences of Shoulder Kinematics Between Baseball Pitching and Football Passing
Parameter
Pitching (n 26) Mean ± SD
Passing (n 26) Mean ± SD
Lead Foot Contact
TABLE 31-6 Differences of Shoulder Kinetics Between Baseball Pitching and Football Passing
Parameter
Pitching (n 26) Mean ± SD
Passing (n 26) Mean ± SD
Arm Cocking Phase
Shoulder abduction (deg)
93 ± 12
96 ± 13
Max shoulder anterior force (N)
310 ± 50
350 ± 80
Shoulder horizontal adduction (deg) (P ⬍ 0.001)
17 ± 12
7 ± 15
Max shoulder horizontal adduction torque (N•m)
82 ± 13
78 ± 19
Shoulder external rotation (deg) (P ⬍ 0.01)
67 ± 24
90 ± 33
Max shoulder internal rotation torque (N•m)
54 ± 10
54 ± 13
850 ± 140
660 ± 120
79 ± 23
58 ± 34
310 ± 110
240 ± 120
85 ± 51
80 ± 34
Arm Deceleration Phase
Arm Cocking Phase Max shoulder horizontal adduction (deg) (P ⬍ 0.001) Max shoulder external rotation (deg) (P ⬍ 0.01)
18 ± 8
32 ± 9
Max shoulder adduction torque (N•m)* 173 ± 10
164 ± 12
Average shoulder abduction (deg) (P ⬍ 0.001)
93 ± 9
108 ± 8
Max shoulder internal rotation velocity (deg/sec) (P ⬍ 0.001)
7±7
26 ± 9
7550 ± 1360
4950 ± 1080
Ball Release
Max, maximum. Data from Fleisig GS, Escamilla R, Andrews J, et al: Kinematic and kinetic comparison between baseball pitching and football passing. J Appl Biomech 12:207-224, 1996.
helps stabilize the glenohumeral joint. Quarterbacks are also less prone to rotator cuff injury because they have less shoulder proximal force than pitchers (660 ± 120 N compared with 850 ± 140 N). The risk of subacromial impingement is also less in quarterbacks, because they do not externally rotate their shoulders as much as pitchers during the arm-cocking stage.48 The analysis of the kinetic data showed that football passing did not produce higher forces or torques compared with baseball pitching. The incidence of shoulder injuries is also much lower for quarterbacks than for pitchers. The fundamental explanation for this is that quarterbacks limit their trunk kinematic parameters. Quarterbacks had less motion in their legs, pelvis, and upper torso compared
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Follow-Through Phase Max shoulder posterior force(N)
Arm Deceleration Phase
Shoulder horizontal adduction (deg) (P ⬍ 0.001)
Max shoulder compressive force (N)*
Max shoulder horizontal abduction torque (N•m)
*P ⬍ 0.01. Max, maximum. Data from Fleisig GS, Escamilla R, Andrews J, et al: Kinematic and kinetic comparison between baseball pitching and football passing. J Appl Biomech 12:207-224, 1996.
with pitchers, and thus quarterbacks were able to limit the amount of forces and torques normally experienced at the shoulder by pitchers. Another explanation for the lower incidence of injury in quarterbacks is that quarterbacks throw much less than pitchers, play in fewer games, and have a greater rest period between games. The quarterbacks thus have less fatigue and instability in the shoulder, with a decreased chance of injury.48
WINDMILL THROWING Underhand pitching has received little attention in sports medicine due to the perception that the windmill throwing motion produces less stress on the arm and thus injuries to the shoulder are less common; however, this might not be true. In one study of eight collegiate softball teams with 24 pitchers in total, the incidence of upper extremity injuries accounted for 17 of the 26 injuries reported.49 In a study conducted by Barrentine and colleagues,49 the pitching motion of eight female pitchers was analyzed
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using a three-dimensional automatic digitizing system. The torque values in this study were normalized as percentages of the body weight times body height, and the forces values were normalized as percentages of the body weight. The results, as presented in Table 31-7, showed that the kinematic and kinetic variables were generally low during the wind-up and stride phases. However, during the delivery phase where the arm accelerated quickly to generate ball velocity, the kinematic and kinetic variable magnitudes were quite high and comparable with or higher than those of male overhand baseball pitchers. Compared with overhand-pitching athletes, the shoulder horizontal abduction torque was lower in windmill pitchers (5.3%-7.2% for overhand compared with 3.3% ± 1.4% for windmill), whereas the shoulder internal rotation torque was comparable with overhand athletes (3.7%-5.9% for overhand compared with 4.4% ± 1.5% for windmill). The high shoulder internal rotation torque was probably generated as a result of the shoulder flexion velocity exceeding 5000 deg/sec. The maximum shoulder medial force was 74% ± 14% and the maximum shoulder anterior force was 38% ± 14%, which was comparable with overhand pitchers (39%-44%). All of these variables occurred from 0% to 55% of the delivery phase.49
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During the latter part of the delivery phase, 75% to 100%, the shoulder of the windmill pitcher experienced a maximum superior force of 98% ± 12% and a maximum lateral force of 50% ± 26%. The shoulder then internally rotated quickly at 4650 ± 1200 deg/sec. The torques at the shoulder were quite high at this point: 9.4% ± 4.0% shoulder abduction torque, and 9.8% ± 3.4% shoulder extension torque. Peak horizontal abduction torque, which was much higher than that for overhand pitchers, occurred after ball release (5.3%-6.0% for overhand compared with 9.0% ± 2.7% for windmill). A shoulder posterior force of 59% ± 13% was also experienced at this time, which was higher than the shoulder posterior force of overhand pitchers (39%-46%).49 Glenohumeral joint stability is of question during windmill pitching, much as in overhand pitching. Unlike with overhand pitching, where the humerus is held in an abducted position during the pitch, leading to shoulder joint instability, the shoulder instability in windmill pitching comes from resistance to distraction and the shoulder’s controlling internal rotation and elbow extension. The arm rotates a total of 485 degrees around the shoulder with the arm fully extended, and this increases shoulder distraction force. Another difference between overhand and windmill
TABLE 31-7 Differences of Shoulder Kinematics and Kinetics Between Female Windmill Softball Pitchers and Male Overhead Baseball Pitchers
Parameter
Windmill (n8) Mean ± SDa
Overhead Range
Shoulder flexion velocity 0%-50% of delivery (deg/sec)
5260 ± 2390
—
Shoulder internal rotation velocity 75%-100% of delivery (deg/sec)
4650 ± 1200
6073-7550b-e
Shoulder horizontal adduction torque 0%-50% of delivery (%bw ⫻ ht)
3.3 ± 1.4
5.3-7.2b,d,e f
Shoulder internal rotation torque 0%-50% of delivery (%bw ⫻ ht)
4.4 ± 1.5
3.7-5.9b,d,e f
Shoulder medial force 0%-50% of delivery (%bw)
74 ± 14
—
Shoulder anterior force 50%-75% of delivery (%bw)
38 ± 14
39-44b,e
Shoulder superior and compressive force 75%-100% of delivery (%bw)
98 ± 12
—
Shoulder abduction torque 75%-100% of delivery (%bw ⫻ ht)
9.4 ± 4.0
—
Shoulder lateral force 75%-100% of delivery (%bw)
50 ± 26
—
Shoulder extension torque 75%-100% of delivery (%bw ⫻ ht)
9.8 ± 3.4
—
Shoulder extension/horizontal abduction torque during arm deceleration (%bw ⫻ ht)
9.0 ± 2.7
5.3-6.0b,e
Shoulder posterior force during arm deceleration (%bw)
59 ± 13
39-46b,e
—
104-126b,d,e
Shoulder superior and compressive force during arm deceleration (%bw)
bw, body weight; ht ⫽ body height. a Barrentine SW, Fleisig GS, Whiteside JA, et al: Biomechanics of windmill softball pitching with implications about injury mechanisms at the shoulder and elbow. J Orthop Sports Phys Ther 28:405-415, 1998. b Campbell KR, Hagood SS, Takagi Y, et al: Kinetic analysis of the elbow and shoulder in professional and little league pitchers. Med Sci Sports Exerc 26: S175, 1994. c Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 18:402-408, 1993. d Feltner M, Dapena J: Dynamics of the shoulder and elbow joints of the throwing arm during a baseball pitch. Int J Sport Biomech 2:235-259, 1986. e Fleisig GS, Andrews JR, Dillman CJ, et al: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233-239, 1995. f Werner SL, Fleisig GS, Dillman CJ, et al: Biomechanics of the elbow during baseball pitching. J Orthop Sports Phys Ther 17:274-278, 1993.
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pitching is that the maximum resistance to distraction occurs during the arm acceleration phase in overhand pitching, but the maximum resistance to distraction occurs during the arm deceleration phase in windmill pitching. The magnitude of distraction in windmill pitching was approximately 80% to 95% of the magnitude of distraction measured in overhand pitching, so the magnitudes were quite similar.49 Anterior shoulder discomfort near the origin of the long head of the biceps tendon is a problem that many windmill pitchers experience. Usually this discomfort is treated with injections of a steroid or analgesic into the bicipital tendon area. However, the discomfort could actually be subscapularis or pectoralis strain due to increased shoulder extension followed by large forces and torques during the delivery motion. In addition, the long head of the biceps acts as a humeral head depressor. The biceps brachii undergoes a lot of strain as it prevents humeral distraction during the delivery phase, and it provides elbow flexion torque to control elbow extension and initiate elbow flexion. This can lead to overuse injury.49 Because both genders were compared in the study, the musculoskeletal differences between the two groups must also be accounted for. Comparisons between windmill and overhand pitching showed similar joint speeds and joint loads. In addition to experiencing high forces and torques, the demands on a female windmill pitcher are much higher than those on a male overhand pitcher. An overhand pitcher might get 3 or 4 days of rest between games, but windmill pitchers might pitch two days in a row and possibly even twice in the same day.49 Thus, the risk of overuse injury is quite high, and it can be speculated that windmill pitching can be quite hard on the pitcher and comparable with overhand pitching.
JAVELIN THROWING Like other types of throws, javelin throwing requires an efficient kinetic chain to generate energy to achieve maximum results. A good indicator of performance in overhead throwing sports is increased external rotation. In a study by Herrington,50 javelin throwers were tested to determine their external rotation and internal rotation angles. Shoulder range of motion was measured with the subject in a supine position with the arm abducted and elbow flexed approximately 90 degrees. Shoulder external rotation was significantly greater in the throwing arm (approximately 90 degrees) than in the nonthrowing arm (approximately 70 degrees), and internal rotation was approximately 50 degrees for both arms. Javelin throwers may be susceptible to over-rotation injuries, much like baseball pitchers. As discussed in the section on shoulder pathomechanics during baseball pitching,
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higher external rotation of the throwing shoulder could increase the chance of injury to the shoulder. Impingement of the rotator cuff can become an issue because it is impinged between the glenoid labrum and the humeral head. This weakens the rotator cuff muscles, which are then less effective to resist anterior humeral head displacement. The end result is increased strain on the glenohumeral joint. Both of these factors can lead to pathologic changes in the shoulder, resulting in an increased chance of injury.36 The weight, size, inertia, and vibration properties of a javelin can also cause problems to the shoulder. A javelin can be 0.4 to 0.8 m long (1.3 to 2.6 feet) and weigh as much as 0.8 kg (28 oz.).51 This is more than five times the weight of a baseball. However, no research has been performed on these subjects, so no definitive statements can be made on how the physical properties of the javelin affect forces and torques on the shoulder.
CRICKET THROWING AND BOWLING The mass of a cricket ball is slightly greater than the mass of a baseball, 5.50 to 5.75 oz for a cricket ball compared with 5.00 to 5.75 oz for a baseball. Although the throwing motion in cricket is quite comparable with the throwing motion in baseball, the cricket bowling motion is quite different from baseball pitching. The demands placed on the shoulder to generate velocity in bowling and throwing in cricket can eventually lead to injury. Fielding in cricket and baseball involves picking up a ball and throwing it to a particular location quickly and accurately. This is especially important in cricket, where the thrower might have to be extremely accurate in throwing out a runner by hitting three small stationary sticks. As in any kind of throwing, a kinematic series of events must occur to throw efficiently. There are quite a few differences in the sport of cricket compared with baseball that could affect athletes. In cricket, the entire field of play is a circle or oval approximately 375 to 525 feet in diameter, whereas the field of play in baseball ranges from 290 to 410 feet from the batter’s box. When in play, cricket batters have to run approximately 60 feet to be safe, and baseball hitters have to run 90 feet to reach a safe base.52 The temporal differences associated with these sports can have a big impact on the athlete. The bowler’s role in cricket is similar to a baseball pitcher’s role. However, unlike baseball pitching, where the pitcher is static on the mound before throwing, the cricket bowler runs up to the bowling location, gradually increasing speed, and leaps into the air to a predelivery phase. This provides additional energy to the kinetic chain of the cricket delivery. The bowler then lands with the back foot down and the upper trunk tilted away from the batter. The hands part, and between the times of rear foot contact and lead foot contact, the arm is rotated and then quickly
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counter-rotated around the glenohumeral joint. The elbow is barely flexed, if it is flexed at all, during this counterrotation, and the arm is accelerated as it circumducts the glenohumeral joint.53 There have been no biomechanical studies that have determined kinematic or kinetic magnitudes of this action. These variables could have been used to determine injury mechanisms associated with cricket bowling such as rotator cuff sprain and subacromial impingement. The bowler’s lead foot has to land behind a marked line. If that line is passed, the throw is deemed illegal. The ball is released a little later in the rotation compared with baseball pitching, as it is usually meant to bounce before reaching the batter. Pitch speeds can exceed 90 mph, as in baseball pitching.53 The bowler has to bowl six legal throws before one over (comparable with an inning in baseball) is complete, after which he is replaced by another bowler. The bowlers may then alternate bowling if they wish to do so. Most bowling injuries are related to the lower back, but many injuries occur at the throwing shoulder as well.54 The injuries to the shoulder in cricket include rotator cuff sprain and subacromial impingement.55 How the shoulder is angled toward the batter is also a key indicator of throwing technique. When the bowler’s shoulders are perpendicular to the batter at rear foot contact, the bowler is said to be a side-on bowler. When the bowler’s shoulders are more rotated toward the batter at rear foot contact (rotated approximately 20 degrees or more toward the pitcher), the bowler is said to be a front-on bowler. A third type of bowler, a mixed bowler, possesses characteristics of both the other types of bowlers, where initially the bowler has a front-on technique at rear foot contact and then changes to a sideon technique during the delivery stride.53 As in baseball, the shoulder externally rotates and prepares for the arm acceleration phase during the arm cocking phase or preparation phase in cricket, as referred to by Cook and Strike.56 In baseball pitching and throwing, the shoulder externally rotates to about 170 degrees.4,15 In cricket throwing, the external rotation is only about 150 degrees.56 Because the elbow is not flexed in the cricket throwing motion, as it is in baseball pitching, the athlete might not be able to externally rotate the shoulder as much. This may be due to the greater inertia of the forearm when the elbow is flexed closer to 90 degrees. On the other hand, the decreased external rotation in cricket bowling might simply be because maximizing external rotation when the elbow is not flexed does not give a biomechanical advantage. This could be due to time limitation placed on a thrower to throw out a runner. In baseball, the pitcher and fielder have more time to externally rotate their shoulders and generate more ball velocity. Cricket throwers only averaged about 68 mph when throwing from the outfield. Once maximum external rotation has been reached, the shoulder quickly internally rotates to accelerate the arm, much as in baseball.56
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HANDBALL Handball places heavy demands on the thrower’s shoulder. This sport is popular mainly in Europe. As in other sports, the thrower activates a kinetic chain of body movements to develop the energy to throw with velocity. One study found that 53% of the resultant ball velocity was due to arm action, and the remaining 47% was due to lower and upper trunk angular velocity.58 This shows the importance of using the entire body to generate ball velocity as opposed to throwing only with the arm. Increased or high range of motion and stability of the shoulder allow the ball to be thrown with higher velocity because the internal and external rotator muscles are more efficient.58 Strengthening these muscles could also help generate higher ball velocity. Bayios and colleagues59 studied the relation between ball velocity in handball and isokinetic strength of the shoulder rotator muscles. Forty-two subjects at three different levels were studied: Division A1, Division A2, and amateur. Shoulder strength during concentric internal and external rotation was measured using an isokinetic dynamometer at three rates: 60 deg/sec, 180 deg/sec, and 300 deg/sec. Shoulder external rotation was measured with the shoulder abducted at 90 degrees and the elbow flexed at 90 degrees. There were no significant differences in any of the variables among the three skill levels (Table 31-8). The shoulder external rotation strength was always less than the shoulder internal rotation strength, ranging anywhere from 47% to 66% of the internal rotation strength. The measured strength of both internal and external rotation decreased as the isokinetic rate of testing was increased. Ball velocity was also measured for each skill level for three different throws: on the spot, crossover step, and vertical jump (Table 31-9). There were significant differences between skill levels for each type of throw. Specifically, as skill level decreased, the throwing velocity decreased regardless of throw type.59 In general, there was no relationship between ball velocity and isokinetic strength of the internal and external rotators regardless of the type of throw or experience level. This was quite surprising because even though ball velocity increased between the groups, no increase in internal or external rotation torque was noticed. The few significant relationships that were discovered occurred during the jump throw for levels A1 and A2. However, these relationships were not very clear and no conclusion could be obtained from the data.59 In a previous study, Fleck and colleagues60 found that there was a relationship between internal rotation strength and ball velocity for the jump shot. This implies that the upper extremity rotation is more important when making a jump shot. The explanation could be that because the feet are off the ground, the lower
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TABLE 31-8 Peak Torque Values of Concentric Internal and External Rotational Shoulder Strength of Three Levels of Skill Shoulder Rotation
Division A1 (n 15)
Division A2 (n 12)
Amateur (n 15)
At 60 deg/sec (N•m) Internal rotation
60.78 ± 10.79
61.63 ± 14.46
53.99 ± 8.87
External rotation
36.44 ± 7.23
37.66 ± 8.88
35.43 ± 6.75
0.60
0.61
0.66
Ratio
At 180 deg/sec (N•m) Internal rotation
52.56 ± 9.23
54.84 ± 16.41
45.60 ± 9.40
External rotation
28.57 ± 5.19
30.41 ± 8.70
25.99 ± 5.33
0.54
0.55
0.57
Ratio
At 300 deg/sec (N•m) Internal rotation
42.99 ± 10.21
47.12 ± 14.20
39.88 ± 8.85
External rotation
20.90 ± 4.85
23.24 ± 8.62
18.56 ± 5.51
0.49
0.49
0.47
Ratio
Data from Bayios IA, Anastasopoulou EM, Sioudris DS, et al: Relationship between isokinetic strength of the internal and external shoulder rotators and ball velocity in team handball. J Sports Med Phys Fitness 41:229-235, 2001.
body is not as able to generate torque to provide energy to increase ball velocity. There appears to be some fundamental difference between handball throwing and the throwing motion seen in baseball. Furthermore, no relationship between range of motion of the shoulder and ball velocity was discovered in handball athletes. Other factors, like lower extremity rotation, perhaps play a bigger role in generating ball velocity, especially when throwing from flat ground.
TENNIS SERVE The tennis serve, much like the other throwing sports, uses a kinetic chain to develop energy to generate ball velocity. However, there are two main differences in the tennis serving motion. In addition to the human kinetic chain involved in the serve, there is another kinetic contribution from the racquet. Furthermore, instead of throwing or releasing the ball, the athlete strikes the ball. These two differences could have varying effects on the shoulder when compared with a typical throwing motion.
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TABLE 31-9 Ball Velocities for Three Throw Types for Division A1, Division A2, and Amateur Athletes Throw Type Division A1 Division A2 (m/sec) (n 15) (n 12)
Amateur (n 15)
Spot throw
23.51 ± 2.23
20.08 ± 1.12* 16.85 ± 1.58*†
Step throw
26.27 ± 3.21
23.22 ± 1.86* 18.90 ± 1.98
Jump throw
22.74 ± 2.16
20.54 ± 1.63* 15.54 ± 1.42*†
*Different from group A1 (P ⬍ 0.001). † Different from group A2 (P ⬍ 0.001). SD, standard deviation. Data from Bayios IA, Anastasopoulou EM, Sioudris DS, et al: Relationship between isokinetic strength of the internal and external shoulder rotators and ball velocity in team handball. J Sports Med Phys Fitness 41:229-235, 2001.
The tennis serve requires the athlete to repetitively strike the tennis ball in a manner that makes the shoulder susceptible to overuse injury. Hill61 reported injury rates as high as 56% in competitive tennis players. They suffered from various injuries, including rotator cuff and shoulder impingement injuries. According to Elliott and colleagues62 up to 50% of the resultant linear racquet head velocity was related to shoulder internal rotation. The forces experienced by the shoulder during the tennis serve can thus cause distraction of the shoulder. Understanding the kinematic and kinetic parameters of the serve motion can lead to a better understanding of the injury mechanism and how to reduce the chance of injury. Fleisig and colleagues63 and Elliott and colleagues62 described kinematic and kinetic variables of the tennis serve. Using two high-speed, electronically synchronized video cameras at the XXVII Olympic Games, data from 20 elite tennis athletes, both male and female, were collected. Using manual digitizing and a computer program that calculated angles, velocities, forces, and torques, the magnitudes of kinematic and kinetic variables were calculated. The shoulder kinematic and temporal values from the study are displayed in Table 31-10. Tennis athletes exhibited a high value of maximum external rotation, 172 ± 12 degrees, which was similar to that of elite baseball pitchers. As in baseball pitching, this large value of external rotation can be attributed to a combination of glenohumeral rotation, scapulothoracic motion, and trunk extension. Maximum external rotation occurred 95 ± 14 msec before ball impact with the racquet. The shoulder was abducted approximately 100 degrees and horizontally abducted about 6 degrees at both maximum external rotation and ball impact.63 The abduction angle of 100 degrees supported the hypothesis made by Atwater and colleagues64 that the arm is usually abducted about 90 degrees in overhand sports. The angle’s magnitude is also similar to that proposed by Matsuo and colleagues65 for maximizing ball velocity and minimizing loading of the shoulder.
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TABLE 31-10 Kinematic and Temporal Parameters Measured in Olympic Tennis Athletes
Parameter
Mean ± SD (n 20)
TABLE 31-11 Differences of Shoulder Kinetics Between Male and Female Tennis Athletes
Parameter
Male (n8) Mean ± SD
Female (n12) Mean ± SD
Shoulder external rotation at maximum shoulder external rotation (deg)
172 ± 12
Internal Rotation Torque at Maximum External Rotation 3.5 ± 1.2
101 ± 13
As a percentage of body weight times height*
4.6 ± 0.9
Shoulder abduction at maximum shoulder external rotation (deg)
In Newton meters*
64.9 ± 15.8
37.5 ± 15.0
Shoulder horizontal adduction at maximum shoulder external rotation (deg)
7±9
Male shoulder internal rotation at maximum angular velocity (deg/sec)
2420 ± 590
Female shoulder internal rotation at maximum angular velocity (deg/sec)
1370 ± 730
Shoulder abduction at instant of ball impact (deg)
Horizontal Adduction Torque at Maximum External Rotation As a percentage of body weight times height
4.2 ± 1.7
3.5 ± 1.4
In Newton meters
61.7 ± 31.0
36.8 ± 16.3
Peak Internal Rotation Torque 101 ± 11
As a percentage of body weight times height
5.1 ± 0.9
4.5 ± 1.3
In Newton meters
71.2 ± 15.1
47.8 ± 16.3
Shoulder horizontal adduction at instant of ball impact (deg)
5 ± 10
Maximum shoulder external rotation as time before ball impact (ms)
95 ± 14
As a percentage of body weight times height*
7.6 ± 0.8
6.5 ± 0.9
Maximum shoulder internal rotation velocity as time before ball impact (ms)
10 ± 18
In Newton meters
107.8 ± 24.9
68.8 ± 14.3
As a percentage of body weight
38.5 ± 14.0
30.5 ± 10.2
In Newtons
291.7 ± 119.8
185.1 ± 60.9
As a percentage of body weight*
79.6 ± 5.3
59.1 ± 8.4
In Newtons*
608.3 ± 109.5
363.7 ± 87.8
Peak Horizontal Adduction Torque
SD, standard deviation. Data from Elliott B, Fleisig GS, Nicholls R, et al: Technique effects on upper limb loading in the tennis serve. J Sci Med Sport 6:76-87, 2003.
After maximum shoulder external rotation, the shoulder internally rotates quickly to generate the energy needed to accelerate the arm and racquet. In Fleisig’s study, shoulder internal rotation angular velocity reached a maximum of 2420 ± 590 deg/sec for men and 1370 ± 730 deg/sec for women approximately 10 msec before ball impact.63 Although the angular velocities were quite high, they were much less than the maximum shoulder internal rotation angular velocity of baseball pitchers (7400 deg/sec).17 This could be attributed to the mass, moment of inertia, and air resistance of the racquet, which slowed down the internal rotation.63 The large difference in internal rotation angular velocity of the two genders is the greater internal rotation strength of male tennis players.62 Because men generate more ball velocity, they are also subjected to larger forces and torques. In the study by Elliott and associates62 shoulder forces and torques in male and female tennis athletes were compared (Table 31-11). The normalized and absolute internal rotation torques of men were found to be significantly greater than those of women when the arm was externally rotated to its maximum position (4.6% ± 0.9% and 64.9 ± 15.8 N•m for men compared with 3.5% ± 1.2% and 37.5 ± 15.0 N•m for women). Peak values for normalized horizontal abduction torque (7.6% ± 0.8% for men compared with 6.5% ± 0.9% for women),
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Peak Anterior Force
Peak Proximal Force
*Significant difference between male and female subjects (P ⬍ 0.01). SD, standard deviation. Data from Fleisig GS, Nicholls R, Elliott B, et al: Kinematics used by world class tennis players to produce high-velocity serves. Sports Biomech 2:51-64, 2003.
normalized shoulder proximal force (79.6% ± 5.3% for men compared with 59.1% ± 8.4% for women), and absolute proximal force (608.3 ± 109.5 N for men compared with 363.7 ± 87.8 N for women) were also higher in the male tennis players.62 The higher forces and torques experienced by the male tennis players were a result of men exerting themselves to a greater degree to generate higher service velocities. The magnitude of shoulder internal rotation torque and shoulder horizontal adduction torque both exceeded Dillman and coworkers’66 implication that any torque greater than 50 N•m was loading the shoulder excessively. According to this assertion, the shoulder is subject to excessive loading, and because of the repetitive nature of the tennis serve, the shoulder could be susceptible to overuse injury.
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Another issue that must be considered is the effect of muscle imbalance. Chandler and colleagues67 found this phenomenon in the college tennis players they tested. In this study, the tennis players had stronger internal rotator muscles compared with external rotator muscles. Specifically, when isokinetic strength testing was performed at a rate of 60 deg/sec, the external rotation peak torque was approximately 60% of the internal rotation peak torque in the dominant arm. When handball athletes performed the same isokinetic exercise, the external rotation peak torque was approximately 60% of the internal rotation peak torque in the dominant arm as well.59 In the nondominant arm of the tennis player, the ratio of external to internal rotation torque was 70%.67 The idea is that the internal rotators increased in strength as serving power increased, but the external rotators that decelerate the arm did not increase in strength enough. This strength difference or imbalance can cause a problem with how the repetitive arm motion is decelerated.
BASEBALL SWING The baseball swing requires the shoulders to accelerate quickly in coordination with the hips and arms to generate energy to hit a baseball. Although the swing is not as hard on the shoulder as a pitch or throw is, there are still numerous problems associated with the swinging mechanism. One such problem is posterior instability of the lead shoulder. To discuss the injury pathology related to the baseball swing, it is important to understand how the baseball swing can be hard on the shoulder. One study by Welch and colleagues68 focused on quantifying the kinematics of the baseball swing. Seven subjects were included in the study. Each batter hit off a tee to minimize the effects of reaction time, pitch type, and pitch speed. The investigators identified three events in the baseball swing: foot off, foot down, and ball contact. The time between the foot off and foot down was the stride phase. Between foot down and ball contact was the swing phase. The follow-through phase was the part of the swing after ball contact. Welch’s group also defined the shoulders, hips, and arms as segments rotating around the spine. They modeled the hips as a vector from the back hip to the leading hip, the shoulders as a vector from the back shoulder to the leading shoulder, and the arms as a vector from the mid shoulders to mid wrists. The rotations of the segments were calculated as rotations around a common spine axis, which was defined as the mid shoulders to the mid hips. For the sake of discussion, clockwise and counterclockwise refer to the direction of rotation of a segment about the common spine axis as viewed from above for a right-handed batter. During the foot-off phase, the batter shifts the weight from the lead leg to the back leg and rotates the upper body (shoulders and arms) clockwise away from the mound. The hips then rotate clockwise as well. This is
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referred to as the coiling process. The batter then shifts the weight forward, planting the lead leg in the ground to provide an axis of rotation during the foot-down phase. During this phase, the hips rotate counterclockwise, and shortly after this, the shoulders and arms rotate counterclockwise as well. The bat is then swung around as the arms rotate counterclockwise.68 The shoulders undergo different motions during batting. During the foot-off phase, when the batter shifts the weight to the back leg, the shoulder vector rotates clockwise about 30 degrees from the initial starting point facing the mound. The batter strides forward, further rotating the shoulders clockwise to increase the coiling effect. At this point, the shoulders are 52 degrees back from the initial starting point. The batter then plants the lead leg, and the shoulders now rotate counterclockwise toward the mound. At foot contact, the shoulders are rotated about 29 degrees clockwise from the initial starting point. The batter then explodes toward the ball by quickly whipping the pelvis and then the upper trunk counterclockwise toward the mound. The shoulder vector reaches a maximum rotational velocity of 937 deg/sec about 65 msec before ball contact. The batter then follows through until the shoulders come to rest at a position ⫺66 degrees from the starting position.68 Posterior instability of the leading shoulder could develop in batters due to the repetitive extreme range of motion while swinging. This effect might be increased when a batter faces an outside pitch where the batter has to extend, having increased horizontal flexion to hit the baseball. This means that there is more shear force acting across the glenohumeral joint. In an unpublished study of two baseball hitters with complaints of posterior instability, the players described a feeling of subluxation after ball contact. Biomechanical data showed that the lead shoulder had 83 degrees and 98 degrees of horizontal flexion when hitting an inside pitch and 98 degrees and 110 degrees of horizontal flexion when hitting an outside pitch. When the batter pulled the ball, horizontal flexion increased to 100 degrees and 115 degrees. In this study of two batters, it was hypothesized that higher horizontal flexion correlated with increased posterior glenoid shear force because of the way the shoulder horizontally flexed. The higher force could cause trauma to the posterior capsular restraints. Additionally, the mass of the bat factors in as a variable and contributes to the increased forces experienced in the glenohumeral joint. Both variables combine to present a condition where the shoulder is subject to laxity that allows periodic subluxation.69
GOLF SWING The golf swing seems harmless, but this is hardly the case. Both shoulders are susceptible to injury either from overuse or from poor technique, especially the lead shoulder. Studies
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show that almost 90% of shoulder injuries in golf are injuries to the leading shoulder. Younger golfers tend to develop shoulder instability, middle-aged golfers are more likely to suffer subacromial impingement, and older golfers are susceptible to arthrosis of the glenohumeral joint.70,71 The golf swing is generally broken up into four phases: set-up, backswing, downswing, and follow-through.72 The chance of injury and injury type vary with each phase. During the set-up phase, where the golfer lines up with the ball, the back shoulder tilts from the combination of spine flexion and the downward rotation of the back arm and scapula. The golfer then initiates the swinging motion by shifting weight to the back foot. When this happens, the right shoulder picks up and the hips rotate as the shoulders rotate. At the top of the back swing, shoulder rotation ranges from 78 to 102 degrees depending on skill level. The left shoulder then rotates internally and adducts horizontally. It is at this position that the left rotator cuff and scapular muscles are stretched, potentially placing the glenohumeral joint in an impinged position.72,73 This stretch also gives a golfer the X-factor, which is the lag of the hips compared with the shoulders. With this lag, energy is transferred from the legs up to the hips, shoulders, arms, and wrists.72 During the downswing, the shoulder accelerates quickly, following the hips to generate energy to drive the ball. In one study, the shoulder angular velocity for professional golfers was 723 deg/sec.74 Hume and colleagues72 found that the shoulders were responsible for about 20% of the club-head speed. The primary contribution came from the wrists (70%). In the follow-through, the lead shoulder externally rotates and abducts while the back shoulder adducts and internally rotates. The motion of the lead shoulder here could lead to anterior instability or biceps tendinitis.73 Golfers work hard to increase shoulder flexibility to maximize their ability to rotate their shoulders to produce maximum club speed. Jobe and colleagues75 found that rotator cuff disease and subacromial impingement were the most common shoulder injuries and accounted for 93% of shoulder injuries. The mechanism for impingement as discussed earlier was the internal rotation and horizontal adduction of the left shoulder across the chest that occurs at the top of the backswing. Sometimes, the capsular and labral structures become injured, and hyperlaxity of the shoulder can also become a problem.76 Instability could also arise due to the adduction across the body in the backswing phase. Anterior instability can occur at the end of the follow-through when the arm experiences maximum abduction and external rotation. Arthritis in old age is another problem. Glenohumeral arthroplasty is usually the treatment, and golfers return to playing within a few months.73 The best way to prevent some of these injuries is to practice proper technique and refrain from playing excessively.
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SWIMMING Swimming is considered to be an overhead sport much like the others sports previously discussed. The shoulder is put through a great deal of stress as the internal rotators fire and the arm abducts during the acceleration phase, and then firing of the external rotators occurs to decelerate the arm.67,77 This can be especially problematic for swimmers who repetitively execute this motion under water, making their shoulders susceptible to injury. The most common ailment of swimmers is impingement associated with glenohumeral instability or too much laxity.77,78 Injury to the shoulder could also be related to an imbalance of external and internal rotator muscles. When compared with nonswimmers, swimmers had a lower external rotation to internal rotation strength ratio (0.75 ratio for nonswimmers and 0.64 in swimmers). This was because the swimmers exhibited higher internal rotation strength.79 This same phenomenon is also measured in people who have impinged shoulders. It has also been noted in numerous studies that overhead athletes have greater external rotation range of motion at the cost of internal rotation range of motion (Table 31-12).79,80 In a study of elite swimmers and nonswimmers, Rupp and colleagues81 measured the shoulder range of motion of swimmers and nonswimmers and compared the values. There was no difference in range of motion between the left and right shoulders for the swimming or nonswimming athlete. However, when the swimming and nonswimming athletes’ shoulder range of motion was compared, significant differences were found. Because differences between the left and right shoulders were insignificant, only measurements for the right shoulder are discussed here TABLE 31-12 Mean and SD Differences of Shoulder Range of Motion Between Swimmers and Nonswimmers RIGHT SHOULDER RANGE OF MOTION (DEGREES)
Parameter
Swimmer
Nonswimmer
Arm adducted
69 ± 14
59 ± 14
Arm adducted 90 deg
115 ± 14
80 ± 12
Arm adducted
96 ± 4
92 ± 5
Arm adducted 90 deg
74 ± 14
63 ± 12
External Rotation
Internal Rotation
SD, standard deviation. Data from Rupp S, Berninger K, Hopf T: Shoulder problems in high level swimmers—impingement, anterior instability, muscular imbalance? Int J Sports Med 16:557-562,1995.
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(see Table 31-12). When looking at shoulder external rotation with the arm adducted 90 degrees, the swimmers had 115 ± 14 degrees of external rotation, whereas the nonswimmers only had 80 ± 12 degrees of external rotation. When looking at shoulder internal rotation with the arm adducted 90 degrees, the swimmers had 74 ± 14 degrees of internal rotation, whereas the nonswimmers only had 63 ± 12 degrees of internal rotation. Rupp and colleagues81 also reported isokinetic strength testing to measure the peak internal and external rotation torques (Table 31-13). There was no difference in external rotation peak torque values. However, the swimmers did have higher internal rotation peak torque values. In general, there appeared to be a 12-N•m difference of strength between the external and internal rotator muscles. Thus, the ratio of external to internal rotator strength was less for swimmers than for nonswimmers. Furthermore, the external to internal ratio of strength in swimming, 0.64,81 was comparable with the external to internal ratio of strength in handball, 0.66 to 0.60,59 and tennis, 0.60.67
SUMMARY Athletic injuries are a serious problem for the shoulder joint. Throwing injuries are of particular concern, because these injuries are common, disabling, and to some extent
TABLE 31-13 Mean and SD Isokinetic Peak Torque Values for External and Internal Rotation for Male Swimmers and Nonswimmers Parameter
Male Swimmer
Male Nonswimmer
External Rotation Peak Torque at 60 deg/sec (N•m) Right
33.16 ± 9.27
32.77 ± 11.84
Left
29.18 ± 6.54
28.99 ± 10.50
External Rotation Peak Torque 180 deg/sec (N•m) Right
32.62 ± 13.49
29.35 ± 9.73
Left
31.04 ± 8.25
29.11 ± 9.21
Internal Rotation Peak Torque 60 deg/sec (N•m) Right
45.43 ± 9.76*
31.17 ± 11.18
Left
45.70 ± 8.70*
33.31 ± 11.13
Internal Rotation Peak Torque 180 deg/sec (N•m) Right
44.34 ± 12.04
34.04 ± 13.32
Left
45.50 ± 10.85*
30.52 ± 11.87
*Significantly different from male nonswimmers (P ⬍ 0.05). SD, standard deviation. Data from Rupp S, Berninger K, Hopf T: Shoulder problems in high level swimmers—impingement, anterior instability, muscular imbalance? Int J Sports Med 16:557-562,1995.
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preventable. During the baseball pitch and other overhand throwing motions, the shoulder is abducted, rotated into maximum external rotation, and then rapidly internally rotated. Large forces and torques are produced to terminate external rotation, initiate internal rotation, prevent distraction, and control abduction and horizontal adduction. These forces and torques may be even larger and more dangerous if the athlete uses improper mechanics. The shoulder also goes through significant range of motion during underhand and striking motions in sports. An understanding of the kinematics and kinetics of the shoulder during athletic activity is essential for good treatment of shoulder injury. The physician, physical therapist, athletic trainer, or other health care professional must design treatment and rehabilitation appropriate for the demands that will be placed on the shoulder. An understanding of biomechanics is just as critical for the strength coach, technique coach, and others who work with the athlete to optimize performance and minimize the risk of injury. Shoulder biomechanics presented in this chapter serve as a foundation to the sports medicine clinician for reading the rest of this book. References 1. Dillman CJ: Proper mechanics of pitching. Sports Med Update 5:15-18, 1990. 2. Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 18:402-408, 1993. 3. Fleisig GS, Dillman CJ, Andrews JR: Proper mechanics for baseball pitching. Clin Sports Med 1:151-170, 1989. 4. Werner SL, Fleisig GS, Dillman CJ, et al: Biomechanics of the elbow during baseball pitching. J Orthop Sports Phys Ther 17:274-278, 1993. 5. Fleisig GS, Escamilla RF, Barrentine SW: Biomechanics of pitching: Mechanism and motion analysis. In Andrews JR, Zarins B, Wilk KE (eds): Injuries in Baseball. Philadelphia, Lippincott–Raven,1998, pp 3-22. 6. Jobe FW, Tibone JE, Perry J, et al: An EMG analysis of the shoulder in throwing and pitching. A preliminary report. Am J Sports Med 11:3-5, 1983. 7. Jobe FW, Moynes DR, Tibone JE, et al: An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 8. Sisto DJ, Jobe FW, Moynes DR: An electromyographic analysis of the elbow in pitching. Am J Sports Med 15:260-263, 1987. 9. Bradley JP, Tibone JE: Electromyographic analysis of muscle action about the shoulder. Clin Sports Med 10:789-805, 1991. 10. DiGiovine NM: An electromyographic analysis of the upper extremity in pitching. J Shoulder Elbow Surg 1:15-25, 1992. 11. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70;220-226, 1988. 12. Gowan ID, Jobe FW, Tibone JE, et al: A comparative electromyographic analysis of the shoulder during pitching. Professional versus amateur pitchers. Am J Sports Med 15:586-590, 1987.
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13. Jacobs P: The overhand baseball pitch: A kinesiological analysis and related strength-conditioning programming. NCSA J 9:5-13, 1987. 14. Feltner M, Dapena J: Dynamics of the shoulder and elbow joints of the throwing arm during a baseball pitch. Int J Sport Biomech 2:235-259, 1986. 15. Fleisig GS, Andrews JR, Dillman CJ, et al: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23:233-239, 1995. 16. Pappas AM, Zawacki RM, Sullivan TJ: Biomechanics of baseball pitching. A preliminary report. Am J Sports Med 13:216-222, 1985. 17. Fleisig GS, Barrentine SW, Zheng N, et al: Kinematic and kinetic comparison of baseball pitching among various levels of development. J Biomech 32:1371-1375, 1999. 18. Dillman CJ, Fleisig GS, Werner SL, et al: Biomechanics of the shoulder in sports: Throwing activities. In Prentice W, Hooker.DN (eds): Postgraduate Studies in Sports Physical Therapy. Berryville, Va, Forum Medicum,1991, pp 1-9. 19. Cosgarea AJ, Campbell KR, Hagood SS, et al: Comparative analysis of throwing kinematics from little league to professional baseball pitchers. Med Sci Sports Exerc 25:S131, 1993. 20. Campbell KR, Hagood SS, Takagi Y, et al: Kinetic analysis of the elbow and shoulder in professional and little league pitchers. Med Sci Sports Exerc 26:S175, 1994. 21. Dun S, Fleisig GS, Loftice JW, et al: The relationship between age and baseball pitching kinematics in professional baseball pitchers. J Biomech 40:265-270, 2007. 22. Escamilla R, Fleisig G, Barrentine S, et al: Kinematic comparisons of throwing different types of baseball pitches. J Appl Biomech 14:1-23, 1998. 23. Fleisig GS, Kingsley DS, Loftice JW, et al: Kinetic comparison among the fastball, curveball, change-up, and slider in collegiate baseball pitchers. Am J Sports Med 34(3):423-430, 2006. 24. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30:136-151, 2002. 25. Fleisig GS, Escamilla RF, Barrentine SW, et al: Kinematic and kinetic comparison of baseball pitching from a mound and throwing from flat ground. American Society of Biomechanics Conference Proceedings of the 20th Annual Meeting, Atlanta, Ga, 1996, pp 153-154. 26. McLeod WD, Andrews JR: Mechanisms of shoulder injuries. Phys Ther 66:1901-1904, 1986. 27. Andrews JR, Kupferman SP, Dillman CJ: Labral tears in throwing and racquet sports. Clin Sports Med 10:901-911, 1991. 28. Andrews JR, Angelo RL: Shoulder arthroscopy for the throwing athlete. Tech Orthop 3;75-81, 1988. 29. Bigliani LU, Codd TP, Connor PM, et al: Shoulder motion and laxity in the professional baseball player. Am J Sports Med 25:609-613, 1997. 30. Brown LP, Niehues SL, Harrah A, et al: Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 16:577-585, 1988. 31. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 30: 20-26, 2002.
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32. Ellenbecker TS, Roetert EP, Bailie DS, et al: Glenohumeral joint total rotation range of motion in elite tennis players and baseball pitchers. Med Sci Sports Exerc 34:2052-2056, 2002. 33. Baltaci G, Johnson R, Kohl H III: Shoulder range of motion characteristics in collegiate baseball players. J Sports Med Phys Fitness 41:236-242, 2001. 34. Reagan KM, Meister K, Horodyski MB, et al: Humeral retroversion and its relationship to glenohumeral rotation in the shoulder of college baseball players. Am J Sports Med 30:354-360, 2002. 35. Meister K, Day T, Horodyski M, et al: Rotational motion changes in the glenohumeral joint of the adolescent/Little League baseball player. Am J Sports Med 33:693-698, 2005. 36. Zheng N, Fleisig GS, Andrews JR: Biomechanics and injuries of the shoulder during throwing. Athletic Therapy Today 4:4-10, 1999. 37. Snyder SJ, Karzel RP, Del Pizzo W, et al: SLAP lesions of the shoulder. Arthroscopy 6:274-279, 1990. 38. Andrews JR, Carson WG Jr, McLeod WD: Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 13:337-341, 1985. 39. Bey MJ, Elders GJ, Huston LJ, et al: The mechanism of creation of superior labrum, anterior, and posterior lesions in a dynamic biomechanical model of the shoulder: The role of inferior subluxation. J Shoulder Elbow Surg 7:397-401, 1998. 40. Morgan CD, Burkhart SS, Palmeri M, et al: Type II SLAP lesions: Three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14:553-565, 1998. 41. Burkhart SS, Morgan CD: The peel-back mechanism: Its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair rehabilitation. Arthroscopy 14:637-640, 1998. 42. Shepard MF, Dugas JR, Zeng N, et al: Differences in the ultimate strength of the biceps anchor and the generation of type II superior labral anterior posterior lesions in a cadaveric model. Am J Sports Med 32:1197-1201, 2004. 43. Jazrawi LM, McCluskey GM III, Andrews JR: Superior labral anterior and posterior lesions and internal impingement in the overhead athlete. AAOS Instr Course Lect 52:43-63, 2003. 44. Sabick MB, Kim YK, Torry MR, et al: Biomechanics of the shoulder in youth baseball pitchers: Implications for the development of proximal humeral epiphysiolysis and humeral retrotorsion. Am J Sports Med 33:1716-1722, 2005. 45. Mair SD, Uhl TL, Robbe RG, et al: Physeal changes and range-of-motion differences in the dominant shoulders of skeletally immature baseball players. J Shoulder Elbow Surg 13:487-491, 2004. 46. Kronberg M, Brostrom LA, Soderlund V: Retroversion of the humeral head in the normal shoulder and its relationship to the normal range of motion. Clin Orthop Relat Res (253):113-117, 1990. 47. Osbahr DC, Cannon DL, Speer KP: Retroversion of the humerus in the throwing shoulder of college baseball pitchers. Am J Sports Med 30:347-353, 2002. 48. Fleisig G, Escamilla R, Andrews J, et al: Kinematic and kinetic comparison between baseball pitching and football passing. J Appl Biomech 12:207-224, 1996. 49. Barrentine SW, Fleisig GS, Whiteside JA, et al: Biomechanics of windmill softball pitching with implications about injury mechanisms at the shoulder and elbow. J Orthop Sports Phys Ther 28:405-415, 1998.
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50. Herrington L: Glenohumeral joint: Internal and external rotation range of motion in javelin throwers. Br J Sports Med 32:226-228, 1998. 51. Morriss C, Bartlett R: Biomechanical factors critical for performance in the men’s javelin throw. Sports Med 21: 438-446, 1996. 52. Melville T: Cricket (game). Microsoft Encarta Online Encyclopedia. Redmond, Wash, Microsoft Corporation, 2006. 53. Bartlett RM, Stockill NP, Elliott BC, et al: The biomechanics of fast bowling in men’s cricket: A review. J Sports Sci 14: 403-424, 1996. 54. Elliott BC: Back injuries and the fast bowler in cricket. J Sports Sci 18:983-991, 2000. 55. Crisp T, King JB: Cricket. In Fu FH, Stone DA (eds): Sports Injuries: Mechanisms, Prevention, Treatment. Baltimore, Williams & Wilkins,1994, pp 283-290. 56. Cook DP, Strike SC: Throwing in cricket. J Sports Sci 18:965-973, 2000. 57. Toyoshima S, Hoshikawa T, Miyashita M, et al: Contribution of the body parts to throwing performance. In Nelson RC, Morehouse CA (eds): Biomechanics IV. Baltimore, University Park Press,1974, pp 169-174. 58. Tullos HS, Erwin WD: Throwing mechanism in sports. Orthop Clin North Am 4:709-720, 1973. 59. Bayios IA, Anastasopoulou EM, Sioudris DS, et al: Relationship between isokinetic strength of the internal and external shoulder rotators and ball velocity in team handball. J Sports Med Phys Fitness 41, 229-235, 2001. 60. Fleck SJ, Smith SL, Craib MW, et al: Upper extremity isokinetic torque and throwing velocity in team handball. J Appl Sports Sci Res 6:120-124, 1992. 61. Hill JA: Epidemiologic perspective on shoulder injuries. Clin Sports Med 2:241-246, 1983. 62. Elliott B, Fleisig G, Nicholls R, et al: Technique effects on upper limb loading in the tennis serve. J Sci Med Sport 6:76-87, 2003. 63. Fleisig G, Nicholls R, Elliott B, et al: Kinematics used by world class tennis players to produce high-velocity serves. Sports Biomech 2:51-64, 2003. 64. Atwater AE: Biomechanics of overarm throwing movements and of throwing injuries. Exerc Sport Sci Rev 7:43-85, 1979. 65. Matsuo T, Matsumoto T, Takada Y, Mochizuki Y: Influence of different shoulder abduction angles during baseball pitching on throwing performance and joint kinetics. Presented at the 23rd annual meeting of the International Society of Biomechanics, 17th Congress, Calgary, Alberta, August 8-13, 1999.
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66. Dillman CJ, Schultheis JM, Hintermeister RA, et al: What do we know about body mechanics involved in tennis skills. In Krahl H, Pieper H, Kibler B, et al (eds): Tennis: Sports Medicine and Science. Düsseldorf, Germany, Society for Tennis Medicine and Science,1995, pp 6-11. 67. Chandler TJ, Kibler WB, Stracener EC, et al: Shoulder strength, power, and endurance in college tennis players. Am J Sports Med 20:455-458, 1992. 68. Welch CM, Banks SA, Cook FF, et al: Hitting a baseball: A biomechanical description. J Orthop Sports Phys Ther 22:193-201, 1995. 69. Philips BB, Andrews JR, Fleisig GS: Batter’s shoulder: Posterior instability of the lead shoulder, a biomechanical evaluation. Birmingham, Alabama Sports Medicine and Orthopaedic Center, 2000. 70. Mallon WJ: Golf. In Hawkins RJ, Misamore GW (eds): Shoulder Injuries in the Athlete: Surgical Repair and Rehabilitation. New York, Churchill Livingstone,1996, pp 427-433. 71. Pink M, Jobe FW, Perry J: Electromyographic analysis of the shoulder during the golf swing. Am J Sports Med 18:137-140, 1990. 72. Hume PA, Keogh J, Reid D: The role of biomechanics in maximising distance and accuracy of golf shots. Sports Med 35:429-449, 2005. 73. Kim DH, Millett PJ, Warner JJ, et al: Shoulder injuries in golf. Am J Sports Med 32:1324-1330, 2004. 74. Geisler PR: Golf. In Shamus E, Shamus J (eds): Sports Injury Prevention and Rehabilitation. New York, McGraw-Hill,2001, pp 185-225. 75. Jobe FW, Moynes DR, Antonelli DJ: Rotator cuff function during a golf swing. Am J Sports Med 14:388-392, 1986. 76. Jobe FW, Pink MM: Shoulder pain in golf. Clin Sports Med 15:55-63, 1996. 77. Jobe FW, Jobe CM: Painful athletic injuries of the shoulder. Clin Orthop Relat Res (173):117-124, 1983. 78. Kennedy JC, Hawkins R, Krissoff WB: Orthopaedic manifestations of swimming. Am J Sports Med 6:309-322, 1978. 79. McMaster WC, Long SC, Caiozzo VJ: Shoulder torque changes in the swimming athlete. Am J Sports Med 20: 323-327, 1992. 80. Kibler WB, Chandler TJ, Livingston BP, et al: Shoulder range of motion in elite tennis players. Effect of age and years of tournament play. Am J Sports Med 24:279-285, 1996. 81. Rupp S, Berninger K, Hopf T: Shoulder problems in high level swimmers—impingement, anterior instability, muscular imbalance? Int J Sports Med 16:557-562, 1995.
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CHAPTER 32 Electromyographic Activity During
Upper Extremity Sports Rafael Escamilla
muscle activity.1 From these initial reports, the baseball pitch was divided into several phases, which later were slightly modified by Escamilla and colleagues6 and Fleisig and colleagues7 as wind-up, stride, arm cocking, arm acceleration, arm deceleration, and follow-through (Fig. 32-1).
Electromyography (EMG) is the science of quantifying muscle activity. Understanding when and how much the shoulder muscles are active during upper extremity sports is helpful to physicians, physical therapists, athletic trainers, and coaches in providing appropriate treatment, training, and rehabilitation protocols to these athletes, as well as helping us to better understand the injury mechanism. EMG data do not always correlate well with muscle force, especially as muscle contraction velocities increase. Nevertheless, EMG is helpful in determining the timing and amount of muscle activation throughout a given movement.
Wind-up Phase Shoulder activity during the wind-up phase, which is from initial movement to maximum knee lift of the stride leg, is generally very low due to the slow movements that occur. As shown in Table 32-1, the greatest activity is from the upper trapezius, serratus anterior, and anterior deltoids, which all contract concentrically to upwardly rotate and elevate the scapula and abduct the shoulder as the arm is initially brought overhead, and then contract eccentrically to control downward scapular rotation and shoulder adduction as the hands are lowered to approximately chest level. The muscles of the rotator cuff, which have a dual function as glenohumeral joint compressors and rotators, have their lowest activity during this phase. Low shoulder activity is not surprising given that the shoulder forces and torques generated during this phase are also low.6,7
The focus of this chapter is on shoulder muscle activity during upper extremity sports. Most of the shoulder movements in the sports discussed here involve overhead throwing–type movements, which are commonly associated with shoulder injuries. Shoulder EMG data are far more extensive for overhead throwing activities, such as baseball pitching and football passing, and therefore much of this chapter focuses on shoulder EMG during activities that involve the overhead throwing motion. Where appropriate and available, shoulder muscle activity is integrated with shoulder joint kinematics (linear and angular shoulder displacements, velocities, and accelerations) and kinetics (shoulder forces and torques) to help better understand why certain muscles are active during different phases of an activity, and the type of muscle action (eccentric or concentric) that occurs. Also, when EMG is integrated with shoulder kinematics and kinetics, it provides insight into the injury mechanism. For a review of shoulder kinetics and kinematics in upper extremity sports, the reader should refer to Chapter 31.
Stride Phase There is a dramatic increase in shoulder activity during the stride phase (see Table 32-1), which is from the end of the balance phase to when the lead foot of the stride leg initially contacts the ground. During the stride the hands separate; the scapula upwardly rotates, elevates, and retracts; and the shoulders abduct, externally rotate, and horizontally abduct due to concentric activity from several muscles, including the deltoids, supraspinatus, infraspinatus, serratus anterior, and upper trapezius. It is not surprising that many more muscles are activated and to a higher degree during the stride compared with the wind-up. Interestingly, the supraspinatus has its highest activity during the stride as it works not only to abduct the shoulder but also to help compress and stabilize the glenohumeral joint. The deltoids also exhibit high activity to initiate and maintain the shoulder in an abducted position.
OVERHEAD BASEBALL PITCH Shoulder muscle activity during baseball pitching has been studied extensively by Jobe and others.1-5 Using 56 healthy male college and professional baseball pitchers, DiGiovine and colleagues1 quantified shoulder muscle activity during baseball pitching, and these EMG data are summarized in Table 32-1. To help generalize phase comparisons in muscle activity from Table 32-1, 0% to 20% of a maximum voluntary isometric contraction (MVIC) is considered low muscle activity, 21% to 40% MVIC is considered moderate muscle activity, 41% to 60% MVIC is considered high muscle activity, and greater than 60% MVIC is considered very high
Arm-Cocking Phase The arm-cocking phase begins at lead foot contact and ends at maximum shoulder external rotation. During this phase the kinetic energy that is generated from the larger lower 385
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TABLE 32-1 Shoulder Activity by Muscle and Phase During Baseball Pitching* PHASE
N
Wind-up (% MVIC)
Stride (% MVIC)
ArmCocking (% MVIC)
Arm Acceleration (% MVIC)
Arm Deceleration (% MVIC)
FollowThrough (% MVIC)
Upper trapezius
11
18±16
64±53
37±29
69±31
53±22
14±12
Middle trapezius
11
7±5
43±22
51±24
71±32
35±17
15±14
Lower trapezius
13
13±12
39±30
38±29
76±55
78±33
25±15
Serratus anterior (6th rib)
11
14±13
44±35
69±32
60±53
51±30
32±18
Serratus Anterior (4th rib)
10
20±20
40±22
106±56
50±46
34±7
41±24
Muscles Scapular
Rhomboids
11
7±8
35±24
41±26
71±35
45±28
14±20
Levator scapulae
11
6±5
35±14
72±54
76±28
33±16
14±13
Anterior deltoid
16
15±12
40±20
28±30
27±19
47±34
21±16
Middle deltoid
14
9±8
44±19
12±17
36±22
59±19
16±13
Posterior deltoid
18
6±5
42±26
28±27
68±66
60±28
13±11
Supraspinatus
16
13±12
60±31
49±29
51±46
39±43
10±9
Infraspinatus
16
11±9
30±18
74±34
31±28
37±20
20±16
Teres minor
12
5±6
23±15
71±42
54±50
84±52
25±21
Subscapularis (lower 3rd)
11
7±9
26±22
62±19
56±31
41±23
25±18
Subscapularis (upper 3rd)
11
7±8
37±26
99±55
115±82
60±36
16±15
Pectoralis major
14
6±6
11±13
56±27
54±24
29±18
31±21
Latissimus dorsi
13
12±10
33±33
50±37
88±53
59±35
24±18
Triceps brachii
13
4±6
17±17
37±32
89±40
54±23
22±18
Biceps brachii
18
8±9
22±14
26±20
20±16
44±32
16±14
Glenohumeral
*Means and standard deviations, expressed for each muscle as a percentage of a maximum voluntary isometric contraction (MVIC). Windup phase: from initial movement to maximum knee lift of stride leg; stride phase: from maximum knee lift of stride leg to when lead foot of stride leg initially contacts the ground; arm-cocking phase: from when lead foot of stride leg initially contacts the ground to maximum shoulder external rotation; arm-acceleration phase: from maximum shoulder external rotation to ball release; arm-deceleration phase: from ball release to maximum shoulder internal rotation; follow-through phase: from maximum shoulder internal roatation to maximum shoulder horizontal adduction. Adapted from DiGiovine NM, Jobe FW, Pink M, Perry J: Electromyography of upper extremity in pitching. J Shoulder Elbow Surg 1:15-25, 1992
Knee Up
Figure 32-1. Pitching phases and key events. ER, external rotation; IR, internal rotation.
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Phases
Wind-up
Foot Contact
Stride
Arm Cocking
Max ER
Release
Max IR
Arm Arm Follow-through Acceleration Deceleration
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ELECTROMYOGRAPHIC ACTIVITY DURING UPPER EXTREMITY SPORTS
extremity and trunk segments is transferred up the body to the smaller upper extremity segments. The pitching arm lags behind as the trunk rapidly rotates forward to face the hitter, generating a peak pelvis angular velocity around 600 deg/sec, occurring 0.03 to 0.05 sec after lead foot contact, followed by a peak upper torso angular velocity of nearly 1200 deg/sec, occurring 0.05 to 0.07 sec after lead foot contact.8 Consequently, high to very high shoulder muscle activity is needed during this phase to keep the arm moving with the rotating trunk as well as to control the resulting shoulder external rotation (see Table 32-1), which peaks near 180 degrees.8 Moderate activity is needed by the deltoids (see Table 32-1) to maintain the shoulder at approximately 90 degrees of abduction throughout the phase.8 Activity from the pectoralis major and anterior deltoid is needed during this phase to horizontally adduct the shoulder to a peak angular velocity of approximately 600 deg/ sec, from a position of approximately 20 degrees of horizontal abduction at lead foot contact to a position of approximately 20 degrees of horizontal adduction at maximum shoulder external rotation.8 Moreover, a large compressive force of approximately 80% of body weight is generated by the trunk onto the upper extremity (UE) at the shoulder to resist the large centrifugal force that is generated as the arm rotates forward with the trunk.7 The rotator cuff muscles (supraspinatus, infraspinatus, teres minor, and subscapularis) achieve high to very high activity to resist glenohumeral distraction and enhance glenohumeral stability. The posterior cuff muscles (infraspinatus and teres minor) and latissimus dorsi also generate a posterior force to the humeral head, which helps resist anterior humeral head translation and perhaps helps unload the anterior capsule and anterior band of the inferior glenohumeral ligament. Although it is widely accepted that strength and endurance in the posterior musculature are very important during the arm-deceleration phase to slow down the UE, they are also important during the arm-cocking phase. During the arm-cocking phase a peak shoulder internal rotation torque of 65 to 70 N•m is generated near the time of maximum shoulder external rotation, which implies that shoulder external rotation is progressively slowing down as maximum shoulder external rotation is approached.7,9 High to very high activity is generated by the shoulder internal rotators (pectoralis major, latissimus dorsi, and subscapularis), which contract eccentrically during this phase to control the rate of shoulder external rotation. The multiple functions of muscles are clearly illustrated during arm cocking. For example, the pectoralis major contracts concentrically to horizontally adduct the shoulder and eccentrically to control shoulder external rotation. This dual function helps this muscle maintain an appropriate length-tension relationship by simultaneously shortening and lengthening, which implies that this muscle might not be changing length much throughout this
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phase but rather maintaining a more constant length and in effect contracting isometrically. Another example is the subscapularis, which contracts concentrically to aid in horizontal adduction, eccentrically to help control external rotation, and may also contract isometrically to help resist glenohumeral joint distraction. The importance of scapular muscles during arm cocking is demonstrated in Table 32-1. High activity from these muscles is needed to stabilize the scapula and properly position the scapula in relation to the horizontally adducting and rotating humerus. The scapular protractors are especially important during this phase in order to resist scapular retraction by contracting eccentrically and isometrically during the early part of this phase, and contracting concentrically during the latter part of this phase to protract the scapula. The serratus anterior generates maximum activity during this phase. Because both the triceps brachii (long head) and biceps brachii (both heads) cross the shoulder, they both generate moderate activity during this phase to provide additional stabilization to the shoulder. In contrast to the triceps EMG reported by DiGiovine,1 which reported only moderate activity during this phase and much higher activity during the arm-acceleration phase, Werner and colleagues10 reported the highest triceps EMG during the arm-cocking phase and relatively little triceps EMG during the arm-acceleration phase. Because elbow extensor torque peaks during this phase,10,11 high eccentric contractions by the triceps brachii are needed to help control the rate of elbow flexion that occurs throughout the initial 80% of this phase.8 High triceps activity is also needed to initiate and accelerate elbow extension, which occurs during the final 20% of this phase as the shoulder continues externally rotating.8 Therefore, during arm cocking, the triceps initially contracts eccentrically to control elbow flexion early in the phase and contracts concentrically to initiate elbow extension later in the phase. Gowan and colleagues3 demonstrated that subscapularis activity is nearly twice as great in professional baseball pitchers compared with amateur pitchers during this phase. In contrast, muscle activity from the pectoralis major, supraspinatus, serratus anterior, and biceps brachii was approximately 50% greater in amateur pitchers compared with professional pitchers. From these data it can be concluded that better throwing efficiency by professional pitchers might require less muscle activity compared with amateurs. Glousman and colleagues2 compared shoulder muscle activity between pitchers with chronic anterior shoulder instability due to anterior glenoid labral tears with healthy pitchers with no shoulder pathology. Pitchers with chronic anterior instability exhibited greater muscle activity from the biceps brachii and supraspinatus and less muscle activity from the pectoralis major, subscapularis, and serratus
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THE ATHLETE’S SHOULDER
anterior. Chronic anterior instability results in excessive stretch of the anterior capsular, which can stimulate mechanoreceptors within the capsule, resulting in excitation in the biceps brachii and supraspinatus and inhibition in the pectoralis major, subscapularis, and serratus anterior. Increased activity from the biceps brachii and supraspinatus helps compensate for anterior shoulder instability because these muscles enhance glenohumeral stability. Decreased activity from the pectoralis major and subscapularis, which contract eccentrically to decelerate the externally rotating shoulder, can accentuate shoulder external rotation and further increase stress on the anterior capsule. Decreased activity from the serratus anterior can cause the scapula to be abnormally positioned relative to the externally rotating and horizontally adducting humerus. A deficiency in scapular upward rotation can decrease the subacromial space and increase the risks of impingement and rotator cuff pathology. Interestingly, infraspinatus activity was less in pitchers with chronic anterior shoulder instability compared with healthy pitchers. During arm cocking, the infraspinatus not only helps externally rotate and compress the glenohumeral joint but also helps generate a small posterior force on the humeral head due to a slight posterior orientation of its fibers as they run from the inferior facet of the greater tubercle to the infraspinous fossa. This posterior force on the humeral head helps resist anterior humeral head translation and unloads strain on the anterior capsule during arm cocking.
Arm-Acceleration Phase The arm acceleration phase only lasts 0.03 to 0.05 sec. It begins at maximum shoulder external rotation and ends at ball release. Like the arm-cocking phase, high to very high activity is generated from the glenohumeral and scapular muscles during this phase in order to accelerate the arm forward (see Table 32-1). Although DiGiovine and colleagues1 reported that the triceps had its highest activity during this phase,1 Werner and colleagues10 reported relatively little triceps EMG during the arm-acceleration phase. In addition, elbow extensor torque is very low during this phase compared with the arm-cocking phase.10,11 Elbow extension initially begins during the arm-cocking phase.6 Kinetic energy that is transferred from the lower extremities and trunk to the arm is used to help generate a peak elbow extension angular velocity of approximately 2300 deg/sec during this phase.6 In fact, a concentric contraction from the triceps brachii alone could not come close to generating this 2300 deg/sec elbow extension angular velocity. This observation is supported by findings by Dobbins and reported by Roberts,12 who had found that subjects who threw with paralyzed triceps muscles could obtain ball velocities greater than 80% of the ball velocities obtained before the triceps were paralyzed.
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This observation is further supported by Toyoshima and colleagues,13 who demonstrated that normal throwing using the entire body generated almost twice the elbow extension angular velocity compared with extending the elbow by throwing without lower extremity, trunk, and shoulder movements. These authors concluded that during normal throwing, the elbow is swung open like a whip, primarily due to linear and rotary contributions from the lower extremity, trunk, and shoulder and, to a lesser extent, a concentric contraction of the triceps. Nevertheless, the triceps help extend the elbow during this phase, as well as contributing to shoulder stabilization by the triceps long head. Moderate activity is generated by the deltoids1 to help produce a fairly constant shoulder abduction of approximately 90 to 100 degrees,8 which is maintained regardless of throwing style (e.g., overhand, sidearm). The glenohumeral internal rotators (subscapularis, pectoralis major, and latissimus dorsi) have their highest activity during this phase1 as they contract concentrically to generate a peak internal rotation angular velocity of approximately 6500 deg/sec near ball release.6 With these rapid arm movements, which are generated to accelerate the arm forward, it is not surprising that the scapular muscles also generate high activity,1 to help maintain proper position of the glenoid relative to the rapidly moving humeral head. Strengthening the scapular musculature is very important. Poor position and movement of the scapula can increase the risk of impingement and other related injuries, as well as reducing the optimal lengthtension relationship of both scapular and glenohumeral musculature. Gowan and colleagues demonstrated that rotator cuff and biceps brachii activity were 2 to 3 times higher in amateur pitchers compared with professional pitchers during this phase.3 In contrast, subscapularis, serratus anterior, and latissimus dorsi activity was much greater in professional pitchers. These results imply that professional pitchers better coordinate their body segment movements to increase throwing efficiency. Enhanced throwing mechanics and efficiency can minimize glenohumeral instability during this phase. This may help explain why professional pitchers generate less activity from the rotator cuff and biceps muscles which help compress the glenohumeral joint and enhance stability. Compared with healthy pitchers, pitchers with chronic anterior shoulder instability due to anterior labral injuries exhibit greater muscle activity from the biceps brachii, supraspinatus, and infraspinatus and less muscle activity from the latissimus dorsi, subscapularis, and serratus anterior.2 The increased activity from rotator cuff and biceps musculature in pitchers with chronic anterior instability is needed to provide additional glenohumeral stability that is lacking in these pitchers due to a compromised anterior labrum.
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With shoulder internal rotation, the long biceps tendon is repositioned anteriorly at the shoulder, providing compressive and posterior forces to the humeral head, which enhance anterior stability. Therefore, throwers with chronic anterior instability activate their biceps to a greater extent (32% vs 12% MVIC), as well as their supraspinatus and infraspinatus (37% vs 13% MVIC), compared with asymptomatic throwers.2 However, increased and excessive biceps activity due to anterior instability results in increased stress to the long biceps anchor at the superior labrum, which over time can result in pathology of the superior labrum anterior to posterior in direction (SLAP [superior anterior-posterior] lesions). In addition, chronic anterior shoulder instability inhibits normal contributions from the internal rotators and serratus anterior, which can adversely affect throwing mechanics and efficiency and increase injury risks at the shoulder.
Arm-Deceleration Phase The arm deceleration phase lasts 0.03 to 0.05 sec. It begins at ball release and ends at maximum shoulder internal rotation. Large loads are generated at the shoulders to slow the forward acceleration of the arm. Posterior shoulder musculature, such as the infraspinatus, teres minor and major, posterior deltoid, and latissimus dorsi, contract eccentrically not only to decelerate horizontal adduction and internal rotation of the UE but also help resist shoulder distraction and anterior subluxation forces. A shoulder compressive force slightly greater than body weight is needed to resist shoulder distraction, and a posterior shear force between 40% and 50% of body weight is generated to resist shoulder anterior subluxation.6,7 Therefore, high activity is generated by posterior shoulder musculature,1 in particular the rotator cuff muscles. In addition, scapular muscles also exhibit high activity to control scapular elevation, protraction, and rotation during this phase. For example, the lower trapezius, which generates a force on the scapula in the direction of depression, retraction, and upward rotation, generates its highest activity during this phase (see Table 32-1). High EMG activity from glenohumeral and scapular musculature illustrates the importance of strength and endurance training of the posterior musculature in the overhead-throwing athlete. Weak or fatigued posterior musculature can lead to multiple injuries, such as tensile overload undersurface cuff tears, labral and biceps pathology, capsule injuries, and internal impingement of the infraspinatus and supraspinatus tendons on the posterosuperior glenoid labrum.7 Compared with healthy pitchers, pitchers with chronic anterior shoulder instability exhibited less muscle activity from the pectoralis major, latissimus dorsi, subscapularis, and serratus anterior, which is similar to what occurred in the armcocking and acceleration phases.2 However, muscle activity from the rotator cuff and biceps brachii are similar between healthy pitchers and pitchers with chronic anterior shoulder
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instability during this phase, which is in contrast to the greater rotator cuff and biceps brachii activity demonstrated in pitchers with chronic anterior shoulder instability during the arm-cocking and acceleration phases.2 This difference in muscle activity may be partially explained by the very high compressive forces that are needed during arm deceleration to resist shoulder distraction, which is a primary function of the rotator cuff and to a lesser extent the biceps brachii. The biceps brachii generate their highest activity during arm deceleration (see Table 32-1). The function of this muscle during this phase to twofold. First, it must contract eccentrically along with other elbow flexors to help decelerate the rapid elbow extension that peaks during arm acceleration. This is an important function because weakness or fatigue in the elbow flexors can result in elbow extension being decelerated by impingement of the olecranon in the olecranon fossa, which can lead to bone spurs and subsequent loose bodies within the elbow. Second, the biceps brachii works synergistically with the rotator cuff muscles to resist distraction and anterior subluxation at the glenohumeral joint. Interestingly, during arm deceleration biceps brachii activity is greater in amateur pitchers compared with professional pitchers,3 which may imply that amateur pitchers employ a less-efficient throwing pattern compared with professional pitchers. Excessive activity from the long head of the biceps brachii can lead to labral pathology.
OVERHEAD FOOTBALL THROW: Only one known study has quantified muscle activity during the football throw.14 Using 14 male recreational and college athletes, these authors quantified activity from nine glenohumeral muscles throughout throwing phases specific for football, and their results are summarized in Table 32-2. The defined phases for football throwing are similar but slightly different than the defined phases for baseball pitching (see Table 32-1). Early arm cocking in the football throw was similar to the stride phase in baseball, and late cocking in the football throw was the same as arm cocking in baseball. The acceleration phase was the same for both the football throw and the baseball pitch. The arm deceleration and follow-through phases in the baseball pitch were combined into a single arm-deceleration and follow-through phase in the football throw. Rotator cuff activity progressively increased in each phase of football throwing, being least in the early cocking phase and peaking in the arm-deceleration and follow-through phases. This is a different pattern than the baseball pitch, where rotator cuff activity was generally greatest during either the arm-cocking phase or the arm-deceleration phase. For baseball pitching and football throwing, deltoid and biceps brachii activity were generally greatest during the arm-deceleration phase. The pectoralis major and latissimus dorsi had their greatest activity during arm-cocking
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TABLE 32-2 Shoulder Activity by Muscle and Phase During the Overhead Football Throw* Early Cocking (% MVIC)
Late Cocking (% MVIC)
Arm Acceleration (% MVIC)
Arm Deceleration and Follow-Through (% MVIC)
Total Throw (% MVIC)
Supraspinatus
45 ± 19
62 ± 20
65 ± 30
87 ± 43
65 ± 22
Infraspinatus
46 ± 17
67 ± 19
69 ± 29
86 ± 33
67 ± 21
Subscapularis
24 ± 15
41 ± 21
81 ± 34
95 ± 65
60 ± 28
Anterior deltoid
13 ± 9
40 ± 14
49 ± 14
43 ± 26
36 ± 9
Middle deltoid
21 ± 12
14 ± 14
24 ± 14
48 ± 19
27 ± 9
Posterior deltoid
11 ± 6
11 ± 15
32 ± 22
53 ± 25
27 ± 11
Pectoralis major
12 ± 14
51 ± 38
86 ± 33
79 ± 54
57 ± 27
Latissimus dorsi
7±3
18 ± 9
65 ± 30
72 ± 42
40 ± 12
Biceps brachii
12 ± 7
12 ± 10
11 ± 9
20 ± 18
14 ± 9
Muscles
*Means and standard deviations expressed for each muscle as a percentage of a maximum voluntary isometric contraction (MVIC). Early cocking phase: from rear foot plant to maximum shoulder abduction and internal rotation; late cocking phase: from maximum shoulder abduction and internal rotation to maximum shoulder external rotation; arm-acceleration phase: from maximum shoulder external rotation to ball release; arm-deceleration and follow-through phases: from ball release to maximum shoulder horizontal adduction; total throw: mean activity throughout the four defined phases. Adapted from Kelly BT, Backus SI, Warren RF, Williams RJ: Electromyographic analysis and phase definition of the overhead football throw. Am J Sports Med 30(6):837-844, 2002.
and arm-acceleration in baseball pitching, whereas peak activity occurred in these muscles during arm acceleration and arm deceleration in football throwing. The greatest activity occurred in the rotator cuff muscles, pectoralis major, and latissimus dorsi during the arm-deceleration and follow-through phases of the football throw. These muscles all work to generate a shoulder-compressive force during this phase to resist shoulder distraction. In fact, the greatest force generated during the football throw is a shoulder-compressive force that occurs during arm deceleration with a magnitude of approximately 80% body weight.15 The different muscle activity patterns between baseball pitching and football throwing are largely because a football weighs three times greater than a baseball. Although there are several kinematic and kinetic similarities between football throwing and baseball pitching, there are also several differences.15 Compared with throwing a football, throwing a baseball produces significantly greater trunk, shoulder, and elbow angular velocities during the arm-cocking and arm-acceleration phases, which lead to significantly greater shoulder forces and torques generated in baseball pitching, especially during the arm-deceleration phase, in order to slow down the rapidly moving arm.15
WINDMILL SOFTBALL PITCHING Maffet and colleagues conducted the only known study that quantified shoulder muscle firing patterns during the softball pitch.16 These authors used 10 female collegiate softball pitchers who all threw the fast pitch and quantified muscle activity in the anterior and posterior deltoid, supraspinatus,
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infraspinatus, teres minor, subscapularis, pectoralis major, and serratus anterior. The fast-pitch motion starts with the throwing shoulder extended, and then as the pitcher strides forward the arm fully flexes, abducts, and externally rotates, and then continues in a circular (windmill) motion all the way around until the ball is released near 0 degrees shoulder flexion and adduction. The six phases that define the pitch are as follows: wind-up, from first ball motion to 6-o’clock position (shoulder flexed and abducted approximately 0 degrees); from 6-o’clock position to 3-o’clock position (shoulder flexed approximately 90 degrees); from 3-o’clock position to 12-o’clock position (shoulder flexed and abducted approximately 180 degrees); from 12-o’clock position to 9-o’clock position (shoulder abducted approximately 90 degrees); from 9-o’clock position to ball release; and from ball release to completion of the pitch. The total circumduction of the arm about the shoulder from the wind-up to the follow-through are approximately 450 to 500 degrees.17 This circumduction occurs while holding a 6.25- to 7-oz ball and with the elbow near full extension, which accentuates the centrifugal distractive force acting at the shoulder. EMG results by muscle and phase during the softball pitch are shown in Table 32-3. Muscle activity was generally lowest during the wind-up and was increased during the 6-o’clock to 3-o’clock phase as the arm begins accelerating upward. Both the supraspinatus and infraspinatus generated their highest activity during this phase. During the 6-o’clock to 3-o’clock phase, the arm accelerates in a circular motion and achieves a peak shoulder flexion
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391
TABLE 32-3 Shoulder Activity by Muscle and Phase During the Windmill Softball Pitch*
Wind-up (%)
6- to 3-o’clock Position (% MVIC)
3- to 12-o’clock Position (% MVIC)
12- to 9-o’clock Position (% MVIC)
9 o’clock to Ball Release (% MVIC)
FollowThrough (% MVIC)
Anterior deltoid
25±11
38 ± 29
17 ± 23
22 ± 24
43 ± 38
28 ± 21
Supraspinatus
34±17
78 ± 36
43 ± 32
22 ± 19
37 ± 27
19 ± 12
Infraspinatus
24±13
93 ± 52
92 ± 38
35 ± 22
29 ± 17
30 ± 15
Posterior deltoid
10±5
37 ± 27
102 ± 42
52 ± 25
62 ± 29
34 ± 29
Teres minor
8±7
24 ± 25
87 ± 21
57 ± 21
41 ± 23
44 ± 11
Muscles
Pectoralis major
18±11
17 ± 12
24 ± 18
63 ± 23
76 ± 24
33 ± 20
Subscapularis
17±4
34 ± 23
41 ± 33
81 ± 52
75 ± 36
26 ± 22
Serratus anterior
23±9
38 ± 19
19 ± 9
45 ± 39
61 ± 19
40 ± 14
*Means and standard deviations, expressed for each muscle as a percentage of a maximum voluntary isometric contraction (MVIC). Adapted from Maffet MW, Jobe FW, Pink MM, et al: Shoulder muscle firing patterns during the windmill softball pitch. Am J Sports Med 25(3):369-374, 1997.
angular velocity of approximately 5000 deg/sec.17 The anterior deltoid was moderately active to help generate this rapid shoulder flexion angular velocity, and the serratus anterior was moderately active in helping to upwardly rotate and protract the scapula. The arm rapidly rotating upward in a circular pattern results in a distractive force of approximately 20% to 40% of body weight, which is resisted in part by the shoulder-compressive action of the supraspinatus and infraspinatus. As the arm continues its upward acceleration during the 3-o’clock to 12-o’clock phase, the posterior deltoid, teres minor, and infraspinatus all achieve their peak activity. These muscles not only help externally rotate the shoulder during this phase but also help compress the glenohumeral joint and resist the progressively increasing shoulder-distractive forces, which are approximately 50% of body weight during this phase.17 These muscles are also in good position to resist shoulder-lateral forces, which peak during this phase.17 The arm begins accelerating downward during the 12-o’clock to 9-o’clock phase. It is during this phase that the shoulder begins to rapidly internally rotate 2000 to 3000 deg/sec.17 It is not surprising that the internal rotators (subscapularis and pectoralis major) exhibit high activity during this phase. High activity from the pectoralis major also helps adduct the shoulder during this phase. The subscapularis also helps stabilize the humeral head and can help unload anterior capsule stress caused by the overhead and backward position of the arm as it begins accelerating forward. The serratus anterior exhibited a marked increase in activity to help stabilize the scapula and properly position the glenoid with the rapidly moving humerus. The subscapularis, pectoralis major, and serratus anterior collectively generat their highest activity during the
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9-o’clock to ball release phase. The serratus anterior continues to work to stabilize the scapula and properly position it in relation to the rapidly moving humerus. High subscapularis and pectoralis major activity is needed during this phase to resist distraction at the shoulder, which peaks during this phase with a magnitude of approximately body weight.17,18 These muscles also help generate a peak shoulder internal rotation of approximately 4600 deg/sec17 and help adduct and flex the UE until the UE contacts the lateral thigh. Not all softball pitchers exhibit the same pattern of motion during this phase, because none of the 53 youth softball pitchers studies by Werner and colleagues18 adopted the release strategy of contacting the lateral thigh at ball release. This might partially explain why the collegiate pitchers in the study by Maffet and colleagues16 generated relatively low posterior cuff activity and relatively low activity in general during the follow-through. With contact of the arm with the lateral thigh near ball release, the deceleration forces and torques generated by muscles to slow down the arm are much less compared with no contact of the arm with the lateral thigh. In the case of no arm contact with the lateral thigh, shouldercompressive and related forces and torques may be higher during follow-through, and relatively high shoulder forces and torques have been reported.17,18 However, these forces and torques are less during follow-through compared with those for the 9-o’clock–to–ball release acceleration phase. This is one major difference between overhand throwing and the windmill motion. In overhead throwing, the deceleration phase after ball release generates greater shoulder forces and torques compared with the acceleration phase up to ball release of the windmill motion. In softball pitching, the greatest forces and torques occur during the acceleration phase of the delivery.
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The rapid shoulder movements and high shoulder forces that are generated during the windmill fast pitch make the shoulder susceptible to injury. There is also a higher risk of subacromial impingement due to the extreme shoulder flexion and abduction that occurs during the pitch. A significant number of shoulder injuries have been reported in softball pitchers, including bicipital and rotator cuff tendinitis, muscle strain, and impingement.19
VOLLEYBALL SERVE AND SPIKE The volleyball serve and spike involve an overhead throwing motion that is similar to baseball pitching and football throwing. Unlike baseball pitching and football passing, there are no known studies that have quantified the shoulder forces and torques that are generated during the volleyball serve and spike. Nevertheless, because the motion is overhead and extremely rapid, similar to baseball pitching, it is hypothesized that high shoulder forces and torques are generated, especially during the volleyball spike. To support this hypothesis, numerous injuries occur each year in volleyball, primarily involving muscle, tendon, and ligament injuries during blocking and spiking.20 It has been reported that approximately one quarter of all volleyball injuries involve the shoulder.20-23 Moreover, in athletes who engage in vigorous upper-arm activities, shoulder pain ranks highest in volleyball players, which is largely due to the repetitive nature of the hitting motion.20-23 Therefore, understanding muscle-firing patterns of the shoulder complex is helpful in developing muscle-specific treatment and training protocols, which may minimize injury and enhance performance. No known studies have quantified muscle activity from the scapular muscles during the volleyball serve or spike. This is surprising given the importance of the scapular muscles in maintaining proper position of the scapula with the humerus. Volleyball players with shoulder pain often have muscle imbalances of the scapular muscles.24 The firing pattern of the scapular muscles during the volleyball serve and spike should be the focus of future research studies. Rokito and colleagues conducted the only known study that quantified muscle-firing patterns of glenohumeral muscles during the volleyball serve and spike.25 These authors used 15 female college and professional volleyball players, who all performed the volleyball serve and spike. The shoulder muscles quantified included the anterior deltoid, supraspinatus, infraspinatus, teres minor, subscapularis, teres major, latissimus dorsi, and pectoralis major. The serve and spike motions were divided into five phases, which collectively are 1.95 sec for the serve25 and 1.11 sec for the spike:25 wind-up, cocking, acceleration, deceleration, and follow-through. The wind-up accounts for 39% of total serve time and 33% of total spike time. It
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begins with the shoulder abducted and extended and ends with the initiation of shoulder external rotation. Cocking accounts for 20% of total serve time and 23% of total spike time and begins with initiation of shoulder external rotation and ends with maximum shoulder external rotation. Acceleration accounts for 6% of total serve time and 8% of total spike time and comprises maximum shoulder external rotation to ball impact. Deceleration accounts for 8% of total serve time and 9% of total spike time and lasts from ball impact to when the upper arm is perpendicular to the trunk. Follow-through accounts for 28% of total serve time and 27% of total spike time and lasts from when the upper arm is perpendicular to the trunk to the end of arm motion. Shoulder EMG results by muscle and phase during the volleyball serve and spike are shown in Table 32-4. Similar to other overhead throwing activities, muscle activity during the serve were relatively low during the wind-up and follow-through phases. However, during the wind-up phase of the spike, peak activity was recorded in the anterior deltoid, infraspinatus, and supraspinatus. These muscles are important to help rapidly elevate the arm overhead (anterior deltoid and supraspinatus) and initiate external rotation (infraspinatus). The rotator cuff muscles are also active to help stabilize the humeral head in the glenoid fossa. During the cocking phase, the shoulder rapidly externally rotates, which helps explain the high activity in the infraspinatus and teres minor during the serve and spike. As in baseball pitching, these muscles also produce a posterior force on the humerus that might help unload the anterior capsule as the humeral head attempts to translate anteriorly while the shoulder externally rotates. Also, the rotator cuff muscles have high activity to generate glenohumeral compression and resist distraction. The relatively high activity from the subscapularis and pectoralis major help provide support to the anterior shoulder (without such support anterior instability can ensue), as these muscles also contract eccentrically to slow down and control the rate of the rapid shoulder external rotation. An important distinction between the serve and spike occurs during the acceleration phase. During the serve, the objective is not to impart maximum velocity to the ball but rather to hit the ball so it floats over the net with a parabolic trajectory in an area that would be most difficult for the opponent to return. In contrast, during the spike the objective typically is to hit the ball as hard as possible so as to impart maximum velocity. Consequently, muscle activity is higher in the powerful acceleratory muscles during the spike compared with the serve. Because overhead throwing motions such as baseball pitching, football passing, and the tennis serve achieve shoulder internal rotation angular velocities between 4000 and 7000 deg/sec,6,15,26 it is reasonable to assume that similar internal rotation angular velocities occur during the volleyball spike. The shoulder internal rotators
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TABLE 32-4 Shoulder Activity by Muscle and Phase During the Volleyball Serve and Spike* Wind-up (% MVIC)
Cocking (% MVIC)
Acceleration (% MVIC)
Deceleration (% MVIC)
Follow-Through (% MVIC)
Serve
21±11
31±13
27±22
42±17
16±16
Spike
58±26
49±19
23±17
27±10
15±7
Serve
25±10
32±18
37±25
45±13
24±16
Spike
71±31
40±17
21±27
37±23
27±15
Serve
17±10
36±16
32±22
39±21
13±11
Spike
60±17
49±16
27±18
38±19
22±11
Serve
7±8
44±20
54±26
30±23
8±9
Spike
39±20
51±17
51±24
34±13
17±7
Muscles Anterior Deltoid
Supraspinatus
Infraspinatus
Teres Minor
Subscapularis Serve
8±8
27±25
56±18
27±15
13±11
Spike
46±16
38±21
65±25
23±11
16±15
Serve
1±1
11±7
47±24
7±8
3±3
Spike
28±14
20±11
65±31
21±18
15±16
Serve
1±2
9±18
37±39
6±9
3±3
Spike
20±13
16±17
59±28
20±21
15±10
Serve
3±6
31±14
36±14
7±11
7±6
Spike
35±17
46±17
59±24
20±16
21±12
Teres Major
Latissimus Dorsi
Pectoralis Major
*Means and standard deviations, expressed for each muscle as a percentage of a maximum voluntary isometric contraction (MVIC). Adapted from Rokito AS, Jobe FW, Pink MM, et al: Electromyographic analysis of shoulder function during the volleyball serve and spike. J Shoulder Elbow Surg 7(3):256-263, 1998.
(teres major, subscapularis, pectoralis major, and latissimus dorsi) all generated their highest activity for both the serve and the spike in order to both internally rotate the shoulder and accelerate the arm forward. During the acceleration phase, teres minor activity peaks to provide a stabilizing posterior restraint to anterior translation. In contrast, infraspinatus activity is relatively low. The differing amounts of EMG activity between the teres minor and infraspinatus throughout the different phases of the serve and spike are interesting to note, especially because the teres minor and infraspinatus provide similar glenohumeral functions and they are located adjacent to each other anatomically. However, the spatial orientations of these two muscles are different: The teres minor is in a better mechanical position to extend the shoulder in a sagittal plane and the infraspinatus is in a
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better mechanical position to extend the shoulder in a transverse plane. There are also clinical differences between these two muscles; they are typically not injured together, but rather one or the other is injured.1,25 This different clinical observation between the teres minor and infraspinatus is consistent with the different muscle-firing patterns that occur within any given phase of overhead throwing, such as what also occurs during baseball pitching (see Table 32-1).1 During the deceleration phase, infraspinatus and supraspinatus activity is greatest during the serve but not during the spike. In fact, rotator cuff activity is generally lower in the spike compared with the serve, which may be counterintuitive. For example, because a primary function of the rotator cuff is to generate shoulder-compressive force to resist shoulder distraction, and because shoulder-compressive
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forces from similar overhead throwing motions (such as baseball pitching and football passing) generate large shoulder-compressive forces during this phase,6,15 it is plausible to assume that large compressive forces are also needed during the spike. The relatively low activity from the rotator cuff muscles during the spike is a different pattern compared with the moderate to high rotator cuff activity generated during the baseball pitch and football pass (see Tables 32-1 and 32-2). The higher rotator cuff activity during baseball pitching and football passing is needed during this phase to resist the large distractive forces that occur at the shoulder, which are near or in excess of body weight. The EMG differences between varying overhead throwing motions may be due to mechanical differences between different activities. For example, in baseball pitching and football passing a weighted ball (5-oz baseball and 15-oz football) is carried in the hands throughout throwing phases but is released just before the beginning of the deceleration phase. With these weighted balls no longer in hand, the arm can travel faster just after ball release (beginning of deceleration phase), and thus more posterior shoulder forces and torques may be generated by the posterior musculature to slow down the rapidly moving arm. In the volleyball spike there is no weighted implement in the hand throughout the entire motion. Moreover, when the hand contacts the ball, the ball generates an equal and opposite force on the hand, which acts to slow down the forward-moving hand. Therefore, a slower-moving arm may result in smaller forces and torques at the shoulder to decelerate the arm and less muscle activity. This explanation might partially explain the lower rotator cuff activity in the volleyball spike compared with baseball pitching and football passing, especially from the posterior musculature (see Table 32-4). However, a biomechanical analysis of the volleyball spike is needed to quantify shoulder forces and torques to help confirm this hypothesis.
TENNIS SERVE AND VOLLEY Tennis Serve The tennis literature is abundant with studies that have examined EMG activity of the elbow and wrist musculature, but data on shoulder EMG during the tennis serve and volley are sparse. Ryu and colleagues27 conducted the only known study that extensively quantified shoulder EMG during the tennis serve. EMG data were collected during the serve from eight shoulder muscles using six male collegiate tennis players. One of the limitations of this study is that no standard deviations were reported and only a few subjects were used. The serve was divided into four phases: wind-up, cocking, acceleration, and deceleration and follow-through. Wind-up is the phase from start of service motion to ball release, cocking is from ball release to maximum shoulder external rotation, acceleration is from maximum shoulder external rotation to racquet contact with the ball, and deceleration and follow-through are from racquet contact with the ball to completion of the serve. Shoulder EMG results during the serve are shown in Table 32-5. Mean EMG peaked for the infraspinatus and supraspinatus during the cocking phase. During this phase, the shoulder externally rotates approximately 170 degrees and the peak shoulder internal rotator torque is approximately 65 N•m.28 These kinematic and kinetic data help explain the high activity from the infraspinatus, which is active in initiating shoulder external rotation during the first half of the cocking phase. The infraspinatus and supraspinatus also contract to resist shoulder-distraction forces during the cocking phase. Although not quantified during the tennis serve, shoulder compressive force (to resist distraction) is approximately 80% of body weight during the cocking phase in baseball pitching, which is a motion similar to the tennis serve.7 The biceps brachii can also help generate shoulder
TABLE 32-5 Shoulder Activity by Muscle and Phase During the Tennis Serve*
Wind-up (% MVIC)
Cocking (% MVIC)
Acceleration (% MVIC)
Deceleration and Follow-Through (% MVIC)
Biceps brachii
6
39
10
34
Middle deltoid
18
23
14
36
Supraspinatus
15
53
26
35
Infraspinatus
7
41
31
30
Subscapularis
5
25
113
63
Pectoralis major
5
21
115
39
Serratus anterior
24
70
74
53
Latissimus dorsi
16
32
57
48
Muscle
*Means (standard deviations not reported), expressed for each muscle as a percentage of a maximum voluntary isometric contraction (MVIC). Adapted from Ryu RK, McCormick J, Jobe FW, et al: An electromyographic analysis of shoulder function in tennis players. Am J Sports Med 16(5):481-485, 1988.
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compressive force during the cocking phase,2 which might help explain the relatively high activity from this muscle. Pectoralis major, latissimus dorsi, and subscapularis activity were greatest during the acceleration phase, as these muscles contract to help generate a peak shoulder internal rotation angular velocity of approximately 2500 deg/sec26 and accelerate the arm forward. The serratus anterior also peaked during the acceleration phase to properly position the scapula relative to the rapidly moving humerus. These EMG findings during the tennis serve are similar to EMG findings during baseball pitching, which is not surprising considering the numerous kinematic and kinetic similarities between the tennis serve and the baseball pitch.6-8,26,28 EMG activity during arm deceleration and follow-through demonstrated moderate to high activity, but activity was less than the EMG observed during baseball pitching and football passing. One reason for this, as for the volleyball spike, is that the force the ball exerts against the racquet acts to slow down the arm, which may result in lower posterior forces and torques needed from muscle contractions. The relatively high activity from the biceps brachii helps stabilize the shoulder (resist distraction) and decelerate the rapid elbow extension angular velocity, which peaks at approximately 1500 deg/sec.26 The moderate to high activity from the rotator cuff muscles generate compressive force to help resist shoulder-distraction forces, in which peak forces have been quantified at approximately 75% of body weight during the serve.28
Tennis Volley A few studies have examined shoulder activity during the tennis backhand and forehand.27,29,30 Ryu and colleagues collected EMG data from eight shoulder muscles using six male collegiate tennis players. This study is weakened by a low number of subjects, no standard deviations reported, and no statistical analyses between the forehand and backhand volleys. The forehand and backhand volleys were divided into three phases: racquet preparation, acceleration, and follow-through.27 Racquet preparation is the phase from shoulder turn to initiation of weight transfer to the front foot, acceleration is from initiation of weight transfer to the front foot to racquet contact with the ball, and deceleration and follow-through are from racquet contact with the ball to completion of the stroke. Shoulder EMG results from Ryu and colleagues27 during forehand and backhand volleys are shown in Table 32-6. Muscle activity was relatively low during the racquetpreparation phase, which is consistent with forehand and backhand shoulder EMG data from Chow and colleagues.30 Relatively large differences in muscle activity have been reported between the forehand and backhand during the acceleration phase.27,30 High activity has been reported in the biceps brachii, anterior deltoid, pectoralis major, and subscapularis during the forehand volley, but these same
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muscles exhibited low activity during the backhand volley.27,29,30 The high activity during the forehand from the pectoralis major, anterior deltoid, and subscapularis is not surprising given their roles as horizontal flexors and internal rotators. However, the high activity from the biceps brachii is somewhat surprising. Morris and colleagues31 also reported high biceps activity during the forehand in the acceleration phase. The biceps is in a mechanically advantageous position to horizontally adduct the shoulder during the forehand motion, and they also work to stabilize both the shoulder and elbow. Moreover, they also can help cause the slight amount of elbow flexion that occurs to stabilize the elbow and keep it from extending (due to inertial forces and torques the upper arm applies to the forearm at the elbow as the arm rapidly horizontally adducts). The serratus anterior is also more active during the forehand compared with the backhand to help protract the scapula during the acceleration phase and help properly position the scapula relative to the rapidly moving humerus. Posterior deltoids, middle deltoids, supraspinatus, infraspinatus, latissimus dorsi, and triceps brachii exhibited high activity during the backhand volley but relatively low activity during the forearm volley.27,30 These muscles all work synergistically during the backhand to horizontally extend and externally rotate the UE. The triceps also work to extend the elbow and help stabilize both the shoulder and elbow. The high activity from the supraspinatus and infraspinatus helps provide shoulder-compression forces to resist shoulder distraction. The supraspinatus and deltoids also help maintain the shoulder in abduction.
BASEBALL BATTING Only one study has quantified muscle activity of the shoulder during baseball hitting.32 Using the swings of 18 professional male baseball players during batting practice, the investigators quantified posterior deltoid, triceps brachii, supraspinatus, and serratus anterior activity during six phases of batting: wind-up, preswing, early swing, middle swing, late swing, and contact of the bat with the ball. Wind-up is from lead heel off to lead forefoot contact; preswing is from lead forefoot contact to the beginning of the swing; early swing is from the beginning of the swing to when the bat is perpendicular to the ground; middle swing is from when the bat is perpendicular to the ground to when the bat is parallel with the ground; late swing is from when the bat is parallel with the ground to bat contact with the ball; and follow-through is from bat contact with the ball to maximum abduction and external rotation of the lead shoulder. Muscle activity was relatively low during the wind-up and follow-through phases, with EMG magnitudes generally
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THE ATHLETE’S SHOULDER
TABLE 32-6 Shoulder Activity by Muscle and Phase During the Tennis Forehand and Backhand Volley*
Racquet Preparation (% MVIC)
Acceleration (% MVIC)
Deceleration and Follow-Through (% MVIC)
Forehand
17
86
53
Backhand
11
45
41
Forehand
27
17
20
Backhand
22
118
48
Forehand
22
25
14
Backhand
10
73
41
Forehand
29
23
40
Backhand
7
78
48
Forehand
28
102
49
Backhand
8
29
25
Forehand
10
85
30
Backhand
15
29
14
Forehand
14
76
60
Backhand
12
45
31
Forehand
6
24
23
Backhand
4
45
10
Muscles Biceps Brachii
Middle Deltoid
Supraspinatus
Infraspinatus
Subscapularis
Pectoralis Major
Serratus Anterior
Latissimus Dorsi
*Means (standard deviations not reported), expressed for each muscle as a percentage of a maximum voluntary isometric contraction (MVIC). Adapted from Ryu RK, McCormick J, Jobe FW, et al: An electromyographic analysis of shoulder function in tennis players. Am J Sports Med 16(5):481-485, 1988.
less than 25% of MVIC. The posterior deltoid peaked at 101% of MVIC during preswing and then progressively decreased throughout early swing (88% MVIC), middle swing (82% MVIC), and late swing (76% MVIC). Triceps brachii activity was 46% of MVIC during preswing, peaked at 92% of MVIC during early swing, and then progressively decreased to 73% of MVIC during middle swing and 38% of MVIC during late swing. Both the supraspinatus and serratus anterior generated relatively moderate and constant activity from preswing to late swing, ranging from 28% to 39% of MVIC throughout these four phases. Compared with overhand throwing, EMG data for hitting are relatively sparse, and thus it is hard to make
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definite conclusions. There are EMG data for only a few shoulder muscles with which to compare. Nevertheless, it does appear that both glenohumeral and scapular muscles generate high activity during the swing, because both concentric and eccentric muscle actions are needed throughout the swing. To make it even more difficult to develop summaries of muscle-firing patterns in hitting, there are currently no shoulder kinetic data in the hitting literature. The focus of future hitting studies should be on quantifying shoulder forces and torques throughout the swing and on acquiring shoulder EMG data for additional shoulder muscles, such as the infraspinatus, teres minor, pectoralis major, latissimus dorsi, biceps brachii, and trapezius.
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397
impact to when the club is horizontal; and follow-through is from when the club is horizontal to the end of the motion.
GOLF SWING Several studies have examined shoulder muscle activity during the golf swing.33-37 Jobe and colleagues34,35 and Pink and colleagues37 used male and female professional golfers to study shoulder musculature activity. These authors quantified both shoulder34,35 and scapular36 muscles of both the leading arm (left for a right-handed golfer) and trailing arm (right for a right-handed golfer), and also reported no significant differences during the swing in shoulder EMG between male and female professional golfers.35 The golf swing has been divided into five phases:34-36 take-away, forward swing, acceleration, deceleration, and follow-through. Takeaway is the phase from ball address to the end of the backswing; forward swing is from the end of backswing to when the club is horizontal; acceleration is from when the club is horizontal to impact with the ball; deceleration is from ball
Shoulder muscle activity during the golf swing is shown in Table 32-7,37 and scapular muscle activity is shown in Table 32-8.36 During the take-away phase, muscle activity is relatively low to moderate, suggesting that lifting the arms and club up during the backswing is not a strenuous activity. The levator scapulae and lower and middle trapezius of the trailing arm exhibit moderate activity during this phase to elevate and upwardly rotate the scapula, and moderate activity from the serratus anterior of the leading arm helps protract and upwardly rotate the scapula. Upper, lower, and middle trapezius activities are highest during this phase compared with the other four phases. Infraspinatus and supraspinatus activities of the trailing arm are also highest during this phase but only fire
TABLE 32-7 Shoulder Activity by Muscle and Phase During the Golf Swing* Take-Away (% MVIC)
Forward Swing (% MVIC)
Acceleration (% MVIC)
Deceleration (% MVIC)
Follow-Through (% MVIC)
Trailing arm
25⫾20
14⫾14
12⫾14
7⫾5
7⫾5
Leading arm
21⫾12
21⫾15
18⫾11
28⫾20
28⫾14
Trailing arm
27⫾24
13⫾16
7⫾8
12⫾13
9⫾10
Leading arm
14⫾12
16⫾13
27⫾25
61⫾32
40⫾24
Trailing arm
16⫾12
49⫾31
68⫾67
64⫾67
56⫾44
Leading arm
33⫾23
29⫾24
41⫾34
23⫾27
35⫾27
Trailing arm
5⫾6
21⫾23
10⫾10
11⫾15
8⫾8
Leading arm
13⫾13
9⫾9
10⫾10
21⫾25
28⫾30
Trailing arm
3⫾3
2⫾3
2⫾5
8⫾10
8⫾8
Leading arm
3⫾3
4⫾6
2⫾2
7⫾8
5⫾3
Trailing arm
17⫾25
10⫾15
9⫾13
17⫾16
11⫾12
Leading arm
5⫾8
24⫾20
11⫾9
9⫾9
8⫾14
Trailing arm
9⫾7
50⫾38
47⫾44
39⫾39
28⫾19
Leading arm
17⫾13
48⫾25
31⫾28
32⫾33
18⫾15
Trailing arm
12⫾9
64⫾30
83⫾55
74⫾55
37⫾35
Leading arm
21⫾32
18⫾14
83⫾75
74⫾74
38⫾23
Muscles Supraspinatus
Infraspinatus
Subscapularis
Anterior Deltoid
Middle Deltoid
Posterior Deltoid
Latissimus Dorsi
Pectoralis Major
*Means and standard deviations, expressed for each muscle as a percentage of a maximum voluntary isometric contraction (MVIC). Adapted from Pink M, Jobe FW, Perry J: Electromyographic analysis of the shoulder during the golf swing. Am J Sports Med 18(2):137-140, 1990.
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THE ATHLETE’S SHOULDER
TABLE 32-8 Scapular Activity by Muscle and Phase During the Golf Swing* PHASE
Take-Away (% MVIC)
Forward Swing (% MVIC)
Acceleration (% MVIC)
Deceleration (% MVIC)
Follow-Through (% MVIC)
Trailing arm
29⫾19
38⫾39
34⫾41
12⫾12
4⫾4
Leading arm
5⫾3
42⫾20
62⫾46
39⫾26
29⫾24
Trailing arm
30⫾18
46⫾27
32⫾24
21⫾12
5⫾4
Leading arm
7⫾13
68⫾27
57⫾46
26⫾26
30⫾33
Trailing arm
24⫾14
4⫾4
13⫾20
23⫾19
5⫾6
Leading arm
5⫾4
29⫾26
42⫾50
34⫾29
27⫾18
Trailing arm
37⫾12
18⫾24
19⫾26
26⫾21
12⫾15
Leading arm
3⫾3
51⫾26
36⫾21
21⫾18
28⫾20
Trailing arm
52⫾28
17⫾12
16⫾28
22⫾22
10⫾15
Leading arm
7⫾10
49⫾27
37⫾28
20⫾16
35⫾18
Muscles Levator Scapulae
Rhomboids
Upper Trapezius
Middle Trapezius
Lower Trapezius
Upper Serratus Anterior Trailing arm
6⫾4
58⫾39
69⫾29
52⫾18
40⫾14
Leading arm
30⫾15
20⫾29
31⫾31
31⫾18
21⫾13
Lower Serratus Anterior Trailing arm
9⫾5
29⫾17
51⫾33
47⫾25
40⫾18
Leading arm
27⫾11
20⫾21
21⫾24
29⫾20
29⫾21
*Means and standard deviations, expressed for each muscle as a percentage of a maximum voluntary isometric contraction (MVIC). Adapted from Kao JT, Pink M, Jobe FW, Perry J: Electromyographic analysis of the scapular muscles during a golf swing. Am J Sports Med 23(1):19-23, 1995.
approximately 25% of a MVIC, which implies relatively low activity from these rotator cuff muscles throughout the golf swing. This is surprising in part because most shoulder injuries are overuse injuries that typically involve the supraspinatus or infraspinatus.38-41 However, these rotator cuff EMG data are only for the trailing arm, which exhibited less overall rotator cuff activity throughout the swing compared with the leading arm. These data imply that rotator cuff injury risk may be higher in the leading arm, but this conclusion might not be valid because it only takes relative muscle activity into account and not other factors, such as impingement risk between shoulders. Another interesting finding is that anterior, middle, and posterior deltoid activities were all relatively low throughout all phases, implying that these muscles are not used much throughout the swing. During the forward swing phase, muscle activity was also relatively low to moderate, except there was relatively high activity from the subscapularis, pectoralis major, latissimus
Ch32_385-400-F06701.indd 398
dorsi, and serratus anterior of the trailing arm to adduct and internally rotate the trailing arm and protract the scapula. There were also relatively high activity from the rhomboids and middle and lower trapezius of the leading arm to help retract and stabilize the scapula. Muscle activity during the acceleration phase was higher overall compared with the forward swing phase. The subscapularis, pectoralis major, latissimus dorsi, and serratus anterior of the trailing arm demonstrated high activity during the acceleration phase to continue adducting and internally rotating the trailing arm. These muscles may be the most important power muscles of the upper extremity to help accelerate the arm during the acceleration phase of the downswing. In addition, using a short or long backswing can affect shoulder activity during the acceleration phase. Slightly greater pectoralis major and latissimus dorsi activity has been reported during the acceleration phase when a short backswing was used compared with a long backswing, suggesting that shoulder injury risk might increase over time.33
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During the deceleration phase, the subscapularis, pectoralis major, latissimus dorsi, and serratus anterior of the trailing arm continued to demonstrate high activity, although now the muscle action is more eccentric and slightly smaller in magnitude compared with the acceleration phase. Low to moderate activity occurred from the scapular muscles of the leading arm, and high pectoralis major and infraspinatus activity occurred in the leading arm. Muscle activity generally decreased from the deceleration phase to the follow-through phase. References 1. DiGiovine NM, Jobe FW, Pink M, Perry J: Electromyography of upper extremity in pitching. J Shoulder Elbow Surg 1:15-25, 1992. 2. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70(2): 220-226, 1998. 3. Gowan ID, Jobe FW, Tibone JE, et al: A comparative electromyographic analysis of the shoulder during pitching. Professional versus amateur pitchers. Am J Sports Med 15(6):586-590, 1987. 4. Jobe FW, Moynes DR, Tibone JE, Perry J: An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12(3):218-220, 1984. 5. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the shoulder in throwing and pitching. A preliminary report. Am J Sports Med 11(1):3-5, 1983. 6. Escamilla RF, Barrentine SW, Fleisig GS, et al: Pitching biomechanics as a pitcher approaches muscular fatigue during a simulated baseball game. Am J Sports Med 35(1):23-33, 2007. 7. Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF: Kinetics of baseball pitching with implications about injury mechanisms. Am J Sports Med 23(2):233-239, 1995. 8. Escamilla RF, Fleisig GS, Barrentine SW, et al: Kinematic comparisons of throwing different types of baseball pitches. J Appl Biomech 14(1):1-23, 1998. 9. Escamilla R, Fleisig G, Barrentine S, et al: Kinematic and kinetic comparisons between American and Korean professional baseball pitchers. Sports Biomech 1(2):213-228, 2002. 10. Werner SL, Fleisig GS, Dillman CJ, Andrews JR: Biomechanics of the elbow during baseball pitching. J Orthop Sports Phys Ther 17(6):274-278, 1993. 11. Feltner M, Dapena J: Dynamics of the shoulder and elbow joints of the throwing arm during a baseball pitch. Inter J Sport Biomech 22:35-59, 1986. 12. Roberts EM: Cinematography in biomechanical investigation. In Selected Topics on Biomechanics: Proceedings of the C.I.C. Symposium on Biomechanics, Indiana University, October 19-20, 1970. Chicago: The Athletic Institute, 1971, pp 41-50. 13. Toyoshima S, Hoshikawa T, Miyashita M, Oguri T: Contribution of the body parts to throwing performance. In Nelson RC, Morehouse CA (eds): Biomechanics IV. Baltimore, University Park Press, 1974, pp 169-74. 14. Kelly BT, Backus SI, Warren RF, Williams RJ: Electromyographic analysis and phase definition of the overhead football throw. Am J Sports Med 30(6):837-844, 2002.
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15. Fleisig GS, Escamilla RF, Andrews JR, et al: Kinematic and kinetic comparison between baseball pitching and football passing. J Appl Biomech 12:207-224, 1996. 16. Maffet MW, Jobe FW, Pink MM, et al: Shoulder muscle firing patterns during the windmill softball pitch. Am J Sports Med 25(3):369-374, 1997. 17. Barrentine SW, Fleisig GS, Whiteside JA, et al: Biomechanics of windmill softball pitching with implications about injury mechanisms at the shoulder and elbow. J Orthop Sports Phys Ther 28(6):405-415, 1998. 18. Werner SL, Guido JA, McNeice RP, et al: Biomechanics of youth windmill softball pitching. Am J Sports Med 33(4):552-560, 2005. 19. Loosli AR, Requa RK, Garrick JG, Hanley E: Injuries to pitchers in women’s collegiate fast-pitch softball. Am J Sports Med 20(1):35-37, 1992. 20. Watkins J, Green BN: Volleyball injuries: A survey of injuries of Scottish National League male players. Br J Sports Med 26(2):135-137, 1992. 21. Chandler TJ, Kibler WB, Uhl TL, et al: Flexibility comparisons of junior elite tennis players to other athletes. Am J Sports Med 18(2):134-136, 1990. 22. Schafle MD: Common injuries in volleyball. Treatment, prevention and rehabilitation. Sports Med 16(2):126-129, 1993. 23. Schafle MD, Requa RK, Patton WL, Garrick JG: Injuries in the 1987 national amateur volleyball tournament. Am J Sports Med 18(6):624-631, 1990. 24. Kugler A, Kruger-Franke M, Reininger S, et al: Muscular imbalance and shoulder pain in volleyball attackers. Br J Sports Med 30(3):256-259, 1996. 25. Rokito AS, Jobe FW, Pink MM, et al: Electromyographic analysis of shoulder function during the volleyball serve and spike. J Shoulder Elbow Surg 7(3):256-263, 1998. 26. Fleisig G, Nicholls R, Elliott B, Escamilla R: Kinematics used by world class tennis players to produce high-velocity serves. Sports Biomech 2(1):51-64, 2003. 27. Ryu RK, McCormick J, Jobe FW, et al: An electromyographic analysis of shoulder function in tennis players. Am J Sports Med 16(5):481-485, 1988. 28. Elliott B, Fleisig G, Nicholls R, Escamilia R: Technique effects on upper limb loading in the tennis serve. J Sci Med Sport 6(1):76-87, 2003. 29. Adelsberg S: The tennis stroke: An EMG analysis of selected muscles with rackets of increasing grip size. Am J Sports Med 14(2):139-142, 1986. 30. Chow JW, Carlton LG, Lim YT, et al: Muscle activation during the tennis volley. Med Sci Sports Exerc 31(6):846-854, 1999. 31. Morris M, Jobe FW, Perry J, et al: Electromyographic analysis of elbow function in tennis players. Am J Sports Med 17(2):241-247, 1989. 32. Shaffer B, Jobe FW, Pink M, Perry J: Baseball batting. An electromyographic study. Clin Orthop Relat Res (292): 285-293, 1993. 33. Bulbulian, R., Ball KA, Seaman DR: The short golf backswing: Effects on performance and spinal health implications. J Manipulative Physiol Ther 24(9):569-575, 2001. 34. Jobe FW, Moynes DR, Antonelli DJ: Rotator cuff function during a golf swing. Am J Sports Med 14(5):388-392, 1986. 35. Jobe FW, Perry J, Pink M: Electromyographic shoulder activity in men and women professional golfers. Am J Sports Med 17(6):782-787, 1989.
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36. Kao JT, Pink M, Jobe FW, Perry J: Electromyographic analysis of the scapular muscles during a golf swing. Am J Sports Med 23(1):19-23, 1995. 37. Pink M, Jobe FW, Perry J: Electromyographic analysis of the shoulder during the golf swing. Am J Sports Med 18(2): 137-140, 1990. 38. Hamilton CD, Glousman RE, Jobe FW, et al: Dynamic stability of the elbow: Electromyographic analysis of the flexor
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pronator group and the extensor group in pitchers with valgus instability. J Shoulder Elbow Surg 5(5):347-354, 1996. 39. Choi CH, Kim SK, Jang WC, Kim SJ: Biceps pulley impingement. Arthroscopy 20(Suppl):280-283, 2004. 40. McHardy, A., Pollard H, Luo K: Golf injuries: A review of the literature. Sports Med 36(2):171-187, 2006. 41. Wiesler ER, Lumsden B: Golf injuries of the upper extremity. J Surg Orthop Adv 14(1):1-7, 2005.
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CHAPTER 33 Shoulder Injuries
in Baseball Kevin E. Wilk, James R. Andrews, E. Lyle Cain, and Kathleen Devine
Injuries to the throwing shoulder occur often. Conte and colleagues1 reported shoulder injuries were the most common injury sustained by professional baseball players and resulted in the most missed playing days. Numerous types of injuries occur to the thrower’s shoulder, including overuse tendinitis, full-thickness rotator cuff tears, fraying of the glenoid labrum, labral detachment, and capsular laxity problems. In this chapter we discuss the various types of injuries and explain their pathomechanics.
contractions of the rotator cuff musculature and the long head of the biceps.4 When the stresses involved in throwing exceed the capability of the muscular system to control these stresses, injury results. Injury can result from improper mechanics, poor dynamic stability, or muscle fatigue. A common injury-producing scenario for the throwing athlete includes the combination of abnormally high stresses that are repeatedly applied to normal tissue, eventually resulting in tissue attenuation and failure. This can be referred to as acquired repetitive microtrauma and can lead to progressive rotator cuff failure, capsular hypermobility, or glenoid labrum fraying or detachment.
Tremendous demands are placed on the shoulder complex during the throwing motion. Throwing is a skilled movement that requires excessive motion, precisely coordinated movement, and a synchronized muscle-firing pattern, all of which must occur at a velocity faster than that of any other movement.2,3 To accomplish this difficult task, the shoulder must have a tremendous amount of passive and dynamic motion (Fig. 33-1). Although excessive motion is required for throwing, the shoulder complex must still maintain stability of the glenohumeral joint. The joint stability required during throwing is accomplished through its capsular ligamentous restraints and by the dynamic contributions of the shoulder’s neuromuscular control system.
This chapter discusses some of the common shoulder injuries seen in the throwing athlete (Box 33-1). In Chapter 31, a thorough discussion of the biomechanics of throwing was discussed. Thus, only specific references are made to specific biomechanics as they relate to different shoulder injuries.
SHOULDER JOINT INJURIES IN THE OVERHEAD ATHLETE
During throwing, the glenohumeral joint receives extremely high forces that often lead to overuse injuries. Angular velocities of the shoulder joint during the acceleration phase of throwing have been documented to exceed 7000 degrees2 (Fig. 33-2). The ball velocity of a professional baseball pitcher can reach 98 to 100 miles per hour. During the acceleration phase, the anterior translation stress placed on the glenohumeral joint can reach one half the thrower’s body weight.2 After ball release, deceleration of the arm occurs, requiring vigorous posterior shoulder musculature eccentric contraction to slow the arm down (see Fig. 33-2). During the deceleration phase, the posterior shoulder muscles contract eccentrically to counteract a glenohumeral joint distraction force equal to the body weight of the thrower.2
Injuries to the throwing shoulder often occur in combination and not in isolation. Internal impingement is a common diagnosis in the overhead athlete and is represented by undersurface rotator cuff fraying of the supraspinatus or infraspinatus (or both), fraying of the posterior superior glenoid labrum, and, often, osseous changes on the posterior humeral head.5,6,7 Several clinicians have suggested that internal impingement is secondary to anterior capsular hypermobility or laxity. Thus, the lesion to the rotator cuff or glenoid labrum did not occur in isolation but rather resulted from a progressive tissue failure phenomenon that occurs due to repetitive microtrauma. Shoulder injuries are listed in Box 33-1.
To facilitate the acceleration forces required during throwing, excessive glenohumeral joint laxity is required during the cocking phase to prestretch the anterior shoulder musculature. The thrower often exhibits in excess of 125 degrees of passive external rotation. Because of this extreme motion seen in the thrower, the muscular system must be capable of providing dynamic glenohumeral joint stability. Dynamic stability is accomplished through the combined stabilizing
ROTATOR CUFF INJURIES The rotator cuff is vital for normal shoulder function, especially in the throwing athlete. It controls the movement of the humeral head and, along with the long head of biceps, serves to steer it during different activities. The larger muscles of the shoulder are the prime movers, which are the pectoralis major, latissimus dorsi, and deltoid. The 401
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BOX 33-1.
Shoulder Injuries in Baseball
Primary Rotator Cuff Injuries Compression cuff disease Internal impingement Overuse tendinitis Primary lesions Rotator cuff tears Tensile failure
Secondary Rotator Cuff Lesions Anterior instability Compressive cuff disease secondary to laxity Multidirectional instability Posterior instability Primary instability (nontraumatic) Tensile failure secondary to laxity
Glenoid Labrum Tears Peel-back lesions SLAP lesions Thrower’s exostosis
Biceps Tendon Pathology Bicipital tendinitis Ruptures and tears
Other
Figure 33-1. During the cocking phase of throwing, the shoulder exhibits a tremendous amount of external rotation.
A
B
Acromioclavicular joint degenerative changes Neurovascular syndromes Scapula disorders Suprascapular nerve entrapment
smaller muscles are classified as the stabilizing muscles. These include the rotator cuff muscles, which function to compress the humeral head into the glenoid fossa, and are dynamic stabilizers.8-10 It is this compression of the articulating surfaces that affords stability to the glenohumeral joint during the throwing motion. The subscapular muscles and the teres minor and infraspinatus muscles form a vital force couple that controls humeral head translation.11,12 The high demands placed on the shoulder musculature during throwing can result in subsequent muscle fatigue, eccentric overload, inflammation, and eventual tendon failure. Once the rotator cuff musculature has been injured, the dynamic stabilizing ability is compromised, and additional injuries such as labrum tears, capsular lesions, and osseous changes can ensue. Poor mechanics often results from this type of chronic inflammation, producing a compensatory mechanism in the throwing act that can contribute to the injuryproducing scenario. These repetitive muscle strains can result in overuse tendinitis of the rotator cuff.
Internal Impingement C
D Figure 33-2. Five phases of throwing: A, wind-up; B, cocking; C, acceleration; and D, deceleration and follow-through.
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Internal impingement is one of the most common shoulder lesions seen in baseball pitchers. This lesion occurs when the athlete abducts the arm to 90 to 100 degrees and maximally
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externally rotates. During this motion, the undersurface of the supraspinatus or infraspinatus tendon (or both) contacts the posterior superior glenoid rim and glenoid labrum. This results in undersurface rotator cuff wear and glenoid labrum fraying and possible detachment. This lesion develops because of the repetitive nature of throwing. Numerous theories propose to explain internal impingement in the overhead athlete, and these are thoroughly discussed in Chapter 11. These theories include anatomic causes,13,14 anterior capsule laxity,15 posterior capsule tightness,16 and over-rotation.17 Several investigators13,18 have shown that there are also injuries to the humeral head. These are cystic changes (Fig. 33-3). The diagnosis of internal impingement is established based on subjective history, imaging studies, and physical examination.
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Weakness or fatigue of the external rotators decreases the muscular efficiency required to decelerate the throwing shoulder properly and can result in tissue damage (Fig. 33-4). A decrease in the power of the infraspinatus and teres minor muscles alters the effectiveness of the subscapular, teres minor, and infraspinatus force couple, and humeral head translation increases (Figs. 33-5 and 33-6). Before musculotendinous inflammation, the posterior glenohumeral capsule often becomes inflamed, which appears to act as a precursor to posterior rotator cuff tendinitis. This inflamed capsule is referred to as posterior capsulitis.
Tensile Lesions A common rotator cuff pathology seen in the thrower is a tensile lesion of the undersurface of the rotator cuff. The mechanism of injury in this instance is deceleration of
Internal impingement is most often managed nonoperatively with rest, stretching, and strengthening. Usually, nonoperative treatment is successful in these athletes. A thorough discussion of the treatment can be found in Chapter 11.
Overuse Tendinitis Overuse tendinitis is commonly seen in the posterior rotator cuff muscles, the infraspinatus, and the teres minor. These occur due to the large stress placed on the shoulder joint during the deceleration phase of throwing. The stresses applied to the posterior rotator cuff musculature effectively exceed the body weight during the deceleration phase.
Figure 33-4. Arthroscopic visualization of the posterior capsule. Note the fraying and capsular failure of the undersurface of the posterior capsule.
Figure 33-3. Magnetic resonance image of a thrower’s shoulder in the ABDER position (abduction to 90 degrees and external rotation). Note the fraying of the posterior superior labrum and undersurface fraying of the rotator cuff muscles. Also note the cystic changes on the posterolateral aspect of the humeral head.
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Figure 33-5. Repetitive microtraumatic forces lead to decreased efficiency of dynamic stability.
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Figure 33-6. Weakness or fatigue of the external rotators decreases the muscular efficiency required to decelerate the throwing shoulder, leading to muscular fatigue and tissue damage.
the arm as the rotator cuff attempts to resist the horizontal adduction, internal rotation, and glenohumeral distraction forces placed on it. Combined, these forces result in an eccentric tensile overload failure and a partial undersurface tear of the rotator cuff caused by repetitive microtrauma.19,20 Most commonly, these lesions are found in the region of the supraspinatus tendon and can extend posteriorly into the infraspinatus tendon. These tears can also be found isolated to the infraspinatus tendon and the posterior glenohumeral capsule. On physical examination, tenderness can be elicited over the supraspinatus or infraspinatus tendon. Obvious gross weakness of the rotator cuff usually is not present, especially in the highly skilled thrower. If weakness is present, it is most often found during isokinetic testing of the external rotators in the 90-degree shoulderabducted position.21 Palpation of the infraspinatus, teres minor, and posterior capsule can be helpful (Fig. 33-7). Computed tomography (CT) or magnetic resonance imaging (MRI) can reveal a partial undersurface tear of the rotator cuff. Initially, the athlete should begin a rehabilitation program with emphasis on rotator cuff strengthening. If no improvement is made over a period of 3 to 6 months, an arthroscopy may be performed to débride the injured tissue and to attempt to promote a healing response.19,22 After
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this procedure, an aggressive rotator cuff strengthening program must be used to minimize the risk of recurrence and maximize a return to symptom-free function. This program should emphasize eccentric strengthening of the posterior rotator cuff musculature.
Compressive Rotator Cuff Disease Compressive rotator cuff disease is an uncommon rotator cuff pathology seen in the overhead athlete.23 This can be a primary pathology when it is associated with a type III hooked acromion,24 os acromiale,24-26 degenerative acromial spurs,27 or congenital thickening of the coracoacromial ligament.20 It can also be caused by an inflamed and thickened subacromial bursa.23 Compressive rotator cuff disease results in an outside type of rotator cuff tear, where the failure begins on the superior bursal surface of the cuff and progresses toward the articular side. In contrast, the tensile overload lesion results in an inside-out type of rotator cuff injury, from the articular to the bursal side. Overhead athletes such as volleyball players and swimmers are more likely to exhibit compressive cuff disease symptoms.
Subacromial Impingement The throwing motion requires the arm to be abducted to 90 degrees while being repetitively submitted to horizontal adduction and internal rotation motions. This repetitive
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motion can produce subacromial impingement symptoms.28 Often the thrower complains of shoulder pain during activity and especially after prolonged throwing. Once the lesion becomes more severe, pain may be present during all throwing activities. An injection of 1% lidocaine into the subacromial space that relieves all symptoms helps to confirm this diagnosis. Other clinical tests performed to determine the degree of involvement and differential diagnosis are specific impingement tests (Fig. 33-8).
Figure 33-7. Palpation of the infraspinatus, teres minor, and posterior capsule can be accomplished with the patient prone and the arm hanging over the side of the examination table. This tractions the arm and allows the clinician to examine the various tissues accurately.
A
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B
Most athletes respond successfully to a conservative program of active rest, nonsteroidal anti-inflammatory medication, and a progressive rotator cuff strengthening and stretching exercise program. In the thrower, external rotation is often excessive and internal rotation is significantly limited.19 This limitation of internal rotation results in posterior capsular tightness, which causes the humeral head to migrate anteriorly during overhead motion.23 Any conservative rehabilitation program should include stretching of the posterior capsule, re-establishing normal internal rotation, and gradual aggressive strengthening of the rotator cuff musculature.30 If the athlete’s symptoms are not relieved by nonoperative measures, surgical treatment may be warranted. The surgical treatment most often performed is an arthroscopic examination to determine the structures involved and the integrity of the rotator cuff.
Figure 33-8. Two clinical provocative tests for compressive cuff pathology. A, The clinician passively elevates the patient’s arm to 90 to 100 degrees while horizontally adducting and internally rotating the arm. B, The clinician passively elevates the patient’s arm with internal rotation while stabilizing the scapulae.
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Rotator Cuff Tears Full-thickness rotator cuff tears are unusual in the throwing athlete. However, it appears that more and more athletes are exhibiting high-grade partial thickness tears, approximately 25% to 50% of the thickness of the rotator cuff. These are usually seen late in the deterioration process of the shoulder.30–32 This type of degenerative process begins with a small partial-thickness rotator cuff tear, which can eventually progress to a complete-thickness tear. Tears of this type can enlarge by additional trauma placed on the rotator cuff tendons during activities. Full-thickness rotator cuff tears are usually seen in older athletes; however, they can occur in the younger thrower. We have seen several throwers who have exhibited full-thickness tears of the supraspinatus or the infraspinatus muscle. Early recognition and treatment can prevent the progression of a partial-thickness tear to a full-thickness rotator cuff tear. Once a full-thickness tear occurs, throwing is often difficult, if possible at all. Significant weakness of the shoulder’s abductors and external rotators can be seen. Often a repair of the rotator cuff is necessary to allow symptom-free return to normal daily activities.20 The surgical procedure of choice to repair a rotator cuff tear in a thrower uses an arthroscopic technique that minimizes scarring of the capsule and soft tissue. This helps in regaining motion in the overhead athlete’s shoulder. This procedure appears to allow an earlier return to functional activities and an accelerated rehabilitation program.
SHOULDER INSTABILITY The throwing motion requires excessive glenohumeral external rotation, which places extreme tension on the anterior stabilizing structures of the glenohumeral joint and especially the anterior capsule and the rotator cuff musculature. The identification of shoulder laxity compared with frank instability is often difficult to assess clinically. The concept of laxity is the ability of the humeral head to be passively translated on the glenoid,33 whereas instability is a clinical condition in which unwanted translation of the humeral head on the glenoid compromises the comfort and function of the shoulder.33 The throwing athlete must exhibit laxity to perform high-performance throwing activities. However, the rotator cuff musculature must control this laxity dynamically for symptom-free throwing. Instability ensues when the dynamic stability is altered and the rotator cuff muscles are unable to control humeral head motion within the glenoid during activities. Thus, the healthy shoulder of the overhead athlete exhibits excessive laxity, but not frank instability. The laxity allows the thrower to reach extreme range of motion without instability as would be seen with subluxation or dislocation from throwing.
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The previously discussed rotator cuff pathologies (compressive cuff disease and tensile failure) can occur as an indirect result of instability. Jobe and colleagues 34,35 provided a classification to evaluate athletes presenting with this type of anterior shoulder pain: • Group I: Athletes with pure impingement • Group II: Athletes who have instability secondary to anterior ligament and labrum injury with secondary impingement • Group III: Athletes who exhibit instability due to hyperelasticity and secondary impingement • Group IV: Athletes who demonstrate pure instability In the thrower, hyperlaxity is a common problem. The shoulder must be loose enough to allow the tremendous motion necessary to throw a baseball but must be tight enough to provide inherent stability. Shoulder instability is restricted by the static stabilizers, the geometry of the joint, and the ligamentous system and labrum. The capsular ligaments act as a buttress to restrict humeral head translation. Repetitive overhead throwing often results in stretching of these capsular restraints and can lead to joint capsule injury. As the capsule becomes more lax, the glenohumeral joint depends on an increase in the dynamic muscular effort to provide the required functional stability required. If the dynamic stabilizers fail because of overuse, injury, or pain, underlying primary instability will result. During the cocking and early acceleration phases of throwing, the anterior and inferior portions of the joint capsule are significantly stressed in a repeated fashion. The anteroinferior glenohumeral ligament (anterior band) provides the static stabilization for this anterior force applied with the shoulder abducted to 90 degrees36 (Fig. 33-9). The dynamic stability required to supplement the anteroinferior glenohumeral ligament is provided through a rotator cuff muscular contraction on both sides of the glenohumeral joint. Also, the inferior glenohumeral ligament complex is prone to considerable plastic deformation before ultimate failure occurs.37 As shoulder laxity increases, labral changes commonly occur. In time, the thrower can develop a loose shoulder joint. Because of this ensuing looseness, the thrower must rely on dynamically controlled stability and thus may be predisposed to musculotendinous injuries caused by overuse, such as secondary internal impingement, tensile failure, and rotator cuff failure. Anterior hyperlaxity is especially common in the thrower. The thrower might complain of anterior or posterior shoulder pain, especially during the late cocking and acceleration phases. Also, the thrower might notice clicking, popping, or early arm fatigue with competitive activities. Several clinical tests are routinely performed to determine the degree of anterior humeral head translation on the glenoid. Anterior laxity is determined with the use of a drawer test (Lachmann’s test of the shoulder) (Fig. 33-10), fulcrum test (Fig. 33-11), or
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A
B
Figure 33-10. Anterior drawer test to determine anterior glenohumeral joint laxity. The humeral head is passively translated on the glenoid at 0, 45, and 90 degrees of elevation.
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Figure 33- 9. A, Three bands of the anterior glenohumeral ligament: superior (A), middle (B), and inferior (C). B, Note the role of the anterior band of the inferior glenohumeral ligament as the arm is abducted and externally rotated (E.R.) (D, d). This band acts as a buttress and restricts anterior humeral head translation. Abd, abduction; I.R., internal rotation. (Figure B from O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18:449-456, 1990; reprinted with permission.)
Figure 33-11. Anterior fulcrum test. The arm is placed into abduction and external rotation. The distal hand horizontally abducts the humerus as the joint line head lifts up on the humerus.
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a relocation test (Fig. 33-12). Routinely, these tests are performed at 45 degrees and 90 degrees of shoulder abduction to test the specific bands of the anterior glenohumeral ligament. Anterior translation testing at 0 degrees of shoulder abduction tests the integrity of the superior glenohumeral ligament, 45 degrees of shoulder abduction tests the middle glenohumeral ligament, and 90 degrees primarily tests the anterior band of the inferior glenohumeral ligament. The amount of translation and end point resistance are determined during these tests. A soft end point would represent end-range elasticity of the capsule, which might imply stretching out of the capsule. Posterior instability can also be seen in the thrower. This occurs during the deceleration and follow-through phases of throwing when the arm horizontally adducts and internally rotates. During this motion, the posterior capsule is stressed and posterior labral injuries can also occur. Stretching of the posterior capsule in this fashion irritates and inflames the capsule, which results in pain and inhibition of the posterior rotator cuff musculature. This muscular inhibition, if unaddressed, eventually results in tendon fatigue and microfailure in addition to increased
instability. Clinically, posterior instability can be determined through a posterior drawer test and a posterior fulcrum test. These tests are usually performed at 90 degrees of shoulder abduction. Posterior instability can also manifest during the hitting motion, especially when the lead shoulder is involved. Most athletes exhibiting glenohumeral laxity without associated labral detachment can be treated with a conservative treatment program. The program consists of temporarily decreasing the stresses from throwing, normalizing the motion of the shoulder, and improving the dynamic stability through muscular strengthening and neuromuscular control. Once the athlete’s shoulder pain has subsided, a gradual return to throwing may begin. If a conservative program is unsuccessful after 2 to 3 months, a surgical procedure may be warranted. An athlete with moderate to severe laxity and functional instability might require an arthroscopic or open stabilization procedure. Surgical procedures to reduce anterior capsular laxity in the throwing shoulder are difficult. Less-than-favorable results have been reported by numerous investigators.38,39 Jobe described the capsulolabral reconstruction procedure39; Andrews discussed the mini–capsular shift procedure40 and the capsular thermal shrinkage procedures.41,42 Today these procedures have been mostly abandoned in favor of arthroscopic plication or arthroscopic capsular shift.43 The goal of the plication or capsular shift procedure is to tighten the capsule just enough to prevent symptomatic humeral head translation.
GLENOID LABRUM TEARS Tears of the glenoid labrum are often seen in the throwing athlete.44,45 During the throwing motion, the glenohumeral joint receives large compressive and shear forces, as well as distraction forces, as the humeral head moves from anterior to posterior during the phases of throwing. These large compressive and shear forces can injure the glenoid labrum, resulting in degenerative tears, frank tears, or labral detachments from the glenoid.
Figure 33-12. The anterior relocation test for anterior instability. The arm is placed in 90 degrees of abduction and maximum external rotation. If the shoulder is painful, the opposite applies. A posterior force is applied to relocate the humeral head with the glenoid, and pain should diminish.
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A common location for labrum tears is in the posterosuperior and superior portion, where the long head of the biceps attaches. During the deceleration and follow-through phases of throwing, the biceps acts at the elbow joint to decelerate the arm, slowing the extensor movement. Because of the large stabilizing muscle activity of the biceps across the glenohumeral joint, an avulsion tear of the biceps or of the biceps-labrum insertion can result.44 Andrews and Carson45 reported on 73 athletes with labrum tears, 83% of whom were found to have an anterosuperior tear. After arthroscopic débridement, 88% exhibited a good-to-excellent result at an average of 13.5 months after surgery.
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A commonly seen labrum tear in the throwing athlete is the posterior or posterosuperior labrum tear. During the follow-through phase, the humeral head translates posteriorly and can cause degenerative tearing of the labrum. Another type of labrum lesion is the superior labrum anterior-posterior (SLAP) lesion.46 The term SLAP refers to a superior labrum tear anterior and posterior to the biceps anchor location. Snyder and colleagues46 classified SLAP lesions into four types. In type I, the superior labrum is frayed and there is no detachment. In type II, the superior labrum is frayed, and the superior labrum is detached. Type III is a bucket-handle tear of the labrum; the labrumbiceps attachment remains intact. Type IV, is similar to the type III, but the labrum tear extends into the biceps tendon, allowing it to sublux into the joint. It appears that SLAP lesions, posterior labrum tears, and some anterior labrum tears may be the result of primary instability of the glenohumeral joint. Labrum tears (other than biceps avulsion) are the result of abnormal translations of the humeral head. Thus, if a labrum tear is present, the clinician must carefully evaluate and treat the shoulder for instability.47 A common type of glenoid labrum tear is the peel-back labrum. This lesion was described by Burkhart and Morgan48 and encompasses several varieties of a Snyder type II SLAP lesion (Fig. 33-13). The pathomechanics of the peel-back lesion result from the torsional force of the long head of the biceps during the throwing motion. Shepard and colleagues49 demonstrated with cadaver shoulders that the force required to create a peel-back SLAP lesion was approximately 262 N during abduction and external rotation (late cocking) compared with 508 N from long-axis traction force, similar to the deceleration phase of throwing.
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We believe the peel-back lesion is probably the result of excessive external rotation during the throwing motion. Physical examination to diagnose SLAP lesions in throwers can be challenging. The athlete often complains of clicking, popping, pain, and a loss of velocity. The most sensitive special tests we have found are the biceps load test,50 the Mimori test, and the resisted external rotation supination (O’Brien) test.51 MR arthrography has been shown to be an accurate and noninvasive technique for evaluating the glenoid labrum. The treatment for frayed glenoid labrum tears without glenohumeral instability is excision of the torn labrum followed by a gradual rehabilitation process and gradual return to throwing. Glenoid labrum detachments are treated with arthroscopic repair using suture anchors.
THROWER’S EXOSTOSIS: BENNETT’S LESION The throwing athlete who experiences persistent posterior shoulder pain can exhibit calcification of the posteroinferior glenohumeral capsule attachment, often termed a thrower’s exostosis. First described by Bennett in 1941,52 this exostosis is normally located at approximately the 8-o’clock position on the right shoulder glenoid rim at the attachment of the posterior band of the inferior glenohumeral ligament. Meister and Andrews53 hypothesized that the lesion is probably a secondary reaction associated with repeated microtrauma and tearing of the posterior and inferior capsule from its glenoid insertion, similar to a traction spur of the plantar fascia.52 For years, it was believed this exostosis was a calcification of the long head of the triceps; however, on surgical inspection, one of us (ELC) has not found this to be true in most cases. This pathology is easily seen on plain radiographs, especially on Stryker’s view (Fig. 33-14), and treatment is usually symptomatic relief. This includes stretching of the posterior structures, improved internal rotation range of motion and strengthening the external rotation. If pain and dysfunction persist, arthroscopic excision and subsequent posterior capsular release may be necessary.
BICEPS BRACHII TENDON PATHOLOGY
Figure 33-13. Snyder type II superior labrum anterior-posterior (SLAP) lesion. Note the detachment of the superior glenoid labrum.
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The role of the biceps brachii during throwing is not fully understood. Jobe and colleagues54 reported modest biceps activity during the cocking and acceleration phases but a high level of biceps activity during the follow-through phase. During this later phase, it is believed the role of the biceps is in deceleration of the elbow joint. Because of the eccentric deceleration action of the biceps brachii, overuse tendinitis of the long head can occur. Also, anterosuperior shoulder stability may be enhanced and assisted by biceps activity,
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A
Figure 33-14. Calcification of the posterior glenohumeral capsule can be seen on a Stryker’s view plain radiograph.
especially during the throwing movement. Therefore, both activities place considerable stress on the biceps musculotendinous unit and can lead to inflammation of the biceps. Biceps pain has a variety of causes, including biceps instability, tendinitis, tendinosis, SLAP lesions, rotator cuff failure, capsular inflammation, and hypermobility of the glenohumeral joint. Furthermore, the treatment for each of these lesions is dramatically different. If the stress is significant and applied repetitively, tendon failure, biceps fraying, or splitting can occur. In many throwers we have observed an obvious split in the long head of the biceps (Fig. 33-15A). The diagnosis of biceps tendinitis is made on clinical examination through palpation, resisted muscle testing, and special tests. Palpation of the biceps tendon can be effectively performed with the patient supine, the shoulder abducted and the forearm fully supinated, and the shoulder internally rotated 30 degrees (see Fig. 33-15B). This clears the biceps tendon from the coracoacromial arch, places the biceps tendon on stretch, and faces the bicipital groove directly superior. The Speed’s test is performed by flexing the shoulder against resistance while the elbow is extended and supinated.55 A positive test localizes pain within the bicipital groove. The Yergasson’s sign is positive when biceps pain is elicited from supination against resistance with the elbow flexed.56 MRI has proved a valuable tool in identifying fluid around the tendon that can indicate inflammation of the biceps or a tear of the tendon.57 Whatever its role in throwing, we believe the biceps should be emphasized in an appropriate exercise program using concentric and eccentric muscle contractions to control the rapid elbow-extension moment during the follow-through phase. The differential diagnosis is the key to a successful treatment program.
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B Figure 33-15. A, Arthroscopic visualization of the biceps brachii tendon (long head). Note the fraying of the tendon and the split in the tendon. B, Palpation of the long head of the biceps brachii. The patient is supine, the arm is abducted approximately 45 to 60 degrees, the shoulder is rotated internally 30 degrees, and the forearm is in full supination. This position clears the biceps tendon from the coracoacromial arch.
OSTEOCHONDRITIS DISSECANS OF THE GLENOID An unusual lesion seen at the glenohumeral joint in the overhead thrower is osteochondritis dissecans of the glenoid. Although this condition is rare, one of us (ELC) has seen this pathology in 17 baseball players out of 1800 shoulder arthroscopies. These athletes all followed conservative treatment consisting of rest, strengthening, and stretching. Surgical treatment included removal of the loose fragments of cartilage and débridement of the osteochondritis dissecans on the glenoid to bleeding bone to stimulate a healing response. Of the 17 athletes treated with débridement, 13 returned to competitive play, 2 failed to return, and 2 gave up baseball to play other sports.
ACROMIOCLAVICULAR JOINT DISORDERS Injuries to the acromioclavicular joint can occur in the throwing athlete. Sprains of the acromioclavicular joint in the thrower usually are caused by a fall or a blow to the
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lateral acromion. Rockwood58 classified acromioclavicular joint sprain into six types. In the throwing athlete, most sprains are of type I or II, or minimally displaced joint. The type III acromioclavicular sprain with rupture of the coracoacromial and acromioclavicular ligaments with displacement presents a significant challenge to the physician treating the throwing athlete. On occasion, surgical intervention is considered earlier in the course of treatment for the throwing athlete compared with the general population. Fortunately, these sprains are rare in the baseball thrower. Most acromioclavicular joint injuries in the baseball player consist of degenerative joint changes. Because of longitudinal shear and compressive forces imparted from the distal clavicle to the acromium during throwing or weight training, degenerative joint changes can occur. These changes include osteolysis and osteophyte formation. The athlete usually complains of a dull ache or pain over the acromioclavicular joint. Conservative treatment is tried initially and consists of nonsteroidal anti-inflammatory medication, physical therapy (including joint mobilization, range of motion, and stretching), modification of physical activity, and steroid injection into the joint. If this fails, open or arthroscopic débridement of the joint may be performed by a direct superior approach. For concomitant subacromial space impingement, this procedure, along with a subacromial decompression, is performed from below. This technique is often best performed arthroscopically. Arthroscopic surgery minimizes the acromioclavicular joint dissection when compared with an open procedure. Also, the arthroscopic débridement allows a more accelerated rehabilitation process.
NEUROVASCULAR SYNDROMES Neurovascular syndromes are rarely seen in the throwing athlete. The syndrome occasionally seen in the thrower is often referred to as thoracic outlet syndrome. This is a complex syndrome with diffuse, inconsistent signs and symptoms caused by compression of the nerves and vessels of the upper extremity as they pass through bony and soft tissue passageways. The three most common sites for compression of the neurovascular structures are the interscalene triangle, the costoclavicular space, and the area posterior to the pectoralis minor.59 Other causes of compression include a seventh cervical rib,59 an anomalous band,60 and variations in the formation of muscles and vessels, but the aforementioned areas of compression are more commonly seen in the thrower. The throwing athlete often exhibits tightness of the pectoralis minor or the anterior and middle scalene muscles. Tightness of these muscles can cause direct compression of the neurovascular structures as they pass through the interscalene triangle or beneath the pectoralis minor. Indirectly, neurovascular compression can result from this muscle tightness because of a structural repositioning of the first rib. Thus, the throwing athlete should consistently
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perform a stretching program for the scalene muscles and the pectoralis minor. Also, insufficiency of the scapular suspensory muscles can contribute to this syndrome.61 Adequate strength and flexibility of the upper trapezius, middle trapezius, rhomboids, levator scapulae, and lower trapezius are required to stabilize the scapulae adequately. Injury to the shoulder girdle muscles that produces local hemorrhage, muscle spasm, and altered shoulder girdle mechanics can also lead to neurovascular compression. The diagnosis of this pathology is difficult because of the nonspecific inconsistent signs and symptoms. Often the thrower complains of a dead or tired arm, numbness, weakness, a fullness or tightness in the arm, or a sudden change in throwing velocity. The manifesting symptoms of this syndrome can be confused with shoulder instability, ulnar nerve neuropathy, rotator cuff injury, or cervical disk pathology. The diagnosis is most often made from an exhaustive workup that includes plain radiographs, electrophysiologic studies, arteriograms, and venographies. These tests are used because of the poor reliability of specific provocation tests such as the Adson maneuver.60,62 Severe cases can lead to vascular thrombosis (clotting) in the thrower’s shoulder, which is a surgical emergency. The clinician treating the overhead athlete is encouraged to evaluate systematically all the structures that can cause neurovascular compression. A program emphasizing stretching and strengthening of the involved structures and postural correction is often adequate in treating symptoms produced by these neurovascular syndromes. Flexibility of the scalene, pectoralis minor, and pectoralis major muscles is extremely valuable. Also, adequate postural strength of the middle trapezius, lower trapezius, rhomboids, posterior deltoid, and levator scapulae muscles is critical in the treatment of any neurovascular syndrome of the shoulder.
SUPRASCAPULAR NERVE ENTRAPMENT Suprascapular nerve entrapment is a rare clinical entity and probably accounts for less than 0.4% of shoulder diagnoses in patients with shoulder pain.63 The suprascapular nerve supplies both the supraspinatus and infraspinatus muscles. When this nerve is compromised, there is significant atrophy of the supraspinatus and infraspinatus muscles, and the superior scapular fossa appears hollow (Fig. 33-16). The pathomechanics of superscapular nerve entrapment can be classified into two main categories: traction injuries and compression injuries. Traction injuries can occur at the suprascapular notch as a result of excessive scapular depression or forced adduction of the upper arm. The nerve becomes kinked by the superior transverse scapular ligament as it passes through the scapular notch. Two other possible sites of traction injuries are the spinoglenoid notch and where the nerve inserts into the mobile infraspinatus muscle.
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because other muscles often compensate for the involved muscles. The athlete might initially complain of a poorly localized posterior shoulder girdle pain that is vague and aching in quality. The cross-arm adduction test causes tension on the suprascapular nerve and may be a provocative test in reproducing symptoms.67 The thrower might also exhibit localized tenderness over the posterior rotator cuff musculature. The use of electromyelogram, nerve conduction velocity tests, and MRI is helpful in determining the site of the lesion. Treatment is focused on strengthening the infraspinatus and supraspinatus muscles and the scapular stabilizing muscles. The flexibility of the scapulothoracic articulation and glenohumeral joint are also emphasized. Occasionally, surgical dissection of the nerve is required to improve the nerve mobility about the soft tissue. The authors have observed this pathology on several occasions in professional baseball pitchers. On isokinetic evaluation, their strength parameters were all within acceptable ranges. All the pitchers observed with this pathology pitched without difficulty or altered mechanics. They presented in our clinic with symptomatic complaints of pain without obvious functional deficits. This diagnosis is often difficult to differentiate.
Figure 33-16. On clinical examination, observation of the posterior scapula indicates a hollowing of the superior and inferior fossa. This observation indicates significant atrophy of the supraspinatus and infraspinatus muscles and can indicate suprascapular nerve entrapment.
Traction injuries at these sites appear to be caused by excessive external rotation of the arm, which places tension on the terminal portion of the suprascapular nerve. These tractiontype injuries usually result in atrophy of both the supraspinatus and infraspinatus muscles. There are several locations for suprascapular nerve compression, but one of the most common sites is at the suprascapular notch next to the superior transverse scapular ligament.63,64 Other causes of compression can involve the inferior transverse scapular ligament, a congenital stenotic suprascapular notch,65 or extrinsic masses.66 Throwers can develop a ganglion cyst of the spinoglenoid notch, causing compression of the suprascapular nerve. The cysts are believed to be formed from glenohumeral synovial fluid leaking through a superior labral tear of capsular hole. Spinoglenoid notch cysts cause atrophy and denervation of the infraspinatus with sparing of the branches to the supraspinatus. Arthroscopic cyst decompression results in return of function in most athletes. Often this diagnosis is overlooked because of the subtle weakness the athlete exhibits on clinical examination and
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SCAPULA DISORDERS The scapula plays a vital role in the throwing athlete. The scapula functions as the proximal stable base of support, allowing distal mobility to the glenohumeral joint and hand. The scapula has numerous muscles attaching to it. The scapula not only acts as a stable base but also must be able to move to maintain a constant length tension relationship for the rotator cuff musculature to function adequately. During the cocking phase of throwing, the scapula must upwardly rotate. The muscles primarily responsible for this motion are the serratus anterior and the middle and upper trapezius. During the acceleration phase, the scapula must forcefully protract and downwardly rotate. The muscles primarily responsible for this motion are the serratus anterior and the pectoralis major and minor. The scapula must be able to rotate upwardly 60 degrees, glide 15 cm laterally, and elevate 10 to 12 cm to allow normal arm elevation.68 Several clinicians have emphasized the importance of the scapular stabilizing muscles in decelerating the arm by dissipating the forces during the follow-through phase of throwing.69,70 Several pathologic forms of scapular motion are seen in the throwing athlete.
Snapping Scapula The scapula disorder termed snapping scapula is a pathology characterized by a loud grating and snapping sound of the scapula as it moves over the thorax. The athlete usually complains of pain in the periscapular region with
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overhead movements and activities. Radiographs or MRI scans are often useful to localize the lesion.71 The treatment is most commonly conservative, consisting of scapula strengthening and modalities such as heat, ultrasound, and occasional use of local steroid injections. Often, as the pain subsides, the athlete continues to notice the snapping noise; this might not warrant treatment.71 The snapping scapula disorder is the result of an osseous or osteocartiliginous lesion of the scapula or the thorax producing this symptomatic crepitus with active scapular motion.
that may be perceived as weak or that plays an extremely important role in throwing.
Scapulothoracic Bursitis
The thrower’s ten program emphasizes the muscles and muscle groups responsible for the throwing movement. The exercise program attempts to re-establish humeral head dynamic stability through rotator cuff musculature strength and neuromuscular control. Also, the prime movers of the shoulder, the accelerators or anterior shoulder muscles, are exercised using concentric and plyometric exercise drills. The posterior cuff muscles, the decelerators, are exercised using an eccentric muscle contraction. The scapulothoracic joint, trunk, and legs are also conditioned in this program. A well-conditioned thrower may be less likely to sustain an injury than an unconditioned athlete.
Scapulothoracic bursitis is a pathology closely associated with snapping scapula. In these instances, one of the scapulothoracic bursae becomes inflamed and swollen, which results in an audible and palpable crepitus with scapula motion. The crepitus is usually localized to the superomedial border of the scapula.72 Repetitive overhead motions, such as throwing, can irritate the soft tissue of the scapulothoracic joint, producing this type of chronic overuse inflammatory reaction. Occasionally, surgery is required to excise the involved thickened bursae.73 Most commonly, this pathology responds well to conservative management, consisting of rest, analgesics, nonsteroidal anti-inflammatory medications, physical therapy, heat, and local steroid injections. Specific exercises designed to strengthen the scapular stabilizers and the shoulders’ internal and external rotators are extremely beneficial in these instances.
REHABILITATION The shoulder joint complex is commonly injured in the throwing athlete. Most injuries to the throwing shoulder are from repetitive microtrauma and rarely require surgical intervention. The throwing athlete should perform specific exercises to strengthen the different muscles of the shoulder complex. These exercises should isolate the rotator cuff, glenohumeral, and scapulothoracic muscles. Also, exercises for the muscles of the core, trunk, and legs should be performed to strengthen all muscle groups of the kinetic chain. The exercises outlined in Figure 33-17 have been developed through the collective works of several investigators who have documented the muscle activity (electromyography) during various exercise movements.74-80 These exercises emphasize the muscles involved in the throwing mechanics and use combined movement patterns and isolated movement patterns. In the combined movement patterns, groups of muscles are exercised to perform a movement pattern that is similar to throwing. This assists in improving neuromuscular control, synchronized movement, and flexibility before throwing is begun. In the isolated movement patterns, a particular muscle or movement is isolated. Isolated movements are performed to overload a particular muscle
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These exercises are called the thrower’s ten program and are prescribed to the throwing athlete as preventive exercises.81 Also, these exercises are often prescribed as strengthening exercises after injuries and when motion and adequate strength have been achieved. Stretching, flexibility, and range-of-motion exercises should also be performed. Emphasis should be on restoring internal-rotation range of motion and horizontal-adduction range of motion.
SUMMARY The shoulder’s angular velocity during throwing often exceeds 7000 deg/sec, which results in increased muscular demands to provide the dynamic stability required by the shoulder complex. The shoulder complex must exhibit excessive motion along with extraordinary strength and neuromuscular control to throw a baseball. As a result of the excessive motion required to throw a baseball, laxity of the shoulder is common. The laxity perceived on clinical examination can progress to frank and symptomatic instability if the thrower cannot exhibit adequate humeral head stabilization. Shoulder instability can lead to various pathologies, including tensile rotator cuff failure, compressive rotator cuff disease, labrum tears, and biceps tendinitis. Further injuries are commonly seen in the throwing athlete other than rotator cuff injuries or instability syndromes. Glenoid labrum tears, biceps tendon pathology, acromioclavicular joint disorders, scapula pain, and different neurovascular pathologies are also common in the throwing athlete. The keys to injury-free throwing are proper mechanics, conditioning, and periodization in training to ensure coordinated muscular contractions of the glenohumeral and scapular muscles. The thrower must have an adequate amount of time to ensure tissue healing between the microtraumatic injury episodes produced while throwing a baseball. Therefore, it may be necessary for the thrower to rest the arm from throwing activities for several days while rehabilitation is being performed through exercises and
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The Thrower’s Ten Program is designed to exercise the major muscles necessary for throwing. The program’s goal is to be organized and concise. All exercises included are specific to the thrower and are designed to improve strength, power, and endurance of the shoulder complex musculature.
1A. Diagonal pattern D2 extension: Involved hand will grip tubing handle overhead and out to the side. Pull tubing down and across your body to the opposite side of leg. During the motion, lead with your thumb. Perform _______ sets of _______ repetitions _______ daily.
1B. Diagonal pattern D2 flexion: Gripping tubing handle in hand of involved arm, begin with arm out from side 45° and palm facing backward. After turning palm forward, proceed to flex elbow and bring arm up and over involved shoulder. Turn palm down and reverse to take arm to starting position. Exercise should be performed _______ sets of _______ repetitions _______ daily.
2A. External rotation at 0° abduction: Stand with involved elbow fixed at side, elbow at 90° and involved arm across front of body. Grip tubing handle while the other end of tubing is fixed. Pull out arm, keeping elbow at side. Return tubing slowly and controlled. Perform _______ sets of _______ repetitions _______ times daily.
2B. Internal rotation at 0° abduction: Standing with elbow at side fixed at 90° and shoulder rotated out. Grip tubing handle while other end of tubing is fixed. Pull arm across body keeping elbow at side. Return tubing slowly and controlled. Perform _______ sets of _______ repetitions _______ times daily.
therapeutic modalities. This can assist in the successful return to throwing after a shoulder injury. Injuries to the throwing shoulder present the clinician with many clinical enigmas. The clinician should carefully
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Figure 33-17. Thrower’s ten exercise program.
examine the involved area with a thorough knowledge of the functional anatomy, the throwing biomechanics, and the pathomechanics of the shoulder complex. An accurate diagnosis of the throwing shoulder is a significant challenge for all clinicians.
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2C. (Optional) External rotation at 90° abduction: Stand with shoulder abducted 90°. Grip tubing handle while the other end is fixed straight ahead, slightly lower than the shoulder. Keeping shoulder abducted, rotate shoulder back keeping elbow at 90°. Return tubing and hand to start position. I. Slow speed sets: (Slow and controlled) Perform _______ sets of _______ repetitions _______ times daily. II. Fast speed sets: Perform _______ sets of _______ repetitions _______ times daily.
2D. (Optional) Internal rotation at 90° abduction: Stand with shoulder abducted to 90°, externally rotated 90° and elbow bent to 90°. Keeping shoulder abducted, rotate shoulder forward, keeping elbow bent at 90°. Return tubing and hand to start position. I. Slow speed sets: (Slow and controlled) Perform _______ sets of _______ repetitions _______ times daily. II. Fast speed sets: Perform _______ sets of _______ repetitions _______ times daily.
3. Shoulder abduction to 90°: Stand with arm at side, elbow straight, and palm against side. Raise arm to the side, palm down, until arm reaches 90° (shoulder level). Perform _______ sets of _______ repetitions _______ times daily.
4. Scaption, external rotation: Stand with elbow straight and thumb up. Raise arm to shoulder level at 30° angle in front of body. Do not go above shoulder height. Perform _______ sets of _______ repetitions _______ times daily.
5. Sidelying external rotation: Lie on uninvolved side, with involved arm at side of body and elbow bent to 90°. Keeping the elbow of involved arm fixed to side, raise arm and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
Figure 33-17. cont’d
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6A. Prone horizontal abduction (neutral): Lie on table, face down, with involved arm hanging straight to the floor, and palm facing down. Raise arm out to the side, parallel to the floor. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
6B. Prone horizontal abduction (full ER, 100° ABD): Lie on table face down, with involved arm hanging straight to the floor, and thumb rotated up (hitchhiker). Raise arm out to the side with arm slightly in front of shoulder, parallel to the floor. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
6C. Prone rowing: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, and bring dumbbell as high as possible. Hold at the top for 2 seconds, then slowly lower. Perform _______ sets of _______ repetitions _______ times daily.
6D. Prone rowing into external rotation: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, up to the level of the table. Pause one second. Then rotate shoulder upward until dumbbell is even with the table, keeping elbow at 90°. Hold at the top for 2 seconds, then slowly lower taking 2–3 seconds. Perform _______ sets of _______ repetitions _______ times daily.
7. Press-ups: Seated on a chair or table, place both hands firmly on the sides of the chair or table, palm down and fingers pointed outward. Hands should be placed equal with shoulders. Slowly push downward through the hands to elevate your body. Hold the elevated position for 2 seconds and lower body slowly. Perform _______ sets of _______ repetitions _______ times daily. Figure 33-17. cont’d
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8. Push-ups: Start in the down position with arms in a comfortable position. Place hands no more than shoulder width apart. Push up as high as possible, rolling shoulders forward after elbows are straight. Start with a push-up into wall. Gradually progress to table top and eventually to floor as tolerable. Perform _______ sets of _______ repetitions _______ times daily.
9A. Elbow flexion: Standing with arm against side and palm facing inward, bend elbow upward turning palm up as you progress. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
9B. Elbow extension (abduction): Raise involved arm overhead. Provide support at elbow from uninvolved hand. Straighten arm overhead. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
10A. Wrist extension: Supporting the forearm and with palm facing downward, raise weight in hand as far as possible. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
10B. Wrist flexion: Supporting the forearm and with palm facing upward, lower a weight in hand as far as possible and then curl it up as high as possible. Hold for 2 seconds and lower slowly. Figure 33-17. cont’d
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10C. Supination: Forearm supported on table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm up. Hold for a 2 count and return to starting position. Perform _______ sets of _______ repetitions _______ times daily.
10D. Pronation: Forearm should be supported on a table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm down. Hold for a 2 count and return to starting position. Perform _______ sets of _______ repetitions _______ times daily.
Figure 33-17. cont’d
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49. Shepard MF, Dugas JR, Zheng N, Andrews JR: Differences in the ultimate strength of the biceps anchor and the generation of type II superior labral anterior posterior lesions in a cadaveric model. Am J Sports Med 32(5):1197-1201, 2004. 50. Kim SH, Ha KI, Ahn JH, et al: Biceps load test II: A clinical test for SLAP lesions of the shoulder. Arthroscopy 17(20):160-164, 2001. 51. Myers TH, Zemanovic JR, Andrews JR: The resisted supination external rotation test: A new test for the diagnosis of superior labral anterior posterior lesions. Am J Sports Med 33(9):1315-1320, 2005. 52. Bennett GE: Elbow and shoulder lesions of the professional baseball pitcher. JAMA 117:510-514, 1941. 53. Meister K, Andrews JR, Batts J, et al: Symptomatic thrower’s exostosis. Arthroscopic evaluation and treatment. Am J Sports Med 27(2):133-136, 1999. 54. Jobe FW, Moynes DR, Tibone JE: An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 55. Crenshaw AH, Kilgore WE: Surgical treatment of bicipital tenosynovitis. J Bone Joint Surg Am 48(8):1496-1502, 1966. 56. Michele AA: Bicipital tenosynovitis. Clin Orthop 18:261267, 1960. 57. Vellet AD, Munk PL, Marks P: Imaging techniques of the shoulder: Present perspectives. Clin Sports Med 10:721-756, 1991. 58. Rockwood CA, Young DC: Disorders of the acromioclavicular joint. In Rockwwod CA, Matsen FA (eds): The Shoulder, Philadelphia: WB Saunders, 1990. 59. Leffert RD: Thoracic outlet syndrome and the shoulder. Symposium on injuries to the shoulder in the athlete. Clin Sports Med 2:439-452, 1983. 60. Roos DB: The thoracic outlet syndrome is underrated. Arch Neurol 47:327-328, 1990. 61. Britt LP: Nonoperative treatment of the thoracic outlet syndrome symptoms. Clin Orthop 51:45-48, 1967. 62. Wright IS: The neurovascular syndrome produced by hyperabduction of the arms. Am Heart J 157:1-19, 1945. 63. Post M, Mayer J: Suprascapular nerve entrapment. Clin Orthop Relat Res (223):126-136, 1987. 64. Callahan JD, Scully TB, Shapiro SA, et al: Suprascapular nerve entrapment. J Neurosurg 74:893-896, 1991. 65. Rengachary SS, Burr D, Lucas S, et al: Suprascapular entrapment neuropathy: Clinical, anatomical and comparative study. Neurosurgery 5:447-451, 1979. 66. Fritz RC, Helms CA, Steinbach LS, et al: Suprascapular nerve entrapment—evaluation with magnetic resonance imaging. Radiology 182:437-444, 1992. 67. Thompson WA, Kopell HP: Peripheral entrapment neuropathies of the upper extremity. N Engl J Med 260:1261-1265, 1959. 68. Kapandji IA: The Physiology of the Joints, vol 1, 5th ed. New York: Churchill Livingstone, 1982. 69. Kibler WB: Rule of the scapula in the overhead throwing motion. Contemp Orthop 22:525-532, 1991. 70. Glousman RE, Jobe FW, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220-226, 1988. 71. Milch H: Snapping scapula. Clin Orthop 20:139-150, 1961. 72. Bigliani LU: Shoulder injuries in athletics. Presentation at Advances of the Shoulder and Knee, Hilton Head, SC, May 30, 1992.
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73. Sisto DJ, Jobe FW: The operative treatment of scapulothoracic bursitis in professional pitchers. Am J Sports Med 14:192-194, 1986. 74. Moseley JB, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. 75. Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19:264-272, 1991. 76. Blackburn TA, McLeod WD, White B: EMG analysis of posterior rotator cuff exercises. Athletic Training 25:40-45, 1990.
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77. Blackburn TA: Off-season program for the throwing arm. In Zarins B, Andrews JR, Carson WG (eds): Injuries to the Throwing Arm. Philadelphia: WB Saunders, 1985. 78. Jobe FW, Bradley JP: Rotator cuff injuries in baseball: Prevention and rehabilitation. Sports Med 6:378-387, 1988. 79. Jobe FW, Moynes DR: Delineation of diagnostic criteria and a rehabilitation program for rotator cuff injuries. Am J Sports Med 10:336-339, 1982. 80. Pappas AM, Zawacki RM: Rehabilitation of the pitching shoulder. Am J Sports Med 13:223-235, 1985. 81. Wilk KE, Arrigo C, Courson R, et al: Preventive and Rehabilitative Exercises for the Shoulder and Elbow, 6th ed. Birmingham, Ala, American Sports Medicine Institute, 2001.
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CHAPTER 34 Shoulder Injuries in Football Brian D. Busconi, Christopher W. Baker, and Thomas J. Gill
Football is one of the most popular sports in the United States. There has been a substantial increase in player participation on the middle school, high school, and college levels since the 1970s. The National Federation of State High School Associations estimates that approximately 1.5 million players from high school, middle school, and nonfederation member schools participated in the 2005 season.1 This includes an increase of 26,200 players compared with the previous year.2 Participation at the college level, including in the National Collegiate Athletic Association (NCAA), National Association of Intercollegiate Athletics (NAIA), and National Junior College Athletic Association (NJCAA), has remained steady since the 1980s at around 75,000 players.1 Semiprofessional, recreational, and flag-football leagues have become more popular; in combination with professional football, the number of these participants is estimated at around 225,000. When school, professional, and other league players are combined, the total number of football participants in the United States for the 2005 football season was around 1.8 million.1 As a result, an increased number of football injuries have been documented.3,4 It has been estimated that 11% to 81% of participants across all levels will be injured at some time while playing the sport.5
positions and making them particularly susceptible to injury. Injury is typically the result of a direct force applied to the injured area or an indirect force transmitted from its point of application and manifesting at the injured area. When assessing shoulder injuries, the mechanism, description of instability, presence of radicular symptoms, and the location of pain are all important.9.18 The vast majority of injuries are acute, resulting from direct forces, but overuse and chronic injuries can also occur.9,11 There are a wide variety of types and locations of injuries about the shoulder, including nerve damage, separation, dislocation, capsular or labral pathology, rotator cuff problems, and fractures.
The shoulder complex trails only the knee, ankle, and hand as the most commonly injured musculoskeletal body parts.2,3,5,6 It is the most common site of injury in the upper extremity, and accounts for roughly 10% to 20% of the total number of football injuries encountered.5 Although the shoulder is extensively protected with pads, it is often the point of first contact in tackling and blocking, making it particularly vulnerable to injury. Extrinsic factors (amount of contact, style of play, type of playing surface, previous injury, and position) have all been reported as risk factors for injury.3,5,9 However, the vast majority of injuries are mild, consisting of sprains/strains, and contusions, and they usually result in minimal loss (less than 1 week) of playing time.3-8 However, up to one third of these athletes eventually require surgery.5,10
Football is the most common sporting activity associated with brachial plexus injury.12 The incidence of plexus injuries in football has been estimated to be as high as 2.2 cases per 100 players.12 Likewise, the incidence among all injuries sustained by elite NCAA college football players has been estimated at about 50%.3,12 The brachial plexus is most often injured by direct traumatic injuries, but traction can also produce a plexopathy.12
The shoulder is a complex joint with multiple articulations and osseous structures surrounded by muscles, tendons, ligaments, cartilage, and nerves. Shoulder injuries can be intra-articular, extra-articular, or both. The shoulder exhibits the greatest degree of mobility and range of motion of all the joints, potentially placing these structures in extreme
Burners and Stingers
BRACHIAL PLEXUS INJURIES The brachial plexus is formed from the nerve roots of C5 to T1 and lies under the clavicle between the anterior and middle scalene muscles. The terminal branches form the five major nerves that innervate the muscles of the arm and hand, including the shoulder. Several peripheral branches originate from the plexus and innervate muscles that are important for shoulder motion, including the rotator cuff. Any of these nerves are susceptible to harm.
Specific peripheral nerve injuries described in football players include those to the axillary nerve, long thoracic nerve, and the suprascapular nerve.12-14 The spinal accessory nerve, although not a true peripheral nerve, can also be injured playing football.12-14 However, the most common brachial plexus injury is the burner or stinger.
The burner or stinger is one of the most common injuries seen in football. Up to 52% of college football players suffer this injury during a single season, and 65% to 70% of collegiate football players suffer this injury during their four-year 421
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college careers.13,19 It accounts for approximately 36% of all neurologic upper extremity injuries in football.12 Burners and stingers are believed to be the result of nerve traction or compression, usually involving the C5 and C6 nerve roots.12,13 Three mechanisms have been described. The first involves neck extension combined with a compression injury on the side the head and neck are tilted toward.12,13 The second mechanism, which is the most common cause of stingers and burners, entails distraction of the shoulder away from the head or neck, commonly occurring during blocking and or tackling.12 The third, and least common, type is a direct blow to the supraclavicular region of the shoulder (Erb’s point), where the brachial plexus is most superficial and vulnerable.13 This typically occurs after a direct blow from a helmet or ground onto a player’s shoulder pads, driving them into the superior scapula and compressing the nerves.13 After suffering this injury, players complain of transient numbness, pain, or paresthesias radiating from the shoulder to the hand on the side of the injury, and they may be unable to move the arm.12,13,19,20 Most symptoms last from a few seconds to a few minutes, although 5% to 10% of patients have a persistent neurologic deficit lasting days or weeks.13,19 Rarely, complete transection of the nerves occurs, requiring urgent surgical repair, and recovery might never be complete.19 The initial examination and treatment begin with observation. The athlete should be removed from competition, and many burners resolve by the time the athlete reaches the sideline.13,19 Some shake their arms and hands, or hold their neck flexed toward the affected side.13 The shoulder pads, helmet, and shirt should be removed as long as cervical-spine injury is not suspected.13 A complete neurologic examination should be performed, including evaluation of strength, reflexes, and sensation.13,19 The shoulder and cervical spine should be examined to rule out concomitant injuries.19,20 Bilateral symptoms, cervical-point tenderness, neck stiffness, bone deformity, fear of moving the head, or complaints of a heavy head warrant immobilization on a spine board and immediate transportation to a medical center.19,20 If symptoms resolve within seconds to minutes and are not associated with loss of strength, neck pain, limitation of neck movement, or signs of shoulder subluxation, the athlete may return to competition the same day.19,20 The athlete should be serially examined for a few successive days to track the duration and resolution of symptoms.13,19 If symptoms persist for longer than a few minutes, a full medical evaluation, including appropriate imaging, is warranted.19,20 Prolonged symptoms should be treated with rest, removal from play, nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy.13 Only after all symptoms have resolved may players return to full sports activity.13
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Axillary Nerve Injures Axillary neuropathies are often associated with a traumatic event, such as anterior glenohumeral dislocation or a direct blow to the anterolateral deltoid region.13 This injury is most commonly secondary to blocking or tackling.12 Initial presentation varies, but usually consists of weakness in shoulder elevation and abduction, accompanied by numbness, pain, or paresthesias about the lateral shoulder and arm.14 However, many of these injuries are initially undetected because other joint or bone injuries dominate the clinical picture.14 Initial management is conservative but should include a well-documented physical and neurologic examination and should rule out more severe injuries, such as those to the cervical spine or the spinal cord. Any other associated injuries, such as fracture or dislocation, should be managed first. After the acute phase of injury, treatment includes rehabilitation to maintain passive and active shoulder range of motion, strength, and proper biomechanics.14 Even though many athletes with axillary neuropathy fail to regain full axillary nerve function, 91% return to a preinjury level of sports activity.15 Return to sport is indicated when the athlete has full shoulder active range of motion and strength is documented to be good or excellent by isokinetic or manual muscle testing.14
Long Thoracic Nerve Injuries Long thoracic nerve injury is another peripheral-nerve shoulder injury seen in football players and can be quite disabling. This nerve innervates the serratus anterior muscle, which is important for scapular stabilization, protraction, and rotation during shoulder abduction. Acute or recurrent trauma is the most common cause of injury.13 The mechanism of injury involves traction to the nerve either when the athlete’s head is tilted or rotated laterally away from the affected extremity with the arm raised overhead, such as when throwing a football, or when the shoulder is depressed in conjunction with contralateral neck bending, as with tackling.13 Athletes initially complain of pain or discomfort in the shoulder, neck, or scapular region. Weakness can also be present, especially with overhead motions and forward elevation. Winging of the scapula medially can also occur. Initial management is conservative but should include a well-documented physical and neurologic examination to help determine the exact cause of the pain or winging.13 Nonoperative management is the mainstay of treatment and includes rest, symptomatic relief, and therapy to maintain shoulder range of motion and
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strength and stability.13 The athlete should avoid heavy lifting or participating in activities that put the nerve at risk.13 Most cases subside within 6 to 9 months, and almost all resolve satisfactorily within 12 months.13,16 Surgery is indicated only after 1 to 2 years of failed conservative management and no improvement in nerve function documented by EMG testing.13
Suprascapular Nerve Injuries Suprascapular nerve injuries have been documented in football players. This nerve innervates the supraspinatus and infraspinatus muscles (part of the rotator cuff) and provides sensation to the proximal one third of the arm. The mechanism of injury varies between repetitive throwing, direct trauma, and traction and has been associated with blocking or tackling.12 Presentation can vary from painless weakness with abduction, external rotation, or both, depending on the location of the injury within the nerve.17 Initially, patients present with a deep, aching pain in the posterior and lateral aspects of the shoulder that radiates from the scapular region to the lateral neck.12,17 Atrophy of the spinati muscles is pathognomonic for this injury.17 Conservative treatment consisting of rest and physical therapy are the initial modalities of treatment.12 Surgery is indicated only after conservative measures have failed.
Spinal Accessory Nerve Injuries The spinal accessory nerve also deserves mention when talking about nerve injuries about the shoulder. It innervates the trapezius muscle, which is important for shrugging the shoulders and for retracting, stabilizing, and rotating the scapula.13 The trapezius resists drooping of the shoulder, assists in abduction of the arm, and allows the arm’s use for overhead activities.13 Injury is typically from blunt trauma, such as a direct blow, or traction during tackling.13 Initial presentation is that of disabling pain, weakness, and deformity. Athletes cannot fully elevate or abduct the shoulder and have drooping of the shoulder, lateral winging of the scapula, and asymmetry of the neckline.13 Initial management again consists of a well-documented physical and neurologic examination to rule out other more acute and serious injuries. Treatment can involve multiple modalities, and includes physical therapy, rest, nerve stimulation, heat and cold therapy, and bracing, all of which have shown mixed results.13 Despite this, a blunt trauma or traction injury to this nerve usually recovers within 12 months. Surgical intervention is indicated only after conservative measures have failed or if the injury is due to penetrating trauma or laceration of the nerve.13
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ACROMIOCLAVICULAR JOINT INJURIES The acromioclavicular joint consists of the articulation of the distal end of the clavicle with the acromion process of the scapula. This joint is surrounded by a capsule that is stabilized by several ligamentous attachments.21,22 Horizontal (anteroposterior) stability is provided by the acromioclavicular ligaments.11,21,22 The superior acromioclavicular ligament, whose fibers blend with the fibers of the deltoid and the trapezius, is the strongest.11,21,22 Vertical (superoinferior) stability is provided by two coracoclavicular ligaments, the conoid and the trapezoid.11,21,22 These function to support the upper extremity to the clavicle and trunk and are the primary support by which the scapula is suspended from the clavicle.11,21,22 Injury to the acromioclavicular joint is one of the most common shoulder injuries reported in football players. Acromioclavicular joint injuries have been shown to account for about 40% of the total shoulder injuries suffered by National Football League (NFL) quarterbacks and between 47% and 70% of shoulder injuries in elite NCAA college football players, depending on position.5,9 Quarterbacks, running backs, and wide receivers had the highest rate of injury, possibly because of the higher incidence of direct contact to the shoulder or from the different type of shoulder pads worn.5 Acromioclavicular dislocation and separation are more common in male athletes and more often involve incomplete injuries.22 Injury can occur in one of two ways. The first is direct impact on the acromion while the humerus is abducted, such as from a helmet or the ground.21 The magnitude of the force determines the severity of the injury and which structures are damaged.21 The second mechanism of injury, which is much less common, is indirect trauma. A fall on the elbow or outstretched arm can direct an upward force through the humeral head and into the acromion, whereas a downward force applied by a pull through the upper extremity can distract and injure the joint.21.22 Acromioclavicular injuries can be classified into six types (I-VI). Type I and II involve a sprain or partial tear of the acromioclavicular ligaments while the coracoclavicular ligaments remain intact, and are the most common types of injury.5,23,24 Type III injuries are true separations, and both the acromioclavicular and coracoclavicular ligaments are disrupted and the clavicle is displaced superiorly.23 Type V injuries are exaggerated type III injuries with more severe displacement.11,21,23 Type IV and type VI injuries involve posterior or inferior displacement of the clavicle and are extremely uncommon.23 Upright x-rays are necessary to determine the exact type.
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Players typically present with pain, swelling, ecchymoses, deformity, abrasion, or abnormal translation, or some combination of these.23 There may be a visible deformity and the patient should be examined either sitting or standing to exaggerate the deformity.22 With more severe grades of injury, the patient might hold the arm adducted and close to the body and supported in an elevated position.22 Initial management involves support for the arm with a sling, a thorough physical examination to check for associated injuries, a complete neurovascular examination, and subsequent transfer for x-ray evaluation of the shoulder. The grade of injury dictates treatment. Type I and II are treated with rest, temporary immobilization with a sling, ice, and early progressive range-of-motion exercises.11,21 Most athletes can return to play in 2 to 6 weeks.11,21 Treatment of type III injuries is controversial, and surgical and nonsurgical treatments are possible.5,21,22 Most surgeons still prefer initial nonoperative management.24 Type IV, V, and VI injuries require operative intervention.5,21-24
GLENOHUMERAL JOINT INJURIES The glenohumeral joint consists of the articulation of the humeral head with the glenoid fossa of the scapula surrounded by multiple soft tissue stabilizers. There is very little bony contact about the shoulder, allowing a large degree of freedom of motion, which is essential for normal shoulder function.11 Because of this, soft tissues about the shoulder provide the majority of the dynamic and static stability to the glenohumeral joint.11,23 These soft tissues are subjected to considerable stresses and are the sources of injury in the athlete’s shoulder.11 Glenohumeral instability is a common shoulder disorder, especially in young, athletic persons, and are typically the result of traumatic dislocation.5,25,26 Atraumatic instability occurs as well. The position of the arm at the time of injury is an important component in determining the injury pattern and the direction of instability.25 Glenohumeral instability can be divided into three main types: anterior, posterior, and multidirectional. The only intra-articular tendon in the shoulder, the biceps tendon, can also be a common source of shoulder pain in athletes.
Anterior Instability Anterior shoulder dislocations are common injuries in athletes, especially football players, and acute anterior instability episodes typically affect those in their early 20s.27 Forty percent of shoulder dislocations occur in patients 22 years old and younger, and the risk of recurrence typically approaches 90% to 95% in this age group.27,28 Recurrence rates typically decrease with age and tend to increase with the activity level of the athlete, the number of recurrences, future athletic participation, and bone
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loss.27,29,30 In elite NCAA college football players, anterior instability was the second most common shoulder injury, with an incidence of 20%.5 It was also found to be primarily a defensive injury, occurring most often in linebackers and defensive backs.5 Anterior instability can result from either a fall or an anteriorly directed force when the arm is abducted and externally rotated.27,30 However, the patient cannot always remember the position of the arm at the time of injury, so a thorough physical examination is recommended, including a neurologic examination documenting axillary nerve function.23,25,26,30 Initial presentation is variable, and can include the arm held at the side, or in abduction and external rotation. Typically, patients present with pain or apprehension when the arm is placed in a position of abduction, external rotation, and extension.25,30 Likewise, the shoulder feels loose or subluxed. If the shoulder is dislocated, on-field reduction is appropriate depending on clinical experience, absence of or concern for concurrent injuries, and specific circumstances; otherwise transfer to an appropriate facility for x-rays (including an axillary lateral film) and reduction is warranted.23 Recurrent dislocations or subluxations often spontaneously reduce.25,26 Initial management includes a brief period of immobilization for comfort, symptomatic relief, and early rehabilitation.23,27,30 However, because of the high rate of recurrence in younger athletes, surgery is often necessary.5,11,23,27,30
Posterior Instability Posterior instability is a rare condition, occurring in only 2% to 5% of those with shoulder instability.31 It is difficult to diagnose and is often missed.32 Approximately 50% of patients recall a distinct traumatic injury, but an associated posterior dislocation is rare.31,32 Repetitive microtrauma might also play a role.31,33 The degree of instability can range from mild subluxation to frank dislocation.31 Recurrent instability most commonly manifests with repeated episodes of subluxation, but there may be no history at all.32,33 In elite NCAA college football players, posterior instability accounts for only 4% of all shoulder injuries.5 Offensive linemen, defensive linemen, and defensive backs are the most commonly injured.5,31,33 Initially believed to be only associated with seizures and electrical shock, posterior shoulder instability among football players typically occurs when a posterior force is applied to the arm when it is forward flexed, adducted, and internally rotated.31,33 This is a common position for offensive lineman while blocking.31,33 Physical examination findings are subtle. Range of motion is often symmetrical and normal, but pain might occur with palpation of the posterior joint line.31 Patients might report feelings of pain
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or weakness with or without instability symptoms, and they typically do not complain of popping, slipping, or giving way.31,33 Initial management involves reduction of dislocations, brief immobilization, rest, and ice followed by early physical therapy. Therapy focuses on strengthening the dynamic muscular stabilizers including the posterior deltoid, the external rotators, and the periscapular muscles.31 A high percentage of players (about 75%) do not respond to conservative treatment and suffer multiple recurrences.5,31,32 For this reason, operative treatment (which usually involves a series of procedures) is increasingly offered at an earlier stage.31,32
Multidirectional Instability As the name implies, multidirectional instability of the shoulder involves an abnormal increase in glenohumeral translation in multiple planes.34 There are two main clinical features. Most symptoms are experienced in the midrange of glenohumeral motion, the physical examination demonstrates the ability to dislocate or subluxate the joint in three directions (anterior, posterior, and inferior); symptoms are reproduced in at least one of the directions.34 Most cases of multidirectional instability are likely the result of repetitive microtrauma such as those found in high-contact sports.35 However, precipitating events tend to be relatively atraumatic, and athletes with a history of lax shoulders are most often found to have multidirectional instability.34 Multidirectional instability is most often found in young adults and those in their third decade, and multidirectional instability is often bilateral.34 Symptoms typically include pain, varying degrees of instability, and intermittent neurologic symptoms. Symptoms are usually experienced during daily activities and are easily provoked.34,35 Initial management includes brief immobilization, NSAIDs, and symptomatic pain relief.34 Rehabilitation is the core of treatment and is successful in about 88% of patients.34,36
BICEPS TENDON DISORDERS Disorders of the biceps tendon can be a source of shoulder pain, especially in overhead athletes such as quarterbacks.5,36 These disorders typically result from overuse and include biceps tendinitis, subluxation, and complete rupture.9,36,37 Biceps tendinitis was found to be the second most common overuse injury in NFL quarterbacks.5 Patients have pain in the bicipital groove and anterior shoulder pain exacerbated by overhead activities.36 Biceps subluxation usually occurs in conjunction with subscapularis tendon
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tears and is typically the result of forceful external rotation or extension of the abducted shoulder.36 Complete tendon rupture is rare and usually due to trauma. The physical examination reveals pain and clicking in the bicepital groove, and palpable subluxation with rotation of the arm.36 In the case of a complete rupture, there may be a visible deformity of the biceps muscle (the Popeye arm) compared with the other side. Treatment consists of rest, activity modification, and rehabilitation.11,36,37 Surgery is rarely indicated. Superior labrum anterior-posterior (SLAP) lesions involve injury to the insertion of the biceps tendon (the anchor) and its surrounding labrum. There are several types. Lesions can result from traction injuries (such as during throwing or after a dislocation), from compression injuries (such as a fall on an outstretched, forward flexed, and abducted arm), or from repetitive microtrauma in the throwing athlete (especially quarterbacks).11,36,37 Patients typically have pain with overhead activities and mechanical symptoms such as clicking, catching, locking, or popping.36,37 The mainstays of treatment are rest, activity modification, and rehabilitation.11,36,37 Surgery is initially warranted for certain types of SLAP lesions or if conservative measures fail.11,36,37
ROTATOR CUFF INJURIES AND IMPINGEMENT The rotator cuff consists of four muscles and their tendinous attachments to the humerus. The supraspinatus, infraspinatus, and teres minor attach to the greater tuberosity, and the subscapularis attaches to the lesser tuberosity. These muscles allow abduction (supraspinatus), external rotation (infraspinatus and teres minor), and internal rotation (subscapularis) of the humerus. The rotator cuff provides dynamic stability to the glenohumeral joint and allows shoulder motion.38 Damage to any of these structures alters the biomechanics of the shoulder.11,36 Injuries to the rotator cuff have been well documented in football players.5,9,39 These include sprains and strains, impingement, and partial and full-thickness tears.5,9,11,36 In elite NCAA college football players, rotator cuff injury was the third most common shoulder injury (12%), and tendinitis was the most common manifestation.5 The injuries were distributed among a variety of positions, including running back, receiver, offensive and defensive linemen, defensive back, linebacker, and quarterback.5 In NFL quarterbacks, rotator cuff tendinitis was the most common injury associated with the throwing motion itself and the second most common shoulder injury overall.9 The mechanism of injury is either direct traumatic rupture of the rotator cuff or chronic microtrauma due to overuse.11,36 Players can have pain in the anterolateral aspect of the
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shoulder, especially with overhead activities; tenderness; or weakness.36,38 Initial management includes rest, activity modification, NSAIDs, occasionally corticosteroid injections, and physical therapy.11,36,38 The vast majority of rotator cuff injuries, including partial-thickness tears, respond favorably to conservative treatment.11,38 However, failure of nonoperative treatment, traumatic rupture, or full-thickness tears usually warrants an operation.11,36,38 Impingement is not a common cause of shoulder pain in football players, but it can occur in overhead athletes, such as quarterbacks.36 There are two main types of impingement: external and internal.36,38 External impingement is caused by contact between the rotator cuff and the structures outside the shoulder joint, such as those in the subacromial space or the coracoid.38 The mechanism of internal impingement involves the surface of the rotator cuff and greater tuberosity coming in contact with the glenoid rim during the late cocking phase of the throwing motion.36,38 Subacromial impingement symptoms include pain in the anterolateral shoulder, are typically present at night, and can be reproduced with forced abduction of the shoulder.36,38 Internal impingement manifests with pain in the posterior shoulder and with decreased internal rotation and excessive external rotation with the patient supine and the arm abducted to 90 degrees.36,38 Initial treatment for both internal and external impingement involves rest, physical therapy, ice, and NSAIDs.36,38 Surgery is warranted after conservative measures fail.36,38
FRACTURES Fractures about the shoulder in football players are uncommon and are usually the result of high-energy trauma.23 Injuries typically occur more often in young, skeletally immature athletes.23,40 The most commonly fractured structure is the clavicle.5,23 In one study of elite NCAA college football players it represented 4.4% of all shoulder injuries.5 Most clavicle fractures are the result of a fall or direct trauma.23 Pain, crepitus, loss of motion, and deformity are all symptoms, and associated structures should also be examined for concomitant injuries.41 Brachial plexus injuries are rare but can occur in conjunction.41 For a true diagnosis, x-rays must be obtained.23,41 There are several possible sites of injury, and the middle third of the clavicle is the most commonly fractured.23,41 Immobilization and pain control are the initial stages of treatment. However, depending on the amount of displacement and location, operative intervention may be warranted.23,41 Fractures of the acromion, scapula, glenoid, and coracoid can also occur. As with the clavicle, initial management includes immobilization, pain control, ice, and appropriate imaging.23,41
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The proximal humerus is rarely injured in the mature football player, but in the skeletally immature shoulder the physis (growth plate) is potentially vulnerable. It is weaker than the surrounding bone and disruptive forces can cause failure or fracture through the physis.40,42 Injury can be the result of direct trauma or overuse.40,42 Long-term implications include loss of function and growth disturbance.40,42 Pain, crepitus, and deformity typically are present. As with any fracture, initial immobilization, symptomatic pain control, and appropriate imaging are customary.23,40,42 As the amount of displacement of the fracture increases, operative intervention may be necessary.40,42 The player may return to contact sports in 4 to 6 months if there is evidence of fracture healing.40,42
SUMMARY The shoulder is a complex joint that can sustain a wide range of injuries while playing football. A thorough history, physical, and neurologic examination are essential for directing treatment. Initial treatment typically includes immobilization as necessary, symptomatic relief, appropriate imaging, and physical therapy. The overwhelming majority of injuries are minor, caused by direct trauma, and do not cause significant loss of playing time.
References 1. National Center for Catastrophic Sport Injury Research. Annual Survey of Football Injury Research 1931-2005. Last updated January 14, 2008. Available at http://www.unc. edu/depts/nccsi/SurveyofFootballInjuries.htm (accessed February 19, 2008). 2. National Federation of State High School Associations: Sports Participation Survey. Kansas City, Mo, National Federation of State High School Associations, 1993. 3. Mueller FO, Zemper ED, Peters A: Football injuries. In Caine D, Caine C, Lindner K (eds.): Epidemiology of Sports Injuries. Champaign, Ill, 1996, pp 41-62. 4. Meeuwisse W, Fowler P: Frequency and predictability of sports injuries in intercollegiate athletics. Can J Sports Med Sci 13(1):35-42; 1988. 5. Kaplan L, Flanigan DC, Norwig J, et al: Prevalence and variance of shoulder injuries in elite college football players. Am J Sports Med 33(8):1142-1146, 2005. 6. Zemper ED: Injury rates in high school and college football: A two year prospective national study. Med Sci Sports Exerc 36(5 Suppl):276; 2004. 7. Stuart MJ, Morrey MA, Smith AM, et al: Injuries in youth football: A prospective observational cohort analysis among players ages 9 to 13 years. Mayo Clin Proc 77(4):317-322, 2002. 8. Adickes M, Stuart M. Youth football injuries. Sports Med 34(3):201-207, 2004. 9. Kelly B, Barnes RP, Powell JW, Warren RF: Shoulder injuries to quarterbacks in the National Football League. Am J Sports Med 32(2):328-331, 2004.
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10. National Collegiate Athletic Association: Annual Sports Sponsorship Survey. Overland Park, Kan: National Collegiate Athletic Association, 2002-2003. 11. Mazoue CG, Andrews JR: Injuries to the shoulder in athletes. South Med J 97(8):748-754, 2004. 12. Toth C, McNeil S, Feasby T: Peripheral nervous system injuries in sport and recreation. Sports Med 35(8): 717-739, 2005. 13. Safran M: Nerve injury about the shoulder in athletes, Part 2. Am J Sports Med 32(4):1063-1076, 2004. 14. Perlmutter GS, Apruzzese W: Axillary nerve injuries in contact sports. Sports Med 26(5):351-361, 1998. 15. Perlmutter GS, Leffeet RD, Zairns B: Direct injury to the axillary nerve in athletes playing contact sports. Am J Sports Med 25(1):65-68, 1997. 16. Foo CL, Swann M: Isolated paralysis of the serratus anterior: A report of 20 cases. J Bone Joint Surg Br 65: 552-556, 1983. 17. Kim DH, Murovic JA, Tiel RL, Kline DG: Management and outcomes of 42 surgical suprascapular nerve injuries and entrapments. Neurosurgery 57(1):120-127, 2005. 18. Metzl JD: Sports-specific concerns in the young athlete: Football. Pediatr Emerg Care 15(5):363-367, 1999. 19. National College Athletic Association: NCAA Guideline 2h. “Burners” (brachial plexus injuries). Overland Park, Kan, National College Athletic Association, 1994, revised June 2003. 20. Torg JS: Cervical spine injuries. In Garrick JG (ed): Orthopaedic Knowledge Update: Sports Medicine 3, vol 3. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 2004, pp 3-19. 21. Nuber GW, Bowen, MK: Acromioclavicular joint injuries and distal clavicle fractures. J Am Acad Orthop Surg 5: 11-18, 1997. 22. Galatz LM, Williams GR: Acromioclavicular joint injuries. In Bucholz RW, Heckman JD (eds): Rockwood and Green’s Fractures in Adults, 6th ed. Philadelphia, Lippincott Williams & Wilkins, 2005, pp 1331-1364. 23. Shaffer BS, Baublitz S: Acute shoulder injuries. In Garrick JG (ed): Orthopaedic Knowledge Update: Sports Medicine 3, vol 3. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 2004, pp 53-77. 24. Bishop JY, Kaeding C: Treatment of the acute traumatic acromioclavicular separation. Sports Med Arthrosc Rev 14(4):237-245, 2006. 25. Pollock RG, Bigliani LU: Glenohumeral instability: Evaluation and treatment. J Am Acad Orthop Surg 1: 24-32, 1993. 26. Paxinos A, Walton J, Tzannes A, et al: Advances in the management of traumatic anterior and atraumatic multidirectional shoulder instability. Sports Med 31(11): 819-828, 2001.
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27. Buss DD, Lynch GP, Meyer CP, et al: Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med 32(6):1430-1433, 2004. 28. Mazzocca AD, Brown FM Jr, Carreira DS, et al: Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am J Sports Med 33(1):52-60, 2005. 29. Pagnani MJ, Dome DC: Surgical treatment of traumatic anterior shoulder instability in American football players. J Bone Joint Surg Am 84(5):711-715, 2002. 30. Bicos J, Mazzocca AD, Arciero RA: Anterior instability of the shoulder. In Schepsis AA, Busconi BD, Tornetta P, Einhorn TA (eds): Sports Medicine (Orthopaedic Surgery Essentials). Philadelphia, Lippincott Williams & Wilkins, 2006, pp 214-230. 31. Millett PJ, Clavert P, Hatch GFR, Warner JP: Recurrent posterior shoulder instability. J Am Acad Orthop Surg 14:464-476⬍,2006. 32. Robinson CM, Aderinto J: Current concepts review: Recurrent posterior shoulder instability. J Bone Joint Surg Am 87(4):883-892, 2005. 33. Guanche CA: Posterior instability of the shoulder. In Schepsis AA, Busconi BD, Tornetta P, Einhorn TA (eds): Sports Medicine (Orthopaedic Surgery Essentials). Philadelphia, Lippincott Williams & Wilkins, 2006, pp 231-243. 34. Schenk TJ, Brems JJ: Multidirectional instability of the shoulder: Pathophysiology, diagnosis, and management. J Am Acad Orthop Surg 6:65-72, 1998. 35. Choi CH, Oglivie-Harris DJ: Inferior capsular shift operation for multidirectional instability of the shoulder in players of contact sports. Br J Sports Med 36:290-294, 2002. 36. Ong BC, Sekiya JK, Rodosky MW: Shoulder injuries in the athlete. Curr Opin Rheumatol 14:150-159, 2002. 37. Mileski RA, Snyder SJ: Superior labral lesions in the shoulder: Pathoanatomy and surgical management. J Am Acad Orthop Surg 6:121-131, 1998. 38. Curtis AS, Shurland AT: Disorders of the rotator cuff. In Schepsis AA, Busconi BD, Tornetta P, Einhorn TA (eds): Sports Medicine (Orthopaedic Surgery Essentials). Philadelphia, Lippincott Williams & Wilkins, 2006, pp 244-253. 39. Foulk DA, Darmelio MP, Rettig AC, Misamore G: Fullthickness rotator cuff tears in professional football players. Am J Orthop 31:622-624, 2002. 40. Caine D, DiFiori J, Maffulli N: Physeal injuries in children’s and youth sports: Reasons for concern? Br J Sports Med 40:749-760, 2006. 41. Lazarus MD, Seon C: Fractures of the clavicle. In Bucholz RW, Heckman JD, Court-Brown C, Tornetta P (eds): Rockwood and Green’s Fractures in Adults, 6th ed. Philadelphia, Lippincott Williams & Wilkins, 2005, pp 1211-1255. 42. Dobbs MB, Luhmann SL, Gordon JE, et al: Severely displaced proximal humeral epiphyseal fractures. J Pediatr Orthop 23:208-215, 2003.
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CHAPTER 35 Shoulder Injuries in Tennis Todd S. Ellenbecker, E. Paul Roetert, and Marc Safran
Court Championships over 2 years.4 Of 370 girls questioned, 35% noted a prevalence of shoulder pain; more than one half noted the pain is anterior in the shoulder and a third complained of pain that is both anterior and posterior about the shoulder. Of 480 boys queried, 24% noted a current or past history of shoulder pain; one third complained of anterior pain, one third of posterior pain, and one third of pain in both locations of the shoulder.
The inherent characteristics of the game of tennis produce specific physiologic and mechanical stresses to the musculoskeletal system. This is particularly evident in the upper extremity. The repetition required for acquiring skills initially and the subsequent practice and competition at all levels of play can subject the shoulder to overuse injury. This chapter provides a review of the injury patterns to the human shoulder and their epidemiology and presents the specific musculoskeletal adaptations to allow clinicians to interpret range of motion and strength tests during the evaluation and treatment of the elite tennis player with a shoulder injury.
In Safran’s study, the shoulder was the second most common location of pain or injury for either gender. When studying the incidence of injuries sustained at those tournaments over a 4-year period, Safran and Hutchinson also found the shoulder the second most common location of injury for boys and the third most common for the girls. During the 4 years studied, they found that 14% of the 960 boys sought evaluation from the athletic trainer at the Boys National Hard Court Championships for new or recurrent shoulder pain. During the same 4 years, the investigators found that 11% of the 741 girls presented to the athletic trainer or physician for evaluation of new or recurrent shoulder pain.4 These epidemiologic studies clearly show the demands placed on the entire upper extremity kinetic chain.
Evaluation and treatment of the tennis player with a shoulder injury requires a total upper extremity approach. An understanding of the sport-specific biomechanical demands placed on the upper extremity with tennis play is of paramount importance. The goal of this chapter is to outline the inherent muscle-activity patterns and joint kinematics in tennis. The specific anatomic upper extremity adaptations found in musculoskeletal evaluation and research in tennis players are presented, followed by application of this information to treatment of the tennis player with overuse shoulder injury.
Most injuries to the shoulder in tennis players are classified as overuse5 and involve the rotator cuff or biceps tendon, or both.6 Because of the overhead nature of the tennis serve, the rotator cuff and biceps tendon can be placed in a compromised position between the humeral head and coracoacromial arch, resulting in subacromial impingement.7,8 This has been shown to be accentuated by posteroinferior capsular tightness and posterior muscle tendon unit tightness.9,10,11 Posteroinferior capsular tightness and posterior muscle tendon unit inflexibility, often seen in tennis players and throwing athletes, can manifest with glenohumeral internal rotation deficit (GIRD).12 With posterior shoulder tightness, externally rotating the abducted arm causes the humeral head to shift posterosuperiorly, resulting in impingement of the rotator cuff and bursa between the humeral head and acromion.
EPIDEMIOLOGY AND CAUSE In a survey of 84 world-class tennis players, Priest and Nagel1 reported that 74% of men and 60% of women had a history of shoulder or elbow pain in the dominant arm that affected tennis play. Injuries to both the shoulder and elbow of the dominant arm were reported by 21% and 23% of the world-class male and female players, respectively. Another survey by Priest and colleagues2 of 2633 recreational tennis players found the incidence of tennis elbow to be 31%. One specific finding was the 63% greater incidence of shoulder injury among players reporting tennis elbow injury. Hutchinson studied the USTA Boys Tennis Championships for 6 years to determine the incidence and distribution of injury in these 14- to 18-year-olds.3 He found the shoulder the third most commonly injured region of the body, accounting for 8% of injuries.3 Safran and Hutchinson studied participants at the Girls 16s National Hard Court Championships and the Boys 16s and 18s National Hard
Reports by Walch and colleagues13 and others14,15 have demonstrated how the position of 90 degrees of glenohumeral joint abduction with external humeral rotation can cause direct contact between the undersurface of the rotator cuff and the posterior superior labrum and glenoid, resulting in posterior or undersurface impingement. 429
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Although this can occur normally,16 there are two theories about how this posterior or undersurface impingement can be exacerbated by anterior glenohumeral joint instability: suboptimal overhead throwing or serving biomechanics, termed the hyperangulation phenomenon,12 and posterior shoulder tightness. The progression of shoulder impingement from tendinitis to partial-thickness and full-thickness tearing of the rotator cuff has been reported in the literature as well.7,17 Superior labrum anterior-posterior (SLAP) lesions also occur more commonly in tennis players.18 There are two leading theories of the cause of SLAP lesions in tennis players. The first is posterior shoulder tightness. As the shoulder is externally rotated in abduction, the posterosuperior humeral head translation leads to a peeling off of the posterosuperior labrum.12 The second is related to the repeated external and internal rotation of the shoulder, and thus biceps tendon, around its anchor, with applied tension leading to the superior labrum pulling off the glenoid.18 Posterior capsular tightness has also been implicated in another common finding in tennis players: infraspinatus atrophy due to suprascapular nerve injury. The suprascapular nerve can become injured, particularly as it passes through the spinoglenoid notch. There are many hypotheses as to the pathophysiology of this nerve injury. One leading theory relates to compression of the nerve as it passes around the base of the spine of the scapula. The spinoglenoid ligament can insert into the posterior glenohumeral capsule. In abduction and internal rotation, this ligament increases tension. This increased tension can lead to intermittent compression of the suprascapular nerve, resulting in injury to the nerve and atrophy of the muscle.19 In addition to the mechanical impingement model, recent reports have focused on the intrinsic tendon overload20,21 from the high-intensity decelerative function of the posterior rotator cuff and anterior shoulder instability17 as the primary mechanisms for shoulder overuse injury in the overhead athlete. Anterior instability of the glenohumeral joint can be caused by insufficiency of the static (inferior glenohumeral ligament and anterior inferior glenoid labrum) and dynamic (rotator cuff complex) stabilizers.17 Progressive attenuation of the static stabilizers is reported with overhead activities such as the tennis serve and overhand throw.21 The increased role of the dynamic stabilizers of the glenohumeral joint can lead to microtraumatic tendon injury and further compromise joint stability and overhead function. It is the challenge of the rehabilitation professional to enhance the dynamic stabilizers of the shoulder without compromising the static stabilizing mechanisms. The enhancement of the dynamic stabilizers is particularly
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challenging during prevention and treatment of overuse shoulder injury in the tennis player because of the physiologic and anatomic demands caused by repetition and high-velocity decelerative function required for biomechanically acceptable tennis play. Additionally, for prevention and rehabilitation, it is imperative for the rehabilitation professional to eliminate the glenohumeral internal rotation deficit. A review of the epidemiology of shoulder injuries in recreational and highly skilled tennis players is presented in Table 35-1. Table 35-1 shows the incidence of shoulder injuries, which is defined as the number or percentage of shoulder injuries sustained over a defined time, and the prevalence of shoulder injuries, which is defined as the percentage of people with past or present shoulder complaints when asked at a specific time.
ANALYSIS OF THE SHOULDER JOINT IN TENNIS-SPECIFIC MOVEMENTS Muscular Activity Patterns The high-velocity dynamic muscle contractions in the tennis serve and ground strokes have been studied in minimally skilled and elite-level tennis players. Yoshizawa and colleagues27 recorded the peak and median muscular activity patterns of the shoulder and forearm muscles during the serve and ground strokes. They found significantly higher muscular activity levels during the serve, indicating that it is the most strenuous stroke in tennis from the standpoint of upper-extremity muscles. The serve can be broken down into four phases: wind-up, cocking, acceleration, and follow-through. The wind-up phase is characterized by the initiation of the serving stance to the toss of the ball by the contralateral extremity. There is very low electromyogram (EMG) activity during this phase in the muscles surrounding the shoulder.28 The cocking phase begins after the ball toss and terminates at the point of maximal external rotation of the glenohumeral joint of the racquet arm. Muscular activity during this phase is moderately high in the supraspinatus, infraspinatus, subscapularis, biceps brachii, and serratus anterior. Muscular activity levels expressed as a percentage of the maximum voluntary isometric contraction (MVIC) were 53% for the supraspinatus, 41% for the infraspinatus, 25% for the subscapularis, 39% for the biceps, and 70% for the serratus.28 The stabilizing and approximating role of the rotator cuff identified by Inman and colleagues29 is clearly shown in the cocking phase of the tennis serve. The moderately high activity during this phase shows the importance of both anterior and posterior rotator cuff strength as well as scapular stabilization for proper execution of the required mechanics.
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TABLE 35-1 Shoulder Injuries in Tennis Players Population
Age (years)
Sample Size
Incidence (%)
Source
Male
14-18
1440
8
Hutchinson et al
Male
14-18
960
14
Safran and Hutchinson
Female
14-16
741
11
Safran and Hutchinson
All
16-20
—
8
Reece et al
14-48
104
17
Winge et al
—
2481
9
Nigg et al
10-60⫹
260
8
Kamien
14-18
480
24
Safran and Hutchinson
Incidence ELITE JUNIORS
Others
Danish elite professionals Competitive Competitive and recreational Prevalence ELITE JUNIORS
Male Female
14-16
370
35
Safran and Hutchinson
All
11-14
97
14
Kibler et al
All
12-19
24
Lehman
OTHER
Competitive Recreational adults
14-63
534
36
Hang and Peng
25-55⫹
2633
7
Priest et al
Hang YS, Peng SM: An epidemiological study of upper extremity injury in tennis players with a particular reference to tennis elbow. J Formosan Med Assoc 83:307-316, 1984. Hutchinson MR, LaPrade RF, Burnett QM II, et al: Injury surveillance at the USTA boys’ tennis championships: A 6 year study. Med Sci Sports Exer 27: 826-830, 1995. Kamien M: The incidence of tennis elbow and other injuries in tennis players at the Royal Kings Park Tennis Club of Western Australia from October 1983 to September 1984. Aust J Sci Med Sport 21:18-22, 1989. Kibler WB, McQueen C, Uhl T: Fitness evaluation and fitness findings in competitive junior tennis players. Clin Sports Med 7:403-416, 1988. Lehman RC: Shoulder pain in the competitive tennis player. Clin Sports Med 7:309-327, 1988. Nigg BM, Frederick EC, Hawes MR, Luethi SM: Factors influencing short term pain and injuries in tennis. Int J Sport Biomech 2:156-165, 1986. Priest JD, Braden V, Gerberich SG: The elbow and tennis. I. An analysis of players with and without pain. Phys Sports Med 8:81-91, 1980. Reece LA, Fricker PA, Maguire KF: Injuries to elite young tennis players at the Australian Institute of Sport. Australian J Sci Med Sport 18:11-15, 1986. Safran MR, Hutchinson MR: Unpublished data, 1995. Winge S, Jorgensen U, Nielsen AL: Epidemiology of injuries in Danish championship tennis. Int J Sports Med 10:368-371, 1989.
The third phase of the tennis serve is acceleration. This phase begins at maximal external rotation and terminates at ball impact. Consistent with EMG recordings during the acceleration phase of throwing,30 high muscular activity was found in the pectoralis major, subscapularis and lattisimus dorsi, and serratus anterior during the forceful concentric internal rotation of the humerus.28 EMG research published by Van Gheluwe and Hebbelinck31 using intermediate tennis players and by Miyashita and colleagues32 using skilled and unskilled tennis players also found high activity levels of the pectoralis major, as well as the deltoid, trapezius, and triceps, during the acceleration phase. Both reports showed a relative silence of electrical activity in the accelerating musculature during impact, and peak levels of muscular activity occurred just before impact. One
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exception is the stabilizing contribution of the infraspinatus, which remained active during impact.31 The fourth phase, the follow-through, occurs after impact. This phase is characterized by moderately high activity of the posterior rotator cuff, serratus anterior, biceps brachii, deltoid, and latissimus dorsi. After the electrical silence of the shoulder musculature during impact or collision,31,32 forceful eccentric muscle contraction is necessary to decelerate the humerus and maintain glenohumeral joint congruity. A relatively consistent pattern of muscular activity is reported for skilled tennis players. The presence of increased, as well as overlapping, muscular activity patterns across the outlined stages in the tennis serve has been reported by untrained27 and less-skilled32 tennis players. This increase
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in the muscular contribution during the serving motion in less-skilled players is a perfect example of how nonoptimal timing and a lack of whole-body contributions to force generation and deceleration subject a player’s shoulder to overuse injury. The contribution of the larger muscle groups in the lower extremities and trunk via proper biomechanical energy transfer during the tennis serve protect the player from injury and optimize performance.33-36
Application of the Kinetic-Chain Concept in Serving Biomechanics The roles of other body segments and their effects on the shoulder and elbow during the tennis serve were studied by Elliott and colleagues.37 They measured kinetic and kinematic variables of the serve in professional tennis players and characterized them as having either an effective leg drive (maximal front knee flexion angle ⬎14.7 degrees) or an ineffective leg drive (maximal front knee flexion ⬍14.7 degrees). Most important from an injury-prevention perspective was the finding of significantly greater medial elbow loading (varus elbow torque 3.9% vs. 5.3%) when comparing the group with greater knee flexion to the group with less knee flexion.37 Additionally, the group with a more effective leg drive showed reduced shoulder internal rotation torques when the shoulder was placed in maximal external rotation than the group of elite players who had less leg drive during their serving motion.37 This study shows the importance of using the entire kinetic chain to produce power during the tennis serve and highlights the
A
B
C
ramifications of using a pattern of serving biomechanics for the shoulder elbow when the lower extremity and trunk are not optimally integrated. In Figure 35-1, we can see an elite player executing a tennis serve. This player’s serve has been clocked at greater than 140 mph, so we can assume this player has an effective transfer of forces. Although in the ground stroke, players transfer forces similarly, we are using the serve as an example because we can clearly see the different body parts involved in a sequential manner. Each of these body parts (or segments) in this coordinated movement is dependent upon the previous segment; otherwise, the overall swing is compromised, which could lead to decreased performance or the risk of injury. As described by Elliott,37 the motion of segments in producing high-speed tennis strokes is generally sequenced in a proximal-to-distal (legs to trunk to arm and racquet) fashion. The proper sequencing of these segments aids in the protection of the shoulder joint as well as the transfer of forces from the ground up. Assuming that the player has the proper equipment, appropriate muscle strength (power as well as endurance), and the coordinated movement described earlier, there are two other major ways to increase the speed of the racquet head during a serve: the use of elastic energy and an increase in the distance of the racquet moving to the ball. The thought behind the use of elastic energy is stretching the muscle followed by a shortening of the muscle. For
D
E
Figure 35-1. Elite tennis player serve sequence. A and B, Wind-up. C, Cocking. D, Acceleration. E, Follow-through. (Photos with permission of United States Tennis Association.).
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example, in the backswing phase of the serve, the shoulders are rotated more than the hips, stretching the muscles across the upper trunk and shoulder area.38,39 This stored energy can then provide force in the forward phase of the swing. If the athlete is not prepared through proper training, these forces could put significant stress on the shoulder joint. Proper strength exercises, particularly of the rotator cuff and scapular stabilizers, are critical for protecting the shoulder joint. Although it makes logical sense to increase the distance the racquet travels to increase the production of force, only recently have researchers and tennis-teaching professionals begun to focus on the distance between the racquet head and the trunk in the backswing. The old backscratch position is counterproductive in producing force. As Elliott37 has pointed out, leg drive forces the racquet in a downward motion and away from the back. This energy is recovered to assist in generating racquet velocity during internal rotation of the upper arm. This increase in the distance of the racquet path in the swing, use of elastic energy, and coordinated use of the kinetic link principle (proper use of the sequencing of body segments initiated by a ground reaction force) help protect the shoulder joint during repeated service actions. Research has compared the traditional service motion, where the racquet arm is brought downward below the waist as the hands separate in the preparation phase, with the abbreviated backswing motion that the player in Figure 35-1 uses, where the racquet is not brought into the downward position in an abbreviated movement pattern. Elliott and colleagues37 and Kibler and colleagues40 have both shown no significant differences in either shoulder or elbow loads comparing the traditional backswing with the abbreviated backswing in players who use proper leg drive. Use of the abbreviated technique in the absence of proper kinetic chain involvement can subject the upper limb to abnormal physiologic loads, however, leading to potential shoulder and upper-extremity injury.
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The follow-through phase of the forehand ground stroke produced moderately high activity of the serratus anterior, subscapularis, infraspinatus, and biceps musculature.28 The continued activity of the infraspinatus was evident during impact and continued into the follow-through phase of the forehand ground stroke.31 Follow-through activity during the backhand was moderately high in the biceps, middle deltoid, supraspinatus, and infraspinatus, but this level of activity was significantly lower than during the acceleration phase. One of the primary changes in the modern game of tennis is the use of lower-extremity open stances.38 An openstance forehand is depicted in Figure 35-2 and shows how, in contrast to more traditional closed or square stances, where the entire body is perpendicular or sideways to the net, the open stance is characterized by the feet being essentially parallel to the net or baseline.38,39 Despite the placement of the feet parallel to the baseline, the shoulders remain rotated such that the degree of separation between the hips and shoulders is optimized. This enables the player to use greater levels of angular momentum during the stroke and facilitates this rotation during the execution of the stroke. This segmental rotation, however, can be a liability when premature opening of the pelvis and early rotation of the shoulders leads to arm lag and hyperangulation at the shoulder joint.38,41,42 This premature opening, similar to that seen in baseball pitchers, can lead to shoulder injury and requires biomechanical intervention to prevent more serious injury and optimize technique.
Joint Kinematics To further understand the demands placed on the upper extremity, shoulder joint angular velocities and ranges of motion incurred during tennis play are analyzed. Angular velocities incurred during the serving motion necessitate high-velocity muscular stabilization (discussed earlier). Biomechanical study of the tennis serve has produced data measuring the speed of internal rotation of the humerus
Ground Strokes The forehand and backhand ground strokes can be broken down into three phases: preparation, acceleration, and follow-through. EMG activity during the preparation phases of both the forehand and backhand is relatively low. Acceleration during the forehand involves very high activity in the subscapularis of 102% of maximum voluntary isometric contraction (MVIC), in the biceps brachii of 86%, in the pectoralis major of 85%, and in the serratus anterior of 76%.28 Acceleration during the backhand stroke consists of high muscular activity levels in the middle deltoid of 118% MVIC, in the supraspinatus of 73%, and in the infraspinatus of 78%.28 The serratus anterior and biceps musculature was active during acceleration for both the forehand and backhand strokes.
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Figure 35-2. Open stance forehand technique.
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during acceleration. Shapiro and Stine36 filmed 14 highly skilled male tennis players and reported a maximum internal rotation velocity of 1074 to 1514 deg/sec. Slightly faster velocities were reported by Dillman43 in a pilot study of professional tennis players with maximal internal rotation velocities up to 2300 deg/sec. Comparable velocities of internal rotation during the acceleration phase of throwing have been reported to exceed 7000 deg/sec.18
the stroke.34 The close association between pronation of the forearm and internal rotation of the shoulder has been reported during the serve.49 Distal upper extremity pronatory acceleration and internal rotation compensation to incorrectly produce topspin increase the demand on the posterior rotator cuff musculature during the followthrough as the external rotators contract to counteract the internally rotating humerus after impact.
Demands placed on the dominant shoulder during the tennis serve are also high with respect to range of motion. Dillman43 reported maximal external rotation values of 154 degrees. Abduction angles at the shoulder in elite Australian players were reported to average 83 degrees during the cocking phase when elbow flexion was 90 degrees.44
Angular velocities of external rotation during the backhand stroke in highly skilled tennis players range between 328 and 1640 deg/sec.36 Rotation of the shoulders into a position perpendicular to the net is of vital importance to optimize the contribution of torso rotation and lower extremity input to generation of force.48 A two-handed backhand has been recommended for players with upper extremity injury, particularly tennis elbow, because the force is generated and the load is shared by both upper extremities.50
These range-of-motion characteristics have definite implications for overuse shoulder injury. Repeated maximal external rotation during the cocking phase of the tennis serve produces adaptations of the glenohumeral joint range of motion on the dominant arm.45,46,47 Greater external rotation of the glenohumeral joint might come at the expense of anterior capsular attenuation and is similar to the range of motion and anterior laxity patterns found in highly skilled baseball players.21 The degree of glenohumeral joint abduction during cocking and acceleration is of prime importance in executing a proper mechanical serve. Increases in glenohumeral joint abduction can lead to placement of the shoulder in a position of subacromial impingement. Initial observation of a highly skilled player’s service motion shows an apparent vertical orientation of the arm to contact the ball overhead. Closer observation reveals that highly skilled players have significant contributions from lateral flexion of the contralateral trunk and abduction of the scapula. These components allow a mid range of glenohumeral joint abduction throughout the four phases of the tennis serve.
ANATOMIC ADAPTATIONS OF THE DOMINANT SHOULDER Postural A characteristic postural adaptation that Priest and Nagel1 found in the clinical evaluation of 84 world-class tennis players is drooping or depression of the dominant shoulder. Priest and Nagel believe that the eccentric stretching of the posterior shoulder and scapular musculature and the increased weight of the playing arm because of muscular hypertrophy cause this adaptation. Presence of the tennis shoulder was reported in all 56 senior tennis players evaluated by Kulund and colleagues.51 The competitive players in their study had an average of more than 50 years of playing experience and ranged in age from 60 to 85 years. Figure 35-3 shows two elite-level players who demonstrate the characteristic depressed dominant shoulder.
Analysis of joint angular velocities during forehand ground strokes shows maximal internal rotation at the shoulder to be between 364 and 746 deg/sec.36 This finding has implications for determining appropriate exercises for preventing and rehabilitating shoulder injuries. Groppel33,48 outlined the rationale and methodology for generating topspin to the forehand ground stroke. Topspin is a desired characteristic used to improve both velocity and control of a shot and has been taught by coaches by emphasizing a low backswing during preparation and a high follow-through. This creates a low-to-high stroke path. This technique requires proper timing and proper positioning and preparation of body segments.35 Many unskilled and intermediate players use a method of rolling over the ball to achieve topspin. This effect increases the pronatory influence of the distal upper extremity and also increases internal rotation acceleration during
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Figure 35-3. Characteristic postural adaptation of two elite players. The player on the left is left-hand dominant and the player on the right is right-hand dominant.
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The downward rotation of the scapula and resultant change in glenoid and acromial positioning might have implications for injury with repeated elevation of the glenohumeral joint. No definitive relationship has been formed regarding this postural adaptation and shoulder injury.
Anthropometric Circumferential measures are commonly used in sports science research to determine externally the presence of hypertrophic muscular development through bilateral comparisons. In a study of 84 world-class players, Chinn and colleagues52 found significantly greater dominant arm proximal humerus girth when compared bilaterally for male and female players. Similar results are reported by Vodak and colleagues53 in 50 middle-aged above-average players. A study of Australian elite junior male and female tennis players found greater upper arm circumference on the dominant arm in female tennis players, with no significant difference between extremities in the male tennis players.54 Muscular adaptation of the dominant arm at both distal and proximal margins supports the EMG findings of dynamic repetitive muscular work required for successful tennis play.
Range of Motion The kinematic analysis presented earlier in this chapter showed the large arcs of humeral rotation required for highly skilled tennis players’ stroke execution. Several clinical studies have presented active range-of-motion measures of the shoulder in elite tennis players. Chandler and colleagues45 measured active range of motion of the shoulder internal and external rotators in 90 degrees of abduction in 86 junior elite tennis players between the ages of 12 and 21 years. They found significantly less mean internal-rotation range in the dominant arm compared with the nondominant arm (65 vs 76 degrees). The dominant shoulder had only slightly greater external-rotation active range of motion (100 vs 103 degrees). Similar findings were reported by Ellenbecker46 in an earlier study of 26 elite junior players ages 11 to 14 years measured at 90 degrees of abduction with scapular stabilization. Significantly greater external rotation was found on the dominant arm of male tennis players only, and both male and female players as young as 11 years showed less internal-rotation active range of motion on the dominant arm. A more recent study by Ellenbecker and colleagues47 again measured humeral rotation with scapular stabilization in elite junior tennis players and professional baseball pitchers. This study also compared humeral rotation using the totalrotation range-of-motion concept. Simply stated, this totalrotation range of motion is obtained by summing the external and internal-rotation measures to obtain a combined or composite total of humeral rotation. The findings of this
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study showed the professional baseball pitchers had greater dominant arm external rotation and significantly less dominant arm internal rotation when compared with the contralateral nondominant or nonthrowing side. The total-rotation range of motion, however, was not significantly different between extremities in the professional baseball pitchers (145 degrees dominant arm, 146 degrees nondominant arm) (Table 35-2). This research showed that despite bilateral differences in the actual internal or external-rotation range of motion in the glenohumeral joints of baseball pitchers, the total arc of rotational motion remained the same.47 In contrast, Ellenbecker and colleagues47 tested 117 elite male junior tennis players. In the elite junior tennis players, significantly less internal-rotation range of motion was found on the dominant arm (45 degrees versus 56 degrees), as well as significantly less total-rotation range of motion on the dominant arm (149 degrees versus 158 degrees) The total-rotation range of motion did differ between extremities (see Table 35-2). Approximately 10 degrees less total-rotation range of motion can be expected in the dominant arm of the uninjured elite junior tennis player, as compared with the nondominant extremity; however, differences of greater than 10 degrees should be cautiously monitored, because healthy uninjured elite players from this study had total-rotation range-of-motion bilateral comparisons within the 10-degree range of their contralateral side. Humeral rotation measured with scapular stabilization is an important part of the evaluation of the elite tennis player during rehabilitation and during preventive screening evaluation (see Table 35-2).41,42
TABLE 35-2 Bilateral Comparison of Humeral Rotation in Professional Baseball Pitchers and Elite Junior Tennis Players Dominant Arm (Mean ± SEM)
Nondominant Arm (Mean ± SEM)
External rotation (deg)
103.2 ± 9.1 (1.34)
94.5 ± 8.1 (1.19)
Internal rotation (deg)
42.4 ± 15.8 (2.33)
52.4 ± 16.4 (2.42)
Total rotation (deg)
145.7 ± 18.0 (2.66)
146.9 ± 17.5 (2.59)
Subject Baseball Pitchers
Elite Junior Tennis Players External rotation (deg)
103.7 ± 10.9 (1.02)
101.8 ± 10.8 (1.01)
Internal rotation (deg)
45.4 ± 13.6 (1.28)
56.3 ± 11.5 (1.08)
Total rotation (deg)
149.1 ± 18.4 (1.73)
158.2 ± 15.9 (1.50)
SEM, standard error of the mean.
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Use of normative data from population-specific research such as this study can assist clinicians in interpreting normal range-of-motion patterns and identify when sportspecific adaptations or clinically significant maladaptations are present. Clinical application of the total-rotation rangeof-motion concept is best demonstrated by a case presentation of a unilaterally dominant upper extremity athlete. If, during the initial evaluation of an elite junior tennis player, the clinician finds a range-of-motion pattern of 120 degrees of external rotation and only 30 degrees of internal rotation, that might or might not represent a range-of-motion deficit in internal rotation that requires rehabilitation with stretching and specific mobilization. However, if measurement of that patient’s nondominant extremity rotation reveals 90 degrees of external rotation and 60 degrees of internal rotation, the current recommendation based on the total-rotation range-of-motion concept would be to avoid extensive mobilization and passive stretching of the dominant extremity, because the total-rotation range of motion in both extremities is 150 degrees (120 degrees’ external rotation ⫹ 30 degrees’ internal rotation ⫽ 150 degrees in the dominant arm; 90 degrees’ external rotation and 60 degrees’ internal rotation ⫽ 150 degrees of total rotation in the nondominant arm). In elite-level tennis players, the total active-rotation range of motion can be expected to be up to 10 degrees less on the dominant arm before a clinical treatment to address internal-rotation range-of-motion restriction would be recommended or implemented.47 This total-rotation range-of-motion concept can be used as illustrated to guide the clinician during rehabilitation, specifically in the area of application of stretching and mobilization, to best determine what glenohumeral joint requires additional mobility and which extremity should not have additional mobility, due to the obvious harm induced by increases in capsular mobility and increases in humeral head translation during aggressive upper-extremity exertion. The loss of internal-rotation range of motion is significant for several reasons. The relationship between internalrotation range-of-motion loss (tightness in the posterior capsule of the shoulder) and increased anterior humeral head translation has been scientifically identified.55,56 The increase in anterior humeral shear force reported by Harryman and colleagues10 was manifested by a horizontaladduction cross-body maneuver, similar to that incurred during the follow-through phase of the throwing motion or tennis serve. Tightness of the posterior capsule has also been linked to increased superior migration of the humeral head during shoulder elevation.57 Koffler and colleagues11 studied the effects of posterior capsular tightness in a functional position of 90 degrees of abduction and 90 degrees or more of external rotation in cadaveric specimens. They found, with imbrication of either the inferior aspect of the posterior capsule or imbrication of
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the entire posterior capsule, that humeral head kinematics were changed or altered. In the presence of posterior capsular tightness, the humeral head shifts in an anteriorto-superior direction, as compared with a normal shoulder with normal capsular relationships.11 With more extensive amounts of posterior capsular tightness, the humeral head was found to shift postero superiorly. These affects of altered posterior capsular tensions experimentally representing in vivo posterior glenohumeral joint capsular tightness highlight the clinical importance of using a reliable and effective measurement methodology to assess internal-rotation range of motion during examination of the shoulder. Additionally, Burkhart and colleagues12 have clinically demonstrated the concept of posteriorsuperior humeral head shear in the abducted externally rotated position with tightness of the posterior band of the inferior glenohumeral ligament. Using a population of 51 elite junior tennis players, Kibler and colleagues58 found significant improvements in shoulder internal-rotation range of motion over a 2-year period. Subjects performed regular internal-rotation stretches as part of a preventive flexibility program. The specific stretch in this study used a tennis racquet to pull the extremity up the back in the combined movement of internal-rotation and shoulder-extension position. Other stretches used and recommended to improve internal rotation include the cross-arm adduction stretch and side-lying sleeper stretch.42 Research has found the cross-arm stretch to be superior to the sleeper stretch in increasing internalrotation range of motion.59 However, we recommend the use of both the cross-arm and the sleeper stretch before and after tennis play to provide a stretch to the posterior capsule and posterior muscle tendon units. Knudson60 has studied the effects of a static shoulder stretching program immediately before maximal effort tennis-serve performance in skilled players. Knudson60 found no increase or decrease in serve performance measured via maximal and average serve velocity immediately following a static-stretching program for the shoulder girdle.
Strength Objective measurement of shoulder strength has been performed in elite and recreational tennis players.46,61-63 Concomitant with range of motion, specific relationships in shoulder strength have been identified in the tennis player that have implications for the development of preventive and rehabilitative exercise programs. Ellenbecker62 used a Cybex II isokinetic dynamometer to measure shoulder internal and external rotation and flexion and extension in 22 highly skilled male adult tennis players. Ellenbecker found significantly greater internal
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isokinetic exercise was performed on a KinCom using 22 collegiate tennis players.61 Results of pre- and posttesting showed statistically significant increases in concentric and eccentric internal-rotation and externalrotation strength in the concentric training group. Subjects in this group also showed a significant increase in maximum serve velocity. The eccentric isokinetic training group also showed significant increases in concentric internal-rotation and external-rotation strength but did not show eccentric strength gains or an increase in functional performance. Similar findings were reported by Mont and colleagues65 using an identical research paradigm. Results from these studies provide a rationale for including isokinetic training of the rotator cuff in rehabilitation and preventive conditioning.
rotation, extension, and flexion in the dominant arm compared with the nondominant arm. No difference between extremities was found in shoulder external rotation. Significantly lower external- and internal-rotation unilateral strength ratios were reported for the dominant arm, showing a relative external-rotation strength deficit on the tennis-playing shoulder. Similar research by Ellenbecker,46 Chandler and colleagues,45 and Koziris and colleagues63 found similar results of greater internalrotation muscular strength on the dominant extremity and no significant difference between extremities in external rotation strength. Table 35-3 displays the most recent data from a larger population of 147 elite junior tennis players by Ellenbecker and Roetert.64 These data are presented for ratios of peak torque to body weight and work to body weight as well as the external-rotation and internal-rotation unilateral strength ratios.
The isokinetic research presented in this chapter clearly shows specific patterns found in the dominant arm of highly skilled tennis players. Care must be taken, however, in the use of normative isokinetic strength data presented in these studies. Research has indicated that isokinetic parameters are both specific to the apparatus66,67 and specific to the position of the shoulder joint during the testing procedure.68,69
The previously reported isokinetic research assessed concentric muscular performance in 90 degrees of abduction of the rotator cuff in highly skilled tennis players. A 6-week training study of concentric or eccentric
TABLE 35-3 Isokinetic Strength Ratios in Elite Junior Tennis Players Dominant Arm
Subject
Peak Torque (%)
Nondominant Arm
Work (%)
Peak Torque (%)
Work (%)
Ratio of Peak Torque to Body Weight and Work to Body Weight* EXTERNAL ROTATION
Male, 210 deg/sec
12
20
11
19
Male, 300 deg/sec
10
18
10
17
Female, 210 deg/sec
8
14
8
15
Female, 300 deg/sec
8
11
7
12
Male, 210 deg/sec
17
32
14
27
Male, 300 deg/sec
15
28
13
23
Female, 210 deg/sec
12
23
11
19
Female, 300 deg/sec
11
15
10
13
INTERNAL ROTATION
†
Ratio of External Rotation to Internal Rotation Male, 210 deg/sec
69
64
81
81
Male, 300 deg/sec
69
65
82
83
Female, 210 deg/sec
69
63
81
82
Female, 300 deg/sec
67
61
81
77
*A Cybex 6000 series Isokinetic Dynamometer and 90 degrees of glenohumeral joint abduction were used. Data are expressed in foot-pounds per unit of body weight for external rotation and internal rotation. † A Cybex 6000 series Isokinetic Dynamometer and 90 degrees of glenohumeral joint abduction were used. Data are expressed as ratios of external rotation to internal rotation representing the relative muscular balance between the external and internal rotators. Data from Ellenbecker TS, Roetert EP: Age specific isokinetic glenohumeral internal and external rotation strength in elite junior tennis players. J Sci Med Sport 6(1):63-70, 2003.
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TREATMENT Evaluation A thorough tennis-specific subjective evaluation is indicated before treatment. This is consistent with orthopedic and sports physical therapy shoulder evaluations41,70; however, the exact relationship between the injured shoulder and tennis play must be determined. Specific questions regarding the player’s tennis history, skill level, stroke mechanics, play frequency and duration, and tournament schedule as well as current racquet type and string tension are of paramount importance.42 Consistent with most musculoskeletal overuse injuries in athletes, a change, however small, has usually been made in one or more of the aforementioned factors before the injury. Often a particular tennis stroke or phase of the stroke can be identified with the onset of injury or with exacerbation of symptoms.
Reduction of Overload and Total Arm Rehabilitation The initial goal of overuse shoulder rehabilitation includes the reduction of pain and inflammation in the involved tissues. Although many methods are appropriate, including physical therapy modalities and anti-inflammatory medications71,72 the injured extremity must be protected from further stress or overload but not from full function. Specific or complete cessation of tennis play is often indicated. Compensation by the upper extremity kinetic chain in persons with shoulder pathology can lead to overuse injury in the elbow, forearm, and wrist.50 Avoidance of overhead movements in activities of daily living and crosstraining activities is also recommended. During the initial phase of shoulder-overuse rehabilitation, stresses imparted to the injured tissues are minimized. Early stress of the distal upper extremity in the forms of isotonic eccentric and concentric elbow, forearm, and wrist exercise is indicated to preserve the important distal musculature. Adaptation of the distal upper extremity in the form of hypertrophy is a consistent finding in the dominant arm of highly skilled tennis players.52,53
Protection and Restoration of Joint Kinematics Presented earlier in this chapter were specific shoulder range-of-motion patterns in elite junior45,46,47 and adult52 tennis players. Shoulder stability must be thoroughly evaluated via assessment of the static and dynamic stabilizers to appropriately base the progression of exercise and range of motion during rehabilitation. Use of the load and shift test,41,73 subluxation relocation test,21,41 and other testing to assess the passive anterior, posterior, and inferior translation of the glenohumeral joint are integral parts in determining the cause of the overuse injury. These findings also
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provide the framework for the use or lack of use of rangeof-motion and mobilization techniques in rehabilitation. The increased external shoulder rotation and reduced internal rotation can indicate anterior capsular laxity and the potential for anterior subluxation.74 Therefore, stretching or mobilization techniques to further increase externalrotation range of motion by attenuating the anterior capsule are not indicated. Posterior capsular mobilization and stretching techniques for the posterior musculature address the lack of glenohumeral joint internal rotation and have been recommended in the treatment of unilaterally dominant upper-extremity athletes.42,75
Upper Extremity Strength Balance and Local Muscular Endurance As the inflammation and pain levels decrease in the injured tissues, early submaximal resistive exercise is initiated. As in the rehabilitation of other musculotendinous injuries, the presence or lack of pain in the joint or over the affected tendon determines the progression or regression of resistive exercise. Research on muscle activity patterns in the tennis strokes highlight concentric as well as eccentric muscle work in the rotator cuff and scapular stabilizers. Treatment of rotator cuff pathology either from primary impingement or impingement secondary to intrinsic tensile overload or joint instability necessitates specific emphasis on strengthening the dynamic stabilizers of the glenohumeral joint both concentrically and eccentrically. The force couple outlined by Inman and colleagues29 and precise function of the deltoid, infraspinatus, supraspinatus, and teres minor delineated by Weiner and MacNab76 reinforce these clinicians’ emphasis on isolated rotator cuff strengthening. Progression of the isolated rotator cuff exercises is predicated on patient signs and symptoms and begins briefly with the isometric and manual resistance mode and progresses rapidly to isotonic concentric and eccentric exercise. Initially, three to four isotonic exercises are recommended for overuse shoulder rehabilitation based on their inherent characteristics of increased rotator cuff activation reported in EMG studies.77-81 These exercises are shown in Figure 35-4 and include side-lying external rotation, prone extension, and prone horizontal abduction with external rotation and prone external rotation. These exercises are performed through a pain-free range of motion and were chosen because of noncompromising glenohumeral joint positions and high EMG activity of the rotator cuff mechanism. Moncrief and colleagues82 has studied the effectiveness of these exercises over a 4-week training period using a 15-repetition-maximum loading scheme and multiple set volume. Significant increases in glenohumeral joint internalrotation and external-rotation strength were measured following the 4-week training program. Based on these results as
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SHOULDER INJURIES IN TENNIS 1. Side-lying External Rotation: Lie on uninvolved side, with involved arm at side, with a small pillow between arm and body. Keeping elbow of involved arm bent and fixed to side, raise arm into external rotation. Slowly lower to starting position and repeat. 2. Shoulder Extension: Lie on table on stomach, with involved arm hanging straight to the floor. With thumb pointed outward, raise arm straight back into extention toward your hip. Slowly lower arm and repeat. 3. Prone Horizontal Abduction: Lie on table on stomach, with involved arm hanging straight to the floor. With thumb pointed outward, raise arm out to the side, parallel to the floor. Slowly lower arm, and repeat. 4. 90/90 External Rotation: Lie on table on stomach, with shoulder abducted to 90 degrees and arm supported on table, with elbow bent at 90 degrees. Keeping the shoulder and elbow fixed, rotate arm into external rotation, slowly lower to start position, and repeat.
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with manual contacts applied directly on the scapula and copious stabilization of the trunk to minimize compensatory muscle activation (Fig. 35-5). Application of isokinetic research on highly skilled tennis players to rehabilitation of overuse shoulder injury assists in determining the focal muscle groups necessary to obtain strength balance. The relative absence of a strength enhancement of the external rotators on the dominant shoulder of highly skilled tennis players highlights the need for specific external-rotation strength training to balance the external-rotation and internal-rotation strength relationship. Isokinetic research also shows dominant arm strength 15% to 30% greater than the nondominant arm,62 indicating a need for postinjury isokinetic strength levels to exceed the healthy, contralateral limb. Continued use of isotonic exercise with weights and elastic tubing is recommended in shoulder rehabilitation with a progression to the isokinetic form of resistance once a
Figure 35-4. Rotator cuff isotonic exercises.
well as the basic science information regarding the muscular activation characteristics of these exercises, we use and advocate a low-resistance and high-repetition format for rehabilitation and preventive condition of the shoulder in tennis players. The low-resistance and high-repetition format we use and recommend minimizes the activation of larger, prime mover muscles whose development can compromise glenohumeral joint stability83 and lead to compensatory movement patterns. This low-resistance and high-repetition format emphasizes local muscle endurance84 and will begin to prepare the athlete for the repetitive nature of the muscular work during tennis play and stroke execution. Concentric and especially eccentric biceps brachii exercise is also emphasized throughout rehabilitation. This is indicated throughout rehabilitation because of the stabilizing nature of the biceps musculature shown in the muscle activity research on tennis strokes. Increased biceps activity has also been reported in overhand throwing of patients with glenohumeral joint instability.85 Early emphasis is also given to the scapulothoracic musculature, particularly the serratus anterior, and lower trapezius force couple. Exercises using noncompromising ranges of glenohumeral joint motion and a low-resistance, high-repetition format are followed, such as rowing combinations, and closed-chain progressions86 with the scapula in the plus protracted position highlighted by the EMG research of Moesley and colleagues87 and Decker and colleagues.88 Manual scapular resistance is used immediately in the rehabilitation program for both protraction and retraction,
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A
B Figure 35-5. Manual scapular resistance. A, Protraction. B, Retraction. Clinician directly resists protraction and retraction of the scapula to increase strength of the scapular stabilizers throughout rehabilitation.
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pain-free range of motion and tolerance to isotonic exercise are shown. Initially, submaximal isokinetic exercise is used in the modified neutral position42,75,89 for internal and external rotation at intermediate contractile velocities. Specific emphasis continues on the external rotators because of their important roles in functional activities28,31 and in the maintenance of dynamic anterior glenohumeral joint stability.90 Rapid progression from intermediate to fast contractile velocities is recommended because of the fast joint kinematic characteristics of the tennis strokes.36 Progression from the modified neutral isokinetic internal and externalrotation position to the 90-degree abducted position is recommended, with tissue tolerance being the limiting factor. The functional rationale for this isokinetic training position is outlined in the earlier discussion of joint kinematics in addition to the known effectiveness of the scapular plane position for joint congruity92 and the ability of the rotator cuff to maintain dynamic stability in this position.93 Isokinetic and manual strength assessments are only two methods used in determining the patient’s readiness to return to tennis play. Isokinetic strength of the internal and external rotators equal to the contralateral limb have been one minimum criterion used by these clinicians for functional return. A goal of achieving a strength level 15% or even 20% greater on the dominant extremity is set based on the literature.46,62 In addition to the isokinetic and isotonic exercise progressions outlined in this chapter, plyometric exercises are used to simulate tennis-specific movement patterns and provide dynamic concentric and eccentric functional movement training. Plyometric exercises begin with medicine balls using simple chest pass and tosses against a rebounder system (Plyoback) mimicking the forehand and backhand ground strokes. In addition to providing a strength stimulus for the injured player, it also reconfirms the importance of trunk rotation. Progression to plyometric exercises that primarily load the posterior rotator cuff are used to determine readiness for the progression to actual tennis play and provide a functionally appropriate training stimulus.94 Figures 35-6 and 35-7 show two plyometric exercises that use the characteristic position of 90 degrees of abduction and 90 degrees of external rotation. A 0.5- to 1-kg medicine ball or soft weight (Hygenic Corp, Akron, Ohio) is used with these exercises to allow explosive muscular contraction without compensation from larger muscle groups. Multipleset, high-volume exercise is targeted, with sets of 20 to 30 seconds applied with these two plyometric exercises. Any localized shoulder discomfort or pain is a contraindication and results in immediate modification of the resistive
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Figure 35-6. The 90/90 prone plyometric exercise for posterior rotator cuff strengthening. The athlete holds a 0.5- to 1-kg medicine ball or soft weight and moves the arm into 90 degrees of abduction and 90 degrees of external rotation. The athlete rapidly drops and catches the ball for sets of 30 seconds. The ball only moves 2-3 inches up and down during the rapid dropping and catching motion used in this exercise.
exercise progression to lighter loads, less-challenging glenohumeral positions, and shortened ranges of motion. Successful completion of the resistive exercise progression with full normalized glenohumeral joint range of motion and capsular tensile relationships as well as normalized scapulohumeral rhythm are all prerequisites for the return to a tennis program.
Return to Functional Activity Analysis of the patient’s objective strength, range of motion, and clinical examination status ultimately determine the return to tennis play. For example, returning an elite player to tennis practice with a 20% deficit in external rotation, a positive subluxation relocation sign, or positive impingement sign ultimately will result in an unsuccessful trial of the interval tennis program and setbacks and possible reaggravation of the injury. Successful completion of a supervised rehabilitation program must occur before beginning an interval tennis program. A submaximal and graded return to tennis is used and is similar to the interval return programs for throwing.18,95 The initial trial of tennis play includes stroke simulation without ball contact and forehand and backhand ground stroke execution with a lightweight foam ball. Proper stroke mechanics are emphasized throughout the interval tennis program. Once a tolerance has been shown with stroke simulation and foam ball contact, the patient is progressed to a standard tennis ball.42 The basic concept applied in the interval tennis program is the progression from situations with low or decreased preimpact ball velocity to situations with functional preimpact ball velocity.42 Application of this concept is evidenced
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A
Once several trials of pain-free ground strokes are achieved, the forehand and backhand volley are initiated. Repetitions of ground strokes and volleys used in the early stages of the interval program are as low as 15 to 30, with gradual progression as signs and symptoms allow. Pain-free execution of volleys and ground strokes is a prerequisite for progression to the serve and overhead smash. Ellenbecker42 gives a more complete description of the authors’ interval tennis program. A submaximal trial is initiated with the serving motion using stroke simulation and foam ball impact. Initial velocity on progression to a standard tennis ball is as low as 30% to 40% of preinjury levels. The player’s velocity and serving repetitions are gradually increased as muscular strength and endurance and subjective tolerance allow. The player’s equipment should be evaluated during the return to tennis. Research indicates that lower string tensions allow greater postimpact ball velocity96 and hence greater power with lower stroke effort from the player. Lowering the racquet’s string tension by several pounds has been recommended in the treatment of tennis elbow.50,71,72 Although a definitive relationship between racquet head size or stiffness and upper extremity injury
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Figure 35-7. The 90/90 reverse-catch plyometric exercise. The athlete prepares to catch a 0.5- to 1-kg medicine ball or soft weight with the arm in 90 degrees of external rotation. (A) A partner tosses the ball from behind the athlete and the athlete catches the ball moving the arm into internal rotation keeping the shoulder in 90 degrees of abduction. (B) The athlete then throws the ball forcefully back to the partner.
B
by the initiation of ground stroke execution from the baseline via ball feeds hit by a partner from the net. This initial activity is built on by progressing to controlled baselineto-baseline rallying with forehand and backhand ground strokes. Partner feeding from the net ensures a controlled and slower preimpact ball velocity, which minimizes impact stress to the injured extremity. A backboard is not initially used because of the fast and continual rebound characteristics that encourage continued, uninterrupted muscle work in the upper extremity.
441
has not been delineated, sports medicine professionals have recommended a midsize racquet head and medium flexibility rating for patients with lateral and medial epicondylitis.71,97 Optimal racquet grip size has been discussed relative to upper extremity injury and muscle activity.98 Proper grip size was described by Nirschl,72 using a measurement from the distal tip of the ring finger along the radial border to the proximal palmar crease.
SUMMARY Thorough knowledge of the mechanical and physiologic demands and subsequent sport-specific adaptations in the upper extremity of the tennis player are required for optimal rehabilitation and performance enhancement. Implementation of the total arm strength program presented in this chapter, integrated with proper stroke mechanics and equipment, are critical components of rehabilitating and preventing overuse shoulder injuries in the tennis player.
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6. Reece LA, Fricker PA, Maguire KF: Injuries to elite young tennis players at the Australian Institute of Sport. Australian J Sci Med Sport 18:11-15, 1986. 7. Bigliani LU, Kimmel J, McCann PD, Wolfe I: Repair of rotator cuff tears in tennis players. Am J Sports Med 20: 112-117, 1992. 8. Neer CS: Impingement lesions. Clin Orthop Relat Res (173):70-77, 1983. 9. Grossman MG, Tibone JE, McGarry MH, et al: A cadaveric model of the throwing shoulder: A possible etiology of superior labrum anterior-to-posterior lesions. J Bone Joint Surg Am 87: 824-831, 2005. 10. Harryman DT, Sidles JA, Clark JM, et al: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334-1343, 1990. 11. Koffler KM Bader D, Eager M, et al: The effect of posterior capsular tightness on glenohumeral translation in the latecocking phase of pitching: A cadaveric study. Abstract (SS-15) presented at Arthroscopy Association of North America Annual Meeting, Washington, DC, April, 2001. 12. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology Part I: Pathoanatomy and biomechanics. Arthroscopy 19(4): 404-420, 2003. 13. Walch G, Boileau P, Noel E, Donell ST: Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: An arthroscopic study. J Shoulder Elbow Surg 1:238-245, 1992. 14. Halbrecht JL, Tirman P, Atkin D: Internal impingement of the shoulder: Comparison of findings between the throwing and nonthrowing shoulders of college baseball players. Arthroscopy 15(3):253-258, 1999. 15. Paley KJ, Jobe FW, Pink MM, et al: Arthroscopic findings in the overhand throwing athlete: Evidence for posterior internal impingement of the rotator cuff. Arthroscopy 16(1):35-40, 2000. 16. Jobe CM: Superior glenoid impingement. Orthop Clin North Am 28(2):137-143, 1997. 17. Jobe FW, Kvitne RS: Shoulder pain in the overhand or throwing athlete: The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18:963-979, 1989. 18. Andrews JR, Kupferman SP, Dillman CJ: Labral tears in throwing and racquet sports. Clin Sports Med 10:901-911, 1991. 19. Safran MR: Peripheral nerve injuries about the shoulder: Part I: Suprascapular nerve, axillary nerve. Current concepts review. Am J Sports Med 32(3):803-819, 2004. 20. Nirschl RP: Shoulder tendinitis. In Pettrone FA (ed): AAOS Symposium on Upper Extremity Injuries in Athletes. St. Louis, Mosby, 1986, pp 332-337. 21. Jobe FW, Bradley JP: The diagnosis and nonoperative treatment of shoulder injuries in athletes. Clin Sports Med 8:419-438, 1989. 22. Nigg BM, Frederick EC, Hawes MR, Luethi SM: Factors influencing short term pain and injuries in tennis. Int J Sport Biomech 2:156-165, 1986. 23. Kamien M: The incidence of tennis elbow and other injuries in tennis players at the Royal Kings Park Tennis Club of Western Australia from October 1983 to September 1984. Aust J Sci Med Sport 21:18-22, 1989. 24. Kibler WB, McQueen C, Uhl T: Fitness evaluation and fitness findings in competitive junior tennis players. Clin Sports Med 7:403-416, 1988.
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25. Hang YS, Peng SM: An epidemiological study of upper extremity injury in tennis players with a particular reference to tennis elbow. J Formosan Med Assoc 83:307-316, 1984. 26. Lehman RC: Shoulder pain in the competitive tennis player. Clin Sports Med 7:309-327, 1988. 27. Yoshizawa M, Itani T, Jonsson B: Muscular load in shoulder and forearm muscles in tennis players with different levels of skill. In Jonsson B (ed): Biomechanics. Champaign, Ill, Human Kinetics, 1987, pp 621-627. 28. Rhu KN, McCormick J, Jobe FW, et al: An lectromyographic analysis of shoulder function in tennis players. Am J Sports Med 16:481-485, 1988. 29. Inman VT, Saunders JB, Abbott LC: Observations on the function of the shoulder joint. J Bone Joint Surg 26:1-30, 1944. 30. Bradley JP, Tibone JE: Electromyographic analysis of muscle action about the shoulder. Clin Sports Med 10:789-805, 1991. 31. Van Gheluwe B, Hebbelinck M: Muscle actions and ground reaction forces in tennis. Int J Sport Biomech 2:88-99, 1986. 32. Miyashita M, Tsunoda T, Sakurai S, et al: Muscular activities in the tennis serve and overhand throwing. Scand J Sports Sci 2:52-58, 1980. 33. Groppel JL: Tennis for Advanced Players and Those Who Would Like to Be. Champaign, Ill, Human Kinetics, 1984. 34. Groppel JL: The utilization of proper racket sport mechanics to avoid upper extremity injury. In Pettrone FA (ed): AAOS Symposium on Upper Extremity Injuries in Athletes. St. Louis, Mosby, 1986. 35. Groppel JL: High Tech Tennis. Champaign, Ill, Human Kinetics, 1992. 36. Shapiro R, Stine RL: Shoulder rotation velocities. Technical report submitted to the Lexington Clinic, Lexington, Ken, 1992. 37. Elliott B, Fleisig G, Nicholls R, Escamillia R: Technique effects on upper limb loading in the tennis serve. J Sci Med Sport 6(1):76-87, 2003. 38. Roetert EP, Groppel J: World Class Tennis Technique. Champaign, Ill, Human Kinetics, 2001. 39. Segal DK: Tenis Sistema Biodinamico. Buenos Aires, Argentina, Tenis Club Argentino, 2002. 40. Seeley MK, Uhl TL, McGinn PA, et al: A comparison of muscle activation patterns during traditional and abbreviated tennis serves. J Appl Biomech (accepted for publication 2008). 41. Ellenbecker TS: Clinical Examination of the Shoulder. Philadelphia, WB Saunders, 2004. 42. Ellenbecker TS: Shoulder Rehabilitation: Non-Operative Treatment. New York, Thieme, 2006. 43. Dillman CJ: The upper extremity in tennis and throwing athletes. Presented to the United States Tennis Association National Meeting, Tucson, Arizona, March, 1991. 44. Elliot B, Marsh T, Blanksby B: A three dimensional cinematographic analysis of the tennis serve. Int J Sport Biomech 2:260-271, 1986. 45. Chandler TJ, Kibler WB, Uhl TL, et al: Flexibility comparisons of junior elite tennis players to other athletes. Am J Sports Med 18:134-136, 1990. 46. Ellenbecker TS: Shoulder internal and external rotation strength and range of motion of highly skilled junior tennis players. Isokinetics Exerc Sci 2:1-8, 1992. 47. Ellenbecker TS, Roetert EP, Bailie DS, et al: Glenohumeral joint total rotation range of motion in elite tennis players and baseball pitchers. Med Sci Sports Exerc 34(12):2052-2056, 2002. 48. Groppel JL: The biomechanics of tennis: An overview. Int J Sport Biomech 2:141-155, 1986.
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49. VanGheluwe B, DeRuysscher I, Craenhals J: Pronation and endorotation of the racket arm in a tennis serve. In Jonsson B (ed): Biomechanics. Champaign, Ill, Human Kinetics, 1987, pp 667-672. 50. Nirschl RP: Tennis elbow. Prim Care 4:367-382, 1977. 51. Kulund DN, Rockwell DA, Brubaker CE: The long-term effects of playing tennis. Physician Sports Med 7:87-92, 1979. 52. Chinn CJ, Priest JD, Kent BE: Upper extremity range of motion, grip strength, and girth in highly skilled tennis players. Phys Ther 54:474-483, 1974. 53. Vodak PA, Savin WM, Haskell WL, Wood PW: Physiological profile of middle-aged male and female tennis players. Med Sci Sports Exerc 12:159-163, 1980. 54. Carlson JS, Cera MA: Cardiorespiratory, muscular strength and anthropoemetric characteristics of elite Australian junior male and female tennis players. Aust J Sci Med Sport 16:7-13, 1984. 55. Tyler TF, Nicholas SJ, Roy T, Gleim GW: Quantification of posterior capsular tightness and motion loss in patients with shoulder impingement. Am J Sports Med 28(5):668-673, 2000. 56. Gerber C, Werner CML, Macy JC, et al: Effect of selective capsulorrhaphy on the passive range of motion of the glenohumeral joint. J Bone Joint Surgery Am 85(1):48-55, 2003. 57. Matsen FA III, Arntz CT, Lippitt SB: Rotator cuff. In Rockwood CA Jr, Matsen FA III (eds): The Shoulder, 2nd ed. Philadelphia, WB Saunders, 1998, pp 755-839. 58. Kibler WB, Chandler TJ: Range of motion in junior tennis players participating in an injury risk modification program. J Sci Med Sport 6(1):51-62, 2003. 59. McClure P, Balaicuis J, Heiland D, et al: A randomized controlled comparison of stretching procedures in recreational athletes with posterior shoulder tightness [abstract]. J Orthop Sports Phys Ther 35(1):A5, 2005. 60. Knudson DV, Noffal GJ, Bahamonde RE, et al: Stretching has no effect on tennis serve performance. J Strength Cond Res 18(3):654-656, 2004. 61. Ellenbecker TS, Davies GJ, Rowinski MJ: Concentric versus eccentric isokinetic strengthening of the rotator cuff: Objective data versus functional test. Am J Sports Med 16:64-69, 1988. 62. Ellenbecker TS: A total arm strength isokinetic profile of highly skilled tennis players. Isokinetics Exerc Sci 1:9-21, 1991. 63. Koziris LP, Kraemer WJ, Triplett NT, et al: Strength imbalances in women in tennis players [abstract]. Med Sci Sports Exerc 23:253, 1991. 64. Ellenbecker TS, Roetert EP: Age specific isokinetic glenohumeral internal and external rotation strength in elite junior tennis players. J Sci Med Sport 6(1):63-70, 2003. 65. Mont MA, Cohen DB, Campbell KR, et al: Isokinetic concentric vs. eccentric training of shoulder rotators with functional evaluation of performance enhancement in elite tennis players. Am J Sports Med 22(4):513-517, 1994. 66. Francis K, Hoobler T: Comparison of peak torque values of the knee flexor and extensor muscle groups using the Cybex II and Lido 2.0 isokinetic dynamometers. J Orthop Sports Phys Ther 8:480-483, 1987. 67. Gross MT, Huffman GM, Phillips CN, Wray A: Intramachine and intermachine reliability of the Biodex and Cybex II for knee flexion and extension peak torque and angular work. J Orthop Sports Phys Ther 13:329-335, 1991. 68. Hageman PA, Mason DK, Rydlund KW, Humpal SA: Effects of position and speed on eccentric and concentric isokinetic
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testing of the shoulder rotators. J Orthop Sports Phys Ther 11:64-69, 1989. Soderberg GJ, Blaschak MJ: Shoulder internal and external rotation peak torque production through a velocity spectrum in differing positions. J Orthop Sports Phys Ther 8:518-524, 1987. Davies GJ, Gould JA, Larson RL: Functional examination of the shoulder girdle. Physician Sports Med 9:82-104, 1981. Nirschl RP, Sobel J: Conservative treatment of tennis elbow. Physician Sports Med 9:43-54, 1981. Nirschl RP: Tennis injuries. In Nicholas JA, Hershman EB (eds): The Upper Extremity in Sports Medicine. St Louis, CV Mosby, 1990, pp 827-843. Abrams JS: Special shoulder problems in the throwing athlete: pathology, diagnosis, and non-operative management. Clin Sports Med 10:839-861, 1991. Warner JJP, Micheli LJ, Arslanian LE, et al: Patterns of flexibility, laxity, and strength in normal shoulders and shoulders with instability and impingement. Am J Sports Med 18:366-375, 1990. Ellenbecker TS, Derscheid GL: Rehabilitation of overuse injuries of the shoulder. Clin Sports Med 8:583-604, 1989. Weiner DS, MacNab I: Superior migration of the humeral head. J Bone Joint Surg Br 52:524-527, 1970. Blackburn TA, McLeod WD, White B, Wofford L: EMG analysis of posterior rotator cuff exercises. Athletic Train 25:40-45, 1990. Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19:264-272, 1991. Ballantyne BT, O’Hare SJ, Paschall JL, et al: Electromyographic activity of selected shoulder muscles in commonly used therapeutic exercises. Phys Ther 73:668-682, 1993. Malanga GA, Jenp YN, Growney ES, An KN: EMG analysis of shoulder positioning in testing and strengthening the supraspinatus. Med Sci Sports Exercise 28(6):661-664, 1996. Reinhold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34(7):385-394, 2004. Moncrief SA, Lau JD, Gale JR, Scott SA: Effect of rotator cuff exercise on humeral rotation torque in healthy individuals. J Strength Cond Res 16(2):262-270, 2002. Lee SB, An KN: Dynamic glenohumeral stability provided by three heads of the deltoid muscle. Clin Orthop Relat Res (400):40-47, 2002. Fleck S, Kraemer W: Designing Resistance Training Programs. Champaign, Ill, Human Kinetics, 1987. Glousman R, Jobe FW, Tibone JE, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral joint instability. J Bone Joint Surg Am 70:220-226, 1988. Ellenbecker TS, Davies GJ: Closed Kinetic Chain Exercise: A Comprehensive Guide to Multiple Joint Exercises. Champaign, Ill, Human Kinetics, 2001. Mosely JB, Jobe FW, Pink M: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. Decker MJ, Hintermeister RA, Faber KJ, Hawkins RJ: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27:784-791, 1999. Davies GJ: A compendium of isokinetics in clinical usage. La Crosse, Wisc, S & S Publishing, 1984.
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90. Cain PR, Mutschler TA, Fu F, Lee SK: Anterior stability of the glenohumeral joint. A dynamic model. Am J Sports Med 15:144-148, 1987. 91. Elliot BC: Biomechanics of the serve in tennis: A biomedical perspective. Sports Med 6:285-294, 1988. 92. Saha AK: Mechanism of shoulder movements and a plea for the recognition of “zero position” of glenohumeral joint. Clin Orthop Relat Res (173):3-10, 1983. 93. Happee R, VanDer Helm CT: The control of shoulder muscles during goal directed movements, an inverse dynamic analysis. J Biomechanics 28(10):1179-1191, 1995.
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94. Davies GJ, Ellenbecker TS: Plyometrics redefine rehab for overhead athletes. Biomechanics 9(9):18-28, 2002. 95. Seto JL, Brewster CE, Randall CC, Jobe FW: Rehabilitation following ulnar collateral ligament reconstruction of athletes. J Orthop Sports Phys Ther 14:100-105, 1991. 96. Brody H: Physics of the tennis racquet. Am J Phys 6:482-487, 1979. 97. Ellenbecker TS, Mattalino AJ: The Elbow in Sport. Champaign, Ill, Human Kinetics, 1997. 98. Adelsberg S: The tennis stroke: An EMG analysis of selected muscles with rackets of increasing grip size. Am J Sports Med 14:139-142, 1986.
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CHAPTER 36 The Shoulder in Swimming George J. Davies, James W. Matheson, Todd S. Ellenbecker, and Robert Manske
swimmer’s shoulder. Emphasis is placed on sport-specific rehabilitation techniques, re-education in proper stroke mechanics, return to activity with an interval-swimming program, and training strategies to prevent reinjury.
Swimming has been around since ancient times. The Hittites, the Minoans, and other early civilizations left behind drawings of swimming and diving skills. In 1696, the French author Thevenot wrote The Art of Swimming. In this text, he described a type of breaststroke done with the face out of the water and an underwater arm recovery.1 Thevenot’s work became the standard swimming reference, and the breaststroke was the most common stroke for centuries. The English are considered the first modern society to develop swimming as a sport. Modern competitive swimming began in 1837 in England, where the National Swimming Society regulated competition.
EPIDEMIOLOGY OF SWIMMER’S SHOULDER Why discuss swimmer’s shoulder as one of the common sports creating shoulder-related problems? Johnson8 describes swimming as one of the most popular recreational activities; more than 100 million Americans classify themselves as swimmers. Thus, with two shoulders required for the execution of the swimming stroke, a potential patient base of 200 million shoulders is created.
In the Western world, the front crawl was first seen in a competition held in London in 1844. The crawl was swum by South American Indians, who easily defeated the British breaststroke swimmers. In the early 1900s, Britishborn Australian swimming teacher and swimmer Richard Cavill brought the front crawl swimming style of the natives of the Solomon Islands back to Australia.1 This stroke, similar to the original Native American style, was known as the Australian crawl. In 1950, its name was shortened to crawl, technically known as front crawl. It remains the fastest swimming style developed. Unlike the backstroke, butterfly, and breaststroke, the front crawl is not regulated by the Fédération Internationale de Natation (FINA) but it is universally swum in freestyle competitions. Because of this, the term “front crawl” is commonly confused with the term “freestyle.”
In addition to the historical popularity of swimming, the growth of the triathlon since the 1980s has certainly led to increased participation in swim training. Many triathletes come from strong running and biking backgrounds. To meet the requirements of triathlon competition, often these experienced athletes must take up swimming as a new activity and skill. In addition, they are taking up an activity where upper extremity strength and power are paramount, something that was not likely emphasized in their running and biking activities. The ability to crosstrain has many advantages for minimizing overuse injuries, but when factored in with the psychology of competition and inexperienced swimming techniques, it can lead to injury. Although a myriad of physiologic and anatomic issues can lead to swimmer’s shoulder, the sport of triathlon has certainly contributed to the increased incidence of this condition.
Although shoulder injury can occur because of one of the other strokes, emphasis throughout this chapter is placed on the most popular stroke, the front crawl. The popularity and use of the front crawl are well documented. Counsilman2,3 and Costill and colleagues4 indicate that 60% to 80% of swim workouts involve front crawl swimming. Fowler5 cites an unpublished study that states that out of 155 swimmers, 99% used the front crawl as their main practice stroke. For more information on the other swimming strokes, the reader is referred to works by Counsilman,2,3 Pink,6,7 and Costill.4
Numerous studies9-12 report the injury rate of swimmer’s shoulder to be approximately 27% to 87%. McMaster and Troup12 report the incidence of shoulder pain interfering with training in 10% of 13- to 14-year-olds, 13% of 15- to 16-year-olds, and 26% of elite college swimmers. Positive histories of shoulder pain were found in 47% of 13- to 14-year-olds, 66% of 15- to 16-year-olds, and 73% of elite college swimmers.12 Master swimmers experience a high incidence of shoulder pain as well. Despite a less-intensive training schedule than their younger counterparts, close to 50% of master swimmers report 3 weeks or more of shoulder pain that interferes with their season.13 There are approximately 200 million shoulders swimming, and a
Swimming the front crawl stroke involves performing a tremendous number of upper-extremity repetitions and places significant stresses on the shoulder joints and tissues. Many competitive and recreational swimmers develop shoulder-related symptoms from swimming. This chapter describes the epidemiology, pathophysiology, swimming stroke pathomechanics, and clinical diagnosis of the 445
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60% injury rate, which translates into potentially 120 million injured shoulders. As a result, the sports medicine clinician with an interest in treating shoulderrelated problems must understand the complexities of this unique diagnosis and the demands of the sport of swimming. Because of the great demands swimming places on the shoulders, the shoulder ranks as the number one anatomic area of musculoskeletal complaint in the competitive swimmer.14-20 Richardson and coworkers20 state that shoulder pain is the most common orthopedic problem in competitive swimming. Moreover, Bak and colleagues21 have described competitive swimming as one of the most demanding and time-consuming sports. On average, swimmers at the elite level practice 20 to 30 hours per week. Thus, during a year of practice, the average elite swimmer performs more than 500,000 stroke revolutions per arm or one million total shoulder revolutions per year. The demands on the competitive swimmer’s shoulders commonly consist of 10 to 12 major competitions per year, training 5 to 7 days per week, several twice-a-day practices, 8000 to 20,000 yards per day of practice, no recovery days, 16,000 arm strokes per day, and approximately 1 million strokes per year.22 Johnson and colleagues8 and Richardson20 state that the average competitive swimmer will perform approximately 1.0 million to 1.3 million stroke revolutions per arm during a year of swimming. Kammer and Young23 use the following example to describe the training loads on a shoulder with swimming. Based on a conservative estimate of eight stroke cycles per 25 yards, a swimmer performing a 10,000-yard workout may expect to complete as many as 3200 overhead cycles with each arm during the workout. In extreme cases, a swimmer can reach overhead as many as 2 million times over the course of one year. Murphy24 indicates that as swimmers fatigue and stroke mechanics break down, they lose efficiency and take more strokes to complete a given distance. This increased stroke frequency results in increased and abnormal loading biomechanical forces that can result in injury. Without question, fatigue is one of the leading factors in stroke breakdown and the onset of shoulder symptoms. Swimmers, in the course of developing overuse problems, relate a history of a gradual onset of symptoms late in their workouts. As the pain progresses and their performance degrades, swimmers report the onset of symptoms occurring progressively earlier in the workout. Knowing when the swimmer has shoulder pain in the workout is a key finding. The temporal onset of symptoms in swim training forms the basis for much of the strategy involved in returning the injured swimmer to fully functional training levels. According to McFarland and colleagues,25 44% of the injuries are due directly to overuse from swimming, 44% are due to cross-training activities and the additional cumulative
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stresses, and 11% are unrelated to swimming or crosstraining. In a comparison of various sports and the stresses to the shoulder, Johnson8 and Pink and colleagues7,26 provide the following examples. A professional golfer usually has approximately 200 revolutions per shoulder in 1 week. A college javelin thrower has approximately 300 revolutions in 1 week. Baseball pitchers throw approximately 1000 pitches involving shoulder revolutions in 1 week. Professional tennis players perform approximately 1000 shoulder revolutions in 1 week. Swimmers have approximately 16,000 shoulder revolutions in 1 week. When comparing the incidence of injuries in different upper extremity–sport athletes, Johnson8 and researchers at the Centinela Hospital Biomechanics Laboratory27 have reported injuries in 7% in professional golfers, 29% in college javelin throwers, 44% in college volleyball players, 57% in professional baseball pitchers, and 66% in elite swimmers.
DEFINITION Swimmer’s shoulder is a condition that has a microtraumatic overuse onset. McMaster12 describes swimmer’s shoulder as a “spectrum of maladies of the shoulder.” Bak28 states that shoulder pain in swimmers has been regarded as synonymous with coracoacromial ligament subacromial impingement, that is, anterior shoulder pain due to rotator cuff or long head biceps tendinopathy. Bak28 also concedes that new knowledge suggests that concomitant glenohumeral instability plays an additional role in creating the clusters of signs and symptoms of swimmer’s shoulder (e.g., secondary rotator cuff impingement due to underlying instability). Weldon and Richardson29 indicate that most of the pain is caused by performance-induced shoulder instability that stems from the specific demands placed on the shoulder during swimming. We think they are in fact describing a group of patients who develop the acquired ligamentous laxity and capsular laxity syndrome. Traditionally, shoulder instability has been divided into two categories. One is the traumatic, unilateral and unidirectional, Bankart lesion, surgery (TUBS) group, and the other is the atraumatic, multidirectional, bilateral, rehabilitation, inferior capsular shift (AMBRI) group. Zemek and colleagues30 show that elite swimmers demonstrate statistically significant greater glenohumeral joint hyperlaxity (multidirectional instability [MDI]) than nonswimmers. The elite swimmers demonstrated positive findings on three of the five laxity tests in the Beighton Scale31 to check for ligamentous laxity. Elite swimmers have increased glenohumeral joint hyperlaxity due to a combination of inherent (self-selection process) and acquired factors described. Allegrucci and coworkers32 and McMaster and coworkers33 stated the repetitive nature of swimming can predispose the shoulder to mechanical impingement
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and microtrauma, which can lead to laxity, rotator cuff fatigue, and subsequent secondary impingement. Often the shoulders of swimmers with increased anterior glenohumeral laxity permit excessive external rotation. This results in a greater demand on the rotator cuff and long head of the biceps, which are attempting to reduce humeral head elevation and anterior translation. Swimmer’s shoulder has been described as an inflammatory condition caused by the mechanical impingement of soft tissue against the coracoacromial arch. When this rotator cuff impingement occurs, it creates a wringing out effect on the supraspinatus tendon.34 The repetitive overhead arm motion of the front crawl stroke most often causes this effect. The pain associated with swimmer’s shoulder may be caused by two commonly described sources of impingement in the shoulder. One type of impingement occurs during the pullthrough phase of the front crawl stroke. The pull-through phase begins when the hand enters the water and terminates when the arm has completed pulling through the water and begins to exit the surface. At the beginning of pull-through, termed hand entry, if a swimmer’s hand enters the water across the midline of the body, the shoulder is placed in a position of horizontal adduction that mechanically impinges the long head of the biceps against the anterior part of the coracoacromial arch. A second type of impingement can occur during the recovery phase of the front crawl stroke. The recovery phase is the time of the stroke cycle when the arm is exiting the water and lasts until the hand enters the water again. As a swimmer fatigues, it becomes more difficult to lift the arm out of the water during the recovery phase. These fatigued muscles of the rotator cuff act to externally rotate and depress the head of the humerus against the glenoid, and they become less efficient. When these muscles are not functioning properly, the supraspinatus muscle becomes mechanically impinged between the greater tuberosity of the humerus and the middle and posterior portions of the coracoacromial arch. Stocker and coworkers13 state that more than 50% of swimmers with shoulder pain in both impingement type groups perceived that increased intensity or distance provoked their shoulder pain. This finding is significant and illustrates that fatigue may be a condition to avoid. Avoiding fatigue may be a primary focus in preventing and rehabilitating swimmer’s shoulder. Tovin35 states the proposed mechanism of failure starts with muscle fatigue. Symptoms that develop as a result of fatigue can also affect stroke mechanics as previously described. Scovazzo and coworkers36 have shown that many swimmers intuitively adjust their stroke to avoid painful movement patterns. According to Murphy,24 the classic symptom complex associated with swimmer’s shoulder pain involves subacromial impingement. In most cases, this is due to fatigue-related changes in stroke mechanics in swimmers with glenohumeral hypermobility or instability. Greipp37
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shows that in a small number of swimmers the impingement is related to hypomobility and inflexibility. Greipp37 also indicates the decreased mobility is usually more a limitation of scapulothoracic mobility (related to scapular retraction and upward rotation), leading to increased subacromial compressive loads. A number of swimmers might also have a primary impingement due to abnormal acromial morphology or a selective hypomobility of the posterior capsule. Tightness of the posterior capsule leads to an obligate translation of the humeral head, which causes the humeral head to migrate superiorly and anteriorly and compresses the structures in the subacromial area.38 However, our experiences indicate this pathoanatomic pattern occurs only in a minority of swimmers with shoulder pain.
CAUSES Bak and colleagues21,39 have stated that the countless repetitions over years of strenuous training combined with an increased muscle imbalance around the shoulder girdle are the main factors in the overuse type of swimmer’s shoulder. The literature contains descriptions of many causes leading to the high incidence of shoulder-related injuries in swimmers, but in any one swimmer the cause is most likely multifactorial. Box 36-1 lists some of the common causes of swimmer’s shoulder. Some of the unique aspects of the shoulder kinematics of swimmers compared with athletes in many other sports include increased internal rotation strength, increased shoulder adduction strength, increased shoulder range of motion, and prolonged, fatiguing shoulder-intensive training sessions.29 Swimmers can have shoulder pain for many reasons (see Box 36-1). Pathomechanics in swimming technique is a major factor in the cause of shoulder pain. As an example, crossing the midline on hand entry can cause impingement of the long head of the biceps tendon. Hand entry with the thumb pointing down and the palm facing outward can result in the same type of impingement. Overtraining can lead to shoulder pain if the swimmer continues to swim with fatigued muscles. As the muscles fatigue, they work less efficiently. This muscular inefficiency has two pathomechanical consequences. First, the muscles have to work harder in a weakened condition. Second, the swimmers have to perform more strokes to cover the same distance. This adds insult to injury, because the muscles are already fatigued. Together, these two consequences of fatigue can result in swimmer’s shoulder. Unilateral breathing can also cause swimmer’s shoulder. Swimmers who consistently turn their heads to the same side to breathe are risking shoulder pain in the opposite shoulder. The swimmer has to work harder to support
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BOX 36-1.
Possible Mechanisms of Shoulder Pain in Swimmers
Training Faulty stroke mechanics
• Muscle strength imbalances • Excessive loading of soft tissue constraints
• Loss of performance • Early fatigue • Abnormal loading of soft tissues
Muscle Weakness
Sudden increase in training loads
• Inadequate scapular stabilization resulting in abnormal loading of glenohumeral joint and surrounding soft tissues
• Abnormal loading of soft tissues • Repetitive microtrauma • Inadequate time for tissue recovery Lack of periodization in training Improper changes in training frequency, duration, or intensity • • • •
Early fatigue Abnormal loading of tissues Repetitive microtrauma Inadequate time for tissue recovery
Serratus anterior and lower trapezius (scapulothoracic muscle weakness)
Weakness of the posterior rotator cuff muscles (supraspinatus, infraspinatus, teres minor) • Inadequate glenohumeral dynamic stability • Early fatigue
Deficits in Neuromuscular Control
Improper or excessive use of training devices (e.g., paddles, kickboards)
Temporal problems with neuromuscular dynamic stability of the scapulothoracic joint can cause inadequate scapular stabilization, resulting in abnormal loading of the glenohumeral joint and surrounding soft tissues.
• Creation of tissue overload response • Abnormal loading of soft tissues • Activation of inflammatory injury response
Temporal problems with the neuromuscular dynamic stability of the glenohumeral joint can cause inadequate glenohumeral dynamic stability.
Higher level of swimming experience • Elite and competitive swimmers train near or at their threshold of injury • Subtle increases in training in elite swimmers can result in tissue injury High percentage of time training with the front crawl stroke
forward movement with the head turned to the side, which leads to overuse conditions. This hypothesis has not been demonstrated in the literature and remains controversial. Overuse of certain training equipment can cause shoulder pain. Paddles that are larger than the swimmer’s hand or that do not have drainage holes place a great strain on the shoulder muscles during the pull-through phase of the front crawl stroke. Using a kickboard with arms fully extended in front of the swimmer can also place the shoulder in a position of impingement. The longer the swimmer uses these training items, or uses them incorrectly, the greater the risk of shoulder pain.
Capsular Abnormalities Posterior capsule tightness (hypomobility) creates obligate translation of the humerus, which can lead to an impingement syndrome. Anterior inferior hypermobility of the glenohumeral joint leads to microinstability, which in turn leads to a secondary impingement syndrome.
symptoms is found in a swimmer presenting with shoulder pain. A better understanding of the clinical diagnosis of swimmer’s shoulder enables the clinician to effectively determine the type of rotator cuff impingement (primary, secondary, or internal) and rule in or out other pathologic findings such as SLAP (superior labral anterior-posterior) lesions.
SIGNS AND SYMPTOMS
So far, the discussion has focused on what signs and symptoms are common in swimmers with shoulder pain. What these swimmers do not have is posterior laxity. Fowler and Webster40 found, in an evaluation of 188 competitive swimmers, that 50% of the swimmers had a history of shoulder pain. Almost 55% of the swimmers and 52% of the control participants had some degree of posterior laxity in one or both shoulders. These results suggest that swimming does not predispose an athlete to increased posterior laxity.
A common constellation of signs and symptoms is seen with a patient with swimmer’s shoulder. These signs and symptoms are described in Box 36-2. The clinician should develop a high index of suspicion if this cluster of signs and
Fowler,5,40 citing an unpublished study, states that pain occurs in the front crawl arm cycle at different points that appeared to correlate with the biomechanical factors in tendinitis. The following describes the position and percentage
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BOX 36-2. Shoulder
Signs and Symptoms of Swimmer’s
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EXAMINATION, EVALUATION, AND DIAGNOSIS
Signs Altered arc of range of motion Reduced arc of range of motion Weakness of the supraspinatus and infraspinatus Weakness of the scapulothoracic stabilizers Poor neuromuscular (temporal) control of scapulothoracic joint Increased shoulder laxity anteroinferiorly Multidirectional instability Trunk and abdominal (core) stability deficits
Symptoms Pain progression • • • • •
Pain Pain Pain Pain Pain
only present after heavy workouts present during and after workouts present that interferes with performance prevents participation at rest or at night
Dead-arm feeling Feelings of instability
of pain during the front crawl stroke: Entry and first half of the pull phase is about 45%; end of pull phase, about 14%; recovery phase, about 23%; and throughout the entire cycle, about 18%. At entry and the first half of the pull phase, the shoulder is in forward flexion, abduction, and internal rotation. This forces the head of the humerus toward the anterior acromion and coracoacromial ligament and can cause impingement of the supraspinatus and the biceps tendons. During the recovery phase, the shoulder is in abduction and external rotation and the head of the humerus comes against the lateral border of the acromion. During the end of the pull phase, the shoulder is in adduction and internal rotation corresponding to the aforementioned wringingout mechanism.34 Costill and colleagues41 state that swimmer’s shoulder progresses through several stages (see Box 36-2) including pain only present after heavy workouts, pain during and after workouts, pain that interferes with performance, and pain that prevents participation. Because of the pathomechanics of the sport of swimming and the high stresses applied to the shoulder complex, Dunn22 indicates the most common shoulder pathologies found in swimmers are multidirectional instability, posterior capsule tightness, rotator cuff dysfunction, and labral tears. Therefore, it is recommended that at the first sign of swimmer’s shoulder symptoms, an evaluation for other symptoms should be undertaken before the condition escalates.
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The diagnostic complexity of the swimmer’s shoulder is as challenging as is the search for the standard of treatment.33,42-44 It is often difficult to distinguish the normal musculoskeletal adaptations of repetitive swimming from the pathologic adaptations that are causing the pathomechanical movement patterns. The increased capsule ligamentous laxity is probably an adaptation that is necessary to provide the excessive range of motion and stresses required by the swimming motion. Dunn22 describes several important considerations in the history and the subjective examination of the patient with a swimmer’s shoulder: • Where in the stroke phase does the swimmer feel pain and where is the pain? • Is there a sense of instability? • Have the stroke mechanics changed with the onset of the pain? • When in the workout does the pain develop? With the history, mechanism of injury, subjective descriptions, and a good clinical physical examination, the clinician should be able to use clinical reasoning to determine the involved structures and the causative factors. Ultimately, the cause must be treated to provide the recreational or elite swimmer with the best care.45
ISOKINETIC SHOULDER STRENGTH IN SWIMMERS McMaster and coworkers46 identified significant increases in torque production in swimmers for most motions tested. The front crawl stroke, because of its repetitive nature, creates muscle imbalances due to the particular activity of certain muscles. McMaster’s group also reported significant shifts in the unilateral ratios of swimmers’ shoulder muscle groups. The front crawl stroke primarily involves adduction and internal rotation, thereby increasing the isokinetic unilateral ratios of the shoulder adductor to abductor and the internal to external rotator. As a result, greater muscle imbalances are created in the shoulders of swimming athletes when compared with controls. This is likely one reason the shoulders of these competitive swimmers are susceptible to injury. An understanding of strength imbalances and shifts in unilateral torque ratios has important implications for the rehabilitation program designed for the swimmer. This concept is further supported by Fowler.5 He performed isokinetic testing of the shoulder’s internal and external rotators on 119 swimmers and 51 controls. The results demonstrated very strong internal rotators, normal strength
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of the external rotators, and an abnormal ratio of internal to external rotators. This study indicates that swimmers have an imbalance in rotation strength ratios when compared with control athletes. The front crawl stroke strengthens the internal rotators, adductors, and extensors, producing this imbalance. Falkel and coworkers47 demonstrated that swimmers who have shoulder pain have significantly lower absolute external rotation endurance and lower externalto-internal rotation endurance than do swimmers without pain and nonswimmers. The ratio of external to internal rotation endurance as measured isokinetically was only 42% in injured swimmers, compared with 56% for swimmers without pain and 68% for nonswimmers. Apparently, once the imbalance of the external rotation to internal rotation endurance falls below 50%, the swimmer no longer has sufficient external rotation muscular endurance to maintain the correct stroke mechanics in the recovery and may be more prone to the cascade of events that result in the impingement syndrome of the swimmer’s shoulder.
ANALYSIS OF NORMAL FRONT CRAWL STROKE BIOMECHANICS Because swimming causes a high number of shoulderrelated syndromes, and because stroke mechanics have been implicated as one of the most common contributing factors, understanding the basic stroke mechanics of the front crawl is critical for treating these patients (Fig. 36-1). The stroke is analyzed from a videotape of the swimmer or through expert analysis while the swimmer is actually performing the stroke. There are several excellent sources for evaluating the other strokes and for a full kinematic analysis of the front crawl stroke.6,26,48,49 The front crawl stroke is divided into different phases. Numerous classifications have been used to divide the phases. One classification system is above the water (early recovery and late recovery phases), approximately 35%, and below the water (early pull-through and late pullthrough phases), approximately 65%. The above-water phase is often described as the recovery phase and is further divided into three components: elbow lift, midrecovery, and hand entry. The arm motions in this phase consist of glenohumeral abduction and external rotation, then elbow flexion to extension. The underwater phase is often described as the pull-through phase and is further divided into three components: hand entry, mid pull-through (down-sweep and in-sweep), and the end pull-through (up-sweep) phases. When the arm is doing most of the work in propelling the body forward using the resistance of the water, the glenohumeral joint is in the adducted, internally rotated, and extended position and the elbow progresses from flexion to extension.
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Figure 36-1. Basic stroke mechanics of the front crawl.
Another classification system with a more thorough description of the front crawl stroke commonly breaks down the front crawl stroke phases into entry, stretch, catch, downsweep, in-sweep, up-sweep, and recovery (Fig. 36-2). Counsilman2,3 and Costill4 have described the importance of head position and breathing patterns. An exaggerated head-down position leads to deeper arm pull and body malalignment during the pull-through and recovery phases. An exaggerated head-up position results in concomitant lowering of the hips in the plane of the water, with excessive drag and water resistance. The side of pain has been inconsistently correlated to the side of breathing in numerous studies,33 but no consensus exists in the literature. Counsilman2,3 and Costill4 recommend body roll of 40 degrees to 60 degrees during the recovery phase, which minimizes the amount of horizontal abduction necessary for initiating the recovery phase and allows the overhead movement of the arm to occur with the necessary external rotation to avoid mechanical and vascular impingement. Excessive roll leads to a crossover during entry, crossover during the propulsive phase, or crossover during both phases. Lack of body roll in the recovery phase prevents full external rotation, increases the degree of mechanical stress, and causes abnormal hand placement during entry. Counsilman2,3 and Costill4 describe the kick as an extremely important component in the propulsive force of the front
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crawl stroke. The kick is also important for stability and mobility of the body roll and maintains the body in an optimal position for efficient use of the arms. A description of the arthrokinematics and osteokimatics of the front crawl stroke is given in Table 36-1.
PATHOMECHANICS OF THE FRONT CRAWL Numerous studies and articles refer to the pathomechanics of the front crawl as being one of the most common causes of developing the painful shoulder in the swimmer. Allegrucci and colleagues32 indicate that improper stroke mechanics can place the swimmer’s shoulder at further risk for developing pain. McMaster and coworkers11,12,33,46 indicate that many injuries originate from faulty techniques or mechanisms, and an assessment must be made of the swimming biomechanics of any injured athlete to identify faults that can contribute to injury. However, McMaster11 recommends evaluating the total training program of the athlete to identify other factors that may be contributing to the injury, such as swimming training, weight training, and dry-land training programs.
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Figure 36-2. Another classification system with a more thorough description of the front crawl stroke commonly breaks down the front crawl stroke phases into entry (1-2), stretch (3-4), catch (4-5), down-sweep (4-7), in-sweep (6-9), up-sweep (9-12), and recovery (13-16).
According to many clinicians,5,8,40,50-53 the most common cause of shoulder pain is improper stroke mechanics. During the extension phase, a greater degree of shoulder roll prevents the rotator cuff muscles from being compressed by the coracoacromial arch. Typically, if there is more room in the subacromial area, there is less compression of painsensitive structures and consequently less pain. Shoulder roll refers to dropping, or rolling down, the shoulder of the arm as the arm enters the water and during the power phase. Shoulder roll also assists in better arm extension. During the recovery phase, the shoulder of the opposite arm should be pointing toward the sky; this makes recovery easier. Thus, one treatment, as part of the total rehabilitation program, is stroke drills. Working with an experienced coach or swimmer to develop better shoulder roll can treat and prevent shoulder pain, as well as making for a more efficient stroke (and thus faster times). Yanai and coworkers54,55 performed three-dimensional videography of male collegiate swimmers during the front crawl stroke. Most commonly, shoulder impingement occurs when the arm is elevated above shoulder level while being internally rotated or when it is forcibly elevated at or beyond the maximum elevation angle. The purpose of the
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TABLE 36-1 Arthrokinematic and Osteokinematic Descriptions of the Front Crawl Stroke Glenohumeral Arthrokinematics
Scapulothoracic Arthrokinematics
Hand entry and early pull-through phase
External rotation and abduction
Scapular downward rotation and adduction
Body roll begins at hand entry
Mid pull-through phase
Neutral rotation and 90 degrees abduction
Scapular protraction and upward rotation
Body roll is at maximum of ⬃40-60 degrees from horizontal position
Late pull-through phase
Internal rotation, extension, and adduction
Scapular downward rotation and adduction
Body returns to the horizontal swimming position in the water
Elbow lift and early recovery phase
External rotation and abduction
Scapular downward rotation and adduction
Body roll begins in the opposite direction from the pull-through phase
Mid-recovery phase
External rotation beyond neutral and abduction to 90 degrees
Scapular protraction and upward rotation
Body roll is at maximum of ⬃40-60 degrees from horizontal position, and breathing occurs by turning the head to the side
Late recovery phase up to hand entry
External rotation and maximal abduction
Scapular protraction and upward rotation
Body returns to the horizontal swimming position in the water
Phase Segment
Function
Pull-through Phase
Recovery Phase
Modified from Richardson AB, Jobe FW, Collins HR: The shoulder in competitive swimming. Am J Sports Med 8(3):159-163, 1980
study was to evaluate the boundary for the shoulder and determine when the shoulder configuration exceeded that boundary and would produce an impingement syndrome. The researchers found that impingement occurs for 12% of the stroke time in each shoulder (24% of the stroke time for both arms); they also found a higher incidence of shoulder impingement on the breathing side. They concluded that the deficits in the front crawl that create shoulder pain are increased internal rotation of the arm during the pull phase of the stroke cycle, late initiation of external rotation of the arm during the recovery phase, and the small amount of tilt angle of the scapula (effect of scapular elevation and abduction on one side and depression and adduction on the other side).
leads to excessive impingement forces (Fig. 36-4). The second example involves the achievement of full external rotation, which does not occur until late in the recovery phase. If the swimmer reaches too far, primarily by reaching past the midline of the body (Fig. 36-5), the upper extremity is placed in excessive elevation. This position is akin to the Neer impingement testing position, therefore resulting in the increased possibility of subacromial impingement. This superior motion also creates an inefficient swimming motion, because the forces are not in a direct line to assist in propelling the body forward. It often leads to a medial and lateral swaying motion and slows down the time in addition to causing an impingement. If the swimmer reaches too short, he or she
There seems to be a consensus that the most common pathomechanics of the swim stroke are dropped elbow, reaching too far (adducting past the midline), and reaching too short. The most common pathomechanical problem is dropping the elbow, particularly in novice swimmers (Fig. 36-3). This occurs during the recovery phase when the swimmer drops the elbow during mid-recovery: Instead of the hand entering the water first, the elbow enters the water before or simultaneously with the hand. The force of the water on the forearm causes an upwardly applied force that causes the humerus to translate superiorly and cause the subacromial impingement. Fakel and colleagues47 postulate that fatigue of the external rotators of the shoulder can account for two potential stroke faults that increase impingement. The first example is when the shoulder completes the recovery phase with decreased external rotation. Consequently, the recovery phase continues with the arm in internal rotation, which
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Figure 36-3. The swimmer has dropped his elbow on entry. (Photograph by Vanessa Polvi and courtesy of Dartfish video analysis software [www.dartfish.com].)
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Fakel and colleagues,50 Counsilman,2,3 Costill,4 and McMaster and colleagues56 have discussed the proper hand placement that allows correct setting of the hand at the catch and assists in establishing optimal elbow and shoulder position to begin pull-through. Poor stroke mechanics during the recovery phase can lead to unfavorable hand placement at the point of catch and therefore reduce the pull efficiency. Crossover placement of the hand at entry or moving across the midline during the early stages of pull-through place the shoulder in a position of horizontal adduction, flexion, and internal rotation. This position of midline crossing in early pull-through has been cited as the position of greatest discomfort by many swimmers.5 Often swimmers with a painful shoulder have a different hand entry (Fig. 36-6): Either the hand enters farther from the midline or the humerus is lower to the water (the droppedelbow position). By keeping the arm lower and shortening the arc of motion, these swimmers are avoiding the painful impingement position. The swim coach might think the swimmer is lazy or getting tired. However, this hand entry can also be a sign of pain or injury, with the swimmer adopting a compensatory stroke to minimize the pain.
Figure 36-4. Shoulder impingement position. The shoulder completes the recovery phase with decreased external rotation (top left), and the recovery phase continues with the arm in internal rotation (top right), which leads to excessive impingement forces. Bottom, Bird’s-eye view. (Photographs by Vanessa Polvi and courtesy of Dartfish video analysis software [www.dartfish.com].)
loses the mechanical advantage of being able to use the leverage of the arms to grab and push the water through a longer distance to propel the body forward. The traditional front crawl stroke requires the hand to enter the water with the thumb side so the entry, stretch, catch, and down-sweep phases can be initiated efficiently. With this position for hand entry, the hand was already in an efficient position to begin the down-sweep or outward motion of the stroke. However, when the hand entry begins with the thumb side, it places the glenohumeral joint into the internally rotated position and increases the likelihood of creating additional stress on the subacromial structures.
Likewise, swimmers with painful shoulders often are over-reaching during hand entry and early pull-through (Fig. 36-7). Swimmers with painful shoulders also often demonstrate a different pattern at the end of pull-through and hand exit. The subscapularis is one of the muscles active throughout the entire swim stroke and consequently fatigues and can also become impinged. To compensate, the infraspinatus demonstrates significantly more activity in the painful shoulder as it externally rotates the humerus even more to try to avoid the painful internal rotation position that is so dominant in the front crawl stroke.
MUSCLE ACTIVITY OF THE FRONT CRAWL Normal Muscle Activity Although it requires technical expertise and laboratory instrumentation, electromyographic (EMG) analysis of shoulder muscle activity during athletic activities can provide the clinician with important information.57-59 Pink
Figure 36-5. Left, The swimmer is crossing his midline with his left arm during the early part of the pull-through phase. Right, The swimmer has good alignment. (Photographs by Vanessa Polvi and courtesy of Dartfish video analysis software [www.dartfish.com].)
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constant activity of the serratus anterior muscle during all phases of the swim cycle. Similar to the subscapularis muscle, the serratus anterior muscle had a constant level of activity greater than 20% MVIC. Monad60 found that 15% to 20% MVIC was the highest level at which sustained activity can be performed without fatigue. With both the subscapularis and the serratus anterior muscles demonstrating EMG activity greater than 20% MVIC throughout the swim stroke, these two muscles appear to be susceptible to fatigue, which has significant implications for rehabilitation.
Muscle Activity in Swimmers with Shoulder Pain Figure 36-6. Poor hand entry. (Photograph by Vanessa Polvi and courtesy of Dartfish video analysis software [www.dartfish.com].)
Figure 36-7. This swimmer is over-reaching with the right upper extremity during hand entry and early pull-through. This places the shoulder in an impingement position of increased internal rotation and flexion. (Photograph by Vanessa Polvi and courtesy of Dartfish video analysis software [www.dartfish.com].)
and coworkers26,49 describe the EMG findings of 12 shoulder muscles in asymptomatic competitive swimmers. This research is unique in that it provides the first look at rotator cuff muscle activity throughout the phases of the front crawl. This research shows that each rotator cuff muscle has different levels of EMG activity throughout the front crawl stroke cycle. This provides support for the theory that each rotator cuff muscle has a unique and specialized role during the front crawl stroke. Of the cuff muscles, the subscapularis was the only one active throughout the entire stroke cycle. Furthermore, the lowest level of EMG activity of the subscapularis throughout the stroke was 26% of a maximum voluntary isometric contraction (MVIC). Pink and coworkers26 also examined the EMG activity of the scapulothoracic muscles, demonstrating
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When the swimmer develops a painful shoulder, regardless of the mechanism(s) of injury, shoulder muscle activity changes.36,61,62 A possible explanation for the change in EMG muscle activity are the affects of pain on stroke mechanics. The stroke mechanics typically change to minimize the pain during the swim stroke. These inhibition-induced compensations begin to develop in the stroke, and changes in muscle-firing patterns are the result. Scovazzo and colleagues36 performed an EMG study of the painful shoulder during front crawl swimming. The following changes were noted when compared with the normal EMG activity in swimmers without pain. All three deltoid muscles maintained a similar EMG pattern throughout the swim stroke, but all three demonstrated decreased EMG activity. The infraspinatus demonstrated statistically significantly more EMG activity, whereas the subscapularis had statistically significantly less activity. This was probably a protective mechanism by the swimmer. The increased EMG activity of the external rotators were probably trying to shield the subacromial area and prevent the powerful and usually overdeveloped internalrotation motions in the swimmer. The scapulothoracic muscles also all demonstrated statistically significantly different EMG activity. The rhomboids and upper trapezius muscles had less EMG activity at hand entry. The rhomboids had significantly more activity at mid pull-through and the serratus anterior had significantly less activity. This again is probably a compensatory protective pattern to try to minimize the pain in the shoulder. In addition to the normal synergistic muscle activity and resultant functioning of the scapulothoracic joint, Wadsworth and Bullock-Saxon62 suggest that the timing of muscle activity during the front crawl is just as important as muscle activity. This control of muscle timing can also be referred to as the temporal recruitment muscle firing patterns. In injured swimmers, the timing of activation varies significantly on the involved side for the upper trapezius, lower trapezius, and the serratus anterior. Consequently, the normal force couple of the scapulothoracic
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joint is dysfunctional. In the painful shoulder, instead of letting the serratus anterior upwardly rotate the scapula, the rhomboids are probably trying to stabilize the scapula and minimize the pain. Therefore, this dysfunctional pattern contributes to the impingement symptoms. The two largest and most powerful internal rotators of the glenohumeral joint, which are also the primary power muscles under the water for the pull-through phase of the swim stroke, demonstrated no significant differences. Consequently, the pectoralis major and the latissimus dorsi muscles functioned similarly as the nonpainful shoulder. To summarize the impairment deficits identified in the research on painful swimmer’s shoulder, there were no significant differences in the EMG activity of the pectoralis muscles, latissimus dorsi, teres minor, posterior deltoid, or supraspinatus. Typically, we would think that because the supraspinatus is the most commonly involved muscle in the impingement syndrome, it would have different EMG responses. However, the research did not demonstrate any significant changes in the EMG activity of the supraspinatus. There were significant changes in the anterior deltoid, middle deltoid, infraspinatus, subscapularis, upper trapezius, rhomboids, and serratus anterior. The three scapular stabilizers that were evaluated all demonstrated significant deficits. These results have obvious implications for rehabilitation of the swimmer with the painful shoulder. Wadsworth and Bullock-Saxon62 showed that athletes with swimmer’s shoulder consistently demonstrate abnormalities in scapular rotator activity, suggesting that muscle dysfunction is a factor to consider in the cause or recurrence of shoulder pain. Empirically, this makes sense, and fatigue of the serratus anterior is probably one of the primary problems leading to the uncoordinated pattern of the scapular motions. The EMG in the serratus anterior decreases during the mid pull-through phase of the swim stroke and the rhomboid EMG activity increases; this probably prevents the normal Codman’s scapulohumeral rhythm and actually causes a downward rotation rather than an upward rotation of the scapula. This rotation produces an impingement to the subacromial contents, leading to the painful shoulder. In addition to the normal synergistic muscle activity and resultant functioning of the scapulothoracic joint, another concern is the temporal recruitment muscle firing patterns.62 In injured swimmers, the timing of activation varies significantly on the involved side for the upper trapezius, lower trapezius, and the serratus anterior. Consequently, the normal synergistic force couple relation of the scapulothoracic joint is compromised. Even more fascinating, there was a significant delay in activation of the serratus anterior on the uninvolved side as well as the involved side. Therefore, the findings of this study
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indicate that a relation does exist between shoulder injury and the temporal recruitment patterns of the scapular rotators, such that injury reduces the consistency of muscle recruitment. This study further suggests that injured subjects have muscle function deficits on their unaffected sides as well.
REHABILITATION Even though we try to emphasize the evidence-based approach to rehabilitation of the swimmer’s shoulder, there are no meta-analyses of current rehabilitation protocols or techniques, systematic reviews, or Cochrane Collaboration reviews to provide the best evidence-based techniques for rehabilitation of this condition. Of course, when research for a topic is limited, then there are many opinions and empirical programs on treatments and rehabilitation for the condition.34,35,42,43,45,50,63,64 Most rehabilitation programs should be based on addressing impairments that develop because of developing swimmer’s shoulder. Examples of impairments include glenohumeral instability, selective hypomobility of the posterior capsule, impaired posture, dysfunctional rotator cuff musculature, altered scapulohumeral rhythm, and poor neuromuscular control. Often the manifesting impairment results from a cascade of impairments. Additionally, progressing to functional specificity training based on the findings in the literature is critical in rehabilitating the swimmer. As an example, it is important to understand the unilateral ratio deficits that develop, but it is also important to work on the neuromuscular dynamic stability and temporal components of the muscular contractions. The first component is to modify the in-water part of the training program. The principle of training specificity suggests that it is most appropriate to train an athlete in a way that most closely duplicates his or her activity. In competitive swimming, although there are numerous stroke specialists, almost all competitive swimmers perform a majority of their training using the front crawl. Although rest or reduced training may be necessary, every effort should be made to keep the swimmer in the water to prevent detraining.11 This also supports the concept of specificity of training. Consequently, we first need to modify other elements of training (e.g., land drills) and training aids (e.g., hand fins). Based on the EMG research and muscle torque analysis, it appears that the key muscles to focus on are serratus anterior and subscapularis. Because of the muscle imbalances created by the repetitive nature of the front crawl stroke, the external rotator and the abductor muscle groups must also be addressed.
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There are imbalances of the scapulothoracic muscles, and the emphasis must be on endurance training because the serratus anterior, in particular, is active throughout the entire stroke cycle. Additionally, due to the temporal components, neuromuscular dynamic stability and motor learning training must be developed. A stable scapula is critical in preventing shoulder injuries. The focus needs to be on restoring the normal force couple relationship, with emphasis on the serratus anterior. No other muscle can substitute for the serratus anterior and provide the same synchronous pattern of muscle firing. In addition to restoring the scapulothoracic muscles, it is important to establish the glenohumeral joint functioning as well as for total shoulder complex functioning in the swimmer’s shoulder. The subscapularis inserts close to the axis of rotation and has a major role in precisely holding the humeral head in the glenoid fossa. The subscapularis forms the first layer of anterior wall musculature for glenohumeral joint protection. The temporal firings of the shoulder muscles are altered; changes in the muscle-firing patterns are the result of a pain-avoidance pattern. Therefore, the emphasis must be on decreasing pain and preventing pain during the swim stroke. Many of the basic principles of rehabilitation for any microtraumatic overuse injury of the shoulder in any athlete would also apply to the swimmer’s shoulder.
Interventions for Impaired Posture Only a few studies demonstrate a correlation between posture and pain,69-72 but empirically it appears that adaptive shortening of some muscles, particularly anterior muscles, can lead to dysfunction. The adaptive postural changes from muscle dysfunction produce changes in the normal physiologic length-tension relationships of the muscles, alter the normal force-couple dynamics, and change the biomechanics of the joint.
Interventions to Address Glenohumeral Instability and Scapulothoracic Control Most swimmers have hypermobility of the anterior-inferior capsule, multidirectional laxity, or both. Laxity that becomes symptomatic results in glenohumeral instability. Interventions to improve dynamic glenohumeral instability and scapulothoracic control are discussed in the exercise section.
EXERCISE PROGRESSION CONTINUUM Training the shoulder muscles for strength and endurance, specifically the muscles shown to have a propensity to fatigue, provides a strong defense against injury, because fatigue of the shoulder muscles may be the initial antecedent to swimmer’s shoulder.
Interventions for Pain and Inflammation Interventions in this phase of rehabilitation include relative rest (attempt to eliminate movements that cause pain), avoidance of aggravating factors (avoid abduction above 90 degrees of glenohumeral abduction), nonsteroidal antiinflammatory drugs (NSAIDs), and various physical therapy modalities (e.g., phonophoresis, iontophoresis, electrical stimulation).
Interventions for Selective Hypomobility of the Posterior Capsule Most swimmers have increased joint laxity and do not need mobilization exercises. However, a small subset of swimmers have selective hypomobility of the posterior capsule. These swimmers need to have heating, stretching, and mobilizations to produce plastic deformation of the noncontractile tissue.65-67
Interventions to Address Flexibility Most swimmers have increased muscle-tendon flexibility and do not need stretching exercises. Selective stretching exercises for the adductor and internal rotator muscle groups are beneficial in some swimmers. The stretching exercises are performed as per recommendations from the research literature.12,20,68
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Scapulothoracic Muscle Strengthening Moseley and colleagues73 identified four core exercises for the scapulothoracic muscles (Fig. 36-8A to D). These include scaption with the thumb up for the upper trapezius; press-ups for the lower trapezius, latissimus dorsi, and teres major; push-up with a plus for the serratus anterior; and scapular retraction for the middle trapezius and rhomboids. There are many different exercises that can be used for strengthening the scapulothoracic muscles.74-76 However, we recommend using super sets and performing the scapulothoracic exercises in Figure 36-8 for isolated strengthening of the respective muscles. Each link in the kinetic chain must be strengthened so they all function normally when integrated back into the activity pattern. If each muscle does not function normally in an isolated pattern, then there is no way the muscles can function normally in a functional pattern.
Scapulothoracic Muscle Recruitment and Endurance Based on the epidemiologic factors associated with swimming, a key emphasis in the rehabilitation program must be on improving endurance of the entire shoulder complex. Furthermore, because of the asynchrony associated with the scapulothoracic joint, specificity of training must
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F Figure 36-8. Core exercises for the scapulothoracic and glenohumeral muscles. A, Push-up with a plus (serratus anterior). B, Scapular retraction (middle trapezius and rhomboids). C, Shoulder scaption (upper trapezius for scapulothoracic; anterior deltoid, middle deltoid, and supraspinatus for glenohumeral joint). D, Press-down (lower trapezius for scapulothoracic; latissimus dorsi, teres major, pectoralis major; and lower fibers of subscapularis, lower fibers of infraspinatus and teres minor for the glenohumeral joint). E, Shoulder flexion (anterior deltoid and coracobrachialis). F, Horizontal extension with external rotation (infraspinatus, teres minor, and posterior deltoid).
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be applied during the rehabilitation program. The actual swimming stroke must be replicated during rehabilitation using such devices as exercise bands, a cable column, or a swim bench.
Glenohumeral Joint Muscle Strengthening Townsend and coworkers77 identified the four core exercises for the glenohumeral muscles. These include scaption with the thumb down for the supraspinatus; anterior and middle deltoids press-ups for the lower fibers of subscapularis, lower fibers of infraspinatus and teres minor; glenohumeral flexion for the anterior deltoid and the coracobrachialis; and external rotation with horizontal extension for the infraspinatus, teres minor, and posterior deltoid (see Fig. 36-8C to F). However, instead of the scaption position with the thumb down, we recommend that scaption be performed with the thumb up based on the studies by Itoi and coworkers,78 Takeda and coworkers,79 and Thigpen and coworkers.80 The study by Itoi’s group78 demonstrated that the EMG activity was similar in both the empty can (thumb down) and full can (thumb up) positions. More importantly, the thumb-up position was more comfortable for all subjects in the study. Takeda’s group79 used magnetic resonance images to indicate that the thumb-up position was as effective as the thumb-down position for activating the supraspinatus. Thigpen’s group80 demonstrated that the thumb-down position produced an anterior tilt to the scapula, narrowing the subacromial space and therefore compromising the rotator cuff structures.
comfortable for the patient than the transverse plane position when performing glenohumeral rotation exercises. Reinold and coworkers83 described the EMG activity of various exercises used to recruit the external rotator muscles. Graichen and colleagues84,85 performed an experimental in vivo study to test the potential changes of the subacromial space width during muscular contractions. Twelve healthy subjects were placed in an open magnetic resonance imaging (MRI) machine at 30 degrees, 60 degrees, 90 degrees, 120 degrees, and 150 degrees of arm elevation. A force of 15 N caused an isometric contraction of the glenohumeral abductors or adductors. The results of the adducting muscle activity led to a statistically significant increase of the subacromial space width in all arm positions. These data show that the subacromial space can be effectively widened by adducting muscle activity and by affecting the position of the humerus relative to the glenoid. As a result, this effect may be employed for treating patients with an impingement syndrome. Box 36-3 summarizes the evidence-based reasons to use the 30/30/30 position. Exercises can be used to strengthen the rotator cuff. Malanga and coworkers,86 Morrison and coworkers,87 and Sharkey and coworkers88 provide examples of exercises effective for isolating the rotator cuff muscles. We then progress the patient to the 90/90 position to advance the rotator cuff strengthening program because the swimmer needs to use the arm in the overhead position, particularly during the recovery phase (Fig. 36-9).
Rotator Cuff Strengthening Exercises Davies and coworkers81 originally described the concept of the 30/30/30 position for rotator cuff strengthening. This position involves 30 degrees of abduction, 30 degrees of scaption, and 30 degrees of a diagonal tilt. The 30 degrees of abduction protects the rotator cuff and prevents the wringing-out effect on the supraspinatus tendon described by Rathbun and McNab.82 If the arm is held in the adducted position, the humeral head pushes on the articular side of the supraspinatus tendon, producing a wringing-out effect on the tendon. With the arm in the 90/90 position (90 degrees of abduction and 90 degrees of external rotation), if the patient has weakness or pain inhibition of the force couple of the glenohumeral joint, reflex inhibition of the rotator cuff muscles, or a superior shear caused by the deltoid muscle, then a wringing-out effect on the bursal side of the supraspinatus is caused by the coracoacromial ligament. The second 30-degree position places the arm into scaption because it is the functional position of the arm, protects the anterior inferior capsule, and prestretches the posterior rotator cuff muscles. Prestretching the posterior rotator cuff muscles (based on the lengthtension curve) facilitates their ability to generate power. The external rotator muscles are the weakest of the six directions of the glenohumeral joint. The 30-degree diagonal tilt prevents creating a posterior internal impingement and is more
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Glenohumeral Muscle Endurance Swimmers who had shoulder pain were placed on training programs designed to improve the muscular endurance of the external rotators. Once they obtained an endurance ratio of greater than 50% in external rotators to internal BOX 36-3. Rationale for Strengthening External Rotators of the Shoulder in a 30/30/30 Position
Scaption position prevents wringing-out effect. Scaption position is a functional arc of motion for the shoulder. Scaption position protects the anterior-inferior capsule. Scaption position pre-stretches the external rotators (which are the weakest of the glenohumeral muscles) based on the physiologic length-tension curve. Scaption position is a comfortable position for performing the internal and external rotation exercises. Glenohumeral adduction to hold towel roll recruits the external rotators. Glenohumeral adduction increases the width of the subacromial space.
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A
459
B
Figure 36-9. Elastic tubing exercises in the prone 90/90 position. Replicating the front crawl position. A, External rotation. B, Internal rotation.
rotators (ER:IR), the shoulders became significantly less painful, and in many cases they became pain free.47,89 Therefore, rehabilitation of the swimmer needs to include endurance training for the shoulder complex muscles and needs to establish the normal unilateral ratios of the ER:IR. Recent fatigue research90,91 further supports the concept of encouraging and training the fatigue resistance of the posterior rotator cuff.
the shoulder complex while accounting for the demands of the sport.32 Nonoperative treatment focuses on scapular stabilizers, stretching the posterior capsule, strengthening the rotator cuff, and improving stroke mechanics, including body roll.22
Ebaugh and coworkers90,91 tested 20 subjects using an external rotation fatigue protocol. Comparison of scapular kinematics before and after external rotation fatigue showed significantly less scapular posterior tilt and upward elevation in the fatigued condition. Similar findings were reported by Tsai and colleagues92; they found upward rotation of the scapula and reductions in posterior tilt following rotator cuff fatigue, but they also found reduced scapular external rotation during arm elevation. These studies cite the importance of rotator cuff endurance and highlight the additional consequences of a fatigued shoulder for a person performing repetitive tasks such as swimming.
The long head of the biceps is an important mover in the early pull-through phase of the swim stroke, and ignoring it in strength training can expose the swimmer to injury and overuse problems. Because the biceps brachii and triceps muscles cross the glenohumeral joint, they have the potential to contribute to dynamic stability of the glenohumeral joint. Davies and Ellenbecker93 described a total arm strengthening effect of the entire upper extremity musculature. Pagnani and colleagues94 show how the biceps brachii functions to provide additional stability in the overhead athlete with underlying anterior glenohumeral joint instability.
Neuromuscular Re-education of Glenohumeral Muscle Recruitment Falkel’s group50 found from their videotape analysis that it is not only the degree but also the timing of external rotation that affects on the impingement process and the swimmer’s shoulder. The dynamic caudal glide and force couple of the glenohumeral joint are critical for a normally functioning shoulder complex. Control of humeral head superior displacement occurs by strengthening the infraspinatus, teres minor, and subscapularis. Secondary impingement in front crawl swimmers suggests that the primary goal of rehabilitation is to promote equilibrium of
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Emphasis on Total Arm Strength, Power, and Endurance
Core Stability in the Swimmer with Shoulder Pain Core stability training of the trunk musculature is important for the swimmer. Core training facilitates total kinetic chain transference and ultimately improves performance.
FUNCTIONAL SPECIFICITY TRAINING Bartels and coworkers recommend adding high-speed isokinetic exercises and diagonal-pattern elastic band exercises for specificity replicating the stroke pattern. Performing isokinetic training at approximately 250 to 300 deg/sec is specific for angular velocity training.95
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PROGNOSIS
might have to stop using hand paddles, stop partnerassisted stretching, and stop overhead weight training.
Swaine and colleagues96 assessed the time course of changes in arm power during recovery from injury. This was a pretest–post-test design, with the performed serial testing at different time intervals. The outcome measures used were 30-second tests on a swim bench evaluating peak power output, mean power output, and power decay. At the 4-week evaluation, the swimmers with swimmer’s shoulder had statistically significant deficits in all parameters. At the 8-week assessment, there were only statistically significant deficits in peak power output. It took 12 weeks before the swimmers had regained the normal force measurements with all parameters. These results suggest that differences in bilateral arm power output after injury persist for at least 8 weeks after return to swim training. This study helps support the rationale and need for prolonged rehabilitation after such injuries. Swaine’s group and others13,63,96,97 have described a high (up to 50%) reoccurrence rate in swimmers with a shoulder injury. Consequently, the efficacy of long-term intervention needs to be evaluated. There are no longitudinal studies regarding the effectiveness of rehabilitation interventions following swimmer’s shoulder and recurrence rate or prevention.
Training considerations to decrease swimmer’s shoulder problems include:
SPECIFICITY
It is important to maintain proper stroke mechanics throughout a training program. The swimmer needs to be educated about the importance of the integrated workouts to minimize shoulder fatigue, including kickboard work, pull-buoy training, and stroke variations to minimize some of the stresses to the shoulder. Bilateral breathing drills may also be of some help in maintaining normal body-roll patterns.
Counsilman2,3 and Costill4 indicate the single most important factor in training the competitive swimmer is technique. Poor technique is a particularly important factor in the evolution of overuse problems that are commonly seen in the swimming athlete. Therefore, it is important to correct technique flaws that produce shoulder stress. One interesting phenomenon with swimmers is the physiology of swim training. Most swimmers, regardless of the length of their competitive events, usually swim megayardage. This is unique to swimmers because no other sport trains in this manner. In running, for example, the miler and the marathoner train at distances related to their events. Neither would train for the distances of the other, because of the potential for stress-related injuries as well as specificity of training. Yet in swimming, most swimmers train at yardage far beyond the actual competitive distances. A team approach is needed to deal with the injured swimmer. In addition to the medical team, proper coaching, without a doubt, is critically important to ensure correct stroke mechanics and to monitor the training programs. The sports medicine team should work closely with the coaching staff to establish training regimens and workouts to optimize performance of the athletes. It is important to consider the entire training program of the swimmer, including additional training load problems that could be exacerbated through the overuse of equipment, such as hand paddles and kickboards. As examples, the swimmer
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• Limit use of hand paddles early in the training season. • Use fins or zoomers (half fins), which can decrease the stress on the swimmer’s shoulder and allow longer pain-free training. • Limit the use of a kickboard with the overhead arm positions. • Avoid sudden increases in workout intensity or mileage. • Mix in other swimming strokes more frequently during a workout and throughout the season. • Monitor and match water and dry-land work in terms of progression, intensity, and load. Upper armbands (Cho-Pat or Levine) can be used to decrease bicipital tendinitis or tendinosis. Although there is no research to support the use of these armbands, many swimmers think it decreases the pain in their shoulder. It may be similar to a counterforce brace in tennis or an infra-patellar tendon strap used for jumper’s knee in jumping sports, whereby it probably distributes the stresses over a larger surface area and consequently decreases pain.
RETURN TO SWIMMING WITH INTERVAL TRAINING PROGRAMS To decrease the effect of overuse on swimmer’s shoulder episodes, appropriate levels of training must be introduced as the swimmer is able to handle them. Too much work too soon, before the body has been prepared for that level of work, can result in recurring swimmer’s shoulder. Allow a gradual return to full activity if symptoms are absent and do not recur. When returning the swimmer back to the pool, the following must all be taken into consideration with the return-to-activity programs: • Follow proper training schedules; modify previous schedules, if necessary. • Practice proper stroke biomechanics and stroke techniques. • Follow a rehabilitation program designed for goals of the swimmer and with cooperation of the coach. • Schedule a progressive return to swimming, including dry-land and pool training in the totals. • Discontinue use of hand paddles.
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• • • •
Discontinue stretching the glenohumeral joint. Use bilateral breathing to protect the shoulder. Increase the amount of body roll. Strengthen the muscles and increase the endurance capacity to prevent the dropped elbow, which lead to fatigue and increased pressure.
Weldon and Richardson29 recommend avoiding all painful activities, taking a 2-week course of NSAIDs, and using cryotherapy frequently. They also recommend decreasing the emphasis on anterior capsule stretching and focusing more on posterior capsule stretching. The athlete should increase rotator cuff–strengthening exercises, with an emphasis on external rotation, and increase the scapularpositioning muscle exercises. The training program should be modified to include increasing body roll in the stroke and taking selective rest. Falkel and colleagues47 recommend individualizing swim training based on stroke and competitive distance, training patterns, age, and competitive level as well as differences in coaching philosophy. Individualized swim training includes a unique return plan for every injured swimmer. It is unlikely that swimmers will successfully complete a progression to unrestricted training if they have not been able to demonstrate good progress in managing symptoms and improving swimming stroke mechanics. Murphy24 recommends the following key criteria for a transitional swimming program: • Full range of motion and adequate upward scapular rotation • Pain-free tolerance of rotator cuff–strengthening routines, resisted movements into provocative overhead positions, and scapulothoracic strengthening routines • Ability to swim at least 500 yards at warm-up intensity (50% of normal training intensity level) without symptoms Murphy24 also describes several examples of specialized training, including in-season management of training errors or progressive overuse, return to training after termination of training, and off-season progression of training.
PREVENTION Numerous recommendations have been made for preventing swimmer’s shoulder. Some examples of commonly cited techniques to prevent swimmer’s shoulder include prehabilitation, education of coaches in primary injury prevention, resistance strength training for prepubescent swimmers, emphasis on improving muscular balance around the glenohumeral joint, and improving muscular balance around the scapulothoracic joint. However, there are no prospective studies to demonstrate the specifics of any one program and its beneficial results over another.
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Weldon and Richardson29 recommend that the swimmer avoid all painful activities and immediately notify the coach of shoulder pain. Swimmers should not use NSAIDs or ice on a chronic basis. They should spend equal time stretching the posterior and anterior capsule (we think that stretching the anterior capsule is not necessary for most swimmers). Swimmers should perform general rotator cuff strengthening exercises and scapular-positioning muscle exercises. Coaches should emphasize the body roll. McMaster and coworkers11,12,33 recommend decreased dry-land weight training, eliminating the use of hand paddles, and decreasing use of the kickboard (or at least using it properly). Stretching should be appropriate, if it is done at all. They prefer resisted specificity training on a swim bench or using exercise bands or a cable column.
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39. Bak K, Magnusson SP: Shoulder strength and range of motion in symptomatic and pain-free elite swimmers. Am J Sports Med 25(4):454-459, 1997. 40. Fowler PJ, Webster MS: Shoulder pain in highly competitive swimmers. Orthop Trans 7:170, 1983. 41. Costill DL, Maglischo EW, Richardson AR: Swimming. Champaign, Ill, Human Kinetics, 1992. 42. Kenal KA, Knapp LD: Rehabilitation of injuries in competitive swimmers. Sports Med 22(5):337-347, 1996. 43. Koehler SM, Thorson DC: Swimmer’s shoulder: Targeting treatment. Phys Sportsmed 24:39-50, 1996. 44. McMaster WC: Painful shoulder in swimmers: A diagnostic challenge. Phys Sportsmed 14:108-122, 1986. 45. Becker TJ: The athletic trainer in swimming. Clin Sports Med 5(1):9-24, 1986. 46. McMaster WC, Long SC, Caiozzo VJ: Shoulder torque changes in the swimming athlete. Am J Sports Med 20(3):323-327, 1992. 47. Falkel JE, Murphy TC, Murray TF: Prone positioning for testing shoulder internal and external rotation of the Cybex II isokinetic dynamometer. J Orthop Sports Phys Ther 8:368-370, 1987. 48. Pink M, Jobe FW, Perry J, et al: The painful shoulder during the butterfly stroke. An electromyographic and cinematographic analysis of twelve muscles. Clin Orthop Relat Res (288):60-72, 1993. 49. Pink MM, Tibone JE: The painful shoulder in the swimming athlete. Orthop Clin North Am 31(2):247-261, 2000. 50. Falkel JE, Murray TF, Malone TR: Case principles: Swimmer’s shoulder. In Malone TR (ed): Shoulder Injuries. Baltimore: Williams and WIlkins, 1988, pp 109-126. 51. Johnson J, Gauvin J, Fredericson M: Swimming biomechanics and injury prevention. Phys Sportsmed 31:41-48, 2003. 52. Johnson JN: Competitive swimming illness and injury: Common conditions limiting participation. Curr Sports Med Rep 2(5):267-271, 2003. 53. Kennedy JC, Hawkins RJ: Swimmer’s shoulder. Phys Sportsmed 2:35-38, 1974. 54. Yanai T, Hay JG: Shoulder impingement in front-crawl swimming: II. Analysis of stroking technique. Med Sci Sports Exerc 32(1):30-40, 2000. 55. Yanai T, Hay JG, Miller GF: Shoulder impingement in frontcrawl swimming: I. A method to identify impingement. Med Sci Sports Exerc 32(1):21-29, 2000. 56. McMaster WC: Anterior glenoid labrum damage: A painful lesion in swimmers. Am J Sports Med 14(5):383-387, 1986. 57. Bradley JP, Tibone JE: Electromyographic analysis of muscle action about the shoulder. Clin Sports Med 10(4):789-805, 1991. 58. Nuber GW, Jobe FW, Perry J, et al: Fine wire electromyography analysis of muscles of the shoulder during swimming. Am J Sports Med 14(1):7-11, 1986. 59. Worrell TW, Corey BJ, York SL, Santiestaban J: An analysis of supraspinatus EMG activity and shoulder isometric force development. Med Sci Sports Exerc 24(7):744-748, 1992. 60. Monad H: Contractivity of muscle during prolonged and static and repetitive activity. Ergonomics 28:81-89, 1985. 61. Su KP, Johnson MP, Gracely EJ, Karduna AR: Scapular rotation in swimmers with and without impingement syndrome: practice effects. Med Sci Sports Exerc 36(7): 1117-1123, 2004.
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62. Wadsworth DJ, Bullock-Saxton JE: Recruitment patterns of the scapular rotator muscles in freestyle swimmers with subacromial impingement. Int J Sports Med 18(8):618-624, 1997. 63. Ciullo JV, Stevens GG: The prevention and treatment of injuries to the shoulder in swimming. Sports Med 7(3): 182-204, 1989. 64. Shrode LW: Treating shoulder impingement using the supraspinatus synchronization exercise. J Manipulative Physiol Ther 17(1):43-53, 1994. 65. Flowers KR, LaStayo P: Effect of total end range time on improving passive range of motion. J Hand Ther 7(3): 150-157, 1994. 66. McClure PW, Flowers KR: Treatment of limited shoulder motion: A case study based on biomechanical considerations. Phys Ther 72(12):929-936, 1992. 67. McClure PW, Flowers KR: Treatment of limited shoulder motion using an elevation splint. Phys Ther 72(1):57-62, 1992. 68. Olsen SJ 2nd, Fleisig GS, Dun S, et al: Risk factors for shoulder and elbow injuries in adolescent baseball pitchers. Am J Sports Med 34(6):905-912, 2006. 69. Bullock MP, Foster NE, Wright CC: Shoulder impingement: The effect of sitting posture on shoulder pain and range of motion. Man Ther 10(1):28-37, 2005. 70. Julius A, Lees R, Dilley A, Lynn B: Shoulder posture and median nerve sliding. BMC Musculoskelet Disord 5:23-29, 2004. 71. Borstad JD, Mathiowetz KM, Minday LE, et al: Clinical measurement of posterior shoulder flexibility. Man Ther 12(4):386-389, 2007. 72. Borstad JD, Ludewig PM: Comparison of three stretches for the pectoralis minor muscle. J Shoulder Elbow Surg 15(3):324-330, 2006. 73. Moseley JB Jr, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20(2):128-134, 1992. 74. Decker MJ, Hintermeister RA, Faber KJ, Hawkins RJ: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27(6):784-791, 1999. 75. Kamkar A, Irrgang JJ, Whitney SL: Nonoperative management of secondary shoulder impingement syndrome. J Orthop Sports Phys Ther 17(5):212-224, 1993. 76. Ludewig PM, Hoff MS, Osowski EE, et al: Relative balance of serratus anterior and upper trapezius muscle activity during push-up exercises. Am J Sports Med 32(2):484-493, 2004. 77. Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19(3):264-272, 1991. 78. Itoi E, Kido T, Sano A, et al: Which is more useful, the “full can test” or the “empty can test,” in detecting the torn supraspinatus tendon? Am J Sports Med 27(1):65-68, 1999. 79. Takeda Y, Kashiwaguchi S, Endo K, et al: The most effective exercise for strengthening the supraspinatus muscle: Evaluation by magnetic resonance imaging. Am J Sports Med 30(3):374-381, 2002.
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80. Thigpen CA, Padua DA, Morgan N, et al: Scapular kinematics during supraspinatus rehabilitation exercise: A comparison of full-can versus empty-can techniques. Am J Sports Med 34(4):644-652, 2006. 81. Davies GJ, Hoffman SD: Neuromuscular testing and rehabilitation of the shoulder complex. J Orthop Sports Phys Ther 18(2):449-458, 1993. 82. Rathbun JB, Macnab I: The microvascular pattern of the rotator cuff. J Bone Joint Surg Br 52(3):540-553, 1970. 83. Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34(7):385-394, 2004. 84. Graichen H, Bonel H, Stammberger T, et al: Subacromial space width changes during abduction and rotation—a 3-D MR imaging study. Surg Radiol Anat 21(1):59-64, 1999. 85. Graichen H, Bonel H, Stammberger T, et al: Threedimensional analysis of the width of the subacromial space in healthy subjects and patients with impingement syndrome. AJR Am J Roentgenol 172(4):1081-1086, 1999. 86. Malanga GA, Jenp YN, Growney ES, An KN: EMG analysis of shoulder positioning in testing and strengthening the supraspinatus. Med Sci Sports Exerc 28(6):661-664, 1996. 87. Morrison DS, Frogameni AD, Woodworth P: Non-operative treatment of subacromial impingement syndrome. J Bone Joint Surg Am 79(5):732-737, 1997. 88. Sharkey NA, Marder RA: The rotator cuff opposes superior translation of the humeral head. Am J Sports Med 23(3):270-275, 1995. 89. Beach ML, Whittney SL, Hoffman SA: Relationship of shoulder flexibility, strength and endurance to shoulder pain in competitive swimmers. J Orthop Sports Phys Ther 16:262-268, 1992. 90. Ebaugh DD, McClure PW, Karduna AR: Effects of shoulder muscle fatigue caused by repetitive overhead activities on scapulothoracic and glenohumeral kinematics. J Electromyogr Kinesiol 16(3):224-235, 2006. 91. Ebaugh DD, McClure PW, Karduna AR: Scapulothoracic and glenohumeral kinematics following an external rotation fatigue protocol. J Orthop Sports Phys Ther 36(8):557-571, 2006. 92. Tsai NT, McClure PW, Karduna AR: Effects of muscle fatigue on 3-dimensional scapular kinematics. Arch Phys Med Rehabil 84(7):1000-1005, 2003. 93. Davies GJ, Ellenbecker TS: Total arm strength for shoulder and elbow overuse injuries. Timm K Orthopaedic Section Home Study Courses. La Crosse: Orthopaedic Section, American Physical Therapy Association, 1993. 94. Pagnani MJ, Deng XH, Warren RF, et al: Role of the long head of the biceps brachii in glenohumeral stability: A biomechanical study in cadavera. J Shoulder Elbow Surg. 5(4):255-262, 1996. 95. Bartels R: Scientists talk about strength training. Swimming Tech 14:14-25, 1980. 96. Swaine IL: Time course of changes in bilateral arm power of swimmers during recovery from injury using a swim bench. Br J Sports Med 31(3):213-216, 1997. 97. McMaster WC: Swimming injuries. An overview. Sports Med 22(5):332-336, 1996.
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CHAPTER 37 Conditioning, Training,
and Rehabilitation for the Golfer’s Shoulder Russell M. Paine and Ron M. Johnson
The game of golf is becoming more and more popular for both spectators and participants and is now one of the top recreational activities in the United States. More than 24 million Americans currently play golf and another 2 million are beginning to play each year. To the nonplayer, golf is often considered a leisure game. However, as all should know, golf is a sport that requires athletic skills such as strength, power, flexibility, and coordination to swing a golf club more than 100 miles per hour and hit the ball more than 300 yards.1
objective evidence has been provided for rehabilitative and preventive exercises, training and conditioning, and surgical procedures for the golfer. For discussion and analysis purposes, the golf swing has been broken down into the following five phases6 (Fig. 37-1): 1. Take-away: From addressing the ball until the club is horizontal 2. Backswing: From club at the horizontal position to the end of the backswing 3. Downswing: From the end of the backswing to club at horizontal 4. Acceleration: From the horizontal position of the club to ball contact 5. Follow-through: From ball contact to the end of the swing
Even though it is not viewed as a vigorous sport, golf cannot be considered a benign activity. Studies have revealed that golf is the contributing factor to injury in 62% of those who play.2 In surveys of the injury rates of golfers, it was concluded that the highest incidence of injury was to the back and upper extremities.3-5 For professional golfers, the shoulders were the third most commonly injured body area; injuries to the lumbar spine and to the wrist and hand occurred more often.4,5 For European amateur golfers, injuries to the shoulders rank third in occurrence behind injuries to the elbow and back.4 Of the shoulder injuries, the lead shoulder (the left shoulder for a right-handed golfer) is three times more likely to be injured than the trailing shoulder.5
When describing shoulder motion in the golf swing, certain kinematic terms are used.7 Vertical elevation is a combination of shoulder forward flexion and shoulder abduction. The angle of the humerus parallel to the trunk and next to the body is described as 0 degrees. Horizontal adduction is motion of the arm in a plane perpendicular to the transverse plane of the body. The angle of the humerus within the frontal plane of the body the body is described as 0 degrees. External rotation is lateral rotation of the humerus determined by the angle of the forearm in the plane perpendicular to the humerus.
This chapter examines the role of the shoulder complex during the different phases of the golf swing. With this understanding, specific flexibility, strengthening, and conditioning exercises are introduced to aid in rehabilitation, preventing injury, and enhancing performance of the golfer with a shoulder injury.
The purpose of this section is to describe and compare the muscle activity patterns and the ranges of motion for the shoulder and trunk during the five phases of the golf swing. The activity patterns for the scapular muscles, the rotator cuff, and the trunk are described in detail. When describing the activity of the shoulders, the leading shoulder is the left shoulder and the trailing shoulder is the right shoulder for a right-handed golfer.
ELECTROMYOGRAPHIC AND KINEMATIC ANALYSIS OF THE GOLF SWING To isolate and identify the functions of the major muscles controlling the various body segments during the golf swing, dynamic electromyographic (EMG) and high-speed motion analysis has often been used. The phases of the golf swing and the EMG recording can be synchronized and studied to reveal specific muscle-firing patterns at specific instances in the golf swing. Motion analysis has also been used to identify the shoulder kinematics involved in the golf swing. Through these investigations,
Take-Away and Backswing The take-away and backswing phases have been described as a coiling or loading of the body in order to enhance the velocity and kinetic energy of the club head.8 Electromyographic analysis of the scapular muscles of the trailing arm reveals relatively high activity of the upper, middle, and 465
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Take-away
Backswing
Downswing
Acceleration
Follow-through
Figure 37-1. The five phases of the golf swing. (From Kim DH, Millett PJ, Warner JP, Jobe FW: Shoulder injuries in golf. Am J Sports Med 32:1324-1330, 2004.)
lower portions of the trapezius during take-away to help the scapula retract and upwardly rotate.9 Similarly, the levator scapulae and rhomboid of the trailing arm are active during this period to help with such scapular movements.9 In the leading arm during take-away and backswing, the activity of the scapular stabilizing muscles is relatively low to allow scapular protraction. EMG analysis of the rotator cuff muscles exhibits contributions from the supraspinatus and infraspinatus in the trailing arm as they act to approximate and stabilize the shoulder.10,11 Of the rotator cuff muscles in the leading arm, only the subscapularis displays marked activity in the take-away phase. EMG analysis reveals relatively low activity of the trunk musculature during this segment of the golf swing, because the trunk is simply preparing for the swing.8 The pectoralis major, the latissimus dorsi, and the deltoid muscles of both arms are relatively inactive in the backswing of the golf club.10,11 When analyzing the motions of the shoulders, Mitchell and coworkers7 documented the extreme ranges that the shoulders incurred at the top of the backswing. They noted that during this phase the lead shoulder reached its maximum horizontal adduction (119-125 degrees) and vertical elevation (94-110 degrees), and the trailing shoulder demonstrated its maximal external rotation (48-86 degrees).
Downswing Analysis of the trailing arm scapular muscles shows that the three portions of the trapezius taper to allow scapular protraction.9 However, the levator scapulae and rhomboid muscles display marked activity to control scapular protraction and rotation of the trailing arm. The serratus anterior muscle in the trailing arm show increased activity during forward swing to aid in scapular protraction.9 EMG studies of the leading arm demonstrate high activity of the trapezius, levator scapulae, rhomboids, and serratus anterior as they all contribute to scapular motion and stabilization as the arms move toward the ball.9
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Of the trailing shoulder muscles during forward swing, the subscapularis, pectoralis major, and latissimus begin firing at marked levels as the trailing arm increasingly accelerates into internal rotation and adduction. The lead shoulder subscapularis and latissimus dorsi are both moderately active during the forward swing phase. During the downswing, trunk rotation movement is initiated. Pink and investigators8 demonstrated backside erector spinae and bilateral abdominal oblique muscle activation to counteract the downward movement of the trunk.
Acceleration In the acceleration phase, the body segments work together in a coordinated sequence to maximize club head speed at ball impact. Only the serratus anterior is significantly active in the trailing arm scapular muscles during acceleration.9 The serratus anterior has high levels of involvement to allow strong scapular protraction and contribute to maximizing club head speed. Conversely, EMG analysis reveals strong contractions of the scapular muscles in the lead arm during acceleration.9 The trapezius, levator scapulae, and rhomboid muscles are firing to aid in scapular retraction, upward rotation, and elevation. The serratus anterior of the lead arm continues to display levels of activation. EMG investigations display high subscapularis, pectoralis major, and latissimus dorsi contractions as they provide power for the trailing arm during the acceleration swing segment.10 The latissimus dorsi and the pectoralis major supply the most power during acceleration.8 The subscapularis, pectoralis major, and latissimus dorsi of the lead arm fire at high rates during the acceleration swing phase.10,11 During this phase there are consistent EMG levels of the erector spinae and abdominal oblique muscle bilaterally. Peak activity of the lead side erector spinae is seen at this time. The erector spinae muscles continue to control the forward fall of the trunk and the oblique muscles are responsible for rotation of the trunk.8 Watkins and colleagues12 established that all trunk muscles are relatively active during the acceleration phase of the golf swing.
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Follow-Through After ball contact has been made, the follow-through phase is initiated. During early follow-through, the body segments work to decelerate their rotatory contributions.10,11 The scapular muscles of the trailing arm display decreased activity throughout the follow-through, allowing coordinated scapular protraction.9 Likewise, the scapular muscles of the lead arm display tapered activity through these swing segments. The serratus anterior muscles of both arms show fairly consistent firing patterns during the follow-through phases.9 In the trailing shoulder, marked activity of the subscapularis, pectoralis major, and latissimus dorsi persist into the early stages of follow-through.10 Only the subscapularis of the trailing shoulder remains highly active throughout this phase.10,11 For the lead shoulder, the subscapularis continues its level of activity during early follow-through. The infraspinatus and the supraspinatus rotator cuff muscles actually increase their contribution during the latter portion of this phase, and the pectoralis major and latissimus dorsi decrease their contributions.10,11 Trunk muscle activity during follow-through, although of low intensity, remains consistent to aid in proper postural control and energy dissipation.8 Analysis of the shoulder motions reveals maximum values for external rotation of the lead shoulder (59-80 degrees) and maximum horizontal adduction (108-121 degrees) and vertical elevation (103-112 degrees) for the trailing shoulder.7
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Table 37-1 summarizes the activity and functions of the shoulder and trunk musculature during the golf swing. Table 37-2 details the maximum ranges of motions the shoulders incur during the golf swing. This information is used as an outline to better develop rehabilitation programs for injured golfers and for those seeking training programs to enhance performance and prevent injuries.
PATHOMECHANICAL ANALYSIS This section describes the proper mechanics of the golf swing and the causes of common shoulder pathologies in relation to the stresses incurred during the golf swing. Common swing faults and mechanical deficiencies are described preparatory to the proper strengthening, conditioning, and flexibility principles that follow. Recommended alterations in the golf swing are given for those who need to compensate for current or chronic orthopedic issues.
Set-up and Take-Away Before initiating the backswing, proper set-up and ball address must be achieved. This initial posture greatly influences the balance of forces throughout the golf swing and is therefore critical to the achievement of the proper swing plane. The most common mistake seen at set-up is using spinal flexion to position over the ball rather than using a hip-hinge motion.13 When this spinal flexion is maintained, the golfer’s center of gravity remains posterior to the base of support. This posture places additional loads through the
TABLE 37-1 Muscle Functions During the Golf Swing Muscle Group
Take-Away and Backswing
Downswing and Acceleration
Follow-Through
Rotator cuff
Stabilize Decelerate
Stabilize
Stabilize Abduct and externally rotate
Scapular
Protract scapula Stabilize
Retract scapula
Retract and elevate scapula
Leading Arm
Pectoralis major and latissimus dorsi
Powerfully adduct
Trailing Arm Rotator cuff
Stabilize Abduct and externally rotate
Subscapularis: powerfully internally rotate
Stabilize Decelerate
Scapular
Retract and elevate scapula
Protract scapula Stabilize
Protract scapula Stabilize
Pectoralis major and latissimus dorsi
Powerfully adduct and internally rotate
Trunk Trunk
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Stabilize
Powerfully rotate
Stabilize
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TABLE 37-2 Maximum Shoulder Joint Angles During the Golf Swing JOINT ANGLES (DEG)
Arm
College (18-24 yrs)
Middle (27-48 yrs)
Senior (50-86 yrs)
Swing Phase
Horizontal Adduction Leading arm
125
126
119
End of backswing
Trailing arm
121
114
108
Follow-through
Leading arm
110
107
94
End of backswing
Trailing arm
112
114
103
Follow-through
Leading arm
80
70
59
Follow-through
Trailing arm
85
71
48
End of backswing
Vertical Elevation
External Rotation
Mitchell K, Banks S, Morgan D, Sugaya H: Shoulder motions during the golf swing in male amateur golfers. J Orthop Sports Phys Ther 33(4):196-203, 2003.
spine and increases the stresses on the spinal structures throughout the swing.2 Without proper maintenance of lumber lordosis, the thoracic spine, cervical spine, scapula, and shoulder postures are altered as well, possibly contributing to impingement-like symptoms in the shoulder. To maintain proper spine angles, use proper rotation, and achieve balance throughout the golf swing, the golfer needs excellent hip and trunk flexibility. Limitations in flexibility can cause the golfer to sacrifice fundamentals and place undue stresses on the lower back during the golf swing.2 For example, a golfer with limited hip and trunk flexibility might compensate by producing more rotation in the lumbar spine and pelvic girdle. This places increased stresses on hypomobile or hypermobile spinal segments. Limitations in hip and trunk flexibility can result in an overcompensation of shoulder turn and increased activation of the shoulder musculature.14 Such alterations in the golf swing can produce stresses to the shoulder complex that are more than the golfer’s body can tolerate.
Take-away and Backswing During the take-away and backswing phases, the lead arm is accelerated into a position of maximal horizontal adduction and elevation, predisposing the golfer to impingement-type problems as the rotator cuff tendons, biceps tendons, and bursae are compressed within the shoulder.15 Indeed, in a review of golfers with shoulder pain, lead arm rotator cuff or subacromial disease (or both) was evident in 93% of the cases.10 Similarly, this end-range position during the backswing can irritate the acromioclavicular joint. Acromioclavicular
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joint pathology is common in the golfer’s shoulder. In a review of elite-level golfers, 53% of those with shoulder pain had pathology of the acromioclavicular joint.16 Although it has not been identified through research, superior labral lesions can occur in the lead shoulder during the backswing. Kim and colleagues6 reported in their practice the diagnosis and treatment of superior labral anterior-posterior (SLAP) lesions. Common complaints from these golfers were pain, clicking, catching, and subjective weakness. The posterior rotator cuff and scapular muscles of the lead arm are also placed at risk for injury at the top of the backswing as they are placed under a stretch load.13 Kao and coworkers9 claimed that the levator scapulae and rhomboid muscles are often injured in this end-range position as well. Pathologic posterior instability of the lead shoulder can also be exacerbated during the backswing. Mallon and Colosimo16 noted a 12% occurrence of posterior instability in their investigation of elite golfers with shoulder pain. Posterior shoulder pain and sensations of instability in the lead arm during the backswing have been associated with this type of shoulder pathology.9
Downswing and Acceleration During downswing and acceleration, high muscular activities and great angular velocities place the golfer at risk for incurring a number of injuries. The downswing period produces the greatest percentage of injuries in golfers today.3,5 During these swing segments, increased stresses on
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the trunk and lower back continue in golfers with improper spinal angles.
and current medical and health concerns should be noted.
Follow-through
Activity Modification
As the swing continues to late follow-through, the golfer can experience pain in the shoulders as they are forced into these end-range positions. For the lead shoulder, maximal abduction and external rotation can be painful, possibly indicating anterior instability.16 Also in the lead shoulder, signs and symptoms of biceps tendinitis have been noted at this point in the swing.6 In the trailing shoulder, this portion of the golf swing can be painful in conditions of subacromial impingement, rotator cuff pathology, or acromioclavicular joint pathology.
One of the cardinal principles of rehabilitation is to avoid overstressing healing or injured tissues. Injuries to the golfer are most often attributed to repetitive overuse from practicing and playing. Unfortunately, the injured golfer often must be reminded of this. The rehabilitation specialist should investigate the patient’s routines, habits, and activities on and off the golf course to ensure that continued tissue trauma does not persist.
Rotational forces continue in the trunk during the followthrough phases of the golf swing. Knowing that the follow-through position should be a mirror image of the downswing, golfers often overcompensate trunk movements to mimic that posture. As a result, physical loads on the spine are increased. Golfers and rehabilitation specialists should be aware of the potential risks involved in the game of golf. The golf swing is an unnatural movement and inherently places significant stresses on the human body. The role of proper body mechanics, adequate strength and flexibility, and sufficient trunk stabilization cannot be overemphasized.
REHABILITATION, CONDITIONING, AND TRAINING In most cases, injuries to the golfer’s shoulder can be successfully treated when a thorough, structured, and carefully implemented program is followed. In general, the rehabilitation program involves a thorough clinical evaluation, pertinent activity modifications, resolution of flexibility and mobility limitations, strength and neuromuscular training, golf swing analysis, correction of harmful swing faults, and gradual return to golf participation.
Clinical Evaluation A detailed and thorough history and examination of the shoulder complex are vital in making an accurate diagnosis of the golfer’s shoulder. Other chapters in this book outline and describe the clinical examination process. Significant to the evaluation of the golfer with shoulder pain is asking the golfer to demonstrate his or her golf swing and note the specific motion that reproduces symptoms. Once a diagnosis has been established, the treating rehabilitation specialist should document the ranges of motion and strengths of the shoulder, trunk, and hip body segments and should evaluate pertinent joint laxity. Current golf participation, training regimens, and previous
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In an epidemiologic study, Gosheger and coworkers4 determined that 92% of shoulder injuries resulted from overuse. Not surprisingly, the number of injuries to the shoulder (and to the back, wrist, and hand) have been shown to increase with increased amounts of time spent playing golf or hitting balls at the driving range.4 Injuries significantly increased for golfers who played more than three rounds a week and for those who hit 200 or more balls in a week. Gosheger’s group also noted that golfers who carried their bags on a regular basis suffered significantly more injuries to their shoulders than those who did not. A reduction or cessation in golfing activity is almost always advised while the injured golfer is rehabilitating and recovering, particularly in the initial phases of the rehabilitation program, when the golfer’s tolerance levels are being established.
Overview Before proceeding, a general overview of important basic rehabilitation principles needs to be outlined. For the golfer who has sustained a shoulder injury, whether a surgical procedure was performed or not, a progressive and systematic approach should be followed. Wilk and colleagues17 have outlined in detail a four-phase approach to the rehabilitation of an athlete with a shoulder injury. The phases are progressive and sequential and should be implemented as such to safely and most effectively return the golfer to playing. Box 37-1 details the phases and general goals for each phase when rehabilitating the injured golfer. Motion restrictions, exercise modifications, and return to activity guidelines are provided within the established rehabilitation protocol for golfers recovering from shoulder surgery. These parameters must be followed to allow sufficient tissue healing and shoulder recovery before amounts of demand and stress on the shoulder complex can be increased. The remainder of our discussion is directed more specifically to the progression of the golfer through the more advanced phases of strength and neuromuscular training. Our goal is to provide the golfer with a training regimen
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BOX 37-1.
Phases of Rehabilitation
Acute Phase
Initiate core training
GOALS
Initiate putting
Diminish pain and inflammation Advance and normalize motion
Advanced Strengthening Phase GOALS
Address limitations on posture and flexibility
Initiate more aggressive strength training
Modify activities
Advance dynamic stability training
FOCUS OF TRAINING
Improve strength, power, and muscle endurance
Modalities as needed
FOCUS OF TRAINING
Flexibility, stretching
Progress above as indicated
Scapular strength and neuromuscular training
Initiate plyometric training
Rotator cuff strength and neuromuscular training
Initiate interval return to golf program
Intermediate Phase
Return To Activity
GOALS
GOALS
Progress strength and neuromuscular training
Progress to golf-specific strength and conditioning program
Advance and normalize motion
Return to competitive golf
Address postural and flexibility limitations
FOCUS OF TRAINING
Promote dynamic stability
Progress above as indicated
FOCUS OF TRAINING
Strength and conditioning
Progress as indicated
Progress to plyometric training
Initiate lower extremity flexibility, stretching
Progress to interval return to golf program
that serves to prevent further injury and enhances performance on the golf course. We have adhered to certain standards in the development of our golf-specific strengthening and conditioning program.17-19
The golfer must train for bilateral strength and flexibility. The left and right sides of the body provide vital contributions and should not be neglected.
The golfer should condition the entire body, not just the upper body. The golfer should be reminded that energy, power, and flexibility are necessary in the legs, trunk, and hips during the golf swing. The golf swing is a full body movement.
Muscular strength is emphasized before dynamic strength and power. A base level of strength is needed before more dynamic and powerful activities can be initiated. Muscular strength and flexibility depend on each other for success. Without the other, strength or flexibility cannot be used in an optimal manner.
The flexibility and exercise program should emphasize multijoint movements and should train the body and the muscles as they function during the golf swing. For example, the large muscles of the upper extremities act as accelerators, and the rotator cuff and scapular muscles work primarily to stabilize and decelerate during the golf swing.
Conditioning and training should be performed year-round and should be periodized. The golfer should have a yearround commitment to training and should vary training volumes and intensities in a systematic manner throughout the year.
The arms should be trained to act through their full range of motion in concert with the legs, hips, and trunk muscles. The rotational components of the legs, hips, and trunk muscles act to enhance clubhead speed through the upper extremities during the golf swing. Core stability must be enhanced to provide optimal swing patterns. Correct postural alignment and a stable base of support provided by the hips, abdominal muscles, spinal stabilizers, and scapular muscles allow the proper swing path to occur.
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The flexibility, conditioning, and training program should be simple and easy to implement in a standard gym and with minimal equipment for training at home and at the golf course. A program is useless if the golfer is unable to comply with the routine.
Flexibility and Mobility Range-of-motion limitations can lead to compensatory swing changes that increase the likelihood of musculoskeletal injuries and can actually impair performance. Additionally, flexibility and mobility limitations simply
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might not allow the golfer to complete his or her swing path optimally or consistently. Optimum flexibility should allow the golfer to develop and maintain a smoother, more efficient, and more effective swing pattern. Consequently, stretching, both active and passive, and manual joint and soft tissue mobilization techniques from the treating clinician should be integral parts of the golfer’s training regimen. Early in the rehabilitation process, one of the major goals is to normalize shoulder motion and address flexibility restrictions in the trunk and hips. Because various disorders are seen in the golfer’s shoulder, it is critical that the clinician fully evaluate range of motion and joint mobility of the shoulder and assess the flexibility of the shoulder complex musculature. Common shoulder motion restrictions seen in golfers in our practices are loss of internal rotation and loss of horizontal adduction, particularly in the lead shoulder. Indeed, Warner and colleagues20 documented limited shoulder internal rotation in patients with shoulder impingement, a common disorder seen in golfers with shoulder pathology. Likewise, Myers and coworkers21 found reduced shoulder internal rotation and shoulder adduction in throwers with internal impingement. Burkhart22,23 reported that a significant loss of internal rotation (⬎25 degrees’ side-to-side difference) was a correlate of glenohumeral posterior-inferior capsular contracture in his series of throwers with arthroscopically proved superior labral lesions. Such capsular shortening has been shown to induce abnormal anterior and superior humeral head translation with shoulder flexion.24 This humeral head motion can lead to the impingement of soft tissues
A
471
in the subacromial space in such motions as shoulder flexion, internal rotation, and horizontal adduction.25 It is obviously noteworthy that these are the motions seen in the lead arm at the top range of the backswing. It is therefore a major goal in the rehabilitation process to address these motion limitations. For the golfer, self-stretching to improve shoulder range of motion is crucial for stimulating long-term soft tissue adaptations that increase flexibility. Stretching in this case is more rehabilitative and corrective and is employed in the more structured phases of a rehabilitation program. Warmup and dynamic flexibility drills, used in pregolf routines, are discussed later. To improve internal rotation motion and posterior shoulder flexibility, we have found it most beneficial to perform internal rotation and horizontal adduction passive stretching while manually stabilizing the scapula (Fig. 37-2A). Stabilizing the scapula in this manner better isolates the stretch to the restricted posterior shoulder structures. If the evaluation of glenohumeral joint mobility reveals loss of posterior humeral head translation, posterior humeral head glides are indicated. Special attention is placed on ensuring the mobilization of the humeral head is directed along the angle of the glenoid fossa in a posterolateral direction (see Fig. 37-2B). We have found it beneficial to initiate these joint mobilizations in the shoulder’s neutral position and advance to increased ranges of internal rotation. The golfer must also perform self-stretches to help correct posterior shoulder tightness. Figure 37-3A depicts the traditional cross-body stretching. A more specific crossbody adduction stretch is performed using the genie stretch. This stretch begins with forearms folded, which
B
Figure 37-2. A, Posterior glide mobilization in neutral. B, Seat the humeral head into the glenoid by lifting the elbow.
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A
B
C Figure 37-3. A, Traditional cross body stretch with no control of internal rotation. B and C, The genie stretch controls internal rotation during cross-body stretching.
allows control of internal rotation as the arm is pulled across the body. The internal rotation is controlled using the elbow of the uninvolved arm as it pushes the hand down, imparting internal rotation of the stretched shoulder. This focuses the cross-body stretch to the posterior cuff musculature (see Fig. 37-3B and C). Side-lying internal rotation stretching, or sleeper stretch (Fig. 37-4), should also be regularly performed by the golfer. In the opposite pocket stretch (Fig. 37-5), the golfer reaches
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across the body and places the fingers in the opposite pocket. An adduction force is then applied to focus on another area of the posterior cuff tightness. Interestingly, of these two stretches (sleeper and traditional cross body), McClure and colleagues26 demonstrated a significantly greater improvement in internal rotation motion with the cross-body adduction stretch only. We have found both of these methods to be effective in enhancing posterior shoulder flexibility.
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is associated with increased upper thoracic kyphosis and scapulae that are protracted, elevated, and anteriorly tilted. In particular, an anteriorly tilted scapula has been associated with subacromial impingement.27, 28 Muscular imbalances and restrictions are also associated with this posture. Tightness of the pectoralis major and minor and latissimus dorsi are coupled with scapular musculature weakness, particularly the middle and lower trapezius.17 For the golfer, a rounded shoulder posture limits the amount of shoulder rotation in the golf swing and acts to further decrease the amount of available subacromial space.
Figure 37-4. The sleeper stretch is a good self-stretch to address an internal rotation deficit.
In an attempt to remedy this posture and decrease symptoms associated with subacromial impingement, we add pectoralis minor stretching (Fig. 37-6) and soft tissue mobilization techniques in addition to pectoralis major and
A
Figure 37-5. The opposite pocket stretch stretches the posterior cuff at a different angle.
Sufficient shoulder external rotation must be obtained for the golfer’s activities of daily living as well as for achieving an optimal golf swing. Manual external rotation stretches, joint mobilizations, and self external rotation stretches with a wand or golf club are performed in increasing ranges of shoulder abduction. Achievement of full external rotation motion in the frontal plane is necessary for ease of shoulder motion during the backswing and follow-through phases of the golf swing. Postural adaptations, scapular resting positions, and scapular mobility should also be assessed. A common postural presentation seen in the golfer with a shoulder disorder is a forward head and rounded shoulders. This slouched posture
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B Figure 37-6. Pectoralis minor assisted stretching techniques.
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minor and latissimus dorsi (Fig. 37-7) stretching to the golfer’s rehabilitation program. In some cases, thoracic spine mobilization techniques are warranted to allow increased mobility and postural correction.
composition, and club head speed after an 8-week strength and flexibility program, dispelling the typical golfer’s concerns that strength training might reduce flexibility and hinder performance on the golf course.
Vad and colleagues29 documented that range-of-motion deficits in lead hip rotation, both internal and external rotation, and lumbar spine extension correlated with a history of low back pain in golfers. Interestingly, no statistically significant difference was noted in nonlead hip range of motion. In separate studies, Mellin30 and BarbeeEllison31 studied hip mobility in patients with recurrent low back pain and showed that those with more external hip rotation than internal hip rotation were more likely to develop low back pain, even though no differences were found between the left and right sides. From these studies, increased forces seem to be transmitted to the lumbar spine when the lead hip rotations are decreased. These observations support the inclusion of hip rotator stretching and lumbar extension stretching in the golfer’s rehabilitation and conditioning to recover from or prevent low back pain. These stretches are outlined later in the flexibility section.
Although expensive gym machines, intricate and detailed routines, and other gimmick devices are available, a conditioning and training program does not need to be elaborate. Programs incorporating body weight, light dumbbells, elastic tubing resistance, and medicine balls are very effective and can easily be implemented.
Strength and Neuromuscular Training The primary goals for advancing a rehabilitation program for the golfer are to safely and effectively return to the previous level of competition, prevent further injury, and enhance performance. Investigators have revealed that appropriate strengthening, conditioning, and flexibility routines improve clubhead speed or driving distances.32-34 Westcott and colleagues34 documented improvements in flexibility, body
Figure 37-7. Self latissimus stretch.
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The components of a successful conditioning and training program include proper warm-up, strengthening, power enhancement, skill training, flexibility enhancement, and cardiovascular conditioning. The golfer should train each component to achieve optimal performance and prevent injuries. Proper Warm-Up It is generally believed that preparing the body before play benefits performance and decreases the risk of injury. However, when investigating the warm-up practices of golfers, it was concluded that only 54.3% performed some form of warm-up activity.35 Air-swings on the tee were the most commonly observed form of warm-up. This is hardly a proper routine. Fradkin and coworkers35 demonstrated that a proper warm-up routine actually increased clubhead speed. Gosheger and colleagues4 found that a warm-up routine of at least 10 minutes had a positive effect on reducing golfing injuries. An appropriate warm-up for golfers should include a period of exercise to increase body temperature, improve dynamic flexibility of the golf muscles, and prepare the body for more vigorous activity. A growing body of research indicates that static stretching before explosive training or competition actually can reduce force production and therefore can reduce explosiveness during movement.36-41 A recent meta-analysis of 361 research papers examining the relation between stretching and injury prevention revealed that static stretching before activity is not associated with a significant reduction in injuries.42 On the other hand, dynamic flexibility—quickly moving a joint through its range of motion with little resistance— improves flexibility, coordination, balance, proprioception, and movement speed. It also raises core body and deep muscle temperatures, elongates active muscles (elasticity), decreases the inhibition of antagonist muscles, stimulates the nervous system (arousal), and helps to decrease the chance of injury.43-45 These findings support the use of dynamic flexibility before training and play and suggest that static stretching should be used for after a workout or after playing, which promotes enhanced flexibility and cools down the body to a preexercise state.
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The routine we prescribe prepares the golfer for strength and neuromuscular training and more specifically for warming up to play. It can also promote decreased injury rates and improved performance. The first goal of the warm-up routine should be to raise the core temperature with a general warm-up. It is important to increase core temperature before moving onto the next phase of the warm-up. As body temperature increases, so does the ability to produce force. Once the core temperature has increased and the joints are lubricated, dynamic stretches should be performed. It is important to start each dynamic stretch with a limited range of motion and then gradually increase the range. The player should
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not force a muscle into a new range by building up too much momentum, or dynamic stretching can backfire. Forcing a muscle into an extreme range too quickly triggers the stretch reflex and the muscles contract instead of relax. The warm-up and flexibility routine are shown in Table 37-3 and Figures 37-8 through 37-15. When strength training, repetitions with lighter resistance should be performed to specifically prepare the muscles and joints for the upcoming task. For days on the golf course, a series of golf swings with a progressive increase in range of motion and vigor should be performed before moving on to the first tee. The specific skills progression is shown in Table 37-4.
TABLE 37-3 General Warm-up and Dynamic Flexibility Routine Exercise
Reps
Time
Description
—
3-5 min
Rotary drill, transverse (Fig. 37-8)
10-20
Hold 3-5 sec
Feet shoulder-width apart, knees slightly bent Rotate trunk and shoulders to the side as far as possible Maintain hip stability
Rotary drill, swing plane (Fig. 37-9)
10-20
Hold 3-5 sec
Begin with golf stance, ensuring proper hip hinge Rotate trunk and shoulders to the side within the swing plane as far as possible Keep head stationary
Side bend and rotation reach (Fig. 37-10)
10-20
Hold 3-5 sec
Raise arms straight up Hold right wrist with left hand Lean over to the left, gently pulling on the right wrist. The stretch should be felt on the right side; then lean over from the waist and turn toward the left, still pulling on the right wrist
Lead arm backswing reach (Fig. 37-11)
10-20
Hold 3-5 sec
Begin with golf stance, ensuring proper hip hinge Rotate trunk, simulating the backswing, and pull and stretch left shoulder across the body as far as possible Keep head stationary
Trailing arm followthrough reach (Fig. 37-12)
10-20
Hold 3-5 sec
Begin with golf stance, ensuring proper hip hinge Rotate trunk, simulating the follow-through, and pull and stretch the right shoulder across the body as far as possible Keep head stationary
Lunge and rotate (Fig. 37-13)
10-20
Hold 3-5 sec
Lunge forward while maintaining trunk stability Rotate to the side of the lunge leg as far as possible
Ball address squats (Fig. 37-14)
10-20
—
Place a golf club behind the back, with the club contacting the buttocks, upper back, and head Maintaining trunk stability, squat down by allowing proper hip hinge to occur With proper posture, the golf club should stay in contact at each point throughout the squat
Forearm and wrist supination and pronation, radial deviation, ulnar deviation (Fig. 37-15)
5-10
—
Hold the golf club with arm extended Perform supination and pronation and radial deviation motions Ulnar deviation is performed with arm extended by the side
Warm-up Jog, bike, or brisk walk
Intense enough to increase body temperature but not to level of fatigue
Dynamic Flexibility
Reps, repetitions.
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A Figure 37-9. Rotary drill swing plane.
B Figure 37-8. Rotary transverse stretch. A, Starting position. B, Ending position. Figure 37-10. Side bend and reach stretch.
Strength Training Strength training includes traditional resistance exercises aimed at increasing the overall strength and athleticism of the golfer. One of the biggest mistakes golfers and those who train golfers make is developing and implementing programs that try to train too specifically for the sport. In most cases, the golfer lacks basic levels of conditioning. It is vital to begin a strength and conditioning program by first establishing a base level of foundational strength.
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Developing such strength better prepares the golfer for advancement to the more intensive golf-specific fitness training programs to follow. Early in the rehabilitation program, one of our goals is to re-establish muscular balance of the shoulder complex. Primarily, initial training targets weak muscles by incorporating exercises that are proved to best isolate specific
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Figure 37-13. Lunge and rotate.
Figure 37-11. Lead arm stretch.
Figure 37-14. Ball address position with squat.
Figure 37 -12. Trail arm stretch.
muscles. In most cases, it is important to train the external rotators and the scapular muscles. The targeted scapular muscles tend to be the serratus anterior, the middle and lower trapezius, and the rhomboids. Isotonic exercise techniques are employed, with the golfer progressing from three sets of 10 repetitions to three sets of 15 to 20 repetitions
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before increasing the resistance. We have established a basic outline of shoulder rehabilitation and training for each training session. Table 37-5 outlines our basic shoulder rehabilitation routine and provides the corresponding EMG research that notes the efficacy of exercise selection. The golf diagonal exercise is shown in Figure 37-16. For strength training in the advanced strengthening and return-to-activity phases, multijoint movements yield far
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B
A
Figure 37-15. Supination strengthening using a club. A, Rotate the club to neutral position. B, Slowly return to 90 degrees.
better results than movements that strive to isolate a single muscle or muscle group. At this stage of the golfer’s rehabilitation program, shoulder-specific training continues, with an additional focus on training movements, not merely muscles. We have outlined our training movements as squatting, lunging, upper body pushing, upper body pulling, and any movements that incorporate trunk rotation or stability (Box 37-2 and Figs. 37-17 and 37-18). When applicable, exercises are performed in manners similar to the golf swing. These exercises are initiated from the trunk and incorporate a weight shift from one leg to the other because the body moves that way on the golf course.
TABLE 37-4 Golf-Specific Skills Progression Skill
Reps or Time
One-half to one-quarter wedge shots
5-10
Full wedge shots
5-10
Mid-iron shots (7 or 5 iron)
5-10
Long iron shots (4 or 3 iron)
5-10
3-wood shots
5-10
Drives
5-10
Putting and chipping reps, repetitions.
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5-10 min
Plyometric Training Once the player’s strength levels have increased and the golfer has sufficiently advanced to more dynamic stabilization training, special resistance exercises can be used to train the athlete for developing muscular power. The goal at this point is to convert general muscular strength to the special quality of power that is relevant to the golf swing. Power is the combination of strength and speed and is incorporated within the rehabilitation and training program as plyometric exercises. Plyometric training, in the form of medicine ball throws (1-3 kg), are used in the training program to mimic the prestretch during the backswing and then activate trunk and shoulder accelerators for the downswing and acceleration phases of the golf swing. Training sequential acceleration of the hips and trunk, shoulders, elbows, and hands with medicine ball throws should enhance the golfer’s power and increase club head speed. Fletcher and Hartwell32 demonstrated that an 8-week combined strengthening and plyometric program for golfers significantly increased the club head speed and driving distance. Front twist throws, side throws, and swing throws (Fig. 37-19) are examples of the plyometric medicine ball exercises used in our program. Optimally, the plyometric exercises should enforce correct golf postures, incorporate weight shifting, promote forceful trunk rotations, and mimic exact golf swing speeds (performed in less than
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TABLE 37-5 Shoulder-Specific Rehabilitation and Training Exercises
Targeted Muscles
References
Light Dumbbell Complex Routine (Choose One Routine) Flexion, scaption, abduction Prone horizontal abduction in 100 degrees, 90 degrees Prone external rotation in 90 degrees of abduction
General rotator cuff and scapular
Blackburn (1990) Bradley (1991) Decker (2003) Donatelli (2003) Malanga (1996) Reinold (2004) Takeda (2002) Townsend (1991)
Infraspinatus, teres minor
Blackburn (1990) Bradley (1991) Greenfield (1990) Reinold (2004) Townsend (1991)
Rhomboids, middle trapezius, lower trapezius
Moseley (1992)
Posterior Cuff Specific (Choose One Exercise) Tubing external rotation Side-lying external rotation Side-lying external rotation in scapular plane
Scapular-Specific Retraction, Downward Rotation Rows
Scapular-Specific Protraction, Upward Rotation (Choose One Exercise) Push-up with a plus Press-up Protraction Dynamic hug D1 PNF
Serratus anterior
Decker (1991) Gross (1998) Moseley (1992)
General rotator cuff and scapular
Eckstrom (2003) Reinold (2004)
Dynamic Overhead (Choose One Exercise) D1 PNF External rotation in 90 degrees of abduction Golf diagonals (see Fig. 37-16) Dribbles
PNF, proprioceptive neuromuscular facilitation. Blackburn TA, McLeod WD, White B, et al: EMG analysis of posterior cuff exercises. Athl Train 25:40-45, 1990. Bradley JP, Tibone JE: Electromyographic analysis of muscle action about the shoulder. Clin Sports Med 10:789-816, 1991. Decker MJ, Hintermeister RA, Faber KJ, Hawkins RJ: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27:784-791, 1999. Decker MJ, Tokish JM, Ellis HB, et al: Subscapularis muscle activity during selected rehabilitation exercises. Am J Sports Med 31:126-134, 2003. Donatelli RA, Ekstrom RA, Soderberg GL: Surface electromyographic analysis of exercises for the trapezius and serratus anterior muscles. J Orthop Sports Phys Ther 33:247-258, 2003. Ekstrom RA, Donatelli RA, Soderberg GL: Surface electromyographic analysis of exercises for the trapezius and serratus anterior muscles. J Orthop Sports Phys Ther 33(5):247-258, 2003. Greenfield BH, Donatelli R, Wooden MJ, Wilkes J: Isokinetic evaluation of shoulder rotational strength between the plane of scapula and the frontal plane. Am J Sports Med 18:124-128, 1990. Gross MT, Lear LJ: An electromyographic analysis of the scapular stabilizing synergists during a push-up progression. J Orthop Sports Phys Ther 28:146-157, 1998. Malanga GA, Jenp YN, Growney EC, et al: EMG analysis of shoulder positioning in testing and strengthening the supraspinatus. Med Sci Sports Exerc 28:661-664, 1996. Moseley JB, Jobe FW, Pink M, et al: EMG analysis of the scapula muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34(7):385-394, 2004. Takeda Y, Kashiwaguchi S, Endo K, et al: The most effective exercise for strengthening the supraspinatus muscle: Evaluation by magnetic resonance imaging. Am J Sports Med 30(3):374-381, 2002. Townsend H, Jobe FW, Pink M, et al: Electromyographic muscle analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19:264-272, 1991.
2 seconds). We find it most beneficial to literally release and throw the medicine ball to ensure the body segments are sufficiently accelerating throughout the entire movement. The medicine ball throws are performed with three sets of five to eight repetitions, with speed and force of movement the main objectives.
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Stability and Core Training Core stability can be defined as the ability to create extremity movement without compensatory movements of the spine or pelvis.46 The golfer must be able to control the movement of one body segment while putting another
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Figure 37-17. Standing chest press strengthens the serratus.
Figure 37-16. Golf diagonal wood chopper. Be sure to maintain core tension and spine angle.
BOX 37-2. Exercises for Advanced Phases of Rehabilitation and Training
Choose one exercise from each group. Exercises may be performed with a barbell, dumbbells, or a machine
Lunge, Hip Extension Dominant, Single Leg Deadlift Romanian deadlift Glute ham raises Step-up, lunge variations Single-leg squat Single-leg leg press
Figure 37-18. Standing row with rotation is excellent for the scapular retractors, which are very active during the backswing.
Squat Squat variations Leg press
Upper Body Pull Rows Pull-ups Pull-downs
Upper Body Push Push-up Bench press Standing chest press with rotation (see Fig. 37-17) Standing row with rotation (see Fig. 37-18)
body segment into motion. The best example of this in golf is the ability to stabilize the lower body during the backswing without swaying or sliding the hips. Spine and trunk stability is provided by the combined coordinated contractions of the musculature responsible for trunk flexion, extension, and lateral bending. The goal of stability and core training for golfers is to improve the muscular activation, strength, and endurance of these trunk muscles to enhance the golfer’s ability to stabilize the spine and produce force during the golf swing.19 The core training program should train the trunk muscles not only to stabilize but also to assist as facilitators of trunk movement. A Swiss ball is very effective when
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A
C performing trunk extensor strengthening. The reverse extension exercise may be one of the most effective exercises for maintaining proper spine posture. This allows the golfer to control the spine angle for address, backswing, and impact. These exercises are shown in Figure 37-20 and are performed in three sets of 10 to 30 repetitions. Other exercises train the core muscles to hold and stabilize isometrically or while the extremities are moved (Fig. 37-21). These exercises are performed by time, beginning with 20 seconds and increasing in holds of up to 1 minute each. Five sets are performed.
Interval Return-to-Golf Program The interval return-to-golf program is initiated when the golfer has full, nonpainful shoulder range of motion, a satisfactory clinical examination, normal strength measures
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B
Figure 37-19. Medicine ball toss. A, Front throw. B, Side throw. C, Swing throw.
for the rotator cuff and scapular musculature, and appropriate progression within the rehabilitation program.17 The objective of the golf interval program (Table 37-6) is to gradually reintroduce the stresses of the golf swing and help the golfer gradually restore the normal biomechanics of the golf swing.47
Golf-Specific Static Stretching Dynamic flexibility movements are performed before training or play, and we suggest that static stretching be implemented after a workout or after playing to further develop long-term flexibility adaptations and to cool down the body to a pre-exercise state. Box 37-3 (Figs. 37-22 through 37-27) outlines a basic stretching routine designed to enhance flexibility of the golf muscles.48 Unless otherwise
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TABLE 37-6 Interval Return-to-Golf Program Monday
Wednesday
Friday
15 putts 15 chips 5-min rest 25 chips
20 putts 20 chips 5-min rest 20 putts 20 chips 5-min rest 10 chips 10 short irons
20 chips 15 short irons 10-min rest 15 short irons 15 chips
15 chips 10 med irons 10-min rest 20 short irons 15 chips
15 short irons 10 med irons 10 long irons 10-min rest 10 short irons 10 med irons 5 long irons 5 woods
15 short irons 10 med irons 10 long irons 10-min rest 10 short irons 10 med irons 10 long irons 10 woods
Play 9 holes
Play 9 holes
Play 9 holes
Play 18 holes
Week 1 10 putts 10 chips 5-min rest 15 chips
A Week 2 20 chips 10 short irons 5-min rest 10 short irons Week 3 15 chips 10 med irons 10-min rest 5 long irons 15 short irons 15 med irons 10-min rest 20 chips
B
Week 4 Figure 37-20. Swiss ball exercises. A, Extensions. B, Crunches.
15 short irons 10 med irons 10 long irons 10 drives 15-min rest Repeat the series Week 5 Play 9 holes
med, medium. Recommended clubs: chips, use wedge; drives, use driver; long irons, use 4, 3, or 2 iron; medium irons, use 7, 6, or 5 iron; short irons, use 9 or 8 iron; woods, use 3 or 5 wood.
A
noted, each stretch should be held for 20 to 30 seconds and repeated three to five times.
Cardiovascular Training Incorporating cardiovascular training into the training regimen is recommended for the reduction of morbidity and mortality.49 Improved cardiovascular fitness can also help to reduce fatigue during the last holes of the round. B Figure 37-21. Abdominal strengthening. A, Side plank. B, Prone plank.
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For more optimal health benefits, the American College of Sports Medicine advises 20 to 30 minutes of activity at heart rate levels greater than 60% of maximal capacity 3 to
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BOX 37-3.
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Golf-Specific Stretching
Hamstring Stretch (See Fig. 37-22) Sit on the edge of a table, bed, or golf cart. Maintain knee extension while leaning forward. Maintain lumbar lordosis and bend at the hips.
Iliotibial Band Stretch (See Fig. 37-23) Lying on your back. Use a golf club to hook and pull the leg toward the opposite shoulder. Keep the leg straight and the back against the surface.
Trunk Rotation (See Fig. 37-24) Lie on your back with your knees bent and feet on the floor. Slowly rotate the knees toward the floor while keeping feet on the floor.
Hip Stretch (See Fig. 37-25) Lie on your back with both knees bent. Place the ankle of one leg on the knee of the other. Grasp the underlying leg and pull it toward the chest to stretch hip rotators to enhance hip external rotation.
Hip and Buttock Stretch (See Fig. 37-26) Lie on your back with both knees bent.
Figure 37-22. In the hamstring stretch, the athlete must maintain lumbar lordosis while hinging at the hip to reach toward the toe.
Place the ankle of one leg on the knee of the other. Grasp knee of the top leg and pull toward the opposite shoulder to stretch hip rotators to enhance hip internal rotation.
Prone Press-up (See Fig. 37-27) Lie on your stomach with hands at shoulder level. Slowly press to extend elbows while keeping hips on surface. Hold 3 to 5 seconds; repeat 5 to 10 times.
5 days per week.50 The golfer is encouraged to participate in a moderate amount of physical activity of at least 30 minutes a day regularly to ensure an adequate level of fitness and promote a healthy quality of life.
SUMMARY AND APPLICATIONS Box 37-4 details a summary of the golfer’s rehabilitation, conditioning, and training program. Once the golfer has sufficiently completed the rehabilitation program and has returned to unrestricted playing, the program involves a year-long, periodized training cycle broken down in to four phases: postseason, offseason, preseason, and inseason. During the postseason and offseason, the golfer’s program is geared toward gaining an overall strength base to prepare
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Figure 37-23. Iliotibial band stretch. A foam roller is also effective in lengthening the iliotibial band.
for the development of power as the golf season nears. Weight training is performed 3 or 4 days a week, with the maximum number of repetitions on the major lifts ranging from 8 to 12. During the preseason phase, the golfer begins power training in the form of plyometric medicine ball throws
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Figure 37-24. Trunk rotation stretch. Unilateral tightness could result in lack of shoulder turn.
Figure 37-27. Prone press-up. This stretch is important for reversing the constant flexed posture used during golf.
and emphasizes increased training loads to further enhance strength development. Weightlifting is performed 3 days per week, with the maximum number of repetitions decreased to 6 to 8. Plyometric training should be performed 2 or 3 days per week. At this phase of the golfer’s year, more time is spent on the course and on the driving range developing golf skills. It is therefore important to monitor training volumes to prevent overuse injuries or exacerbations to previous shoulder pathology. During the golf inseason, weight training is reduced to 2 days per week, with the primary goals of maintaining and gradually improving levels of strength, conditioning, and fitness. Repetitions remain in the 6 to 8 range, with
Figure 37-25. Hip-piriformis stretch.
BOX 37-4.
Summary of Golfer’s Program
Warm-up General Dynamic Golf-specific skill progression before play or lifting with light loads before strength training
General Strength and Neuromuscular Training Squat dominant Upper body push Lunge, hip dominant, single leg Upper body pull Shoulder-specific rehabilitation and training
Stability and Core Training Golf-specific and shoulder-specific flexibility training Plyometric training and cardiovascular training (may be performed separately to avoid overtraining) Figure 37-26. Hip-gluteal stretch.
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decreased levels of intensity. Plyometric drills continue to be performed 1 or 2 days a week. Box 37-5 provides a general outline of the yearly periodization program for the golfer.
MODIFICATIONS TO THE GOLF SWING Many golfers with orthopedic problems experiment with their swings to reduce strain on vulnerable parts. Adjustments to the swing can aid in reducing stresses to the shoulder and allow the golfer to play golf more safely and effectively.
Low Back Pain Proper swing mechanics and potential swing modifications can ensure that incorrect compensation patterns do not overload other body segments, in particular, the shoulders. One of the most common strategies to decrease stresses on the spine is to shorten the swing in an attempt to reduce twisting of the trunk and spine. A study by Bulbulian and colleagues14 suggests that shortening the backswing can have a beneficial effect on the trunk and can reduce the potential for back problems. They found that the shortened backswing did reduce trunk muscle activation without reducing clubhead velocity or
BOX 37-5.
Strength-Training Program
Postseason (10 Weeks) 8-12 RM (major lifts)
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ball-contact accuracy. However, the short swing increased shoulder muscle activation and can increase the risk of shoulder injury. The golfer might attempt to compensate for the shortened backswing by excessive arm movement or overactivation, which can be detrimental to the shoulders. The therapist should closely monitor the backswing and stress that the backswing is being shortened for the overall benefit of the golfer. Lindsay and Horton51 compared the spinal motion in 12 male professional golfers: six with low back pain and six without low back pain. They found increased lumbar flexion in golfers with low back pain at ball address. These golfers also demonstrated greater side bending toward the lead side on the backswing. On examination, golfers with low back pain also had less trunk rotation. Lindsay and Horton proposed this limitation would force the golfer to rotate to extremes of motion, resulting in a relative overrotation of the spine when swinging. The golfer’s spine flexion angle at set-up must be evaluated and corrected as needed. The most common mistake at set-up is forward flexion at the spine instead of the proper hip hinge. When a proper hip hinge is used, the golfer flexes through the hip and maintains a neutral spine position. Club length may be modified when considering stresses placed on the spine during the golf swing. For example, when comparing the spine angles of the golf swing when using a 7 iron or when using a driver, spinal flexion and side bending were increased with the shorter 7 iron. Therefore, modifications of club length can help prevent or control low back pain.
70%-80% 1 RM 3-4 days/week
Shoulder Pathology
Offseason (12 Weeks)
The lead arm of the golf swing is the most common site of shoulder problems. This is probably due to the extreme horizontal adducted position at the end of the backswing. From this position at the top, there is a violent move toward the ball that is accelerated using the trunk musculature. At impact, the shoulder places the club in a position to strike the ball solidly. The load is then lifted from the lead shoulder. Common shoulder pathology in golfers includes labral tears, rotator cuff tears, and internal or mechanical impingement. Because of this horizontal position during the backswing, there can be coracoid or coracoacromial ligament impingement causing bursal inflammation.
8-12 RM, progressing to 6-8 RM (major lifts) 70%-80% 1 RM, progressing to 80%-90% 3-4 days/week Initiate plyometric drills
Preseason (14 Weeks) 6-8 RM (major lifts) 80%-90% 1 RM 3 days/week Initiate plyometric drills 2 days/week
Season (16 Weeks) 6-8 RM (major lifts) 60%-80% 1RM 2 days/week Plyometric drills 1-2 days/week RM, repetition maximum.
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The typical evaluation of the golfer’s lead shoulder involvement might not show typical loss of horizontal adduction, as is commonly seen with internal impingement. This is because of the horizontally adducted position the golfer assumes during the golf swing, which creates a natural ballistic stretch while swinging. If the golfer has
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normal range of motion, the next objective measurement is rotator cuff strength. This often shows a significant weakness in the lead shoulder. Verification of pathology can obviously be assisted with imaging studies, but posterior cuff weakness can be diagnosed with physical examination and is easily treatable with rehabilitation. Rotator cuff weakness can be attributed to many factors. Pain can be a leading contributor to rotator cuff weakness. This has been demonstrated clinically by a study we performed measuring rotator cuff weakness immediately before and immediately after xylocaine or cortisone injection into the shoulder. Our study showed a 35% improvement in posterior cuff strength when pain was blocked by xylocaine. Because pain has been proved to inhibit the rotator cuff, and the downswing causes high EMG activity of the rotator cuff, it is crucial that rotator cuff strength be restored. This is initiated with internal rotation and external rotation activity using exercise bands and, later, dumbbell exercises to focus on isolating the rotator cuff. If the golfer has lost internal rotation or horizontal adduction, there must be a concerted effort to mobilize and stretch the soft tissue of the posterior shoulder. This can be performed using contract-relax techniques and posterior glide mobilizations. In addition to traditional rehabilitation methods, alterations in the golf swing can influence shoulder pain. When initiating the golf swing following rotator cuff repair surgery, it is imperative that the golfer maintain a swing and posture that reduces the load on the repair. This is achieved by keeping the elbows tucked to the body during the backswing and downswing. Drills to emphasize this motion are shown in Figure 37-28. In this drill, the golfer can use either golf tees or small towels placed under the arms. During the swing, the player must keep the tees in position under the arm so they don’t drop to the ground. This posture removes the stress from the shoulders and uses the trunk musculature to accelerate the club. Many golfers have noted that adopting this swing immediately reduces shoulder pain. Acceleration of the golf club is primarily influenced by increased trunk and hip rotation. Players who use the trunk for increased speed have fewer shoulder problems. Golfers who use arm speed to increase the swing speed tend to load the rotator cuff and can develop more shoulder pathology. This type of swing is recognized by the flying elbow during the backswing. The farther away the golf club is positioned from the spine’s rotation, the less centripetal force is used and the more force is placed on the rotator cuff. Posterior instability can be a problem for the golfer. The symptoms can include popping during the transition from the top of the backswing to initiation of the downswing. Improvement of posterior instability symptoms can be of
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A
B Figure 37-28. Tee drill. This exercise is excellent for alleviating shoulder pain during the golf swing. The golfer holds the tee under the arm while taking the club back. A, Starting position. B, Ending position.
great benefit to the golfer. Unlike other sports where athletes can push through some discomfort, golfing requires intense mental concentration. Pain during this transition phase of the golf swing will cause frustration and an inability to play the sport if the problem is not resolved. An outline of rotator cuff strengthening exercises is shown in Figure 37-29.
SUMMARY Golf is increasingly being enjoyed throughout the world. As the frequency and intensity of play increase, more and more golfers seem to be incurring injuries from the game they have come to enjoy. With a good understanding of the biomechanics and kinematics of the golf swing, medical
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A
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B
D
C
and rehabilitation specialists can better diagnose and treat the shoulder injuries sustained by golfers at all levels of play. A thorough and well-structured rehabilitation program focused on the specific needs of the golfer can prevent further injuries and can enhance performance and prolong the golfer’s playing career.
References 1. Miburm PD: Summation of segmental velocities in the golf swing. Med Sci Sports Exerc 32(14):60-64, 1982. 2. Mallare C: Golf’s contribution to low back pain. Sports Med Update 11(2):20-25, 1997.
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Figure 37-29. Rotator cuff strengthening routine. Notice the 45-degree angle of the elastic resistance. This will focus on posterior cuff activation and fatigue.
3. Duda M: Golf injuries: They really do happen. Phys Sports Med 15(7):190-196, 1987. 4. Gosheger G, Liem D, Ludwig K, et al: Injuries and overuse syndromes in golf. Am J Sports Med 31(3):438-443, 2003. 5. McCarroll JR, Gioe TJ: Professional golfers and the price they pay. Phys Sports Med 10(7):64-70, 1982. 6. Kim DH, Millett PJ, Warner JP, Jobe FW: Shoulder injuries in golf. Am J Sports Med 32:1324-1330, 2004. 7. Mitchell K, Banks S, Morgan D, Sugaya H: Shoulder motions during the golf swing in male amateur golfers. J Orthop Sports Phys Ther 33(4):196-203, 2003. 8. Pink M, Perry J, Jobe FW: Electromyographic analysis of the trunk in golfers. Am J Sports Med 21(3):385-3881, 1993.
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9. Hovis WD, Dean MT, Mallon WJ, et al: Posterior instability of the shoulder with secondary impingement in elite golfers. Am J Sports Med 30; 886-890, 2002. 10. Jobe FW, Moynes DR, Antonelli DJ: Rotator cuff function during a golf swing. Am J Sports Med 14(5):388-392, 1986. 11. Pink M, Jobe FW, Perry J: Electromyographic analysis of the shoulder during a golf swing. Am J Sports Med 18(2):137-140, 1990. 12. Watkins RG, Uppal GS, Perry J, et al: Dynamic electromyographic analysis of trunk musculature in professional golfers. Am J Sports Med 24:535-538, 1996. 13. Geisler P: Kinesiology of the full golf swing. Implications for intervention and rehabilitation. Sports Med Update 11(2):9-19, 1997. 14. Bulbulian R, Ball KA, Seaman DR: The short golf backswing: Effects on performance and spinal health implications. J Manipulative Physiol Ther 24(9):569-575, 2001. 15. Mallon WJ: Golf. In Hawkins RJ, Misamore GW (eds): Shoulder Injuries in the Athlete. New York, Churchhill Livingstone, 1996. 16. Mallon WJ, Colosimo AJ: Acromioclavicular joint injury in competitive golfers. J South Orthop Assoc 4:277-282, 1995. 17. Wilk KE, Meister K, Andrews JR: Current concepts on the rehabilitation of the overhead throwing athlete. Am J Sports Med 30:136-151, 2002. 18. Wilk KE: Conditioning and training techniques. In Hawkins RJ, Misamore GW (eds): Shoulder Injuries in the Athlete. New York, Churchhill Livingstone, 1996. 19. Lehman GJ: Resistance training for performance and injury prevention in golf. J Can Chiropr Assoc 50:27-42, 2006. 20. Warner JJ, Micheli LJ, Arslanian LE, et al: Patterns of flexibility, laxity, and strength in normal shoulders and shoulders with instability and impingement. Am J Sports Med 18: 366-375, 1990. 21. Meyers JB, Laudner KG, Pasquale MR, et al: Glenohumeral range of motion deficits and posterior shoulder tightness in throwers with pathological internal impingement. Am J Sports Med 34:385-391, 2006. 22. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: A spectrum of pathology Part I: Pathoanatomy and biomechanics. Arthroscopy 19:404-420, 2003. 23. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: A spectrum of pathology Part II: Evaluation and treatment of SLAP lesions in throwers. Arthroscopy 19: 531-539, 2003. 24. Harryman DT 2nd, Sidles JA, Clark JM, et al: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72:1334-1343, 1990. 25. Warner JJ, Allen AA, Marks PH, Wong P: Arthroscopic release of postoperative capsular contracture of the shoulder. J Bone Joint Surg Am 79:1151-1158, 1997. 26. McClure P, Balaicuis J, Heiland D, et al: A randomized controlled comparison of stretching procedures for posterior shoulder tightness. J Orthop Sports Phys Ther 37:108-114, 2007. 27. Borstad JD, Ludewig PM: The effect of long versus short pectoralis minor resting length on scapular kinematics in healthy individuals. J Orthop Sports Phys Ther 35:227-238, 2005.
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28. Lukasiewicz AC, McClure P, Michener L, et al: Comparison of 3-dimensional scapular position and orientation between subjects with and without shoulder impingement. J Orthop Sports Phys Ther 29:574-586, 1999. 29. Vad VB, Bhat AL, Basrai D, et al: Low back pain in professional golfers: The role of associated hip and low back rangeof-motion deficits. Am J Sports Med 32(2):494-497, 2004. 30. Mellin G: Correlation of hip mobility with degree of back pain and lumbar spinal mobility in chronic low back pain patients. Spine 13:668- 670, 1988. 31. Barbee-Ellison JB, Rose SJ, Sahrmann SA: Patterns of hip rotation range of motion: Comparison between healthy subjects and patients with low back pain. Phys Ther 70: 537-541, 1990. 32. Fletcher IM, Hartwell M: Effect of an 8-week combined weights and plyometrics training program on golf drive performance. J Strength Cond Res 18(1):59-62, 2004. 33. Thompson CJ, Osness WH: Effects of an 8-week multimodal exercise program on strength, flexibility, and golf performance in 55- to 79-year-old men. J Aging Phys Act 12(2):144-156, 2004. 34. Westcott WL, Dolan F, Cavicchi T: Golf and strength training are compatible activities. Strength Cond 18:54-56, 1996. 35. Fradkin AJ, Sherman CA, Finch CF: How well does club head speed correlate with golf handicaps? J Sci Med Sport 7(4):465-472, 2004. 36. Church BJ, Wiggins MS, Moode FM, Crist R: Effect of warm-up and flexibility treatments on vertical jump performance. J Strength Cond Res 15:332-336, 2001. 37. Cornwell A, Nelson AG, Heise GD, Sidaway B: Acute effects of passive muscle stretching on vertical jump performance. J Hum Mov Stud 40:307-324, 2001. 38. Cramer JT, Housh TJ, Johnson GO, et al: Acute effects of static stretching on peak torque in women. J Strength Cond Res 18:236-241, 2004. 39. Evetovich TK, Nauman NJ, Conley DS, Todd JB: Effect of static stretching of the biceps brachii on torque, electromyography, and mechanomyography during concentric isokinetic muscle actions. J Strength Cond Res 17:484-488, 2003. 40. Fletcher IM, Jones B: The effect of different warm-up stretch protocols on 20-meter sprint performance in trained rugby union players. J Strength Cond Res 18:885-888, 2004. 41. Fowles JR, Jones B: Time course of strength deficit after maximal passive stretch in humans. Med Sci Sports Exerc 29:526, 1997. 42. Thacker SB, Gilchrist J, Stroup DF, Kimsey CD Jr: The impact of stretching on sports injury risk: A systematic review of the literature. Med Sci Sports Exerc 36:371-378, 2004. 43. Coleman AE: A baseball conditioning program for all seasons. In Andrews JR, Zarins B, Wilk KE (eds): Injuries in Baseball. Philadelphia, Lippincott Williams & Wilkins, 1998 pp 537-545. 44. Gambetta V: Get ready, get set. Training Cond 9:19-21, 1999. 45. Gambetta V: Stretching the truth. Training Cond 7:25-31, 1997. 46. Boyle M: Core training. In Boyle M (ed): Designing Strength Training Programs and Facilities. E-book available for purchase from http://www.michaelboyle.biz/ebook.htm (accessed February 27, 2008). 47. Reinold MM, Wilk KE, Reed J, et al: Interval sport programs: Guidelines for baseball, tennis, and golf. J Orthop Sports Phys Ther 32(6):293-298, 2002.
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48. Serlo M: Avoid and prevent. Steps for preventing low back pain in golfers. Sport Med Update 14:19-22, 1999. 49. Dawes J: General golf conditioning program. NSCA Performance Training Journal 4(3):7-13. Available at http://www. nsca-lift.org/Perform/articles/04033.pdf (accessed March 1, 2008).
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50. American College of Sports Medicine: Guidelines for Exercise Testing and Prescription, 7th ed. Philadelphia, Lippincott Williams & Wilkins, 2006. 51. Lindsay D, Horton J: Comparison of spine motion in elite golfers with and without low back pain. J Sports Med Sci 20:599-605, 2002.
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CHAPTER 38 The Artistic Gymnast’s Shoulder Larry Nassar and William Sands
Artistic gymnastics is the ultimate test of the strength, flexibility, and stability of the human shoulder complex. The complexity of the mechanics of the shoulder is as difficult to understand as the sport of artistic gymnastics. The average sports medicine professional has a fairly good understanding of the development, rules, and activities involved in such sports as football, basketball, baseball, hockey, soccer, track and field, cycling, swimming, and tennis. Gymnastics, however, is a sport that most medical professionals know by watching the Olympics and have little concept of the overall sport. The purpose of this chapter is to describe the sport of male and female artistic gymnastics and its effect on the shoulder complex.
Training and Progression The progression to becoming a member of the national team has been developed in great detail in an effort to ensure proper physical and mental preparation to perform the difficult skills needed to succeed at the elite level. To regulate this progression to the Olympics, the USAG has divided the women’s and men’s programs into the Junior Olympic and the Elite programs. The Junior Olympic program is designed to prepare a gymnast from the beginning to advanced levels of gymnastics. It is within these two programs that the split between the organization of men and women differs. Girls and Women The girls’ and women’s Junior Olympic program consists of ten progressive levels. Levels 1 to 4 are noncompetitive. These four levels are designed to develop the athletes’ strength, flexibility, and coordination. Gymnasts at these levels are not allowed to compete for rankings or places at a competition. They are allowed to compete for a judge’s score, and every participant receives a ribbon after each event she performs. This allows the gymnast to experience the effect of competing without the full mental stress of a meet. The awarding of ribbons to all competitors allows a sense of reward and accomplishment. Levels 5 and 6 are competitive levels, but the athlete performs compulsory routines on all events to ensure a baseline of skill performance progressing to the optional levels. Levels 7 to 10 are competitive levels where optional routines are performed, allowing the coach and athlete to select the skills they use for competition. The selection of skills at these levels is restricted to a certain list that allows the gymnast to gradually increase her skill level as she progresses up through the ranks to level 10. Only at level 10 do the gymnasts compete at a national championship. Each level is divided into age groups in an attempt to allow a fair competitive field. A child must be at least 7 years old to compete at levels 5 through 7, at least 8 years old to compete at level 8 or 9, and at least 9 years old to compete at level 10.2
OVERVIEW Overuse injuries are a large part of injury to the shoulder complex in the competitive artistic gymnast. To understand how overuse can occur, it is important to understand the development of gymnasts as they progress through the sport to the ultimate level of international elite gymnastics. This progression is similar, yet different between the genders, and therefore both will be outlined here. A basic understanding of a sport enhances the sports medicine professional’s doctor–patient relationship and instills further confidence in the athlete’s feeling toward the practitioner. USA Gymnastics (USAG) is the national governing body of artistic gymnastics, trampoline and tumbling, sport acrobatics, and rhythmic gymnastics. There were 4000 recorded gymnastics clubs in the United States in 2006. Recreational gymnastics accounts for the largest group, with 3 million participants. USAG has 1300 clubs registered as members, with 85,000 competitive athletes.1 Because USAG is the national governing body, their members are the only athletes allowed to represent the United States at international events. High school and collegiate gymnasts are not regulated by USAG but their rules are derived from the USAG rules. High school and collegiate gymnasts may participate with the USAG. Many of the male gymnasts on the national team also participate in college gymnastics. It is rare for a female gymnast to compete in both venues. For the purpose of this chapter, USAG gymnasts are considered club gymnasts.
The girls’ and women’s Elite program currently consists of the Talent Opportunity Program (TOP), pre-elite program, and elite program. The elite national team program consists of 12 seniors (age 16 years and older) and 16 juniors (age 11-15 years). The pre-elite and TOP programs have no set number of members and are designed to enhance 491
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an athlete’s physical and mental skills to prepare for the elite national team. The pre-elite level is grouped into child (ages 10-12 years), junior (ages 13-15 years), and senior (ages 16 years and older) divisions. The addition of TOPs in 1992 has been an excellent way for coaches and gymnasts to prepare for the pre-elite and elite levels. A gymnast must be between the ages of 7 and 11 years to be a member of the TOP.3 The TOP is based on physical abilities testing and skill testing to progress to a yearly National TOP Team Training Camp. If an athlete qualifies for this training camp yet is only 7 or 8 years old, the athlete’s coach is invited to the camp. The athlete is still too young to attend the camp herself; she must be at least 9 to personally attend the camp. The true purpose of the camp is to train the coaches how to progress their gymnasts safely to the elite national team. Since the addition of TOPs, gymnasts have been able to stay at their local clubs and train instead of leaving home to train at one of the few programs around the country. Now gymnasts can very easily live at home and train all the way up to the Olympics. Education of coaches is one of the greatest means of reducing injuries in gymnastics. Boys and Men The boys’ and men’s Junior Olympic program consists of 10 levels similar to the girls’ and women’s program. They are also divided into age groups at all levels. The boys and men compete starting at level 4, exercises in levels 4 through 7 are compulsory, and levels 8 through 10 allow optional routines. Levels 9 and 10 have a national championship competition. The minimum age to compete at level 4 is 6 years and at level 10 is 14 years.4 The boys do not have levels 1 through 3. The boys and men’s Elite Program consists of senior and junior elites. The senior elites are 18 years and older. The Junior Elite program consists of level 10 gymnasts who have qualified for the elite national championships based on their ranking at the level 10 national championships. Similar to the girls’ TOP, the boys have a Future Stars Program5 for 10- to 12-year-old gymnasts. This program began in 1995 and has stressed education of coaches and athletes to prepare safely for the elite level of competition.
Events The events that the men and women compete in are different. The men compete in six events: vault, parallel bars, pommel horse, rings, high bar, and floor exercise mat. The women perform the vault, uneven bars, balance beam, and floor exercise mat. The difference between these events allows the men to take advantage of their upper extremity strength with the parallel bars, pommel horse, rings and high bar. Shoulder injuries have traditionally been more common with the men due to these event differences.
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CAUSES OF INJURY The International Gymnastics Federation (FIG) regulates the rules for international competition worldwide. The rules change every 4 years based on the Olympic cycle. This is very important to understand. Injuries may be related to these rule changes.6 For example, before 1996 it was relatively rare for a female gymnast to sustain a knee or shoulder injury.7 From 1996 to 2000 the number of anterior cruciate ligament knee injuries in female gymnasts exploded.7 From 2000 to 2004 the number of shoulder injuries in women’s gymnastics became very large at the club level, and at the collegiate level it became a very serious issue, limiting full participation in the sport. Even men are now sustaining more shoulder injuries as a result of these rule changes. However, due to a new national team strength program that was instituted in 2000, the number of shoulder injuries on the women’s national team has dramatically declined.7 Proper conditioning is vital for injury prevention. Most medical practitioners consider spondylolysis to be a major problem in gymnastics, limiting an athlete’s ability to compete. This thought is greatly outdated. It is the shoulder that currently carries the most devastating injuries and that prevents a gymnast from further full participation in the sport. It is our belief that this trend is occurring because the level of difficulty in competition has increased at a rate faster than most athletes can safely improve their physical preparation. No other major sport in the United States changes its rules and raises the level of competition every 4 years. Imagine the result if basketball changed the size of the ball, the height of the rim, the length and width of the court, the number of fouls allowed, and the number of steps allowed every 4 years. The coaches would have to change their coaching plans constantly and the athletes’ risk for injury would also change. The equipment design has also changed over the years in both men’s and women’s artistic gymnastics. These equipment changes have radically changed the skills that the athlete can perform and has allowed more difficult skills to be practiced. Between the rule changes and the changes in equipment, it is extremely difficult to compare injuries sustained by today’s gymnast with those of gymnasts from before 2000. Unfortunately, as the FIG raises the level of competition, this trend filters down to the lower levels of competition and even affects collegiate and high school gymnastics. Thus, the gymnastics injury statistics published in the medical literature become outdated almost by the time the data are published and read. Some features of gymnastics make it different from most sports when it comes to injuries to the shoulder. First, gymnasts can sustain enough force through their twisting and flipping to dislocate their shoulders in mid air, and noncontact shoulder dislocations do occur in this sport.
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The best-known incident occurred when a U.S. Olympian dislocated her shoulder performing a triple layout twist (rotating along the midsagittal axis three times while rotating along the midtransverse axis one time) on the floor exercise mat while competing at the 2000 Olympic Games. These noncontact dislocations mainly occur with twisting skills; however an unpublished case did occur with a cheerleader from the New England area while performing a back tucked salto (rotating around the midtransverse axis of the body once) in which she dislocated both her shoulders at the same time. In both of these cases, the athlete had no prior shoulder pathology. The dislocation occurs from the forces the shoulder endures in creating the rotation of the body. Shoulder dislocations, however, do occur more commonly from the positions of the shoulders while the gymnast is holding onto an apparatus such as the rings, high bar, or uneven bars. One of us (LN) has 20 years of experience working with the USAG national teams. Even though these data have not been published,7 based on this experience with gymnasts, we recommend looking for two additional unique injuries. First, due to the forces sustained with upper-extremity straight-arm mechanics, gymnasts tend to have a greater incidence of posterior shoulder capsule injury than nongymnasts. Second, gymnasts are known to have shoulder labral pathology without a known episode of shoulder subluxation or dislocation. Be aware of this during the physical examination of the gymnast’s injured shoulder. As with other athletes in other sports, gymnasts have a tendency to overuse injuries in the shoulder. Biceps tendinitis, rotator cuff tendinitis, and shoulder impingement are common in both male and female gymnasts. According to Caine and Nassar,6 the shoulder is the most commonly injured joint in men’s gymnastics. In women’s gymnastics the ankle, wrist, and knee are more commonly injured than the shoulder.
MECHANICS OF THE SHOULDER IN GYMNASTICS The high-speed movements of throwing often result in shoulder injury. Gymnastics does not provide angular velocities as high as throwing, but the loads on the shoulder can be enormous.8 Gymnastics provides opportunities for the development and display of thousands of skills that involve movements of, and support by, the shoulder and nearby joints. At present, experience with the men’s Junior and Senior National Teams at the United States Olympic Training Center has revealed that shoulder injuries and resulting surgeries are extremely common: Nearly all of the members of the Senior National Team have had at least one surgery. Men’s gymnastics in particular appears to tax the shoulder, shoulder girdle, and upper extremity to the point where acute and chronic injuries are rampant.9
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Unfortunately, characterizing forces applied to the shoulder alone is astonishingly difficult. According to Bruggemann and colleagues, standard inverse dynamics techniques, although powerful, do not achieve sufficiently high levels of validity without extensive anatomic imaging of each subject and thorough understanding of the underlying calculation model.10-13 The methods used to determine the forces working through a joint involve two steps. The first step is to calculate the resultant moments and forces in the joint via inverse dynamics. Then the calculated moments and forces must be applied to the existing load-carrying structures. The load-carrying structures can involve an enormous degree of variability in dozens of factors. This results in an indeterminate system of equations. Although mathematical approaches have been undertaken to solve the resulting system of equations, they all rely on reducing the number of factors involved to a more manageable number. These approaches therefore rely heavily on the model used and the assumptions made. Moreover, there are a number of potential models from which to choose.14 Short of performing investigations involving high-quality medical images and sophisticated mathematical analysis techniques, can a physician get an idea of the types of loads presented to the shoulder during gymnastics activities? Fortunately, there are a number of tangential studies that may help the physician piece together a better understanding of the mechanical loads that might be seen by the shoulder in gymnastics training and performance. The following divides the problem of shoulder mechanics and characteristics by exploiting the available literature categorized by gymnastics events.
Locomotion on the Hands and Arms Glasheen and McMahon studied human locomotion by use of the hands and arms in a circumstance where part of their subject’s weight was supported while the subject walked and ran on his hands.15 Gymnasts also walk, run, and jump from their hands, although similar movements by gymnasts usually involve single efforts of no more than a few dozen steps. However, a notable exception to this is Glenn Sundby’s incredible feat of walking down the 898 steps of the Washington Monument on his hands. Glasheen and McMahon found that locomotion on the upper extremity was four to five times more metabolically costly than locomotion using the lower extremities.
Tumbling In gymnastics, the upper extremity is a supporting limb, as opposed to a limb used primarily for reaching, grasping, and carrying. In the classic handstand position, the primary determinant of balance control in terms of correcting torques comes from the wrists and shoulders.16 Although the wrists
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dominate, the shoulders provide another degree of freedom for balance correction and can often be seen as a relatively more dominant control strategy while young gymnasts learn a handstand.17 Advanced handstands require greater strength, proprioception, and range of motion (Fig 38-1). Gymnastics involves many skills that result in heavy impacts that are absorbed by the upper extremities. Studies of arm impact have shown that the initial impact has a high-frequency component that is quickly followed by a low-frequency component, which is due to the deceleration of the descending torso.18 The magnitude and timing of the force components seen during upper-extremity impacts appear to be highly dependent on the stiffness and damping of the wrist and shoulder joints.18 The differences in stiffness and damping might also be due to available muscle mass and thus can vary depending on age and size. A study of upper-extremity stiffness and damping during a dive roll and back handspring among boys and girls showed maximum impact velocities of these maneuvers. In the dive roll, maximum impact velocity for the wrist was 2.5 ± 0.5 m/sec and for the torso was 1.6 ± 0.5 m/sec. In the back handspring, maximum impact velocity of the wrist was 2.7 ± 0.3 m/sec and for the torso was 2.6 ± 0.2 m/sec. Impact forces for the dive roll were 1.5 ± 0.4 times body weight and for the back handspring were 2.0 ± 0.3 times body weight.18 Interestingly, the only significant relationship seen with the shoulder occurred in the back handspring among the studied children, showing that for every kilogram increase in mass, the shoulder damping increased 2.7 N/m. This points to the shoulder as being one of the primary joints for absorption of impact during these skills.
Horizontal Bar and Uneven Bars In a kinematic study of skilled and unskilled performers of the kip on the horizontal bar,Yamada, Ae, and Fujii19 showed that the shoulder reached more than 4 rad/sec in extension and less than 1 rad/sec in flexion, with more than 100 N•m torque in extension, nearly 100 N•m torque in flexion, and power of more than 400 W. This study was based only on kinematics; no medical images were included. A kinetic study of the backward giant swing on the horizontal bar resulted in forces ranging from 3.5 to 4.9 times body weight,20 with the peak forces being experienced slightly beyond the bottom (lowest point) of the swing. A study of the Stalder movement (straddle-piked circling motion to and from a handstand) by Daniels21 showed that inexperienced gymnasts reached forces of approximately 1.7 times body weight and skilled gymnasts reached peak forces of 2.5 times body weight. An unusual study of female gymnasts was seeking data on rail kinetics and athlete kinematics when a chance occurrence of a dangerous release and flyaway occurred from the uneven bars. The dangerous flyaway dismount was compared with a more typical technique for the same skill captured from a different athlete during the same test session. The results showed marked differences in rail forces, timing, and shoulder movement.22 The primary force- and torque-time pattern differences were shown during the upswing before the flyaway release. The errors made during the dangerous flyaway included grip release too late, rapidly increasing shoulder extension, leading to a center of mass flight trajectory that directed the athlete’s head toward the upper rail rather than away, and slightly lower but uniformly later peak forces and torques. The peak forces for the dangerous flyaway still remained around 2 to 3 times body weight, slightly less than the typical flyaway. The durations of the upswings differed between the superior and dangerous flyaways (0.33 sec and 0.42 sec, respectively). One of the lessons from this study was that high forces and torques might not be the major cause of a serious technique error and a serious injury near miss.
Vaulting
Figure 38-1. The Japanese handstand is an advanced handstand position on the floor exercise mat requiring great upper extremity strength and control.
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In a study of vaulting aptitude among 8- to 14-year-old female gymnasts,23 the investigators included a test item that is also a common drill in gymnastics training, which includes kicking to a handstand and bouncing off the hands to land in a second handstand after a brief flight phase from the hands (handstand push-off). The Bradshaw and Rossignol23 study used a portable force platform to determine the hand contact time during the handstand push-off. The authors found that the handstand push-off predicted vaulting ability and that the support time on the hands decreased with increasing age and ability. The ground contact times ranged from 0.239 sec (8- to 10-year-olds)
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to 0.194 sec (13- to 14-year-olds). Decreased contact time is a direct consequence of increased shoulder and shoulder girdle explosiveness. In a study of a specific upper-extremity joint, elbow forces were calculated from kinematic data by Panzer and colleagues on the Tsukahara vault, showing estimated forces at the elbow from 1.7 to 2.2 times body weight.24 Although the study did not specifically address the shoulder, this study was somewhat unusual in that a specific joint was addressed and the vault studied involved alternate rather than simultaneous hand placement. The Tsukahara vault was considered a difficult vault at that time.
Still Rings The still rings have become notorious for contributing to shoulder injury.8,25 The gymnast’s body can be characterized as a multiple pendulum with the shoulder serving as one of the axes. In a study of still ring forces in a long swing, Niu and colleagues26 found that peak forces during the gymnast’s swing past the bottom (lowest point) reached 4.27 to 4.66 times body weight. Cheetham and Sreden found peak forces ranging from 5.1 to 7.9 times body weight among 10- to 12-year-old male gymnasts.27 A study designed to assess how forces are minimized during the backward long swing on the still rings sought to explain how technique and elasticity of the gymnast and the ring apparatus serve to reduce forces at the shoulder.28 The researchers used computer simulation techniques to show that the peak combined forces at the shoulders were approximately 8.5 times body weight. They found that although the elasticity of the gymnasts and of the apparatus contributes to the peak forces seen at the shoulders, the primary contributor is the gymnast’s technique. Interestingly, when the gymnast’s body and the ring apparatus were modeled as rigid structures, the shoulder force reached 24.05 times body weight. Clearly, the gymnast and ring elasticity and the gymnast’s technique work together to reduce the shoulder forces that are seen to peak during the bottom of the swing.28 An EMG study of shoulder muscles during backward giant swings on the rings showed that the shoulder muscles examined tended to show a dramatic reduction in muscle tension during the latter phase of the fall to a vertical hanging position, declining to only 10% of the activation seen during the early stages of the fall.8 The authors speculated that the reduction in tension combined with a mistake in technique could lead to a SLAP (superior labral anteriorposterior) lesion or other shoulder injury. The authors also indicated that proprioceptive training might be helpful in teaching the gymnast to recognize the position of the head of the humerus in the glenoid fossa and labrum.
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A kinematic and kinetic study of shoulder and hip torques during a still rings backward giant swing showed that whereas the hips were net energy sinks at the bottom of the swing, the shoulders were a source of energy generation in the system.29 This study included a load cell in one of the ring cables and high-speed video. Peak shoulder torques were approximately 450 N•m. Tension on the cables reached approximately 6.5 times body weight. According to the authors, the muscular action at the shoulder joint as the gymnast passed the bottom of the swing was one of continuous shoulder-flexor activity. The muscle action helps the gymnast hold a position where the arms are pressed behind the head. After the gymnast swings through the bottom, the gymnast’s shoulder muscle activity continues in the shoulder flexors, but the tension shifts to eccentric. Bernasconi and colleagues30 undertook a study of the muscle activation characteristics of nine shoulder muscles during a cross on the still rings in men’s gymnastics (Fig. 38-2). The muscles investigated included the pectoralis major, latissimus dorsi, teres major, infraspinatus, rhomboideus and middle trapezius, lower trapezius, serratus anterior, biceps brachii, and triceps brachii. The largest muscular contributors to the cross were, in order of importance, the biceps brachii, triceps brachii, teres major, pectoralis major, latissimus dorsi, infraspinatus, serratus anterior, rhomboideus and middle trapezius, and lower trapezius. They found that the stabilizer muscles of the shoulder were highly active during the performance of the cross. More advanced positions are the inverted cross (Fig. 38-3) and the Maltese cross (Fig. 38-4).
Flexibility Shoulder range of motion and injury symptoms were assessed in female gymnasts and controls.31 Gymnasts were more flexible than controls in shoulder flexion and horizontal abduction. Flexibility between regions was not highly correlated, nor were there clear relations between flexibility
Figure 38-2. The iron cross is an icon in men’s gymnastics. It is a classic display of the strength and control of the gymnast’s shoulders.
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and injury symptoms except toe touching ability and low back pain. A comparison of male and female gymnasts, dancers, and controls in shoulder flexibility showed that active and passive ranges of motion were statistically different in gymnasts and dancers, whereas both gymnasts and dancers had greater shoulder ranges of motion when compared with the controls.32 Male gymnasts showed a more restricted range of motion in shoulder flexion that the authors thought might be due to the male gymnast’s emphasis on strength in the upper extremity. However, the authors noted that of the nine male gymnasts assessed in their study, six had already undergone shoulder surgery.
The mechanical loads on the shoulder can be astonishingly high. Moreover, the positions and postures of the gymnast while receiving these loads can be difficult for the gymnast to achieve and for the physician to anticipate. Gymnasts support themselves in inverted handstand positions and full hanging positions with the shoulder fully internally rotated and externally rotated. These positions are called elgrip (Fig. 38-5), eagle grip, or inverted grip (Fig. 38-6). Gymnasts also hang in a variety of positions including all of the foregoing plus positions called a German grip and a back lever position. All of these
Figure 38-3. The inverted cross is an advanced skill requiring exceptional control of the trunk and upper extremities. Figure 38-5. In the elgrip, the gymnast places the shoulder into a fully internally rotated position and is shown here in a hanging position on the high bar.
Figure 38-4. The Maltese cross is a very difficult skill on the still rings apparatus. As seen in the photograph, a crutch is often used to assist in training due to the incredible stress this position places on the gymnast.
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Figure 38-6. In the inverted grip, the gymnast places the shoulder into a fully internally rotated position. The gymnast is shown here in a handstand position on a floor rail bar used for training.
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positions take maximum advantage of the large range of motion of the shoulder while largely ignoring the concomitant instability of the shoulder. Gymnasts, coaches, and physicians should carefully balance the movement freedom of the shoulder with its instability.
REHABILITATION TECHNIQUES FOR THE INJURED GYMNAST’S SHOULDER In general, rehabilitation of the injured gymnast’s shoulder is similar to the rehabilitation of any other athlete’s shoulder. The important factor with all overuse injuries in any athlete is to look for the biomechanical imbalance and attempt to correct this imbalance. In addition to the glenohumeral joint, the thoracic spine, cervical spine, ribs, scapula, and clavicle might be involved and should be evaluated and manipulated to encourage more efficient shoulder mechanics and enhanced rehabilitation. Taping of the shoulder can be useful in the early rehabilitation phases. Variations of the principles McConnell (Fig 38-7) and Kinesio taping can be used to assist with the function of the shoulder. The reader is referred to Chapter 59 for further information on this topic. Scapulothoracic mechanics are vital for shoulder rehabilitation, and scapular stabilization exercises should be included in any program. Proprioceptive neuromuscular facilitation (PNF) patterns for the shoulder and scapula are helpful techniques. Additional rehabilitation protocols
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and exercises are discussed in the “Rehabilitation Principles” section of this book.
Phases In general, the rehabilitation of the injured gymnast’s shoulder is divided into five phases. Progression through the five phases varies depending on the gymnast’s injury. Specific limitations should be imposed by the attending physician based on the severity of the injury. This is meant to be a template that should be customized according to the physician’s treatment guidelines for the specific injury. Gymnasts recovering from their injury should continue to strengthen their trunk and lower extremities and work on their lower-extremity flexibility. They should be allowed to stay as active in the gymnastics club as possible without risking further injury to their shoulder (Fig. 38-8). Phase 1 Phase 1 exercises are specific to the injury and restricted range of motion. We recommend shoulder external rotation and internal rotation with arm in neutral; specific range of motion following subluxation or dislocation must be stated by the attending physician. We also recommend shoulder scaption, shoulder abduction to 90 degrees, shoulder adduction to 90 degrees, shoulder flexion to 90 degrees, shoulder extension, scapular retraction, rowing, shoulder protraction, scapular PNF patterns, elbow flexion (use caution in patients with a SLAP injury), and elbow extension. Phase 2 Phase 2 is a progression as the gymnast is released to work through the full range of motion. The following exercises may be included: prone shoulder flexion, overhead triceps extension, overhead straight-arm pulls (Fig. 38-9), shoulder pull-down into extension (Fig. 38-10), whole body band (Fig. 38-11), shoulder internal and external rotation at 90 degrees of abduction, and shoulder PNF patterns. Continuation from phase 1 of scapular stabilization and scapular PNF may be beneficial during phase 2. Rhythmic stabilization may also be started during this phase. A Bodyblade may be useful. The gymnast may begin with rhythmic stabilization exercises with the elbow kept next to the side, progressing to 90 degrees of abduction and then to overhead activity.
Figure 38-7. This is the anterior view of the tape application used to assist a member of the 2000 U.S. Olympic Team after she dislocated her shoulder on the floor exercise mat.
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The use of a slide board of a Total Gym or similar type of equipment can be very useful for straight-arm pulls and shoulder pull-downs to simulate skills on the uneven bars, high bar, and parallel bars. This type of equipment is also very helpful for male gymnasts as they return to rings. This slide-board pulley apparatus is useful in training and rehabilitating injured gymnasts by allowing a gradual progression of resistance to the upper extremities as they simulate their skills.
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Phase 1 Basic strength within a limited range of motion
Phase 2 Advanced strength through full range of motion including rhythmic stabilization
Phase 3 Closed-chain weight-bearing progression
Phase 2 Continue
Phase 4 Proprioception/ balance training
Phase 3 Continue
Phase 5 Upper extremity plyometrics
Phase 4, Part 1 Wobble board
Phase 4, Part 2 Swiss ball
Figure 38-8. Overview of the gymnast’s shoulder rehabilitation template.
Combining shoulder rehabilitation exercises with sitting on a Swiss ball may be beneficial for the gymnast (Fig. 38-12). Most of the exercises in phases 1 and 2 may be performed with the gymnast using the Swiss ball. This will challenge the gymnast to maintain good trunk form while doing shoulder exercises. Phase 3 Phase 3 is a closed-chain weight-bearing progression (Box 38-1 and Figs. 38-13 to 38-16). This phase may be started once the treating physician has given the gymnast permission to start closed-chain weight-bearing exercises. The gymnast should still be doing the phase 2 exercises, including rhythmic stabilization exercises, while performing this weight-bearing progression. The purpose of this phase is to gradually increase the forces imposed on the gymnast’s upper extremities. It also helps to guide the athlete on his or her return to performing gymnastics skills. The gymnast should progress through these exercises from phases 1 through 8. The gymnast should be able to
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Phase 2 (Con’t) Add event-specific rehabilitation. (e.g., Total Gym for rings and bars) Phase 2 Continue
Continue with a maintenance rehab program for an entire year.
Phase 4, Part 3 Advanced combinations
perform three sets of 5 to 15 repetitions of each exercise. Once the gymnast has accomplished three sets of 15 repetitions without difficulty or pain, then he or she may progress to the next exercise. Always wait at least 1 day before progressing to see how the injured shoulder feels before progressing. It is not uncommon to feel fine while doing the exercise but then having increased soreness the next day. The injured gymnast should not progress until it hurts. By the time the shoulder hurts, further damage may have occurred. The goal is to challenge the shoulder but not cause insult to the recovering injury. The progression stops at piked handstand push-ups. The handstand pushup is not needed in a progression like this because it can stress the injured shoulder too much. Phase 4 Phase 4 is designed to help the injured gymnast enhance proprioception and balance training. This is the most difficult phase for the injured gymnast to perform. The gymnast should not start this phase until adequate strength has been developed through the first three phases. In addition,
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Figure 38-9. Overhead straight-arm pulls using weights. The athlete starts with the weights at his or her sides. Keeping the arms straight, the athlete lifts the weight over the head and then slowly lowers it back to the starting position. This exercise can also be done supine with the band.
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Figure 38-10. Shoulder pull down into extension. Using bands attached to a rail, the gymnast stands or lies supine and pulls the band from over the head to the waist. The gymnast must keep the elbows straight.
the gymnast should continue with phases 2 and 3 exercises while progressing through phase 4. Phase 4 is broken into three parts. Each part is harder than the prior part. The gymnast progresses through each part as the strength and balance improve. Core strength is vital for the successful completion of this phase and for the completion of the injured gymnast’s shoulder rehabilitation program. Phase 4, part 1 (Box 38-2 and Fig. 38-17), is a set of exercises very similar to the phase 3 exercises. The gymnast may start this progression after the comparable phase 3 exercise has been successfully completed. For example, the mini trampoline on knees push-up should not be done until the phase 3 exercise, press-up in a push-up position, is completed. The mini trampoline exercises should always be one to two steps behind the phase 3 exercises in the progression. This allows proper strength to develop before starting the more challenging phase 4 exercises. The mini trampoline creates an unstable surface for the gymnast to work from. This enhances the gymnast’s proprioception and balance.
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Figure 38-11. Whole-body band exercise. Using a strong band of resistance, tie an 8- to 10-foot piece into a circle. Either standing or lying supine, the gymnast places the band around the feet and hands and shrugs the shoulders upward. The whole-body band is a way to strengthen the last portion of the shoulder shrug to help the gymnast to block and push through the shoulders. The gymnast should keep the axillae, ribs, and hips flat to maintain a good body alignment while performing this exercise.
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BOX 38-1. Closed-Chain Weight-Bearing Progression
Progress through these exercises in order from 1 through 8. Perform three sets of 5 to 15 repetitions of each exercise. 1. Wall press-out (Fig 38-13) • Place hands flat on a wall, shoulder-width apart and elbows extended. • Perform scapular protraction and retraction action, pushing through your arms into the wall. • Your hands should stay in contact with the wall and elbows remain extended throughout this drill. 2. Wall push-up with a press-out • Place hands flat on a wall, shoulder-width apart, elbows extended. • Perform a push-up against the wall and finish with a press-out. 3. Bent over press-out • Place hands flat on a table or the top of a mat. • Place hands shoulder-width apart and keep elbows extended. • Perform a press-out. Figure 38-12. The gymnast may combine trunk stabilization with shoulder rehabilitation by performing band or weight exercises while sitting on a Swiss ball. Here the gymnast is performing a Swiss ball proprioceptive neuromuscular facilitation D2 bilateral flexion exercise.
In phase 4, part 2, the gymnast uses a wobble board (round board with a round bottom) (Box 38-3 and Figs. 38-18 and 38-19). The wobble board is more advanced than the mini trampoline. It is preferable to have the gymnast start with the mini-trampoline progression and then add the wobble board progression so it lags behind by one step. For example, the gymnast who has progressed to doing the mini-trampoline push-up can start the wobble board circles on knees; the gymnast who has started the minitrampoline elevated push-up can start the wobble board circles in the push-up position. The wobble board exercises are performed by keeping the elbows straight and pushing through the arms into the board using scapular protraction and retraction as the main actions. The hands should be placed shoulder-width apart. The trunk should remain in a neutral to a posterior pelvic position. The gymnast should rock the board into clockwise and counterclockwise circles, performing three sets of 30 to 60 seconds of circles in each direction and progressing through the four main wobble board exercises. Variations of the wobble board exercises may be performed to make them more challenging for the gymnast if the basic exercises are too simple. Exercises with the foam rollers in combination with the wobble board are described in Box 38-3.
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4a. Press-up in a push-up position • In the push-up position, place your hands shoulderwidth apart with elbows extended. • Perform a press-out. 4b. Doggy rock (see Fig. 38-14) • Position yourself on the floor with your hands shoulder-width apart and your knees hip-width apart. • Dog rock back and forth while maintaining a stable trunk. • Keep the scapulae protracted while rocking. 5a. Dips reclined • Lean back onto a spotting block or platform table. • Keep feet on the floor. • Perform a dip action within a pain-free range of motion. 5b. L-Seat (sitting press-up) (see Fig. 38-15) • Using floor parrallette bars or just using a firm mat, press down with your arms to lift your body up in a pike position. • Your elbows should remain straight throughout the exercise. 6a. Push-up with a press-up • Perform a push-up with hands shoulder-width apart. • Perform a floor press-up at the end of the push-up. 6b. Pull-ups • Perform pull-ups on the uneven bars with your feet resting on the low bar and your body in an incline position so you lift only partial body weight up to the high bar (straight body pull).
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BOX 38-1. Closed-Chain Weight-Bearing Progression—cont’d
• Next add regular pull-ups. • As you become stronger you can change grip positions to make the push-ups more difficult. 7. Elevated push-up with a press-up • Place feet up on an 18- to 24-inch spotting block. • Perform a push-up with hands shoulder-width apart. • Perform a press-up at the end of the push-up. 8. Piked handstand push-up with a press-up (see Fig. 38-16) • Place feet up on a spotting block to position the body in a piked handstand position • Perform a push-up with hands shoulder-width apart. • Perform a press-up at the end of the push-up.
Figure 38-15. L-seat.
Figure 38-13. Wall press out.
Figure 38-14. Doggy rock.
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Figure 38-16. Piked handstand push-up with a press-up.
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BOX 38-2.
Mini Trampoline Exercises
Progress from 1 through 4, performing 3 sets of 8-15 repetitions with good form. 1. Mini tramp on knees push-up • In a kneeling position, perform a push-up with a press-out. 2. Mini tramp push-up • Perform a regular push-up with a press-out. 3. Mini tramp elevated push-up • Perform an elevated push-up with a press-out. 4. Mini tramp piked handstand push-up (see Fig. 38-17) • Perform a piked handstand push-up with a press-out.
Mini tramp, mini trampoline.
BOX 38-3.
Wobble Board Circles
Basic Place the hands shoulder-width apart. Keep the elbows straight and push through the arms into the board. Rock the board into clockwise and counterclockwise circles for 30 to 60 seconds so that the outer edge of the board makes contact with the floor throughout the circular motion. Progress through the following levels of difficulty: • On knees • In full push-up position • In elevated push-up position • In piked handstand position (the gymnast might need a spot).
With Foam Roller These are performed just like the basic wobble board on knees exercise, except the gymnast kneels on a foam roller to increase the difficulty. Place the hands shoulder-width apart. Keep the elbows straight and push through the arms into the board. Rock the board into clockwise and counterclockwise circles for 30 to 60 seconds so that the outer edge of the board makes contact with the floor throughout the circular motion. Progress through the following levels of difficulty: • Kneeling on a cut foam roller • Kneeling on a foam roller (see Fig. 38-19).
Figure 38-17. Mini trampoline piked handstand push-up.
Phase 4, part 3, uses combinations of equipment to enhance the difficulty of the balance and proprioception training. These are the most advanced exercises and should not be performed unless the athlete has properly progressed through the prior phases and has adequate strength and control (Box 38-4 and Fig. 38-20). Phase 5 Phase 5 consists of upper-extremity plyometrics (Box 38-5 and Fig. 38-21). Plyometrics are designed to transition strength into power. There is no value in doing these exercises if the athlete has not regained his or her strength. These exercises should be added in preparation for tumbling and vaulting. Plyometrics should be done at the
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Figure 38-18. Wobble board circles in elevated push-up position.
beginning of practice while the gymnast is rested. These exercises should not be done if the gymnast is fatigued. The gymnast must have explosive action when doing these exercises. The gymnast rotates through the four exercises in circuit fashion with a 2- to 3-minute rest between exercises. During
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Figure 38-20. Swiss ball push-ups with hands on volleyballs. Figure 38-19. Wobble board circles on knees with foam roller.
BOX 38-4.
Swiss Ball Push-ups
Basic Lay your chest on the Swiss ball and then walk on your hands until the ball reaches your feet. Hold the hollow body position while doing push ups. Perform 1 to 3 sets of 5 to 10 reps.
With Wobble Board Place your hands on a wobble board Perform clockwise and counterclockwise circles. Perform 1 to 3 sets of 20 to 40 seconds of circles.
Elevated Kneel on a spotting block or panel mat stack. Place your hands and chest on a Swiss ball. Roll the ball away from the mats. Hold the hollow body position while doing push-ups. Perform 1 to 3 sets of 5 to 10 reps.
With Cut Foam Rollers Place your hands on two cut foam rollers. Hold the hollow body position while doing push-ups. Perform 1 to 3 sets of 5 to 10 reps.
With Full Foam Roller Place your hands on a full foam roller. Hold the hollow body position while doing push-ups. Perform 1 to 2 sets of 5 to 10 reps.
With Volleyballs (see Fig. 38-20) Place your hands on two volleyballs. Hold the hollow body position while doing push-ups. Perform 1 to 2 sets of 3 to 7 reps.
rep, repetition.
the rest time the gymnast may stretch. Plyometrics should be done only twice a week (e.g., Monday and Thursday). This is the last phase of the rehabilitation program. The gymnast in phase 5 should be following a maintenance strength program composed of select exercises from the
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BOX 38-5.
Plyometrics
Rotate through the four exercises in circuit fashion, with a 2- to 3-minute rest between exercises. During the rest time the gymnast may stretch. 1. Plyometric wall push-away • Lean forward and fall toward a wall. • Catch yourself with your hands against the wall and then quickly push away from the wall and repeat. • Allow your elbows to bend close to 90 degrees. • Perform 3 sets of 10 reps. 2. Plyometric push-up with a blocking action • Start in the push-up position • Quickly snap arms over head and return to the push-up position. • Maintain a tight and stable trunk. • Perform 3 sets of 10 reps. 3. Plyometric hops with feet on a block • Start in a piked position. • Place feet up on a spotting block or locked into a stall bar. • Perform 5 short quick hops forward and then back again. • Perform 3 sets. 4. Plyometric hops in push-up position (wheelbarrow exercise) (see Fig 38-21) • Have a partner hold your feet and travel forward as you block the floor. • Perform 10 short, very quick forward hops forward. • Try not to bend your elbows greater than 45 degrees and try to maintain your trunk in a hollow body pushup position. • Repeat 3 sets of 5 reps.
rep, repetition.
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Figure 38-22. Shoulder hyperflexion supine stretch.
Figure 38-21. Plyometric hops with feet on a block.
first four phases. Chapter 55 gives further examples and details on upper extremity plyometrics.
Flexibility Flexibility of the shoulder is vital for successful gymnastics. There is a delicate balance between flexibility and instability. The two should not be confused. Gymnasts need to counteract the need for flexibility with their strength. Without the strength, the strain on the shoulders during gymnastics skills will convert the flexibility into instability. With adequate strength through the full range of motion, the shoulder capsule is protected and instability is less likely. The rehabilitation section in this book describes a generalized shoulder flexibility program. One specific stretch that is very useful for gymnasts is the supine hyperflexion shoulder stretch. The gymnast lies supine on a spotting block, panel mats, table, or other suitable elevated surface. The shoulders are supported by the edge of the surface, and the neck is unsupported and lying off the edge of the surface (Fig. 38-22). The gymnast grasps a dowel rod and stretches the arms overhead into hyper flexion. A weight may be wrapped around the dowel rod to increase the stretch. The athlete relaxes the arms and shoulders yet tightens the trunk by performing a posterior pelvic tilt to flatten the rib cage and hips. This gives the best overall stretch to the shoulders while maintaining good form and not overstressing the shoulder capsule. Following surgery, all stretches should be overseen by the physician, therapist, or certified athletic trainer to prevent complications with overstretching too early in the postoperative phase.
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TEMPLATE FOR RETURN TO GYMNASTICS AFTER A SHOULDER INJURY Here we list some generalized guidelines to help coaches make a more informed choice about how to progress the injured gymnast back to gymnastics. The attending physician, in consultation with the coach and athlete, should try and customize this template based on the gymnast’s skill level and injury. This program relates the strength needed to perform the exercise drills with gymnastics skills. In this manner, the gymnast should regain confidence in the injured shoulder and the coach can assess the gymnast’s ability to support his or her own body weight again to safely execute the gymnastics skills. The exercise drills listed in this section refer to the above closed-chain weight-bearing progression discussed earlier. 1. Once the gymnast has enough strength to perform a press-up in a push-up position, then the gymnast may try to hold a handstand against the wall (10-60 sec). The gymnast may also try hanging from the high bar at this time. 2. Once the gymnast can hold a handstand, he or she progresses to front and back walkovers on the floor mat. This helps to make sure the gymnast has enough arm strength so that the shoulder will not collapse as they do the walkovers. The athlete is still supporting the body weight with both arms at this stage. 3. When the gymnast can perform 3 sets of 10 back walkovers and front walkovers with no pain, he or she may start cartwheels on the floor mat during the next practice session. Cartwheels do require singlearm loading, so this may be difficult to do. Therefore, it is recommended that the gymnast be able to perform a push-up with a press-up before doing the cartwheels. The gymnast needs enough strength so the arm will not collapse during the single-arm phase of the cartwheels.
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4. Once the gymnast can perform 3 sets of 10 cartwheels he or she may attempt roundoffs and back and front handsprings on the TumblTrak (a long trampoline designed for performing tumbling passes) at the next practice. If the injured shoulder is on the lead arm for the roundoffs, then the roundoffs might be more difficult, and the gymnast might have to start with back and front handsprings. The gymnast should have enough strength to perform a piked handstand push-up with a press-up before attempting the roundoffs and front and back handsprings on the TumblTrak. 5. Once the gymnast can perform 10 roundoffs, 10 back handsprings, and 10 front handsprings on the TumblTrak with good form and strength, he or she may start performing combinations, such as roundoff– back handspring, on the TumblTrak. The gymnast should be increasing the force of the tumbling. Once the coach and athlete feel the gymnast has proper technique, the gymnast may start back tuck and layout saltos on the TumblTrak, landing into a safety pit. At the same time, individual skills may be added on the floor (roundoffs, back handsprings, front handsprings), and back walkovers, front walkovers, and cartwheels may be started on a line on the floor, then progressed to the low beam for the female athlete. More shoulder range of motion is needed to perform on the balance beam than on the floor because the narrow width of the beam requires greater shoulder abduction to grasp the beam. Thus, the gymnast must master the skills on the floor before attempting them on the beam. It may be possible to start tap swings on bars and rings now, also. 6. When the gymnast can do tumble passes into the pit off the TumblTrak, he or she should be able to start combinations on the floor. If the injured shoulder is the lead arm for a roundoff, torque will be greater and the roundoff may be more difficult than back and front handsprings. 7. Once the gymnast can do two sets of 10 combinations on the floor with good technique and good power, he or she can finish the passes with back tuck or layout saltos. During this time, the gymnast is increasing the difficulty of the tumbling passes on the TumblTrak. During this same phase, he or she may start individual skills (roundoffs, back handsprings, front handsprings) on a line, then on the low beam, then on the high beam. The gymnast should be able to do at least 10 of each skill before progressing from low to high beam. The gymnast may be able to do floor rail work during this phase to assist with bars. Progression must be pursued with caution. Do not overload the gymnast with too many new skills and drills on the same day. Try to stagger the addition of new skills and drills so that not too much is being added at one time. 8. Once the gymnast can do back tucked saltos and layouts on the floor, he or she should be ready to start vault drills. Start with handstand pop drills and
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progress to simple handspring vaults. We like to see 10 good handspring vaults with power and good technique before progressing to more difficult skills. If the lead arm for round-offs is the injured arm, it may take longer for the gymnast to be ready to start Yurchenko vaults. 9. Following a shoulder injury, parallel bars, pommel horse, uneven bars, and the high bar are more difficult to return to than the floor, balance beam, and vault. Therefore, we like to have the gymnast work on the floor, beam, and vault first before adding the events that can cause the most problems. So far the gymnast has only hung from the bar, worked tap swings, and done floor rail work. Now he or she may start to add skills to these events in a logical order. Add single arm skills, pirouettes, release moves, and complex grips, in that order, to the progression. Add one event at a time to prevent overuse problems or reinjury secondary to too much stress to the shoulder complex. These events place greater strain on the shoulder complex than the floor, vault, and balance beam. It is beneficial to build a good strength base back on floor and vault before attempting these more stressful events. 10. Still rings is the most difficult event to return to after a shoulder injury and should be the last event that is added back. Obviously, skills are added back in order of difficulty.
SUMMARY The key to a successful return to gymnastics is for the gymnast to first regain the range of motion of the shoulder. Next, the gymnast must regain strength and proprioception. The addition of plyometrics then helps convert the strength to power. Finally, the gymnastics skills are added in a logical order to complete the rehabilitation of the injured gymnast’s shoulder. It is highly recommended that the injured gymnast perform a maintenance program of shoulder exercises for an entire year before abandoning the rehabilitation program. Once the athlete is pain free for an entire year, the rehabilitation maintenance program may be discontinued. Due to the intense stress on the gymnast’s shoulder, a year-long maintenance program can help prevent a recurrence of the injury. The injured gymnast should not focus on what he or she cannot do but on what he or she can do.
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3. USA Gymnastics: Talent Opportunity Program goals and objectives. Available at: http://www.usa-gymnastics.org/ women/tops/05manualgoals.pdf (accessed March 1, 2008). 4. USA Gymnastics: General age group competition program information. Available at: http://www.usa-gymnastics.org/ men/2005/m-chapter1-replacementpages.pdf (accessed March 1, 2008). 5. USA Gymnastics: USA Gymnastics Men’s Program: Future Stars. Available at http://www.usa-gymnastics.org/men/ future-stars/ (accessed March 1, 2008). 6. Caine, DJ, Nassar, L: Gymnastics injuries. In Caine DJ, Maffulli N (eds): Epidemiology of Pediatric Sports Injuries: Individual Sports. Basel, Karger, 2005, pp 18-58. 7. Nassar L: Unpublished review of unpublished private medical records of the USAG Women’s Artistic National Team, TOPS, and Junior Olympic Nationals. 8. Cerulli G, Caraffa A, Ragusa F, et al: A biomechanical study of shoulder pain in elite gymnasts. In Riehle HJ, Vieten MM (eds): ISBS ‘98 XVI International Symposium on Biomechanics in Sports. Konstanz, Germany, University of Konstanz, 1998, pp 308-310. 9. Silvij S, Nocini S: Clinical and radiological aspects of gymnast’s shoulder. J Sports Med 22:49-53, 1982. 10. Ai K, Janshen L, Bruggemann, GP: Techniques for analyzing muscular activity and stress. In Leglise M (ed): Symposium Medico-Technique. Lyss, Switzerland, International Gymnastics Federation, 1999, pp 47-53. 11. Bruggemann GP: Mechanical load in artistic gymnastics and its relation to apparatus and performance. In Leglise M (ed): Symposium Medico-Technique. Lyss, Switzerland, International Gymnastics Federation, 1999, pp 17-27. 12. Bruggemann GP: Mechanical load and stress on the muscular skeletal system in gymnastics. In Robin J-F (ed): Actes des 2èmes Journées Internationales d’Etude de l’AFRAGA. Rennes, France, Association Française de Recherche en Activités Gymniques et Acrobatiques, 2000, pp 42-43. 13. Brüggemann GP: Mechanical loading and tissue response in young elite gymnasts. In Prassas S, Gianikellis K (eds): Applied Proceedings: Gymnastics, July 1-July 5, 2002. Caceres, Spain, Universidad de Extremadura, International Society on Biomechanics in Sports, 2002, pp 10-22. 14. Bruggemann GP: Biomechanical and biological limits in artistic gymnastics. In Wang Q (ed): Proceedings of the XXIII International Symposium on Biomechanics in Sports. Beijing, China Institute of Sport Science, 2005. 15. Glasheen JW, McMahon TA: Arms are different from legs: Mechanics and energetics of human hand running. J Appl Physiol 78(4):1280-1297, 1995. 16. Kerwin DG, Trewartha G: Strategies for maintaining a handstand in the anterior-posterior direction. Med Sci Sports Exerc 33(7):1182-1188, 2001. 17. George GS (ed): Biomechanics of Women’s Gymnastics. Englewood Cliffs, New Jersey, Prentice-Hall, 1980. 18. Davidson PL, Mahar B, Chalmers DJ, Wilson BD: Impact modeling of gymnastic back-handsprings and dive-rolls in children. J Appl Biomech 21:115-128, 2005. 19. Yamada T, Ae M, Fujii N: Comparison of the kip maneuver at the horizontal bar between the skilled and unskilled subjects. In Gianikellis KE (ed): Scientific Proceedings of the XXth International Symposium on Biomechanics in
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Sports. Caceres, Spain, Universidad de Extremadura, International Society of Biomechanics in Sports, 2002, pp 163-166. Ishii K, Komatsu T: Changes of kinematic parameters and forces on the horizontal bar backward giant swing. In Hoshizaki TB, Salmela JH, Petiot B (eds): Diagnostics, Treatment and Analysis of Gymnastic Talent. Montreal, Sport Psyche Editions, 1987, pp 107-117. Daniels DB: Identification of critical features in gymnastics skills through biomechanical and statistical analysis. In Hoshizaki TB, Salmela JH, Petiot B (eds): Diagnostics, Treatment and Analysis of Gymnastic Talent. Montreal, Sport Psyche Editions, 1987, pp 76-96. Sands WA, Smith SL, Westenburg TM, et al: Kinematic and kinetic case comparison of a dangerous and superior flyaway dismount—women’s uneven bars. In Hubbard M, Metha RD, Pallis JM (eds): The Engineering of Sport 5. Sheffield, UK, International Sports Engineering Association, 2004, pp 414-420. Bradshaw EJ, Rossignol PL: Identification of floor and vaulting aptitude in 8-14 year old talent selected female gymnasts. In Gianikellis, KE (ed): Scientific Proceedings of the XXth International Symposium on Biomechanics in Sports. Caceres, Spain, Universidad de Extremadura, International Society of Biomechanics in Sports, 2002, pp 171-174. Panzer VP, Bates BT, McGinnis PM: A biomechanical analysis of elbow joint forces and technique differences in the Tsukahara vault. In Hoshizaki TB, Salmela JH, Petiot B (eds): Diagnostics, treatment and analysis of gymnastic talent. Montreal, Sport Psyche Editions, 1987, pp 37-46. Caine DJ: Injury epidemiology. In Sands WA, Caine DJ, Borms J (eds): Scientific Aspects of Women’s Gymnastics. Basel, Karger, 2002, pp 72-109. Niu J, Lu X, Xu G, et al: Study on gymnastics ring movements using force measuring system. In Hong Y, Johns DP (eds): Proceedings of XVIII International Symposium on Biomechanics in Sports, 1st ed. Hong Kong, The Chinese University of Hong Kong, International Society for Biomechanics in Sports, 2000, pp 321-324. Cheetham PJ, Sreden HI, Mizoguchi H: Preliminary investigation of forces produced by junior male gymnasts on the rings. In Hoshizaki TB, Salmela JH, Petiot B (eds): Diagnostics, Treatment and Analysis of Gymnastic Talent. Montreal, Sport Psyche Editions, 1987, pp 99-106. Brewin MA, Yeadon MR, Kerwin DG: Minimizing peak forces at the shoulders during backward longswings on rings. Hum Mov Sci 19:717-736, 2000. Sprigings EJ, Lanovaz JL, Russell KW: The role of shoulder and hip torques generated during a backward giant swing on rings. J Appl Biomech 16:289-300, 2000. Bernasconi S, Tordi N, Parratte B, et al: Surface electromyography of nine shoulder muscles in two iron cross conditions in gymnastics. J Sports Med Phys Fitness 44:240-245, 2004. Kirby RL, Simms FC, Symington VJ, Garner JB: Flexibility and musculoskeletal symptomatology in female gymnasts and age-matched controls. Am J Sports Med 9(3):160-164, 1981. Gannon LM, Bird HA: The quantification of joint laxity in dancers and gymnasts. J Sports Sci 17:743-750, 1999.
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CHAPTER 39 Pediatric Shoulder Injuries Peter D. Asnis, Eric M. Berkson, and Thomas J. Gill
Youth participation in sports has changed dramatically since the 1970s.1,2 Not only has participation in sports grown, but the level of competition and the intensity of play have increased. Youth athletes are more likely to participate in high-impact sports and are more likely to specialize in a sport at a young age.3 This earlier specialization has led to year-round training by younger and stronger athletes who compete in more extensive ways.4 As this participation with increased physical stress has become more common, injuries to the upper extremity and shoulder have become more prevalent.5-7
BIOMECHANICS The skeletally immature athlete differs from the adult because of fundamental physiologic differences. In comparison with adult bones, pediatric bones have less mineral content, more porosity, and more flexibility. Children’s bones have a thicker periosteum that can stabilize fractures and increased vascularity that provides rapid rates of healing. Immature cartilage at the physis, at the joint surface, and at apophyseal insertions of tendons are subject to damage from direct injuries and overuse injuries. The physis is the weakest periarticular structure. Thus, the immature shoulder can suffer physeal fractures rather than ligamentous injuries. Growth plate fractures often occur through the hypertrophic zone and can produce growth disturbances or angular deformities.
Athletic injuries to the pediatric shoulder result from both macrotrauma and microtrauma and are largely sport specific.8-10 Shoulder fractures and dislocations occur most often in contact sports such as football and wrestling.11 Shoulder injuries remain the most common site of injury in hockey. About 85% of cycling injuries involve the upper extremity and lateral clavicle; acromioclavicular joint injuries are prevalent.12 Up to 11% of all pediatric skiing injuries and 20% of snowboarding injuries involve the shoulder.9
The young athlete has several predisposing factors to injury. Children often have underdeveloped musculature and less capacity to absorb energy of direct trauma and of repetitive overuse insults. Flexibility imbalances can also increase susceptibility to injury.16 Because the musculotendinous unit elongates in response to the growth of the long bones, the process of rapid growth itself can lead to further flexibility and strength imbalances. This can place the child at risk during these times.17,18
Overuse injuries to the shoulder in the pediatric population are seen in sports requiring overhead activities. Almost 80% of swimmers report a shoulder problem some time during their career.13 Microtrauma from repetitive rotational force places the proximal humerus at risk in baseball and other throwing sports. The number of high school and college pitchers needing surgery has increased secondary to a rise in the prevalence of these overuse injuries.6,14
THE THROWING ATHLETE The throwing motion of the young athlete is similar in both temporal parameters and kinematic relationships to that of the professional pitcher.19 The phases of the throwing motion and the relative timing through these phases remain unchanged. However, arm angular velocities, lever arm length, and resultant joint forces depend on age, physical maturity, and strength. These parameters are relatively lower in younger athletes.19 The velocity, acceleration, and force produced in the upper extremities of young pitchers are still considerable. Fleisig and colleagues calculated shoulder internal rotation velocities during arm acceleration at 6900 ± 1050 deg/sec in a youth population between 10 and 15 years of age.19 In a similarly aged population, Sabick and colleagues cited distraction forces at the shoulder of 1090 N
Injuries to the immature shoulder are often unique to the pediatric population; they are not simple corollaries of adult injuries. There are distinct differences in the physiology and biomechanics of the child, the adolescent, and the adult. Youth athletes are more susceptible to fractures and overuse injuries from lower forces. They have specific fracture patterns and possess a rapid healing and remodeling potential around open growth plates.15 In this population, glenohumeral instability is more likely than rotator cuff injuries. In addition, the treatment for these conditions differs from their adult counterparts. This chapter discusses the biomechanics of the immature shoulder and injuries resulting from both microtrauma and macrotrauma in the youth athlete. 507
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(108% body weight) and peak humeral torques of 18 N•m.20 Applied alone, this peak humeral torque is 400 times the sheer strength of epiphyseal cartilage.20 Routine exposure to forces of this magnitude has been postulated to affect the development of the retroversion of the humeral head.20-23 Although there is some variability in measurements, the humeral head normally anteverts during development from an average of 78 degrees of retroversion in preterm skeletons to 25 degrees to 30 degrees of retroversion in adulthood.24 Most of this anteversion of the humeral head occurs by the age of 8 years, but it continues until approximately 16 years of age.25 Several researchers have suggested that during this vulnerable period, external forces on the shoulder lead to the development of retroversion by hindering the progression of anteversion.20,26 This observation is supported by range-of-motion findings in professional pitchers. Side-to-side differences in shoulder external rotation appear to increase with age between populations of youth, adolescent, college, and professional pitchers.21,27 This external rotation occurs at the expense of internal rotation and shifts the arc of motion in these throwing athletes.21,27 An increase in retroversion in the dominant arm of these pitchers seems to explain these findings. In youth pitchers, osseous adaptations of the humeral head due to stresses at a young age lead to increased external rotation and a resultant increase in pitch velocity. However, these same forces place Little League pitchers at higher risk for injury than their professional counterparts.Youth pitchers have shorter strides that might not dissipate forces as well from the upper extremity to the trunk and legs.8 Forces may be less absorbed by underdeveloped musculature. The more upright posture, poorer balance, and inadequate flexibility of youth pitchers can also contribute to alterations from optimal throwing mechanics. EMG analysis of amateur pitchers reveals increased muscle activity of the rotator cuff and biceps and less activity in the latissimus and pectoralis, suggesting a less efficient transfer of energy to the ball.28 Several authors have attempted to define risk factors for injury in the young throwing athlete. Lyman and colleagues examined risk factors for shoulder and elbow pain in youth baseball players ages 9 to 14 years.29,30 Increased shoulder pain was related to decreased satisfaction with pitching, pitching with arm fatigue, number of pitches per game, and number of pitches per season. Risks for elbow pain were similar and also related to increased age and weight. Breaking pitches and high pitch counts significantly increased risk of shoulder and elbow pain.29 Based on these studies, the USA Baseball Medical and Safety Advisory Committee advised that young pitchers should focus on pitching mechanics and should control pitch counts.31 Returning to the mound after being removed from a game, pitching more than 9 months of the year, showcase pitching, and playing through pain should all be avoided.
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In a case-control study of adolescent pitchers (14-20 years of age) undergoing surgery, Olsen and colleagues noted that the overriding risk of injury was overuse. Pitching more than 80 pitches per game resulted in a fourfold increased risk of injury. Increased risks for injury were seen in taller, heavier pitchers who pitched harder. One half of the injured players perceived their coaches to be more concerned about winning than concerned about the player. Based on these findings, and on the authors’ opinions, safety recommendations for adolescent baseball pitchers were offered (Box 39-1).
LITTLE LEAGUER’S SHOULDER Little Leaguer’s shoulder was first described in 1953 by W.E. Dotter.32 Since this initial case report, several different terms have been used to describe this overuse condition found in the adolescent overhead athlete. Little Leaguer’s shoulder has also been called proximal humeral epiphyseolysis,33 osteochondrosis of the proximal humeral epiphysis,34 stress fracture of the proximal humeral epiphyseal plate,35 and rotational stress fracture of the proximal humeral epiphyseal plate.36 Although the cause of this condition continues to be a source of debate, the clinical picture of an adolescent with Little Leaguer’s shoulder has been fairly well established. Little Leaguer’s shoulder occurs in youth overhead athletes. Pain is localized to the proximal
BOX 39-1. Safety Recommendations for Adolescent Baseball Pitchers
Pitchers should avoid pitching with arm fatigue or arm pain. Pitchers should avoid pitching too much. Further research is needed on this topic, but reasonable limits are as follows: • Avoid pitching more than 80 pitches per game. • Avoid pitching competitively more than 8 months per year. • Avoid pitching more than 2500 pitches in competition per year. Monitor pitchers with the following characteristics closely for injury: • Pitchers who regularly use anti-inflammatories or ice to “prevent” an injury • Regularly starting pitchers • Pitchers who throw with velocity ⬎85 mph • Taller and heavier pitchers • Pitchers who warm up excessively • Pitchers who participate in showcases
Modified from Olsen SJ 2nd, Fleisig GS, Dun S, et al: Risk factors for shoulder and elbow injuries in adolescent baseball pitchers. Am J Sports Med 34(6):905-912, 2006.
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509
humerus and radiographic findings include widening of the proximal humeral physis (Fig. 39-1).37
describe swelling, weakness, atrophy, and decreased range of motion.7,37
In 1998, Carson and Gasser published their findings of one of the largest series of 23 patients with Little Leaguer’s shoulder.37 The average age in this series was 14 years. All patients were male baseball players. The average duration of symptoms for these patients was 7.7 months. About 83% of the patients were pitchers, 65% played baseball continually for at least 12 months, and 26% played on two different teams at the same time. In this series, players threw an average of 4.5 times per week. From these data, the authors conclude that Little Leaguer’s shoulder is an overuse injury to the proximal humeral epiphysis and physis and that there is a relation between the development of this condition and the amount and intensity of activity to which the shoulder is exposed.37 The researchers note that although this condition occurs more often than it is reported, it does not affect all adolescents who throw hard and often. It is difficult to quantify the amount and intensity of overuse that causes damage to the growth plate.
Radiographs are critical to making the diagnosis of Little Leaguer’s shoulder. Internal rotation and external rotation anteroposterior radiographs should be obtained of both the affected shoulder and the contralateral shoulder in order to compare the two sides.7,37 The radiographic hallmark of Little Leaguer’s shoulder is an increase in the width of the proximal humeral physis.37 This finding was present in 100% of the cases described by Carson and Gasser. Other, less common radiographic findings associated with Little Leaguer’s shoulder include demineralization,34 fragmentation of the lateral proximal humeral metaphysis,39 sclerosis of the proximal humeral metaphysis,33 and cystic changes. At least one of these findings was present in 52% of the cases described by Carson and Gasser.37 In cases where there is a high degree of suspicion for Little Leaguer’s shoulder but inconclusive x-rays, MRI may be helpful in making the diagnosis.40
Patients with Little Leaguer’s shoulder usually present with the chief complaint of gradual onset of pain in the proximal humerus with throwing or serving.37 Pain has been described with various stages of throwing. On physical examination, 87% of patients have tenderness over the proximal humerus, and 70% have more specific pain over the lateral aspect of the proximal humerus.37 The periosteum is thickest over the posteromedial aspect of the proximal humerus.38 This explains why the lateral physis is most commonly involved. Less commonly, patients
Figure 39-1. X-ray of Little Leaguer’s shoulder.
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Little Leaguer’s shoulder has been compared with a SalterHarris I fracture through the proximal humeral physis.37 In an acute Salter-Harris I fracture, there is a plane of separation through the hypertrophic zone of the growth plate. This zone represents the weakest part of the epiphyseal plate. After an acute injury, there is a widening of the physis as growth cartilage is produced at the site of injury. After several weeks, vessels infiltrate the area of injury, and the physis narrows as it heals.37 With Little Leaguer’s shoulder, radiographic changes take much longer to develop and resolve.33,41 In addition, other associated radiographic changes are more common with Little Leaguer’s shoulder than a simple acute SalterHarris I fracture. The difference in the radiographic appearance between a Salter-Harris I fracture and Little Leaguer’s shoulder is believed to be secondary to the different mechanism by which the pathology occurs. A Salter-Harris I fracture is an acute injury. Little Leaguer’s shoulder is caused by gradual and repetitive microtrauma, which leads to a more chronic radiographic appearance.37 The mechanism of injury leading to Little Leaguer’s shoulder has been studied. Sabick and colleagues evaluated the shoulder biomechanics of young baseball pitchers to look for a cause.20 They found that a combination of unique conditions of the developing shoulder in youth pitchers created a situation where the proximal humeral physis is prone to injury. Among the unique aspects are joint laxity, open epiphyseal plates, and underdeveloped musculature.8 In the adolescent patient, the epiphyseal plate is weaker than the surrounding musculoskeletal structures. Thus, an injury that can damage a ligament or tendon in an adult athlete can lead to an epiphyseal plate injury in the skeletally immature athlete.20
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Two types of mechanical loading can lead to Little Leaguer’s shoulder.20 The first type of loading is external rotational torque applied to the proximal humeral physis.42 During the act of throwing, the distal aspect of the humerus is externally rotated relative to the proximal end. This external rotational torque peaks just before maximal shoulder external rotation (at the end of arm cocking and the beginning of the acceleration phase of throwing).20 This torsional force is exerted over the epiphyseal plate. The shear stress caused by torsion alone represents approximately 400% of the shear strength of the epiphyseal cartilage and is probably enough to deform the cartilage of the proximal humeral epiphysis.20 The second type of loading during pitching is distraction of the shoulder at the time of ball release.36,41 In response to this distraction force, the rotator cuff exerts a proximally directed force to maintain the integrity of the glenohumeral joint.14 Because the rotator cuff inserts proximal to the proximal humeral physis, this distraction force acts across the physis. It has been estimated that the stress caused by distraction alone during pitching accounts for only 5% of the cartilage strength.20 During the act of pitching, the magnitude of peak stress caused by torsion is much greater than distraction. In addition, the growth plate is most resistant to tension and least resistant to torsion.20 Thus, repetitive rotational stress is the more likely cause of Little Leaguer’s shoulder. The growth plate is also known to be weakest in periods of rapid growth.17 In the proximal humeral epiphyseal plate, this occurs in the 13- to 16-year-old group, which coincides with the peak incidence of Little Leaguer’s shoulder. The treatment of Little Leaguer’s shoulder consists of activity modification, nonsteroidal anti-inflammatory drugs (NSAIDs), and shoulder-flexibility exercises.43 In particular, patients with Little Leaguer’s shoulder should rest from throwing for at least 3 months or until there is no pain with throwing.37 At that time, the adolescent athlete may gradually return to throwing activity. Once the athlete returns to play, the throwing technique should be modified, and the intensity and frequency of throwing should be limited until the growth plates close.43 In terms of activity modification, other recommendations have included rest from throwing until the following season39,42 and rest from throwing until the proximal humeral physis closes.34 The injury might heal clinically much sooner than the radiographs normalize. Thus, return to throwing is most often based on the resolution of clinical symptoms.44 Perhaps the best treatment of Little Leaguer’s shoulder is prevention. Little Leaguer’s shoulder is an overuse injury resulting from poor throwing technique, a developing skeleton that is prone to injury, and throwing with excessive frequency and intensity. In a time when Little League competition is taken much more seriously than originally intended, players and their parents must be taught about good and reasonable throwing habits. In most youth baseball leagues, there are rules limiting the number of innings
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pitched and regulating the number of rest days required between appearances. However, these rules do not limit the players’ pitch count or their ability to practice on their own time. Future research into the biomechanics of youth pitching and the risk factors for injury offers promise for preventing overuse injuries such as Little Leaguer’s shoulder.
ROTATOR CUFF INJURY The cause of rotator cuff disease in the pediatric population is clearly different from that in the adult. Rotator cuff disease in an adult has been described as a progressive continuum, ranging from the extremes of rotator cuff tendinitis to rotator cuff arthropathy. The underlying problem in adults is generally attributed to outlet impingement with extrinsic compression on the rotator cuff from the coracoacromial arch.10,45 In the pediatric population, however, rotator cuff disease is often attributed to secondary impingement.10,46 This may be due to the many unique anatomic aspects in the development of the musculoskeletal system in the skeletally immature patient. These patients commonly have general hyperlaxity of the shoulder joint and muscle imbalance.10 With excessive overuse of the shoulder in activities such as repetitive high-velocity throwing, the patient can develop a subtle anterior shoulder instability secondary to progressive attenuation of the anterior static restraints.47 In turn, this can lead to anterior subluxation of the humeral head when throwing, which can cause secondary impingement of the rotator cuff.35 A forceful eccentric load during throwing or swimming can cause further damage to the weakened rotator cuff.10 If left untreated, this can ultimately lead to a rotator cuff tear. Thus, rotator cuff disease in the pediatric and adult populations is represented by a progressive continuum of pathology. However, the underlying pathology is quite different. In the adult population, rotator cuff disease is attributed to degenerative changes and outlet impingement, resulting from extrinsic compression on the rotator cuff by the coracoacromial arch. In the pediatric patient, rotator cuff disease is attributed to microtrauma from repetitive overuse on a generally lax shoulder joint, which leads to subtle anterior instability and secondary impingement. Repetitive overuse is proved to cause histologic changes to tendons in animal studies.48 Soslowsky and colleagues studied an overuse running regimen in 36 rats.48 After daily running for at least 4 weeks, the histologic analysis of the supraspinatus tendons in these rats revealed increased cellularity, an increased number of active fibroblasts, and a disorganized pattern of collagen fibers. Biomechanical testing revealed a decrease in the modulus of elasticity and a decrease in the maximum stress to failure.48 Overuse of an animal tendon causes histologic changes to that tendon similar to what has been seen in humans with tendinopathy.48 Clearly, this predisposes the rotator cuff to further damage and tearing.
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Rotator cuff tears are very common in adults. In contrast, rotator cuff tears have very rarely been reported in the pediatric population. It has been reported that less than 1% of rotator cuff tears occur in patients younger than 20 years of age.45,49 For this reason, a rotator cuff tear in an adolescent may be overlooked, and it can be very disabling. Tarkin and colleagues point out that there is often a delay in diagnosis secondary to the rarity of the disease.49 This delay can lead to progressive exacerbation of the condition. They reported on four patients ages 12 to 14 years with rotator cuff tears.49 They suggest that a rotator cuff tear in a pediatric population may be secondary to either significant trauma or to chronic overuse. In terms of overuse, a rotator cuff can tear as a result of secondary impingement or internal impingement of the rotator cuff on the posterior glenoid rim.50,51 Yamanaka and Matsumoto studied 40 patients with partial thickness articular sided rotator cuff tears. They found that when these partial thickness tears were treated conservatively, 21 of 40 experienced enlargement of the tear and 11 of 40 progressed to full-thickness tears.52 Although they were studying an adult population, it seems that younger, more active patients can also have problems with untreated rotator cuff tears. Thus, it is important to make an early and accurate diagnosis. Patients with rotator cuff tears typically present with shoulder pain and weakness. Overuse of the shoulder can predispose the tendon to tear. Thus, rotator cuff tears should be suspected in adolescents who participate in repetitive activities with shoulder pain and weakness. A careful physical examination can reveal focal weakness of the rotator cuff, a positive lift-off or belly-press test, impingement signs, and change in range of motion compared with the contralateral shoulder. An x-can may reveal an avulsion of the tuberosity.53,54 Repeat x-rays at a later date can reveal calcification as the repair process begins.55 MRI is very helpful in confirming the diagnosis. The treatment of rotator cuff disease in the pediatric population depends on the extent of the injury. In general, the treatment of rotator cuff tendinitis in the pediatric population is to evaluate the biomechanics of the shoulder and address any underlying problems. Physical therapy remains the mainstay of treatment for these patients.43 Because rotator cuff tears are so rare in the pediatric population, the literature regarding the treatment of this injury is scarce. Tarkin and colleagues report that for fullthickness tears, primary repair seems to yield a good result.49 The treatment of partial-thickness tears is more controversial. There is no current literature comparing the results of nonoperative with operative treatment of partial-thickness rotator cuff tears in the pediatric population. When considering treatment options for these patients, each case must be analyzed individually in terms of the activity level of the patient, the level of disability, and the pattern of the tear.
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GLENOHUMERAL INSTABILITY Generalized shoulder laxity is a common finding in the pediatric population. There is an important difference between laxity and instability. Laxity has been defined as asymptomatic passive translation of the humeral head on the glenoid.56,10 Instability has been defined as “abnormal translation of the humeral head on the glenoid, which causes pain with active shoulder motion.”56,10 In any given position, only 25% to 30% of the humeral head is covered by the glenoid.10 This is one of the reasons that the glenohumeral joint can function through a very wide range of motion. However, there is a very delicate balance in the glenohumeral joint between passive mobility and stability.
Static and Dynamic Constraints The shoulder is a very complex structure, with both static and dynamic constraints that allow great mobility without sacrificing stability. The static constraints include the labrum, the bony articular anatomy, the capsuloligamentous structures (coracohumeral ligament, superior glenohumeral ligament, middle glenohumeral ligament, and inferior glenohumeral ligament), and negative intra-articular pressure.10 The dynamic constraints include the rotator cuff and the biceps tendon. Any injury to these constraints can interfere with the delicate balance between mobility and stability and can lead to an unstable shoulder. The labrum stabilizes the glenohumeral joint via several mechanisms. The labrum forms a ring around the glenoid and anchors the capsuloligamentous structures to the glenoid. It also deepens the fossa of the glenoid and increases the surface area between the glenoid and humeral head.10 When the labrum is detached from the glenoid anteriorly, the depth of the glenoid fossa is reduced by more than 50% in the anteroposterior dimension.57 This is why a Bankart lesion so often leads to anterior instability. The articular components of the glenohumeral joint are also important providers of shoulder stability. Patients with developmental hypoplasia or dysplasia of the glenoid are prone to instability. Similarly, patients with version abnormalities of the glenohumeral joint are prone to instability.58,59 Patients with a Hill-Sachs lesion involving more than 30% of the humeral head are also at risk for anterior instability.7,60 Although the capsuloligamentous structures must be somewhat loose to allow normal motion, any injury to one of the ligaments can lead to instability.10 With the shoulder in a position of abduction and external rotation, the IGHL has proved to be the primary restraint to anterior instability.61 Damage to this ligament can lead to instability. The vacuum effect created by negative intra-articular pressure also serves to stabilize the shoulder joint.62 When the
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capsule is penetrated, this stabilizing effect is lost, which can lead to instability.10,62 The rotator cuff and biceps tendon cause joint compression, leading to increased bony congruity and stability. Loss of rotator cuff function can lead to joint instability secondary to fatigue of the static stabilizers.10
Instability Pediatric patients with general shoulder laxity do not necessarily have shoulder instability. In this population, instability can result from several mechanisms. Instability can occur when an acute force that exceeds the ultimate failure strength of the shoulder stabilizers is placed across the glenohumeral joint.10 This usually results in a traumatic anterior dislocation. Instability can also occur as the result of repetitive forces below the ultimate failure strength. These submaximal forces can gradually lead to instability secondary to attenuation of the static soft tissue stabilizers of the glenohumeral joint.10 This is referred to as atraumatic instability and is often multidirectional. Repetitive motions such as throwing and swimming have been linked to multidirectional instability. There may also be a genetic component to shoulder instability. Patients who require a shoulder stabilization procedure have a higher incidence of a positive family history of shoulder instability. Dowdy and O’Driscoll found that 24% of patients who required a shoulder stabilization for recurrent instability had a first-degree relative with shoulder instability.63 Voluntary glenohumeral instability occurs in patients who can dislocate their shoulders at will. Although this condition may be associated with a history of emotional or psychiatric disorders, the instability can depend on position or be under muscular control.64 The most common type of shoulder instability in the pediatric population is traumatic anterior dislocation. The usual mechanism leading to dislocation is an indirect force to the arm in the abducted, extended, and externally rotated position.7 When these patients are seen in the emergency department or clinic, it is essential to obtain multiple radiographic views including anteroposterior, axillary, and scapular Y views to confirm or rule out dislocation. A good neurovascular examination must be performed, because a high incidence of neurologic deficit (especially to the axillary nerve) is associated with this injury.65 The acute treatment for a traumatic dislocation is a gentle reduction of the glenohumeral joint, followed by another set of x-rays to confirm that the reduction was successful. A postreduction neurovascular examination should be performed and documented as well.
Sequelae The most common sequela of a primary anterior shoulder dislocation is recurrence. The rate of recurrent dislocation in adolescent patients has been reported to be
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between 55% and 100%.7,66-70 The most common underlying pathology leading to this high recurrence rate is an anteroinferior glenoid labral tear. Hovelius and colleagues reported on 247 primary anterior dislocations that they followed for 10 years after the injury.71 The age range of their patients was 12 to 40 years. At 10 years’ follow-up, 48% of their patients had recurrent instability. When analyzed according to age, the younger patients in their study had a higher incidence of recurrence, and they more often required surgery secondary to their instability.71 Although the incidence of recurrence differs slightly from study to study, it is clear that there is a high rate of recurrence after a primary anterior dislocation in the pediatric population. Another common complication after primary anterior dislocation is development of arthropathy. Hovelius and colleagues reported a 20% incidence of post-dislocation arthropathy within 10 years of the injury.71 They suggested that the initial dislocation was responsible for most of the arthropathy and that later recurrences were much less important.
Treatment The definitive treatment of glenohumeral instability in the pediatric population is controversial. The most important factor in deciding how to treat these patients is the type of instability. For patients with recurrent traumatic unidirectional instability, surgical stabilization is often recommended.72 The goal of stabilization is to prevent recurrence and further arthropathy. Definitive treatment after the initial dislocation is less clear. The patient’s age, activity level, and mechanism of injury should all be taken into account when deciding whether to treat these shoulders with rehabilitation or stabilization. Regardless of the chosen treatment, Deitch and colleagues suggest that the prognosis for full recovery after a primary anterior shoulder dislocation is guarded.66 For a patient with atraumatic multidirectional instability, the mainstay of treatment is prolonged rehabilitation. Conditions that can lead to generalized laxity, such as Marfan’s syndrome and Ehlers-Danlos syndrome, should be ruled out.10 If conservative treatment is truly exhausted, then an inferior capsular shift may be indicated.72 Patients with voluntary instability are another very difficult group to treat. These patients should also be treated with prolonged rehabilitation. If these patients have positional instability, then surgery may be beneficial. In patients with voluntary instability secondary to muscular control, there is a high rate of recurrence after stabilization procedures.10 Thus, caution is required when recommending these patients for surgery.
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FRACTURES Pediatric fractures about the shoulder are relatively uncommon, and they are unique in several ways. Because of their proximity to the open physis, fractures in this region possess a rapid healing and remodeling potential. Fractures can usually be treated nonoperatively, but knowledge of operative indications is important for optimal outcomes. Fractures in the female athletic population must be assessed for the female triad.73,74 This triad includes osteoporosis, disordered eating, and amenorrhea. The female athlete’s triad should be suspected in female athletes with low body fat, poor nutrition, and a history of exercising intensely. Female patients who suffer from this condition are prone to fractures. Fractures of any kind in women or girls can signal these problems. These patients should be treated not only for their fracture but also for their other related problems.
Proximal Humerus The four articulations around the shoulder and their respective centers of ossification appear in predictable sequences and possess implications for the types of injuries to this region (Fig. 39-2). The proximal humeral epiphyseal ossification center appears by 6 months of age. The greater tuberosity forms between 7 months and 3 years, and the lesser tuberosity appears by age 5 years. These three secondary ossification centers coalesce between ages 5 and 7 years to form the proximal humeral epiphysis.75 The physis is extra-articular, except medially, where the capsule extends beyond the anatomic neck. The epiphysis fuses to the metaphysis between ages 14 and 17 years in girls and ages 16 and 18 years in boys. About 80% of humeral growth occurs from the proximal growth plate, offering great remodeling potential in this area.75,76
3m
Salter-Harris type I fractures typically occur in patients younger than 5 years. After coalescence of the proximal epiphyseal ossification centers, which occurs around age 5 years, metaphyseal fractures begin to become more common. Salter-Harris type II fractures predominate after age 11 years. These fractures occur secondary to a disruption of the weakest portion of the periosteum in the anterolateral aspect of the humerus. Salter-Harris types III and IV fractures are usually caused by high-energy trauma (Fig. 39-3). The proximal humerus has great remodeling potential. Thus, most minimally displaced or angulated fractures can be treated with sling-and-swathe immobilization and early motion.78 Shortening of the extremity 1 to 3 cm can be seen with premature closing of the physis. However, this is usually not clinically significant.76,78,79 Partial arrest of the growth plate can lead to varus deformity and resultant shoulder impingement.80 Fractures with significant angulation or displacement (⬎75 degrees in children younger than 7 years, ⬎60 degrees in children between 8 and 11 years, and ⬎45 degrees in children 12 years and older), are treated with closed reduction and percutaneous pinning.81 Failure of closed reduction can be due to interposition of the long head of the biceps, periosteum, or capsule and requires open reduction.81
1y
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Proximal humerus fractures in the pediatric population are relatively rare. They represent 4% of all physeal fractures and are usually secondary to direct contact. Indirect trauma such as a fall onto an outstretched hand can result in a fracture of the proximal humerus as well. In the adult population, this same indirect trauma is more likely to produce a glenohumeral dislocation. Approximately 20% of proximal humerus fractures in young patients occur during sporting activities.77 About 25% of pediatric proximal humerus fractures occur through unicameral bone cysts.77
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Figure 39-2. A, Average ages of appearance of epiphyseal ossification center about the shoulder girdle for greater tuberosity, proximal humerus, proximal and distal clavicle, acromion, coracoid, medial scapula, and glenoid ossification center. B, Fusion of these ossification center ages are shown for proximal and distal clavicles, coracoid, acromion, glenoid, medial scapula, and proximal humerus.
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A
C
B
Figure 39-3. A, Anteroposterior (AP) x-ray showing a high-energy Salter-Harris type II fracture in a 14-year-old skateboarder. B, AP view of internal fixation. C, Final result after removal of hardware.
Lesser tuberosity avulsion fractures in the pediatric population represent an apophyseal injury. Open reduction and internal fixation are performed for acute displaced fractures.82 Operative reduction of fractures in adolescents may be more important than in younger patients.81 In a series of 18 patients 15 years and older with highgrade proximal humerus fractures, no operative or postoperative complications were noted, and postoperative glenohumeral motion was almost normal in this group of patients.81
Clavicle Fractures Clavicle fractures are the most common fractures of childhood. About 85% are midshaft and are usually due to direct trauma. These fractures heal rapidly. Nearly all can be treated nonoperatively with a sling. Sporting activities may be difficult for 6 to 8 weeks. The lateral clavicle accounts for 20% to 30% of clavicle growth and closes at 20 years of age. For this reason, a direct fall onto the shoulder in a child usually results in a physeal fracture instead of a true acromioclavicular dislocation. The classification of these fractures is similar to that in adults. However, it does recognize that a fracture to the distal clavicle disrupts the periosteal sleeve instead of the coracoclavicular ligaments.83 Minimally displaced injuries of the distal clavicle (types I, II, and III) are managed with sling and early motion. Remodeling of these fractures is excellent because the periosteum usually remains intact.5 There is some controversy regarding the treatment of displaced distal clavicle fractures. Good results have been seen with both operative and nonoperative treatments.5,84 Osteolysis of the distal clavicle can be seen as a late sequela of grades I and II acromioclavicular joint sprains. This can also be a result of repetitive microtrauma in younger athletes
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with year-round weight training. Rest, rehabilitation, and injections are usually successful in treating this condition. The medial clavicle secondary ossification center appears at age 17 years and closes between ages 18 and 24 years. It is responsible for 80% of the clavicle’s growth. True dislocations of this joint are rare, and most fractures are physeal disruptions. The epiphysis remains attached, and the medial clavicular shaft displaces anteriorly or posteriorly. This usually occurs from a lateral blow to the shoulder and depends on the position of the shoulder at the time of impact. If the shoulder is driven anteriorly, then posterior displacement occurs. Determination of the direction of displacement may be difficult due to swelling. Tangential radiologic views of the joint or a CT scan can assist in the diagnosis. Although anterior dislocations require a subacute reduction, posterior dislocations can impinge on major vessels, the trachea, or the esophagus.85 An emergent reduction is usually performed with a thoracic surgeon available to assist if needed. Catastrophic pin migration and hardware complications prevent use of internal fixation for these fractures.86 Return to sports requires 3 to 4 months.
SUMMARY There are fundamental differences in the anatomic and biomechanical properties between the pediatric and the adult athlete. Several unique properties of the developing shoulder in the skeletally immature population predispose this group to specific injuries. Little Leaguer’s shoulder is one condition seen specifically in the pediatric population. Rotator cuff disease, glenohumeral instability, and shoulder fractures occur in both the adult and pediatric populations. However, the underlying pathology and treatment algorithms differ between these age groups.
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Other less-common conditions can also lead to shoulder pain in pediatric patients. Conditions such as long thoracic nerve palsy, snapping scapula, acromial apophysitis,87 cervical spine disease, and others can lead to shoulder pain in youth athletes. Bone and soft tissue tumors should always be considered and ruled out in pediatric patients with shoulder pain; although these conditions are beyond the scope of this chapter, it is important to consider all possible causes for shoulder pain in young athletes. Understanding the fundamental anatomic and biomechanical differences in the developing shoulder of the youth athlete will lead to a more accurate diagnosis and appropriate treatment in this patient population.
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17. Bright RW, Burstein AH, Elmore SM: Epiphyseal-plate cartilage. A biomechanical and histological analysis of failure modes. J Bone Joint Surg Am 56(4):688-703, 1974. 18. Gill TJ, Micheli LJ: The immature athlete. Common injuries and overuse syndromes of the elbow and wrist. Clin Sports Med 15(2):401-423, 1996. 19. Fleisig GS, Barrentine SW, Zheng N, et al: Kinematic and kinetic comparison of baseball pitching among various levels of development. J Biomech. 32(12):1371-1375, 1999. 20. Sabick MB, Kim YK, Torry MR, et al: Biomechanics of the shoulder in youth baseball pitchers: Implications for the development of proximal humeral epiphysiolysis and humeral retrotorsion. Am J Sports Med 33(11):1716-1722, 2005. 21. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 30(1):20-26, 2002. 22. Pieper HG: Humeral torsion in the throwing arm of handball players. Am J Sports Med 26(2):247-253, 1998. 23. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30(1):136-151, 2002. 24. Edelson G: Variations in the retroversion of the humeral head. J Shoulder Elbow Surg 8(2):142-145, 1999. 25. Edelson G: The development of humeral head retroversion. J Shoulder Elbow Surg 9(4):316-318, 2000. 26. Osbahr DC, Cannon DL, Speer KP: Retroversion of the humerus in the throwing shoulder of college baseball pitchers. Am J Sports Med 30(3):347-353, 2002. 27. Mair SD, Uhl TL, Robbe RG, et al: Physeal changes and range-of-motion differences in the dominant shoulders of skeletally immature baseball players. J Shoulder Elbow Surg 13(5):487-491, 2004. 28. Gowan ID, Jobe FW, Tibone JE, et al: A comparative electromyographic analysis of the shoulder during pitching. Professional versus amateur pitchers. Am J Sports Med 15(6):586-590, 1987. 29. Lyman S, Fleisig GS, Andrews JR, et al: Effect of pitch type, pitch count, and pitching mechanics on risk of elbow and shoulder pain in youth baseball pitchers. Am J Sports Med 30(4):463-468, 2002. 30. Lyman S, Fleisig GS, Waterbor JW, et al: Longitudinal study of elbow and shoulder pain in youth baseball pitchers. Med Sci Sports Exerc 33(11):1803-1810, 2001. 31. American Sports Medicine Institute: USA Baseball Medical & Safety Advisory Committee: Guidelines, May 2006. Position Statement on Youth Baseball injuries. Available at http://www.asmi.org/asmiweb/usabaseball.htm (accessed March 1, 2008). 32. Dotter WE: Little Leaguer’s shoulder: A fracture of the proximal epiphysial cartilage of the humerus due to baseball pitching. Guthrie Clin Bull 23(1):68-72, 1953. 33. Barnett LS: Little League shoulder syndrome: Proximal humeral epiphyseolysis in adolescent baseball pitchers. A case report. J Bone Joint Surg Am 67(3):495-496, 1985. 34. Adams JE: Little League shoulder: Osteochondrosis of the proximal humeral epiphysis in boy baseball pitchers. Calif Med 105(1):22-25, 1966. 35. Ireland ML, Andrews JR: Shoulder and elbow injuries in the young athlete. Clin Sports Med 7(3):473-494, 1988. 36. Cahill BR, Tullos HS, Fain RH: Little League shoulder: Lesions of the proximal humeral epiphyseal plate. J Sports Med 2(3):150-152, 1974.
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37. Carson WG Jr, Gasser SI: Little Leaguer’s shoulder. A report of 23 cases. Am J Sports Med 26(4):575-580, 1998. 38. Curtis R, Rockwood CA: Fractures and dislocations of the shoulder in children. In Rockwood CA, Matsen FA, 3rd, (eds): The Shoulder, vol 2. Philadelphia, WB Saunders, 1990, pp 991-1032. 39. Lipscomb AB: Baseball pitching injuries in growing athletes. J Sports Med 3(1):25-34, 1975. 40. Song JC, Lazarus ML, Song AP: MRI findings in Little Leaguer’s shoulder. Skeletal Radiol 35(2):107-109, 2005. 41. Tibone JE: Shoulder problems of adolescents. How they differ from those of adults. Clin Sports Med 2(2):423-427, 1983. 42. Albert MJ, Drvaric DM: Little League shoulder: Case report. Orthopedics 13(7):779-781, 1990. 43. Hogan KA, Gross RH: Overuse injuries in pediatric athletes. Orthop Clin North Am 34(3):405-415, 2003. 44. Adams JE: Bone injuries in very young athletes. Clin Orthop 58:129-140, 1968. 45. Itoi E, Tabata S: Rotator cuff tears in the adolescent. Orthopedics 16(1):78-81, 1993. 46. Neer CS: Cuff tears, biceps lesions, and impingement. In Neer CS (ed): Shoulder Reconstruction. Philadelphia, WB Saunders, 1990, pp 41-142. 47. Jobe FW, Kvitne RS, Giangarra CE: Shoulder pain in the overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18(9):963-975, 1989. 48. Soslowsky LJ, Thomopoulos S, Tun S, et al: Neer Award 1999. Overuse activity injures the supraspinatus tendon in an animal model: A histologic and biomechanical study. J Shoulder Elbow Surg 9(2):79-84, 2000. 49. Tarkin IS, Morganti CM, Zillmer DA, et al: Rotator cuff tears in adolescent athletes. Am J Sports Med 33(4):596-601, 2005. 50. McFarland EG, Hsu CY, Neira C, et al: Internal impingement of the shoulder: A clinical and arthroscopic analysis. J Shoulder Elbow Surg 8(5):458-460, 1999. 51. Paley KJ, Jobe FW, Pink MM, et al: Arthroscopic findings in the overhand throwing athlete: Evidence for posterior internal impingement of the rotator cuff. Arthroscopy 16(1):35-40, 2000. 52. Yamanaka K, Matsumoto T: The joint side tear of the rotator cuff. A followup study by arthrography. Clin Orthop Relat Res (304):68-73, 1994. 53. Klasson SC, Vander Schilden JL, Park JP: Late effect of isolated avulsion fractures of the lesser tubercle of the humerus in children. Report of two cases. J Bone Joint Surg Am 75(11):1691-1694, 1993. 54. Paschal SO, Hutton KS, Weatherall PT: Isolated avulsion fracture of the lesser tuberosity of the humerus in adolescents. A report of two cases. J Bone Joint Surg Am 77(9):1427-1430, 1995. 55. Uhthoff HK, Sano H: Pathology of failure of the rotator cuff tendon. Orthop Clin North Am 28(1):31-41, 1997. 56. Harryman DT 2nd, Sidles JA, Clark JM, et al: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72(9):1334-1343, 1990. 57. Howell SM, Galinat BJ: The glenoid-labral socket. A constrained articular surface. Clin Orthop Relat Res (243): 122-125, 1989. 58. Brewer BJ, Wubben RC, Carrera GF: Excessive retroversion of the glenoid cavity. A cause of non-traumatic posterior instability of the shoulder. J Bone Joint Surg Am 68(5): 724-731, 1986.
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59. Hill JA, Tkach L, Hendrix RW: A study of glenohumeral orientation in patients with anterior recurrent shoulder dislocations using computerized axial tomography. Orthop Rev 18(1):84-91, 1989. 60. Connolly J: Humeral head defects associated with shoulder dislocation: Their diagnostic and surgical significance. Instr Course Lect 21:42-52, 1972. 61. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18(5):449-456, 1990. 62. Warner JJP DX, Warren RF, Torzilli PA.: Superior-inferior translation in the intact and vented shoulder. J Shoulder Elbow Surg 2:99-105, 1993. 63. Dowdy PA, O’Driscoll SW: Shoulder instability. An analysis of family history. J Bone Joint Surg Br 75(5):782-784, 1993. 64. Rowe CR, Pierce DS, Clark JG: Voluntary dislocation of the shoulder. A preliminary report on a clinical, electromyographic, and psychiatric study of twenty-six patients. J Bone Joint Surg Am 55(3):445-460, 1973. 65. Visser CP, Coene LN, Brand R, et al: The incidence of nerve injury in anterior dislocation of the shoulder and its influence on functional recovery. A prospective clinical and EMG study. J Bone Joint Surg Br 81(4):679-685, 1999. 66. Deitch J, Mehlman CT, Foad SL, et al: Traumatic anterior shoulder dislocation in adolescents. Am J Sports Med 31(5):758-763, 2003. 67. Hovelius L: Anterior dislocation of the shoulder in teenagers and young adults. Five-year prognosis. J Bone Joint Surg Am 69(3):393-399, 1987. 68. Marans HJ, Angel KR, Schemitsch EH, et al: The fate of traumatic anterior dislocation of the shoulder in children. J Bone Joint Surg Am 74(8):1242-1244, 1992. 69. Postacchini F, Gumina S, Cinotti G: Anterior shoulder dislocation in adolescents. J Shoulder Elbow Surg 9(6):470-474, 2000. 70. Rowe CR: Prognosis in dislocations of the shoulder. J Bone Joint Surg Am 38-A(5):957-977, 1956. 71. Hovelius L, Augustini BG, Fredin H, et al: Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J Bone Joint Surg Am 78(11):1677-1684, 1996. 72. Thomas SC, Matsen FA 3rd: An approach to the repair of avulsion of the glenohumeral ligaments in the management of traumatic anterior glenohumeral instability. J Bone Joint Surg Am 71(4):506-513, 1989. 73. Nattiv A, Agostini R, Drinkwater B, et al: The female athlete triad. The inter-relatedness of disordered eating, amenorrhea, and osteoporosis. Clin Sports Med 13(2):405-418, 1994. 74. Yeager KK, Agostini R, Nattiv A, et al: The female athlete triad: Disordered eating, amenorrhea, osteoporosis. Med Sci Sports Exerc 25(7):775-777, 1993. 75. Dameron TB Jr, Reibel DB: Fractures involving the proximal humeral epiphyseal plate. J Bone Joint Surg Am 51(2): 289-297, 1969. 76. Neer CS, 2nd, Horwitz BS: Fractures of the proximal humeral epiphysial plate. Clin Orthop Relat Res 41:24-31, 1965. 77. Kohler R, Trillaud JM: Fracture and fracture separation of the proximal humerus in children: Report of 136 cases. J Pediatr Orthop 3(3):326-332, 1983. 78. Beringer DC, Weiner DS, Noble JS, et al: Severely displaced proximal humeral epiphyseal fractures: A follow-up study. J Pediatr Orthop 18(1):31-37, 1998. 79. Sherk HH, Probst C: Fractures of the proximal humeral epiphysis. Orthop Clin North Am 6(2):401-413, 1975.
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80. Gill TJ, Waters P: Valgus osteotomy of the humeral neck: A technique for the treatment of humerus varus. J Shoulder Elbow Surg 6(3):306-310, 1997. 81. Dobbs MB, Luhmann SL, Gordon JE, et al: Severely displaced proximal humeral epiphyseal fractures. J Pediatr Orthop 23(2):208-215, 2003. 82. Levine B, Pereira D, Rosen J: Avulsion fractures of the lesser tuberosity of the humerus in adolescents: Review of the literature and case report. J Orthop Trauma 19(5):349-352, 2005. 83. Dameron TB Jr, Rockwood CA: Fractures and dislocations of the shoulder. In Rockwood CA, Wilkins B, King R, (eds): Fractures in Children. Philadelphia, JB Lippincott, 1984, pp 624-653.
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84. Havranek P: Injuries of distal clavicular physis in children. J Pediatr Orthop 9(2):213-215, 1989. 85. Waters PM, Bae DS, Kadiyala RK: Short-term outcomes after surgical treatment of traumatic posterior sternoclavicular fracture-dislocations in children and adolescents. J Pediatr Orthop. 23(4):464-469, 2003. 86. Clark RL, Milgram JW, Yawn DH: Fatal aortic perforation and cardiac tamponade due to a Kirschner wire migrating from the right sternoclavicular joint. South Med J 67(3): 316-318, 1974. 87. Morisawa K, Umemura A, Kitamura T, et al: Apophysitis of the acromion. J Shoulder Elbow Surg 5(2 Pt 1):153-156, 1996.
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CHAPTER 40 Female Shoulder Injuries Jo A. Hannafin, Monique A. Sheridan, and Theresa A. Chiaia
Since the enactment of Title IX in 1972, there has been an explosion of women’s participation in sports at all levels. Women’s significantly increasing involvement in sports is especially evident at the Olympic level,1 where female participation has doubled since the Olympic Games in 1976 and tripled since 1964. In the 2004 Olympic Games in Athens, women competed in every sport except baseball (softball for women) and boxing.
lacrosse, and softball); new datasets are being collected for swimming, tennis, golf, and rowing. Two military studies have evaluated gender as a variable affecting injury rate. A study of army parachutists10 from 1985 to 1994 found that rates of injury did not differ significantly by gender; however, sites of injury were different. Upper-body injuries were reported in 43% of the men and 27% of the women. Male shoulder dislocations were most prevalent in an Israeli military study.11 There was a male dominance of shoulder injuries (30% of total injuries) when compared with women (5% of total injuries). The authors postulated that the 6:1 ratio might reflect the role of trauma in recurrent shoulder dislocation.
Along with the growth in popularity of women’s sports, the incidence of female athletic injuries has increased considerably. In addition, there is growing concern that female athletes may be at higher risk for certain types of injuries than male athletes. Much attention has been paid to the female athlete’s knee.2-7 This chapter, however, explores the published data available concerning athletic injuries in the female shoulder.
There is inconclusive evidence that gender correlates to athletic shoulder injury. Macnab,12 in a study of alpine skiers and snowboarders, reported that head, face, and shoulder injuries were more common in men, and knee injuries were more common in women. Similarly, Kocher13 reported that 11% of total injuries in alpine skiers were shoulder injuries, accounting for 39% of all upper extremity injuries. A male dominance of shoulder injury was reported with a male-to-female ratio of 3:1. In contrast, Aargard and Jorgensen,14 in a year-long questionnaire study of elite Danish volleyball players, found a slight increase in overuse shoulder injuries in female athletes, but the incidence of overall shoulder injury was similar in men and women.
Shoulder injuries in female athletes are common and are often attributed to a combination of increased ligamentous and joint laxity, relatively weaker upper body strength, and shorter bone length as compared with those of male athletes.8 However, there are limited published data that evaluate the role of gender in the incidence and treatment of female shoulder injuries.
EPIDEMIOLOGY Shoulder instability and impingement syndrome are the most common injuries seen in the athletic shoulder. The incidence of shoulder instability (traumatic and atraumatic) and impingement syndrome (primary and secondary) in female athletes is unknown. Numerous studies report the prevalence of male and female injuries, but few evaluate gender-specific variables affecting type or incidence of injury.10-14,16,17 The National Collegiate Athletic Association (NCAA) Injury Surveillance System, the largest continuous collection of injury statistics in college athletics, discloses sport-specific data categorized by body part injured and injury mechanism, as reported by team athletic trainers in both practice and competition. Data since 19989 indicate that shoulder injuries are the first or second most common injury in women’s softball practices, totaling between 10% and 20% of softball injuries per year. The NCAA Injury Surveillance System currently includes 8 out of 16 women’s collegiate sports (soccer, volleyball, field hockey, basketball, gymnastics, ice hockey,
In a retrospective cohort study, Sallis15 reviewed athletic injuries at an NCAA Division III college from 1980 to 1995 to determine whether gender-specific factors existed in location and pattern of injury. The authors’ objective was to formulate gender-specific recommendations in the hope of reducing future risk for injury. More than 3700 participants from a total of seven sports (basketball, cross country, soccer, swimming, tennis, track, and water polo) were included in the study. Women had a greater incidence of shoulder injury (52.5/100 participant-years) than men (47.7/1000 participant-years), but the gender difference was not statistically significant when all sports were combined. A statistically significant (P ⬍ 0.001) gender difference in injury pattern was found for female swimmers and water polo players. In both groups, shoulder injuries were more prevalent in the female athletes, which the authors suggested may have been the result of the rigorous training philosophy of the coach. The study 519
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did not assess injury trends or the severity of injury. Shoulder injuries are common in both male and female elite swimmers, but the published data do not explore the role of gender as an independent variable in injury or response to treatment.16,17
MULTIDIRECTIONAL INSTABILITY Multidirectional instability (MDI) of the shoulder is a complex entity, characterized by symptomatic global laxity of the glenohumeral joint, and is believed to be more common in women than in men. It is known that in general, women tend to have greater ligamentous laxity than men, but do women therefore have greater shoulder laxity? If so, female athletes may be more prone to overuse and repetitive microtrauma, with an increased risk of converting global laxity to symptomatic instability. In a study evaluating 51 asymptomatic physically active men (n ⫽ 24) and women (n ⫽ 27), women demonstrated significantly more anterior glenohumeral joint laxity (P ⫽ 0.001), less anterior joint stiffness (P ⫽ 0.01), and more joint hypermobility (P ⫽ 0.01) than men.18 These physically active men and women reported no regular long-term experience in overhead-throwing sports. Overhead-throwing athletes tend to have greater joint laxity on average than nonthrowing athletes.19,20 These data combined with the data on the physically active women suggest that female athletes participating in sports such as swimming, water polo, softball, volleyball, and tennis have greater joint laxity when compared with their male counterparts, but further research is needed. Brown21 extensively reviewed the existing literature on shoulder laxity in female athletes and found insufficient data to confirm that female shoulders exhibit more laxity than male shoulders. Therefore, the mixed data reported by Brown do not indicate that MDI is more prevalent in female athletes. No significant conclusions can be made based on the available literature. There is evidence that proprioception is reduced in overhead-throwing athletes or those with recurrent anterior dislocation. A single published study examines proprioception in the female athlete. Dover22 reported a significant decrease in external joint position sense in female softball players when compared with nonthrowing female athletes (soccer and track). The study suggests that regardless of arm dominance, external joint position sense is reduced in female overhead athletes. Warner23 proposed that gradual development of shoulder instability may be the result of cumulative injury to the capsuloligamentous structures, with loss of its proprioceptive feedback mechanism and subsequent loss of reflexive muscular protection against excessive humeral head translation and rotation. The mechanism for reduced proprioception must be examined more closely.
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FLEXIBILITY AND JOINT LAXITY Limited published data are available that systematically compare flexibility in men and women, although it is commonly believed that women have more flexible joints than men. Some evidence supports an increased incidence of generalized ligamentous laxity in women. Grana and Moretz24 reported that high school girls, when evaluated by an overall grading of laxity, had more ligamentous laxity than boys, and they confirmed these findings in high school male and female basketball players. McFarland25 reported that asymptomatic high school and college female athletes demonstrated an increase in posterior and inferior laxity compared with male subjects. More female shoulders (65%) could be subluxated posteriorly than male shoulders (51%). A statistically significant increase in the incidence of generalized ligamentous laxity was also found in the female athletes. Marshall26 reported increased joint laxity in the hip and elbow related to female gender. Normative data for sit-and-reach tests support the concept that girls and women in the general population are more flexible than boys and men.
TREATMENT The role of gender in patient response to conservative and surgical treatment has not been defined in the literature. Although hundreds of studies report the results of surgical treatment for impingement syndrome, instability, labral pathology, and rotator cuff tear, few include gender-specific variables in their analysis.
Impingement Syndrome Morrison27 examined the outcome of conservative treatment of impingement syndrome in 616 patients. The patients were of mixed age, activity level, and gender, and were treated with a uniform rehabilitation protocol. In this study, gender did not appear to affect outcome: 68% of the 386 men and 66% of the 230 women achieved satisfactory results. To our knowledge, this is the only published study that evaluates the role of gender in response to conservative treatment of impingement syndrome. Numerous studies report the results of surgical treatment of impingement syndrome, but data evaluating the role of gender in outcome are limited. Sperling28 examined the long-term success of full-thickness rotator cuff repair in young patients (ⱕ50 years). Twenty-two male shoulders and seven female shoulders were graded for postoperative pain, active abduction, and external rotation over a minimum period of 13 years or until revision surgery. Although long-term results were not as successful as in a mixed-age population, gender did not appear to be a significant variable in this small study.
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521
Gill29 reviewed the results of 523 patients who had arthroscopic or open shoulder surgery and reported that a larger percentage of male patients (76.4%; P ⫽ 0.019) had full-thickness rotator cuff tears than female patients. Although there was an independent association between rotator cuff pathology and gender, the relation does not necessarily imply causation. It is possible that the mechanisms of injury or response to conservative treatment varied by gender. In both studies, patients were derived from the general population and were not athletes.
them to shoulder injury and subsequent treatment. Of the 14 studies reporting operative treatment of MDI, 35.7% of patients were female. Why does the percentage of female patients in these studies not reach 50%? Is there a selection bias in surgical treatment? Do female patients respond better to conservative treatment than men or are women undertreated for MDI and thus underreported? With the rise of the female athletic population, further research is necessary to determine the role of gender in the incidence and treatment of shoulder injury.
Shoulder Instability
Few reports include more female subjects than male and even fewer examine the role of gender when assessing clinical outcome. Cooper45 studied 38 patients (22 female, 16 male) treated with an anterior-inferior capsular shift. Improvement occurred in 86% of patients and generalized ligamentous laxity was found in 76% of patients. Steinbeck46 evaluated the outcome of a modified capsular shift as treatment for MDI in 19 patients (17 female, 2 male). The authors reported no recurrent dislocations in 17 out of the 19 total patients. A separate study evaluated the outcome of an inferior capsular shift for MDI in contact-sport athletes (29 female, 18 male).47 The patients were professional or highly competitive athletes (college, high school, or club) involved in ice hockey, rugby, soccer, football, or basketball. The study achieved excellent results, with 92% of anterior repairs and 81% of posterior repairs reported as successful. Return to sports was noted in 82% of anterior repairs and 75% of posterior repairs. Gender was not evaluated as an independent variable, but the results appear positive in the female athletes. Although these studies suggest that a capsular shift is an effective treatment for MDI in female athletes, future protocols must examine gender stratification more closely before conclusions can be made about the effectiveness of capsular shifts in the treatment for MDI in male versus female patients.
Nonsurgical management of shoulder instability has been evaluated in numerous studies, but the role of gender has not been addressed. Kronberg30 suggested that muscle strengthening and coordination training may be a more effective treatment than soft-tissue reconstruction to improve shoulder stability in patients with generalized joint laxity and shoulder instability. Burkhead and Rockwood31 reported similar results in patients with MDI. Eighty-eight percent of 33 patients with MDI reported improvement in shoulder stability following a conservative strengthening and exercise treatment. A study by Buss32 evaluated the effectiveness of nonoperative treatment in in-season athletes with symptomatic instability. Twenty-four male and six female subjects, ages 14 to 20 years, were treated with physical therapy in which range-of-motion and rotator cuff–strengthening exercises were emphasized. Eighty-seven percent of the subjects successfully returned to competition within the season without any period of immobilization. In these studies, gender was not evaluated as an independent variable in outcome of conservative management of MDI. The literature on the surgical management of shoulder instability does not consistently stratify results by gender. Neer and Foster33 reported the results of treatment of patients with MDI with an anterior capsular shift; one of 36 patients experienced recurrent subluxation. The study included equal numbers of male and female patients. Although gender was not evaluated as a factor in response to treatment, the study suggests that gender was not a significant variable. In the majority of the literature discussing surgical treatment of MDI, including results for open capsular shifts,34-36,39 arthroscopic stabilization,37-39 and thermal capsulorrhaphy,40-43 the number of female patients is significantly lower than that of male patients. In 2002, Hiemstra44 reviewed the available literature examining the operative treatment of anterior and multidirectional instability. Of the 43 studies reporting results for surgical treatment of anterior instability, women accounted for 22.3% of all subjects. Hiemstra noted that male athletes may be more likely to participate in overheadthrowing sports or high-risk activities, thus predisposing
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The results of thermal capsular shrinkage have been reported recently,40-43,48,49 but gender has not been examined as a variable related to outcome. In a study of 19 young, physically active patients (13 female, 6 male), Miniaci48 reported recurrent instability in more than 50% of patients and concluded that thermal capsular shrinkage was not a recommended treatment for young patients. Although there were more female patients than male, the role of gender in the outcome of thermal capsular shrinkage for treatment of shoulder instability has not been defined. To our knowledge, a single study assesses the role of gender in outcome of arthroscopic treatment for shoulder instability. Hayashida49 reported on the results of arthroscopic transglenoid suture repair for traumatic anterior shoulder instability in 82 patients (63 male, 19 female). The authors reported 67% excellent, 17% good, and 16% poor results. Gender was not found to be a statistically significant parameter.
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SUMMARY The role of gender in an individual response to pharmacologic intervention, physical therapy, and operative treatment of shoulder injury remains a wide open field of research. Gender differences in response to treatment have been identified in all fields of medicine, and it remains our responsibility to evaluate gender as an independent variable in outcome of treatment. Gender has routinely been ignored in the research of incidence and response to treatment for athletic shoulder injuries. Clearly, as the gap in participation between male and female athletes narrows, gender is an increasingly important variable that warrants careful investigation.
References 1. International Olympic Committee, Promotion of Women in Sport: New record participation of women at the olympic games. August 19, 2004. Available at http://www.olympic. org/uk/organisation/missions/women/full_story_uk .asp?id⫽1017 (accessed February 21, 2008). 2. Arendt E, Dick R: Knee injury patterns among men and women in collegiate basketball and soccer: NCAA data and review of literature. Am J Sports Med 23:694-701, 1995. 3. Zelisko JA, Noble HB, Porter M: A comparison of men’s and women’s professional basketball injuries. Am J Sports Med 10:297-299, 1982. 4. Hutchinson MR, Ireland ML: Knee injuries in female athletes. Sports Med 19:288-302, 1995. 5. Hewett TE, Myer GD, Ford KR: Anterior cruciate ligament injuries in female athletes: Part 1, mechanisms and risk factors. Am J Sports Med 34:299-311, 2006. 6. Ergström B, Johansson C, Törnkvist H: Soccer injuries among elite female players. Am J Sports Med 19:372-375, 1991. 7. Agel J, Arendt EA, Bershadsky B: Anterior cruciate ligament injury in National Collegiate Athletic Association basketball and soccer: A 13-year review. Am J Sports Med 33:24-531, 2005. 8. Holschen JC: The female athlete. South Med J 97:852-858, 2004. 9. National Collegiate Athletic Association: Injury Surveillance System: Sport-specific injury data 2003-2004, Women’s softball, Injury summary 1986-2003. PDF available at http:// www1.ncaa.org/membership/ed_outreach/health-safety/iss/ Injury_Reports_2004/Softball_Summary_2004.pdf (accessed February 20, 2008). 10. Amoroso PJ, Bell NS, Jones BH: Injury among female and male army parachutists. Aviat Space Environ Med 68:1006-1011, 1997. 11. Milgrom C, Mann G, Finestone A: A prevalence study of recurrent shoulder dislocations in young adults. J Shoulder Elbow Surg 7:621-624, 1998. 12. Macnab AJ, Cadman R: Demographics of alpine skiing and snowboarding injury: Lessons for prevention programs. Inj Prev 2:286-289, 1996. 13. Kocher MS, Dupre MM, Feagin JA Jr: Shoulder injuries from alpine skiing and snowboarding: Aetiology, treatment and prevention. Sports Med 25:201-211, 1998.
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14. Aagaard H, Jorgensen U: Injuries in elite volleyball. Scand J Med Sci Sports 6:228-232, 1996. 15. Sallis RE, Jones K, Sunshine S, et al: Comparing sports injuries in men and women. Int J Sports Med 22:420-423, 2001. 16. Bak K, Magnusson SP: Shoulder strength and range of motion in symptomatic and pain-free elite swimmers. Am J Sports Med 25:454-459, 1997. 17. Bak K, Fauno P: Clinical findings in competitive swimmers with shoulder pain. Am J Sports Med 25:254-260, 1997. 18. Borsa PA, Sauers EL, Herling DE: Patterns of glenohumeral joint laxity and stiffness in healthy men and women. Med Sci Sports Exerc 32:1685-1690, 2000. 19. Bigliani LU, Codd TP, Connor PM, et al: Shoulder motion and laxity in the professional baseball player. Am J Sports Med 25:609-613, 1997. 20. Kvitne RS, Jobe FW, Jobe CM: Shoulder instability in the overhand or throwing athlete. Clin Sports Med 14:917-935, 1995. 21. Brown GA, Tan JL, Kirkley A: The lax shoulder in females: Issues, answers, but many more questions. Clin Orthop Relat Res (372):110-122, 2000. 22. Dover GC, Kaminski TW, Meister K, et al: Assessment of shoulder proprioception in the female softball athlete. Am J Sports Med 31:431-437, 2003. 23. Warner JJ, Lephar S, Fu FH: Role of proprioception in pathoetiology of shoulder instability. Clin Orthop 330:35-39, 1996. 24. Grana WA, Moretz JA: Ligamentous laxity in secondary school athletes. JAMA 240:1975-1976, 1978. 25. Marshall JL, Johanson N, Wickiewicz TL, et al: Joint looseness: A function of the person and the joint. Med Sci Sports Exerc 12:189-194, 1980. 26. McFarland EG, Campbell G, McDowell J: Posterior shoulder laxity in asymptomatic athletes. Am J Sports Med 24:468-471, 1996. 27. Morrison DS, Frogameni AD, Woolworth P: Non-operative treatment of subacromial impingement syndrome. J Bone Joint Surg Am 79:732-737, 1997. 28. Sperling JW, Cofield RH, Schleck C: Rotator cuff repair in patients fifty years of age and younger. J Bone Joint Surg Am 86:2212-2215, 2004. 29. Gill TJ, McIrvin E, Kocher MS, et al:: The relative importance of acromial morphology and age with respect to rotator cuff pathology. J Shoulder Elbow Surg 11:327-330, 2002. 30. Kronberg M, Brostrom LA, Nemeth G: Differences in shoulder muscle activity between patients with generalized joint laxity and normal controls. Clin Orthop 269:181-192, 1991. 31. Burkhead WZ Jr, Rockwood CA Jr: Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg Am 74:890-896, 1992. 32. Buss DD, Lynch GP, Meyer CP, et al: Nonoperative management for in-season athletes with anterior shoulder instability. Am J Sports Med 32:1430-1433, 2004. 33. Neer CS, Foster CR: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. J Bone Joint Surg Am 62:897-908, 1980. 34. Bigliani LU, Kurzweil PR, Schwartzbach CC, et al: Inferior capsular shift procedure for anterior-inferior shoulder instability in athletes. Am J Sports Med 22:578-584, 1994. 35. Pollock RG, Owens JM, Flatow EL, Bigliani LU: Operative results of the inferior capsular shift procedure for
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36.
37.
38.
39.
40.
41.
42.
multidirectional instability of the shoulder. J Bone Joint Surg Am 82:919-928, 2000. Bak K, Spring BJ, Henderson IJP: Inferior capsular shift procedure in athletes with multidirectional instability based on isolated capsular and ligamentous redundancy. Am J Sports Med 28:466-471, 2000. Gartsman GM, Roddey TS, Hammerman SM: Arthroscopic treatment of anterior-inferior glenohumeral instability: Two to five-year follow-up. J Bone Joint Surg Am 82:991-1003, 2000. Treacy SH, Savoie FH, Field LD: Arthroscopic treatment of multidirectional instability. J Shoulder Elbow Surg 8:345-350, 1999. Cole BJ, L’Insalata J, Irrgang J, Warner JJP: Comparison of arthroscopic and open anterior shoulder stabilization: A two to six-year follow-up study. J Bone Joint Surg Am 82: 1108-1114, 2000. Chen S, Haen PS, Walton J, Murrell GAC: The effects of thermal capsular shrinkage on the outcomes of arthroscopic stabilization for primary anterior shoulder instability. Am J Sports Med 33:705-711, 2005. Fitzgerald BT, Watson BT, Lapoint JM: The use of thermal capsulorrhaphy in the treatment of multidirectional instability. J Shoulder Elbow Surg 11:108-113, 2002. Frostick SP, Sinopidis C, Al Maskari S, et al: Arthroscopic capsular shrinkage of the shoulder for the treatment of
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43.
44. 45.
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patients with multidirectional instability: Minimum 2-year follow-up. Arthroscopy 19:227-233, 2003. Anderson K, Warren RF, Altchek DW, et al: Risk factors for early failure after thermal capsulorrhaphy. Am J Sports Med 30:103-107, 2002. Hiemstra LA, Kirkley A: Shoulder instability in female athletes. Sports Med Arthrosc Rev 10:50-57, 2002. Cooper RA, Brems JJ: The inferior capsular-shift procedure for multidirectional instability of the shoulder. J Bone Joint Surg Am 74:1516-1521, 1992. Steinbeck J, Jerosch J: Surgery for atraumatic anterior-inferior shoulder instability: A modified capsular shift evaluated in 20 patients followed for 3 years. Orthop Scand 68:447-450, 1997. Choi CH, Ogilvie-Harris DJ: Inferior capsular shift operation for multidirectional instability of the shoulder in players of contact sports. Br J Sports Med 36:290-294, 2002. Miniaci A, McBirnie J: Thermal capsular shrinkage for treatment of multidirectional instability of the shoulder. J Bone Joint Surg Am 85:2283-2287, 2003. Hayashida K, Yoneda M, Nakagawa S, et al: Arthroscopic Bankart suture repair for traumatic anterior shoulder instability: Analysis of the causes of a recurrence. Arthroscopy 14:295-301, 1998.
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CHAPTER 41 Nonoperative Treatment
of Shoulder Impingement Michael A. Keirns and Julie M. Whitman
DEFINITION
CAUSES OF IMPINGEMENT
There are two types of shoulder impingement: internal impingement and subacromial impingement syndrome (SAIS).1-5 Internal impingement has been recognized by more recent studies describing the encroachment of the cuff and the labral complex between the humeral head and the glenoid fossa.6-8 This chapter focuses on SAIS, which is the traumatizing of subacromial structures from a mechanical narrowing of the subacromial space and is diagnosed with three of the six signs and symptoms seen in Box 41-1.9-11 (See Chapter 4 for a review of the shoulder diagnostic test.
As with any pathologic condition, it is important for the rehabilitation team to determine and treat the cause of the problem and not just eliminate the symptoms. This strategy has shown positive outcomes in long-term management of patients with shoulder impingement.33 Once the diagnosis of impingement is made, it is often helpful to distinguish whether the mechanical impingement is occurring secondary to structural or functional causes, or perhaps secondary to a combination of structural and functional causes. Structural causes of impingement encompass congenital abnormalities or degenerative alterations (or both) in the subacromial arch. Whether these transformations are the cause or consequence of impingement is difficult to determine. Bigliani and Morrison34,35 described a high correlation (0.95) between the types of acromion processes and impingement diagnosis with rotator cuff involvement. In their morphologic study, type III anterior hooked acromion processes (Fig. 41-2) were found to be associated with rotator cuff tears in 70% of the cases; however, a causal relation could not be determined. In other words, did the rotator cuff tear, with subsequent humeral head elevation, cause the proliferation of the acromion process, or did the hooked acromion process cause the rotator cuff tear? Or did both elevation of the humerus and mechanical rubbing of the acromion on the subacromial tissue cause the resultant findings of rotator cuff pathology and the signs and symptoms of impingement?
Using the arm in a repetitive overhead activity can compromise the structures in the subacromial space, thus causing injury to the rotator cuff and subsequent shoulder dysfunction.11-16 Several authors recognized this subacromial entrapment; however, we are indebted to Charles Neer for popularizing this pathologic mechanism of injury and classifying subacromial impingement as impingement syndrome.17-18 The impingement syndrome is characterized as a continuum beginning with an inflammatory process, progressing to fibrosis, and ending in rotator cuff rupture.19-22 There is good evidence to demonstrate successful nonoperative treatments for the patient with SAIS.23-26 The subacromial space that becomes compromised in SAIS normally measures 7 to 12 mm and is bordered superiorly by the acromion, acromioclavicular joint, and coracoacromial ligament.27,28 Inferiorly, this space is bound by the head of the humerus (Fig. 41-1). As the acromiohumeral distance becomes narrowed with elevation of the arm, especially when poor posture is present and the upperextremity motion involves internal rotation, the structures within the subacromial space can become pinched against the anterior edge of the acromion and the coracoacromial ligament.29,30
Uhthoff and colleagues36 showed that most rotator cuff tears are degenerative and are present on the articular side of the muscle (on the side facing the humeral head). Ozaki and colleagues37 presented a cadaver study indicating that these tears on the articular side of the muscle were not associated with degeneration of the acromion undersurface. In contrast, they found that complete and bursal rotator cuff tears were associated with pathologic changes of the acromion. They postulated that a vicious cycle develops, beginning with a tear of the rotator cuff on the bursal side of the muscle, followed by pathologic changes of the undersurface acromion, and ending with the subsequent acromion lesion abrading the rotator cuff and therefore facilitating the degenerative process. Consequently, it is important to break this cycle by restoring the humeral head depression and minimizing the impact of this degenerative
The structures in the subacromial space that become compromised during the impingement process include the supraspinatus tendon, the long head of the biceps tendon, the subacromial bursa, and, to a lesser extent, the infraspinatus tendon.13,30 The greatest encroachment occurs near the attachment of the supraspinatus to the greater tuberosity, often called the critical zone.31,32 The possibility of diminished blood flow to the critical zone emphasizes its significance as a precursor for pathology. 527
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BOX 41-1. Shoulder Impingement Tests for Diagnosis of SAIS
Positive Neer’s impingement test Positive Hawkins impingement test
in diminished humeral head depression. Good history taking followed by thorough examination will provide the practitioner with appropriate screening and delineation of functional predispositions for shoulder impingement. This examination and reassessments guide the treatment plan during each phase of patient management.
Positive horizontal adduction Pain with resistive abduction Painful arc test Pain in the C5-C6 dermatome region
cycle. Should patients with structural changes in the subacromial arch not respond to alterations in activity and interventions adequately addressing contributing factors, more invasive management such as shoulder injection or possibly surgical intervention may be appropriate.38-43 Functional causes of impingement include a combination of many interrelated factors: glenohumeral capsular laxity or tightness, cervical spine dysfunction with or without radiculopathy, postural deviations, altered mechanics of the thoracic spine and rib cage, scapular dyskinesis potentially due to altered motor control or unsuitable joint movements, and inadequate rotator cuff function resulting
Capsular laxity, which is prevalent in an athletic population, can alter normal humeral head translations during overhead activity. During athletic endeavors, such as the acceleration phase of a baseball pitch, the glenohumeral joint’s static stabilizers must withstand tremendous torques (ⱖ71 N•m) as the arm accelerates 7000 deg/sec2.44,45 Anterior capsular tension and the articular congruencies, not the contraction of the muscles, mediate humeral translation during the late cocking and early acceleration of this pitch.46 With capsule laxity, this accessory movement cannot be controlled by the static constraints, thereby allowing the humeral head to slide forward and potentially cause shoulder impingement.47 If a diagnosis of impingement syndrome secondary to hypermobility is established, treatment should focus on the primary diagnosis of subluxating shoulder with a glenohumeral stabilization program.14,48-49 Just as hypermobility can be a precursor for impingement, so too can the hypomobility of the glenohumeral joint lead to SAIS. Cofield and Simonet50 described how the patient
Supraspinatus m.
A.C. joint Acromion
Coracoacromial ligament Subacromial bursa Coracoid process
Infraspinatus m.
Biceps tendon
Subscapularis m. Teres minor m.
Figure 41-1. Anatomic predispositions of impingement. A.C., acromioclavicular.
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529
subsequent diminished humeral head depression.56-57 There is evidence to support rehabilitative interventions such as manual therapy, re-education of deep neck flexors, and cervical traction for treating cervical dysfunctions and associated radiculopathies.58-62 Altered thoracic and rib movements can also hinder the correct function of the shoulder girdle, thereby causing potential subacromial impingement. When treating the patient with shoulder impingement, it is critical to examine and treat related joint dysfunctions such as the thoracic or cervical mechanical limitations in movement. Mobilization/ manipulations of the thoracic spine to improve movement can be helpful, potentially through enhanced scapula positions and facilitation of the lower trapezius muscle.63-66 An example of intervention to the thoracic spine and rib cage, which can be used throughout the treatment plan, is the thoracic spine extension technique seen in Figure 41-4.
Figure 41-2. Type III hooked acromion (arrow), which predisposes to impingement of structures in the subacromial space.
with adhesive capsulitis might be predisposed to shoulder entrapment in the subacromial space. Stiffness involving the posterior capsule can cause the humeral head to migrate superiorly (Fig. 41-3). Subsequent humeral pressure is placed upward against the anteroinferior acromion. It is important for the treating clinician to understand the role and influence of static constraints on glenohumeral mobility.51,52 Treatment of this patient should focus on increasing the mobility of the static constraints, especially the posterior capsule.53,54 The differential diagnosis should include the possibility of spinal dysfunction causing functional entrapment of the subacromial space. Nerve root entrapment at the C5-C6 level can facilitate weakness of the rotator cuff, with
Normal posterior capsule
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In connection with the importance of spinal movements, there may also be nerve root entrapment affecting the scapular stabilizers with subsequent scapular dyskinesia.67-72 To rule out possible nerve involvement, the practitioner needs to evaluate for long thoracic nerve entrapment, suprascapular nerve entrapment, or axillary nerve involvement. In addition to nerve involvement, correct motor control and refinement of scapular movement need to be addressed to include evaluation and interventions for acromioclavicular joint, scapulothoracic joint, and sternoclavicular joint dysfunctions. Poor scapulothoracic movements can alter correct scapulohumeral rhythm and hinder the correct spacing of the subacromial space opening.73 The direct influence of scapular dyskinesis on humeral head neutralization with the glenoid may be caused by modification of the lengthtension relationship of the deltoid and rotator cuff musculature, tension changes of the glenohumeral static constraints, incorrect position of the glenoid under the humerus during full elevation, and bringing the acromion process closer to the humerus. There is evidence supporting the premise that scapular dyskinesis can be a primary cause of shoulder injuries and dysfunctions.74-76
Tight posterior capsule
Figure 41-3. Influences (arrows) of the posterior capsule on forcing humeral head elevation, causing impingement. Left, Normal posterior capsule allowing normal humeral head translation. Right, Tight posterior capsule causing humeral head elevation and impingement (star).
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Figure 41-4. Thoracic spine mobilization and manipulation to improve joint movement.
The correct scapulothoracic movement can be influenced by posture. The classic rounded or forward shoulder posture can bring the acromion process closer to the humeral head and can influence movement of the scapulae on the thoracic spine and rib cage.27 Posture can influence thoracic and cervical spine dysfunction and correct positioning of the scapula. The patient with postural deviation or spinal dysfunction should respond favorably to conservative therapy and manual interventions to address the shortening of tissue and to improve joint mobility and motor control.23-26,77-82 The final, and often the most important component in understanding the cause of the impingement syndrome is the influence of the rotator cuff tendons in maintaining the position of the humeral head in the glenoid fossa.83-86 The rotator cuff is the prime mover in the depressor mechanism of the humeral head.87-88 McMasters89 has shown normal tendons to be exceedingly strong and resistant to pathology. However, in the case of the rotator cuff, light and scanning electron microscopes have confirmed rotator cuff microtears and hyalinization.90 The pathogenesis of the rotator cuff tendon failure comes from a combination of adverse effects: repeated mechanical trauma from pinching or rubbing, ischemia causing predisposition to injury, and diminished healing secondary to compromised vascularity.19,91-95 Deficiency of the rotator cuff allows the upward vector pull of the deltoid to elevate the humeral head (Fig. 41-5).96-97 When not addressed through rehabilitation, these functional causes of impingement can cause elevation of the humeral head, with associated rotator cuff trauma. This is a self-perpetuating process that facilitates an impingement
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Figure 41-5. Diagram of force vectors (arrows) showing how the influences of the deltoid resultant vector (heavy arrow) can cause humeral elevation. Impingement can be magnified with diminished rotator cuff influences.
cycle (Fig. 41-6). As the subacromial structures become compromised, structural changes are often forthcoming.
IMPORTANCE OF SUBACROMIAL SPACE VASCULARITY In 1939, Lindbloom98 suggested that the Codman’s critical zone of the supraspinatus tendon was avascular. Through evaluation with laser Doppler ultrasound, Iannotti and colleagues99 and Moseley and Goldie31 later found that there actually is adequate blood supply to this area; however, it is a zone of anastomoses between the osseous vessels (the anterior and posterior humeral circumflex) and tendinous vessels (the suprascapular and subscapular) (Fig. 41-7). The classic study of Rathbun and MacNab32 showed attenuation of this blood supply during certain activities. Essentially, there is a diminished filling of the blood quantity when the arm is held in an adducted and neutral rotation position. It was then proposed that the tendon failure is eminent when the humerus is allowed to wring out the underdeveloped blood supply to the critical zone. Diminished vascularity
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NONOPERATIVE TREATMENT OF SHOULDER IMPINGEMENT
Humeral head elevation
Functional causes of impingement
531
NONOPERATIVE MANAGEMENT Overview Emerging evidence shows nonoperative treatment is very effective and is the treatment of choice in rehabilitation of patients with impingement syndrome.23-26,33,66,102-110
Impingement cycle
Structural changes of impingement
Subacromial space compromised
Figure 41-6. The impingement cycle is a continuum that can begin anywhere in the sequence and can cause a vicious succession.
to the arm decreases the blood supply for nutrition and oxidation necessary to the healing process. Another important finding in vascularity with respect to rehabilitation was the study performed by Sigholm and colleagues,100 in which the subacromial pressure was measured during shoulder elevation. By using a micropipette infusion technique, it was found that the pressure in the subacromial space was raised from 8 mm Hg to 56 mm Hg with 45 degrees of shoulder flexion with a 1-kg weight. This magnitude of elevation is sufficient to compromise the microvascularity of the arm held in an elevated position.101
Two randomized clinical trials compared programs of manual physical therapy interventions combined with exercise with exercise alone.33,66 In the study by Conroy and Hayes, 14 patients with shoulder impingement were randomized to undergo either a supervised exercise program or supervised exercise plus glenohumeral joint mobilization.66 At the completion of nine therapy sessions over 3 weeks, the group receiving the manual therapy and exercise had less pain compared with the supervised exercise group. In a larger study several years later, Bang and Deyle compared outcomes of patients randomized into either an exercise group or manual therapy plus exercise.33 Patients were treated for six sessions over 3 to 4 weeks. The exercise group performed stretching exercises targeting the anterior chest musculature and posterior shoulder capsule and musculature. The manual therapy plus exercise group followed the same exercise program, but they also received manual physical therapy addressing impairments identified in the entire upper quarter including the neck, thoracic spine, and rib cage, and the glenohumeral, acromioclavicular, and sternoclavicular joints. Outcomes were assessed at baseline, the end of the
Suprascapular artery Tendon Muscle
Critical zone anastomoses Subscapular artery
Bone
Anterior circumflex artery (osseous artery)
Figure 41-7. Vascularity of the critical zone is a period of transition.
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treatment session, and 1 month after treatment. At the end of treatment and at the 1-month follow-up, the manual therapy plus exercise group achieved superior gains in pain, function, and strength compared with the exercise group. Three other large, multisite, pragmatic randomized controlled trials have been conducted with patients recruited directly from the primary care or general practitioner’s office.108-110 In the study by Bergman ‘s group, 150 patients were randomized to receive usual medical care or manipulative therapy plus usual medical care. Manipulative therapy included manual therapy to the neck, thoracic spine, ribs, and shoulder girdle.108 After completion of care, and up to 1 year, the group receiving manual therapy plus usual medical care achieved greater rates of recovery and improvements in severity of symptoms and disability when compared with the group receiving only usual medical care. In a large trial by Winters and colleagues, just under 200 patients were randomized to receive either steroid injection, manipulation therapy (for the spine, rib cage, and shoulder girdle), or a program including exercise, massage, and physical modalities.109 Patients without significant impairments identified in the cervicothoracic or scapular region were defined as the synovial group, and patients in this group who were treated with steroid injection improved to a greater degree than those treated with manipulation. Further, patients treated with manipulation improved to a greater degree than the patients receiving only exercise, massage, and physical modalities. For patients with both glenohumeral joint and upper quarter findings (the shoulder girdle group), the patients receiving manipulation achieved superior outcomes compared with those treated with only exercise, massage, and physical modalities. Finally, Hay and colleagues conducted a randomized controlled trial comparing corticosteroid injection with community physical therapy.110 The physical therapy program included education, active shoulder exercises, and a home exercise program at a minimum; manual physical therapy (manipulation and mobilization) was included approximately 75% of the time. Although both groups of patients achieved similar outcomes at 6 weeks and 6 months (pain, disability, function), the patients receiving the community physical therapy used fewer health care resources (reconsultation, other interventions). The common denominator for all five of these trials is the superiority of a comprehensive intervention program that addresses identified impairments in the entire upper quarter, including the cervical and thoracic spine, rib cage, and entire shoulder girdle. Based on this evidence, we advocate a comprehensive examination of the upper quarter and use of physical therapy treatments, including manual physical therapy interventions and exercise, to address identified impairments. In our proposed treatment program, the emphasis is not only on direct treatment to the
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glenohumeral joint but also on proposed treatments for the other regions of the upper quarter.
Rehabilitation Many rehabilitation programs have been outlined for treatment of impingement, and these programs commonly include allowing adequate rest, restoring mechanical incriminators, and promoting rotator cuff strengthening.102-106 The goal of our rehabilitation program is to highlight the evidence in treating shoulder impingement and present a goal-oriented, sequenced treatment plan and criteria for progression. The main emphasis is on the vascularity influences and outlined progression. A basic rationale in developing a rehabilitation protocol is that compromised circulation diminishes the healing capabilities of the shoulder. This reduction in vascularity is particularly important with respect to accelerating rotator cuff healing, chiefly because the rotator cuff communicates with the joint fluid and bursal fluid that remove any hematoma, contributing to cuff healing. The program proposed in this chapter places the primary focus of rehabilitation on facilitating subacromial tissue healing and addressing mechanical deficits that can facilitate incorrect humeral head position on the glenoid fossa. Attention is focused on correcting mechanical deficits and facilitating vascularity in the subacromial space. Targeting the mechanical deficits should optimize more biomechanically correct humeral head position on the glenoid fossa. This along with increasing subacromial space vascularity should facilitate healing and minimize continued ischemic pathology. This program has four phases, with established goals and criteria for each stage that the patient should achieve before moving to the next stage. When initiating the rehabilitation program, it is first important to confirm the diagnosis. Then one must assess where the patient is in the rehabilitation program and how far the impingement pathology has progressed according to Neer’s19 classification. This rehabilitation protocol will, through systematic re-evaluations, progress the surgical and nonsurgical patients quickly and safely through their rehabilitation program. Stage I: Acute Inflammatory Stage During this stage, an acute inflammatory process exists in the shoulder. There is bleeding into the tissue with subsequent impaired healing secondary to increased capillary pressure on the damaged tissue.111 The stage I inflammatory process is characterized by inability to sleep on the affected extremity, discomfort at rest, warmth felt with palpation of the joint, pain and weakness with isolated muscle evaluation, diffuse tenderness with palpation, positive impingement signs, and pain with overhead activity.112-116 The rehabilitation goals during this stage include decreasing the inflammatory process; educating the patient; maintaining glenohumeral joint mobility; treating spinal dysfunctions
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such as hypomobility in the cervical spine, thoracic spine, or rib cage; and preventing atrophy of the upper quarter musculature. It is important to avoid exacerbating impingement symptoms during this stage. Decreasing the Inflammatory Process. Adjuncts in diminishing the chemical reaction of the inflammatory process are rest, therapeutic modalities, and nonsteroidal antiinflammatory agents. When the inflammatory mechanism is inhibited, the patient should experience an associated decrease in pain and swelling. Success in achieving these goals has been accomplished through an array of modalities to include laser, microcurrent, pulsed electromagnetic field therapy, iontophoresis, and phonophoresis.117 My (MAK) anecdotal choice of modalities to treat the acute inflamed shoulder include cryotherapy and low-frequency transcutaneous electrical nerve stimulation (TENS). Cold applications diminish the inflammatory condition by acting as vasoconstrictors and reducing metabolic activity.118,119 Cooling also diminishes discomfort associated with the acute shoulder injury by increasing the threshold of pain in stimulated nerve fibers.120,121 Through this cold-induced analgesia, normal shoulder motion can be facilitated.122 Cold therapy can be effective with ice massage for 15 to 20 minutes with the arm positioned in abduction (Fig. 41-8).
Figure 41-8. Ice massage performed with shoulder abduction.
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Classically, TENS has been used for the purpose of pain alleviation. Low-frequency TENS has also been found effective to increase microcirculation and facilitate the absorption of calcific deposits in the shoulder tendons.123,124 The most effective treatment points are believed to be associated with stimulation of the acupuncture points.125 Figure 41-9 displays a possible electrode placement using acupuncture sites. The points used in this arrangement include Jianjing (GB 21), Binao (LI 14), Juga (LI 16), and Jianya (LI 15).126 Any physical modality is only an adjunct in a physical therapy clinic and should be used with prudence. Although injections can be a useful tool in decreasing the inflammatory process and differentiating the impingement diagnoses, caution must be exercised in recommending steroid injections. Steroid injection in or near the cuff and biceps tendons can produce tendon atrophy or can reduce the capability of damaged tendon to repair itself.127-129 Kennedy and Willis130 concluded that collagen necrosis occurred with steroid injection. Controlled studies have been performed showing minimal effectiveness alone with the use of steroid injections.131,132 Patient Education. Patient education begins with instruction as to the pathogenesis of the injury. Understanding the problem can clarify for the patient the therapeutic rationale
Figure 41-9. Successful method of transcutaneous electrical nerve stimulation setup.
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for avoiding activities that can cause persisting shoulder pathology. The rehabilitation program should be outlined with the short-term and long-term goals emphasized; the criteria for the stage advancement should be highlighted. Educating the patient can also promote compliance throughout the rehabilitation program. When outlining motions to refrain from, it is particularly important to advise the patient to avoid activities where the humerus is elevated 10 degrees higher than the scapular spine. Higher angles approximate the humerus with the acromion and can impede the microvascularity of the subacromial space.30 If symptoms persist with the arm at the waist level, the overhead limitation is set at that height. Avoidance of reaching and lifting activities should be emphasized to prevent traumatizing the associated structures.133 The inflammatory process needs rest and protection to heal, and any activity causing pain should be avoided.134 Besides emphasizing the don’ts, it is also equally important to inform patients of how they should protect the arm by emphasizing optimal posture. A critical part of the home care is to advise the patient to minimize the time that the arm rests at the side. When sitting, the patient should have the arm propped and supported approximately 45 degrees away from the side (Fig. 41-10). When
Figure 41-10. Preferred position of shoulder during daily activities of living.
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sleeping, the patient should lie on the contralateral side with a pillow under the arm to maintain the desired position (Fig. 41-11). These recommendations facilitate circulation to the hypovascular zone of the subacromial space.32,108 Active rest is important in the rehabilitation of the patient with impingement symptoms, although the clinician should outline activities that the patient may engage in. Aerobic non–weight-bearing arm activities, such as running in the pool, stationary bike riding, and stair-climbing exercises, are indicated. The vascularity improvement in the nonexercising extremity can promote the healing process and facilitate progression in the rehabilitation process.135 It is important for the therapist to observe and modify the exercise program and activity to minimize stress to shoulder. Maintaining Joint Mobility. Immobility and the inflammatory process associated with stage I can result in increased scar tissue formation and eventual joint capsule contracture.134 Therefore, during the early stages of rehabilitation, it is important to maintain the mobility of the associated joints.136-140 These are to include the spinal, glenohumeral, scapulothoracic, acromioclavicular, and sternoclavicular joints. Grades I and II caudal glides to the glenohumeral joint in the scapular plane can help to decrease the discomfort associated with the inflammatory process of the joint.141 Grades III and IV joint mobilizations can help to address any hypomobile portions of the glenohumeral joint as long as the clinician takes care not to aggravate the shoulder symptoms. Maintenance of the humeral depression and evaluation of capsular tightness may also be addressed, with ensuing treatments as indicated and tolerated.142
Figure 41-11. Preferred position of shoulder during sleeping; the affected shoulder is resting on the pillow.
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535
Adequate spinal, scapulothoracic, acromioclavicular, and sternoclavicular joint mobility’s are essential for assurance of normal joint play and upper quarter movement.143-146 Joint mobilization/manipulations are indicated to allow normal arthrokinematics during range-of-motion exercises and during activities of daily living.147-149 Through joint mobilization and manipulations, a skilled manual therapist may be able to prevent complications of abnormal shoulder rhythms and ensuing diminished shoulder mechanics.33,148-152 While performing the joint mobilization and manipulations, it is critical to avoid irritating the shoulder and potentially intensify the inflammatory process. In addition to the manual therapy strategies to maintain shoulder girdle joint mobility, it is important for the physical therapist to assess and treat associated thoracic and cervical spine mobility issues. Figures 41-12 and 41-13 show examples of the manual physical therapy techniques we often use to address limitations in mobility of the glenohumeral joint and the thoracic spine and rib cage. Finally, the therapist should instruct the patient in exercises that the patient can perform at home to maintain the gains achieved through the use of manual therapy techniques. Along with joint mobilization and manipulations, manual strategies to address connective tissue dysfunctions should be addressed at this time. Restoring the joint functions can reflexively assist with improving motor control of the upper quarter movements and can help restore normal connective tissue status.66 Still, there may be areas with myofascial dysfunctions in the upper trapezius, levator scapulae, subscapularis, pectoralis minor, and midscapular regions. According to several authors, restoring normal myofascial performance can be accomplished with connective tissue strategies such as manual stretching of the muscles, myofascial release, dry needling or intramuscular stimulation, and trigger point therapy.153-155 These interventions can assist with the correct
Figure 41-13. Rib joint mobilization and manipulation.
neurologic input and motor control of the scapulothoracic and glenohumeral joint complexes.154 Additionally, active assisted range-of-motion exercises should be introduced to help maintain and increase soft tissue flexibility. It is often helpful to begin with pendulum activity, followed by progression to rope-and-pulley motion. The rope-and-pulley exercise should begin with the flexion motion, performed with the palm supinated and the humerus externally rotated. Keeping the shoulder in external rotation with this exercise allows the greater tuberosity to glide laterally on the anterior acromion, thereby lessening the chance of subacromial impingement. The pulley maneuver is an advantageous way to perform range-of-motion exercise because it allows gravity to assist with humeral depression. The goal of the active assisted range of motion is not to accomplish soft tissue remodeling, and therefore performing these exercises requires only a pause at the extremes of motion. The purpose of the rangeof-motion exercises is to accomplish a pumping action with redistribution of the waste products and neuromodeling of the associated musculature. Full flexion is the goal; however, as with any activity, it is crucial to avoid any discomfort associated with the movement.
Figure 41-12. Thoracic extension joint mobilization and manipulation.
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After the pulley exercise, an appropriate progression of exercise is flexion and scapular-plane external rotation with a T-bar or cane. Just as in the pulley-flexion motion, the contralateral extremity should assist with the flexion
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action and the arm should maintain external rotation and supination throughout the motion (Fig. 41-14). External rotation is then performed with the T-bar by placing the shoulder in the scapular plane with 45 degrees of abduction (Fig. 41-15).157-159 Preventing Muscle Atrophy. The next goal of stage I is to retard muscular atrophy. When shoulder injury occurs, muscle atrophy occurs secondary to reflexive retardation and disuse.160-163 Costill and colleagues164 have shown the physiologic characteristics of this atrophy to be a decrease in the muscle oxidative enzyme system with a predilection for effects on volume and diameter of type I slow-twitch fibers. The shoulder muscles that are affected most substantially are the tonic rotator cuff musculature.165 Consequently, when addressing beginning shoulder rehabilitation, it is important to emphasize the preservation of rotator cuff strength and endurance. Because recruitment order begins with the type I fibers, submaximal modified isometrics are indicated to support the rotator cuff musculature. Modified isometrics are illustrated as standing motions of 10 degrees or less in a slow rhythmic action with submaximal effort. The modified isometrics are performed with the arm supported at 45 degrees of abduction and are preferable because they facilitate a concentric contraction that exercises the contraction component of the muscle.166 This in turn should promote an increase in vascularity and minimize the stress at the tendinous junction, which needs protection at this point in rehabilitation. Three sets of 12 to 20 repetitions are recommended to facilitate a pumping action and enhance recruitment of the
Figure 41-15. External rotation with the arm in the scapular plane using a T-bar.
mitochondria and vascular energy system. The motions performed are listed in Table 41-1. Active rest and using the arm below 90 degrees in pain-free motion during the normal activities of daily living will help minimize atrophy by recruiting the rotator cuff for stabilization and promoting vascularity of the rotator cuff. Stage II: Subacute Stage The criteria for progress into stage II of the rehabilitation program are decreased signs of inflammation characterized by no discomfort at rest, no warmth felt with palpation of the joint, and good tolerance of stage I program. Although the patient may still have the other signs and symptoms of stage I, he or she may progress to stage II within a week. We advocate progressing from stage to stage based on achievement of set goals and criteria and not according to a strict time-based schedule. One of us (MAK) has observed that 70% of the patients fit the
TABLE 41-1 Stage I: Modified Isometrics Exercises with Good Posture
Figure 41-14. Flexion exercise with correct arm position using a T-bar.
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Position
Activity
Limitation
Standing
External rotation
Submaximal
Standing
Internal rotation
Moderate
Standing
Adduction
Moderate
Standing
Abduction
Submaximal
Standing
Flexion
Submaximal
Standing
Extension
Moderate
Standing
Scapular motions
Moderate
Side-lying
Scapular motions
Submaximal
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standard program, 15% need to speed up progress through the program, and another 15% need to be slowed down. The goals of stage II are the same as those for stage I, with the primary difference being an emphasis on circulatory advancement. At this stage, pathogenesis of the rotator cuff tendons is considered a tendinopathy and is treated accordingly. The primary focus of this stage is circulation enhancement to the subacromial space. This may be facilitated by ultrasound to the supraspinatus fossa,167-171 by effleurage massage proximal to distal to the supraspinatus and infraspinatus muscles while the patient’s arm is in an abducted position (Fig. 41-16),172,173 and by ice to the supraspinatus and infraspinatus fossa and insertions with the patient’s arm in the abducted position.174,175 Transverse friction massage may be indicated in cases involving superficial lesion at the tenoperiosteal junction116 (the scenario in which a painful arc is present and the pinching occurs between the greater tuberosity and the acromion). Rationale for using transverse friction massage centers on causing tissue hyperemia and assisting with remodeling of the lesion.172,116 Joint mobility is advanced as tolerated with abduction movement with the rope and pulley; T-bar external rotation at 90 degrees of abduction; self-stretch for anterior, posterior, and inferior capsule; and progressive joint mobilization. The prevention-of-atrophy exercise program is the same as outlined in stage I with the addition of total arm strengthening. Exercises in this stage may include scapular stabilization with submaximal proprioceptive neuromuscular facilitation in mid range of motion, submaximal biceps with dumbbell, submaximal triceps dumbbell kick-
Figure 41-16. Massage to supraspinatus and infraspinatus fossae.
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back, and dumbbell forearm exercises. A light resistance should be used for all isotonic exercises, beginning with three sets of 10 repetitions, progressing to 20 repetitions. Stage III: Progressive Exercise Stage The criteria for advancing into stage III include normal range of motion, no symptoms during activities of daily living, and improved muscular performance. Resolution of pain and disability does not mean the lesion has healed.18,133 We believe that premature progression into this stage of rehabilitation is one of the most important factors leading to a dissatisfactory rehabilitation process. It is more beneficial to delay progression into this stage, especially with the aging population, who may have diminished healing capabilities. Brewer177 and Meyer178 have shown age-related changes in the rotator cuff to include diminution of vascularity and loss of normal organizational characteristics of tendon. The goals during this stage include normalizing the arthrokinematics of the shoulder complex, regaining and improving strength, and improving neuromuscular control of the shoulder. Normalize Range of Motion. The range of motion and arthrokinematics may be normalized through aggressive joint mobilization, self-stretching of the glenohumeral joint capsule, and T-bar active assisted range of motion in all planes. Joint mobilization is performed to address limitations found in glenohumeral joint mobility detected in the clinical evaluation. The keys for joint mobilization include oscillations in caudal motion to treat abduction, ventral and anterior accessory glides to increase external rotation, dorsal and posterior accessory glides to increase internal rotation, and lateral distraction to increase general motions. After completing glenohumeral joint mobilization in the cardinal planes, the therapist might need to progress this treatment by mobilizing in the directions of any noted direction of hypomobility, with the glenohumeral joint positioned in combined motions. Self-capsule stretches are performed to specifically address limitations found in clinical evaluation with inferior, anterior, and posterior regions outlined (Figs. 41-17 and 41-18). It is often helpful to perform the range-of-motion exercises before and after an arm ergometer warm-up.179,180 Regain and Improve Strength. The main emphasis of stage III is restoration of the rotator cuff effectiveness and total arm strength. Many references show improvement in the SAIS patient through specific exercise programs.143,146,147 In the early stages of the progressive exercise program, endurance of the rotator cuff is emphasized. This may be accomplished by performing arm ergometry and initiating an isotonic dumbbell program for the shoulder musculature (Table 41-2). If available, a cable system is often effective in progressing the shoulder-strengthening program by adjusting the lever arm and minimizing the stress on the humeral depressors.
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TABLE 41-2 Stage III: Isotonic Shoulder Exercise Program
Figure 41-17. Posterior capsule self-stretch.
Position
Motion
Limitation
Prone
Extension
Pain
Prone
Horizontal abduction
Pain
Standing
Flexion
90 deg
Standing
Abduction
90 deg
Standing
Supraspinatus
80 deg
Side-lying
Rotations
Arm abducted
Proximal stability with scapular stabilization is also emphasized early on in the exercise plan. Proximal stability for distal mobility is important to allow total arm strengthening without exacerbating the impingement syndrome.186,187 This may be accomplished with exercises such as scapular proprioceptive neuromuscular facilitation patterns and wall push-ups.188 If the patient has difficulty with the scapular recruitment pattern and correct movement pattern, scapular taping for kinesthetic awareness and biofeedback systems may be of benefit.189,190 As the progressive exercise program is accelerated, the concept of specificity of training should dominate the choices of exercise. Ten variables should be focused on to organize the appropriate strength training program (Box 41-2). Understanding the needs of the shoulder will dictate the optimal manipulation of these 10 parameters. The needs of the shoulder might include type of muscle involved (phasic versus tonic),191,192 energy system used,193,194 demands to be placed on the shoulder with return to individual activities
BOX 41-2. Program
Variables for Strength Training
Number of repetitions Amount of weight Number of sets Concentric versus eccentric contractions Figure 41-18. Inferior capsule self-stretch.
Amount of rest between exercises and sets Type of exercise (e.g., dumbbell, isokinetic, tubing)
Surgical tubing can also be an important adjunct in designing an adaptable exercise program. However, clinicians should be cautious to instruct the patient to perform the exercises only in the pain-free range of motion. Full range of motion occasionally aggravates shoulder symptoms, especially at end range of motion, where undue stress may be placed on the musculotendinous junctures.181-185
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Level of intensity Order of exercises Frequency of workouts Isolation of muscle or muscle groups
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of daily living (including manual labor or athletic participation),195,196 and prevention of exercises or activities that permit the impingement cycle. In the advanced stages of the progressive exercise program, strength and power of the shoulder musculature should be emphasized. Exercises should focus on duplicating the stresses that will be placed on the shoulder when the patient returns to his or her normal upper extremity activities. The concept of specialization is used during this latter part of stage III.197 Plyometrics may be used to duplicate the explosive dynamics of overhead athletic participation.198-204 Stage IV: Return to Activity The guidelines for return to activity include full nonpainful range of motion, no pain or tenderness, satisfactory strength evaluation (isokinetic test), and satisfactory clinical examination. The goal of unrestricted symptom-free activity can be accomplished with a functional interval program progressing back to full activity. It is important to adapt the activity and make appropriate changes in the movement pattern to avoid predisposing to recurrence of impingement.205,206 During the return to activity, we recommend instituting a maintenance program to include flexibility exercises, rotator cuff strengthening, and total arm strengthening exercises.207
SUMMARY The program emphasizes treating the cause and not just the symptoms associated with SAIS. For optimal outcome, a thorough examination with subsequent treatment of the key impairments in the entire upper quarter are often necessary. Successful patient management is contingent on adequate examination that delineates deficits and appropriate interventions to address identified limitations. To accomplish optimal outcomes, a progressive-stage protocol uses goal orientation and criteria progression. Every rehabilitation program must be individualized during the progression back to normal activity by monitoring outcomes to ensure the efficacy of the treatment plan.208-216 Practitioners should consult the available evidence and modify their practice in accordance with Sackett’s model of evidence-based practice. 217
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157. Saha AK: Mechanism of shoulder movements and a plea for the recognition of “zero position” of glenohumeral joint. Indian J Surg 12:153-165, 1950. 158. Freedman L, Monro RR: Abduction of the arm in the scapular plane: Scapular and glenohumeral movements. J Bone Joint Surg Am 48:1503-1510, 1966. 159. Das SP, Roy GS, Saha AK: Observations on the tilt of the glenoid cavity of scapula. J Anat Soc India 15:114, 1966. 160. Cardenas DD, Stolov WC, Hardy R: Muscle fiber number in immobilization atrophy. Arch Phys Med Rehabil 58: 423-426, 1977. 161. Currier DP, Petrilli CR, Threlkeld AJ: Effect of graded electrical stimulation of blood flow to healthy muscle. Phys Ther 66:937-943, 1986. 162. Gould N, Donnermeyer D, Pope M, Ashikaga T: Transcutaneous muscle stimulation as a method to retard disuse atrophy. Clin Orthop Relat Res (164):215-220, 1982. 163. Wolf E, Magora A, Gonen B: Disuse atrophy of the quadriceps muscle. Electromyography 11:479-490, 1971. 164. Costill DL, Fink WJ, Habansly AJ: Muscle rehabilitation after knee surgery. Physician Sportsmed 5:71-74, 1977. 165. Granit R: The Basis of Motor Control. New York, Academic Press, 1970. 166. Curin S, Stanish WD: Tendinitis: Its Etiology and Treatment. Toronto, DC Heath, 1984. 167. Abramson KI, Burnett C, Bell Y, et al: Changes in blood flow, oxygen uptake and tissue temperatures produced by therapeutic physical agents. Am J Phys Med 39:51-62, 1960. 168. Griffin JE, Karselis TC: Physical Agents for Physical Therapists. Springfield, Ill, Charles C Thomas, 1978. 169. Griffin JE: Physiological effects of ultrasonic energy as it is used clinically. J Am Phys Ther Assoc 46:18-26, 1966. 170. Lehmann JF, Delateur BJ, Stonebridge JB, Warren CG: Therapeutic temperature distribution produced by ultrasound as modified by dosage and volume of tissue exposed. Arch Phys Med Rehabil 48:662-666, 1967. 171. Lota MJ: Electric plethysmographic and tissue temperature studies of effect of ultrasound on blood flow. Arch Phys Med Rehabil 46:315-322, 1965. 172. Beard G, Wood EC: Massage: Principles and Techniques. Philadelphia, WB Saunders, 1974. 173. Hovind H, Nielsen SL: Effect of massage on blood flow in skeletal muscle. Scand J Rehabil Med 6:74-77, 1974. 174. Kowal MA: Review of physiological effects of cryotherapy. J Orthop Sports Phys Ther 5:66-73, 1983. 175. Singh H, Osbahr DC, Holovacs TF, et al: The efficacy of continuous cryotherapy on the postoperative shoulder: A prospective, randomized investigation. Shoulder Elbow Surg.10(6):522-525, 2001. 176. Cyriax J: Textbook of Orthopaedic Medicine: Treatment by Manipulation, Massage and Injection, vol 2, 10th ed. London, Bailliere Tindall, 1980. 177. Brewer BJ: Aging of the rotator cuff. Am J Sports Med 7:102-110, 1979. 178. Meyer AW: The minute anatomy of attrition lesions. J Bone Joint Surg Am 13:341-348, 1931. 179. Moore MA, Hutton RS: Electromyographic investigation of muscle stretching techniques. Med Sci Sports Exerc 12:322-329, 1980. 180. De Vries HA: Physiology of Exercise for Physical Education and Athletics. Dubuque, Iowa, Brown, 1980.
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CHAPTER 42 Nonoperative Rehabilitation
for Traumatic and Congenital Glenohumeral Instability Kevin E. Wilk, Leonard C. Macrina, and Michael M. Reinold
Shoulder instability is a common pathology often seen in the orthopedic and sports medicine setting. The glenohumeral joint allows tremendous amounts of joint mobility, thus making the shoulder inherently unstable and the most frequently dislocated joint in the body.1 Due to the joint’s poor osseous congruency and capsular laxity, it greatly relies on the dynamic stabilizers and neuromuscular system to provide functional stability.2 Therefore, differentiating between normal translation and pathologic instability is often difficult. There exists a wide range of shoulder instabilities, from subtle subluxations to gross instability. Often the success of the rehabilitation program is based on the recognition and treatment program designed to treat the specific type of instability.
subluxated the shoulder. A first-time episode of dislocation is generally more painful than the repeat event. Rehabilitation progresses based on the patient’s symptoms, with emphasis on early controlled range of motion, reduction of muscle spasms and guarding, and relief of pain. Conversely, a patient presenting with atraumatic instability often presents with a history of repetitive injuries and symptomatic complaints. Often the patient does not complain of a single instability episode but rather a feeling of shoulder laxity or an inability to perform specific tasks. Rehabilitation for this patient should focus on early proprioception training, dynamic stabilization drills, neuromuscular control, scapular muscle exercises, and muscle strengthening exercises to enhance dynamic stability due to the unique characteristic of excessive capsular laxity and capsular redundancy in this type of patient.
Nonoperative rehabilitation is often implemented in patients with a variety of shoulder instabilities. These instability patterns can range from congenital multidirectional instabilities to traumatic unidirectional dislocations. We have classified glenohumeral joint instabilities into two broad categories: traumatic and atraumatic. Based on the classification system of glenohumeral instability as well as several other factors, a nonoperative rehabilitation program may be developed. This chapter discusses these factors along with the nonoperative rehabilitation programs for the various types of shoulder instability to return the patient to the previous level of function.
The second factor is the degree of instability and its effect on the patient’s function. Varying degrees of shoulder instability exist, such as a subtle subluxation or gross instability. Subluxation refers to the complete separation of the articular surfaces with spontaneous reduction. Dislocation is a complete separation of the articular surfaces and requires a specific movement or manual reduction to relocate the joint. Dislocation results in underlying capsular tissue trauma. Thus, with shoulder dislocations the degree of trauma to the glenohumeral joint’s soft tissue is much more extensive. For a shoulder dislocation to occur, a Bankart lesion must be present and soft tissue trauma must be present on both sides of the glenohumeral joint capsule.3 In an acute traumatic dislocation, the anterior capsule may be avulsed off the glenoid (Bankart lesion) and the posterior capsule may be stretched, allowing the humeral head to dislocate. Warren and colleagues call this the circle stability concept.4 The rate of progression varies based on the degree of instability and persistence of symptoms. For example, a patient with mild subluxations and muscle guarding might initially tolerate strengthening exercises and neuromuscular control drills more than a patient with a significant amount of muscle guarding.
REHABILITATION FACTORS Seven key factors should be considered when designing a rehabilitation program for a patient with an unstable shoulder (Box 42-1). We will briefly discuss these factors and their significance to the rehabilitation program. The first factor to consider in the rehabilitation of a patient with shoulder instability is the onset of the pathology. Pathologic shoulder instability can result from an acute, traumatic event or chronic, recurrent instability. The goal of the rehabilitation program can vary greatly based on the onset and mechanism of injury. Following a traumatic subluxation or dislocation, the patient typically presents with significant tissue trauma, pain, and apprehension. The patient who has sustained a dislocation often exhibits more pain due to muscle spasm than a patient who has
The next factor to influence the rehabilitation program is the frequency of dislocation or subluxation. The primary traumatic dislocation is most often treated conservatively with immobilization in a sling and early controlled passive 545
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BOX 42-1. Key Factors in Rehabilitation of the Unstable Shoulder
goal is to enhance strength, proprioception, dynamic stability, and neuromuscular control, especially in the specific points of motion or direction result in instability.
Onset of the pathology • Traumatic • Congenital Degree of instability • Dislocation • Subluxation • Silent subluxation Frequency of dislocation • Chronic • Acute Direction of instability • Anterior • Posterior • Multidirectional Concomitant pathologies • • • • •
Bankart lesion SLAP lesion Hill-Sach lesion Rotator cuff Mechanoreceptor disruption
End range neuromuscular control Premorbid activity level • High-level athlete • Recreational athlete • Sedentary
range-of-motion (ROM) exercises. The incidence of recurrent dislocation ranges from 17% to 96%, with a mean of 67% in patient populations between the ages of 21 and 30 years.10,49 Therefore, the rehabilitation program should progress cautiously in young athletic patients. Hovelius and colleagues8,16,17 demonstrated that the rate of recurrent dislocations is based on the patient’s age and is not affected by the length of postinjury immobilization. Persons between the ages of 19 and 29 years are the most likely to experience multiple episodes of instability. Hovelius and colleagues8,16,17 noted patients in their 20s exhibited a recurrence rate of 60%, whereas patients in their 30s and 40s had a less than 20% recurrence rate. In adolescents, the recurrence rate is as high as 92%,18 and the rate is 100% with an open physis.19 Chronic subluxations, as seen in the atraumatic, unstable shoulder, may be treated more aggressively due to the lack of acute tissue damage and less muscle guarding and inflammation. Rotator cuff and periscapular strengthening activities should be initiated while ROM exercises are progressed. The patient must avoid excessive stretching of the joint capsule through aggressive ROM activities. The
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The fourth factor is the direction of instability. The three most common are anterior, posterior, and multidirectional. Anterior instability is the most common traumatic type of instability seen in the general orthopedic population. It has been reported that this type of instability represents approximately 95% of all traumatic shoulder instabilities.12 However, the incidence of posterior instability appears to depend on the patient population. For example, in professional or collegiate football, the incidence of posterior shoulder instability is higher than in the general population. This is especially true in linemen. Mair and coworkers20 reported on nine athletes with posterior instability in which eight of nine were linemen and seven were offensive linemen. Often, these patients require surgery: Mair’s group20 also reported that 75% required surgical stabilization. Kaplan and colleagues21 reported in a study of collegiate football players that 78% required surgical stabilization. Following a traumatic event in which the humeral head is forced into extremes of abduction and external rotation or into horizontal abduction, the glenolabral complex and capsule can become detached from the glenoid rim, resulting in anterior instability. This type of detachment is a Bankart lesion (Fig. 42-1). There are numerous types of Bankart lesions. Baker and coworkers22 have identified four types of Bankart lesions based on the size and the degree of tissue involvement. Conversely, rarely does a patient with atraumatic instability due to capsular redundancy dislocate a shoulder. It is our opinion that they are more likely to repeatedly sublux the joint without complete separation of the humerus from the glenoid rim. Capsular avulsions can occur on the glenoid side (Bankart lesion) or on the humeral head side (HAGHL lesion: humeral avulsion of the inferior glenohumeral ligament).24-25,42 Posterior instability occurs less commonly, accounting for less than 5% of traumatic shoulder dislocations.26,27 This type of instability is often seen following a traumatic event such as falling onto an outstretched hand or from a pushing mechanism. However, patients with significant atraumatic laxity might complain of posterior instability, especially with shoulder elevation, horizontal adduction, or excessive internal rotation because of the strain placed on the posterior capsule in these positions. Multidirectional instability (MDI) can be identified as shoulder instability in more than one plane of motion. Patients with MDI have a congenital predisposition and exhibit ligamentous laxity due to excessive collagen elasticity of the capsule. Rodeo and colleagues28 reported that this type of patient turns over collagen at a faster rate. We consider an inferior displacement of greater than 8 to 10 mm during the sulcus maneuver (Fig. 42-2) with the
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A
Figure 42-2. Sulcus maneuver to assess inferior capsular laxity.
B
Glenoid
C Figure 42-1. Bankart lesion commonly observed with a traumatic dislocation. A, Drawing illustrating a Bankart lesion. The arrow denotes the avulsed capsule from the glenoid. B, Computed tomographic arthrogram of a bony Bankart lesion. The large arrow shows the dye that has leaked out of the capsule. The small arrow shows the bony lesion which has pulled away from the glenoid rim. C, an arthroscopic view of a Bankart lesion (arrow).
arm adducted to the side to be significant hypermobility, thus suggesting significant congenital laxity.2 Due to the atraumatic mechanism and lack of acute tissue damage, ROM is often normal to excessive. Patients with recurrent shoulder instability due to MDI generally have
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weakness in the rotator cuff and the deltoid and scapular stabilizers, with poor dynamic stabilization and inadequate static stabilizers. Initially, the focus is on maximizing dynamic stability, scapula positioning, and proprioception and improving neuromuscular control in mid ROM. Also, rehabilitation should focus on improving the efficiency and effectiveness of glenohumeral joint force couples through co-contraction exercises, rhythmic stabilization, and neuromuscular control drills. Isotonic strengthening exercises for the rotator cuff, deltoid, and scapular muscles are also emphasized to enhance dynamic stability. Morris and coworkers29 reported the EMG activity of the rotator cuff and deltoid muscle in MDI and asymptomatic subjects. They noted the most significant difference was in the deltoid muscles compared with the rotator cuff muscles in their groups. The fifth factor involves considering other tissues that might have been affected and the premorbid status of the tissue. Disruption of the anterior capsulolabral complex from the glenoid commonly occurs during a traumatic injury, resulting in an anterior Bankart lesion. Osseous lesions are often present, such as a concomitant Hill-Sachs lesion caused by an impaction of the posterolateral aspect of the humeral head as it compresses against the anterior glenoid rim during relocation. This has been reported in up to 80% of dislocations.30-32 Conversely, a reverse Hill-Sachs lesion may be present on the anterior aspect of the humeral head because of a posterior dislocation.33 Occasionally, a bone bruise is present in persons who have sustained a shoulder dislocation as well as pathology to the rotator cuff. In rare cases of extreme trauma, the brachial
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plexus also becomes involved.34 Other common injuries in the unstable shoulder can involve the superior labrum. A type V SLAP (superior labral anterior-posterior) lesion is characterized by a Bankart lesion of the anterior capsule extending into the anterior-superior labrum.35 These concomitant lesions affect the rehabilitation significantly.
also significantly influence the successful outcome. The recurrence rates of instabilities vary based on age, activity level, and arm dominance. In athletes involved in collision sports, the recurrence rates have been reported between 86% and 94%.6,41-43
The sixth factor to consider is the patient’s level of neuromuscular control, particularly at end range. Neuromuscular control may be defined as the efferent, or motor, output in reaction to an afferent, or sensory, input.2,10 The afferent input is the ability to detect the glenohumeral joint position and motion in space with resultant efferent response by the dynamic stabilizers as they blend with the joint capsule to assist in stabilizing the humeral head. Injury with resultant insufficient neuromuscular control could have deleterious effects. The humeral head might not center itself within the glenoid, thereby compromising the surrounding static stabilizers. The patient with poor neuromuscular control can exhibit excessive humeral head migration, with the potential for injury, an inflammatory response, and reflexive inhibition of the dynamic stabilizers.
REHABILITATION GUIDELINES
Several clinicians have reported that neuromuscular control of the glenohumeral joint may be negatively affected by joint instability.10,36-39 Lephart and colleagues10 compared the ability to detect passive motion and the ability to reproduce joint positions in normal, unstable ,and surgically repaired shoulders. They reported a significant decrease in proprioception and kinesthesia in the shoulders with instability when compared with normal shoulders and with shoulders undergoing surgical stabilization procedures. Smith and Brunoli38 reported a significant decrease in proprioception following a shoulder dislocation. Blasier and colleagues36 reported that patients with significant capsular laxity exhibited a decrease in proprioception compared with patients with normal laxity. Zuckerman and coworkers39 noted that proprioception is affected by the patient’s age: Older subjects exhibited diminished proprioception compared with a younger population. Thus, the patient presenting with traumatic or acquired instability can present with poor neuromuscular control. The final factor to consider in the nonoperative rehabilitation of the unstable shoulder is the arm dominance and the desired activity level of the patient. If the patient often performs overhead motions or plays sports such as tennis, volleyball, or a throwing sport, then the rehabilitation program should include sport-specific dynamic stabilization exercises, neuromuscular control drills, and plyometric exercises in the overhead position once full, pain-free ROM and adequate strength have been achieved. Patients whose functional demands involve below-shoulder-level activities will follow a progressive exercise program to return full ROM and strength. The success rates of patients returning to overhead sports after a traumatic dislocation of their dominant arm are extremely low.40 Arm dominance can
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Shoulder instability may be classified into two common forms: traumatic and atraumatic.
Traumatic Shoulder Instability Phase I: Acute Phase Following a first-time traumatic shoulder dislocation or subluxation, the patient often presents in considerable pain, with muscle spasm and an acute inflammatory response. The patient usually limits motion by guarding the injured extremity in an internally rotated and adducted position against the side of the body to protect the injured shoulder. The goals of the acute phase are to decrease pain, inflammation, and muscle guarding; promote healing and protect the healing soft tissues; prevent the negative effects of immobilization; re-establish baseline dynamic joint stability; and prevent further damage to the glenohumeral joint capsule (Box 42-2). We allow immediate limited and controlled motion following a traumatic dislocation in some patients (ages 18-28 years) but we immobilize patients between the ages of 29 and 54 years. Motion is restricted so as to prevent further tissue attenuation. A short period of immobilization in a sling to control pain and to allow scar tissue to form for enhanced stability may be necessary for 7 to 14 days, although no long-term benefits regarding recurrence rates and immobilization have been found in younger patients between the ages of 17 and 29 years.8,44 Patients older than 29 years are usually immobilized for 2 to 4 weeks to allow scarring of the injured capsule. The ideal position to immobilize the glenohumeral has traditionally been in internal rotation with the arm close to the body. A recent study by Itoi and colleagues45,46 examined positional differences of immobilization and compared the rates of recurrent dislocations. They concluded that immobilization in external rotation significantly reduced the recurrence rate of instability in chronic and firsttime dislocators. They have recommended immobilization with the arm in 30 degrees of abduction and 10 degrees external rotation,46 whose results were superior to those in a group of patients immobilized in internal rotation. The results indicated a 0% recurrence rate in external rotation and 30% incidence of instability in the group immobilized in internal rotation. The resultant Bankart lesion had improved coaptation to the glenoid rim with immobilization in external rotation versus conventional immobilization in
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BOX 42-2.
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The program will vary in length for each patient depending on several factors: severity and onset of symptoms, degree of instability symptoms, direction of instability, concomitant pathologies, age and activity level of the patient, arm dominance, and desired goals and activities.
Phase I: Acute Motion GOALS
Protect healing capsular structures Re-establish nonpainful range of motion Decrease pain, inflammation, and muscle spasms Retard muscle atrophy and establish voluntary muscle activity Re-establish dynamic stability Improve proprioception Note: During the early rehabilitation program, the capsule must not be placed under stress until dynamic joint stability is restored. It is important to refrain from activities in extreme ranges of motion early in the rehabilitation process. PROGRAM
• • • •
Internal rotation (multiple angles) External rotation (multiple angles) Biceps Scapular retraction and protraction, elevation and depression (seated manual resistance) • Electrical muscle stimulation may be used to ER during isometrics • Rhythmic stabilizations • ER and IR in the scapular plane (pain-free multiple angles) • Flexion and extension in the scapular plane (pain-free multiple angles) • Weight shifts • Standing hands on table (CKC exercises) for anterior instability only • Proprioception training drills • Active joint reproduction proprioceptive drills (ER, IR, flexion)
Phase II: Intermediate GOALS
Regain and improve muscular strength Normalize arthrokinematics
Decrease pain and inflammation:
Enhance proprioception and kinesthesia
• Sling or ER brace for comfort and depending on the age of the patient and physician preference • Therapeutic modalities such as ice and TENS • NSAIDs • Gentle joint mobilizations (grades I-II) for pain neuromodulation • Caution: Do not stretch the injured capsule!
Enhance dynamic stabilization
Range-of-motion exercises
Good MMT of IR, ER, flexion, and abduction
• • • • • •
Baseline proprioception and dynamic stability
Gentle ROM only, no stretching Pendulums Rope and pulley Elevation in scapular plane to tolerance Active-assisted ROM using L-bar to tolerance Flexion • IR with arm in scapular plane at 30 degrees of abduction • ER with arm in scapular plane at 30 degrees of abduction • Caution: Motion is performed in a nonpainful arc of motion only. Do not push into ER or horizontal abduction with anterior instability. Avoid excessive IR or horizontal adduction with posterior instability. Strengthening and proprioception exercises • Isometrics (performed with arm at side) • Flexion • Abduction • Extension
Improve neuromuscular control of shoulder complex CRITERIA TO PROGRESS TO PHASE II
Nearly full to full passive ROM (ER may be still limited) Minimal pain or tenderness
PROGRAM
Progress range-of-motion activities at 90 degrees of abduction to tolerance (pain free) Initiate isotonic strengthening • Emphasis on ER and scapular strengthening • ER and IR with tubing • Scaption raises (full can) • Abduction to 90 degrees • Side-lying external rotation to 45 degrees • Standing ER with tubing with manual resistance • Hand on ball against wall resistance stabilization • Prone extension to neutral • Prone horizontal adduction • Prone rowing • Lower and middle trapezius • Side-lying neuromuscular exercise drills • Push-ups onto table Continued
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BOX 42-2.
Nonoperative Rehabilitation for Traumatic Dislocation of the Shoulder—cont’d
• Seated manual scapular resistance • Biceps curls • Triceps pushdowns • Electrical muscle stimulation may be used to ER during exercises Improve neuromuscular control of shoulder complex • Initiate proprioceptive neuromuscular facilitation • Rhythmic stabilization drills • ER and IR at 90 degrees of abduction (limit degree of ER) • Flexion at 100 degrees, horizontal abduction at 10 degrees • Progress to mid and end ROM • Progress OKC program • PNF • Manual resistance ER (supine → side-lying → eccentrics), prone row • ER/IR tubing with stabilization • Progress CKC exercises with rhythmic stabilizations • Wall stabilization on ball • Hand on wall: wall circles for rotator cuff endurance • Hand on wall: side-to-side motion for scapular muscles and deltoid • Static holds in push-up position on ball • Push-ups on tilt board • Core • Abdominal strengthening • Trunk strengthening and low back • Gluteal strengthening Continue use of ice and electrotherapy as needed
Phase III: Advanced Strengthening GOALS
Improve strength, power, and endurance Improve neuromuscular control Enhance dynamic stabilizations
• Progress to bench press in restricted ROM (restrict horizontal abduction ROM) • Progress to flat and inclined chest press (weighted); restrict motion • Progress to seated rowing and latissimus pull down (in front) in restricted ROM Emphasize PNF • Manual D2 with rhythmic stabilization at 45, 90, and 145 degrees Advanced neuromuscular control drills (for athletes) • Ball flips on table • ER tubing at 90 degrees of abduction with manual resistance and rhythmic stabilization at end range • Push-ups on ball or rocker board with rhythmic stabilizations • Manual scapular neuromuscular control drills • Initiate perturbation activities (ER with exercise tubing with end-range rhythmic stabilization) Endurance training • Timed bouts of exercises: 30-60 sec • Increase number of repetitions (sets of 15-20) • Multiple bouts throughout the day (three times) Initiate plyometric training • Two-hand drills: • Chest pass throw • Side-to-side throw • Overhead soccer throw • Progress to one-hand drills: • 90/90 baseball throws • Wall dribbles • 90/90 baseball throws against wall • Caution: Continue to avoid excessive stress on joint capsule.
Phase IV: Return to Activity
Prepare patient or athlete for activity
GOALS
CRITERIA TO PROGRESS TO PHASE III
Maintain optimal level of strength, power, and endurance
Full nonpainful range of motion No palpable tenderness Continued progression of resistive exercises Good to normal muscle strength, dynamic stability, and neuromuscular control PROGRAM
Progressively increase activity level to prepare the athlete for full functional return to activity and sports CRITERIA TO PROGRESS TO PHASE IV
Full ROM No pain or palpable tenderness Satisfactory isokinetic test
Continue use of modalities (as needed)
Satisfactory clinical exam
Continue isotonic strengthening (progress resistance)
PROGRAM
• Continue Thrower’s Ten • Progress to end range stabilization drills • Progress to full ROM strengthening
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Continue all exercises as in phase III Progress isotonic strengthening exercises Resume normal lifting program (physician will determine)
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BOX 42-2.
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Initiate interval sport program as appropriate Continue ice and electrical stimulation as needed Consider GH joint stabilizing brace for contact sports
Follow-up Isokinetic test (ER and IR; abduction and adduction) Progress interval program Maintain exercise program
CKC, closed kinetic chain; ER, external rotation; GH, glenohumeral; IR, internal rotation; MMT, manual muscle testing; NSAIDs, nonsteroidal antiinflammatory drugs; OKC, open kinetic chain; PNF, proprioceptive neuromuscular facilitation; ROM, range of motion; TENS, transcutaneous electrical stimulation.
a sling. Seybold and colleagues13 found similar results after immobilizing primary anterior dislocations in 10 to 20 degrees of external rotation. Miller and colleagues 47 found improved contact forces between the glenoid and the labrum as the glenohumeral joint went from full internal rotation to neutral followed by 45 degrees of external rotation. They concluded that the improvement in contact forces might influence the healing of a Bankart lesion. Potential complications with immobilization can include a decrease in joint proprioception, muscle disuse and atrophy, and a loss of ROM in specific age groups. Therefore, prolonged use of immobilization following a traumatic dislocation might not be recommended in all patients. Passive ROM is initiated in a restricted and protected range based on the patient’s symptoms. The early motion is intended to promote healing, enhance collagen organization, stimulate joint mechanoreceptors, and aid in decreasing the patient’s pain through neuromuscular modulation.14,48-50 Pain-free active-assisted ROM exercises, such as pendulums and external and internal rotation at 45 degrees of abduction using an L-bar (Breg Corp, Vista, Calif), might also be initiated. Passive ROM exercises are also performed in a pain-free arc of motion. In addition, passive and active joint positioning is also performed in a restricted motion. Modalities such as ice, transcutaneous electrical nerve stimulation (TENS), and high-voltage stimulation might also be beneficial to decrease pain, inflammation, and muscle guarding.
static position as the rehabilitation specialist performs manual rhythmic stabilization drills to facilitate muscle cocontractions. These manual rhythmic stabilization drills are performed for the shoulder internal and external rotators in the scapular plane at 30 degrees of abduction and are performed at pain-free angles that do not compromise the healing capsule. Rhythmic stabilizations for flexion and extension may also be performed with the shoulder at 100 degrees of flexion and 10 degrees of horizontal abduction. Strengthening exercises are also performed for the scapular retractors and depressors to reposition the scapula in its proper position. Scapula strengthening is critical for successful rehabilitation. Closed-kinetic-chain exercises such as weight shifting on a ball are performed to produce a co-contraction of the surrounding glenohumeral musculature and to facilitate joint mechanoreceptors to enhance proprioception. Weight shifts can usually be performed immediately following the injury unless posterior instability is present. Phase II: Intermediate Phase During the intermediate phase, the program emphasizes regaining full ROM along with progressing strengthening exercises of the rotator cuff, and re-establishing muscular
Strengthening exercises are initially performed through submaximal, subpainful isometric contractions to initiate muscle recruitment and retard muscle atrophy. Electrical stimulation of the posterior cuff musculature may also be incorporated to enhance this muscle fiber recruitment process early on in the rehabilitation process and also in the next phase when the patient initiates isotonic strengthening activities (Fig. 42-3). Reinold and colleagues23 believe that the use of electrical stimulation might improve force production of the rotator cuff, particularly the external rotators, immediately after an acute injury. Dynamic stabilization exercises are also performed to reestablish dynamic joint stability. The patient maintains a
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Figure 42-3. Electrical stimulation to the posterior rotator cuff during exercise activity to improve muscle fiber recruitment and contraction.
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balance of the glenohumeral joint, scapular stabilizers, and surrounding shoulder muscles. Before the patient enters phase II, certain criteria must be met, which include diminishing pain and inflammation, satisfactory static stability, and adequate neuromuscular control. To achieve the desired goals of this phase, passive ROM is performed to the patient’s tolerance with the goal of attaining nearly full ROM. Active-assisted ROM exercises are performed using a rope and pulley. Flexion and externaland internal-rotation exercises at 90 degrees of abduction are performed using an L-bar. These exercises may be progressed to tolerance without stressing the involved tissues. External rotation at 90 degrees of abduction is generally limited to 65 to 70 degrees to avoid overstressing the healing anterior capsuloligamentous structures for approximately 4 to 8 weeks. ROM is eventually increase to full motion as the patient tolerates it. Isotonic strengthening exercises are also initiated during this phase. Emphasis is placed on increasing the strength of the internal and external rotators and scapular muscles to maximize dynamic stability.The ultimate goal of the strengthening phase is to re-establish muscular balance following the injury. Kibler and colleagues1 noted that scapular position and strength deficits have been shown to contribute to glenohumeral joint instability. Exercises initially include external and internal rotation with exercise tubing at 0 degrees of abduction, side-lying external rotation, and prone rowing. During the latter part of this phase, exercises are progressed to include the progressive isotonic strengthening program (Box 42-3) to emphasize rotator cuff and scapulothoracic muscle strength. Manual resistive exercises such as side-lying external rotation and prone rowing may also prove beneficial by having the clinician vary the resistance throughout the ROM. Incorporating concentric and eccentric manual exercises and rhythmic stabilization drills at end range to enhance neuromuscular control and dynamic stability is also recommended (Fig. 42-4). Closed kinetic chain exercises are progressed to include hand-on-the-wall stabilization drills in the plane of the scapular at shoulder height as the patient tolerates (Fig. 42-5). Push-ups are performed first with hands on a table then progressed to a push-up on a ball or unstable surface while the rehabilitation specialist performs rhythmic stabilizations to the involved and uninvolved upper extremity along with the trunk to integrate dynamic stability and core strengthening (e.g., tilt board, Swiss ball) (Fig. 42-6). Caution should be used while performing closed-kinetic-chain exercises in patients with posterior instability for 6 to 8 weeks to allow adequate healing and strength gains. Patients with significant scapular winging should perform push-ups until adequate scapular strength is attained. Core stabilization drills should be performed to enhance scapular control. Resistance, repetitions, and sets of strengthening exercises may be advanced as the
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patient improves. End-range rhythmic stabilization drills with the arm at 0 degrees of adduction or at 45 degrees of abduction are also performed. Exercises such as tubing with manual resistance and end-range rhythmic stabilization drills are also performed (Fig. 42-7). The goal of these exercise drills is to improve proprioception and neuromuscular control at end range. Phase III: Advanced Strengthening In the advanced strengthening phase, the focus is on improving strength, dynamic stability, and neuromuscular control near end range through a series of progressive strengthening exercises for a gradual return to the patient’s activity. Criteria to enter this phase include minimal pain and tenderness, full range of motion, symmetrical capsular mobility, good (at least 4/5 manual muscle test) strength, endurance, and dynamic stability of the scapulothoracic and upper extremity musculature. Muscle fatigue has also been associated with a decrease in neuromuscular control. Carpenter and coworkers51 observed the ability to detect passive motion of shoulders positioned at 90 degrees of abduction and 90 degrees of external rotation. The investigators reported a decrease in both the detection of external and internal rotation movement following an isokinetic fatigue protocol. Thus, exercises designed to enhance endurance in the upper extremity, such as low resistance and high repetitions (20-30 repetitions per set), are incorporated during this phase. Exercise sets using time may be incorporated, such as 30-second or 60-second exercise bouts. These exercises may include tubing external and internal rotation, medicine ball wall dribbling, and submaximal manual resistance drills. Aggressive upper body strengthening through continuing a progressive isotonic resistance program is recommended. A gradual increase in resistance as well as a progression to a more functional position by performing tubing exercises at 90 degrees of abduction to strengthen the external and internal rotators is also recommended. More aggressive isotonic strengthening exercises such as bench presses, seated rows, and latissimus pull-downs may be incorporated in a protected range of motion during this phase. During bench presses and seated rows, the patient is instructed to not extend the upper extremities beyond the plane of the body to minimize stress on the shoulder capsule. Latissimus pulldowns are performed in front of the head, and the patient is instructed to avoid full extension of the arms to minimize the amount of traction force applied to the shoulder joint. Also during this phase, the patient continues to perform rhythmic stabilization drills with the rehabilitation specialist and gradually progresses to a position of apprehension using tubing at 90 degrees of abduction with end-range rhythmic stabilization drills to enhance dynamic stability. A patient wishing to return to athletic participation may be instructed to perform plyometric exercises for the upper
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BOX 42-3.
Progressive Isotonic Strengthening Program
This program is designed to exercise the major muscles of the shoulder joint. All exercises are specific to improving strength, power, and endurance of the shoulder complex musculature.
1. Diagonal Pattern D2 Flexion
5. Side-lying External Rotation Lie on uninvolved side, with involved arm at side of body and elbow bent to 90 degrees. Keeping the elbow of involved arm fixed to side, raise arm.
Grip tubing handle in hand of involved arm.
Hold seconds and lower slowly.
Begin with arm out from side 45 degrees and palm facing backward
Perform _____ sets of _____ repetitions _____ times daily.
Turn palm forward, flex the elbow, and bring arm up and over the involved shoulder. Turn palm down and reverse to take arm to starting position.
6A. Prone Horizontal Abduction (Neutral) Lie on table, face down, with involved arm hanging straight to the floor and palm facing down. Raise arm out to the side, parallel to the floor. Hold 2 seconds and lower slowly.
Perform _____ sets of _____ repetitions _____ daily.
Perform _____ sets of _____ repetitions _____ times daily.
2A. External Rotation at 0 Degrees of Abduction
6B. Prone Horizontal Abduction (Full External Rotation, 100 Degrees of Abduction)
Stand with involved elbow fixed at side, elbow at 90 degrees, and involved arm across the front of body.
Lie on table face down, with involved arm hanging straight to the floor and thumb rotated up (hitchhiker).
Grip tubing handle while the other end of tubing is fixed.
Raise arm out to the side with arm slightly in front of shoulder, parallel to the floor.
Pull out arm, keeping elbow at side.
Hold 2 seconds and lower slowly.
Return tubing in a slow and controlled fashion.
Perform _____ sets of _____ repetitions _____ times daily.
Perform _____ sets of _____ repetitions _____ times daily.
6C. Prone Rowing
2B. Internal Rotation at 0 Degrees of Abduction
Lie on stomach with involved arm hanging over the side of the table, dumbbell in hand, and elbow straight.
Stand with elbow at side fixed at 90 degrees and shoulder rotated out.
Slowly raise arm, bending elbow, and bring dumbbell up as high as possible.
Grip tubing handle while other end of tubing is fixed.
Hold at the top for 2 seconds, then slowly lower.
Pull arm across body, keeping elbow at side.
Perform _____ sets of _____ repetitions _____ times daily.
Return tubing in a slow and controlled fashion.
6D. Prone Rowing into External Rotation
Perform _____ sets of _____repetitions _____ times daily.
3. Shoulder Abduction to 90 Degrees Stand with arm at side, elbow straight, and palm against side. Raise arm to the side, palm down, until arm reaches 90 degrees (shoulder level). Perform _____ sets of _____ repetitions _____ times daily.
Lie on stomach with involved arm hanging over the side of the table, dumbbell in hand, and elbow straight. Slowly raise arm, bending elbow, up to the level of the table. Pause one second. Rotate shoulder upward until dumbbell is even with the table, keeping elbow at 90 degrees. Hold at the top for 2 seconds, then slowly lower, taking 2-3 seconds.
4. Scaption, External Rotation
Perform _____ sets of _____ repetitions _____ times daily.
Stand with elbow straight and thumb up.
7. Press-ups
Raise arm to shoulder level at 30-degree angle in front of body. Do not go above shoulder height. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily.
Sit on a chair or table. Place both hands firmly on the sides of the chair or table, palm down and fingers pointed outward. Hands should be placed equal with shoulders. Slowly push downward through the hands to elevate your body. Continued
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BOX 42-3.
Progressive Isotonic Strengthening Program—cont’d
Hold the elevated position for 2 seconds and lower body slowly. Perform _____ sets of _____ repetitions _____ times daily.
8A. Seated Rowing Sit in a chair. Grip the handles of a cable pulley or of tubing that is fixed in front of you with your elbows in at your side. Pull elbows back until in line with your trunk, squeezing shoulder blades together. Slowly return to starting position. Perform _____ sets of _____ repetitions.
8B. Seated Machine Bench Press (Restricted Motion) Sit in a chair.
Start with a push-up into wall. Gradually progress to table top and eventually to floor as tolerable. Perform _____ sets of _____ repetitions _____ times daily.
10A. Elbow Flexion Stand with arm against side and palm facing inward. Bend elbow upward, turning palm up as you progress. Hold 2 seconds and lower slowly. Perform _____ sets of _____ repetitions _____ times daily.
10B. Elbow Extension (Abduction) Raise involved arm overhead. Provide support at elbow from uninvolved hand. Straighten arm overhead. Hold 2 seconds and lower slowly.
Grip the handles of the machine and extend the elbows straight forward.
Perform _____ sets of _____ repetitions _____ times daily.
Pause, then return back to the starting position.
Support the forearm and with palm facing downward.
Avoid extending beyond the plane of the body to avoid excessive capsular stress.
Raise weight in hand as far as possible.
Perform ____ sets of ____ repetitions _____ times daily.
Perform _____ sets of _____ repetitions _____ times daily.
11A. Wrist Extension
Hold 2 seconds and lower slowly.
8C. Latissimus Dorsi Pulldown (Restricted Motion)
11B. Wrist Flexion
Sit at a latissimus pulldown machine and grip the bar just wider than shoulder width.
Lower a weight in hand as far as possible and then curl it up as high as possible.
Recline the upper body back approximately 45 degrees.
Hold for 2 seconds and lower slowly.
Pull bar to chest, then return to starting position.
Support the forearm and with palm facing downward.
Perform _____ sets of _____ repetitions _____ times daily.
11C. Supination
Do not allow the elbows to go beyond the plane of the body while pulling the bar to the chest.
Support the forearm on a table with wrist in neutral position.
Avoid extending the elbows completely when returning to the starting position.
Using a weight or hammer, roll wrist, taking palm up.
Perform _____ sets of ______ repetitions ______ times daily.
9. Push-ups Lie facedown with arms in a comfortable position. Place hands no more than shoulderwidth apart. Push up as high as possible, rolling shoulders forward after elbows are straight.
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Hold for a 2 count and return to starting position. Perform _____ sets of _____ repetitions _____ times daily.
11D. Pronation Support the forearm on a table with wrist in neutral position. Using a weight or hammer, roll wrist, taking palm down. Hold for a 2 count and return to starting position. Perform _____ sets of _____ repetitions _____ times daily.
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Figure 42-4. The athlete performs side-lying manual external rotation while the clinician imparts rhythmic stabilization drills at end range.
Figure 42-6. Rhythmic stabilization drill. The athlete performs push-ups on an unstable surface (tilt board) to challenge neuromuscular control and improve dynamic stabilization.
Figure 42-5. Wall stabilization drill. The athlete holds the hand on the ball in the plane of the scapula while rhythmic stabilization drills are performed.
extremity. These activities are incorporated to regain any remaining functional ROM, as well as improving neuromuscular control, and to train the extremity to produce and dissipate forces.62 Initially, two-handed drills close to the body, such as chest pass, side-to-side, and overhead soccer throws (Fig. 42-8) using a 3- to 5-lb medicine ball may be performed to enhance dynamic stabilization of the glenohumeral joint. Exercises are initiated with two-hand drills close to the center of gravity and gradually progressed to longer lever arms away from the patient’s body. Drills are progressed to challenge the dynamic stabilizers of the shoulder. After approximately 2 weeks of pain-free two-handed drills, the athlete progresses to one-handed plyometric drills using a small medicine ball (1-2 lb) and throwing into a Plyoback. Medicine-ball wall dribbles in the 90/90
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Figure 42-7. The athlete performs external rotation with tubing while the therapist applies a manual resistance throughout the range of motion.
position (Fig. 42-9) to improve overhead muscle endurance may also be incorporated. Phase IV: Return to Activity In the return-to-activity phase, the goal is to increase, gradually and progressively, the functional demands on the shoulder in order for the patient to return to unrestricted
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may begin functional sport activities through an interval return-to-sport program. These activities are designed to gradually return motion, function, and confidence in the upper extremity by progressing through graduated sportspecific activities.52-54 These interval sport programs are set up to minimize the chance of reinjury while training the patient for the demands of each individual sport. Each program should be individualized based on the patient’s injury, skill level, and goals. The duration of each program is based on several factors including the extent of the injury, the sport and level of play, and the time of season.
Figure 42-8. Two-handed overhead plyometric throw into a Plyoback (Exertools, Inc., San Carlos, Calif).
The athlete is allowed to return to unrestricted sports activities after completing an appropriately designed rehabilitation program and a successful clinical examination including full ROM, strength, and adequate dynamic stability and neuromuscular control. We routinely perform a combination of isokinetic testing for our overhead athletes, which we refer to as the thrower’s series.55,56 Criteria to begin an interval sport program include an external rotation–to–internal rotation strength ratio of 66% to 76% or higher at 180 deg/sec and an external rotation–to– abduction ratio of 67% to 75% or higher at 180 deg/sec.55,56 Patients returning to contact sports such as hockey, football, or rugby may be required to wear a shoulder stability brace (Don-Joy) in the beginning (Fig. 42-10).
Rehabilitation for Congenital Shoulder Laxity Rehabilitation of the patient with congenital shoulder instability poses a significant challenge for the rehabilitation specialist. Patients typically present with several episodes of instability that prevent them from performing certain tasks, which can include daily work tasks or recreational or
Figure 42-9. Wall dribbles with a 2-pound medicine ball in the 90/90 position for shoulder muscle endurance.
sport or daily activities. Other goals of this phase are to maintain the patient’s muscular strength and endurance, dynamic stability, and functional range of motion. The criteria to progress into this phase include full functional ROM, adequate static stability, satisfactory muscular strength and endurance, adequate dynamic stability, and a satisfactory clinical examination. The general orthopedic patient continues to perform a maintenance program to improve strength, dynamic stability, and neuromuscular control as well as maintaining full, functional, and pain-free ROM. The athlete continues to perform aggressive strengthening exercises such as plyometrics, proprioceptive neuromuscular facilitation drills, and isotonic strengthening. In addition, the athlete
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Figure 42-10. Don-Joy (Vista, Calif) shoulder-stabilizer brace used during sports activities to prevent excessive shoulder range of motion.
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sports activities. This type of instability can arise from several factors, including excessive capsular redundancy, laxity due to increased elastin density and decreased collagen density,28 poor osseous configuration such as a flattened glenoid fossa, or weakness in the glenohumeral and scapular musculature that results in poor neuromuscular control. Any of these factors, individually or in combination, can contribute to pathologic glenohumeral instability. The focus of the rehabilitation program for the patient with atraumatic instability is similar to that for the traumatically unstable shoulder, but it involves a slower progression with careful consideration to avoid excessive stretching of the capsular tissue. Early goals include improving proprioception, dynamic stability, neuromuscular control, and scapular muscle strengthening to gradually return the patient to functional activities without limitations. The early phase of rehabilitation involves reducing shoulder pain and muscular inhibition while abstaining from activities that produce apprehension. Shoulder muscle activation in patients with congenital laxity has been shown to differ from that in persons with a normal, stable shoulder.29,57-60 Normal force coupling that dynamically stabilizes the glenohumeral joint is altered, resulting in excessive humeral head migration and a feeling of subluxation by the patient. Rockwood and Burkhead40 found that an exercise program was effective in managing 80% of atraumatic instability. Misamore and colleagues61 found improved results in 28 of 59 patients in a long-term follow-up study of atraumatic instability in athletic patients. The rehabilitation program (Box 42-4) for patients with atraumatic instability involves regaining full ROM without excessive stress to the involved tissues. The patient often presents with excessive ROM, and therefore PROM activities are not the focus of the rehabilitation program, and excessive stretches to the involved tissues are avoided. Modalities such as cryotherapy, phonophoresis, high-voltage stimulation, and TENS may be used to minimize pain and inflammation. Shoulder pain can also be reduced through practicing gentle motion activities to neuromodulate pain, taking prescription nonsteroidal anti-inflammatory drugs, and abstaining from painful arcs of active and passive ROM. The focus of the early phase of the rehabilitation program is to minimize any further muscle atrophy and reflexive inhibition resulting from disuse, repeated subluxation episodes, and pain. Isometric contraction exercises may be performed for the glenohumeral muscles, particularly the rotator cuff. Rhythmic stabilization drills may also be performed to facilitate a muscular co-contraction and co-activation to improve neuromuscular control and enhance the sensitivity of the afferent mechanoreceptors (Fig. 42-11).10 The goal is to create a more efficient agonist-antagonist co-contraction to improve force coupling and joint stability during active movements.
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We believe that exercises such as rhythmic stabilization drills and closed-kinetic-chain exercises to promote a cocontraction and improve proprioception are beneficial for this patient population. Axial compression exercises are progressed from standing weight shifts on a table top to performing the quadruped and tripod positions (except in patients with posterior instability). Rhythmic stabilizations of the involved extremity as well as at the core and trunk may be applied during these closed-kinetic-chain drills to further challenge the patient’s dynamic stability and neuromuscular control. Unstable surfaces such as tilt boards, foam, large exercise balls, and the Biodex stability system (Biodex Corp, Shirley, NY) may be incorporated to further challenge the patient’s dynamic stability while in the closed-chain position to further promote a co-activation or co-contraction of the surrounding musculature (Fig. 42-12). Patients with congenital laxity often present with significant rotator cuff and scapular strength deficits, particularly the external rotators, scapular retractors, and scapular depressors. A progressive isotonic strengthening program may be initiated to improve rotator cuff and scapular musculature strength, endurance, and dynamic stability. Proper scapula stability and movement are vital for asymptomatic function. Scapula strengthening improves proximal stability and therefore enables distal segment mobility for the patient’s functional tasks. These exercises may include external rotation at 0 degrees of abduction, side-lying external rotation, standing external rotation at 90 degrees of abduction, prone external rotation, prone rowing, prone extension, and prone horizontal abduction at 100 degrees with external rotation. Other scapular training exercises commonly incorporated include supine serratus punches and a dynamic hug for serratus anterior strengthening. Bilateral external rotation with scapular retraction and table lifts may also be performed to strengthen the lower trapezius. Neuromuscular control drills are performed for the scapular musculature by having the rehabilitation specialist manually resist scapula movements. The goals of these drills are to enhance strength and endurance and to improve scapula proprioception. The function of the neuromuscular control system must not be overlooked in this patient population. Functional exercise drills that include positions of instability to induce a reflexive muscular response2,54,62 can protect against future injury or recurring episodes of instability. Active joint repositioning tasks, proprioceptive neuromuscular facilitation (PNF), and plyometric exercises may be beneficial, as well, to evoke a neuromuscular response. Once sufficient strength of the scapular stabilizers and posterior cuff has been achieved, the patient is encouraged to use the shoulder only in the most stable positions: those in the plane of the scapular during humeral elevation. Activities that promote a feeling of joint instability with or without subluxation or dislocation should be avoided. Only when coordination and confidence are achieved through progressive strengthening should the patient
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BOX 42-4.
Nonoperative Rehabilitation for Atraumatic Instability
This multiphased program allows the athlete to return to the previous functional level as quickly and safely as possible. Each phase varies in length for each athlete depending on the severity of injury, ROM and strength deficits, and the required activity demands of the patient.
• Caution: It is important to refrain from activities and motion in extreme ROM early in the rehabilitation process to minimize stress on the joint capsule. Proprioception and kinesthesia • Active joint reposition drills for ER and IR
Phase I: Acute
Phase II: Intermediate
GOALS
GOALS
Decrease pain and inflammation
Normalize arthrokinematics of shoulder complex
Re-establish functional range of motion
Regain and improve muscular strength of glenohumeral and scapular muscle
Establish voluntary muscular activation Re-establish muscular balance Improve proprioception PROGRAM
Decrease pain and inflammation • Therapeutic modalities: ice, electrotherapy • NSAIDs • Gentle joint mobilizations (Grades I and II) for neuromodulation of pain ROM exercises • • • • • • • • •
Gentle ROM exercises—no stretching Pendulum exercises Rope and pulley Elevation to 90 degrees, progressing to 145-150 degrees flexion L-bar Flexion to 90 degrees, progressing to full ROM Internal rotation with arm in scapular plane at 45 degrees of abduction External rotation with arm in scapular plane at 45 degrees of abduction Progress arm to 90 degrees of abduction
Improve neuromuscular control of shoulder complex Enhance proprioception and kinesthesia CRITERIA TO PROGRESS TO PHASE II
Full functional ROM Minimal pain or tenderness Good MMT PROGRAM
Initiate isotonic strengthening • • • • • • • •
IR and ER (side-lying dumbbell) Scaption to 90 degrees Abduction to 90 degrees Prone horizontal abduction Prone rows Prone extensions Biceps Lower trapezius strengthening
Initiate eccentric (surgical tubing) exercises at 0 degrees of abduction • Internal rotation • External rotation
Strengthening exercises
Improve neuromuscular control of shoulder complex
• • • • • • • • • • •
• Rhythmic stabilization drills at inner, mid, and outer ranges of motion (ER and IR, flexion and extension)
Isometrics (performed with arm at side) Flexion Abduction Extension External rotation at 0 degrees of abduction Internal rotation at 0 degrees of abduction Biceps Scapular isometrics Retraction and protraction Elevation and depression Weight shifts with arm in scapular plane (closed-chain exercises) • Rhythmic stabilizations (supine position) • ER and IR at 30 degrees of abduction • Flexion and extension at 45 and 90 degrees of flexion
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Initiate proprioceptive neuromuscular facilitation • Scapulothoracic musculature • Glenohumeral musculature Open kinetic chain at beginning and mid ranges of motion • • • • • •
PNF Manual resistance External rotation Begin in supine position progress to sidelying Prone rows ER and IR using tubing, with rhythmic stabilization
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BOX 42-4.
559
Nonoperative Rehabilitation for Atraumatic Instability—cont’d
Closed kinetic chain Wall stabilization drills • Initiated in scapular plane • Progress to stabilization onto ball • Weight shifts with hand on ball Initiate core stabilization drills • Abdominal • Erector spinae • Gluteal strengthening Continue therapeutic modalities (ice, electrotherapy) as needed
Phase III: Advanced Strengthening GOALS
Enhance dynamic stabilization Improve strength and endurance Improve neuromuscular control Prepare patient for activity CRITERIA TO PROGRESS TO PHASE III
Full non-painful ROM
• Open kinetic chain • PNF and manual resistance exercises at outer ranges of motion • Closed kinetic chain • Push-ups with rhythmic stabilization • Progress to unsteady surface: medicine ball, rocker board • Push-ups with stabilization onto ball • Wall stabilization drills onto ball Program scapular neuromuscular control training • Side-lying manual drills • Progress to rhythmic stabilization and movements (quadrant) Emphasize endurance training • Time bouts of exercise, 30-60 sec • Increase number of repetitions • Multiple bouts, three times a day
Phase IV: Return to Activity GOALS
Maintain levels of strength, power, and endurance
No pain or tenderness
Progress activity level to prepare athlete for full functional return to activity and sports
Continued progression of resistive exercises
CRITERIA TO PROGRESS TO PHASE IV
Good to normal muscle strength PROGRAM
Continue therapeutic modalities (ice, electrotherapy) as needed Continue isotonic strengthening
Full, pain-free ROM No pain or tenderness Satisfactory isokinetic test Satisfactory clinical examination PROGRAM
• Fundamental shoulder exercises II
Continue all exercises as in phase III
Continue eccentric strengthening
Initiate interval sport program (if appropriate)
Emphasize PNF exercises (D2 pattern) with rhythmic stabilization hold
Patient education
Continue to progress to neuromuscular control drills
Continue fundamental shoulder exercises as in phase II
ER, external rotation; IR, internal rotation; MMT, manual muscle testing; NSAIDs, nonsteroidal anti-inflammatory drugs; PNF, proprioceptive neuromuscular facilitation; ROM, range of motion.
attempt activities in an intrinsically unstable position. Bracing of the glenohumeral joint for return to sporting activities might also be necessary to provide immobilization or controlled ROM to protect against further injury.
and sufficient strength has been achieved, the patient may resume normal shoulder function, which may include sports activities.
The primary focus of the rehabilitation program for the patient with a congenitally unstable shoulder is to enhance strength and balance in the rotator cuff, improve scapular position and core stability, and improve proprioception and neuromuscular control. Once symptoms have subsided
SUMMARY
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The glenohumeral joint is an inherently unstable joint that relies on the interaction of the dynamic and static stabilizers to maintain stability. Disruption of this interplay or poor
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gradual return to athletics. The focus of the program should minimize the risk of reinjury and ensure that the patient can safely produce and dissipate forces at the glenohumeral joint.
References
Figure 42-11. Manual rhythmic stabilization drills. External-rotation and internal-rotation rhythmic stabilization in neutral rotation to promote a co-contraction and improve dynamic stability.
Figure 42-12. Axial compression drill. The athlete shifts weight on an unstable surface (medicine ball) while the clinician performs rhythmic stabilizations to the patient’s involved shoulder and trunk.
development of any of these factors can result in instability, pain, and a loss of function. Rehabilitation varies based on the type of instability present and the key principles described. A comprehensive program designed to establish full ROM, balance capsular mobility, and maximize muscular strength, endurance, proprioception, dynamic stability, and neuromuscular control is essential. A functional approach to rehabilitation using movement patterns and sport-specific positions along with an interval sport program will allow a
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1. Kibler WB: The role of the scapular in athletic shoulder function. Am J Sports Med 26(2):325-337, 1998. 2. Wilk KE, Arrigo CA, Andrews JR: Current concepts: The stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther 25(6):364-379, 1997. 3. Speer KP, Deng X, Borrero S, et al: Biomechanical evaluation of a simulated Bankart lesion. J Bone Joint Surg Am 76(12):1819-1826, 1994. 4. Warren RF, Kornblatt IB, Marchand R: Static factors affecting posterior shoulder instability. Orthop Trans 8:89, 1984. 5. Aronen JG, Regan K: Decreasing the incidence of recurrence of first time anterior dislocations with rehabilitation. Am J Sports Med 12:283-291, 1984. 6. Henry JH, Genung JA: Natural history of glenohumeral dislocation revisited. Am J Sports Med 10:135-137, 1982. 7. Hoelen MA, Burgers AMJ, Rozing PM: Prognosis of primary anterior dislocations in young adults. Arch Orthop Trauma Surg 110:51-54, 1990. 8. Hovelius L, Augustini BG, Fredin H, et al: Primary anterior dislocation of the shoulder in young patients: A ten-year prospective study. J Bone Joint Surg Am 78(11):1677-1684, 1996. 9. Kazar B, Relouszky E: Prognosis of primary dislocation of the shoulder. Acta Orthop Scand 40:216-219, 1969. 10. Lephart SM, Warner JJP, Borsa, PA, Fu FH: Proprioception of the shoulder joint in healthy, unstable, and surgically repaired shoulders. J Shoulder Elbow Surg 3:371-380, 1994. 11. McLaughlin HL, MacLellan DI: Recurrent anterior dislocation of the shoulder: A comparative study. J Trauma 7: 191-201, 1967. 12. Rowe CR: Prognosis in dislocations of the shoulder. J Bone Joint Surg Am 38:957-977, 1956. 13. Seybold D, Gekle C, Fehmer T, et al: Immobilization in external rotation after primary shoulder dislocation. Chirurg 77(9):821-826, 2006. 14. Tipton CM, MattesRD, Maynard JA: The influence of physical activity on ligaments and tendons. Med Sci Sports Exerc 7:165-175, 1975. 15. Yoneda B, Welsh RP, MacIntosh DL: Conservative treatment of shoulder dislocations in young males. J Bone Joint Surg Br 64:254-255, 1982. 16. Hovelius L: Anterior dislocation of the shoulder in teenagers and young adults. Five year prognosis. J Bone Joint Surg Am 69:393-399, 1987. 17. Hovelius L, Eriksson K, Fredin H, et al: Recurrences after initial dislocation of the shoulder. Results of a prospective study of treatment. J Bone Joint Surg Am 65(3):343-349, 1983. 18. Postacchini F, Gumini S, Cinotti G: Anterior shoulder dislocation in adolescents. J Shoulder Elbow Surg 9(6):470-474, 2000. 19. Marans HJ, Angel KR, Schmeitsch EH, et al: The fate of traumatic anterior dislocation of the shoulder in children. J Bone Joint Surg Am 74(8):1242-1244, 1992.
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20. Mair SD, Zarzour R, Speer KP: Posterior labral injury in contact athletes. Am J Sports Med 26:753-758, 1998. 21. Kaplan LD, Flanigan DC, Norwig J, et al: Prevalence and variance of shoulder injuries in elite collegiate football players. Am J Sports Med 33:1142-1146, 2005. 22. Baker CL, Uribe JW, Whitman C: Arthroscopic evaluation of acute initial anterior shoulder dislocations. Am J Sports Med 18(1):25-28, 1990. 23. Reinold MM, Wilk KE, Macrina LC, et al: The effect of electrical stimulation of the infraspinatus on shoulder external rotation force production following rotator cuff repair surgery. Presented at American Physical Therapy Association Combined Sections Meeting, New Orleans, 2005. 24. Spang JT, Karas SG: The HAGL lesion: An arthroscopic technique for repair of humeral avulsion of the glenohumeral ligaments. Arthroscopy 21(4):498-502, 2005. 25. Wolf EM, Cheng JC, Dickson K: Humeral avulsion of glenohumeral ligaments as a cause of anterior shoulder instability. Arthroscopy 11(5):600-607, 1995. 26. Blaiser RB, Burkus K: Management of posterior fracturedislocations of the shoulder. Clin Orthop 232:197-204, 1988. 27. Schwartz E, Warren RF, O’Brien SJ, et al: Posterior shoulder instability. Orthop Clin North Am 18:409-419, 1987. 28. Rodeo SA, Suzuki K, Yamauchi M, et al: Analysis of collagen fibers in shoulder capsule in patients with shoulder instability. Am J Sports Med 26:634-643, 1998. 29. Morris AD, Kemp GJ, Frostick SP: Shoulder electromyography in multidirectional instability. J Shoulder Elbow Surg 13(1):24-29, 2004. 30. Caspari RB, Geissler WB: Arthroscopic manifestations of shoulder subluxation and dislocation. Clin Orthop Relat Res (291):54-66 1993. 31. O’Brien SJ, Warren RF, Schwartz E: Anterior shoulder instability. Orthop Clin North Am 18:395-408, 1987. 32. Warner JJ, Flatbow EL: Anatomy and biomechanics. In Bigliani LU (ed): The Unstable Shoulder. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1996. 33. Beltran J, Rosenberg ZS, Chandnani VP, et al: Glenohumeral instability: Evaluation with MR arthrography. Radiographics 17(3):657-573, 1997 34. Goubier JN, Duranthon LD, Vandenbussche E, et al: Anterior dislocation of the shoulder with rotator cuff injury and brachial plexus palsy: A case report. J Shoulder Elbow Surg 13(3):362-363, 2004. 35. Maffet MW, Gartsman GM, Moseley B: Superior labrum– biceps tendon complex lesions of the shoulder. Am J Sports Med 23(1):93-98, 1995. 36. Blasier RB, Carpenter JE, Huston LJ: Shoulder proprioception. Effect of joint laxity, joint position, and direction of motion. Orthop Rev 23(1):45-50, 1994. 37. Myers JB, Lephart SM: The role of the sensorimotor system in the athletic shoulder. J Athl Train 35(3):351-363, 2000. 38. Smith RL, Brunoli J: Shoulder kinesthesia after anterior glenohumeral joint dislocation. Phys Ther 69(2):106-112, 1989. 39. Zuckerman JD, Gallagher MA, Lehman C, et al: Normal shoulder proprioception and the effect of lidocaine injection. J Shoulder Elbow Surg 8(1):11-16, 1999. 40. Rockwood CA, Burkhead WZ: Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg Am 74:890-896, 1992.
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41. Arciero RA, Wheeler JH, Ryan JB, et al: Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am J Sports Med 22(5):589-594, 1994. 42. Larrain MV, Botto GJ, Montenegro HJ, et al: Arthroscopic repair of acute traumatic anterior shoulder dislocation in young athletes. Arthroscopy 17(4):373-377, 2001. 43. Wheeler JH, Ryan JB, Arciero RA, et al: Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy 5(3):213-217, 1989. 44. Kiviluoto O, Pasila M, Jaromea H, Sundholm A: Immobilization after primary dislocation of the shoulder. Acta Orthop Scand 51:915-919, 1980. 45. Itoi E, Sashi R, Minigawa H, et al: Position of immobilization after dislocation of the glenohumeral joint. A study with use of magnetic resonance imaging. J Bone Joint Surg Am 84(5):873-874, 2002. 46. Itoi E, Hatakeyama Y, Kido T: A new method of immobilization after traumatic anterior dislocation of the shoulder: A preliminary study. J Shoulder Elbow Surg 12(5):413-415, 2003. 47. Miller BS, Sonnabend DH, Hatrick C et al: Should acute anterior dislocations of the shoulder be immobilized in external rotation? A cadaveric study. J Shoulder Elbow Surg 13(6):589-592, 2004. 48. Dehre E, Tory R: Treatment of joint injuries by immediate mobilization based upon the spinal adaption concept. Clin Orthop 77:218-232, 1971. 49. Haggmark T, Eriksson E, Jansson E: Muscle fiber type changes in human muscles after injuries and immobilization. Orthopaedics 9:181-189, 1986. 50. Salter RB, Hamilton HW, Wedge JH: Clinical application of basic science research on continuous passive motion for disorders of injuries and synovial joints. J Orthop Res 1: 325-333, 1984. 51. Carpenter JE, Blaiser RB, Pellizon GG: The effects of muscle fatigue on shoulder joint position sense. Am J Sports Med 26:262-265, 1998. 52. Ellenbecker TS, Mattalino AJ: The elbow in sport. Champaign, Ill, Human Kinetics 1997, pp 171-177. 53. Reinold MM, Wilk KE, Reed J, et al: Interval sport programs: Guidelines for baseball, tennis and golf. J Orthop Sports Phys Ther 32:293-298, 2002. 54. Wilk KE, Reinold MM, Andrews JR: Postoperative treatment principles in the throwing athlete. Sports Med Arthrosc Rev 9:69-95; 2001. 55. Wilk KE, Andrews JR, Arrigo CA, et al: The strength characteristics of internal and external rotator muscles in professional baseball pitchers. Am J Sports Med 21:61-66, 1993. 56. Wilk KE, Andrews JR, Arrigo CA: The abductor and adductor strength characteristics of professional baseball pitchers. Am J Sports Med 23:307-311, 1995. 57. Barden JM, Balyk R, Raso VJ, et al: Atypical shoulder muscle activation in multidirectional instability. Clin Neurophysiol 116(8):1846-1857, 2005. 58. Kronberg M, Brostrom LA, Nemeth G: Differences in shoulder muscle activity between patients with generalized joint laxity and normal controls. Clin Orthop Relat Res (269):181-192, 1991. 59. Myers JB, Ju YY, Hwang JH, et al: Reflexive muscle activation alterations in shoulders with anterior glenohumeral instability. Am J Sports Med 32(4):1013-1021, 2004.
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60. von Eisenhart-Rothe R, Jager A, Enlmeier KH, et al: Relevance of arm position and muscle activity on three-dimensional glenohumeral translation in patients with traumatic and atraumatic shoulder instability. Am J Sports Med 30: 514-522, 2002. 61. Misamore GW, Sallay PI, Didelot W: A longitudinal study of patients with multidirectional instability of the shoulder
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with seven- to ten-year follow-up. J Shoulder Elbow Surg 14(5):466-470, 2005. 62. Wilk KE, Arrigo CA: Current concepts in the rehabilitation of the athletic shoulder. J Orthop Sports Phys Ther 18: 365-378, 1993.
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CHAPTER 43 Strength and Conditioning
for the Preadolescent and Adolescent Athlete Leonard C. Macrina and Michael M. Reinold
Strength and conditioning programs have become an integral training component in the well-being of most athletes. An increase in participation and competitiveness in youth sports has produced a new interest in strength and conditioning programs in preadolescent and adolescent players. Proper physical training can enhance the young athlete’s sports performance and abilities to compete at their highest levels against their peers. This chapter outlines guidelines for a strength and conditioning program that is appropriate for the young athlete. Goals of these programs for these young athletes may include improved muscular strength, power, and endurance, with a focus on injury prevention, all leading to an enhanced performance by the athlete.
two 20-second sets per session, three times per week for 4 to 6 weeks. Although the results of these studies do not show benefits of strength training, the volume of exercise might have been too low to cause significant changes. More recent studies have shown that strength and conditioning programs can have a beneficial and safe outcome in preadolescents and adolescents. Sewall and Micheli3 studied the effects of a progressive resistance training program over a 9-week period. Exercises were performed three times per week and consisted of knee extension, chest press, and rowing. Eighteen prepubescent boys and girls between the ages of 10 and 11 years performed three sets of 10 repetitions at 50%, 80%, and 100% of their 10-repetition maximum. Significant increases in strength (42.9% vs. 9.5%) were reported, and no injuries occurred during the training period.
It is believed that most strength and conditioning programs for preadolescent and adolescent athletes should include many of the fundamental components seen at the higher levels of training. Resistance training may be included to increase strength and power production, along with a good stretching program to maintain flexibility. Neuromuscular control drills may also be included to improve the athlete’s reaction times. Cardiovascular and endurance training allow the athlete to maintain a high level of participation into the late innings. Speed and agility drills, plyometric training, and core stabilization all can be included as parts of the strengthening program.
Weltman and colleagues4 studied the effects of a 14-week concentric resistance program on 26 prepubescent boys with a mean age of 8.2 years. His results showed significant increases in strength, vertical jump, flexibility, and maximal oxygen consumption compared with a control group. Subjects in the study demonstrated no damaging effects to epiphyses, bone, or muscle as a result of the strengthening program. Ramsay’s group5 investigated the effects of 20 weeks of progressive resistance training three times a week on 13 male subjects between 9 and 11 years of age. Significant increases in strength were demonstrated when compared with the control group.
EFFICACY OF STRENGTH TRAINING IN ADOLESCENTS Controversy in the literature does exist regarding the efficacy and safety of strength and conditioning programs in preadolescent and adolescent athletes. Many studies have been performed and varying results have been reported. One of the first studies was performed by Vrijens and colleagues,1 who looked at the effects of an 8-week isotonic strengthening program consisting of 8 to 12 repetitions performed three times per week by 10- to 17-year-old boys. The study concluded that no strength gains were observed in the muscle groups of the upper and lower extremities, although their back and abdominal strength increased significantly. An older group of adolescent boys (mean age, 16.7 years) made significant strength gains in all areas tested. A study by Docherty2 also concluded that there were no significant strength gains after 12-year-old male athletes performed
Rians and coworkers6 compared the effects of a progressive concentric training program versus a control group. Eighteen boys with a mean age of 8.3 years old demonstrated significant increases in strength, flexibility, and vertical jump over a 14-week period. The authors reported no adverse effects on growth, flexibility, bone, muscle, or epiphyses as a result of the study. Pfeiffer and Francis7 compared repetitive strength training in prepubescent, pubescent, and post-pubescent male subjects using free weights and weight-stack machines. Weight training was done three days a week for 8 weeks. Nine exercises were performed at 50%, 75%, and 90% of 563
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the 10-repetition maximum. Their findings indicated that the greatest relative strength gains occurred in the prepubescent boys, which contradicted the Vrijens study. Similar results have been demonstrated by Payne and colleagues,8 Falk and Tenenbaum,9 and Faigenbaum.10 It appears that a well-designed program can benefit children using similar concepts regarding repetitions, sets, and weight as adult programs. These studies have shown strength training to be successful and safe for children who are still developing.
BENEFITS OF STRENGTH TRAINING Many potential benefits are associated with strength and conditioning in preadolescent and adolescent athletes. These include increases in muscular function and performance, significant hypertrophy, soft tissue flexibility, and enhanced muscular and cardiovascular endurance. Several authors have studied the effects of strength and conditioning on muscle function in preadolescent and adolescent athletes.2,4,5,7,11-16 Ozmun and colleagues15 and Ramsay and colleagues5 have documented significant increases in muscle strength despite no changes in anthropometric measurements. Earlier studies by Weltman’s group4 and Blimkie’s group11 also demonstrated significant strength gains in adolescent populations. Studies on muscle performance as a result of strength and conditioning have also demonstrated positive results in the youth population. These changes are most commonly attributed to changes in neuromuscular control rather than hypertrophy. Ozmun and colleagues15 demonstrated a 17% increase in electromyographic activity versus a control. In an earlier study from Blimkie’s group,11 there was an increase in motor unit activation as measured by interpolar twitch following a strength-training program. As important as strength gains are in the youth athlete, the ability to remain flexible will ensure that muscle strains do not occur. A study published by Weltman4 in 1986 determined that resistance training with a stretching regimen increased the sit-and-reach test by 8.4% in 26 boys with a mean age of 8.2 years. Coinciding with Weltman’s data was a study published by Rians and coworkers6 in 1987 in which 18 male subjects performed a 14-week strengthening and flexibility program. There was an increase of 8.4% on the sit-and-reach test in the study group as compared with the control group, which showed a 1.2% decrease in flexibility. Lillegard and colleagues14 published a study in 1997 in which the effects of a 12-week progressive resistance exercise program demonstrated a significant increase in the sit-and-reach test for both boys and girls versus a control group. Throughout these studies, the benefits of a controlled and supervised fitness program are witnessed in strength gains and in increased flexibility.
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Strength and conditioning training might also benefit the muscular and cardiovascular endurance of the athlete. Faigenbaum and colleagues17 observed the heart rates of children to be between 130 and 150 beats per minute throughout an entire strengthening workout. The effects of this prolonged increase in heart rate have been shown to enhance left ventricular structure and contractility . while eliciting a larger stroke volume and increased peak V O2. Enhanced muscular and cardiovascular endurance could help the athlete prevent overuse injuries, which are common when fatigue sets in late in a competition. Enhanced motor coordination, neuromuscular control, and dynamic stabilization may be developed to withstand detrimental forces during competition and control normal arthrokinematics. Hewett and coworkers18 studied the effects of a 6-week strengthening and plyometric program on 11 female volleyball players with a mean age of 15 years. The authors observed a 22% decrease in ground reaction forces and a 50% decrease in the abduction and adduction moments at the knee. In another study, Hewett and colleagues19 tried to determine the effects of a 6-week strengthening and plyometric program on preventing injury. In total, 366 high school female athletes were followed through the soccer, volleyball, and basketball seasons. A 3.6 times increase in knee injuries was observed in the untrained group, and a significant decrease in the incidence of noncontact knee injuries was noted in the experimental group. It is imperative that preadolescent and adolescent athletes maintain their flexibility and range of motion along with a supervised muscular and cardiovascular endurance program. With this training, normal arthrokinematics may be maintained and overuse injuries can be prevented during competition. Preadolescent and adolescent participation in athletics requires similar physiologic stress; however, children are metabolically less efficient than adults and require more oxygen to maintain a certain pace. An increase in performance may be attributed to a strength and conditioning program that enhances the anaerobic component of baseball by developing explosive strength. Hitting a baseball, throwing from the outfield, running to make a tackle, or chasing the soccer ball all require a sudden burst of power and strength to perform safely and injury free. This is essentially accomplished through motor coordination and neuromuscular control with an efficient transfer of potential energy through the kinetic chain resulting in the act performed. Gorostiaga and colleagues20 studied whether the effects of a 6-week heavy resistance training program could increase the throwing velocity of 19 male handball players. The participants ranged from 14 to 16 years of age and demonstrated a significant increase in velocity from 71.7 km/hr to 74.0 km/hr as compared with no change in the control group. Increases in power production have also been studied by various authors. Weltman and colleagues4
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in 1986 determined that a 10.4% increase in vertical jump height could result from a strength and conditioning program. Rians and coworkers6 had similar conclusions in 1987, along with Hewett and colleagues18 in 1996, in a study in which a 9.2% increase in vertical jump height was observed. Other general health-related benefits also result from a supervised strength and conditioning program in preadolescent and adolescent athletes. Increases in bone mineral density, improved body composition, and immune system along with the positive psychosocial benefits all contribute to the well-being of the youth.17 This attitude might also carry over into adulthood and prevent future conditions such as cardiovascular disease from occurring. The development of muscular strength, flexibility, and endurance helps maintain force production and stability for longer durations throughout the course of a game and season.
GENERAL GUIDELINES General guidelines should be developed before beginning a strength and conditioning program for the young athlete. Of particular importance is the close supervision and progression by an appropriately trained strength coach, therapist, or athletic trainer. The young athlete should also obtain medical clearance from a doctor. Although injuries such as growth plate fractures have been reported in rare circumstances, the majority of injuries sustained are softtissue injuries. In 2001, The American Academy of Pediatrics21 reported that 40% to 70% of injuries are muscle strains, most likely due to improper supervision, instruction, or technique. Therefore, injuries of this nature are usually avoidable. Proper training advice on technique during a strength and conditioning program is critical if injuries are to be averted. A warm-up and cool-down period should precede each session in which the athlete performs at least 10 minutes of light aerobic and stretching exercises. Exercises should be performed in a controlled manner, and ballistic motions are avoided to prevent excessive forces on muscles and joints. Fundamental fitness skills such as running, jumping, and throwing should be taught before sport-specific skills are incorporated. Early exercises may include working large muscle groups with progression to smaller muscle groups. Maximum amounts of weight that allow fewer than eight repetitions to be completed per set should be avoided initially. The focus should be on high repetitions with low resistance to increase endurance and neuromuscular adaptations. As the athlete matures, lower repetitions with increased weight may be incorporated to build more strength. In a study by Faigenbaum and colleagues,13 43 boys and girls
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between 5.2 and 11.8 years of age exercised two times per week for 8 weeks. One group performed 6 to 8 repetitions with a heavy load and the other performed 13 to 15 repetitions with a moderate load. There was a significantly greater increase in strength observed in the high-repetition group as compared with the heavy-load group. This study confirms the idea that strength gains are attainable with lower loads while keeping in mind that injury prevention is the key to all exercises. To maintain these strength gains, the athlete needs to continue with the strength and conditioning program on a regular basis. Faigenbaum and coworkers22 determined that gains in strength, muscle size, or power are lost 6 weeks following the cessation of resistance training. Ideally, exercises should be performed 3 to 5 times per week, allowing a day of rest between each session for the muscle group that was worked. Although strength and conditioning can aid the preadolescent and adolescent athlete during competition, specific guidelines vary depending on the age, maturity, and mental preparation of the youth. There is no standard age to begin a strengthening program, and the supervising coach, trainer, or therapist should use discretion. General stages23 have been developed to correspond with the age and maturity of the athlete (Table 43-1). Preadolescence refers to the athlete who has yet to develop sexual characteristics. This usually lasts to approximately 11 years of age in girls and 13 years of age in boys. This preadolescent period comprises Tanner stages I and II. Adolescence refers to the time between puberty and adulthood and usually occurs at ages 12 to 18 years of age in girls and 14 to 18 years of age in boys. Adolescence comprises Tanner stages III and IV. The youth is developing sexual characteristics and is physically maturing. Finally, Tanner stage V refers to adulthood and is the time after adolescence when full maturity is achieved, generally after age 18 years in both men and women. These stages can be used as a general guideline when developing a strength and conditioning program to fit the needs and safety of the athlete. TABLE 43-1 Tanner Stages Stage
Boys
Girls
1
Prepubertal (age ⬍7 years)
Prepubertal (age ⬍7 years)
2
Age 8-12 years
Age 8-10 years
3
Age 12-14 years
Age 10-16 years
4
Age 14-18 years
Age 12-18 years
5
Age ⬎18 years
Age ⬎18 years
From Tanner JM: Growth at Adolescence. Oxford, Blackwell Scientific, 1962.
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AGE-SPECIFIC GUIDELINES The athlete who is 7 years old or younger may be introduced to basic exercises with little to no weight. Begin with a bicycling or jogging program as a general warm up and cardiovascular conditioning. Teach proper exercise techniques using active range of motion followed by low-volume resistance training. Exercises such as push-ups (Fig. 43-1), pull-ups, abdominal crunches, and mini squats that incorporate body weight may be ideal for this age group. Also, introduce the athlete to the benefits of stretching before and after exercising or competing in an event. Generally, holding the stretch for 20 to 30 seconds is most beneficial after the muscle has been warmed up.24 The goals of this phase are to introduce the child to strength and conditioning, teach the basic principles of movement, and instruct in proper technique during exercises. In children 8 to 10 years of age, the number of exercises may gradually be increased while maintaining the simplicity of the exercises. Continue the progression of cardiovascular exercises using a bicycle, treadmill, or elliptical trainer followed by a flexibility program. Exercises may be balanced to contain both upper- and lower-extremity activities such as bench press, seated row or biceps curls, triceps curls, hamstring curls, leg press, and calf raises. Begin by establishing the 10-repetition maximum, which allows the athlete to perform 1 or 2 sets of 10 to 15 repetitions of each exercise. Preadolescent children should never lift maximum or nearmaximum weights due to excessive strain on developing muscles and epiphyseal plates. Teaching proper form and educating the athlete on the body’s response to exercise should make the experience educational and beneficial while maintaining the safety of the youth.
Figure 43-1. Push-up performed using the athlete’s body weight to enhance upper body strength.
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With the onset of adolescence at around 11 to 13 years of age, the athlete may progress to more advanced exercises and should progress the loading of each exercise. Begin by introducing more advanced exercises with little or no weight, with gradual progression of resistance. Isotonic exercises for a full-body workout may begin at this age. Exercises such as latissimus pulldowns, hip abduction and adduction, and hip flexion and extension are indicated. Quadriceps strengthening by knee extension, wall squats (Fig. 43-2), and lateral step-ups may also be added to the workout regimen. Further advancement may involve basic proprioceptive drills. Begin with proximal joint reproduction and continue distally on both the upper and lower extremities, advancing to rhythmic stabilizations to continue strengthening. Further challenging exercises may include tilt-board squats, with single-leg balance on a solid surface progressing to an unstable surface. The athlete should be supervised for any unusual musculoskeletal pains such as delayed-onset muscle soreness lasting longer than 48 hours after the exercise session. Middle adolescent athletes at around 14 to 15 years of age should continue to focus on full-body fundamental exercises. Advance to 2 or 3 sets of 8 to 12 repetitions of resistive
Figure 43-2. Wall squats using the athlete’s body weight to enhance overall lower-extremity strength.
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exercises while including sport-specific exercises. Baseball players may perform side-lying rotator cuff exercises, beginning with little or no weight and progressing 1 lb every 10 to 14 days to strengthen the external rotators.25 Resisted shoulder elevation in the scaption plane (full-can exercises) isolates the supraspinatus muscle. Scapular stabilization exercises such as seated rows, push-ups with a plus, and prone elevation in the scaption plane may also be included. In addition, basic running and agility focusing on proper technique to increase speed and power production may be essential in this age group. Light plyometric drills for the upper and lower extremities to strengthen the body’s ability to dissipate, control, and produce forces may be initiated. Exercises with a 2- to 3-lb medicine ball such as the two-hand chest pass, the two-hand side throw, and the two-hand overhead throw are examples. Plyometrics for the lower extremity such as leg press jumps, jumping in place, jumping rope, and two-leg box jumps are just a few strengthening exercises that may be included. Delayedonset muscle soreness is common after plyometric exercises for 24 to 48 hours, so exercises in moderation will most benefit the athlete while maintaining safety. Throughout all these exercises, the athlete should be focusing on core stabilization by maintaining a neutral or slight posterior pelvic tilt for the duration of the exercise. The athlete in late adolescence, generally older than 16 years, may begin a basic adult program if the athlete is competent in strength and conditioning principles. These may include a deltoid press, dumbbell fly, pullovers and the squat. The Thrower’s Ten program (Appendix III) to strengthen the rotator cuff and scapular stabilizers along with elbow and wrist exercises may also be included. In addition, eccentric and high-speed training similar to plyometric exercises might also benefit the athlete in this age group. Exercises such as tape hops, box drills, and sport cord lunges will increase speed and agility, which are necessary for the athlete in all sports. Advance these exercises by adding a manual perturbation or by performing the exercises on an unstable surface to increase dynamic stabilization of the upper and lower extremities (Fig. 43-3). Performing the 90/90 one-hand ball toss into a trampoline or performing a wall dribble using a 1- to 2-lb ball may also advance plyometric drills. Lower-extremity plyometric drills such as single leg bounding and rotational jumps further challenge the athlete’s strength and agility demands.
SUMMARY Strength and conditioning in preadolescent and adolescent have proved to be a safe and effective component to baseball training programs in young athletes. These programs should vary based on the age, physical maturity, and experience of the athlete. Simple light-weight exercises that emphasize the entire body may be progressed to sport-specific exercises for the young athlete, including a
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Figure 43-3. Proprioceptive neuromuscular facilitation D2 pattern on a foam surface to further challenge dynamic and core stability.
gradual increase in intensity, duration, and frequency to assure a progressive accommodation to heavy and dynamic loading. Most importantly, all programs should be closely supervised by a medical professional to avoid potential injuries.
References 1. Vrijens J: Muscle strength development in the pre-and postpubescent age. Med Sport 11:152-158, 1978. 2. Docherty D, Wenger HA, Collis ML, Quinney HA: The effects of variable speed resistance training on strength development in prepubertal boys. J Hum Mov Stud 13:377-382, 1987. 3. Sewall L, Micheli LJ: Strength training for children. J Ped Orthop 6:143-146, 1986. 4. Weltman A, Janney C, Rians CB, et al: The effects of hydraulic resistance strength training in pre-pubertal males. Med Sci Sports Exerc 18(16):629-638, 1986. 5. Ramsay JA, Blimkie CJ, Smith K, et al: Strength training effects in prepubescent boys. Med Sci Sports Exerc 22: 605-614, 1990. 6. Rians, CB, Weltman A, Cahill BR, et al: Strength training for prepubescent males: Is it safe? Am J Sports Med 15:483-489, 1987.
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7. Pfeiffer RD, Francis RS: Effects of strength training on muscle development in prepubescent, pubescent, and postpubescent males. Physician Sportsmed 14:134-143, 1986. 8. Payne VG, Morrow JR, Johnson L, Dalton SN: Resistance training in children and youth: A meta-analysis. Res Q Exerc Sport 68:80-88, 1997. 9. Falk B, Tenenbaum G: The effectiveness of resistance training in children: A meta-analysis. Sports Med 22:176-186, 1996. 10. Faigenbaum, AD, Zaichkowsky LD, Westcott WL, et al: The effects of a twice per week strength training program on children. Ped Exerc Sci 5:339-346, 1993. 11. Blimkie CJ, Ramsay J, Sale D, et al: Effects of 10 weeks of resistance training on strength development in prepubertal boys. In Oseid S, Carlsen K-H (eds): Children and Exercise XIII. Champaign, Ill, Human Kinetics Publishers, 1989, pp 183-197. 12. Blimkie CJ: Resistance training during pre- and early puberty: efficacy, trainability, mechanisms, and persistence. Can J Sport Sci 17(4):264-279, 1992. 13. Faigenbaum AD, Westcott WL, Loud RL, Long C: The effects of different resistance training protocols on muscular strength and endurance development in children. Pediatrics 104(1):e5, 1999. 14. Lillegard WA, Brown EW, Wilson DJ, et al: Efficacy of strength training in prepubescent to early postpubescent males and females: Effects of gender and maturity. Pediatr Rehabil 1(3):147-157, 1997. 15. Ozmun JC, Mikesky AE, Surburg PR: Neuromuscular adaptations following prepubescent strength training. Med Sci Sports Exerc 26(4):510-514, 1994. 16. Blimkie CJ: Resistance training during preadolescence. Issues and controversies. Sports Med 15(6):389-407, 1993.
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17. Faigenbaum AD: Strength training for children and adolescents Clin Sports Med 19(4):593-619, 2000. 18. Hewett TE, Stroupe AL, Nance TA, Noyes FR: Plyometric training in female athletes. Decreased impact forces and increased hamstring torques. Am J Sports Med 24:765-773, 1996. 19. Hewett TE, Lindenfeld TN, Riccobene JV, Noyes FR: The effect of neuromuscular training on the incidence of knee injury in female athletes: A prospective study. Am J Sports Med 27(6):699-706, 1999. 20. Gorostiaga EM, Izquierdo M, Iturralde P, et al: Effects of heavy resistance training on maximal and explosive force production, endurance and serum hormones in adolescent handball players. Eur J Appl Physiol Occup Physiol 80(5):485-493, 1999. 21. Bernhardt DT, Gomez J, Johnson MD, et al; Committee on Sports Medicine and Fitness: Strength training by children and adolescents. Pedatrics 107(6):1470-1472, 2001. 22. Faigenbaurn AD, Westcott WL, Micheli LJ, et al: The effects of strength training and detraining on children. J. Strength Cond Res 10(2):109-114, 1996. 23. Tanner JM: Growth at Adolescence. Oxford, UK, Blackwell Scientific, 1962. 24. Bandy WD, Irion JM: The effect of time on static stretch on the flexibility of the hamstring muscles. Phys Ther 74(9):845-850, 1994. 25. Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34(7):385-394, 2004.
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CHAPTER 44 Injuries and Rehabilitation of the
Overhead Female Athlete’s Shoulder Airelle O. Hunter-Giordand, Wendy J. Hurd, Michael J. Axe, and Lynn Snyder-Mackler
across a broad spectrum of sports.8-11 Only Sallis and colleagues12 identified differences in the number of shoulder injuries in female athletes compared with male athletes. They tracked injuries in seven matched sports over 15 years at a single NCAA Division III school; all injuries were evaluated by the same certified athletic trainer. They reported a significantly greater number of shoulder injuries among female athletes participating in swimming and water polo compared with their male counterparts. When interpreting the potential source of the discrepancy of injury rates between the two genders, the authors proposed the coach’s more rigorous training regimen might have contributed to the higher number of female shoulder injuries in this cohort. When taken in context with other epidemiologic studies, the work by Sallis’s group suggests that training errors can be more likely to contribute to injuries than that female athletes have a higher susceptibility to shoulder injury.
Participation in competitive and recreational sports among female athletes in the United States has increased dramatically in recent decades. Title IX is a legislative act providing an increased number of women the opportunity to compete in collegiate sports; passed in 1972, it is commonly seen as a major turning point in women’s sports. As a result of this dramatic increase in sports participation by female athletes, injury patterns are emerging for women that are distinct from those of men.1 For example, higher rates of noncontact anterior cruciate ligament (ACL) injuries among women versus men have been well documented.2-4 Female-oriented injury prevention and rehabilitation programs have been developed to address this so-called ACL epidemic.5-7 This leads to the question, do similar gender differences in injury patterns exist in the upper extremity? Compared with the lower extremity, relatively little research has been performed on upper-extremity injury patterns or rehabilitation needs for female athletes. A review of the literature combined with clinical experience suggests there are in fact more similarities than differences in the patterns, types, and rehabilitation of shoulder injuries when comparing male and female athletes. Subtle differences in physiologic makeup and sport demands do, however, often result in a unique presentation of the female athlete’s shoulder. The ability to accurately diagnose shoulder injuries and appreciate the rehabilitation needs of the female athlete are necessary for the clinician to return the athlete to play as quickly and safely as possible. Therefore, the purpose of this chapter is to review common female athletic shoulder injuries and their causes and to describe unique shoulder rehabilitation interventions when treating the female athlete.
Overuse injuries are more common than traumatic shoulder injuries in the female athlete. The potential for a traumatic shoulder injury (e.g., dislocation) does exist in an impact sport such as gymnastics or while performing a skill like a headfirst dive in softball. Collisions between players and their environment that can contribute to a traumatic shoulder injury, however, are relatively uncommon. Overuse shoulder injuries such as tendinitis and glenohumeral instability are more commonplace in female athletes who participate in overhead sports. This is secondary to the repetitive nature and extreme arm positions associated with overhead motions. Tendinitis and subsequent impingement are common pathologies of the supraspinatus and biceps tendons among participants in sports such as volleyball, softball, and swimming,11,13-15 and they occur when the demands of the sport exceed the tensile abilities of these muscles. The combination of an inherently unstable joint, increased ligamentous laxity, and extreme arm positioning make glenohumeral instability another common pathology in the female overhead athlete. Glenohumeral instability can range from multidirectional instability secondary to contributing congenital factors to subtle subluxations that occur secondary to the acquisition of increased anterior capsular laxity.
SHOULDER INJURIES IN THE FEMALE ATHLETE Injury Patterns A number of investigations have compared injury rates in female and male athletes. The evidence predominantly suggests male and female athletes sustain a comparable number of shoulder injuries when examining injuries per exposure hour while participating in matched sports (e.g., baseball or softball, gymnastics). This includes studies performed on high school, collegiate, and professional level athletes and
The incidence of tendinitis versus instability or the combination in female athletes is difficult to discern from the literature. Injury data for female athletes are often vague, with the injury described ambiguously as a strain, sprain, 569
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or tendinitis of the shoulder. Meister and Andrews16 have described an injury classification system that distinguishes primary tendinitis from tendinitis that is occurring secondary to an underlying instability. Secondary tendinitis can occur as the muscles surrounding the glenohumeral joint are taxed in an attempt to compensate for the lack of static joint stability. When an athlete presents acutely with significant pain and inflammation, instability may be missed secondary to guarding. Injuries in many female athletes are therefore misdiagnosed as shoulder tendinitis and anterior impingement, and these athletes often are considered to have inadequate shoulder mobility. In our clinical experience, we have identified a degree of glenohumeral instability in the majority of female patients presenting with an overuse injury.
Contributing Injury Factors Training errors and faulty mechanics can contribute to shoulder injury in any athlete. Depending on the environment and funding situation, female athletes might not have coaches or trainers to provide education regarding exercise periodization, injury prevention, sport-specific training, and proper weight-lifting techniques. Furthermore, not all coaches have the ability to teach sport-specific skills such as the windmill softball pitch. The rehabilitation specialist must be part of a team prepared to address training errors and sport mechanics as the athlete transitions to sports activities, or injury recurrence is inevitable. For female athletes, increased ligamentous laxity has been proposed as a risk factor for shoulder injury. Although women are considered to have greater laxity than men, it has not been established that generalized ligamentous laxity correlates with increased shoulder laxity. Emery and colleagues17 measured generalized ligament laxity and shoulder laxity in 150 adolescents. General joint laxity was assessed by measuring index finger hyperextension, and shoulder laxity was evaluated with drawer and sulcus tests. Generalized ligament laxity did not correlate with shoulder laxity. McFarland and colleagues18 also measured general joint laxity and shoulder laxity but reported contrasting results. Hyperlaxity of other joints was determined by the presence of hyperextension of the knees and elbows, the ability to touch thumb to forearm, and the ability to sublux other joints. Posterior shoulder laxity was assessed with a drawer test. A total of 356 shoulders on 178 asymptomatic high school and college athletes were tested. They reported a significantly larger number of female athletes demonstrating generalized ligamentous laxity than male athletes, and more female shoulders (65%) could be posteriorly subluxed than male shoulders (51%) (P ⬍ 0.05). The studies by Emery17 and McFarland18 not only report contrasting results but also include methodologic limitations: Emery17 used only index finger hyperextension as a measure of generalized ligamentous laxity, and both studies
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assessed shoulder mobility with manual examination.17,18 Comparisons of shoulder laxity between examiners has been shown to have poor reliability and are only as good as the examiner.19 Borsa and colleagues1 measured glenohumeral laxity, stiffness, and generalized joint hypermobility on 51 uninjured subjects with no history of participation in overhead sports. Glenohumeral laxity and stiffness were measured with an instrumented arthrometer, and hyperextension was measured with a goniometer. Borsa1 reported that female subjects exhibited significantly greater anterior laxity and less anterior stiffness of the glenohumeral joint (i.e., the amount of force required to displace the joint was lower) as well as greater generalized laxity than men. The clinicians concluded that these findings might indicate a possible increased risk for joint instability in women, especially those participating in overhead sports. Although women might exhibit increased ligament laxity when compared with men, this does not equate to instability: Laxity is the amount of physiologic motion that is present; instability is when the amount of motion present becomes symptomatic. Future investigations are needed to determine if there is a correlation between glenohumeral laxity and injury.
Presentation of the Female Athlete’s Shoulder In our clinical experience, the majority of female athletes with a shoulder complaint present with an overuse injury and participate in an overhead sport. Acute patient presentation typically consists of anterior shoulder pain emanating from biceps irritation, supraspinatus tendinitis, posterior rotator cuff weakness, an abducted scapular position at rest with poor dynamic scapulothoracic rhythm, decreased glenohumeral motion secondary to pain and guarding, and an increase in capsular laxity (globally or isolated to the anterior aspect of the glenohumeral joint). According to the Meister and Andrews16 classification system, this injury would be described as tendinitis secondary to instability. We have coined the term female athlete’s shoulder to describe this presentation. Although the injured female athlete can sustain a broad range of shoulder injuries, the numerous pathologies (e.g., acute dislocation, glenoid labrum injury) have a similar clinical presentation. Therefore, the remainder of this chapter addresses unique nonoperative rehabilitation concerns when treating the female athlete’s shoulder.
REHABILITATION OF THE FEMALE ATHLETE’S SHOULDER Multiphased Rehabilitation We use a multiphased rehabilitation program to treat the female athlete’s shoulder. This program is based on the nonoperative thrower’s rehabilitation protocol developed by Wilk and colleagues20 and the University of Delaware throwing programs38 and implements criteria-based advancement with respect for tissue-healing time frames.
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One of the recurrent themes emphasized during rehabilitation of the female athlete’s shoulder is avoidance of activities and arm positions that exacerbate pain symptoms. Primarily emanating from the biceps, this pain can be difficult to resolve. Many clinicians choose to advance the rehabilitation program in an eager attempt to get the athlete back to sports as quickly as possible. We believe to normalize shoulder motion and strength and to enhance dynamic joint stability ultimately with a successful return to sports; resolving biceps pain should be the clinician’s priority even if this results in the patient’s remaining in the acute stage of rehabilitation for several weeks.
muscle groups that serve as prime movers might need to be addressed to assist with appropriate sport biomechanics for this population. Lack of prior participation in weight training and poorly scaled machinery might also necessitate instruction in technique and equipment use. The final step in rehabilitation comes when the athlete begins the appropriate interval sport program. Few interval sports programs have been developed for women’s sports. The University of Delaware has developed position-specific interval sports programs for softball38 and volleyball.39 These programs take into account game and training volume and intensity for each overhead skill.
Another challenge in the acute stage of rehabilitation is determining what constitutes normal shoulder motion in the female athlete. In male overhead athletes, the total shoulder rotation motion (internal rotation plus external rotation) should be equal on both upper extremities.20 The presence of an increase in external rotation and a corresponding decrease in internal rotation on the dominant arm is an expected adaptation associated with overhead throwing. Limited data are available describing shoulder range of motion in the uninjured female overhead athlete. Dover and colleagues21 measured active shoulder rotation motion in healthy collegiate softball athletes and reported a shift in rotational motion on the dominant arm similar to that seen in male overhead athletes. In contrast, Hurd and coworkers22 measured passive shoulder rotation motion in healthy female college softball players and found no difference between arms in external and internal glenohumeral rotation motions. One possible explanation for the difference in findings between the studies is that with active range-of-motion testing, both muscle strength and capsular laxity play roles in the amount of motion observed, whereas with passive motion testing only capsular laxity is a factor. Hurd and colleagues22 proposed that the nondominant arm be used to identify normal shoulder motion for individual female athletes; however, further research in this field is necessary to determine what constitutes normal shoulder motion in this population.
Box 44-1 includes treatment strategies and interventions for nonoperative rehabilitation of the female athlete’s shoulder and was developed to complement the thrower’s rehabilitation program developed by Wilk and coworkers.20 The remainder of this chapter describes in detail the points of emphasis during this rehabilitation program.
As the female athlete progresses into the subacute and advanced stages of rehabilitation, her treatment closely resembles that of the male overhead athlete. Exercises to improve rotator cuff and scapular strength are performed, and dynamic joint control is emphasized during neuromuscular control drills. When the athlete approaches return to sport readiness, there are again unique concerns when treating the female athlete. Many male athletes are regular participants in a weight-training program. Large muscles groups such as the latissimus dorsi, pectoralis major, and biceps brachii are well developed and sometimes do not need to be specifically addressed in rehabilitation; the stabilizing rotator cuff and scapular musculature are the focal points during treatment. Conversely, fewer female athletes participate in weight-training programs. Large
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Biceps Tendon Dysfunction The long head of the biceps tendon contributes to glenohumeral stability by centralizing the humeral head within the glenoid fossa and serving as a dynamic restraint to external rotation with the arm in an abducted position.23 The anatomic location of the long head of the biceps tendon allows it to serve as a stabilizer to the anterior aspect of the glenohumeral joint. After originating superiorly from the supraglenoid tubercle and the glenoid labrum, the course of the tendon is oblique over the top of the humeral head and then inferior to the bicipital groove. The long head of the biceps tendon then exits the shoulder joint through the rotator interval before extending toward its distal attachment site at the elbow.24 In the lateral aspect of the rotator interval, the superior glenohumeral ligament forms a U-shaped sling, crossing under the biceps tendon and inserting into the proximal aspect of the intertubercular groove.25 This anatomic feature of the superior glenohumeral ligament allows it to function as an intra-articular stabilizer for the long head of the biceps tendon and protects the tendon against anterior shearing stress. Werner25 proposed that a lesion in this area might lead to anterior instability of the long head of the biceps tendon in external rotation and be a source of anterior shoulder pain. The underlying source of anterior shoulder pain in the female athlete therefore appears to be biceps tendon pathology secondary to congenital or acquired increases in glenohumeral ligament laxity. The tendon involvement may be a result of inadequate biceps tendon stabilization within the rotator interval, biceps overuse to compensate for a lack of ligamentous and posterior rotator cuff joint stabilization, or a combination of both factors. Although joint instability may be the primary cause underlying bicipital pain in the female athlete, the early stages of
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BOX 44-1.
Nonoperative Rehabilitation of the Female Athlete’s Shoulder
Acute Phase
STRENGTHENING
GOALS
Initiate isotonics for rotator cuff
Resolve pain and inflammation Normalize motion
• Tubing, dumbbells • Limited-arc and full-arc motion
Retard muscle atrophy
Bias key muscle groups
Re-establish neuromuscular base THERAPEUTIC MODALITIES
• Shoulder external rotators • Scapular depressors, retractors, protractors
Cryotherapy
NEUROMUSCULAR CONTROL
Ultrasound
End-range joint control with rhythmic stabilizations
Phonophoresis
Dynamic joint control with PNF patterns
Electrical modalities
FLEXIBILITY AND STRETCHING
• Isolated pain: →Noxious stimulation • Nonspecific pain: TENS
Restore thrower’s motion
CONTROL STRESS
No overhead sports activities Avoid painful activities of daily living Safe arc of motion • Avoid painful arm positions • Shoulder extension to midline • Limited rotational movements NORMALIZE MOTION
Determine source of motion limitation • Capsular restriction: Joint mobilizations • Musculotendinous tightness: Stretching • Pain and guarding: Symptom resolution Determine amount of motion to restore STRENGTHENING
Rotator cuff isometrics augmented with electrical stimulation Scapular strengthening • Isometrics • Tubing versus dumbbells NEUROMUSCULAR CONTROL
Avoid positions that promote impingement
Advanced Strengthening Phase GOALS
Aggressive strengthening Progress dynamic neuromuscular control Improve strength, power, endurance Initiate light throwing activities STRENGTHENING
Continue bias of rotator cuff, scapular muscles Train large muscle groups • Supervision for weight-lifting technique • Modifications for congenitally lax joint Move into overhead strengthening positions Upper extremity plyometrics • Two-handed and one-handed • Below and above shoulder Endurance component to overhead activities NEUROMUSCULAR CONTROL
Functional positions for rhythmic stabilizations PNF variations for glenohumeral, scapulothoracic joints
Rhythmic stabilizations for glenohumeral and scapulothoracic joints
INITIATE INTERVAL SPORTS PROGRAM
Pattern reproduction
Return to Activity Phase
Joint repositioning
Biomechanical analysis GOALS
Scapular taping
• Progress to sports • Continue strengthening and flexibility drills
Intermediate Phase
EXERCISES
GOALS
Progress strengthening exercise
Stretching and flexibility drills
Restore muscle balance
Maintenance program for strength
Enhance dynamic neuromuscular control
Plyometrics
Practice controlled flexibility and stretching PNF, proprioceptive neuromuscular facilitation; TENS, transcutaneous electrical nerve stimulation.
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rehabilitation must focus on resolving soft tissue pain and inflammation. Activity modification is one of the keys to controlling stress to the healing tissue and includes rest from painful sports and daily activities. Athletes who are in season may continue to participate in their sports without extending the injury, but it is unlikely the pain complaints will be resolved until the athlete can cease the offending activities. Prolonging soft tissue pain and inflammation can extend the time necessary to completely recover from the injury. Another form of activity modification is limiting arm motions that stress the long head of the biceps tendon, including arm extension beyond the midline of the body, external rotation beyond 0 degrees with the arm by the side, and resisted elbow flexion. In acute cases, any arm motion causes persistent biceps pain. In these cases, strengthening exercises must first be performed isometrically before progressing to nonpainful limited-arc isotonic exercise. Some treatments can hasten the resolution of biceps pain. In addition to cryotherapy for pain control, electrical modalities can be extremely useful in resolving pain complaints. In our experience, the most effective electrical modality to resolve focal soft tissue pain is noxious stimulation (Table 44-1),26 which is so named because the electrical stimulation intensity level during treatment is painful. Noxious stimulation is produced with long pulse durations of up to 1 second and amplitudes that produce pain beneath the electrodes. The electrodes are often smaller (1 cm ⫻ 1 cm) and the stimulus is often more tolerable if it is placed over a more superficial surface (long head of the biceps tendon) rather than over a muscle belly (biceps) where muscle contraction can occur (Fig. 44-1). Eliciting muscle contraction is acceptable, although it may be less tolerable for the patients. The only requirement for this treatment is for the patient to perceive the stimulus as painful at the site in question.
573
Figure 44-1. Noxious stimulation to the long head of the biceps tendon.
Because the electrodes used for noxious stimulation are relatively smaller than those used for other applications of electrical stimulation, current density is increased and the clinician should take care to investigate patient sensations of burning. In these instances, the electrodes should be investigated for appropriate positioning and contact. If necessary, current intensity might have to be decreased to avoid a skin burn. Pain levels should be tested before and after the treatment to assess whether the stimulation is beneficial. Pain relief is often immediate with noxiouslevel stimulation. In patients who complain of global rather than local shoulder pain, transcutaneous electrical nerve stimulation (TENS) (see Table 44-1) may be better used in place of noxious stimulation. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used to control shoulder inflammation, which is often
TABLE 44-1 Electrical Stimulation Protocols
Protocol
Pad Placement
Carrier Frequency
Ramp Treatment Time Time
Pad Size
12/8sec.
2 sec
10-15 min
1.5 cm ⫻ 1.5 cm
Frequency On/Off Time
Noxious stimulation
1 pad on both sides of the painful area and secured with tape
2500 Hz
50 bps
TENS
2-4 pads placed on and around the painful area
4500 Hz
50-100 bps
Continuous/0
None
ⱖ15 min
Depends on the size of the area
Isometric muscle strengthening
Depends on area of rotator cuff intended to strengthen
2500 Hz
50-75 bps
12/50sec
2 sec
12 contractions/ 10 min
2 cm ⫻ 2-3 cm
Functional electrical stimulation
Depends on area of rotator cuff intended to strengthen
2500 Hz
50-75 bps
Length of exercise Ex. 10/5sec
2 sec
30 reps/ 10 min
2 cm ⫻ 2-3 cm
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associated with an athlete’s pain. Use of NSAIDs should be directed by a physician. Patients typically take NSAIDs for 7 to 14 days and then taper their use of the medication until there is no pain with activity. If the patient does not show any difference in pain levels in this time period, a drug from a different NSAID family may be warranted.
Rotator Cuff Strengthening One of the main functions of the rotator cuff musculature is to provide dynamic stability to the glenohumeral joint. Several force couples help establish dynamic equilibrium of the glenohumeral joint in any arm position.27 These force couples help to compress the humeral head centrally within the glenoid fossa, which maximizes joint congruency and minimizes humeral head translation during all motions. Demands on glenohumeral joint dynamic muscle stabilizers are especially pronounced during overhead throwing motions. With repetitive fatigue of these muscles, injury often occurs not only to the rotator cuff as an overuse syndrome but also to the capsule in the form of microtraumatic laxity secondary to subtle subluxations of the humeral head. Due to the extreme amounts of motion required by overhead athletes, the rotator cuff has to be exceptionally strong and enduring to maintain glenohumeral joint stability. This is especially important for female athletes because their shoulders often exhibit greater laxity when compared with the shoulders of male athletes. In the acute phase after injury, rotator cuff strength must be addressed immediately to minimize atrophy and prevent further weakening of this muscle complex. Strengthening in the acute phase is often difficult because of the athlete’s pain; therefore, modifications addressed earlier in this chapter (e.g., limited arc isotonics) should be implemented to maintain muscle strength and minimize pain. Because of the internal rotation strength bias typically seen in the overhead athlete,28,29 strengthening of the external rotator muscle group is an early goal of the rehabilitation specialist. These muscles function eccentrically to slow the arm after ball release and follow-through phases of overhead sports motions. Weakness or fatigue of the posterior rotator cuff can contribute to inadequate dynamic glenohumeral stabilization. Typical rehabilitation exercises such as external rotation with tubing can exacerbate pain due to the increased stress on the biceps tendon. Therefore, alternative methods of strengthening these muscles may include isometric (with and without electrical stimulation) and rhythmic stabilization exercises. When using electrical stimulation to augment external rotation strength, two electrodes are positioned over the infraspinatus while the athlete is seated and the muscle is held isometrically in neutral or slight internal rotation (Fig. 44-2; see Table 44-1). The stimulation intensity is increased until a
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Figure 44-2. Patient position for isometric external rotation exercise with electrical stimulation to the infraspinatus.
full tetanic contraction is seen or the athlete is at her maximum tolerance.30 As a home program, the athlete can continue to do isometrics against the wall for all muscles surrounding the shoulder complex, increasing the repetitions and time of the holds as long as pain is absent. Rhythmic stabilization exercises can promote joint stability via co-contraction of the muscles surrounding a joint. The clinician can also use this exercise to promote external rotation strength by biasing resistance (time, magnitude, and frequency of resistance is applied to emphasize external rotation muscle activity) during the exercise. The exercise can be initiated in the supine position and progressed to side lying, and the amount of arm rotation may vary. Positioning the arm in either slight internal rotation or a neutral rotation (0 degrees) is recommended to avoid biceps stress. As the athlete moves from the acute to the intermediate phase of rehabilitation, the anterior shoulder pain subsides and pain-free range of motion is restored. Consequently, rotator cuff strengthening is advanced to include light isotonics and rhythmic stabilization exercises performed at various angles with the arm in external rotation. Electrical stimulation may be used to complement active movements, with the athlete using a hand-held device to trigger the onset of electrical stimulation as she begins to move through the range of motion (Fig. 44-3; see Table 44-1). Conventional rotator cuff–strengthening exercises included in the Thrower’s Ten31 program are also performed in these phases of rehabilitation. Criteria including no pain, a manual muscle test grade of least a 4/5, full range of motion, and no substitution patterns are used to determine if the athlete is ready to progress from below- to above-shoulder strengthening exercises. The higher-level strengthening activities performed in the advanced and return-to-activity phases are consistent with
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575
abducted scapular position, with weakened posterior scapular musculature, which can contribute to an increased risk of anterior impingement. It is therefore important for the rehabilitation specialist to instruct the female athlete in appropriate posture and address scapula stability early in the rehabilitation process.
Figure 44-3. Isotonic external rotation exercise with functional electrical stimulation to the infraspinatus. The patient triggers the stimulator manually with a hand-held device.
exercises performed by the male overhead athlete during these same time intervals.20
Scapula Dysfunction
Early goals after injury (acute phase) include re-establishing scapular stability and normalizing muscle activation patterns. A stable scapula with correct arthrokinematics permits normal activation of the rotator cuff and decreases the chance of further injury. Exercises in the acute phase often consist of scapular isometrics and shrugs. Scapular taping may be used in this phase to assist with scapular position and control (Fig. 44-4). Taping helps to retract and depress the scapula and promotes more normal scapular muscle– firing patterns, which are often quite disorganized and inhibited after injury.33 Altered arthrokinematics in the form of increased scapular motion or altered timing of scapular motion are the manifestation of altered muscle-firing patterns. To further help with normalization of muscleactivation patterns, closed-chain exercises are also included. The closed-chain position enhances sensory feedback and facilitates neuromuscular control. These exercises are usually done with one hand stabilized on a table or ball, with
The scapula performs four pivotal roles relative to shoulder function during overhead activities. First, the scapula acts as a stabilizer to the glenohumeral articulation. Proper orientation of this stable scapula base allows the most efficient performance of the rotator cuff musculature. The second role of the scapula is retraction and protraction along the thoracic wall. To reach the cocking position during overhead sports motions, the scapula must retract. This position allows optimum length-tension relationships for shoulder girdle muscles as they prepare for the explosive phase of overhead sports actions. As the arm begins to accelerate, the scapula must then protract laterally and then anteriorly around the thoracic wall, which allows maintenance of a normal scapular humeral position and also dissipates some of the deceleration forces that occur in follow-through.32 Active acromial elevation is the third important role of the scapula. The scapula must rotate in the cocking and acceleration phases to clear the acromion from the rotator cuff to decrease impingement and coracoacromial arch compression.33 The last pivotal role of the scapula is to serve as a kinetic link by delivering energy and force from the trunk and legs to the arm and hand. The multiple roles of the scapula in the overhead athlete necessitate considerable emphasis early in rehabilitation to restore normal shoulder function. One factor that contributes to scapular dysfunction in the female athlete and that is often not addressed is the female athlete’s posture. As female athletes begin to physically mature, they are often sensitive about their chest size and they develop a posture with more rounded shoulders and forward head. This then leads to a protracted and
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Figure 44-4. Scapular tape application. Tape is applied in the directions of the arrows.
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the athlete performing isolated scapular movements including elevation, depression, protraction, and retraction. Once the scapular base is restored and muscle activation is normalized, advancement of rehabilitation during the intermediate and advanced phases includes more openchain, isotonic exercises to advance scapular strength. Short-arc isotonic exercises for scapular muscles can be initiated early during the acute stage of rehabilitation because these exercises do not typically provoke anterior pain complaints. Patients should consciously focus on scapula setting (i.e., retracting and depressing the scapula) during these active arm movements to promote dynamic scapula stability. Initially, these exercises are performed with tubing while standing, and they may include shoulder extensions and rows to enhance scapular muscle strength. Initially, these exercises may be performed in a limited arc of motion to avoid biceps irritation (Fig. 44-5). Ultimately the athlete advances to the prone position and performs multiple exercises with dumbbells to improve scapular strength.
A
B Figure 44-5. Scapular strengthening exercises performed with tubing to the midline of the trunk to avoid irritating the biceps. A, Starting position. B, Ending position.
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Closed-chain neuromuscular control drills may also be advanced to include proprioceptive neuromuscular facilitation (PNF) drills subsequent to restoring the scapular base and resolving anterior shoulder pain; these concepts are addressed further under the next section.
Neuromuscular Re-education Neuromuscular control involves the subconscious integration of sensory information that is processed by the central nervous system, resulting in controlled movement through coordinated muscle activity.35 Dynamic joint stability is the result of coordinated muscle activity achieved through neuromuscular control. In the shoulder, dynamic stability accounts for the bulk of the joint’s stability in the face of limited static stabilizing structures. For overhead athletes, enhanced proprioception (defined as a product of sensory information gathered by mechanoreceptors)36 is necessary for the dynamic structures to stabilize the glenohumeral joint in the presence of significant capsular laxity and excessive range of motion.20 Inadequate proprioception may be a contributing factor to shoulder injuries in the overhead athlete. Dover and coworkers21 measured shoulder proprioception in 50 collegiate softball athletes and 50 nonthrowing athletes during active repositioning tests. They found the softball athletes had a significantly greater error when attempting to reposition the arm in external rotation compared with the nonthrowing athletes. These findings suggest that female softball athletes might have an increased risk of shoulder injury secondary to diminished proprioception. For the injured female athlete, proprioceptive and neuromuscular control drills are a critical component of the rehabilitation process. Both the glenohumeral and scapulothoracic joints should be addressed through all stages of rehabilitation. In the early stages of rehabilitation, joint repositioning tasks, pattern reproduction (i.e., PNF patterns), and rhythmic stabilization exercises with the arm in a stationary position are effective ways to enhance joint position sense and promote muscle co-contraction around the joint. Exercise modification is often necessary to prevent joint and soft tissue pain. Common modifications include performing internal and external rhythmic stabilization exercises with the arm in less than 60 degrees of abduction and in neutral or internal rotation and performing closed-chain scapula drills with the arm by the side versus in an abducted position (Fig. 44-6). Advancing to external rotation and increased abduction angles for rhythmic stabilization exercises should coincide with decreasing pain levels. During dynamic neuromuscular control drills, we prefer the D2 PNF pattern to the D1 pattern for limb repositioning because the D2 pattern is a more functional movement for overhead athletes and does not promote anterior impingement. However, the arc of motion may be limited to mid range of the pattern in early rehabilitation stages to minimize pain levels.
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577
A Figure 44-7. Patient performing external rotation against manual resistance while stabilizing her humeral head against an anteriorly directed force.
train the athlete to avoid over-rotation of the glenohumeral joint and thus avoid anterior humeral head subluxation. Another training technique employs a rhythmic stabilization with tubing as added resistance performed in functional positions to facilitate carry-over of joint stability as the patient prepares for a return to sport (Fig. 44-8). PNF exercises for the glenohumeral and scapulothoracic joints that incorporate rhythmic stabilization, rhythmic B Figure 44-6. Patient positioning for closed-chain scapular neuromuscular control drills with the arm abducted (A), and modified with the arm by the side (B) to avoid anterior impingement.
As patient status progresses, neuromuscular control drills should be advanced to include more challenging arm positions and situations for rhythmic stabilization exercises and should include drills that require joint stabilization during dynamic movements. Controlling anterior humeral head translation during rotational motions and overhead positions is a key training concept. One training technique is to have the patient perform resisted external rotation while the clinician applies an anteriorly directed force to the humeral head. The patient is instructed to keep her shoulder back while performing the rotational movement (Fig. 44-7).20 This drill may be performed with the patient in side-lying or standing position, using tubing as extra resistance during external rotation. Initially the active rotational movement should be limited from full internal rotation to neutral to prevent an exacerbation of biceps symptoms, and then progressing to full external rotation motion as symptom status allows. The clinician may also implement a rhythmic stabilization at the end range of external rotation during these drills to
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Figure 44-8. Rhythmic stabilization exercise performed with tubing as added resistance in a functional position for a windmill softball pitcher.
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THE ATHLETE’S SHOULDER
initiation, slow reversal hold, and timing for emphasis techniques may be used to bias selective muscle activity, promote dynamic joint stability, and enhance joint awareness. Once the patient’s goals and any treatment limitations (e.g., pain) have been identified, the only limiting factor to implementing neuromuscular training drills is the clinician’s creativity.
Return to Sport On successful completion of the early phases of the rehabilitation program, a gradual and controlled return to sportspecific activities is advocated.37 Use of an interval sport program facilitates a return to sports, promotes confidence in the athlete, and minimizes the risk of reinjury. Although the female athlete participates in sports that are similar to those male athletes compete in, there are different sport demands that necessitate interval sport programs designed specifically for the female athlete. Few interval sport programs have been developed, but the University of Delaware has developed interval sport programs for return to play for collegiate softball38 players. These programs were based on game and practice data and are representative of the demands placed on athletes in these sports. After analyzing our data, we concluded at least four programs required development to meet the sport’s demands for pitchers, catchers, outfielders, and infielders (Boxes 44-2 to 44-5). We have developed similar position-specific interval sport programs for collegiate volleyball players (Boxes 44-6 to 44-9).39
BOX 44-2.
Successful patient progression through an interval sport program depends on many factors. Cutting corners to inappropriately move onto higher steps and improperly implementing the protocols can result in re injury. Significant internal and external pressure to return to play quickly after an injury can prompt the athlete to skip steps in the interval sport program. Awareness of this pressure is an important consideration for health care providers and sport organizations when assessing whether an athlete is medically and psychologically ready to play.40 Successful completion of all steps of an interval sport program is one method of assessing an athlete’s readiness for return to play. We recommend the rehabilitation specialist take the athlete through the beginning stages of the interval sport program protocols to educate the athlete regarding correct performance of her interval sport training and assess the athlete’s biomechanics. The athlete should warm up, stretch, and perform one set of each of her advancedphase exercises before and two sets of each exercise after the interval sport program.37 This provides an adequate warm-up but also ensures maintenance of necessary ROM and flexibility of the upper extremity as the athlete returns to sport.37 Reinold and colleagues37 recommend that the rehabilitation program be performed on alternating days. All strengthening, plyometric, and neuromuscular control drills should be preformed three times per week (with a day off in between) and on the same day as the interval sport program.
Softball Pitcher’s Interval Sport Program
Phase I: Early Throwing All throws are to tolerance to a maximum of 50% effort All long tosses should begin with a crow-hop L N,I éð
Warm-up toss to 30 ft
Rest 8 min 10 throws to 60 ft 10 long tosses to 75 ft L N,I é´
Warm-up toss to 75 ft
10 throws to 30 ft
10 throws to 75 ft
Rest 8 min
Rest 8 min
10 throws to 30 ft
10 throws to 75 ft
10 long tosses to 40 ft
10 long tosses to 90 ft
L N,I éó
L N,I é‰
Warm-up toss to 45 ft
Warm-up toss to 90 ft
10 throws to 45 ft
10 throws to 90 ft
Rest 8 min
Rest 8 min
10 throws to 45 ft
10 throws to 90 ft
10 long tosses to 60 ft
10 long tosses to 105 ft
L N,I éí
L N,I éã
Warm-up toss to 60 ft
Warm-up throws to 105 ft
10 throws to 60 ft
10 throws to 105 ft
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BOX 44-2.
579
Softball Pitcher’s Interval Sport Program—cont’d
Rest 8 min
10 pitches to 46 ft (50%)
10 throws to 105 ft
Rest 8 min
10 long tosses to 120 ft
10 throws to 60 ft (75%)
Phase II: Initiation of Pitching
10 pitches to 46 ft (50%)
All pitches are fast balls (no off-speed pitches)
15 long tosses to 120 ft
All pitches to tolerance or maximum effort level specified
Phase III: Intensified Pitching
All long tosses should begin with a crow-hop
Pitch steps 11-15 should consist of 1 fastball to 1 off-speed pitch at the effort level specified
L N,I éå
10 throws to 60 ft (75%)
Pitch steps 16-21 should consist of a percentage of pitches that match the preinjury pitch mix specific to the athlete at the effort level specified
10 pitches to 20 ft (50%)
Begin each step with a warm-up toss to 120 ft
10 throws to 60 ft (75%)
End each step with 20 long tosses to 120 ft
10 pitches to 35 ft (50%)
L N,I éðð
Warm-up toss to 120 ft
Rest 8 min 10 throws to 60 ft (75%) 5 pitches to 20 ft (50%) 10 long tosses to 120 ft L N,I é†
Warm-up toss to 120 ft
2 throws to each base (75%) 15 pitches (50%), rest 8 min 15 pitches (50%), rest 8 min 1 throw to each base (75%) 15 pitches (50%), rest 8 min L N,I éðó
2 throws to each base (75%)
10 throws to 60 ft (75%)
15 pitches (50%), rest 8 min
10 pitches to 35 ft (50%)
15 pitches (50%), rest 8 min
Rest 8 min
15 pitches (50%), rest 8 min
10 throws to 60 ft (75%)
1 throw to each base (75%)
10 pitches to 35 ft (50%)
15 pitches (50%), rest 8 min
10 long tosses to 120 ft
SN,I
L N,I é±
2 throws to each base (75%)
Warm-up toss to 120 ft
15 pitches (50%), rest 8 min
10 throws to 60 ft (75%)
15 pitches (75%), rest 8 min
10 pitches to 46 ft (50%)
15 pitches (75%), rest 8 min
Rest 8 min
1 throw to each base (75%)
10 throws to 60 ft (75%)
15 pitches (50%), rest 8 min
10 pitches to 46 ft (50%)
L N,I éð´
15 long tosses to 120 ft L N,I éðȜ
13
2 throws to each base (75%) 15 pitches (50%), rest 8 min
Warm-up toss to 120 ft
15 pitches (75%), rest 8 min
10 throws to 60 ft (75%)
15 pitches (75%), rest 8 min
10 pitches to 46 ft (50%)
20 pitches (50%), rest 8 min
Rest 8 min
1 throw to each base (75%) Continued
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BOX 44-2. L N,I
Softball Pitcher’s Interval Sport Program—cont’d
15
2 throws to each base(100%) 15 pitches (75%), rest 8 min 15 pitches (75%), rest 8 min 15 pitches (75%), rest 8 min
15 pitches (100%), rest 8 min 20 pitches (100%), rest 8 min 15 pitches (75%), rest 8 min 20 pitches (100%), rest 8 min L N,I
19
15 pitches (75%), rest 8 min
1 throw to each base (100%)
1 throw to each base (75%)
15 pitches (100%), rest 8 min
15 pitches (75%), rest 8 min
1 throw to each base (100%)
L N,I
20 pitches (100%), rest 8 min
16
15 pitches (50%), rest 8 min 1 throw to each base (100%) 15 pitches (100%), rest 8 min 20 pitches (75%), rest 8 min
15 pitches (100%), rest 8 min 20 pitches (100%), rest 8 min 15 pitches (100%), rest 8 min L N,I
20
15 pitches (100%), rest 8 min
20 pitches (100%), rest 8 min
20 pitches (75%), rest 8 min
15 pitches (100%), rest 8 min
1 throw to each base (75%)
1 throw to each base (100%)
20 pitches (75%), rest 8 min
15 pitches (100%), rest 8 min
L N,I
L N,I
17
21
1 throw to each base (100%)
Batting practice
15 pitches (100%), rest 8 min
100-120 pitches
20 pitches (75%), rest 8 min
1 throw to each base per 25 pitches
15 pitches (100%), rest 8 min
Simulated game
15 pitches (100%), rest 8 min
7 innings
20 pitches (75%), rest 8 min
18-20 pitches/inning
1 throw to each base (100%)
8-min rest between innings
15 pitches (75%), rest 8 min
Preinjury pitch mix
L N,I
18
1 throw to each base (100%) 20 pitches (100%), rest 8 min
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BOX 44-3.
Softball Catcher’s Interval Sport Program
Phase I: Beginning Throwing Throws to 50% effort All long tosses should begin with a crow-hop L N,I
1
Warm-up toss to 30 ft 10 throws to 30 ft Rest 8 min 10 throws to 30 ft 10 long tosses to 45 L N,I
2
Warm-up toss to 45 ft 10 throws to 45 ft Rest 8 min 10 throws to 45 ft 10 long tosses to 60 ft L N,I
3
10 throws to pitcher (50%)* 10 long tosses to 120 ft L N,I
6
Warm-up toss to 90 ft 10 throws to pitcher (50%)* 15 throws to pitcher (50%)* 10 throws to pitcher (50%)* 15 throws to pitcher (50%)* 15 long tosses to 120 ft L N,I
7
Warm-up toss to 90 ft 10 throws to pitcher (75%) 2 throws to 1st and 3rd base (50%)* 15 throws to pitcher (50%)* 10 throws to pitcher (75%)* 15 throws to pitcher (50%)*
Warm-up toss to 60 ft
20 long tosses to 120 ft
10 throws to 60 ft
L N,I
Rest 8 min 10 throws to 60 ft 10 long tosses to 75 ft L N,I
581
4
8
Warm-up toss to 90 ft 10 throws to pitcher (75%) 2 throws to 1st and 3rd base (75%)* 15 throws to pitcher (75%)*
Warm-up toss to 75 ft
10 throws to pitcher (75%)*
10 throws to 75 ft
15 throws to pitcher (75%)*
Rest 8 min
20 long tosses to 120 ft
10 throws to 75 ft
L N,I
10 long tosses to 90 ft
Phase II: Catching Practice Complete warm-up lap around the field before each step All throws completed to tolerance, not to exceed the effort level specified All throws are made after squatting 8 seconds to simulate receiving a pitch
9
Warm-up toss to 90 ft 10 throws to pitcher (75%) 2 throws to 1st and 3rd bases (75%)* 10 throws to pitcher (75%) 15 throws to pitcher (75%)* 10 throws to pitcher (75%)* 15 throws to pitcher (75%)*
All long tosses should begin with a crow-hop
20 long tosses to 120 ft
L N,I
L N,I
5
10
Warm-up toss to 90 ft
Warm-up toss to 90 ft
10 throws to pitcher (50%)*
10 throws to pitcher (75%)
10 throws to pitcher (50%)*
2 throws to 1st and 3rd bases (100%)* Continued
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BOX 44-3.
Softball Catcher’s Interval Sport Program—cont’d
10 throws to pitcher (75%)
2 throws to 1st and 3rd bases (100%)*
3 throws to 2nd base (75%)*
15 throws to pitcher (75%)*
15 throws to pitcher (75%)*
10 throws to pitcher (75%)*
10 throws to pitcher (75%)*
15 throws to pitcher (75%)*
15 throws to pitcher (75%)*
10 throws to pitcher (75%) 3 throws to 2nd base (100%)*
20 long tosses to 120 ft L N,I éðð{ éL 5>P< N,+
é3
10 throws to pitcher (75%)*
>,
Warm-up toss to 90 ft
10 throws to pitcher (75%)*
10 throws to pitcher (75%)
20 long tosses to 120 ft
*Complete a 60-ft sprint and then rest 8 minutes after these sets.
BOX 44-4.
Softball Infielder’s Interval Sport Program
General Guidelines
Step 4
Complete a warm-up lap around the field before each step
Warm-up toss to 90 ft
Complete a 60-ft sprint before each set of throws
20 throws to 60 ft (75%)
Rest 8 minutes between sets
Field practice (75%)
All throws are with a limited arc
5 throws to 60 ft
All long tosses should begin with a crow-hop
5 throws to 84 ft
Step 1
5 throws to 120 ft
Warm-up toss to 45 ft
20 long tosses to 120 ft
15 throws to 40 ft (50%)
Step 5
Field practice (50%)
Warm-up toss to 120 ft
5 throws to 35 ft
20 throws to 60 ft (75%)
5 throws to 45 ft
Field practice (100%)
20 long tosses to 60 ft
5 throws to 60 ft
Step 2
5 throws to 84 ft
Warm-up toss to 60 ft 20 throws to 45 ft (50%)
5 throws to 120 ft
Field practice (50%)
20 long tosses to 150 ft
Step 6: Simulated Game
5 throws to 45 ft
Warm-up toss to 120 ft
10 throws to 60 ft
20 throws at 60 ft (100%)
20 long tosses to 75 ft
Field practice (100%)
Step 3 Warm-up toss to 75 ft
5 throws to 60 ft
20 throws to 60 ft (50%)
5 throws to 84 ft
Field practice (75%)
5 throws to 120 ft
5 throws to 60 ft
1 throw to each base from position (100%)
10 throws to 75 ft
20 tosses to 150 ft
20 long tosses to 90 ft
582
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BOX 44-5.
583
Softball Outfielder’s Interval Sport Program
General Guidelines
Rest 1 min between throws
Complete a warm-up lap around the field before each step
15 tosses to 150 ft
Tosses are with limited arc
Step 5
All long tosses should begin with a crow-hop
Warm-up toss to 120 ft
Step 1 Warm-up toss to 45 ft
Field ground balls and throw to cutoff at 90 ft (100% effort) ⫻5
Catch fly balls or field ground balls and throw to cutoff at 45 ft (50% effort) ⫻5
Catch fly balls and throw to base at 120 ft (75% effort) ⫻5
Rest 1 min between throws
Rest 1 min between throws
15 tosses to 60 ft
20 tosses to 180 ft
Step 2
Step 6
Warm-up toss to 60 ft
Warm-up toss to 150 ft
Catch fly balls or field ground balls and throw to cutoff at 60 ft (50% effort) ⫻5
Catch fly balls and throw to base at 150 ft (100% effort) ⫻5
Rest 1 min between throws
Field ground balls and throw to cutoff at 90 ft (100% effort) ⫻5
15 tosses to 90 ft
Step 3
Rest 1 min between throws
Warm-up toss to 90 ft
20 tosses to 180 ft
Catch fly balls or field ground balls and throw to cutoff at 90 ft (75% effort) ⫻5
Step 7: Simulated Game
Rest 1 min between throws
Field ground balls and throw to cutoff at 120 ft (100% effort) ⫻5
15 tosses to 120 ft
Step 4 Warm-up toss to 120 ft Field ground balls and throw to cutoff at 90 ft (75% effort) ⫻5
Warm-up toss to 180 ft
Catch fly balls and throw to base at 180 ft (100% effort) ⫻5 Rest 1 min between throws 20 tosses to 180 ft
Catch fly balls and throw to base at 120 ft (75% effort) ⫻5
BOX 44-6.
Volleyball Outside Attacker Hitting Program
Step 1
Step 3
20 warm-up hits (40%-50%)
20 warm-up hits (50%)
8 attack hits (50%), 2 sets*
8 attack hits (50%), 3 sets*
10 easy full court hits
4 serves (50%), 2 sets†
Step 2
10 easy full court hits
20 warm-up hits (40-50%) 10 attack hits (50%), 2 sets* †
Step 4 20 warm-up hits (50%)
4 serves (50%)
10 attack hits (50%), 3 sets*
10 easy full court hits
4 serves (50%), 3 sets† 10 easy full court hits Continued
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BOX 44-6.
Volleyball Outside Attacker Hitting Program—cont’d
Step 5
Step 8
20 warm-up hits (50%-75%)
30 warm-up hits (50%-75%)
8 attack hits (75%), 3 sets*
8 attack hits (75%-100%), 4 sets*
3 serves (75%), 3 sets†
5 serves (75%), 4 sets†
15 easy full court hits
20 easy full court hits
Step 6
Step 9
30 warm-up hits (50%-75%)
30 warm-up hits (50%-75%)
9 attack hits (75%), 3 sets*
10 attack hits (75%-100%), 4 sets*
3 serves (75%), 3 sets†
5 game placement serves, 4 sets†
15 easy full court hits
20 easy full court hits
Step 7
Step 10
30 warm-up hits (50%-75%)
30 warm-up hits (50%-75%)
10 attack hits (75%), 4 sets*
12 attack hits (75%-100%), 4 sets*
†
4 serves (75%), 3 sets
5 game placement serves, 4 sets†
15 easy full court hits
20 easy full court hits
*Rest 45-60 sec between hits, 6-8 min between sets. † Rest 30 sec between serves, 6 min between sets.
BOX 44-7.
Volleyball Setter and Defensive Specialist Hitting Program
Step 1
Step 4
20 warm-up hits (40%-50%)
25 warm-up hits (50%)
3 attack hits (50%), 2 sets*
4 attack hits (75%), 4 sets*
5 serves (50%), 2 sets†
5 serves (75%), 3 sets†
10 easy full court hits
15 easy full court hits
Step 2
Step 5
20 warm-up hits (40%-50%)
25 warm-up hits (50%-75%)
4 attack hits (50%), 3 sets*
4 attack hits (75%), 4 sets*
†
6 serves (50%), 2 sets
6 game placement serves, 3 sets†
10 easy full court hits
15 easy full court hits
Step 3
Step 6
20 warm-up hits (50%)
30 warm-up hits (50%-75%)
4 attack hits (75%), 3 sets*
4 attack hits (75%-100%), 4 sets*
6 serves (50%), 3 sets†
6 game placement serves, 4 sets†
10 easy full court hits
20 easy full court hits
Note: Average increase per step ⫽ 26%. *Rest 45 sec between hits, 10 min between sets. † Rest 30 sec between serves, 6-8 min between sets.
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INJURIES AND REHABILITATION OF THE OVERHEAD FEMALE ATHLETE’S SHOULDER
BOX 44-8.
585
Volleyball Middle Attacker Program
4 serves (75%), 3 sets†
Step 1 20 warm-up hits (40%-50%)
15 easy full court hits
8 attack hits (50%), 2 sets
Step 6
10 easy full court hits
30 warm-up hits (50%-75%)
Step 2
10 attack hits (75%), 3 sets
20 warm-up hits (40%-50%)
4 serves (75%), 3 sets†
10 attack hits (50%), 2 sets*
15 easy full court hits
4 serves (50%)†
Step 7
10 easy full court hits
30 warm-up hits (50%-75%)
Step 3
10 attack hits (75%), 4 sets*
20 warm-up hits (50%)
4 serves (75%), 4 sets†
9 attack hits (50%), 3 sets*
15 easy full court hits
4 serves (50%), 2 sets†
Step 8
10 easy full court hits
30 warm-up hits (50%-75%)
Step 4
8 attack hits (75%-100%), 4 sets*
20 warm-up hits (50%)
5 serves (75%), 4 sets†
10 attack hits (50%), 3 sets*
20 easy full court hits
5 serves (50%), 3 sets†
Step 9
10 easy full court hits
30 warm-up hits (50%-75%)
Step 5
10 attack hits (75%-100%), 4 sets*
20 warm-up hits (50%-75%)
6 game placement serves, 4 sets†
8 attack hits (75%), 3 sets*
20 easy full court hits
Note: Average increase per step ⫽ 21%. *Rest 45-60 sec between hits, 6-8 min between sets. † Rest 30 sec between serves, 6 min\ between sets.
BOX 44-9.
Volleyball Right Side Attacker Program
Step 1
4 serves (50%), 3 sets†
20 warm-up hits (40%-50%)
10 easy full court hits
6 attack hits (50%), 2 sets*
Step 4
10 easy full court hits
20 warm-up hits (50%)
Step 2
6 attack hits (75%), 3 sets*
20 warm-up hits (40%-50%)
4 serves (50%), 3 sets†
6 attack hits (50%), 2 sets*
15 easy full court hits
†
4 serves (50%), 2 sets 10 easy full court hits
Step 5 25 warm-up hits (50%-75%)
Step 3
6 attack hits (75%), 3 sets*
20 warm-up hits (50%)
4 serves (75%), 3 sets†
6 attack hits (50%), 3 sets*
15 easy full court hits Continued
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BOX 44-9.
Volleyball Right Side Attacker Program—cont’d
Step 6
Step 7
30 warm-up hits (50%-75%)
30 warm-up hits (50%-75%)
6 attack hits (75%), 4 sets*
7 attack hits (75%-100%), 4 sets* †
4 game placement serves, 4 sets
4 game placement serves, 4 sets†
20 easy full court hits
20 easy full court hits
Note: Average increase per step ⫽ 26%. *Rest 45-60 sec between hits, 6-8 min between sets. † Rest 20 sec between serves, 6 min between sets.
BOX 44-10.
Injury Classification for Interval Sport Program Progression
Nonthrowing or Hitting-Arm Injury After medical clearance, begin with step 1. Advance 1 step daily, following soreness rules.
Throwing or Hitting Arm: Bruise or Bone Involvement
Throwing or Hitting Arm: Tendon, Ligament, Nerve Injury (Moderate, Severe, Postoperative) After medical clearance, begin with step 1.
After medical clearance, begin with step 1.
For the first 2 weeks (days 1-14) hit every 3-4 days, and do not advance beyond step 1.
Advance every other day, following soreness rules, to end of program.
On days 15-28, begin hitting step 2 every 2-3 days, but do not advance beyond step 2.
Throwing or Hitting Arm: Tendon, Ligament, or Nerve Injury (Mild)
On days 29-42, use soreness rules to advance program, hitting every third day.
After medical clearance, begin with step 1. For the first week, hit every third day, following soreness rules.
If no soreness, hit the warm-up and easy full court hits of the previous days workout on off days.
After the first 2 weeks, advance program as soreness rules allow, hitting every other day, to end of program.
BOX 44-11.
Soreness Rules
If no soreness, advance 1 step every throwing day. If sore during warm-up but soreness is gone within the first 15 throws, repeat the previous workout. If shoulder becomes sore during this workout, stop and take 2 days off. On return to throwing, drop down 1 step. If sore more than 1 hour after throwing or the next day, take 1 day off and repeat the most recent throwing program workout. If sore during warm-up and soreness continues through the first 15 throws, stop throwing and take 2 days off. On return to throwing, drop down 1 step.
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With interval sport programs, program progression is tailored to each athlete. The rate of progression of the interval sport program varies based on the degree of the shoulder injury and persistence of symptoms (Box 44-10).41 The universal soreness rules govern progression through the interval sport program and a rapid return to play without risking reinjury (Box 44-11).41
SUMMARY Overall, the treatment approach during rehabilitation of the female athlete’s shoulder has more similarities with than differences from treatment of the injured male athlete. Successful outcomes for the female athlete depend on thoroughly evaluating the athlete to identify the involved structures and the cause of the pathology and then implementing a multiphased rehabilitation program using criteria-based advancement. Greater awareness of physiology and sport demands aids the clinician in addressing unique rehabilitation needs when treating the injured female athlete.
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References 1. Borsa PA, Sauers EL, Herling DE: Patterns of glenohumeral joint laxity and stiffness in healthy men and women. Med Sci Sports Exerc 32:1685-1690, 2000. 2. Arendt E, Dick R: Knee injury patterns among men and women in collegiate basketball and soccer. NCAA data and review of literature. Am J Sports Med 23:694-701, 1995. 3. DeHaven KE, Lintner DM: Athletic injuries: Comparison by age, sport, and gender. Am J Sports Med 14: 218-224, 1986. 4. Cox JS, Lenz HW: Women midshipmen in sports. Am J Sports Med 12:241-243, 1984. 5. Hewett TE: Neuromuscular and hormonal factors associated with knee injuries in female athletes. Strategies for intervention. Sports Med 29:313-327, 2000. 6. Soderman K, Werner S, Pietila T, et al: Balance board training: Prevention of traumatic injuries of the lower extremities in female soccer players? A prospective randomized intervention study. Knee Surg Sports Traumatol Arthrosc 8: 356-363, 2000. 7. Mandelbaum BR, Silvers HJ, Watanabe DS, et al: Effectiveness of a neuromuscular and proprioceptive training program in preventing anterior cruciate ligament injuries in female athletes: 2-year follow-up. Am J Sports Med 33: 1003-1010, 2005. 8. Bahr R, Reeser JC: Injuries among world-class professional beach volleyball players. The Fédération Internationale de Volleyball beach volleyball injury study. Am J Sports Med 31:119-125, 2003. 9. Whiteside PA, Albohm MJ, Ritter MA: Men’s and women’s injuries in comparable sports. Physician Sportsmed 8(3):130-140, 1980. 10. Shively RA, Grana WA, Ellis D: High school sports injuries. Physician Sportsmed 9(8):46-50, 1981. 11. Agel J, Palmieri-Smith RM, Dick R, et al: Descriptive epidemiology of collegiate women’s volleyball injuries: National Collegiate Athletic Association Injury Surveillance System, 1988-1989 through 2003-2004. J Athl Train 42:295-302, 2007. 12. Sallis RE, Jones K, Sunshine S, et al: Comparing sports injuries in men and women. Int J Sports Med 22:420-423, 2001. 13. Beasley L, Faryniarz DA, Hannafin JA: Multidirectional instability of the shoulder in the female athlete. Clin Sports Med 19:331-349, x, 2000. 14. Meyers MC, Brown BR, Bloom JA: Fast pitch softball injuries. Sports Med 31:61-73, 2001. 15. Bahr R, Bahr IA: Incidence of acute volleyball injuries: A prospective cohort study of injury mechanisms and risk factors. Scand J Med Sci Sports 7:166-171, 1997. 16. Meister K, Andrews JR: Classification and treatment of rotator cuff injuries in the overhand athlete. J Orthop Sports Phys Ther. 18: 413-21, 1993. 17. Emery RJ, Mullaji AB: Glenohumeral joint instability in normal adolescents. Incidence and significance. J Bone Joint Surg Br 73: 406-408, 1991. 18. McFarland EG, Campbell G, McDowell J: Posterior shoulder laxity in asymptomatic athletes. Am J Sports Med 24: 468-471, 1996. 19. Ellenbecker TS, Roetert EP, Bailie DS, et al: Glenohumeral joint total rotation range of motion in elite tennis players and baseball pitchers. Med Sci Sports Exerc 34:2052-2056, 2002.
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20. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30:136-151, 2002. 21. Dover GC, Kaminski TW, Meister K, et al: Assessment of shoulder proprioception in the female softball athlete. Am J Sports Med 31:431-437, 2003. 22. Hurd WJ, Axe MJ, Snyder-Mackler L: Adaptive shoulder range of motion in collegiate softball players. Presented at American Physical Therapy Association’s Combined Sections Meeting, Nashville, Tenn, February 4-8, 2004. 23. Kuhn JE, Huston LJ, Soslowsky LJ, et al: External rotation of the glenohumeral joint: Ligament restraints and muscle effects in the neutral and abducted positions. J Shoulder Elbow Surg. 14:39S-48S, 2005. 24. Paynter KS: Disorders of the long head of the biceps tendon. Phys Med Rehabil Clin N Am. 15: 511-528, 2004. 25. Werner A, Mueller T, Boehm D, Gohlke F: The stabilizing sling for the long head of the biceps tendon in the rotator cuff interval. A histoanatomic study. Am J Sports Med 28:28-31, 2000. 26. Delitto A, Snyder-Mackler L, Robinson AJ: Electrical stimulation of muscle: Techniques and applications. In Robinson AJ, Snyder-Mackler L (eds): Clinical Electrophysiology. Baltimore, Williams & Wilkins, 1995, pp 121-154. 27. Wilk KE, Arrigo C: Current concepts in the rehabilitation of the athletic shoulder. J Orthop Sports Phys Ther 18: 365-378, 1993. 28. Wilk KE, Andrews JR, Arrigo CA, et al: The strength characteristics of internal and external rotator muscles in professional baseball pitchers. Am J Sports Med 21:61-66, 1993. 29. Ellenbecker TS, Mattalino AJ: Concentric isokinetic shoulder internal and external rotation strength in professional baseball pitchers. J Orthop Sports Phys Ther 25:323-328, 1997. 30. Snyder-Mackler L, Delitto A, Stralka SW, Bailey SL: Use of electrical stimulation to enhance recovery of quadriceps femoris muscle force production in patients following anterior cruciate ligament reconstruction. Phys Ther 74: 901-907, 1994. 31. Wilk KE, Andrews JR, Arrigo A, et al: Preventive and Rehabilitative Exercises for the Shoulder and Elbow, 6th ed. Birmingham, Ala, American Sports Medicine Institute, 2001. 32. Pink MM, Perry J: Biomechanics. In Jobe FW (ed): Operative Techniques in Upper Extremtiy Sports Injuries. St Louis, Mosby, 1996, pp 109-123. 33. Kibler WB: The role of the scapula in athletic shoulder function. Am J Sports Med 26:325-337, 1998. 34. Fleisig GS, Dillman CJ, Andrews JR: Biomechanics of the shoulder during throwing. In Andrews JR, Wilk KE (eds): The Athlete’s Shoulder. New York, Churchill Livingstone, 1994, pp 355-368. 35. Williams GN, Chmielewski T, Rudolph K, et al: Dynamic knee stability: Current theory and implications for clinicians and scientists. J Orthop Sports Phys Ther 31:546-566, 2001. 36. Sherrington CS: The Integrative Action of the Nervous System. New Haven, Yale University Press, 1906. 37. Reinold MM, Wilk KE, Reed J, et al: Interval sport programs: Guidelines for baseball, tennis, and golf. J Orthop Sports Phys Ther 32:293-298, 2002.
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38. Axe MJ, Windley TC, Snyder-Mackler L: Data-based interval throwing programs for collegiate softball players. J Athl Train 37:194-203, 2002. 39. Hurd WJ, Axe MJ, Snyder-Mackler L: Data based interval hitting program for collegiate volleyball players. Presented at American Physical Therapy Association’s Combined Sections Meeting. Tampa, Fla, February 12-16, 2003.
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40. Bauman J: Returning to play: The mind does matter. Clin J Sport Med 15:432-435, 2005. 41. Axe MJ, Wickham R, Snyder-Mackler L: Data-based interval throwing programs for little league, high school, college, and professional baseball pitchers. Sports Med Arthrosc Rev 9:24-34, 2001.
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CHAPTER 45 Biomechanical Considerations
in Shoulder Rehabilitation Exercises Michael M. Reinold and Edgar T. Savidge
The biomechanical analysis of rehabilitation exercises has gained recent attention in sports medicine and orthopedic practice. Several investigators have sought to quantify the kinematics, kinetics, and electromyographic (EMG) activity during common rehabilitation exercises in an attempt to fully understand the implications of each exercise on the arthrokinematics and soft tissues of the shoulder. Advances in the understanding of the biomechanical factors of rehabilitation have led to the enhancement of rehabilitation programs that place minimal strain on specific healing structures while returning the injured athlete to competition as quickly and safely as possible. This chapter provides an overview of the biomechanical implications associated with rehabilitation of the athlete’s shoulder.
Dynamic fine wire EMG activity of the four rotator cuff muscles, the pectoralis major, the latissimus dorsi, and three portions of the deltoid were studied in 15 healthy male subjects during 17 common shoulder exercises. The authors quantified the exercises that produced the most activity for each specific muscle (Table 45-1). For the anterior deltoid, exercises involving elevation of the shoulder, such as scaption with internal rotation (empty can), scaption with external rotation (full can), and forward flexion produced the greatest amount of activity at approximately 70% manual muscle test (MMT). This was also consistent with the middle deltoid, although exercises in the prone position involving horizontal abduction produced approximately 80% MMT. The posterior deltoid showed the greatest amount of activity in the prone position during exercises such as horizontal abduction and rowing at approximately 90% MMT.
BIOMECHANICAL IMPLICATIONS OF SHOULDER REHABILITATION The glenohumeral joint exhibits the greatest amount of motion of any articulation in the human body, although little inherent stability is provided by its osseous configuration. Functional stability is accomplished through the integrated functions of the joint capsule, ligaments, and glenoid labrum, as well as the neuromuscular control and dynamic stabilization of the surrounding musculature, particularly the rotator cuff muscles.1-4 The rotator cuff musculature maintains stability by compressing the humeral head into the concave glenoid fossa during upper-extremity motion.5 Thus, the glenohumeral muscles play a vital role in normal arthrokinematics and symptomatic shoulder function.
Similar to the anterior deltoid, the supraspinatus muscle was most active during shoulder-elevation movements, although the military press (from 0 to 30 degrees) produced the greatest amount of supraspinatus activity, with 80% MMT. Comparing the empty can and full can exercises, the authors found 74% MMT during empty can and 64% MMT during full can. The exercises with the most activity of the subscapularis also included those involving shoulder elevation, although at moderate intensity of approximately 55% MMT. Interestingly, the side-lying internal rotation exercise was not found to produce significant activity of the subscapularis, although the similar exercise of internal rotation at 0 degrees of abduction with exercise tubing was shown to have 52% maximal voluntary contraction by Hintermeister and colleagues.7 Others have recommended motions involving lifting the hand off the lower back and motions that replicate a tennis forehand with internal rotation and horizontal adduction.
Rehabilitation programs for the shoulder joint often focus on restoring maximum strength and muscle balance, particularly of the rotator cuff and scapulothoracic joint. The majority of research regarding shoulder biomechanics has focused on quantifying the electromyographic (EMG) activity of particular muscles during common rehabilitation exercises. The goal of this research is to determine the most optimal exercise to recruit specific muscle activity.
The infraspinatus and teres minor muscles showed similar results with high activity during the side-lying external rotation exercise (85% for infraspinatus and 80% for teres minor). Exercises in the prone position involving horizontal abduction also produced high activity of the external rotators with up to 88% MMT (range, 68%-88% MMT) activity of the infraspinatus during prone horizontal abduction with external rotation.
ELECTROMYOGRAPHIC ANALYSIS OF SHOULDER EXERCISES Townsend and colleagues6 conducted one of the first comprehensive studies analyzing the electromyographic activity of the shoulder musculature during rehabilitation exercises. 589
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TABLE 45-1 Electromyographic Analysis of Glenohumeral Musculature by Intensity of Peak Arc Peak (% MMT ± SD)
Duration (% Exercise)
Peak Arc Range (Degrees)
Scaption IR
72 ± 23
50
90-150
Scaption ER
71 ± 39
30
90-120
Flexion
69 ± 24
31
90-120
Military press
62 ± 26
50
60-90
Abduction
62 ± 28
31
90-120
Scaption IR
83 ± 13
70
90-120
Horiz abd IR
80 ± 23
38
90-120
Horiz abd ER
79 ± 20
57
90-120
Flexion
73 ± 16
31
90-120
Scaption ER
72 ± 13
58
90-120
Rowing
72 ± 20
43
90-120
Military press
72 ± 24
38
90-120
Abduction
64 ± 13
31
90-120
Deceleration
58 ± 20
27
90-60
Horiz abd IR
93 ± 45
63
90-120
Horiz abd ER
92 ± 49
57
90-120
Rowing
88 ± 40
57
90-120
Extension
71 ± 30
44
90-120
External Rot.
64 ± 62
43
60-90
Deceleration
63 ± 28
27
60-90
Military press
80 ± 48
50
0-30
Scaption IR
74 ± 33
40
90-120
Flexion
67 ± 14
31
90-120
Scaption ER
64 ± 28
25
90-120
Exercise Anterior Deltoid
Middle Deltoid
Posterior Deltoid
Supraspinatus
Subscapularis Scaption IR
62 ± 33
22
120-150
Military press
56 ± 48
50
60-90
Flexion
52 ± 42
23
120-150
Abduction
50 ± 44
23
120-150
Horiz abd ER
88 ± 25
71
90-120
External rotation
85 ± 26
43
60-90
Horiz abd IR
74 ± 32
38
90-120
Abduction
74 ± 23
31
90-120
Infraspinatus
Continued
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591
TABLE 45-1 Electromyographic Analysis of Glenohumeral Musculature by Intensity of Peak Arc—cont’d Flexion
66 ± 15
23
90-120
Scaption ER
60 ± 21
38
90-120
Deceleration
57 ± 17
27
90-60
Push-up (hands together)
54 ± 31
38
90-60
External rotation
80 ± 14
57
60-90
Horiz abd ER
74 ± 28
57
60-90
Horiz abd IR
68 ± 36
43
90-120
Press-up
84 ± 42
75
Push-up (hands apart)
64 ± 63
50
60-30
55 ± 27
50
peak 1 sec
Teres Minor
Pectoralis Major 1
⁄2 peak to peak
Latissimus Dorsi Press-up
ER, external rotation; horiz abd, horizontal abduction; IR, internal rotation; MMT, manual muscle test; SD, standard deviation. Reprinted with permission from Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19(3):264-272, 1991.
The press-up exercise was found to elicit the most activity of the latissimus dorsi (55% MMT) and the pectoralis major (84%). This is consistent with the prime function of shoulder depression for each of these muscles. In comparison, the push-up produced 64% MMT for the pectoralis major. Of the 17 exercises studied by Townsend and colleagues,6 the authors recommend the inclusion of the empty can exercise, shoulder flexion, prone horizontal abduction with external rotation, and the press-up in shoulder rehabilitation programs based on the high activity for each muscle examined during these exercises. It should be noted that the work of Townsend’s group6 did not include statistical analysis between exercises, and thus comparison of muscle activity between exercises—for example, supraspinatus during the empty and full can exercises—cannot be considered conclusive. Several studies have since expanded on the work of Townsend and colleagues.6 In particular, they have sought to compare the effectiveness of several exercises for the external rotators, supraspinatus, and scapulothoracic musculature. The following sections discuss each one in detail.
External Rotators The overhead athlete requires the rotator cuff to maintain an adequate amount of glenohumeral joint congruency for asymptomatic function.8 Strength of the infraspinatus and teres minor is integral during the overhead throwing
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motion to develop a compressive force equal to body weight at the shoulder joint to prevent distraction.9 Andrews and Angelo10 found that overhead throwers most often present with rotator cuff tears located from the midsupraspinatus posterior to the midinfraspinatus area, which they believe to be a result of the compressive force produced to resist distraction, horizontal adduction, and internal rotation at the shoulder during arm deceleration. Thus, the external rotators are muscles that often appear weak and affected by different shoulder pathologies such as internal impingement,11,12 joint laxity, labral lesions, and rotator cuff lesions,13,14 particularly in overhead athletes.15,16 Consequently, many clinicians have advocated emphasizing external rotation strengthening during rehabilitation or athletic conditioning programs to enhance muscular strength, endurance, and dynamic stability in overhead athletes. Several studies have been published to document the electromyographic (EMG) activity of the glenohumeral musculature during specific shoulder exercises.6,17-25 Variations in experimental methodology have resulted in conflicting outcomes and controversy in exercise selection. Townsend and colleagues6 evaluated the infraspinatus and teres minor activity during 17 shoulder exercises. They determined that the exercise that elicited the most EMG activity for the infraspinatus muscle was prone horizontal abduction with external rotation (88% MMT), and the most effective exercise for the teres minor muscle was side-lying external rotation (80% MMT).
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Similarly, Blackburn and colleagues18 performed EMG analysis of rotator cuff muscles in 28 healthy subjects during a series of 23 common posterior rotator cuff–strengthening exercises. The authors reported high levels of EMG activity of the infraspinatus (80% EMG) and teres minor (70% EMG) when performing the prone horizontal abduction movement at 90 and 100 degrees of abduction with full external rotation in 28 healthy subjects. Conversely, Greenfield and colleagues20 compared shoulder rotational strength in the scapular and frontal planes during isokinetic testing in 20 healthy subjects. They reported that there were no significant differences in internal rotation strength between positions; however, external rotation strength was significantly higher in the scapular plane, suggesting that the plane of the scapula may be a more effective position for exercising the external rotators. Ballantyne and colleagues17 compared the EMG activity of the external rotators during side-lying and prone positions at 90 degrees of abduction in 40 subjects. They reported similar EMG findings of the infraspinatus and teres minor during both exercises with approximately 50% normalized activity for each muscle. Blackburn’s group,18 however, compared the side-lying and prone exercises and noted greater activity in the prone position for the infraspinatus (prone 80%, side 30% EMG) and teres minor (prone 88%, side 45% EMG). Reinold and colleagues26 analyzed several different exercises commonly used to strengthen the external rotators to determine the most effect exercise and position to recruit muscle activity of the posterior rotator cuff. The authors sought to eliminate the confusion of past research and include a comprehensive study that documented the statistical differences in EMG activity during a variety of commonly performed exercises. Integrated EMG of the infraspinatus, teres minor, supraspinatus, posterior deltoid, and middle deltoid of 10 asymptomatic subjects (five male, five female; mean age, 28.1 years; age range 22-38 years) was analyzed during seven exercises: prone horizontal abduction at 100 degrees of abduction and full abduction, prone at 90 degrees of abduction, standing at 90 degrees of abduction, standing at 45 degrees in the scapular plane, standing at 0 degrees of abduction, standing at 0 degrees of abduction with a towel roll, and sidelying at 0 degrees of abduction. In this study, the exercise that elicited the most combined EMG activity for the infraspinatus and teres minor was side-lying external rotation (infraspinatus, 62% maximum voluntary isometric contraction [MVIC]; teres minor, 67%), followed closely by in the scapular plane (infraspinatus, 53%; teres minor, 55%), and prone in the 90-degree abducted position (infraspinatus, 50%; teres minor, 48%) (Table 45-2). Exercises in the 90-degree abducted position are often incorporated to simulate the position and strain on the shoulder during similar overhead activities such as
Ch45_589-602-F06701.indd 592
throwing. This position produced moderate activity of the external rotators but also increased activity of the deltoid and supraspinatus in order to stabilize the shoulder. It appears that the amount of infraspinatus and teres minor activity progressively decreases as the shoulder moves into an abducted position, while activity of the supraspinatus and deltoid increases. This might imply that as the arm moves into a position of less shoulder stability, the supraspinatus and deltoid are active to assist in the external rotation movement while providing some degree of glenohumeral stability through muscular contraction. Standing external rotation at 90 degrees abduction might have a functional advantage over 0 degrees of abduction and in the scapular plane because of the close replication of this position in sporting activities. However, the combination of abduction and external rotation places strain on the shoulder’s capsule, particularly the anterior band of the inferior glenohumeral ligament.27,28 When the arm is not in an abducted position, external rotation places less strain on this portion of the joint capsule. Therefore, although muscle activity was low to moderate during external rotation at 0 degrees of abduction, this rehabilitation exercise may be worthwhile when strain of the inferior glenohumeral ligament is of concern. Sidelying may be the most optimal exercise to strengthen the external rotators based on the highest amount of EMG activity observed during this study. Theoretically, external rotation at 0 degrees of abduction with a towel roll provides minimal capsular strain and provides a good balance between the muscles that externally rotate the arm and the muscles that adduct the arm to hold the towel. Our clinical experience has shown that adding a towel roll to the external rotation exercise provides assistance to the patient by ensuring that proper technique is observed without muscle substitution. Adding a towel roll to the exercise consistently exhibited a tendency toward higher activity of the posterior rotator cuff as well. Approximately 20% to 25% increase in infraspinatus and teres minor EMG activity was noted with the use of a towel roll. External rotation in the scapular plane can serve as an effective rehabilitation exercise due to the moderate amount of activity of each of the muscles tested, with a moderate amount of capsular strain in the 45-degree abducted position. This exercise might offer a compromise between strengthening and stabilization.
Supraspinatus and Deltoid Numerous investigators have studied the electromyographic activity of the supraspinatus during rehabilitation exercises. The optimal exercise to elicit muscle activity is controversial. Jobe and Moynes29 were the first to recommend elevation in the scapular plane with internal rotation, the empty can exercise. They recommended this exercise for supraspinatus strengthening due to the high EMG activity observed
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82 ± 32 88 ± 33 39 ± 17 44 ± 25
Middle deltoid
Posterior deltoid
Infraspinatus
Teres minor
48 ± 27
50 ± 23
79 ± 31
49 ± 15
68 ± 33
39 ± 13
50 ± 25
59 ± 33
55 ± 23
57 ± 32
55 ± 30
53 ± 25
43 ± 30
38 ± 19
32 ± 24
34 ± 13
40 ± 14
27 ± 27
11 ± 7
41 ± 38
46 ± 21
50 ± 14
31 ± 27
11 ± 6
41 ± 37
67 ± 34
62 ± 13
52 ± 42
36 ± 23
51 ± 47
P ⬍ 0.050 h
P ⬍ 0.050 a, c, d, f, g
P ⬍ 0.050 a, b, c, f
P ⬍ 0.050 a, c, d, e
*% maximum voluntary isometric contraction, mean ± standard deviation. a, Prone horizontal abduction ⬎ ER 90, ER scapular plane, ER 0, ER 0 with towel, side-lying ER; b, Prone horizontal abduction ⬎ Prone ER; c, Prone ER ⬎ ER 0 and 0 with towel; d, Prone ER ⬎ ER scapular plane; e, Prone ER ⬎ side-lying ER; ER, external rotation ;f, 90 ER ⬎ ER 0 and ER 0 with towel; g, Side-lying ER ⬎ ER 0 and ER 0 with towel; h, Side-lying ER ⬎ prone horizontal abduction.
82 ± 37
Prone Horizontal Abduction Prone ER ER 90º ER Scapular ER 0 deg (100-deg, full ER) (90-deg abduction) (90-deg abduction) Plane ER 0 deg with Towel Side-lying ER Significance
Supraspinatus
Muscle
TABLE 45-2 Peak Muscle Activity During External Rotation Exercises* BIOMECHANICAL CONSIDERATIONS IN SHOULDER REHABILITATION EXERCISES
593
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THE ATHLETE’S SHOULDER
during this movement. The recommendation of the empty can exercise was further strengthened by the work of Townsend and colleagues,6 who reported greater EMG activity of the supraspinatus and deltoid muscle during the empty can exercise when compared with elevation in the scapular plane with external rotation (the full can exercise), although statistical analysis was not performed to compare exercises (see Table 45-1). Many clinicians have suggested that the empty can exercise can provoke pain in many patients by trapping the soft tissue within the subacromial space during this impingementtype maneuver. Numerous clinicians have since compared the empty can exercise with several other common supraspinatus exercises to determine if exercises that place the shoulder in less of a disadvantageous position elicit similar amounts of supraspinatus activity. Blackburn and coworkers18 compared the EMG activity of the rotator cuff during several exercises and reported no significant differences in supraspinatus activity during the empty can and full can exercises. However, the authors did report a statistically significant increase in supraspinatus activity during the prone horizontal abduction at 100 degrees with full external rotation exercise (Fig. 45-1). Worrell and colleagues25 compared the amount of supraspinatus activity during the empty can exercise recommended by Jobe and Moynes29 and the prone horizontal abduction exercise recommended by Blackburn and colleagues.18 They used fine-wire EMG and hand-held dynamometer measurements in 22 healthy subjects. The authors reported greater supraspinatus activity during the prone exercise but less total force production than the empty can exercise. They hypothesized that although supraspinatus activity was greater in the prone position, a greater amount of surrounding muscular activity was noted during the empty can exercise.
The effect of increased deltoid activity during arm elevation is a concern to the rehabilitation specialist, especially when rehabilitating a patient with subacromial impingement or rotator cuff pathology. Morrey and colleagues30 examined the resultant force vectors of the deltoid and supraspinatus during arm elevation at various degrees of motion. Deltoid activity alone exhibited a superiorly orientated force vector from 0 to 90 degrees and a compressive force on the glenohumeral joint at 120 to 150 degrees. Conversely, the supraspinatus muscle produced a consistent compressive force throughout the range of elevation (Fig. 45-2). In patients with inefficient subacromial impingement, weak posterior rotator cuff muscles, inefficient dynamic stabilization, or rotator cuff pathology, exercises that produce high levels of deltoid activity can be detrimental because of the amount of superior humeral head migration when the rotator cuff does not efficiently compress the humeral head within the glenoid fossa. Therefore, exercises are often chosen to minimize the opportunity for the deltoid to overpower the rotator cuff musculature during arm elevation. Based on the hypothesis of Worrell and colleagues,25 Malanga’s group22 examined the EMG activity of the supraspinatus and deltoid muscles during the empty can and prone exercises in 17 healthy subjects. The authors reported no significant differences in supraspinatus activity during the two exercises (107% EMG during empty can, 94% EMG during prone). However, a statistically significant increase in posterior deltoid activity was observed during the prone exercise (76% EMG during empty can, 76% during prone) and significantly greater anterior deltoid activity during the empty can exercise (96% EMG during empty can, 65% during prone). Middle deltoid activity was high during both exercises (104% EMG during empty can, 111% during prone). In a similar study by Kelly and colleagues,31 the authors compared the supraspinatus and deltoid EMG activity during the full can and empty can exercises in 11 healthy subjects. The authors again reported no significant difference in supraspinatus activity, but they did note that the least amount of surrounding muscle activity was observed during the full can exercise. They therefore recommended the full can position for manual muscle testing of the supraspinatus exercise.
Figure 45-1. Prone horizontal abduction at 110 degrees of abduction and full external rotation.
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Takeda and coworkers32 examined the most effective exercise for strengthening of the supraspinatus using magnetic resonance imaging (MRI) T2 relaxation times in the shoulders of six healthy subjects. An increase in relaxation time correlated well with concentric and eccentric muscle contractions. Subjects performed the empty can, full can, and prone exercises with MRI scans taken immediately before and after each exercise. Change of relaxation for the supraspinatus was significantly higher during empty can (10.5 ms) and full can (10.5 ms) when compared with
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BIOMECHANICAL CONSIDERATIONS IN SHOULDER REHABILITATION EXERCISES
595
30 60
30
90 120 150
Deltoid muscle alone
120 90 150 60 30
Supraspinatus muscle alone
the prone exercise (3.6 ms). The least amount of deltoid activity was observed during the full can exercise. Reinold and colleagues33 were the first to examine both supraspinatus and deltoid muscle activity dynamically during all three exercises (empty can, full can, and prone). They used fine-wire EMG in the dominant shoulder of 22 healthy subjects (15 male, seven female; mean age, 27.5 years) (see Table 45-1). EMG activity was normalized to MVIC and analyzed using a one-way repeated-measure analysis of variance. They found no significant difference in supraspinatus activity, which ranged from 62% to 67% MVIC during each exercise. However, the activity of the middle deltoid and posterior deltoid was significantly greater during the empty can and prone exercise when compared with the full can exercise. Biomechanically, Poppen and Walker34 examined the resultant force vectors of the glenohumeral joint during elevation with the arm position in neutral, internal rotation, and external rotation, similar to the empty can and full can, respectively. At angles below 90 degrees of abduction, the empty can position resulted in a superiorly orientated force vector and the full can position produced a compressive force from 0 to 120 degrees (Fig. 45-3). These results correlate well with the previously mentioned studies reporting increased deltoid activity, and thus superior humeral head migration, during the empty can exercise. The empty can and full can exercises have also been examined to determine the accuracy of each when detecting lesions of the supraspinatus tendon. Itoi and colleagues35 performed the two tests in 143 shoulders before MRI testing to detect a full-thickness tear of the rotator cuff. The authors considered a test positive if the subject exhibited pain, weakness, or both. The authors reported 75% accuracy with the full can test compared with 70% with the empty can test. The empty can test also provoked greater pain. Therefore, based on the numerous EMG investigations, the full can exercise may be the best exercise for the
Ch45_589-602-F06701.indd 595
60 90 120
150
Deltoid and supraspinatus muscles together
Figure 45-2. Direction of the magnitude of the resultant force vectors (arrows) for different glenohumeral joint positions as a function of different muscle activity. Numbers indicate the angle of the arm position. (Reprinted with permission from Morrey BF, Itoi E, An KN: Biomechanics of the shoulder. In: Rockwood CA, Matsen FA (eds): The Shoulder, 2nd ed. Philadelphia: WB Saunders, 1998, pp 233-276.)
supraspinatus due to the moderate amounts of muscle activity with the least amount of pain provocation and surrounding muscle activation.
Subscapularis The subscapularis provides anterior stabilization and assists the posterior rotator cuff with compression of the humeral head in the glenoid fossa during overhead and throwing activities.5,28,36 Although many shoulder rehabilitation programs integrate internal rotation strengthening in the neutral position, evidence suggests that this might not be the most effective exercise for selectively strengthening the subscapularis. Several EMG studies have identified exercises and shoulder positions that elicit the most muscle activity and may be important to consider in developing rehabilitation programs.37,38 Decker and colleagues37 evaluated EMG data for seven shoulder exercises with 15 healthy subjects in seven muscles including both upper and lower portions of the subscapularis. They found that the push-up with a plus and a diagonal exercise moving from flexion, abduction, and external rotation to extension, adduction, and internal rotation (Fig. 45-4) consistently elicited the most subscapularis activity in both the upper and lower portions. Furthermore, they found that the upper and lower portions of the subscapularis might function independently. Upper subscapularis activity was greater during internal rotation at 90 degrees of abduction, and the lower portion was more active at neutral abduction. Suenaga and coworkers38 examined subscapularis activity during isometric and active internal rotation at 0 and 90 degrees of abduction. Using fine-wire EMG, they found subscapularis activity at 12.1% of maximum MMT at 90 degrees of abduction compared with 2.0 % at 0 degrees of abduction. Pectoralis major activity was greater than all other internal rotators for active and isometric contractions at 0 degrees of abduction. The results of this study suggest that larger muscle groups, such as the pectoralis, latissimus
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THE ATHLETE’S SHOULDER I I N N X
N
I X
0°
Figure 45-3. The position of the resultant force vector of the shoulder for different positions of arm elevation with (N) neutral rotation, (I) internal rotation, and (X) external rotation. (Reprinted with permission from Poppen NK, Walker PS: Forces at the glenohumeral joint in abduction. Clin Orthop Relat Res (135):165-170, 1978.)
Figure 45-4. Diagonal exercise moving from flexion, abduction, and external rotation, into extension, adduction, and internal rotation against resistance. A, Starting position. B, Ending position.
30°
60°
N X
I N
90°
A
dorsi, and anterior deltoid, likely have a greater effect on glenohumeral internal rotation at 0 degrees of abduction. These studies suggest that internal rotation exercises at 90 degrees of abduction may be the most advantageous position to strengthen the subscapularis while minimizing contributions from larger muscle groups. Functional exercises such as the diagonal and push-up with a plus exercises should be considered at the appropriate stage of
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X
X
120°
N 150°
B
rehabilitation to strengthen the subscapularis and enhance glenohumeral stability.
SCAPULOTHORACIC JOINT The function of the scapulothoracic joint is critical for normal shoulder function. Several clinicians have noted that scapular dyskinesis and weakness can lead to altered
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BIOMECHANICAL CONSIDERATIONS IN SHOULDER REHABILITATION EXERCISES
scapular position and possible shoulder impingement.39 The EMG activity of muscles of the scapulothoracic joint has also been studied by several authors. Moseley and colleagues40 examined eight muscles: the upper, middle, and lower trapezius, levator scapula, rhomboids, pectoralis minor, and middle and lower serratus anterior, during 16 commonly performed exercises in nine healthy subjects (Table 45-3). The authors reported the peak EMG activity for each muscle and noted that the majority of the muscles had assisted in more than one scapular function. Based on the
597
results of the study, the authors recommended that a core program of exercises including shoulder scaption, prone rowing, push-ups with a plus, and press-ups should be included in shoulder and scapular rehabilitation programs.
Serratus Anterior More specifically, Decker and colleagues41 documented the EMG activity of the serratus anterior during several different scapulohumeral rehabilitation exercises. They analyzed
TABLE 45-3 Electromyographic Analysis of Scapulothoracic Musculature Duration Qualified (% of exercise)
Peak Arc (% MMT ± SD)
Rowing
75
Military press
Exercise
Peak Arc Range
Function
112 ± 84
Isometric*
Retraction
27
64 ± 26
150-peak
Up rot
Horiz abd w/ER
33
75 ± 27
Isometric*
Retraction
Horiz abd (neutral)
33
62 ± 53
90-peak
Retraction
Scaption
23
54 ± 16
120-150
Up rot
Abduction
31
2 ± 30
90-120
Up rot
108 1/- 63
90-peak
Retraction
Horiz abd w/ER
67
96 ± 73
Peak-90
Retraction
Extension (prone)
27
77 ± 49
Neutral-30
Retraction
Rowing
33
59 ± 51
90-120
Retraction
Abduction
50
68 ± 53
90-150
Up rot
Rowing
50
67 ± 50
120-150
Retraction
Horiz abd w/ER
33
63 ± 41
90-peak
Retraction
Flexion
23
60 ± 18
120-150
Up rot
Horiz abd (neutral)
33
56 ± 24
90-peak
Retraction
Scaption
23
60 ± 22
120-150
Up rot
Rowing
78
114 ± 69
Isometric*
Retraction
Horiz abd (neutral)
67
96 ± 57
Isometric*
Retraction
Shrug
63
88 ± 32
Isometric*
Elevation
Horiz abd w/ER
33
87 ± 66
Isometric*
Retraction
Extension (prone)
36
81 ± 76
Isometric*
Elevation
Scaption
46
69 ± 46
120-150
Retraction
Horiz abd (neutral)
33
66 ± 38
90-peak
Retraction
Scaption
25
65 ± 79
120-150
Retraction
Abduction
31
64 ± 53
90-150
Retraction
Rowing
30
56 ± 46
Isometric*
Retraction
Upper Trapezius
Middle Trapezius Horiz abd (neutral) 78
Lower Trapezius
Levator Scapulae
Rhomboids
Continued
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THE ATHLETE’S SHOULDER
TABLE 45-3 Electromyographic Analysis of Scapulothoracic Musculature—cont’d Middle Serratus Anterior Flexion
69
96 ± 45
120-150
Up rot and protract
Abduction
54
96 ± 53
120-150
Up rot and protract
Scaption
58
91 ± 52
120-150
Up rot and protract
Military press
64
82 ± 36
150-peak
Up rot and protract
Push-up with a plus
28
80 ± 38
Plus man.
Up rot and protract
Push-up with hands apart
21
57 ± 36
Last arc of push-up
Up rot and protract
Scaption
50
84 ± 20
120-150
Up rot and protract
Abduction
54
74 ± 65
120-150
Up rot and protract
Flexion
31
72 ± 46
120-150
Up rot and protract
Push-up with a plus
67
72 ± 3
Chest moving away from floor
Up rot and protract
Push-up with hands apart
21
69 ± 31
Isometric as the chest was near the floor
Up rot and protract
Military press
36
60 ± 42
120-150
Up rot and protract
Press-up
75
89 ± 62
Isometric*
Depression
Push-up with a plus
34
58 ± 45
Plus man.
Protraction
Push-up with hands apart
50
55 ± 34
2nd to last arc
Protraction
Lower Serratus Anterior
Pectoralis Minor
*Isometric contractions were at the extreme of the range of motion. ER, external rotation; horiz abd, horizontal abduction; IR, internal rotation; MMT, manual muscle test; protract, protraction; SD, standard deviation; up rot, upward rotation. Adapted from 40. Moseley JB Jr, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20(2):128-134, 1992.
serratus anterior activity during eight common rehabilitation exercises in 20 healthy subjects. They developed a rank order of exercises that elicited the greatest amount of serratus activity. The three exercises that were suggested were the push-up with a plus, dynamic hug (Fig. 45-5), and a standing serratus anterior punch exercise. Ekstrom and coworkers42 studied EMG activity of the trapezius and serratus anterior in 30 subjects for 10 different exercises. They identified two exercises that yielded significantly higher EMG activity in serratus anterior than the other eight. Specifically, a diagonal exercise into shoulder flexion, horizontal flexion, and external rotation produced 100% MVIC (Fig. 45-6). Standing shoulder scaption above 120 degrees produced EMG of 96% MVIC. EMG activity was greater for both exercises than with traditional straightplane scapular protraction, suggesting that strengthening programs for the serratus anterior should incorporate an element of protraction combined with elevation.
Lower Trapezius Exercises designed to strengthen the lower trapezius are often desired in rehabilitation settings. One of the most effective exercises is the prone horizontal abduction
Ch45_589-602-F06701.indd 598
Figure 45-5. The dynamic hug exercise. Using resistance, the patient horizontally adducts the shoulder at 60 degrees of elevation while protracting the scapula.
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BIOMECHANICAL CONSIDERATIONS IN SHOULDER REHABILITATION EXERCISES
599
in EMG activity from 60 to 90 degrees of elevation in patients with impingement. Reddy and colleagues suggest that the decreased EMG activity of the shoulder musculature observed during arm elevation can lead to subacromial impingement. Furthermore, the decreased activity of the infraspinatus and subscapularis force couple with normal activity of the supraspinatus can allow superior migration of the humeral head, rather than glenohumeral joint compression, causing impingement within the subacromial space.
Figure 45-6. Diagonal exercise moving into flexion, horizontal flexion, and external rotation against resistance.
with full glenohumeral external rotation. This exercise is often performed at 100 to 110 degrees of abduction; however, Ekstrom and colleagues42 identified the prone arm raise in line with the fibers of the lower trapezius as the most effective exercise to recruit lower trapezius. They demonstrate EMG activity of 101% MVIC during this exercise, significantly greater than in the other nine exercises. Thus, it is important to watch the patient perform the exercise, with direct visualization of the scapula to determine the specific angle of lower trapezius insertion.
THE BIOMECHANICAL EFFECTS OF SHOULDER PATHOLOGY Although most biomechanical research on shoulder rehabilitation has included healthy subjects, certain pathologies can effect the biomechanical function of the shoulder, requiring modification to the rehabilitation program. Reddy and colleagues43 evaluated the electromyographic activity of the four rotator cuff muscles and middle deltoid in 15 healthy subjects and 15 subjects with subacromial impingement during elevation in the scapular plane. Impingement was diagnosed based on radiographs and confirmed after testing at the time of arthroscopic subacromial decompression. The authors report an overall decrease in EMG activity of each muscle throughout the exercise in patients with impingement. A statistically significant decrease in EMG was observed for the infraspinatus, subscapularis, and middle deltoid from 30 to 60 degrees of elevation. In addition, the infraspinatus muscle demonstrated a statistically significant decrease
Ch45_589-602-F06701.indd 599
McMahon and colleagues44 compared the EMG activity of the rotator cuff and scapulothoracic muscles in 15 normal shoulders and 23 shoulders with anterior instability. Subjects performed EMG testing of abduction, scaption, and forward flexion before surgical intervention for unidirectional anterior stabilization. The authors reported a statistically significant decrease in supraspinatus activity during abduction and scaption from 30 to 60 degrees in subjects with instability. During all three movements, a statistically significant decrease in serratus anterior activity was also observed in subjects with instability. This occurred in the range of 30 to 120 degrees of abduction and at 0 to 120 degrees of scaption. McMahon and colleagues suggest that the decreased amount of supraspinatus activity can result in disadvantageous superior humeral head migration and can affect the amount of abnormal glenohumeral translation. Blaiser and colleagues45 reported that the supraspinatus muscle is highly active in shoulder joint stabilization, with an 18% reduction of force needed to sublux the glenohumeral joint when the supraspinatus muscle was not active. The finding of decreased serratus anterior activity is also important in patients with shoulder instability. Decreased serratus anterior activity has also been observed in baseball pitchers with anterior instability36 and swimmers with shoulder pain.28 Blaiser and colleagues suggest that the decreased amount of serratus anterior activity can result in the inability to position the scapula in an upward position during shoulder elevation, thus altering the position and length-tension relationship of the static and dynamic stabilizers of the shoulder. A summary of the clinical implications of shoulder rehabilitation is given in Table 45-4.
SUMMARY A thorough understanding of the biomechanical factors associated with rehabilitation is necessary to return the injured athlete to competition as quickly and safely as possible. Various factors are associated with specific pathologies that will alter the rehabilitation program in order to minimize stress on healing structures. Knowledge of the
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THE ATHLETE’S SHOULDER
TABLE 45-4 Peak Muscle Activity During Supraspinatus Exercises MEAN PERCENTAGE MVIC ± SD
Muscle
Full Can
Empty Can
Prone
Supraspinatus
62.2 ± 39.9
62.7 ± 45.2
66.8 ± 50.1
Middle deltoid
52.2 ± 26.6
76.9 ± 43.9*
63.1 ± 30.8*
Posterior deltoid
37.8 ± 32.0
54.1 ± 28.3*
86.7 ± 52.7*
*Significant greater muscle activity compared with full can exercise (p ⱕ 0.017) empty can, scaption with internal rotation; full can, scaption with external rotation; MVIC, maximal voluntary isometric contraction; prone, prone horizontal abduction at 100 degrees with external rotation; SD, standard deviation.
biomechanical implications discussed in this chapter may be used when designing injury prevention and rehabilitation programs for patients with shoulder pathology. References 1. Apreleva M, Hasselman CT, Debski RE, et al: A dynamic analysis of glenohumeral motion after simulated capsulolabral injury. A cadaver model. J Bone Joint Surg Am 80(4):474-480, 1998. 2. Cain PR, Mutschler TA, Fu FH, Lee SK: Anterior stability of the glenohumeral joint. A dynamic model. Am J Sports Med 15(2):144-148, 1987. 3. Harryman DT 2nd, Sidles JA, Clark JM, et al: Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg Am 72(9):1334-1343, 1990. 4. Saha AK: Dynamic stability of the glenohumeral joint. Acta Orthop Scand 42(6):491-505, 1971. 5. Wilk KE, Arrigo CA, Andrews JR: Current concepts: The stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther 25(6):364-379, 1997. 6. Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19(3):264-272, 1991. 7. Hintermeister RA, Lange GW, Schultheis JM, et al: Electromyographic activity and applied load during shoulder rehabilitation exercises using elastic resistance. Am J Sports Med 26(2):210-220, 1998. 8. Wilk KE, Arrigo C: Current concepts in the rehabilitation of the athletic shoulder. J Orthop Sports Phys Ther 18(1):365-378, 1993. 9. Fleisig GS, Barrentine SW, Escamilla RF, Andrews JR: Biomechanics of overhand throwing with implications for injuries. Sports Med 21(6):421-437, 1996. 10. Andrews JR, Angelo RL: Shoulder arthroscopy for the throwing athlete. Tech Orthop 3(1):75-82, 1988. 11. Jobe FW, Kvitne RS, Giangarra CE: Shoulder pain in the overhand or throwing athlete: The relationship of anterior instability and rotator cuff impingement. Orthop Rev 18:963-975, 1989. 12. Walch G, Boileau P, Noel E, Donell T: Impingement of the deep surface of the infraspinatus tendon on the posterior glenoid rim. J.Shoulder Elbow Surg 1:239-245, 1992.
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13. Neer CS 2nd, Craig EV, Fukuda H: Cuff-tear arthropathy. J Bone Joint Surg Am 65(9):1232-1244, 1983. 14. Rockwood CA, Matsen FA: The Shoulder. 2nd ed. Philadelphia: WB Saunders, 1990. 15. Wilk KE, Andrews JR, Arrigo CA, et al: The internal and external rotator strength characteristics of professional baseball pitchers. Am J Sports Med 1(21):61-66, 1993. 16. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30(1):136-151, 2002. 17. Ballantyne BT, O’Hare SJ, Paschall JL, et al: Electromyographic activity of selected shoulder muscles in commonly used therapeutic exercises. Phys Ther 73(10):668-677, 1993. 18. Blackburn TA, McLeod WD, White B: EMG analysis of posterior rotator cuff exercises. J Athl Train 25:40-45, 1990. 19. Bradley JP, Tibone JE: Electromyographic analysis of muscle action about the shoulder. Clin Sports Med 10(4):789-805, 1991. 20. Greenfield BH, Donatelli R, Wooden MJ, Wilkes J: Isokinetic evaluation of shoulder rotational strength between the plane of scapula and the frontal plane. Am J Sports Med 18(2):124-128, 19990. 21. Kronberg M, Nemeth G, Brostrom LA: Muscle activity and coordination in the normal shoulder. an electromyographic study. Clin Orthop Relat Res (257):76-85, 1990. 22. Malanga GA, Jenp YN, Growney ES, An KN: EMG analysis of shoulder positioning in testing and strengthening the supraspinatus. Med Sci Sports Exerc 28(6):661-664, 1996. 23. McCann PD, Wootten ME, Kadaba MP, Bigliani LU: A kinematic and electromyographic study of shoulder rehabilitation exercises. Clin Orthop Relat Res (288):179-188, 1993. 24. Moynes DR, Perry J, antonelli DJ, et al: Electromyographic motion analysis of the upper extremity in sports. Phys Ther 66:1905-1911, 1986. 25. Worrell TW, Corey BJ, York SL, Santiestaban J: An analysis of supraspinatus EMG activity and shoulder isometric force development. Med Sci Sports Exerc 24(7):744-748, 1992. 26. Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34(7):385-394, 2004. 27. O’Brien SJ, Neves MC, Arnoczky SP, et al: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 18(5):449-456, 1990. 28. Scovazzo ML, Browne A, Pink M, et al: The painful shoulder during freestyle swimming: An electromyographic cinematographic analysis of twelve muscles. Am J Sports Med 19(6):577-582, 1991. 29. Jobe FW, Moynes DR: Delineation of diagnostic criteria and a rehabilitation program for rotator cuff injuries. Am J Sports Med 10(6):336-339, 1982. 30. Morrey BF, Itoi E, An KN: Biomechanics of the shoulder. In: Rockwood CA, Matsen FA (eds): The Shoulder, 2nd ed. Philadelphia: WB Saunders, 1998, pp 233-276. 31. Kelly BT, Kadrmas WR, Speer KP: The manual muscle examination for rotator cuff strength: An electromyographic investigation. Am J Sports Med 24(5):581-588, 1996. 32. Takeda Y, Kashiwaguchi S, Endo K, et al: The most effective exercise for strengthening the supraspinatus muscle: Evaluation by magnetic resonance imaging. Am J Sports Med 30(3):374-381, 2002.
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BIOMECHANICAL CONSIDERATIONS IN SHOULDER REHABILITATION EXERCISES
33. Reinold MM, Macrina LM, Wilk KE, et al: Electromyographic analysis of the supraspinatus and deltoid muscles during three common rehabilitation exercises. J Athl Train 42(4): 464-469, 2007. 34. Poppen NK, Walker PS: Forces at the glenohumeral joint in abduction. Clin Orthop Relat Res (135):165-170, 1978. 35. Itoi E, Kido T, Sano A, et al: Which is more useful, the “full can test” or the “empty can test,” in detecting the torn supraspinatus tendon? Am J Sports Med 27(1): 65-68, 1999. 36. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70(2):220-226, 1988. 37. Decker MJ, Tokish JM, Ellis HB, et al: Subscapularis muscle activity during selected rehabilitation exercises. Am J Sports Med 31(1):126-134, 2003. 38. Suenaga N, Minami A, Fujisawa H: Electromyographic analysis of internal rotational motion of the shoulder in various arm positions. J Shoulder Elbow Surg 12(5):501-505, 2003. 39. Kibler WB, McMullen J: Scapular dyskinesis and its relation to shoulder pain. J Am Acad Orthop Surg 11(2):142-151, 2003.
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40. Moseley JB Jr, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20(2):128-134, 1992. 41. Decker MJ, Hintermeister RA, Faber KJ, Hawkins RJ: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27(6):784-791, 1999. 42. Ekstrom RA, Donatelli RA, Soderberg GL: Surface electromyographic analysis of exercises for the trapezius and serratus anterior muscles. J Orthop Sports Phys Ther 33(5):247-258, 2003. 43. Reddy AS, Mohr KJ, Pink MM, Jobe FW: Electromyographic analysis of the deltoid and rotator cuff muscles in persons with subacromial impingement. J Shoulder Elbow Surg 9(6):519-523, 2000. 44. McMahon PJ, Jobe FW, Pink MM, et al: Comparative electromyographic analysis of shoulder muscles during planar motions: Anterior glenohumeral instability versus normal. J Shoulder Elbow Surg 5(2 Pt 1):118-123, 1996. 45. Blasier RB, Guldberg RE, Rothman ED: Anterior shoulder stability: Contributions of rotator cuff forces and the capsular ligaments in a cadaveric model. J Shoulder Elbow Surg 1:140-150, 1992.
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CHAPTER 46 Open- and Closed-Chain Rehabilitation
for the Shoulder Complex Rafael Escamilla and Kyle Yamashiro
This chapter focuses on the scientific rationale behind choosing and progressing exercises during shoulder rehabilitation and training. Specifically, the rotator cuff, deltoid, and scapular muscles will be discussed in terms of biomechanics, function, and muscle activation patterns during shoulder exercises. The two types of general classification of shoulder exercises used in the clinic are open and closed kinetic chain. Most clinicians define an open kinetic chain upper extremity exercise as a combination of links in which the distal segment (the hand) moves freely with or without external resistance (e.g., shoulder flexion and abduction exercises). A closed kinetic chain exercise is commonly defined as a combination of links in which the distal segment meets considerable external resistance that restrains motion (e.g., push-up).1 These definitions are actually modifications of the original definitions of the open and closed kinetic chains,1 which has led to the development of new terminology.2,3
exercises that are commonly used in rehabilitation, with varying intensities and resistive devices. Some of the commonly used and effective shoulder rehabilitation exercises in terms of glenohumeral and scapular muscle recruitment and amplitude are shown in Figures 46-1 to 46-10. Numerous exercises currently used in rehabilitating the athlete’s shoulder are believed to be more functional and sport specific compared with many of the other exercises described in the literature. Several of these exercises are shown in Figures 46-11 to 46-17. Unfortunately, there is little or no research to support the effectiveness of these newer more functional exercises, and therefore research is needed for functional exercises. These more functional exercises exhibit movements patterns that are sport specific (such as the overhand throwing motion), and they are believed to develop not only upper-extremity musculature but also lower-extremity and trunk musculature.
The original definition of open kinetic chain does not cover conditions in which the distal segment moves against resistance, therefore representing a gray area between the traditional definitions of open- and closed-chain exercises.1-3 In addition, it has been demonstrated that exercises with similar biomechanical motions and external loading have comparable electromyography (EMG) values regardless of whether the exercise is closed or open chain.3 In terms of EMG and functional activity, external load is more important compared with whether or not the hand is restrained.3 Therefore, a case can be made to minimize or eliminate, where appropriate, the use of sometimes confusing terminology and instead classify an exercise by its biomechanical and muscular demands.2,3
ROTATOR CUFF BIOMECHANICS AND FUNCTION The rotator cuff has been shown to be a substantial stabilizer of the glenohumeral joint in numerous shoulder positions.5 Appropriate rehabilitation progression and strengthening of the rotator cuff muscles is important to provide appropriate force to help elevate and move the arm, compress and center the humeral head within the glenoid fossa during shoulder movements, and resist humeral head superior translation due to deltoid activity.6-10 This latter function is important in early arm elevation when the resultant force vector from the deltoids is directed in a more superior direction.
Although weight-bearing closed-chain positions do occur in sports, such as a wrestler in a quadriceps position with hands fixed to the ground, it is more common in sports for the hand to move freely in space against varying external loads, such as in throwing a football or shot put, passing a basketball, pitching a baseball, swinging a tennis racket or golf club, or lifting a weight overhead. The movements performed in these activities are similar to the movements that occur in open-chain exercises. Nevertheless, weight-bearing exercises are still used in the shoulder rehabilitation setting for a variety of reasons, such as faciliting proprioceptive feedback mechanisms, co-contraction, and dynamic joint stability.4
Supraspinatus The supraspinatus compresses, abducts, and provides a small external rotation torque to the glenohumeral joint. From three-dimensional biomechanical shoulder models, predicted supraspinatus force during maximum-effort isometric scapular plane abduction (90 degrees position) was 117 N (approximately 26 pounds, since 1 N equals 0.22 pounds).6 Moreover, supraspinatus activity increases as resistance increases during abduction and scaption movements, peaking at 30 to 60 degrees for any given resistance. At lower scaption angles, supraspinatus activity increases to provide additional humeral head compression within the glenoid fossa to counter the humeral head superior translation from the deltoids. (see Table 46-9).11
Tables 46-1 to 46-9 list glenohumeral and scapular muscle activity during numerous closed- and open-chain shoulder 603
Ch46_603-626-F06701.indd 603
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Ch46_603-626-F06701.indd 604
46⫾29
300⫾90
Push-up plus
122⫾22
39⫾26
60⫾34a
270⫾30
D2 diagonal pattern extension, horizontal adduction, internal rotation (throwing acceleration)
There were no significant differences (p ⫽ 0.122) in tubing force among exercises. There were significant differences (p ⬍ 0.001) in EMG activity among exercises.
99⫾36
Adapted from Decker MJ, Tokish JM, Ellis HB, et al: Subscapularis muscle activity during selected rehabilitation exercises. Am J Sports Med 31(1):126-134, 2003.
Note: Muscles whose EMG activity was greater than 45% of a MVIC are bolded, and these exercises are considered to be an effective challenge for that muscle.
94⫾27
76⫾32
⬍20a
54⫾35a
104⫾54
46⫾24a,d
⬍20a
62⫾31a
Significant differences between exercises (p ⬍ 0.002): a) Significantly less EMG activity compared with push-up plus. b) Significantly less EMG activity compared with standing scapular dynamic hug. c) Significantly less EMG activity compared with standing internal rotation at 0° abduction. d) Significantly less EMG activity compared with D2 diagonal pattern extension, horizontal abduction, internal rotation. e) Significantly less EMG activity compared with standing forward scapular punch.
†
*
38⫾20
58⫾32a
260⫾50
Standing scapular dynamic hug
51⫾24a,d
⬍20a
⬍20a, b, d, e
40⫾27
50⫾23a
270⫾40
Standing internal rotation at 0° abduction
39⫾22a,d
⬍20a
33⫾25a, b
26⫾19
53⫾40a
260⫾40
Standing internal rotation at 45° abduction
25⫾12a,b,c,d
Pectoralis Major EMG (% MVIC)†
⬍20a,b,c,d
28⫾12a
Infraspinatus EMG (% MVIC)†
⬍20a
40⫾23a
⬍20a, b, c, d
58⫾38a
270⫾30
Standing internal rotation at 90° abduction
46⫾24a
⬍20a, b, c, d
33⫾28a
260⫾50
Supraspinatus EMG (% MVIC)†
Standing forward scapular punch
Exercise
Tubing Force (N)*
Lower Subscapularis EMG (% MVIC)†
Upper Subscapularis EMG (% MVIC)†
47⫾26
⬍20a
⬍20a
⬍20a
⬍20a
⬍20a
⬍20a
Teres Major EMG (% MVIC)†
TABLE 46-1 Mean (⫾SD) Tubing Force and Glenohumeral EMG (Normalized by a Maximum Voluntary Isometric Contraction, MVIC) During Shoulder Exercises Using Elastic Tubing and Body Weight Resistance with Intensity for Each Exercise Normalized by a 10-Repetition Maximum
49⫾25
21⫾12a
⬍20a,d
⬍20a,d
⬍20a,d
⬍20a,d
⬍20a,d
Latissimus Dorsi EMG (% MVIC)†
604 THE ATHLETE’S SHOULDER
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OPEN- AND CLOSED-CHAIN REHABILITATION FOR THE SHOULDER COMPLEX
605
TABLE 46-2 Mean (⫾SD) Rotator Cuff and Deltoid EMG (Normalized by a Maximum Voluntary Isometric Contraction, MVIC) During Shoulder External Rotation Exercises Using Dumbbell Resistance with Intensity for Each Exercise Normalized by a 10-Repetition Maximum Infraspinatus EMG (% MVIC)*
Teres Minor EMG (% MVIC)*
Supraspinatus EMG (% MVIC)*
Middle Deltoid EMG (% MVIC)*
Posterior Deltoid EMG (% MVIC)*
Side-lying external rotation at 0° abduction
62⫾13
67⫾34
51⫾47e
36⫾23e
52⫾42e
Standing external rotation in scapular plane at 45° abduction and 30° horizontal adduction
53⫾25
55⫾30
32⫾24c,e
38⫾19e
43⫾30e
Prone external rotation at 90° abduction
50⫾23
48⫾27
68⫾33
49⫾15e
79⫾31
Standing external rotation at 90° abduction
50⫾25
39⫾13a
57⫾32
55⫾23e
59⫾33e
Standing external rotation at approximately 15° abduction with towel roll
50⫾14
46⫾41
41⫾37c,e
11⫾6c,d,e
31⫾27a,c,d,e
Standing external rotation at 0° abduction without towel roll
40⫾14a
34⫾13a
41⫾38c,e
11⫾7c,d,e
27⫾27a,c,d,e
Prone horizontal abduction at 100° abduction with external rotation (thumb up)
39⫾17a
44⫾25
82⫾37
82⫾32
88⫾33
Exercise
*There were significant differences (p ⬍ 0.01) in EMG activity among exercises. Significant differences between exercises (p ⬍ 0.05): a) Significantly less EMG activity compared with side-lying external rotation at 0° abduction. b) Significantly less EMG activity compared with standing external rotation in scapular plane at 45° abduction and 30° horizontal adduction. c) Significantly less EMG activity compared with prone external rotation at 90° abduction. d) Significantly less EMG activity compared with standing external rotation at 90° abduction. e) Significantly less EMG activity compared with prone horizontal abduction at 100° abduction with external rotation (thumb up). Note: Muscles whose EMG activity was greater than 45% of a MVIC are bolded, and these exercises are considered to be an effective challenge for that muscle. Adapted from Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34(7):385-394, 2004.
Due to a decreasing moment arm with abduction, the supraspinatus is a more effective abductor in the scapular plane at smaller abduction angles, but it still generates abductor torque (a function of both moment arm and muscle force) at larger abduction angles.6-8 The abduction moment arms peak at approximately 3 cm near 30 degrees of abduction, but the supraspinatus maintains an abduction moment arm of greater than 2 cm throughout shoulder abduction range of motion.7,8 Its ability to generate abduction torque in the scapular plane appears to be greatest with the shoulder in neutral rotation or in slight internal or external rotation.7,8 This is consistent with both EMG and magnetic resonance imaging (MRI) data obtained while performing exercises such as the empty can (humerus elevated in internal rotation)12,13 and full can (humerus elevated in external rotation)14 exercises, with both exercises producing similar amounts of supraspinatus activity.14-16
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Even though supraspinatus activity is similar between the empty can and full can exercises, there are several reasons why the full can exercise may be preferred over the empty can during rehabilitation and supraspinatus testing. Firstly, the humerus in internal rotation during the empty can does not allow the greater tuberosity to clear from under the acromion during arm elevation, which can increase risk of subacromial impingement because of decreased subacromial space width.17,18 Secondly, abducting in extreme internal rotation progressively decreases the abduction moment arm of the supraspinatus from 0 to 90 degrees of abduction.7 A diminished mechanical advantage can require the supraspinatus to work harder, thus increasing the tensile stresses in the healing tendon. Thirdly, scapular kinematics are different between these two exercises. Scapular internal rotation and anterior tilt
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606
THE ATHLETE’S SHOULDER
TABLE 46-3 Mean (⫾SD) Trapezius and Serratus Anterior Muscle Activity (EMG was Normalized by a Maximum Voluntary Isometric Contraction, MVIC) During Shoulder Exercises Using Dumbbell or Similar Resistance with Intensity for Each Exercise Normalized by a 5-Repetition Maximum
Exercise
Upper Trapezius EMG (% MVIC)*
Middle Trapezius EMG (% MVIC)*
Lower Trapezius EMG (% MVIC)*
Serratus Anterior EMG (% MVIC)*
Shoulder shrug
119⫾23
53⫾25b,c,d
21⫾10b,c,d,f,g,h
27⫾17c,e,f,g,h,i,j
Prone rowing
63⫾17a
79⫾23
45⫾17c,d,h
14⫾6c,e,f,g,h,i,j
Prone horizontal abduction at 135° abduction with external rotation (thumb up)
79⫾18a
101⫾32
97⫾16
43⫾17e,f
Prone horizontal abduction at 90° abduction with external rotation (thumb up)
66⫾18a
87⫾20
74⫾21c
9⫾3c,e,f,g,h,i,j
Prone external rotation at 90° abduction
20⫾18a,b,c,d,e,f,g
45⫾36b,c,d
79⫾21
57⫾22e,f
D1 diagonal pattern flexion, horizontal adduction, and external rotation
66⫾10a
21⫾9a,b,c,d,f,g,h
39⫾15b,c,d,f,g,h
100⫾24
Scaption above 120° with ER (thumb up)
79⫾19a
49⫾16b,c,d
61⫾19c
96⫾24
Scaption below 80° with ER (thumb up)
72⫾19a
47⫾16b,c,d
50⫾21c,h
62⫾18e,f
Supine scapular protraction with shoulders horizontally flexed 45° and elbows flexed 45°
7⫾5a,b,c,d,e,f,g,h
7⫾3a,b,c,d,f,g,h
5⫾2b,c,d,f,g,h
53⫾28e,f
Supine upward scapular punch
7⫾3a,b,c,d,e,f,g,h
12⫾10b,c,d
11⫾5b,c,d,f,g,h
62⫾19e,f
*The were significant difference (p ⬍ 0.05) in EMG activity among exercises. Significant differences between exercises (p ⬍ 0.05): a) Significantly less EMG activity compared with shoulder shrug. b) Significantly less EMG activity compared with prone rowing. c) Significantly less EMG activity compared with prone horizontal abduction at 135° abduction with external rotation. d) Significantly less EMG activity compared with prone horizontal abduction at 90° abduction with external rotation. e) Significantly less EMG activity compared with D1 diagonal pattern flexion, horizontal adduction, and external rotation. f) Significantly less EMG activity compared with scaption above 120° with ER (thumb up). g) Significantly less EMG activity compared with scaption below 80° with ER (thumb up). h) Significantly less EMG activity compared with prone external rotation at 90° abduction. i) Significantly less EMG activity compared with supine scapular protraction with shoulders horizontally flexed 45° and elbows flexed 45°. j) Significantly less EMG activity compared with supine upward scapular punch. Note: Muscles whose EMG activity was greater than 50% of a MVIC are bolded, and these exercises are considered to be an effective challenge for that muscle. Adapted from Ekstrom RA, Donatelli RA, Soderberg GL: Surface electromyographic analysis of exercises for the trapezius and serratus anterior muscles. J Orthop Sports Phys Ther 33(5):247-258, 2003.
are greater in the empty can than in the full can.19 Scapular internal rotation, or winging, occurs in the transverse plane with the scapular medial border moving posteriorly away from the trunk; anterior tilt occurs in the sagittal plane with the scapular inferior angle moving posteriorly away from the trunk. This occurs in part because humeral internal rotation in the empty can tensions both the posteroinferior capsule and rotation cuff (infraspinatus, primarily), which originate from the posterior glenoid and infraspinous fossa. Tension in these structures contributes to an anterior tilted and internally rotated scapula, which protract the scapula. This is clinically important because scapular protraction has been shown to decrease the width of the subacromial space, increasing subacromial
Ch46_603-626-F06701.indd 606
impingement risk.20 In contrast, scapular retraction has been shown to increase subacromial space width20 and increase supraspinatus strength potential (enhanced mechanical advantage) when compared with a more protracted position.21 These data emphasize the importance of strengthening the scapular retractors and maintaining good posture. Fourthly, although both the empty can and full can test positions have been shown to be equally accurate in detecting a torn supraspinatus tendon, the full can test position may be desirable in the clinical setting because it provokes less pain22 and it has been shown to be a more optimal position for isolating the supraspinatus.14
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OPEN- AND CLOSED-CHAIN REHABILITATION FOR THE SHOULDER COMPLEX
TABLE 46-4 Mean (⫾SD) Ground Reaction Force on Hand (Normalized by Body Weight, BW) and Glenohumeral EMG (Normalized by a Maximum Voluntary Isometric Contraction, MVIC) During Low- to High-Demand Weight Bearing Shoulder Exercises Ground Reaction Force on Hand (% BW)*
Supraspinatus EMG (% MVIC)†
Infraspinatus EMG (% MVIC)†
Anterior Deltoid EMG (% MVIC)†
Posterior Deltoid EMG (% MVIC)†
Pectoralis Major EMG (% MVIC)†
Prayer
6⫾3a,b,c,d,e,f
2⫾2a,b,c,d
4⫾3a,b,c,d,e
2⫾4a,b,c
4⫾3a,d,e
7⫾4a,b,c
Quadruped
19⫾2a,b,c,d,e
6⫾10a,b
11⫾8a,b,c,d,e
6⫾6a,b,c
6⫾4a,d,e
10⫾4a,b,c
Tripod
32⫾3a
10⫾11a
37⫾26a
12⫾10a,b
27⫾16a
16⫾8a,b
Bipod (alternating arm and leg)
34⫾4a
12⫾13a
42⫾33a
18⫾10a
28⫾16a
22⫾10a
Push-up
34⫾3a
14⫾14a
44⫾31a
31⫾16
18⫾12a
33⫾20
Push-up with feet elevated
39⫾5a
18⫾16a
52⫾32a
37⫾15
23⫾14a
42⫾28
One-arm push-up
60⫾6
29⫾20
86⫾56
46⫾20
74⫾43
44⫾45
Exercise
There were significant differences (p ⬍ 0.001) in ground reaction force among exercises. There were significant differences (p ⬍ 0.001) in EMG activity among exercises.
*
†
Significant differences between exercises (p ⬍ 0.002): a) Significantly less compared with the one-arm push-up. b) Significantly less compared with the push-up feet elevated. c) Significantly less compared with the push-up. d) Significantly less compared with the pointer. e) Significantly less compared with the tripod. f) Significantly less compared with the quadruped. Note: Muscles whose EMG activity was greater than 40% of a MVIC are bolded, and these exercises are considered to be an effective challenge for that muscle. Adapted from Uhl TL, Carver TJ, Mattacola CG, et al: Shoulder musculature activation during upper extremity weight-bearing exercise. J Orthop Sports Phys Ther 33(3):109-117, 2003.
The supraspinatus is active in numerous shoulder exercises other than the empty can and full can exercises. Relatively high supraspinatus activity has been quantified in several common rotator cuff exercises, such as prone horizontal abduction at 100 degrees of abduction with external rotation, prone external rotation at 90 degrees of abduction, standing external rotation at 90 degrees of abduction, flexion above 120 degrees with external rotation, military press, side-lying abduction, proprioceptive neuromuscular facilitation (PNF) scapular clock, and D2 diagonal pattern flexion and extension (see Tables 46-1, 46-2, 46-5, and 46-7).16,23-31 When these shoulder exercises are compared with each other, mixed results have been reported. Some EMG data support prone horizontal abduction at 100 degrees of abduction with external rotation over the empty can in supraspinatus activity,24,29 whereas other EMG data show no difference in supraspinatus activity between these two exercises.26 In contrast, MRI data support both empty can and full exercises can over prone horizontal abduction at 100 degrees of abduction with external rotation in activating the supraspinatus.15 Interestingly, relatively high supraspinatus activity has also been reported in several exercises that are not commonly thought of as rotator cuff exercises, such as standing forward scapular punch, rowing exercises, push-up exercises, and two-hand overhead medicine ball throws (see Tables 46-1, 46-4, and 46-7).4,30,32,33
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The supraspinatus also provides weak rotational torques due to small rotational moment arms.8 From three-dimensional biomechanical shoulder models, predicted supraspinatus force during maximum-effort external rotation in 90 degrees of abduction was 175 N.6 The anterior portion, which is considered the strongest,34 has been shown to be a weak internal rotator at 0 degrees of abduction (0.2-cm moment arm), no rotational ability at 30 degrees of abduction, and a weak external rotator at 60 degrees of abduction (⬃0.2-cm moment arm).8 In contrast, the posterior portion of the supraspinatus has been shown to provide an external rotation torque throughout shoulder abduction, with an external rotation moment arm that progressively decreases as abduction increases (approximately 0.7 cm at 0 degrees of abduction and approximately 0.4 cm at 60 degrees of abduction).8 When the anterior and posterior portions of the supraspinatus are viewed as a whole, this muscle provides weak external rotation regardless of abduction angle, although it appears to be a more effective external rotator at smaller abduction angles.8
Infraspinatus and Teres Minor The infraspinatus and teres minor make up the posterior cuff, which provides glenohumeral compression and resists superior and anterior humeral head translation by Text continued on p. 612
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72⫾24 80⫾23
79⫾20
72⫾23 71⫾39 62⫾26 ⱕ50
ⱕ50
Scaption above 120° with IR (thumb down)
Scaption above 120° with ER (thumb up)
Military press
Prone horizontal abduction at 90° abduction with IR (thumb down)
Prone horizontal abduction at 90° abduction with external rotation (thumb up)
ⱕ50 58⫾20
ⱕ50 ⱕ50
Side-lying external rotation at 0° abduction
Side-lying eccentric control of 0-135° horizontal adduction (throwing deceleration)
ⱕ50
74⫾33 64⫾28 80⫾48
ⱕ50
ⱕ50 ⱕ50 ⱕ50
63⫾28
64⫾62
88⫾40
ⱕ50
92⫾49
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
67⫾14
ⱕ50
93⫾45
Supraspinatus EMG (% MVIC)
Posterior Deltoid EMG (% MVIC)
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
56⫾48
ⱕ50
62⫾33
50⫾44
52⫾42
Subscapularis EMG (% MVIC)
57⫾17
85⫾26
ⱕ50
ⱕ50
88⫾25
74⫾32
ⱕ50
60⫾21
ⱕ50
74⫾23
66⫾15
Infraspinatus EMG (% MVIC)
ⱕ50
80⫾14
ⱕ50
ⱕ50
74⫾28
68⫾36
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
Teres Minor EMG (% MVIC)
ⱕ50
ⱕ50
ⱕ50
84⫾42
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
Pectoralis Major EMG (% MVIC)
ⱕ50
ⱕ50
ⱕ50
55⫾27
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
Latissimus Dorsi EMG (% MVIC)
Adapted from Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19(3):264-272, 1991.
Note: Muscles whose EMG activity was greater than 50% of a MVIC over at least three consecutive 30° arcs of motion are bolded, and these exercises are considered to be an effective challenge for that muscle.
ⱕ50 92⫾20
ⱕ50 ⱕ50
Press-up
Prone rowing
72⫾13
83⫾13
64⫾13
62⫾28
Abduction above 120° with ER (thumb up)
73⫾16
69⫾24
Middle Deltoid EMG (% MVIC)
Flexion above 120° with ER (thumb up)
Exercise
Anterior Deltoid EMG (% MVIC)
TABLE 46-5 Peak (⫾SD) Glenohumeral EMG (Normalized by a Maximum Voluntary Isometric Contraction, MVIC) Over 30° Arc of Movement During Shoulder Exercises Using Dumbbells
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96⫾73
ⱕ50
75⫾27
ⱕ50
Prone horizontal abduction at 90° abduction with ER (thumb up)
77⫾49 ⱕ50 ⱕ50
ⱕ50 ⱕ50 ⱕ50
Prone extension at 90° flexion
Push-up plus
Push-up with hands separated
ⱕ50
ⱕ50
ⱕ50
67⫾50
ⱕ50
63⫾41
56⫾24
ⱕ50
ⱕ50
81⫾76
114⫾69
ⱕ50
87⫾66
96⫾57
ⱕ50
69⫾46
ⱕ50
ⱕ50
Levator Scapulae EMG (% MVIC)
ⱕ50
ⱕ50
ⱕ50
56⫾46
ⱕ50
ⱕ50
ⱕ50
57⫾36
80⫾38
69⫾31
73⫾3
ⱕ50
ⱕ50
ⱕ50 ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
66⫾38
84⫾20
74⫾65
72⫾46
Lower Serratus Anterior EMG (% MVIC)
60⫾42
91⫾52
96⫾53
96⫾45
Middle Serratus Anterior EMG (% MVIC)
82⫾36
ⱕ50
65⫾79
64⫾53
ⱕ50
Rhomboids EMG (% MVIC)
55⫾34
58⫾45
ⱕ50
ⱕ50
89⫾62
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
ⱕ50
Pectoralis Minor EMG (% MVIC)
Adapted from Moseley JB Jr, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20(2):128-134, 1992.
Note: Muscles whose EMG activity was greater than 50% of a MVIC over at least three consecutive 30° arcs of motion are bolded, and these exercises are considered to be an effective challenge for that muscle.
59⫾51
112⫾84
Prone rowing
Press-up
108⫾63
62⫾53
Prone horizontal abduction at 90° abduction with IR (thumb down)
ⱕ50
ⱕ50
64⫾26
Military press
60⫾22
ⱕ50
54⫾16
Scaption above 120° with ER (thumb up)
68⫾53
ⱕ50
52⫾30
60⫾18
ⱕ50
ⱕ50
Abduction above 120° with ER (thumb up)
Flexion above 120° with ER (thumb up)
Exercise
Lower Trapezius EMG (% MVIC)
Middle Trapezius EMG (% MVIC)
Upper Trapezius EMG (% MVIC)
TABLE 46-6 Peak (⫾SD) Scapular EMG (Normalized by a Maximum Voluntary Isometric Contraction, MVIC) Over 30° Arc of Movement During Shoulder Exercises Using Dumbbells with Intensity Normalized for Each Exercise by a 10-Repetition Maximum
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27⫾20
30⫾17
30⫾11
13⫾8
13⫾7 12⫾8 16⫾8 16⫾11 21⫾11 26⫾12 15⫾11 15⫾11 12⫾8 19⫾11
D2 diagonal pattern extension, horizontal adduction, internal rotation (throwing acceleration)
Eccentric arm control portion of D2 diagonal pattern flexion, abduction, external rotation (throwing deceleration)
Standing external rotation at 0° abduction
Standing external rotation at 90° abduction
Standing internal rotation at 0° abduction
Standing internal rotation at 90° abduction
Standing extension from 90-0°
Flexion above 120° with ER (thumb up)
Standing high scapular rows at 135° flexion
Standing mid scapular rows at 90° flexion
Standing low scapular rows at 45° flexion
Standing forward scapular punch
36⫾24
34⫾23
26⫾16
34⫾17
32⫾14
27⫾16
41⫾21
4⫾3
50⫾22
8⫾7
44⫾16
22⫾12
Middle Deltoid EMG (% MVIC)
69⫾47
69⫾50
81⫾65
74⫾53
99⫾38
97⫾55
71⫾43
74⫾47
57⫾50
72⫾55
69⫾48
94⫾51
Subscapularis EMG (% MVIC)
46⫾31
46⫾38
40⫾26
42⫾28
42⫾22
30⫾21
41⫾30
10⫾6
50⫾21
20⫾13
64⫾33
36⫾32
Supraspinatus EMG (% MVIC)
Adapted from Meyers JB, Pasquale MR, Laudner KG, et al: On-the-field resistance-tubing exercises for throwers: An electromyographic analysis. J Athl Train 40(1):15-22, 2005.
69⫾40
109⫾58
98⫾74
101⫾47
112⫾62
96⫾50
63⫾38
93⫾41
89⫾47
84⫾39
90⫾50
89⫾57
Teres Minor EMG (% MVIC)
Note: Muscles whose EMG activity was greater than 45% of a MVIC are bolded, and these exercises are considered to be an effective challenge for that muscle.
45⫾36
19⫾13
18⫾10
31⫾25
61⫾41
19⫾15
28⫾18
6⫾6
22⫾12
6⫾6
Anterior Deltoid EMG (% MVIC)
Exercise
Tubing Force (N)
35⫾17
29⫾16
27⫾17
31⫾15
47⫾34
50⫾57
24⫾21
32⫾51
51⫾30
46⫾20
45⫾21
33⫾22
Infraspinatus EMG (% MVIC)
TABLE 46-7 Mean (⫾SD) Tubing Force and Rotator Cuff and Deltoid EMG (Normalized by a Maximum Voluntary Isometric Contraction, MVIC) During Shoulder Exercises Using Elastic Tubing
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22⫾28
13⫾8
13⫾7 12⫾8 16⫾8 16⫾11 21⫾11 26⫾12 15⫾11 15⫾11 12⫾8 19⫾11
Eccentric arm control portion of D2 diagonal pattern flexion, abduction, external rotation (throwing deceleration)
Standing external rotation at 0° abduction
Standing external rotation at 90° abduction
Standing internal rotation at 0° abduction
Standing internal rotation at 90° abduction
Standing extension from 90-0°
Flexion above 120° with ER (thumb up)
Standing high scapular rows at 135° flexion
Standing mid scapular rows at 90° flexion
Standing low scapular rows at 45° flexion
Standing forward scapular punch
32⫾35
35⫾26
40⫾42
36⫾36
33⫾34
64⫾53
22⫾48
34⫾34
19⫾16
33⫾39
35⫾48
26⫾37
Latissimus Dorsi EMG (% MVIC)
12⫾9
21⫾50
17⫾32
7⫾4
22⫾15
10⫾27
9⫾6
11⫾7
10⫾8
7⫾4
11⫾7
6⫾4
Biceps Brachii EMG (% MVIC)
27⫾28
21⫾13
21⫾22
19⫾8
22⫾12
67⫾45
13⫾12
21⫾19
15⫾11
22⫾17
22⫾16
32⫾15
Triceps Brachii EMG (% MVIC)
39⫾32
44⫾32
39⫾27
51⫾34
49⫾35
53⫾40
54⫾39
44⫾31
88⫾51
48⫾25
63⫾42
54⫾46
Lower Trapezius EMG (% MVIC)
52⫾43
57⫾38
59⫾44
59⫾40
52⫾54
66⫾48
65⫾59
41⫾34
77⫾53
66⫾49
86⫾49
82⫾82
Rhomboids EMG (% MVIC)
Adapted from Meyers JB, Pasquale MR, Laudner KG, et al: On-the-field resistance-tubing exercises for throwers: An electromyographic analysis. J Athl Train 40(1):15-22, 2005.
Note: Muscles whose EMG activity was greater than 45% of a MVIC are bolded, and these exercises are considered to be an effective challenge for that muscle.
19⫾33
17⫾32
18⫾34
29⫾56
19⫾13
22⫾37
18⫾23
36⫾31
34⫾65
10⫾9
36⫾30
30⫾11
D2 diagonal pattern extension, horizontal adduction, internal rotation (throwing acceleration)
Exercise
Pectoralis Major EMG (% MVIC)
Tubing Force (N)
67⫾45
22⫾14
24⫾20
38⫾26
67⫾37
30⫾21
54⫾32
21⫾14
66⫾39
18⫾19
48⫾32
56⫾36
Serratus Anterior EMG (% MVIC)
TABLE 46-8 Mean (⫾SD) Tubing Force and Glenohumeral and Scapular EMG (Normalized by a Maximum Voluntary Isometric Contraction, MVIC) During Shoulder Exercises Using Elastic Tubing
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TABLE 46-9 Mean (⫾SD) Glenohumeral EMG (Normalized by a Maximum Voluntary Isometric Contraction, MVIC) During Scaption with Neutral Rotation and Increasing Load Using Dumbbells Anterior Middle Posterior Deltoid EMG Deltoid EMG Deltoid EMG (% MVIC) (% MVIC) (% MVIC)
Supraspinatu EMG (% MVIC)
Infraspinatus Teres Minor Subscapularis EMG EMG EMG (% MVIC) (% MVIC) (% MVIC)
0% NMW* 0-30°
22⫾10
30⫾18
2⫾2
36⫾21
16⫾7
9⫾9
6⫾7
30-60°
53⫾22
60⫾27
2⫾3
49⫾25
34⫾14
11⫾10
14⫾13
60-90°
68⫾24
69⫾29
2⫾3
47⫾19
37⫾15
15⫾14
18⫾15
90-120°
78⫾27
74⫾33
2⫾3
42⫾14
39⫾20
19⫾17
21⫾19
120-150°
90⫾31
77⫾35
4⫾4
40⫾20
39⫾29
25⫾25
23⫾18
0-30°
42⫾14
55⫾28
5⫾11
64⫾37
39⫾16
17⫾16
14⫾10
30-60°
82⫾20
81⫾21
6⫾8
79⫾29
64⫾23
24⫾23
32⫾15
60-90°
97⫾33
87⫾26
4⫾4
65⫾21
60⫾24
23⫾21
34⫾18
90-120°
96⫾30
85⫾28
4⫾4
53⫾18
49⫾24
21⫾17
28⫾18
71⫾39
70⫾36
10⫾6
41⫾23
43⫾30
32⫾26
18⫾19
0-30°
68⫾21
79⫾30
12⫾18
89⫾45
69⫾27
36⫾28
31⫾14
30-60°
113⫾33
96⫾24
11⫾14
98⫾35
93⫾27
45⫾33
54⫾24
60-90°
113⫾41
91⫾26
10⫾11
82⫾27
80⫾30
40⫾27
50⫾31
90-120°
90⫾34
79⫾28
9⫾10
53⫾17
56⫾28
27⫾22
28⫾22
47⫾38
44⫾35
14⫾15
29⫾8
40⫾28
30⫾22
16⫾18
0-30°
81⫾18
88⫾30
14⫾19
99⫾45
85⫾30
48⫾34
40⫾20
30-60°
127⫾44
104⫾33
13⫾14
109⫾37
108⫾33
61⫾37
61⫾32
60-90°
121⫾45
97⫾27
14⫾13
91⫾25
96⫾35
54⫾30
50⫾31
90-120°
88⫾35
79⫾28
15⫾16
56⫾17
63⫾28
39⫾27
27⫾22
38⫾33
35⫾26
20⫾22
28⫾12
32⫾18
36⫾23
18⫾15
0-30°
96⫾33
108⫾43
14⫾14
120⫾49
93⫾16
41⫾28
54⫾19
30-60°
129⫾47
115⫾45
15⫾9
122⫾37
104⫾24
56⫾27
78⫾41
60-90°
135⫾53
102⫾36
13⫾11
104⫾33
86⫾20
54⫾22
67⫾40
90-120°
97⫾41
78⫾30
12⫾6
67⫾31
47⫾12
32⫾20
41⫾29
120-150°
26⫾14
19⫾14
16⫾9
22⫾19
26⫾15
23⫾12
26⫾17
25% NMW*
120-150° *
50% NMW
120-150° *
75% NMW
120-150° *
90% NMW
NMW ⫽ normalized maximum weight lifted in pounds, where 100% of NMW was calculated pounds by the peak torque value (in foot-pounds) that was generated from a 5 s maximum isometric contraction in 20° scaption divided by each subject’s arm length (in feet). Mean (⫾SD) NMW was 21⫾8 pounds (approx 93⫾36 N). *
Adapted from Alpert SW, Pink MM, Jobe FW, et al: Electromyographic analysis of deltoid and rotator cuff function under varying loads and speeds. J Shoulder Elbow Surg 9(1):47-58, 2000.
exerting an inferoposterior force to the humeral head.10 The posterior cuff muscles also provide lateral rotation, which helps clear the greater tuberosity from under the coracoacromial arch during overhead movements, minimizing subacromial impingement.
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From three-dimensional biomechanical shoulder models, the maximum predicted isometric infraspinatus force was 723 N for external rotation at 90 degrees of abduction and 909 N for external rotation at 0 degrees of abduction.6 The maximum predicted teres minor force was much less than
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613
Figure 46-2. Press-up.
Figure 46-1. D2 diagonal pattern extension.
the infraspinatus during maximum external rotation at both 90 degrees of abduction (111 N) and 0 degrees of abduction (159 N).6 The effectiveness of the posterior cuff to laterally rotate depends on glenohumeral position. For the infraspinatus, its superior, middle, and inferior heads all generate the largest external rotation moment arm (approximately 2.2 cm) and torque at 0 degrees of abduction.8 As the abduction angle increases, the moment arms of the inferior and middle heads stay relatively constant but decrease slightly, while the moment arm of the superior head progressively decreases until it is about 1.3 cm at 60 degrees of abduction.8 These data imply that the infraspinatus is a more effective external rotator at lower abduction angles compared with higher abduction angles.
Figure 46-3. Prone external rotation at 90 degrees of abduction.
Although infraspinatus activity during external rotation has been shown to be similar at 0 degrees, 45 degrees, and 90 degrees of abduction (see Table 46-2),14,27,28 external rotation at 0 degrees of abduction is the optimal position to isolate the infraspinatus muscle,14 and there is a trend toward greater infraspinatus activity during external rotation at lower abduction angles compared with higher abduction angles.28,35 For the teres minor, it generates a relatively constant external rotation moment arm (approximately 2.1 cm)
and torque throughout arm abduction movement, which implies that abduction angle does not affect the effectiveness of the teres minor to generate external rotation torque.8 Teres minor activity during external rotation is similar at 0 degrees, 45 degrees, and 90 degrees of abduction (see Table 46-2).27,28 In addition, infraspinatus and teres minor activities are similar to each other during external rotation movements regardless of abduction positions.16,23,28
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Figure 46-6. Push-up with a plus.
Figure 46-4. Prone horizontal abduction at 90 to 135 degrees of abduction with external rotation.
Figure 46-7. Scaption with external rotation (full can). Figure 46-5. Rowing.
What is not readily apparent is the significant role of the infraspinatus as a shoulder abductor in the scapular plane.6-8 From three-dimensional biomechanical shoulder models, predicted infraspinatus force during maximum isometric effort scapular plane abduction (90 degrees position) was 205 N, nearly twice the predicted force from the supraspinatus in this position.6 Liu and colleagues7 reported that in scapular plane abduction with neutral rotation, the infraspinatus generated an abductor moment arm that was small at 0 degrees of
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abduction but increased to 1 cm at 15 degrees of abduction and remained fairly constant throughout increasing abduction angles. Moreover, infraspinatus activity increases as resistance increases, peaking at 30 to 60 degrees for any given resistance (see Table 46-9).11 As resistance increases, infraspinatus activity increases to help generate a higher scaption torque, and at lower scaption angles infraspinatus activity increases to resist superior humeral head translation due to the increased activity from the deltoids.10
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Figure 46-8. Flexion. Figure 46-10. Standing scapular dynamic hug–forward scapular punch.
45 degrees of external rotation, 0.5 to 1.7 cm at neutral rotation, and 0.8 to 2.4 cm at 45 degrees of internal rotation. These data imply that the infraspinatus is more effective as a scapular plane abductor with the shoulder internally rotated and is not as effective with the shoulder externally rotated. However, in terms of infraspinatus activity, MRI data demonstrate similar activity during abduction with internal rotation and abduction with external rotation.15 Moreover, greater infraspinatus activity has been reported with the full can exercise compared with the empty can exercise.16
Figure 46-9. Side-lying external rotation at 0 degrees of abduction.
Another interesting finding is that the abductor moment arm of the infraspinatus generally increased as abduction with internal rotation increased,7 such as performing the empty can exercise. In contrast, the abductor moment arm of the infraspinatus generally decreased as abduction with external rotation increased,7 similar to performing the full can exercise. Otis and colleagues8 reported similar findings in that the abductor moment arms for the three heads of the infraspinatus (greatest in the superior head and least in the inferior head) were approximately 0.3 to 1.0 cm at
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The infraspinatus is active in numerous shoulder exercises other than empty can, full can, and external rotation exercises. Relatively high infraspinatus activity has been quantified in prone horizontal abduction at 100 degrees of abduction with external rotation and internal rotation, abduction, flexion, side-lying abduction, standing extension from 90 to 0 degrees, and D1 and D2 diagonal pattern flexion (see Tables 46-5 and 46-7).15,16,24-28,35,36 When these shoulder exercises are compared with one another, mixed results have been reported. Some EMG data support prone horizontal abduction at 100 degrees of abduction with external rotation over the empty can and full can in infraspinatus activity,24 and other EMG data and MRI data show no difference in infraspinatus activity between these exercises.15,26
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A A
B Figure 46-12. A, Throwing deceleration, starting position. B, Throwing deceleration, ending position.
B Figure 46-11. A, Throwing acceleration, starting position. B, Throwing acceleration, ending position.
Interestingly, relatively high infraspinatus activity has been reported in several closed-chain weight-bearing exercises, such as a variety of push-up exercises and when assuming a bipod (alternating arm and leg) position (see Table 46-4).4,30 In contrast to the infraspinatus, the teres minor generates a weak shoulder adductor torque due to its relatively lower
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A
A
B Figure 46-13. A, Push and pull, starting position. B, Push and pull, ending position.
attachments to the scapula and humerous.6-8 A threedimensional biomechanical model of the shoulder reveals that the teres minor does not generate scapular plane abduction torque when it contracts, but rather generates an adduction torque and 94 N of force during maximum-effort scapular plane adduction.6 Otis and colleagues8 reported the adductor moment arm of the teres minor was approximately 0.2 cm at 45 degrees of internal rotation and approximately 0.1 cm at 45 degrees of external rotation. These data imply that the teres minor is a weak adductor of the humerus regardless of the rotational position of the humerus. In addition, because of its posterior position at the shoulder, it also helps generate a weak horizontal abduction torque. Therefore, although its activity is similar to that of the infraspinatus during external rotation, it is hypothesized that the teres minor would not be as active as the infraspinatus during scaption, abduction, and flexion movements but would show activity similar to that of the infraspinatus during horizontal abduction–type movements.
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B Figure 46-14. A, Low to high twist, starting position. B, Low to high twist, ending position.
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A
A
B B
Figure 46-16. A, High to low chop, starting position. B, High to low chop, ending position.
Figure 46-15. A, Low to high lift, starting position. B, Low to high lift, ending position.
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This hypothesis is supported by EMG and MRI data, which show that teres minor activity during flexion, abduction, and scaption is drastically less than the infraspinatus activity (see Tables 46-5 and 46-9).11,15,16,23,24,26 Even though the teres minor generates an adduction torque, it is active during these different elevation-type movements as it contracts to enhance joint stability by resisting superior humeral head translation and providing humeral head compression within the glenoid fossa.10 This is especially true at lower abduction angles and when abduction and scaption movements encounter greater resistance (see Table 46-9).11 In contrast to arm abduction, scaption, and flexion, teres minor activity is much higher during prone horizontal abduction at 100 degrees of abduction with external rotation, exhibiting activity similar to that of the infraspinatus (see Tables 46-2 and 46-5).15,16,24,26,28 Teres minor activity is also relatively high during standing high, mid, and low scapular rows and standing forward scapular punch and, surprisingly, even during internal rotation exercises.27
Subscapularis
A
B Figure 46-17. A, D1 diagonal extension, starting position. B, D1 diagonal extension, ending position.
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The subscapularis provides glenohumeral compression, internal rotation, and anteroinferior stability. Numerous exercises produce high activity in the subscapularis, such as the exercises listed in Tables 46-1 and 46-7.10,27,30,35,37-39 From three-dimensional biomechanical shoulder models, predicted subscapularis force during maximum effort internal rotation was 1725 N at 90 degrees of abduction and 1297 N at 0 degrees of abduction.6 Its superior, middle, and inferior heads all generate the largest internal rotation moment arm (approximately 2.5 cm) and torque at 0 degrees of abduction.8 As the abduction angle increases, the moment arms of the inferior and middle heads stay relatively constant, and the moment arm of the superior head progressively decreases until it is about 1.3 cm at 60 degrees of abduction.8 These data imply that the upper portion of the subscapularis muscle (innervated by the upper subscapularis nerve) is a more effective internal rotator at lower abduction angles compared with higher abduction angles. However, there is no significant difference in upper subscapularis activity among internal rotation exercises at 0 degrees, 45 degrees, or 90 degrees of abduction (see Table 46-1).30,38 Abduction angle does not appear to effect the ability of the lower subscapularis (innervated by the lower subscapularis nerve) to generate internal rotation torque.8 However, lower subscapularis muscle activity is affected by abduction angle. Some EMG data show significantly greater activity with internal rotation at 0 degrees of abduction compared with internal rotation at 90 degrees of abduction (see Table 46-1),30 whereas other EMG data show greater activity with internal rotation at 90 degrees of abduction compared to 0 degrees of abduction.38 Performing internal rotation at 0 degrees of abduction produces similar amounts of upper and lower subscapularis activity.30,37,38
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The movement most optimal for isolation and activation of the subscapularis muscle is the Gerber lift-off against resistance,14,37,39 which is performed by lifting the dorsum of the hand off the mid lumbar spine (against resistance) by simultaneously extending and internally rotating the shoulder.40 Although this was originally developed as a test (using no resistance) for subscapularis tendon ruptures,40 it can be used as an exercise because (a) it tends to isolate the subscapularis muscle by minimizing pectoralis major, teres major, latissimus dorsi, supraspinatus, and infraspinatus activity when performed with no resistance;14,37 (b) it generates as much or more subscapularis activity compared with resisted internal rotation at 0 degrees or 90 degrees of abduction;14,37,39 and (c) it avoids the subacromial impingement position associated with internal rotation at 90 degrees of abduction.14 It is important to begin the Gerber lift-off test (or exercise) with the hand in the mid lumbar spine, because lower and upper subscapularis activity decreases approximately 30% when the test (or exercise) begins at the buttocks level.37 Performing the Gerber lift-off test produces similar amounts of upper and lower subscapularis activity.37 The subscapularis also generates an abduction torque during arm elevation.7,8 From three-dimensional biomechanical shoulder models, predicted subscapularis force during maximum effort scapular plane abduction (90 degrees of isometric position) was 283 N, approximately 2.5 times the predicted force from the supraspinatus in this position.6 Liu and colleagues7 reported that in scapular plane abduction with neutral rotation, the subscapularis generated a peak abductor moment arm of 1 cm at 0 degrees of abduction and then slowly decreased to 0 cm at 60 degrees of abduction. Moreover, the abductor moment arm of the subscapularis generally decreased as abduction with internal rotation increased,7 such as performing the empty can exercise. In contrast, the abductor moment arm of the subscapularis generally increased as abduction with external rotation increased, similar to performing the full can exercise. These data imply that the full can exercise may be more effective in generating subscapularis activity compared with the empty can exercise. Whereas most studies that have examined the empty can exercise have reported relatively low subscapularis activity,15,25,26 Townsend and colleages16 reported relatively high subscapularis activity during the empty can exercise and relatively low subscapularis activity during the full can exercise (see Table 46-5). In contrast, scaption with neutral rotation as well as flexion and abduction above 120 degrees with external rotation generated relatively high subscapularis EMG activity (see Tables 46-5, 46-7, 46-9).11,16,27 The subscapularis is active in numerous shoulder exercises other than flexion, abduction, scaption, and internal rotation exercises. Relatively high subscapularis activity has been quantified in side-lying abduction, standing extension from 90 to 0 degrees, military press, D2 diagonal pattern flexion and extension, and PNF scapular clock, depression,
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elevation, protraction, and retraction movements (see Tables 46-1, 46-5, and 46-7).16,25,27,30,31,35 Surprisingly, even external rotation exercises have generated relatively high subscapularis activity (see Table 46-7).27 Although prone horizontal abduction at 90 degrees of abduction with external rotation was an effective exercise for the supraspinatus, infraspinatus, and teres minor, it is not an effective exercise for the subscapularis (see Table 52-5).16,26 Moreover, relatively high subscapularis activity has been reported in the push-up with a plus, standing scapular dynamic hug, standing forward scapular punch, standing high, mid, and low scapular rows, and two-hand overhead medicine ball throw (see Tables 46-1 and 46-7).27,30,32,33 In contrast to overhead throwing, during the two-hand overhead medicine ball throw, peak lower subscapularis was greater than peak upper subscapularis during the acceleration phase of the throw. Otis and colleagues8 reported that the superior, middle, and inferior heads of the subscapularis all generate abductor moment arms (greatest in the superior head and least in the inferior head) that vary as a function of humeral rotation. These moment arm lengths for the three muscle heads are approximately 0.4 to 2.2 cm at 45 degrees of external rotation, 0.4 to 1.4 cm at neutral rotation, and 0.4 to 0.5 cm at 45 degrees of internal rotation. These data imply that the subscapularis is most effective as a scapular plane abductor with the shoulder in external rotation and least effective with the shoulder in internal rotation. The simultaneous activation of the subscapularis and infraspinatus during arm elevation generates abductor moments and inferior directed force to the humeral head to resist superior humeral head translation.10 These muscles also neutralize the internal rotation and external rotation torques they generate, further enhancing joint stability.
DELTOID BIOMECHANICS AND FUNCTION The abductor moment arms in the scapular plane are approximately 0 cm for the anterior deltoid and 1.4 cm for the middle deltoid at 0 degrees of abduction with neutral rotation, progressively increasing with increasing abduction.7,8 By 60 degrees of abduction, the moment arms increase to approximately 1.5 to 2 cm for the anterior deltoid and 2.7 to 3.2 cm for the middle deltoid. From 0 to 40 degrees of abduction, the moment arms for the anterior and middle deltoids are less than the moment arms for the supraspinatus, subscapularis, and infraspinatus.7,8 These data imply that the anterior and middle deltoids are not effective abductors at low abduction angles with neutral rotation, especially the anterior deltoids, whereas the supraspinatus and to a lesser extent the infraspinatus and subscapularis are more effective abductors at low abduction angles. These biomechanical data are supported by EMG data, in which anterior and middle deltoid activity generally peaks between 60 and 90 degrees of abduction
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in the scapular plane, and supraspinatus, infraspinatus, and subscapularis activity generally peaks between 30 and 60 degrees of abduction in the scapular plane (see Table 46-9).11 The abductor moment arm for the anterior deltoid changes considerably with humeral rotation, increasing with external rotation and decreasing with internal rotation.7 At 60 degrees of external rotation and 0 degrees of abduction, a position similar to the beginning of the full can exercise, the anterior deltoid moment arm was 1.5 cm (compared with 0 cm in neutral rotation), which makes the anterior deltoid an effective abductor even at small abduction angles.7 By 60 degrees of abduction with external rotation, its moment arm increased to approximately 2.5 cm (compared with approximately 1.5-2 cm in neutral rotation).7 In contrast, at 60 degrees of internal rotation at 0 degrees of abduction, a position similar to the beginning of the empty can exercise, its moment arm was 0 cm (the same as with neutral rotation), which implies that the anterior deltoid is not an effective abductor with humeral internal rotation.7 By 60 degrees of abduction and internal rotation, its moment arm increased to only about 0.5 cm.7 Although the abductor moment arms for the middle and posterior deltoids did change significantly with humeral rotation, the magnitude of these changes were too small to be clinically relevant. From EMG and MRI data, it is surprising that both the anterior and middle deltoids exhibit similar activity between scaption with internal rotation and scaption with external rotation (see Table 46-5).15,16 Additional exercises that have exhibited relatively high anterior and middle deltoid activity are shown in Tables 46-4, 46-5, and 46-7.4,16,27,32,35,36,41-44 These include the D1 and D2 diagonal pattern flexion, flexion, push-up exercises, bench press, dumbbell fly, military press, two-hand overhead medicine ball throws, press-up, dynamic hug, and standing forward scapular punch. Comparing exercises, anterior and middle deltoid activity was significantly greater performing a free-weight bench press compared with a machine bench press.44 There was no difference in mean anterior deltoid activity among the dumbbell fly and barbell and dumbbell bench press, but both the anterior deltoid and pectoralis major were activated for longer periods of time in the barbell and dumbbell bench press compared with the dumbbell fly.42 Bench press (horizontal, inclined, or declined) and military (trunk vertical) technique variations also affect deltoid activity. Anterior deltoid activity increased as the trunk became more vertical, such as performing the incline and military press.43 Compared with the incline and military press, anterior deltoid activity was less in the horizontal press and lowest in the decline press.43 Hand grip also affects shoulder biomechanics and deltoid activity during the bench press. Compared with a narrow hand grip, employing a wider hand grip resulted in slightly
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greater anterior deltoid activity during the incline and military press.43 In contrast, compared with a wide hand grip, employing a narrow hand grip resulted in greater anterior deltoid and clavicular pectoralis activity during the decline and horizontal press.43 This is consistent with biomechanical data during the horizontal bench press, in which a greater shoulder extension torque is generated by the load lifted with a narrower (95% biacromial breadth) hand grip (peak torque of approximately 290 N•m occurred when the bar was near the chest) compared with a wider (270% biacromial breadth) hand grip (peak torque of approximately 210 N•m occurred when the bar was near the chest), which must be countered by a shoulder flexor torque generated by the shoulder flexors (primarily the anterior deltoid and to a lesser extent the clavicular pectoralis major).45 The greater shoulder flexor torque during the narrower hand grip occurred because throughout the bench press movement the load was held farther away from the shoulder axis with a narrower hand grip (moment arm of approximately 7 cm at the beginning and end of the bench press and approximately 21 cm when the bar was near the chest) compared with a wider hand grip (moment arm of approximately 4 cm at the beginning and end of the bench press and approximately 15 cm when the bar was near the chest).45 Push-up technique variations also affect deltoid activity.4,46 Anterior deltoid activity was least in a standard push-up, greater in a push-up with feet elevated, and greatest in a one-arm push-up. Moreover, anterior deltoid activity was 60% to 70% of MVIC during a plyometric push-up (clapping) and one-arm push-up, but only 40% to 50% of MVIC during the standard push-up, during push-ups with hands staggered (left or right hand forward relative to other hand), and while performing push-ups with one or both hands on a basketball.46 However, performing the plyometric and one-arm push-ups generated approximately twice as much spinal compressive load compared with performing standard, ball, or staggered-hand push-ups, which may be problematic for persons with spinal problems.46 The posterior deltoids do not effectively contribute to scapular plane abduction from 0 to 90 degrees, but they function more effectively as scapular plane adductors due to an adductor moment arm.7,8 Because this moment arm decreases as abduction increases, this muscle becomes less effective as a scapular plane adductor at higher abduction angles and can change to a scapular plane abductor beyond 110 degrees of abduction.7,8 These biomechanical data are consistent with EMG and MRI data, in which posterior deltoid activity is relatively low not only during scaption but also during flexion and abduction (see Tables 46-5 and 46-9).11,15,16 However, relatively high posterior deltoid activity has been reported in the empty can exercise when compared with the full can exercise, which implies that humeral rotation during scaption affects posterior deltoid activity.15,26 During rowing exercises and prone horizontal abduction at 100 degrees of abduction with external rotation and internal rotation, both the posterior and middle
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deltoids produced relatively high activity (see Tables 46-2 and 46-5) but relatively low anterior deltoid activity.16,26,28 Posterior and middle deltoid activity remains similar in performing prone horizontal abduction at 100 degrees of abduction with internal rotation compared with performing with external rotation (see Table 46-5).16 Other exercises that have exhibited relatively high posterior and middle deltoid activity include D1 diagonal pattern extension and D2 diagonal pattern flexion, push-up exercises, shoulder extension, and side-lying external rotation at 0 degrees of abduction (see Tables 46-4 and 46-5).4,16,27,35,36 It has been reported that given a peak isometric abduction torque of 25 N•m at 0 degrees of abduction and neutral rotation, up to 35% to 65% of this torque may be generated by the middle deltoid, up to 30% by the subscapularis, up to 25% by the supraspinatus, up to 10% by the infraspinatus, up to 2% by the anterior deltoid, and 0% by the posterior deltoid.7 Interestingly, the rotator cuff provides significant abduction torque. The ineffectiveness of the anterior and posterior deltoids in generating abduction torque with neutral rotation might appear surprising.7,8 However, it is important to understand that the low abduction torque for the anterior deltoid does not mean that this muscle is only minimally active. In fact, because the anterior deltoid has an abductor moment arm near 0 cm, the muscle could be very active and generating very high force (in 0 degrees of abduction, this force attempts to translate the humeral head superiorly), but very little torque. The aforementioned torque data are complemented and supported by muscle force data from Hughes and An.6 These authors reported predicted forces from the deltoids and rotator cuff during maximum effort abduction with the arm 90 degrees abducted and in neutral rotation. Posterior deltoid and teres minor forces were only 2 N and 0 N, respectively, which further demonstrates the ineffectiveness of these muscles as shoulder abductors. In contrast, middle deltoid force was the highest at 434 N, which confirms the high activity in this muscle during abduction. The anterior deltoid generated the second highest force of 323 N. This might appear surprising given the low abductor torque for this muscle, but force and torque are not the same, and the shoulder was positioned at 90 degrees of abduction in this study but at 0 degrees of abduction in the torque data from Liu and colleagues.7 As previously mentioned, the moment arm of the anterior deltoid progressively increases as abduction increases, and it becomes a more effective abductor. It is also important to remember that muscle force is generated not only to generate joint torque but also to provide stabilization such as joint compression. Also of interest is the 608 N of force collectively generated by the subscapularis (283 N), infraspinatus (205 N), and supraspinatus (117 N). These large forces are generated not only to abduct the shoulder but also to compress and stabilize the joint and neutralize the
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superior-directed force generated by the deltoids at lower abduction angles.
SCAPULAR MUSCLE FUNCTION Appropriate scapular muscle strength and balance are important because the scapula and humerus move together as a unit during arm movement, referred to as scapulohumeral rhythm. Near 30 to 40 degrees of humeral elevation, the scapula begins to upwardly rotate in the frontal plane, rotating approximately 1 degree for every 2 degrees of humeral elevation until 120 degrees humeral elevation, and thereafter rotating approximately 1 degree for every 1 degree of humeral elevation until maximal arm elevation, for a total of approximately 45 to 55 degrees of upward rotation.47,48 Scapulohumeral rhythm is affected by humeral rotation. For example, it has been demonstrated that from 0 to 90 degrees of scapular plane abduction, the scapula rotates upward 28 to 30 degrees with neutral humeral rotation, 36 to 38 degrees with humeral external rotation, and 40 to 43 degrees with internal rotation.49 From 0 to 90 degrees of scapular plane abduction, scapular internal rotation and anterior tilt are greater (decreasing subacromial space width) with humeral internal rotation (empty can exercise) compared with humeral external rotation (full can exercise). During humeral elevation, in addition to scapular upward rotation, the scapular also normally posterior tilts approximately 20 to 40 degrees in the sagittal plane and externally rotates approximately 15 to 35 degrees in the transverse plane.47,48 If these three-dimensional sequences of normal scapular movements are disrupted by abnormal scapular muscle firing patterns, fatigue, or injury, the shoulder complex functions less efficiency and injury risk is enhanced. The primary muscles that control scapular movements include the trapezius, serratus anterior, levator scapulae, rhomboids, and pectoralis minor.
Serratus Anterior The serratus anterior works with the pectoralis minor to abduct (protract) the scapula and with the upper and lower trapezius to upwardly rotate the scapula. The serratus anterior is an important muscle because it contributes to all components of normal three-dimensional scapular movements during arm elevation, which includes upward rotation, posterior tilt, and external rotation.47,48 The serratus anterior also helps stabilize the medial border and inferior angle of the scapula, preventing scapular internal rotation (winging) and anterior tilt. Tables 46-3, 46-6, and 46-8 show several exercises that elicit high serratus anterior activity.27,33,41,50,51 These include D1 and D2 diagonal pattern flexion; D2 diagonal pattern extension; supine scapular protraction; supine
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upward scapular punch; military press; push-up with a plus; internal and external rotation at 90 degrees of abduction; and flexion, abduction, and scaption above 120 degrees with external rotation. Serratus anterior activity tends to increase in a somewhat linear fashion with arm elevation (see Tables 46-3 and 46-6).48,50-53 However, increasing arm elevation increases subacromial impingement risk,17,18 and arm elevation at lower abduction angles also generates relatively high serratus anterior activity (see Table 46-3).50 It is interesting that performing internal rotation and external rotation at 90 degrees of abduction generates relatively high serratus anterior activity (see Tables 46-3 and 46-8), because these exercises are usually believed to primarily work rotator cuff muscles.27,50 Not surprising is the high activity generated during the push-up. When performing the standard push-up, push-up on knees, and wall push-up, serratus activity is greater when full scapular protraction occurs after the elbows fully extend (push-up with a plus).54 Serratus anterior activity is lowest in the wall push-up with a plus, exhibits moderate activity during the push-up with a plus on knees, and relatively high activity in the standard push-up with a plus.41,54 Compared with the standard push-up, performing a push-up with a plus with the feet elevated produces significantly greater serratus anterior activity.55 Additional exercises that have been shown to be effective in activating the serratus anterior are the prone horizontal abduction at 90 degrees of abduction with external rotation,26 standing scapular dynamic hug,41 PNF scapular depression and protraction movements,31 empty can,26 and wall slide.53 The wall slide begins by slightly leaning against the wall with the ulnar border of the forearms in contact with wall, elbows flexed 90 degrees, and shoulders abducted 90 degrees in the scapular plane. From this position the arms slide up the wall in the scapular plane while leaning into wall. The wall slide produces serratus anterior activity similar to scaption above 120 degrees with no resistance. One advantage of the wall slide compared with scaption is that, anecdotally, patients report that the wall slide is less painful to perform compared with scaption.53 This may be because during the wall slide the upper extremities are supported against the wall, making it easier to perform.
Trapezius General functions of the trapezius include scapular upward rotation and elevation for the upper trapezius, retraction for the middle trapezius, and upward rotation and depression for the lower trapezius. The inferomedialdirected fibers of the lower trapezius might also contribute to posterior tilt and external rotation of the scapula during arm elevation,48 which decreases subacromial impingement risk.56,57 Tables 46-3, 46-6, and 46-8 show several
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exercises that elicit high trapezius activity. Relatively high upper trapezius activity occurs in the shoulder shrug; prone rowing; prone horizontal abduction at 90 degrees and 135 degrees of abduction with external rotation and internal rotation; D1 diagonal pattern flexion; standing scapular dynamic hug; PNF scapular clock; military press; two-hand overhead medicine ball throw; and scaption and abduction below 80 degrees, at 90 degrees, and above 120 degrees with external rotation.31,32,41,50,51 During scaption, upper trapezius activity progressively increases from 0 to 60 degrees, remains relatively constant from 60 to 120 degrees, and continues to progressively increase from 120 to 180 degrees.52 Relatively high middle trapezius activity occurs in the shoulder shrug, prone rowing, and prone horizontal abduction at 90 degrees and 135 degrees of abduction with external rotation and internal rotation.50,51 Some studies have reported relatively high middle trapezius activity during scaption at 90 degrees and above 120 degrees,41,50,52 and other EMG data show low middle trapezius activity during this exercise.51 Relatively high lower trapezius activity occurs in the prone rowing, prone horizontal abduction at 90 degrees and 135 degrees of abduction with external rotation and internal rotation; prone and standing external rotation at 90 degrees of abduction; D2 diagonal pattern flexion and extension; PNF scapular clock; standing high scapular rows; and scaption, flexion, and abduction below 80 degrees and above 120 degrees with external rotation.27,31,50,51 Lower trapezius activity tends to be relatively low at less than 90 degrees of scaption, abduction, and flexion, and then it increases exponentially from 90 to 180 degrees.31,50-53,58 Significantly greater lower trapezius activity has been reported in prone external rotation at 90 degrees of abduction compared with the empty can exercise.23
Rhomboids and Levator Scapulae Both the rhomboids and levator scapulae function as scapular adductors (retractors), downward rotators, and elevators. Relatively high rhomboid activity has been reported during D2 diagonal pattern flexion and extension; standing external rotation at 0 degrees and 90 degrees of abduction; standing internal rotation at 90 degrees of abduction: standing extension from 90 to 0 degrees; prone horizontal abduction at 90 degrees of abduction with internal rotation; scaption, abduction, and flexion above 120 degrees with external rotation; prone rowing; and standing high, mid, and low scapular rows (see Tables 46-6 and 46-8).27,51 Relatively high levator scapulae activity has been reported in scaption above 120 degrees with external rotation, prone horizontal abduction at 90 degrees of abduction with external rotation and internal rotation, prone rowing, and prone extension at 90 degrees flexion (see Table 46-6).51
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References 1. Steindler A: Kinesiology of the Human Body. Springfield, Ill: Charles C Thomas, 1995. 2. Blackard DO, Jensen RL, Ebben WP: Use of EMG analysis in challenging kinetic chain terminology. Med Sci Sports Exerc 31(3):443-448, 1999. 3. Dillman CJ, Murray TA, Hintermeister TA: Biomechanical differences of open and closed chain exercises with respect to the shoulder. J Sport Rehab 3:228-238, 1994. 4. Uhl TL, Carver TJ, Mattacola CG, et al: Shoulder musculature activation during upper extremity weight-bearing exercise. J Orthop Sports Phys Ther 33(3):109-117, 2003. 5. Lee SB, Kim KJ, O’Driscoll SW, et al: Dynamic glenohumeral stability provided by the rotator cuff muscles in the mid-range and end-range of motion. A study in cadavera. J Bone Joint Surg Am 82(6):849-857, 2000. 6. Hughes RE, An KN: Force analysis of rotator cuff muscles. Clin Orthop Relat Res (330):75-83, 1996. 7. Liu J, Hughes RE, Smutz WP, et al: Roles of deltoid and rotator cuff muscles in shoulder elevation. Clin Biomech (Bristol, Avon) 12(1):32-38, 1997. 8. Otis JC, Jiang CC, Wickiewicz TL, et al: Changes in the moment arms of the rotator cuff and deltoid muscles with abduction and rotation. J Bone Joint Surg Am 76(5):667-676, 1994. 9. Burke WS, Vangsness CT, Powers CM: Strengthening the supraspinatus: A clinical and biomechanical review. Clin Orthop Relat Res (402):292-298, 2002. 10. Sharkey NA, Marder RA: The rotator cuff opposes superior translation of the humeral head. Am J Sports Med 23(3):270-275, 1995. 11. Alpert SW, Pink MM, Jobe FW, et al: Electromyographic analysis of deltoid and rotator cuff function under varying loads and speeds. J Shoulder Elbow Surg 9(1): 47-58, 2000. 12. Jobe FW, Moynes DR: Delineation of diagnostic criteria and a rehabilitation program for rotator cuff injuries. Am J Sports Med 10(6):336-339, 1982. 13. Rowlands LK, Wertsch JJ, Primack SJ, et al: Kinesiology of the empty can test. Am J Phys Med Rehabil 74(4):302-304, 1995. 14. Kelly BT, Kadrmas WR, Speer KP: The manual muscle examination for rotator cuff strength. An electromyographic investigation. Am J Sports Med 24(5):581-588, 1996. 15. Takeda Y, Kashiwaguchi S, Endo K, et al: The most effective exercise for strengthening the supraspinatus muscle: Evaluation by magnetic resonance imaging. Am J Sports Med 30(3):374-381, 2002. 16. Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19(3):264-272, 1991. 17. De Wilde L, Plasschaert F, Berghs B, et al: Quantified measurement of subacromial impingement. J Shoulder Elbow Surg 12(4):346-349, 2003. 18. Roberts CS, Davila JN, Hushek SG, et al: Magnetic resonance imaging analysis of the subacromial space in the impingement sign positions. J Shoulder Elbow Surg 11(6):595-599, 2002. 19. Thigpen CA, Padua DA, Morgan N, et al: Scapular kinematics during supraspinatus rehabilitation exercise: A comparison of full-can versus empty-can techniques. Am J Sports Med 34(4):644-552, 2006.
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20. Solem-Bertoft E, Thuomas KA, Westerberg CE: The influence of scapular retraction and protraction on the width of the subacromial space. An MRI study. Clin Orthop Relat Res (296):99-103, 1993. 21. Kibler WB, Sciascia A, Dome D: Evaluation of apparent and absolute supraspinatus strength in patients with shoulder injury using the scapular retraction test. Am J Sports Med 34(10):1643-1647, 2006. 22. Itoi E, Kido T, Sano A, et al: Which is more useful, the “full can test” or the “empty can test,” in detecting the torn supraspinatus tendon? Am J Sports Med 27(1):65-68, 1999. 23. Ballantyne BT, O’Hare SJ, Paschall JL, et al: Electromyographic activity of selected shoulder muscles in commonly used therapeutic exercises. Phys Ther 73(10):668-677; discussion 677-682, 1993. 24. Blackburn TA, McLeod WD, White B, Wofford L: EMG analysis of posterior rotator cuff exercises. Athl Train 25(1):40-45, 1990. 25. Horrigan JM, Shellock FG, Mink JH, Deutsch AL: Magnetic resonance imaging evaluation of muscle usage associated with three exercises for rotator cuff rehabilitation. Med Sci Sports Exerc 31(10):1361-1366, 1999. 26. Malanga GA, Jenp YN, Growney ES, An KN: EMG analysis of shoulder positioning in testing and strengthening the supraspinatus. Med Sci Sports Exerc 28(6):661-664, 1996. 27. Meyers JB, Pasquale MR, Laudner KG, et al: On-the-field resistance-tubing exercises for throwers: An electromyographic analysis. J Athl Train 40(1):15-22, 2005. 28. Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34(7):385-394, 2004. 29. Worrell TW, Corey BJ, York SL, Santiestaban J: An analysis of supraspinatus EMG activity and shoulder isometric force development. Med Sci Sports Exerc 24(7):744-748, 1992. 30. Decker MJ, Tokish JM, Ellis HB, et al: Subscapularis muscle activity during selected rehabilitation exercises. Am J Sports Med 31(1):126-134, 2003. 31. Smith J, Dahm DL, Kaufman KR, et al: Electromyographic activity in the immobilized shoulder girdle musculature during scapulothoracic exercises. Arch Phys Med Rehabil 87(7):923-927, 2006. 32. Cordasco FA, Wolfe IN, Wootten ME, Bigliani LU: An electromyographic analysis of the shoulder during a medicine ball rehabilitation program. Am J Sports Med 24(3):386-392, 1996. 33. Hintermeister RA, Lange GW, Schultheis JM, et al: Electromyographic activity and applied load during shoulder rehabilitation exercises using elastic resistance. Am J Sports Med 26(2):210-220, 1998. 34. Itoi E, Berglund LJ, Grabowski JJ, et al: Tensile properties of the supraspinatus tendon. J Orthop Res 13(4):578-584, 1995. 35. Kronberg M, Nemeth G, Brostrom LA: Muscle activity and coordination in the normal shoulder. An electromyographic study. Clin Orthop Relat Res (257):76-85, 1990. 36. Ekholm J, Arborelius UP, Hillered L, Ortqvist A: Shoulder muscle EMG and resisting moment during diagonal exercise movements resisted by weight-and-pulley-circuit. Scand J Rehabil Med 10(4):179-185, 1978.
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37. Greis PE, Kuhn JE, Schultheis J, et al: Validation of the lift-off test and analysis of subscapularis activity during maximal internal rotation. Am J Sports Med 24(5):589-593, 1996. 38. Kadaba MP, Cole A, Wootten ME, et al: Intramuscular wire electromyography of the subscapularis. J Orthop Res 10(3):394-397, 1992. 39. Suenaga N, Minami A, Fujisawa H: Electromyographic analysis of internal rotational motion of the shoulder in various arm positions. J Shoulder Elbow Surg 12(5):501-505, 2003. 40. Gerber C, Krushell RJ: Isolated rupture of the tendon of the subscapularis muscle. Clinical features in 16 cases. J Bone Joint Surg Br 73(3):389-394, 1991. 41. Decker MJ, Hintermeister RA, Faber RA, Hawkins RJ: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27(6):784-791, 1999. 42. Welsch EA, Bird M, Mayhew JL: Electromyographic activity of the pectoralis major and anterior deltoid muscles during three upper-body lifts. J Strength Cond Res 19(2):449-452, 2005. 43. Barnett C, Kippers V, Turner P: Effects of variations of the bench press exercise on the EMG activity of five shoulder muscles. J Strength Cond Res 9(4):222-227, 1995. 44. McCaw ST, Friday JJ: A comparison of muscle activity between a free weight and machine bench press. J Strength Cond Re2 8(4):259-264, 1994. 45. Wagner LL, Evans SA, Weir JP, et al: The effect of grip width on bench press performance. Int J Sport Biomech 8:1-10, 1992. 46. Freeman S, Karpowicz A, Gray J, McGill S: Quantifying muscle patterns and spine load during various forms of the push-up. Med Sci Sports Exerc 38(3):570-577, 2006. 47. McClure PW, Michener LA, Sennett BJ, Karduna AR: Direct 3-dimensional measurement of scapular kinematics during dynamic movements in vivo. J Shoulder Elbow Surg 10(3):269-277, 2001. 48. Ludewig PM, Cook TM, Nawoczenski DA: Three-dimensional scapular orientation and muscle activity at selected positions
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of humeral elevation. J Orthop Sports Phys Ther 24(2):57-65, 1996. Sagano M, Magee MD, Katayose M: The effect of glenohumeral rotation on scapular upward rotation in different positions of scapular-plane elevation. J Sport Rehab 15: 144-155, 2006. Ekstrom RA, Donatelli RA, Soderberg GL: Surface electromyographic analysis of exercises for the trapezius and serratus anterior muscles. J Orthop Sports Phys Ther 33(5):247-258, 2003. Moseley JB Jr, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20(2):128-134, 1992. Bagg SD, Forrest WJ: Electromyographic study of the scapular rotators during arm abduction in the scapular plane. Am J Phys Med 65(3):111-124, 1986. Hardwick DH, Beebe JA, McDonnell MK, Lang CE: A comparison of serratus anterior muscle activation during a wall slide exercise and other traditional exercises. J Orthop Sports Phys Ther 36(12):903-910, 2006. Ludewig PM, Hoff MS, Osowski EE, et al: Relative balance of serratus anterior and upper trapezius muscle activity during push-up exercises. Am J Sports Med 32(2):484-493, 2004. Lear LJ, Gross MT: An electromyographical analysis of the scapular stabilizing synergists during a push-up progression. J Orthop Sports Phys Ther 28(3):146-157, 1998. Graichen H, Bonel H, Stammberger T, et al: Threedimensional analysis of the width of the subacromial space in healthy subjects and patients with impingement syndrome. AJR Am J Roentgenol 172(4):1081-1086, 1999. Ludewig PM, Cook TM: Alterations in shoulder kinematics and associated muscle activity in people with symptoms of shoulder impingement. Phys Ther 80(3):276-291, 2000. Wiedenbauer MM, Mortensen OA: An electromyographic study of the trapezius muscle. Am J Phys Med 31(5): 363-367, 1952.
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CHAPTER 47 Neuromuscular Control Exercises
for Shoulder Instability Steven Hoffman, Christopher Hughes, Gordon Riddle, and Omar Ross
NEUROMOTOR CONTROL
The concept of shoulder instability has received a significant amount of attention in the literature in recent years.1,2,4-7 Two basic types of shoulder instability have been identified: static instability and functional subluxation.
Payton and colleagues10 define neuromotor control as a purposeful act initiated at the cortical level. They state that “motor control is an involuntary associated movement organized subcortically that results in a well learned skill operating without conscious guidance.”The basic component of neuromotor control is the ability to discriminate joint position and movement, which is defined as proprioception or kinesthesia. Freeman and Wyke11 identified muscle and joint afferents, which are present in ligaments and synovial tissue. Newton12 described kinesthesia as “the ability to discriminate joint position, relative weight of body parts, and joint movement including direction, amplitude, and speed.” Joint proprioceptors are responsible for signaling a stretch reflex when the shoulder capsule becomes taut and prevent translation at extremes of movement. The tremendous amount of mobility that the shoulder possesses requires that joint proprioceptors be active, because motor control occurs at the subcortical level and the neuromuscular component must be activated to control dynamic stability of the glenohumeral joint. This enables the glenohumeral joint to function through a large range of motion without becoming unstable. A summary of the typical joint receptors found in ligaments and the synovial capsule is presented in Table 47-1.
Static instability is a result of structural damage to the glenohumeral joint resulting in functional glenohumeral instability. Static instability is defined as insufficiency of the static restraining structures such as the glenohumeral capsule, glenoid labrum, and supporting ligaments. It can also be a result of glenohumeral arthritis due to poor geometric articulation. A shoulder that is statically unstable can be subluxed during clinical examination and does not function well in an active person. The fine coordinated action of the rotator cuff and scapulothoracic articulations cannot be maintained secondary to loss of static support. The second type of instability is functional subluxation, and it is a more dynamic form of instability that commonly results from of a loss of neuromotor control, proprioception, or from muscle weakness.2-4,8 Dynamic or functional instability results from a lack of kinesthetic awareness, proprioceptive control, and an inability of the person to maintain the glenohumeral joint in a neutral position.29 An inability to seat the scapula firmly against the thorax can result in uncoordinated movement patterns and muscle weakness.2-4 Clinical manifestations of the subluxation phenomenon can cause minor inflammatory changes such as subacromial impingement or more serious damage to the rotator cuff or glenoid labrum. In the active shoulder, proper and precise coordinated action of the glenohumeral and scapulothoracic stabilizers are important for facilitating synchronous function of the glenohumeral joint. Without proper neuromuscular control, muscles fire asynchronously, which can result in suprahumeral elevation, eventual impingement, rotator cuff arthropathy, and a lack of shoulder function.4,8
KINESIOLOGY AND NEUROMUSCULAR CONTROL OF THE SHOULDER The shoulder is composed of four independent articulations that move synchronously via a force-couple arrangement between muscles attaching to the joints. These include the glenohumeral, acromioclavicular, sternoclavicular, and scapulothoracic joints. An abnormal pattern of movement caused by static or dynamic imbalances can result in excessive stress being placed on the soft tissue, manifesting in an inflammatory response.5,10-13,22,23 This joint interdependence is a unique method for maintaining neuromuscular control of the shoulder.
The purpose of this chapter is to review some of the basic concepts of neuromotor control and how it relates to functional instability. Following this review, a sequence of exercises is described so that they can be used in the clinical setting to facilitate neuromuscular control. These exercises are useful in facilitating dynamic stability of the glenohumeral and scapulothoracic joints, which can prevent the functional subluxation phenomenon.
The scapulothoracic joint is controlled by the levator scapulae, trapezius, rhomboids, and serratus anterior muscles (Fig. 47-1). Without adequate stability of the base of the shoulder girdle complex by the scapula, the glenohumeral joint can become unstable and the joint proprioceptors will
We would like to acknowledge Danny Hoffman’s input in developing some of the figures in the chapter.
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TABLE 47-1 Characteristics of Joint Receptors Type
Location
Physiologic Function
I
Stratum fibrosum of ligaments
Active at rest and during movement
II
Junction of synovial and fibrosum of capsule
Active at onset and termination of movement
III
Collateral ligaments
Active at end of joint range
IV
Ligaments, capsule
Active only to extreme mechanical irritation
Levator scapulae
Trapezius
Serratus anterior
Adapted from Freeman MAR, Wyke B: The innervation of the knee joint: An anatomical and histological study in the cat. J Anat 101:505-532, 1967, with permission.
fire erratically. Therefore, the basis for establishing a neuromuscular control program for shoulder instability is predicated on the scapulothoracic articulation.
TORQUE, FORCE, AND LEVERAGE Torque is defined as a force that is applied perpendicular around an axis of rotation. Torques generated on the shoulder by loads or muscles ultimately depend on arm position in relation to gravity. Maximum resistive torque about the glenohumeral joint is greatest at 90 degrees of elevation with the elbow fully extended.15 Resultant torques and joint reaction forces generated by muscle forces at the shoulder girdle represent the net effect of individual cuff and scapular muscles at any instant in time. Small changes in the direction of force application can significantly affect contact forces at the joint and influence joint stability (Fig. 47-2). Due to its positioning on the rib cage, the scapula is offset 30 degrees from the frontal plane (Fig. 47-3). This position is termed the scapular plane. Arthokinematically, the scapular plane position has been shown to be an important factor in joint stability. Unfortunately, most active persons do not function in this plane of motion, and therefore it is critical that neuromotor training eventually leave the scapular plane and move toward functional movement patterns, so the shoulder can maintain stability in its original position of neutrality. The ideal position of glenohumeral stability occurs when the center point on the glenoid is in line with the center point of the humerus (Figs. 47-3 and 47-4). Because articulation and compression of the glenohumeral joint also depend on the lever arm, position of the arm does not change the length-tension relationship of the capsule. Research has shown that the 90-degree position of elevation is the one that promotes maximum stability of the glenohumeral joint.13,15 Muscle weakness can result
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Figure 47-1. Anatomy and kinesiology of the scapulothoracic joint. (From Tullos HS, Bennett JB: The shoulder in sports. In Norman SW, Niconson B, Nicholas JA (eds): Sports Medicine. Baltimore, Williams & Wilkins, 1985, with permission.)
Direction of joint contact force fo
Direction of force application
of joint Direction o contact force Change in direction of force application Figure 47-2. Contact forces at the glenohumeral joint.
in abnormal compression and shear forces that must be balanced to create stability of the path of the humeral head in the glenoid fossa. A favorable balance between compression and shear forces makes the shoulder position of 90 degrees of elevation the optimal position for joint stability (Fig. 47-5).8,10,13-15
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Horizontal flexion
Neutral-plane of the scapula (“SCAPTION”)
30–45° Balanced net force Horizontal extension
A
Scapular plane
Rib cage
Humerus 60°
A Scapula
30°
B
Frontal plane
Figure 47-3. The scapular plane and position of glenohumeral stability.
Dynamic control of the glenohumeral joint depends on the ability of the rotator cuff and biceps tendon to apply compression and depression to the humerus in the glenoid.13-15 Without adequate dynamic control of the rotator cuff and biceps stabilizers, the glenohumeral joint can become unstable. If the scapulothoracic muscles are also weak, the entire shoulder complex functions abnormally, producing instability due to abnormal positioning of the scapula in relation to the humerus. The purpose, therefore, of neuromuscular conditioning and control of the glenohumeral joint is to facilitate dynamic coordination of the rotator cuff and scapulothoracic stabilizers.19-22,24
EXERCISES TO ENHANCE NEUROMUSCULAR CONTROL When establishing a program for the dynamically or functionally unstable shoulder, the goals should include proximal stability, glenohumeral control at the desired angle and functional position, eccentric strength of the posterior shoul-
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Figure 47-4. The ideal position of glenohumeral stability occurs when the center point on the glenoid is in line with the center point of the humerus. (From Burstein AH, Wright TM: Fundamentals of Orthopaedic Biomechanics. Baltimore, Williams & Wilkins, 1994, with permission.)
der girdle, compressive stability, force couple enhancement, rapid acceleration and deceleration, progressive overload, and adequate flexibility of the shoulder capsule relative to function. The purpose of an exercise program for neuromuscular control is to maintain dynamic muscle balance and flexibility. This program incorporates the SAID principle (specific adaptation for imposed demand). Specificity refers to the concept that to be proficient at a skill or task, that specific task must be practiced. Demand means that the system must be stressed beyond its normal limits for an improvement in skill to occur. This directly relates to the concept of overload. The exercises discussed in this section combine Resultant force Shear force
Compression force
90° Abduction Figure 47-5. Leverage and torque of the glenohumeral joint at varying degrees of abduction (From Rowe CR: The Shoulder. New York, Churchill Livingstone, 1988, pp 735, with permission.)
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eccentric loading, plyometric conditioning (quick acceleration and deceleration), open- or closed-chain facilitation to enhance dynamic stability, and compression and shear force balance with repetition.
Stability Exercises
adduction, and internal rotation, all encompassing different components of the capsule (Figs. 47-26 to 47-35).
CLINICAL APPLICATION OF EXERCISES
Stability exercises can be performed in either the open- or closed-chain position. Closed-chain training enhances static stability by facilitating compression of the glenohumeral joint capsule and stimulating neuromuscular proprioceptors to provide static control. Examples of closed-chain and dynamic-stabilization exercise progressions are shown in Figures 47-6 to 47-14.
One of the most common diagnoses that a physical therapist is likely to see related to shoulder pathology is that of impingement. In its simplest of form, impingement is the result of approximation of subacromial tissues against the acromion process or the glenoid labrum, resulting in tissue inflammation, possible tissue disruption, and ultimate failure.
Open-chain exercises facilitate dynamic control and kinesthetic awareness. It is critical that the scapula remain fixed along the rib cage and the glenohumeral joint remain in neutral so that when these exercises are performed, the humerus does not traverse outside the glenoid labrum. Examples of open-chain exercises for neuromuscular control are shown in Figures 47-15 to 47-25.
Many causes of impingement have been identified. These include overt instability of the glenohumeral joint, weakness of the scapular stabilizers and rotator cuff complex, and poor mechanics during activity. Using proper exercise and technique is critical in treating mechanical impingement of the shoulder. If the shoulder can be trained to maintain a position
Flexibility Exercises Flexibility of the capsule and rotator cuff is important for maintaining mobility of the glenohumeral joint. The shoulder is the most mobile and least stable joint of the body. The stability of the joint capsule and enhancement of neuromotor awareness helps to maintain the glenohumeral joint in neutral, allowing it to perform extremes of motion without subluxing. In the active person, it is critical that the shoulder capsule flexibility be maintained without compromising the integrity of the collagen.25 To achieve improvements in motion without provoking an inflammatory reaction, it is imperative to maintain glenohumeral alignment. Stretching exercises that can be employed to facilitate elevation include external rotation, cross-body
A
B
Figure 47-6. Closed-chain co-contraction with ball on the wall.
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Figure 47-7. Closed-chain protraction in prone plank position on wobble board, with scapulae protracted and retracted. A, Starting position. B, Ending position.
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A Figure 47-8. Closed-chain stabilization on Fitter (Fitter International, Calgary, Alberta).
B Figure 47-11. Prone on elbows on Dyna Disc (A) and Swiss ball (B).
Figure 47-9. Closed-chain iron cross bilateral hook-lying bridge, Bosu (OPTP, Minneapolis, Minn).
Figure 47-12. Closed-chain lateral stabilization.
Figure 47-10. Closed-chain iron cross on foam roller with trunk rotation.
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A
A
B
B
Figure 47-13. Plyometric push-ups on Swiss ball. A, Starting position. B, Ending position.
Figure 47-14. Dynamic stabilization in push-up position catch and toss with soccer ball. A, Starting position. B, Ending position.
of glenohumeral neutrality without exaggerated compensation, impingement symptoms typically abate. If an improvement in flexibility, strength, and proprioceptive awareness does not help to alleviate impingement pain in the active person, other problems probably exist that can require surgical intervention. Typical problems that require surgery are superior labrum anterior-posterior (SLAP) lesions (biceps tendon labral complex insufficiency), rotator cuff tears, overt capsular laxity, and subacromial spurs. Once the anatomic abnormalities have been corrected surgically, the exercise program can be used to facilitate dynamic function and neuromotor control, which should yield a positive functional outcome.
SUMMARY Dynamic instability of the shoulder is the result of abnormal flexibility, lack of proprioception, and muscle weakness. These parameters can be trained by applying the SAID principle, which specifically encourages repetition and training that mimic the functional activity that it is
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Figure 47-15. Scapular retraction and depression.
going to be performed. Because most movement of the shoulder involves quick acceleration and deceleration, rapidity of movement is a necessity. The physiologic factors of speed and reaction time need to be considered to enhance neuromuscular control. Exercising the position
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A Figure 47-17. Elevation in scapular plane.
B
Figure 47-18. Supine protraction.
C Figure 47-16. Prone on Swiss ball scapular retraction and lower trapezius sequence. A, Scapular retraction; B, Prone extension; C, Lower trapezius.
of function is necessary to educate the joint receptors, which should result in a well-learned skill operating without conscious guidance. Summation of all of these activities results in a finely coordinated glenohumeral and scapulohumeral joint acting in concert and thus providing a fine-tuned mechanism for dynamic function without any sense of dynamic instability.
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Figure 47-19. Scapular retraction with external rotation.
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A Figure 47-20. External rotation/internal rotation oscillation with Body Blade (Hymanson, Inc, Playa Del Rey, Calif).
Figure 47-21. Resisted scapular retraction, depression, and glenohumeral external rotation with surgical tubing.
B Figure 47-22. Dynamic stabilization wall dribble (A) and wall clock (B).
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A Figure 47-23. Plyometric chest pass.
B Figure 47-25. Manual perturbation in the scapular plane (A) and the 90/90 position (B).
Figure 47-24. Plyometric chop toss.
Figure 47-26. Lateral capsule scoop.
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Figure 47-27. Inferior capsule stretch with lateral scapula stabilization.
Figure 47-30. Posterior capsule stretch.
Figure 47-28. External rotation stretch.
Figure 47-31. Sleeper stretch for the posterior capsule.
Figure 47-29. Elevation with external rotation.
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Figure 47-32. Horizontal adduction stretch for the posterior capsule.
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Figure 47-33. Inferior capsule stretch.
Figure 47-34. Internal rotation stretch with a wand.
Figure 47-35. Supine external rotation stretch with a wand.
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References 1. Cain PR, Mutschler TA, Fu FH: Anterior stability of the glenohumeral joint: A dynamic model. Am J Sports Med 15: 144-148, 1987. 2. Norwood LA, Del Pizzo W, Jobe FW, Kerlan RK: Anterior shoulder pain in baseball players. Am J Sports Med 6: 103-105, 1978. 3. Pappas AM, Gross TP, Kleinman PK: Symptomatic shoulder instability due to lesions of the glenoid labrum. Am J Sports Med 1:279-288, 1983. 4. Rowe CR, Zarins B: Recurrent transient subluxation of the shoulder. J Bone Joint Surg Am 63:863-872, 1981. 5. Smith RL, Brunolli J: Shoulder kinesthesia after anterior glenohumeral joint dislocation. Phys Ther 69:106-112, 1989. 6. Albright JA, Jokl P, Shaw R, et al: Clinical study of baseball pitchers: correlation of injury to the throwing arm with method of delivery. Am J Sports Med 6:15-21, 1978. 7. Atwater AE: Biomechanics of overarm throwing movements and of throwing injuries. Exerc Sport Sci Rev 7:43-85, 1979. 8. Andrews JR, Carson WG, McLeod WD: Glenoid labrum tears related to the biceps. Am J Sports Med 13:337-341, 1985. 9. Jobe FW, Moynes DR, Tibone JE, et al: An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 10. Payton OD, Hirt S, Newton RA (eds): Scientific Bases for Neurophysiologic Approaches to Therapeutic Exercise. Philadelphia, FA Davis, 1977. 11. Freeman MAR, Wyke B: The innervation of the knee joint: An anatomical and histological study in the cat. J Anat 101:505-532, 1967. 12. Newton RA: Joint receptor contributions to reflexive and kinesthetic responses. Phys Ther 62:22-29, 1982. 13. Jobe FW, Tibone JE, Perry J, et al: An EMG analysis of the shoulder in throwing and pitching. A preliminary report. Am J Sports Med 11:3-5, 1983. 14. Dillman CJ, Fleisig GS, Werner SL, Andrews JR: Biomechanics of the Shoulder in Sports: Throwing Activities. Post Graduate Studies in Physical Therapy. Pennington, NJ, Forum Medicum, 1990. 15. Pappas AM, Zawacki RM, Sullivan TJ: Biomechanics of baseball pitching. A preliminary report. Am J Sports Med 13: 216-222, 1985. 16. Nicholas JA, Hershman EB (eds): The Upper Extremity in Sports Medicine. St Louis, CV Mosby, 1990. 17. Siewert MW, Ariki PK, Davies GJ, et al: Isokinetic torque changes based on lever arm placement. Phys Ther 65:715, 1985. 18. Sanders B (ed): Sports Physical Therapy. East Norwalk, Conn, Appleton & Lange, 1990. 19. Scott NW, Nisonson B, Nicholas JA: Sports Medicine. Baltimore, Williams & Wilkins, 1984. 20. Wyke B: Articular neurology: A review. Physiotherapy 58: 94-99, 1972. 21. Zarins B, Andrews JR, Carson WG: Injuries to the Throwing Arm. Philadelphia, WB Saunders, 1985. 22. Tullos HS, Bennett JB: The shoulder in sports. In Norman SW, Niconson B, Nicholas JA (eds): Sports Medicine. Baltimore, Williams & Wilkins, 1985. 23. Perry J, Glousman R: Biomechanics of throwing. In Nicholas JA, Hershman EB (eds): The Upper Extremity in Sports Medicine. St Louis, CV Mosby, 1990.
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24. Rowe CR: The Shoulder. New York, Churchill Livingstone, 1988, p 735. 25. Lippitt S, Matsen F: Mechanisms of glenohumeral stability Clin Orthop Rel Res (291):20-28, 1993. 26. Glousman R: Electromyographic analysis and its role in the athletic shoulder Clin Orthop Rel Res (288):27-34, 1993. 27. Barden JM, Balyk R, Raso VJ, et al: Atypical shoulder muscle activation in multidirectional instability Clin Neurophysiol 116 (8):1846-1857, 2005. 28. Ginn KA, Cohen ML: Exercise therapy for shoulder pain aimed at restoring neuromuscular control: A randomized comparative clinical trial J Rehabil Med 37(2):115-122, 2005.
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29. Myers JB, Lephart SM: Sensorimotor deficits contributing to glenohumeral instability Clin Orthop Relat Res (400):98-104, 2002. 30. Myers JB, Ju YY, Hwang JH, et al: Reflexive muscle activation alterations in shoulders with anterior glenohumeral instability Am J Sports Med 32(4):1013-1021, 2004. 31. Tyler TF, Mullaney MJ: Adolescent shoulder treatment. Phys Ther Products (Jul/Aug):26-30, 2005. Available at http:// www.ptproductsonline.com/issues/articles/2005-07_05.asp (accessed March 14, 2008). 32. Tyler TF, Roy T, Nicholas SJ, Gleim GW: Posterior capsule tightness and range of motion loss in patients with shoulder impingement Am J Sports Med 28(5):668-673, 2000.
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CHAPTER 48 Proprioceptive Neuromuscular
Facilitation for the Shoulder Bruce Greenfield
The shoulder consists of several joints that function optimally when there are precise recruitment and coordination of the muscles attaching to these joints. Perry1 describes 17 muscle groups that contribute in varying proportions to the composite movement of the scapula and humerus during movement of the upper extremity.
promote functional progression. Modifications to the original patterns of movement of Knott and Voss5 can be performed for select shoulder pathologies while considering the same neurophysiologic concepts. This chapter reviews the theoretical basis of PNF, describes the guidelines for the clinical use of PNF in shoulder rehabilitation, describes the use of PNF techniques to address common impairments and functional losses associated with shoulder conditions, and reviews the current evidence for the use of PNF on shoulder outcomes. Although there are many excellent courses that teach precise PNF techniques, and I encourage readers to pursue such training, my clinical experience indicates that one does not have to be an expert in PNF to successfully integrate many of its techniques into a shoulder rehabilitation program.
The recruitment and timing of muscle activity during function must be consistently precise, because the bone stability of the primary joints of the shoulder is not particularly good compared with most of the other major joints in the body. The scapula is a sesamoid bone embedded in muscles and without direct articulation with the posterior thorax. To complicate matters, the bones and soft tissues around the glenohumeral joint provide little support for the relatively long lever of the rotating upper extremity. These factors have led many researchers to conclude that the shoulder represents one of the best examples of dynamic stability in the human body. Dynamic stability results in neuromuscular recruitment of muscles to stabilize and coordinate movement around a joint complex.2 Specifically, the muscles and their synergistic actions (muscle working in concert to produce a particular motion) around the shoulder provide its inherent stability.
THEORETICAL BASIS The theoretical basis of PNF for affecting motor changes is a controversial subject. We should remember that PNF is promoted as an example of a neurofacilitation approach to motor control. Motor control is the ability to regulate or direct the mechanism essential to movement.6 Neurofacilitation techniques such as PNF are largely associated with both the reflex and hierarchical theories of motor control.7 These approaches in general suggest that normal movement results from a chain of reflexes organized hierarchically within the central nervous system (CNS). According to these theories, normal movement is organized at higher and higher levels in the spinal cord and brain neuronal circuits. A great emphasis is placed on the understanding that incoming sensory information stimulates and thus drives a normal movement pattern.
Lephart and colleagues3 reported that neuromotor control impairments are ubiquitous after shoulder injury and surgery. Although isolated strengthening of weak muscles is important in shoulder rehabilitation, the key to rehabilitation of the shoulder, particularly for the overhead athlete, is to restore the precise temporal pattern of muscle recruitment necessary for smooth coordinated shoulder movement. Rehabilitation specialists should have the requisite skills and knowledge to integrate patterns of muscle activity throughout all stages of shoulder rehabilitation. Fortunately, we have a strategy to facilitate neuromuscular control of the shoulder.
Although new research shows that motor control is more complex than reflex or hierarchical theories suggest,6 the importance of sensory input for stimulating movement is still widely accepted and integrated into clinical practice. Such PNF techniques as repeated quick stretches are believed to stimulate muscle spindles that enhance input and excitation of the alpha motor neuron to the targeted agonist muscles for optimal muscle fiber recruitment and contractions.8 Conversely, elongation and stretching of muscles that are antagonistic to a particular PNF pattern can facilitate the Golgi tendon organs of those muscles,
Proprioceptive neuromuscular facilitation (PNF) is a neurophysiologic approach to therapeutic exercises that can be used during all phases of shoulder rehabilitation to address multiple and different impairments and functional losses. PNF applies neurophysiologic principles of the sensory and motor system to coordinate and efficiently perform purposeful movements at the shoulder.4 PNF can be used effectively as part of an overall progressive rehabilitation program for the shoulder to facilitate neural adaptation and motor control, to improve strength and flexibility, and to 639
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resulting in inhibition and relaxation of the antagonist muscle groups. Finally, techniques such as joint compression and traction used during active PNF patterns are believed to excite joint mechanoreceptors such as Pacinian corpuscles and Ruffini endings that respond to joint angle changes, velocity, and direction of movement and can enhance joint position sense and dynamic reflect stabilization.9 In recent years, the use of PNF has evolved to put greater emphasis on explicitly training function and less emphasis on inhibiting reflexes and retraining normal patterns of movement.
strengthening performed in the OKC group (both groups demonstrated a 15% increase in rotational strength). The authors concluded that by improving shoulder rotation strength as well as functional performance, PNF exercise appears to be the most efficient of the training methods used in their study. The results of this study seem to support the use of manually resisted PNF techniques to selectively strengthen the rotator cuff muscles while working functional movements.
EVIDENCE
Several basic procedures promote the effective use of PNF during rehabilitation. These procedures should be used to optimize the desired movement pattern and should be practiced for consistent application. Clinicians performing PNF procedures use basic techniques to facilitate or inhibit smooth coordinated movement patterns. These techniques include the proper manual contacts, resistance, quick stretch, irradiation, traction and approximation, verbal commands, and visual cues.13,14
A 1997 survey by Surburg and Schrader10 indicated the wide application of PNF techniques by athletic trainers to treat various musculoskeletal conditions using PNF. In addition, one of us (BHG) has observed during years of academic and clinical practice the integration of PNF into therapeutic applications in both orthopedic and neurologic practice settings. Despite the ubiquitous use of PNF for shoulder rehabilitation, evidence is scant on its effectiveness. In an earlier study, Surberg11 examined the effects of PNF on reaction time, movement time, and response time in the shoulders of 42 subjects. Subjects were randomly assigned to one of three training groups: weight training, target throwing, and PNF. Subjects engaged in three training sessions a week for 6 weeks. Analysis revealed a significant improvement for the PNF group compared with the other groups in response time and movement time of the shoulders. Perhaps the most compelling study of the effectiveness of PNF in shoulder outcomes measures was presented by Padua and coworkers.12 The authors randomly assigned 54 healthy subjects to one of three groups: closed kinetic chain (CKC), open kinetic chain (OKC), and upper-extremity PNF diagonal patterns to compare the effectiveness of these exercises on select upper-extremity performance outcomes including isokinetic rotator cuff strength, active angle reproduction, single-arm dynamic stability, and functional throwing performance. Groups trained three times a week for 6 weeks. Outcomes indicated that the OKC and PNF groups demonstrated significant pretest to post-test improvement for isokinetic rotational strength, but only the PNF group demonstrated significant improvement in functional performance. The fact that the PNF improved functional throwing capabilities might not be surprising given the similarities in the PNF D2 flexion pattern and the overhand throwing motion. Both motions require reciprocal patterns of shoulder external rotation, abduction, and flexion (wind-up and cocking phases of throwing), followed rapidly by internal rotation, adduction, and extension (acceleration and deceleration phases of throwing). What may be more surprising is that PNF was as effective as isolated rotator-cuff
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BASIC PROCEDURE
Manual Contacts Many clinicians prefer to use PNF techniques throughout treatment because of their ability to manually guide and control movement. Manual control may be particularly important when certain ranges of motion need to be limited in the presence of healing tissue or pain. In postsurgical shoulder cases, the rehabilitation specialist should have a clear understanding of the progression of range-ofmotion (ROM) constraints for proper tissue healing. In the presence of muscle weakness, proper use of hand contacts can provide the patient with sensory cues that purportedly enhance neuromuscular control and eliminate, correct, or minimize substitution patterns. A lumbrical grip is usually a preferred method of applying manual contacts, particularly when resistance is required. Ideally, the clinician should touch only the surface of the area to be facilitated. Usually one manual contact is placed distally and one manual contact is placed proximally on a segment to facilitate distal-to-proximal movement.
Resistance Clinicians apply manual resistance to strengthen weak muscles in isolation or in functional patterns of movement. A common question is how much resistance is appropriate? A simple answer is that optimal resistance is defined as resistance that is graded appropriately for the intended movement.14 A rule of thumb is that optimal resistance should be the maximum resistance that results in a smooth, coordinated movement pattern. The clinician should remember when working with a movement pattern of the upper extremity, it is the quality of movement that is the desired outcome. Once a patient is
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smoothly and effortlessly moving his or her upper extremity, the clinician may choose to apply increased resistance to that pattern. Too much manual resistance applied too early can result in substitution patterns of movement, muscle juddering, loss of control, pain, and, at times, injury. To apply the proper amount of resistance, the clinician considers the patient’s age, general health, gender, comorbidities, stage of healing, the muscle performance deficits, and functional needs. Early in rehabilitation, clinicians often apply submaximal resistance to overcome muscle inhibition due to pain. In addition, submaximal resistance tends to recruit type 1 or slow twitch muscle fibers that facilitate stability and postural control.15 As strength and motor control improve, resistance can be applied maximally using concentric, eccentric, and isometric muscle contractions, or in combinations. Saliba and colleagues14 summarized the uses of appropriate resistance: to teach and increase awareness of a movement, to stimulate appropriate irradiation from strong to weak components, and to reinforce weak patterns by irradiation from strong patterns.
Traction and Approximation The use of joint traction (separation) and approximation (compressive forces) further stimulates facilitation of the desired response through the joint receptor system and can be used to protect healing tissue. Stimulation of these mechanoreceptors helps to signal the muscle for a response. This is critical in the shoulder for enhancing stability (approximation) and mobility (traction). For example, early application of manual approximation of the humerus into the glenoid fossa is used to facilitate co-contraction of the musculature in patients with multidirectional instability (MDI) in the glenohumeral joint.16 Conversely, the clinician may choose to provide tractive forces on the humerus during a diagonal pattern to protect a healing labrum in a patient with a superior labral anterior-posterior tear (SLAP lesion).
Quick Stretch Quick stretch is a neurophysiologic technique that is used to increase excitation to the muscle before a concentric contraction. The clinician applies a gentle quick nudge or tap to the muscle under tension to use the muscle’s stretch reflex for excitation of a specific movement response. The shoulder joint is taken into a position to apply a controlled manual stretch to all components of the movement. Often, in the presence of a patient presenting with muscle weakness throughout his or her ROM, I apply a consistent series of quick stretches to facilitate movement, an advantage that manually applied PNF has that is not offered by traditional muscle training.
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Verbal Commands Verbal communication further enhances the facilitation process by increasing muscle excitation. Directions to patients are also more clearly defined. Verbal tone might also be important to monitor, because it can serve an excitation role. An important consideration is the consistency of the verbal stimuli. The clinician should use the same simple understandable cues each time a movement is performed.
Visual Stimuli Visual cues and stimuli help the patient learn movement patterns more easily, coordinating the head, trunk, and extremities. During upper extremity diagonal patterns, early on, it is often useful for the clinician to encourage the patient to coordinate head movement with the extremity elevation to maintain visual contact. Eventually, however, the patient should be encouraged to perform movement patterns using only proprioceptive input by eliminating all visual cues.
Irradiation Conceptually, irradiation occurs at the level of the anterior horn cell and is the spread of facilitation with increased effort across muscles that work in synergy to produce a particular movement pattern. The practical application of irradiation occurs with the clinician’s judicious use of quick stretches and resistance. Typically, overflow is directly proportional to the amount of strength in the resisted muscle groups and the amount of resistance the clinician applies. The advantage of irradiation in a patient with shoulder weakness in the rotator cuff and deltoid muscles is to resist the stronger distal muscles around the elbow and the wrist and hand during a particular diagonal motion to reinforce the weaker proximal muscles. As in much PNF, the application of the right amount of resistance and quick stretch to produce the appropriate amount of irradiation is more art than not, so the clinician should practice these techniques but be careful to closely monitor the patient’s responses and modify the amount of resistance for the best results. The basic precept of “do no harm” should always guide treatment, particularly after surgery. If the clinician is not sure about the status of the healing tissue, the best advice is to err on the side of less resistance.
PATTERNS OF FACILITATION FOR THE UPPER EXTREMITIES This section describes the classic upper extremity and shoulder PNF patterns. The objective is for the interested reader to practice and master these patterns so as to be able to integrate and modify them for individual shoulder rehabilitation programs.
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Performance of PNF revolves around specific spiral and diagonal patterns that include three integrated mechanical motions: flexion and extension, abduction and adduction, and internal and external rotation. There are four shoulder patterns: flexion–abduction–external rotation, extension– adduction–internal rotation, flexion–adduction–external rotation, and extension–abduction–internal rotation.4 Classically, the patterns of movement are named by two different ways: either by diagonal (e.g., D1 flexion pattern) or, more simply, for the motion occurring at the proximal joint. Table 48-1 lists the components for the two upper extremity motions. Table 48-2 lists the classic scapular patterns. Initially, four isolated scapular diagonal patterns can be incorporated, including anterior elevation, posterior depression, and posterior elevation and anterior depression. Figures 48-1 through 48-8 illustrate the PNF patterns listed in the tables. Box 48-1 lists several strategies that should be used by clinicians to optimize their patients’ performances of PNF patterns.13 These strategies should be modified depending on the impairments and functional needs of a particular patient. For example, the sequencing of motions associated with normal timing is recruitment of the distal joint segments (such as the fingers, wrist, and hand) to proximal segments (elbow, glenohumeral joint, and scapulothoracic joint) of a freely moving multiple joint segment and proximal to distal with a fixed multiple joint segment. Changes in normal timing can be used, however, to emphasize a specific component of the movement pattern. For example, a clinician may choose to isolate glenohumeral joint external rotation at the beginning of the flexion–abduction– external rotation upper extremity D2 diagonal pattern. In the upper extremity, I recommend correcting proximal impairments before correcting distal impairments by working isolated scapular and glenohumeral patterns before commencing with entire upper-extremity diagonal patterns. In that way, the clinician restores scapular stability in preparation for exercising distal patterns. In additions to these strategies, the clinician should practice some of the basic PNF techniques.13 These techniques
require the clinician to control the patient’s muscular effort, movement patterns, and joint position. The patterns of movement are designed to rhythmically stimulate the agonist of the movement while causing relaxation of the antagonist.
Rhythmic Initiation The purpose of rhythmic initiation is to passively move a segment through a ROM to assess the available amount of motion and to help the patient learn a direction of motion that is supposedly normal. I use rhythmic initiation as a form of passive ROM and warm-up before active and active-resistive ROM. As rhythmic initiation progresses, the patient slowly assists the direction of movement through concentric muscle contractions.
Repeated Quick Stretch In repeated quick stretch, the therapist applies a stretch force to invoke a reflex to further stimulate muscular contraction. The stretch mechanism stimulates a response by the gamma system in the musculotendinous unit. This technique is helpful in cases of fatigue and specific areas of inhibition. Repeated quick stretch is useful as the patient progresses from rhythmic initiation to active and activeresistive concentric contractions.
Combination of Isotonics The use of concentric, eccentric, and maintained isotonic techniques facilitates control of movement. Combination of isotonics is a progression from rhythmic initiation and can be used throughout the available ROM of a particular segment.
Reversal of Antagonists Reversal of antagonists is crucial in normal function to allow a movement to occur without excessive resistance of the antagonistic muscle. The technique consists of reciprocal isometric (stabilizing reversal) or isotonic (isotonic reversal)
TABLE 48-1 Upper Extremity PNF Diagonal Patterns
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Glenohumeral Joint
Elbow
Forearm
Wrist
Fingers
D1 Flexion: Flexion, adduction, external rotation
Varies
Supination
Radial deviation
Flexion
D1 Extension: Extension, abduction, internal rotation
Varies
Pronation
Ulnar deviation
Extension
D2 Flexion: Flexion, abduction, external rotation
Varies
Supination
Radial deviation
Extension
D2 Extension: Extension, adduction, internal rotation
Varies
Pronation
Ulnar deviation
Flexion
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TABLE 48-2 Scapular Patterns
Relaxation Techniques
Exercise
Location
Motion
D1 Flexion
Scapula
Anterior elevation
D1 Extension
Scapula
Posterior depression
D2 Flexion
Scapula
Posterior elevation
D2 Extension
Scapula
Anterior depression
contractions through the desired ROM. The goal is to work on facilitation of the agonist and antagonist.
Rhythmic Stabilization Rhythmic stabilization employs isometric contractions of the agonist and antagonist muscles in different points of the ROM. Rhythmic stabilization results in a buildup of holding power around a joint. The patient must not be defeated with so much resistance that he or she finds it necessary to contract isotonically to recover or maintain position. The grading of resistance will be as accurate as the clinician’s ability to feel the patient’s response. Rhythmic stabilization is particularly useful with joint compression in the presence of MDI to facilitate co contractions and stabilization of the glenohumeral joint.
A
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Relaxation of synergistic muscle groups stimulates the agonist and inhibits the antagonist to increase ROM. Hold-relax, and contract-relax techniques are used to relax muscles that exhibit increased tone or increased passive resistance to elongation (stretch). Hold-relax should produce an isometric muscle contraction resulting in negligible movement of the targeted segment. During hold-relax, the clinician should take care to build up resistance slowly by telling the patient,“Give me what I give you.” Contractrelax produces a more abrupt contraction, and the clinician imparts enough force to move the segment, producing an eccentric contraction. I use hold-relax earlier in rehabilitation in the presence of pain and tissue healing. The amount of time to ask the patient to hold or contract varies from a few seconds to 10 seconds.
TECHNIQUES AND PROGRESSIONS The clinician faces several decisions about performing these patterns. These decisions are predicated on firmly establishing a physical therapy diagnosis that includes stage of healing, biomechanical constraints of surgery, nature and extent of impairments, functional losses, and functional needs to return to full activity.
B
Figure 48-1. Scapular anterior elevation. Purpose is to facilitate the D2 upper extremity flexion pattern by improving neuromuscular control of the scapula through strengthening the levator scapulae and serratus anterior muscles in a diagonal pattern. Concomitantly, this pattern stretches and elongates the rhomboids, latissmus dorsi, and lower trapezius muscles. A, The patient is placed side lying with the clinician standing behind the patient’s hips in the line of motion, facing the patient’s head. Both hands overlap on the anterior glenohumeral joint and acromion. B, The clinician gently takes up the slack, moving the scapula into a posterior depressed position (starting position), and applies a quick stretch. The patient anteriorly elevates the scapula against appropriate resistance. Movement is a diagonal arc up toward the patient’s nose.
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Figure 48-2. Scapular posterior depression. Purpose is to facilitate the D2 upper extremity extension pattern by improving neuromuscular control of the scapula through strengthening the rhomboids, lower trapezius, and latissimus dorsi muscles in a diagonal pattern. This pattern stretches and elongates the levator scapulae, upper trapezius, and serratus anterior muscles. A, The patient is placed side lying with the clinician standing behind the patient’s hips in the line of motion, facing the patient’s head. Both hands are flat palmed on the middle to lower scapulae, along the vertebral border. B, Movement is down to the ipsilateral ischial tuberosity.
Figure 48-3. Scapular posterior elevation. Purpose is to facilitate the D1 upper extremity flexion pattern by improving neuromuscular control of the scapula through strengthening the trapezius and levator scapula muscles in diagonal plane of the scapula. A, Client is side lying. The clinician stands at the client’s head, facing the hips. Manual contacts are placed on the distal edge of the upper trapezius, close to the acromion. B, Movement is an arc as the client shrugs up toward the ear.
A
B
A
B
Procedures for Shoulder Impairments and Functional Losses Patterns can be altered by choosing among unilateral or bilateral, symmetrical or asymmetrical, elbow straight or flexionextension, timing for emphasis, submaximal or maximal efforts, and full range or partial range of motion. For example, linear patterns instead of the classic diagonal patterns are sometimes necessary postoperatively when scapula and
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clavicle rotation produces pain at the rotator cuff, acromioclavicular joint, or capsular restraints. The use of linear patterns can also help when diagonal patterns are limited by soft tissue and myofascial restrictions secondary to chronic postural impairments. Shirley Sahrmann17 observed that clinically most movement impairment syndromes involving the shoulder arise
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Figure 48-4. Scapular anterior depression. Purpose is to facilitate the D1 upper extremity extension pattern by improving neuromuscular control of the scapula through strengthening the rhomboids and pectoralis minor and major muscles in the diagonal plane of the scapula. A, Client is side lying. The clinician stands at the client’s head, facing the hips. Manual contacts are placed on either side of the axilla, on the pectoral muscle and corocoid process anteriorly and on the lateral border of the scapula posteriorly. B, The patient pulls the shoulder down toward the umbilicus.
B
A
A
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B
Figure 48-5. Upper extremity flexion–adduction–external rotation (D1 flexion). This pattern facilitates the function of the upper extremity in reaching up and across the body while facilitating external rotation at the glenohumeral joint. This pattern is useful early in rehabilitation for initiating rotator cuff activities while minimizing the shear forces of the humeral head along the glenoid fossa produced by deltoid muscle activity. However, the clinician must be certain that the patient has adequate humeral head external rotation and scapular anterior elevation to avoid shoulder impingement at end range of flexion. A, The client lies supine with the shoulder in slight extension with the hand near the hip. The clinician stands at the client’s elbow, facing the feet. Distal manual contact on the palm provides most of the traction and rotatory control. Proximal contact can be on the biceps or the pectorals. B, The patient is told, “Turn and squeeze my hand then pull up and across your nose.”The clinician pivots toward the patient’s head as the arm moves past. The diagonal movement ends with the elbow crossing the midline around the nose.
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A
B
Figure 48-6. Upper extremity extension–abduction–internal rotation (D1 extension). This pattern facilitates the function of the upper extremity reaching down and back, similar to leaning back on the arm to support oneself while sitting. This technique is useful to activate the posterior deltoid muscle to counteract anterior shear forces of the humeral head in a patient with anterior glenohumeral joint instability. Other muscles activated during this pattern are the teres major, the latissimus dorsi, and the long head of the triceps. A, The patient lies supine. The clinician stands at the patient’s side near the head. The patient’s upper extremity is flexed and adducted. Manual contacts are placed along the dorsal surface of the hand (distal) and on the posterior surface of the humerus or scapula (proximal). B, A quick stretch, especially in the form of traction, can be applied simultaneously to the hand and shoulder. The patient is told, “Pull your wrist up and push your arm down to the side.” As the upper extremity moves past the clinician, traction can be switched to approximation to increase recruitment of the proximal muscles. The pattern ends with the wrist extended and the upper extremity at the patient’s hip.
from impairments in the timing and control of scapular motion. I have found it useful to begin most shoulder rehabilitation programs by focusing on restoring scapular control. It is particularly important to restore the counterbalancing forces of the muscles that attach to the scapula. Two muscles in particular—the serratus anterior and lower trapezius—seem to lose strength after surgery or immobilization. These muscles are critical to restore the correct force-couple mechanism to the scapula during overhead elevation. In particular, these muscles produce scapular outward rotation during upper extremity elevation. Early application of PNF can be applied in the classic side-lying position (see Figs. 48-1 to 48-4) immediately after surgery without fear of injuring healing tissue. The clinician can begin with rhythmic initiation to mediate losses of ROM and slowly progress to passive and active resistance, initially in limited ranges and progressively working the patterns into larger ROMs. Contract or hold-relax techniques are useful in producing reciprocal inhibition of shortened and tight antagonist muscles.18 Patients with the forward-head and rounded-shoulder posture often exhibit an abducted and elevated position of the scapulae. These patients exhibit elongation and weakness in
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their rhomboid, middle trapezius and lower trapezius muscles and shortening and tightness in their pectoralis major, levator scapulae, serratus anterior, and subscapularis muscles.17 Scapular adduction in prone (Fig. 48-9) and sitting (Fig. 48-10) can assist in correcting this type of upper quarter alignment. Resistance of the shoulder extensors at end range of the extension and abduction pattern can facilitate middle and lower trapezius activity via posterior depression of the scapula. The serratus anterior can be facilitated in several ways. Early in rehabilitation, scapular anterior depression with the patient side lying activates the lower and middle fibers of the serratus anterior, which are critical to produce outward rotation of the scapula during overhead elevation. Anterior elevation can help recruit the upper fibers of the serratus anterior, which contract along with the upper trapezius muscle to produce elevation and the upward portion of the scapular force-couple during overhead elevation. Input to the lower trapezius muscle can be initially facilitated using the pattern of posterior depression in a side-lying position. The clinician may also choose to exercise the serratus anterior as an abductor or protractor by resisting scapular abduction with a combination of
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A
647
B
Figure 48-7. Upper-extremity flexion–abduction– external rotation (D2 flexion). This pattern facilitates the functional movement of reaching up and out and helps to restore external rotation early in rehabilitation. To avoid potential subacromial impingement, the clinician should restore scapula posterior elevation before working toward the end range of flexion associated with this pattern. Because the movement of this pattern mimics the overhead throwing motion, clinicians use this pattern to promote muscle timing and recruitment during the functional stages of rehabilitation. A, The patient lies supine with the clinician standing at the patient’s shoulder facing the patient’s feet with a wide base of support in the diagonal of movement. The patient’s upper extremity starts from across the body in an elongated, extended position, with the elbow crossing the body near the hip. Distal manual contact is placed on the dorsal hand, and contact either on the proximal humerus or on the scapula emphasizes shoulder and scapular motion. B, The clinician takes the patient’s upper extremity to a fully elongated position, taking up all the slack in the muscle groups, and gently applies a quick stretch. The patient is told, “Pull your wrist up and reach.” The wrist completes extension before the other components.
A
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B
Figure 48-8. Upper-extremity extension–adduction–internal rotation (D2 extension). This pattern facilitates the movement of the upper extremity to move down and across the body and mimics the acceleration and deceleration phases of the overhead throwing motion. A, The patient lies supine while the clinician stands near the patient’s shoulder. The clinician applies distal manual contact palm to palm with the patient. The clinician applies proximal contact on the pectoral muscles to emphasize recruitment of the trunk and scapula or on the proximal humerus. B, The clinician applies initial elongation and a quick stretch. The patient is told, “Squeeze and turn your hand.” The clinician pivots slightly as the limb passes the clinician’s center of gravity. The pattern ends in shoulder extension, forearm pronation, with the elbow across the midline.
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BOX 48-1. Strategies to Enhance PNF Performance
Clinician’s Position • Faces the direction of motion • Shoulders and pelvis face the line of movement • Take up all the slack in all components of motion Patient’s Position • Close to the clinician • Starting position is one of optimal elongation Manual Contacts • Combinations of proximal and distal Quick Stretch • Use body weight, no arm strength • Nudge Move with the Patient • Clinician’s center of gravity must move • Distal component initiates motion When Performing Reversals • Change distal contact first
Figure 48-9. Prone scapular adduction with glenohumeral joint external rotation.
PNF, proprioceptive neuromuscular facilitation.
isotonic techniques at various angle positions (Figs. 48-11 and 48-12). As strength and healing improve, the patient can be instructed in performing a standard push-up with a plus with pronounced scapular protraction. When the patient has adequate strength and scapular and upperextremity control, the clinician can apply resistance to both upper extremities simultaneously with the patient supine to produce cross facilitation in shoulder elevation. This pattern produces posterior elevation of the scapulae as well as strength in the upper extremities in flexion, abduction, and external rotation. Bars of varying weights can offer resistance in addition to that provided by the clinician. While the clinician concentrates initially on restoring scapular control and movement, input to the rotator cuff can be increased by having the patient hold the shoulder isometrically at one point in the ROM while performing synergistic scapular movements. This is a particularly useful technique for the baseball pitcher. For example, scapular elevation patterns with the shoulder maintained in 90 degrees includes the deltoid and supraspinatus in the exercise pattern with the serratus anterior and the upper trapezius and levator scapulae muscles. The clinician can gauge improvement in rotator-cuff muscle control by watching for the onset of a lag sign (loss of shoulder external rotation) over exercise sessions. As rotator cuff muscle strength increases, the clinician can use combined isotonics and progress from
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Figure 48-10. Sitting scapular adduction with slight elevation.
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A
A
B
B
isometric and concentric contractions to eccentric contraction of the posterior cuff and deltoid muscles (Fig. 48-13). Rhythmic stabilization exercises can be used to facilitate rotator cuff and deltoid muscle activity during isometric contraction of the protracted scapula (Figs. 48-14 and 48-15). As adjuncts to the manual techniques, scapular exercises can be performed with dumbbells or elastic cords. Individual components of the scapula in throwing movements can be facilitated. After re-establishing normal scapular mobility, strength, and stability in this manner, the
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Figure 48-11. Resisted scapular abduction. A, Initiating scapular protraction with patient supine using quick stretch. B, End range of scapular protraction.
Figure 48-12. Resisted scapular abduction. A, Initiating scapular protraction with patient sitting using quick stretch. B, End range of scapular protraction.
scapula treatment can be integrated with treatment of the glenohumeral joint. Each exercise technique and pattern must have a specific goal, and the clinician must consider its effect on various structures (primarily the rotator cuff, capsuloligamentous stabilizers, acromioclavicular joint, and the upper quarter of the body). The flexion–abduction–external rotation and extension–adduction–internal rotation diagonals are the most commonly used PNF diagonals for the overhead
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Figure 48-13. Resisted external rotation with scapular patterns.
Figure 48-15. Rhythmic stabilization of the upper extremity with isometric scapular protraction (patient sitting).
athlete because they mimic the throwing motion. Resistance to external rotation motion in the flexion–abduction– external rotation pattern can be modified to be isometric as well as isotonic. This is especially important in cases of infraspinatus tendinitis or partial tears in which overload must be avoided. Full glenohumeral elevation can create subacromial impingement of the rotator cuff against the coracoacromial arch. Predictably, this leads to far greater problems than it solves, especially in patients with partial or full rotator cuff tears, history of classic impingement syndrome, and encroachment of the supraspinatus outlet secondary to acromial morphology or bony changes. When applied appropriately, this pattern can be extremely useful in facilitating the shoulder elevators. Supine, prone, or upright positioning of the patient can be used as well as bilateral and asymmetrical techniques. Slight modification of this pattern can put the patient in an elevation and planeof-scapula movement, which is also very effective and usually less stressful to the rotator cuff than beginning from an adducted position. Bilateral techniques for cross facilitation and positioning the glenohumeral joint in midranges from a supine position are good starting points for scapula and rotator cuff stabilization in elevation. Figure 48-14. Rhythmic stabilization of the upper extremity with isometric scapular protraction (patient supine).
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Extension–adduction–internal rotation is the diagonal pattern opposite to flexion–abduction–external rotation. It has mechanical characteristics similar to the acceleration, follow-through, and deceleration phases of throwing. Again, as in flexion and abduction, this pattern is excellent
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for subscapularis facilitation in conjunction with other glenohumeral components. Patients with posterior shoulder instabilities must be monitored carefully to avoid subluxation and overloading of the capsuloligamentous restraints. Supine, standing, and sitting positions may also be used for this exercise. In the throwing athlete, the flexion–adduction–external rotation and extension–abduction–internal rotation are more important for the glove or nonthrowing side because that extremity functions opposite to the throwing side. Endrange flexion and adduction can produce overcompression or repetitive microtrauma at the acromioclavicular joint. The end range of extension and abduction resisted in an upright position with trunk rotation can assist in facilitation of the posterior glenohumeral, scapular adductor and depressor, and trunk rotator muscle groups used during the course of the throwing motion. From this same position, reciprocal shoulder flexion and extension motions can be facilitated with concentric and eccentric techniques through an appropriate ROM synergistically with trunk rotation. Facilitation of the shoulder rotators in isolated patterns is extremely important because the rotator cuff muscles are directly affected. Initially, the shoulder is positioned slightly abducted in the plane of the scapula (approximately 30 degrees of forward flexion at 70 degrees of abduction) (Fig. 48-16). This position has been shown by
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Greenfield and colleagues19 to be optimal for rotational strengthening over the more traditional neutral arm at the side position. Similarly, the shoulder can be manually resisted for both internal and external rotation at 90 degrees of abduction. This position is associated with anterior instability and is used for strengthening the subscapularis as described in many rehabilitation programs with various exercise devices (free weights, tubing, mechanical weights). External rotation in this position is associated with cocking phases of throwing and can be important for facilitation of the posterior rotator cuff. Maximal external rotation at 90 degrees of abduction, however, stresses the inferior glenohumeral ligament complex, which is the main restraint to anterior instability and is often associated with patient apprehension. External rotation at 90 degrees of flexion is a component of the flexion and abduction diagonal. Flexion and abduction is isometrically resisted at 90 degrees of flexion while working isotonically in external rotation. Maximal internal rotation ROM will impinge the rotator cuff against the coracoacromial arch and is a contraindication. Over-resistance to a weak external rotator group should also be avoided. Infraspinatus and teres minor strengthening in this pattern is an effective technique for the posterior subluxation patient when applied correctly.
Trunk and Neck Patterns Patterns that include the upper extremities with the trunk and neck provide a higher functional level of neuromuscular training and movement re-education. These procedures, however, demand a higher degree of skill on the part of clinician and patient. Normal functional activity includes whole body involvement, making this type of treatment pattern very valuable in rehabilitation programs.
Adjunctive Procedures The principles and specific techniques presented may be enhanced by using more effective exercise devices as well as manual techniques. On the market today are a variety of elastic cords, weights, resistive exercise machines, and other equipment that can be modified for rehabilitation of the shoulder patient (Figs. 48-17 and 48-18). Plyometric exercise activities can also be applied in diagonal patterns and other components of shoulder complex motion. The goals of adding resistance are to build strength, endurance, stabilization, and coordination at higher velocities, which are considered more functional.
CASE STUDY Figure 48-16. Isolated upper shoulder external rotation in the plane of the scapula.
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A 19-year old male competitive football quarterback presented on referral from his orthopedist with a diagnosis of secondary impingement to his dominant (right) shoulder.
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A
A
B
B
He reported anterior shoulder pain during the cocking and acceleration phases of throwing. Examination indicated that the right scapular was in a downwardly rotated position compared with the left. Repetitive overhead elevation indicated increased winging of the medial border of both scapulae. The inferior angle of the scapula did not reach the axillary midline of the chest
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Figure 48-17. D2 flexion and abduction pattern with the use of a Theraband. A, Beginning position. B, Ending position.
Figure 48-18. Shoulder external rotation in the 90/90 position. A, Beginning position. B, Ending position.
with full overhead elevation. Manual active assist for scapular upward rotation applied during overhead elevation eliminated much of the right shoulder pain. The full can test recommended by Itio and colleagues20 to isolate the supraspinatus indicated pain and weakness. Both the Neer and Hawkins-Kennedy impingement tests were positive.21 The Jobe subluxation-relocation test was positive for anterior shoulder pain.22
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The manual muscle test (MMT) indicated the following: serratus anterior, 3⫹/5; lower trapezius, 4/5; middle trapezius, 4/5; teres minor and infraspinatus, 4/5.
Assessment The patient presented with occult subluxation that contributed to overuse and impingement of the supraspinatus tendon. Primary impairments contributing to his pathology included reduced upward scapular rotation during elevation and concomitant muscle weakness. The initial goals of treatment were to reduce pain and inflammation at the tendinous insertion of the supraspinatus muscle; to improve scapular control, including upward scapular rotation during overhead elevation, by increasing muscle strength and control of the serratus anterior, lower trapezius, and middle trapezius muscles; and to improve dynamic stability of the glenohumeral joint by increasing muscle strength and control of the supraspinatus, infraspinatus, and teres minor muscles.
Intervention The patient was directed to apply ice to the affected shoulder. PNF was initiated. The PNF pattern of anterior elevation and posterior depression and posterior elevation and anterior depression of the right scapula began with the patient side lying. The clinician began with rhythmic initiation and progressed to slow reversals, emphasizing concentric activity of muscles. Quick stretches were used throughout the ROM to facilitate muscle activity. The clinician used no set recommended number of repetitions but gauged the number of repetitions based on the patient’s fatigue and ability to produce a smooth coordinated contraction. Isolated manual scapular protraction in supine and sitting was instituted. The patient performed isolated external rotation in the plane of the scapula using isometrics in various points in the range followed by concentric and then eccentric contractions (combined isotonics). The patient progressed to isolated external and internal rotation in prone and standing positions using combined isotonics in pain-free ranges. The home program included corrective taping for downward rotation, various scapular exercises including shoulder pinches (scapular retraction) and wall push-ups with a plus, and isolated rotator cuff strengthening in a side-lying position using a 1-lb weight to fatigue.
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Clinic treatment continued with manually resisted PNF patterns, progressing to unilateral full-range D2 flexion and extension for the right upper extremity, using combination isotonics. Standing activities were introduced, including PNF D2 flexion and extension diagonals and 90/90 external rotation using a Theraband to produce concentric and eccentric contractions. Treatment was supplemented with highspeed isokinetic training for external and internal rotation. The home program consisted of various exercises for the rotator cuff muscles and scapular muscles, emphasizing light weights (⬍5 lbs) with high repetitions to produce muscle fatigue. Two Weeks after Initial Examination After 2 weeks of intervention, examination indicated painfree ROM in the right upper extremity and improving strength. All provocation tests for impingement were negative. Functionally, the patient reported that he had begun throwing the football without pain. The goals at this time were to continue to strengthen the rotator cuff and scapular muscles and progress functional training to the right upper extremity (see Chapter 50).
SUMMARY The specific techniques of PNF combining diagonal patterns with facilitatory and inhibitory input using manual contact makes this approach extremely useful for rehabilitating the shoulder. Selected techniques that are modified to limit range and resistance appropriately facilitate muscle activity early in rehabilitation while protecting healing tissue and controlling pain. The clinician can slowly elicit different muscle contractions combined with more complex movement patterns as pain and tissue healing improve. Integrated upper-extremity diagonal patterns in different positions are particularly useful to restore the motor needs for the throwing athlete.
ACKNOWLEDGMENT The author would like to acknowledge the late Robert P. Engle, PT, ATC. I incorporated sections of his chapter “Proprioceptive Neuromuscular Facilitation for the Shoulder,” which appeared in the first edition, for this updated chapter. His expertise in the application of PNF for the athlete was well recognized and highly respected by many members of the orthopedics and sports rehabilitation communities.
Progression
References
One Week after Initial Treatment At the time of re-examination, the patient presented with pain-free active overhead elevation of his right upper extremity with improving strength in all muscles to 4/5 ranges.
1. Perry J: Muscle control of the shoulder. In Rowe C (ed): The shoulder. New York, Churchill Livingstone, 1988. 2. Davies G, Dickoff-Hoffman S: Neuromuscular testing and rehabilitation of the shoulder complex. J Orthop Sports Phys Ther 18:449-458, 1993.
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3. Lephart SM, Pincivero DM, Giraldo JL, Fu FH: The role of proprioception in the management and rehabilitation of athletic injuries. Am J Sports Med 25(1):130-137, 1997. 4. Voss DE, Ionta MK, Myers BJ: Proprioceptive Neuromuscular Facilitation, 3rd ed. Philadelphia, Harper and Row, 1985. 5. Knott M, Voss DE: Proprioceptive Neuromuscular Facilitation. New York, Harper and Row, 1968. 6. Shumway-Cook A, Woollacott MH: Motor Control: Theory and Practical Applications, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 2001. 7. Kabat H: Central mechanisms for recovery of neuromuscular function. Science 112:23-24, 1950. 8. Gordon J, Ghez C: Muscle receptors and spinal reflexes: The stretch reflex. In Kandel E, Schwartz JH, Jessel TM (eds): Principles of Neural Science. New York, Elsevier, pp 564-580. 9. Minaki Y, Yamashita T, Takebayashi T, Ishii S: Mechanosensitive afferent units in the shoulder and adjacent tissues. Clin Orthop Relat Res (369):349-356, 1999. 10. Surburg PR, Schrader JW: Proprioceptive neuromuscular facilitation techniques in sports medicine: A reassesment. J Athletic Train 32(1):34-39, 1997. 11. Surburg PR: The effect of proprioceptive facilitation patterning upon reaction, response, and movement times. Phys Ther 57(5):513-517, 1977. 12. Padua D, Guskiewicz KM, Prentice WE, et al: The effect of select shoulder exercises on strength, active angle reproduction, single-arm balance, and functional performance. J Sport Rehabil 13:75-95, 2004. 13. Stalvey MH: Proprioceptive neuromuscular facilitation. In Bandy W, Sanders, B (eds): Therapeutic Exercise: Techniques for Intervention. Philadelphia, Lippincott Williams & Wilkins, 2001, pp 145-177.
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14. Saliba V, Johnson GS, Wardlaw C. Proprioceptive neuromuscular facilitation. In Basmajian JV, Nyberg RE (eds): Rational Manual Therapies. Baltimore, Williams & Wilkins, 1983, pp 243–285. 15. Milner-Brown H, Stein RB, Yemm R: The contractile properties of human motor units during voluntary isometric contraction. J Physiol (London) 228:285-306, 1973. 16. Lephart SM, Warner JP, Borsa PA, Fu FH: Proprioception of the unstable shoulder joint in healthy, unstable and surgically repaired shoulders. J Shoulder Elbow Surg 3: 371-380, 1994. 17. Sahrmann S: Diagnosis and Treatment of Movement Impairments. St. Louis, Mosby, 2002. 18. Sherrington C: Integrative activity of the nervous system. New Haven, Yale University Press, 1960. 19. Greenfield BH, Donatelli R, Wooden MJ, Wilkes J: Isokinetic evaluation of shoulder rotational strength between the plane of scapula and the frontal plane. Am J Sports Med 18(2):124-128, 1990. 20. Itoi E, Kido T, Sano A, et al: Which is more useful, the “full can test” or the “empty can test,” in detecting the torn supraspinatus tendon? Am J Sports Med 27(1):65-68, 1999. 21. Tennent T, Beach WR, Meyers, JF: Current concepts: Clinical sports medicine update: A review of the special tests associated with shoulder examination Part I: The rotator cuff tests. Am J Sports Med 31:154-160, 2003. 22. Tennent T, Beach WR, Meyers, JF: Current concepts: Clinical sports medicine update. A review of the special tests associated with shoulder examination. Part II: Laxity, instability, and superior labral anterior and posterior (SLAP) lesions. Am J Sports Med 31:301-307, 2003.
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CHAPTER 49 Sensorimotor Contribution
to Shoulder Joint Stability Joseph B. Myers, Craig A. Wassinger, and Scott M. Lephart
Glenohumeral joint stability is provided by both mechanical and dynamic restraints that result in the humeral head remaining or promptly returning to proper alignment within the glenoid fossa through an equalization of forces.1 Functional joint stability is defined as maintaining joint stability during body movements and results from the complementary interaction between the mechanical and dynamic restraints. As separate entities, neither the mechanical nor dynamic restraints can effectively act alone in providing functional joint stability.
contractile muscles responses vital to coordinated movement patterns and joint stability.3
Proprioception Proprioception is defined as the afferent information, arising from peripheral areas of the body (including the mechanical and dynamic restraints about the shoulder) that contributes to joint stability, postural control, and motor control.1-3 Proprioception has three submodalities: joint position sense, kinesthesia, and sensation of force.1,2 Joint position sense is the appreciation and interpretation of information concerning joint position and orientation in space.4 Kinesthesia is the ability to appreciate and interpret joint motions.4 Sensation of force is the ability to appreciate and interpret force applied to or generated within a joint.4 The CNS uses all of this proprioceptive information collectively to elicit appropriate neuromuscular control over the shoulder musculature that is important for joint stability and coordinated movement of the shoulder complex.
The necessary interaction between mechanical and dynamic restraint is mediated by the sensorimotor system. The purpose of this chapter is to describe the sensorimotor system and how proprioception and neuromuscular control mediate functional joint stability of the shoulder, describe how the sensorimotor system is altered with shoulder injury, and provide evidence regarding the effect of treatment (both surgical and conservative) in restoring the sensorimotor mechanisms responsible for functional joint stability.
Proprioceptive information originates at the level of the mechanoreceptor. Mechanoreceptors are sensory neurons or peripheral afferents present within muscle, tendons, fascia, joint capsule, ligaments, and skin about a joint.5-7 Mechanoreceptors are mechanically sensitive and transduce mechanical tissue deformation into frequency-modulated neural signals that travel to the CNS through afferent sensory pathways.5 Deformation of the tissues causes a mechanically gated release of stored sodium from the mechanoreceptors, eliciting an action potential.8 An increase in tissue deformation causes an increase in action potentials, thereby increasing neural input to the CNS.5,8 The mechanoreceptors responsible for proprioception include Pacinian corpuscles, Ruffini endings, Golgi-tendon like organs, Merkel discs, Messner corpuscles, Golgi-tendon organs, and muscle spindles.
COMPONENTS OF SHOULDER STABILITY Although a majority of this chapter focuses on the dynamic restraint components associated with functional shoulder stability, an outline of the mechanical restraints is necessary given the role that these structures play in influencing dynamic stability. The roles mechanical and dynamic restraints play are often discussed as separate processes, yet they must work synergistically to maintain joint stability. The mechanical restraints include osseous geometry, negative intra-articular pressure, the glenoid labrum, tenomuscular structures, and capsuloligamentous restraints. These are described at length elsewhere in this book. Dynamic restraint results from neuromuscular control over the shoulder muscles. This neuromuscular control is facilitated by the sensorimotor system. The sensorimotor system is defined as all of the sensory, motor, and central integration and processing components involved in maintaining joint stability (Fig. 49-1).1,2 Sensory information (proprioception) travels from the shoulder joint through afferent pathways to the central nervous system (CNS), where it is processed and integrated with input from other levels of the nervous system (central processing), eliciting
Type I Ruffini endings are clustered, encapsulated endings that are slow adapting and have a low threshold to mechanical stress.9 The Ruffini endings are believed to provide information concerning static joint position, intra-articular pressure, joint-limit detection, and amplitude and velocity of joint rotation.5,10 Histologic studies have demonstrated that Ruffini endings are present within the subacromial bursa, glenohumeral ligaments, and the shoulder capsule.7,11-14 Pacinian corpuscles are dispersed throughout 655
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Central nervous system
Neuromuscular control
Voluntary motor commands
Proprioception
Proprioception
Vestibular and visual input
Dynamic restraints
Mechanical restraints
Shoulder functional joint stability Figure 49-1. The contribution of the mechanical and dynamic restraints to functional joint stability and how the sensorimotor system mediates their interaction.
articular tissues. Type II Pacinian corpuscles are encapsulated conical corpuscles9,15 present within the glenohumeral ligaments of the shoulder.7,11 Pacinian corpuscles are characterized as low threshold and fast adapting, and they are sensitive to joint acceleration and deceleration.16,17 Golgi-tendon organs are thin, encapsulated, fusiform corpuscles, characterized as slow adapting with a high threshold to mechanical deformation.18,19 These receptors contribute to direction of motion and joint position.20,21 Golgi-tendon organs are present within the glenohumeral ligaments of the shoulder.22 Unlike the mechanoreceptors just described, the mechanoreceptors present within the cutaneous portion of a joint provide information exclusively about external events (externoreceptors) that affect the joint.15 These receptors provide afferent information regarding an organism’s interactions with the environment. There are four types of mechanoreceptors in the skin. Merkel discs and Meissner corpuscles are located in the superficial layers. Merkel discs are quick-adapting receptors sensitive to tissue compression. Like Merkel discs, Meissner corpuscles are also sensitive to local pressure but are slow adapting, allowing for maintenance of pressure sensitivity.15 Deep to the Merkel and Meissner receptors within cutaneous structures are the Ruffini and Pacinian receptors. The Ruffini endings are sensitive to unidirectional skin stretch and the Pacinian receptors are sensitive to rapid tissue movements.15,23 Embedded within the collagen of the musculotendinous junction are Golgi tendon organs (GTOs). These lowthreshold, dynamically sensitive receptors signal tension development within the musculotendinous structure, especially under active contraction conditions.24 In addition, stimulation of the GTOs elicits relaxation of the agonist muscle groups being stretched and contraction of their antagonist muscle groups.9
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The intrafusal muscle spindle lies parallel to the extrafusal contractile elements of muscle.9 Because the intrafusal muscle spindles are innervated by gamma motor neurons and the extrafusal contractile elements are innervated by alpha motor neurons, muscle spindle sensitivity is adjusted during the entire range of motion, continuously signaling both the changes in muscle length and rate of length changes.9,23 Afferent proprioceptive information originating from musculotendinous, capsuloligamentous, and cutaneous receptors is integrated with messages descending from higher levels of the CNS at the fusimotor neurons influencing the muscle spindle.16,25-27 An adjustment is made to all incoming input, where a single composite signal is passed from the muscle spindle to the CNS and directly to the alpha motor neurons of the muscle.25,26,28 The adjustment mechanism is termed the final common input hypothesis.26 This final outcome of this proprioceptive input to the CNS results in joint movement and position sense, reflexive muscle contraction, and regulation of muscle stiffness.23,25,29 Because the capsuloligamentous and cutaneous afferents influence the muscle spindle, it appears that musculotendinous, capsuloligamentous, and cutaneous mechanoreceptors play a complementary role in providing proprioceptive input to the CNS.25
Central Nervous System Processing The proprioceptive information provided by the mechanoreceptors is processed at three distinct levels of motor control within the CNS. Those levels of motor control include the spinal level, the brain stem, and cerebellum and higher levels of the CNS such as the cerebral cortex.20,23,30,31 Each level provides unique neural control over the muscles about the shoulder joint vital to joint stability. Neural control is later referred to as neuromuscular control. The first level of processing is at the spinal cord. The spinal cord is a primitive but powerful mechanism for rapid tactical responses to a wide range of inputs.32 Afferent information from the periphery travels to the spinal cord, where it enters through the dorsal roots.33 From the dorsal root, the afferent information can be transmitted through several pathways. First, the afferent information can bifurcate directly with alpha motor neurons.33,34 This bifurcation leads to a reflexive response by the musculature innervated by the alpha motor neuron.9,33,34 Given that the afferent neuron synapses directly with the efferent motor neuron, this reflex is termed monosynaptic.34 An example of this type of reflex is the stretch reflex. Stretching of a muscle stimulates the muscle spindle, which in turn provides afferent information that synapses with the alpha motor neuron of the stretched muscle, stimulating reflexive muscle contraction. Afferent information from the periphery, either from the muscle or joint, can also connect with the alpha motor neuron through interneurons.33 Interneurons also receive information from descending CNS pathways and project directly or indirectly with motor nuclei.32 Upon arrival, the afferent
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neuron synapses with an interneuron, and that interneuron then synapses with the alpha motor neuron. The result is a polysynaptic (more than one synapse) reflex.34 The information from proprioceptive afferents, as well as descending information from higher centers, also affects the gamma motor system.16,25-28,33,35,36 The gamma motor system plays a significant role in reflexive muscle activity and muscle stiffness. The role that reflexive activity and muscle stiffness plays in joint stability is described in subsequent sections. Afferent information is also transported to the second level of motor control, higher in the CNS, by ascending tracts. Information from the periphery travels up the dorsal and spinocerebellar tracts. From a joint-stability perspective, the spinocerebellar tract seems more likely to provide supraspinal control over dynamic restraints.3 Information from the periphery arrives at the cerebellum through both the dorsal and ventral spinocerebellar tracts.37 The dorsal spinocerebellar tract provides information concerning joint position, rate of change in joint movement, tension of muscle, and forces acting on the musculoskeletal system.37 Information concerning the actual motor sequences is transported up the ventral spinocerebellar tract.37 Working entirely subconsciously, the cerebellum has an essential role in planning and modifying motor activities by comparing the intended movement with the outcome movement.3,15,33,38,39 The cerebellum is involved with the timing of motor activity and adjusts decisions made via the motor cortex by deciding on the best plan of action for the desired movement.33 The cerebellum assists the motor cortex in planning the next movement while a simultaneous movement is occurring, allowing smooth movement transition. It can produce more efficient movement patterns resulting from lessons learned from previous errors.33 The cerebellum is divided into three functional areas.37 The first division, the vestibulocerebellum, is primarily responsible for controlling the axial muscles largely concerned with postural equilibrium. The second division, the cerebrocerebellum, is mainly involved with the planning and initiating movements requiring precise and rapid dexterous limb movements.37,38 The third division, the spinocerebellum, receives afferent information from the somatosensory, visual, and vestibular systems.37 The output from the spinocerebellum serves to adjust ongoing movements through influential connections with the brain stem and motor cortex. Additionally, this division of the cerebellum uses somatosensory inputs for the feedback regulation of muscle tone through control of gamma motor neuron drive to the muscle spindles.3,26,38-40 At the brain stem, information from the periphery is integrated with information from both the visual and vestibular centers to control automatic and stereotypic movement patterns as well as modulating balance and posture.20,23
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The third level of motor control is the higher regions of the CNS such as the cerebral cortex. Tibone and colleagues41 demonstrated an afferent pathway from the mechanoreceptors present in the joint capsule to the cerebral cortex using somatosensory evoked potentials. Evidence of this pathway indicates that conscious awareness of proprioception can occur at the cortical level. At this level, proprioceptive information is integrated and plays a role in voluntary movements that are stored as central commands for later movements.42 The cortical level initiates and modulates complex and discrete movements and organizes and prepares motor commands.33 Motor programs initiated from the motor cortex are transmitted directly to the spinal cord through the corticospinal tracts (pyramidal tracts), where they eventually terminate at interneurons. This allows higher centers to influence the spinal reflexes by affecting the gamma motor neurons as well as eliciting the desired movement patterns through excitation of the alpha motor neurons.33 This control by the higher systems of the CNS permits some level of control over the dynamic restraints that cross the joint, thereby affecting joint stability.
Neuromuscular Control The processing of proprioceptive information by the CNS results in neuromuscular control over the dynamic restraints about the shoulder. Neuromuscular control is defined as the subconscious activation of the dynamic restraints in preparation for and in response to joint motion and loading for the purpose of maintaining joint stability.4 Neuromusclar control over the dynamic restraints, independent of the motor control level, can be considered to occur in both feedforward and feedback manners. Feedforward controls are the anticipatory actions occurring on the identification of the beginning, as well as the effects, of an impending event or stimulus, whereas feedback controls describe the actions occurring in direct response to sensory detection of effects from the arrival of the event or stimuli.26,39,40 Open- and closed-loop processes affect both control of dynamic restraints and movement. In a closed-loop system, there is ongoing input concerning the state of movement, whereas an open-loop system works without such input.43,44 Because both feedforward and feedback mechanisms rely on proprioceptive input either as identification of an impending stimulus or as a direct response to sensory detection, both are considered closed-loop systems. Feedforward and feedback control have unique, but interrelated, roles in control over the dynamic restraints. The neuromuscular control mechanisms responsible for shoulder stability include co-activation of the shoulder musculature and resulting force couples, muscle reflexes, and regulation of muscle stiffness.4,45 Due to the insertion point of the rotator cuff musculature attaching on the humerus, these muscles collectively act as compressors of the humeral head into the glenoid fossa through the action of force couples.46 Co-activation of the
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rotator cuff muscles at the shoulder joint is vital to dynamic stabilization. Inman and colleagues47 first described force couples providing joint stability. Contraction of the subscapularis counteracts contraction of the infraspinatus and teres minor in the frontal plane, and contraction of the deltoid counteracts contraction of the lower rotator cuff muscles (infraspinatus, teres minor, and subscapularis) in the transverse plane.47 These force couples are believed to produce joint compression, which in turn increases congruency of the articulating surfaces.30 The rotator cuff is essential for dynamic stability by centralizing the humeral head within the glenoid fossa, thus preventing excessive humeral translation.48 Wilk and colleagues49 refer to the resulting vector forces that stabilize the humeral head within the glenoid as a “balance of forces.”This balance of forces suggests that there is coordinated synergistic action of all glenohumeral musculature, providing joint stability. When those forces are not properly balanced or equalized, abnormal glenohumeral mechanics and glenohumeral instability can result.49 Cadaveric models have been used extensively to assess the contribution of muscle force for maintaining glenohumeral stability and function. Halder and colleagues50 demonstrated that the infraspinatus and subscapularis have a humeral head depressor function, thus providing superior glenohumeral stability. Interestingly, the inferior portion of the subscapularis is the more effective humeral head depressor.50 Similar results demonstrating the importance of the subscapularis-infraspinatus force couple were reported by Thompson and colleagues51 and Parsons and colleagues.52 Through selective sectioning of the cuff tendons, significant alterations in joint stability were reported only when the infraspinatus or subscapularis was disrupted. Very little disruption of humeral motion was appreciated when the supraspinatus was lesioned.51 Like Thompson and colleagues,51 Halder and colleagues53 demonstrated that the inferior stabilizing effect of the supraspinatus is minimal. These results suggest that the transverse force couple (subscapularis–infraspinatus–teres minor) is more important for stability. Others have demonstrated that all muscles of the rotator cuff are equally important rather than just the transverse force couple in maintaining concavity-compression.54-61 In addition to the synergistic action of glenohumeral musculature, the common insertion of the rotator cuff tendons within the joint capsule provides an element of dynamic capsular tension. As the cuff muscles simultaneously contract, the forces generated in their tendinous insertion applies tension to the joint capsule.62-64 This increased capsular tension aids in drawing the humeral head into the glenoid fossa, supplementing joint stability. In addition to the rotator cuff, numerous studies have also demonstrated that the biceps brachii plays a vital role as a humeral head depressor within the glenohumeral joint.50,65-69
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Muscle reflexes also play an essential role in dynamic stability of the shoulder. Several investigators have demonstrated that a reflex loop exists between the joint capsule and the musculature surrounding the feline glenohumeral joint using electrical stimulation of the joint capsule.11,70,71 Jerosch and coworkers72 arthroscopically demonstrated that a similar reflex arc exists between the shoulder capsule and the deltoid, trapezius, pectoralis major, and rotator cuff musculature in the human shoulder. These results demonstrated the presence of a ligament-muscular reflex between the mechanical restraints and dynamic restraints of the shoulder. Several investigators have studied the reflexive mechanism at the shoulder joint in vivo. Brindle and colleagues73 measured latent muscle reaction time between trained (baseball pitchers) and untrained subjects during ballistic internal rotation perturbations. The researchers demonstrated that shorter latencies were present in the supraspinatus and posterior deltoid, leading to altered deceleration, which in turn resulted in faster pitching velocities. Latimer and coworkers74 measured muscle latencies of the shoulder resulting from an anterior translation force. Their results demonstrated that on average, the anterior deltoid was the first to fire (110 msec). Overall, when an apprehension perturbation similar to a shoulder dislocation-subluxation injury mechanism is applied to the shoulder, the anterior muscles fired first followed by the posterior muscles. The authors concluded that the reflexive actions might be too slow and too short to protect the joint in a traumatic instability episode because the shortest latency was approximately 110 msec. Our laboratory assessed shoulder muscle reflex latencies of the shoulder and demonstrated significantly shortened muscle reflex latencies (latencies of approximately 75 msec) when muscle was preactivated.75 The results suggest that if muscle preactivation levels can be increased (possibly through rehabilitation), the resulting reflexes can be much faster, possibly assisting with joint stability. Traditionally, the ligament-muscular reflex research has centered around the alpha motor neuron being the efferent path to the muscle. Although these afferent alpha motor neuron reflexes do exist, another plausible role of shoulder reflexes is the gamma motor–muscle spindle system, specifically how reflexes influence muscle stiffness and ultimately joint stability.26,35,76,77 As humans interact with the environment, they constantly experience forces acting on the body.78 To interact successfully, the joint must have enough stiffness to counteract and coexist with forces encountered.78,79 From an engineering perspective, stiffness is calculated as the change in force divided by the change in length80-82 or angular rotation displacement.83,84 From a musculoskeletal perspective, joint stiffness is defined as resistance provided by tissue, joint, or limb to a change in shape and position.85 Ultimately, joint stiffness provides the first line of defense for joint stability when force is applied to the joint.78,79,82,86-88 It provides an
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immediate and substantial response to perturbation and decreases the latency of the reflexive response, thus improving joint stability.32 The stiffness provided by the muscles about the shoulder plays a substantial role in how effectively external forces imposed on the musculoskeletal system are transmitted.89 Muscle stiffness is strongly influenced by the level of contraction present.90 As muscle contraction increases, so does stiffness.78,91-94 Louie and Mote95 demonstrated that eliciting muscle contraction increased joint stiffness by as much as 314%. Olmstead and colleagues96 reported an increase of 200% to 250% from increased muscle contraction. Muscle contraction creates stable cross bridges that resist stretch, thereby resisting a perturbing episode to the joint.97,98 Mechanoreceptors play a significant role in regulating muscle stiffness. The muscle spindle system contributes to preprogramming muscle stiffness.77 Ligament mechanoreceptors can also regulate stiffness by heightening muscle spindle sensitivity via increased gamma motor neuron excitation, which influences both the amount of muscle stiffness and quickens the stiffness achieved from reflexive muscle activation.26,27,35,76,77,99
SENSORIMOTOR ALTERATIONS WITH SHOULDER INJURY Lephart and Henry30 presented a shoulder functional joint stability paradigm illustrating the cyclic role that joint injury plays on functional joint stability (Fig. 49-2). Injury to the stabilizing structures (capsuloligamentous and musculotendinous), whether caused by a traumatic or an atraumatic mechanism, can compromise stability of the shoulder joint. Accompanying the disruption of the mechanical stabilizing structures is decreased capsuloligamentousmusculotendinous mechanoreceptor stimulation, thus
Shoulder injury
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Proprioception alterations
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Functional instability Figure 49-2. Mechanism of shoulder joint injury.
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altering the sensorimotor contributions to joint stability. The combination of mechanical deficiency and sensorimotor alterations contributes to deficits in functional joint stability. Ultimately, these deficiencies can contribute to reinjury patterns often seen at the shoulder joint.
Proprioception Alterations Several studies have shown that instability at the shoulder has deleterious effects on proprioception.100-103 Joint position sense and kinesthesia are altered in patients with glenohumeral instability.100-103 Accompanying the disruption of the mechanical stabilizing structures is decreased capsuloligamentous mechanoreceptor stimulation resulting from tissue deafferentation or the increased tissue laxity limiting mechanoreceptor stimulation, thus decreasing proprioception.30,41 Barden and colleagues100 demonstrated errors bilaterally in joint position sense in subjects exhibiting unilateral instability. These results suggest that alterations in the central processing mechanisms may also be present. Proprioceptive deficits have also been identified in patients with osteoarthritis.104 Proprioceptive deficits were attributed to decreases in shoulder muscle activity levels combined with local muscle atrophy.104 Additionally, the increased afferent signals sent by pain receptors about the shoulder were believed to override and subsequently decrease proprioception afferents. The work by Safran and colleagues105 supports the role of pain in adversely affecting proprioception. These results demonstrated that baseball players with shoulder pain have decreased proprioception most likely due to increased nociceptor activity in the painful shoulder.105 Subacromial impingement has also been linked to proprioceptive deficits. Machner and coworkers106 demonstrated decreased kinesthesia in subjects with unilateral stage II subacromial impingement. The authors theorized that the subacromial bursa was deficient in relaying the movement sense signals.106
Neuromuscular Control Alterations Given the proprioceptive deficits associated with shoulder joint injury, neuromuscular control is hypothesized to be altered as well.4,45 Several investigators have assessed the neuromuscular control component of dynamic joint stability in subjects presenting with glenohumeral instability.107-110 Muscle activation alterations were identified in patients with glenohumeral instability during simple elevation tasks108,109 and while throwing a baseball.110 Deficits in co-activation of the rotator cuff and primary humeral movers were present, possibly leading to compromised dynamic joint stability and further exacerbating the existing instability. Our laboratory has assessed reflexive characteristics of the shoulder muscles in patients with anterior glenohumeral
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instability.107 The patients with instability demonstrated suppressed pectoralis major and biceps brachii mean reflexive activation, significantly slower biceps brachii reflex latency, and suppressed supraspinatus-subscapularis coactivation. The results suggested that in addition to the capsuloligamentous deficiency and proprioceptive deficits present in patients with anterior glenohumeral instability, muscle activation alterations are also present. The suppressed rotator cuff coactivation, slower biceps brachii activation, and decreased pectoralis major and biceps brachii mean activation can contribute to the recurrent instability episodes seen in patients with glenohumeral instability. Muscle activation abnormalities associated with subacromial impingement and rotator cuff lesions have also been identified.111-113 Common findings include altered activity of the primary humeral movers; decreased activity in the supraspinatus, infraspinatus, and subscapularis; decreased co-activation of the rotator cuff musculatur;, and suppressed scapular stabilization by the trapezius and serratus anterior muscles during elevation. Kelly and colleagues113 assessed activation of the rotator cuff during functional tasks and demonstrated that patients with symptomatic rotator cuff tears exhibit activation alterations that can limit functional performance compared to both asymptomatic and normal subjects. Our laboratory has found that patients with subacromial impingement exhibited less subscapularis-infraspinatus, supraspinatus-subscapularis, and supraspinatus-infraspinatus co-activation.114 Increased middle deltoid and latissimus dorsi activity was exhibited by the impingement patients. The results indicate that patients with subacromial impingement exhibit suppressed rotator cuff co-activation and abnormal humeral mover alterations during humeral elevation. These muscle activation alterations can contribute to impingement of the subacromial structures and subsequent pain during overhead elevation in patients with subacromial impingement.
SENSORIMOTOR RESTORATION Following shoulder injury, the goal of management should be restoration of functional joint stability. Functional joint stability encompasses the interplay of both the mechanical restraints (joint capsule, ligamentous structures, and glenoid labrum) and dynamic restraints (neuromuscular control of the shoulder musculature). To restore functional joint stability, both constituents must be restored. Evidence suggests that the sensorimotor contributors to joint stability can be restored. Surgical intervention to restore mechanical stability has a demonstrated benefit in restoring proprioception.101,102,104,115,116 The main goal of surgery for glenohumeral instability is to re-establish mechanical restraint to the humeral head. Yet as reported by several investigators, the surgery was also successful at restoring proprioception.101,102,104,115,116 It is believed that
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by re-establishing tension within the glenohumeral joint capsule and ligaments, mechanoreceptor stimulation is also reestablished.101,102,104,115,116 Mechanoreceptors might also repopulate the joint capsule, allowing reinnervation following surgery as a normal part of the histologic healing process.102,115 Potzl and colleagues116 found an increase in proprioception bilaterally following unilateral surgical intervention, hypothesizing that an alteration in central mediation of proprioception also contributes to normalization of proprioception. Subacromial decompression was also found to restore proprioception in patients with subacromial impingement.106 It was suggested that the painful subacromial bursa was the cause of the initial deficit, and subsequent restoration of proprioception was due to resection of this structure. These results are supported by Cuomo and colleagues,104 who found that both measures of kinesthesia and joint position sense returned to normal levels following total shoulder arthroplasty.104 It was suggested that a decrease in pain afferents with greater mechanoreceptor afferent activity following surgery was the mechanism for improved proprioception.104,106 Other potential mechanisms for restoration of proprioception following surgery included retensioning the joint capsule and surrounding musculature and restoring anatomic alignment through greater joint congruence following arthroplasty.104 As with any injury, rehabilitation should address reduction of inflammation and pain, a return to normal range of motion and flexibility, and restoration of strength through traditional rehabilitation exercises. Yet return to vigorous physical activity and athletic participation requires additional rehabilitation considerations. Lephart and Henry31 promote the use of functional rehabilitation for return to athletic and highly demanding activities of daily living.30 A large component of functional rehabilitation is the ability to replicate the demands placed on the joint in a controlled manner to decrease the initial impact on return to physical activity. Some of the expected benefits of functional rehabilitation include increasing proprioceptive awareness, increasing dynamic stabilization, eliciting preparatory and reactive muscle activation, and restoring functional movement patterns.30 Proprioceptive awareness training is believed to re-establish afferent pathways from the mechanoreceptors to the CNS and to facilitate supplementary afferent pathways as a compensatory mechanism for proprioceptive deficits that resulted from joint injury.4 Dynamic stabilization is paramount in restoring functional joint stability and should focus on restoring coordinated muscle activation patterns during functional tasks and restoring muscle co-activation and the resulting force-coupling restraint. Eliciting preparatory and reactive muscle activation around the shoulder helps to establish reflex loops and muscle stiffness around the joint, thus creating stability during destabilizing events.
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To further ease the transition from rehabilitation to the functional demands of sports or occupation, allowing controlled simulation of tasks is beneficial. Re-creating in the clinical setting the activities that will be required of the joint during sports allows a controlled environment to practice and evaluate techniques before actual specific performance. There is some evidence of the effectiveness of exercise in restoring sensorimotor mechanisms at the shoulder. Shoulder plyometric training has been shown to increase proprioception in swimmers.117 It was theorized that repeated eccentric loading and subsequent length and tension changes in the shoulder stabilizers at end range of motion created increased proprioceptive awareness of the mechanical and dynamic stabilizers.117 Additionally, increases in central processing might have resulted from performing the repetitive, perturbing plyometric tasks. This creates increased muscle tension in preparation for the task being performed, which can elicit increased awareness of joint position.117 Furthermore, both open- and closed-kinetic-chain exercises have been shown to cause improvements in joint position sense at the shoulder.118 It has also been shown that closed-kinetic-chain upperextremity activities facilitate co-activation of the muscles around the shoulder, increasing functional joint stability.119,120 By using closed-chain exercises, an increase in joint stability can be obtained by creating greater joint congruency and stimulation of articular mechanoreceptors.119,120 There also appears to be a central component trained during closed-chain exercise, because increases in joint stability were seen in both shoulders in subjects training unilaterally.120 It has also been shown through a randomized controlled trial that enhancing neuromuscular control through exercises designed to enhance co-activation about the shoulder leads to faster recovery from chronic shoulder pain than the natural course of recovery.121 Recovery time with enhanced neuromuscular control was also shown to be equivalent to that with steroid injection and physical modalities. The authors advocate retraining because it is more cost effective than the other modalities and has less inherent risk than steroid injection.121
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Thus, we highlight only some common assessments as they relate to important findings for understanding shoulder joint stability. Proprioception is defined as the afferent information concerning the three submodalities of kinesthesia, joint position sense, and sensation of force. Assessment techniques attempt to quantify these submodalities. Kinesthesia is commonly assessed by determining one’s ability to detect motion of the shoulder joint. For example, Lephart and colleagues quantified one’s ability to consciously detect shoulder movement using a proprioception-testing device (Fig. 49-3).105,115,117,124 Typically, the test assesses the amount of time or joint displacement that occurs before movement is appreciated. Joint position sense has been measured in the laboratory and clinical setting with a number of assessment tools including isokinetic dynamometry,117,125,126 clinical goniometry,127,128 proprioceptive testing devices,105,115,117,124 and motion-analysis systems (Fig. 49-4).100,115,129 Joint position sense testing protocols typically measure the ability to appreciate where one’s extremity is oriented in space. Testing protocols usually begin by passively or actively placing the upper limb in some standardized position, having the subject appreciate its spatial orientation, then asking the subject to either actively reproduce the presented joint position or provide a response once the joint position is replicated passively. Variations in testing include reproduction of movement patterns rather than specific joint position100,115 and assessment of accuracy in reproducing joint velocity.25,130,131 Sensation of joint force by the upper extremity has also been assessed.4,132-136 Dover and Powers128 have described a force-reproduction test that can be reliably performed in the laboratory and clinic using a dynamometer to determine
SENSORIMOTOR ASSESSMENTS Given the complexity of the sensorimotor system and all of the specific components associated with joint stability, assessment can be extremely difficult. Most assessment techniques evaluate the integrity and function of sensorimotor components by measuring variables along the afferent or efferent pathways or by measuring the final outcome of skeletal muscle activation.123 An entire book could be devoted to describing sensorimotor assessments.
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Figure 49-3. Assessment of proprioception (joint position sense or kinesthesia) using a proprioception testing device.
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Figure 49-4. Assessment of proprioception using electromagnetic tracking motion analysis instrumentation. Participant (A) places his arm with the help of a guide (B) into a standardized position. C, The participant attempts to reproduce the standardized position without assistance from the guide. D, The motion analysis instrumentation provides three-dimensional quantification in joint-position sense error.
one’s ability to reproduce standardized amounts of torque generation at the shoulder. Somatosensory evoked potentials (SEP) provide a means of assessing the integrity of afferent pathways to the cerebral cortex. SEP can be elicited either through transcutaneous electrical stimulation of peripheral nerves and sensory organs or through more physiologic stimuli such as joint movement.137 Once a stimulus is applied peripherally, measurements can be made along the course of the afferent pathways. For example, following the delivery of an electrical stimulus to the wrist (median nerve), the nerve action potentials can be detected as they propagate at the level of the brachial plexus, midcervical spinal cord, upper midbrain and thalamus, and somatosensory cortex.138 SEP techniques are performed by introducing an electrical potential with known characteristics (amplitude, wavelength) to the afferent pathway123 and measuring the changes (or lack of changes) in these characteristics. Tibone and colleagues41 used SEP to demonstrate that that in patients with shoulder instability, the afferent pathway is intact, suggesting that the proprioceptive deficits seen in this patient population result from decreased mechanical stimulation of the mechanoreceptors rather than deafferentation. Similar to SEP, nerve conduction study testing is an objective method of assessing the functional status of the peripheral alpha motor neuron system.139 The basis for nerve conduction study testing resides with the proximal and distal reaction propagation that occurs along an entire nerve following electrical stimulation.123 An electrical current with known characteristics (amplitude, wavelength) is applied to the efferent neural pathway, usually on the innervating nerve. Electromyographic recordings are then taken distal to the applied current, usually on the desired muscle.123 Di Benedetto and Markey140 used nerve conduction velocity testing to identify motor deficits in football players with brachial plexopathies. Neuromuscular control is defined as the unconscious activation of dynamic restraints occurring in preparation for
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and in response to joint motion and loading for the purpose of maintaining functional joint stability. Thus, assessments of neuromuscular control ultimately focus on quantifying muscle activation. Electromyography (EMG) provides a means of measuring the myoelectrical events associated with muscle contraction including the initiation, cessation, and magnitude of muscle activity.141,142 Specifically at the shoulder joint, EMG has been used to investigate muscle activation during athletic activity,143-149 neuromuscular alterations following injury,107-110,150 and shoulder rehabilitation.122,151-155 Our laboratory recently used EMG to evaluate the muscle activation of 12 resistance-tubing exercises commonly used by throwers for warm-up (Fig. 49-5).122 Seven exercises
Figure 49-5. Assessment of shoulder muscle activation using electromyography in a thrower performing a resistance-tubing exercise. (Reprinted with permission from Myers JB, Pasquale MR, Laudner KG, et al: On-the-field resistance tubing exercises for throwers: An electromyographic analysis. J Athletic Train 40:15-22, 2005).
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(external rotation at 90 degrees of abduction, throwing deceleration, humeral flexion, humeral extension, low scapular rows, throwing acceleration, and scapular punch) resulted in at least moderate activation (⬎20% maximal voluntary isometric contraction) in each muscle of the rotator cuff, the primary humeral movers, and the scapular stabilizer muscles (Fig. 49-6 to 49-12). The implications are that these exercises are most effective in activating the muscles important to the throwing motion and may be beneficial for throwers during their prethrowing warm-up routine.
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Although assessing muscle activity provides valuable information, one must remember that EMG measures activation of muscle, not the actual force production that is vital to joint stability.156 It is force production that is most important in protecting the joint from injury or applying force to a limb for movement to occur. Several sensorimotor assessments have been used at the shoulder to better understand the force generation associated with joint stability and function. Those assessments include but are not limited to isokinetics, musculoskeletal imaging such as ultrasound or magnetic resonance imaging (MRI),
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Figure 49-6. A thrower performing the external rotation at 90 degrees of abduction exercise. A, Starting (A) and ending (B) positions. B, Direction reversed.
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Figure 49-7. A thrower performing the throwing acceleration exercise. A, Starting (A) and ending (B) positions. B, Direction reversed.
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Figure 49-8. A thrower performing the throwing deceleration exercise. A, Starting (A) and ending (B) positions. B, Direction reversed.
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B Figure 49-9. A thrower performing the shoulder extension exercise. A, Starting (A) and ending (B) positions. B, Direction reversed.
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B Figure 49-11. A thrower performing the scapular punch exercise. A, Starting (A) and ending (B) positions. B, Direction reversed.
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B Figure 49-12. A thrower performing the scapular row exercise. A, Starting (A) and ending (B) positions. B, Direction reversed.
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and indirect measures of neuromuscular control through measures of joint function. Variables assessed during isokinetic testing represent the resulting body segment torque produced by voluntary skeletal muscle activation. Isokinetic torque does not immediately or directly reflect individual muscle force production but
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rather reflects the final outcome of all muscles across a limb segment.123 Torque is a function of many factors such as level of muscle activation, muscle dynamics (length and velocity), and joint geometry (moment arm length and joint congruency).15 Numerous studies have used isokinetic dynamometry to answer questions related to the shoulder joint.157-172
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Novel in vivo imaging techniques have provided ways of assessing muscle function. Boehm and colleagues173 used dynamic ultrsonography to investigate the effect of different contraction patterns on shoulder function in patients with rotator cuff tears. In patients with a supraspinatus tear, the contraction type of the supraspinatus correlated significantly with the Constant function score, indicating better shoulder function. Graichen and colleagues174 assessed that potential changes of the subacromial space width, scapular kinematics, and glenohumeral translation that result from shoulder muscle activity using open MRI. They reported that the subacromial space can be effectively widened by eliciting adducting muscle activity. Graichen and colleagues175 also analyzed the influence of shoulder muscle activity on the three-dimensional motion pattern of the shoulder girdle with an open MRI system. The study demonstrated that muscle activity leads to an alteration of shoulder girdle motion patterns at higher degrees of abduction, with increased rotation of the scapula and an altered spatial relationship between the supraspinatus and humerus. Neuromuscular control can indirectly be assessed through functional performance tests. Functional performance tests at the shoulder have been limited but include functional throwing performance indices, single-arm dynamic stability tests, and single-arm hop tests.125,126,176,177
SUMMARY Functional joint stability at the shoulder joint results from an interaction between the mechanical and dynamic restraints about the shoulder. The sensorimotor system plays an integral role by mediating mechanical and dynamic restraints through the appreciation of afferent proprioceptive information concerning joint position sense, kinesthesia, and sensation of force and the efferent neuromuscular control over the dynamic stabilizers that result. Following shoulder joint injury, proprioceptive input appears to be disrupted, which in turn affects neuromuscular control. Restoration of functional joint stability in the shoulder requires attention to both the anatomic structures that are compromised, whether with surgical intervention or a conservative approach, and the neuromuscular mechanisms vital to joint stability.
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4. Myers JB, Lephart SM: The role of the sensorimotor system in the athletic shoulder. J Athletic Train 35:351-363, 2000. 5. Grigg P: Peripheral neural mechanism in proprioception. J Sport Rehabil 3:2-17, 1994. 6. Kikuchi T: Histological studies on the sensory innervation of the shoulder joint. J Iwate Med Assoc 20:554-567, 1968. 7. Vangsness CT, Ennis M, Taylor JG, Atkinson R: Neural anatomy of the glenohumeral ligaments, labrum, and subacromial bursa. Arthroscopy 11:180-184, 1995. 8. Martini F: Fundamentals of Anatomy and Physiology. New York, Prentice Hall, 1997. 9. Guyton AC (ed): Textbook of Medical Physiology. Philadelphia, WB Saunders, 1991. 10. Barrack RL, Lund PJ, Skinner HB: Knee joint proprioception revisited. J Sport Rehabil 3:18-42, 1994. 11. Solomonow M, Guanche CA, Wink CA, et al: Shoulder capsule reflex arc in the feline shoulder. J Shoulder Elbow Surg 5:139-146, 1996. 12. Gohlke F, Muller T, Sokeland T, et al: Distribution and morphology of mechanoreceptors in the rotator cuff. J Shoulder Elbow Surg 5:S72, 1996. 13. Gohlke F, Janssen E, Leidel J, Eulert J: Histopathological findings in the proprioception of the shoulder joint. Orthopade 27:510-517, 1998. 14. Ide K, Shirai Y, Ito H: Sensory nerve supply in the human subacromial bursa. J Shoulder Elbow Surg 5:371-382, 1996. 15. Enoka RM: Neuromechanical Basis of Kinesiology. Champaign Ill, Human Kinetics, 1994. 16. Johansson H, Sjolander P: The neurophysiology of joints. In Wright V, Radin E (eds): Mechanics of Joints: Physiology, Pathophysiology, and Treatment. New York, Marcel Dekker, 1993, pp 243-290. 17. Boyd IA: The histological structures of the receptors of the knee joint of cat correlated with their physiological response. J Physiology 124:476-488, 1954. 18. Wyke B: The neurology of joints: A review of general principles. Clin Rheum Dis 7:223-239, 1981. 19. Zimny ML: Mechanoreceptors in articular tissues. Am J Anat 182:16-32, 1988. 20. Tyldesling B, Grieves JI: Muscle, Nerve, and Movement, Kinesiology in Daily Living. Boston, Blackwell Scientific, 1989. 21. Hall LA, McCloskey DI: Detection of movement imposed on the finger, elbow, and shoulder joints. J Physiol 335: 519-533, 1983. 22. Guanche CA, Solomonow M, D’Ambrosia RD: Peripheral afferents of the shoulder: Relationship between active and passive restraints regulating muscle activation. In Lephart SM, Fu FH (eds): Proprioception and Neuromuscular Control in Joint Stability. Champaign, Ill, Human Kinetics, 2000, pp 99-107. 23. Riemann BL, Guskiewicz KM: Contribution of the peripheral somatosensory system to balance and postural equilibrium. In Lephart SM, Fu FH (eds): Proprioception and Neuromuscular Control in Joint Stability. Champaign, Ill, Human Kinetics, 2000, pp 37-52. 24. Jami L: Golgi tendon organs in mammalian skeletal muscle: functional properties and central actions. Physiolo Rev 72:623-666, 1992. 25. Pedersen J, Lonn J, Hellstrom F, et al: Localized muscle fatigue decreases the acuity of the movement sense in the human shoulder. Med Sci Sports Exerc 31:1047-1052, 1999.
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107. Myers JB, Ju YY, Hwang JH, McMahon PJ, et al: Reflexive muscle activation alterations in shoulders with anterior glenohumeral instability. Am J Sports Med 32:1013-1021, 2004. 108. McMahon PJ, Jobe FW, Pink MM, et al: Comparative electromyographic analysis of shoulder muscles during planar motions: Anterior glenohumeral instability versus normal. J Shoulder Elbow Surg 5:118-123, 1996. 109. Kronberg M, Brostrom LA, Nemeth G: Differences in shoulder muscle activity between patients with generalized joint laxity and normal controls. Clin Orthop Relat Res (269):181-192, 1991. 110. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220-226, 1988. 111. Ludewig PM, Cook TM: Alterations in shoulder kinematics and associated muscle activity in people with symptoms of shoulder impingement. Phys Ther 80:276-291, 2000. 112. Reddy AS, Mohr KJ, Pink MM, Jobe FW: Electromyographic analysis of the deltoid and rotator cuff muscles in persons with subacromial impingement. J Shoulder Elbow Surg 9:519-523, 2000. 113. Kelly BT, Williams RJ, Cordasco FA, et al: Differential patterns of muscle activation in patients with symptomatic and asymptomatic rotator cuff tears. J Shoulder Elbow Surg 14:165-171, 2005. 114. Myers JB, Hwang JH, Pasquale MR, et al: Shoulder muscle coactivation alterations in patients with subacromial impingement. Paper presented at the American College of Sports Medicine Annual Meeting. San Francisco, Calif, May 28-31, 2003. 115. Lephart SM, Myers JB, Bradley JP, Fu FH: Shoulder proprioception and function following thermal capsulorraphy. Arthroscopy 18:770-778, 2002. 116. Potzl W, Thorwesten L, Gotze C, et al: Proprioception of the shoulder joint after surgical repair for instability: A longterm follow-up study. Am J Sports Med 32:425-430, 2004. 117. Swanik KA, Lephart SM, Swanik CB, et al: The effects of shoulder plyometric training on proprioception and selected muscle performance characteristics. J Shoulder Elbow Surg 11:579-586, 2002. 118. Rogol IM, Ernst GP, Perrin DH: Open and closed kinetic chain exercises improve shoulder joint reposition sense equally in healthy subjects. J Athletic Train 33:315-318, 1998. 119. Henry TJ, Lephart SM, Giraldo J, et al: The effect of muscle fatigue on muscle force-couple activation of the shoulder. J Sport Rehabil 10:246-256, 2001. 120. Ubinger ME, Prentice WE, Guskiewicz KM: Effects of closed kinetic chain training on neuromuscular control in the upper extremity. J Sport Rehabil 8:184-194, 1999. 121. Ginn KA, Cohen ML: Exercise therapy for shoulder pain aimed at restoring neuromuscular control: A randomized comparative clinical trial. J Rehabil Med 37:115-122, 2005. 122. Myers JB, Pasquale MR, Laudner KG, et al: On-the-field resistance tubing exercises for throwers: An electromyographic analysis. J Athletic Train 40:15-22, 2005. 123. Riemann BL, Myers JB, Lephart SM: Sensorimotor system measurement techniques. J Athletic Train 37:85-98, 2002. 124. Allegrucci M, Whitney SL, Lephart SM, et al: Shoulder kinesthesia in healthy unilateral athletes participating in upper extremity sports. J Ortho Sport Phys Ther 21:220-226, 1995.
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125. Myers JB, Guskiewicz KM, Schneider RA, Prentice WE: Proprioception and neuromuscular control of the shoulder after muscle fatigue. J Athletic Train 34:362-367, 1999. 126. Padua DA, Guskiewicz KM, Prentice WE, et al: The effect of select shoulder exercises on strength, active angle reproduction, single-arm balance, and functional performance. J Sport Rehabil 13:75-95, 2004. 127. Dover GC, Kaminski TW, Meister K, et al: Assessment of shoulder proprioception in the female softball athlete. Am J Sports Med 31:431-437, 2003. 128. Dover GD, Powers ME: Reliability of joint position sense and force-reproduction measures during internal and external rotation of the shoulder. J Athletic Train 38:304-310, 2003. 129. Slobounov SM, Poole ST, Simon RF, et al: The efficacy of modern technology to improve healthy and injured shoulder joint position sense. J Sport Rehabil 8:10-23, 1999. 130. Jerosch J, Brinkmann T, Schneppenheim M: The angle velocity reproduction test (AVRT) as sensorimotor function of the glenohumeral complex. Arch Orthop Trauma Surg 123:151-157, 2003. 131. Lonn J, Djupsjobacka M, Johansson H: Replication and discrimination of limb movement velocity. Somatosens Mot Res 18:76-82, 2001. 132. Brockett C, Warren N, Gregory JE, et al: A comparison of the effects of concentric versus eccentric exercise on force and position sense at the human elbow joint. Brain Res 771:251-258, 1997. 133. Jones LA, Hunter IW: Effect of muscle tendon vibration on the perception of force. Exp Neurol 87:35-45, 1985. 134. Jones LA, Hunter IW: Effect of fatigue on force sensation. Exp Neurol 81:640-650, 1983. 135. Jones LA: Role of central and peripheral signals in force sensation during fatigue. Exp Neurol 81:497-503, 1983. 136. Gandevia SC, Kilbreath SL: Accuracy of weight estimation for weights lifted by proximal and distal muscles of the human upper limb. J Physiol 423:299-310, 1990. 137. Mima T, Terada K, Mackawa M, et al: Somatosensory evoked potentials following proprioceptive stimulation of finger in man. Exp Brain Res 111:233-245, 1996. 138. Nuwer M: Fundamentals of evoked potentials and common clinical applications today. Electroenceph Clin Neurophysiol 106:142-148, 1998. 139. DeLisa J, Mackenzie K, Baran E: Manual of nerve conduction velocity and clinical neurophysiology. New York, Raven Press, 1994. 140. Di Benedetto M, Markey K: Electrodiagnostic localization of traumatic upper trunk brachial plexopathy. Arch Phys Med Rehabil 65:15-17, 1984. 141. Winter DA: Biomechanics and motor control of human movement. New York, John Wiley & Sons, 1990. 142. Basmajian JV, DeLuca CJ: Muscles Alive. Their Functions Revealed by Electromyography. Baltimore, Williams & Wilkins, 1985. 143. Heise GD: EMG changes in agonist muscles during practice of a multijoint throwing skills. J Electroymyo Kinesiol 5:81-94, 1995. 144. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the shoulder in throwing and pitching: a preliminary report. Am J Sport Med 11:3-5, 1983. 145. Jobe FW, Moynes DR, Tibone JE, Perry J: An EMG analysis of the shoulder in pitching: A second report. Am J Sport Med 12:218-220, 1984.
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146. Gowan ID, Jobe FW, Tibone JE, et al: A comparative electromyographic analysis of the shoulder during pitching: professional versus amateur pitching. Am J Sport Med 15:586-590, 1987. 147. Nuber GW, Jobe FW, Perry J, Moynes DR, Antonelli D: Fine wire electromyography analysis of muscles of the shoulder during swimming. Am J Sport Med 14:7-11, 1986. 148. Pink M, Jobe FW, Perry J: Electromyographic analysis of the shoulder during the golf swing. Am J Sports Med 18: 137-140, 1990. 149. Scovazzo ML, Brown A, Pink M, et al: The painful shoulder during freestyle swimming: An EMG and cinematographic analysis of twelve muscles. Am J Sport Med 19:577-582, 1991. 150. Wallace DA, Beard DJ, Gill RH, et al: Reflex muscle contraction in anterior shoulder instability. J Shoulder Elbow Surg 6:150-155, 1997. 151. Moseley JB, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sport Med 20:128-134, 1992. 152. Litchfield R, Hawkins R, Dillman CJ, et al: Rehabilitation of the overhead athlete. J Orthop Sport Phys Ther 18:433-441, 1993. 153. Blackburn TA, McLeod WD, White B, Wofford L: EMG analysis of posterior rotator cuff exercise. Athletic Train 25: 40-45, 1990. 154. McCann PD, Wootten ME, Kadaba MP, Bigliani LU: A kinematic and electromyographic study of shoulder rehabilitation exercises. Clin Orthop 288:179-188, 1993. 155. Worrell TW, Corey BJ, York SL, Santiestaban J: An analysis of supraspinatus EMG activity and shoulder isometric force development. Med Sci Sport Exerc 24:744-748, 1992. 156. Bochdansky T, Kollmitzer J, Ebinbechler G: The role of electromyography in the assessment of neuromuscular control. In Lephart SM, Fu FH (eds): Proprioception and Neuromuscular Control in Joint Stability. Champaign, Ill, Human Kinetics, 2000, pp 145-160. 157. Heiderscheit BC, McLean KP, Davies GJ: The effects of isokinetic versus plyometric training on the shoulder internal rotators. J Orthop Sport Phys Ther 23:125-133, 1996. 158. Mont MA, Cohen DB, Campbell KR, et al: Isokinetic concentric versus eccentric training of shoulder rotators with functional evaluation of performance enhancement in elite tennis players. Am J Sport Med 22:513-517, 1974. 159. Greenfield B, Donatelli R, Wouden M: Isokinetic evaluation of shoulder rotational strength between the plane of scapula and the frontal plane. Am J Sport Med 18:124-148, 1990. 160. Miyahara M, Sleivert GG, Gerrard DF: The relationship of strength and muscle balance to shoulder pain and impingement syndrome in elite quadriplegic wheelchair rugby players. Int J Sports Med 19:210-214, 1998. 161. Powers CM, Newsam CJ, Gronley JK, et al: Isometric shoulder torque in subjects with spinal cord injury. Arch Phys Med Rehabil 75:761-765, 1994.
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162. Rokito AS, Zuckerman JD, Gallagher MA, Cuomo F: Strength after surgical repair of the rotator cuff. J Shoulder Elbow Surg 5:12-17, 1996. 163. Ben-Yishay A, Zuckerman JD, Gallagher M, Cuomo F: Pain inhibition of shoulder strength in patients with impingement syndrome. Orthopedics 17:685-688, 1994. 164. Kirschenbaum D, Coyle MP Jr, Leddy JP, et al: Shoulder strength with rotator cuff tears. Pre- and postoperative analysis. Clin Orthop Relat Res (288):174-178, 1993. 165. Walker SW, Couch WH, Boester GA, Sprowl DW: Isokinetic strength of the shoulder after repair of a torn rotator cuff. J Bone Joint Surg Am 69:1041-1044, 1987. 166. Swanik KA, Swanik CB, Lephart SM, Huxel K: The effect of functional training on the incidence of shoulder pain and strength in intercollegiate swimmers. J Sport Rehabil 11:140-154, 2002. 167. Hinton RY: Isokinetic evaluation of shoulder rotational strength in high school baseball pitchers. Am J Sports Med 16:274-279, 1988. 168. Brown LP, Niehues SL, Harrah A, et al: Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 16:577-585, 1988. 169. Malerba JL, Adam ML, Harris BA, Krebs DE: Reliability of dynamic and isometric testing of shoulder external and internal rotators. J Orthop Sports Phys Ther 18:543-552, 1993. 170. McMaster WC, Long SC, Caiozzo VJ: Isokinetic torque imbalances in the rotator cuff of the elite water polo player. Am J Sports Med 19:72-75, 1991. 171. Warner JJ, Micheli LJ, Arslanian LE, et al: Patterns of flexibility, laxity, and strength in normal shoulders and shoulders with instability and impingement. Am J Sports Med 18:366-375, 1990. 172. Treiber FA, Lott J, Duncan J, et al: Effects of Theraband and lightweight dumbbell training on shoulder rotation torque and serve performance in college tennis players. Am J Sports Med 26:510-515, 1998. 173. Boehm TD, Kirschner S, Mueller T, et al: Dynamic ultrasonography of rotator cuff muscles. J Clin Ultrasound 33: 207-213, 2005. 174. Graichen H, Hinterwimmer S, von Eisenhart-Rothe R, et al: Effect of abducting and adducting muscle activity on glenohumeral translation, scapular kinematics and subacromial space width in vivo. J Biomechan 38:755-760, 2005. 175. Graichen H, Stammberger T, Bonel H, et al: Threedimensional analysis of shoulder girdle and supraspinatus motion patterns in patients with impingement syndrome. J Orthop Res 19:1192-1198, 2001. 176. Davies GJ, Dickoff-Hoffman S: Neuromuscular testing and rehabilitation of the shoulder complex. J Orthop Sport Phys Ther 18:449-458, 1993. 177. Falsone SA, Gross MT, Guskiewicz KM, Schneider RA: One-arm hop test: Reliability and effects of arm dominance. J Orthop Sports Phys Ther 32:98-103, 2002.
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CHAPTER 50 The Role of the Scapula
in Rehabilitation Tim L. Uhl and W. Ben Kibler
The body functions as an integrated system in all aspects of sport and work. This integrated system allows variability so that we can respond to specific tasks in an efficient manner. Understanding how the entire system works as a functional unit within its environment is indispensable for appropriate evaluation and intervention to restore patients to their full functional level. Individual patients develop movement patterns and resting postures dependent on their physical characteristics, the demands of the particular task, the environment of the task, and their psychological state. The goal of the treating clinician is to identify these factors as they relate to physical impairments, functional limitations, and particular pathology. Once the factors are identified, there are several ways to intervene. Through our clinical experience we have found that exercises that integrate the entire body and address scapular motion and control have helped our patients return to their normal function. The primary goals of this chapter are to describe our clinical assessment of the scapula and to provide our rehabilitation approach in the upper extremity of a throwing athlete.
clinical symptoms has not been identified, and ultimately the rehabilitation program will fail. Lower-body strength has been positively correlated with terminal ball velocity and is more highly correlated than upper body strength.8 A critical segment or link in transferring this force is the scapula, which is the attachment site for approximately 17 muscles involved in upper-extremity motion. Many of the muscles that attach to the scapula, such as the trapezius, serratus anterior, latissimus dorsi, and rhomboids, have proximal attachments to the axial skeleton and are instrumental in maximizing mobility of the upper extremity. The interaction of trunk, scapular, and humeral motion provides a dynamic linked system that is used in many ways in numerous sport activities, from providing a stable base for archery to providing a very mobile system in throwing. The motion provided by the scapula allows the glenohumeral articulation to be the most mobile joint in the human body.9 The scapula provides a dynamic base for humeral motion. The interactive coupling of the scapula and humerus, scapulohumeral rhythm, maintains an optimal muscle length relationship in the rotator cuff musculature and avoids excessive tension on the glenohumeral ligaments.10,11
BIOMECHANICS In overhead throwing sports the goal is to throw the ball accurately, for a great distance or at maximum speeds. To impart the necessary force to the ball the entire body is used sequentially in a general proximal-to-distal manner.1-3 This system is commonly referred to as the kinetic chain, which is a coordinated activation of body segments (e.g., leg, trunk, upper arm) that are connected at articulations. To throw a ball at a high rate of speed, the proximal segments of the kinetic chain initiate motion of the entire system. As a proximal segment, such as the front leg of a pitcher, decelerates, momentum is transferred to the next distal segment, the trunk. This process continues throughout the entire kinetic chain until the ball is released. As momentum is transferred to the arm segments (which are smaller in mass), the velocity of the segment increases.4,5 By using the summation of the entire kinetic chain, all segments contribute to the performance of the task. Segment drop out or kinetic chain breakage requires other segments to increase force production or increase loads in distal segments.4,6,7 This is why the evaluation of the injured patient has to be so comprehensive. If the examiner focuses on a sore shoulder and does not discover that the athlete has a weak front leg, the primary culprit of the
This sequencing of events not only occurs biomechanically but also occurs in the neuromuscular control of human motion. Activation of proximal trunk musculature, such as the transverse abdominus and multifidius muscles, has been demonstrated to precede activation of distal muscles, such as the anterior deltoid, to prepare the body for positional changes due to the moving segment.12,13 These anticipatory postural adjustments occur both in sitting and standing and occur regardless of the direction of the movement.14,15 These normal motor control patterns are exaggerated in our approach to shoulder rehabilitation by incorporating the entire kinetic chain and focusing the patient’s abilities to activate proximal muscle to control the trunk and scapula before placing demands on more distal musculature. Proximal control for distal mobility is a basic concept taught in many biomechanics and kinesiology courses. One of us (WBK) put this to work clinically in the 1980s when he started investigating the role of the scapula in upper-extremity pathologies. In observing a swimmer with chronic shoulder pain from the rear while she was wearing a swimming suit, he noted significant scapular winging. 671
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By evaluating and appreciating the relationship between symptoms of shoulder impingement and proximal scapular dysfunction, he was able to identify all physical impairments contributing to her pathology. The assessment of scapular dysfunction as part of the clinical examination of the upper extremity is still a relatively new idea to many clinicians. However, since the 1980s the literature on the role of the scapula and the surrounding muscular in shoulder dysfunction and the importance of considering the scapula in treatment interventions has dramatically increased. A Medline search of the word scapula between 1966 and 1988 (22 years) retrieved 1647 citations; the same search between the years 1989 and 2006 (17 years) returned 2281 citations. Advances in biomechanical techniques that allow evaluation of scapular motion have opened many doors of investigation. Critical research by Karduna and McClure demonstrated that scapular motion could be evaluated with skin sensors attached to the scapula, increasing our understanding of scapular biomechanics. In a series of studies, they instrumented subjects with electromagnetic sensors attached to the skin overlying the scapula and to bone pins placed in the spine of the scapula. They demonstrated that sensors attached to the skin could accurately measure scapular motion during arm motions.16,17 From their research they identified that the scapula rotates about three axes; upward and downward rotation, internal and external rotation, and anterior and posterior tilt (Fig. 50-1).
Internal/external rotation
Anterior/ posterior tilt
Upward/downward rotation
Karduna and McClure found that at maximal humeral elevation in the scapular plane the scapula upwardly rotated 50 ± 5 degrees, externally rotated 24 ± 13 degrees, and posteriorly tilted 30 ± 13 degrees. This motion occurs simultaneously in all three planes, but they demonstrated that the greatest amount of external rotation and posterior tilting occurred above 90 degrees of humeral elevation.17 In addition to these rotations, translatory motion of the scapula occurs. Superior scapular translation along the thoracic wall occurs during forward reaching tasks. Anterior translation around the thoracic wall occurs during forward reaching tasks, and the scapula translates posteriorly during pulling tasks. Medial and lateral translation, the third translation, is limited due to the clavicle strut effect and does not occur unless there is a high-grade acromioclavicular joint separation.17 Understanding the anatomy and biomechanics of the scapula provides the clinician with a firm base to better understand the function and the evaluation of scapular dysfunction. Chapters 1 and 2 address the anatomy and biomechanics of the shoulder complex thoroughly; therefore, we direct the reader to those chapters for further information.
ASSESSMENT OF SCAPULAR DYSKINESIS The term scapular dyskinesis was coined by JP Warner. He found scapular dyskinesis in 64% of his patients with glenohumeral instability and in nearly 100% of his patients with rotator cuff impingement.18 Several factors can contribute to scapular dyskinesis. They are categorized into two groups: proximal causes and distal causes.19 Proximal categories include neuropathy,20,21 muscle weakness,22 muscle tightness,23 muscle fatigue,24,25 pain,26 and loss of neuromuscular control,27,28 which can respond to physical therapy interventions. Distal categories include glenohumeral pathology29-32 and acromioclavicular joint separations, which usually require surgical intervention to return the patient to full function. Each of these potential factors needs to considered during physical examination of scapular dyskinesis. The goals of the physical examination of the scapula are to determine the presence or absence of scapular dyskinesis, to evaluate proximal and distal causative factors, and to employ dynamic maneuvers to assess the effect of correction of dyskinesis. The results of the examination help in establishing the complete diagnosis and in guiding rehabilitation.
Posture Figure 50-1. This diagram illustrates the three rotational axes of the scapula and the motions that occur around them.
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To evaluate scapular dyskinesis, the scapula, spine, and clavicle must be adequately exposed and the examiner must view the patient from the posterior aspect.
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Observation of resting posture of the spine and scapula should be the first assessment. Resting posture has been implemented as a cause of shoulder and neck pain.33 Thoracic kyphosis has been demonstrated to decrease scapular and humeral motion while also decreasing shoulder strength.34 Rounded shoulder posture is often present in athletes, such as weightlifters and swimmers, who have developed muscle imbalances due to their sport.35 One factor contributing to protracted shoulders can be a shortened or tight pectoralis minor. A short pectoralis minor has been demonstrated to reduce scapular motion during active arm elevation.36 Another factor contributing to scapular dyskinesis is internal rotation deficiency due to tight posterior structures of the glenohumeral joint. This can restrict humeral motion and potentially place increased compressive and tensile loads on glenohumeral tissues. Incorporation of legs and trunk observation in a bipedal and single leg stance is important to evaluate core stability and the lower extremity balance. The patient should perform a single leg squat. This allows the clinician to screen for poor trunk and hip control, which might need further isolated examination. In clinical assessment of throwing athletes, poor hip and trunk stability are commonly found in the presence of shoulder pain.32 The direct correlation is not currently known, but a significant force contribution originating in the legs has been demonstrated.5,6,8 Therefore, proximal deficiencies must be identified so they can be addressed during the rehabilitation program. Resting scapular position can be assessed with the patient’s arms at the sides. Excessive scapular internal rotation and lateral translation will be noted as prominence of the medial scapular border. A semidynamic assessment of scapular position using a tape measure is called the lateral scapular slide.37 The distance between the inferior angle of the scapula and a thoracic spinous process is measured in three arm positions; at rest, hands on hips, and arms abducted to 90 degrees and maximally internally rotated. A difference of greater than 1.5 cm suggests a loss of muscular control of the involved shoulder.37 The ability to discriminate this difference in symptomatic and asymptomatic subjects has been supported by Odom.38
Active Range of Motion Assessment of active and passive range of motion is critical in evaluating shoulder impairments. Assessment of dynamic scapular motion allows the examiner to appreciate scapulohumeral rhythm during arm motion. This dynamic assessment can be facilitated by having the subject perform multiple3-10 repetitions of active arm elevation in both flexion and abduction. By watching the patient move slowly through the range of motion, subtle anomalies can be identified. Additionally, adding 2 to 5 lbs in the hand increases the distal load and can elicit more scapular dysfunction. A categorization of this dynamic scapular observation has been reported and found to have a moderate inter- and
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intrarater reliability of 40% to 50%.39 The four categories described were normal, superior border pattern, medial border pattern, and inferior angle pattern (Box 50-1). These patterns of scapular motion have not been found to be associated with any specific glenohumeral injury. Further investigations into the patterns of scapular motion have demonstrated that altered scapular motion does not occur in isolation but more commonly occurs in combination. By modifying the categories to a simpler description of whether scapular dyskinesis is present or absent, the sensitivity of clinical observation reached 76% when compared with three-dimensional kinematic assessment of scapular motion (unpublished data). Corrective maneuvers during the assessment of dynamic scapular motion can help the clinician estimate the effect of the scapular dyskinesis. The scapular assistance test may be used in patients with impingement symptoms. The examiner applies a firm upward rotation and posterior tilt to the scapula’s inferior angle and superior border as the patient elevates the arm (Fig. 50-2).40 The test is positive when the patient’s symptoms of a painful arc are reduced during active elevation with the scapula supported. The scapular assistance test validity has not been quantified.
BOX 50-1. Scapular Dyskinesis System Used to Categorize Abnormal Scapular Motion
Inferior Angle Pattern (Type I) At rest, the inferior medial scapular border may be prominent dorsally. During arm motion, the predominant movement is that the inferior angle tilts dorsally and the acromion tilts ventrally over the top of the thorax. The axis of rotation for this pattern is in the horizontal plane.
Medial Border Pattern (Type II) At rest, the entire medial border may be prominent dorsally. During arm motion, the predominant movement is that the medial scapular border tilts dorsally off the thorax. The axis of rotation is vertical in the frontal plane.
Superior Border Pattern (Type III) At rest, the superior border of the scapula may be elevated, and the scapula can also be anteriorly displaced. During motion, the predominant movement is that a shoulder shrug initiates movement without significant winging of the scapula. The axis of this motion occurs in the sagittal plane.
Symmetrical Scapulohumeral Pattern (Type IV) At rest, the positions of both scapulae are relatively symmetrical, taking into account that the dominant arm may be slightly lower. During arm motion, the scapulae rotate symmetrically upward so that the inferior angles translate laterally away from the midline and the scapular medial border remains flush against the thoracic wall. The reverse occurs during lowering of the arm.
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Figure 50-2. The scapular assistance test is positive when shoulder symptoms are reduced during the maneuver.
The scapular retraction test may be used in demonstrating rotator cuff weakness (Fig. 50-3).40 The test is positive when rotator cuff strength is increased during the scapular retraction test as compared with rotator cuff strength without the scapula retracted. If either test is positive, rehabilitation of scapular retraction or external rotation should precede rotator cuff–focused exercises.
Proximal Stability Proximal factors influencing scapular dyskinesis are critical components in evaluating and treating scapular problems. Proximal hip and trunk stability can be screened by having the subject stand on one leg. Poor balance and Trendelenberg (hip-adducted) posture should be noted. A squat maneuver to 60 degrees of knee flexion evaluates dynamic control of the pelvic region. Dramatic loss of hip control such as excessive pelvic rotation in any plane (Fig. 50-4) and poor balance indicates poor dynamic pelvic control
Figure 50-3. The scapular retraction test is positive when elevation strength is stronger with the scapula stabilized.
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Figure 50-4. Single leg squat with poor hip stability.
and merits further examination of hip and trunk muscular strength and flexibility.41
Strength Scapular muscle strength can be screened with a wall push-up for gross serratus dysfunction such as is found in long thoracic palsy. A shoulder shrug has been demonstrated to be a valid assessment upper trapezius strength.42 The test originally described by Kendall43 for the lower trapezius has also been found to be a very good assessment of lower trapezius strength and preferentially activates the lower trapezius muscle.42,44 The patient lies prone with arm abducted to 135 degrees and thumb pointing toward the ceiling. A force is applied to the scapula or to the arm to cause shoulder extension. A weak lower trapezius is diagnosed if the subject is unable to hold this position or unable to hold it against minimal resistance. The middle trapezius is best tested by positioning the patient prone with elbow extended and shoulder externally rotated (thumb up) and applying a downward force at the forearm to make the patient produce scapular adduction.45 Various positions of prone horizontal abduction to discriminate the rhomboids from other synergistic muscles have not been able to isolate rhomboid activation.45 Therefore, weakness with shoulder horizontal abduction can be attributed to several muscles, including the middle trapezius and posterior deltoid, along with the rhomboids.
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All complete shoulder evaluations include testing of the rotator cuff musculature. A modification of the supraspinatus strength test, the scapular retraction test, has been proposed by one of us (WBK).40 The purpose of this test is to better determine if rotator cuff weakness is true or apparent. The test is performed by first examining the strength of the supraspinatus in the typical manner. Then the patient retracts the scapula and, with the assistance of the examiner, maintains scapular retraction. The test is positive when strength is improved in the retracted position. This is considered an apparent rotator cuff weakness but not a true weakness because the performance improves with additional stabilization of the proximal attachment of the supraspinatus, the scapula. A negative test indicates a true rotator cuff weakness if the patient’s strength did not improve with the scapula stabilized.40 Through the use of a hand-held dynamometer, the scapular retraction test has been found to improve elevation strength by 24% over the traditional empty can strength test for the supraspinatus.46 Following a complete examination of the shoulder including glenohumeral instability, labral pathology, tendinopathy, and acromioclavicular and sternoclavicular joint integrity, a treatment plan to address scapular dysfunction is developed. The first step in an effective intervention is a thorough understanding of normal function and identification of deficits during the examination.47 This allows the clinician to develop a specific rehabilitation program.
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exercises to decrease thoracic kyphosis in concert with scapular retraction exercises.
Posture Thoracic kyphosis reduces humeral elevation and limits normal scapular motion in such a manner to cause the scapula to be more protracted.34 A protracted scapula has been demonstrated by MRI to reduce the subacromial space49 and diminish humeral elevation strength.50 To address these common problems we recommend a program that facilitates trunk extension and scapular retraction. This can be accomplished in a variety of ways. A dynamic exercise that is commonly attempted initially is called “elbows in the back pocket” (Fig. 50-5). This exercise starts with a forward flexed trunk and protracted scapula and ends with the patient in thoracic extension and scapular retraction. The patient is instructed to tuck the elbows into the back pocket during this maneuver and is closely watched to ensure he or she is getting good scapular retraction without excessive lumbar lordosis. Key teaching points are not shrugging the shoulders and not overly extending the lumbar spine. If the back pocket exercise is too painful for the patient or the scapular control is not adequate, this exercise can be simplified to a low row exercise (Fig. 50-6). This exercise also incorporates both trunk and scapular motion simultaneously but has a smaller magnitude of motion and is
The body functions as an integrated system. Rehabilitation, like evaluation, needs to incorporate the entire functional unit. During rehabilitation our focus needs to shift from isolating the problem to providing interventions that address the athlete’s impairments and functional limitations. We take an integrated approach incorporating the kineticchain model, the motor-control pattern of proximal to distal activation, and many principles of proprioceptive neuromuscular facilitation to achieve the goals of restoring function. Consideration of the athlete’s impairments and environment must be integral to the intervention because the athlete is often attempting to return to the same activity that might have precipitated the initial injury. From the comprehensive evaluation we have identified physical impairments such as tight or weak musculature and specific functional limitations of the patient that are going to be addressed during the rehabilitation program. Often the first two areas to address are posture and proximal stability. As we have mentioned, proximal dysfunctions can contribute to scapular dyskinesis. The position of the spine is intimately involved with the position and motion of the scapula and the humerus.34,48 Therefore, we often address proximal control of the trunk with trunk extension
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Figure 50-5. Trunk extension and scapular retraction.
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Figure 50-7. Biceps stretch to stretch the anterior shoulder musculature attaching to the scapula. It is critical that the scapula stays retracted and no neurologic symptoms are present during the maneuver.
Figure 50-6. Low row.
more of an isometric exercise. The patient places the hand on either an immovable object (e.g., countertop) or uses a heavy elastic resistance. With the arm at the side, the patient extends the shoulder and depresses the scapula as he or she steps forward with the ipsilateral leg. This exercise has been found to produce low to moderate activation of the serratus anterior, lower trapezius, and posterior deltoid without significant activation of the upper trapezius (unpublished observation). Both of these exercises incorporate one of the fundamental principles in kinetic chain rehabilitation: facilitating distal motion by initially activating the proximal musculature.51,52 Proximal activation of leg and trunk musculature before activating primary movers in to prepare the entire system for motion is called anticipatory postural adjustment.12,13 We emphasize trunk and leg motion to use this natural motor control pattern and to be sure the trunk is properly positioned to allow arm motion. Flexibility of the surrounding shoulder musculature and spine is addressed early in the rehabilitation program in association with strengthening exercises. Stretching exercises such as corner stretch, scapular retraction on a roll, and biceps stretch (Fig. 50-7) are used to lengthen tight pectoral musculature, which has been demonstrated to negatively affect scapular kinematics.36 Each stretch should be held for 30 seconds and performed two or three times at least once a day.53 Cervical, thoracic, and lumbar spine flexibility exercises are prescribed to address mobility restrictions identified in the examination.
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The combination of stretching and strengthening exercises has been found to positively affect posture. Wang and colleagues54 demonstrated that a program of progressive resistive exercises using elastic resistance of horizontal abduction, scapular retraction with external rotation, shrugs, and shoulder abduction in the scapular plane along with corner stretching performed independently decreased thoracic kyphosis and improved scapular stability. A similar study performing shoulder external rotation, shoulder flexion, and horizontal adduction using elastic resistance exercises three times a week for 3 sets of 10 to 15 repetitions in combination with passively lengthening pectoralis minor and major musculature reduced forward scapular displacement by almost 1 cm in young competitive swimmers.35 Unfortunately, not all patients respond to stretching and strengthening exercises. In some chronic pain conditions, patients cannot correct their own posture and need external assistance. In the past, figure-of-eight clavicle straps and other braces reminding patients of their posture have been used. McConnell taping to either facilitate or inhibit scapular musculature might decrease pain and improve function.55-57 Scapular taping is typically applied to retract, posteriorly tilt, and externally rotate the scapula (Fig. 50-8) to allow the patient to perform functional activities with less pain.55 The tape is applied and left on for several days at a time until the patient demonstrates adequate neuromuscular control of the scapula independent of the tape. One drawback of taping is that the patient requires the assistance of another to apply the tape. Therefore, the patient has to return to the clinic frequently or have another person trained to tape the scapula. Another drawback is that the tape is expensive and occasionally can irritate the patient’s skin. The spine and scapula stabilizing brace (Scapula Stabilizing System [S3], Alignmed, Santa Ana, Calif) corrects postural alignment of the scapular and spine by simulating the effects of taping (Fig. 50-9). The
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that incorporate the entire length of the arm with resistance applied distally. The load of arm alone is approximately 5% of a person’s body weight.58 The often-inflamed structures about the shoulder are further aggravated when exercises that use even the weight of the arm alone are initiated. We attempt to reduce this occurrence in three ways: Strengthen proximal muscles first to avoid inflaming healing tissues further, use the proximal muscles to assist in moving the distal extremity through momentum, and support the weight of the upper arm by keeping it in contact with a surface during large arcs of motion initially until proper mechanics and neuromuscular control of the motion are demonstrated. Figure 50-8. Scapular taping to retract the scapula during scaption exercise.
Figure 50-9. Spine and scapula stabilizing brace from a posterior view with all support strapping applied.
initial results of the brace on scapular kinematics suggest that the brace alters scapular posterior tilt and scapular external rotation in the lower ranges of arm elevation. Anecdotal reports from our patients with scapular dyskinesis are mixed; however, some patients do have good relief of symptoms from this orthosis. Further research is necessary to determine its effectiveness.
Proximal Stability Proximal leg, trunk, and scapular musculature is activated to prepare the system for higher demanding distal loads. The proximal-to-distal muscle activation pattern is a normal motor-activation pattern for upper-extremity motions.12,14 To promote a functional rehabilitation approach, we attempt to recreate this activation approach. A common mistake in treating shoulder injuries is the early use of exercises
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Trunk strength and stability are initially screened during the examination with the single leg stance and squat. In patients demonstrating poor stability, specific strength tests are performed on hip musculature to identify specific strength deficits. The hip deficits are incorporated with the core stabilization exercise program, focusing on activating transverse abdominus and multifidus muscles by performing a drawing in maneuver. Activation of these muscles always precedes distal arm motion.13,59 In patients with significant core stabilization deficits, a basic mat program should be initiated, progressing to functional motions. An ideal period to focus on core stabilization exercises is in the immobilization period following a shoulder surgery or significant injury, when shoulder activities are limited. The core stabilization program can be emphasized on alternating days to break up the redundancy of a rehabilitation program in an athletic environment when patients are seen frequently. Kinetic chain shoulder exercises attempt to use the trunk and legs to gain control of the trunk and facilitate scapula and shoulder motion. Knott and Voss call this irradiation, a process of facilitating inhibited muscle by activating stronger muscles that are synergistic for a movement pattern.60 We focus on facilitating scapular retraction (external rotation, posterior tilt, depression) as our primary goal to gain proximal stability for the shoulder. The treating clinician needs to have several methods to facilitate this control and progressively increase the demands to strengthen the periscapular musculature. Use of sagittal trunk motion, by starting with trunk flexed and moving into extension, to facilitate scapular retraction is a first-line activity. Integrating horizontal rotation or frontal plane motions can be incorporated to provide variety or if sagittal motions do not produce the desired scapular retraction with correct trunk posture. Incorporating a 4- to 6-inch step into an exercise engages the lower extremity and trunk musculature involuntarily. This additional demand recruits a greater neuromotor pool of the proximal musculature to assist stabilization and requires patients to work on postural stability by challenging their balance. The individual needs of the patient, the fundamental principles of physiologic healing tissue restrictions, and
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BOX 50-2.
Scapular Retraction Exercises
Isometric Exercises Isometric exercises are used for patients to activate scapular retractors in a controlled environment requiring minimal to no glenohumeral motion. LOW ROW (SEE FIG. 50-6)
The low row produces scapular retraction and depression. With the hand at the side, extension of the shoulder is coordinated with a forward weight shift to the opposite leg. This can be performed isometrically and progressed to an isotonic exercise. Be certain the lower trapezius is activated and the scapula is depressing. INFERIOR GLIDE (SEE FIG. 50-10)
The inferior glide produces scapular retraction with shoulder adduction with the arm abducted to approximately 90 degrees. Be certain the lower trapezius is activated and the scapula is depressing.
Dynamic Standing Exercises Dynamic standing exercise is the most common. The patient takes an astride athletic position to perform these exercises with the opposite side leg slightly forward. LAWNMOWER (IN SLING)
The patient starts with the trunk flexed and rotated slightly toward the opposite leg. The scapula is retracted and the arm is supported in a sling. The motion is the same as in the standard lawnmower exercise but with small amplitude and low intensity. LAWNMOWER SUPPORTED (SEE FIG. 50-11)
The patient strives for the same scapular retraction end position, but the arm is free to move and the weight of the arm is supported so as not to overload inflamed tissues in the glenohumeral joint. LAWNMOWER ON A STEP (SEE FIG. 50-12)
The patient starts with the trunk flexed and rotated trunk the opposite leg. The scapula is retracted with the arm
externally rotating. The addition of the step is to facilitate more trunk and pelvic muscle activation to encourage better scapular retraction during the maneuver. SHOULDER DUMP
The patient starts with the trunk flexed and rotated toward the opposite leg just as in the lawnmower exercises. The scapula is retracted with the arm abducting and externally rotating within a pain-free range. This activity simulates the cocking phase of a throwing motion.
Dynamic Sitting Exercises Dynamic sitting exercises are for patients who have lowerextremity limitations that preclude them from dynamic standing activities or who need to perform a significant component of their sports in a nonstanding phase such as swimming, water polo, and volleyball. Dynamic sitting activities can be started on a stable chair and progressed to a Swiss ball or a wobble board for home therapy. The patient is progressed to place the feet on the unstable surface to increase trunk demand. SCAPULAR RETRACTION ON BALL (SEE FIG. 50-13)
The lawnmower exercise is performed in a sitting position to facilitate scapular retraction with greater emphasis placed on trunk and scapular musculature, because the legs cannot contribute as much. The patient sits on a Swiss ball and reaches with the affected arm down toward the weight-bearing ankle. The patient retracts and depresses the scapula while pulling the elbow toward the back pocket and shifting the weight toward the opposite leg. DIAGONAL ROTATIONS ON BALL
Perform a diagonal resistance pattern while sitting on a ball. This exercise simulates throwing activities such as arm cocking, pulling arm into abduction, and external rotating and it simulates the acceleration phase of throwing, bringing the arm from overhead diagonally across the body.
progressing from low- to high-demand activities are always respected during the course of rehabilitation. Examples of scapular retraction exercises are provided in attempt to meet the goals outlined earlier (Box 50-2 and Figs. 50-10 to 50-13) Typically, the patient can control the scapula with these integrative techniques; however, some patients require manual assistive and resistive techniques described as rhythmic initiation and reversal of antagonists.60 These techniques can be performed with the patient side lying, if necessary, to isolate scapular muscle control as described by Adler,61 or they can be performed standing, applying resistance to the scapula through the motion.
Overhead Elevation Progression Arm elevation progression can begin when a patient demonstrates adequate scapular stability with retraction. It is not expected that the athlete will go through an entire
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Figure 50-10. Inferior glide with the scapula posteriorly tilting due to activation of the lower trapezius muscle.
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B
A
Figure 50-11. Lawnmower exercise, supported, allows the patient to start moving through the functional range of motion but does not overload healing tissues by keeping the weight of the arm supported on the Swiss ball. A, Starting position, to be adjusted to limits of comfort and motion restrictions. B, Ending position to emphasize scapular retraction.
Figure 50-12. Lawnmower exercise on a step to facilitate core muscle activation. A, Starting position to prestretch target musculature, B, Finishing position incorporates lower extremity stability with trunk and scapular retraction in a single exercise.
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A
B
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B
A
Figure 50-13. Scapular retraction on a Swiss ball. A, Start by reaching toward the ipsilateral leg with weight on the ipsilateral foot and the contralateral foot slightly off the ground. B, Finish by retracting the scapula and tucking elbow into the back pocket as weight is shifted off the ipsilateral foot onto the contralateral foot.
A
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B
Figure 50-14. Kinetic chain wall slides. Overhead reach with towel slide starting in crouched position (A) and using the legs to drive the arm up while simultaneously reaching overhead (B).
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retraction program before initiating elevation exercises. However, it is a common rehabilitation error that patients are given elevation exercises that are too demanding, which result in scapular substitutions and inflamed shoulder tissues. The primary aim during this progression is to gain the pain-free and substitution-free full active arm elevation unsupported. Once this is obtained, moredemanding strengthening programs are initiated, leading to task- and sport-specific activities.
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The initial arm elevation exercises should be performed with the arm supported and initiated by the trunk and legs. Support of the arm can be easily obtained by sliding the hand along a surface. Lephart described this type of motion as a “movable boundary with axial load.”62 The friction between these two surfaces should be minimized to allow the patient to move the arm freely. This can be obtained by using a towel on a glass or smooth wooden door or using lotion or powder on a treatment plinth. The arm load is diminished
TABLE 50-1 Exercise Progression for Shoulder Musculature Exercise
Deltoid
Supraspinatus
Upper Trapezius
Serratus Anterior
Lower Trapezius
Rows with elastic tubing1,2
NA
Peak: 39 ± 16 Avg: 9 ± 2
Peak: 34 ± 23 Avg: 9 ± 6
Peak: 10 ± 6 Avg: 5 ± 4
NA
Unilateral rows3,4
72 ± 20
NA
63 ± 17
14 ± 6
45 ± 17
Standing press-up with elbow bent 5
30 ± 11
30 ± 17
24 ± 8
29 ± 13
9±5
Peak: 39 ± 23 Avg: 9 ± 4
Peak: 48 ± 83 Avg: 8 ± 3
NA
Peak: 49 ± 14 Avg: 10 ± 3
NA
Prone flexion at 135 deg of abduction3
NA
NA
79 ± 18
43 ± 17
97 ± 16
Prone ER at 90 deg3,6
NA
50
20 ± 18
57 ± 22
79 ± 21
Unilateral shoulder press supine w/a plus3
N.A
NA
7± 3
62 ± 19
11 ± 5
Scaption ⬍80 deg3,7
Forward punch2
91 ± 26
82 ± 27
72 ± 19
62 ± 18
50 ± 21
4,8
72 ± 24
56 ± 48
64 ± 26
82 ± 36
NA
Scaption ⬎120 deg3,4
72 ± 13
64 ± 28
79 ± 19
96 ± 24
61 ± 19
Diagonal flexion, horizontal adduction, ER3
NA
NA
66 ± 10
100 ± 24
39 ± 15
Push-up with a plus9
NA
NA
50
140
30
Military press
Note: This exercise progression for shoulder musculature is based on published EMG literature and is organized based on the serratus anterior musculature. The percentage of the maximal voluntary isometric contraction plus or minus standard deviation is that reported in the cited reference. Caution should be used in interpreting this table because different loads were used in different studies, which can account for EMG variations. 1. Decker MJ, Hintermeister RA, Faber KJ, et al: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27:784-791, 1999. 2. Hintermeister RA, Lange G, Schultheis J, et al: Electromyographic activity and applied load during shoulder rehabilitation exercises using elastic resistance. Am J Sports Med 26:210-220, 1998. 3. Ekstrom RA, Donatelli RA, Soderberg G: Surface electromyographic analysis of exercises for the trapezius and serratus anterior muscles. J Orthop Sports Phys Ther 33:247-258, 2003. 4. Townsend H, Jobe FW, Pink M, et al: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19:264-272, 1991. 5. Lawson L, Klare K, Uhl TL: Electromyographic assessment of 13 shoulder rehabilitation exercises. Unpublished data, 2003. 6. Blackburn TA, McLeod WD, White B, et al: EMG analysis of posterior rotator cuff exercises. J Athl Train 25:40-45, 1990. 7. Alpert SW, Pink MM, Jobe FW, et al: Electromyographic analysis of deltoid and rotator cuff function under varying loads and speeds. J Shoulder Elbow Surg 9:47-57, 2000. 8. Moseley JB, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. 9. Lear JL, Gross MT: An electromyographical analysis of the scapular stabilizing synergists during a push-up progression. J Orthop Sports Phys Ther 28:146-157, 1998. avg, average EMG amplitude occurring during the exercise by a particular muscle; EMG, electromyography; ER, external rotation; NA, not available; peak, peak EMG amplitude reached during exercise performed by a particular muscle.
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and the demand is lessened on shoulder musculature by placing the hand in contact with a surface.63 Progressing from horizontal limited flexion angle (⬃ 60 degrees) to a vertical surface allowing full flexion is a logical progression. However, in arm-elevation exercises that are near 90 degrees, the load of the arm is the greatest and increases the demand on shoulder musculature.63,64 In some cases, patients tolerate vertical motions before they tolerate more diagonal reaching motions that place the arm at 90 degrees. These arm elevation motions are initiated by placing the patient in the astride athletic position, with the hips and knees flexed, and instructing the patient to drive the arm up by extending the lower legs and continuing the reaching task through the upper extremity (Fig. 50-14). This allows momentum to be used. As strength of the shoulder increases, less use of trunk motion is encouraged to decrease the use of momentum. Removal of the support surface makes the exercise a more-functional open-kinetic-chain strengthening exercises.
Strengthening Progression Patients can progress to traditional long-lever-arm resistance exercises to strengthen and gain endurance once they demonstrate proper control of shoulder and scapular motion during both retracting and overhead reaching activities. The patient should be able to elevate at least to 120 degrees without resistance without scapular winging or shrugging (dyskinesis). The exercises described to this point have focused on gaining neuromuscular control of the scapula through using the kinetic chain. Incorporating resistive exercises that have been found to activate shoulder and scapular musculature by electromyographical (EMG) studies is important. The challenge of increasing load, repetitions, and speed are all factors that should be incorporated into the recovery and sport-specific phases of rehabilitation after a solid base of the spine and scapula are established. EMG studies have focused on identifying which exercise maximally activates the scapular musculature. In 1992, Moseley65 published core exercises to maximally activate the trapezius, serratus anterior, and rhomboids. Other researchers have investigated other shoulder exercises to help develop an exercise progression for clinicians to strengthen scapular and shoulder musculature.44,66-68 One major underlying principle of rehabilitation is to progress from lowerdemand to higher-demand activities without overloading healing tissues. This guiding principle in rehabilitation has led us to develop a scapular strengthening exercise progression based on the available literature. The exercise progression starts from the point of the patient demonstrating controlled active forward elevation without scapular substitutions and pain (Table 50-1). The exercise order is changed depending on the target musculature; for this table we targeted the serratus anterior.
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SUMMARY It is important to evaluate dynamic function of the scapula with and without load and evaluate trunk position and control during dynamic activities such as a single-leg squat. If all impairments are not identified in a complete assessment, the athlete is likely to return with similar complaints. Our rehabilitation approach addresses the deficits identified in the examination with particular focus on improving trunk and scapular posture. Rehabilitation that focuses on enhancing proximal stability and control of pelvis, trunk, and scapula should establish a foundation; then, patient-specific exercises that gradually increase the demands of the scapular and shoulder musculature can be built on this foundation.
References 1. Feltner ME, Dapena J: Three-dimensional interactions in a two-segment kinetic chain. Part I: General model. Int J Sport Biomech 5:403-419, 1989. 2. Putnam CA: Sequential motions of body segments in striking and throwing skills: Description and explanations. J Biomech 26:125-135, 1993. 3. Hirashima M, Kadota H, Sakurai S: Sequential muscle activity and its function role in the upper extremity and trunk during overarm throwing. J Sports Sci 20:301-310, 2002. 4. Fleisig GS, Barrentine SW, Escamilla RF, et al: Biomechanics of overhand throwing with implications for injuries. Sports Med 21:421-437, 1996. 5. Toyoshima S, Hoshikawa T, Miyashita M: Contributions of Body Parts to Throwing Performance. Biomechanics IV. Baltimore, University Park Press, 1974, pp 169-174. 6. Kibler WB. Biomechanical analysis of the shoulder during tennis activities. Clin Sports Med 14:79-85, 1996. 7. Davids K, Glazier P, Arajuo D, et al: Movement systems as dynamic systems: The functional role of variability and its implications for sports medicine. Sports Med 33:245-260, 2003. 8. Kraemer WJ, Triplett NT, Fry AC: An in-depth sports medicine profile of women college tennis players. J Sport Rehabil 4:79-88, 1995. 9. Inman VT, Saunders M, Abbott LC: Observations of the function of the shoulder joint. J Bone Joint Surg Am 26:1-31, 1944. 10. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics, and tennis. Clin Sports Med 2:247-270, 1983. 11. Davidson PA, El Attrache NS, Jobe CM et al: Rotator cuff and posterior-superior glenoid labrum injury associated with increased glenohumeral motion: A new site of impingement. J Shoulder Elbow Surg 4:384-390, 1995. 12. Zattara M, Bouisset S: Posturo-kinetic organisation during the early phase of voluntary upper limb movement. 1 Normal subjects. J Neurol Neurosurg Psychiatry 51: 956-965, 1988. 13. Cordo PJ, Nashner LM: Properties of postural adjustments associated with rapid arm movements. J Neurophysiol 47:287-308, 1982.
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14. Bouisset S, Zattara M: A sequence of postural movements precedes voluntary movement. Neurosci Lett 22:263-270, 1981. 15. Le Bozec S, Lesne J, Bouisset S: A sequence of postural muscle excitation precedes and accompanies isometric ramp efforts performed while sitting in human subjects. Neurosci Lett 303:72-76, 2001. 16. Karduna AR, McClure PW, Michener LA, et al: Dynamic measurements of three-dimensional scapular kinematics: A validation study. J Biomech Eng 123:184-190, 2001. 17. McClure PW, Michener LA, Sennett BJ, et al: Direct 3-dimensional measurement of scapular kinematics during dynamic movements in vivo. J Shoulder Elbow Surg 10: 269-277, 2001. 18. Warner JJP, Micheli LJ, Arslanian LE, et al: Scapulothoracic motion in normal shoulders and shoulders with glenohumeral instability and impingement syndrome. A study using Moiré topographic analysis. Clin Orthop Rel Res (285): 191-199, 1992. 19. Rubin BD, Kibler WB: Fundamental principles of shoulder rehabilitation: Conservative to postoperative management. Arthroscopy 18:29-39, 2002. 20. Schultz JS, Leonard A Jr: Long thoracic neuropathy from athletic activity. Arch Phys Med Rehabil 73:87-90, 1992. 21. Warner JJ, Navarro RA: Serratus anterior dysfunction. Recognition and treatment. Clin Orthop Rel Res (349): 139-148, 1998. 22. Cools AM, Witvrouw E, Declercq GA et al: Evaluation of isokinetic force production and associated muscle activity in the scapular rotators during a protraction-retraction movement in overhead athletes with impingement symptoms. Br J Sports Med 38:64-68, 2004. 23. Borstad JD, Ludewig PM: The effect of pectoralis minor length on scapular kinematics in subjects without shoulder pathology [abstract]. J Orthop Sports Phys Ther 34(1):A16, 2004. 24. McQuade KJ, Dawson JD, Smidt GL: Scapulothoracic muscle fatigue associated with alterations in scapulohumeral rhythm kinematics during maximum resistive shoulder elevation. J Orthop Sports Phys Ther 28:74-80, 1998. 25. Tsai L, Wredmark T, Johansson C, et al: Shoulder function in patients with unoperated anterior shoulder instability. Am J Sports Med 19:469-473, 1991. 26. Brox JI, Roe C, Saugen E, et al: Isometric abduction muscle activation in patients with rotator tendinosis of the shoulder. Arch Phys Med Rehabil 78(11):1260-1267, 1997. 27. Scovazzo ML, Browne A, Pink M, et al: The painful shoulder during freestyle swimming, an electromyographic cinematographic analysis of twelve muscles. Am J Sports Med 19:577-582, 1991. 28. Wadsworth DJ, Bullock-Saxton JE: Recruitment patterns of the scapular rotator muscles in freestyle swimmers with subacromial impingement. Int J Sports Med 18:618-624, 1997. 29. Glousman R, Jobe FW, Tibone JE, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral instability. J Bone Joint Surg Am 70:220-226, 1988. 30. Ludewig PM, Cook TM: Alterations in shoulder kinematics and associated muscle activity in people with symptoms of shoulder impingement. Phys Ther 80:276-291, 2000. 31. Lukasiewicz AC, McClure P, Michener L, et al: Comparison of 3-dimensional scapular position and orientation between
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subjects with and without shoulder impingement. J Orthop Sports Phys Ther 29:574-586, 1999. Burkhart SS, Morgan CD, Kibler WB: The disabled throwing shoulder: Spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 19:404-420, 2003. Kamkar A, Irrgang JJ, Whitney SL: Nonoperative management of secondary shoulder impingement syndrome. J Orthop Sports Phys Ther 17:212-224, 1993. Kebaetse M, McClure P, Pratt N: Thoracic position effect on shoulder range of motion, strength, and three-dimensional scapular kinetics. Arch Phys Med Rehabil 80:945-950, 1999. Kluemper M, Uhl TL, Hazelrigg H: Effect of stretching and strengthening shoulder muscles on forward shoulder posture in competitive swimmers. J Sport Rehabil 15:58-70, 2006. Borstad JD, Ludewig PM: The effect of long versus short pectoralis minor resting length on scapular kinematics in healthy individuals. J Orthop Sports Phys Ther 35:227-238, 2005. Kibler WB: Role of the scapula in the overhead throwing motion. Contemp Orthop 22:525-532, 1991. Odom CJ, Taylor AB, Hurd CE, et al: Measurement of scapular asymmetry and assessment of shoulder dysfunction using the lateral scapular slide test: A reliability and validity study. Phys Ther 81:799-809, 2001. Kibler WB, Uhl TL, Maddux JQ, et al: Qualitative clinical evaluation of scapular dysfunction. A reliability study. J Shoulder Elbow Surg 11:550-556, 2002. Kibler WB, McMullen J: Scapular dyskinesis and its relation to shoulder pain. J Am Acad Orthop Surg 11:142-151, 2003. DiMattia MA, Livengood AL, Uhl TL, et al: What are the validity of the single-leg squat test and its relationship to hip abduction strength. J Sport Rehab 14:108-123, 2005. Michener LA, Boardman ND, Pidcoe PE, et al: Scapula muscle tests in subjects with shoulder pain and functional loss: reliability and construct validity. Phys Ther 85: 1128-1138, 2005. Kendall FP, McCreary EK, Provance PG: Upper extremity and shoulder girdle strength test. In Butler JP (ed): Muscle Testing and Function. Baltimore, Williams & Wilkins, 1993, pp 235-298. Ekstrom RA, Donatelli RA, Soderberg G: Surface electromyographic analysis of exercises for the trapezius and serratus anterior muscles. J Orthop Sports Phys Ther 33:247-258, 2003. Smith J, Padgett DJ, Kaufman KR, et al: Rhomboid muscle electromyography activity during 3 different manual muscle tests. Arch Phys Med Rehab 85:987-992, 2004. Kibler WB, Sciascia A, Dome D: Evaluation of apparent and absolute supraspinatus strength in patients with shoulder injury using the scapular retraction test. Am J Sports Med 34:1643-1647, 2006. Kibler WB, Livingston B, Bruce R: Current concepts in shoulder rehabilitation. Adv Oper Orthop 3:249-299, 1995. Kapandji IA: The shoulder. In Kapandji IA (ed): The Physiology of the Joints. New York, Churchill Livingstone, 1982, pp 2-71. Solem-Bertoft E, Thuomas KA, Westerberg CE: The influence of scapular retraction and protraction on the width of the subacromial space. An MRI study. Clin Orthop Relat Res (296):99-103, 1993.
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50. Smith J, Kotajarvi BR, Padgett DJ, Eischen JJ: Effect of scapular protraction and retraction on isometric shoulder elevation strength [abstract]. Arch Phys Med Rehab 83:367-370, 2002. 51. McMullen J, Uhl TL: A kinetic chain approach for shoulder rehabilitation. J Athl Train 35:329-337, 2000. 52. Kibler WB, McMullen J, Uhl T: Shoulder rehabilitation strategies, guidelines, and practice. Orthop Clin North Am 32:527-538, 2001. 53. Bandy WD, Irion JM, Briggler M: The effect of time and frequency of static stretching on flexibility of the hamstring muscles. Phys Ther 77:1090-1096, 1997. 54. Wang C-H, McClure P, Pratt N et al: Stretching and strengthening exercises: Their effect on three-dimensional scapular kinematics. Arch Phys Med Rehabil 80:923-929, 1999. 55. Host HH: Scapular taping in the treatment of anterior shoulder impingement. Phys Ther 75:803-811, 1995. 56. Cools AM, Witvrouw EE, Danneels LA, et al: Does taping influence electromyographic muscle activity in the scapular rotators in healthy shoulders? Man Ther 7:154-162, 2002. 57. Ackermann B, Adams R, Marshall E: The effect of scapula taping on electromyographic activity and musical performance in professional violinists. Aust J Physiother 48: 197-203, 2002. 58. Dempster WT: Space requirements of the seated operator: Geometrical, kinematic, and mechanical aspects of the body, with special reference to the limbs. Technical Report TR-55-159. Wright-Patterson Air Force Base, Ohio, 1955.
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59. Hodges PW, Richardson CA: Feedforward contraction of transversus abdominus is not influenced by the direction of arm movement. Exp Brain Res 114:362-370, 1997. 60. Knott M, Voss DE: Proprioceptive Neuromuscular Facilitation Patterns and Techniques. Philadelphia, Harper & Row, 1968. 61. Adler SS, Beckers D, Buck M: PNF in Practice: An Illustrated Guide. New York, Springer-Verlag, 1993. 62. Lephart SM, Henry TJ: The physiological basis for open and closed kinetic chain rehabilitation for the upper extremity. J Sport Rehabil 5:71-87, 1996. 63. Wise MB, Uhl TL, Mattacola CG, et al: The effect of limb support on muscle activation during shoulder exercises. J Shoulder Elbow Surg 13:614-620, 2004. 64. Poppen N, Walker P: Forces at the glenohumeral joint in abduction. Clin Orthop Rel Res (135):165-170, 1978. 65. Moseley JB, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. 66. Decker MJ, Hintermeister RA, Faber KJ, et al: Serratus anterior muscle activity during selected rehabilitation exercises. Am J Sports Med 27:784-791, 1999. 67. Decker MJ, Tokish JM, Ellis HB, et al: Subscapularis muscle activity during selected rehabilitation exercises. Am J Sports Med 31:126-134, 2003. 68. Ekstrom RA, Bifulco KM, Lopau CJ, et al: Comparing the function of the upper and lower parts of the serratus anterior muscle using surface electromyography. J Orthop Sports Phys Ther 34:235-243, 2004.
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CHAPTER 51 Alternative Techniques
for the Motion-Restricted Shoulder Robert E. Mangine, Matthew J. Ernst, and Marsha Eifert-Mangine
TREATMENT OF ARTHROFIBROSIS
factors associated with loss of range of motion, postoperative complications leading to motion loss, manual therapy principles of restriction, the patient’s clinical response, and the connective tissue’s response to factors associated with restricted motion.
Loss of motion of the glenohumeral joint caused by the development of arthrofibrosis often occurs after injury or surgery of the shoulder. Establishing range of motion after a joint trauma is the earliest goal of rehabilitation. When treating the motion-restricted shoulder, it does not take long to realize that many possible pathologies are associated with this complication. The most common pathologies correlating to frozen shoulder include adhesive capsulitis, periarthritis, painful shoulder syndrome, periarticular adhesions, short rotator tendinitis, bicipital tenosynovitis, subacromial bursitis, fibromyositis, supraspinatus tendinitis, and reflex sympathetic dystrophy.1-8
HISTORICAL PERSPECTIVE To provide an adequate treatment approach to the motion-restricted shoulder, it is necessary to identify structures involved in the injury process. A review of the literature provides a capsulized version of the advanced research performed. Codman,1 in 1934, identified the frozen shoulder. He attributed the decrease in range of motion to the painful, stiff shoulder associated with a short rotator tendinitis. McLauglin,2 in 1939, used surgical exploration of frozen shoulders to reveal no histologic evidence of inflammation. The loss of range of motion was correlated with a loss of elasticity in the redundant fold of the inferior capsule. Shortening of the rotator cuff kept the humeral head position tight in the glenoid, and with prolonged disuse of the shoulder, it appeared to precede the stiff shoulder. Changes in the periarticular connective tissue collagen were believed to be related to effects of immobility.
These pathologies would be considered primary diagnoses that can lead to a motion complication; therefore, adequate differential diagnosis is critical in determining the primary lesion. There does seem to be some recognized predisposing factors. Adhesive capsulitis appears to affect middleaged patients, from 45 to 70 years of age; the mean age for men is 55 years, and mean age for women is 52 years.9-12 In 1000 nondiabetic patients, the incidence was approximately 2%. Among diabetic patients, 10% to 20% have adhesive capsulitis, and the rate among insulin-dependent diabetics is 36%.13-17 To attempt to progress the patient into the strength or functional activities portion of the program can exacerbate the motion restriction. All too often clinicians intervene with strengthening exercises as a means of establishing motion, with the reverse effect as the end result. To understand motion complications, the therapist must consider the causal factors. These include arthrokinematic disruption in the direction of the restriction, biomechanics of surgical intervention, adaptation of musculotendinous fibers in a shortened position, scar tissue development involving capsular or ligamentous tissue, and pathomechanics within the joint.
Lippman,3 in 1943, performed surgical examinations to diagnose frozen shoulders. He observed tenosynovitis of the long head of the biceps and thickening of the sheath as well as edema of the tendon, which was roughened and adherent to the sheath. As the condition advanced, it was associated with increased adhesions. An upward spread of the tenosynovitis into the shoulder created intracapsular adhesions of the tendon. Work by Neviaser4 in 1945 revealed decreased synovial fluid in the glenohumeral space and associated thickening of the auxiliary fold of the capsule. The capsule became adherent to the humeral head, thus defining the term adhesive capsulitis.
Following a logical progress of evaluation, these indications can help the therapist initiate a treatment program to prevent the secondary diagnosis from occurring. Secondary diagnoses include those associated with loss of joint range of motion (frozen shoulder or adhesive capsulitis) or those associated with an abnormal response to pain (reflex sympathetic dystrophy).
Simmonds,5 in 1949, suggested that a loss in range of motion was associated with rotator cuff inflammation. Impingement of the supraspinatus tendon created degenerative changes within the tendon caused by impaired circulation. Further impingement of this decreased vascular area was the cause of partial tears of the rotator cuff.
Review of the motion-restricted shoulder requires detailing of the historical perspective of motion loss theories, general 685
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In 1966, Reeves6 substantiated the concept of the capsular pattern with the use of the arthrogram. Contrast dye was used to show an increased deposit of the dye in the posterior aspect of the shoulder. The joint capsule size was reduced, and the inferior capsular fold, subscapularis bursa, and biceps sheath were obliterated. By assessing the arthrokinematics, joint motion restrictions became clear. Involvement of the anterior capsule results in loss of external rotation. The decrease in abduction is consistent with inferior capsular involvement. Turek,7 in 1977, indicated that repetitive trauma of the rotator cuff and biceps tendon against the acromion results in degeneration and inflammation. With persistent trauma, granular scar tissue occurs during healing, which leads to fibrous adhesions of the rotator cuff, biceps, subacromial bursa, and capsule. The resulting scar lesions lead to a decrease in range of motion. DePalma,8 in 1983, suggested that a frozen shoulder involves a fibrous capsule. The capsular tissues shrink and become nonelastic. As the inflammatory process progresses, it involves the synovial fluid, fascia, rotator cuff, biceps tendon, biceps sheath, and subacromial bursa. The inferior redundant fold of the capsule becomes constrained initially. The synovial lining thickens and becomes hypervascular. The coracohumeral ligament also thickens. The subscapularis, infraspinatus, and supraspinatus become tight and also lead to decreased rotation.
CAUSATIVE FACTORS ASSOCIATED WITH MOTION LOSS Factors associated with motion loss can be addressed on both a nonsurgical and surgical basis. Nonsurgical factors include severity of the injury, joint effusion, pain, upper extremity swelling, joint inflammation, patient compliance, delayed mobilization, and muscle weakness. Postsurgical factors include the type of surgery performed (arthroscopy versus arthrotomy), postoperative hemarthrosis, pain, reflex sympathetic dystrophy, muscle shutdown, infection, postoperative neurapraxia, and patient compliance.
Stage I restrictions are those in which the complaints of pain are limited to the shoulder region. The patient exhibits no pain at rest and limited pain with movement. The patient can sleep or lie on the involved shoulder. With passive range of motion, the capsular end feel is a soft springy restriction that is encountered before eliciting the pain response. Muscle spasm is limited and does not interfere with range of motion. Stage II restrictions are evident by several combinations of one or more of the symptoms in stage I (positive rest pain, inability to sleep or lie on the involved side, pain to the elbow). With passive movement, pain is elicited at the same time the capsular restriction is achieved. Muscle spasm can also limit range immediately on entering the restricted range. Stage III restrictions are exhibited by the patient’s complaint of radiating pain into the entire distal segment. The patient also has pain at rest and occasional waking pain. With passive movement, pain increases before the capsular restriction is reached. Once the end range is reached, a hard, leathery end feel stops movement. If pain becomes disproportionate to the pathology, it is crucial to evaluate for other neurologic problems.
CONNECTIVE TISSUE RESPONSE Connective tissue elasticity is decreased in response to immobilization. With immobilization, structural and cellular alterations are seen that result in decreased range of motion, In 1972, Enneking19 described an increase in proliferation of fibrofatty tissue within the joint space. During immobilization, the ground substance of connective tissue undergoes reduction of water, glycosaminoglycans, and lubricating action.20 This results in alteration of the gel-to-fiber ratio, correlating with joint stiffness. Range of motion is important to maintain the normal glycosaminoglycans buffer between the collagen fibers.
CLINICAL PRESENTATION
Another tissue response to restricted motion is random collagen alignment secondary to loss of stress application during normal motion. This leads to adhesions within the connective tissue. Again, fibrofatty deposits within the joint interfere with normal joint range of motion.19
The clinical presentation of patients with arthrofibrosis or motion restrictions displays a capsular pattern (restricted external rotation greater than abduction greater than internal rotation).18 However, other pathologies can mimic these capsular patterns. Therefore, a differential diagnosis must rule out myeloma, reflex sympathetic dystrophy, arthritis, intra-articular lesions, and capsular inflammatory lesions. Nonmuskulosketal conditions such as referred visceral pain and cancer have also been reported to mimic the classic frozen shoulder.
Muscle shortening is also associated with prolonged immobilization. This is evidenced by a decrease in the number of sarcomeres.21 This process also appears to be correlated with age. Muscle response can be reversed by initiating an active range of motion program. This may be one of the advantages with continuous passive motion after surgery. Unfortunately, if immobilization is left unchecked, the result is continued movement dysfunction, which typically leads to a vicious cycle of pain, decreased range of motion, and muscle spasm.22 The clinician must
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define the physiologic component for a motion complication. Total range of motion is defined by arthrokinematic versus osteokinematic movement. The noncontractile soft tissue component that limits range of motion includes all the periarticular structures that came under stress during movement of the joint. The second component controlling joint motion is the contractile component of the muscletendon unit.23 Joint motion results in the muscle-tendon unit’s adapting to a lengthened state to allow the joint or series of joints to move freely. After trauma or surgery, changes in either component of the surrounding soft tissue can result in a motion complication. Early motion intervention is crucial to avoid tissue length changes and development of bridge adhesions in the inferior glenohumeral capsule. The small acromioclavicular and sternoclavicular joints require motion for normal glenohumeral motion. Because the total amount of laxity at the joints is small, they can become easily involved. Structural changes, which commonly occur to joints with immobilization, need to be reversed as soon as possible. The physiologic alterations associated with motion limitation include decreased collagen length in the shortened tissue position,24 fibrofatty infiltration into the capsular recesses,19 ligament atrophy resulting in decreased stress absorption,25 collagen bands bridging across recesses,19 collagen production that is random in orientation,26 and altered sarcomere number in muscle tissue (increase in sarcomeres in the lengthened tissue, decreased sarcomeres in the shortened tissue).24
MOTION RESTRICTIONS In the shoulder with loss of motion, specific patterns of range loss in external rotation, abduction, and flexion are associated with the complication. This is a physiologic response secondary to the position of immobilization and comfort on the part of the patient. Restrictions in these patterns of motion can begin as soon as 24 hours after the onset Pain vs. restricted motion BR
P
RM
687
of immobilization, with or without an injury or surgical procedure. Therefore, early intervention of a motion program to place tension on the periarticular structures should be used. A successful approach after surgery is the use of continuous passive motion. This allows gentle motion to be placed across the healing tissue and avoids high stresses. Manual therapy as a treatment technique for motion complications is also well established in the literature. These techniques are divided into tractions (prolonged holds) or oscillations. Treatment intervention by manual therapy is meant to apply passive movement to restricted joints. Techniques are often based on clinical trials and kinematic knowledge. The mobilization technique chosen by the therapist is based on the clinical evaluation, the primary cause of motion restriction, and the primary diagnosis that led to the motion restriction. A crucial factor for the clinician during manual therapy is application of force. Unfortunately, the literature is subjective in reference to the amount of force applied during mobilization techniques. The clinician applies a force correlated to the degree of motion in the joint. This occurs through evaluating the amount of accessory motion glide obtained in the normal shoulder or based on the preoperative evaluation. Borsa and colleagues attempted to quantify the amount of force needed to reach capsular end feel in the nonimpaired shoulder. The amount of force needed was 181 to 203 N, with anterior translation requiring higher force than inferior translation. This study also supported the circle concept of stability. Average displacement values for the three directions were separated by less than 1 mm (mean anterior, 14.5 mm; posterior, 14 mm; inferior, 13.9 mm).27 An example of motion versus restriction correlation is displayed in Figure 51-1. When moving a joint through accessory motion glides, the total amount of displacement may be broken into four ranges, as described in the literature (Box 51-1). An initial amount of force is needed to move the joint the
Restriction stage
ER Stage I oscillation and traction if pain occurs before restriction
Pain before restricted motion P and RM Stage II oscillation and traction if pain occurs simultaneous to restriction Pain same time as restriction RM
P Stage III oscillation and traction if pain occurs after restriction
Pain after restriction
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Figure 51-1. Range of motion versus restriction stages. BR, beginning range; ER, end range; P, pain; RM, restricted motion.
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BOX 51-1.
Mobilization Grades
BOX 51-2.
Treatment Stages
Grade I Minimal Overpressure
Stage I Treatment
Range limited by 25%
Moist heat with NMES phase I (see Fig. 51-4A)
Pain after restriction
Grades I and II oscillation
Muscle spasm minimal
Pulley program
Soft end point
Pendulum motions
Grade II Moderate
Cane program
Range limited by 25%-75%
Isometrics, shortened range
Pain restriction simultaneous
Muscular strengthening
Muscle spasm moderate
Light-resistance exercises
Hard end point after restriction is encountered
Muscular stretching
Grade III Severe
Ice in the stretch position
Range ⬍75% Pain before restrictions Muscle spasm severe Hard end point as restriction is encountered
Grade IV Maximum Range 90% to ⬍100% Pain after restriction Muscle spasm might limit range Hard end point
Stage II Treatment Moist heat in stretch position with NMES phase II (see Fig. 51-4B) Grade I oscillation or traction Passive motion devices with overpressure (Biodex Isokinetic Dynamometer) Pulley program Cane program Muscular strengthening Grade I oscillation Ice in the stretch position
first 10% of available displacement (grade I motion). The second grade of motion is to move the joint up to 50% of the total displacement. Grade III motion is to move it up to 75% of displacement, and grade IV is to the maximum. Force application beyond this is grade V, or manipulation.
Stage III Treatment
The second factor the clinician accounts for is end feel of the periarticular tissue at the end range. Patterns to end feels in patients with contractures include soft leathery (tissue is resisting movement but might respond well to manual techniques), spasm secondary muscular protection or internal impingement, and hard leathery (tissue is resisting motion but might require a high force or longer periods of mobilization).18,23
Grades II and III mobilization once pain is controlled
In the first part of the range, when applying small traction or oscillation forces, the clinician is primarily affecting the neurologic system or mechanoreceptors.28 These smallamplitude forces can cause relaxation of the surrounding musculature through type I and type II receptors. In the beginning range, it is considered the elastic end of the range where capsular tissue easily elongates and returns. This is an excellent clinical treatment that can be used regardless of what stage of restriction the patient feels (Boxes 51-1 and 51-2).
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Moist heat in the stretch position with NMES phase III (see Fig. 51-4C) Grade I oscillation and traction Passive motion devices with overpressure (Biodex Isokinetic Dynamometer)
Pulley program Isometrics in shortened position Muscle strength Grade I oscillation Ice in the stretch position NMES, neuromuscular electrical stimulation.
Grade I treatment movements can be implemented within the first 3 weeks after immobilization, and only 25% of the range is restricted. Grades I and II mobilization forces can occur for up to 50% of the treatment time. Stage I restrictions can occur very quickly and are not always associated with injury or surgery. This often occurs even with simple overuse syndrome injuries.
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689
Grade II movements take the joint into the 50% point of the range and apply a force on the collagen into a stretched position. If the joint shows restrictions to 50% of the range, a moderate amount of force will be needed to accomplish this. Postscapsular shift patients often show restrictions into this range.
distraction, anterior and posterior glide, inferior glide, and internal and external rotation.
Grade III restrictions are characterized by greater than 50% motion loss, muscle guarding, and a painful examination. The restriction is highlighted by a hard, leathery end feel, which results in pain as the restriction is entered. Aggressive mobilization might only cause a secondary muscle response of spasm to protect the joint. Low force to moderate pain with long hold periods is generally used to avoid the muscle response. Care must be taken to avoid triggering an inflammatory response of the synovial tissue with treatment.
Anterior and Posterior Glide Anterior and posterior glide is a movement in the sagittal plane. The common position for the therapist is to stabilize the arm in 30 degrees of flexion and 70 degrees of abduction. A slight amount of distraction is applied to the joint before the gliding movement (Fig. 51-2). For cases of isolated anterior capsular tightness a better anterior glide can be accomplished with the patient in the prone position and the arm resting on the therapist’s thigh.
NEUROMUSCULAR ELECTRICAL STIMULATION
Distraction Distraction is a movement in which the therapist applies a traction in the long-axis direction of the lever arm.
Inferior Glide Inferior glide is a movement in the coronal plane. Again, the arm is stabilized in 30 degrees of flexion and 70 degrees of abduction, while distraction is applied before moving into the inferior direction (Fig. 51-3).
Advances in portable electrical stimulation devices have allowed us to be more liberal in introducing these devices into the patient’s home program. We also use the smaller devices for a more functional progression. Treatment of the frozen shoulder as a secondary diagnosis in the postoperative patient begins on day 1 with prevention and education. The use of neuromuscular electrical stimulation (NMES) postoperatively has been supported in the literature.29-31 When applied to the postoperative shoulder, NMES helps to decrease hemarthrosis through muscle pumping, prevents muscle shutdown by improving rotator cuff activation, and decreases postoperative pain. These all improve postoperative ROM, preventing a secondary frozen shoulder. The use of NMES is not limited to prevention of adhesive capsulitis. It can also be an effective modality for treating decreased ROM. Improved muscle activation of the rotator cuff helps to establish a normal glenohumeral rhythm, improves inferior glide of the humeral head, and assists in restoring normal joint kinematics. Muscle re-education also helps carry over ROM gained from one treatment to the next. We have found benefit in using NMES in functional positions to achieve greater overhead range of motion.
Figure 51-2. Distraction technique with shoulder held in 30 degrees of forward flexion and 70 degrees of abduction.
MOBILIZATION POSITIONS AND DIRECTION Single-Plane Movements The simplest of all mobilization techniques are single plane. These movements are designed to follow the arthrokinematics of the joint. The movements revolve around
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Figure 51-3. Inferior glide with arm abducted to 70 degrees and neutral flexion.
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Internal and External Rotation Internal and external rotation is a movement in the transverse plane. The therapist may elect to perform these movements in the 90/90-degree position. Slight distraction is applied before beginning to mobilize. The therapist may choose between long-axis or short-axis force application. Long-axis forces can result in a higher joint force because of the lever arm. The side-lying position can also be an effective way to mobilize inferiorly while maintaining good scapular stabilization. By having the patient place the hand palm down on the treatment table, you can fix the upper extremity and achieve greater force production for the inferior glide.
Multiplane Movements The scientific knowledge of collagen tissue adaptation and stress capabilities has become well established. Work by Butler and colleagues32 defined the structural matrix of collagen and the effects of single-plane versus multiple-plane
A
force application. Based on this work and on soft tissue healing (extra-articular) and scar remodeling, the amount of force and the positions might need to be varied in the late states of motion complications. Therefore, one of us (MEM) developed a series of mobilization positions defined as multiplane movements (Fig. 51-5). Greater force can be achieved by using the therapist’s hip in the patient’s axilla to create a fulcrum for generating force (see Fig. 51-5A, B, and D). This position allows the therapist to grade force application by applying trunk rotation away from the patient and using the therapist’s body to stabilize the scapula. The purpose of these movements is to replicate normal arthrokinematic motions that occur at the joint articular surface. Also, by applying multiplane movements, the amount of force needed can be lower based on adaptation of collagen tissue as shown in laboratory research.32
B
C
D Figure 51-4. Augmentation of the treatment plan with the use of NMES can be done in all stages of the treatment. A, Stage I. B, Stage II, position of stretch. C, Stage III, stretch into abduction and ER. D, Stage III, NMES with active elevation of arm.
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A
B
C
D
E
F
691
Figure 51-5. Multiple plane mobilizations with maximum force achieved by therapist through fulcrum. A, Distraction and posterior glide using therapist’s hip as fulcrum. B, Distraction and anterior glide using fulcrum. C, Inferior glide in the plane of scaption. D, Distraction and posterior glide in maximum ER. E, Distraction and inferior glide applied with the patient in side-lying and ER of the GH joint. F, Inferior glide and internal rotation in 90 degrees of abduction.
Many patients who are at this stage of treatment are into stage II or III restriction and are advanced in their motion restriction. Single-plane techniques often work well in the initial phase of manual therapy, and excellent results to regain motion are seen. However, these techniques are often in a plateau effect after 2 or 3 weeks. The therapist must now be able to apply a greater force to maintain motion gains using single-plane techniques. Because collagen responds to lower forces if multiplane movements are used, the patient can be treated more comfortably with multiplane therapy to reach the same goal.
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By this stage of treatment, the key factors are force and time of application. Studies have shown the need for long periods of manual techniques in order to be effective. In congruence with manual techniques in the clinic, the patient must also follow a home program to maintain motion between manual treatment bouts. The patient is asked to perform this home program four to six times per day between clinic visits. Position 1: Distraction, posterior glide, and external rotation. The patient’s arm is placed at an end range (where restriction
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is first encountered). Distraction is the initial force, followed by posterior glide and finally an external rotation force. Both oscillations and holds are applied, and low force is applied first, followed by high force (see Fig. 51-5D). Position 2: Distraction, posterior glide, and internal rotation (see Fig. 51-5F). Again the arm is placed at the end of the available range and distraction is applied.
the patient can be managed effectively to prevent the progressive stages of motion complications. The therapist must also be able to communicate the patient’s needs to the physician for early intervention once problems are recognized. Treatment of these conditions requires input from the entire health care team to provide the most effective care for the patient.
Position 3: Distraction, inferior glide, and external rotation. In some patients, scarring in the subdeltoid space can lead to motion complications secondary to impingement. This maneuver is useful to facilitate inferior capsule mobilization. The patient’s arm is in a flexed position. Distraction is applied in the long axis, inferior glide is next applied, and finally external rotation is applied. Care is taken with this position because pain can easily be elicited and a low force is used to avoid secondary muscle spasm (Fig. 51-5E).
The outcome of the program is a functional joint, which is able to achieve full range of motion without substitution of the normal arthrokinematics, normal tissue length of the capsule and other extra-articular tissues, functional length of the musculotendinous structures without reflex spasm, and correct management of the primary diagnosis if it is something other than adhesive capsulitis. The focus of this program is to evaluate, recognize, treat, and educate.
It is important for the clinician to recognize that these techniques are end-stage treatment methods. They are used in a motion complication in which scarring is the primary cause of motion loss. The scar that is encountered by this is maturing, but it might have a random orientation of the collagen fibers, requiring higher stresses in multiple planes.
References
Soft Tissue Mobilization and Proprioceptive Neuromuscular Facilitation Techniques A study focusing on the effects of soft tissue mobilization to the subscapularis and proprioceptive neuromuscular facilitation to the shoulder rotators has offered promising results on shoulder external rotation and overhead reach. Godges and colleagues demonstrated a mean increase of 16.4 degrees in the treatment group compared with less than 1 degree in the control group. The treatment group received soft tissue mobilization of the subscapularis followed by contract-relax techniques to the internal rotators at end range of external rotation. The subjects were then asked to perform proprioceptive neuromuscular facilitation patterns (flexion-abduction and external rotation diagonal pattern) with manual facilitation. Although these results offer initial promise for the manual therapy sequence, the article was limited to only one treatment. This sequence should be carried out and studied over a course of treatment to determine its true effectiveness.33
SUMMARY The most effective treatment of arthrofibrosis of any joint is prevention. In today’s protocols, faster, more efficient, and highly scientific levels of knowledge are used. The clinician must be in a position to evaluate the patient as soon as possible after injury or surgery and recognize the early motion complication. With immediate evaluation,
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1. Codman EA: The Shoulder. Robert E. Malabar, Fla, Kreiger, 1934. 2. McLaughlin HL: The “frozen shoulder.” Clin Orthop 20: 126-131, 1961. 3. Lippmann RK: Frozen shoulder, periarthritis, bicipital tenosynovitis. Arch Surg 47:283-296, 1943. 4. Neviaser JS: Adhesive capsulitis of the shoulder: study of pathological findings in periarthritis of the shoulder. J Bone Joint Surg 27:211-222, 1945. 5. Simmonds FA: Shoulder pain with particular reference to the “frozen” shoulder. J Bone Joint Surg Br 31:426-432, 1949. 6. Reeves B: Arthrographic changes in frozen shoulder and posttraumatic stiff shoulders. Proc Soc Med 59:827-830, 1966. 7. Turek S: Orthopaedics: Principles and Their Application. Philadelphia, JB Lippincott, 1977. 8. DePalma AF: Surgery of the Shoulder. Philadelphia, JB Lippincott, 1983. 9. Bruckner FE, Nye CJS: A prospective study of adhesive capsulitis of the shoulder in a high risk population. Q J Med 198:191-204, 1981 10. Harmon PH: Methods and results in the treatment of 2560 painful shoulders. AM J Surg 95:527-544, 1958. 11. Reaves B: The natural history of the frozen shoulder syndrome. Scand J Rheumatol 4:193-196, 1975. 12. Lundberg BJ: The frozen shoulder. Acta Orthop Scand 119(suppl):1-59, 1969. 13. Bridgeman JF: Periarthritis of the shoulder and diabetes mellitus. Ann Rheum Dis 31:69-71, 1972. 14. Fisher L, Kurtz A, Shipley M: Association between cheiroarthropathy and frozen shoulder in patients with insulin dependant diabetes mellitus. Br J Rheumatol 25: 141-146, 1986. 15. Moren-Hybbinette I, Moritz V, Schersten B: The clinical pictures of a painful diabetic shoulder: Natural history, social consequences and analysis of concomitant hand syndrome. Acta Med Scand 221:73-82, 1987. 16. Laquesne M, Dang M, Bensasson M, Mery C: Increased association of diabetes mellitus with capsulitis of the shoulder and shoulder-hand syndrome. Scand J rheumatol 6:53-56, 1977.
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17. Satter MA, Lugman WA: Periarthritis: Another duration related complication of diabetes mellitus. Diabetes Care 8:507-510, 1985. 18. Cyriax J: Textbook of Orthopaedic Medicine, 7th ed, vol 1. London, Bailliere Tindall, 1978. 19. Enneking WF, Horowitz M: The intra-articular effects of immobilization on the human knee. J Bone Joint Surg Am 54:973-985, 1972. 20. Lundberg BJ: Glycosaminoglycans of the normal and frozen shoulder-joint capsule. Clin Orthop 69:279-284, 1970. 21. Akeson WH, Woo SLY, Amiel D, et al: Biomechanical and biochemical changes in the periarticular connective tissue during contracture development in the immobilized rabbit knee. Connect Tissue Res 2:315-323, 1974. 22. Donatelli R: Physical Therapy of the Shoulder, 2nd ed. New York, Churchill Livingstone, 1991. 23. Zachazewski JE: Improving flexibility. In Scully RM, Barnes MR (eds): Physical Therapy. Philadelpia, JB Lippincott, 1989. 24. Lavigne AB, Watkins RP: Preliminary results of immobilization-induced stiffness in monkey knee joints and posterior capsule. Perspectives in Biomedical Engineering: Proceedings of a Symposium, Biological Engineering Society, University of Strathclyde, Glasgow, Scotland. Baltimore, University Park Press, 1972. 25. Noyes FR, Butler DL, Paulos LE, et al: Intra-articular cruciate reconstruction: Part I. Perspectives on graft strength, vascularization and immediate motion after replacement. Clin Orthop Relat Res (172):71-77, 1983. 26. Wojtys EM, Noyes FR, Gikas P: Patella Baja syndrome. Presented at the Annual Meeting of the American Academy of Orthopaedic Surgeons, New Orleans, February, 1986.
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27. Borsa PA, Sauers EL, Herling DE, Manzour WF: In vivo quantification of capsular end-point in the nonimpaired glenohumeral joint using an instrumented measurement system. J Orthop Sports Phys Ther 31(8):419-431, 2001. 28. Newton RA: Joint receptor contributions to reflexive and kinesthetic responses. Phys Ther 62:22-29, 1982. 29. Gotlin RS, Hershowitz S, Juris PM, et al: Electrical stimulation effect on extensor lag and length of hospital stay after total knee arthroplasty. Arch Phys Med Rehab 75:957-959, 1994. 30. Snyder-Mackler L, Delitto A, Stralka SW, Bailey SL: Use of electrical stimulation to enhance recovery of quadriceps femoris muscle force production in patients following anterior cruciate ligament reconstruction. Phys Ther 74: 901-907, 1994. 31. Snyder-Mackler L, Delitto A, Stralka SW, Bailey SL: Strength of the quadriceps femoris muscle and functional recovery after reconstruction of the anterior cruciate ligament. A prospective, randomized clinical trail of electrical stimulation. J Bone Joint Surg Am 77:1166-1173, 1995. 32. Butler DL, Grood ES, Noyes, FR, Zernicke RF: Biomechanics of ligaments and tendons. Exerc Sports Sci Rev 6:125-182, 1979. 33. Godges JJ, Mattson-Bell M, Thorpe D, Shah D: The immediate effects of soft tissue mobilization with proprioceptive neuromuscular facilitation on glenohumeral external rotation and overhead reach. J Orthop Sports Phys Ther 33(12):713-718, 2003.
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CHAPTER 52 The Decelerator Mechanism:
Eccentric Muscular Contraction Applications at the Shoulder J. Gregory Bennett
It has long been appreciated that a good follow-through demanding a rapid deceleration of the internal rotation component of shoulder motion is essential in sports. This is especially true in activities such as pitching, golf, and tennis. One might question this conventional wisdom by pointing out that the action on the ball has already been accomplished and its trajectory is already determined. This observation clearly misses an important point: To excel at such sports, one must repetitively accelerate and then abruptly decelerate the arm in a consistent pattern that does not cause injury. The accomplishment of only one satisfactory golf swing or pitch is never enough, although often that is all that may be achieved if pathology develops. This chapter focuses on the deceleration or eccentric component of sports performance, especially as it relates to the shoulder (Fig. 52-1).
DECELERATOR (ECCENTRIC) MECHANISM Errors in deceleration, regardless of the joint or muscle groups involved, have long been identified with orthopedic injuries, especially sports. Hughston and colleagues6 first spoke of the body’s deceleration mechanism relative to the quadriceps femoris musculature in anterior knee pain (Fig. 52-2). Since that time, errors in the deceleration phenomena, or eccentric muscle action, have received increased scrutiny in the scientific literature.4-12 Eccentric muscle action is muscular lengthening while resisting a load, whether it is the weight of a body part or the body part plus a foreign object such as a tennis racket. Negative work is performed and energy is absorbed. Eccentric muscle action functions to decelerate a load or body parts, or both, in activities of daily living and is often accentuated in sports. Eccentric muscle action also functions as the shock-absorption mechanism in activities such as walking and running. By comparison, concentric muscle action involves shortening of a muscle’s length and functions to accelerate the body part or external load. Positive work is performed.13-15 The third type of muscular action, isometric action, involves active tension of the muscle without changing the muscle’s length. No external work is performed, and isometric muscle action functions to stabilize body parts.
In throwing sports, the shoulder rotates at 6000 to 7000 deg/sec and then decelerates over a very brief interval.1-4 The muscles that accomplish the acceleration are relatively large: the pectorals major and minor, the latissimus dorsi, the triceps, and the anterior deltoid muscles.5 After release, the rapidly moving extremity has principally the supraspinatus, teres minor, and infraspinatus muscles—short and relatively small muscles—to rely on to decelerate a limb with a very large moment of inertia. These muscles accomplish this task by contracting while they are lengthening (an eccentric muscle action) and they replicate this motion many dozens or even hundreds of times in a single athletic session. Repetitive deceleration activities are required for most activities of daily living and are not limited to athletic applications. This is why physical therapy paradigms emphasizing eccentric muscle exercise have potential for helping the throwing athlete and the nonathlete in the rehabilitation and training settings.
Most activities require combinations of concentric, eccentric, and isometric muscle action. For instance, when throwing a baseball, the rotator cuff musculature performs all three muscular actions. The subscapularis muscle is involved in acceleration (concentric action), the supraspinatus stabilizes the humerus (isometric action), and the supraspinatus, infraspinatus, and teres minor are active in deceleration (eccentric action).
This chapter explores the physical and physiologic components of concentric and eccentric muscle actions and how exercise affects motor adaptation. The reader is given applications and implications for injury and rehabilitation specifically as they are affected by concentric versus eccentric exercise. Mechanisms and rehabilitation of specific pathologies are explored, in particular as they apply to the shoulder.
The advent of isokinetic dynamometry in the late 1960s allowed, for the first time, the study of maximal muscle force production in vivo. Research in the area of muscle dynamics has been prolific; however, much of the early scientific data reflected only concentric muscle action because of the limitations of early dynamometry. Devices capable of measuring eccentric activity have allowed further 695
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exploration of human muscle action by allowing maximal testing of both the concentric and the eccentric components of muscle action.7,9,11 The importance of eccentric analysis becomes obvious given the instances of eccentric or deceleration variances that can occur. The importance of including eccentric analysis is further compounded by several physiologic differences between concentric and eccentric muscular action. Physiologic differences can preclude inferences regarding eccentric muscle function from data derived from concentric muscle action. An appropriate model using eccentric muscle action analysis is required for thoroughness. A
B
PHYSIOLOGY Numerous studies have been conducted comparing energy demand, electromyographic (EMG) output, and force production between concentric and eccentric muscle action. Studies have also been published comparing relative muscle soreness and the effect of speed on force output during concentric versus eccentric muscle action (Table 52-1). Understanding similarities and differences helps the clinician make appropriate decisions when applying specific exercise to the pathology being treated.
C
D Figure 52-1. Deceleration (eccentric muscle action) plays a major role in most athletic events and activities of daily living. Sports with major deceleration activity at the shoulder include, but are not limited to, tennis, baseball, golf, and fast-pitch softball.
Figure 52-2. Running and walking require coordinated deceleration action by the quadriceps femoris, gluteal, and trunk extensor muscles.
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The first and most striking difference between concentric and eccentric muscle action is the maximal tension each is capable of producing. The layperson would readily agree it is much easier to go down steps (eccentric muscle action) than it is to go up steps (concentric muscle action). The amount of work performed in both cases is similar (i.e., moving the weight of the body the distance of a flight of steps). Work in this instance is relative and excludes the effect of gravity and potential energy. The perceived exertion is much lower when descending stairs. Laboratory research has substantiated this perception. Komi and colleagues, as well as others, demonstrated in several instances that eccentric muscle actions are capable of producing the greatest tensile force (Fig. 52-3).16-19 In other words, less muscle activation is required to do the same amount of work when the muscle is functioning eccentrically. In fact, eccentric contractions have been shown to invoke 40% less EMG activity compared with concentric contractions at similar loads.20 Clinicians can exploit this phenomenon clinically. Persons with difficulty in muscle activation can benefit from early emphasis on concentric exercise. More of the muscle is activated to move an object concentrically. Postoperative muscle inhibition may be overcome more rapidly by emphasizing concentric exercise, assuming the exercise is appropriate for the pathology being addressed. Concentric and eccentric contractions also react differently in different velocities of contraction. A particularly interesting study performed by Komi examined the force–velocity relationship of concentric and eccentric muscle actions.16 In all instances, eccentric muscle actions produced the greatest
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TABLE 52-1
697
Concentric versus Eccentric Muscle Action
Property
Concentric versus Eccentric Comparison
Clinical Application
Electromyography (EMG)
More concentric muscle fiber activation is required (higher-amplitude EMG signal) at the same resistance when compared with eccentric fiber activation
Concentric exercise recruits more of the muscle at the same resistance
Energy
More energy (as reflected by oxygen demand) is used for concentric work compared with the same amount of eccentric work
Patients with endurance and energy deficits can exercise longer by doing eccentric exercise
Muscle soreness
Eccentric exercise is far more likely to create muscle soreness than similar amounts of concentric exercise
Repeated eccentric bouts diminish soreness progressively and are required for sports and activities of daily living
Force
More force can be generated eccentrically than can be developed concentrically
Compressive load (joint reaction force) may be less in concentric exercise
Force/velocity
As velocity increases, concentric force capacity decreases and eccentric force capacity increases
Isokinetic speed must be adjusted differently for eccentric force control
amount of tension. As velocity increased, concentric tension decreased but eccentric tension increased. This is critically important to clinicians using isokinetic exercise. Therapists often increase the speed of exercise to diminish force, a method that is only appropriate concentrically. The tension ratio of eccentric to concentric contraction at higher velocities Force
(7 cm/sec) became nearly 2:1 (Fig. 52-4).21 Cress and colleagues,22 in a similar study using isokinetic dynamometry, found that during increases in eccentric velocities, force levels remained consistent; however, increases in concentric speed led to diminished force production. Pathologies in which joint compression forces should be minimized (e.g., arthritis) might be better treated with higher-speed concentric action but lower-speed eccentric action, and therefore lower force transmission through the joint.
1.8
Because eccentric muscle actions produce greater tension than their concentric counterpart, the metabolic demand during eccentric muscle action would be expected to be greater. However, extensive research on the subject has
1.4
Maximal 1.0 isometric force 9 0.6
0.2 0.6 0.2 Velocity of lengthening
0
0.2
0.6
Velocity of shortening
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Eccentric 5 3
Max
Power absorbed
Figure 52-3. The classic force-velocity curve (solid line) obtained on an isolated muscle. It shows the maximal force that can be developed when a muscle is contracting at different speeds. The maximal force in a concentric activity is less than in an isometric contraction. A rapid eccentric contraction produces the highest force. The maximal power (i.e., the force times the velocity of contraction) is represented by the dashed line.
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Concentric
7 Force
Power produced
1 8
6
4
2
0
2 4
6
8
Velocity Figure 52-4. Relationship of force attained by an isolated muscle during maximal stimulation at various velocities: for concentric contractions, velocity of shortening; for isometric contractions, zero velocity; and for eccentric contractions, velocity of lengthening. Each point represents the force the muscle generates in a single experiment. The muscle length remains constant. (From Knuttgen HG, Kraemer WJ: Terminology and measurement in exercise performance. J Applied Sport Sci Res 1:1-10, 1987, used with permission.)
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shown the opposite to be true.21,23-26 Knuttgen and colleagues26 compared oxygen consumption, heart rate, and pulmonary ventilation during concentric and eccentric bicycling. Oxygen consumption increased with intensity for both concentric and eccentric activity, but it increased at a far greater rate during concentric exercise. Similar results were found for heart rate and pulmonary reactions. This study in essence showed that when generating the same tension, eccentric muscle actions caused smaller circulatory and pulmonary reactions and used a much smaller volume of oxygen (Fig. 52-5).26 Similar results have been substantiated by Newham and colleagues27 in the comparison of ultrastructural changes caused by concentric and eccentric muscle actions. Metabolic costs were less during eccentric exercise, and EMG activity was diminished at the same tension. EMG activity, which is a reflection of muscle fiber electrical activity and not strength, suggests that fewer fibers are producing equal tension to the concentric counterpart. In other words, fewer fibers contract eccentrically than concentrically to produce equal amounts of tension. Given that fewer muscle fibers are activated, eccentric activity must create a lower metabolic demand. This, too, can be exploited clinically. By using primarily eccentrically loaded exercises, patients with poor endurance should be able to tolerate longer workouts. This could be particularly applicable in neurologic cases and in early orthopedic rehabilitation, when emphasis is placed on endurance and not on strength. Another consideration in a metabolic comparison is the work performed by Friden and colleagues regarding adaptive responses to eccentric exercise.28 They found eccentric strength to be remarkably trainable and showed strength gains of 375% during their experimental period of 8 weeks. The rapid adaptation and change in eccentric muscle behavior have been used clinically in evaluation and rehabilitation.14,29 Coinciding with these gains was the confirmation of decreased oxygen consumption during eccentric exercise, which they expressed as improved nervous coordination.28
The final physiologic difference found when comparing concentric and eccentric muscle actions is the production of delayed-onset muscle soreness (DOMS). A study by Newham and colleagues30 comparing pain and fatigue secondary to concentric and eccentric exercise found that only the eccentrically trained group experienced DOMS. Although many authors and clinicians believe that only eccentric exercise causes muscle soreness, this belief is not without controversy.27,31,32 Tiidus and lanuzzo33 found that overall intensity was the primary factor in creating DOMS, especially as compared with duration. Their work, though, also substantiates the previously established premise that eccentric exercise is the primary cause of soreness. Given the previously established information that eccentric muscle action creates the greatest tension, eccentric exercise would create more profound DOMS. It is important to note that DOMS is not necessarily harmful. There is no evidence that DOMS causes any long-term damage or leads to long-term functional impairment.21,31 In fact, the best way to avoid DOMS is through repetitive exercise, which might in fact protect the muscle against other and more serious injury.14,31 The ability of eccentric exercise to improve strength is well established and accepted.14,16,21,23,28,29 In summary, it becomes apparent that different forms of exercise have vastly different effects on skeletal muscle. Although the same muscle is involved in both eccentric and concentric activity, several important differences occur between concentric and eccentric action. Eccentric action produces significantly greater tension with maximal voluntary effort. At equal tension, eccentric contractions use less oxygen, place lower demand on the cardiorespiratory system, and show lower EMG activity.
PATHOLOGY Eccentric muscle function and the deceleration mechanism throughout the body play important roles in many pathologies and rehabilitation paradigms. Although this chapter focuses on the shoulder, the deceleration mechanism 3,000
Figure 52-5. Oxygen uptake in positive (upper curve) and negative (lower curve) work. The work consisted of riding a bicycle on a motor-driven treadmill. Uphill was positive work and downhill was negative work (with the movements of the pedals reversed). The work load equals the product of the weight of the subject plus the bicycle times the vertical distance that this weight was lifted or lowered. Oxygen uptake was also measured at zero load (free wheeling). Rate of pedaling ⫽ 45 rpm. The average cost of positive work was 5.9 times higher than that of negative work. (From Asmussen E: Positive and negative muscular work. Acta Physiol Scand 28:364-382, 1953, with permission.)
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O2, mL • min–1
2,500
Positive work pos = 5.9 neg
2,000
y = 1.95x + 479
1,500 1,000
Negative work y = 0.33x + 451 150 200 W
500 50
100
0 0
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particularly as related to shoulder pathologies such as rotator cuff injuries and instability must be connected and applied to the body as a whole. Rapid deceleration must occur at the glenohumeral joint during many overhead activities, especially throwing. However, the deceleration system is not limited to the glenohumeral joint. A link-sequencing system has been described for effective force generation and deceleration in athletic shoulder function (Fig. 52-6).34 The link-sequencing system is the interrelationship required for efficient creation and transfer of acceleration and deceleration forces and involves the lower extremities, trunk, scapula, and upper extremities.34-36 Successful sequencing requires rapid and effective translation of forces from a concentric to an eccentric phased deceleration activity. The trunk and scapula are pivotal in transferring forces to and from the glenohumeral joint, and successful deceleration is necessary for injury prevention and successful follow-through. Rehabilitation paradigms, therefore, must emphasize not only deceleration training for the posterior rotator cuff muscles involved with slowing the translation of the humerus but also those muscles that serve as decelerators for the trunk and scapula. These muscles include (but are not limited to) the erector spinae muscles and the middle and lower trapezius as prime movers and decelerators.11,34-37 The applications and implications of deceleration activity specific to the shoulder are numerous. Increasingly, applications for eccentric rehabilitation are found in the
A
699
literature.9,11,28,29,37-39 Dynamometers capable of measuring and training deceleration (eccentric) capacity have furthered research and improved rehabilitation techniques. The throwing shoulder is an area of particular interest. Because shoulder injuries often involve deceleration (especially the rotator cuff), muscle-specific activity, capacity, and rehabilitation are necessary. Specifically, impingement syndromes and rotator cuff injuries require closer analysis. Many authors consider the two intricately linked, particularly in instances of overuse or chronic stress injuries. Most examples found in the scientific literature show the efficacy of exercise programs only in terms of general applications for prophylactic or rehabilitative applications. Increasing examples of specific programs and their efficacy are encountered, but more are needed.5,7,29,37-40 Patients with rotator cuff tendinitis or an inadequate subacromial space often benefit from rehabilitation of the cuff muscles in their eccentric phase of muscle action. It is important that high-velocity eccentric exercise be restricted until after the acute inflammatory phase subsides; thereafter, eccentric rehabilitation becomes useful at increasingly greater velocities. We have not seen exacerbation of symptoms in this situation from the rehabilitation itself, and we have not seen rotator cuff inflammation or rupture. Patients with overt subacromial crepitus and type III acromions41,42 have been excluded from this type of exercise until the underlying pathology was relieved.
B
Figure 52-6. Link sequencing describes the development and transfer of forces in serial linkage (legs, trunk, scapula, and arms) to accomplish acceleration (A) in throwing. Equally, the links must be decelerated rapidly in follow-through using eccentric muscle action (B).
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Eccentric muscle action has many unique properties that make eccentric exercise paramount to the requirements of sport. In the shoulder, relatively small muscle groups with low oxygen demand can function repetitively at high velocities of rotation to result in a smooth, balanced throw. In some disease states, rehabilitation of the eccentric muscles may be useful in restoring improved kinematics of the shoulder, provided the cuff is not inflamed, grossly damaged, or impinging severely. In such cases, rehabilitation alone may be detrimental to treatment.
resistances, such as elastic. Possible exceptions to including eccentric training are some isokinetic programs and isometric and some rhythmic stabilization exercises. Even programs that do include eccentric training often can be modified to enhance the eccentric component of the exercise. Parameters that can be adjusted include the speed of the contraction, the range of motion of the contraction, and the resistance. This is equally appropriate for the examination process and analysis that include mechanical and physiologic factors discussed previously.
The optimal paradigm for spectral application of eccentric exercise has yet to be identified. Present technology partially emulates the throwing motion and does succeed in placing eccentric load on the muscles (Fig. 52-7). Future research might result in even better models so that rehabilitation of the deceleration mechanism more closely approximates its function in sport. As this goal is achieved, it should be possible to obtain better measurements of muscle function during the throwing motion and to analyze patterns of weakness requiring treatment.
Symptoms in the rotator cuff muscles are multifactorial and can originate from factors that are primarily mechanical (acromial morphology), vascular, or traumatic. Impingement syndromes have been separated into two classifications, primary and secondary.
APPLICATIONS AT THE SHOULDER This section focuses on eccentric exercise. However, a comprehensive approach to evaluation and rehabilitation including a variety of exercise options is unequivocally advocated. Rehabilitative exercises specific for a variety of pathologies are addressed specifically in other chapters of this book. Most exercise paradigms used clinically have patients performing exercises using both concentric and eccentric muscle action. This is obviously true for most isotonic exercise programs as well as those that feature varying
Figure 52-7. Isokinetics are used extensively as a training modality. Diagonal exercises train not only the posterior glenohumeral musculature but also the scapular decelerators. These exercises can be performed either seated or standing, with the standing exercise less specific but including more musculature and specifically the trunk decelerators.
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Primary impingement refers to diminished clearance in the subacromial space, often as a result of bone spurs, and is usually seen in middle-aged patients.41,42 Secondary impingement syndromes have been described in persons with shoulder instability, muscle weakness, or capsule tightness, all of which play a role in deceleration.39,43-46 Loss of stability requires general increases in muscle strength and motor control of the glenohumeral joint in order to limit or prevent humeral migration.39,45,46 In cases in which impingement is the primary problem, the glenohumeral musculature requires retraining to achieve better kinematics. Even in instances where impingement is subsequent pathology (caused by microsubluxation), rehabilitation usually provides a satisfactory outcome as long as the capsular tissues maintain their competency.39,46,48,49 Comprehensive rehabilitation requires inclusion of scapular mechanics, mobility, and strength. Scapular strengthening should also be enhanced in the deceleration phrase of follow-through.39,46,47 Glenohumeral internal rotation deficit (GIRD) plays a significant role in many shoulder pathologies. GIRD also has a secondary relationship and direct impact on deceleration function. Pathologies associated with GIRD could be accentuated in the presence of an eccentric motor deficit. The loss of internal rotation range of motion (GIRM) is a relatively recent observation and is associated with many shoulder pathologies.47,50,51 GIRD can originate either from capsular and muscular changes in the shoulder or from osseous changes as an adaptation in throwing athletes.47,51 GIRD has been described as both a contributing and a secondary factor in shoulder pathology.47,50,51 In either instance, patients are left with a decreased range of motion in internal rotation (Fig. 52-8). This loss of motion then requires an enhanced deceleration mechanism in which the slowing down of a rotating shoulder occurs more quickly than in a person with normal range of motion. Posterior capsular tightness (GIRD) therefore plays a significant role because tightness in this area results in a diminished arc of motion in which deceleration can take place.47 Because of this phenomenon, a key component of
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A
701
B
Figure 52-8. Glenohumeral internal rotation deficit (GIRD) often requires very efficient deceleration. However, exercise alone may be inadequate and appropriate range of motion and stretching may be needed. Side-lying (A) and standing (B) “sleeper” stretches are part of the comprehensive management of follow-through dysfunction and GIRD.
the pathology associated with GIRD may be comparative analysis of concentric internal rotation with eccentric external rotation. Isokinetic evaluations (Fig. 52-9) have demonstrated significantly lower eccentric external rotation versus concentric internal rotation ratios in throwers versus nonthrowers in their dominant limbs. Nondominant limbs, however, showed no significant statistical difference in the ratios between internal rotation peak torque verses external rotation eccentric peak torque.9 The potential for this deficit was first identified by Wilk and colleagues52 in their analysis of the strength characteristics of internal and external rotator muscles in professional athletes. As noted in the Noffal study, the ratio deficit is due to increased training
efforts in acceleration activities, namely the internal rotation musculature, without concomitant strengthening of the deceleration or eccentric mechanism.9 Therefore, isokinetic testing focusing on only involved and noninvolved or body-weight comparisons can miss a significant deficit. Several parameters are tested and evaluated in our clinics. Test speeds were arbitrarily chosen to be 50 and 150 deg/sec. Many clinicians choose to test at higher velocities to be more functional, but because we test the eccentric component, lower velocities were chosen. Motions tested include flexion, abduction, internal rotation, and external rotation. Also, horizontal flexion is often tested from 90 degrees of abduction, especially in patients doing a lot of overhead activity (Box 52-1; see Fig. 52-9). It is our opinion that the ability to work overhead for sustained periods is often overlooked in testing and rehabilitation programs.
BOX 52-1. Select Isokinetic Test Parameters for Concentric and Eccentric Evaluation
Velocities 50 deg/sec 150 deg/sec
Positions Abduction Internal rotation Figure 52-9. Isokinetic rotation activities can be done seated or standing. In a standing posture, the patient is more inclined to use the scapular and the trunk musculature. When specific isolation (especially when testing) is desired, then a seated posture with appropriate stabilization is appropriate.
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Horizontal flexion Flexion External rotation
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capacity paramount to preventing or relieving shoulder symptoms (Fig. 52-10).38,39,48,49,56
ECCENTRIC CONTRACTION AND SHOULDER DYSFUNCTION
As noted earlier, examination of isokinetic data that only provide the concentric component of rotator cuff action can lead to errors in strength analysis and therefore errors in rehabilitation.9,52 This is particularly true for analysis of external rotation. Because the supraspinatus is not primarily an external rotator and the rest of the cuff musculature acts primarily eccentrically, concentric analysis of external rotation may be inadequate. Ideally, isokinetic or even isotonic studies allow the clinician to
Eccentric muscle action plays an important role in shoulder function. EMG studies by Jobe and colleagues53 and others54,55 demonstrated that the musculature of the rotator cuff functions primarily eccentrically in sports. This phenomenon probably extends to activities of daily living as well but is not documented in the literature. It is well documented that the rotator cuff is often involved in shoulder pathology, making adequate eccentric or deceleration
COMPREHENSIVE EVALUATION: EXCEL REHABILITATION Name: Jane Doe Gender: Female Mode: Isokinetic
Session: 2/9/06 Weight: 125 Joint: Shoulder
Diagnosis: Impingement left shoulder Windowing: Isokinetic Contraction: CON/ECC
Protocol: Isokinetic bilateral
Pattern: Ext/int rotation modified neutral
ISOKINETIC BILATERAL 6 REPS AT 60/60 DEG/SEC 240 180 120 60 0 –60 –120 –180 –240 –300 –360
Legend Uninvolved (right) Involved (left)
10 0 –10 –20 0
0.5
1.0
1.5
2.0
2.5
3.0
Position in degrees
Torque in ft-lbs
20
3.5
Time in seconds Concentric ER 60 degrees/sec # of reps: right 6 # of reps: left 6 Peak torque Peak tq/bw Time to pk tq
Involved
Right
Left
16.4
15.2
Deficit
7.4
Uninvolved
Involved
Right
Left
12.7
10.2
%
11.7
10.9
9.0
7.3
Msec
630.0
160.0
390.0
1680.0
Deficit
19.7
Deg
–35.0
–8.0
–85.0
–8.0
Ft-lbs
0.0
0.0
0.0
0.0
0.0
0.0
Torq @ 0.18 sec
Ft-lbs
13.3
151
–13.7
0.0
0.0
0.0
%
9.6
4.4
8.6
13.0
Ft-lbs
20.7
16.4
14.8
11.7
Coeff. of var. Max rep tot work
20.5
Max work rep #
#
4
6
1
Wrk/bodyweight
%
14.8
11.7
10.6
Ft-lbs
113.7
95.8
%
9.7
–2.2
Avg. power
Watts
16.0
13.6
9.1
6.1
Acceleration
Msec
80.0
60.0
350.0
370.0
Deceleration
Msec
90.0
90.0
160.0
160.0
ROM
Deg
89.5
89.4
89.5
89.4
Ft-lbs
15.0
14.1
11.7
8.5
Total work Work fatigue
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Uninvolved
Torq @ 30.0 deg
Angle of pk tq
Figure 52-10. Sample isokinetic test data demonstrating a force output deficit in the shoulder external rotators. Note the increased amplitude of the deficit during eccentric muscle action.
Ft-lbs
Eccentric IR 60 degrees/sec
Avg peak tq
15.7
15.3
2 8.3
78.4
578
14.3
18.2
20.9
26.3
32.6
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compare and analyze the eccentric action of the rotator cuff with appropriate rehabilitation and re-examination (testing) at appropriate intervals. An approach to rehabilitation of rotator cuff tendinitis emphasizing eccentric action has been followed in our clinic for some time, especially for throwing athletes. A comprehensive approach to rehabilitation is advocated and must be undertaken. This chapter focuses only on the unique applications of our program, and a comprehensive approach is discussed elsewhere in this text. The unique application of our program is the rapid application of eccentric or deceleration forces to the rotator cuff in external rotation. An outline of this program is presented in Box 52-2. This component is part of a comprehensive program including modalities and concentric exercise. All types of exercise, including isometric and isotonic muscle actions, are thoroughly incorporated. The purpose of this program is to simulate the rapid reversal from concentric internal rotation to eccentric external rotation that occurs at ball release. Isokinetic machines cannot switch muscle action in mid arc of motion, so a slight modification was made. Patients are positioned in a seated posture with the actuator aligned with the plane of the scapula. In cases of instability, care is taken to protect the patient from recurrence by positioning the humerus in a more stable position, such as 45 degrees of flexion. The patient experiences a concentric external rotation muscle action at a relatively slow speed, which is doubled when the eccentric action begins (see Box 52-2). By doing this, the patients are taught rapid activation of eccentric muscle action, as is required in throwing sports. The results of this type of rehabilitation in addition to traditional intervention have been encouraging.
Figure 52-11. Our facilities use a number of exercises to enhance the eccentric component of rehabilitation. One is a weighted ball drop. The position chosen depends upon which muscles are being addressed, but common applications include the supraspinatus, infraspinatus, and teres minor. The patient elevates the ball to approximately 90 degrees in the scaption position (45 degrees of adduction combined with 45 degrees of horizontal flexion). The patient drops the ball and attempts to catch it before it reaches the table or floor. When the ball is caught, rapid deceleration is required to slow the ball down. The same exercise can be accomplished for external rotation by placing the patient in a prone position. The weight of the ball is adjusted as the patient progresses, and rapid improvements in both skill and deceleration weight have been observed.
Eccentric muscle action is routinely incorporated into our spectrum approach to rehabilitation (Figs. 52-11 and 52-12).
BOX 52-2. A Novel Protocol to Adjunct Rotator Cuff Rehabilitation Emphasizing Rapid Deceleration
Dynamometer Mode Isokinetic concentric/eccentric or passive
Motion External rotation
Concentric Velocity (deg/sec) 50 75 100
Eccentric Velocity (deg/sec) 100 150 200
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Figure 52-12. Compound rowing is a good exercise for training the posterior glenohumeral musculature and the scapular muscles. Similar exercises that can emphasize the deceleration component include the upright row, the bent-over row, and scapular depression such as using a dips machine.
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Our approach is to exercise muscles comprehensively, that is, both concentrically and eccentrically for each muscle group. Additional emphasis is then placed on that component in which the muscle most commonly is used. The internal rotators primarily accelerate and receive concentric emphasis, depending on the musculature. As with all rehabilitation programs, exercise must be modified according to the patient’s pathologies, with appropriate modification made for healing tissues or altered mechanics.
SUMMARY Eccentric muscle action has several unique features compared with its concentric counterpart. At equal external loads, less muscle activation (based on EMG) occurs and less energy is expended during eccentric muscle action. Many sports injuries are identified as occurring during deceleration, requiring strong eccentric muscle action. However, most activities of daily living require both concentric and eccentric muscle action. A cup of coffee must be successfully accelerated and decelerated to drink it. Stairs must be both ascended and descended. It would, therefore, be an error to only exercise the concentric or eccentric component of muscular action. A comprehensive program emphasizing both concentric and eccentric muscle action is advocated. Special emphasis can then be added to that component of muscle behavior that is sports-specific or lifestyle-specific.
References 1. Perry J: Anatomy and biomechanics of the shoulder in throwing, swimming, gymnastics, and tennis. Clin Sports Med 2:247-270, 1983 2. Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis upon shoulder kinematics. J Orthop Sports Phys Ther 18:402-408,1993. 3. Escamilla RF, Fleisig GS, Barrentine SW, et al: Kinematic comparisons of throwing different types of baseball pitches. J Appl Biomech 14:1-23,1998. 4. Fleisig GS, Escamilla RF, Andrews JR, et al: Kinematic and kinetic comparison between baseball pitching and football passing. J Appl Biomech 12:207-224,1996. 5. Ryu RKN, McCormick J, Jobe FW, Moynes DR, Antonelli DJ: An EMG analysis of shoulder function in tennis players. Am J Sports Med 16:481-485, 1988 6. Hughston JC, Walsh WM, Puddu G: Patellar Subluxation and Dislocation. Philadelphia, WB Saunders, 1984. 7. Ellenbecker TS, Davies GS, Rowinski MS: Concentric versus eccentric isokinetic strengthening of the rotator cuff: Objective data versus functional tests. Am J Sports Med 16:64-69, 1988. 8. Highgenboten CL, Jackson AW, Meske NB: Concentric and eccentric torque comparisons for knee extension and flexibility in young adult males and females using the Kinetic Communicator. Am J Sports Med 64:234-237, 1985. 9. Noffal GJ: Isokinetic eccentric-to-concentric strength ratios of the shoulder rotator muscles in throwers and nonthrowers. Am J Sports Med 31(4):537-541, 2003.
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10. Nosaka K, Clarkson PM: Muscle damage following repeated bouts of high force eccentric exercise. Med Sci Sports Exerc 27:1263-1269, 1995. 11. Sirota SC, Malanga GA, Eischen JJ, Laskowski ER: An eccentric and concentric profile of shoulder external and internal rotator muscles in professional baseball players. Am J Sports Med 25(1): 59-64, 1997. 12. Tomberlin JP, Basford JR: A comparative study of eccentric and concentric quadriceps strengthening [abstract]. Phys Ther 67:790, 1987 13. Åstrand P, Rodahl K: Textbook of Work Physiology. New York, McGraw-Hill, 1977. 14. Proske U, Morgan DL: Muscle damage from eccentric exercise: Mechanism, mechanical signs, adaptation and clinical applications. J Physiol 537(2):333-345, 2001 15. Wackerhage H: Recovering from eccentric exercise: Get weak to become strong. J Physiol 553(3):681, 2003. 16. Komi PV: Measurement of the force-velocity relationship in human muscle under concentric and eccentric contraction. Med Sport 8:224-229, 1973. 17. Komi PV, Burkirk ER: Effect of eccentric and concentric muscle conditioning on tension and electrical activity of human muscle. Ergonomics 15:417-434, 1972. 18. Komi PV, Rusko H: Quantitative evaluation of mechanical and electrical changes during fatigue loading of eccentric and concentric work. Scand J Rehabil Med 3:121-126, 1974. 19. Rogers KL, Berger RA: Motor unit involvement and tension during maximum voluntary concentric, eccentric, and isometric contractions of the elbow flexors. Med Sci Sports Exerc 6:253-259, 1974 20. Gibala M, MacDougall D, Tarnopolsky M, et al: Changes in human skeletal muscle ultra-structure and force production after acute resistance exercise. J Appl Physiol 78:702-708, 1995. 21. Komi PV: Relationship between muscle tension, EMG and velocity of contraction under concentric and eccentric work. In Desmedt JD (ed): New Developments in Electromyography and Clinical Neurophysiology, vol. 6. Basel, Karger, 1973. 22. Cress NM, Peters KS, Chandler JM: Eccentric and concentric force-velocity relationships of the quadriceps femoris muscles. J Orthop Sports Phys Ther 16:82-86, 1992. 23. Asmussen E: Positive and negative muscular work. Acta Physiol Scand 28:364-382, 1953. 24. Bigland B, Lippold OC: The relation between force, velocity and integrated electrical activity in human muscles. J Physiol (Lond) 123:214-224, 1954. 25. Horstman T, Mayer F, Maschmann J, et al: Metabolic reaction after concentric and eccentric endurance-exercise of the knee and ankle. Med Sci Sports Exerc 33(5): 791-795, 2001. 26. Knuttgen HG, Nadel ER, Pandolf KB, Patton JF: Effects of training with eccentric muscle contraction on exercise performance, energy expenditure and body temperature. Int J Sports Med 3:13-17, 1982. 27. Newham DJ, McPhail G, Mills KR, Edwards RHT: Ultrastructural changes after concentric and eccentric contractions of human muscle. J Neurol Sci 61:109-122, 1983. 28. Fridén J, Seger J, Sjöström M, Ekblom B: Adaptive response in human skeletal muscle subjected to prolonged eccentric training. Int J Sports Med 4:177-183, 1983.
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29. Bennett JG, Stauber WT: Evaluation and treatment of anterior knee pain using eccentric exercise. Med Sci Sports Exerc 18:526-530, 1986. 30. Newham DJ, Mills KR, Quigley BM, Edwards RHT: Pain and fatigue after concentric and eccentric muscle contractions. Clin Sci (Lond) 64:55-62, 1983. 31. Armstrong RB: Mechanisms of exercise-induced delayed onset muscular soreness: A brief review.Med Sci Sports Exerc 16(6):529-538, 1984. 32. Byrnes WC, Clarkson PM, Katch FI: Muscle soreness following resistance exercises with and without eccentric contraction. Res Q Exer Sport 56:283-285, 1985. 33. Tiidus PM, Ianuzzo ED: Effects of intensity and duration of musclar exercise on delayed soreness and serum enzyme activities. Med Sci Sports Exer 15:461-465, 1983. 34. Kibler WB: The role of the scapula in athletic shoulder function. Am J Sports Med 26:325-337, 1998. 35. Fleisig GS, Dillman CJ, Andrews JR: Biomechanics of the shoulder during throwing. In Andrews JR, Wilk KE (eds): The Athlete’s Shoulder. New York, Churchill Livingstone, 1994, pp 355-368. 36. Pink MM, Perry J: Biomechanics. In Jobe FW (ed): Operative Techniques in Upper Extremity Sports Injuries. St Louis, Mosby, 1996, pp 3-14. 37. Cools AM, Witvrouw EE, Declercq GA, et al: Evaluation of isokinetic force production and associated muscle activity in the scapular rotators during a protraction-retraction movement in overhead athletes with impingement symptoms Br J Sports Med 38(1):64-68, 2004. 38. Curwin S, Stanish W: Tendinitis: Its Etiology and Treatment. Torontoa, Collamore Press, 1984. 39. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30:136-151, 2002. 40. Cools AM, Witvrouw EE, Declercq GA, et al: Scapular muscle recruitment patterns: Trapezius muscle latency with and without impingement symptoms Am J Sports Med 31(4):542-549, 2003. 41. Bigliani LU: The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 10:228, 1986. 42. Bigliani LU, Ticker JB, Flatow EL, et al: The relationship of acromial architecture to rotator cuff disease. Clin Sports Med 10:823-838, 1991.
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43. Altchek DW, Warren RF, Ortiz G et al: T-plasty: A technique for treating multidirectional instability in the athlete. Orthop Trans 13:560-561, 1989. 44. Bowen MK, Warren RF: Ligamentous control of shoulder stability based on selective cutting and static translation experiments. Clin Sports Med 10:757-782, 1991. 45. Lyons PM, Orwin JF: Rotator cuff tendinopathy and subacromial impingement syndrome. Med Sci Sports Exerc 30:512-517, 1998. 46. Schmitt L, Snyder-Mackler L: Role of scapular stabilizers in etiology and treatment impingement syndrome. J Orthop Sports Phys Ther 29:31-38, 1999. 47. Tyler TF, Nicholas SJ, Roy T, Gleim GW: Quantification of posterior capsule tightness and motion loss in patients with shoulder impingement. Am J Sports Med 28:668-673, 2000. 48. Hawkins RJ, Kennedy JC: Impingement syndrome in athletes. Am J Sports Med 8:151-158, 1980. 49. Neer CS II: Impingement lesions. Clin Orthop Relat Res (173):70-77, 1983. 50. Borsa PA, Wilk KE, Jacobsen JA, et al: Correlation of range of motion and glenohumeral translation in professional baseball pitchers. Am J Sports Med 33(9):1392-1399, 2005. 51. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the glenohumeral joint in professional baseball pitchers. Am J Sports Med 30(1):20-26, 2002. 52. Wilk KE, Andrews JR, Arrigo CA et al: The strength characteristics of internal and external rotator muscles in professional baseball pitchers. Am J Sports Med 21:61-66, 1993. 53. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the shoulder in throwing and pitching. A preliminary report. Am J Sports Med 11:3-5, 1983. 54. Chandler TJ, Kibler WB, Stracener EC, et al: Shoulder strength, power, and endurance in college tennis players. Am J Sports Med 20:455-458, 1992. 55. Jobe FW, Moynes DR, Tibone JE, et al: An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 56. Tibone JE, Elrod B, Jobe FW, et al: Surgical treatment of tears of the rotator cuff in athletes. J Bone Joint Surg am 68:887-891, 1986
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CHAPTER 53 Neurodynamic Techniques
for the Athlete’s Shoulder John Tomberlin
median nerve and the upper limb and its movements.4 The focus in this chapter is on the peripheral nerve tissues of the shoulder.
Clinical management of the shoulder complex in athletes would not be complete without consideration of the regional peripheral nerve tissues. This chapter discusses the peripheral nerve structures pertinent to the maintenance of healthy shoulder function in athletes, with a focus on the clinical evaluation and management of pain and dysfunction of neuropathic origin. Peripheral neuropathic pain describes situations in which peripheral nerve trunks (or nerve roots) contribute to pain states, usually from mechanical or chemical stimuli that exceed the physical tolerance of the nervous system.1-4
Neurodynamic tests are becoming more integrated into clinical practice.10 Physical examination to assess the health and mobility of the relevant nerves in the shoulder region should include physical testing of regional neurodynamics. These neurodynamic tests should always be accompanied by a traditional neurological examination (deep tendon reflexes, sensory and motor testing). Clinical physical examination of the nerves traditionally has focused solely on elongation and gliding of nerve tissues.4 Clinicians are reminded to consider the relevant tissues surrounding the nerves and their affects on the nerve tissues when they are shortened (producing compressive loads) or lengthened (producing tension loads). Glenohumeral instability and scapular instability are examples of clinical shoulder problems that can contribute to mechanical overload of the peripheral nerve tissues of the upper limb. The relative health of the nerves in relation to the neighboring tissues could be described in terms of nerve tissue requiring a dynamic roominess.11 This term might facilitate clinical awareness when attempting to understand the relative movement of nerves to their neighboring tissues in both a static and dynamic sense when performing neurodynamic tests.4 Topps and Boyd elucidate peripheral nerve responses to physical stresses, which can aid clinicians in the understanding of the physical examination of nerve tissues and the implications for clinical practice.12
Injured athletes might describe symptoms consistent with a pattern of peripheral neuropathic pain. Those patterns commonly include symptom complaints of numbness and tingling, pins and needles, burning, electric shock, or shooting pains. In fact, any symptom complaint in the distribution of a nerve root, along the path of a peripheral nerve trunk, or in a regional cutaneous nerve field could arouse suspicion for pain of neuropathic origin. The distribution and type of symptom complaints of neuropathic pain associated with musculoskeletal dysfunction can be quite variable.1-4 Severe cases of peripheral neuropathic involvement can lead to complaints of sensory loss or even motor weakness; these should always be investigated thoroughly by the sports medicine team (physician, physical therapist, and athletic trainer).
NEURODYNAMICS Peripheral nerve tissues are well equipped to function and tolerate the various postures and movements of the body while adapting to the unique stresses placed on them during athletic activities.1,4-8 The term used to describe the intricate relationships among neuroanatomic structures, neurophysiologic processes, and functional mechanics of nerve movement is neurodynamics.9
Anatomic Considerations: Nerves of the Shoulder Complex Musculocutaneous Nerve The musculocutaneous nerve (Fig. 53-1) arises from the lateral cord of the brachial plexus, opposite the lower border of the pectoralis minor. Its fibers originate from the fifth, sixth, and seventh cervical nerves. It pierces the coracobrachialis muscle and passes obliquely between the biceps brachii and the brachialis to the lateral side of the arm. It pierces the deep fascia lateral to the tendon of the biceps brachii just above the elbow and continues into the forearm as the lateral antibrachial cutaneous nerve. This nerve innervates the coracobrachialis, biceps brachii, and the greater part of the brachialis muscles.
A neurodynamic test aims to evaluate the mechanics and underlying physiology of a particular part of the nervous system. For example, median nerve tissue strain and motion relative to the pectoralis minor muscle during an upper limb neurodynamic test (discussed later) challenge the mechanical component of the nerve. Physiologic components tested can relate to blood flow, ion channel activity, and nerve inflammation, as well as to central nervous system changes in the representation of the 707
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Anterior view*
Medial Posterior Lateral
Musculocutaneous nerve (C5, C6, C7) Coracobrachialis muscle
Cords of brachial plexus
Medial brachial cutaneous nerve
Biceps brachii muscle (retracted)
Ulnar nerve
Medial antebrachial cutaneous nerve
Median nerve Radial nerve Axillary nerve
Brachialis muscle Articular branch Lateral antebrachial cutaneous nerve Anterior branch
Cutaneous innervation (via lateral antebrachial cutaneous nerve)
Posterior branch
Figure 53-1. Regional anatomy of the musculocutaneous nerve. (Source: Elsevier, Inc. Netter Images. Available at www.netterimages.com.)
∗ Note: Only muscles innervated by musculocutaneous nerve are shown
Nerve dysfunction (entrapment) of the musculocutaneous nerve can occur proximally where it pierces the coracobrachialis muscle or distally in the deep fascia lateral to the biceps tendon at the elbow. Athletes involved in overhead throwing sports and intense training (especially bicepsintense training) activities may be especially at risk for problems with this nerve. Long Thoracic Nerve The long thoracic nerve (Fig. 53-2) arises by three roots from the fifth, sixth, and seventh cervical nerves; on occasion, the root from the seventh nerve is absent. The roots from the fifth and sixth nerves can pierce the scalenus medius, and the root from the seventh passes in front of the muscle. The nerve then descends behind the brachial plexus and the axillary vessels, coursing between the thoracic cage and the scapula to innervate the serratus anterior muscle. It extends along the side of the thorax to the lower border of that muscle, supplying filaments to each of the digitations of the serratus anterior. Nerve dysfunction (entrapment) of the long thoracic nerve can occur proximally where it pierces the middle scalene, or between the anterior and middle scalenes, or distally in the subscapular space between the scapula and the thorax. Athletes involved in forceful protraction and retraction activities may be at risk for problems with this nerve.
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Anterior (palmar) view
Posterior (dorsal) view
Axillary Nerve The axillary nerve (Fig. 53-3) arises from the roots of the fifth and sixth cervical roots and passes backward from the posterior cord of the brachial plexus (at the level of the axilla). It crosses the inferolateral surface of the subscapularis muscle, 3- to 5-mm medial to the musculotendinous border. It courses along the inferior border of the shoulder capsule and through the quadrangular space below the lower border of the teres minor, where it passes around the posterior and lateral humerus on the deep surface of the deltoid muscle. The axillary nerve has four terminal branches: the superior-lateral cutaneous branch, which supplies the skin overlying the deltoid on the lateral upper arm; the anterior branch to the anterior and middle deltoid; the posterior branch to the posterior deltoid; and a branch to the teres minor. Nerve dysfunction (entrapment) can occur anteriorly and inferior to the glenohumeral capsule and posteriorly in the quadrangular space. Athletes with a history of anterior and inferior dislocation of the glenohumeral joint may be at risk for injury to this nerve. Suprascapular Nerve The suprascapular nerve (see Fig. 53-3) arises from the upper trunk of the brachial plexus, typically receiving fibers from the roots of C5 and C6. It sends sensory branches to both the glenohumeral and acromioclavicular joints, but it does not innervate the skin. It passes downward, laterally
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NEURODYNAMIC TECHNIQUES FOR THE ATHLETE’S SHOULDER
709
Levator scapulae muscle Phrenic nerve Scalene muscles
Accessory nerve (XI)
Anterior Middle Posterior
Brachial plexus Subclavian artery and vein Scapula (retracted) Subscapularis muscle Teres major muscle
External intercostal muscle
Long thoracic nerve
Figure 53-2. Regional anatomy of the long thoracic nerve. (Source: Elsevier, Inc. Netter Images. Available at www.netterimages.com.)
Serratus anterior muscle
Dorsal scapular nerve (C5)
Suprascapular nerve (C5, C6)
Supraspinatus muscle
Lower subscapular nerve (C5, C6)
Infraspinatus muscle
Axillary nerve (C5, C6) Superior lateral cutaneous nerve of arm Radial nerve (C5, C6, C7, C8, T1) Inconstant contribution
Figure 53-3. Regional anatomy of the axillary nerve and suprascapular nerve. (Source: Elsevier, Inc. Netter Images. Available at www.netterimages.com.)
(deep to the omohyoid and trapezius) then posteriorly to run under the cover of the trapezius muscle. It then reaches the suprascapular notch on the scapula and travels beneath the suprascapular notch. It then has two branches that innervate the supraspinatus muscle. Finally, it passes around the lateral border of the scapular spine (spinoglenoid notch) in the infraspinatus fossa to innervate the infraspinatus muscle. Nerve dysfunction (entrapment) can occur at the suprascapular notch and, less commonly, the spinoglenoid
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notch. Athletes involved in repetitive overhead and throwing activities are at risk for injury to this nerve.
Current Concepts in Neurodynamic Testing Neurodynamic tests challenge the physical capabilities of the nervous system. Clinicians should attempt to gain an appreciation of the sequential movements of the spine and limbs during testing as they alter the dimensions of the
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nerve bed surrounding the nerve structure.1,4-6,9,10,13-16 Neurodynamic tests challenge movements that are related to a sensitive nervous system. This includes appreciation of the resistance encountered by the examiner as he or she carries out the neurodynamic tests. Physical examination of the nervous system should first include active testing (where possible) to provide a baseline of responses before passive testing.4 This allows the clinician to observe what range of motion and functional movement patterns the athlete is willing to perform. It sets the stage for the passive examination and can stand alone if analysis provides elements of a positive test. For example, an athlete complains of shoulder pain following a “sprain” on the playing field. Active elevation produces pain in the posterolateral arm radiating into the lateral elbow. The addition of contralateral side bending of the neck increases this pain; release of it eases the pain. The clinician now suspects a neurodynamic dysfunction contributing to the athlete’s symptom complaints (radial nerve distribution). Follow-up neurodynamic testing is necessary for an appropriate diagnosis. Manual nerve palpation is also a key part of physically assessing mechanosensitivity of the peripheral nervous system. Manual palpation of the nerves assists the clinician in two distinct ways. First, manual nerve palpation supplements the physical examination by directly challenging the mobility of nerve tissue and testing its sensitivity to touch. Second, manual palpation of the nerves gives guidance toward treatment strategies by identifying any restrictions in movement relative to the surrounding
tissues. The innervated connective tissue sheath surrounding peripheral nerves may be the source of symptoms of a local, sometimes intense pain when a nerve is palpated.6,8
The Upper Limb Neurodynamic Test (Base Test) Four neurodynamic tests are suggested for examination of the physical health of the nervous system of the upper quarter.4,17 The base test, previously familiar to many clinicians as the upper limb tension test,4 is currently referred to as the upper limb neurodynamic test (ULNT). ULNT has been described as the straight leg raise of the upper quarter.18 This test is useful as a screening tool for the shoulder complex when examining mechanosensitivity of the nervous system in the upper quarter. An active test should be performed first, and any symptom complaints noted. The clinical test is shown in Figure 53-4. It is important to note responses and document these symptom complaints during testing (increases or changes in any symptom complaints) at each step of the test to allow the results to be analyzed. Starting Position The athlete lies comfortably supine with the clinician (facing the athlete) in a stride stance close to the side of the table (see Fig. 53-4A). If testing the athlete’s left upper limb, then the clinician grasps the hand and wrist with his or her right hand. The clinician’s left hand rests at the upper trapezius to gently stabilize the shoulder girdle. This
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Figure 53-4. Clinical performance of the upper limb neurodynamic test (ULNT) (base test). A, Starting position. B, Shoulder abduction. C, Wrist and finger extension. D, Forearm supination. E, Shoulder external rotation. F, Elbow extension. G, Cervical lateral flexion (away). H, Cervical lateral flexion (toward).
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hand can be used to palpate muscle reactivity in the upper trapezius muscle that might represent the flexor withdrawal response related to the athlete’s perception of first onset neurogenic pain in the upper limb.19-21 The patient’s wrist is held in neutral and the patient’s upper arm rests on the clinician’s thigh. A comfortable and controllable starting position should enhance the clinician’s handling ability and increase the likelihood of retest reliability.4 Shoulder Abduction The support of the clinician’s thigh allows the athlete’s shoulder to be abducted by walking up the arm at the side of the table as the clinician shifts his or her weight toward the front leg (see Fig. 53-4B). The shoulder can be abducted up to 110 degrees of abduction, and the clinician should be sensitive to the first onset of pain, apprehension, or guarding and any significant resistance to movement.4 Wrist and Finger Extension While maintaining the shoulder-abduction position, the patient’s wrist and fingers (including the thumb) are extended to the point of any change in pain or new onset of pain (see Fig. 53-4C). The clinician should appreciate any resistance to movement. Forearm Supination Maintaining the previous components of the test, the patient’s forearm is supinated to the point of any change in pain or new onset of pain (see Fig. 53-4D). The clinician should appreciate any resistance to movement. Shoulder External Rotation Maintaining the previous components of the test, the clinician moves the patient’s shoulder into external rotation (see Fig. 53-4E). The movement is taken to the point of change in pain or new onset of pain. The clinician should appreciate any resistance to movement. Elbow Extension The final upper limb movement of the test is elbow extension (see Fig. 53-4F). All other limb positions need to be maintained. The clinician should note the areas and quality of responses. Cervical Lateral Flexion Away Cervical movements can be added at any point in the test procedure. Commonly, cervical lateral flexion away (from the involved limb) is added as a sensitizer to particularly challenge the middle and lower cervical nerve roots (see Fig. 53-4G).4 Responses should be noted. Cervical Lateral Flexion Toward It is appropriate to follow up cervical lateral flexion away with a movement toward the side of complaints in the case of an athlete exhibiting enhanced sensitivity (see Fig. 53-4H). This maneuver slackens the ipsilateral middle and lower cervical nerve roots. Responses should be noted.
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Specific Neurodynamic Tests Musculocutaneous Nerve An active test is performed first and responses are noted. The clinical test is shown in Figure 53-5. Starting position: The athlete should lie at an angle across the table so that the involved glenohumeral joint is slightly over the edge of the examination table (see Fig. 53-5A). The clinician stands at the head end of the table and contacts the patient’s shoulder girdle with the clinician’s thigh. The test arm should be supported at the elbow by the clinician’s arm closest to the athlete; the other hand holds the athlete’s wrist in a neutral position. Shoulder depression: The clinician leans his or her thigh into the athlete’s shoulder girdle to gently guide the shoulder girdle into depression (see Fig. 53-5B). Elbow extension: While maintaining the shoulder girdle depression, the involved elbow is guided into elbow extension (see Fig. 53-5C). Shoulder extension: While maintaining the previous positions, the shoulder is guided into up to 30 degrees of extension (see Fig. 53-5D).4 Wrist ulnar deviation: The wrist is moved into ulnar deviation (see Fig. 53-5E). The specifics of the hand-hold are shown in Figure 53-5F. Cervical lateral flexion away and toward: Adding neck movements assists with evidence of structural differentiation, showing that the problem is indeed in the nervous system. Shoulder abduction and external rotation of the shoulder can be used as sensitizers as needed.4 Axillary Nerve An active test can be performed first. Any glenohumeral joint symptoms should be noted; use caution if the patient has a history of glenohumeral subluxation or dislocation. The clinical test is shown (Fig. 53-6). Starting position: The athlete is supine on the table, and the clinician stands by the side of the examination table holding the involved limb at the elbow and cradling the entire arm. Internal rotation of the shoulder: The glenohumeral joint is internally rotated. Shoulder depression: The shoulder girdle is guided into shoulder depression. Cervical lateral flexion away and toward: The cervical spine can be laterally flexed away, then toward, the involved limb.
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Figure 53-5. Specific neurodynamic testing of the musculocutaneous nerve. A, Starting position. B, Shoulder girdle depression. C, Elbow extension. D, Shoulder extension. E, Ulnar deviation of the wrist (plus circle inset).
Suprascapular Nerve This nerve is not easily challenged in an active test. The clinical test is shown (Fig. 53-7). Starting position: The athlete is supine on the examination table and the clinician stands on the opposite side of the table from the involved arm. The examiner brings the arm across the patient’s midline in horizontal adduction and rests the athlete’s elbow on the sternum. The examiner places his or her hands on the scapula.
Figure 53-6. Specific neurodynamic testing of the axillary nerve.
Cervical lateral flexion away: The athlete’s head and neck are guided into lateral flexion away from the injured side. Humeral drive through: The examiner leans into the athlete’s elbow while maintaining support of the athlete’s scapula to simulate a drive-through action. Shoulder girdle depression: The shoulder girdle is guided into depression. Medial rotation of the scapula: The examiner guides the athlete’s scapula into medial rotation. Long Thoracic Nerve This nerve is not easily challenged in an active test. The clinical test is shown (Fig. 53-8).
Figure 53-7. Specific neurodynamic testing of the suprascapular nerve.
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Starting position (see Fig. 53-8A): The athlete is lying on his or her side opposite the involved limb. The examiner
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stands behind the athlete, supporting the shoulder girdle and the arm. Cervical lateral flexion away (see Fig. 53-8B): The athlete’s head and neck are guided into lateral flexion away from the injured side as the pillow support is gradually released. Shoulder girdle depression (see Fig. 53-8C): The shoulder girdle is guided into depression. Scapular lift (not shown): The examiner gently lifts or pulls the scapula away from the chest wall at the medial border of the scapulothoracic joint. Lateral rotation of the scapula (optional): The scapula can be carefully rotated laterally to tolerance.
NEURODYNAMIC TEST FINDINGS Analysis Without any other clinical information, all a neurodynamic test can tell you is that your athlete has a sensitive movement.4 Neurodynamic tests alone do not give specific information about the sources or mechanisms of the symptoms that an athlete is experiencing. They do not give any direct information about where along the nervous system a pathology might exist. Any symptoms produced during the test do not necessarily indicate that a pathologic process is occurring. Neurodynamic tests do give insight into
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Figure 53-8. Specific neurodynamic testing of the long thoracic nerve. A, Starting position. B, Cervical lateral flexion (away). C, Shoulder girdle depression.
the hypotheses that the nervous system may be involved in generating neurogenic symptoms in the athlete. The results of neurodynamic tests need to be considered as only one aspect of the bigger clinical picture. Making Test Findings Relevant Structural Differentiation. Structural differentiation refers to the initial analysis of the test performance that occurs during neurodynamic testing. For example, when testing the musculocutaneous nerve, adding contralateral side bending of the cervical spine, which then increases symptoms in the distribution of the nerve, adds more support to the interpretation that the test is provocative for neurogenic symptoms. It is recommended that clinicians perform structural differentiation analysis with all neurodynamic tests, including active and passive maneuvers.4,17,22 There is evidence that structural differentiation can preferentially provoke responses in the nervous system.22 Test Positivity. There are several key features of a positive neurodynamic test. The first feature is that the test provokes or reproduces the symptoms that the athlete complains of or are in a relevant distribution to the nerve being tested. The second feature of a positive test is that the response (sensory symptoms or range of motion or resistance perceived by the examiner) is different from that of the opposite (asymptomatic) limb and different from what is known to be a normal response. Structural differentiation is the final feature of a positive test; it supports the premise that the symptoms provoked from a neurodynamic test are most likely of neurogenic origin.4,5,13,17,22
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Neurogenic Source Considerations. Clear cut nerve root disorders can often be readily determined clinically by interpreting the location of the area of symptoms (dermatome), the spinal segmental level of motor loss if present (myotome), and suppression of a relevant reflex. These can be easily tested by carrying out a thorough traditional neurologic examination. When multiple spinal levels or tissues are involved, or where there are maladaptive sensitivities in the central nervous system, interpretation of the sources of the peripheral neurogenic symptoms is a much more difficult endeavor for the clinician.4 Possible sources of peripheral neurogenic symptoms in an athlete can be indicated by the area of the symptoms, motor loss, history, pain behavior, and objective studies.4 The area of symptoms in an identifiable dermatome or cutaneous neural zone can assist the clinician, because cutaneous neural zones are more nerve trunk in origin and dermatomes are more nerve root in origin. The presence of motor loss may point to either a nerve root or nerve trunk; loss of a reflex points more to a nerve root origin. Palpation of the nervous system can allow the examiner to put a finger directly on the peripheral nerve that has become an abnormal impulse-generating site of symptoms. Mechanical symptoms and sensitivity anywhere along the nerve in response to palpation should be investigated as contributing factors. Skilled examination of tissue surrounding the nervous system can give insights into the relevant dysfunction of the regional muscle, fascia, or joints that act as container tissues to the nervous system. History of the site of the injury may be enough in some cases to point out the source of the peripheral neurogenic mechanisms involved. Pain behavior, including the quality and type of symptoms, aggravating and easing movements and positions, and 24-hour pain behavior can help link the overall pattern of symptoms to a peripheral neurogenic pain source. External evidence should be considered in the form of nerve conduction and imaging studies when neurologic pathology is suspected. Normal Physiologic Responses Pullos23 tested 100 asymptomatic subjects and reported a range of elbow-extension deficit of 16.5 to 53.2 with ULNT testing. Clinical experts have stated that only hypermobile persons exhibit full asymptomatic elbow extension.4 Kenneally and colleagues tested 400 asymptomatic subjects.18 Figure 53-9 provides a reference of these sensory responses.4 The Kenneally group summarized their findings of the responses to the ULNT as follows: Deep ache or stretch in the cubital fossa extending down the anterior or radial aspect of the forearm into the radial side of the hand (see Fig. 53-9B) was found in 99% of subjects. Tingling sensation was found in the thumb and first three fingers (see Fig. 53-9C). Stretch sensation in the anterior shoulder was found in a small percentage of subjects (see Fig. 53-9A). Cervical lateral flexion away from the side of the side tested increased evoked responses in 90% of subjects.
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Figure 53-9. Normal responses in healthy university students to ULNT. (Adapted from Kenneally M, Rubenach H, Elvey R: The upper limb tension test: the SLR of the arm. In Grant R [ed]: Physical Therapy of the Cervical and Thoracic Spine. New York, Churchill Livingstone, 1988, pp 167-194.)
Cervical lateral flexion toward the side being tested decreased the evoked responses in 70% of subjects. Progressive muscle reactivity in the upper trapezius is considered normal during ULNT1 testing, as shown by several authors.19-21,24 It may be useful for clinicians to manually monitor this trapezius reactivity as reflecting the flexorwithdrawal response, at the point where the athlete perceives the stretch sensation as pain during testing.19-21,24
Clinical Management Neurodynamic test results reflect an athlete’s problems with movement in sports. Clinicians need to determine if these test movements should be used to reduce symptoms and restore movement patterns or if they should be used as indicators of improvement toward specific outcomes for return to sports practice or competition. Some evidence in the literature supports the use of specific nerve mobilization treatment for upper quarter disorders. Several clinicians have shown the cervical lateral glide technique25 (Fig. 53-10) to be effective in reducing neurogenic pain and decreasing signs of neural tissue sensitivity in patients with lateral epicondylgia and neck and arm pain.26-28 Shoulder girdle oscillation techniques have been incorporated with the cervical lateral glide technique and shown
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Figure 53-10. Cervical lateral glide technique. A, Cervical lateral glide technique. B, Cervical lateral glide, hand position on spine mode.
to be effective in reducing neurogenic neck and arm pain.28 Clinical trials of nerve gliding mobilization in the management of carpal tunnel syndrome have shown mixed results; one study combining nerve mobilization with tendon mobilization showed a 30% reduction in the need for surgical intervention,22 but another showed no additional benefit in reducing pain or improving function when used with a splinting program.18 Traditional medical advice can lead us to believe that we can clinically diagnose and treat the specific tissues and structures of the shoulder. Neuropathic disorders that have little or no evidence of pathology via medical tests (e.g., imaging studies, nerve-conduction tests) but significant symptom complaints from an athlete might seem to contradict this type of traditional advice. When a neurodynamic test for shoulder complaints finds pathology in an athlete, it is easier to treat the faulty movement(s) and sensitivity of structures associated with those movement(s) rather than any specific structural pathology itself. Treatment in the form of nerve tissue mobilization can be used as a passive or active movement applied to the nervous system. The goals are to restore the ability of the nervous system to tolerate all of the potential compressive, tensile, and friction forces associated with sports activities. Neurodynamic Test Findings as a Reassessment Tool It can be quite useful to treat the tissues contributing to the shoulder pain and dysfunction and use the neurodynamic test findings as a reassessment tool only. This is particularly true if the clinician is unfamiliar with nerve mobilization techniques or if the mechanosensitivity of the nerve tissues in the area are extremely irritable. An example is a baseball pitcher complaining of posterior shoulder pain with a suspected suprascapular nerve problem (a positive suprascapular neurodynamic test and no detection of motor loss on physical examination). The clinician may
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choose a soft-tissue mobilization of the infraspinatus muscle to free up any restriction in the myofascial tissues interfering with blood flow to the suprascapular nerve bed to reduce pain and promote a healing environment for the nerve. The specific neurodynamic test for the suprascapular nerve could be then repeated and any progress noted. Neurodynamic Treatment: Passive Techniques The results of a neurodynamic test used as a reassessment tool can plateau. The clinician could then choose to mobilize the suprascapular nerve as treatment technique. Three options should be considered. Sliders are a form of neurodynamic technique used to encourage movement and avoid tensile loading of the nerve tissues. In the case of the pitcher with posterior shoulder pain, the clinician could move the shoulder girdle into depression while simultaneously moving the head and neck toward the involved shoulder and then move in an opposite manner to effectively slide the suprascapular nerve bed (see Fig. 53-7). Tensioners are a form of tensile-loading neurodynamic technique that effectively lengthen the nerve bed and apply a normal physiologic tensile load on the nerve itself. Tensioners are more aggressive than sliders. In the case of the pitcher with suprascapular nerve problems, the clinician could move the shoulder girdle into shoulder depression with the head and neck in cervical lateral flexion to the contralateral side to effectively tension the suprascapular nerve bed (see Fig. 53-7). With neurogenic massage, direct mobilization of the nerve itself can be used to control symptoms, ultimately reducing mechanosensitivity of the nerve bed. Jabre29 showed that patients with a clinical diagnosis of ulnar neuropathy (supported by EMG findings) had self-rated symptom relief of up to 50% in daily activities with ulnar nerve
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massage and significantly fewer complaints of nighttime waking. Neurodynamic Treatment: Active Self-Care Techniques Functional exercise in any form can be used to mobilize the nervous system and promote a healing environment for the suspected nerve tissues. The concept of sliders and tensioners can be applied to any active movements as a self-treatment option for athletes. Care should be taken to evaluate the ultimate effect of any rehabilitation prescription for the postures, positions, or creative movement patterns on the specific nerve tissues being treated and the nervous system as a whole.
NEUROGENIC PAIN SYNDROMES FOLLOWING SHOULDER SURGERY A sports medicine conference discussed the potential deleterious effects on the upper quarter nervous system as a result of undergoing a surgical procedure at the shoulder.30 A review of the literature reveals numerous factors that could contribute to neuropathic pain or pathology to the nervous system following shoulder surgery. Three main causative factors are associated with the onset of postoperative neurogenic shoulder pain. The first consideration reported in the literature was the position of the shoulder during the procedure.31 Many surgeons agree that the position of the shoulder during the procedure (lateral decubitus vs. beach chair) can put excessive stress on the nervous system and contribute to neurogenic symptoms and even motor loss.32-36 The second consideration noted in the literature points to the type of shoulder surgery, ranging from arthroscopic surgery to open surgical procedures.35-38 The final consideration is the delivery of an interscalene block. Complications with an interscalene block for shoulder surgery range from minor neuropathic pain complaints (up to 10%) to cardiac arrest, phrenic nerve palsy, and brachial plexus neuropathy.39-53 This evidence should justify a neurologic screen and neurodynamic testing in any athlete following shoulder surgery.54 Abnormal mechanosensitivity can develop in the nervous system following a period in a sling or immobilizer, given the deleterious effects on the nerve tissues themselves following a period of immobilization after a surgical procedure.12 Early mobilization is essential in rehabilitation following any injury or procedure so long as there is no risk to the healing tissues.
SUMMARY Consideration of the nervous system in athletic injury has long been overlooked except in cases where there is obvious clinical evidence of neurologic impairment suggesting
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severe pathology. The clinician must consider examining and treating the regional neural tissues in athletes with shoulder pain and dysfunction after acute injury, after shoulder surgery, after any period of immobilization, and in a chronic injury state.
References 1. Nee RJ, Butler D: Management of peripheral neuropathic pain: Integrating neurobiology, neurodynamics, and clinical evidence. Phys Ther Sport 7:36-49, 2006. 2. Merskey H, Bogduk N: Classification of chronic pain: Descriptions of chronic pain syndromes and definitions of pain terms, 2nd ed. Seattle, IASP Press, 1994. 3. Gifford L, Butler D: The integration of pain sciences into clinical practice. J Hand Ther 10:86-95, 1997. 4. Butler D: The Sensitive Nervous System. Adelaide, Australia, NOIgroup Publications, 2000. 5. Butler D: Mobilisation of the Nervous System. Melbourne, Churchill Livingstone, 1991. 6. Butler DS, Tomberlin J: Peripheral nerve: Structure, function and physiology. In Magee DJ, Zachazewski JE, Quillen WS (eds): Musculoskeletal Rehabilitation, vol 2. New York, Elsevier, 2007. 7. Sunderland S: The anatomy and physiology of nerve injury. Muscle Nerve 13:771-784, 1990. 8. Sunderland S: Nerve Injuries and Their Repair: A Critical Appraisal. Edinburgh, Churchill-Livingstone, 1991. 9. Shacklock M: Neurodynamics. Physiotherapy, 81:9-16, 1995. 10. Coppieters M, Stappaerts K, Evaraert D, Staes F: Addition of test components during neurodynamic testing: Effect on range of motion and sensory responses. J Orthop Sports Phys Ther 31: 226-237, 2001. 11. Penning L: Functional pathology of lumbar spinal stenosis. Clin Biomech 7: 3-17, 1992. 12. Topps KS, Boyd BS: Structure and biomechanics of peripheral nerves; nerve responses to physical stresses and implications for physical therapy practice. Phys Ther 86:92-109, 2006. 13. Elvey R: Physical evaluation of the peripheral nervous system in disorders of pain and dysfunction. J Hand Ther 10:122-129, 1997. 14. Millesi H, Zoch G, Rath T: The gliding apparatus of peripheral nerve and its clinical significance. Ann Hand Surg 9: 87-97, 1990. 15. Beith L, Robins E, Richards P: An assessment of the adaptive mechanisms within and surrounding the peripheral nervous system, during changes in nerve bed length resulting from underlying joint movement. In M Shacklock (ed): Moving in on Pain. Sydney, Butterworth Heinemann 1995, pp 194-203. 16. Hall T, Elvey R: Nerve trunk pain: Physical diagnosis and treatment. Man Ther 4:63-73, 1999. 17. Shacklock M: Clinical Neurodynamics: A New System of Musculoskeletal Treatment. Edinburgh, Butterworth Heinemann, 2005. 18. Kenneally M, Rubenach H, Elvey R: The upper limb tension test: the SLR of the arm. In Grant R (ed): Physical Therapy of the Cervical and Thoracic Spine. New York, Churchill Livingstone, 1988, pp 167-194. 19. Tomberlin JP: Towards a clinical test: Monitoring muscle responses during media nerve palpation in asymptomatic
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subjects. Presented at the International Federation of Manipulative Therapists, Perth, Australia, November 6, 2000. Edgar D, Jull G, Sutton S: Relationship between upper trapezius muscle length and upper quadrant neural extensibility. Aust J Physiother 40:99-103, 1994. van der Heide B, Allison G, Zusman M: Pain and muscular responses to a neural tissue provocation test in the upper limb. Man Ther 6:154-162, 2001. Coppieters M, Kurz K, Mortenson T, et al: The impact of neurodynamic testing on the perception of experimentally induced muscle pain. Man Ther 10:52-60, 2005. Pullos J: The upper limb tension test. Aust J Physiother 32:258-259, 1986. Balster S, Jull G: Upper trapezius muscle activity during the brachial plexus tension test in asymptomatic subjects. Manual Therapy 2:144-149, 1997. Elvey R: Treatment of arm pain associated with abnormal brachial plexus tension. Aust J Physiother 32:225-230, 1986. Vincenzino B, Collins D, Wright A: The initial effects of a cervical spine manipulative physiotherapy treatment on the pain and dysfunction of lateral epicondylalgia. Pain 68:69-74, 1996. Coppieters M, Stappaerts K, Wouters L, et al: Aberrant protective force generation during neural provocation testing and the effect of treatment in patients with neurogenic cervicobrachial pain. J Manipulative Physiol Ther 26(2):99-106, 2003. Allison G, Nagy B, Hall T: A randomized clinical trial of manual therapy for cervicobrachial pain syndrome: A pilot study. Man Ther 7:95-102, 2002. Jabre JF: “Nerve rubbing” in the symptomatic treatment of ulnar nerve parasthesiae. Muscle Nerve 17:1237, 1994. Tomberlin JP: Neurogenic Upper Quarter Pain Shoulder Surgery: Incidence, Detection, Treatment. Presented at the Southwest Sports Medicine Conference, Banner Health System, Mesa, Ariz, March 3-5, 2006. Coppieters MW, Van de Velden M, Stappaerts KH: Positioning in anesthesiology: Toward a better understanding of stretch-induced perioperative neuropathies. Anesthesiology 97(1):75-81, 2002. Klein AH, France JC, Mutschler TA, et al: Measurement of brachial plexus strain in arthroscopy of the shoulder: Arthroscopy 3:45-52, 1987. Cooper DE, Jenkins RS, Bready L, et al: The prevention of injuries of the brachial plexus secondary to malposition of the patient during surgery. Clin Orthop Relat Res (228):33-41, 1988. Park T, Kim Y: Neuropraxia of the cutaneous nerve of the cervical plexus after shoulder arthroscopy. Arthroscopy 21(5):631, 2005. Segmuller H, Alfred SP, Zilio G, et al: Cutaneous nerve lesions of the shoulder and arm after arthroscopic surgery. J Shoulder Elbow Surg 4:254-258, 1995. Stanish D, Peterson DC: Shoulder arthroscopy and nerve injury: Pitfalls and prevention. Arthroscopy 11:458-466, 1995.
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37. Lynch NA, Cofield RH, Silbert PL, Hermann RC: Neurologic complications after total shoulder arthroplasty. J Shoulder Elbow Surg 5:53-60, 1996. 38. Richards RR, Hudson AR, Bertoia JT, et al: Injury to the brachial plexus during Putti-Platt and Bristow procedures. Am J Sports Med 15:374-380, 1987. 39. Winnie AP: Interscalene brachial plexus block. Anesth Analg 49:455-466, 1970. 40. Passannante A: Spinal anesthesia and permanent neurologic deficit after interscalene block. Anesth Analg 82:873-874, 1996. 41. Walton JS, Folk JW, Friedman RJ: Complete brachial plexus palsy after TSA done with interscalene block anesthesia. Reg Anesth Pain Med 25:318-321, 2000. 42. Pavlik A, Ang KC, Bell SN: Contralateral brachial plexus neuropathy after arthroscopic shoulder surgery. Arthroscopy 18:658-659, 2002. 43. Dutton R, Eckhardt W, Sunder N: Total spinal anesthesia after interscalene plexus blockade of the brachial plexus. Anesthesiology 80:939-941, 1994. 44. Seltzer J: Hoarseness and Horner’s syndrome after interscalene brachial plexus block. Anesth Analg 56:585-586, 1977. 45. Stadlmeyer W, Neubauer J, Finkl RO, et al: Unilateral phrenic nerve paralysis after vertical infraclavicular plexus block. Anaesthesist 49:1030-1033, 2000. 46. Rosenberg PH, Lamberg TL, Tarkkila P, et al: Auditory disturbance associated with interscalene brachial plexus block. Br J Anaesth 74:89-91, 1995. 47. Korman B, Riley RH: Convulsions induced by ropivacaine during interscalene brachial plexus block. Anesth Analg 85:1128-1129, 1997. 48. Benumof JL: Permanent loss of cervical spinal cord function associated with interscalene block performed under general anesthesia. Anesthesiology 93:1541-1545, 2000. 49. Candido KD, Sukhani R, Doty R, et al: Neurologic sequelae after interscalene brachial plexus block for shoulder/upper arm surgery: The association of patient, anesthetic, and surgical factors to the incidence and clinical course. Anesth Analg 100:1489-1495, 2005. 50. Shaw WM: Paralysis of the phrenic nerve during brachial plexus anesthesia. Anesthesiology 10:627-628, 1949. 51. Hood J, Knoblanche G: Respiratory failure following brachial plexus block. Anesth Intensive Care 7:346-349, 1979. 52. Horlocker TT, O’Driscoll SW, Dinapoli RP: Recurring brachial plexus neuropathy in a diabetic patient after shoulder surgery and continuous interscalene block. Anesth Analg 91:688-690, 2000. 53. Deruddre S, Vidal D, Benhamou D: A case of persistent hemidiaphragmatic paralysis following interscalene brachial plexus block. J Clin Anesth 18:238-239, 2006. 54. Weber SC, Jain R: Scalene regional anesthesia for shoulder surgery in a community setting: An assessment of risk. J Bone Joint Surg Am 84:775-778, 2002.
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CHAPTER 54 Isokinetic Testing and Rehabilitation
of the Shoulder Complex George J. Davies, Todd S. Ellenbecker, and Kevin E. Wilk
Conceived in 1969 by James Perrine, isokinetics became extremely popular during the late 1970s and the 1980s. In the early 21st century, the clinical trend appears to be favoring a decrease in isokinetic exercise and a greater focus on functional activities. We still believe isokinetics should be an important component of patient care, because isokinetic exercise provides the clinician with objective reproducible clinical outcome measurements relating to muscular performance. Furthermore, in our opinion, next to the clinician’s hands, isokinetic exercises are one of the safest types of exercises due to the accommodating resistance. Accommodating resistance occurs when the force applied by the patient is directly matched (accommodated) by the isokinetic resistance. Isokinetics is one of the safest modes of resistance testing and training when used appropriately.2,3 Moreover, several research studies demonstrate the efficacy of isokinetics in rehabilitation.
It is a capital mistake to theorize before one has data. Sir Arthur Conan Doyle
A curious phenomenon occurring in health care is an emphasis on evidence-based practice and documentation of outcome studies, yet many clinicians do not use isokinetics for either documentation or treatment interventions. The use of isokinetic exercise and testing appears to be in a period of flux. Conceived in 1969 by James Perrine, isokinetics became extremely popular during the late 1970s and 1980s. In the past several years, the clinical trend appears to be using isokinetic exercises less with a greater focus on functional activities. Although ultimately the patient must return back to function, it is also important to evaluate and rehabilitate each link in the kinetic chain so the functional unit is normalized. This is one of the primary roles of isokinetic testing. Sackett and colleagues1 have described evidence-based practice as the integration of clinical experience and expertise, patient values, and the best evidence (research) into the decision-making process for patient care. Yet many clinicians perform interventions and perhaps never critically evaluate the literature for the same documentation or efficacy regarding clinical applications and outcomes of Kinesio taping, Swiss ball exercises, upper-extremity closed-kinetic-chain exercises, and plyometrics. However, when we perform a literature search, we find four articles on Kinesio taping, five articles on Swiss ball exercises, six articles on upper-extremity closed-kinetic-chain exercises, and five articles on plyometrics. We performed a Medline search on August 20, 2007, and found 3319 articles on isokinetics; 272 of those specifically deal with testing for documentation or outcome measures or treatment interventions for the shoulder. We are not saying the other interventions are not effective, but only that we use them with less documented evidence, and we do not use isokinetics, which has a much larger evidence base. Several books are devoted exclusively to isokinetics, and these have provided the applications of isokinetics in clinical practice and performance enhancement.2-7
The glenohumeral joint is an inherently unstable joint.9-12 It consists of a large oval humeral head articulating with a small convex glenoid fossa, a ball-and-socket joint. This type of joint allows a tremendous amount of movement, but stability is compromised. The functional stability of the glenohumeral joint is accomplished through the joint’s dynamic stabilizing components. The dynamic stabilizers of the shoulder complex are the rotator cuff musculature, the long head of the biceps brachii, the deltoid, and some of the scapulothoracic musculature. The primary function of the rotator cuff muscles is one of dynamic glenohumeral stability.9,11 These muscles steer the humeral head and control humeral head displacement through a co-contraction of these muscles, which results in increased joint compression forces. The rotator cuff also functions as a fine tuner during strenuous activities, especially overhead motions such as throwing, tennis, or elevated work activities. The rotator cuff’s secondary function is one of primary movement, such as with external and internal rotation of the shoulder. It is obvious that the glenohumeral joint must rely extensively on the shoulder musculature and rotator cuff for dynamic stability during different strenuous activities. Therefore, the objective documentation of the strength, power, and endurance of the shoulder musculature is necessary to predict a return to injury-free sporting activities or strenuous activities.
Isokinetic test results document objective patient status at the initial examination, progression or regression, and criteria for discharge regarding muscular performance. This ability to document results is important in the examination, evaluation, and treatment of the patient with a shoulder problem.8 719
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THE ATHLETE’S SHOULDER
ISOKINETICS IN ASSESSING AND REHABILITATING THE SHOULDER COMPLEX Isokinetics in shoulder examination and treatment are often used in testing to determine the patient’s dynamic muscular power (as part of a functional testing algorithm) and establish a database, in rehabilitation techniques, and in testing as part of a functional testing algorithm for discharge.2-7,13
BOX 54-2. Criteria for Progression of Functional Testing for the Shoulder Complex
Sport-specific testing: specificity for sport Functional throwing performance index • Male athletes: 33%-60% accuracy of throws • Female athletes: 17%-41% accuracy of throws Closed-kinetic-chain upper-extremity stability test • Male athletes: 21 touches • Female athletes: 23 touches
Functional Testing Algorithm
Isokinetic testing
We often use a functional testing algorithm as the basis for examination and rehabilitation intervention strategies for patients with shoulder injuries.14-20 Examples of functional testing algorithms that we use for examining and treating the shoulder complex are shown in Boxes 54-1 and 54-2.
⬍15% bilateral difference: Normative data for functional throwing performance test ⬍25% bilateral difference: Normative data for closedkinetic-chain test Kinesthetic and proprioceptive testing
Physical Examination and the Role of Isokinetics22-26
• ⬍3º ± 2º males • ⬍4º ± 3º females
Isokinetic testing should be one part of the patient’s objective dynamic muscular power (database). Testing includes observation of posture, referral and related joints, neurologic examination, sensation and reflexes, kinesthetic and proprioceptive testing,27,28 palpation, scapular assessment,27-30 active range of motion (ROM),31,32 physiologic passive ROM flexibility tests, resisted ROM and manual muscle testing (MMT),33-45 special tests,27,46 computerized isokinetic testing and reliability,47-55 functional testing, and imaging studies.
Basic measurements
When a clinician refers to the assessment of muscular strength, one often thinks of the MMT techniques. The earliest description of MMT was by Robert Lovett in 1912.34 Since its conception, there have been several revisions in this technique. Two of the most popular versions of MMT have been developed by Kendall35 and by Daniels and Worthingham.36 Several inconsistencies are found in the application and grading of these two techniques.36,37 Also, BOX 54-1. Functional Testing Algorithm for the Shoulder Complex
Sport-specific testing Functional throwing performance index Closed-kinetic-chain upper-extremity stability test Isokinetic testing Kinesthetic and proprioceptive testing Basic measurements Visual analog scale
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⬍10% bilateral difference Visual analog scale (0-10) • ⬍3 out of 10
inter-rater reliability is poor,38,39 and the grading is relatively subjective.40,41 Wilk and colleagues38 demonstrated bilateral isokinetic knee extension deficits ranging from 23% to 31% in 176 arthroscopic knee patients who exhibited bilaterally equal and normal grade (5/5) MMT. MMT tells the examiner nothing regarding muscular performance parameters such as work, power, and endurance; rather, it determines the ability of the subject to exert force at one particular point in the ROM.37 Thus, the validity of MMT for the orthopedic and sports medicine patient might not be completely acceptable in all instances.36,37 Isokinetic testing is used in the examination because of the limitations of MMT or hand-held dynamometry. MMT is based on performing an isometric test at one point in the ROM. It is a subjective test on the part of the examiner, and it is not really a functional indicator of the muscle’s performance capabilities. Ellenbecker and colleagues56 compared MMT with isokinetic testing of patients’ glenohumeral internal rotation (IR) and external rotation (ER). Although the patients demonstrated MMT results of 5/5 for the shoulder IR and ER, when isokinetic testing was performed the patients demonstrated a 10% to 30% deficit. Therefore, isokinetic testing of the shoulder is a practical clinical addition to MMT. Isokinetic testing allows the
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clinician to document dynamic muscular performance objectively in a safe and reliable way using either isolated or combined movement patterns. This objectivity ensures appropriate patient progression or regression and helps the clinician answer such functional questions as: When can I hit a golf ball? Begin throwing? Begin hitting a tennis ball? Return to overhead work activities? Isokinetics affords the clinician objective dynamic muscle performance criteria and provides reproducible data to monitor patient function and plan patient progression. We think the circle concept of dynamic muscle balance is important in assessing the patient. The circle concept also applies to examining the shoulder, where one needs to test both sides of the joint for a unilateral ratio. One rationale for the circle concept is the contre-coup concept: Injury or weakness can occur opposite to the side of the obvious injury. As an example, the patient who has an anterior injury (e.g., anterior inferior subluxation) might also demonstrate a contre-coup weakness of the rotator cuff external rotators.
ISOKINETIC TESTING OF THE SHOULDER
Figure 54-1. The 90-degree abducted position for shoulder external and internal rotation.
To assess the muscular performance characteristics of the shoulder joint that has sustained a repetitive microtraumatic injury57 or a macrotraumatic injury,58 the clinician should consider the patient’s activities of daily living, ergonomic considerations, and the sports activities the patient participates in. This type of information provides the clinician with the rationale for choosing the position for testing the shoulder. Most commonly, the shoulder is placed at risk for sustaining a microtraumatic injury when elevation, abduction, and rotation are required while performing a wide variety of activities. Examples of these activities include throwing, tennis, swimming, volleyball, and workrelated activities such as painting and construction work. In the overhead athlete or worker, the authors recommend testing in the 90-degree abducted and 90-degree elbow flexed position for shoulder internal and external rotation (Fig. 54-1). In contrast, for the patient who has sustained a macrotraumatic shoulder injury that involves the capsule or rotator cuff and whose daily activities do not necessitate repetitive overhead motions, testing is recommended in a lessdemanding or less-stressful position. This position is referred to as a modified neutral position2,3 (Fig. 54-2) or the 30/30/30 position. (This position is described in detail later with specific rationale and justification.) We recommend using this testing position in the low-demand patient, the patient who uses the arm most commonly below 90 degrees of elevation, or when objective data are necessary earlier in the rehabilitation program before the patient has dynamic control in the 90/90 position.
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Figure 54-2. Modified neutral position (30/30/30 position) for shoulder external and internal rotation. Dynamometer is tilted 30 degrees and the shoulder is abducted 30 degrees and placed in scaption of approximately 30 degrees.
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ISOKINETIC TESTING CONSIDERATIONS FOR THE SHOULDER COMPLEX Several testing protocols have been recommended.2,3,59 Davies2,3 and Wilk and colleagues59 suggested a standardized isokinetic testing protocol for the shoulder. Wilk referred to this standardized isokinetic testing protocol as the thrower’s series.59 The goals of a standardized testing protocol are to improve the quality, consistency, and testto-retest reliability47-55,60 and to allow clinicians to share test data.37,50 We present an expanded thrower’s series and explain the modifications of this protocol to the general orthopedic patient. Several variables must be standardized and controlled to ensure an objective, consistent, and reliable isokinetic evaluation of the patient’s shoulder complex (Box 54-3).
BOX 54-3. Protocol
Standardized Isokinetic Testing
Patient education
Patient Education Once the clinical decision has been made that it is appropriate to perform an isokinetic test of the shoulder, the first variable is to educate the patient so he or she understands the purpose and intent of the test as well as what is expected in their performance of the test. The patient should be familiarized with the testing equipment, how it functions, what results will be provided, and how the results will be used in the patient’s evaluation and treatment planning. An informed client is less apprehensive and produces more consistent, reproducible results. Two investigators61 demonstrated that subjects allowed previous isokinetic exposures show significantly favorable responses on isokinetic testing. Mawdsley and Knapik61 reported significant differences between values demonstrated in the first testing session and those of the remaining six test trials. Wilk (unpublished data) has shown that subjects allowed one practice session before testing produced more consistent torque values in 83% to 88% of all test trials. Therefore, it is recommended that, whenever possible, clients undergo at least one isokinetic exposure before testing.
System stabilization
System Stabilization
System calibration
Patient interface with the proper instant axis of rotation of the joint motion
Because of the forces that can potentially be generated and to improve the reliability and consistency of the test data, the testing system should be level and adequately stabilized to the floor. A level and stable system minimizes artifact, overshoot, and oscillation interference during testing. Each of these aberrant recordings can lead to misinterpretation of test data, especially during shoulder abduction and adduction testing.59,62,63
Four progressive submaximal to maximal active warm-ups at each test velocity
System Calibration
Planes of motion to be tested Testing position of the patient Stabilization of the patient
Testing environment • Testing environment that is consistent and free of distractions • Standardized verbal commands to the patient • Standardized visual feedback • Consistent and experienced tester
Although most manufacturers recommend calibration every 30 days to ensure reliability and validity in testing measures, we recommend calibrating the testing system every 2 weeks or before testing many subjects in any session, such as screening a team.
Standardized testing protocol
Planes of Motion
• • • •
In the overhead athlete, the shoulder’s external and internal rotators, adductors and abductors, and horizontal abductors and adductors are the most critical to be tested.2,3,59,64-68 Therefore, isokinetic testing in the thrower’s series should include evaluation of the shoulder’s internal and external rotators as well as the abductors and adductors.59 Because isokinetic testing of the horizontal abductors and adductors is performed in either the supine or prone position, these nonfunctional postures are not recommended in the testing sequence for the microtraumatically injured shoulder. In the low-demand shoulder patient, routine tests should include
Test velocities Test repetitions performed Rest intervals Uninvolved side tested first
Data analysis Gravity compensation of data Consistency in data collection (use of windowed data) Consistency in data analysis
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internal and external rotation and occasionally shoulder flexion and extension. The testing sequence is standardized so that the internal and external rotators are always evaluated first, followed by either shoulder abduction and adduction or flexion and extension.
Testing Position2,3,59 It is necessary to test the shoulder in a position that closely resembles the position of function during activity, while isolating the specific muscle groups desired. To approximate functional positioning and ensure isolation of the muscle, most testing is performed in the seated position. This position allows normal gravitational forces to act on the trunk and upper extremities and enhances glenohumeral joint stabilization. Stabilization of the trunk, hips, and lower extremities during isokinetic testing of the shoulder is highly recommended (Fig. 54-3). Testing of the shoulder’s external and internal rotators can be performed in several test positions. These positions include the 90/90-degree seated test position (see Fig. 54-1), modified neutral position (30/30/30 position; see Fig. 54-2), scapular plane position, and neutral position. Several authors demonstrated significant torque value variations by altering the subjects’ test positions.69-74 Greenfield and colleagues 70 tested external and internal rotation in both the scapular and frontal planes. They found no significant internal rotation peak torque difference but did find increased external rotation torque values in the scapular
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plane. Walmsley and Szybbo74 assessed external and internal rotation peak torque values in three test positions: neutral, 90-degree abduction, and 90-degree flexion. They found increased internal rotation torque values in the neutral position and the highest external rotation values in the 90degree position. Hinton71 reported increased torque for internal rotation in the neutral position compared with the 90-degree abducted position, and external rotation was found to be equal in both positions.
Stabilization of the Patient2,3,59 The patient must be adequately stabilized based on the testing position to be used. The stabilization can be accomplished through proper patient positioning: supine where the body weight helps stabilize the patient, or against a testing chair or table for securing the patient to minimize compensatory movements (see Fig. 54-3). This is obviously important for the reliability of the testing results.
Proper Instant Axis of Rotation2,3,59 It is critical to ensure that the axis of joint motion is aligned with the axis of rotation of the shaft of the dynamometer. This alignment is necessary for accuracy in torque measurement.37 Although the phenomenon is not yet documented for the shoulder, changes in lever arm length of 2.5 in. or greater during knee extension and flexion testing have been shown to significantly alter torque production.75-77 When testing shoulder abduction and adduction, the axis of the dynamometer should be aligned 1 to 2 cm distal to the acromioclavicular joint. In testing the internal and external rotation, the axis of rotation is aligned through the center of the olecranon and the shaft of the humerus.
Submaximal to Maximal Active Warm-ups2,3 An active warm-up before isokinetic testing is important for several reasons. Several studies have shown no direct relation between a warm-up and increased isokinetic torque production.78,79 There is definitely basic science research that documents the need for an active warm-up from a physiologic basis; however, this has not been found to enhance isokinetic testing.80-83 Nevertheless, based on these basic exercise physiology principles, a standardized upper extremity warm-up is performed before isokinetic testing of the shoulder. This graded active warm-up activity includes a 5-minute upper-body ergometer session at 90 repetitions per minute at a 60 kg/m work load.
Figure 54-3. Trunk, hip, and lower extremity stabilization to eliminate substitution during glenohumeral testing.
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An isokinetic warm-up or familiarization period before testing includes four progressive gradient submaximal to maximal isokinetic repetitions at each angular test velocity before testing at that velocity.2,3,61 The repetitions are performed at a 25%, 50%, 75%, and 100% gradient effort. Our clinical decision has determined it was appropriate to test the patient; however, by having the patient perform the
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gradient warm-ups we confirm our decision, and if the patient has pain on the gradient warm-ups, it may be a contraindication to testing the patient on that day. This provides a fail-safe system so a patient who is not ready for testing will not be tested. Performing only submaximal warm-ups and then performing maximal tests creates a negative transfer of learning. If one is performing maximal volitional testing, then it is appropriate to have the patient perform the maximal activity in the warm-up phase. Mawdsley and Knapik61 have demonstrated improved reliability when the warm-up activity replicates the test activity.
Testing Environment2,3,59 Consistent and Distraction-Free Testing Environment59 The testing environment should be one that promotes concentration and assists in eliminating distractions. A designated room or specified area of the clinic for testing is encouraged to isolate the patient from interruptions, distractions, or additional activities that can prevent a consistent test effort. Standardized Verbal Commands2,3,59 Verbal commands to each patient should be standardized to improve reproducibility. Johansson and colleagues84 demonstrated that loud verbal commands resulted in greater isometric torque values compared with softer verbal commands. This has been seen during manual resistance techniques.85 Thus, verbal commands during isokinetic testing should be consistent, encouraging, and moderate in intensity. Standardized Visual Feedback The subject’s knowledge of results of torque production during testing is the next component of the testing environment to control. Several investigators reported that knowledge of results during strength testing can enhance some parameters of performance.86-89 Therefore, visual feedback in the form of knowledge of results can significantly influence testing performance and must be consistently used or not used during isokinetic testing. Because visual feedback has been shown to enhance torque values and promote earlier fatigue, its use is not recommended.37,89 Consistent and Experienced Tester2,3,59 The final component of the testing environment is the skill and experience of the examiner. An experienced examiner can greatly allay a subject’s apprehension, improve reproducibility of testing, and maximize the efficiency and efficacy of isokinetic shoulder assessment.
Standardized Testing Protocol2,3,59 Test Velocities2,3,59 The next guideline is the selection of the angular velocities to be used during shoulder testing. Box 54-4 illustrates the current angular velocity classifications for isokinetic testing
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BOX 54-4. Isokinetic Angular Velocity Classification
Slow: 0-60 deg/sec Intermediate: 60-180 deg/sec Fast: 180-300 deg/sec Functional: 300-450 deg/sec
devices. Because of the extremely high angular velocities the shoulder obtains during throwing, golf, or tennis,68,90,91 testing at slow isokinetic speeds may be inappropriate and, in fact, can impart undue forces on the glenohumeral joint.92 Therefore, we recommend testing the shoulder at faster angular velocities of 180, 210, 300, 360, and 450 deg/ sec. For the general orthopedic patient being tested in the 30/30/30 position, testing at 60, 180, and 300 deg/sec is appropriate because of the shorter arc of motion, free limb acceleration, and less stressful position to the shoulder. Test Repetitions Performed2,3,59 The number of repetitions performed during isokinetic shoulder testing should be standardized. Davies2,3 has found that ten isokinetic repetitions produce an optimal training effect for both peak torque and average power parameters. Based on this observation, isokinetic evaluation of the shoulder is performed using 5-10 repetitions at 180, 300, and 450 deg/sec. Although it has been demonstrated that peak torque for both internal and external rotation, as well as the abductors and adductors of the shoulder, is produced during the second or third test repetition in 96% of all cases,93 10 to 15 test repetitions are used during isokinetic shoulder testing to ensure the optimal assessment of total work, average power parameters, and endurance parameters. Often, for the orthopedic patient, we recommend five repetitions at each speed and perform velocity spectrum testing. Rest Intervals3 Controlling the rest interval during testing is the next factor that must be addressed to ensure reproducibility. Ariki and colleagues94,95 showed that the optimal period of rest between each isokinetic test speed is 90 seconds. In evaluating the shoulder isokinetically, this period of rest should be used between each test speed. Uninvolved Side Tested First2,3,59 Which side to test first is the next parameter to standardize. Testing the uninvolved side first serves three important functions: it establishes a baseline of data for the involved side, it evaluates the client’s willingness to be tested, and it decreases the patient’s apprehension by allowing exposure to an isokinetic movement in the contralateral extremity first.2,3,37
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During shoulder abduction and adduction testing, error can be caused by end-stop oscillation and torque curve spiking.62,63 These torque spikes are produced by combining the long lever arm, high test speeds, and large torque values demonstrated during testing with an abrupt terminal end point. Any abrupt end point results in spiking of the torque curve graph far beyond the actual values produced. These spikes are not valid indicators of true force production.
Gravity Compensation2,3,59,100 The effects of gravity must be addressed, and therefore, we recommend gravity compensation of the limb before testing. Significant differences have been demonstrated during isokinetic testing of muscle groups that were gravitycompensated when compared with those that were not.96,97 Although no specific investigations have shown this fact during shoulder testing, it is generally accepted that when gravity compensation is not used, the muscles assisted by gravity show higher torque values, whereas the muscles working against gravity show significantly lower torque values. Also, as isokinetic angular velocities increase, so does the relative effect of gravity on torque values.98,99 Therefore, gravity compensation should be performed before each test on every patient.
Consistency in Data Collection59,100 We recommend controlling aberrant data production by using a semihard (firm) end stop and windowing the isokinetic data collection during shoulder abduction and adduction or shoulder flexion and extension testing. An end stop is used to cushion the end range and decelerate the lever arm during testing. A firm end stop results when the end-stop control is turned one-quarter turn from the hard end point. This type of end stop prevents excessive deceleration produced by a soft stop or the abrupt endstop oscillation that occurs when a hard end stop is used.62 End-stop oscillation is also prevented by windowing the test results so that any data not obtained at the preset isokinetic test speed or at 95% of that speed will not be recorded.
Consistency in Data Analysis Using a standardized method of isokinetic assessment of the shoulder addresses one of the main pitfalls inherent in isokinetic testing: not using a standardized testing protocol with each evaluation. Our isokinetic testing protocol satisfies this limitation by outlining a clinically functional, activity-specific, and consistent means to evaluate the shoulder isokinetically. We recommend testing the overhead athlete in the 90/90-degree seated position and testing the lower-demand shoulder patient in a more inherently
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stable, modified neutral or scapular plane position. The tester should use a position that places the client in the most common functional position for that particular client.
INTERPRETING ISOKINETIC TEST DATA An advantage and disadvantage of isokinetic testing is the copious amounts of data typically generated by the computer. Many isokinetic parameters can be used for examining and assessing patients and athletes.2,3,59,100,101,102 Data analysis for isokinetic testing involves specific angular velocities, peak torque, ratio of peak torque to body weight (normalized data), total work, average power, and torque acceleration energy. The results of these data can then further be analyzed by bilateral comparison, unilateral ratio, ratio of peak torques to body weight to normalize the data to the individual patient, total arm strength, and normative data.2, 3, 60,103
Interpreting Test Data2,3,59,100 The data can be subdivided into topics identifying torque parameters, acceleration and deceleration characteristics, and muscular performance parameters. A sample isokinetic graph and data are illustrated in Figure 54-4. Torque Parameters Torque is defined as force times the perpendicular distance from the axis of rotation. The term peak torque expresses a single repetition event that is the highest point on the graph regardless of where it occurs in the ROM.2,3,60,103
EXTERNAL ROTATORS 96
80
64 Torque ft-lbs
Data Analysis2,3,59,96-100
725
48
32
16
–70°
–35°
0°
35°
70°
105°
Position (7°/division) Figure 54-4. Sample isokinetic torque curve.
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The average torque of all the test repetitions performed during one set is the mean peak torque. Mean peak torque values can provide more valuable information to the clinician regarding muscular performance than a single repetition peak torque value. Acceleration and Deceleration Characteristics The test parameter referred to as time rate to torque development is an example of an acceleration parameter.2,3,59,100 This test parameter represents how quickly the subject can generate torque. The time rate to torque development can be expressed as a factor of time, such as at 0.2 seconds, or as a factor of joint position at any specific joint angle or predetermined torque value. This test parameter can be beneficial to the clinician in determining the acceleration capability of the shoulder’s internal rotators, particularly in the overhead-throwing athlete. Torque acceleration energy (TAE) is another example of measuring explosive muscle performance. TAE is the total work in 1⁄8 second. Force decay rate of the torque curve or the deceleration of the muscle group2,3,100 is the down slope of the curve from the peak torque. On torque curve observation, the down slope of the torque curve should appear straight or slightly convex. A torque curve whose force decay rate is concave indicates an inability or difficulty in producing force near the end of the ROM. Muscular Performance Parameters The next area of data interpretation is the muscular performance parameters.2,3,59,100 These include total work, average power, and muscular endurance characteristics. Total work is defined as torque times ROM. It represents the volume of area contained in the torque curve. Maximum work repetition is the single repetition during which the maximum amount of work occurred. Average power is torque times an arc of movement divided by time, or work divided by time. This parameter is represented in watts. Work and power can also be expressed in relation to body weight, such as work–to–body-weight ratios. There are numerous methods to assess muscular endurance with isokinetic testing. In one commonly used method, work in the first third and work in the last third of the repetition set is calculated as a muscular endurance measurement. This represents the total amount of work performed in the first 33.3% of the set, and work in the last third is the last 33.3%. The work fatigue percentage is the ratio of change between the first third and the last third of any test. A tremendous amount of data can be produced by an isokinetic shoulder test. These data can create a paradox for the tester. Three commonly used parameters for data interpretation of the shoulder are bilateral comparison, unilateral data comparison, and torque-to-body-weight ratios.2,3,59,100 The current literature has produced significant
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controversy in data comparison. Some of this confusion may be attributed to the inconsistencies in the test positions used and differences in testing apparatus. Several investigators have shown significant differences between results gathered on different testing devices.104-107 Results of isokinetic testing cannot be compared from one device or system with results from another device or system. Bilateral Comparison In regard to bilateral comparison of peak torque of the dominant versus nondominant shoulder, Wilk and colleagues108 reported their results of isokinetic testing in 150 professional baseball pitchers. The results indicate, with regard to bilateral comparison of external and internal rotation testing, that the throwing shoulder is equal to the nonthrowing shoulder (Table 54-1). The bilateral comparison of abduction and adduction indicated no significant differences in peak torque for the shoulder’s abductors, whereas the adductors exhibited a significant difference at both test speeds (180 and 300 deg/sec) (Table 54-2).63 Table 54-3 illustrates the collective work of different investigators who have documented bilateral peak torque comparisons of the shoulder. Unilateral Ratios Unilateral muscle ratios express the balance between the agonist and antagonist muscle groups. Several investigators have published data regarding ER/IR ratios of the shoulder.2,3,109-112 Ivey and colleagues113 reported a ratio of 66% at 60, 180, and 300 deg/sec. Cook and colleagues111 demonstrated an ER/IR ratio of 70% at 180 deg/sec and 300 deg/sec for the throwing shoulder and ratios of 83% and 87% at the respected speeds for the nonthrowing shoulder. Davies2,3 reported a ratio of 66.6% at 60 and 300 deg/sec. Table 54-4 presents the ER/IR unilateral muscle ratios for the shoulder from different investigators.2,3,71,108-112 TABLE 54-1 Shoulder External and Internal Rotation in Throwing Athletes (Mean Peak Torque ± SD) Angular Velocity (deg/sec) Dominant Arm Nondominant Arm External Rotation (%) 180
34.5 ± 6.2
36.5 ± 6.8*
300
29.3 ± 5.1
30.1 ± 6.3
180
53.9 ± 8.8
52.4 ± 9.5
300
49.0 ± 8.5
48.0 ± 10.4
Internal Rotation (%)
Data from Biodex isokinetic dynamometer. *Statistically significant difference (P ⬍ .05) between respective pairs. Data from Wilk KE, Andrews JR, Arrigo CA, et al: The internal and external rotator strength characteristics of professional baseball pitchers. Am J Sports Med 21:61-66, 1993.
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TABLE 54-2 Shoulder Abduction and Adduction in 131 Throwing Athletes (Mean Peak Torque ± SD) Angular Velocity (deg/sec)
Dominant Arm
Nondominant Arm
180
56.1 ± 12.5
58.6 ± 9.7
300
40.3 ± 15.7
38.4 ± 14.7
180
68.1 ± 12.6
62.5 ± 10.5*
300
61.0 ± 12.5
54.6 ± 13.2*
TABLE 54-3 Bilateral Peak Torque in the Shoulder Test Position
Dominant Stronger
Equal Bilateral
Nondominant Stronger
External rotation
Brown
Cook et al Ivey et al Jobe and Moynes Wilk et al
Alderink and Kuck Hinton
Internal rotation
Brown et al Cook et al Hinton
Alderink and Kuck Ivey Jobe and Moynes Wilk et al
—
Abduction
—
Alderink and Kuck Wilk et al
—
Adduction
Alderink and Kuck Wilk
—
—
Flexion
—
Alderink and Kuck Cook et al
—
Extension
Alderink and Kuck
Cook et al
—
Abduction (ft-lbs)
Adduction (ft-lbs)
Data collected with a Biodex isokinetic dynamometer. Shoulders were tested in 90 degrees of glenohumeral joint abduction. *Statistically significant difference (P ⬍ .05) between respective pairs. Data from Wilk KE, Arrigo CA, Keirns MA: Shoulder abduction/adduction isokinetic test results: Window vs unwindow data collection. J Orthop Sports Phys Ther 15:107, 1992.
Tables 54-5, 54-6, and 54-7 list the ratios of torque and work to body weight from studies on elite junior tennis players and professional baseball pitchers. Tables 54-8 and 54-9 give the ratios of external to internal rotation for elite junior tennis players and baseball pitchers. The unilateral muscle ratio for the shoulder abductors and adductors has been reported as 2:1 by several authors.107,112 Wilk and colleagues63 found the abduction-to-adduction ratio for the dominant shoulder (throwing shoulder) to be 83% at 180 deg/sec and 94% at 300 deg/sec. The nondominant shoulder abduction-to-adduction ratio is 66% at 180 deg/sec and 70% at 300 deg/sec.63 Table 54-10 represents the collective work values of different authors regarding the abduction-to-adduction muscle ratios of the shoulder.2,3,109,112 Ratios of Torque to Body Weight The last torque parameter is the ratio of torque to body weight. Tables 54-5 to 54-7 and Table 54-11 present torqueto-body-weight ratios for shoulder external rotation and internal rotation and for abduction and adduction.109 Differences occur in isokinetic muscular performance among different types of sporting athletes, subject’s age and skill, and pathologic conditions. Tables 54-5 and 54-8 and Tables 54-12 to 54-14 present descriptive data from several studies regarding elite junior and collegiate tennis players,114-117 professional baseball pitchers, and swimmers.118 These data can help one interpret the isokinetic shoulder test data in different overhead athletic populations.
Load Range Load range119 refers to the percentage of motion at the preset isokinetic speed. During an isokinetic test, the subject accelerates to the preset isokinetic speed, engages the speed
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Alderink GJ, Kuck DJ: Isokinetic shoulder strength of high school and college aged pitchers. J Orthop Sports Phys Ther 7:163-172, 1986. Brown LP, Niehues SL, Harrah A, et al: Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 16:577-585, 1988. Cook EE, Gray VL, Savinor-Nogue E, Medeiros J: Shoulder antagonistic strength ratios: a comparison between college level baseball pitchers. J Orthop Sports Phys Ther 8:451-461, 1987. Hinton RY: Isokinetic evaluation of shoulder rotational strength in high school baseball pitchers. Am J Sports Med 16:274-249, 1988. Ivey FM, Calhoun JH, Rusche K, et al: Normal values for isokinetic testing of shoulder strength [abstract]. Med Sci Sports Exerc 16:274, 1988. Jobe FW, Moynes DR: Delineation of diagnostic criteria and a rehabilitation program for rotator cuff injuries. Am J Sports Med 10:336, 1982. Wilk KE, Andrews JR, Arrigo CA, et al: The internal and external rotator strength characteristics of professional baseball pitchers. Am J Sports Med 21:61-66, 1993. Wilk KE: Dynamic muscle strength testing. In Amundsen LR (ed): Muscle Strength Testing: Instrumented and Noninstrumented Systems, New York, Churchill Livingstone, 1990.
(load range), and then decelerates near the end range. The preset ROM is then divided by the load range to obtain a percentage. Brown and colleagues119 have used this parameter to study elite junior tennis players. We use this parameter to monitor patient progression from test to retest.
Concentric Versus Eccentric Considerations120-128 Although many shoulder activities involve eccentric muscle actions, research is more limited regarding some of the applications with eccentric exercise. Some of the research on eccentric muscle actions has evaluated its reliability,53-55 muscle functions,129,130 documentation of deficits in select
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TABLE 54-4 Ratios of External and Internal Rotation Torque and Work–to–Body Weight DOMINANT ARM (%)
Angular Velocity (deg/sec)
A
B
C
60 66
120
68
180
I
W
B
C
71
81
D
H
I
W
70 72
70
66
65
71
64
76 61
70
A
66 69
67
240 300
H
64
90
210
D
NONDOMINANT ARM (%)
65
71 70
66
66.6
61
76
80
65
81
70
A, Alderink and Kuck; B, Brown et al; C, Cook et al; D, Davies et al[?]; H, Hinton; I, Ivey et al; W, Wilk et al. Alderink GJ, Kuck DJ: Isokinetic shoulder strength of high school and college aged pitchers. J Orthop Sports Phys Ther 7:163-172, 1986. Brown LP, Niehues SL, Harrah A, et al: Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 16:577-585, 1988. Cook EE, Gray VL, Savinor-Nogue E, Medeiros J: Shoulder antagonistic strength ratios: a comparison between college level baseball pitchers. J Orthop Sports Phys Ther 8:451-461, 1987. Davies GJ: A Compendium of Isokinetics in Clinical Usage, 3rd ed. S & S Publishers, Onolaska, WI, 1987. Hinton RY: Isokinetic evaluation of shoulder rotational strength in high school baseball pitchers. Am J Sports Med 16: 274-249, 1988. Ivey FM, Calhoun JH, Rusche K, et al: Normal values for isokinetic testing of shoulder strength [abstract]. Med Sci Sports Exerc 16:274, 1988. Wilk KE, Andrews JR, Arrigo CA, et al: The internal and external rotator strength characteristics of professional baseball pitchers. Am J Sports Med 21:61-66, 1993. Data from Ellenbecker T, Roetert EP: Age specific isokinetic glenohumeral internal and external rotation strength in elite junior tennis players. J Sci Med Sport 6(1):63-70, 2003.
TABLE 54-5 Isokinetic Peak Torque–to–Body Weight Ratios and Single-Repetition Work–to–Body Weight Ratios in Elite Junior Tennis Players DOMINANT ARM
Angular Velocity (deg/sec)
NONDOMINANT ARM
Peak Torque (%)
Work (%)
Peak Torque (%)
Work (%)
210
12
20
11
19
300
10
18
10
17
210
8
14
8
15
300
8
11
7
12
210
17
32
14
27
300
15
28
13
23
210
12
23
11
19
300
11
15
10
13
External Rotation MALE SUBJECTS
FEMALE SUBJECTS
Internal Rotation MALE SUBJECTS
FEMALE SUBJECTS
Note: Data were collected with a Cybex 6000 series isokinetic dynamometer. The shoulder was tested in 90 degrees of glenohumeral joint abduction. Data are expressed in foot-pounds per unit of body weight. Data from Ellenbecker T, Roetert EP: Age specific isokinetic glenohumeral internal and external rotation strength in elite junior tennis players. J Sci Med Sport 6(1):63-70, 2003.
728
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the greater tension being generated in the SEC and PEC, which creates microtrauma to those tissues. With the microtrauma to the SEC and PEC, this tissue releases hydroxyproline as a by-product of connective tissue breakdown. The hydroxyproline produces a noxious stimulus to the surrounding tissues that begins at 12 hours, peaks at 72 hours, and resolves by approximately 7 to 10 days.141 Many clinicians recommend performing concentric isokinetic testing and rehabilitation before performing eccentric isokinetic testing and rehabilitation. However, there is limited research regarding the applications of eccentric isokinetics and its full potential.
TABLE 54-6 Isokinetic Peak Ratios of Torque and Work–to–Body Weight from 150 Professional Baseball Pitchers Angular Velocity (deg/sec)
Dominant Arm
Nondominant Arm
180
18
19
300
15
15
180
27
17
300
25
25
729
External Rotation (%)
Internal Rotation (%)
ISOKINETICS IN UPPER-EXTREMITY FATIGUE TESTING
Note: Data were obtained on a Biodex isokinetic dynamometer. Data from Wilk KE, Andrews JR, Arrigo CA, et al: The strength characteristics of internal and external rotator muscles in professional baseball pitchers. Am J Sports Med 21:61-66, 1993.
Isokinetic testing has been used to measure muscle fatigue.142,143 The clinical implications of this are important because many functional and sports activities require multiple repetitions or prolonged activity times, which leads to fatigue. Various testing protocols are described in the literature for measuring isokinetic muscle fatigue (also see “Muscular Performance Parameters” earlier).
pathologies,131 effectiveness of strengthening particular muscles,132-134 correlation to sports performance and performance enhancement,134-137 normative data that are sport specific,120-127 and used for outcome measures.138-140 Use of eccentric testing and exercise is clearly indicated because of the prevalence of so many functional activities that involve eccentric muscle actions in the shoulder complex. However, one of the limitations of performing isolated joint eccentric testing is an unusual feeling is an unnatural motion. The most EMG activity of the rotator cuff occurs during the eccentric deceleration follow-through phase of the throwing cycle.64
The most commonly used fatigue-testing protocols involve operational definitions of measuring the number of repetitions of maximum effort required to reach a 50% reduction in torque, work, or power. The other commonly used operational definition is a relative fatigue ratio, which usually compares the work performed in a certain number of repetitions at the beginning of the test with the work performed in a certain number of repetitions at the end of the test.
Most of the research demonstrates that the greater force production with eccentric muscle actions is due to the contributions of the noncontractile tissue (series elastic components [SEC] and parallel elastic components [PEC]).141 Likewise, there appears to also be a greater incidence of delayed-onset muscle soreness (DOMS) due to
Burdett and Van Swearingen142 studied the reliability of isokinetic fatigue tests that had intraclass correlation coefficients of 0.48 to 0.73 for work-fatigue ratios. Montgomery and colleagues143 reported similar test-to-retest reliability
TABLE 54-7 Isokinetic Peak Ratios of Torque and Work–to–Body Weight from 147 Professional Baseball Pitchers DOMINANT ARM
Angular Velocity
Peak Torque (%)
NONDOMINANT ARM
Work (%)
Peak Torque (%)
Work (%)
External Rotation 210
13
25
14
25
300
13
23
13
23
210
21
41
19
38
300
20
37
18
33
Internal Rotation
Note: Data were obtained on a Cybex 350 isokinetic dynamometer. Data from Ellenbecker TS, Mattalino AJ: Concentric isokinetic shoulder internal and external rotation strength in professional baseball pitchers. J Orthop Sports Phys Ther 25:323-328, 1997.
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THE ATHLETE’S SHOULDER
TABLE 54-8 Isokinetic External–to–Internal Rotation Ratios in Elite Junior Tennis Players DOMINANT ARM
Angular Velocity (deg/sec)
NONDOMINANT ARM
Peak Torque (%)
Work (%)
Peak Torque (%)
Work (%)
210
69
64
81
81
300
69
65
82
83
210
69
63
81
82
300
67
61
81
77
Male Players
Female Players
Note: Data were collected with a Cybex 6000 series isokinetic dynamometer. The shoulder was tested in 90 degrees of glenohumeral joint abduction. Data are expressed as ratios of external rotation to internal rotation representing the relative muscular balance between the external and internal rotators. Data from Ellenbecker T, Roetert EP: Age specific isokinetic glenohumeral internal and external rotation strength in elite junior tennis players. J Sci Med Sport 6(1):63-70, 2003.
TABLE 54-9 Unilateral External–to–Internal Rotation Ratios in Professional Baseball Pitchers DOMINANT ARM
Angular velocity (deg/sec)
Peak Torque (%)
NONDOMINANT ARM
Work (%)
Peak Torque (%)
Work (%)
Ellenbecker and Mattalino 210
64
61
74
66
300
65
62
72
70
180
64
—
64
—
300
61
—
70
—
Wilk et al
Ellenbecker TS, Mattalino AJ: Concentric isokinetic shoulder internal and external rotation strength in professional baseball pitchers. J Orthop Sports Phys Ther 25:323-328, 1997. Wilk KE, Andrews JR, Arrigo CA, et al: The strength characteristics of internal and external rotator muscles in professional baseball pitchers. Am J Sports Med 21:61-66, 1993.
values, with intraclass correlation coefficients of 0.67 to 0.78 for relative tests of isokinetic muscular endurance. These studies demonstrate the important role of isokinetic fatigue testing, its significance in guiding the clinician in designing a rehabilitation program, and its potential as a parameter for measuring outcomes in rehabilitation.
PARAMETERS TO INTERPRET ISOKINETIC TESTING When interpreting the results of an isokinetic shoulder test, several key parameters have been identified for routine evaluation and interpretation. These are identified in Table 54-15.2,3,59,100
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Several pitfalls should be avoided when performing an isokinetic shoulder test. First, the test and retest should be performed in the identical position, at the same speeds, and using the same testing protocol.2,3,37,59,60,100 If the test position or protocol is altered, the test results are significantly affected. The second pitfall is only interpreting bilateral peak torque comparisons to determine the patient’s progress.37 Review of the literature shows that bilateral comparisons are inconsistent and specifically are altered by test position. The third is relying on torque curve shapes to determine different pathologies. We have found, after several hundred preoperative tests, that torque curves are not consistently generated by any specific shoulder pathologies. Fourth, do not solely rely on peak torque measurements to determine a patient’s
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731
TABLE 54-10 Unilateral Muscle Ratios for Abduction and Adduction DOMINANT ARM
Angular Velocity (deg/sec)
NONDOMINANT ARM
Peak Torque (%)
Work (%)
Peak Torque (%)
Work (%)
210
64
61
74
66
300
65
62
72
70
180
64
—
64
—
300
61
—
70
—
180
64
—
64
—
300
61
—
70
—
Alderink and Kuck
Davies
Ivey et al
Wilk 180
64
—
64
—
300
61
—
70
—
Alderink GJ, Kuck DJ: Isokinetic shoulder strength of high school and college aged pitchers. J Orthop Sports Phys Ther 7:163-172, 1986. Davies GJ: A Compendium of Isokinetics in Clinical Usage, 3rd ed. S & S Publishers, Onolaska, WI, 1987. Ivey FM, Calhoun JH, Rusche K, et al: Normal values for isokinetic testing of shoulder strength [abstract]. Med Sci Sports Exerc 16:274, 1988. Wilk KE: Isokinetic testing and exercise for the shoulder complex. Presented at annual conference of Biodex Corporation, Ft. Lauderdale, FL, October 3, 1991.
status. Power, work, and time parameters must be considered to determine muscular performance. Last, the examiner should window all test data to prevent misinterpretation. Dynamic isokinetic testing is only one part of a comprehensive clinical examination. The final clinical decisionmaking is predicated on evaluating the history, subjective examination, special tests, physical examination, dynamic isokinetic muscular testing, and functional testing to help determine the condition of the patient’s shoulder complex.
ISOKINETIC REHABILITATION PRINCIPLES Based on the examination findings, including the dynamic isokinetic muscle testing, the rehabilitation program is customized to the patient. A total body rehabilitation program is the focus. This incorporates leg strength, core stability, and scapulothoracic, glenohumeral, and total arm strength. Many rehabilitation and conditioning programs for the shoulder complex are in widespread use. There are no meta-analyses or systematic reviews that clearly demonstrate the superiority of any one method. Therefore, most rehabilitation and conditioning programs have a multimodal approach including isolated joint exercises,144-150
Ch54_719-748-F06701.indd 731
multijoint exercises,26,151-156 proprioceptive and kinesthetic exercises,27,157 plyometrics,27,138,158-162 neuromuscular dynamic stability,27,163 and functional activities. Scapulothoracic rehabilitation focuses on the specific exercises that provide dynamic stability and the foundation for the functioning of the glenohumeral joint. Moseley and colleagues145 have described the foundation exercises they found from fine-wire EMG testing. The four exercises identified as foundation exercises were scaption with the thumb up for the top of the scapula, press-up for the bottom of the scapula, scapular protraction for the front of the scapula, and rowing for scapular retraction for the back of the scapula. Townsend and colleagues144 also used fine-wire EMG testing and identified the four exercises that functioned as foundation exercises for the glenohumeral joint. For the top of the glenohumeral joint, scaption with the thumb up was originally recommended. The original Townsend and colleagues article recommended the thumb down (empty-can) position, but because of the potential to impinge the subacromial space, we now recommend the thumb up (full-can) position. For the bottom of the glenohumeral joint, the press-up; for the front of the glenohumeral joint, flexion in the sagittal plane with the thumb up; and for the back of the glenohumeral joint, prone-lying, external rotation with horizontal extension.
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THE ATHLETE’S SHOULDER
TABLE 54-11 Isokinetic Shoulder Torque–to–Body Weight Ratios Angular Velocity (deg/sec)
Dominant Arm
Nondominant Arm
90
27
26
120
25
25
210
21
21
300
18
18
90
50
46
120
47
45
210
43
41
300
36
36
90
15
15
120
14
15
210
13
14
300
13
13
90
22
22
120
21
21
210
19
19
300
18
18
Abduction (%)
ISOKINETICS FOR DESIGNING REHABILITATION TRAINING PROGRAMS Although numerous exercise programs are currently in widespread use for rehabilitation of the shoulder complex, there is no evidence that clearly distinguishes one program as the best. Because the focus of this chapter is on isokinetics, this section focuses on the applications of isokinetics for rehabilitation of the shoulder complex. Unfortunately, many clinicians do not regularly use isokinetics in the rehabilitation of the shoulder complex, yet Moncrief and colleagues164 and Malliou and colleagues165 demonstrated the superiority of using isokinetics for training the rotator cuff muscles. Malliou and colleagues randomly divided 48 subjects into four groups: control group; experimental group 1, which used multijoint exercises; experimental group 2, which used progressive resistive exercises for the rotator cuff; and experimental group 3, which trained with isokinetics for the rotator cuff. Malliou and colleagues165 concluded that “isokinetic strengthening is the most effective method of altering strength ratios of the rotator cuff muscles.”
Adduction (%)
External Rotation (%)
Internal Rotation (%)
This section focuses on the resisted-exercise progression continuum that can be used for rehabilitation or performance enhancement.2,3 Resisted-exercise programs are usually multimodal and consist of isometrics, isotonics, isokinetics, concentric training, eccentric training, and plyometrics as well as hybrids of these. The safer forms of exercise, such as isometrics and short-arc training, should be used in the earlier stages of rehabilitation, and the more aggressive exercises should be used in the latter stages of rehabilitation
Data from Alderink GJ, Kuck DJ: Isokinetic shoulder strength of high school and college aged pitchers. J Orthop Sports Phys Ther 7:163-172, 1986.
TABLE 54-12 Isokinetic Muscular Performance of Collegiate Tennis Players RATIOS (%)
Angular Eccentric Eccentric Concentric Velocity PT/BW PT/BW in PT/BW (deg/sec) in ER IR in ER
Concentric PT/BW in IR
Eccentric ER/IR
Concentric ER/IR
Eccentric to Eccentric to Concentric Concentric in ER in IR
Men 60
80
99
43
59
84
59
202
183
180
80
91
41
49
92
49
206
202
210
77
96
40
50
81
50
202
201
60
46
56
25
34
87
80
103
123
180
47
56
22
27
93
82
107
143
210
46
57
22
25
89
89
119
173
Women
BW, body weight; ER, external rotation; IR, internal rotation; PT, peak torque. Data from Ellenbecker TS: A total arm strength profile of highly skilled tennis players. Isokin Exerc Sci 1:9-21, 1991.
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TABLE 54-13 Isokinetic Muscular Performance of Collegiate Tennis Players Angular Velocity (deg/sec)
Dominant
Nondominant
Internal Rotation (Peak Torque) (ft-lbs)
733
isokinetics as an integral part of the rehabilitation or performance-enhancement program for the shoulder complex.
Patient Progression Criteria
60
18
17
300
13
11
Progression of the patient through a rehabilitation program is predicated on numerous factors166 including the patient’s clusters of signs and symptoms, time since surgery, soft tissue healing limitations, and the type of surgical procedure. The patient’s progression through the exercise progression continuum is determined by continual reassessment of the signs and symptoms.
60
30
24
300
21
16
External Rotation (Peak Torque) (ft-lbs)
Internal Rotation Torque-to-Body-Weight % 60
20
15
Resistive-Exercise Progression Continuum
300
13
10
Davies2,3 first described the resistive-exercise progression continuum more than 20 years ago. The current model has been modified to incorporate the advances in exercise and is shown in Box 54-5. This progression is designed to progress from the least stressful and safest forms of exercise to the more aggressive forms of exercise.
External Rotation Torque-to-Body-Weight % 60
12
11
300
8
7
External Rotation to Internal Rotation % 60
61
70
300
65
69
Data from Chandler TJ, Kibler WB, Stracener EC, et al: Shoulder strength, power, and endurance in college tennis players. Am J Sports Med 20: 455-458, 1992.
TABLE 54-14 Isokinetic Muscular Performance of Scholastic Swimmers Angular Velocity (deg/sec)
Before Training
After 3-Week Training Program
120
20
32
180
19
93
120
36
42
180
32
41
External Rotation (ft-lbs)
Internal Rotation (ft-lbs)
Multiple-Angle Isometric Exercises The progression begins with multiple-angle isometric exercises because these are the safest and least stressful to the patient. It helps prevent reflex dissociation, begins motor-learning response, and assists with mechanical effects to decrease swelling. Short-Arc Exercises The next step in the progression is to incorporate dynamic short-arc (ROM) isokinetic exercises.167,168 Short-arc isokinetic exercises are used for several reasons: to accommodate resistance, to avoid symptomatic areas in the ROM, and to protect healing soft tissue. Due to the accommodating resistance inherent in isokinetic muscle loading, short-arc exercises are safe and do not stress the healing soft tissue. Based on the patient’s response and signs and symptoms, the exercises are progressed to maximal intensity without pain. The short-arc isokinetic exercises use the intermediate velocity-spectrum rehabilitation protocol (VSRP), 60 to 180 deg/sec (Fig. 54-5).
External Rotation/Internal Rotation (%) 120
57
75
180
58
73
From TS Murphy, unpublished data.
or performance enhancement training. More aggressive exercises include full-arc exercises, maximal intensity, plyometrics, neuromuscular dynamic stability exercises, and functional simulations or specificity exercises. We discuss the scientific and clinical rationale for the progression through a resisted-exercise program, including the specific progressions, with emphasis on implementing
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The intermediate VSRP uses 60 to 180 deg/sec for the following reasons. Velocities slower than 60 deg/sec increase joint compressive forces and often produce an inhibition response; they are also unnatural angular velocities. Velocities faster than 180 deg/sec in a short arc of motion cause free limb acceleration: In a short arc of motion, the patient cannot accelerate the extremity fast enough to develop isokinetic muscle loading in that ROM, resulting in insufficient loading of the muscles. Consequently, isokinetic exercise involves three components: acceleration up to the isokinetic speed, the load range where the patient meets the isokinetic velocity and creates the accommodating resistance, and deceleration. Brown and colleagues117 described the isokinetic load
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THE ATHLETE’S SHOULDER
TABLE 54-15 Parameters for Interpreting Isokinetic Shoulder Test Results at 180 Deg/Sec Bilateral Peak Torque Comp
Unilateral Muscle Ratio
Torque-toBody-Weight Ratio
Bilateral Total Work Comp
Bilateral Total Power Comp
Torque at 0.2 sec for IR
Work-toEndurance Ratio
External rotation (%)
100-110
66-70
18-23
105-115
107-118
80-85
60-68
Internal rotation (%)
115-125
66-70
28-33
118-128
119-139
65-75
Abduction (%)
100-110
82-88
26-32
110-119
110-120
60-68
Adduction (%)
120-135
82-88
32-38
115-130
118-128
68-78
Test Position
comp, comparison; IR, internal rotation.
range as inversely related to isokinetic speed. A larger load range occurs at slower angular velocities, and significantly shorter load ranges occur at faster contractile velocities. Physiologic Overflow: Range of Motion. Based on the patient’s condition and his or her available ROM, the short-arc isokinetic program is customized to the patient. With short-arc isokinetic exercise, there is approximately a 30-degree physiologic overflow through the ROM (Fig. 54-6).2,3,167 Consequently, a patient’s rehabilitation program can use short-arc exercises with a concomitant overflow into the painful ROM without ever exercising in that ROM. Consequently, exercising in the safe short arc of motion protects the patient and avoids problems caused by the exercise program.
BOX 54-5. Resistive-Exercise Progression Continuum
Multiple-angle isometrics • Submaximal intensity, pain free • Maximal intensity, pain free Short arc (ROM) exercises • Isokinetics, submaximal intensity, pain free • Isotonics, submaximal/maximal intensity, pain free • Isokinetics, maximal intensity, pain free Full arc (ROM) exercises
Another example of the short-arc exercise concept with the resultant physiologic overflow is rehabilitating an overhead-throwing athlete who has significant anterior shoulder laxity. Exercising in the short arc of motion and avoiding the exercise stresses on the anterior capsule still allow a concomitant strengthening into the additional ROM without actually exercising there and potentially stretching the capsule further through repetitive exercises. Velocity Spectrum Overflow. When performing the short arc VSRP, another important consideration is how frequently through the velocity spectrum the patient should exercise. The research has demonstrated the patient should exercise every 30 deg/sec through the velocity spectrum.2,3 This is because there is a 30-deg/sec physiologic overflow producing an isokinetic strengthening effect. Optimal Number of Repetitions. Davies and colleagues169-171 performed several randomized training studies that compared a control group and training groups that used 3 sets of 5 repetitions, 3 sets of 10 repetitions, 3 sets of 15 repetitions, or 3 sets of 20 repetitions. The results showed that the group training with 10 repetitions had more significant improvement in several measured parameters. For clinical efficiency, 10 repetitions are used at each angular velocity, and the patient gains in torque, power, and endurance. Rest Intervals. If the patient has progressed to maximalintensity isokinetic exercise using a VSRP, research by Ariki and colleagues94,95 indicates the rest interval between each
• Isokinetics, submaximal intensity, pain free • Isotonics, submaximal/maximal intensity, pain free • Isokinetics, maximal intensity, pain free
180 150
Plyometrics
120
Neuromuscular dynamic stabilization exercises Functional simulation exercises (specificity exercises)
ROM, range of motion.
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90 60
180 150 120 90 60
Figure 54-5. Short-arc isokinetic velocity spectrum rehabilitation protocol (VSRP) performed at intermediate contractile velocities.
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ISOKINETIC TESTING AND REHABILITATION OF THE SHOULDER COMPLEX
735
5° ROM-deceleration!
30° ROM
20°–25° ROM to accelerate extremity fast enough to “catch” machine and create isokinetic muscle loading.
set of 10 training repetitions may be as long as 90 seconds. However, this is not a clinically practical rest time because it would take the patient too much time to complete the exercise session. Consequently, the patient performs the next set of repetitions based on a symptom-limited rest interval. Then, research by Ariki and colleagues95 recommends a rest interval of 3 minutes between sets. The rest intervals can also be based on the concept of specificity relative to the demands of the patient or particular demands of the athletic activity. Full-Arc Exercises When it is appropriate, the patient is progressed to fullROM submaximal to maximal isokinetic exercises. Initially, straight planar movements are performed through the ROM because the stresses can be controlled on the involved area. The patient then progresses to functional diagonal patterns through the full ROM. Because the diagonal patterns incorporate multiple planes of motion and increase stresses on the patient, they are performed after the patient has demonstrated tolerance to the isolated planar movements. Because a larger ROM is available, the patient has more time to generate the power, and because of the faster angular velocities with functional activities, most full-ROM exercises are performed at the fast VSRP (180-300 deg/sec) (Fig. 54-7) or at the functional angular velocities. The rationale for using the faster angular velocities in the isolated joint movements is physiologic overflow to slower velocities, specificity response, neurophysiologic motor learning response, and decreased joint-compressive forces.172 The decreased joint-compressive forces are based on Bernoulli’s principle, which states that surface pressure on the articular surfaces is decreased due to the synovial fluid interface at faster angular velocities.172
Figure 54-6. Acceleration and deceleration range of motion (ROM) with short-arc isokinetic exercises.
effects on improving scapular plane (scaption) elevation. There was no carryover from training internal rotation and external rotation and the improvement of scaption power. The results of these studies conflict with the findings of the Quincy and colleagues173 study. Quincy and colleagues demonstrated that training in the 90/90 position of internal and external rotation position did demonstrate a power improvement in most other straight planes of movement. However, the Durall and colleagues study evaluated unique positions that were off-axis movements and not straight planar movements. Furthermore, the sample size and training durations might have limited the statistical power to demonstrate a training response. On-Axis Planes and Movements The final component of the rehabilitation program consists of one of the most important parts of shoulder rehabilitation, which focuses on the rotator cuff muscles specifically. Because the rotator cuff muscles are so important in providing neuromuscular dynamic stability to the shoulder complex, it is important to rehabilitate them in the most optimal way. Consequently, we use the concept described by Davies2,3,27 of the modified neutral position (30/30/30 position) to begin rotator cuff strengthening in the beginning and then progress to the 90/90 position when it is appropriate. The 30/30/30 position places the shoulder joint into 30 degrees of abduction, 30 degrees of forward flexion into scaption, and 30 degrees of diagonal tilt. The 30 degrees of abduction position prevents the wringing out effect on the supraspinatus tendon. This is based on the seminal paper by Rathbun and MacNab,174 which demonstrated that working with the arm in the adducted position produced a wringing out effect because the humeral head compresses the articular side of the rotator cuff. When the arm is elevated to 90/90 (and with weakness of the
Functional Training Positions. Functional training in the clinic is designed to replicate the ultimate functional performance activities of the athlete. Simulating the biomechanics of the joints, the length-tension curves of the muscles, and the angular velocities as closely as possible is one of the focuses of the terminal stages of rehabilitation; the other is return to functional activities. Training Specificity. Durall and colleagues149 performed a pretraining and post-training study on training the shoulder internal rotators and external rotators and their
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Figure 54-7. Full range-of-motion isokinetic velocity spectrum rehabilitation protocol (VSRP) performed at fast contractile velocities.
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rotator cuff muscles, reflex inhibition, or pain inhibition), the deltoid overpowers the lower rotator cuff muscles and causes a compression on the bursal side of the supraspinatus tendon, causing the wringing out effect. Holding the arm in 30 degrees of abduction also facilitates the blood flow to the tendon to help with the healing process. Glenohumeral adduction increases the EMG activity of the external rotators in this position.175-176 The scaption plane is the functional arc of motion of the shoulder. Holding the arm in 30 degrees of scaption decreases stress on the anterior capsule, protecting it. This position also prestretches the infraspinatus and teres minor on the physiologic length-tension curve to increase power. In 30 degrees of diagonal tilt on the transverse plane, forces are diagonally aligned along the direction of the muscle fibers. This position is more comfortable for the patient and prevents injury to the posterior shoulder. Reinold and colleagues175 completed an EMG analysis of the rotator cuff and deltoid musculature during common shoulder ER exercises and identified the optimum positions to recruit the infraspinatus and teres minor muscles. Using the adduction motion increases the EMG activity of the external rotator muscles due to a synergistic recruitment response.
head and the infraspinatus contraction causes posterior translation of the humeral head. The descriptive norms for ER/IR unilateral ratios are 60% to 70% (⬃66%). The contre-coup concept of shoulder stability is to create dynamic stability with a posterior dominant shoulder. Because the normal unilateral ratio for the IR/ER is 3/2 or 100%:66%, the operational definition of the posterior dominant shoulder is to increase the ER by 10%, thereby creating a 4/3 or 100%:76% ratio.27 Soderberg and Blaschek69 tested external and internal rotation in six different test positions. They concluded that the internal rotation exhibited increased torque production in a neutral position, defined as 0 to 20 degrees of shoulder abduction, and external rotation torque was enhanced in the 90-degree abducted position or neutral position.69 Hellwig and Perrin73 reported no significant differences in external and internal rotation in the frontal plane compared with the scapular plane during concentric and eccentric muscular contractions. Considering these investigations, the pathophysiology of rotator cuff injuries, and the function of the shoulder muscles, a continuum of external and internal rotation exercise positions can be developed (Figs. 54-8 and 54-9). The natural progression of this continuum is from 0 degrees of
Graichen and colleagues176 performed a study to test the potential changes of the subacromial space width (during muscular contractions), which are caused by alterations of scapular kinematics or glenohumeral translation, or both. Open magnetic resonance imaging (MRI) was performed on 12 healthy subjects at 30, 60, 90, 120, and 150 degrees of arm elevation. They had the subjects perform isometric contraction of the glenohumeral abductors or adductors at 15 N. Adducting muscle activity led to significant increases of the subacromial space width in all arm positions. Scapulohumeral rhythm and tilting were constant during adduction and abduction. These data show that the subacromial space can be effectively widened by adducting muscle activity and by affecting the position of the humerus relative to the glenoid fossa. The results of this study suggest that this effect of opening the subacromial space may be employed to treat the impingement syndrome.
Contre-Coup Concept of Posterior Dominant Shoulder28 If we were to ask most clinicians to select only one muscle to rehabilitate in a patient with an anterior instability, most would answer the subscapularis, because it is the only anterior dynamic stabilizer of the glenohumeral joint. Cain and colleagues177 demonstrated that the subscapularis contraction causes anterior translation of the humeral
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Figure 54-8. Continuum of rotator cuff strengthening.
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Figure 54-9. External and internal rotation rehabilitation position continuum.
adduction through the scapular plane and up to the functional 90-degree abducted position, which maximizes the external and internal rotation length-tension relationship. This position also maximally stresses the dynamic stabilizing function of the rotator cuff musculature. This exercise continuum allows the progression of static shoulder stability from a position of maximal joint stability to one of minimal stability. As with any form of exercise, if symptoms develop at any stage, the activity is regressed to an asymptomatic level and progressed only when appropriate. The clinician should be aware that the test results generated in any one specific position cannot be compared with test results obtained in a different test position.
CATEGORIES OF ISOKINETIC EXERCISES
Figure 54-10. Shoulder abduction and adduction in seated position.
athlete. We also believe that the shoulder adductors serve a vital role in glenohumeral joint stability. Shoulder Internal and External Rotation Shoulder external and internal rotation is a commonly tested movement of the shoulder. Positions to isolate the external and internal rotation of the shoulder include the modified-neutral position (30/30/30) (see Fig. 54-2), scapular plane (Fig. 54-11), and 90-degree abducted position (see Fig. 54-1). These positions are listed from maximal inherent stability to minimal inherent stability. Each position
The three basic categories of isokinetic exercise for the shoulder complex are on-axis planes and movements, scapulothoracic patterns, and off-axis planes and movements. On-axis planes or movements are isolated movement patterns in which the axis of rotation of the dynamometer is aligned with the axis of the joint motion. The scapulothoracic patterns are isolated movements for the scapular muscles, and the off-axis movements are movements in which the axis of the dynamometer is not aligned with the axis of joint motion, which usually results in multijoint combined movement patterns.
On-Axis Planes and Movements178 Shoulder Abduction and Adduction Shoulder abduction and adduction is a movement that we commonly use in the seated position (Fig. 54-10). This movement pattern attempts to isolate the shoulder abductors (deltoid, supraspinatus) and the adductors (pectoralis major, latissimus dorsi, teres major). Several authors have demonstrated a positive correlation between isokinetic shoulder adduction strength and arm velocity during throwing.179,180 This correlation makes isokinetic exercise of this movement pattern extremely beneficial in functional strengthening of the shoulder complex in the throwing
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Figure 54-11. Internal and external rotation in the scaption plane.
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renders different torque measurements compared with another position, and the clinician should be aware of these torque results and should employ consistency when comparing data from one test with another. Shoulder Flexion and Extension Shoulder flexion and extension can be accomplished in several positions: seated (Fig. 54-12), supine (Fig. 54-13), and modified supine (Fig. 54-14). The supine position is commonly used to emphasize the shoulder flexors and to provide scapular stability (through the contact of the scapula on the chair). Conversely, the prone position is used to emphasize the shoulder extensors and to challenge the scapula-stabilizing muscles. Shoulder Horizontal Abduction and Adduction Shoulder horizontal abduction and adduction can be used in the supine position (Fig. 54-15). This movement is important to the overhead athlete such as the thrower or the tennis player or other racquet sport athletes to simulate the follow-through phase. The clinician must proceed with care when using horizontal adduction because this movement can cause impingement syndrome. Scapulothoracic Patterns27,29,30 Adequate scapulothoracic muscular performance is essential to the symptom-free function of the shoulder complex. A proper exercise regimen to strengthen the scapular muscles ensures the maintenance of the normal length-tension relationship of the glenohumeral joint, a
Figure 54-12. Shoulder flexion and extension in seated position.
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Figure 54-13. Shoulder flexion and extension in supine position.
stable base from which the upper extremity can function. These components ensure that the scapulothoracic musculature provides proximal stability for the scapula to allow distal mobility of the arm. Two commonly used scapular patterns are scapular protraction and scapular retraction. Scapular Protraction.27,29,30 A standing modified unilateral push-up activity performed isokinetically can mimic the function of the serratus anterior performing a wall push-up
Figure 54-14. Shoulder flexion and extension in modified supine position; chair is tilted approximately 45 degrees.
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B
Figure 54-15. Shoulder horizontal abduction (A) and adduction (B) in supine position.
maneuver. (Fig. 54-16). It can be used concentrically and eccentrically for serratus strengthening. The serratus anterior muscle is an important element of scapular motion and control and must be exercised adequately to improve shoulder function.145 Scapular Retraction.27,29,30 Scapular retraction can be accomplished by shortening the lever arm of motion above the elbow in the sagittal plane; the scapular retractors can be adequately strengthened isokinetically (Fig. 54-17). This motion loads the rhomboids, middle trapezius, and posterior deltoid during scapular retraction.145
Off-Axis (Multiple Joint) Planes181 As described by Jobe and colleagues146 the supraspinatus scaption isokinetic exercise position approximates the muscle testing position for the supraspinatus at a 45-degree oblique plane (Fig. 54-18).144,146-158 This off-axis pattern for the supraspinatus muscle can be used for isometric or isotonic muscular contraction.
Proprioceptive Neuromusuclar Facilitation Patterns182 Diagonal combined movement patterns are exercise movements to replicate many dynamic upper-extremity work and sports activities. These movements use reciprocal movement patterns and emphasize functional movements for the entire shoulder complex. The D2 flexion pattern (abduction, flexion, external rotation) is
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Figure 54-16. Scapular protraction (pushing movement) performed seated.
used to strengthen the posterior rotator cuff muscles and scapular retractors (Fig. 54-19). The D2 extension pattern (extension, adduction, internal rotation) is used to strengthen the adductor and internal rotators of the shoulder (Fig. 54-20).
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REHABILITATION GUIDELINES The angular velocities (isokinetic speeds) commonly used during the rehabilitation process are shown in Figures 54-5 and 54-7 and Box 54-6. These pyramids are isokinetic VSRPs.2,3 The patient performs 10 repetitions at each of the predetermined speeds, followed by 90 seconds of rest and then 10 repetitions at the next isokinetic velocity.2,3 This process is continued until all the prescribed speeds have been performed. Figure 54-5 illustrates the intermediatevelocity spectrum used for short movement patterns such as shoulder external and internal rotation and scapular patterns. Figure 54-7 illustrates the fast-velocity spectrum most often used for larger movement patterns such as shoulder flexion and extension and abduction and adduction. The functional velocity spectrum (see Box 54-6) is used for the upper extremity athletic patient and can be used for any single-plane movement or diagonal pattern.
Figure 54-17. Scapular retraction (pulling movement) performed seated.
RELATIONSHIP OF ISOKINETIC TESTING TO FUNCTIONAL PERFORMANCE Although many clinicians do not appreciate the relationship of isolated joint testing to functional activities, several studies demonstrate this relationship in the shoulder complex.179-189 Bartlett and colleagues179 also demonstrated a relationship between shoulder adductor peak torque and throwing speed. Pedegana and colleagues180 identified a significant correlation with elbow extension, wrist flexion, and shoulder flexion, extension and external rotation strength measured isokinetically, and throwing speed in professional baseball pitchers.
Figure 54-18. Isolation of the supraspinatus muscle is performed in the plane of the scapula. This is an off-axis scaption isokinetic motion.
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Ellenbecker and colleagues135 demonstrated that 6 weeks of concentric isokinetic training of the rotator cuff musculature resulted in a significant improvement in serving velocity in collegiate tennis players. However, those who trained with eccentric isokinetics did not demonstrate a significant improvement in the serving velocity. Mont and colleagues134 essentially replicated the Ellenbecker and colleagues study and found significant improvements in serving velocity after concentric and eccentric internal and external rotation training. Trieber and colleagues188 used isokinetic testing to measure the effectiveness of training the rotator cuff internal and external rotators with isotonic dumbbell or resistance tubing exercise programs. In addition to documenting significant strength improvements with isokinetic testing, they also found a significant increase in tennis serve velocity in the training groups. Most functional movement patterns of the upper extremities are a summation of the forces generated through the entire kinetic chain. Because of this complex biomechanical relationship of segmental velocities and the interrelationship of the entire kinetic chain, including the lower
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B
Figure 54-19. Diagonal D2 flexion pattern for shoulder abduction, flexion and external rotation. A, Total body stabilization. B, Full ROM exercise for D2 flexion pattern.
A
B
Figure 54-20. Diagonal D2 extension pattern for the shoulder. This movement consists of shoulder extension, adduction, and internal rotation. A, Total body stabilization. B, Full ROM exercise for D2 extension pattern.
extremities and the trunk (core), establishing a direct relationship between an isolated joint movement and the complex functional activities is difficult. However, testing each link of the kinetic chain to make sure it is contributing its share to the total composite movement pattern is an
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important concept of isolated joint testing. If a muscle group cannot function normally in an isolated pattern, then there is no way that the muscle group can function normally in a functional movement pattern. The testing and then rehabilitation of each link of the kinetic chain, which
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BOX 54-6. Functional Velocity Spectrum Rehabilitation Program for the Shoulder
Perform 10 repetitions at the following speeds (deg/sec): 450
420
390
360
330
450
420
390
360
References
330
300
300
is then integrated back into the functional movement patterns, provide the optimal rehabilitation for the patient.
ISOKINETIC TESTING AND OUTCOMES DOCUMENTATION Isokinetic testing plays an important part in the measurement of dynamic muscular performance following an injury or surgery or in evaluating performance enhancement. The objective documentation with isokinetic testing provides evidence-based outcome measures.190-200 Davies196 has described torque acceleration energy as a measure of the patient’s ability to generate force quickly, which is the most functional measure of muscular performance. Additional terms that have been used to describe this measurement of muscle performance is time rate of torque development, force development rate, and force development quickness. Manske and Davies191 demonstrated that torque acceleration energy deficits are common in a heterogeneous group of patients. With a multimodal rehabilitation approach using isokinetics as part of the rehabilitation program, the torque acceleration energy deficits were resolved as one of the parameters monitored during the rehabilitation program.
SUMMARY The shoulder exhibits tremendous motion with inherently poor stability. The dynamic stabilizers (neuromuscular control) provide the shoulder with much-needed stability during different functional activities. Because of the greatly imposed demands on the shoulder musculature, the clinician must routinely assess the status of the neuromuscular
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system in an objective, reliable, and reproducible manner. Isokinetics provides the clinician with a reproducible, objective, and safe muscular performance testing and exercise tool. The clinician is encouraged to use a standardized testing protocol to improve test-to-retest reproducibility. A standardized testing protocol also allows clinicians to compare and share data, opening effective communication among sports medicine practitioners. When reviewing published data, the reader must consider test position and the testing protocol before using those data. Isokinetics should remain a vital tool for the rehabilitation team.
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58. Davies GJ, Manske R, Schulte R, DiLorenzo C, et al: Rehabilitation of macro-instability. In Ellenbecker TS (ed): Shoulder Rehabilitation: Current Concepts in Non-Operative Treatment. New York, Thieme, 2006, pp 39-63. 59. Wilk KE, Arrigo CA, Andrews JR: Standardized isokinetic testing protocol for the throwing shoulder: The thrower’s series. Isokin Exerc Sci 1:63, 1991. 60. Byl NN, Wells L, Grady D, et al: Consistency of repeated isokinetic testing: Effect of different examiners, sites, and protocols. Isokin Exerc Sci 1:122, 1991. 61. Mawdsley RH, Knapik JJ: Comparison of isokinetic measurements with test repetitions. Phys Ther 62:169-172, 1982. 62. Wilk KE, Arrigo CA, Keirns MA: Shoulder abduction/ adduction isokinetic test results: Window vs unwindow data collection. J Orthop Sports Phys Ther 15:107, 1992. 63. Wilk KE, Andrews JR, Arrigo CA, et al: The abductor and adductor strength characteristics of professional baseball pitchers. Am J Sports Med 23:307-311, 1995. 64. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the shoulder in throwing and pitching. A preliminary report. Am J Sports Med 11:3-5, 1983. 65. Jobe FW, Moynes DR, Tibone JE, Perry J: An EMG analysis of the shoulder in pitching. A second report. Am J Sports Med 12:218-220, 1984. 66. Figoni SF, Morris AF: Effects of knowledge of results on reciprocal isokinetic strength and fatigue. J Orthop Sports Phys Ther 6:190-197, 1984. 67. Pappas AM, Zawacki RM, McCarthy CF: Rehabilitation of the pitching shoulder. Am J Sports Med 13:223-235, 1985. 68. Pappas AM, Zawacki RM, Sullivan TJ: Biomechanics of baseball pitching. A preliminary report. Am J Sports Med 13:216-232, 1985. 69. Soderberg GJ, Blaschek MJ: Shoulder internal and external rotation peak torque production through a velocity spectrum in differing positions. J Orthop Sports Phys Ther 8:518, 1987. 70. Greenfield BH, Donatelli R, Wooden MJ, Wilkes J: Isokinetic evaluation of shoulder rotational strength between plane of the scapula and functional plane. Am J Sports Med 18:124-128, 1990. 71. Hinton RY: Isokinetic evaluation of shoulder rotational strength in high school baseball pitchers. Am J Sports Med 16:274-249, 1988. 72. Hageman PA, Mason DK, Rydlund KW, et al: Effects of position and speed on eccentric and concentric isokinetic testing of the shoulder rotators. J Orthop Sports Phys Ther 11:64-69, 1989. 73. Hellwig EV, Perrin DH: A comparison of two positions for assessing shoulders rotator peak torque: The traditional frontal plane versus the plane of the scapula. Isokin Exerc Sci 1:202-206, 1991. 74. Walmsley RP, Szybbo C: A comparative study of the torque generated by the shoulder internal and external rotators in different positions and at varying speeds. J Orthop Sports Phys Ther 9:217-222, 1987. 75. Johnson RJ, Wilk KE: The effect of lever arm pad placement upon the isokinetic torque during knee extension and flexion. Phys Ther 68:779, 1988. 76. Siewert MW, Ariki PK, Davies GJ, et al: Isokinetic torque changes based on lever arm placement. Phys Ther 65: 715, 1985.
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77. Taylor RC, Casey JJ: Quadriceps torque production on the Cybex II dynamometer as related to changes in lever arm length. J Orthop Sports Phys Ther 8:147, 1986. 78. Davies GJ, et al: Cybex II isokinetic dynamometer measurements on the acute effects of direct active warmups and direct passive warmups (selected physical therapy modalities) on knee extension and knee flexion strength and power. Presented at the APTA National Conference, Las Vegas, NV, 1978. 79. Wiktorsson-Möller M, Oberg B, Ekstrand J, Gillquist J: Effects of warming up, massage, and strengthening on range of motion and muscle strength in the lower extremity. Am J Sports Med 11:249-252, 1983. 80. Asmussen E, Boje O: Body temperature and capacity for work. Acta Physiol Scand 10:1-22, 1945. 81. Astrand PO, Rodahl K: Textbook of Work Physiology: Physiologic Basis of Exercise, 2nd ed. New York, McGraw-Hill, 1977. 82. Franks DB: Physical warm-up. In Morgan WP (ed): Ergogenic Aids and Muscular Performance. Orlando, Fla, Academic Press, 1972. 83. Martin BV, Robinson S, Wiogoma DC, et al: Effect of warmup on metabolic responses to strenuous exercise. Med Sci Sports Exerc 7:146, 1975. 84. Johansson CA, Kent BE, Shepard KF: Relationship between verbal command volume and magnitude of muscle contraction. Phys Ther 63:1260-1265, 1983. 85. Knott M, Voss D: Proprioceptive Neuromuscular Facilitation. New York, Harper & Row, 1968. 86. Hald RD, Bottken EJ: Effects of visual feedback on maximal and submaximal isokinetic test measurements of normal quadriceps and hamstring. J Orthop Sports Phys Ther 9:86, 1987. 87. Manzer CW: The effect of knowledge of output on muscle work. J Exp Psychol 18:80, 1935. 88. Pierson WR, Rasch PJ: Effect of knowledge of results on isometric strength scores. Res Q 35:313-315, 1964. 89. Ulrich C, Burke RK: Effect of motivational stress on physical performance. Res Q 28:403, 1957. 90. Figoni SF, Christ CB, Massey BH: Effects of speed, hip and knee angle, and gravity on hamstring to quadriceps torque ratios. J Orthop Sports Phys Ther 9:287-291, 1988. 91. Bradley JP, Tibone JE: Electromyographic analysis of muscle action about the shoulder. Clin Sports Med 10:789-805, 1991. 92. Elsner RC, Pedegana LR, Lang J: Protocol for strength testing and rehabilitation of the upper extremity. J Orthop Sports Phys Ther 4:229-235, 1983. 93. Arrigo CA, Wilk KE, Andrews JR: Peak torque and maximum work repetition during isokinetic testing of the shoulder internal and external rotators. Isokin Exerc Sci 4(4):171-175, 1994. 94. Ariki PK, Davies GJ, Siewert MW, et al: Optimum rest interval between isokinetic velocity spectrum rehabilitation speeds. Phys Ther 65(5):735-736, 1985. 95. Ariki PK, Davies GJ, Siewert MW, et al: Optimum rest interval between isokinetic velocity spectrum rehabilitation sets. Phys Ther 65(5): 733-734, 1985. 96. Caizzo VJ: Alterations in the in vivo force velocity curve. Med Sci Sports Exerc 12:134, 1980. 97. Fillyaw M, Bevins T, Fernandez L: Importance of correcting isokinetic peak torque for the effect of gravity when calculating knee flexor to extensor muscle ratios. Phys Ther 66:23-31, 1986.
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98. Nelson SG, Duncan PW: Correction of isokinetic and isometric torque recordings for the effects of gravity. Phys Ther 63:674-676, 1983. 99. Winter DA, Wells RP, Orr GW: Errors in the use of isokinetic dynamometers. Eur J Appl Physiol Occup Physiol 46:397408, 1981. 100. Davies GJ, Heiderscheidt B, Brinks K: Isokinetic test interpretation. In Brown L (ed): Isokinetics in Human Performance. Champaign, Ill, Human Kinetics, 2000, pp 3-24. 101. Ivey FM, Calhoun JH, Rusche K, et al: Isokinetic testing of shoulder strength: Normal values. Arch Phys Med Rehabil 66:384-386, 1985. 102. Newsham KR, Keith CS, Saunders JE, Goffinett AS: Isokinetic profile of baseball pitchers’ internal/external rotation 180, 300, 450 degrees s-1. Med Sci Sports Exerc 30:1489-1495, 1998. 103. Francis K, Hoobler T: Comparison of peak torques of the knee flexor and extensor muscle groups using the Cybex II and Lido 2.0 isokinetic dynamometers. J Orthop Sports Phys Ther 8:480-483, 1987. 104. Wilk KE, Johnson RJ, Levine B: A comparison of peak torque values of knee extensors and flexor muscle groups using the Biodex, Cybex, Kin-Com isokinetic dynamometer. Phys Ther 67:789-790, 1987. 105. Wilk KE, Johnson RJ: A comparison of peak torque values of knee extensor and flexor muscle groups using the Biodex, Cybex, and Lido isokinetic dynamometer. Phys Ther 68:792, 1988. 106. Thompson MC, Shingleton LG, Kegerreis ST: Comparison of values generated during testing of the knee using the Cybex 11⫹ and Biodex mode B-2000 isokinetic dynamometers. J Orthop Sports Phys Ther 11:108-115, 1989. 107. Gross MT, Huffman GM, Phillips CN, Wray JA: Intramachine and intermachine reliability of the Biodex, Cybex for knee flexion and extension peak torque and angular work. J Orthop Sports Phys Ther 13:329-335, 1991. 108. Wilk KE, Andrews JR, Arrigo CA, et al: The internal and external rotator strength characteristics of professional baseball pitchers. Am J Sports Med 21:61-66, 1993. 109. Alderink GJ, Kuck DJ: Isokinetic shoulder strength of high school and college aged pitchers. J Orthop Sports Phys Ther 7:163-172, 1986. 110. Brown LP, Niehues SL, Harrah A, et al: Upper extremity range of motion and isokinetic strength of the internal and external shoulder rotators in major league baseball players. Am J Sports Med 16:577-585, 1988. 111. Cook EE, Gray VL, Savinor-Nogue E, Medeiros J: Shoulder antagonistic strength ratios: a comparison between college level baseball pitchers. J Orthop Sports Phys Ther 8:451-461, 1987. 112. Williams M: Manual muscle testing, development and current use. Phys Ther Rev 36:797-805, 1956. 113. Ivey FM, Calhoun JH, Rusche K, et al: Normal values for isokinetic testing of shoulder strength [abstract]. Med Sci Sports Exerc 16:274, 1988. 114. Ellenbecker TS: A total arm strength profile of highly skilled tennis players. Isokin Exerc Sci 1:9-21, 1991. 115. Chandler TJ, Kibler WB, Stracener EC, et al: Shoulder strength, power, and endurance in college tennis players. Am J Sports Med 20:455-458, 1992.
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116. Kibler WB, McQueen C, Uhl T: Fitness evaluations and fitness findings in competitive junior tennis players. Clin Sports Med 7:403-416, 1988. 117. Ng LR, Kramer JS: Shoulder rotator torques in female tennis and non-tennis players. J Orthop Sports Phys Ther 13:40-47, 1991. 118. Falkel JE, Murphy TC, Murray TF: Prone positioning for testing shoulder internal and external rotation on the Cybex II isokinetic dynamometer. J Orthop Sports Phys Ther 8:368-370, 1987. 119. Brown LE, Whitehurst M, Findley BW, et al: Isokinetic load range during shoulder rotation exercises in elite male junior tennis players. J Strength Cond Res 9:160-164, 1995. 120. Shklar A, Dvir Z: Isokinetic strength relationships in shoulder muscles. Clin Biomech 10:369-373, 1995. 121. Noffal GJ: Isokinetic eccentric-to-concentric strength ratios of the shoulder rotator muscles in throwers and nonthrowers. Am J Sports Med 31:537-541, 2003. 122. Ng GY, Lam PC: A study of antagonist/agonist isokinetic work ratios of shoulder rotators in men who play badminton. J Orthop Sports Phys Ther 32:399-404, 2002. 123. Wang HK, Macfarlane A, Cochrane T: Isokinetic performance and shoulder mobility in elite volleyball athletes from the United Kingdom. Br J Sports Med 34:39-43, 2000. 124. Alfredson H, Pietila T, Lorentzon R: Concentric and eccentric shoulder and elbow muscle strength in female volleyball players and non-active females. Scand J Med Sci Sports 8:265-270, 1998. 125. Scoville CR, Arciero RA, Taylor DC, et al: End range eccentric antagonistic/concentric agonist strength ratios: A new perspective in shoulder strength assessment. J Orthop Sports Phys Ther 25:203-207, 1997. 126. Sirota SC, Malanga GA, Eischen JJ, et al: An eccentric and concentric strength profile of shoulder external and internal rotator muscles in professional baseball pitchers. Am J Sports Med 25:59-64, 1997. 127. Mikesky AE, Edwards JE, Wiggleworth JK, et al: Eccentric and concentric strength of the shoulder and arm musculature in collegiate baseball pitchers. Am J Sports Med 23:638-642, 1995. 128. Hollander DB, Kraemer RR, Kilpatrick MW, et al: Maximal eccentric and concentric strength discrepancies between young men and women for dynamic resistance exercise. J Strength Cond Res 21(1):34-40, 2007. 129. David G, Magarey ME, Jones MA, et al: EMG and strength correlates of selected shoulder muscles during rotations of the glenohumeral joint. Clin Biomech 15:95-102, 2000. 130. Weltman A, Janney C, Rians CB, et al: The effects of hydraulic resistance strength training in pre-pubertal males. Med Sci Sports Exerc 18:629-638, 1986. 131. Wang HK, Cochrane T: Mobility, impairment, muscle imbalance, muscle weakness, scapular asymmetry and shoulder injury in elite volleyball athletes. J Sports Med Phys Fitness 41:403-410, 2001. 132. Bast SC, Vangsness CT, Takemura J, et al: The effects of concentric versus eccentric isokinetic strength training of the rotator cuff in the plane of the scapula at various speeds. Bull Hosp Jt Dis 57:139-144, 1998. 133. Heiderscheit BC, McLean KP, Davies GJ: The effects of isokinetic vs plyometric training on the shoulder internal rotators. J Orthop Sports Phys Ther 23:125-133, 1996.
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134. Mont MA, Cohen DB, Campbell KR, et al: Isokinetic concentric versus eccentric training of shoulder rotators with functional evaluation of performance enhancement in elite tennis players. Am J Sports Med 22:513-517, 1994. 135. Ellenbecker TS, Davies GJ, Rowinski MJ: Concentric versus eccentric isokinetic strengthening of the rotator cuff. Objective data versus functional test. Am J Sports Med 16:64-69, 1988. 136. Forthomme B, Croisier JL, Ciccarone G, et al: Factors correlated with volleyball spike velocity. Am J Sports Med 33:1513-1519, 2005. 137. Kennedy K, Altchek DW, Glick IV: Concentric and eccentric isokinetic rotator cuff ratios in skilled tennis players. Isokinet Exerc Sci 3:155-159, 1993. 138. Hartsell HD, Forwell L: Postoperative eccentric and concentric isokinetic strength for the shoulder rotators in the scapular and neutral planes. J Orthop Sports Phys Ther 25-19-25, 1997. 139. Martin DR, Garth WP: Results of arthroscopic debridement of glenoid labrum tears. Am J Sports Med 23:447-451, 1995. 140. MacDonald PB, Alexander MJ, Frejuk J, et al: Comprehensive functional analysis of shoulders following complete acromioclavicular separation. Am J Sports Med 16:475-480, 1988. 141. Davies GJ, Ellenbecker TS: Eccentric isokinetics. Orthop Phys Ther Clin North Am 1:297-336, 1992. 142. Burdett RG, Van Swearingen J: Reliability of isokinetic muscular endurance tests. J Orthop Sports Phys Ther 8:484-488, 1987. 143. Montgomery LC, Douglass LW, Duester PA: Reliability of an isokinetic test of muscle strength and endurance. J Orthop Sports Phys Ther 10:315-322, 1989. 144. Townsend H, Jobe FW, Pink M, Perry J: Electromyographic analysis of the glenohumeral muscles during a baseball rehabilitation program. Am J Sports Med 19:264-272, 1991. 145. Moseley JB, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. 146. Jobe FW, Bradley JP: Rotator cuff injuries in baseball. Prevention and rehabilitation. Sports Med 6:378-387, 1980. 147. Jobe FW, Moynes DR: Delineation of diagnostic criteria and a rehabilitation program for rotator cuff injuries. Am J Sports Med 10:336-339, 1982. 148. De Luca CJ, Forrest WJ: Force analysis of individual muscles acting simultaneously on the shoulder joint during isometric abduction. J Biomechanics 6:385-393, 1973. 149. Durall C, Davies GJ, Kernozek TW, et al: The effects of training the humeral rotator musculature on scapular plane humeral elevation. J Sport Rehab 10:79-92, 2001. 150. Sporrong H, Styf J: Effects of isokinetic muscle activity on pressure in the supraspinatus muscle and shoulder torque. J Orthop Res 19:337-338, 2001. 151. Schneider MA, Catlin PA, Davies GJ, Mattson PA: An isokinetic estimation of total arm strength. Isokinet Exerc Sci 1(3):117-121, 1991. 152. Davies GJ, Ellenbecker TS: Total Arm Strength for Shoulder and Elbow Overuse Injuries. In Timm K (ed): Upper Extremity. La Crosse, Wisc, APTA Home Study Course, Orthopaedic Section, 1993. 153. Di Lorenzo CE, Parkes JC, Chmelar RD: The importance of shoulder and cervical dysfunction in the etiology and treatment of athletic elbow injuries. J Orthop Sports Phys Ther 11:402-409, 1990.
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154. Ellenbecker TS: A total arm strength isokinetic profile of highly skilled tennis players. Isokinet Exerc Sci 1:9-21, 1991. 155. Strizak AM, Gleim GW, Sapega A, et al: Hand and forearm strength and its relation to tennis. Am J Sports Med 11: 234-239, 1983. 156. Durall C, Manske R, Davies GJ: Avoiding shoulder injury from resistance training. Strength Cond J 23:10-18, 2001. 157. Hatterman D, Kernozek TW, Palmer-McLean K, Davies GJ: Proprioception and its application to shoulder dysfunction. Critical reviews. Phys Rehabil Med 15:47-64, 2003. 158. Davies GJ, Matheson JW: Shoulder plyometrics. Sports Med Arthrosc Rev 9:1-18, 2001. 159. Davies GJ, Ellenbecker TS, Bridell D: Upper extremity plyometrics as a key to functional shoulder rehabilitation and performance enhancement. Biomechanics. 9:18-28, 2002. 160. Schulte-Edelmann JA, Davies GJ, Kernozek TW, Gerberding ED: The effects of plyometric training of the posterior shoulder and elbow. J Strength Cond Res 19: 129-134, 2005. 161. Fortun CM, Davies GJ, Kernozck TW: The effects of plyometric training on the internal rotators of the shoulder. Phys Ther 78:S87, 1998. 162. Nichols, J, Howard, Z, Davies, GJ, et al: Plyometric training study of the shoulder complex to identify optimum training parameters. Presented at the American Physical Therapy Association meeting, Orlando, Fla, June, 2006. 163. Davies GJ, Kraushar D, Brinks K, Jennings J: Neuromuscular stability of the shoulder complex. In Manske RC (ed): Postsurgical Orthopedic Sports Rehabilitation: Knee and Shoulder. St Louis, Mosby, 2006. 164. Moncrief SA, Lau JD, Gale JR, et al: Effect of rotator cuff exercise on humeral rotation torque in healthy individuals. J Strength Cond Res 16:262-270, 2002. 165. Malliou PC, Giannakopoulos K, Beneka AG, et al: Effective ways of restoring muscular imbalances of the rotator cuff muscle group: A comparative study of various training methods. Br J Sports Med 38:766-772, 2004. 166. Davies GJ, Zillmer DA: Functional progression of a patient through a rehabilitation program. Orthop Phys Ther Clin North Am 9:103-118, 2000. 167. Halbach JW, Davies GJ, Gould J: Effect of limited ROM on non-exercised ROM strength. Phys Ther 65(5):732-733, 1985. 168. Seehaver JI, May KL, Kernozek TW, Davies GJ: Short arc isokinetic training’s effect on the full range of motion power of shoulder rotators. J Orthop Sports Phys Ther 29: A49, 1999. 169. Davies GJ, et al: The optimum repetitions to increase total work in the quadriceps and hamstrings. Phys Ther 66(5), 1986. 170. Davies GJ, et al: The optimum repetitions to increase average power in the quadriceps and hamstrings. Physical Therapy, 66(5), 1986. 171. Davies GJ, et al: The optimum repetitions to increase peak torque to body weight in the quadriceps and hamstrings. Med Sci Sports Exerc 18(2), 1986. 172. Barnham JN: Mechanical Kinesiology. St Louis, CV Mosby, 1978. 173. Quincy R, Davies GJ, et al: Isokinetic exercise: The effects of training specificity on shoulder torque. J Athletic Train 35:S64, 2000.
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174. Rathbun JB, MacNab I: The microvascular pattern of the rotator cuff. J Bone Joint Surg Br 52:540-553, 1970. 175. Reinold MM, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the rotator cuff and deltoid musculature during common shoulder external rotation exercises. J Orthop Sports Phys Ther 34(7):385-394, 2004. 176. Graichen H, Hinterswimmer S, von Eisenhart-Rothe R, et al: Effect of abducting and adducting muscle activity on glenohumeral translation, scapular kinematics and subacromial space width in vivo. J Biomechanics 38(4): 755-760 2005. 177. Cain PR, Mutschler TA, Fu FH, Lee SK: Anterior stability of the glenohumeral joint: A dynamic model. Am J Sports Med 15:144-148, 1987. 178. Doorenbosch CA, Mourits AJ, Veeger DH, et al: Determination of functional rotation axes during elevation of the shoulder complex. J Orthop Sports Phys Ther 31:133-137, 2001. 179. Bartlett LR, Storey MD, Simons BD: Measurement of upper extremity torque production and its relationship to throwing speed in the competitive athlete. Am J Sports Med 17:89-91, 1989. 180. Pedegana LR, Elsner R, Roberts D, et al: The relationship of upper extremity strength to throwing speed. Am J Sports Med 10:352-354, 1982. 181. Baltaci G, Tunay VB: Isokinetic performance at diagonal pattern and shoulder mobility in elite overhead athletes. Scand J Med Sci Sports 14:231-238, 2004. 182. Signorile JF, Sandler DJ, Smith WN, et al: Correlation analyses and regression modeling between isokinetic testing and on-court performance in competitive adolescent tennis players. J Strength Cond Res 19: 519-526, 2005. 183. Forthomme B, Croisier JL, Ciccarone G, et al: Factors correlated with volleyball spike velocity. Am J Sports Med 33:1513-1519, 2005. 184. Tunstall H, Mullineaux DR, Vernon T: Criterion validity of an isokinetic dynamometer to assess shoulder function in tennis players. Sports Biomech 4:101-111, 2005. 185. Mulligan IJ, Biddington WB, Barnhart BD, et al: Isokinetic profile of shoulder internal and external rotators of high school aged baseball players. J Strength Cond Res 18: 861-866, 2004. 186. Manske RC, Tajchman CS, Stranghoner TA, et al: Differences in isokinetic torque acceleration energy of the rotator cuff: Competitive male pitchers versus male nonathletes. J Strength Cond Res 18:447-450, 2004. 187. Pugh SF, Kovaleski JE, Heitman RJ, et al: Upper and lower body strength in relation to ball speed during a serve by male collegiate tennis players. Percept Mot Skills 97:867-872, 2003.
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188. Treiber FA, Lott J, Duncan J, et al: Effects of Theraband and lightweight dumbbell training on shoulder rotation torque and serve performance in college tennis players. Am J Sports Med 26:510-515, 1998. 189. Bayios IA, Anastasopoulou EM, Sioudris DS, et al: Relationship between isokinetic strength of the internal and external shoulder rotators and ball velocity in team handball. J Sports Med Phys Fitness 41:229-235, 2001. 190. Davies GJ, et al: A Descriptive Muscular Power Analysis of the United States Cross Country Ski Team. Med Sci Sports Exerc, 12(2):441, 1980. 191. Manske RC, Davies GJ: Post-rehabilitation outcomes of muscle power (torque acceleration energy) in patients with selected shoulder conditions. J Sport Rehabil 12:181-198, 2003. 192. Davies GJ, Giangara C: Open antero-capsulolabral reconstruction and rehabilitation. In DeCarlo M, Oneacre K (eds): Current Topics in Musculoskeletal Medicine: A Case Study Approach. Thorofare, NJ, Slack, 2001, pp 75-88. 193. van Meeteren J, Roebroeck ME, Selles RW, Stam H: Responsiveness of isokinetic dynamometry parameters, pain and activity level scores to evaluate changes in patients with capsulitis of the shoulder. J Clin Rehabil. 20(6):496-501, 2006. 194. Davies GJ, et al: A descriptive study of selected parameters of open versus arthroscopic bankart shoulder reconstructions: A preliminary report [abstract]. Phys Ther 72(6): S80, 1992. 195. Davies GJ, et al: Computerized isokinetic testing of patients with rotator cuff (RTC) impingement syndromes demonstrates specific RTC external rotators power deficits. Phys Ther 77(5):5106, 1997. 196. Davies GJ, Manske RC: The importance of evaluating muscle power (torque acceleration energy) in patients with shoulder dysfunctions. Phys Ther 79:S81, 1999. 197. Manske RC, Davies GJ: Rehabilitation outcomes assessing muscular power in patients with selected shoulder dysfunctions. Phys Ther 79:S81, 1999. 198. Kollwelter K, Davies GJ, et al: Effects of impulse inertial training of the shoulder internal and external rotators of the shoulder. J Orthop Sports Phys Ther 30:A39, 2000. 199. MacDermid JC, Ramos J, Drosdowech D, et al: The impact of rotator cuff pathology on isometric and isokinetic strength, function, and quality of life. J Shoulder Elbow Surg 13:593-598, 2004. 200. Jennings, J, Davies, GJ, Tanner, S, et al: Examination, surgery and rehabilitation of patients with superior labrum anterior and posterior (SLAP) lesions. In Manske R (ed): Postsurgical Orthopedic Sports Rehabilitation: Knee & Shoulder. St Louis, Mosby, 2006.
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CHAPTER 55 Plyometrics for the
Shoulder Complex Kevin E. Wilk and Michael L. Voight
similar results.10 Swanik and colleagues stated that after an 8-week plyometric training program, proprioception and kinesthesia also were improved; plyometrics might therefore have neuromuscular benefits as well.11
The rehabilitation process has changed dramatically since the 1990s. A relatively newer concept in the rehabilitation of the athletic shoulder is plyometrics. This concept was made popular by several clinicians during the early 1990s.1-4 In the rehabilitation of athletic injuries and in sports training, the concept of specificity has emerged as an important parameter in determining the proper choice of an exercise program.5 The imposed demands during training must mirror those incurred during athletic competition. In many athletic events, these stresses center around a muscle’s capacity to exert its maximal force output in a minimal amount of time. Success depends on the speed at which muscular force can be generated.
Although the term plyometrics is relatively new, the basic concepts are old. The roots of plyometric training can be traced to Eastern Europe, where it was simply known as jump training. The actual roots of the word plyometric are a little confusing. “Plyo” comes from the Greek word plythein, which means to increase. Plio is the Greek word for “more,” and metric literally means “measure.” The practical definition of plyometrics is a quick powerful movement involving a prestretching of the muscle, thereby activating the stretchshortening cycle. As the Eastern European countries began to dominate sports requiring power, their training methods became the focus of attention. After the 1972 Olympics, articles began to appear in coaching magazines outlining an unusual program of leaps and bounds used to increase speed. As it turns out, the Eastern European nations were not the originators of plyometrics, they were the ones who developed organized programs.
A form of exercise training that attempts to combine strength with speed of movement is plyometrics. We have used plyometrics for the upper extremity as a functional transitional exercise drill before initiating an interval throwing or interval sports program, and we have used it as a drill to enhance strength, power, and neuromuscular control. Plyometrics can be used to train contact and collision athletes who have to use their upper extremities in quick forceful movements. We strongly encourage the clinical use of plyometrics applied to appropriate athletic patients.
This system of hops and jumps has been used by American coaches for years as a form of conditioning. Rope jumping and bench hops have been used for years as a method to increase reaction time and quickness. The organization of this method of conditioning has been credited to the legendary Soviet jump coach Yuri Verkhoshanski, who, during the late 1960s, began to incorporate this miscellaneous program of hops and jumps into an organized plan of training.12 The actual term plyometrics was first introduced in 1975 by American track coach Fred Wilt.13 A literature review shows that since 1969, many trainers have used variances of Verkhoshanski’s method in an attempt to establish the best plyometrics technique and training program.14-18 Although there is agreement on the benefits of basic plyometric principles, there is controversy regarding an optimal training routine19-22 Today, the chief proponents of plyometrics are still in the track and field community, and they continue to use Verkhoshanski’s “reactive neuromuscular apparatus” for reproducing and enhancing the reactive properties of the lower extremity musculature.17,18,23 Numerous articles have been published discussing upper extremity plyometric training techniques. The main purpose of plyometric training is to increase the excitability of the neurologic receptors for improved reactivity of the neuromuscular system.
This chapter explains the theoretical basis of plyometrics and presents a philosophy for using the stretch reflex to produce an explosive reaction in the upper extremity. Stretch-shortening exercise drills are classified into two categories: sports-enhancement training and neuromuscular control. This chapter primarily discusses sportsenhancement training for the upper quadrant.
HISTORY AND DEFINITION Plyometrics was initially used for lower extremity training for several years. After numerous years of success, several clinicians, trainers, and conditioning experts advocated using plyometrics to train the upper extremity.3 Since then, many clinicians have advocated plyometrics and have discussed using these drills clinically, with specific recommendations for programs and movements.3,6-8 Investigators have documented the efficiency of plyometrics for the upper extremity. Carter and colleagues have documented that after an 8-week plyometric training program, strength and power improved.9 Schulte-Edelmann and colleagues reported 749
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Most of the literature to date on plyometric training has been focused on the lower quarter. Adaption of plyometric principles can be used to enhance the specificity of training in other sports or activities that require a maximum amount of muscular force in a minimal amount of time. All movements in competitive athletics involve a repeated series of stretch-shortening cycles. The musculature surrounding the shoulder girdle possesses the same physiologic characteristics as the musculature of the lower extremity. Therefore, different forms of plyometric exercises can be applied to the upper quarter to exploit the stretch-shortening cycle. The intensity of the upper-quarter plyometrics program is much less due to the small muscle mass as compared with the program for the lower quarter, but the basic concepts and principles are the same. Perhaps in no one single athletic endeavor is the use of elastic loading to produce a maximal explosive concentric contraction and the rapid decelerative eccentric contraction seen more than in the violent activity of throwing a baseball. Similar stretch-shortening movements can be seen in such sports as tennis, swimming, and golf. To replicate these forces during rehabilitation is beyond the scope of every traditional exercise tool. For example, the isokinetic dynamometer that reaches maximal velocities of 450 to 500 deg/sec is not specific to the velocities greater than 7000 deg/sec seen during a baseball pitch.24 Consequently, to exercise with the philosophy of specificity, drills such as plyometrics should be an intrinsic part of every upper extremity training program to facilitate a complete return to athletic participation.
NEUROPHYSIOLOGIC BASIS OF PLYOMETRICS Plyometrics is a form of exercise that uses the elastic and reactive properties of a muscle to generate a maximal force. In normal muscle function, the muscle is stretched before it contracts concentrically. This eccentric-concentric coupling is also referred to as the stretch-shortening cycle. Plyometrics uses the stimulation of the body’s proprioceptors to facilitate an increase in muscle recruitment over a minimal amount of time. The proprioceptors of the body include the muscle spindle, the Golgi tendon organ, and the joint capsule and ligamentous receptors.25,26 Stimulation of these receptors can cause facilitation, inhibition, and modulation of agonist and antagonist muscles. Both the muscle spindle and Golgi tendon organ provide the proprioceptive basis for plyometric training. The muscle spindle functions mainly as a stretch receptor. The muscle spindle components that are primarily
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sensitive to changes in velocity are the nuclear bag intrafusal muscle fibers, which are innervated by a group la phasic nerve fiber. This response is provoked by a quick stretch, which reflexively produces a quick contraction of the agonistic and synergistic extrafusal muscle fibers (Fig. 55-1). The firing of the type la phasic nerve fibers is influenced by the rate of stretch; the faster and greater the stimulus, the greater the effect of the associated extrafusal fibers.27,28 This cycle occurs in 0.3 to 0.5 msec and is mediated at the spinal cord level in the form of a monosynaptic reflex such as the knee jerk (Fig. 55-2). The Golgi tendon unit is located at the junction between the tendon and muscle at both the origin and insertion and is sensitive to tension.29 It is arranged in series with the extrafusal muscle fibers and therefore becomes activated with stretch. Unlike the muscle spindle, the Golgi tendon organ has an inhibitory effect on the muscle. On activation, impulses are sent to the spinal cord, causing an inhibition of the alpha motor neurons of the contracting muscle and its synergists and thereby limiting the force produced. It has been postulated that the Golgi tendon organ is the mechanism that protects against overcontraction or stretch of the muscle.30 Because the Golgi tendon organ uses at least one interneuron in its synaptic cycle, inhibition requires more time than the type la monosynaptic interneuron excitation.31 During concentric muscle contraction, the muscle spindle output is reduced because the muscle fibers are either shortening or attempting to shorten. During eccentric contraction, the muscle stretch reflex serves to generate more tension in the lengthening muscle. When the muscle tension increases to a high or potentially harmful level, the Golgi tendon organ fires, thereby generating a neural pattern that reduces the excitation of the muscle. Consequently, although the Golgi tendon organ receptors are a protective mechanism, in the correctly carried out plyometric exercise, their influences are overshadowed by the reflex arc pathway incorporated with excitation of type 1a nerve fibers (Fig. 55-3). Another principle to consider when discussing the quickexplosion philosophy of plyometrics is which muscles can be best affected. Patten embryologically classified muscles into phasic and tonic groups according to how they arise from the myotomes.32 Group 1 muscles (phasic or fast twitch) are innervated by anterior divisions of the plexuses and include the flexors, adductors, and internal rotators. Also included in this category are most two-joint muscles.30 Group II muscles (tonic or static) include the extensors, external rotators, and abductors. The group I muscles will possess more influence by the type 1a phasic nerve endings, resulting in a greater chance of being facilitated
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Alpha motor neuron to extrafusal muscle fiber end plates
Efferent fibers Afferent fibers Gamma motor neuron to intrafusal muscle fiber end plates II (Aβ) fiber from flower spray endings I (Aα) fiber from annulospiral endings
Extrafusal muscle fiber Intrafusal muscle fibers Sheath Lymph space Nuclear bag fiber Nuclear chain fiber
Detail of muscle spindle
Figure 55-1. The muscle spindle complex is a receptor consisting of intrafusal muscle fibers. Each spindle receives different innervation from group la (A␣) fibers and group II (A) fibers. The purpose of the muscle spindle is to provide information regarding muscle length to the central nervous system.
lb fibers la fibers ⫹⫹⫹⫹ Extrafusal muscle fiber Intrafusal muscle fiber
Alpha motor neurons ⫹⫹⫹ Gamma motor neurons
Golgi tendon organ
by the plyometric mechanism. The muscles responsible for arm acceleration and ball velocity are the adductors and internal rotators of the glenohumeral joint (pectoralis major, latissimus dorsi, subscapularis). These muscles are important to focus on with plyometric training drills. Along with the neurophysiologic stimulus, the positive results of plyometrics also come from the recoil action of elastic tissues.16,19 Several clinicians have shown that an eccentric contraction immediately preceding a concentric contraction significantly increases the force generated concentrically because of the storage of elastic energy.14,15 The mechanism for this increased concentric
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Figure 55-2. Passive stretch (knee jerk). Both intrafusal and extrafusal muscle fibers are stretched, and the spindle is activated. Reflex via group la fibers and alpha motor neurons causes secondary contraction (basis of stretch reflex) stretch too weak to activate Golgi tendon organs.
force is the ability of the muscle to use the force produced by the elastic component. During the loading of the muscle, when the stretch occurs, the load is transferred to the elastic component and stored as elastic energy. The elastic elements can then deliver increased energy as it is recovered and used for the concentric contraction.14 The muscle’s ability to use the stored elastic energy is affected by time, magnitude of stretch, and velocity of stretch. Increased force generation during the concentric contraction is most effective when the preceding eccentric contraction is of short range and performed quickly without delay.14,15
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lb fibers ⫹⫹⫹ la fibers ⫹⫹⫹⫹
Alpha and gamma activation from brain
Extrafusal muscle fiber
Intrafusal muscle fiber Alpha motor neurons ⫹⫹⫹⫹ Gamma motor neurons ⫹⫹⫹⫹ Figure 55-3. Active contraction. Intrafusal and extrafusal fibers contract. Spindles are activated and, with increased resistance, group 1a fibers are activated. The Golgi tendon organ is activated if the load is too great, causing relaxation.
Golgi tendon organ
The improved or increased muscle performance that occurs with the prestretching of the muscle is the result of the combined effects of the storage of elastic energy and the myotatic reflex activation of the muscle.14,15,19 The percentage of contribution from each component is not known.15 The degree of improvement depends on the time frame between the eccentric and concentric contractions.19 Plyometric exercise has three phases: the setting or eccentric phase, the amortization phase, and the concentric response phase (Box 55-1). The eccentric or setting phase begins when the athlete mentally prepares for the activity and lasts until the stretch stimulus is initiated. Advantages of a correct setting stage include increasing the muscle spindle activity by prestretching the muscle before activation and mentally biasing the alpha motor neuron for optimal extrafusal muscle contraction.21,33 The duration of the setting phase is determined by how much impulse is desired for facilitating the contraction. With too much or prolonged loading, the elapsed time from eccentric to concentric contraction prevents exploitation of the stretch-shortening myotatic reflex.28,34
BOX 55-1.
Plyometrics Phases
Phase 1 Eccentric phase (setting): Preloading period
Phase 2 Amortization phase: Time between eccentric and creative phases
Phase 3 Concentric phase: Facilitated contraction (payoff)
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The second phase of the plyometric response is the amortization phase. This phase is the amount of time between undergoing the yielding eccentric contraction and initiating a concentric overcoming force. By definition, it is an electromechanical delay between the eccentric and concentric contractions during which the muscle must switch from overcoming work to imparting the necessary amount of acceleration in the required direction. The final period of the plyometric exercise is the concentric response phase. During this phase the athlete concentrates on the effect of the exercise and prepares for initiating the second repetition. Plyometric exercise helps to improve physiologic muscle performance in several ways. Although increasing the speed of the myotatic stretch-reflex response would increase performance, it has not been documented in the literature. It has been documented that the faster a muscle is loaded eccentrically, the greater the concentric force that is produced. Eccentric loading places stress on the elastic components, thereby increasing the tension of the resultant rebound force. A second possible mechanism for the increased force production involves the inhibitory effect of the Golgi tendon organs on force production. Because the Golgi tendon organ serves as a protective mechanism limiting the amount of force produced within a muscle, its stimulation threshold becomes the limiting factor. It may be possible to desensitize the Golgi tendon organ, thereby raising the level of inhibition and ultimately allowing increased force production with greater loads applied to the musculoskeletal system.
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SCIENTIFIC EVIDENCE TO SUPPORT CLINICAL USE OF PLYOMETRICS Several studies have documented the efficiency of plyometric training for the upper extremity. Carter and colleagues compared two training programs in collegiate baseball players: a twice-weekly plyometric training program and a twice-weekly concentric training program.9 Both programs lasted 8 weeks. The plyometric training group exhibited greater throwing velocity (2 mph faster); isokinetic strength parameters were similar between groups. Schulte-Edelmann and colleagues studied the effects of plyometrics on collegeaged volunteer subjects (not athletes).10 The investigators implemented a 6-week plyometric training program and compared them with a control group not practicing plyometrics. The plyometrics group exhibited greater elbow extensor strength, but there were no differences in posterior shoulder musculature or in a closed-kinetic-chain test. Swanik and colleagues studied the effects of plyometrics on proprioception and isokinetic muscular performance in collegiate female swimmers. Following a 6-week plyometric training program, the plyometrics group exhibited improved proprioception, kinesthesia, and dynamometer strength values compared with a control group.11 The last mechanism by which plyometric training can increase muscular performance centers around neuromuscular coordination. Explosive plyometric training can improve neural efficiency and thereby increase neuromuscular performance. Neural adaptation allows the athlete to better coordinate the activities of the muscle groups, thereby affecting a greater net force even in the absence of morphologic change within the muscles themselves. The neurologic system is enhanced to become more automatic. Successful plyometric training relies heavily on the rate of stretch rather than the length of stretch. If the amortization phase is slow, elastic energy is wasted because heat and the stretch reflex are not activated. The more quickly the athlete can switch from yielding work to overcoming work, the more powerful the response.
UPPER-EXTREMITY PLYOMETRIC PROGRAM The implementation of the plyometric program begins initially with the development of an adequate strength base. The development of a greater strength base results in greater force generation due to both the increased crosssectional area and the resultant elastic component. To produce optimal strength gains, a structured plan must be instituted to prevent overuse injuries.
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Plyometric exercise trains the neuromuscular system by teaching it to better accept the increased strength loads. Using the stretch reflex helps to improve the ability of the nervous system to react with maximal speed to the lengthening muscle. This allows the muscle to contract concentrically with maximal force. Because the plyometric program attempts to modify and retrain the neuromuscular system, the exercise program should be designed with sport specificity in mind. The upper extremity program is organized into four exercise groupings: warm-up exercises, throwing movements, trunk extension and flexion exercises, and medicine ball wall exercises (Box 55-2).
Warm-up Exercises These exercises provide the body and especially the shoulder, arm, and trunk with an adequate physiologic warm-up before beginning a plyometric program. An active warm-up should facilitate muscular performance by increasing blood flow, muscle and core temperature, speed of contraction, oxygen use, and nervous system transmission.23,27,29,35,36 The warm-up exercises are listed in Box 55-2. The first three warm-up exercises use a 9-lb medicine ball or a rubber coated ball called a Plyoball. These warm-up exercises include trunk rotations (Fig. 55-4), trunk side bends (Fig. 55-5), and trunk wood chops (Fig. 55-6). The next two warm-ups are performed with exercise tubing for internal and external rotation movements of the shoulder with the arm in 90 degrees of shoulder abduction and 90 degrees of elbow flexion (Fig. 55-7) to simulate the throwing position. The last warm-up exercise is push-ups with both hands on the ground. Athletes perform 2 or 3 sets of 10 repetitions for each of these warm-up exercises.
Throwing Movements The exercises in this group attempt to isolate the muscles and muscle groups necessary for throwing. These exercises are performed in movement patterns similar to the throwing motion. Box 55-2 lists these plyometric exercises. The first four drills are throwing movement plyometrics using a 6- to 8-lb Plyoball. The first drill is a two-hand overhead soccer throw (Fig. 55-8) followed by a two-hand chest pass (Fig. 55-9). The next two throws incorporate a step and pass (Fig. 55-10) and a side throw (Fig. 55-11). These exercises can be performed with a partner or with a spring-loaded bounce-back device called the Plyoback (Exertools, Novato,Calif). The next four plyometric drills require exercise tubing. The first movement is plyometrics for the external rotators (Fig. 55-12). In this exercise, the athlete stands, bringing the tubing back into external rotation, and
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BOX 55-2.
Upper Extremity Plyometrics Drills
Tubing plyos diagonals
Warm-up Exercises Medicine ball rotation
Tubing plyos biceps
Medicine ball side bends
Plyo push-up (boxes)
Medicine ball wood chops
Push-up (clappers)
Tubing external and internal rotation
Medicine Ball Trunk Extension and Flexion Movements
Tubing diagonal patterns (D2)
Sit-ups
Tubing biceps
Long seating trunk twists
Push-ups
Throwing Movements
Side throws in long seating
Medicine ball soccer throw
Back extension
Medicine ball chest pass
Medicine Ball Wall Exercises Soccer throw
Medicine ball step and pass
Chest pass
Medicine ball side throw
Side-to-side throw
Medicine ball side-lying external rotation ball flips
Wall dribble
Medicine ball prone horizontal abduction ball flips Medicine ball standing external rotation side throws
Wall dribble circular motion
Medicine ball standing internal rotation side throws
Wall dribble side throws with opposite hand holding ball
Lunge and medicine ball soccer throw
Backward side-to-side throw
Lunge onto box and medicine ball soccer throw
Forward two hands through legs
Tubing plyos interior rotation and external rotation
One-hand baseball throw
Figure 55-5. Warm-up plyometrics. Trunk side bends with an 8-lb. medicine ball.
Figure 55-4. Warm-up plyometrics. Trunk rotations with an 8-lb. medicine ball.
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A
B
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Figure 55-6. Warm-up plyometrics. Wood chops with an 8-lb. medicine ball. A, Starting position. B, Ending position.
arm reaches horizontal, the external rotators then contract concentrically to bring the tubing back into external rotation. This constitutes one plyometric repetition. This movement is continued for 6 to 8 repetitions. Similar movements are performed for the internal rotators and for proprioceptive neuromuscular facilitation diagonal patterns including D2 flexion and D2 extension of the upper extremities.37-39 Plyometrics is also performed for the elbow flexors, using exercise tubing. Push-ups to strengthen the serratus anterior, pectoralis major, deltoid, triceps, and biceps musculature are also performed. Plyometric contractions for push-ups are performed using a 6- to 8-in. box or the ground in a depth-jump training manner (Fig. 55-13). All these exercises are performed for 2 to 4 sets of 6 to 8 repetitions two to three times weekly. Several plyometric drills can be performed to enhance performance and endurance (Figs. 55-14 and 55-15). A two-hand soccer throw can be used to enhance performance and acceleration rate (Fig. 55-16). Figure 55-7. Warm-up plyometrics. Exercise tubing external and internal rotation at 90 degrees of shoulder abduction.
holds that position for 2 seconds. Then the athlete allows the external rotation musculature to release this isometric contraction, thus allowing the tubing to pull the arm into internal rotation. Thus, the external rotators are eccentrically controlling this movement. Once the
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The purpose of these exercises is to provide the athlete with advanced strengthening exercises that are more aggressive and at higher exercise levels than those provided by a simple dumbbell exercise program. These programs can only be used once the athlete has performed a strengthening program for an extended period and has a satisfactory clinical examination.
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A
B
Figure 55-8. Plyometric drill. Two-hand overhead soccer throw. A, Starting position. B, Ending position.
A
B
Figure 55-9. Plyometric drill. Two-hand chest pass with an 8-lb ball. A, Starting position. B, Ending position.
Figure 55-11. Plyometric drill. Two-hand side throws with an 8-lb ball. Figure 55-10. Plyometric drill. One-hand step and throw with a 2-lb ball.
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Figure 55-14. Plyometric drill. Side-lying ball flips into external rotation with a 2-lb medicine ball. Figure 55-12. Plyometric drill. External-rotation plyometric exercise drill with tubing.
Trunk Extension and Flexion The next two groups of plyometric drills are for trunk strengthening, emphasizing the abdominals and trunk extensors. The exercises in this group are medicine ball sit-ups (Fig. 55-17), prone back extension (Fig. 55-18), and sideto-side throws to train the oblique muscles (Fig. 55-19).
Medicine Ball Wall Exercises The last group of exercises or drills uses a 2- or 4-lb medicine ball or Plyoball and a wall, which allows the athlete the opportunity to perform plyometric medicine ball drills without a partner. Alternatively, these exercises can be performed with the Plyoback. This allows the athlete to train alone. The first five exercises in this session include a two-handed overhead soccer throw (Fig. 55-20), a two-handed chest pass (Fig. 55-21), a two-handed side-to-side throw, a backward
A
Figure 55-15. Plyometric drill. Prone horizontal abduction ball flips with a 2-lb medicine ball.
two-handed side-to-side throw, and a forward two-handed pass through the legs . Lastly, using a 2-lb medicine ball, the athlete performs a one-handed plyometric baseball throw (Fig. 55-22). Plyoball wall dribbling may be used to throw for endurance (Fig. 55-23). These drills are usually performed
B
Figure 55-13. Plyometric push-up drill onto boxes. A, Starting position. B, Ending position.
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Figure 55-16. Plyometric drill. Lunge step onto box during two-hand overhead soccer throw.
Figure 55-18. Plyometric drill. Back extensions with a 10-lb medicine ball.
for time, not repetitions; sets of 30 seconds to 1 minute are encouraged. These exercises can be performed in the kneeling position to eliminate the use of the lower extremities and to increase the demands on the trunk and upper extremities.
This form of exercise should not be performed for an extended period because of the large stresses that occur during plyometric exercise. Rather, plyometrics is appropriately used during the first and second preparation phases of periodized training (Fig. 55-24).40
CONTRAINDICATIONS
SUMMARY
The first contraindication to plyometric exercise is inadequate physical conditioning. Other contraindications to plyometric upper-extremity exercises include acute inflammation or pain and gross shoulder or elbow instabilities. Plyometrics is contraindicated in patients immediately following surgery.
We encourage the clinician to implement some of these concepts when rehabilitating the competitive athlete. We also suggest alterations in this program while using the plyometric concepts. We strongly recommend clinical research to document the efficiency of this training program. The authors of this chapter have used plyometrics for the upper extremity for 20 years with excellent results. We strongly believe for the overhead athlete and for contact and collision athletes that plyometrics is extremely beneficial and functional. Plyometrics has been documented to improve muscular strength, power, endurance and improve the neuromuscular system.
This exercise program is intended to be an advanced strengthening program for the competitive athlete. The clinician should be aware of the adverse reactions secondary to this form of exercise, such as postexercise soreness and delayed onset muscular soreness (DOMS).
A
B
Figure 55-17. Plyometric drill. Sit-ups with medicine-ball throw. A, Starting position. B, Ending position.
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A
759
B
Figure 55-19. Plyometric drill. Side-to-side throws with a 10-lb medicine ball. A, Starting position. B, Ending position.
Figure 55-21. Plyometric wall drill. Two-hand chest pass into wall. Figure 55-20. Plyometric wall drill. Two-hand soccer throws.
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Figure 55-22. Plyometric wall drill. Side-to-side rotation throws.
Figure 55-24. Plyometric wall drill. One-hand wall dribbling drill for endurance.
References
Figure 55-23. Plyometric wall drill. One-hand baseball throws.
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1. Chu D: The language of plyometrics. Natl Strength Cond Assoc J 6(5):30-31, 1984. 2. Gambetta V: Plyometrics for beginners—basic considerations. New Studies in Athletics 4(1):61-66, 1989. 3. Wilk KE, Arrigo C: Current concepts in the rehabilitation of the athletic shoulder. J Orthop Sports Phys Ther 18(1): 365-378, 1993. 4. Wilk KE, Voight ML, Keirns MA, et al: Stretch-shortening drills for the upper extremities: Theory and clinical application. J Orthop Sports Phys Ther 17(5):223-239, 1993. 5. Allman FL: Sports Medicine. Orlando, Fla, Academic Press, 1974. 6. Pezzullo DJ, Karas S, Irrgang JJ: Functional plyometric exercises for the throwing athlete. J Athl Train 30(1):22-26, 1995. 7. Chmielewski TL, Myer GD, Kauffman D, Tillman SM: Plyometric exercise in the rehabilitation of athletes: Physiological responses and clinical applications. J Orthop Sports Phys Ther 36(5):308-319, 2006. 8. Wilk KE, Meister K, Andrews JR: Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30(1):136-151, 2002. 9. Carter AB, Kaminski TW, Douex AT, et al: Effects of high volume upper extremity plyometric training on throwing velocity and functional strength ratios of the shoulder rotators in collegiate baseball players. J Strength Cond Res 21(1):208-215, 2007. 10. Schulte-Edelmann JA, Davies GJ, Kernozek TW, Gerbering ED: The effects of plyometric training of the posterior shoulder and elbow. J Strength Cond Res 19(1): 129-134, 2005. 11. Swanik KA, Lephart SM, Swanik CB, et al: The effects of shoulder plyometric training on proprioception and selected
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12.
13. 14. 15.
16. 17. 18.
19. 20. 21. 22. 23.
24.
25.
muscle performance characteristics. J Shoulder Elbow Surg 11(6):579-586, 2002. Verkhoshanski Y: Perspectives in the improvement of speed-strength preparation of jumpers. Yessis Rev Soviet Phys Educ Sports 4:28-35, 1969. Wilt F: Plyometrics, what it is and how it works. Athletic J 55:76-90, 1975. Assmussen E, Bonde-Peterson F: Storage of elastic energy in skeletal muscles in man. Acta Physiol Scand 91:385-392, 1974. Bosco C, Komi P: Potentiation of the mechanical behavior of the human skeletal muscle through pre-stretching. Acta Physiol Scand 106:467-472, 1979. Cavagna G: Elastic bounce of the body. J Appl Physiol 29:279-282, 1970. McGarlane B: Special strength: Horizontal and vertical. Track Field Q Rev 83:51-00, 1983. Polhemus R, Osina M, Burkhardt E, Patterson M: The effects of plyometric training with ankle and vest weights on conventional weight training programmes for men. Track Field Q Rev 80(4):59-61, 1980. Cavagna D, Disman B Margari R: Positive work done by a previously stretched muscle. J Appl Physiol 24:21-00, 1968. Chu D: Plyometric exercise. Natl Strength Cond Assoc J 6:56-62, 1984. Lundin PE: A review of plyometric training. Natl Strength Conditioning Assoc J 7:65-74, 1985. Scoles G: Depth jumping! Does it really work? Athletic J 58:48-75, 1978. Adams T: An investigation of selected plyometric training exercises on muscular leg strength and power. Track Field Q Rev 84:36-39, 1984. Pappas AM, Zawacki RM, Sullivan TJ: Biomechanics of baseball pitching. A preliminary report. Am J Sports Med 13: 216-222, 1985. Buchwald JS: Exteroceptive reflexes and movement. Am J Phys Med 46:121-128, 1967.
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26. Granit R: Receptors and Sensory Perception. New Haven, Yale University Press, 1962. 27. Astrand P, Rodahl K: Textbook of Work Physiology. New York, McGraw-Hill, 1970. 28. O’Connel A, Gardner E: Understanding the Scientific Bases of Human Movement. Baltimore, Williams & Wilkins, 1972. 29. Franks BD: Physical warm-up. In Morgan WP (ed): Ergogenic Aids and Muscular Performance. Orlando, Fla, Academic Press, 1972. 30. Granit R: The Basis of Motor Control. Orlando, Fla, Academic Press, 1970. 31. Brodal A: Neurological Anatomy in Relation to Clinical Medicine. New York, Oxford University Press, 1969. 32. Patten BM: Human Embryology. New York, McGraw-Hill, 1953. 33. Eldred E: Functional implications of dynamic and static components of the spindle response to stretch. Am J Phys Med 46:129-140, 1967. 34. Komi P. Bosco U: Utilization of stored elastic energy in leg extensor muscles by men and women. Med Sci Sports 10:261-265, 1978. 35. DeVries HA: Physiology of exercise for physical education and athletics. Dubuque, WV Brown, 1974. 36. McArdle WD, Katch FI, Katch VL: Exercise Physiology: Energy, Nutrition, and Human Performance. Philadelphia, Lea & Febiger, 1981. 37. Knott M, Voss DE: Proprioceptive Neuromuscular Facilitation. New York, Harper & Row, 1968. 38. Sullivan PE, Markos PD, Minor MD: An Integrated Approach to Therapeutic Exercise: Theory and Clinical Application. Reston, Va, Reston Publishing Co, 1982. 39. Voss DE, Knott M, Kabat N: Application of neuromuscular facilitation in the treatment of shoulder disabilities. Phys Ther Rev 33:536-541, 1953. 40. Matveyev L: Fundamentals of Sports Training. Moscow, Russia, Progress Publishers, 1977.
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CHAPTER 56 Core Stabilization: Integration
with Shoulder Rehabilitation Sue Falsone and Mark Verstegen
Many years ago, we were working with a baseball pitcher who began to have immense right shoulder pain with a resultant rotator cuff tear and rotator cuff surgery. He missed the second half of his season. He could not figure out why his shoulder began to hurt him. He did not change his mechanics (that he knew of), he did not change his velocity, he had been doing his shoulder program as he always did. His routine had not varied, and his shoulder pain seemingly began for no reason. As he was voicing his frustration, he removed his shoe and sock, and began talking about an ingrown toenail he had on the first toe of his right leg; it wouldn’t go away and had been bothering him for quite some time. Anyone who has ever had an ingrown toe nail knows that it can cause significant pain. An ingrown toenail can hurt so badly that you’ll do anything to get off of it, because it hurts with every step. Now imagine trying to pitch off that right leg with the ingrown toenail. Could it be possible that his toe hurt him so much that he changed his push-off, altering his transfer of force through the kinetic chain, in a way that was so subtle that his pitching coaches did not notice? Could he alter his delivery so subtly that even he did not notice? We believe an ingrown toenail was the cause of subtle changes in his kinetic chain that led to the eventual breakdown of his rotator cuff. We cannot prove it, but we believe it.
A combination of mobility, stability, and strength at the shoulders, trunk, and hips is needed to efficiently transfer force from the lower body to the upper body or vice versa.1-4 These three definable, yet integrated areas are the foundation for all human movement. A lot of research has been done on the shoulder, spine, and pelvis, with their associated musculatures and functions. Countless protocols focus on the rehabilitation or performance enhancement of these areas, but the true synergy lies within their seamless integration. We need to move past the simplistic view of the core and look to a more integrated view of pillar strength. Pillar strength is the complete integration of our shoulders, trunk, and hips. Mobility, stability, and strength at each of these individual areas are needed so they can come together to create a conduit for power production and force transfer in the body. When discussing pillar strength, there are several things to consider in regard to their relationship with one another. In the pillar, there are approximately 63 joints and more than 71 muscles, depending on how we count the individual spinal intrinsics and pelvic floor muscles. All of these are connected via fascial slings that run in the sagittal, coronal, and transverse planes.1 This massive amount of mobile structure creates an intricate symphony of motor programs, conducting dozens of force couples to work seamlessly together to create a diverse set of harmonious and fluid movements throughout the kinetic chain.
That was our first lesson in the power of the kinetic chain. From that day forward, if an athlete came to us complaining of pain, we would start at the toes and work our way up to find the cause. Often the area that is hurt is not the problem. The area that hurts is the source of tissue pathology. The actual cause of this tissue pathology is often coming from somewhere else in the body.
INDIVIDUAL UNITS IN RELATION TO EACH OTHER
This chapter reviews the basic concepts of core stability and the role core stability plays in force transfer, production, and absorption as it relates to rehabilitation of the shoulder.
We know the foundation for the shoulder relies heavily on the function of the torso, specifically with its relationship to the cervical and thoracic segments of the spine.5 The lumbar spine, integrated with the pelvis, heavily influences the function of these areas. With extensive mobility, stability, and strength, as well as cognitive postural awareness in both static and dynamic movement, we can create a great foundation that the shoulder can work efficiently from.
TERMINOLOGY Core training has gained a tremendous amount of attention in the literature from sports medicine through the latest Hollywood craze. Athletes and professionals alike often equate core stability with abdominal strength. A strong core, or strong abdominals, is often believed to be all that is necessary to prevent injury and improve performance. In theory, we all realize that injury prevention and optimal performance lie much deeper than simple abdominal strength.
Shoulder The importance of shoulder function in the overhead athlete is obvious. The rotator cuff is the main stabilizing muscle group of the glenohumeral joint, and it originates 763
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from the scapula. If the rotator cuff has an unstable base to work from, then it cannot be an efficient stabilizer of the glenohumeral joint. This can be related to a squat. Someone can be a very good back squatter, but place him or her on one leg, and squatting becomes very difficult. This is not because the person physically can’t squat, but because he or she has a less stable base to work from. The rotator cuff and scapula have a very similar relationship. The rotator cuff needs a stable base to work from to efficiently stabilize the glenohumeral joint. The shoulder girdle has a similar relationship to the trunk. If the trunk is unstable, the shoulder girdle does not have a stable base from which to work.6-9
Trunk Newton’s third law tells us that every action has an equal and opposite reaction. If we are throwing a baseball toward home plate, and all of our force is directed exactly to where we need it and want it to go, then 100% of our effort is directed at home plate. An athlete who cannot stabilize the spine during this motion will have tiny energy leaks at each segment. This can quickly add up to a significant amount of wasted energy. The trunk must be an efficient, stable base from which to work. Excessive, extraneous movement causes an overall decrease in ability to efficiently transfer force to where we need it to go. This loss of energy can translate into inefficient movement, decreased performance, and ultimately injury from trying to compensate for this energy loss.
Hips Much time is spent discussing the rotator cuff, but we need to begin to direct our energies to the hip as well. Thirty-seven muscles, not including the pelvic floor, attach to the hip and pelvis. Sixteen of these muscles externally or internally rotate the hip; that is approximately 42% of lumbar-pelvic-hip musculature affecting rotation. We refer to these muscles as the hip cuff. Considering the huge rotational component of throwing or of swinging a bat, golf club, or tennis racquet, one cannot deny the involvement of the hips. Biomechanical analysis has shown that during a golf swing, the first segment of the kinetic chain that begins to move is the hip.10 As the hips move, force is transferred through the spine, out the arms, and into the club. It is this summation of force that creates such a huge rotational club head speed, translating into the distance the golf ball moves. If the hips did not initiate this movement, or if forces were not added throughout the kinetic chain, the club head speed would decrease, decreasing the distance the ball is driven off the tee, thus decreasing the performance of the golfer. This is very similar to the baseball pitch. Force is generated through the lower extremities, hips, and trunk and finally through the upper extremities.11 The velocity produced is a
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result of the force generated through the entire kinetic chain. In fact, the rotator cuff muscles are active during the pitch to control the forces produced by the lower extremity and trunk. This allows the rotator cuff to function more to dissipate energy. The rotator cuff then acts as a defensive mechanism to injury rather than a muscle group that produces energy.12
Pelvic Floor The pelvic floor is often left out of discussion during the education of our athletes. Voluntary contraction of the pelvic floor has been shown to increase EMG activity of the abdominal musculature.13 Palpate just medial to your anterior superior iliac spine. Now contract your pelvic floor. You should feel almost a flattening, or a pulling away, of your abdominals from your fingers. But by contracting your pelvic floor, you feel activity at your abdominals. This demonstrates the direct connection of your pelvic floor to your abdominals and how contraction of these muscles can directly affect the contraction of your abdominal intrinsics.
Fascial Slings and Muscle Fiber Orientation Fascial slings have been described throughout the body and documented in the literature.1,14,15 Fascial slings and muscle fiber orientation demonstrate that truly there is no individual action of a muscle or joint. Consider the fiber orientation and fascial attachments of the rectus abdominus, how they run superior to inferior and attach onto the pubic bone. The pelvic floor creates a sling beneath us and runs in the same direction into the lumbodorsal fascia. Similarly, the transverse abdominus muscle fibers run around us and have an attachment onto the lumbodorsal fascia, creating what McGill describes as an abdominal hoop.14 Finally, we have diagonal slings that run in the direction of the rhomboids, into the serratus anterior, to the external oblique. Then the internal oblique runs into the anterior gluteus medius, completing these diagonal slings.15 These slings that run throughout the body demonstrate the intricate linking of our shoulders, trunk, and hips. We cannot discuss one of these parts without considering the other two.
FOUNDATION FOR ALL MOVEMENT PATTERNS Efficient movement patterns can improve performance and decrease injury potential. If we know, from basic laws of physics, that energy is never created or destroyed, it is merely transferred or exchanged, then we know when we move, we transfer energy from ourselves to something or someone else, from our lower body, through our trunk and out our upper body, or vice versa. Also, if every action has an equal and opposite reaction, then the more efficiently we apply our energy into the ground, the faster we can be
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propelled forward. The more efficiently we transfer energy into a ball, the further it will go. If we are running, we direct all of our energy into the ground, we will have an equal and opposite reaction to propel ourselves forward, which possibly means us getting to the ball quicker than someone else; then we can theoretically improve our performance and, we hope, decrease our injury potential. Decreasing extraneous movement at the trunk while throwing allows the muscles of the shoulder to pull from a stable base and more efficiently perform the task at hand.12 A stable trunk will allow the scapula to move in a controlled fashion, maintaining the optimal length-tension relationship of the shoulder girdle. This optimal length-tension relationship is necessary for proper force production, absorption, and energy transfer throughout the kinetic chain.16-18
COMMON PROBLEMS RELATED TO MOVEMENT DYSFUNCTION Short Muscles Short muscles reach the end of their length before a normal length muscle, causing a joint to move sooner than normally required during an efficient movement pattern. This early, extraneous movement causes an energy leak at the segment that is moving too early or too much and decreases the amount of energy actually being directed where it was originally intended to go. This inefficiency leads to an apparent weakness, decrease in power, or decrease in speed.2,19
Muscle-Firing Patterns Muscles need to fire in a very specific order for efficient movement. When synergistic muscles of a joint become prime movers, synergistic dominance occurs, placing undue stress on muscles and joints.2,19,20 When a muscle becomes a prime mover for a joint it was never meant to be a prime mover for, it becomes stressed and overworked. For example, we have all seen the athlete who extends the hip by extending the back. When the paraspinals and hamstrings become the prime movers for hip extension, they become overworked. A person with chronic low back pain or chronic proximal hamstring strains will continue to deal with these issues if he or she does not re-educate the gluteal musculature to become the prime mover for hip extension.
Arthrokinematic Dysfunctions Arthrokinematic dysfunction can occur for several reasons. Long-term dysfunction of muscle-firing patterns, weak muscles, or short muscles can lead to altered joint movement and eventual loss of capsular mobility, leading to altered arthrokinematics.2,19 When joint function is altered, structures such as cartilage can be worn down, causing
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pain. With pain, movement patterns are altered yet again, setting into motion a cycle that is difficult to break. For example, an athlete has a short psoas muscle. When the athlete extends the hip, the muscle becomes taut sooner than is considered normal. In an attempt to achieve normal hip extension, the athlete compensates with an increase in low back extension. Doing this repetitively at high intensities or velocities can eventually result in abnormal wearing of the lumbar facet joint and low back pain. Back pain can inhibit spinal intrinsic and abdominal musculature, altering fundamental movement patterns of the trunk, and therefore altering the fundamental movement patterns of the upper and lower extremities.2
HOW DO WE TURN CONCEPT INTO REALITY? Our philosophy is: Isolate, in order to innervate, to better integrate into functional movement patterns. Many athletes are great compensators, being able to perform just about any movement asked of them. When considering a gross movement pattern, we must consider the intricacies of that movement and how it is being performed. Are they firing the right muscles to produce the movement? Are they firing these muscles in the proper order? Many times athletes skip the “easy” exercises and go right into the multijoint, multiplanar exercises because they are “harder” and more fun to perform. If we bring athletes back to the fundamentals, requiring them to concentrate on the quality of the movement versus the quantity of the exercise, we can get more from our training and rehabilitation programs. This can allow us to maximize the potential the athlete already has. We believe, whether training for performance, rehabilitating from an injury, or preventing injury, a multifaceted approach is needed. A combination of mobility, stability, and strength at each segment is needed for proper kinetic linking to occur. If this is achieved, optimal power can be produced and energy can be transferred efficiently and effectively. The exercises described here are samples of mobility, stability, and strength at each segment, building on each other to eventually integrate the entire body. Although the exercises are divided into categories, many exercises could justifiably be in several categories. There is much overlap, even in what may be considered an isolation exercise. Organize your typical exercise selections according to what makes sense to you and your methodology. The realities of training do not allow us to always work on these things at individual stages, meeting the requirements of one before moving on to the next. Often these things are worked on simultaneously. Once the
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fundamental, isolated exercises are mastered, they can continue to be used as a warm-up, to activate the muscles before more complicated activity, or on regeneration days, when volume and intensity of exercise need to be low.
Mobility Proper muscle length, capsule mobility, nerve gliding, and fascial stretching are necessary at each portion of the pillar (shoulders, trunk, and hips) to allow proper movement. Adhesions or abnormal tissue shortening inhibits proper movement patterns and causes early or altered movements of joints. All tissues must be considered, although only a few examples are offered here. Shoulders Active latissimus dorsi stretch (Fig. 56-1). The athlete should be in a neutral spine position, actively lifting the arms above the head to feel a stretch in the latissimus dorsi. Trunk extension should not be allowed and indicates either a lack of latissimus dorsi length or lack of trunk stabilization as the shoulders are brought into flexion. Trunk Thoracic rotation (Fig. 56-2). The shoulder girdle has a direct musculature attachment to the thoracic spine. Thoracic spine mobility is crucial to normal shoulder function. The entire spine needs proper mobility in all directions. Hips Quadruped rocking (Fig. 56-3). Performed as an active posterior hip capsule mobilization, quadruped rocking provides a posterior translation of the femoral head in the acetabulum, decreasing the anterior pinch often felt at the hips during hip flexion activities. A neutral spine should be maintained as the hips move into a flexed
Figure 56-1. Active latissimus dorsi stretch. The athlete lies supine with knees bent, actively flexing the arms overhead to stretch the latissimus dorsi, maintaining an element of external rotation to his humerus.
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Figure 56-2. Thoracic rotation. Sitting on the heels takes the lumbar spine into a position of lumbar flexion, allowing the rotation to become more concentrated in the thoracic spine.
position. A common compensatory pattern includes moving into trunk flexion as the hips flex.
Stability Postural muscles and stabilizing muscles of the shoulders, trunk, and hips must activate reflexively before movement of the limbs.21,22 Efficient movement is difficult without a stable base from which to move. These exercises are examples of stability-based movements you can use throughout the pillar during shoulder rehabilitation. Shoulders Wall walk (Fig. 56-4). It is important here to have the wrists as wide as or wider than the elbows to activate the infraspinatus and teres minor. If the elbows are wider than the wrists, the middle deltoid can dominate the movement.
Figure 56-3. Quadruped rocking. The hips should be in a relatively neutral position, or slightly internally rotated as the athlete rocks back, maintaining a neutral spine. This femur position stretches the posterior hip capsule more effectively and affects the tracking of the femoral head.
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Figure 56-4. Wall walk. The athlete externally rotates his shoulders throughout this range of motion to activate the posterior cuff. Typically, an athlete walks his or her arms up the wall until the elbows reach eye level, and then walks back down. Working up to 3 sets of 5 and gradually increasing the resistance is desirable.
Figure 56-5. Leg lowering. As the athlete lowers and raises the legs, the pelvis and lumbar spine should not move. The motion should occur only at the hip joint. The legs should only be lowered as far as the athlete can control the lumbar spine and pelvis.
Trunk Leg lowering (Fig. 56-5).21 Begin with a neutral spine, abdominals drawn in, and pelvic floor activated. Lift the legs so the hips are at a 90-degree angle. Push the heels toward the ceiling to give a feeling of lengthening both legs through the entire exercise. Lower one leg toward the ground, keeping both legs straight. Only lower the leg as far as possible while keeping a neutral spine. This exercise focuses on active hamstring lengthening along with dissociating hip movement from the spine.
connections that run throughout the body, an exercise considered isolated is truly not. A seemingly isolated exercise is simply less complex than what most would consider an integrated exercise. When training for strength, keep in mind the ultimate goal for most athletes: power. Strength is the foundation for power and the goal of training should be to improve relative, or pound-for-pound, strength. Power is what allows the athlete to move mass with speed. The stronger we are per pound and the quicker we can apply and reapply these movements, the more powerful we are. This is one of the core fundamentals in sports and life.
Hips Stride-length stance. This exercise is used throughout clinics and can be progressed accordingly. A patient can stand on a stable surface or unstable surface, can turn the head to stimulate the vestibular system, or can perform upper extremity exercises while in this position. Any modification is appropriate for the situation as long as some fundamental posturing is being followed. The foot is in a neutral, short foot position23 with the first metatarsal and phalanx placed on the ground for balance. The knee should be aligned with the second toe, engaging the posterior gluteus medius for femoral control. Do not overuse the quadratus lumborum, or the pelvis can drop. As the athlete progresses, he or she might fight through these compensations, but the athlete should be able to spend their time as close to the desired position as possible, despite the external challenge this position gives them.
When progressing our strength exercises, we begin with each individual joint, then progress to combining joints, providing more complex exercises that bias the joints we are focusing on (Fig 56-6). This exercise progression follows this progressive system of relative isolation to more-integrated exercises. Shoulders Y, T, W, L, and M exercises (Figs. 56-7 to 56-11).24,25 We use these exercises as scapular activation exercises for the lower trapezius, the middle trapezius, the rhomboids,
Shoulders/ trunk
Shoulders
Hips/knees/ ankles
Trunk/hips
Trunk
Hips
Knees
Ankles
Strength Individual strength at each muscle is needed, as well as integrated strength within the kinetic chain. “Isolate in order to innervate in order to integrate” is a concept we adhere to in our practice. Keeping in mind the neural and fascial
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Foundation of stability, mobility, and strength at each individual joint Figure 56-6. When progressing strength exercises, we begin with each individual joint, then progress to combining joints, providing more complex exercises that bias the joints we are focusing on.
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Figure 56-7. Y exercise. The motion should be initiated by the lower trapezius, with a relative position of external rotation at the shoulders.
Figure 56-8. T exercise. The motion should be initiated by the middle trapezius, not the middle deltoid. Rotation of the humerus can vary: with the thumbs pointing to the ceiling or floor or with the palms facing the floor.
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Figure 56-9. W exercise. The elbows should not rise above the plane of the body during this exercise. A helpful verbal cue is to tell the athlete to think about lifting the forearms to the ceiling, not the elbows. Palms face the floor during the exercise, with a variation including thumbs pointing to the ceiling.
Figure 56-10. L exercise. Scapular tilting should not be allowed to substitute for glenohumeral joint rotation.
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Shoulders and Abdominals Swiss ball cable chop (Fig. 56-13), Swiss ball lift (Fig. 56-14), wobble board twists (Fig. 56-15).21 The Swiss ball cable chop and lift begin to introduce a rotational stability and strength component during a strength activity for the upper extremity. The core board twists also introduce trunk stability with upper extremity strength, focusing on the athlete’s ability to disassociate upper extremity movement from trunk movement. Compensatory patterns include trunk side bending during shoulder flexion and pelvic dropping.
Figure 56-11. M exercise. Scapular tilting should not be allowed to substitute for glenohumeral joint rotation.
the infraspinatus, the teres minor, and the subscapularis, respectively. Trunk Swiss ball plate crunch (Fig. 56-12). This exercise focuses on sagittal plane trunk strength. The coronal plane must also be considered. We address rotational trunk strength below. Hips Side-lying gluteal series: hip abduction, adduction, and external and internal rotation. Quality of movement is important here, focusing on the prime mover. Do not let the synergistic muscle groups become dominant during these seemingly simple exercises. Athletes often perform these exercises quickly and recruit the synergistic muscles early, causing poor motor patterns to develop.
Abdominals and Hips Bridge progression. Beginning in a hook-lying position, with a neutral spine, the abdominals should be drawn in and the pelvic floor engaged. Lift the hips using the gluteal muscles until the pelvis places the hips in a neutral position. Lift the left foot off the ground one inch, maintaining a neutral pelvis. Do not let the pelvis drop on the side with the lifted foot. Repeat on the other side. Shoulders, Abdominals, and Hips Standing stability chop (Fig. 56-16) and standing stability lift (Fig. 56-17).21 These exercises progress the patient into standing, introducing an element of hip stability, trunk stability. and upper extremity strength. Abdominals, Hips, Knees, and Feet Band walks (Fig. 56-18).24,25 Band walks can be performed with bent or straight legs and moving forward, backward, laterally, or diagonally. The band can be placed at the ankles to increase the lever arm, if desired. We prefer to have a band just above the knee joint for femoral control feedback. Adding a second band at the ankles can increase the resistance and difficulty of the exercise. Shoulders, Abdominals, Hips, Knees, and Feet Cable chop (Fig. 56-19) and cable lift (Fig. 56-20).24,25 During the propulsive chop, the athlete initiates the movement with scapular retraction, then pulls the rope into the body. At this time, he or she rotates through the movement and pushes the arms down toward the floor. This is a powerful movement, intended to be performed with speed. During the propulsive lift, the athlete sits into a regular squat with hips back. The rope pulls the arms toward the machine, but the hips should stay back. Drive through the hips to rotate the body through the movement, arms reaching toward the ceiling. This is a powerful movement and intended to be performed with speed.
SUMMARY
Figure 56-12. Swiss ball plate crunch. Use a burst-resistant Swiss ball with this exercise. Place appropriate weight behind the head as shown or on the chest. Crunch up and perform a posterior pelvic tilt at the same time.
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The shoulder may be the weakest link in the system and simply where the pain is located. Often, a more global issue is the actual cause of the more local shoulder derangement. Pillar strength is defined as the interplay of mobility, (Text continues on page 773)
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A
B
Figure 56-13. Swiss ball cable chop. The movement includes pulling the bar with the outside hand (A) and pushing down with the inside hand to finish the movement (B). The trunk does not move.
A
B
Figure 56-14. Swiss ball lift. The movement includes pulling the bar with the outside hand, like an upright row with one arm (A). The inside arm pushes toward the ceiling as the outside elbow drops (B).
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Figure 56-15. Wobble board twists. The athlete is in a pillar bridge position and turns the wobble board. No trunk movement should occur. This exercise can also be performed from the knees.
Figure 56-17. Standing stability lift. This is the same exercise as seen in Figure 56-14 except the athlete is standing. The arm movement is the same and there should be no trunk movement.
Figure 56-16. Standing stability chop. This is the same exercise as seen in Figure 56-13 except the athlete is standing. The arm movement is the same and there should be no trunk movement.
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Figure 56-18. Band walks. Instruct the athlete to think about pushing him- or herself across the floor with the back leg, versus pulling with the front leg.
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A
B
Figure 56-19. Cable chop. The propulsive rotational chop calls in all the elements of stability, mobility, and strength throughout the shoulders, trunk, and hips. This exercise teaches force transfer throughout the kinetic chain. A, Starting position. B, Ending position.
A
B
Figure 56-20. Cable lift. The propulsive rotational lift calls in all the elements of stability, mobility, and strength throughout the shoulders, trunk, and hips. This exercise teaches force transfer throughout the kinetic chain. A, Starting position. B, Ending position.
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stability, and strength at the shoulder, trunk, and hips. Concepts of pillar strength can be placed in all training and rehabilitation programs. The more global issues of force transfer and kinetic linking need to be addressed so the athlete does not keep breaking down the next weakest link in a fragile and volatile system. It is important to integrate pillar strength training into shoulder programs. The concepts reviewed may be applied to both rehabilitation and injury reduction programs to ensure athletes are performing with optimal function. References 1. Myers TW: The World According to Fascia. In Myers TW: Anatomy Trains. New York, Churchill Livingstone, 2001, pp 9-50. 2. Sahrmann,SA: Concepts and principles of movement. In Sahrmann, SA: Diagnosis and Treatment of Movement Impairment Syndromes. St Louis, Mosby, 2002, pp 9-50. 3. Wight J, Richards J, Hall S: Influence of pelvis rotation styles on baseball pitching mechanics. Sports Biomech 3(1):67-83, 2004. 4. Young JL, Herring SA, Press JM, Casazza BA: The influence of the spine on the shoulder in the throwing athlete. J Back Musculoskeletal Rehabil 7:5-17, 1996. 5. McMullen J, Uhl TL: A kinetic chain approach for shoulder rehabilitation. J Athl Train 35:329-337, 2000. 6. Moseley JB Jr, Jobe FW, Pink M, et al: EMG analysis of the scapular muscles during a shoulder rehabilitation program. Am J Sports Med 20:128-134, 1992. 7. Guanche C, Knatt T, Solomonow M, et al: The synergistic action of the capsule and the shoulder muscles. Am J Sports Med 23:301-306, 1995. 8. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic analysis of the throwing shoulder with glenohumeral joint instability. J Bone Joint Surg Am 70: 70:220-226, 1988. 9. Wilk K, Arrigo C, Andrews J: Current concepts: The stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther 25:364-379, 1997. 10. Hume PA, Keogh J, Reid D: The role of biomechanics in maximizing distance and accuracy of golf shots. Sports Med 35:429-449, 2005.
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11. Watkins RG, Dennis S, Dillin WH, et al: Dynamic EMG analysis of torque transfer in professional baseball pitchers. Spine 14:404-408, 1989. 12. Fleisig G, Barrentine S, Escamilla R, Andrews J: Biomechanics of overhand throwing with implications for injuries. Sports Med 21:421-437, 1996. 13. Sapsford R, Hodges P, Richardson C, et al: Co-activation of the abdominal and pelvic floor muscles during voluntary exercises. Neurourol Urodyn 20:31-42 2001. 14. McGill S: Functional anatomy of the lumbar spine. In McGill S: Low Back Disorders. Champaign, Ill, Human Kinetics, 2002, pp 45-86. 15. Tittle K: Describing functional anatomy in humans. In Benninghoff A, Drenckhahn D, Zenker W (eds): Benninghoff Anatomy, 13th ed, vol 1. Munich, Urban & Fischer Verlag, 1994, pp 304-307. 16. Kamkar A, Irrang J, Whitney S: Nonoperative management of secondary shoulder impingement syndrome. J Orthop Sports Phys Ther 17:212-224, 1993. 17. Paine R, Voight M: The role of the scapula. J Orthop Sports Phys Ther 18:386-391, 1993. 18. Wilk K, Arrigo C: Current concepts in rehabilitation of the athletic shoulder. J Orthop Sports Phys Ther 18:365-378, 1993. 19. Janda V: Evaluation of muscular imbalance. In Liebenson C (ed): Rehabilitation of the Spine: A Practitioner’s Manual. Baltimore, Lippincott Williams & Wilkins, 1996, pp 97-112. 20. Alexander RM: Optimum timing of muscle activation for simple models of throwing. J Theor Biol 150:349-372, 1991. 21. Cook, G: Movement imbalance training. In Cook G: Athletic Body in Balance. Champaign, Ill, Human Kinetics, 2003, pp 97-107. 22. Hodges PW, Richardson CA: Delayed postural contraction of transversus abdominis in low back pain associated with movement of the lower limb. J Spinal Disord 11:46-56, 1998. 23. Janda, V, Va’Vrova, M: Sensory motor stimulation. In Liebenson C (ed): Rehabilitation of the Spine: A Practitioner’s Manual. Baltimore, Lippincott Williams & Wilkins, 1996, pp 319-328. 24. Verstegen, M: Prehab and strength. In Verstegen M: Core Performance. Emmaus, Penn, Rodale, 2004, pp 55-71, 113-137. 25. Verstegen M: Core movements. In Verstegen M: Core Performance Essentials. Emmaus, Penn, Rodale, 2006, pp 109-178.
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CHAPTER 57 Conditioning of the Shoulder
Complex for Specific Sports Ken Crenshaw, Kevin Harmon, Jamie Reed, and Dave Donatucci
Function of the shoulder complex in the athlete, and more specifically the overhead athlete, requires synchrony of multiple neuromuscular components. The precise timing of shoulder neurodynamics, osteodynamics, and neuromuscular dynamics depends on function of the entire kinetic chain. In-depth understanding of how the shoulder complex functions in relation to the torso and lower extremities (kinetic chain) allows adequate conditioning in preparation for competitive sports or rehabilitation from injury.
require specific soft tissue manipulation (flexibility, manual therapy) and activation of specific musculature (strengthening exercises). Isolation for activation of specific musculature should be accomplished before sports-specific movements for synchrony. If not, the neuromuscular system will find a means of compensation around the deficient components. When looking at sport-specific motions, the range of motion, the speed of movement, the muscles activated, and how they are activated (concentrically, eccentrically, isometrically) all must be understood to create a proper conditioning program. Because all movements have an optimal biomechanical position, it is imperative to aim to achieve biomechanical efficiency, which eases stress on tissues and improves function. It is important to emphasize quality of effort and proper intensity to gain optimum results from exercises in any conditioning program.
The specific movements of the overhead athlete create numerous adaptations throughout the kinetic chain. Adaptation and compensation are the processes that athletes use to respond to many demands of their given sport. As clinicians and sports trainers we can aid in this adaptation through proper conditioning methods. Specific exercises to promote healthy adaptation are paramount to the success of any program.
ADAPTATION
Injury prevention is the primary objective of a properly applied conditioning program; performance enhancement and return from injury are secondary objectives. This chapter gives the practitioner a solid foundation for creating a program that fits the needs of each athlete.
All athletes develop physiologic adaptations to their given sports, some more drastically than others. Influences from daily living habits can also modify the way an athlete functions, for good or ill. Repetitive stresses, which are all too common in sports, can compromise tissues that are shortened or weakened from environmental influences. An in-depth understanding of interaction and adaptation from psychosocial, biochemical, and biomechanical demands allows proper program design.
KINETIC CHAIN CONCEPTS AND CONNECTIONS An athlete’s body may be required to move or react in various ways to accomplish sport-specific movements. A perfectly executed movement is the result of several body parts working in synchrony. This synergy is accomplished by precise function of the neuromuscular system. The movement in the overhead athlete begins in the foot, is transferred through the torso, and ends with a force being applied by the hand. As clinicians and sports trainers we must understand how function in one part of the neuromuscular system can affect function in others. The function of the entire kinetic chain is paramount in injury prevention, performance enhancement, and return from injury. The sum of the whole may be more important than the individual components, although each individual component must be evaluated for proper function.
Understanding the sport and the position-specific demand is critical to good program design. A feel for the tissue stresses that the athlete is being exposed to will help prevent overuse injuries. Misuse or abuse of tissue from sportspecific skill work may be helped or hindered by exercise regimens; therefore, the conditioning program must be carefully selected. The balancing act of loading the tissue to maximize the training response without overloading the adaptive potentials must be constantly monitored. Selye’s1 specific adaptation to imposed demand (SAID) principle describes the changes that occur throughout the body in response to training or athletic demands. Wilk2 demonstrated that the baseball player has a specific adaptation about the throwing shoulder. As different researchers have tried to determine the exact cause of this adaptation,3-6 it has become apparent that each athlete adapts in a similar
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pattern depending on the sport and the position within the sport. Although similar patterns of adaptation do occur, each athlete responds in his or her own unique way. Evaluating each athlete allows a path to preventive exercise programs that have a more specific approach. How much to incorporate in an attempt to prevent the adaptation process is an intriguing question. The adaptation might help the athlete to meet the demands of the game or prevent injury, and clinicians and sports trainers must carefully select their therapeutic interventions. A look specifically at the overhead throwing athlete shows adaptation occurring throughout the kinetic chain. Scapular, torso, and hip adaptations all appear to play roles in the athlete’s success from a performance and well-being standpoint. Because more distal adaptation can ultimately affect the shoulder or elbow, it is necessary to look at all aspects of the body. Promoting a healthy adaptation can require attention to exercise, flexibility, soft tissue therapy, recovery, and proper nutrition.
EVALUATION The idea that connectivity exists between the shoulder and the rest of the kinetic chain requires a look at proper length-tension relationships. This in turn allows the best chance for optimal movement patterns. An evaluation of the entire body is imperative because it can identify and help correct any problems before implementing a conditioning program. A misguided program can actually promote dysfunction or necessitate new adaptation patterns, either of which could result in injury. The evaluation should take into account overall gross movement dysfunction, postural abnormalities, flexibility, bilateral symmetry, and muscle and joint function. This evaluation should give the practitioner a reasonable picture of an athlete’s current state of function and direction for program design. It is very common for athletes to develop muscle imbalances that are often overlooked until the athlete has an injury. A thorough evaluation of posture (static, dynamic), muscle tension, and functional movement will help identify abnormalities, which will allow a corrective exercise strategy that can offset any associated muscle imbalances. The corrective exercise program should strive to obtain optimal posture and alignment, which will lead to functional efficiency. Optimal posture can be viewed as alignment of each component of the kinetic chain. This alignment allows optimal length-tension relationships and force couples from the myofascial components. Adequate joint kinematics will also be optimized. Optimal static posture
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(viewed in the coronal plane) should reveal a line of gravity passing from the earlobe through the glenohumeral joint and the greater trochanter of the hip and finishing just anterior to the lateral malleolus of the ankle. Dynamic posture is the ability to maintain optimal force couples and length-tension relationships regardless of body position. In the presence of poor posture, dysfunctional muscle patterns can develop. These dysfunctions may be responses to overuse, misuse, abuse, or disuse.7 A normal response of muscle to any stress is to increase tightness. A chain reaction then occurs whereby the stressed muscles tighten and their antagonists weaken, which creates altered movement patterns.8 Many times these chain reactions create predictable patterns of dysfunction. Vladimir Janda has described them as upper and lower crossed syndromes. These syndromes can have detrimental effects on the shoulder of any athlete. Sherrington’s law of reciprocal innervation indicates that tight muscles act in an inhibitory fashion to their antagonists.9 Therefore, it is prudent to stretch the tightened muscles before strengthening the weakened muscles. It is important to evaluate all athletes for postural abnormalities, proper length-tension relationships, and proper muscle-firing patterns. A program to correct flexibility deficits, activate neuromuscular isolation, and integrate exercises can then be developed for each athlete depending on the athlete’s individual needs.
PROGRAM COMPONENTS To design a specific program for conditioning the shoulder complex, several components must be developed. These components require different degrees of emphasis and specificity depending on the athlete and his or her adaptational patterns, evaluation results, demands of the sport, and goals of the program (injury prevention, improved performance, rehabilitation). Each component depends on the others, on skill development, and on health status.
Strength Strength is the ability of a muscle or group of muscles to generate muscular force under specific resistive conditions.10 Although there are many types of strength, this chapter only discusses strength in a general sense as it relates to conditioning the shoulder complex. Some sports depend on strength more than others. Because developing power critically depends on maximal strength, most athletes need some type of strength training to help
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improve this quality. Strength development can increase the use of muscular motor units through increased intensity. Intensities must be carefully planned (periodized) to gain optimal training effects. Shoulder complex exercises many times use very small and specific musculature; therefore, using maximum strength training exercises might not be advantageous.
Flexibility and Mobility
Power
The goal of flexibility training is to correct specific muscle tightness that can inhibit optimum neuromuscular function and to improve extensibility of specific soft tissues.13 A thorough evaluation will help determine specifically which myofascial or neural components need improved flexibility. This will minimize the chance of a hit or miss approach by a general overall body flexibility program. Optimum performance and injury prevention depend on proper length-tension relationships of muscles, and therefore the flexibility and mobility component must address any deficiencies.
Power can be explained as the ability to produce force in a short period of time, which is vital to most sport skills.11 Power is highly related to strength and more specifically at the higher levels of force. Power depends on the stretch-shortening cycle of muscular contraction. Power (plyometric) development can be done in a specific component that is developed in conjunction with the other components or simply intertwined into the strength development component.
This component can be seen as the extensibility of all connective tissues that allow joint range of motion while still maintaining joint integrity. Mobility can refer to the extensibility of a group of muscles and joints rather than a single muscle or joint.
The ability to maintain power output is critical to sport success and represents a portion of one’s work capacity. The combination of strength, speed, and endurance yields the most productive use of power. To create an effective power-plyometric program, the exercises should exhibit patterns of movement, speed, and frequency similar to the actual sport movement. These exercises help make the neuromuscular system more efficient at storing and releasing energy. In essence, plyometric training improves the relation between maximum strength and power. The exercises also improve the ability of the tissues to tolerate the higher forces that are common in sports. Many times, less is more with this component of training. An adequate strength base is essential before initiating plyometric exercises.
Flexibility and mobility can be achieved by many different methods such as static stretching, myofascial release, muscle energy techniques, proprioceptive neuromuscular facilitation (PNF) stretching, dynamic stretching, and functional movement stretching. A thorough understanding of each type of stretching allows the trainer to integrate the proper method into the overall conditioning program.
Endurance (Work Capacity)
Stabilization and Neuromuscular Control
This component may be defined as the capacity to resist fatigue. This may be a cumulative process from one repetition to another, from exercise to exercise, or from day to day. The ability to recover and allow more work of higher quality is the goal. Obviously, recovery is a critical variable in this process. Understanding the requirements of the sport and the position of the athlete within the sport determines the importance of training for endurance and more specifically what type of endurance. It is the opinion of many strength and conditioning professionals that endurance work for an anaerobic athlete must be carefully selected because it can prevent the conversion of transitional or intermediate muscle fiber to red endurance fibers.12 Hence, if improved aerobic endurance damages the athlete’s power, then volume and intensity might need to be manipulated. Therefore, when designing a program, make sure it fits the athlete’s needs.
It is our view that stabilization is fundamental to injury prevention and proper neuromuscular function. Stabilization is the ability of the neuromuscular system to allow agonists, antagonists, synergists, stabilizers, and neutralizers to work synergistically.
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Athletes are master compensators. They devise compensation patterns, muscle imbalances, and postural abnormalities that can in turn create joint dysfunction and decreased neuromuscular control. A properly designed flexibility and mobility program can be the determining factor in the health or illness of the athlete.
Core stabilization allows proximal stability, which in turn allows a stable fulcrum for efficient extremity motion. It also provides force reduction capabilities and hence injury prevention. The shoulder girdle has very little static or ligamentous stability. Therefore, the stability required is dynamic and requires specific synergism of all neuromuscular components. It is essential to understand the difference between muscles that provide power for shoulder motion (deltoid, latissimus dorsi, and pectoral muscles) and those that provide shoulder stability (subscapularis, infraspinatus, teres
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minor, and supraspinatus).14 Stabilization of the shoulder complex is critical to the overall conditioning program. When reactivity is added to the stabilization exercises, the shoulder complex becomes more adept at handling the forces that sporting activities cause. Improved stabilization, neuromuscular control, and reactivity enhance performance and prevent injury.
Coordination or Skill Movements Coordination or skill movements show how well neuromuscular firing patterns are working. It also shows motor unit recruitment for producing force and for timing of movement qualities. In essence, a specific movement with a specific force with the proper timing is the byproduct of properly executed skill movements. It is neuromuscular control and proprioception that allow these movements to happen efficiently. It is very important to improve all physical conditioning components of the shoulder complex, but ultimately it is the skill movements that are required for success. Skill movements should be classified as exercise in themselves; for example, a throwing or hitting program designed by the skills coach must be considered an exercise. Skill movements are normally practiced repetitiously for maximum biomechanical efficiency. With this in mind, the skills coach is vital to the success of any athlete. A properly designed conditioning program must take into account the volume, frequency, and intensity of skills training and implement the conditioning program around these variables for best results.
Recovery The most overlooked area of training is recovery. As in any sport, it is not the amount of work the athlete does that determines good health and improved performance, instead it is the recovery that takes place between bouts of exercise and between athletic competitions. The process of recovery, or more specifically regeneration, is a complex biologic reaction influenced by both external and internal environments. Unfortunately, at present there is a greater emphasis on stressing the body than on recovery. There are many methods that can be used to promote recovery. Proper nutrition and hydration, hot and cold hydrotherapies, sports massage, relaxation techniques, and rest and sleep can be used to aid an athlete’s recovery.15 Lymphatic drainage techniques may also be beneficial. Planning recovery is a critical component to maximizing the overall conditioning effect.
GUIDELINES FOR SPECIFIC EXERCISES Several basic guidelines should be followed when designing an exercise program for the shoulder complex.
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Selection Age In our opinion, it is important for the prepubescent athlete to be able to control body weight before performing a resistance program involving weights. The neuromuscular control that is required to perform push-ups, press-ups, pull-ups, body squats, lunges, and lateral lunges needs to be developed. This allows the adolescent the opportunity to develop intramuscular coordination that may be overlooked if the training only consists of traditional stabilized weight training that occurs when using benches and machines. Another aspect of age is the effect of overtraining on bone growth plates. Any exercise or sports participation that causes abnormal responses from the epiphysis or apophysis of bone should be discontinued until the symptoms resolve, and return to that activity should be gradual. Evaluation of Range of Motion An exercise program should strive to increase the desired response from the targeted muscle group. Before embarking on a designed program, an evaluation to assess posture, scapulothoracic motion, scapulohumeral motion, and muscular strength should be performed by a trained professional. For example, in annual physicals in professional baseball before spring training, each player is evaluated by an orthopedic physician, deficits in strength and range of motion are brought to the attention of the athletic training and strength and conditioning staffs, and individual programs are established for players who have specific needs. Previous Injuries and Surgeries An athlete who is returning from a recent injury or surgery must be cleared to participate by the team physician. Any deficits must be corrected before the player embarks on more sport-specific activity. Two common shoulder adaptations that are encountered in the throwing athlete are changes in glenohumeral internal rotation (measured with the scapula stabilized) and weakness or deficits in the rotator cuff. When a decrease in internal rotation is accompanied by a decrease in the total range of motion of the glenohumeral joint it would be advantageous to stretch the involved extremity. Isokinetic testing devices are helpful in providing objective numbers that can be used to motivate an athlete to improve strength deficits. Completion of a properly designed physical therapy program (isotonic through plyometric exercises) should also be completed before beginning a throwing progression. Training Age Before a program is designed for an athlete, the athlete’s athletic history and level of training should be determined. Proficiency in tasks (body control exercises) should be determined and a functional screening (posture and functional strength) should be carried out to address any potential weaknesses.
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Exercise Selection The goal of any exercise program should be to increase performance and reduce the probability of injury. An understanding of risk versus reward should be considered when evaluating any exercise. In our experience, athletes are exposed to many training philosophies and might have performed exercises in their training routines that can be considered risk-versus-reward exercises. Over the course of a long career, the cumulative effects of repetitive motion (overhand throwing of an implement or ball) and the added effects of some exercises can place undue stress on the joints and soft tissue. In our opinion, certain exercises can have undesirable effects.
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peak levels of fitness for the most important competitions.16 Before beginning a periodized program it is important to look at two factors: the athlete’s training experience and body mechanics and the specific demands of the sport.
Military Press. The act of overhead pressing can decrease the amount of space in the subacromial area. A throwing athlete might already have some chronic changes in the subacromial space. Adding the stress of the overhead press can cause further irritation.
Training needs for an athlete are different from the training needs for a person who is training for aesthetics (bodybuilding) or Olympic lifting. Aesthetic lifters train body parts in stabilized environments to exhaustion to stimulate growth. Olympic lifters train to perform specific one-repetition maximum lifts for competition. The goal for an athlete needs to be specific to the demands of the sport. Athletes should strive to stimulate not only the prime movers or agonists but also the antagonists, synergists, stabilizers, and neutralizers by performing exercises that stimulate the nervous system to fire stabilizing muscle groups. Anecdotal evidence of the inability of exercises to protect athletes from injuries are numerous. Hamstring curls are not the panacea for hamstring injuries, four-way hip machines do not prevent groin strains, and the list can go on and on. An athlete training for a sport needs a good base of general strength and also needs sportspecific training to ensure training the body for the desired response.
Bench Press. Performing the bench press with a bar (as opposed to using dumbbells) places the arms in essentially the same working plane, which can cause some acromioclavicular joint stress with time. Using dumbbells, an athlete can vary the angles at which the exercise is performed, and the arms work as individual units. It is also recommended that the athlete not lower the upper arms below the level of the trunk to place less stress on the anterior shoulder capsule and ligaments, preserving the static stabilizers of the anterior shoulder.
Periodization The training cycle is divided into mesocycles.16 These cycles revolve around the dates that the athlete wants to be at his or her peak, such as major competition dates. The training cycle as a whole, generally 1 year, is a macrocycle. The mesocycles are the preparatory period and the competitive period. The preparatory period (the off-season or noncompetition season) includes the hypertrophy phase, the strength phase, and the power phase.
Latissimus Pull-downs. Performing the latissimus pulldown exercise by pulling the bar behind the head can place the anterior structures of the glenohumeral joint in a stretched position at 90 degrees of flexion and 90 degrees of abduction. Performing the exercise with the bar in front of the head trains the targeted muscle groups with less anterior stresses.
Preparatory Period. The hypertrophy phase lasts from 1 to 6 weeks. It begins at a low intensity (weights, running intensity) and a high volume (repetitions per set). This allows the muscles and soft tissues to adapt to the stresses of training that will be increased in the next phase. The exercises can be general or can be specific to the sport. Continued work to improve deficits addressed in the corrective exercises phase can be beneficial (Table 57-1).
Knee Extension. The patellofemoral joint is subjected to very high forces when performing open-chain kneeextension exercises. In addition, training the quadriceps with knee extension eliminates recruitment of other muscle groups that occurs in athletic activity.
Olympic Lift. Olympic lifts can place a significant demand on the glenohumeral, elbow, and wrist joints. The technical demands of these lifts require extensive coaching and supervision. The potential for incorrect mechanics, combined with heavy loads, necessitates a decision regarding the benefits of the exercises.
Design of an Exercise Program Periodized training is the gradual cycling (allocation of a specific period of time, whether days, weeks, or months) of specificity, intensity, and volume of training to achieve
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In the strength phase, running progresses to interval sprints at moderate distances, weight training becomes more specific, and intensity level increases. Loads of more than 80% of the athlete’s one-repetition maximum (1 RM) are used, and the volume is reduced from the hypertrophy phase (see Table 57-1). In the power phase, loads increase to more than 90% of 1 RM and running speedwork is at a near-contest pace. Plyometric exercises can be implemented to take
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TABLE 57-1 Exercise in the Preparatory Period Phase
Reps
Sets
Intensity of 1 RM (%)
Rest Interval
Total Volume
Velocity (sec)*
Hypertrophy
12-25
2-3
50%-70%
30-60 sec
36-75 reps/exercise
3/2/1
Strength
6-8
3-4
80%-85%
2-3 min
18-24 reps/exercise
3/1/1
Power
1-5
4-8
85%-100%
3-5 min
12-20 reps/exercise
1/1/1
*Velocity is the time for the eccentric/isometric/concentric contractions rep, repetition; 1 RM, one-repetition maximum weight. Adapted from Clark M: Optimum Performance Training for the Performance Specialist. Home Study Course. Calabasas, Calif, National Academy of Sports Medicine, 2002.
advantage of increased strength gains made in the strength phase. Plyometrics uses the stretch reflex and the accompanying stretch-shortening cycle to elicit more powerful concentric contractions. This type of training includes bounding, hopping, jumping, and throwing. Plyometric training requires sufficient recovery and should be used 1 to 3 days per week for 15- to 20-minute sessions (see Table 57-1)
Another postural fault is pronation syndrome, in which subtalar pronation can lead to tibial internal rotation, knee flexion, and femoral internal rotation. Because the tibia does not sufficiently externally rotate during knee extension (with excessive subtalar pronation), the femur must accommodate by internal rotation. Correction of foot biomechanics can greatly enhance the proper function of the kinetic chain.
Competitive Period. The competitive period is often preceded by a transition period, at which time the athlete usually performs all activities at a low level of intensity and volume. This allows some physical recuperation before competition. The competition period is characterized by very high intensity and low volume training, in essence a maintenance of strength and power, with a minimum of energy expended in the weight room. Periodization or cycling is more complex when the competitive season is long, as in professional sports, or when there are two or more competitive seasons, as in college baseball, which has fall, spring, and summer competitions.
Injury Prevention, Performance, and Rehabilitation Factors include work, rest, and weight work. Training sessions should not exceed 90 minutes.18 The number of training sessions per week is influenced by training goals,
Corrective Exercises Before starting a comprehensive periodized conditioning program, it might be beneficial to correct any postural deficits in the athlete. When attempting to correct what may be seen as a structural abnormality, remember that the neuromuscular system is an unknown variable. The neuromuscular system can adapt significantly to limit dysfunction.17 A common postural fault is what is commonly known as upper cross syndrome,8 which is characterized by rounded shoulders (protracted scapula) and a forward head. Lower cross syndrome is characterized by lumbar lordosis and an anterior pelvic tilt. Contributing factors are a group of muscles that are prone to be tight and a group of muscles prone to be weak and inhibited (Fig. 57-1 and Box 57-1). If these postural deficits are not addressed then some common injury patterns, such as rotator cuff impingement and thoracic outlet syndrome can emerge. Some corrective strategies for these syndromes are shown in Box 57-2:
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Figure 57-1. Forward head posture.
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BOX 57-1.
Postural Faults
Upper Cross Syndrome
Lower Cross Syndrome
TIGHT AND SHORTENED MUSCLES
TIGHT AND SHORTENED MUSCLES
Pectoralis major and minor
Iliopsoas
Latissimus dorsi
Rectus femoris
Teres major
Tensor fascia latae
Upper trapezius
Short adductors
Levator scapulae
Erector spinae
Sternocleidomastoid
WEAK AND LENGTHENED MUSCLES
Scalenes
Gluteus maximus
WEAK AND LENGTHENED MUSCLES
Hamstrings
Rhomboids
Gluteus medius
Teres minor
Transverse abdominus
Infraspinatus
Multifidus
Serratus anterior
Internal oblique
Middle and lower trapezius Longus colli
BOX 57-2. Faults
training age, general health, work capacity, nutritional status, recoverability, lifestyle, and other stressors. Other factors to consider are mechanics (poor vs. perfect), work load (learning a new skill, such as pitches, arm angle) and rehabilitation. It is important not to move too quickly through the rehabilitation process for throwing athletes. The athlete may begin a strengthening program when cleared to do so by the physician.
Corrective Exercises for Postural
Upper Cross Syndrome FOAM ROLL OR STRETCH
Upper trapezius Levator scapulae Sternocleidomastoid
Resistance and Endurance Working with the scapular muscle groups is extremely important during the rehabilitation process. Endurance is trained by strengthening using isometric exercises with a 5- to 6-second hold for 10 repetitions using fatigue as a guideline. These exercises are performed for forward flexion, abduction, extension, internal rotation, and external rotation below the level of discomfort (Box 57-3).
Latissimus dorsi Pectorals CORE STABILIZATION
Cervical retraction Prone cobra Scaption Proprioception neuromuscular facilitation
If the throwing athlete is allowed in an aquatic environment (no risk of infection), performing isotonic exercises in chest-deep water eliminates the weight of the arm. Exercising in chest-deep water allows the athlete to begin forward flexion, scapular plane, empty can and full can, abduction, and extension exercises. The athlete can also perform range-of-motion exercises such as writing the alphabet and using PNF patterns. The speed of the exercise or the addition of aquatic dumbbells can increase the amount of resistance (Box 57-4).
Lower Cross Syndrome FOAM ROLL OR STRETCH
Iliopsoas Rectus femoris Adductors Erector spinae CORE STABILIZATION
Bridging Physioball crunches with proper abdominal maneuver
Isotonic exercises with dumbbells can be initiated when the athlete is able to perform the exercises with proper form and without substituting synergistic muscles
Activation of transverse abdominus and internal obliques
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BOX 57-3.
Tubing Exercises for the Scapula
BOX 57-5.
Rotator Cuff Isotonic Exercises
Perform 10 repetitions with 6-second holds
90 degrees of abduction
Shrug with retraction
Full-can to empty-can scaption
Wide row: squeeze and hold
Prone abduction
Retraction with extension
Prone extension
Retraction with T
Prone 90/90
Retraction with external rotation
Side-lying external rotation with deceleration
Retraction with Y
Prone scaption (110 degrees of abduction)
Bear hug with protraction Seated press-up External rotation at 0 degrees (holding tubing between hands) Horizontal abduction (holding tubing between hands) Elevation and protraction Protraction and depression
repetitions for all exercises before increasing by 1 pound. We have found that using this method, the athlete is less likely to increase resistance than when doing 3 sets of 10 to 15 repetitions. Performing each exercise correctly with 5 pounds for 30 repetitions is a good indicator that the athlete is ready to move on to more sport-specific strengthening. Power Plyometric Exercises See Box 57-6 and Figures 57-2 to 57-9.
BOX 57-4.
Pool Exercises
Shoulder exercises, with or without water dumbbells • Flexion in all planes • Horizontal abduction • ER/IR at 0 degrees • ER/IR at all angles • Punches • Circles (change angle at GH joint) • Wrist curls • Pronation and supination • Flexion and extension • Radial and ulnar • Elbow flexion and extension • Patterns (alphabet writing, PNF)
Neuromuscular Control and Stabilization Exercises Neuromuscular control exercises allow the body to produce force and dynamically stabilize and reduce external forces, essentially to maintain balance during movement. Traditional machine-based strength training eliminates the need for neuromuscular control. The antagonists, stabilizers, and neutralizers are not called on to balance the movement produced by the prime movers (agonists and synergists). Machine-based training also generally exercises prime movers in only one plane instead of in the multiplane mode that sports activities are performed in.
BOX 57-6.
Upper Body Plyometrics
Swimming: Front crawl
Two-Hand Exercises
Running
Soccer throw Chest pass
Note: Use time instead of number of repetitions. ER, external rotation; GH, glenohumeral; IR, internal rotation; PNF, proprioceptive neuromuscular facilitation.
Side-to-side throws Trunk rotation
One-Hand Exercises Wrist flips
(Box 57-5). We have found it useful to start with the weight of the arm for 1 set of 30 repetitions to develop endurance. Once all the exercises can be completed for 30 consecutive repetitions, then 1 pound is added and the athlete is required to complete 30 consecutive
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Reverse wrist flips 90/90 throws Eccentric catches
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CONDITIONING OF THE SHOULDER COMPLEX FOR SPECIFIC SPORTS
Figure 57-2. Socccer throw.
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Figure 57-4. Side-to-side throw.
Figure 57-3. Chest pass. Figure 57-5. Trunk rotation.
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Figure 57-6. Wrist flip.
Figure 57-8. 90/90 throw.
Injuries cause altered sensory afferent feedback to the central nervous system. This alters neuromuscular control, which can lead to tissue overload and further injury. Neuromuscular control training may be done in functional movement patterns and in a multisensory environment. Exercise progression should occur from slow to fast, from using one extremity to using both, from performing simple movements to performing complex ones, and from performing movements with eyes open to performing them with eyes closed. Sport-Specific Drills See Box 57-7 and Figure 57-10. BOX 57-7.
Sport-Specific Drills
Medicine ball throws against a wall or a Plyoback Cable machine exercises Body blade exercises Impulse exercises Sock throwing Throwing programs Figure 57-7. Reverse wrist flip.
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Throwing from different arm angles after completing a throwing program
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A
785
B
C Figure 57-9. Eccentric catches.
Skill Development as an Exercise One of the most critical components of success for a throwing athlete is performing the throwing motion as efficiently and stress free as possible. Proper mechanics decrease the probability of injury more than all other aspects of the conditioning program. The ability to repeat the correct mechanics is essential to successful overhead throwing. Evaluation by a skilled coach or
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biomechanist can help correct mechanical flaws that can predispose an athlete to injury. Throwing a baseball is an extremely fast motion, and the ability to watch for certain body positions at different points in the delivery is crucial. Several skills are important to develop in the throwing athlete. The throwing athlete must develop the ability
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to balance over the back leg during the wind-up phase. Hand separation should take place at the same time as the lead leg begins moving toward the plate. The hand should be on top of the ball during the windup phase and the planted leg should be pointed
A
toward home plate. The front arm (glove hand) must remain in front of the body during delivery. The elbow position of the throwing arm should remain above the shoulder. The whole body must be used during follow-through.
B
C Figure 57-10. Row to external rotation. A, Starting position. B, Mid-row. C, Ending position.
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References 1. Selye H: The Stress of Life. New York, McGraw Hill, 1956. 2. Wilk KE: Rehabilitation guidelines for the thrower with internal impingement. Presented at the American Sports Medicine Institute Injuries in Baseball Course, January 23, 2004. 3. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and range of motion at the gleno-humeral joint in professional baseball pitchers. Am J Sports Med 30(1): 20-26, 2002. 4. Reagan KM, Meister K, Horodyski MB, et al: Humeral retroversion and its relationship to gleno-humeral rotation in the shoulder of college baseball players. Am J Sports Med 30(3):354-360, 2002. 5. Osbahr DC, Cannon DL, Speer KP: Retroversion of the humerus in the throwing shoulder of college baseball pitchers. The Am J Sports Med 30(3):347-353, 2002. 6. Borsa PA, Wilk KE, Jacobson JA, et al: Correlation of range of motion and glenohumeral translation in professional baseball pitchers. Am J Sports Med 33:1392-1399, 2005. 7. Chaitow L: Muscle energy techniques, 2nd ed. Edinburgh, Churchill Livingstone, 2001. 8. Janda V: Muscles central nervous regulation and back problems. In Korr I (ed): Neurobiological mechanisms in manipulative therapy. New York, Plenum Press, 1978. 9. Chaitow L, Delany JW: Clinical Application of Neuromuscular Techniques, vol 1: The Upper Body. Edinburgh, Churchill Livingstone, 2001. 10. Siff MC: Supertraining, 6th ed. Denver, Mel C Siff, 2004. 11. Kraemer WJ, Gomez AL: Establishing a solid-fitness base. In Foran B (ed): High-Performance Sports Conditioning. Champaign, Ill, Human Kinetics, 2001. 12. Francis C: Training for Speed. Canberra, Canadian Faccioni Speed & Conditioning Consultants, 1997. 13. Jull G, Janda V: Muscles and motor control in low back pain: assessment and management. In Twomey L (ed): Physical Therapy of the Low Back. New York, Churchill Livingstone, 1987. 14. Hammer WI: Functional Soft Tissue Examination and Treatment by Manual Methods: New Perspectives, 2nd ed. Gaithersburg, Md, Aspen Publishers, 1999. 15. Calder A: Recovery: Restoration and regeneration as essential components within training programs. Excel 6(3):15-19, 1990. 16. Baechle TR: Essentials of Strength Training and Conditioning. Champaign, Ill, Human Kinetics, 1994 17. Brownstein B, Bonner S: Functional Movement in Orthopedic and Sports Physical Therapy. New York, Churchill Livingston, 1997 18. Clark M: Optimum Performance Training for the Performance Specialist. Home Study Course. Calabasas, Calif, National Academy of Sports Medicine, 2002.
Suggested Reading Anderson JE: Grant’s Atlas of Anatomy, 8th ed. Baltimore, Williams & Wilkins, 1983. Anderson MK, Hall SJ: Sports Injury Management. Baltimore, Williams & Wilkins, 1995.
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Andrews JR, Harrelson GL, Wilk KE: Physical Rehabilitation of the Injured Athlete, 3rd ed. Philadelphia, WB Saunders, 2004. Apostolopoulos N: Performance flexibility. In Foran B (ed): High Performance Sports Conditioning. Champaign, Ill, Human Kinetics, 2001, pp 49-61. Bandy WD, Irion JM, Briggler M: The effect of static stretch and dynamic range of motion training on the flexibility of hamstring muscles. J Orthop Sports Phys Ther 27(4):295-300, 1998. Barlow W: Anxiety and muscle tension pain. Br J Clin Pract 13(5):339-350, 1959. Basmajian JV, DeLuca CJ: Muscles Alive, 5th ed. Baltimore, Williams & Wilkins, 1985. Brotzman SB, Wilk KE: Clinical Orthopaedic Rehabilitation. Philadelphia, Mosby, 2003. Chaitow L: Integrated neuromuscular inhibition technique. Br J Osteop 13:17-20, 1994. Chaitow L, Delany JW: Clinical Application of Neuromuscular Techniques. Vol 2: The Lower Body. Edinburgh, Churchill Livingstone, 2002. Chaitow L: Positional Release Techniques, 2nd ed. Edinburgh, Churchill Livingstone, 2002. Chaitow L: Palpation and assessment skills, 2nd ed. Edinburgh, Churchill Livingstone, 2003. Church JB, Wiggins MS, Moode FM, et al: Effect of warm-up and flexibility treatments on vertical jump performance. J Strength Cond Res 15(3):332-336, 2001. Cramer JT, Housh TJ, Johnson GO, et al: Acute effects of static stretching on peak torque in women. J Strength Cond Res 18(2):236-241, 2001. Ellenbecker TS: Restoring performance after injury. In Foran B (ed): High Performance Sports Conditioning. Champaign, Ill, Human Kinetics, 2001 pp 327-344. Farfan HF: Biomechanics of the spine in sports. In Watkins RG (ed): The Spine in Sports. St Louis, Mosby, 1996, pp 13-20. Frederick GA, Syzmanski DJ: Baseball (part I): Dynamic flexibility. Strength Cond J 23(1):21-30, 2001. Fritz S, Grosenbach JM: Mosby’s Essential Sciences for Therapeutic Massage, 2nd ed. St Louis, Mosby, 2004. Fritz S: Mosby’s Fundamentals of Therapeutic Massage, 2nd ed. St Louis, Mosby, 2000. Gleim GW, McHugh MP: Flexibility and its effects on sports injury and performance. Sports Med 24(5):289-299, 1997. Gracovetsky SA: The Spinal Engine. New York, Springer-Verlag, 1998. Greenfield B, Catlin PA, Coats PW, et al: Posture in patients with shoulder overuse injuries and healthy individuals. J Orthop Sports Phys Ther 21(5):287-295, 1995. Greenman P: Principles of Manual Medicine. Baltimore, Williams & Wilkins, 1991. Hodges PW, Richardson CA, Jull G: Evaluation of the relationship between laboratory and clinical tests of transverse abdominus function. Physiother Res Int 1:30-40, 1996. Janda V: Janda Compendium (2 vols). Minneapolis, OPTP, 1997. Jones LH, Kusunose R, Goering E: Jones strain-counterstrain. Boise, Idaho: Jones Strain-Counterstrain, Inc., 1995. Kendall FP, McCreary EK: Muscle testing and function, 3rd ed. Baltimore, Williams & Wilkins, 1983. Knudson DV, Noffal GJ, Bahamonde RE, et al: Stretching has no effect on tennis serve performance. J Strength Cond Res 18(3):654-656, 2004. Korr I: Neurobiological mechanisms in manipulation. New York, Plenum Press, 1980.
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Kurz T: Stretching Scientifically: A Guide to Flexibility Training, 4th rev ed. Island Pond, Vt, Stadion Publishing, 2003. Lacote M, Chevalier AM, Miranda A, et al: Clinical Evaluation of Muscle Function. Edinburgh, Churchill Livingstone, 1987. Lee D: The Pelvic Girdle, 2nd ed. Edinburgh, Churchill Livingstone, 1999. Lewit K: Manipulative Therapy in Rehabilitation of the Motor System, 3rd ed. London, Butterworths, 1999. Liebenson C: Muscular relaxation techniques. J Manip Physiol Ther 12(6): 446-454, 1990. Liebenson C: Active muscular relaxation techniques (Part 2). J Manip Physiol Ther 13(1): 2-6, 1990. Liebenson C: (ed): Rehabilitation of the Spine. Baltimore, Williams & Wilkins, 1996. Liebenson C: Sensory motor training. Journal of Bodywork and Movement Therapies 5(1):21-27, 2001. Lukasiewiscz AC, McClure P, Michener L, et al: Comparison of 3-dimensional scapular position and orientation between subjects with and without shoulder impingement. J Orthop Sports Phys Ther 29(10):574-586, 1999. Magee D: Orthopedic Physical Assessment, 3rd ed. Philadelphia, WB Saunders, 1997. Mangine B, Nuzzo G, Harrelson GL: Physiologic factors of rehabilitation. In Andrews JR, Harrelson GL, Wilk KE (eds) Physical Rehabilitation of the Injured Athlete, 3rd ed. Philadelphia, WB Saunders, 2004, pp 13-33. McAtee RE: Facilitated Stretching. Champaign, Ill, Human Kinetics, 1993. McGill S: Ultimate Back Fitness and Performance. Waterloo, Ont, Wabbuno Publishers, 2004. McGill S: Low Back Disorders: Evidence-Based Prevention and Rehabilitation. Champaign, Ill, Human Kinetics, 2002. Merrick MA: Therapeutic modalities as an adjunct to rehabilitation. In Andrews JR, Harrelson GL, Wilk KE: (eds) Physical Rehabilitation of the Injured Athlete, 3rd ed. Philadelphia, WB Saunders, 2004, pp 51-98. Myers T: Anatomy Trains: Myofascial Meridians for Manual and Movement Therapists. Edinburgh, Churchill Livingstone, 2002. Norris CM: Sports Injuries: Diagnosis and Management, 3rd ed. London, Butterworth-Heinemann, 2004. Norris C: Back Stability. Champaign, Ill, Human Kinetics, 2000. O’Sullivan PB, Twomey LT, Allison GT: Altered abdominal muscle recruitment in patients with chronic back pain following a specific exercise intervention. J Orthop Sports Phys Ther 27(2):114-124, 1998.
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Porterfield JA, Derosa C: Mechanical Low Back Pain: Perspectives in Functional Anatomy, 2nd ed. Philadelphia, WB Saunders, 1998. Richardson C, Jull G, Hodges P, Hides J: Therapeutic Exercise for Spinal Segmental Stabilization in Low Back Pain. Edinburgh, Churchill Livingstone, 1999. Rothbart BA: Medial column foot systems: An innovative tool for improving posture. Journal of Bodywork and Movement Therapies 6(1):37-46, 2002. Sahrmann SA: Diagnosis and treatment of movement impairment syndromes. Baltimore, Williams & Wilkins, 2002. Shrier I: Stretching before exercise does not reduce the risk of local muscle injury: A critical review of the clinical and basic science literature. Clin J Sports Med 9(4):221-227, 1999. Simons D, Travell J, Simons L: Myofascial Pain and Dysfunction: The Trigger Point Manual, vol 1: Upper Half of Body, 2nd ed. Baltimore, Williams & Wilkins, 1999. Solem-Bertott E, Thuomas KA, Westerberg CE: The influence of scapular retraction and protraction on the width of the subacromial space: An MRI study. Clin Orthop Relat Res (296):99-103, 1993. Thacker SB, Gilchrist J, Stroup DF, et al: The impact of stretching on sports injury risk: A systematic review of the literature. Med Sci Sports Exerc 36(3):371-378, 2004. Thompson B: Ankle pain (chronic) with associated low back pain. In Chaitow L, DeLany J (eds): Clinical Application of Neuromuscular Techniques: Practical Case Study Exercises. Edinburgh, Churchill Livingstone, 2005. Travell J, Simons D: Myofascial Pain and Dysfunction: The Trigger Point Manual, vol 2: The Lower Extremities. Baltimore, Williams & Wilkins, 1993. Warner JJ, Micheli LJ, Arslanian LE, et al: Scapulothoracic motion in normal shoulders and shoulders with glenohumeral instability and impingement: A study using Moiré topographic anaylsis. Clin Orthop Relat Res (285):191-199, 1992. Wenos DL, Konin JG: Controlled warm up intensity enhances hip range of motion. J Strength Cond Res 18(3):529-533, 2004. Watkins RG (ed): The Spine in Sports. St Louis, Mosby, 1996. Young WB, Behm DG: Should static stretching be used during a warm up for strength and power activities? Strength Cond J 24(6):33-37, 2002.
9/19/08 7:16:32 PM
CHAPTER 58 Interval Sport Programs
for the Shoulder Kevin E. Wilk, Michael M. Reinold, and Adam C. Olsen
Rehabilitation specialists commonly observe injuries to the upper extremities of overhead athletes. Traditional nonoperative and postoperative rehabilitation programs for these athletes involve a gradual restoration of range of motion (ROM), strength, muscular endurance, dynamic stabilization, and neuromuscular control.1,2 On successful completion of the early phases of the rehabilitation program, a gradual, controlled return to sports activities has been advocated by several clinicians.1-7
exercise program such as the Thrower’s 10 Program (Appendix III).2,6,7 The strengthening program should achieve a balance between anterior and posterior musculature, but special emphasis should be given to the posterior rotator cuff and scapular musculature for any strengthening program.1,2 The rehabilitation program should follow a sequential order of alternating days.6 All strengthening, plyometric, and neuromuscular control drills should be performed three times per week (with a day off in between) on the same day as the ISP. The athlete should warm up, stretch, and perform one set of each exercise before the ISP, followed by two sets of each exercise after the ISP. This provides an adequate warm-up but also ensures maintenance of necessary range of motion and flexibility of the upper extremity. Cryotherapy may be used after the rehabilitation program to minimize pain and inflammation.
An interval sport program (ISP) is a functional rehabilitation course that simulates sport activities. These programs progressively apply forces to the healing structures and are intended to gradually return the athlete to full athletic competition as quickly and safely as possible. This chapter describes specific interval sport programs to return athletes in baseball, softball, football, tennis, and golf to competition following an injury or surgery.
The alternate days are used for lower extremity, cardiovascular, and core stability training. The athlete also performs ROM and light strengthening exercises emphasizing the posterior rotator cuff and scapular muscles.6 The cycle is repeated throughout the week with the seventh day designated for rest and light ROM and stretching exercises. To advance to the next step of the ISP, the athlete must be able to perform it a set number of consecutive sessions without pain at the surgical or injury site. If pain or difficulty occurs, the athlete returns to the previous level or attempts the same step during the next ISP session.
PRINCIPLES OF INTERVAL SPORT PROGRAMS ISPs are used to return upper extremity function after injury or surgery by gradually progressing through graduated sport-specific activities. An athlete can begin an ISP following a satisfactory clinical examination demonstrating full ROM, minimal pain or tenderness, adequate dynamic stabilization, and sufficient strength and muscular endurance.8,9 The ISP is initiated on clearance by the athlete’s physician to resume sport activities and is performed under the supervision of the rehabilitation team (physician, physical therapist, and athletic trainer).
INTERVAL BASEBALL THROWING
The ISP is set up to minimize the chance of reinjury and emphasizes warm-up and stretching. There is no set timetable for completing the program because the athlete’s age, skill level, goals, injury, and timing within the competitive season vary for each athlete. The athlete should follow the program rigidly, because this is the safest route to return to competition. Highly competitive athletes who wish to return to competition quickly tend to increase the intensity of the ISP. This can increase the incidence of reinjury and can hinder the rehabilitation process.
For the throwing athlete, the number of throws, distances, intensities, and types of throws are monitored and progressed to facilitate a successful return to competition.10,11 The baseball throwing program is organized into two phases: phase I, a long-toss program and flat ground throwing program (Box 58-1), and phase II, an off-themound program for pitchers (Box 58-2).
Long Toss The interval long-toss program is performed by all baseball players, positional or pitchers. The throwing mechanics performed in the long-toss program uses a crow-hop
Each ISP has a general activity outline. The athlete should supplement the ISP with a high-repetition, low weight 789
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THE ATHLETE’S SHOULDER
BOX 58-1.
Interval Throwing Program for Baseball Players, Phase I
All throws are on an arc with a crow-hop. Warm-up throws consist of 10 to 20 throws at approximately 30 feet. The throwing program is performed every other day, 3 times per week, unless otherwise specified by your physician or rehabilitation specialist. Perform each step _____ times before progressing to next step.
45-Foot Phase STEP 1
90-Foot Phase STEP 5
Warm-up throwing 25 throws to 90 ft Rest 5-10 min Warm-up throwing 25 throws to 90 ft STEP 6
Warm-up throwing
Warm-up throwing
25 throws to 90 ft
25 throws to 45 ft
Rest 5-10 min
Rest 5-10 min
Warm-up throwing
Warm-up throwing
25 throws to 90 ft
25 throws to 45 ft
Rest 5-10 min
STEP 2
Warm-up throwing
Warm-up throwing 25 throws to 45 ft Rest 5-10 min
25 throws to 90 ft
120-Foot Phase STEP 7
Warm-up throwing
Warm-up throwing
25 throws to 45 ft
25 throws to 120 ft
Rest 5-10 min
Rest 5-10 min
Warm-up throwing
Warm-up throwing
25 throws to 45 ft
25 throws to 120 ft
60-Foot Phase
STEP 8
STEP 3
Warm-up throwing
Warm-up throwing
25 throws to 120 ft
25 throws to 60 ft
Rest 5-10 min
Rest 5-10 min
Warm-up throwing
Warm-up throwing
25 throws to 120 ft
25 throws to 60 ft
Rest 5-10 min
STEP 4
Warm-up throwing 25 throws to 60 ft Rest 5-10 min
Warm-up throwing 25 throws to 120 ft
150-Foot Phase STEP 9
Warm-up throwing
Warm-up throwing
25 throws to 60 ft
25 throws to 150 ft
Rest 5-10 min
Rest 5-10 min
Warm-up throwing
Warm-up throwing
25 throws to 60 ft
25 throws to 150 ft
Continued
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INTERVAL SPORT PROGRAMS FOR THE SHOULDER
BOX 58-1.
Interval Throwing Program for Baseball Players, Phase I—cont’d
STEP 10
Warm-up throwing 25 throws to 150 ft Rest 5-10 min Warm-up throwing 25 throws to 150 ft Rest 5-10 min Warm-up throwing 25 throws to 150 ft
180-Foot Phase STEP 11
25 throws to 180 ft Rest 5-10 min Warm-up throwing 25 throws to 180 ft Rest 5-10 min Warm-up throwing 15 throws, progressing from 120 ft to 90 ft STEP 14
Return to respective position or
Warm-up throwing
Progress to Flat-Ground Throwing for Baseball Pitchers
25 throws to 180 ft
Flat-Ground Throwing for Baseball Pitchers
Rest 5-10 min Warm-up throwing 25 throws to 180 ft STEP 12
STEP 14
Warm-up throwing 10-15 throws to 60 ft 10 throws to 90 ft
Warm-up throwing
10 throws to 120 ft
25 throws to 180 ft
20-30 throws to 60 ft (flat ground) using pitching mechanics
Rest 5-10 min
STEP 15
Warm-up throwing
Warm-up throwing
25 throws to 180 ft
10-15 throws to 60 ft
Rest 5-10 min
10 throws to 90 ft
Warm-up throwing
10 throws to 120 ft
25 throws to 180 ft
20-30 throws to 60 ft (flat ground) using pitching mechanics
STEP 13
Warm-up throwing 25 throws to 180 ft
10-15 throws to 60 ft
Rest 5-10 min
20 throws to 60 ft (flat ground) using pitching mechanics
Warm-up throwing
Progress to Phase II—Throwing Off the Mound
45 ft ⫽ 13.7 m; 60 ft ⫽ 18.3 m; 90 ft ⫽ 27.4 m; 120 ft ⫽ 36.6 m; 150 ft ⫽ 45.7 m; 180 ft ⫽ 54.8 m.
technique similar to throwing from the outfield. This technique uses a hop, skip, and throw to accentuate lower body and trunk involvement in the throwing motion. The crow-hop method simulates the throwing act, allowing an emphasis on proper body mechanics. Throwing flatfooted encourages improper body mechanics and places increased stresses on the throwing shoulder. The thrower progresses through each step with the ultimate goal of throwing 75 repetitions at 180 feet without pain (step 13)
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for positional players and 120 feet without pain (step 8) for most pitchers.
Off-the-Mound Throwing Once the pitcher can perform 75 throws from 120 feet along with flat-ground throwing without pain, most pitchers may begin throwing from the mound. Occasionally, a specific athlete is accustomed to throwing from
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THE ATHLETE’S SHOULDER
BOX 58-2.
Interval Throwing Program for Baseball Players, Phase II: Throwing Off the Mound
All throwing off the mound should be done in the presence of your pitching coach or sport biomechanist to stress proper throwing mechanics.
Stage Two: Fastballs Only
Use speed gun to aid in effort control.
15 throws in batting practice
Use interval throwing 120 ft (36.6m) phase as the warm-up.
STEP 10
Stage One: Fastballs Only
STEP 9
60 throws off mound at 75% effort
50-60 throws off mound at 75% effort
STEP 1
30 throws in batting practice
Interval throwing
STEP 11
15 throws off mound at 50% effort
45-50 throws off mound at 75% effort
STEP 2
45 throws in batting practice
Interval throwing
Stage Three
30 throws off mound at 50% effort
STEP 12
STEP 3
Warm-up: 30 throws off mound at 75% effort
Interval throwing 45 throws off mound at 50% effort
15 throws off mound at 50% effort (begin breaking balls)
STEP 4
45-60 throws in batting practice (fastball only)
Interval throwing
STEP 13
60 throws off mound at 50% effort
30 throws off mound at 75% effort
STEP 5
30 breaking balls 75%
Interval throwing
30 throws in batting practice
70 throws off mound at 50% effort
STEP 14
STEP 6
30 throws off mound at 75% effort
45 throws off mound at 50% effort 30 throws off mound at 75% effort
60-90 throws in batting practice (gradually increase breaking balls)
STEP 7
STEP 15
30 throws off mound at 50% effort
Simulated game, progressing by 15 throws per workout (pitch count)
45 throws off mound at 75% effort STEP 8
10 throws off mound at 50% effort 65 throws off mound at 75% effort
longer distances. In this situation, the athlete continues to progress the long toss program as outlined to 150 or 180 feet. In the phase II throwing program from the mound, the number of throws, intensity (speed), and type of pitch are monitored and systematically progressed. The phase II program is subdivided into three progressive components that allow the pitcher to return to symptom-free athletic participation. In stage I, mechanics and velocity are emphasized during fastball pitching only. In stage II, mechanics, ball location, and confidence are emphasized as the pitcher begins throwing to the hitter. In stage III, breaking balls (curve balls, sliders) are initiated as the final progression before return to competition. If the athlete complains of pain or an inability to throw at a particular stage, we encourage a
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light toss program. This program is performed at about 70% intensity from 60 to 75 feet, allowing the pitcher to continue to throw while symptoms dissipate.
Accelerated Throwing Programs Certain in-season injuries require an accelerated throwing program to expedite a return to sport. Depending on the severity of the injury, an athlete can follow a shorter throwing program, such as 14- or 21-day interval throwing programs (Boxes 58-3 and 58-4). Each program integrates portions of the interval throwing program with shoulder flexibility and strengthening exercises. The athlete’s symptoms are monitored throughout and guide the throwing progression. Unlike the extended version,
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INTERVAL SPORT PROGRAMS FOR THE SHOULDER
BOX 58-3.
Interval Throwing Program: 14-Day Progression
Days 1-3 Stretching • ER/IR at 90 degrees of abduction, flexion, horizontal adduction Strengthening • • • • •
793
ER/IR tubing Full can Prone rowing Biceps Side-lying ER dumbbells
• Throw on a line to 90 ft, 2 sets of 25-30 throws
Day 12 Thrower’s 10 Program • Plyometrics
Day 13 Stretching • ER/IR at 90 degrees of abduction, flexion, horizontal adduction STRENGTHENING
• Scapular strengthening • Core stabilization
• • • • •
Stretching
Throwing
Throwing
• Throw on a line to 90 feet, 3 sets of 25-30 throws
• Play catch 30-45 ft, 25-30 throws
Day 14
Days 4-6 Thrower’s 10 Program
Days 7-9 Thrower’s 10 Program • Rhythmic stabilization • Plyometrics
Day 10 Thrower’s 10 Program Stretching Throwing • Play catch 45-60 ft, 2 sets of 25-30 throws
Day 11 Thrower’s 10 Program
ER/IR tubing Full can Prone rowing Biceps Side-lying ER dumbbells
Stretching • ER/IR at 90 degrees of abduction, flexion, horizontal adduction Strengthening • ER/IR tubing • Full can • Prone rowing • Biceps • Side-lying ER dumbbells Throwing • Throw from mound at 50% effort, 45-50 throws • Progress throwing program from mound or position as tolerated according to symptom
Stretching Throwing
ER, external rotation; IR, internal rotation.
throwing may occur on consecutive days within the prescribed intervals.
Little League The adolescent baseball player presents a different challenge for the clinician. The Little League interval throwing program is similar to the previously discussed throwing program, with two distinct differences: The throwing distances are shorter and the number of throws is smaller (Box 58-5). The young thrower is encouraged to progress slowly though these steps and re-establish good throwing mechanics before any return to competitive activity. The
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adolescent thrower is encouraged to master control and change of velocity in place of breaking balls, which can cause deleterious stress on the elbow and shoulder complex.
Interval Hitting Program Generally, before the athlete is ready to begin throwing, he or she is able to return to team hitting activities. In preparation for full-force swings, the interval hitting program is broken down into three phases (Box 58-6). The phase progression provides the gradual tissue load necessary to condition the shoulder for the dynamic
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THE ATHLETE’S SHOULDER
BOX 58-4.
Interval Throwing Program: 21-Day Progression
Day 1 30 throws to 45 ft 30 throws to 60 ft
Day 2 45 throws to 45 ft
60 throws to 120 ft 20 throws to 60 ft
Day 12 Rest
Day 13
45 throws to 60 ft
100 throws to 60 ft
Day 3
Bullpen pitching (fastballs only)
125 throws to 60 ft
Day 4 85 throws to 60 ft
25 pitches at 75% effort
Day 14 50 throws to 45 ft
30 throws to 90 ft
30 throws to 90 ft
20 throws to 60 ft
20 throws to 120 ft
Day 5
50 throws to 45 ft
Rest
Day 6 100 throws to 60 ft 30 throws to 90 ft 20 throws to 60 ft
Day 7 50 throws to 60 ft
Day 15 100 throws to 60 ft Bullpen pitching (fastballs and change-ups) 35 pitches at 80% effort
Day 16 Rest
Day 17
50 throws to 90 ft
100 throws to 60 ft
50 throws to 60 ft
Bullpen pitching (all pitches)
Day 8
45 pitches at 100% effort
50 throws to 60 ft
Day 18
50 throws to 90 ft
50 throws to 45 ft
25 throws to 120 ft
30 throws to 90 ft
20 throws to 60 ft
20 throws to 120 ft
Day 9
50 throws to 45 ft
Rest
Day 10 50 throws to 60 ft
Day 19 Simulated game (25 pitches)
Day 20
20 throws to 90 ft
50 throws to 45 ft
50 throws to 120 ft
30 throws to 90 ft
20 throws to 60 ft
20 throws to 120 ft
Day 11
50 throws to 45 ft
50 throws to 60 ft 20 throws to 90 ft
Day 21 Game (25-35 pitches)
45 ft ⫽ 13.7 m; 60 ft ⫽ 18.3 m; 90 ft ⫽ 27.4 m; 120 ft ⫽ 36.6 m; 150 ft ⫽ 45.7 m; 180 ft ⫽ 54.8 m.
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INTERVAL SPORT PROGRAMS FOR THE SHOULDER
BOX 58-5.
795
Little League Interval Throwing Program
30-Foot Phase STEP 1
Warm-up throwing 25 throws to 30 ft Rest 15 min
Rest 15 min Warm-up throwing 25 throws to 60 ft STEP 6
Warm-up throwing
Warm-up throwing
25 throws to 60 ft
25 throws to 30 ft
Rest 10 min
STEP 2
Warm-up throwing 25 throws to 30 ft Rest 10 min Warm-up throwing 25 throws to 30 ft Rest 10 min
Warm-up throwing 25 throws to 60 ft Rest 10 min Warm-up throwing 25 throws to 60 ft
90-Foot Phase STEP 7
Warm-up throwing
Warm-up throwing
25 throws to 30 ft
25 throws to 90 ft
45-Foot Phase
Rest 15 min
STEP 3
Warm-up throwing 25 throws to 45 ft Rest 15 min
Warm-up throwing 25 throws to 90 ft STEP 8
Warm-up throwing
Warm-up throwing
20 throws to 90 ft
25 throws to 45 ft
Rest 10 min
STEP 4
Warm-up throwing 25 throws to 45 ft Rest 10 min Warm-up throwing 25 throws to 45 ft Rest 10 min Warm-up throwing 25 throws to 45 ft
Warm-up throwing 20 throws to 60 ft Rest 10 min Warm-up throwing 20 throws to 45 ft Rest 10 min Warm-up throwing 15 throws to 45 ft
60-Foot Phase STEP 5
Warm-up throwing 25 throws to 60 ft 30 ft, 9.1 m; 45 ft ⫽ 13.7 m; 60 ft ⫽ 18.3 m; 90 ft ⫽ 27.4 m.
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THE ATHLETE’S SHOULDER
BOX 58-6.
Interval Hitting Program
Hit 3 times per week with 1 day off between workouts. Perform each step for 2 days before progressing to the next step.
Off a Tee Stand STEP 1
15-20 swings at 50% effort
STEP 6
15-20 swings at 50%-60% effort STEP 7
2 sets of 20-25 swings at 65%-70% effort STEP 8
2 sets of 25 swings at 80%-90% effort
STEP 2
Batting Practice Swings
2 sets of 15 swings at 50% effort
Warm-up with soft toss swings
STEP 3
STEP 9
2 sets of 15 swings at 65%-70% effort
2 sets of 25 swings at 50%-65% effort
STEP 4
STEP 10
2 sets of 20-25 swings at 70%-75% effort
2 sets of 30 swings at 70%-75% effort
STEP 5
STEP 11
2 sets of 25 swings at 80%-90% effort
2 sets of 30-35 swings at 80%-90% effort
Soft Toss Swings Warm-up using a tee stand
force of the swing. The athlete begins in phase I with hitting off a tee stand. Dry swinging (without making contact with a ball) is not encouraged for most athletes because the motion is often jerky and does not simulate the natural swing motion that occurs when contact is made. The intensity of swing and number of swings are progressed through a series of five steps. For the athlete to progress, he or she must perform the step for 2 days without pain or tenderness. The hitting athlete progresses to soft-toss swings during phase II. In preparation for game hitting, phase III of the hitting program involves batting practice swings. The athlete progresses to a swing up to 80% to 90% intensity against live pitching. On successful completion of the interval hitting program, the patient should be ready to fill a designated-hitter role with the team while progressing through the throwing program.
Softball A growing number of adolescents are playing softball, and with this growth comes a greater incidence of injury to these athletes. The softball thrower begins at 35 feet and progresses through a series of eight steps up to 100-foot throws (Box 58-7). The program controls for the number of throws and for distance. The softball pitcher must successfully complete the phase I long toss program before beginning windmill throws from the mound. Number of throws and intensity of throws are controlled for, as well as type of pitch. The throwing progression from the mound mirrors that of the baseball mound throwing program. Pitchers begin with fastballs during the first two stages before beginning breaking balls in
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stage III. The pitcher throws batting practice in stage II and performs simulated game pitching in phase III. During the interval pitching phase, proper mechanics must be stressed to prevent reinjury.
INTERVAL FOOTBALL THROWING For the football interval throwing program, a unique dilemma occurs. Unlike a pitcher who throws from a consistent stance and surface, the quarterback must be trained to throw from different angles and stances. No matter the situation, the quarterback must be coached to establish a base of support before throwing to decrease the forces at the shoulder. Power should be gathered from the core. The thrower begins each step with light warm-up tossing through an arc (Box 58-8). The throwing program controls for number and distance of throws. During steps 12 through 14, the quarterback begins with roll-out passes for game-like situations.
INTERVAL TENNIS The same principles of the interval program can be followed for racquet sports such as tennis or racquetball (Table 58-1). The program for the tennis player progresses from a limited number of forehand and backhand ground strokes, gradually increasing the number of these strokes over a period of 2 to 3 weeks. During this time, the player gradually initiates overhead and service strokes in combination with ground strokes. The athlete begins playing games during the fourth week of this
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INTERVAL SPORT PROGRAMS FOR THE SHOULDER
BOX 58-7.
797
Softball Interval Throwing Program
35-Foot Phase STEP 1
Warm-up throwing 25 throws to 35 ft Rest 10 min Warm-up throwing 25 throws to 35 ft STEP 2
Warm-up throwing
Rest 5-10 min Warm-up throwing 25 throws to 65 ft STEP 6
Warm-up throwing 25 throws to 65 ft Rest 5-10 min Warm-up throwing
25 throws to 35 ft
25 throws to 65 ft
Rest 10 min
Rest 5-10 min
Warm-up throwing
Warm-up throwing
25 throws to 35 ft
25 throws to 65 ft
Rest 10 min
100-Foot Phase
Warm-up throwing 25 throws to 35 ft
50-Foot Phase STEP 3
STEP 7
Warm-up throwing (65 ft) 25 throws to 100 ft Rest 5-10 min
Warm-up throwing (35 ft)
Warm-up throwing
25 throws to 50 ft
25 throws to 100 ft
Rest 10 min
STEP 8
Warm-up throwing 25 throws to 50 ft STEP 4
Warm-up throwing 20 throws to 100 ft Rest 5-10 min
Warm-up throwing
Warm-up throwing
25 throws to 50 ft
20 throws to 65 ft
Rest 10 min
Rest 5-10 min
Warm-up throwing
Warm-up throwing
25 throws to 50 ft
20 throws to 50 ft
Rest 5-10 min
Rest 5-10 min
Warm-up throwing
Warm-up throwing
25 throws to 50 ft
15 throws to 50 ft
65-Foot Phase STEP 5
Warm-up throwing (50 ft) 25 throws to 65 ft
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THE ATHLETE’S SHOULDER
BOX 58-8.
Football Throwing Program
Throw every other day, unless directed otherwise by your physician, therapist, or trainer.
Step 10
Step 1
20-25 throws to 20-25 yd
Warm-up tossing
Warm-up tossing
20-25 throws to 45-55 yd
20-25 throws to 15-20 yd
Step 2
20-25 throws to 30-35 yd
Warm-up tossing
20-25 throws to 10-15 yd (on a line)
25-30 throws to 15-25 yd
Step 11
Step 3
Warm-up tossing
Warm-up tossing
15-20 throws to 20-30 yd
2 sets of 25 throws to 20-25 yd
20-25 throws to 40-50 yd
Step 4
20-25 throws to 30-40 yd
Warm-up tossing 2 sets of 25-30 throws to 25 yd
Step 5 Warm-up tossing 25-30 throws to 30-35 yd
Step 6
20-25 throws to 10-20 yd (on a line) 15-20 throws to 20-30 yd (on a line)
Step 12 Warm-up tossing 15 throws to 20-30 yd
Warm-up tossing
20 throws to 40-50 yd
2 sets of 30 throws to 35 yd
20 throws to 30-40 yd
Step 7
20 throws to 10-20 yd (on a line)
Warm-up tossing 10-15 throws to 40 yd 20 throws to 25-30 yd
20 throws to 20-30 yd (on a line) 15 throws (roll out to throwing side)
Step 13
20 throws to 20-25 yd (on a line)
Warm-up tossing
Step 8
15 throws to 20-30 yd
Warm-up tossing 20 throws to 40-50 yd 20 throws to 25-30 yd 20 throws to 20-25 yd
20 throws to 40-50 yd 20 throws to 30-40 yd 20 throws to 10-20 yd (on a line)
Step 9
20 throws to 20-30 yd (on a line)
Warm-up tossing
15 throws (roll out to throwing side)
20 throws to 25-35 yd
15 throws (roll to nonthrowing side)
20 throws to 40-50 yd
Step 14
20 throws to 20 yd (on a line)
Warm-up tossing
10-15 throws to 10-15 yd out (on a line)
Progress to practice situation
interval program. Occasionally, it is necessary to delay this activity because of the patient’s individual rehabilitation progression and underlying pathology. The clinician is encouraged to monitor the athlete’s signs and symptoms as the athlete progresses through the stages of functional rehabilitation.
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INTERVAL GOLF One of the most common programs is the interval golf program (Table 58-2). This program begins with chipping and putting, followed by a gradual progression to
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TABLE 58-1 Interval Tennis Program Monday
Wednesday
Friday
Week One
TABLE 58-2 Interval Golf Program Monday
Wednesday
Friday
25 putts 15 chips Rest 5 min 25 chips
20 putts 20 chips Rest 5 min 20 putts 20 chips 10 irons off tee Rest 5 min 10 chips 5 irons off tee
20 chips 15 short irons Rest 10 min 15 short irons 15 chips putting 15 med irons
15 short irons 10 medium irons Rest 10 min 20 short irons 15 chips
15 short irons 10 med irons 10 long irons Rest 10 min 10 short irons 10 med irons 5 long irons 5 woods
15 short irons 15 med irons 10 long irons Rest 10 min 10 short irons 10 med irons 10 long irons 10 woods
Play 9 holes
Play 9 holes
Play 9 holes
Play 18 holes
Week One
12 FH
15 FH
15 FH
8 BH
8 BH
10 BH
Rest 10 min
Rest 10 min
Rest 10 min
13 FH
15 FH
15 FH
7 BH
7 BH
10 BH
25 FH
30 FH
30 FH
15 BH
20 BH
25 BH
Rest 10 min
Rest 10 min
Rest 10 min
25 FH
30 FH
30 FH
15 BH
20 BH
25 BH
20 putts 15 chips Rest 5 min 15 chips
Week Two
Week Three
Week Two 20 chips 10 short irons Rest 5 min 10 short irons 15 med irons (5 irons off tee)
30 FH
30 FH
30 FH
25 BH
25 BH
30 BH
Week Three
10 SR
15 SR
15 SR
Rest 10 min
Rest 10 min
Rest 10 min
30 FH
30 FH
30 FH
25 BH
25 BH
15 SR
10 SR
15 SR
Rest 10 min 30 FH 30 BH 15 SR
15 short irons 20 med irons Rest 10 min 5 long irons 15 short irons 15 med irons Rest 10 min 20 chips
Week Four 30 FH
30 FH
30 FH
30 BH
30 BH
30 BH
10 SR
10 SR
10 SR
Rest 10 min
Rest 10 min
Rest 10 min
Play 3 games
Play 1 set
Play 11⁄2 sets
10 FH
10 FH
10 FH
10 BH
10 BH
10 BH
5 SR
5 SR
3 SR
BH, backhand shots; FH, forehand shots; SR, serves.
short and medium iron strokes. The golfer is encouraged to use a tee with all shots to prevent the deleterious effects of a divot to the shoulder. Once a confident, painfree swing has been re-established, long irons and woods are initiated. The purpose of the interval golf program is to allow golfers time to re-establish their swing pace, weight transfer, and proper mechanics before resuming play. Once play is resumed, the golfer is encouraged to progress to 9 holes twice per week, to 9 holes four or five
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Week Four 15 short irons 10 med irons 10 long irons 10 drives Rest 5 min repeat Week Five Play 9 holes
Note: As you start your program, remember that mechanics plays an important role in your recovery. If you have questions, contact your physician or rehabilitation specialist. Perform flexibility exercises before hitting and use ice after hitting. Recommended clubs: chips, use wedge; drives, use driver; long irons, use 4, 3, or 2 iron; medium irons, use 7, 6, or 5 iron; short irons, use wedge, 9, or 8 iron; woods, use 3 or 5 wood. med, medium.
times per week, to 18 holes several times per week. This allows a gradual improvement of endurance and strength as well as an increase in the player’s tolerance to the microtraumatic stresses of the golf swing. The same principles should be followed with the interval golf program as with the interval baseball program. Proper warm-up, stretching, and strengthening should still be implemented throughout the entire interval golf rehabilitation program.
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INTERVAL JAVELIN THROWING Rehabilitation of the javelin thrower presents a unique set of challenges to the therapist as the athlete returns to throwing. Because the javelin thrower does not seek to hit a target but rather throws for distance, intensity of throw BOX 58-9.
and mass of implement must be controlled for. The athlete begins by warming up with football throws for distance and repetition through a series of six steps before the javelin is introduced (Box 58-9). The second phase uses a 400-g safety javelin. Intensity is controlled for through distance and number of throws. Next, the athlete continues to throw the 400-g javelin but uses a
Interval Javelin Throwing
Football Throws STEP 1
Warm-up throwing 25 throws to 45 ft Rest 10 min Warm-up throwing 25 throws to 45 ft STEP 2
Warm-up throwing
Rest 10 min Warm-up throwing 25 throws to 90 ft STEP 6
Warm-up throwing 25 throws to 90 ft Rest 10 min Warm-up throwing
25 throws to 45 ft
25 throws to 90 ft
Rest 10 min
Rest 10 min
Warm-up throwing
Warm-up throwing
25 throws to 45 ft
25 throws to 90 ft
Rest 10 min
400-g Safety Javelin Throws
Warm-up throwing 25 throws to 45 ft STEP 3
Warm-up throwing 25 throws to 60 ft Rest 10 min Warm-up throwing 25 throws to 60 ft STEP 4
STEP 7
Warm-up throwing* 25 throws to 45 ft Rest 10 min Warm-up throwing* 25 throws to 45 ft STEP 8
Warm-up throwing 25 throws to 45 ft
Warm-up throwing
Rest 10 min
25 throws to 60 ft
Warm-up throwing
Rest 10 min
25 throws to 45 ft
Warm-up throwing
Rest 10 min
25 throws to 60 ft
Warm-up throwing
Rest 10 min
25 throws to 45 ft
Warm-up throwing
STEP 9
25 throws to 60 ft STEP 5
Warm-up throwing 25 throws to 60 ft
Warm-up throwing
Rest 10 min
25 throws to 90 ft
Warm-up throwing
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BOX 58-9.
801
Interval Javelin Throwing—cont’d
25 throws to 60 ft
Warm-up throwing
STEP 10
25 throws at 50% effort
Warm-up throwing
STEP 15
25 throws to 60 ft
Warm-up throwing
Rest 10 min
25 throws at 75% effort
Warm-up throwing
Rest 10 min
25 throws to 60 ft
Warm-up throwing
Rest 10 min
25 throws at 75% effort
Warm-up throwing
STEP 16
25 throws to 60 ft STEP 11
Warm-up throwing 25 throws at 75% effort
Warm-up throwing
Rest 10 min
25 throws to 90 ft
Warm-up throwing
Rest 10 min
25 throws at 75% effort
Warm-up throwing
Rest 10 min
25 throws to 90 ft
Warm-up throwing
STEP 12
25 throws at 75% effort
Warm-up throwing
STEP 17
25 throws to 90 ft
Warm-up throwing
Rest 10 min
25 throws at 100% effort
Warm-up throwing
Rest 10 min
25 throws to 90 ft
Warm-up throwing
Rest 10 min
25 throws at 100% effort
Warm-up throwing
STEP 18
25 throws to 90 ft
400-g Safety Javelin Throws STEP 13
Warm-up throwing 25 throws at 100% effort Rest 10 min
Warm-up throwing
Warm-up throwing
25 throws at 50% effort
25 throws at 100% effort
Rest 10 min
Rest 10 min
Warm-up throwing
Warm-up throwing
25 throws at 50% effort
25 throws at 100% effort
STEP 14
Warm-up throwing
600-g Safety Javelin Throws STEP 19
25 throws at 50% effort
Warm-up throwing
Rest 10 min
25 throws at 50% effort
Warm-up throwing
Rest 10 min
25 throws at 50% effort
Warm-up throwing
Rest 10 min
25 throws at 50% effort
Continued
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BOX 58-9.
Interval Javelin Throwing—cont’d
STEP 20
Warm-up throwing 25 throws at 50% effort Rest 10 min Warm-up throwing
25 throws at 75% effort Rest 10 min Warm-up throwing 25 throws at 75% effort STEP 23
25 throws at 50% effort
Warm-up throwing
Rest 10 min
25 throws at 100% effort
Warm-up throwing
Rest 10 min
25 throws at 50% effort
Warm-up throwing
STEP 21
Warm-up throwing 25 throws at 75% effort Rest 10 min Warm-up throwing 25 throws at 75% effort
25 throws at 100% effort STEP 24
Warm-up throwing 25 throws at 100% effort Rest 10 min Warm-up throwing
STEP 22
Warm-up throwing
25 throws at 100% effort
25 throws at 75% effort
Rest 10 min
Rest 10 min
Warm-up throwing
Warm-up throwing
25 throws at 100% effort
*May warm up with football throws to 60-75 ft.
percent-intensity scale to control distance. Phase IV uses a 600-gram javelin and perceived intensity to progress the athlete. Throwing is performed every other day, and two consecutive symptom-free sessions are necessary to progress to the next step. The javelin thrower should work closely with a throwing coach to stress proper mechanics to prevent reinjury.
SUMMARY The purpose of interval sport programs is to provide the athlete with established time frames for a gradual, progressive return to sport activities. Athletes are encouraged to progress at their own rate and to regress or stay at the same phase if pain or dysfunction occurs. The athlete is instructed to perform specific flexibility and strengthening exercises before the interval program as a warm-up and afterward as part of a cool-down. Initially, cryotherapy may be used after the interval program if pain or soreness develops. The use of these interval sport programs is encouraged for the competitive or recreational athlete.
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The athletic patient must be encouraged to continue strengthening and flexibility exercises during this returnto-activity phase of rehabilitation. The interval sport programs are not meant to rehabilitate or to get the athlete in shape for competition. The athlete must be in good physical condition to participate in this type of program. The interval program is used for sport-specific training. Therefore, a basic principle supported by the use of these programs is that an athlete must rehabilitate to train for a sport and then perform sport-specific training to participate in sporting activities.
References 1. Wilk KE, Arrigo CA: Current concepts in the rehabilitation of the athlete shoulder. J Orthop Sports Phys Ther 18:365-378, 1993. 2. Wilk KE, Reinold MM, Andrews JR: Postoperative treatment principles in the throwing athlete. Sports Med Arthrosc Rev 9:69-95, 2001. 3. Axe MJ, Snyder-Mackler L, Konin JG, Strube MJ: Development of a distance-based interval throwing program for little league-aged athletes. Am J Sports Med 24:594-602, 1996.
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INTERVAL SPORT PROGRAMS FOR THE SHOULDER
4. Axe MJ, Wickham R, Snyder-Mackler L: Data-based interval throwing programs for little league, high school, college, and professional baseball pitchers. Sports Med Arthrosc Rev 9: 24-34, 2001. 5. Ellenbecker TS, Mattalino AJ: The Elbow in Sport. Champaign, Ill, Human Kinetics; 1997, pp 171-177. 6. Wilk KE, Andrews JR, Arrigo CA, et al: Preventive and Rehabilitative Exercises for the Shoulder and Elbow, 6th ed. Birmingham, Ala, American Sports Medicine Institute, 2001. 7. Wilk KE, Reinold MM, Dugas JR, Andrews JR: Rehabilitation following thermal-assisted capsular shrinkage of the glenohumeral joint: Current concepts. J Orthop Sports Phys Ther 32:268-292, 2002. 8. Wilk KE, Andrews JR, Arrigo CA, et al: The strength characteristics of the internal and external rotator muscles in professional baseball pitchers. Am J Sports Med 21:61-69, 1993.
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9. Wilk KE, Arrigo CA, Andrews JR: The abductor and adductor strength characteristics of professional baseball pitchers. Am J Sports Med 23(3):307-311, 1995. 10. Fleisig GS, Escamilla RF, Barrentine SW, et al: Kinematic and kinetic comparison of baseball pitching from a mound and throwing from flat ground. Presented at the 20th Annual Meeting of the American Society of Biomechanics, Atlanta, Georgia, October 17-19, 1996. 11. Fleisig GS, Zheng, Barrentine SW, et al: Kinematic and kinetic comparison of full-effort and partial-effort baseball pitching. Presented at the 20th Annual Meeting of the American Society of Biomechanics, Atlanta, Georgia, October 17-19, 1996.
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CHAPTER 59 Taping, Padding, and Bracing
for the Shoulder Complex Jeff G. Konin, Thomas J. Kuster III, and Mark D. Miller
HISTORY OF PROTECTIVE EQUIPMENT
schools where coaches, managers, and student assistants are responsible for adequately fitting equipment, although they might not have the proper training, knowledge, and techniques for this task. A qualified professional must fit any type of preventive equipment and each athlete must be fitted individually.
Protective equipment, taping, padding, and bracing are commonly performed treatment adjuncts for the sports medicine professional. The lack of documentation makes it unclear when protective equipment was first used. As described by Plutarch, it is believed that protective equipment was first used in ancient times when Termerus destroyed his enemies by running into them head first. The first use of adhesive substances as external devices can be dated back to ancient times as well. The Greeks have been credited with formulating a healing paste composed of lead oxide, olive oil, and water, which was used for many different skin conditions.1
Protective equipment can be manufactured commercially or it can be fabricated on the spot by the fitter. Regardless of the nature of production, five basic concepts should be addressed with each piece of material or equipment:2 • Does the equipment protect the area of concern appropriately? • Can the athlete perform the skills required for his or her sport and position while wearing the device? • Will the device maintain a proper anatomic position? • Is the device potentially hazardous or injurious to other participants? • Is the device legal by the rules and regulations of the athlete’s particular sport?
Today, the difficulty lies not in finding protective equipment or padding but instead in choosing an appropriate, costeffective device that is appropriate to a specific function and protects an athlete from injury. Manufacturers have progressed in technology, and variously designed forms of athletic tapes, pads, and equipment are commercially available. Many organizations and committees have also been formed to provide rules for the use and conditions of these products.
Fitting Football Shoulder Pads Shoulder pads provide four main functions: absorb shock, protect the shoulders, protect the chest, and fit the midcervical spine to the trunk.3-7
PURPOSE OF PROTECTIVE EQUIPMENT
Proper fit to the chest is important in distributing the shock to the shoulders evenly. Better shoulder protection should allow one to de-emphasize the use of the head as a blocking and tackling instrument. Improperly fitted equipment can cause injury or increase the severity of an injury. Those who fit the shoulder pads must be extremely knowledgeable about fitting techniques.
The primary purpose of protective equipment and padding is to disperse and absorb forces of a blow by spreading them over a larger area than the initial point of contact, thus reducing the number and severity of injuries. For many sports, particularly those involving high levels of contact (e.g., football, lacrosse, ice hockey), protective equipment is part of the uniform. The idea behind this concept is to protect body parts prone to repeated blows or traumatic contact by the nature of the sport.
There are two basic types of shoulder pads: flat pads and cantilever pads (Fig. 59-1).5 Quarterbacks and receivers use flat pads because they allow greater glenohumeral motion. The cantilever pads are named for the bridge that extends over the superior portion of the shoulder and are worn by players who are in constant contact. There are two components of cantilever pads, the inside and the outside. The inside cantilever is more common, but the outside cantilever provides more protection with a larger blocking surface, and thus are used by linemen. Some pads are specifically designed with larger anterior surfaces that are
PREVENTIVE AND PROTECTIVE EQUIPMENT Injuries can be caused not only by inadequate protection from equipment but also by improper fitting of the equipment. An example of this takes place at many secondary 805
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Figure 59-1. Two types of shoulder pads: flat (A) and cantilever (B).
A
slanted slightly forward for players who receive blows in a standing position. In some cases, anthropometric calipers may be used to help properly fit shoulder pads. With this device, a measurement is taken from the edge of the shoulder across to the opposite shoulder. A similar measurement is then made on the undersurface of the pad and etched on the anterior surface of the pad. These measurements are then used to derive a correct size. Calipers are primarily used to speed the process of fitting. However, all principles of fitting should still be followed for a complete and proper fit. When applying shoulder pads for a fitting evaluation, the following points should be addressed:1,3,4 • The tip of the shoulder pad should fit just to the lateral edge of the shoulder • The neck opening should be large enough for a player to extend the arm overhead without impinging the neck and not allowing any excessive sliding about the shoulder. Neck openings that are too small can compress the cervical or deltoid regions. Pads with excessively large neck openings can cause cervical or acromioclavicular injuries. • Elastic straps holding the pads to the chest and back must be tight yet comfortable, allowing equal distribution of forces. • The flaps (epaulets) on the lateral aspects of the pads should completely cover the deltoid region. Additional epaulets may be attached to cover the deltoids adequately. • The anterior portion of the pads must adequately cover the sternum and clavicle and the posterior aspect of the pads must completely cover the scapulae. In addition to the two standard types of shoulder pads for football players, there are a few commercially manufactured devices that further protect specific areas of the shoulder complex and surrounding areas (discussed later). There are also differently designed forms of shoulder girdle protection for those playing men’s lacrosse and ice hockey. Because these sports have a high contact and collision
Ch59_805-816-F06701.indd 806
B
component, men’s lacrosse and ice hockey shoulder pads are designed similar to football pads. Men’s football, ice hockey, and lacrosse pads are all designed to provide chest protection and glenohumeral protection while allowing a functional range of motion. Ice hockey pads protect against high collision forces, much like football pads. In men’s lacrosse, it has been demonstrated that a high percentage of acromioclavicular joint dislocations and clavicular fractures occur in attackmen who are struck in the clavicular region by defensemen.8 As a result, lacrosse shoulder pads allow greater protection of the clavicular region with highdensity polyethylene covering the clavicle and acromioclavicular joint.
Maintenance of Equipment All equipment should be inspected with documentation at the beginning and end of each season. Equipment should be constantly observed for damaged parts such as cracks, missing or loose rivets, and nonelastic or fraying straps. All defective equipment should be properly repaired by the manufacturer. Taking time to inspect and recondition faulty equipment adequately is significantly worthwhile because it allows the equipment to provide optimal protection.
Roles and Relationships with the Equipment Manager With organized sports, someone is often designated to oversee equipment. In the high school, college, university, and professional settings, this person is referred to as an equipment manager. The training and experience of an equipment manager vary widely throughout settings. In a high school setting, it is not uncommon to see coaches or parents serve as equipment managers. The same holds true in many recreational sports leagues. So long as the person responsible for ensuring that the equipment is properly maintained and meets current safety standards is competent, then equipment can be properly fitted and used. Otherwise, risk of injury and potential liability issues can arise.
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TAPING, PADDING, AND BRACING FOR THE SHOULDER COMPLEX
Many colleges, universities, and professional teams employ full-time equipment managers who receive formal training. The American Equipment Managers’ Association (AEMA) is the national governing body for equipment managers.9 The purpose of the AEMA is to promote, advance, and improve the equipment managers’ profession in all of its many aspects. This includes improving equipment for the greater safety of all participants in sports and recreation. In 1991, the AEMA initiated a certification program. The educational focus was targeted toward the five major domains equipment managers identified routinely in their jobs: purchasing (17.6%), fitting (22.2%), maintenance and repair (23.4%), management (17.6%), and accountability (19.2%). It is important to have a good relationship with the equipment manager. Communication between the clinician and the equipment manager can ensure the safest care to an athlete at all times. Appropriate modifications can be made to standard equipment to accommodate an athlete who might not otherwise be able to participate in a sporting event due to injury.
TAPING Taping of the shoulder can be a valuable adjunct to properly supervised therapeutic exercise for an injury. Taping is a skill that one can master only with extensive practice. Although at present there is minimal research on the effectiveness of taping the shoulder complex, some important functions of tape have been reported in the literature. These functions include increasing joint stability, limiting joint range of motion, improving kinesthetic awareness, stabilizing compressive-type bandages or padding, and preventing further insult to injury.1,4
Taping Materials Elastic Tape Elastic tape comes in many forms; some common brands are Conform (Bike), Elastikon (Johnson & Johnson), Lightplast (Beiersdorf), and Coban (3M). Elastic tape is made to stretch, so it is highly conforming to the affected area. Elastic tape should to be used when attempting to provide a gentle compressive force on tissues. For the shoulder complex, a rugged yet conforming tape should be used. Elastic tapes can be used to secure protective padding around the areas of the shoulder to which adhesive tape do not conform well. Adhesive Tape The primary use for adhesive (linen) tape is to prevent excessive motion of the joints and to aid in the stability of the functioning ligaments. This type of tape is much
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stronger than elastic tape and is better able to withstand vigorous athletic competition. Like most other types of tape, adhesive tape comes in many colors, sizes, and strengths. Tape width can vary from 0.5 to 3 inches. The most commonly used adhesive tape in athletic training is the cloth-backed variety, which comes in tubes or speed packs. Speed packs are wound more loosely than tubes and can be damaged more easily. Three factors should be considered when purchasing adhesive tape: tape grade, adhesive mass, and winding tension. The strength of linen or cloth-backed tape is graded by the number of longitudinal and vertical threads per inch. A stronger grade of tape backing contains in excess of 85 longitudinal fibers and 65 vertical fibers. In comparison, weaker cloth-backed tape contains 65 longitudinal and 45 vertical fibers or less per inch. Tape grade is always considered in the manufacturer’s expenses.3 Adhesive mass is simply the tape’s ability to adhere to skin surface despite circumstances such as perspiration and physical activity. It is important that the materials composing this mass contain as few irritants as possible and do not damage superficial layers of skin on removal. One of the most important concepts often overlooked when purchasing adhesive tape is the winding tension of each brand. Adhesive tape must contain an even and constant unwinding tension. All principles of taping applications to joints encompass anatomy, biomechanics, and tensile strength of the supporting structures. These techniques are designed with the simple fact that external supportive structures such as tape are of equal tension throughout, therefore not altering any mechanical characteristics of application. Leukotape is a form of hypoallergenic adhesive tape designed to assist with postural deviations by facilitating realignment of structures. This type of tape comes in a number of forms classified by its various label names and is reported to have an elasticity of 130% to 140% of its original length. It is often developed with a rayon backing and a zinc oxide adhesive component, yielding a high tensile strength. Common areas of the shoulder complex where Leukotape is used for treatment include the scapulothoracic, acromioclavicular, and glenohumeral joints. Leukotape is not applied directly to the skin, but rather is placed over another form of tape referred to as CoverRoll Stretch, designed to enhance localized adherence of the taping technique for longer-lasting postural changes.
Principles of Taping A complete taping application for any structure involving the shoulder complex should be effective and comfortable while affording consistent, compressive tension.
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The most important aspect of taping is to have a thorough understanding of why a certain technique is being used based on the anatomy and biomechanics of the involved structure. As with taping of any joint, the athlete should be in a comfortable position, and the shoulder should be easily accessible for taping. As long as the athlete has no open wounds, the area may be cleansed and prepared with a skin adherent. If the adherent or tape causes skin irritation, an underwrap may be used before applying the tape. This is usually made of a thin, porous, polyurethane foam. However, the effectiveness of the supporting tape is maximized when applied directly to the skin. All tape should be applied when the skin is at normal body temperature, and any excess body hair should be shaved. Just as important as applying tape correctly is the art of removing tape. Tape can be removed with the aid of bandage scissors (sharks) or by manual methods and should always be pulled off from the skin in a linear fashion. This is performed in a slow, controlled manner. After the tape is removed, the skin should be cleansed with soap and water to rid the surface of tape residue. A moisturizing cream or antibiotic ointment may then be applied to prevent skin abrasions. The area to be taped should be adequately prepared and positioned for easy access. Always observe the skin before application and after removal of tape for any irritations. Only apply tape and adhesive products when the area of concern is at normal skin temperature. The effectiveness of any taping application lies in the understanding of why it is being performed and the art of its completeness. Tape should be applied by following the natural contours of the athlete’s anatomy. The tension of application should be performed in a smooth, equal, and firm manner. Each athlete is taped individually according to his or her anatomy, and each strip of tape must be individualized to the anatomic location. Continuous strips of tape may be constricting and lead to circulatory problems. Each strip of tape applied in sequence should overlap the previous strip by one half. Follow each strip of tape by smoothing it down, being careful to avoid any wrinkles or gaps. Removal of tape should be slow and controlled, being careful not to damage superficial layers of the skin.
PROTECTIVE PADDING MATERIALS The athletic trainer must be skilled at recognizing the indications for using protective padding and must also be aware of the types of materials available. Pads absorb
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shock through closed-cell foam or water cells or through a semiliquid high-viscosity material. Materials can also be combined for functional purposes. For example, a pad can be fabricated with a rigid outer layer and a softer inner layer.
Rigid Materials Many rigid materials are used to fabricate custom padding. Often, a plastic material is used because of its chemical composition and reaction to heat. Three common types are thermoforming plastics, thermosetting plastics, and thermoplastic foams.3 The most popular plastics in athletic training are thermoforming. This plastic can be molded to the body part when heated to between 140° and 180° F. The most common brands are Orthoplast (synthetic rubber thermoplast) and Aquaplast (a polyester sheet). A more rigid and difficult to form plastic is the thermosetting type. This is usually formed from a mold rather than being formed directly on the body part. Thermosetting plastics require higher temperatures to alter the material for fabrication. Examples of this type of plastic are polyvinyl chloride (high-impact vinyl), polyvinyl chloride acrylic (Kydex), and thermoplaster acrylic (Myoplex). Plastics containing additional liquids and gases, or crystals that alter their density, are called thermoplastic foams. Polyethylene foams such as alloplast and Plastazote are two of the most common types. Other products often used as rigid outer layers of padding are Lighcast (Merck Sharpe Dohne, West Point, Penn), Hexalite (Hexcel, Dublin, Calif), and RTV-11 (Genulastic Silicone Products, Waterford, NY). Prefabricated rigid pads can be used to protect the shoulder. Cramer produces OSi protective padding. This is a precut, customized, lightweight, and breathable low-profile pad that can be custom molded to specific body parts such as the acromioclavicular joint and deltoid. To activate the curing process one wets the pad with water at any temperature and applies the pad to the body part. Within five minutes the pad becomes firm and is molded and conformed to the body part. These pads are NCAA compliant to standards for rigid protective devices. The Impact AC (acromioclavicular) pad (Fig. 59-2) uses a dome design that when applied rests over (not on) the injured area, allowing greater dispersion of force. This padding is easily moldable by immersion in a hydrocollator and is secured to the athlete with hook-and-loop tape straps.
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aids in the dispersion of forces. It is heat sensitive, so it responds to the body heat of the athlete as it molds to the contours of the body.
PROTECTING AND PADDING JOINTS IN THE SHOUDLER Protection of the Acromioclavicular Joint In many contact sports such as football, lacrosse, and ice hockey, the acromioclavicular joint is susceptible to frequent injury.8 Athletes with acromioclavicular joint sprains can return to competition with satisfactory functional testing and with the approval of the team physician. However, adequate protection should be provided to the acromioclavicular joint to prevent further injury.
Figure 59-2. Impact AC (acromioclavicular) prefabricated pad.
Soft Materials Soft materials are equally important for preventive measures. These can vary in shape and size and are easy to mold to the contours of the body. Foam rubber is particularly effective because of its variety of thicknesses. It protects the body area from force and is resilient and nonabsorbent. Ther-o-foam (Cramer Products, Gardner, Kan) and Ensolite (Whiroyal, Mishawka, Ind) are two of the most common types of foam used today. Felt is another popular soft material. Felt produces a firmer pressure than most foam rubbers because of its comfortable, semi-resilient surface. This type of material is composed of matted wool fibers pressed into varying degrees of thickness. Felt can absorb perspiration and therefore must be replaced daily to allow it to be fully effective. However, its ability to absorb moisture allows it to keep better skin contact, thus decreasing the tendency of the pad to migrate. Other soft materials such as adhesive felt (moleskin), gauze, cotton, and lamb’s wool can also be used as adjuncts to protective devices. Viscoelastic polyurethane foam (memory foam) is a relatively new type of foam available to the clinician and comes with either an adhesive or nonadhesive backing. It has great shock-absorbing properties and is moldable and conformable. It is available in soft, medium, or firm density. This open-cell foam recovers its shape slowly, which
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One form of protection is by using a foam pad insert called a shoulder injury pad or a spider pad (Adams Plastics, Cookeville, Tenn) (Fig. 59-3). This type of pad is lightweight yet directs the attention of a blow to the acromioclavicular joint toward the elevated foam pad.10 This is commercially available and should be properly fitted to the individual athlete. A specialized pad for the acromioclavicular joint can also be made.10-12 This is done to provide a more custom fit for the athlete. Many types of material have been recommended for construction of the pad. The pad basically takes on an elevated donut or dome shape with a rigid outer shell and a softer inner padding. The rigid material is molded to the athlete’s acromioclavicular joint region. When doing this, a dome of 1.5 inches should be constructed, so the acromioclavicular joint itself is not directly in contact with the pad (Fig. 59-4). A softer material made of foam is then used as a dispersive medium between the athlete’s shoulder and the rigid dome. This pad can be held in place by taping it to the skin with adhesive tape, by creating a strap or belt system, or by using an elastic bandage and applying a spica-type wrap to the shoulder. The key to making a successful acromioclavicular pad is to make sure that the pad is raised off the injured area to distribute the force of a blow around that area, allowing the force to be absorbed by the pad itself.
Taping the Acromioclavicular Joint Taping of the acromioclavicular joint has been used for first- or second-degree sprains, because it can provide some external support while not limiting the athlete’s range of motion. The area of involvement should be cleansed and shaved to allow good contact surfaces. The nipple can be protected with an adhesive bandage or a small piece of felt or gauze. Initially, two anchors are applied. The first is
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A
B
Figure 59-3. Spider pad. A, Side view. B, Anterior view.
More support strips are applied in a diagonally from the arm to the shoulder anchors. These strips are applied in a fanning pattern, both anterior to posterior and posterior to anterior (see Fig. 59-5C). Anchor strips can then be applied from the chest to the back, attaching to the initial anchor. These should be overlapped halfway, allowing a more stable support (see Fig. 59-5D). Strips are then applied completely around the chest and arm to close off the taping procedure (see Fig. 59-5E and F).12
Protecting the Sternoclavicular Joint Although the sternoclavicular joint can be injured in numerous sporting activities, mostly from the result of a direct force, it can actually be protected quite well following an injury through the use of assistive protective devices. Injuries to the sternoclavicular joint involve either an anterior or posterior subluxation or dislocation to the medial end of the clavicle as it displaces from the stable sternum.
Figure 59-4. Custom acromioclavicular pad.
placed from the chest at its midline, over the shoulder to the back, and ending just below the tip of the scapula. A second anchor is applied from the anterior to the posterior aspect of the thorax (Fig. 59-5A). A series of nonelastic support strips are then placed upward from the arm to the anchor strips on the shoulder (see Fig. 59-5B).
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Historically, athletes with sternoclavicular joint sprains have been withheld from physical participation when contact is involved until the area is stable enough to reduce the risk of recurrence. With return to participation, it is a good idea to provide a protective covering in the form of a shell made of thermoplastic materials (Fig. 59-6). The shell appears much more effective in preventing against posterior sternoclavicular instability because the mechanism for that type of injury would be a direct blow to the medial end of the sternum or
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A
C
E
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F
Figure 59-5. Taping the acromioclavicular joint. A, Anchor strips. B, Fan is applied. C, Fan is reinforced. D, Anterior/posterior anchors applied. E, Transverse anchors applied. F, Completed procedure.
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Protecting the Glenohumeral Joint By nature of its anatomic design and the forces applied to it during athletic activity, the glenohumeral joint is susceptible to numerous conditions. Most notable of these are contusions and glenohumeral instability issues.
Figure 59-6. Sternoclavicular pad.
forceful horizontal adduction of the humerus, of which the latter is not as often seen. When using a shell to protect against further sternoclavicular joint injuries, it is important to maintain adequate functional mobility and not compromise movements necessary for participation. Such compromise can lead to additional injuries and create a vulnerable situation in general with respect to the ability to protect oneself from further damage to the preexisting injury. Athletes who return to participation with a shell to protect the sternoclavicular joint should do so after a careful screening of abilities and potential vulnerability considerations, always under the final clearance of a physician.
Figure 59-7. A, Donut-shaped pad to protect the lateral aspect of the humerus from direct forces. B, Close-up view.
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Contusions Direct blows to the glenohumeral joint are common in contact sports. Complications such as tackler’s exostosis and myositis ossificans can be prevented with proper protection to the glenohumeral region.1,13 Often, the area of concern is just distal to the glenohumeral joint, near the insertion of the deltoid muscle and the origin of the brachialis muscle. This is an area that might not be adequately protected with football shoulder pads. Protective donut-shaped pads can be designed to cover the lateral humerus in a manner similar to those for contusion of the acromioclavicular joint (Fig. 59-7). Anterior Instability One of the most difficult challenges that a medical team faces is how to adequately prevent an athlete from recurrent anterior instability of the glenohumeral joint. Because of the complexity of the capsuloligamentous structures, there is no true device or taping procedure guaranteed to protect the unstable shoulder. Because the mechanism of injury for anterior subluxation or dislocation is external rotation and abduction of the shoulder, braces have been designed to limit these motions while allowing an athlete to return to competition.14 However, an athlete who must compete by bringing his or her shoulder into external rotation and abduction is a viable candidate for a reinjury regardless of the type of brace being worn. Many sports,
B
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such as skiing, are somewhat style conscious, and the likelihood of gaining acceptance for any type of brace may be impractical.15 Many different types of shoulder braces have been designed to prevent recurrent episodes of anterior subluxation and dislocation. The Shoulder Subluxation Inhibitor (SSI, Physical Support Systems, Inc, Windham, NH) (Fig. 59-8) is custom-fitted and made of low- and high-density polyethylene.16 It is designed with a hyperextension strap used to restrict excessive external rotation about the shoulder (Fig. 59-9). The C.D. Denison–Duke Wyre Shoulder Vest (C.D. Denison Orthopaedic Appliance Co, Baltimore, Md) (see Fig. 59-9) is constructed of sturdy canvas and is chrome leather stitched with nylon.17 This harness contains a biceps cuff, with a lacer attachment to the chest vest used to limit abduction and extension of the shoulder. Also, laces can be threaded to limit horizontal adduction and shoulder elevation. The Sawa Shoulder Orthosis (BRACE International, Scottsdale, Ariz) is an off-the-shelf brace made of a hypoallergenic blend of cotton and rubber material.18 It is reinforced for strength, shape, and form with hookand-loop tape front closures and fasteners. A glenohumeral hook-and-loop strap attached to the humeral cuff limits adduction, abduction, flexion, and extension. (Fig. 59-10).
Figure 59-9. C.D. Denison–Duke Wyre shoulder brace.
Newer braces include the Sully Shoulder Stabilizer, the Cadlow Shoulder Stabilizer, the Simply Stable Shoulder Stabilizer, the MAX Brace, and the Donjoy Shoulder Brace (Fig. 59-11). The Sully Shoulder Stabilizer provides support while allowing some restricted range of motion. Elastic straps attach with hook-and-loop tape to a neoprene vest at any point, in any direction, and with varied
Figure 59-10. Sawa shoulder orthosis.
Figure 59-8. Shoulder subluxation inhibitor.
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amounts of force to allow the clinician to selectively and functionally stabilize or restrict movement according to each patient’s needs. The Cadlow is a unique brace that uses a pull system of elastic tubes to provide glenohumeral stability while allowing a full range of motion. In addition, the tubes have graduated resistance that allows the athlete to strengthen the shoulder. The Simply Stable Shoulder Stabilizer is designed for simplicity and ease of use. It consists of an elastic strap that attaches directly to the shoulder pads and encircles the humeral head, restricting the motions of abduction and external rotation. For athletes
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Figure 59-12. Simply Stable Shoulder Stabilizer. Figure 59-11. The Donjoy shoulder brace.
not involved with football, there is a harness that can be attached to the humeral strap (Fig. 59-12). The MAX Brace facilitates and controls glenohumeral range of motion and can also be used to support acromioclavicular separations. Studies have shown minimal effects on shoulder positioning sense and glenohumeral joint active and passive range of motion using a variety of shoulder braces.19-21 The ultimate preventive brace for recurrent anterior instability is one that would allow enough motion for the athlete to be as functional as possible in his or her particular sport, yet provide restricted support to stabilize the glenohumeral joint. Because no surgery or rehabilitative protocol can ever replace the original anatomic and biomechanical functions of the shoulder, more research is needed to help create an individualized shoulder restrictor that is lightweight, comfortable, functional, and effective.
Postoperative Shoulder-Bracing Options There are basically four different options for postoperative bracing. The simplest and most useful brace for most procedures is a sling (Fig. 59-13). This affords the patient some protection but also can be easily removed for early postoperative range of motion. Most surgeons allow early passive motion after most procedures, and this can easily be done with a sling. If additional protection is desired, a shoulder immobilizer can be used. This holds the shoulder in a position similar to a sling, but it is more stable. For open posterior capsulorraphy procedures, a gunslinger type brace may be necessary. This brace puts less strain on the posterior capsule in the early postoperative period.
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Figure 59-13. Shoulder sling.
The shoulder is positioned in slight abduction, external rotation, and flexion. Typically, these braces are used for 4 to 6 weeks, and shoulder motion is discouraged. Elbow motion can be allowed by removing the forearm from the brace. With the advent of arthroscopic procedures, many surgeons are electing not to routinely use these braces.
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A variation of the traditional gunslinger brace is an external rotation brace that uses a soft wedge to hold the arm in external rotation. These braces may be useful in the acute management of anterior shoulder instability.
Calleghan reported taping techniques to inhibit trapezius tone when there is a hitching associated with rotator cuff pathology resulting in a decreased humeral inferior glide.25
The final commonly used postoperative brace is an abduction brace. This is a popular soft wedge-type brace. These braces have traditionally been used following rotator cuff repair. Recently, however, their use has been discouraged, because surgeons have recognized that if the cuff can not be repaired without tension in adduction, then the repair is unlikely to be successful.
Not all studies measuring the effects of scapular taping have shown beneficial results. Cools and colleagues looked at taping techniques for the trapezius and serratus anterior muscles during dynamic full range of motion abduction and forward flexion and found no significant influence of tape application on electromyographic activity in healthy subjects.26 As with all other treatment interventions, scapular taping may play an assistive role with certain populations of athletes while not necessarily being as beneficial for others. It is up to the clinician to identify the athletes who can benefit from scapular taping procedures.
There are many factors to consider when prescribing a postoperative brace. These include tissue quality, surgical technique, patient compliance, and goals. Close cooperation and communication among the surgeon, clinician, and patient allow team approach and successful postoperative management.
Taping for Rehabilitative Purposes Studies have shown using Kinesiotape can be effective in assisting with rehabilitation programs. In 2005, Keirns and colleagues demonstrated effective treatment interventions for recruiting suprascapular and infrascapular muscle firing using scapular taping techniques.22 Effects were optimal during forward reaching motion below the horizontal plane (Fig. 59-14). Others have identified scapular taping as an effective measure to treat anterior shoulder impingement when returning athletes to overhead sports activities.23 Methods of scapular taping have even been shown to be effective with performing artists. Ackermann and colleagues identified a 49% increase in electromyographic activity of the left trapezius muscle in professional violinists with the intervention of scapular taping.24
LEGAL AND ETHICAL CONSIDERATIONS A substantial amount of controversy exists regarding the effectiveness of external devices used to protect the athlete’s shoulder. When considering the use of any protective equipment, one should always be aware of the concerns in the specific sport and any ethical ramifications that may arise in regard to the design and application of the equipment itself. Liability is defined as the legal responsibility of a person in a certain situation to do a particular task in a reasonable and prudent manner.3 Failure to perform such action in a reasonable and prudent manner can make the person legally liable for the results of that action. The courts can hold the person negligent when it is shown that the person has done something that a reasonable and prudent person would not do.3 More specifically, knowingly using dangerous or faulty equipment is a type of negligence that an athletic trainer, therapist, coach, or team physician can be held accountable for should an accident result. All athletes and medical personnel should be aware that no single piece of equipment can be 100% reliable in terms of injury or reinjury. The statement that a piece of equipment can treat or prevent a certain injury should be completely avoided in all discussion. The implication of such a statement can lead to implied liability should an injury occur in this situation.
Figure 59-14. Using tape to assist in the rehabilitation of scapular muscles.
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Special care is required with any device made by the medical staff. No piece of equipment should predispose an athlete to further injury. Of primary concern are devices constructed to limit an athlete’s range of motion. The following is a list of suggestions to help maintain safety parameters with the use of protective equipment.3
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• Maintain accurate records of each athlete’s injuries, both present and past. • Establish qualified and adequate supervision of all equipment. • Properly instruct the medical staff, the coaches, the equipment managers, and the athletes themselves on correct procedures for equipment fitting. • Thoroughly inspect equipment on a regular basis, looking for faulty or hazardous parts. • Inform all athletes that no piece of equipment is 100% able to prevent injury. • Use sound, logical judgment when applying any type of external device. • Have a thorough understanding of the rules of the sport your athlete is participating in. It is the ultimate responsibility of the medical staff to ensure that every athlete is treated in a reasonable and prudent manner. Any person deviating from this principle is subject to ethical and legal complications.
SUMMARY The complexity of the shoulder joint has caused many of us to use different methods of prevention and protection through the use of external protective devices. Taping, padding, and bracing of the shoulder complex have become skills in which all of us involved in sports medicine are attempting to become more proficient. An external protective device will never replace a thorough rehabilitation program, nor will it restore normal biomechanics of the injured shoulder. However, performed within the guidelines of one’s qualifications and legal considerations, external protective devices for the shoulder can be a valuable adjunct for returning an athlete to competition.
References 1. Kuland D: The Injured Athlete. Philadelphia, JB Lippincott, 1988. 2. Miller R: Protective Padding. Presented at the NATA National Convention and Symposium, Columbus, Ohio, June 1987. 3. Arnheim DD: Modern Principles of Athletic Training. St Louis, Mosby, 1985. 4. Fahey TD: Athletic Training: Principles and Practice. Palo Alto, Calif, Mayfield Publishing, 1986. 5. Gieck J, McCue FC III: Fitting of protective football equipment. Am J Sports Med 8(3):192-196, 1980. 6. Malacrea R: Protective equipment fit. Proceedings of the NATA Professional Preparation Conference. Nashville, NATA Professional Education Committee, 1978. 7. Watkins RG: Neck injuries in football players. Clin Sports Med 5(2):215-246, 1986.
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8. Silloway KA, McLaughlin RE, Edlich RC, Edlich RF: Clavicular fractures and acromioclavicular joint dislocations in lacrosse: Preventable injuries. J Emerg Med 3(2):117-121, 1985. 9. Athletic Equipment Managers’ Association: Home page. Available at http://www.aema1.com/ (accessed March 26, 2008). 10. Biron SA: Acromioclavicular protection of ice hockey players. Athletic Training 18:103, 1983. 11. Deutch B, Fashour T: MA, Fashover T: Football hip pad protection for hip pointers and AC sprains on ice hockey players. Athletic Training 16:2-00, 1981. 12. Wershing CE: A specialized pad for the acromioclavicular joint. Athletic Training 15:102-103, 1980. 13. Booher JM, Thibodeau GA: Athletic Injury Assessment. St Louis, Mosby, 1985. 14. Rovere GD, Curl WW, Brownig DG: Bracing and taping in an office sports medicine practice. Clin Sports Med 8(3):497-515, 1989. 15. Weaver JK: Skiing-related injuries to the shoulder. Clin Orthop Relat Res (216):24-28, 1987. 16. Physical Supports Systems: Shoulder subluxation inhibitor (information packet). Windham, NH, Physical Supports Systems, Inc, 1989. 17. Denison Orthopedic Appliance Corp: CD Denison-Duke Wyre Shoulder Vest (information packet). Baltimore, CD Denison Orthopedic Appliance Corp, 2005. 18. Brace International: Sawa shoulder orthosis (information packet). Scottsdale, Ariz, Brace International, 2005. 19. Chu JC, Kane EJ, Arnold BL, Gansneder BM: The effect of a neoprene shoulder stabilizer on active joint-reposition sense in subjects with stable and unstable shoulders. J Ath Train 37(2):141-145, 2002. 20. Ulkar B, Kunduracioglu B, Cetin C, Guner RS: Effect of positioning and bracing on passive position sense of shoulder joint. Br J Sports Med 38(5):549-552, 2004. 21. Weise K, Sitler MR, Tierney R, Swanik KA: Effectiveness of glenohumeral-joint stability braces in limiting active and passive shoulder range of motion in collegiate football players. J Ath Train 39(2):151-155, 2004. 22. Keirns MA, Taylor M, Bailey-Carter D: The effects of scapular taping on the suprascapular and infrascapular muscle recruitment in individuals with forward head/rounded shoulder posture [abstract]. Phys Ther, 2005. Available at http://www.apta.org/AM/abstracts/pt2005/abstractsPt. cfm?pubNo⫽PO-RR-107-TH (accessed March 26, 2008). 23. Host HH: Scapular taping in the treatment of anterior shoulder impingement. Phys Ther 75(9):803-812, 1995. 24. Ackermann B, Adams R, Marshall E: The effects of scapula taping on electromyographic activity and musical performance in professional violinists. Aust J Physiother 48(3):197-203, 2002. 25. Callaghan MJ: Role of taping and bracing in the athlete. Br J Sports Med 31(2):102-108, 1997. 26. Cools AM, Witvrouw EE, Danneels LA, Cambier DC: Does taping influence electromyographic muscle activity in the scapular rotators in healthy subjects? Man Ther 7(3):154-162, 2002.
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CHAPTER 60 Shoulder Outcome Measures Tara Ridge and James J. Irrgang
Outcome measures are important tools for quantifying, standardizing, and judging the results of medical treatment.1 Function of the shoulder has traditionally been assessed with objective measures such as range of motion (ROM), strength, and pain, which often do not accurately reflect a patient’s functional limitation of the involved upper extremity. In addition, results of therapeutic or surgical interventions have often been described as poor, fair, good, or excellent based on poorly defined criteria, usually established by an investigator with little supporting evidence of reliability or validity of the measure. However, as third party payers and educated patients demand data regarding treatments that have been proved to be cost effective and efficacious, the use of disease- or regionspecific and generic health status measures has been advocated to evaluate the effectiveness of treatments for shoulder conditions.1 This has given rise to the systematic development of patient-reported outcome measures to assess symptoms, function, and activity level from the patient’s perspective.
Important outcomes in sports medicine include clinical outcomes, process outcomes, patient satisfaction, and costs.3 Among these four areas of outcomes, clinical outcomes are most often the primary outcome of interest. Disablement models, such as the Nagi disablement model2 and the International Classification of Functioning, Disability and Health (ICF) proposed by the World Health Organization,4 provide frameworks that are useful for identifying relevant clinical outcome measures and are discussed in greater detail later. Process outcomes include measures such as duration of care, length of hospital stay, number of outpatient visits, and number and type of interventions provided to the patient. The evaluation of process outcomes provides important information on clinician and organizational performance by assessing if the services that were provided to the patient, including diagnostic tests and therapeutic interventions, were appropriate for the patient’s condition based on the findings from the history and physical examination. The basis for using process outcomes to judge clinician performance is that expert clinicians would be expected to more often choose diagnostic procedures and therapeutic interventions that match the patient’s presentation. Many of the outcome measures that have been proposed for Medicare’s pay-for-performance program are examples of process outcomes. In this system, clinicians are rewarded when the care provided to the patient matches evidence-based guidelines for care. The basis for an emphasis on process outcomes is that clinical outcomes are optimized when the “right care” is provided to the patient; however, there is little empirical evidence to support this. The sources of process outcomes data can include scheduling and billing databases and patient records.
Currently, more than twenty different measurement tools have been proposed to determine functional outcomes of shoulder procedures. Because of the absence of a single universally accepted scale, numerous different scales continue to be reported in the literature despite the lack of information on their validity, reliability, and responsiveness. We think the measurements of activity and participation should make use of patient-reported outcome measures that have been shown to be reliable, valid, and responsive. This chapter reviews the issues related to measurement of clinical outcomes for patients with shoulder dysfunction and compares commonly reported shoulder outcomes scales.
OVERVIEW OF OUTCOMES MANAGEMENT
Patient satisfaction is another important outcome measure that includes the patient’s satisfaction with the caregiver, the support staff, and the clinical result. Patient satisfaction can be measured via written surveys or personal interviews; however, written surveys offer the added benefit of patient anonymity. Aspects of patient satisfaction that are commonly assessed include access to care, physical environment, patient care, billing, and the overall experience throughout the episode of care. Instruments for measuring patient satisfaction commonly make use of Likert-type scales, whereby the degree of satisfaction or dissatisfaction is rated on a scale that ranges from “strongly agree” to “strongly disagree” or from “excellent” to “poor.” Patient-satisfaction instruments
Outcomes management is the process of data collection, analysis, and interpretation of the efficiency and effectiveness of patient treatment, with the intent of improving quality of care and lowering health care costs.2 The importance of outcome measures lies in using them to manage patients, evaluate clinician performance and organization performance, and provide evidence on the effectiveness of interventions. Outcomes data and the process by which the data are collected weigh heavy in the decisions that can be made from such data. 817
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are often developed by individual users and therefore are not likely to have undergone psychometric testing. Thus, there is little standardization among satisfaction surveys. A standardized patient satisfaction instrument to measure the outcomes of patients with shoulder injuries would be a valuable tool to permit benchmarking between health care providers and organizations. The cost of care is another important outcome measure for management of shoulder injuries. The patient’s total costs of a shoulder injury include the direct costs for medical care and indirect costs. The direct costs include the costs for diagnosis, medical and surgical management, and rehabilitation. The indirect costs are related to decreased work hours, decreased productivity, and the assistance required from others to perform activities of daily living or household activities. When discussing costs of care, one must first differentiate costs from charges, but one must also remember that there are two different perspectives to consider. From the perspective of the health care provider, costs are related to the expense of providing a service, including personnel, space, equipment, and supplies. From the perspective of the patient or payer, costs are the charges for the services that are rendered. Charges are closely related to the services (the process outcomes) that are provided during the episode of care. Costs can be used to calculate the value of treatment of a shoulder injury, which is defined as the ratio of the benefit of care to the costs of providing that care. When managing shoulder injuries, one should aim for high value, which is a large benefit at a relatively low cost. The remainder of this chapter focuses on clinical outcomes. This includes a discussion of a framework for identifying important clinical outcomes and considerations for selecting outcome measures.
FRAMEWORK FOR IDENTIFYING CLINICAL OUTCOMES Disablement models provide a useful framework for identifying relevant clinical outcomes for evaluating shoulder dysfunction and the results of medical intervention. Dis-
ablement models have been proposed by Nagi,5,6 the National Center for Medical Rehabilitation Research (NCMRR),7 and the World Health Organization.8 Disablement is the impact of injury or illness on the function of specific body systems, on basic human performance, and on a person’s role in society.9,10 Although the proposed models differ in the terminology they use, each defines disablement at four basic levels: the tissue and cellular level, the organ and body system level, the personal level, and the societal level (Table 60-1). The four levels of disablement defined by the Nagi scheme are active pathology, impairment, functional limitations, and disability. Active pathology describes processes that can interrupt or interfere with normal cellular processes, such as those resulting from trauma or degenerative disease conditions. Active pathology also includes the simultaneous efforts by the organism to regain homeostasis. Impairment is the loss or abnormal function at the organ or body system level. Functional limitations are the manifestations of pathology and impairment on the function of the person as a whole and can include limitation in physical or psychological function. Disability refers to the function of the person within society and is defined as “the inability or limitation experienced by the person in performing socially defined roles and tasks within the context of a socio-cultural and physical environment.”6 Disability can affect many aspects of a person’s life. Often it affects family and other interpersonal interactions, work and other economic pursuits, education, recreation, and the ability to take care of oneself. The World Health Organization (WHO) has introduced a revision of the International Classification of Impairments, Disabilities and Handicaps (ICIDH), the International Classification of Functioning, Disability and Health (ICF).4 The ICF provides a unified and standard language and framework for describing health and health-related states that can be used as a framework to measure health outcomes. In the ICF disablement model, health domains are described from the corporal, personal, and societal perspectives in terms of body structure, function, activity, and participation. In the ICF, function is an umbrella term that
TABLE 60-1 Comparison of Disablement Schemes System
Tissue and Cellular Level
Organ and System Level
Personal Level
Societal Level
Nagi
Active pathology
Impairment
Functional limitation
Disability
ICIDH
Disease
Impairment
Disability
Handicap
NCMRR
Pathophysiology
Impairment
Disability
Societal limitation
ICF
Impairment of body structure and function
Impairment of body structure and function
Activity limitation
Participation restriction
ICF, International Classification of Functioning, Disability and Health; ICIDH, International Classification of Impairments, Disabilities, and Handicaps; NCMRR, National Center for Medical Rehabilitation Research.
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refers to all body functions, activities, and participation. Disability is the umbrella term for impairments, activity limitations, and participation restrictions. Body structures are the anatomic parts of the body, such as organs, limbs, and their components. Body function refers to function of the body systems including both physiologic and psychological function. Impairments are problems in body structure or function. Activity is the execution of a task or action by an individual person, and participation is involvement in life situations. Activity limitations are difficulties a person has in executing activities, and participation restrictions are the limitations a person experiences in life situations. The ICF model of functioning and disability provides a detailed description of body structure and function, activity, and participation. The descriptions of body structure and function, activity, and participation provided by the ICF can be used to identify important clinical outcomes following a shoulder injury. For example, following a shoulder dislocation, impairment of body structure might include disruption of the glenohumeral ligaments and possible injury to the labrum, articular cartilage, or subchondral bone. Clinical outcome measures to evaluate body structure can include magnetic resonance imaging and arthroscopy. Impairment of body function can include pathologic laxity of the glenohumeral joint, limited ROM, or rotator cuff weakness. Measures of clinical outcome at the level of impairment of body function for a patient with a shoulder injury can include manual testing of capsular laxity, goniometry to measure the range of shoulder motion, and isometric or isokinetic testing to measure rotator cuff performance. Activity limitations experienced by a person with a shoulder injury can include difficulty sleeping, bathing, dressing, grooming, reaching overhead to change a light bulb, opening a heavy door, or performing household chores and recreational activities. The resulting participation restrictions might include the inability to participate in sports or work. Clinical outcome in terms of activity and participation can be measured by observing and rating the patient executing a variety of activities or by using standardized self-reports of activity limitations and participation restrictions.
CLINICAL OUTCOME MEASURES FOR SHOULDER INJURIES The most important clinical outcome following a shoulder injury for an athlete is whether he or she can return to his or her prior levels of activity and participation with the same intensity, frequency, duration, and skill without symptoms and risk of reinjury. This outcome should be achieved in the shortest time possible. Although on the surface this outcome appears easy to determine, it is difficult to quantify due to the varying demands of daily activity, sports, and levels of participation. Thus, function
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(the activity and participation) of the athlete is an important clinical outcome following a shoulder injury. In addition to being an important outcome of treatment, sports activity is also an important prognostic factor for the sports medicine population, because people who are very active have different expectations and demands than those who are less active. Defining outcome only in terms of the absence of symptoms may be misleading if the level of sports activity is not considered. For example, the outcome would be considered suboptimal if the athlete before injury could participate in very strenuous sports that require the arm to move freely or to take some force or impact through the arm, but after surgery and rehabilitation can only return to activities that involve little effort from the upper extremity. In measuring outcome, it is important to know if a patient has returned to his or her preinjury level of sports activity in terms of the frequency, intensity, and duration of participation as well as the length of time needed to return to this level. Because the frequency, intensity, and duration of sports participation vary widely among individual athletes, it is important to consider the level of sports activity when critically evaluating upper extremity clinical outcome studies. For example, a study describing outcome following anterior shoulder dislocation should document the patient’s activity level to ensure that the results can be applied to the appropriate patient population. For studies comparing two groups of patients, the activity levels of the two groups should be similar to avoid a biased comparison.
Measures of Body Structure and Function for Shoulder Injuries Impairment of body structure associated with rotator cuff injuries for example, may include a partial or full-thickness tear of the supraspinatus or infraspinatus as well as injury to the surrounding structures such as the glenoid labrum. Clinical outcome measures to evaluate the integrity of the rotator cuff and other intra-articular structures include arthroscopy, radiographs, and magnetic resonance imaging. Impairment of body function associated with rotator cuff injury includes ROM and weakness. Active and passive ROM can be reliably measured with a goniometer.11 Riddle and colleagues examined passive ROM of shoulder measurements by physical therapists in a clinical setting and did not control for patient position during the measurements or for each examiner’s placement technique. Intraclass correlation coefficients for intratester reliability were 0.98 for flexion, 0.98 for abduction, 0.94 for extension, 0.90 for horizontal abduction, 0.95 for horizontal adduction, 0.99 for lateral rotation, and 0.94 for medial rotation. Intraclass correlation coefficients reflecting intertester reliability were notably lower, ranging from
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0.26 to 0.90.12 Similarly, Myers and colleagues reported test-to-retest intrasession and intersession reliability as well as the precision for a single examiner performing assessments for ROM, yielding intrasession intraclass correlations ranging from 0.85 to 0.94 with a standard error of measurement of approximately 3 degrees.13 Ellenbecker reported values related to internal and external ROM when measured in the supine position at 90 degrees of shoulder abduction while providing scapular stabilization to be consistent with the other examiners. Test-to-retest reliability (Pearson correlation) results were r ⫽ 0.94 for external rotation and r ⫽ 0.89 for internal rotation.14 Manual muscle testing (MMT) is the traditional method for clinical assessment of muscular strength in patients with orthopedic pathology.15,16 The criterion for a normal strength grade states that the “muscle can hold the test position against strong resistance”and“might be described as strength that is adequate for ordinary functional activities.”17 This method however, challenges a clinician to detect subtle weakness that might exist between sides. In addition, the reliability of MMT is compromised by clinician size and strength differences and the subjective nature of the grading system.18 Ellenbecker compared isokinetic testing of the shoulder’s internal and external rotators with MMT in 54 subjects exhibiting manually assessed symmetrical normal-grade (5/5) strength.18 On isokinetic testing, 13% to 15% bilateral differences in external rotation and 15% to 28% bilateral differences in internal rotation were found. In addition to the bilateral comparison of rotator strength, a clinically significant isokinetic finding is the ratio between external and internal rotation strength. The ratio is used to estimate the degree of muscular balance between the larger anterior muscle group (internal rotators) and the posterior cuff.18 External and internal rotation ratios measured in normal healthy subjects has been reported at 66% at multiple contractile velocities.18 Ratios of less than this 66% standard indicate a relative imbalance of the posterior rotator cuff. Clinically, isokinetic testing is expensive, requires a large amount of space for the dynamometer, and involves timeconsuming testing sessions. Manual muscle testing with a hand-held dynamometer is an alternative means of objectively determining shoulder strength. Tyler and colleagues assessed strength of the internal and external rotators of subjects with and without shoulder impingement, all of whom had normal shoulder strength bilaterally according to MMT.19 Strength of the internal and external rotators was tested isokinetically at 60 deg/sec and 180 deg/sec, as well as manually with a hand-held dynamometer in 17 patients and 22 control subjects. Testing was performed with the shoulder positioned in the scapular plane and in 90 degrees of shoulder abduction with 90 degrees of elbow flexion (90/90). Despite a normal muscle grade, patients had marked weakness in external rotators at the 90/90 position tested
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with the hand-held dynamometer. In contrast, external rotation weakness was not evident with isokinetic testing at the 90/90 position. In control subjects, greater internal rotator strength in the dominant arm compared with the nondominant arm was evident with the hand-held dynamometer at the 90/90 position and in the scapular plane.19 Given these results, internal and external strength should be assessed, and quantified when possible, to direct decisions regarding rehabilitation and return to play and work. In addition to the methods described here, a variety of functional strength tests, such as sport- and work-specific tasks, including examples such as throwing and lifting objects, can be performed to direct functional training and facilitate the return to work and sport.
Measures of Activity and Participation for Shoulder Injuries Activity and participation of the athlete after a shoulder injury or surgery can be measured by directly observing and rating the athlete’s performance or by using standardized self-reports of activity limitations and participation restrictions. Direct observation and measurement of an athlete’s performance can include tests such as the ability to participate in a short-toss throwing program, serve a tennis ball, or swim freestyle 100 meters. However, performance-based measures of activity and performance are limited by the ability to observe and quantify the full range of activity and participation of the athlete, and it might not be possible to observe the full range of athletic activities in which an athlete participates in a clinical setting. As a result of these limitations, there has been greater reliance on and acceptance of patient-reported measures of activity and participation to measure clinical outcomes following a shoulder injury. This has led to efforts to develop and validate a wide variety of patientreported outcome instruments to measure an athlete’s activity and participation. Some instruments that have been reviewed most often in the literature20 include Disabilities of Arm Shoulder and Hand (DASH),21 Simple Shoulder Test (SST),22,23 American Shoulder and Elbow Surgeons Shoulder Score Index (ASES),24 and the Shoulder Pain and Disability Index (SPADI).25 The DASH is a 30-item questionnaire that evaluates symptoms and physical function (at the level of disability) with a five-response option for each item. The tool is scored by summing the responses and subtracting 30. This figure is divided by 1.2 to get a DASH function and symptom score out of a possible 100. A higher score on the DASH reflects greater disability and is designed to be used for single or multiple disorders in the upper limb.21 The SST is a quick, subjective questionnaire composed of 12 yes-or-no questions that measure pain and function of the shoulder. Although no formal scoring system is
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described for the SST, some researchers have reported total scores for this scale.22,23 The ASES was designed to provide a standard method for evaluation of shoulder through assessment of pain and activities of daily living. The ASES is derived from an equation that incorporates a visual analogue pain scale and functional ability questions. Both components have a maximum score of 50. Pain is calculated by subtracting the visual analogue score from 10 and then multiplying by 5 for a total of 50 points. The function component is calculated by adding the points and multiplying by 5/3 for a maximum of 50 points. The subscores for pain and function are then added for the total score. The maximum possible score is 100, representing less pain and greater function.24 The SPADI is a subjective questionnaire that has pain and disability or function components. Roach and colleagues developed this scale using visual analogue scales to measure pain and function of the shoulder.25 The pain index of this scale is made up of five visual analogue scales (minimum ⫽ 0, maximum ⫽ 11). The sum of the scores on the five visual analogue scales is divided by 55, and the quotient is multiplied by 100. The same procedure is used to calculate the score for eight questions in the function component. However, the sum of the visual analogue scale is divided by 88 because the functional index is based on eight scales. The total score is found by averaging the two component scores. A higher score on the SPADI indicates greater pain and disability.25
Health-Related Quality of Life Health-related quality of life is a person’s perception of his or her health. Broadly, health-related quality of life encompasses a person’s perception of his or her physical, emotional, and social function. Health-related quality of life deals with what people perceive their health condition to be and the consequences of it; hence, it is the person’s subjective sense of well-being.4 Because health-related quality of life encompasses a person’s physical, emotional, and social function, it overlaps with the activity and participation domains of the ICF model. As such, health-related quality of life measures can be used to measure the athlete’s perception of his or her activity and participation. Numerous health-related quality-of-life measures have been developed. These can be classified as general or specific measures of health-related quality of life. General measures of health-related quality of life are designed to be applicable across a number of disease processes and interventions and across demographic and cultural subgroups.26 General health-related quality-of-life instruments are designed to give a comprehensive and general overview of healthrelated quality of life. General health-related quality of life measures are usually multidimensional, and scores can be obtained for each dimension or they can be combined to
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provide an overall score. The most widely known and accepted general measure of health-related quality of life is the Medical Outcomes Study Short Form—36 (SF-36).27 General measures of health-related quality of life permit comparisons across populations with different health conditions26 and are more likely to detect unexpected effects of intervention.26 An important limitation of general health-related quality of life measures is that they tend to be less responsive to changes in health status than specific measures of health-related quality of life.28 Therefore, use of general health-related quality of life measures might make it more difficult to detect the effects of shoulder injuries and surgery. General measures of health-related quality of life are also susceptible to ceiling effects. The presence of ceiling effects limits the ability to detect the effects of intervention, especially when used by young, healthy, high-functioning patients such as athletes who have sustained a shoulder injury. Because general measures of health-related quality of life assess a broad range of health including emotional function, the content may appear less relevant to patients and clinicians. Finally, general measures of health-related quality of life tend to be longer and more difficult to score. Specific health-related quality-of-life measures are designed to focus on aspects of health that are directly related to the primary condition or population of interest, with the intent of creating a more responsive measure.28 Specific measures of health-related quality of life have been developed for specific diseases (e.g., rotator cuff disease), specific populations of patients (e.g., the frail elderly), specific functions (e.g., physical function), or symptoms (e.g., pain).28 Specific measures of health-related quality of life are responsive to small changes in the patient’s condition and are easy to administer and interpret.26 The increased responsiveness of specific measures of health-related quality of life stems from the fact that they include only those aspects that are relevant to the condition or population being studied.28 Specific health-related quality-of-life measures usually relate closely to areas commonly assessed by clinicians, and therefore they are more likely to be accepted by clinicians for routine use. Additionally, because specific health-related quality-of-life measures relate more closely to a particular condition, they are also more likely to be accepted by patients. Disadvantages of specific measures of health-related quality of life are that they do not measure all aspects of health status and they do not allow comparisons between different disease states or populations. Specific health-related quality-of-life measures include disease- and region-specific measures. Disease-specific measures are developed for a particular injury or illness. The content of disease-specific, health-related, quality-of-life
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measures include the symptoms, activity limitations, and participation restrictions commonly experienced by athletes with the injury or illness for which the instrument was developed. The Western Ontario Rotator Cuff (WORC) Index is a selfreport questionnaire that measures health-related quality of life in persons with injuries and conditions of the rotator cuff.29 Kirkley and colleagues wanted the measure to represent the impact of the condition on health as defined by the World Health Organization: “a state of complete physical, mental and social well-being.” Therefore, included were items in five domains: pain and physical symptoms, sports and recreation, work, lifestyle, and emotions. The result is 21 items that are answered on visual analogue scales with answers such as no pain or difficulty and extreme pain or difficulty. Two studies30 have examined the responsiveness of the WORC Index and other shoulder measures by calculating the standardized response mean (SRM). The SRM of the WORC Index was not noticeably different from the comparative measures of the SST and DASH. It has been argued that disease-specific measures to evaluate orthopedic treatment are more responsive than global health measures.29 However, some reports suggest that regionspecific tools might perform as well. The WORC Index was highly correlated with both the DASH and SST30 and had an SRM similar to that of both instruments. Therefore, it might not be necessary to have various tools specific to a particular condition in the shoulder. Region-specific, health-related, quality-of-life measures have been developed to determine the effects of a variety of pathologies and impairments affecting a particular region. The content of region-specific measures of healthrelated quality of life reflects the symptoms, activity limitations, and participation restrictions commonly experienced by patients with impairment of the particular region for which the instrument was developed. The measurement of disability or capacity to function is critical to a comprehensive assessment of outcome following an injury in the upper limb. However, measuring disability in patients with upper limb disorders can be challenging because several questionnaires target a specific region of the upper limb (e.g., shoulder), but many patients have multiple affected areas (e.g., shoulder and elbow) that alter upper extremity function. The DASH can be used for single or multiple disorders in the upper limb, providing the possibility of a single questionnaire for measuring disability for any upper-limb region.31 The DASH, SPADI, and ASES have been evaluated most often, and overall, the DASH received the best ratings for its clinimetric properties.20 The DASH and SPADI are recommended for evaluations in outpatient clinics, because they have received positive ratings for responsiveness and do not exhibit floor or ceiling effects.31
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SELECTING CLINICAL OUTCOME MEASURES When selecting clinical outcome measures, one must consider the purpose for which the information will be used as well as practical and psychometric considerations of the instrument. Kirshner and Guyatt (1985)32 classified health indices according to their purpose as discriminative, predictive, or evaluative measures of health status. Evaluative health status measures are most appropriate for measuring clinical outcome following rotator cuff injuries, for example, because they measure change of an athlete or group over time on the dimension of interest. To demonstrate effectiveness for the management of rotator cuff injuries, one is interested in measuring change in body structure and function, activity, and participation over time. Thus, measuring clinical outcomes for rotator cuff injuries and surgery requires evaluative health indices that can measure change over time.
Practical Considerations for Selecting Clinical Outcomes Practical considerations for selecting clinical outcome measures include ease of use, acceptance, and costs.26 Attractive clinical outcome measures are ones that require minimal resources to administer. Ease of use is determined by the time required for administration and scoring as well as the effort required to interpret and use the data. The time and costs for administering and scoring an outcomes instrument greatly influence acceptance of the outcome measure in clinical practice and research. Clinical outcome measures that require special expertise or equipment to administer, score, and interpret are likely to be more costly and less readily accepted than measures that can be scored manually.26 Similar arguments for practicality must be considered when selecting clinical measures of body structure and function. Generally, clinical measures of body structure and function that can be measured as part of routine clinical practice with minimal effort and costs are more acceptable than those that require special equipment and are time consuming and expensive.
Psychometric Considerations for Selecting Outcomes Measures A number of investigators have discussed psychometric considerations for selecting a clinical outcome measure (Table 60-2).26,32-38 Reliability, validity, and responsiveness are important psychometric considerations to include when selecting a clinical outcome measure that is designed to measure change over time. In validity theory, validity is defined as “the degree to which empirical evidence and theoretical rationales support the adequacy and appropriateness of the inferences and actions based on the test scores.”39 Knowledge of the psychometric
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TABLE 60-2 Psychometric Considerations for the Selection of Outcomes Measures Scale
Content
Format
Scoring
American Shoulder and Elbow Surgeons Shoulder Form (ASES) Richards RR et al (1994)
Self-administered questionnaire to assess pain and function of ADL
100-point scale (50% pain, 50% function) 1 pain item, 10 function items 10-cm VAS for pain 4-point Likert scale for function
Visual analogue pain scale with a maximum score of 50 points. Pain is calculated by subtracting the VAS from 10 and multiplying by 5. Function component is calculated by adding the points and multiplying by 5/3 for a maximum of 50. Pain and function scores are added for a possible 100 representing less pain and more function.
Constant-Murley Score Constant CR (1987)
Assess pain, function, ROM, and strength
100-point scale Self-report: pain (15%) and function (20%) Clinical measures: ROM (40%) and strength (25%)
Pain has a maximum score of 15 points, function (ADL) 20 points, ROM 40 points, and strength 25 points. The component scores are summed for a maximum total score of 100. Maximum score indicates greater function.
Disabilities of the Arm, Shoulder, and Hand (DASH) Hudak PL et al (1996)
Self-administered questionnaire to assess pain and function related to upper extremity function. Optional Sports and Work Module
100-point scale 30 items: four items for sports module; four items for work module 5-point Likert scale
Scores are calculated by summing the responses and subtracting 30 and dividing the total by 1.2. Higher scores indicate greater disability
Modified Rowe Scale Jobe et al (1991)
Assesses stability, motion, function, pain and ability to throw/ return to prior level of competition. Designed specifically to assess outcome of treatment for anterior shoulder instability in athletes
100-point scale
Pain (10 points), stability (30 points), ROM (10 points), function (50 points) Specific to shoulder instability and an athletic population
Rowe Scale Rowe CR et al (1978)
Assess stability, motion, and function Designed specifically to assess outcome of treatment for anterior shoulder instability
100-point scale
Stability (50 points), ROM (20 points), function (30 points) Higher score indicates less disability and greater function
Shoulder Pain and Disability Index (SPADI) Roach KE et al (1991)
Self-administered questionnaire to assess pain, disability, and function
100-point scale (50% pain and 50% function) Five pain items, eight function items
Originally each item was scored on a VAS with a maximum score of 11 points. The sum of scores on the five scales is divided by 55 and the quotient is multiplied by 100. The same procedure is used to calculate the score for the eight function questions. The total score is the average of the two components. Maximum score indicates greater pain and disability.
Shoulder Disability Questionnaire (SDQ) van der Heijden G et al (2000)
Self-administered questionnaire to assess pain-related shoulder function
100-point scale 16 items
Dichotomous questions (yes or no)
Continued
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TABLE 60-2 Psychometric Considerations for the Selection of Outcomes Measures—cont’d Scale
Content
Format
Scoring
Simple Shoulder Test (SST) Lippitt SB et al (1993)
Self-administered questionnaire to assess pain and function of the shoulder
100-point scale 12 items
No formal scoring system. Some researchers have allocated 1 point for “yes” and 0 for “no” answers. This results in a maximum score of 12 points, indicating greater function.
Western Ontario Rotator Cuff Index (WORC) Kirkley et al (2003)
Self-administered questionnaire to assess pain, function (sports, work, lifestyle), and emotions Developed to specifically evaluate persons with rotator cuff pathology
100-point scale VAS-type response option 21 items Five domains: pain and physical symptoms, sports and recreation, work, lifestyle, emotions
The highest or most symptomatic score is 2100, and the best or asymptomatic score is 0. To present this in a more clinically meaningful format, the score can be reported as a percentage of normal by subtracting the total from 2100, dividing by 2100, and multiplying by 100. 100% represents the greatest amount of function with the fewest symptoms.
University of California Los Angeles Shoulder Score (UCLA) Amstutz et al (1981)
Assess pain, function, ROM, strength, and patient satisfaction Initially described in the assessment of outcome of shoulder arthroplasty
35-point scale
Pain and function have maximum value of 10; other components have maximum value of 5. Component values are added to achieve a total score of 35. Higher score indicates increased function.
ADL, activities of daily living; ROM, range of motion; VAS, visual analogue scale. Amstutz HC, Sew Hoy AL, Clarke IC: UCLA anatomic total shoulder arthroplasty. Clin Orthop Relat Res (155):7-20,1981. Constant CR, Murley AH: A clinical method of functional assessment of the shoulder. Clin Orthop Relat Res (214):160-164, 1987. Hudak PL, Amadio PC, Bombardier C; Upper Extremity Collaborative Group (UECG): Development of an upper extremity outcome measure: The DASH (Disabilities of the Arm, Shoulder, and Hand). Am J Industrial Med 29:602-608, 1996. Jobe FW, Giangarra CE, Kvitne RS, Glousman RE: Anterior capsulolabral reconstruction of the shoulder in athletes in overhand sports. Am J Sports Med 19:428-434, 1991. Kirkley A, Alvarez C, Griffin S: The development and evaluation of a disease-specific quality-of-life questionnaire for disorders of the rotator cuff: The Western Ontario Rotator Cuff Index. Clin J Sport Med 13:84-92, 2003. Lippitt SB, Harryman DT II, Matsen FA III: A practical tool for evaluating function: The simple shoulder test. In Matsen FA III, Fu FH, Hawkins RJ (eds): The Shoulder: A Balance of Mobility and Stability. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1993, pp 501-518. Richards RR, An K-N, Bigliani LU, et al: A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg 3:347-352, 1994. Roach KE, Budiman-Mak E, Songsiridej N et al: Development of a shoulder pain and disability index. Arthritis Care Res 4:143-149, 1991. Rowe CR, Patel D, Southmayd WW: The Bankart procedure: a long-term end-result study. J Bone Joint Surg Am 60:1-16, 1978. van der Heijden GJ, Leffers P, Bouter LM: Shoulder disability questionnaire design and responsiveness of a functional status measure. J Clin Epidemiol 53:29-38, 2000.
characteristics of a clinical outcomes measure allows one to interpret the appropriateness and usefulness of the inferences and actions that are based on the scores from the measure. Validity evidence to support use and interpretation of a clinical outcomes instrument to measure change should include demonstration of test-to-retest reliability and responsiveness. In other words, scores should remain stable when the underlying condition measured by the outcome instrument remains stable (test-to-retest reliability), and the scores should change with improvement or worsening of the condition measured by the instrument (responsiveness). Reliability and responsiveness are important aspects of validity for clinical outcome measures and are discussed in greater detail below. Reliability Reliability of a clinical outcomes measure implies consistency of measurement. Measures of reliability include internal consistency and test-to-retest reliability. Internal
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consistency is the degree to which all items on the scale consistently measure the underlying condition and is concerned with measurement errors related to the sampling of items that are included on the instrument.40 Internal consistency is most commonly estimated with coefficient alpha. Test-to-retest reliability is the degree to which scores remain stable when there is no change in the underlying construct that is being measured. Test-to-retest reliability for a clinical outcomes measure is estimated by measuring athletes two or more times over a period when the athlete’s condition is expected to remain stable. The amount of time between repeat measurements is an important issue when determining test-to-retest reliability.41 The length of time should not be so short that memory or recall artificially inflates the testto-retest reliability estimate. Conversely, the length of time between repeat administrations of the clinical outcomes measure should not be too long to avoid change in the
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condition that is being measured. In general, the length of time between repeat administrations should be relatively short (1-3 days) when the condition being measured is expected to change rapidly (e.g., the first 4-6 weeks following rotator cuff repair). The time between repeat administrations of the clinical outcome measure should be longer (e.g., ⱖ4 weeks) when the condition is not expected to change (e.g., 3-5 years after rotator cuff repair). Test-to-retest reliability should not be considered a property of the instrument itself but rather the degree of consistency of measurement when applied to certain populations under particular measurement conditions.42 The DASH outcome measure exceeded recommended standards for test-to-retest reliability. Generally, test-to-retest coefficients need to exceed 0.90 or 0.95 before interpretation on an individual level can be considered. For group-level interpretation, lower coefficients (0.75) are acceptable. Beaton demonstrated a coefficient of 0.96 of the DASH, which was consistent with other studies.31 The type of reliability coefficient used to estimate test-toretest reliability depends on the nature of the data. Percent agreement and Cohen’s kappa statistic, which is the agreement above chance agreement, are recommended for nominal- or ordinal-level data, and the intraclass correlation coefficient43 is recommended for interval- or ratiolevel data. Because test-to-retest reliability is concerned not only with the relative standing of athletes on repeated measurement but also with the degree to which the repeated measurement yields the same score, the intraclass correlation coefficient is recommended over the Pearson correlation coefficient when estimating test-to-retest reliability for continuous data. However, this statistic gives the clinician or researcher a measure of the stability of the scale; it does not give an estimate of the error associated with its obtained score. Responsiveness Responsiveness is the degree to which a clinical outcome score changes as the underlying condition that is measured by the scale changes. The score of a responsive clinical outcome measure improves as an athlete’s condition improves and likewise worsens as the athlete’s condition deteriorates. Demonstration of responsiveness for a clinical outcome measure requires evidence that the measure accurately detects change when change has occurred. Studies to demonstrate responsiveness of a clinical outcome measure should link the amount of change in the outcome score to a construct of change. The construct of change is the way that was used to demonstrate that change has in fact occurred.44 The construct of change is defined by the answers to: Who is the focus of the analysis? Which scores are being compared? and, What kind of change or difference is being examined? Examples of a construct for change include change from before to after treatment of a known efficacy or change in those deemed to be better or worse based on an external marker of change.44,45
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Factors that affect the magnitude of change for a given instrument include the patient group under study, the type of treatment being studied, timing of the data collection, and the construct for change.44 For example, one would expect greater change over a similar time frame for those with an acute condition compared with those with a chronic condition. The patient group, type of treatment, and timing of data collection must be comparable before the results of a responsiveness study can be applied to a particular clinical setting or used to judge the meaningfulness of a change score.44 When selecting an outcome instrument to measure the outcomes of patients with shoulder instability, one should review the evidence to support its reliability and responsiveness for patients with unstable shoulders. This evidence should be provided in a sample that has characteristics similar to those of the sample in which the outcome measure will be applied. For example, it would not be appropriate to use evidence for reliability and responsiveness of an outcome measure that was established in an older, lessactive population to support use of the outcome measure in a younger, more-active population.
LIMITATIONS AND FUTURE DIRECTIONS Impairment Outcomes The relationship between restoration of ROM and strength and return to activity and participation following a shoulder injury remains unclear. In theory, restoring strength and ROM should allow the athlete to return to throwing a baseball, spiking a volleyball, or serving a tennis ball and ultimately to sports such as baseball, volleyball, or tennis. The lack of a direct relationship between impairment of body structure and function and limitations of activity and participation is inherent in the ICF model (Fig. 60-1).
Health condition (disorder or disease)
Body functions and structures
Environmental factors
Activities
Participation
Personal factors
Figure 60-1. International Classification of Functioning, Disability and Health proposed by the World Health Organization.
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In this model, disability is the outcome of a complex interaction between the athlete’s health condition and contextual factors.4 Contextual factors include environmental and personal factors. Environmental factors are the makeups of the physical, social, and attitudinal environments in which athletes live and conduct their lives. Personal factors include gender, race, age, health conditions, fitness, lifestyle, habits, upbringing, coping styles, social background, education, profession, and past and current experiences, any of which can play a role in disability.4,46 Thus, research exploring the relationships between impairment of shoulder joint structure and function with the activity and participation of the athlete should make use of modeling techniques that account for environmental or personal factors that could moderate or mediate these relationships. The lack of a direct relationship between impairment of body structure and function and the resulting activity limitations and participation restrictions imply that measures of impairment should not be combined with measures of activity limitations and participation restrictions into a single composite score. Rather, reports of clinical outcome should include separate summaries of relevant measures of impairment of body structure and function that are appropriate for the interventions that were provided, which would include strength and ROM and valid measures of activity limitations and participation restrictions. Activity limitations and participation restrictions may be measured either through direct observation of performance or by general or specific measures of healthrelated quality of life.
Measures of Activity and Participation A limitation of currently available patient-reported clinical outcome instruments is their relatively imprecise measurement. Two values are used to determine the amount of error associated with a patient’s score on a self-report form—the standard error of the mean (SEM) and the minimal detectable change (MDC). The SEM is used to ascertain the associated error when a patient completes a shoulder-specific scale one time. The MDC indicates the error associated with multiple completions of the same scale (e.g., when the same patient completes a shoulder-specific scale at initial evaluation and at discharge.)47 The SEM for most patient-reported outcomes measures that have been developed and tested for measuring outcomes of upper extremity disability are on the order of 7 to 11 points on a 100-point scale. These values can be interpreted and applied in the clinical setting when making decisions about a patient’s care. For example, a patient completes the ASES and obtains a score of 50 out of 100. From a prior study48 the SEM was calculated to be 6.7 ASES points, with the 90% confidence bounds of ±11 points. Applying these
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values to this patient, the clinician can be 90% confident that the patient’s actual score falls within ±11 points of the patient’s score of 50. The clinician can also use the MDC value. For example, if the patient who scored 50 points on the initial evaluation scores 72 points on a reassessment 2 weeks later, the clinician can be 90% confident that the patient has shown true improvement, because the change (22 points) is greater than the MDC value of 15.5 points.
FUTURE DIRECTIONS IN MEASURING PATIENT-REPORTED OUTCOME Advancements in test theory and computer technology have recently led to the development of computeradaptive tests to measure patient-reported outcomes.49 Computer-adaptive tests make use of item-response theory to tailor the patient-reported outcome measure to the unique abilities of the athlete responding to the outcome measure. A computer algorithm selects from a large bank of questions that have been calibrated using itemresponse theory to select the “best” questions to measure an athlete’s ability, given the athlete’s responses to previous questions. For example, in an 18-year-old male collegiate baseball player who has pain only when pitching, the computer might begin by asking the athlete how much difficulty he has with recreational activities that require little effort. If the athlete indicates that he can participate without any limitations, the computer bypasses easier questions and asks a more difficult question, such as how much difficulty the athlete has when participating in recreational activities that require the generation of force or to take some impact through the arm, shoulder, or hand. If the athlete indicates he is unable to participate in activities that require the upper extremity to move freely, the computer asks an easier question, such as how much difficulty the athlete has washing his back. The computer algorithm continues iteratively until a predefined number of questions have been asked or until ability is measured with a predefined level of precision. Computer-adaptive tests that have been tested for use in athletes who have had a shoulder injury or surgery could lead to more efficient and precise measurements of patient-reported symptoms, activity, and participation.
SUMMARY Clinical outcomes data can be used to facilitate patient management decisions, to assess clinician and organizational performance, and to provide evidence for the effectiveness of surgery and rehabilitation. The validity of the inferences made from outcomes data depends on the validity of the outcomes measures themselves and the circumstances under which the data were collected, analyzed, and interpreted.
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Clinical outcomes can include measures of impairment of body structure and function, activity limitation, and participation restriction. However, because the relationship between impairment and the resulting activity limitation and participation restriction are not direct, and because activity limitations and participation restrictions are of the utmost concerns to the athlete, the primary clinical outcome should be measures of activity limitation and participation restriction. Activity limitation and participation restriction may be measured either through direct observation of performance or by general or specific measures of health-related quality of life. Clinical outcomes data must be collected systematically to ensure valid inferences from the data.
14.
15.
16.
17.
18. References 1. Placzek JD, Lukens SC, Badalanmenti S et al: Shoulder outcome measures: A comparison of 6 functional tests. Am J Sports Med 32:1270-1277, 2004. 2. Dobrzykowski EA: The methodology of outcomes measurement. J Rehabil Outcomes Meas 1:8-17, 1997. 3. Irrgang JJ: Outcomes in sports medicine: Classification schemes for physical impairments, functional limitations, and disability. Project Focus ‘96: The Conference on Sports Related Injury. Atlanta, Foundation for Physical Therapy, 1996, pp 9-12. 4. World Health Organization: International Classification of Functioning Disability and Health. Geneva, World Health Organization, 2001. 5. Nagi SZ: Some conceptual issues in disability and rehabilitation. In Sussman MB (ed): Sociology and Rehabilitation. Washington, DC, American Sociological Association, 1965, pp 100-113. 6. Nagi SZ: Disability concepts revisited: Implication for prevention. In Pope AM, Tarlov AR (eds): Disability in America: Toward a National Agenda for Prevention. Washington, DC, National Academies Press, 1991, pp 309-327. 7. National Institutes of Health 1992 National Advisory Board on Medical Rehabilitation Research: Draft V: Report and plan for medical rehabilitation research. Bethesda, Md, National Institutes of Health, 1992. 8. World Health Organization: International Classification of Impairments, Disabilities and Handicaps: A Manual of Classification Relating to the Consequences of Disease. Geneva, World Health Organization, 1980. 9. Jette AM: Physical disablement concepts for physical therapy research and practice. Phys Ther 74:380-386, 1994. 10. Verbrugge LM, Jette AM: The disablement process. Soc Sci Med 38:1-14, 1994. 11. Watkins MA, Riddle DL, Lamb RL, Personius WJ: Reliability of goniometric measurements and visual estimates of knee range of motion obtained in a clinical setting. Phys Ther 71:90-96, 1991. 12. Riddle DL, Rothstein JM, Lamb RL: Goniometric reliability in a clinical setting: Shoulder measurements. Phys Ther 67:668-673, 1987. 13. Myers JB, Laudner KG, Pasquale MR, et al: Glenohumeral range of motion deficits and posterior shoulder tightness in
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throwers with pathologic internal impingement. Am J Sports Med 34:385-391, 2006. Ellenbecker TS, Elmore E, Bailie DS: Descriptive report of shoulder range of motion and rotational strength 6 and 12 weeks following rotator cuff repair using a mini-open deltoid splitting technique. J Orthop Sports Phys Ther 36:326-335, 2006. Aitkens S, Lord J, Bernauer E et al: Relationship of manual muscle testing to objective strength measurements. Muscle Nerve 12:173-177, 1989. Beasley WC: Quantitative muscle testing: Principles and application to research and clinical services. Arch Phys Med Rehab 42:398-425, 1961. Kendall FP, McCreary EK, Provance PG: Muscles: Testing and function with posture and pain, Baltimore, Williams & Wilkins, 1993. Ellenbecker TS, Davies GJ: The application of isokinetics in testing and rehabilitation of the shoulder complex. J Athl Train 35:338-350, 2000. Tyler TF, Nahow RC, Nicholas SJ, et al: Quantifying shoulder rotation weakness in patients with shoulder impingement. J Shoulder Elbow Surg 14:570-574, 2005. Bot SDM, Terwee CB, van der Windt DAWM, et al: Clinimetric evaluation of the shoulder disability questionnaires: A systematic review of the literature. Ann Rheum Dis 63:335-341, 2004. Hudak PL, Amadio PC, Bombardier C; Upper Extremity Collaborative Group (UECG): Development of an upper extremity outcome measure: The DASH (Disabilities of the Arm, Shoulder, and Hand). Am J Industrial Med 29: 602-608, 1996. Beaton DE, Richards RR: Measuring function of the shoulder. A cross-sectional comparison of five questionnaires. J Bone Joint Surg Am 78:882-890, 1996. Lippitt SB, Harryman DT II, Matsen FA III: A practical tool for evaluating function: The simple shoulder test. In Matsen FA III, Fu FH, Hawkins RJ (eds): The Shoulder: A Balance of Mobility and Stability. Rosemont, Ill, American Academy of Orthopaedic Surgeons, 1993, pp 501-518. Richards RR, An K-N, Bigliani LU, et al: A standardized method for the assessment of shoulder function. J Shoulder Elbow Surg 3:347-352, 1994. Roach KE, Budiman-Mak E, Songsiridej N et al: Development of a shoulder pain and disability index. Arthritis Care Res 4:143-149, 1991. McSweeney AJ, Creer TL: Health related quality-of-life assessment in medical care. Dis Month 41:6-71, 1995. McHorney CA, Ware JE Jr, Raczek AE: The MOS 36-Item Short-Form Health Survey (SF-36): II Psychometric and clinical tests of validity in measuring physical and mental health constructs. Med Care 31:247-263, 1993. Guyatt GH, Feeny DH, Patrick DL: Measuring healthrelated quality of life. Ann Intern Med 118:622-629, 1993. Kirkley A, Alvarez C, Griffin S: The development and evaluation of a disease-specific quality-of-life questionnaire for disorders of the rotator cuff: The Western Ontario Rotator Cuff Index. Clin J Sport Med 13:84-92, 2003. Wessel J, Razmjou H, Mewa Y, et al: The factor validity of the Western Ontario Rotator Cuff Index. BMC Musculoskelet Dis 6:1-7, 2005. Beaton DE, Katz JN, Fossel AH et al: Measuring the whole or the parts? Validity, reliability, and responsiveness of the
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Disabilities of the Arm, Shoulder and Hand outcome measure in different regions of the upper extremity. J Hand Ther 14:128-146, 2001. Kirshner B, Guyatt G: A methodological framework for assessing health indices. J Chron Dis 38:27-36, 1985. Guyatt GH, Sackett DL, Cook DJ: Users’ guides to the medical literature: II. How to use an article about therapy or prevention: A. Are the results of the study valid? JAMA 270:2598-2601, 1993. Hoffman LG, Rouse MW, Brin BN: Quality of life: A review. J Am Optometric Assoc 66:281-289, 1995. Kessler RC, Mroczek DK: Measuring the effects of medical interventions. Med Care 33:AS109-AS119, 1995. Lohr KN, Aaronson NK, Alonso J, et al: Evaluating qualityof-life and health status instruments: Development of scientific review criteria. Clin Ther 18:979-992, 1996. Testa MA, Nackley JF: Methods for quality of life studies. Annu Rev Public Health 15:535-559, 1994. Testa MA, Simonson DC: Assessment of quality-of-life outcomes. N Engl J Med 334:835-840, 1996. Messick S: Validity. In Linn RL (ed): Educational Measurement. New York, American Council on Education/Macmillan Series on Higher Education, 1989, pp 13-103. Crocker L, Algina J: Introduction to classical and modern test theory. Fort Worth, Tex, Harcourt Brace Jovanovich College Publishers, 1986. Marx RG, Menezes A, Horovitz L et al: A comparison of two time intervals for test-retest reliability of health status instruments. J Clin Epidemiol 56:730-735, 2003.
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42. Streiner DL, Norman GR: Health Measurement Scales: A Practical Guide to their Development and Use. New York, Oxford University Press, 1995. 43. Shrout PE, Fleiss JL: Intraclass correlation: Uses in assessing rater reliability. Psychol Bull 86:420-428, 1979. 44. Beaton DE: Understanding the relevance of measured change through studies of responsiveness. Spine 25: 3192-3199, 2000. 45. Stratford PW, Binkley JM, Riddle DL: Health status measures: Strategies and analytic methods for assessing change scores. Phys Ther 76:1109-1123, 1996. 46. Classification, Assessment, Surveys and Terminology Team: International Classification of Functioning, Disability and Health 2. Geneva, World Health Organization, 2001. 47. Michener LA, Leggin BG: A review of self-report scales for the assessment of functional limitation and disability of the shoulder. J Hand Ther 14:68-76, 2001. 48. Michener LA, McClure PW, Sennett BJ: American Shoulder and Elbow Surgeons standardized shoulder assessment form: Reliability, validity and responsiveness. J Orthop Sports Phys Ther 30:A30, 2000. 49. Jette AM, Haley SM, Tao W, et al: Research reports: Prospective evaluation of the AM-PAC-CAT in outpatient rehabilitation settings. Phys Ther 87:385-398, 2007.
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APPENDIX I Shoulder Outcome Rating Scales
TABLE A-1 Simple Shoulder Test* 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.
Is your shoulder comfortable with your arm at rest by your side? Does your shoulder allow you to sleep comfortably? Can you reach the small of your back to tuck in your shirt with your hand? Can you place your hand behind your head with the elbow straight out to the side? Can you place a coin on a shelf at the level of your shoulder without bending your elbow? Can you lift 1 lb (a full pint container) to the level of your shoulder without bending your elbow? Can you lift 8 lb (a full gallon container) to the level of the top of your head without bending your elbow? Can you carry 20 lb (a bag of potatoes) at your side with the affected extremity? Do you think you can toss a softball underhand 10 yards with the affected extremity? Do you think you can throw a softball overhand 20 yards with the affected extremity? Can you wash the back of your opposite shoulder with the affected extremity? Would your shoulder allow you to work full-time at your regular job?
Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes Yes
No No No No No No No No No No No No
*The Simple Shoulder Test (SST) is used for patient self-assessment of general shoulder function. (From Lippitt SB, Harryman DT II, and Matsen FA III: A practical tool for evaluation function: the simple shoulder test. In Matsen FA III, Fu FH, and Hawkins RJ [eds]: The Shoulder: A Balance of Mobility and Stability. Rosemont, IL: American Academy of Orthopaedic Surgeons, 1993, pp 501–518.)
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TABLE A-2 Rowe Scoring System SCORING SYSTEM
EXCELLENT UNITS (100–90)
Stability, no recurrence, subluxation, or apprehension Apprehension when placing arm in certain positions
50
Subluxation (not requiring reduction) Motion 100% of normal external rotation, internal rotation, and elevation 75% of normal external rotation, and normal elevation and internal rotation 50% of normal external rotation, 75% of internal rotation and elevation 50% of normal external and internal rotation; no elevation Function: No limitation in work or sports; little or no discomfort
10
Mild limitation in work or sports; little or no discomfort Moderate limitation and discomfort Marked limitation and pain Total units possible
25
30
20
15
No recurrences
GOOD (89–75)
FAIR (74–51)
No recurrences
No recurrences
POOR (50 or less)
Recurrence of dislocation Moderate apprehension Marked apprehension Mild apprehension No apprehension during elevation during elevation and when placing the when placing arm in and extension external rotation arm in elevation and complete elevation external rotation and external rotation No subluxation No subluxation No subluxation 75% of normal 100% of normal external rotation, external rotation, internal rotation, internal rotation, and and complete complete elevation elevation
50% of normal external No external rotation; 50% of elevation rotation, 75% of (can get hand only internal rotation and to face) and 50% elevation of internal rotation
5
0
30
Marked limitation; Moderate limitation Performs all work and Mild limitation in unable to perform doing overhead work work and sports; sports; no limitation overhead work and and heavy lifting; shoulder strong; in overhead activities; lifting; cannot minimum discomfort unable to throw, shoulder strong in throw, play tennis, serve hard in tennis, lifting, swimming, or swim; chronic or swim; moderate tennis, throwing; no discomfort disabling pain discomfort
10 0 100
*The Rowe scoring system is used for evaluating the results of Bankart repairs. (From Rowe CR, Patel D, and Southmayd WW: The Bankart procedure: A long-term end-result study. J Bone Joint Surg 60A:1–16, 1978.)
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TABLE A-3 UCLA Scoring System*† FUNCTION/REACTION MEASURED
POINTS
Pain Present all of the time and unbearable; strong medication frequently Present all of the time but bearable; strong medication occasionally None or little at rest, present during light activities, salicylates frequently Present during heavy or particular activities only; salicylates occasionally Occasional and slight None
1 2 4 6 8 10
Function Unable to use limb Only light activities possible Able to do light housework or most activities of daily living Most housework, shopping, and driving possible; able to fix hair and dress and undress, including fastening brassiere Slight restriction only; able to work above shoulder level Normal activities
1 2 4 6 8 10
Active Forward Flexion 150 degrees or more 120 to 150 degrees 90 to 120 degrees 45 to 90 degrees 30 to 45 degrees Less than 30 degrees
5 4 3 2 1 0
Strength of Forward Flexion (Manual Muscle Testing) Grade Grade Grade Grade Grade Grade
5 4 3 2 1 0
(normal) (good) (fair) (poor) (muscle contraction) (nothing)
5 4 3 2 1 0
Satisfaction of the Patient Satisfied and better Not satisfied and worse
5 0
*The University of California–Los Angeles (UCLA) scoring system is used for evaluating shoulder function and patient satisfaction. (From Ellman H, Hanker G, and Bayer M: Repair of the rotator cuff: End-result study of factors influencing reconstruction. J Bone Joint Surg 68A:1136–1144, 1986.) † Maximum score of 35 points.
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TABLE A-4 Hospital for Special Surgery Scoring System* NO. OF POINTS Pain (30 points) None ⫽ 6 points, mild ⫽ 3, moderate ⫽ 2, severe ⫽ 0 during: 1. Sports 2. Non-sports overhead reaching 3. Activities of daily living 4. Sitting at rest 5. Sleeping Total
______ ______ ______ ______ ______ ______
Functional limitation (28 points) None ⫽ 7 points, mild ⫽ 4, moderate ⫽ 2, severe ⫽ 0 during: 1. Sports with hand overhead 2. Sports not involving use of the shoulder 3. Reaching overhead 4. Nonspecific activities of daily living Total
______ ______ ______ ______ ______
Tenderness (5 points) None ⫽ 5 points, at one or two sites ⫽ 3, at more than two sites ⫽ 0 Total
______
Impingement maneuvers (32 points) Indicated numbers of points are assigned for each maneuver in an allor-none fashion, 0 points being assigned if the maneuver is: 1. Impingement sign (15) 2. Abduction sign (12) 3. Adduction sign (5) Total
______ ______ ______ ______
Range of motion (5 points) One point is assigned for each 20-degree loss of motion in any plane, to a maximum of 5 points Total
______
*The Hospital for Special Surgery (HSS) scoring system is used for evaluating the results of acromioplasty. (From Altchek DW, Warren RF, Wickiewicz TL, et al: Arthroscopic acromioplasty: Technique and results. J Bone Joint Surg 72A:1198–1207, 1990.)
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TABLE A-5 Constant Scoring System* PAIN
POINTS
None Mild Moderate Severe
15 10 5 0
ACTIVITIES OF DAILY LIVING Activity Level Full work Full recreation/sport Unaffected sleep
Points 4 4 2
Positioning Up to waist Up to xiphoid Up to neck Up to top of head Above head
Points 2 4 6 8 10
Total for activities of daily living: 20 POINTS FOR FORWARD AND LATERAL ELEVATION Elevation (Degrees) 0–30 31–60 61–90 91–120 121–150 151–180
0 2 4 6 8 10
EXTERNAL ROTATION SCORING Position Hand behind head with elbow held forward Hand behind head with elbow held back Hand on top of head with elbow held forward Hand on top of head with elbow held back Full elevation from on top of head Total: 10 INTERNAL ROTATION SCORING Position Dorsum Dorsum Dorsum Dorsum Dorsum Dorsum
of of of of of of
hand hand hand hand hand hand
Points
to to to to to to
lateral thigh buttock lumbosacral junction waist (3rd lumbar vertebra) 12th dorsal vertebra interscapular region (DV 7)
Points 2 2 2 2 2
Points 0 2 4 6 8 10
*The Constant scoring system is used for evaluating general shoulder function both objectively and subjectively. (From Constant CR and Murley AHG: A clinical method of functional assessment of the shoulder. Clin Orthop 214:160–164, 1987.)
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TABLE A-6 ASES Scoring System* ASES PATIENT SELF-EVALUATION: INSTABILITY QUESTIONNAIRE Does your shoulder feel unstable (as if it is going to dislocate)?
YES
NO
How unstable is your shoulder (mark line)? 0 Very Stable
10 Very Unstable
ASES PATIENT SELF-EVALUATION: ACTIVITY OF DAILY LIVING QUESTIONNAIRE Circle the number in the box that indicates your ability to do the following activities: 0 ⫽ unable to do; 1 ⫽ very difficult to do; 2 ⫽ somewhat difficult; 3 ⫽ not difficult Activity 1. Put on a coat 2. Sleep on your painful or affected side 3. Wash back or do up bra in back 4. Manage toileting 5. Comb hair 6. Reach a high shelf 7. Lift 10 lb above the shoulder 8. Throw a ball overhand 9. Do usual work—list: 10. Do usual sport—list:
Right Arm 0123 0123 0123 0123 0123 0123 0123 0123 0123 0123
Left Arm 0123 0123 0123 0123 0123 0123 0123 0123 0123 0123
ASES PHYSICIAN ASSESSMENT: RANGE OF MOTION Range of Motion
Right
Total shoulder motion; goniometer preferred
Active
Passive
Left Active
Passive
Forward elevation (maximum arm-trunk angle) External rotation (arm comfortably at side) External rotation (arm at 90 degrees of abduction) Internal rotation (highest posterior anatomy reached with the thumb) Cross-body adduction (antecubital fossa to the opposite acromion)
ASES PHYSICIAN ASSESSMENT: SIGNS
0 ⫽ none; 1 ⫽ mild; 2 ⫽ moderate; 3 ⫽ severe Sign
Right
Left
Supraspinatus/greater tuberosity tenderness
0123
0123
Acromioclavicular joint tenderness
0123
0123
Biceps tendon tenderness (or rupture)
0123
0123
Other tenderness—list:
0123
0123
Impingement I (passive forward elevation in slight internal rotation)
YN
YN
Impingement II (passive internal rotation with 90 degrees of flexion)
YN
YN
Impingement III (90 degrees of active abduction—classic painful arc)
YN
YN
Subacromial crepitus
YN
YN
Scars—location:
YN
YN
Atrophy—location:
YN
YN
Deformity—describe:
YN
YN
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TABLE A-6 ASES Scoring System*—cont’d ASES PHYSICIAN ASSESSMENT: STRENGTH (RECORD MRC GRADE) 0 ⫽ no contraction; 1 ⫽ flicker; 2 ⫽ movement with gravity eliminated; 3 ⫽ movement against gravity; 4 ⫽ movement against some resistance; 5 ⫽ normal power Testing affected by pain?
Right
Left
YN
YN
Forward elevation
012345
012345
Abduction
012345
012345
External rotation (arm comfortably at side)
012345
012345
Internal rotation (arm comfortably at side)
012345
012345
ASES PHYSICIAN ASSESSMENT: INSTABILITY 0 ⫽ none; 1 ⫽ mild (0–1 cm translation) 2 ⫽ moderate (1–2 cm translation or translates to glenoid rim) 3 ⫽ severe (⬎2 cm translation or over rim of glenoid) Anterior translation
0123
0123
Posterior translation
0123
0123
Interior translation (sulcus sign)
0123
0123
Anterior apprehension
0123
0123
Reproduces symptoms?
YN
YN
Voluntary instability?
YN
YN
Relocation test positive?
YN
Generalized ligamentous laxity?
YN YN
Other physical findings:
Examiner’s name:
Date
*The American Shoulder and Elbow Surgeons (ASES) scoring system is used for evaluating general shoulder function both objectively and subjectively. (From Richards RR, An K-N, Bigliani LU, et al: A standardized method for assessment of shoulder function. J Shoulder Elbow Surg 3:347–352, 1994.)
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TABLE A-7 Health Status Questionnaire (SF-36©)* This survey asks for your views about your health. Please answer every question by circling the appropriate number: 1, 2, 3, etc. If you are unsure about how to answer a question, please give it the best answer you can and make a comment in the left margin, or on the back. Thank You. 1. In general, would you say your health is (circle one number): Excellent 1 Very good 2 Good 3 Fair 4 Poor 5 2. Compared to one year ago, how would you rate your health in general now? (Circle one number.) Much better now than 1 year ago 1 Somewhat better now than 1 year ago 2 About the same 3 Somewhat worse now than 1 year ago 4 Much worse now than 1 year ago 5 3. The following questions are about activities you might do during a typical day. Does your health limit you in these activities? If so, how much? (Circle 1, 2, or 3 on each line.) Yes, Limited a Lot Yes, Limited a Little No, Not Limited At All a. Vigorous activities, such as running, lifting heavy 1 2 3 objects, participating in strenuous sports b. Moderate activities, such as moving a table, 1 2 3 pushing a vacuum cleaner, bowling, or playing golf c. Lifting or carrying groceries 1 2 3 d. Climbing several flights of stairs 1 2 3 e. Climbing one flight of stairs 1 2 3 f. Bending, kneeling, or stooping 1 2 3 g. Walking more than 1 mile 1 2 3 h. Walking several blocks 1 2 3 i. Walking one block 1 2 3 j. Bathing and dressing yourself 1 2 3 4. During the past 4 weeks, have you had any of the following problems with your work or other regular daily activities as a result of your physical health? (Please answer YES or NO for each question by circling 1 or 2 on each line.) Yes No a. Cut down on the amount of time you spent on work 1 2 or other activities b. Accomplished less than you would like 1 2 c. Were limited in the kind of work or other activities 1 2 d. Had difficulty performing the work or other activities 1 2 (e.g., it took extra effort) 5. During the past 4 weeks, have you had any of the following problems with your work or other regular daily activities as a result of any emotional problems (e.g., feeling depressed or anxious)? (Please answer YES or NO for each question by circling 1 or 2 on each line.) Yes No a. Cut down on the amount of time you spent on 1 2 work or other activities b. Accomplished less than you would like 1 2 c. Didn’t do work or other activities as carefully 1 2 as usual 6. During the past 4 weeks to what extent have your physical health or emotional problems interfered with your normal social activities with family, friends, neighbors, or groups? (Circle one number.) Not at all 1 Slightly 2 Moderately 3 Quite a bit 4 Extremely 5
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TABLE A-7 Health Status Questionnaire (SF-36©)*—cont’d 7. How much body pain have you had during the past 4 weeks? (Circle one number.) None 1 Very mild 2 Mild 3 Moderate 4 Severe 5 Very severe 6 8. During the past 4 weeks, how much did pain interfere with your normal work (including work both outside the home and housework)? (Circle one number.) Not at all 1 A little 2 Moderately 3 Quite a bit 4 Extremely 5 9. These questions are about how you feel and how things have been with you during the past month. For each question, please indicate the one answer that comes closest to the way you have been feeling. How much of the time during the past month All of Most of A Good Bit Some of A Little of None of the Time the Time of the Time the Time the Time the Time a. Did you feel full of pep? 1 2 3 4 5 6 b. Have you been a very nervous person? 1 2 3 4 5 6 c. Have you felt so down in the dumps nothing could 1 2 3 4 5 6 cheer you up? d. Have you felt calm and peaceful? 1 2 3 4 5 6 e. Did you have a lot of energy? 1 2 3 4 5 6 f. Have you felt downhearted and blue? 1 2 3 4 5 6 g. Did you feel worn out? 1 2 3 4 5 6 h. Have you been a happy person? 1 2 3 4 5 6 i. Did you feel tired? 1 2 3 4 5 6 j. Has your health limited your social activities 1 2 3 4 5 6 (like visiting your friends or close relatives)? 10. Please choose the answer that best describes how true or false each of the following statements is for you. (Circle one number on each line.) Definitely Mostly Mostly Definitely True True Not Sure False False a. I seem to get sick a little easier than other people 1 2 3 4 5 b. I am as healthy as anybody I know 1 2 3 4 5 c. I expect my health to get worse 1 2 3 4 5 d. My health is excellent 1 2 3 4 5 11. Please answer YES or NO for each question by circling 1 or 2 on each line. Yes No a. In the past year, have you had 2 weeks or more during which you felt sad, blue, or depressed; or 1 2 when you lost all interest or pleasure in things you usually care about or enjoyed? b. Have you had 2 years or more in your life when you felt depressed or sad most days, even if you 1 2 felt okay sometimes? c. Have you felt depressed or sad much of the time in the past year? 1 2 *The Health Status Questionnaire (SF-36©) form is used for patient self-assessment of overall health status. (From Ware JE and Sherbourne CD: The MOS 36 item short-form health survey [SF-36]. I. Conceptual framework and item selection. Med Care 30[6]:473–481, 1992.)
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APPENDIX II Shoulder Rehabilitation
Exercise Programs
Fundamental Shoulder Exercises Range of Motion Exercises 1. L-Bar Flexion: Lie on back and grip L-Bar between index finger and thumb, elbows straight. Raise both arms overhead as far as possible keeping thumbs up. Hold for _____ seconds and repeat _____ times.
2. L-Bar External Rotation, Scapular Plane: Lie on back with involved arm 45° from body and elbow bent at 90°. Grip L-Bar in the hand of involved arm and keep elbow in flexed position. Using uninvolved arm, push involved arm into external rotation. Hold for ____ seconds, return to starting position. Repeat _____ times.
3. L-Bar Internal Rotation, Scapular Plane: Lie on back with involved arm 45° from body and elbow bent at 90°. Grip L-Bar in the hand of involved arm and keep elbow in flexed position. Using the uninvolved arm, push involved arm into internal rotation. Hold for ______ seconds, return to starting position. Repeat ______ times.
839
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Strengthening Exercises 1. Tubing, External Rotation: Standing with involved elbow fixed at side, elbow bent to 90° and involved arm across the front of the body. Grip tubing handle while the other end of tubing is fixed. Pull out with arm, keeping elbow at side. Return tubing slowly and controlled. Perform _____ sets of _____ reps.
2. Tubing, External Rotation: Standing with elbow at side fixed at 90° and shoulder rotated out. Grip tubing handle while other end of tubing is fixed. Pull arm across body keeping elbow at side. Return tubing slowly and controlled. Perform _____ sets of _____ reps.
3. Lateral Raises to 90°: Standing with arm at side, elbow straight, and palm against side. Raise arm to side, rotating palm up as arm reaches 90°. Do not go above shoulder height. Hold for _____ seconds and lower slowly. Perform _____ sets of ____ reps.
4. “Full Can”: Stand with elbow extended and thumb up. Raise arm to shoulder level at 30° angle in front of body. Do not go above shoulder level. Hold for _____ seconds and lower slowly. Perform _____ sets of ______ reps.
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841
5. Side-Lying External Rotation: Lie on uninvolved side, with involved arm at side of body and elbow bent to 90°. Keeping the elbow of involved arm fixed to side, raise arm. Hold ____ seconds and lower slowly. Perform _____ sets of _____ reps.
6. Prone Horizontal Abduction: Lie on table, face down, with involved arm hanging straight to floor and palm facing down. Raise arm out to the side, parallel to the floor. Hold _____ seconds and lower slowly. Perform _____ sets of ____ reps.
7. Prone Rowing: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, and bring dumbbell as high as possible. Hold at the top for _____ seconds then lower slowly. Perform ____ sets of _____ reps.
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APPENDIX III Thrower’s Ten Exercise Program
The Thrower’s Ten Program is designed to exercise the major muscles necessary for throwing. The program’s goal is to be organized and concise. All exercises included are specific to the thrower and are designed to improve strength, power, and endurance of the shoulder complex musculature.
1A. Diagonal pattern D2 extension: Involved hand will grip tubing handle overhead and out to the side. Pull tubing down and across your body to the opposite side of leg. During the motion, lead with your thumb. Perform _______ sets of _______ repetitions _______ daily.
1B. Diagonal pattern D2 flexion: Gripping tubing handle in hand of involved arm, begin with arm out from side 45° and palm facing backward. After turning palm forward, proceed to flex elbow and bring arm up and over involved shoulder. Turn palm down and reverse to take arm to starting position. Exercise should be performed _______ sets of _______ repetitions _______ daily.
2A. External rotation at 0° abduction: Stand with involved elbow fixed at side, elbow at 90° and involved arm across front of body. Grip tubing handle while the other end of tubing is fixed. Pull out arm, keeping elbow at side. Return tubing slowly and controlled. Perform _______ sets of _______ repetitions _______ times daily.
2B. Internal rotation at 0° abduction: Standing with elbow at side fixed at 90° and shoulder rotated out. Grip tubing handle while other end of tubing is fixed. Pull arm across body keeping elbow at side. Return tubing slowly and controlled. Perform _______ sets of _______ repetitions _______ times daily.
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THE ATHLETE’S SHOULDER
2C. (Optional) External rotation at 90° abduction: Stand with shoulder abducted 90°. Grip tubing handle while the other end is fixed straight ahead, slightly lower than the shoulder. Keeping shoulder abducted, rotate shoulder back keeping elbow at 90°. Return tubing and hand to start position. I. Slow speed sets: (Slow and controlled) Perform _______ sets of _______ repetitions _______ times daily. II. Fast speed sets: Perform _______ sets of _______ repetitions _______ times daily.
2D. (Optional) Internal rotation at 90° abduction: Stand with shoulder abducted to 90°, externally rotated 90° and elbow bent to 90°. Keeping shoulder abducted, rotate shoulder forward, keeping elbow bent at 90°. Return tubing and hand to start position. I. Slow speed sets: (Slow and controlled) Perform _______ sets of _______ repetitions _______ times daily. II. Fast speed sets: Perform _______ sets of _______ repetitions _______ times daily.
3. Shoulder abduction to 90°: Stand with arm at side, elbow straight, and palm against side. Raise arm to the side, palm down, until arm reaches 90° (shoulder level). Perform _______ sets of _______ repetitions _______ times daily.
4. Scaption, external rotation: Stand with elbow straight and thumb up. Raise arm to shoulder level at 30° angle in front of body. Do not go above shoulder height. Perform _______ sets of _______ repetitions _______ times daily.
5. Sidelying external rotation: Lie on uninvolved side, with involved arm at side of body and elbow bent to 90°. Keeping the elbow of involved arm fixed to side, raise arm and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
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THROWER’S TEN EXERCISE PROGRAM
845
6A. Prone horizontal abduction (neutral): Lie on table, face down, with involved arm hanging straight to the floor, and palm facing down. Raise arm out to the side, parallel to the floor. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
6B. Prone horizontal abduction (full ER, 100° ABD): Lie on table face down, with involved arm hanging straight to the floor, and thumb rotated up (hitchhiker). Raise arm out to the side with arm slightly in front of shoulder, parallel to the floor. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
6C. Prone rowing: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, and bring dumbbell as high as possible. Hold at the top for 2 seconds, then slowly lower. Perform _______ sets of _______ repetitions _______ times daily.
6D. Prone rowing into external rotation: Lying on your stomach with your involved arm hanging over the side of the table, dumbbell in hand and elbow straight. Slowly raise arm, bending elbow, up to the level of the table. Pause one second. Then rotate shoulder upward until dumbbell is even with the table, keeping elbow at 90°. Hold at the top for 2 seconds, then slowly lower taking 2–3 seconds. Perform _______ sets of _______ repetitions _______ times daily.
7. Press-ups: Seated on a chair or table, place both hands firmly on the sides of the chair or table, palm down and fingers pointed outward. Hands should be placed equal with shoulders. Slowly push downward through the hands to elevate your body. Hold the elevated position for 2 seconds and lower body slowly. Perform _______ sets of _______ repetitions _______ times daily.
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THE ATHLETE’S SHOULDER
8. Push-ups: Start in the down position with arms in a comfortable position. Place hands no more than shoulder width apart. Push up as high as possible, rolling shoulders forward after elbows are straight. Start with a push-up into wall. Gradually progress to table top and eventually to floor as tolerable. Perform _______ sets of _______ repetitions _______ times daily.
9A. Elbow flexion: Standing with arm against side and palm facing inward, bend elbow upward turning palm up as you progress. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
9B. Elbow extension (abduction): Raise involved arm overhead. Provide support at elbow from uninvolved hand. Straighten arm overhead. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
10A. Wrist extension: Supporting the forearm and with palm facing downward, raise weight in hand as far as possible. Hold 2 seconds and lower slowly. Perform _______ sets of _______ repetitions _______ times daily.
10B. Wrist flexion: Supporting the forearm and with palm facing upward, lower a weight in hand as far as possible and then curl it up as high as possible. Hold for 2 seconds and lower slowly.
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THROWER’S TEN EXERCISE PROGRAM
847
10C. Supination: Forearm supported on table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm up. Hold for a 2 count and return to starting position. Perform _______ sets of _______ repetitions _______ times daily.
10D. Pronation: Forearm should be supported on a table with wrist in neutral position. Using a weight or hammer, roll wrist taking palm down. Hold for a 2 count and return to starting position. Perform _______ sets of _______ repetitions _______ times daily.
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Index
Note: Page numbers followed by b indicate boxed material; those followed by f indicate figures; those followed by t indicate tables.
A Abdominal(s), core stabilization exercises for, 769, 770f–772f Abdominal oblique muscle in golf swing, 466 Abduction bilateral peak torque and, 726, 727t clavicular, 23 coracoacromial arch and, 12 coracohumeral ligament and, 9 deltoid muscles and, 620–621, 622 glenohumeral capsule and, 8 glenohumeral ligaments and, 10 horizontal isokinetic exercise and, 738, 739f neutral, electromyographic analysis of scapulothoracic musculature during, 597t at 135 degrees of abduction with external rotation, trapezius and serratus anterior activity during, 606t following posterior instability repair, 223, 224f prone. See Prone horizontal abduction. isokinetic exercise and, 737, 737f isokinetic shoulder torque to body weight ratios and, 732t isokinetic testing and, bilateral comparison of, 726, 727t neurodynamic testing in, 711 to 90 degrees, in thrower’s 10 program, 844 above 120 degrees with external rotation glenohumeral muscle activity during, 608t scapular muscle activity during, 609t resisted, in upright position, end range of, throwing motion and, 651 scapular, 19f, 20 in scapular plane, infraspinatus and, 614–615 of sternoclavicular joint, 23 and subscapularis muscle, 620 supraspinatus muscle and, 605 teres minor muscle and, 617, 619 Abduction braces, postoperative, 815 Abduction exercise(s) electromyographic analysis of scapulothoracic musculature during, 597t, 598t horizontal, prone, 841 with full glenohumeral external rotation, 598–599 horizontal, with external rotation, electromyographic analysis of scapulothoracic musculature during, 597t Accelerated throwing interval programs, 792–793, 793b, 794b
Acceleration in isokinetic testing, interpretation of, 726 Acceleration phase of baseball pitching biomechanics of, 366t, 367 electromyography during, 386t, 388–389 of golf swing electromyography during, 397t, 398, 398t, 466 kinematic analysis of, 466, 467t of tennis serve electromyography during, 394t, 395 muscular activity patterns in, 431 of tennis volley, electromyography during, 395, 396t of throwing football, electromyography during, 390t instability and, 406, 407f of volleyball serve and spike, electromyography during, 392–393, 393t Acquired repetitive microtrauma, 401 Acromioclavicular joint anatomy of, 4–5, 5f, 116, 303, 304f biomechanics of, 23–24, 24f injuries of. See Acromioclavicular joint injuries. innervation of, 14 movement of, total arm movement and, 5 protection of, 809, 810f taping of, 809–810, 811f Acromioclavicular joint injuries, 303–312 baseball and, 410–411 classification of, 303–304, 305f diagnosis of, 304–306, 305f examination for, 57–58 in football, 423–424 incidence of, 304 mechanisms of injury and, 303, 304f radiographic evaluation of, 306 rehabilitation for, 311–312 treatment of, 306–311 operative arthroscopy for, 103 type I, 303, 304f, 305, 305f, 306, 423, 424 type II, 303, 304f, 305, 305f, 306–307, 307f, 423, 424 type III, 303, 304f, 305, 305f, 306, 307–308, 423, 424 type IV, 303, 304f, 305f, 305–306, 308, 423, 424 type V, 303, 304f, 305, 305f, 308, 423, 424 type VI, 303, 304f, 305f, 308, 423, 424 Acromion anatomy of, 116 variations of, 116–117, 117f deformity of, 6 fractures of, in football, 426
Acromion (Continued) shapes of, 6, 7f type II anterior hooked acromion process and, impingement and, 527, 529f Acromioplasty anterior, for subacromial impingement, 120, 121f arthroscopic, for subacromial impingement, 120 for compressive cuff disease, 99 Active pathology, definition of, 818 Active range of motion as body function measure, 819–820 in scapular dyskinesis assessment, 673b, 673–674, 674f Active rest for impingement, 534 Active-assisted range-of-motion exercises for impingement, 535 for instability, 551, 552 following posterior instability repair, 222–223 for superior labral anterior-posterior lesions, 138 Activity definition of, 819 limitations for, definition of, 819 measures of, 820–821, 826 as prognostic factor, 819 Adaptation, 629–630, 775–776 Adduction bilateral peak torque and, 726, 727t horizontal in golf swing, 465 isokinetic exercise and, 738, 739f light adduction stretching following posterior instability repair and, 223, 224f 0-135 degrees of, side-lying eccentric control of, glenohumeral muscle activity during, 608t isokinetic exercise and, 737, 737f isokinetic shoulder torque to body weight ratios and, 732t isokinetic testing and, bilateral comparison of, 726, 727t scapular, 19f, 20 of sternoclavicular joint, 23 teres minor muscle and, 616–617 Adhesion-cohesion mechanism, glenohumeral stability and, 33 Adhesive capsulitis, 293–301, 685 causes of, 293 diagnosis of, 293–294 imaging in, 75–76 natural history of, 294
849
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850
INDEX
Adhesive capsulitis (Continued) pathogenesis of, 293 stage I (painful stage), 294 treatment of, 295b, 295–296 stage II (adhesion stage), 294 treatment of, 295b, 296, 296f stage III (frozen stage), 294 treatment of, 295b, 296, 297f, 298f stage IV (chronic or thawing stage), 294 treatment of, 294–301 arthroscopic capsular release for, 298–300, 300f manipulation under anesthesia for, 296–298, 299f open surgical release for, 300–301 physical therapy in, 295b, 295–296, 296f–298f Adhesive felt for padding, 809 Adhesive tape, 807 Adolescents, 563–567 definition of adolescence and, 565 safety recommendations for baseball pitchers and, 508, 508b strength training in age-specific guidelines for, 566f, 566–567, 567f benefits of, 564–565 efficacy of, 563–564 guidelines for, 565, 565t Adson test in thoracic outlet syndrome, 327, 327f Adson’s maneuver, 69 Afferent information, central nervous system processing of, 656–657 Age. See also Adolescents; Children; Preadolescents. age-specific rehabilitation guidelines and, 566f, 566–567, 567f baseball pitching biomechanics and, 368–370, 369t conditioning program for shoulders and, 778 training, conditioning program for shoulders and, 778 Alloplast, 809 Alpha motor neuron, muscle reflexes and, 658 ALPSA. See Anterior labroligamentous periosteal sleeve avulsion lesions. American Equipment Managers’Association, 807 American Shoulder and Elbow Surgeons Shoulder Score Index, 820, 823t, 834t–835t Amortization phase of plyometric exercise, 752 Anatomic theory of internal impingement pathology, 123 Anatomy of shoulder joint complex, 3–14 of acromioclavicular joint, 4–5, 5f, 116, 303, 304f of acromion, 116–117, 117f arthroscopic, normal. See Arthroscopy, normal shoulder anatomy on. of bursae, 12–13, 13f of coracoacromial arch, 12, 12f of coracohumeral ligament, 9, 9t external, arthroscopic, 105–106, 106f of glenohumeral capsule, 7–9, 8f, 9f, 192–193 of glenohumeral joint, 3, 5–7, 6b, 6f, 7f of glenohumeral ligaments, 9–10, 93, 93f, 209–210
Index_849-876-F06701.indd 850
Anatomy of shoulder joint complex (Continued) of glenoid labrum, 7, 7f, 92–93, 192, 193f of nerves, 13–14 of rotator cuff, 10–12, 11t, 94, 95f, 116 variations of, 116–117, 117f stability and, 191–197, 192f–196f dynamic stabilizers and, 192 glenohumeral capsule and, 192–193 glenohumeral ligaments and, 193f–196f, 193–196 glenoid fossa and, 192 glenoid labrum and, 192, 193f osseous adaptation and, 192 rotator interval and, 196f, 196–197 static stabilizers and, 192 of sternoclavicular joint, 3–4, 4f upper extremity function related to, 3 of vascular supply, 13 Anesthesia examination under in anterior acute dislocation of shoulder, for arthroscopic treatment, 246 for arthroscopic rotator cuff repair, 180 manipulation under, for adhesive capsulitis, 296–298, 299f Aneurysms of axillary artery, 329–330 Angiography, magnetic resonance, 73–74 in posterior instability, 214–215, 215f Annulus fibrosus, 351 Antagonists, reversal of in proprioceptive neuromuscular facilitation, 642–643 for scapular dyskinesia, 678 Anterior dislocation of shoulder, acute, 239–254 acute anterior instability algorithm for, 234 arthroscopic treatment of, 245–251 with acute osseous Bankart lesions, 251 Bankart repair with suture anchors for, 248–249 examination under anesthesia in, 246 with extension of anterior inferior labrum tear into superior labrum, 250–251 with extension of capsulolabral injury posteriorly, 250, 251f outcomes with, 253–254 rotator interval closure for, 249–250, 250f technical errors in, 252–253 causes and epidemiology of, 242–243 classification of, 239 diagnosis of, 243 evaluation and physical examination in, 243 radiologic features in, 243, 244f nonoperative treatment of, 244–245, 245f pathoanatomy of, 239–242 Bankart lesion and, 239–240, 240f glenoid bone lesions and, 242, 242f humeral avulsion of glenohumeral ligament lesions and, 241, 241f humeral head lesions and, 241–242 superior labrum extension and, 240, 240f traumatic bone lesions and, 241 postoperative care for, 251–252 treatment of, 244–251 Anterior instability of shoulder. See Instability of shoulder, anterior. Anterior interval slide, 168–169
Anterior labroligamentous periosteal sleeve avulsion lesions dislocation and, 240, 240f imaging of, 77, 79f Anterior laxity theory of internal impingement pathology, 123–124, 124f Anterior release test in multidirectional instability, 231t Anthropometric adaptation in tennis players, 435 Anticoagulation for axillary artery compression and aneurysm, 330 Apprehension test(s), 46, 67f, 67–68, 68f for glenohumeral laxity, 101 in multidirectional instability, 229, 231t in PASTA lesions, 144 in tensile failure of rotator cuff, 113 Approximation for proprioceptive neuromuscular facilitation, 641 Aquaplast, 809 Aquatic dumbbells, isotonic exercises with, in conditioning program for shoulder, 781–782, 782b Arc of rotation, total, assessment of, 58–59, 59f Arm(s). See also Forearm(s). locomotion on, shoulder mechanics and, 493 Arm acceleration exercise, 616f Arm acceleration phase. See Acceleration phase. Arm cocking. See Cocking phase. Arm deceleration. See Deceleration phase. Arteriography, subclavian, in quadrilateral space syndrome, 332, 333f Arthritis. See Adhesive capsulitis; Osteoarthritis. Arthrofibrosis, 685–692 causative factors in, 686 clinical presentation of, 686 connective tissue response and, 686–687 historical background of, 685–686 mobilization positions and direction for, 689–692 multiplane, 690f, 690–692 proprioceptive neuromuscular facilitation techniques and, 692 single-plane, 689–690 soft tissue, 692 neuromuscular electrical stimulation for, 689 restrictions in, 687f, 687–689, 688b stages of, 686 treatment of, 685 Arthrography, 73 magnetic resonance, 73 of biceps tendon dislocation, 81, 81f of labral injuries, 77–78, 78f, 79f of loose bodies, 75, 76f of rotator cuff tears, 83–85, 84f, 85f in PASTA lesions, 145 Arthrokinematic dysfunctions, 765 Arthrokinematics. See also Kinematics. of front crawl stroke, 452t of scapulothoracic joint. See Biomechanics, of scapulothoracic joint. Arthropathy. See also Adhesive capsulitis; Osteoarthritis. arthroplasty of the shoulder for, 315 Arthroplasty of the shoulder, 315–323 for capsulorrhaphy arthropathy, 315 degenerative osteoarthritis and, 315, 316f indications for, 316–317
9/19/08 7:17:23 PM
INDEX Arthroplasty of the shoulder (Continued) surgical considerations and, 316–317, 317f, 318f obligate translation and, 316 outcomes of, 322, 322t rehabilitation following, 317–322, 318t capsular relationship optimization and, 318 range of motion and, 318 rotator cuff and scapular exercise progression for, 320–322, 321f strengthening and, 319–320, 320f subscapularis precautions for, 318, 319b surgical approaches for, 317–318 Arthroscopic débridement, for PASTA lesions débridement-only technique for, 146–147 with subacromial decompression, 146–147 Arthroscopic drive-through sign, 199 Arthroscopic rotator cuff repair, 101, 159, 177–188 anchor placement for, 179, 179f examination under anesthesia for, 180 knot placement for, 179–180 mini-open repair versus, 165–167, 173–174 patient positioning and draping for, 180, 180f portal placement for, 180–181, 181f rehabilitation following, 186–187 results and outcomes with, 187–188 surgical indications and contraindications and, 180 surgical techniques for, 182–186 diagnostic arthroscopy as, 182 subacromial inspection and decompression as, 182 tear configuration and repair determination and, 182–186 for tuberosity insertion site preparation, 182, 182f suture type for, 179 tear pattern and size and, 179 tear pattern classification and, 177, 178f Arthroscopy diagnostic in internal impingement, 130–131, 135–136 for posterior instability, 218, 218f for rotator cuff tears, 182 in rotator cuff tears, 159 skybox view on, 218, 218f examination for glenohumeral translation using, 67 examination under anesthesia using, 105 normal shoulder anatomy on, 91–96 of biceps tendon, 91, 92f of glenohumeral ligaments, 93, 93f of glenoid labrum, 92–93 of humeral head and glenoid, 91 of rotator cuff, 94, 95f of rotator interval, 94 of subscapularis tendon and bursa, 93, 94f of superior recess and subacromial space, 94–96, 95f, 96f treatment using. See Operative arthroscopy. Artistic gymnastics. See Gymnastic injuries; Gymnastics. ASES Shoulder Score Index, 820, 823t, 834t–835t Atmospheric pressure, glenohumeral stability and, 33 Australian crawl, 445. See also Swimmer’s shoulder; Swimming.
Index_849-876-F06701.indd 851
Avascular necrosis, imaging in, 74, 76f Average power in isokinetic testing, 726 Axillary artery anatomy of, 329, 329f occlusion and aneurysm of, 329–330 Axillary nerve anatomy of, 13, 708, 709f injuries of, 354 in football, 422 neurodynamic testing of, 711, 712f Axillary pouch, 10 Axillosubclavian vein, compression of, 330–332, 331f Axioclavicular muscles, biomechanics and, 33–35, 34f, 35f Axiohumeral muscles. See also Latissimus dorsi muscle; Pectoralis major muscle. biomechanics of, 37 Axioscapular muscles, biomechanics and, 33–35, 34f, 35f Axon(s), Wallerian degeneration of, 337 Axonotmesis, 337
B Back, low, golf swing modifications with, 485 Back extension, prone, in plyometric program, 757, 758f Back lever position, shoulder mechanics and, 496–497 Back palsy, 341 Backpack paralysis, 341 Backswing phase of golf swing electromyographic and kinematic analysis of, 465–466, 467t pathomechanical analysis of, 468 Balance of forces, stability of shoulder and, 658 Ball(s). See Medicine ball; Physioball exercises for internal impingement; Plyoball; Swiss ball; specific sports. Ball address position squats for warm-up for golf, 475t, 477 Band walk exercise, 769, 771f Bankart lesions, 7, 7f, 257–265, 258f bony, 267 causative factors for, 259–260 diagnosis and assessment of, 260f, 260–261 dislocation and, 239–240, 240f imaging of, 77, 78f instability and, 197, 545 literature review for, 258–260 of basic science, 258–259 of causative factors and natural history, 259–260 natural history of, 259–260 pathoanatomy of, 257–258, 258f, 259f rehabilitation for, 263–264, 546, 547f reverse, 210 imaging of, 78, 79f osseous, 78, 79f, 211 Bankart repair anchor fixation for, 200 arthroscopic, 102, 261–262 benefits of, 262 open repair versus, 202–204 procedural approaches for, 261–262 staple capsulorrhaphy for, 199–200
851
Bankart repair (Continued) complications of, 264–265 indications for, 261, 261b open, 198–199, 199f, 262–263 anatomic repairs as, 262–263 arthroscopic repair versus, 202–204 recommended technique for, 263, 264f with suture anchors, for anterior dislocation of shoulder, 248–249, 249f tight, scapulohumeral rhythm and, 23 Baseball acromioclavicular joint disorders and, 410–411 batting in. See Baseball swing. biceps brachii tendon pathology and, 409–410, 410f glenoid labrum tears in, 408–409, 409f hitting in. See Baseball swing. instability of shoulder in, 406, 407f, 408, 408f Little Leaguer’s shoulder and, 508–510, 509f neurovascular syndromes and, 411 osteochondritis dissecans and, 410 pitching in. See Baseball pitching; Baseball throwing; Softball pitching. rotator cuff injuries in, 401–406 compressive, 404 internal impingement as, 402–403, 403f overuse tendinitis as, 403, 403f, 404f subacromial impingement as, 404–405, 405f tears as, 406 tensile lesions as, 403–404, 405f scapula disorders and, 412–413 scapulothoracic bursitis as, 413 snapping scapula as, 412–413 suprascapular nerve entrapment and, 411–412, 412f throwing in. See Baseball pitching; Baseball throwing; Softball pitching. Baseball hitting interval program, 793, 796, 796b Baseball pitching. See also Softball pitching. anterior instability and, 387–389 biomechanics of, 365–373 arm acceleration and, 366t, 367 of arm cocking, 366t, 366–367, 368f, 374t arm deceleration and, 366t, 367–368, 374t of changeup, 370t, 370–371, 371t comparison among levels of development and, 368–369, 369t comparison among pitch types and, 370t, 370–371, 371t of curveball, 370t, 370–371, 371t of fastball, 370t, 370–371, 371t flat ground throwing and, 371 of follow-through, 368, 374t football throwing compared with, 373–374, 374t humeral retroversion and, 373 normal, 365–368, 366t pathomechanics and, 371–373 rotator cuff injuries and, 372 shoulder-grinding factor and, 372 SLAP lesions and, 372–373 of slider, 370t, 370–371, 371t stride and, 365–366, 367f subacromial impingement and, 372 of wind-up, 365, 367f
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852
INDEX
Baseball pitching. See also Softball pitching. (Continued) electromyography during, 385, 386f, 386t, 387–389 in arm acceleration phase, 386t, 388–389 in arm cocking phase, 385, 386t, 387–388 in arm deceleration phase, 386t, 389 in stride phase, 385, 386t in wind-up phase, 385, 386t humeral rotation and, 435, 435t safety recommendations for, for adolescents, 508, 508b thrower’s exostosis and, 409, 410f thrower’s 10 program for, 413–414, 414f–415f, 416 Baseball swing baseball hitting interval program and, 793, 796, 796b bat contact phase of, 395 biomechanics of, 380 coiling process in, 380 electromyography during, 395–396 follow-through phase of, 380 stride phase of, 380 swing phase of, 380 Baseball throwing. See also Baseball pitching; Softball pitching. interval program in, 789, 790b–792b, 791–796 accelerated throwing programs and, 792–793, 793b, 794b hitting program and, 793, 796, 796b Little League, 793, 795b long toss in, 789, 791 off-the-mound, 791–792 softball, 796, 797b one-handed, in plyometric program, 757, 760f Bat contact phase of baseball batting, 395 Batting in baseball. See Baseball swing. Belly press test, 63, 63f Bench press exercise in conditioning program for shoulders, 779 deltoid activity and, 621 Bennett lesion, 214 baseball and, 409, 410f imaging of, 77, 77f operative arthroscopy for, 102–103 Biceps brachii exercise for tennis injuries, 439 Biceps brachii muscle activity of, in shoulder exercises, 611t anatomy of, 284 in baseball pitching, 386t, 387, 388, 389 biomechanics of, 37 cross-sectional area of, 11t disorders of assessment for, 63–65, 64f, 65f examination in, 63–65, 64f, 65f in football throwing, 389, 390t function of, in baseball pitching, 372 long head of function of, 11 tenosynovitis of, 685 strengthening of, for superior labral anteriorposterior lesions, type II, 139 tendon of. See Biceps tendinitis; Biceps tendinosis; Biceps tendon. in tennis serve, 394t, 394–395 in tennis volley, 395, 396t
Index_849-876-F06701.indd 852
Biceps load test(s), 47–48 in multidirectional instability, 231t in SLAP lesions, 409 Biceps stretch for scapular dyskinesis, 676, 676f Biceps tendinitis, 284–286 biceps tendon subluxation and dislocation and, 285 clinical presentation of, 284 in football, 425 nonoperative treatment of, 285–286, 286b, 286f pathology of, 285 radiographic evaluation of, 284–285 Biceps tendinosis imaging of, 80 treatment of, 286 Biceps tendon, 7, 283–287 anatomy of, 8–9 arthroscopic, 91, 92f functional, 284 dislocation of, 285 imaging of, 81, 81f disorders of. See also Biceps tendinitis; Biceps tendinosis. baseball and, 409–410, 410f in female athlete, rehabilitation for, 571, 573f, 573t, 573–574 in football, 425 of long head in baseball pitching, 389 rupture of, 286–287 palpation of, 57, 57f repetitive trauma of, restriction of motion due to, 686 rupture of imaging of, 80–81 long head, 286–287 subluxation of, 285 tendinitis of. See Biceps tendinitis. Biceps tenodesis for biceps long head ruptures, 287 Biceps tenosynovitis. See Adhesive capsulitis. Biceps tenotomy for biceps long head ruptures, 287 Bicipital groove palpation of, 57 tenderness of, in multidirectional instability, 232t Bilateral comparison, in isokinetic testing, 726, 726t, 727t Biomechanics, 17–37 of acromioclavicular joint, 23–24, 24f of arthroscopic rotator cuff repairs, 179f, 179–180 of baseball pitching. See Baseball pitching, biomechanics of. of baseball swing, 380 in children, 507 of cricket throwing and bowling, 376–377 of football throwing, 373–374, 374t of front crawl, 450f, 450–451, 451f, 452t of glenohumeral joint, 24–26, 25f–27f of golf swing, 380–381 of handball, 377–378, 378t of javelin throwing, 376 muscle activity and, 33–37, 34b axiohumeral, 37 axioscapular and axioclavicular, 33–35, 34f, 35f
Biomechanics (Continued) biceps brachii, 37 coracobrachialis, 37 scapulohumeral, 35–36, 36f triceps brachii, 37 planes of motion and, 17–18, 18f of scapula, 17–18, 18f, 19f in resting position, 17 of rotator cuff, 603, 605–620 of infraspinatus and teres minor, 607, 612–619 of subscapularis, 617, 619–620 of supraspinatus, 603, 605–607 of scapula, 671–672, 672f of scapulothoracic joint, 18–23, 19f abduction and, 19f, 20 adduction and, 19f, 20 depression and, 19, 19f downward and upward rotation and, 19f, 20, 20f elevation and, 19, 19f internal and external rotation and, 20, 20f posterior and anterior tilt and, 20, 20f scapulohumeral rhythm and, 20–23, 21t shoulder rehabilitation exercises and, 589–600 effects of shoulder pathology and, 599, 600t electromyographic analysis of exercises and, 589, 590t–591t, 591–596 lower trapezius and, 597b, 598–599 scapulothoracic joint and, 596–599, 597t–598t serratus anterior and, 597–598, 598f, 598t, 599f stability and, 26–33 adhesion-cohesion mechanism and, 33 articular surfaces and, 26–27 atmospheric pressure and, 33 capsuloligamentous complex and, 28–31, 29f dynamic, 31f, 31–33 labrum and, 27–28, 28f of sternoclavicular joint, 23, 23f of swimming, 381t, 381–382, 382t of tennis serve, 378–380, 379t of windmill throwing, 374–376, 375t Bipod exercise, glenohumeral muscle activity during, 607t Blood supply of shoulder, 13. See also specific blood vessels. vascular examination and, 69–70, 70f Body Blade, external rotation with, 634f Body function definition of, 819 measures of, 819–820 Body roll in front crawl stroke, 450 Bone block procedures for anterior instability, 201, 202 Bowling, cricket, biomechanics of, 376–377 Boys, gymnastic training and progression for, 492 Brace(s) abduction, postoperative, 815 gunslinger, postoperative, 814–815 postoperative, of shoulder, 814f, 814–815 to prevent anterior subluxation and dislocation, 813, 813f
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INDEX Brace(s) (Continued) spine and scapula stabilizing, for scapular dyskinesis, 676–677, 677f Brachial neuropathy, acute, 341–342 Brachial plexus anatomy of, 13, 337–338, 338f, 339f injuries of. See Brachial plexus injuries. interaction between cervical spine and shoulder girdle and, 352 posterior cord of, 708 Brachial plexus injuries, 337–342 acute brachial neuropathy as, 341–342 back palsy as, 341 burners (stingers) as, 339–341, 354, 421–422 classification of, 337, 338f in football, 421–423 of axillary nerve, 422 burners (stingers) as, 421–422 of long thoracic nerve, 422–423 of spinal accessory nerve, 423 of suprascapular nerve, 423 grade I, 340–341 grade II, 340–341 grade III, 340, 341 high-velocity, 338–339 management of for acute brachial neuropathy, 342 for back palsy, 341 for burners (stingers), 340–341 for high-velocity injuries, 338–339 Bracing. See Brace(s). Brain, processing at level of, shoulder stability and, 656–657 Breathing patterns of, in front crawl stroke, 450 unilateral, swimmer’s shoulder and, 447–448 Bristow procedure, 262 glenohumeral arthritis following, 315 Bristow-Latarjet procedure for anterior instability, 202 Bupivacaine for subacromial impingement, 120 Burners, 339–341, 354 in football, 421–422 Bursectomy for subacromial impingement, 120, 121f Bursitis, 283 scapulothoracic, baseball and, 413 subdeltoid, obliterative. See Adhesive capsulitis. Bypass grafting, for axillary artery compression and aneurysm, 330
C Cable chop exercise, 769, 772f Cable lift exercise, 769, 772f Cable tensiometry, 50 Cadlow Shoulder Stabilizer, 813 Calcific tendinitis, 155–158, 156f evaluation for, 156f, 156–157 historical background of, 155 imaging of, 83, 83f pathogenesis of, 155–156 degenerative calcification in, 155 reactive calcification in, 155–156 radiographic types of, 157 stages of, 155–156, 157 treatment of, 157
Index_849-876-F06701.indd 853
Calcification degenerative, calcific tendinitis and, 155 reactive, calcific tendinitis and, 155–156 Capsular laxity, impingement and, 528 Capsular plication diagnostic arthroscopy prior to, 136 postoperative rehabilitation following, 137 Capsular relationships, optimization of, following arthroplasty of the shoulder, 318 Capsular shift procedure, anterior, postoperative rehabilitation following, 138 Capsular shrinkage, thermal for instability, in female athletes, 521 for internal impingement, postoperative rehabilitation following, 137 Capsular tightness, posterior, tennis and, 430 Capsular-labral complex, defect of. See Bankart lesions. Capsule scoop, lateral, 635f Capsule stretch inferior, with lateral scapula stabilization, 636f posterior, 636f Capsulitis adhesive. See Adhesive capsulitis. posterior, baseball and, 403 Capsulolabral plication, open, for posterior instability, 218–220, 219f Capsulorrhaphy staple, arthroscopic, 199–200 thermal, 200 for multidirectional instability, 235–236, 236f Capsulorrhaphy arthropathy, arthroplasty of the shoulder for, 315 Cardiovascular endurance for preadolescent and adolescent athletes, 564 Cardiovascular training for golf, 482–483 Carpal tunnel syndrome, cervical lateral glide technique for, 715, 715f Catching, softball, interval sport program for, 581b–582b C.D. Denison-Duke Wyre Shoulder Vest, 813, 813f Central nervous system processing, shoulder stability and, 656–657 Cerebellum, afferent information processing and, 657 Cerebral cortex, afferent information processing and, 657 Cerebrocerebellum, 657 Cervical cord neurapraxia, 354–355 Cervical lateral flexion away, neurodynamic testing in, 711, 712, 713, 713f toward, neurodynamic testing in, 711 Cervical lateral glide technique, neurodynamic testing and, 714–715, 715f Cervical nerve(s), pinch injuries of, 339–341 Cervical nerve roots brachial plexus and, 337–338, 338f, 339f burners (stingers) and, 354 high-velocity injuries of, 338–339 Cervical radiculopathy, shoulder pain caused by, 352–353 Cervical spine anatomy of, 351–352 degenerative changes in, contact sports and, 354, 355 examination of, 69, 69f
853
Cervical spine (Continued) interaction with shoulder girdle, 351–352 joint movement in, 351 shoulder disease due to. See Cervicogenic shoulder disease. Cervicogenic shoulder disease, 351–359 axillary nerve injury and, 354 cervical anatomy and, 351–352 contact sport injuries causing, 354–355, 355f differential diagnosis of, 352–354 electromyelography in, 353–354 imaging studies in, 353 musculocutaneous nerve injury and, 354 neurapraxias as, 354 overhead athlete injuries causing, 355–356 posture and, 356 quadrilateral space syndrome as, 354 rehabilitation for, 357–359, 358f, 359f spinal accessory nerve injury and, 354 treatment of, 356, 357f, 358f Changeup, biomechanics of, 370t, 370–371, 371t “Check rein” shoulder. See Adhesive capsulitis. Chest pass in conditioning program for shoulder, 783f plyometric, 635f two-hand, in plyometric program, 753, 756f, 757, 759f Chest press, standing, with rotation, for golf, 480, 480f Children, 507–515. See also Preadolescents. age-specific rehabilitation guidelines for, 566, 566f fractures in, 513–514 of clavicle, 514 of proximal humerus, 513f, 513–514, 514f glenohumeral instability in, 511–512 sequelae of, 512 static and dynamic constraints in, 511–512 treatment of, 512 Little Leaguer’s shoulder in, 508–510, 509f rotator cuff injury in, 510–511 shoulder biomechanics of, 507 throwing motion in, 507–508, 508b Chop exercise, high to low, 618 Chop pass, plyometric, 635f Circle stability concept, 545 Clavicle fractures of brachial plexus injuries with, 341 in children, 514 in football, 426 scapular plane movement and, 20 Clinical outcomes, 818–827 activity and participation measures and, 826 framework for identifying, 818t, 818–819 impairment and, 825f, 825–826 measures of, 819–822, 829–837 activity and participation measures as, 820–821 body structure and function measures as, 819–820 health-related quality of life as, 821–822 patient-reported, future directions in measuring, 826 selecting measures for, 822–825 practical considerations for, 822 psychometric considerations in, 822, 823t–824t, 824–825
9/19/08 7:17:23 PM
854
INDEX
Closed kinetic chain exercise(s) definition of, 603 deltoid activity during, 605t, 610t glenohumeral muscle activity during, 603, 604t, 607t, 608t, 611t, 612t for instability, 551, 552, 555f proprioceptive neuromuscular facilitation compared with, 640 for proprioceptive restoration, 661 rotator cuff biomechanics and function and, 603, 605–620 of deltoids, 620–622 of infraspinatus and teres minor, 607, 612–619 of levator scapulae, 623 of rhomboids, 623 of serratus anterior, 622–623 of subscapularis, 617, 619–620 of supraspinatus, 603, 605–607 of trapezius, 623 rotator cuff muscle activity during, 605t, 610t scapular muscle activity during, 609t, 611t serratus anterior activity during, 606t for stability, 630, 630f–632f trapezius activity during, 606t Closed-chain neuromuscular control drills for female shoulder injuries, 576 Closed-chain scapula drills for female shoulder injuries, 576, 577f Closed-chain weight-bearing progression for gymnastic injuries, 498, 500b–501b, 501f Clunk test for glenohumeral laxity, 101 for glenoid labral tears, 102 in labral pathology, 58 in multidirectional instability, 229, 231t Cocking phase of baseball pitching biomechanics of, 366t, 366–367, 368f, 374t electromyography during, 385, 386t, 387–388 of baseball throw, instability and, 406, 407f of football throw early, electromyography during, 390t late, electromyography during, 390t of tennis serve electromyography during, 394t, 394–395 muscular activity patterns in, 430 of volleyball serve and spike, electromyography during, 392, 393t Co-contraction, closed-chain, with ball on the wall, 630f Cohen’s kappa statistic, 825 Cold application for impingement, 533, 533f, 537 Compression rotation test in multidirectional instability, 232t Compression testing in cervicogenic injuries, 357, 358f Computed tomography, 73 in anterior dislocation of shoulder, 243, 244f in Bankart lesions, 260 in Bennett lesion, 77, 77f of dislocations, 74, 75f of fractures, of humerus, 74 in multidirectional instability, 230 in neck and shoulder pain, 352–353
Index_849-876-F06701.indd 854
Computed tomography (Continued) in osteoarthritis, 74 in posterior instability, 214 in rotator cuff calcific tendinitis, 83 in suprascapular nerve entrapment, 345 Concavity-compression, 31–32 Concentric muscle action eccentric muscle action contrasted with, 696–698, 697f, 697t, 698f in isokinetic testing, 732t eccentric muscle action versus, 727, 729 muscle spindles and, 750, 752f plyometric exercises and. See Plyometric exercise(s). Concentric response phase of plyometric exercise, 752 Concept rotator cuff repair system kit, 170 Conditioning for preadolescent and adolescent athletes, 563–567 age-specific guidelines for, 566f, 566–567, 567f benefits of, 564–565 efficacy of, 563–564 guidelines for, 565, 565t Conditioning program for shoulder complex, 775–786 adaptation and, 775–776 coordination or skill movements component of, 778 endurance (work capacity) component of, 777 evaluation and, 776 flexibility and mobility component of, 777 guidelines for specific exercises in, 778–786 for injury prevention, performance, and rehabilitation, 780–786 for program design, 779–780 for selection, 778–779 kinetic chain concepts and connection and, 775 power component of, 777 recovery component of, 778 stabilization and neuromuscular control component of, 777–778 strength component of, 776–777 Connective tissue, restricted motion and, 686–687 Conoid ligament, anatomy of, 5 Constant Scoring System, 833t Constant-Murley Score, 823t Contact sports. See also specific sports. cervicogenic shoulder pain and, 354–355, 356f Contre-coup concept, isokinetic exercise and, of posterior dominant shoulder, 736f, 736–737, 737f Contusion of glenohumeral joint, protecting against, 812, 812f Conventional radiography, 73 in anterior dislocation of shoulder, 243 in Bankart lesions, 260 in biceps tendinitis, 284–285 in calcific tendinitis, 156, 156f in internal impingement diagnosis, 127–128, 128f in Little Leaguer’s shoulder, 509 in multidirectional instability, 229–230 in neck and shoulder pain, 352–353
Conventional radiography (Continued) in osteoarthritis, 74 in PASTA lesions, 144–145 in posterior instability, 214 in suprascapular nerve entrapment, 345 in tensile failure of rotator cuff, 113 in thoracic outlet syndrome, 328, 328f Coordination in conditioning program for shoulders, 778 Coracoacromial arch anatomy of, 12, 12f subacromial impingement and, 115–116 Coracoacromial joint, anatomy of, 81, 82f Coracoacromial ligament anatomy of, 12, 12f resection and decompression of, for subacromial impingement, 120, 121f in throwing, 117 Coracobrachialis muscle, biomechanics of, 37 Coracoclavicular ligament, anatomy of, 5 Coracoclavicular reconstruction, anatomic, for acromioclavicular joint injuries, 308, 308b Coracohumeral ligament anatomy of, 9, 9t glenohumeral stability and, 28–30, 29f Coracoid fractures in football, 426 Core stability in swimmers, 459 Core stabilization, 763–771 arthrokinetic dysfunctions and, 765 in conditioning program for shoulders, 777 exercises for, 765–769 for mobility, 766 for stability, 766–767 for strength, 767f, 767–769 fascial slings and muscle fiber orientation in, 764 as foundation for movement patterns, 764–765 hips in, 764 muscle-firing patterns and, 765 pelvic floor in, 764 short muscles and, 765 shoulder in, 763–764 terminology for, 763 trunk in, 764 Core training for golf, 480–481, 482f Corrective exercises in conditioning program for shoulders, 780, 780f, 781b Correlation coefficient, 825 Cost of care, 818 Costoclavicular ligament, anatomy of, 3, 4, 4f Costoclavicular space, axillosubclavian vein compression in, 330, 331f Cotton for padding, 809 Crank test, 47, 58, 58f Crawl, 445. See also Swimmer’s shoulder; Swimming. Cricket throwing and bowling, biomechanics of, 376–377 Critical zone, 527 Cross-arm adduction test, 47 for acromioclavicular joint injury, 58, 58f in impingement, 61 Cross-body stretch for golf injuries, 472, 472f Curveball, biomechanics of, 370t, 370–371, 371t
9/19/08 7:17:23 PM
INDEX Cysts ganglion of spinoglenoid notch, suprascapular nerve compression due to, 412 suprascapular nerve entrapment by, 345 paralabral, imaging of, 80
D DASH, 820, 822, 823t, 825 Dead arm syndrome, 65, 101, 112–113 Débridement, arthroscopic, for PASTA lesions débridement-only technique for, 146–147 with subacromial decompression, 146–147 Deceleration in isokinetic testing, interpretation of, 726 Deceleration phase of baseball pitching biomechanics of, 366t, 367–368, 374t electromyography during, 386t, 389 eccentric muscle action and. See Eccentric muscle action. of football throw, electromyography during, 390t of golf swing, electromyography during, 397t, 398t, 399 of tennis serve, electromyography during, 394t, 395 of tennis volley, electromyography during, 396t of volleyball serve and spike, electromyography during, 393, 393t Decelerator mechanism, 695–696, 696f Deltoid muscle(s) abduction and, 620–621, 622 activity of in shoulder exercises, 605t, 607t, 608t, 610t, 612t in throwing, 112 anterior activity of, in shoulder exercises, 607t, 608t, 610t, 612t assessment of, 59–60 in baseball pitching, 386t, 387 exercise of, electromyographic analysis of, 589, 590b in football throwing, 389, 390t in front crawl, 455 in golf swing, 397t in tennis volley, 395, 396t in volleyball serve and spike, 392, 393t in windmill pitching, 391, 391t biomechanics of, 35 cross-sectional area of, 11t dynamic stability and, 33 exercise of electromyographic analysis of, 589, 590b, 594 external rotation, peak muscle activity during, 593t exercise progression for, 681t–682t in front crawl, 454 in golf swing, 466 middle activity of, in shoulder exercises, 605t, 608t, 610t, 612t in baseball pitching, 386t electromyographic analysis of exercise of, 590b
Index_849-876-F06701.indd 855
Deltoid muscle(s) (Continued) external rotation exercise of, peak muscle activity during, 593t in football throwing, 389, 390t in front crawl, 455 in golf swing, 397t in tennis serve, 394t in tennis volley, 395, 396t posterior activity of, in shoulder exercises, 605t, 607t, 608t, 612t in baseball pitching, 386t electromyographic analysis of exercise of, 590b external rotation exercise of, peak muscle activity during, 593t in football throwing, 389, 390t in golf swing, 397t in tennis volley, 395, 396t in windmill pitching, 391, 391t Demyelination, 337 Depression neurodynamic testing in, 711, 712f scapular, 19, 19f of shoulder girdle, neurodynamic testing in, 712, 713, 713f of sternoclavicular joint, 3, 4, 4f, 23 Dermatomal sensory examination, 69 Dexamethasone for biceps long head ruptures, 287 for snapping scapula syndrome, 290 Diabetes mellitus, adhesive capsulitis in, 293 Diagnostic arthroscopy in internal impingement, 130–131, 135–136 for posterior instability, 218, 218f in rotator cuff tears, 159, 182 skybox view on, 218, 218f Diagonal patterns D1 extension, 642t, 643t, 645f, 646f D2 extension, 613f, 642t, 643t, 644f, 647f glenohumeral muscle activity during, 604t, 611t rotator cuff and deltoid muscle activity during, 610t scapular muscle activity during, 611t in thrower’s 10 program, 843 D2 extension, eccentric arm control portion of glenohumeral muscle activity during, 611t rotator cuff and deltoid muscle activity during, 610t scapular muscle activity during, 611t D1 flexion, 642, 642t, 643t, 644f, 645f trapezius and serratus anterior activity during, 606t D2 flexion, 642, 642t, 643t, 647f, 652f, 653 in thrower’s 10 program, 843 extension, 619f flexion, horizontal adduction, external rotation, for scapular dyskinesia, 682t serratus anterior muscle and, 598, 599f subscapularis muscle and, 595, 596f Diagonal rotation exercise on ball for scapular dyskinesia, 678b Disabilities of Arm, Shoulder and Hand, 820, 822, 823t, 825
855
Disability definition of, 818, 819 frequency of, instability and, 545–546 Disablement, levels of, 818 Disablement models, 817 Dislocation arthropathy, arthroplasty of the shoulder for, 315 Dislocation of shoulder anterior acute. See Anterior dislocation of shoulder, acute. anterior instability and, 197, 197f braces to prevent, 813, 813f imaging of, 74, 75f instability and, 545 posterior, locked, 212, 212f, 214 Distraction technique for motion restriction, 689–689f Distraction test in neck and shoulder pain, 352–353 Doggy rock for gymnastic injuries, 500b, 501f Donjoy Shoulder Brace, 813, 814f Dorsal root ganglion, interaction between cervical spine and shoulder girdle and, 352 Downswing phase of golf swing, electromyographic and kinematic analysis of, 466, 467t Drawer test(s) anterior, 67 in anterior instability, 406 posterior, 46–47, 67 in posterior instability, 212, 213 Drop arm test, 48–49 in subacromial impingement, 119 Drop signs, 62 Dumbbells aquatic, isotonic exercises with, in conditioning program for shoulder, 781–782, 782b scaption with neutral rotation and increasing load using, glenohumeral muscle activity during, 612 Dyna Disc, prone on elbows on, 631f Dynamic flexibility, golf injuries and, 474–475, 475t Dynamic hug exercise, serratus anterior muscle and, 598, 598f Dynamic roominess, 707 Dynamic sitting exercises, for scapular dyskinesia, 678b, 680f Dynamic stabilization exercises, 551, 551f, 634f for instability, 551 progressions for, 630, 630f–632f in push-up position catch and toss with soccer ball, 632f wall dribble and, 634f Dynamic stabilization wall dribble, 634f Dynamic standing exercises for scapular dyskinesia, 678b, 679f Dynamometers hand-held, 50 for monitoring weakness, in cervicogenic injuries, 359, 359f for strength assessment, in tennis injuries, 436–437 in vivo study of maximal muscle force production using, 695–696
9/19/08 7:17:23 PM
856
INDEX
E Eagle grip, shoulder mechanics and, 496, 496f Early swing phase of baseball batting, 395 Eccentric exercise(s) applications for, 699–701, 701b, 701f for rotator cuff tendinitis, 703b, 703f, 703–704 Eccentric muscle action, 695–704, 696f concentric muscle action contrasted with, 696–698, 697f, 697t, 698f eccentric exercise and, 700–701, 701b, 701f in isokinetic testing, 732t concentric muscle action versus, 727, 729 mechanism of, 695–696, 696f pathology affecting, 698–700, 699f, 700f physiology of, 696–698, 697f, 697t, 698f plyometric exercises and. See Plyometric exercise(s). shoulder dysfunction and, 702f, 702–704, 703b, 703f Eccentric phase of plyometric exercise, 752 Eden-Hybbinette procedure for anterior instability, 202 Effleurage massage for impingement, 537, 537f Effort thrombosis, 330–332, 331f Elastic tape, 807 Elastic tissues, recoil action of, plyometrics and, 751–752 Elbow dropped, in front crawl stroke, 452, 452f extension of, neurodynamic testing in, 711, 712f flexion of, in thrower’s 10 program, 846 proprioceptive neuromuscular facilitation pattern for, 642t “Elbows in the back pocket” exercise for scapular dyskinesis, 675, 675f, 676 Electrical stimulation for female shoulder injuries, 573, 573f–575f, 573t, 574 for internal impingement, 129, 130f for motion restriction, 689 transcutaneous electrical nerve stimulation as for female shoulder injuries, 573, 573t to reduce inflammatory process, in impingement, 533, 533f Electromyelography in neck and shoulder pain, 353–354 Electromyography during baseball batting, 395–396 in brachial neuropathy, 341 in brachial plexus injuries, 338 concentric versus eccentric muscle action and, 697t, 698 during golf swing, 397t, 397–399, 398t acceleration phase of, 466, 467t downswing phase of, 466, 467t follow-through phase of, 467, 467t, 468t take-away and backswing phase of, 465–466, 467t neuromuscular control assessment using, 662f–664f, 662–663 during overhead baseball pitch, 385, 386f, 386t, 387–389
Index_849-876-F06701.indd 856
Electromyography (Continued) in arm acceleration phase, 386t, 388–389 in arm cocking phase, 385, 386t, 387–388 in arm deceleration phase, 386t, 389 in stride phase, 385, 386t in wind-up phase, 385, 386t during overhead football throw, 389–390, 390t shoulder exercise analysis using, 589, 590t–591t, 591–596 external rotators and, 591–592, 593t lower trapezius and, 598–599 serratus anterior and, 597–598, 598f, 599f subscapularis and, 595–596, 596f supraspinatus and deltoid and, 592, 594f–596f, 594–595 in suprascapular nerve entrapment, 345, 346–347 during tennis serve, 394t, 394–395 during tennis volley, 395, 396t in thoracic outlet syndrome, 328 during throwing, 111–112 during volleyball serve and spike, 392–394, 393t during windmill softball pitching, 390–392, 391t Elevation conoid ligament and, 5 planes of motion and, 17–18, 18f, 19f scapular, 19, 19f in scapular plane, 17–18, 19f scapulohumeral rhythm and, posture and, 22–23 of sternoclavicular joint, 23 sternoclavicular joint and, 3, 4, 4f Elgrip, shoulder mechanics and, 496, 496f Empty can exercise electromyographic activity during, 592, 594f–596f, 594–595 supraspinatus muscle and, 605 Endurance exercise(s) in conditioning program for shoulders, 777, 781–782, 782b plyometric exercises for, 755, 757f for swimmers, 458–459 Energy, concentric versus eccentric muscle action and, 697t Ensolite, 809 Epiphyseal plate, humeral, proximal, stress fractures of, 508–510, 509f Epiphysiolysis, humeral, proximal, 508–510, 509f Equipment manager, 806–807 Erector spinae muscle in golf swing, 466 Ethical issues with protective equipment, 815–816 Evidence-based practice, 719 Examination of shoulder, 45–52, 55–70. See also specific disorders and tests. acromioclavicular and labral assessment in, 47–48 Adson’s maneuver in, 69, 70f apprehension test in, 46, 67f, 67–68, 68f, 113 arthroscopy in in internal impingement, 130–131, 135–136 for posterior instability, 218, 218f in rotator cuff tears, 159, 182 skybox view on, 218, 218f belly press test in, 63
Examination of shoulder (Continued) in biceps disorders, 63–65, 64f, 65f biceps load tests in, 47–48 cable tensiometry in, 50 capsular tests in, 46–47 case study of, 52 clunk test in, 58, 58f crank test in, 47, 58, 58f cross-arm adduction test in, 61 crossed arm adduction in, 47 drawer tests in anterior, 67 posterior, 46–47, 67 drop arm test in, 48–49, 119 drop sign in, 62 external rotation lag sign in, 119 functional assessment in, 51, 52 in glenohumeral instability, 65–68, 66f–69f hand-held dynamometry in, 50 Hawkins test in, 60, 61f, 118, 119f, 144 Hawkin’s (Kennedy) test in, 48 hornblower’s sign in, 119 in impingement, 60–63, 61f–63f internal, 48, 126–127, 127f impingement testing in, 48 initial impression in, 55–56 initiating, 45 inspection in, 56, 56f internal rotation lag sign in, 63, 119 Jahnke (jerk) test in, 68, 69f Jobe test in, 61, 62f, 113, 144 labral tests in, 47–48 lag signs of rotator cuff in, 49 liftoff test in, 62f, 62–63, 119 load and shift test in, 46, 66f, 66–67 of muscle actions, 49–51, 50t isokinetic, 51 isometric techniques for, 50 isotonic, 50–51 Neer’s sign in, 48, 60, 61, 61f, 118 Neer’s test in, 118 neurological, 69, 69f O’Brien test in, 47, 64, 65f, 113, 127, 232t, 409 observation in, 56, 56f, 57f O’Driscoll test in, 64 painful arc test in, 48, 60–61, 61f palpation in, 47, 57f, 57–58, 58f range-of-motion, 58–59, 59f, 60f relocation test in, 46, 68, 68f, 113 resisted external rotation in, 49, 61–62, 62f Roos test in, 70, 70f rotator cuff assessment in, 48–49 in rotator cuff disorders, 60–63, 61f–63f screen in, 45–46, 46t sequence for, 45–49, 46b Speed’s test in, 63, 64f, 232t, 284, 410 strength assessment in, 49, 52, 59–60, 60t sulcus sign in, 46, 65–66, 66f, 113, 212, 229, 231t in superior labral pathology lesions, 63–65, 64f, 65f supraspinatus test in, 61, 62f in tensile failure of rotator cuff, 113 thoracic outlet tests in, 69–70, 70f vascular, 69–70, 70f Yergasson’s test in, 63, 64f, 232t, 284, 410
9/19/08 7:17:24 PM
INDEX Examination under anesthesia in anterior, acute dislocation of shoulder, for arthroscopic treatment, 246 for arthroscopic rotator cuff repair, 180 Exercise(s). See also Conditioning entries; Rehabilitation; Training; specific muscles and exercises. abduction electromyographic analysis of scapulothoracic musculature during, 597t, 598t horizontal, prone, 598–599, 841 horizontal, with external rotation, electromyographic analysis of scapulothoracic musculature during, 597t biomechanics of, 589–600 effects of shoulder pathology and, 599, 600t electromyographic analysis of exercises and, 589, 590t–591t, 591–596 lower trapezius and, 597b, 598–599 scapulothoracic joint and, 596–599, 597t–598t serratus anterior and, 597–598, 598f, 598t, 599f for cervicogenic injuries, 356 closed kinetic chain. See Closed kinetic chain exercise(s). in conditioning program for shoulders, 778–786 injury prevention, performance, and rehabilitation and, 780–786 program design and, 779–780 selection of, 778–779 for core stabilization, 765–769 for mobility, 766 for stability, 766–767 for strength, 767f, 767–769 of deltoid muscles anterior, electromyographic analysis of, 589, 590b middle, electromyographic analysis of, 590b posterior, electromyographic analysis of, 590b dynamic stabilization progressions and, for stability, 630, 630f–632f endurance in conditioning program for shoulders, 777, 781–782, 782b plyometric exercises for, 755, 757f for swimmers, 458–459 to enhance neuromuscular control, 629–630 clinical application of, 630, 632 flexibility exercises as, 630, 635f–637f stability exercises as, 630, 630f–635f external rotation. See External rotation exercise(s). flexibility, 630, 635f–637f flexion, 615f electromyographic analysis of scapulothoracic musculature during, 597t, 598t L-bar, 839 full-arc, 735 of infraspinatus muscle, electromyographic analysis of, 589, 590b–591b, 591, 592
Index_849-876-F06701.indd 857
Exercise(s). See also Conditioning entries; Rehabilitation; Training; specific muscles and exercises. (Continued) isokinetic. See Isokinetic exercise(s). isometric multiple-angle, 733 for scapular dyskinesia, 676f, 678, 678f subscapularis activity during, 595–596 for superior labral anterior-posterior lesions, type II, 139 isotonic for female shoulder injuries, 576, 576f in pool, in conditioning program for shoulder, 781–782, 782b for posterior instability, 217 strengthening, for instability, 551, 551f for tennis injuries, 438, 439f, 439–440 of latissimus dorsi muscle, electromyographic analysis of, 591b mobility, for core stabilization, 766 open kinetic chain. See Open kinetic chain exercise(s). for PASTA lesions, 146 of pectoralis major muscle, electromyographic analysis of, 591b plyometric. See Plyometric exercise(s). pool, isotonic, in conditioning program for shoulder, 781–782, 782b range-of-motion. See Range-of-motion exercise(s). rotator cuff following arthroplasty of the shoulder, 320–322, 321f isotonic, in conditioning program for shoulder, 782b scaption. See Scaption exercise(s). scapular following arthroplasty of the shoulder, 320–322, 321f for internal impingement, 130, 135f scapular retraction. See Scapular retraction exercise(s). scapular row. See Scapular row exercise(s). scapulothoracic joint during, electromyographic analysis of, 596–599, 597t–598t short-arc, 733, 734f, 735 stability, 630, 630f–635f stabilization. See Stabilization exercises. strengthening. See Strength training; Strengthening exercises. of subscapularis muscle, electromyographic analysis of, 589, 590b, 595–596, 596f of supraspinatus muscle, electromyographic analysis of, 589, 592, 593t, 594f, 594–595, 596f of teres minor muscle, electromyographic analysis of, 589, 591, 591b, 592 thrower’s 10 program of, 843–847 for adolescents, 567 for baseball injuries, 413–414, 414f–415f, 416 for instability, 556 for internal impingement, 130, 131f–135f warm-up for golf injuries, 474–475, 475t, 476f–478f, 478t for isokinetic testing, 723–724
857
Exercise(s). See also Conditioning entries; Rehabilitation; Training; specific muscles and exercises. (Continued) muscle activation of, 662, 662f for plyometric program, 753, 754f, 755f Exercise tubing in plyometric program, 753, 755, 757f Extension. See also Diagonal patterns. bilateral peak torque and, 726, 727t of elbow, neurodynamic testing in, 711, 712f finger, neurodynamic testing in, 711 isokinetic exercise and, 738, 738f of knee, in conditioning program for shoulders, 779 prone electromyographic analysis of scapulothoracic musculature during, 597t at 90 degrees of flexion, scapular muscle activity during, 609t resisted, in upright position, end range of, throwing motion and, 651 of shoulder, neurodynamic testing in, 711, 712f standing, from 90 to 0 degrees glenohumeral and scapular muscle activity during, 611t rotator cuff and deltoid muscle activity during, 610t of trunk, in plyometric program, 757, 758f of wrist neurodynamic testing in, 711 in thrower’s 10 program, 846 External rotation in baseball players, 125, 125f bilateral peak torque and, 726, 727t with Body Blade, 634f eccentric control for, following posterior instability repair, 223, 224f eccentric versus concentric, in throwers, 701, 701f elevation with, 636f in golf swing, 465 infraspinatus muscle and, 612–613 isokinetic exercise and, 737f, 737–738 continuum of exercise positions for, 736f, 736–737, 737f isokinetic muscular performance in, 733t isokinetic shoulder torque to body weight ratios and, 732t isokinetic testing and, bilateral comparison of, 726, 726t loss of, with Bankart repair, 265 for motion restriction, 690 neurodynamic testing in, 711 at 90 degrees of abduction muscle activation of, 663f in thrower’s 10 program, 844 in 90/90 position, 652f peak torque-body weight ratio and, 728t following posterior instability repair, 223, 224f prone. See Prone external rotation. resisted, 49, 61–62, 62f with scapular patterns, 650f scaption, in thrower’s 10 program, 844 scapular, 20, 20f in scapular plane, electromyographic analysis of, 592
9/19/08 7:17:24 PM
858
INDEX
External rotation (Continued) scapular retraction with, 633f standing. See Standing external rotation. strengthening of external rotators and, 591–592, 593t with surgical tubing, 634f teres minor muscle and, 612–613 upper shoulder, isolated, in scapular plane, 651, 651f at 0 degrees of abduction electromyographic analysis of, 592 in thrower’s 10 program, 843 External rotation exercise(s). See also specific exercises. of infraspinatus muscle, peak muscle activity during, 593t of middle deltoid muscle, peak muscle activity during, 593t peak muscle activity during, 592, 593t of posterior deltoid muscle, peak muscle activity during, 593t range-of-motion, for superior labral anterior-posterior lesions, type II, 139 side-lying. See Side-lying external rotation exercise(s). of supraspinatus, peak muscle activity during, 593t of teres minor muscle, peak muscle activity during, 593t with tubing, 840 External rotation lag sign in subacromial impingement, 119 External rotation stretch, supine, with wand, 637f External rotation supination, resisted (O’Brien test), 47 in labral pathology, 64, 65f in multidirectional instability, 232t in SLAP lesions, 127, 409 in tensile failure of rotator cuff, 113 External rotators, plyometrics for, 753, 755, 757f Extracorporeal shock wave therapy for calcific tendinitis, 157
F Facet joints, anatomy of, 351 Fascial slings, core stabilization and, 764 Fastball, biomechanics of, 370t, 370–371, 371t Fatigue testing, isokinetic, 729–730 Faulty mechanics, female shoulder injuries and, 570 Feedback, visual, for isokinetic testing, 724 Feedback control, neuromuscular control and, 657 Feedforward control, neuromuscular control and, 657 Feet, core stabilization exercises for, 769, 771f Felt for padding, 809 Female shoulder injuries, 519–522, 569–586 epidemiology of, 519 flexibility and joint laxity and, 520 impingement as epidemiology of, 519 treatment of, 520–521 injury patterns and, 569–570 contributing injury factors and, 570 presentation of, 570
Index_849-876-F06701.indd 858
Female shoulder injuries (Continued) instability as epidemiology of, 519 multidirectional, 520 treatment of, 521 rehabilitation for, 570–586 biceps tendon dysfunction and, 571, 573f, 573t, 573–574 injury classification for interval sport program progression and, 586b multiphased, 570–571, 572b neuromuscular re-education in, 576–578, 577f return to sport and, 578, 578b–586b rotator cuff strengthening in, 574f, 574–575, 575f scapula dysfunction and, 575f, 575–576, 576f softball catcher’s interval sport program for, 581b–582b softball infielder’s interval sport program for, 582b softball outfielder’s interval sport program for, 583b softball pitcher’s interval sport program for, 578b–580b soreness rules for, 586b volleyball middle attacker program for, 585b volleyball outside attacker hitting program for, 583b–584b volleyball right side attacker program for, 585b–586b volleyball setter and defensive specialist hitting program for, 584b Final common input hypothesis, 656 Fingers extension of, neurodynamic testing in, 711 proprioceptive neuromuscular facilitation pattern for, 642t Fitter, closed-chain stabilization on, 631f 5 o’clock portal for operative arthroscopy, 108 Flat ground throwing, biomechanics of, 371 Flexibility in conditioning program for shoulders, 777 dynamic, golf injuries and, 474–475, 475t in female athletes, 520 gymnastics and, 495–497, 496f, 504, 504f in rehabilitation, for golf injuries, 470–474, 471f–474f in swimmers, interventions for, 456 Flexibility exercises, 630, 635f–637f Flexion. See also Diagonal patterns. bilateral peak torque and, 726, 727t clavicular, 23 coracoacromial arch and, 12 of elbow, in thrower’s 10 program, 846 isokinetic exercise and, 738, 738f above 120 degrees with external rotation glenohumeral and scapular muscle activity during, 611t glenohumeral muscle activity during, 608t rotator cuff and deltoid muscle activity during, 610t scapular muscle activity during, 609t prone, at 135 degrees of abduction, for scapular dyskinesia, 681t
Flexion. See also Diagonal patterns. (Continued) teres minor muscle and, 617, 619 of trunk, in plyometric program, 757, 759f of wrist, in thrower’s 10 program, 846 Flexion exercise(s), 615f electromyographic analysis of scapulothoracic musculature during, 597t, 598t L-bar, 839 Foam(s), thermoplastic, for padding, 809 Foam rubber for padding, 809 Follow-through phase in baseball pitching, biomechanics of, 368, 374t of golf swing electromyographic and kinematic analysis of, 467, 467t, 468t electromyography during, 397t, 398t, 399 pathomechanical analysis of, 469 of tennis serve electromyography during, 394t, 395 muscular activity patterns in, 431 of tennis volley, 396t of volleyball serve and spike, electromyography during, 393t of windmill throw, electromyography during, 391t Football, 421–426 acromioclavicular nerve injuries in, 423–424 biceps tendon disorders in, 425 brachial plexus injuries in, 421–423 of axillary nerve, 422 burners (stingers) as, 421–422 of long thoracic nerve, 422–423 of spinal accessory nerve, 423 of suprascapular nerve, 423 fractures in, 426 glenohumeral joint injuries in, 424–425 anterior instability as, 424 multidirectional instability as, 425 posterior instability as, 424–425 impingement in, 426 rotator cuff injuries in, 425–426 Football shoulder pads, fitting of, 805–806, 806f Football throw biomechanics of, 373–374, 374t interval program in, 796, 798b overhead, electromyography during, 389–390, 390t Force. See Muscle force. Forearm(s) proprioceptive neuromuscular facilitation pattern for, 642t supination of, neurodynamic testing in, 711 Forearm supination and pronation for warm-up for golf, 475, 478t Forward punch exercise for scapular dyskinesia, 681t Forward swing phase of golf swing, electromyography during, 397t, 398, 398t Fracture(s) of acromion, in football, 426 avulsion, of lesser tuberosity, in children, 514 in children, 513–514 of clavicle, 514 of proximal humerus, 513f, 513–514, 514f
9/19/08 7:17:24 PM
INDEX Fracture(s) (Continued) of clavicle brachial plexus injuries with, 341 in children, 514 in football, 426 of coracoid, in football, 426 in football, 426 of glenoid bone dislocation and, 241, 242, 242f in football, 426 of glenoid rim with Bankart repair, 265 dislocation and, 242, 242f of humerus imaging of, 74 proximal, in children, 513f, 513–514, 514f stress fractures of proximal humeral epiphyseal plate as, 508–510, 509f of lesser tuberosity, in children, 514 Salter-Harris type I, 509, 513 type II, 513, 514f type III, 513 of scapula, in football, 426 of shoulder complex, imaging of, 74, 75f stress, of proximal humeral epiphyseal plate, 508–510, 509f Friar Tuck wear pattern, 315, 316f Front crawl stroke. See also Swimmer’s shoulder; Swimming. biomechanics of, 450f, 450–451, 451f, 452t historical background of, 445 muscle activity with shoulder pain and, 454–455 normal muscle activity of, 453–454 pathomechanics of, 451–453, 452f–454f Front-on bowlers, 377 Frozen shoulder, 685, 686 Fulcrum test in anterior instability, 406, 407f Full can exercise, 840 electromyographic activity during, 594–595 supraspinatus muscle and, 605–606 Full-arc exercises, 735 Functional assessment, 51, 52 Functional limitations, definition of, 818 Functional performance, isokinetic resting related to, 740–742 Functional specificity training for swimmers, 459 Functional testing algorithm, 720, 720b progression of, criteria for, 720, 720b
G Gallie procedure for anterior instability, 202 Gamma motor system, afferent information processing and, 657 Ganglion cysts of spinoglenoid notch, suprascapular nerve compression due to, 412 suprascapular nerve entrapment by, 345 treatment of, 347 Gauze for padding, 809 Gender. See Boys; Female shoulder injuries; Girls; Men; Women. Genie stretch for golf injuries, 472f Gerber lift-off exercise (test), subscapularis muscle and, 620 German grip, shoulder mechanics and, 496–497
Index_849-876-F06701.indd 859
GIRD, 31, 125 eccentric exercise for, 700–701, 701f total arc of motion in, 58, 59f Girls. See also Female shoulder injuries. gymnastic training and progression for, 491–492 GLAD lesions, imaging of, 77–78, 79f Glenohumeral instability. See Instability of shoulder. Glenohumeral internal rotation deficit, 31, 125 eccentric exercise for, 700–701, 701f total arc of motion in, 58, 59f Glenohumeral joint anatomy of, 3, 5–7, 6b, 6f, 7f. See also Anatomy of shoulder joint complex. axes of motion of, 24 biomechanics of, 24–26, 25f–27f injuries of. See specific injuries and sports. movement of, retroversion and, 6 protecting, 812–814 against anterior instability, 812–814, 813f, 814f against contusions, 812 stability of. See Instability of shoulder; Stability of shoulder. Glenohumeral joint capsule. See also Capsular entries; Capsule entries. anatomy of, 7–9, 8f, 9f, 192–193 glenohumeral stability and, 28–31, 29f inferior stretch, 637f movement and, 8 negative intra-articular pressure in, 10 posterior horizontal adduction stretch for, 636f sleeper stretch for, 636f Glenohumeral laxity definition of, 511 in female athletes, 520 normal, instability differentiated from, 191 operative arthroscopy for, 99, 101–102 Glenohumeral ligaments, 193f, 193–196 anatomy of, 7–8, 8f, 9–10, 209–210 arthroscopic, 93, 93f attachments to humerus, 8–9, 9f inferior, 193f–196f, 194–196 anatomy of, 8, 8f, 10, 93, 93f, 209–210 glenohumeral stability and, 30–31 injuries of, 80, 81f, 197–198 middle, 193f, 193–194 anatomy of, 8, 8f, 9–10, 93, 93f glenohumeral stability and, 30 superior, 193, 193f anatomy of, 8, 8f, 9, 93, 93f glenohumeral stability and, 30 Glenohumeral noise, postoperative, 253, 254f Glenoid fossa of scapula anatomy of, 6, 6f, 192, 209 arthroscopic, 91 congruency between humeral head and, 27 fractures of dislocation and, 241, 242, 242f in football, 426 inverted-pear, 267 labrum of. See Glenoid labrum. osteochondritis dissecans of, baseball and, 410 posterior, exostosis of, 214
859
Glenoid fossa of scapula (Continued) baseball and, 409, 410f imaging of, 77, 77f operative arthroscopy for, 102–103 surface of, glenohumeral stability and, 26–27 version of, 209 Glenoid labrum. See also Labral entries. abnormalities of, imaging of, 77–80, 78f–80f anatomy of, 7, 7f, 192, 193f arthroscopic, 92–93 anteroinferior avulsion of. See Bankart lesions; Bankart repair. chondrolabral lesions of, 211 dynamic stability and, 33 glenohumeral stability and, 27–28, 28f Kim lesions as, 211 lesions of, types of, 211 peel-back, 409 posterior tears of, imaging of, 78, 79f SLAP lesions of. See SLAP lesions. tears of baseball and, 408–409, 409f flap, 211 nondisplaced, 211 operative arthroscopy for, 101, 101f, 102, 102f, 103f Glenoid rim, fracture of, with Bankart repair, 265 Glenolabral articular disruption lesions, imaging of, 77–78, 79f Glide anterior, for motion restriction, 689–689f of glenohumeral joint, 24–26, 26f inferior for motion restriction, 689–690 for scapular dyskinesia, 678b, 678f posterior, for motion restriction, 689–689f Golf, 465–487 injuries in. See Golf injuries. interval program in, 798–799, 799t swing in. See Golf swing. Golf diagonals, 479t, 480f Golf injuries, 469–485 rehabilitation for, 469–485 activity modification and, 469 applications of, 483–485, 485b cardiovascular training in, 482–483 clinical evaluation and, 469 flexibility and mobility and, 470–474, 471f–474f golf-specific static stretching in, 481–482, 483b, 483f, 484f interval return-to-golf program and, 481, 482t overview of, 469–470, 470b plyometric training in, 478–479, 481f stability and core training in, 479–481, 482f strength and neuromuscular training in, 474–478 summary of, 483, 484b Golf swing biomechanics of, 380–381 electromyographic and kinematic analysis of, 465–467, 466f during acceleration phase, 466, 467t during downswing phase, 466, 467t
9/19/08 7:17:24 PM
860
INDEX
Golf swing (Continued) during follow-through phase, 467, 467t, 468t during take-away and backswing phase, 465–466, 467t electromyography during, 397t, 397–399, 398t modifications to, 485–486 with low back pain, 485 with shoulder pathology, 485–486, 486f, 487f pathomechanical analysis of, 467–469 during downswing and acceleration phase, 468–469 during follow-through phase, 469 during set-up and take-away phase, 467–468 during take-away and backswing phase, 468 Golgi tendon organs force production and, 752 proprioception and, 656, 750 Gravity, compensation for, for isokinetic testing, 725 Grip, inverted, shoulder mechanics and, 496, 496f Gunslinger brace, postoperative, 814–815 Gymnastic injuries causes of, 492–493 rehabilitation for, 497f, 497–504 flexibility and, 504, 504f phases of, 497–504, 498f return to gymnastics after, template for, 504–505 Gymnastics, 491–505 events in, 492 injuries in. See Gymnastic injuries. shoulder mechanics and, 493–497 flexibility and, 495–497, 496f horizontal bar and uneven bars and, 494 locomotion on hands and arms and, 493 still rings and, 495, 495f, 496f tumbling and, 493–494, 494f vaulting and, 494–495 training and progression in, 491–492 for boys and men, 492 for girls and women, 491–492
H HAGHL lesions dislocation and, 241, 241f imaging of, 80, 81f, 243, 244f reverse, 211, 211f Hamstring stretch, for golf, 483, 483f Hand(s) locomotion on, shoulder mechanics and, 493 manipulation of, shoulder complex and, 3 Hand entry in swimming, 447, 453, 454f Hand grip during bench press, deltoid activity and, 621 Handball, biomechanics of, 377–378, 378t Hand-held dynamometry, 50 Handstands, shoulder mechanics and, 494, 494f Hawkins impingement test in impingement, 60, 61f subacromial, 118, 119f in PASTA lesions, 144
Index_849-876-F06701.indd 860
Hawkin’s (Kennedy) test, 48 Head position in front crawl stroke, 450 Health Status Questionnaire (SF-36), 836t–837t Health-related quality of life, 821–822 Hemiarthroplasty, humeral, indications for, 316 Hexalite, 809 Hill-Sachs lesion(s), 257–258, 259f dislocation and, 241–242 engaging, 198, 258 instability and anterior, 198 rehabilitation for, 547–548 nonengaging, 258 reverse, 209, 210f imaging studies of, 214 reverse (bony), 78, 79f Hip(s), core stabilization and, 764 exercises for, 766, 766f, 767, 769, 771f, 772f Hip cuff, 764 Hip stretch for golf, 483, 484f Hip-gluteal stretch for golf, 483, 484f Histamine skin testing in brachial plexus injuries, 338 Hitting in baseball. See Baseball swing. Horizontal abduction exercise, prone, 841 Horizontal adduction stretch for posterior capsule, 636f Horizontal bar, shoulder mechanics and, 494 Hornblower’s sign in subacromial impingement, 119 Hospital for Special Surgery Scoring System, 832t Humeral avulsion of the glenohumeral ligament lesions. See HAGHL lesions. Humeral drive through, neurodynamic testing in, 712 Humeral epiphyseal plate, proximal, stress fractures of, 508–510, 509f Humeral epiphysiolysis, proximal, 508–510, 509f Humeral head anatomy of, 24 arthroscopic, 91 axillary artery compression by, 330 compression of, by rotator cuff muscles, 657–658 congruency between glenoid and, 27 Hill-Sachs lesion of. See Hill-Sachs lesion(s). obligate translation and, 316 Humeral hemiarthroplasty, indications for, 316 Humeral retroversion, baseball pitching and, 373 Humeroscapular periarthritis. See Adhesive capsulitis. Humerus. See also Humeral entries; Scapulohumeral entries. fractures of imaging of, 74 proximal, in children, 513f, 513–514, 514f glenohumeral ligament attachments to, 8–9, 9f head of. See Humeral head. rotation of, in tennis players and baseball pitchers, 435, 435t Hyperangulation, internal impingement and, 124, 124f Hyperangulation phenomenon, 430 Hyperlaxity. See Instability of shoulder.
Hypomobility impingement and, 528–529, 529f in swimmers, interventions for, 456
I Ice application for impingement, 533, 533f, 537 ICF, 817, 818, 818t Iliotibial band stretch for golf, 483, 483f Imaging of shoulder complex, 73–85 in adhesive capsulitis, 75–76 in Bennett lesion, 77, 77f in biceps tendon injury, 80–81, 81f of bone and articular cartilage abnormalities, 74–75, 76f of fracture and dislocation, 74, 75f in impingement and rotator cuff abnormalities, 81–85, 82f–85f in labral injury, 77–80, 78f–80f in muscle injuries, 85, 85f, 86f techniques for, 73–74. See also specific imaging modalities. in vivo, for muscle function assessment, 665 Immobilization for anterior dislocation of shoulder, 244, 251 connective tissue response to, 686–687 for instability, 548, 551 complications with, 551 posterior, 215, 215f following posterior instability repair, 222 for superior labral anterior-posterior lesions, type II, 139 Impact AC pad, 808, 809f Impairment(s) definition of, 818, 819 relationship to function and limitations of activity and participation, 825f, 825–826 Impingement, 527–539, 685 biomechanics of, 35 causes of, 527–530, 529f–531f of coracoacromial arch, 12 definition of, 527, 528b, 528f eccentric exercise for, 699, 700 examination in, 60–63, 61f–63f extrinsic, secondary, imaging of, 81 in female athletes epidemiology of, 519 treatment of, 520–521 in football, 426 imaging of, 81–85, 82f–85f internal. See Internal impingement. mechanical model of, 429–430 nonoperative management of, 531–539 overview of, 531–532 rehabilitation for, 532–539 primary, eccentric exercise for, 700 rehabilitation for, 532–539 stage I (acute inflammatory stage) of, 532–536 stage II (subacute state) of, 536–537, 537f stage III (progressive exercise stage) of, 537–539 stage IV (return to activity stage) of, 539 scapulohumeral rhythm and, 22 secondary, eccentric exercise for, 700 subacromial, 115–121, 527 anatomic variations and, 116–117, 117f baseball pitching and, 372
9/19/08 7:17:24 PM
INDEX Impingement (Continued) baseball throwing and, 404–405, 405f biomechanical effects of, 599 cause and pathology of, 115–116 clinical correlation of, 118 evaluation of, 118–119, 119f functional causes of, 528–530, 529f, 530f neuromuscular control alterations due to, 660 nonoperative management of, 531–539 normal anatomy and, 116 pathophysiology of, 117–118 structural causes of, 527–528, 529f subacromial space vascularity and, 530–531, 531f tensile failure of rotator cuff and, 112 treatment of, 119–120, 120f, 121f subacromial space vascularity and, 530–531, 531f swimmer’s shoulder and. See Swimmer’s shoulder. tennis and, 429–430 testing for, 48 Impingement signs, 48, 60, 61, 61f in PASTA lesions, 144 in subacromial impingement, 118 Inferior glide for scapular dyskinesia, 678b, 678f Infielding, softball, interval sport program for, 582b Inflammation of rotator cuff, 685 in swimmer’s shoulder, interventions for, 456 Inflammatory response bursitis and, 282 decreasing, in impingement, 533, 533f tendinitis and, 282 Infraspinatus muscle activity of exercises eliciting, 607, 612–613, 614–616 in shoulder exercises, 604t, 605t, 607t, 608t, 610t, 612t assessment of, 48–49 attachment to capsule, 10 in baseball pitching, 386t, 388 biomechanics of, 36, 607, 612–619 cross-sectional area of, 11t dynamic stability and, 32–33 exercise of electromyographic analysis of, 589, 590b–591b, 591, 592 eliciting activity of, 604t, 605t, 607, 607t, 608t, 610t, 612t, 612–613, 614–616 external rotation, peak muscle activity during, 593t external rotation and, 612–613 peak muscle activity during, 593t in football throwing, 390t in front crawl, 454, 455 function of, 607, 612–619 in golf swing, 397t, 397–398, 399, 466 maximum predicted isometric force for, 612 in tennis serve, 394, 394t in tennis volley, 395, 396t testing of, 61–62, 62f in volleyball serve and spike, 392, 393t wasting of, conditions associated with, 56, 56f in windmill pitching, 390, 391, 391t
Index_849-876-F06701.indd 861
Initiation, rhythmic, in proprioceptive neuromuscular facilitation, 642 Injuries. See also specific injuries. classification of, for interval sport program progression, for female athletes, 586b previous, evaluation of, for conditioning program for shoulders, 778 Innervation reciprocal, law of, 776 of shoulder, 13–14. See also specific nerves. Instability of shoulder anterior, 191–205 anatomy of, 191–197, 192f–196f arthroscopic repair of, 199–201, 200f baseball pitching and, 387–389 baseball throwing and, 406, 407f, 408, 408f biomechanical effects of, 599 in football, 424 neuromuscular control alterations due to, 659–660 nonanatomic reconstructions for, 201–202, 202f open repair techniques for, 198–199, 199f open versus arthroscopic stabilization for, 202–204 pathologic lesions and, 197f, 197–198 protecting against, 812–814, 813f, 814f rehabilitation for, 205, 546, 547f subdeltoid arthroscopic stabilization for, 204f, 204–205 arm dominance and, rehabilitation and, 548 atraumatic, in children, 512 atraumatic, multidirectional, bilateral, rehabilitation, inferior capsular shift group of, 446 in children, 511–512 atraumatic, 512 sequelae of, 512 static and dynamic constraints in, 511–512 treatment of, 512 congenital, rehabilitation for, 556–557, 558b–559b, 559, 560f definition of, 511 degree of, rehabilitation and, 545 desired activity level and, rehabilitation and, 548 direction of, rehabilitation and, 546–547, 547f dislocation frequency and, rehabilitation and, 545–546 dynamic (functional), 627 neuromuscular control exercises for, 629–630, 630f–637f examination in, 65–68, 66f–69f in female athletes epidemiology of, 519 multidirectional, 520, 521 treatment of, 521 multidirectional, 229–236 anatomy of, 229, 230t biomechanics of, 229 clinical presentation of, 229–230, 231t–232t in female athletes, 520, 521 in football, 425 nonoperative treatment of, 230, 232–233 operative treatment of, 233–236 rehabilitation for, 546–547, 547f sulcus sign in, 65–66, 66f
861
Instability of shoulder (Continued) neuromuscular control and alterations in, 659 rehabilitation and, 548 normal laxity differentiated from, 191 onset of, rehabilitation and, 545 posterior, 209–227, 210f anatomy of, 209–210 athletes affected by, 211–212, 212f atraumatic, 209, 212, 212f baseball throwing and, 408 biomechanics of, 210 in football, 424–425 imaging studies in, 214f, 214–215, 215f nonoperative management of, 215f–217f, 215–217, 217t operative arthroscopy for, 102, 226 operative management of, 217–222, 218f, 225–226 outcomes with, 225–226 pathomechanics of, 210–211, 211f physical examination in, 212–214, 213f rehabilitation for, 222–225, 546 traumatic, 209, 212, 212f voluntary, 212, 212f proprioception alterations due to, 659 rehabilitation for, 545–560 for anterior instability, 547f, 201540 arm dominance and, 548 for congenital shoulder laxity, 556–557, 558b–559b, 559, 560f degree of instability and, 545 desired activity level and, 548 direction of instability and, 546–547, 547f factors to consider in, 545–548, 546b, 547f frequency of dislocation or subluxation and, 545–546 for multidirectional instability, 546–547, 547f neuromuscular control and, 548 onset of instability and, 545 phase I (acute phase) of, 548, 549b, 551, 551f phase II (intermediate phase) of, 549b–550b, 551–552, 553b–554b, 555f phase III (advanced strengthening phase) of, 550b, 552, 555, 556f phase IV (return to activity phase) of, 550b–551b, 555–556, 556f for posterior instability, 222–225, 546 tissues affected and, 547–548 for traumatic instability, 548–556 scapulohumeral rhythm and, 22 static, 627 subluxation frequency and, rehabilitation and, 545–546 in swimmers, interventions for, 456 tissues affected in, rehabilitation and, 547–548 traumatic, rehabilitation for, 548–556 traumatic, unilateral and unidirectional, Bankart lesion, surgery group of, 446 Interclavicular ligament, anatomy of, 4 Internal impingement, 123–139, 124f, 527 baseball and, 402–403, 403f examination in, 126–127, 127f imaging of, 81–83, 82f operative arthroscopy for, 100 overhead sports and, 144
9/19/08 7:17:25 PM
862
INDEX
Internal impingement (Continued) PASTA lesions and, 144 pathology of, 123–126 anatomic theory of, 123 anterior laxity theory of, 123–124, 124f microinstability-over-rotation theory of, 126 posterior capsular tightness theory of, 124–126, 125f postoperative rehabilitation for, 137–139 following anterior capsular shift procedure, 138 following capsular plication, 137 following superior labral surgery, 138–139 following thermal capsular shrinkage, 137 radiographic diagnosis of, 127–128, 128f tensile failure of rotator cuff and, 112 testing for, 48 treatment of, 128–137 nonoperative, 128–130, 129f–136f surgical, 130–131, 135–137 Internal impingement sign, 126–127, 127f Internal rotation in baseball players, 125f, 125–126 bilateral peak torque and, 726, 727t coracoacromial arch and, 12 elevation in scapular plane with. See Empty can exercise. glenohumeral internal rotation deficit and, 31, 125 eccentric exercise for, 700–701, 701f total arc of motion in, 58, 59f isokinetic exercise and, 737f, 737–738 continuum of exercise positions for, 736f, 736–737, 737f isokinetic muscular performance in, 733t isokinetic shoulder torque to body weight ratios and, 732t isokinetic testing and, bilateral comparison of, 726, 726t for motion restriction, 690 at 90 degrees abduction, in thrower’s 10 program, 844 peak ratio of torque and work to body weight and, 729t peak torque-body weight ratio and, 728t scapular, 20, 20f standing. See Standing internal rotation. subscapularis activity during, 595–596 at 0 degrees abduction, in thrower’s 10 program, 843 Internal rotation lag sign, 63, 63f in subacromial impingement, 119 Internal rotation range-of-motion exercises for superior labral anterior-posterior lesions, type II, 139 Internal rotation stretches side-lying, for golf injuries, 472, 473f with wand, 637f International Classification of Functioning, Disability and Health, 817, 818, 818t International Classification of Impairments, Disabilities and Handicaps, 818, 818t Interneurons, afferent information processing and, 656–657 Interval sport programs, 789–802 baseball throwing, 789, 790b–792b, 791–796 accelerated throwing programs and, 792–793, 793b, 794b
Index_849-876-F06701.indd 862
Interval sport programs (Continued) hitting program and, 793, 796, 796b Little League, 793, 795b long toss in, 789, 791 off-the-mound, 791–792 softball, 796, 797b definition of, 789 for female shoulder injuries for softball catcher, 581b–582b for softball infielders, 582b for softball outfielders, 583b for softball pitchers, 578b–580b football throwing, 796, 798b golf, 481, 482t, 798–799, 799t javelin throwing, 800, 800b–802b, 802 principles of, 789 progression and, injury classification for, for female athletes, 586b return to swimming with, 460–461 tennis, 796, 798, 799t Intervertebral discs, anatomy of, 351 Intervertebral foramen, 351 Inverted cross, shoulder mechanics and, 495, 496f Inverted grip, shoulder mechanics and, 496, 496f Iontophoresis, for internal impingement, 128 Iron cross closed-chain bilateral hood-lying bridge and, 631f on foam roller with trunk, 631f shoulder mechanics and, 495, 495f Irradiation, 677 for proprioceptive neuromuscular facilitation, 641 Isokinetic exercise(s), 731–740 contre-coup concept of posterior dominant shoulder and, 736f, 736–737, 737f decrease in use of, 719 off-axis (multiple-joint) planes and, 739, 740f on-axis planes and movements and, 737f, 737–739 patient progression criteria for, 733 proprioceptive neuromuscular facilitation patterns and, 739, 741f rehabilitation guidelines for, 740, 742b rehabilitation principles for, 731 resistive-exercise progression continuum for, 733–736, 734b Isokinetic testing, 51, 664, 719–742, 721f, 820 concentric and eccentric evaluation using, 701, 701f functional performance related to, 740–742 functional testing algorithm for, 720, 720b interpretation of test data and, 725f, 725–729 of acceleration and deceleration characteristics, 726 bilateral comparison and, 726, 726t, 727t concentric versus eccentric considerations in, 727, 729 of load range, 727 of muscular performance parameters, 726 parameters for, 730–731, 734t of ratios of torque to body weight, 727, 732t, 733t of torque parameters, 725–726
Isokinetic testing (Continued) of unilateral ratios, 726–727, 728t–731t outcomes documentation and, 742 physical examination and, 720–721 rehabilitation principles and. See Isokinetic exercise(s). standardized protocol for, 722b, 722–725 consistency in data analysis in, 725 consistency in data collection in, 725 data analysis in, 725 gravity compensation in, 725 instant axis of rotation in, 723 patient education in, 722 planes of motion in, 722–723 stabilization of patient in, 723 submaximal to maximal active warm-ups in, 723–724 system calibration in, 722 system stabilization in, 722 testing environment in, 724 testing position in, 723, 723f testing protocol and, 724, 724b in upper-extremity fatigue testing, 729–730 Isometric exercise(s) multiple-angle, 733 for scapular dyskinesia, 676f, 678, 678f subscapularis activity during, 595–596 for superior labral anterior-posterior lesions, type II, 139 Isometric muscle testing, 50 Isotonic exercise(s) for female shoulder injuries, 576, 576f for instability posterior, 217 strengthening, 551, 551f, 552, 553b–554b in pool, in conditioning program for shoulder, 781–782, 782b for tennis injuries, 438, 439f, 439–440 Isotonic muscle testing, 50–51 Isotonic resistance program, for instability, 552 Isotonic techniques, combination of, in proprioceptive neuromuscular facilitation, 642
J Jahnke test, 68, 69f Javelin throwing biomechanics of, 376 interval program in, 800, 800b–802b, 802 Jerk test, 68, 69f in posterior instability, 212, 213f, 213–214 Jobe test, 61, 62f in PASTA lesions, 144 in tensile failure of rotator cuff, 113 Joint mobility, maintaining, for impingement, 534–536, 535f, 536f Joint position sense, 655, 661, 662f Jump training. See Plyometric exercise(s).
K Keukotape, 807 Kick in front crawl stroke, 450–451 Kim lesions, 211 arthroscopic treatment of, 221–222, 222f Kim test in posterior instability, 212, 213, 214
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INDEX Kinematics arthrokinematics as of front crawl stroke, 452t of scapulothoracic joint. See Biomechanics, of scapulothoracic joint. during golf swing acceleration phase of, 466, 467t downswing phase of, 466, 467t follow-through phase of, 467, 467t, 468t take-away and backswing phase of, 465–466, 467t osteokinematics as of front crawl stroke, 452t of scapulothoracic joint. See Biomechanics, of scapulothoracic joint. in tennis, 433–434 Kinesiotape, 815 Kinesthesia, 655, 661, 661f Kinetic chain evaluation and, 776 length-tension relationships and, 776 tennis serve and, 432f, 432–433 Kinetic chain concept, 775 Kinetic chain exercises. See also Closed kinetic chain exercise(s); Open kinetic chain exercise(s). for scapular dyskinesia, 677 Knee(s) core stabilization exercises for, 769, 771f extension of, in conditioning program for shoulders, 779 Kneeling on foam roller for gymnastic injuries, 502b, 503f Knot placement, arthroscopic, for arthroscopic rotator cuff repairs, 179–180 Knot tying for anterior dislocation of shoulder, 253, 253f Kyphosis, thoracic rehabilitation of scapular dyskinesis and, 675f–677f, 675–677 scapulohumeral rhythm and, 22
L L exercise, 767, 768f, 769 Labral grinding, 58 Labral surgery, superior, postoperative rehabilitation following, 138–139 Labral tests, 47–48 Labrum, glenoid. See Glenoid labrum; Labral entries. Lachman’s test in anterior instability, 406, 407f for glenohumeral capsule laxity, 99 Lag signs of rotator cuff, 49 Lamb’s wool for padding, 809 Langer’s lines, 106 Latarjet procedure, 262 glenohumeral arthritis following, 315 Late swing phase of baseball batting, 395 Lateral raises to 90 degrees, 840 Lateral scapular slide, 673 Latissimus dorsi muscle abnormalities of, imaging of, 85, 85f activity of, in shoulder exercises, 604t, 608t, 611t in baseball pitching, 386t biomechanics of, 37
Index_849-876-F06701.indd 863
Latissimus dorsi muscle (Continued) cross-sectional area of, 11t exercise of, electromyographic analysis of, 591b in football throwing, 389–390, 390t in front crawl, 455 in golf swing, 397t, 398, 399, 466, 467, 467t middle, 394t in tennis volley, 395, 396t in volleyball serve and spike, 392, 393t Latissimus dorsi stretch(es) active, 766, 766f for golf injuries, 474, 474f Latissimus pull-down exercise in conditioning program for shoulders, 779 Lavage for calcific tendinitis, 157 Lawnmower exercise in sling, for scapular dyskinesia, 678b on a step, for scapular dyskinesia, 678b, 679f supported, for scapular dyskinesia, 678b, 679f Laxity, ligamentous examination for, 56, 57f female shoulder injuries and, 570 Laxity of shoulder definition of, 511 in female athletes, 520 hyperlaxity as. See Instability of shoulder. normal, instability differentiated from, 191 operative arthroscopy for, 99, 101–102 L-bar external rotation exercise, scapular plane, 839 L-bar flexion exercise, 839 L-bar internal rotation exercise, scapular plane, 839 Lead arm backswing reach for warm-up for golf, 475t, 477 Leg drive in tennis serve, 432 Leg lowering exercise, 767, 767f Legal issues with protective equipment, 815–816 Length-tension relationships, kinetic chain, 776 Lesser tuberosity, fractures of, in children, 514 Levator scapulae muscle activity of exercises eliciting, 623 in shoulder exercises, 609t in baseball pitching, 386t exercise of electromyographic analysis of, 597t eliciting activity, 623 in golf swing, 398t, 466 scapulothoracic joint motion and, 11 Leverage, joint stability and, 628–629, 629f Liability with protective equipment, 815 Lidocaine for biceps long head ruptures, 287 for snapping scapula syndrome, 290 for subacromial impingement, 120 Lift exercise, low to high, 618 Liftoff test, 62f, 62–63 in subacromial impingement, 119 Ligament(s). See also specific ligaments. laxity of examination for, 56, 57f female shoulder injuries and, 570 of vertebral column, 351 Lighcast, 808 Limited joint motion syndrome, 293
863
Link sequencing, eccentric muscle action and, 699, 699f Little League interval program, 793, 795b Little Leaguer’s shoulder, 508–510, 509f diagnosis of, 509 mechanism of injury of, 509–510 prevention of, 510 treatment of, 510 Load and shift test, 46, 66f, 66–67 in multidirectional instability, 231t Load range in isokinetic testing, 727 Load test in posterior instability, 212 Locomotion on hands and arms, shoulder mechanics and, 493 Long thoracic nerve anatomy of, 708, 709f injuries of, in football, 422–423 neurodynamic testing of, 712–713, 713f Long thoracic nerve palsy, 35 Long toss interval program, 789, 791 Loose bodies, imaging of, 75, 76f Low back, golf swing modifications with, 485 Low row exercise for scapular dyskinesis, 675–676, 676f, 678b Lower cross syndrome, 780, 781b L-seat for gymnastic injuries, 500b, 501f Lunge and rotate for warm-up for golf, 475t, 477
M M exercise, 767, 769, 769f Magnetic resonance angiography, 73–74 in posterior instability, 214–215, 215f Magnetic resonance arthrography, 73 of biceps tendon dislocation, 81, 81f of labral injuries, 77–78, 78f, 79f of loose bodies, 75, 76f of rotator cuff tears, 83–85, 84f, 85f Magnetic resonance imaging, 73 in adhesive capsulitis, 76, 294 in anterior dislocation of shoulder, 243, 244f of Bankart lesions, 260, 260f of Bennett lesion, 77, 77f in biceps tendinitis, 285 in calcific tendinitis, 156 of dislocations, 74 of fractures, of humerus, 74 in internal impingement, 127–128, 128f in multidirectional instability, 230 in neck and shoulder pain, 352–353 in osteoarthritis, 74 of osteochondral lesions, 75, 76f in osteonecrosis, 74, 76f of PASTA lesions, 145, 145f in posterior instability, 214, 214f of rotator cuff abnormalities, 81, 82f calcific tendinitis as, 83, 83f rotator cuff tears as, 83 tendinosis as, 83, 83f tensile failure of rotator cuff as, 113 of SLAP lesions, 79–80, 80f of subacromial tendon distention and inflammation, 83 in suprascapular nerve entrapment, 346, 346f in thoracic outlet syndrome, 328 Magnuson-Stack procedure, 262 scapulohumeral rhythm and, 23 Males. See Boys; Men.
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864
INDEX
Maltese cross, shoulder mechanics and, 495, 496f Manipulation under anesthesia for adhesive capsulitis, 296–298, 299f Manual contacts for proprioceptive neuromuscular facilitation, 640 Manual muscle testing, 820 isokinetic testing as useful addition to, 720 Manual therapy for motion restriction, 687f, 687–689, 688b stages of, 688b, 690f Massage for impingement, 537, 537f neurogenic, 715–716 MAX Brace, 813, 814 Maximum voluntary isometric contraction, 430 Maximum work repetition in isokinetic testing, 726 Mean peak torque, 726 Mechanoreceptors, 655 muscle stiffness and, 659 Medical Outcomes Study Short Form—36, 821 Medicine ball sit-ups using, in plyometric program, 757, 758f wall exercises using, in plyometric program, 757–758, 759f, 760f Medicine ball throws for golf, 478–479, 481f Meissner corpuscles, proprioception and, 656 Memory foam for padding, 809 Men, gymnastic training and progression for, 492 Merkel discs, proprioception and, 656 Metabolic demand, concentric versus eccentric muscle action and, 697–698, 698f Methylprednisolone for subacromial impingement, 120 Microinstability-over-rotation theory of internal impingement pathology, 126 Microtrauma, repetitive, acquired, 401 Military press exercise in conditioning program for shoulders, 779 deltoid activity during, 621 electromyographic analysis of scapulothoracic musculature during, 597t, 598t glenohumeral muscle activity during, 608t for scapular dyskinesia, 682t scapular muscle activity during, 609t Mimori test in multidirectional instability, 231t Mimori test in SLAP lesions, 409 Minimal detectable change, 826 Mini-open rotator cuff repair, 159, 160f, 161f, 165–174 arthroscopic repair versus, 165–167, 173–174 open technique versus, 165 rehabilitation following, 171–172 results of, 172–174 surgical technique for, 167–171, 168f–172f Mini-trampoline exercises for gymnastic injuries, 502b, 502f Mixed bowlers, 377 Mobility in conditioning program for shoulders, 777 in rehabilitation for golf injuries, 470–474, 471f–474f Mobility exercises for core stabilization, 766 Modified neutral position, 721, 721f Modified Rowe Scale, 823t
Index_849-876-F06701.indd 864
Moleskin for padding, 809 Monosynaptic reflex, 656 Motion of shoulder complex. See also Abduction; Adduction; Depression; External rotation; Flexion; Internal rotation; Protraction; Protrusion; Range of motion; Retraction; Rotation; Tilt. planes of, 17–18, 18f Motion-restricted shoulder. See Arthrofibrosis; specific conditions. Multidirectional instability. See Instability, multidirectional. Multiplane movements for motion restriction, 690f, 690–692 Multiple-angle isometric exercises, 733 Muscle(s). See also specific muscles. actions of. See Muscle action(s); specific muscles. atrophy of, prevention of, in impingement, 536, 536t contraction of concentric muscle action and, 696–698, 697f, 697t, 698f eccentric muscle action and. See Eccentric muscle action. electromyography data collected during throwing and, 111–112 fatigue of, isokinetic testing for, 729–730 firing patterns of, 765 short, 765 soreness of concentric versus eccentric muscle action and, 697t, 698 soreness rules for, for female athletes, 586b stiffness of, level of contraction and, 659 of vertebral column, 351 wasting of, conditions associated with, 56, 56f Muscle action(s). See also specific muscles. assessment of, 49–51, 50t isokinetic, 51 isometric techniques for, 50 isotonic, 50–51 characteristics of, 49, 50t eccentric, 695–704, 696f concentric muscle action contrasted with, 696–698, 697f, 697t, 698f eccentric exercise and, 700–701, 701b, 701f mechanism of, 695–696, 696f pathology affecting, 698–700, 699f, 700f physiology of, 696–698, 697f, 697t, 698f shoulder dysfunction and, 702f, 702–704, 703b, 703f Muscle activation pattern, proximal-to-distal, for scapular dyskinesia, 677 Muscle fatigue, isokinetic testing for, 729–730 Muscle fibers during concentric muscle contraction, 750, 752f orientation of, core stabilization and, 764 Muscle force balance of forces and, stability of shoulder and, 658 concentric versus eccentric muscle action and, 697t maximum predicted isometric force and for infraspinatus muscle, 612 for teres minor muscle, 612–613
Muscle force (Continued) sensation of, 655, 661–662 in vivo study of maximal muscle force production using dynamometers and, 695–696 Muscle reflexes, dynamic stability of shoulder and, 658–660 Muscle spindle, as stretch receptor, 750, 751f Muscle strength. See also Strengthening exercises. assessment of, 49, 52, 59–60, 60t Muscle tone, feedback regulation of, 657 Muscular endurance for preadolescent and adolescent athletes, 564 tennis injuries and, 438–440, 439f–441f Muscular performance parameters in isokinetic testing, interpretation of, 726 Musculocutaneous nerve anatomy of, 13, 707–708, 708f injuries of, 354 neurodynamic testing of, 711, 712f
N Nagi disablement model, 817, 818, 818t National Center for Medical Rehabilitation Research disablement scheme, 818t Neck. See also Cervical entries. in proprioceptive neuromuscular facilitation, 651 Necrosis, avascular, imaging in, 74, 76f Neer’s impingement test in subacromial impingement, 118 Neer’s sign, 48, 60, 61, 61f, 118 Nerve(s). See also specific nerves. cervical, pinch injuries of, 339–341 dynamic roominess and, 707 injury of, with Bankart repair, 265 Nerve conduction studies afferent pathway assessment using, 662 in brachial neuropathy, 341–342 in suprascapular nerve entrapment, 346–347 Nerve mobilization treatment, neurodynamic testing and, 714, 715f Nerve roots cervical brachial plexus and, 337–338, 338f, 339f burners (stingers) and, 354 high-velocity injuries of, 338–339 disorders of, neurodynamic test findings in, 714 entrapment of, impingement and, 529 Nerve supply of shoulder, 13–14. See also specific nerves. Nerve tension testing in cervicogenic injuries, 357, 358f Neurapraxia(s), 337, 354 cervical cord, 354–355 Neurodynamic testing, 707 active, 710 of axillary nerve, 711, 712f current concepts in, 709–710 findings of, 713–716 analysis of, 713–714 clinical management and, 714–716, 715f neurogenic source considerations and, 714 normal physiologic responses and, 714, 714f as reassessment tool, 715
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INDEX Neurodynamic testing (Continued) structural differentiation and, 713 test positivity and, 713 of long thoracic nerve, 712–713, 713f manual nerve palpation and, 710 of musculocutaneous nerve, 711, 712f of suprascapular nerve, 712, 712f upper limb (base test), 710f, 710–711 Neurodynamic treatment, 714–716, 715f active self-care techniques for, 716 passive techniques for, 715–716 Neurodynamics, 707–716 anatomic considerations in axillary nerve and, 708, 709f long thoracic nerve and, 708, 709f musculocutaneous nerve and, 707–708, 708f suprascapular nerve and, 708–709, 709f definition of, 707 testing and. See Neurodynamic testing. treatment and. See Neurodynamic treatment. Neurogenic massage, 715–716 Neurogenic pain following shoulder surgery, 716 Neurological examination, 69, 69f Neuromuscular control, 627–633 alterations in, with shoulder injury, 659–660 co-activation to improve, exercises to enhance, 661 in conditioning program for shoulder, 777–778, 782, 784 definition of, 662 electromyography to assess, 662f–664f, 662–663 exercises to enhance, 629–630 clinical application of, 630, 632 flexibility exercises as, 630, 635f–637f stability exercises as, 630, 630f–635f kinesiology and, 627–628, 628f leverage and, 628–629, 629f neuromotor control and, 627, 628t proprioceptive neuromuscular facilitation for. See Proprioceptive neuromuscular facilitation (PNF) patterns. sensorimotor facilitation of, 655, 656f stability of shoulder and, 657–659 in throwing, 671–672 torque and, 628, 628f Neuromuscular electrical stimulation for motion restriction, 689 Neuromuscular re-education for female shoulder injuries, 576–578, 577f of glenohumeral muscle recruitment, for swimmers, 459 Neuromuscular training for golf injuries, 474–478 warm-up and, 474–475, 475t, 476f–478f, 478t Neuropathic pain, peripheral, 707. See also Neurodynamic testing; Neurodynamics. Neurovascular compression syndromes, 325–333. See also Thoracic outlet syndrome. axillary artery occlusion and aneurysm and, 329f, 329–330 baseball and, 411 effort thrombosis as, 330–332, 331f historical background of, 325 quadrilateral space syndrome as, 332f, 332–333, 333f Nevaiser’s portal for operative arthroscopy, 108
Index_849-876-F06701.indd 865
Nicola procedure for anterior instability, 202 90/90 throws in conditioning program for shoulder, 784f Noise, glenohumeral, postoperative, 253, 254f Nonsteroidal anti-inflammatory drugs for female shoulder injuries, 573–574 Noxious stimulation for female shoulder injuries, 573, 573f, 573t Nucleus pulposus, 351 Numbness with burners (stingers), 422
O Obesity, arthroscopic rotator cuff repairs and, 180 Obligate translation, 316 O’Brien test, 47 in labral pathology, 64, 65f in multidirectional instability, 232t in SLAP lesions, 127, 409 in tensile failure of rotator cuff, 113 O’Driscoll SLAP test, 64 Off-the-mound throwing interval program, 791–792 Olympic lift exercise in conditioning program for shoulders, 779 On-axis planes and movements in isokinetic exercises, 735–736 One-handed baseball throw in plyometric program, 757, 760f Open kinetic chain exercise(s) definition of, 603 proprioceptive neuromuscular facilitation compared with, 640 for proprioceptive restoration, 661 rotator cuff biomechanics and function and, 603, 605–620 of deltoids, 620–622 of infraspinatus and teres minor, 607, 612–619 of levator scapulae, 623 of rhomboids, 623 of serratus anterior, 622–623 of subscapularis, 617, 619–620 of supraspinatus, 603, 605–607 of trapezius, 623 for stability, 630, 632f–635f Open stance in tennis, 433, 433f Operative arthroscopy, 99–103, 105–108 for acromioclavicular joint injuries, 103 for acute dislocation of shoulder, 245–251 with acute osseous Bankart lesions, 251 Bankart repair with suture anchors for, 248–249 examination under anesthesia in, 246 with extension of anterior inferior labrum tear into superior labrum, 250–251 with extension of capsulolabral injury posteriorly, 250, 251f rotator interval closure for, 249–250, 250f for adhesive capsulitis, capsular release as, 298–300, 300f for anterior instability, 199–201, 200f open versus arthroscopic stabilization and, 202–204 subdeltoid arthroscopic stabilization and, 204f, 204–205 subdeltoid stabilization and, 204f, 204–205
865
Operative arthroscopy (Continued) for Bankart lesions. See Bankart repair, arthroscopic. for calcific tendinitis, 157 for compressive cuff disease, 99–100 primary, 99 secondary, 99–100 débridement of PASTA lesions using, 146–147 external anatomy and, 105–106, 106f for ganglion cysts, 347 for glenohumeral laxity, 101–102 for glenoid labral tears, 102, 102f, 103f for impingement, internal, 100 for instability in female athletes, 521 multidirectional, 234–236, 235f posterior, 220–222, 221f, 222f, 226 for Kim lesions, 221–222, 222f operative technique for, 105, 106f for rotator cuff repair. See Arthroscopic rotator cuff repair. for subacromial impingement, 120, 121f for suprascapular nerve entrapment, 347–348 for tensile lesions, 100f, 100–101, 101f for thrower’s exostosis, 102–103 Opposite pocket stretch for golf injuries, 472, 473f Orthoplast, 809 Os acromiale, 6 Osseous adaptation, 192 Osseous lesions. See also Fracture(s); specific bones and lesions. instability and, rehabilitation for, 547–548 Osteoarthritis of glenohumeral joint, 315, 316f primary and secondary, 315 imaging in, 74 proprioception alterations due to, 659 Osteochondral lesions, imaging of, 74–75, 76f Osteochondritis dissecans of glenoid, baseball and, 410 Osteochondrosis of the proximal humeral epiphysis, 508–510, 509f Osteokinematics. See also Kinematics. of front crawl stroke, 452t of scapulothoracic joint. See Biomechanics, of scapulothoracic joint. Osteolysis of distal clavicle in children, 514 Osteonecrosis, imaging in, 74, 76f Outcome measures, 817–827 clinical outcomes and. See Clinical outcomes. cost of care and, 818 isokinetic testing and, 742 patient satisfaction and, 817–818 process outcomes and, 817 Outfielding, softball, interval sport program for, 583b Overhead elevation progression, rehabilitation of scapular dyskinesis and, 678, 680f, 681 Overhead reach with towel slide for scapular dyskinesia, 680f, 681–682 Overhead soccer throw, two-hand, in plyometric program, 753, 756f, 757, 759f Overhead sports. See also Baseball pitching; Serve(s); Swimming; Throwing. cervicogenic shoulder pain and, 355–356 coracoacromial ligament and, 117
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866
INDEX
Overhead sports. See also Baseball pitching; Serve(s); Swimming; Throwing. (Continued) internal impingement and, 144. See also Internal impingement. rotator cuff lesions and. See Rotator cuff, tensile failure of. Overhead straight-arm pulls for gymnastic injuries, 497, 499f Overtraining, swimmer’s shoulder and, 447 Overuse injuries in children, 507 in female athletes, 569 reduction of overuse and, in tennis, 438 tendinitis as, baseball and, 403, 403f, 404f Oxygen consumption, concentric versus eccentric muscle action and, 698, 698f
P Pacinian corpuscles, proprioception and, 655–656 Padding of acromioclavicular joint, 809, 810f protective, materials for, 808–809 Paget-Schroetter syndrome, 330–332, 331f diagnosis of, 331, 331f physical signs in, 331, 331f treatment of, 331–332 Pain with acromioclavicular joint injuries, 304–305 biceps, baseball and, 410 in biceps tendon dysfunction, 571, 573 tendinitis as, 284, 285–286, 286b in brachial neuropathy, 341 with burners (stingers), 339–340, 422 in cervical radiculopathy, 352–353 in internal impingement, 126 in Little Leaguer’s shoulder, 509 neurogenic, following shoulder surgery, 716 neuropathic, peripheral, 707. See also Neurodynamic testing; Neurodynamics. in quadrilateral space syndrome, 332 in radiculopathy, 352 referred, 352 in suprascapular nerve entrapment, 412 in swimmer’s shoulder, 447, 448–449, 449b, 451 interventions for, 456 muscle activity and, 454–455 in tensile failure of rotator cuff, 112 Painful arc test, 48, 60–61, 61f Paralabral cysts, imaging of, 80 Paralysis in brachial neuropathy, 341 Paresthesia with burners (stingers), 339, 422 Partial articular supraspinatus tendon avulsion lesions. See PASTA lesions. Participation definition of, 819 measures of, 820–821, 826 restrictions on, definition of, 819 Passive range of motion as body function measure, 819–820 Passive range of motion into internal rotation stretch for internal impingement, 128, 129f Passive range-of-motion exercises for instability, 551, 552 for superior labral anterior-posterior lesions, 138
Index_849-876-F06701.indd 866
PASTA lesions, 143–152 classification of, 145–146 clinical diagnosis of, 144 imaging studies in, 144–145, 145f pathogenesis of, 143–144 treatment of, 146–152 algorithm for, 147f, 147–149, 148f arthroscopic débridement-only technique for, 146–147 nonoperative, 146 open repair for, 147 PASTA transtendon repair for, 147–152, 148f–152f with subacromial decompression, 146–147 PASTA transtendon repair, 147–149, 147–152, 148f–152f Patient education about isokinetic testing, 722 in impingement, 533–534, 534f Patient satisfaction, 817–818 Pavlov’s ratio, 354 Paxinos test for acromioclavicular joint injury, 58 Peak torque, 725–726 mean, 726 Pearson correlation coefficient, 825 Pectoralis major muscle, 287–289 activity of, in shoulder exercises, 604t, 607t–609t, 612t anatomy and function of, 287–288 in baseball pitching, 386t biomechanics of, 37 cross-sectional area of, 11t exercise of, electromyographic analysis of, 591b in football throwing, 389–390, 390, 390t in front crawl, 455 in golf swing, 397t, 398, 399, 466, 467, 467t middle, 394t rupture of, 288–289 causes of, 287 presentation of, 287, 287f, 289f treatment of, 289 in tennis volley, 395, 396t in volleyball serve and spike, 392, 393t in windmill pitching, 391, 391t Pectoralis major musculotendinous abnormalities, imaging of, 85, 85f Pectoralis minor muscle activity of, in shoulder exercises, 609t exercise of, electromyographic analysis of, 598t scapulothoracic joint motion and, 12 Pectoralis minor stretching for golf injuries, 473f, 473–474 Peel-back labrum, 409 Peel-back mechanism, SLAP lesions and, 372 Pelvic floor, core stabilization and, 764 Performance, plyometric exercises for, 755, 757f Periarthritis. See Adhesive capsulitis. Pericapsulitis. See Adhesive capsulitis. Periodization in conditioning program for shoulders, 779–780 Peripheral nerve injuries. See also Brachial plexus injuries. classification of, 337, 338f Peripheral neuropathic pain, 707. See also Neurodynamic testing; Neurodynamics.
Perthes lesion, imaging of, 77, 78f Perturbation drills for internal impingement, 130 Physical therapy for adhesive capsulitis, 295b, 295–296, 296f–298f Physioball exercises for internal impingement, 130, 135f Piked handstand push-ups for gymnastic injuries, 501b, 502f Pitching. See Baseball pitching; Throwing; Windmill pitching. Planes of motion, isokinetic testing and, 722–723 Plank exercises for internal impingement, 130, 136f Plastazote, 809 Plastics for padding, 809 Plus position, 320 Plyoback, 753 Plyoball wall dribbling using, in plyometric program, 757, 760f wall exercises using, in plyometric program, 757–758, 759f, 760f Plyometric exercise(s), 749–760 chest pass as, 635f chop pass as, 635f in conditioning program for shoulders, 782b, 783f–785f, 784 contraindications to, 758, 760f definition of, 749 for golf, 478–479, 481f for gymnastic injuries, 503b, 504f historical background of, 749–750 for instability, 552, 555, 556f for internal impingement, 130 neurophysiologic basis of, 750–752, 751f, 752b, 752f phases of, 752, 752b for posterior instability, 217, 217f for proprioceptive restoration, 661 push-ups as, on Swiss ball, 632f scientific studies supporting clinical use of, 753 for superior labral anterior-posterior lesions, 138–321 for tennis injuries, 440, 440f, 441f upper-extremity program for, 753, 754b, 755–758 medicine ball wall exercises in, 757–758, 759f, 760f throwing movements in, 753, 755, 756f–758f trunk extension and flexion in, 757, 758f, 759f warm-up exercises in, 753, 754f, 755f Plyometrics, quick-explosion philosophy of, 750–751 PNF patterns. See Proprioceptive neuromuscular facilitation patterns. Polyethylene forms for padding, 809 Polyvinyl chloride acrylic for padding, 809 Polyvinyl chloride for padding, 809 Pool exercises, isotonic, in conditioning program for shoulder, 781–782, 782b Popeye sign, 81 Port of Washington portal for operative arthroscopy, 108
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INDEX Portals for operative arthroscopy, 106–108 accessory superolateral, 181, 181f anterior, 107, 181 for anterior dislocation of shoulder, 247f, 247–248 incorrect placement of, 252 anterosuperolateral, 108 5 o’clock, 108 lateral, 181 Nevaiser’s, 108 Port of Washington, 108 posterior, 106–107, 181 posterolateral, 108 for rotator cuff repair, 180–181, 181f subacromial, 107–108, 108f Posterior capsular tightness theory of internal impingement pathology, 124–126, 125f Posterior capsulitis, baseball and, 403 Posterior instability of shoulder. See Instability of shoulder, posterior. Posterolateral portal for operative arthroscopy, 108 Posture adaptations of in golfers, 473f, 473–474, 474f in tennis players, 434f, 434–435 in female athletes, scapular dysfunction and, 575 forward-head, 780, 780f, 781b forward-head and rounded-shoulder, impairments in timing and control of, 646, 648f impaired, in swimmers, interventions for, 456 impingement and, 530 lower cross syndrome and, 780, 781b optimal, 776 poor, dysfunctional muscle patterns and, 776 pronation syndrome and, 780, 781b rehabilitation of scapular dyskinesis and, 675f–677f, 675–677 in scapular dyskinesis assessment, 672–673 shoulder dysfunction related to, 356 upper cross syndrome and, 780, 780f, 781b Power average, in isokinetic testing, 726 in conditioning program for shoulders, 777 Prayer exercise, glenohumeral muscle activity during, 607t Preadolescents, 563–567. See also Children. definition of preadolescence and, 565 strength training for age-specific guidelines for, 566f, 566–567, 567f benefits of, 564–565 efficacy of, 563–564 guidelines for, 565, 565t Press-up exercise(s), 613f electromyographic analysis of scapulothoracic musculature during, 598t glenohumeral muscle activity during, 608t prone, for golf, 483, 484f scapular muscle activity during, 609t standing, with elbow bent, for scapular dyskinesia, 681t in thrower’s 10 program, 845 Preswing phase of baseball batting, 395 Previous injuries, evaluation of, for conditioning program for shoulders, 778
Index_849-876-F06701.indd 867
Previous surgeries, evaluation of, for conditioning program for shoulders, 778 Process outcomes, 817 Pronation in thrower’s 10 program, 847 Pronation syndrome, 780, 781b Prone back extension in plyometric program, 757, 758f Prone external rotation at 90 degrees, for scapular dyskinesia, 681t at 90 degrees of abduction, 613f rotator cuff and deltoid activity during, 605t trapezius and serratus anterior activity during, 606t at 100 degrees of abduction, rotator cuff and deltoid activity during, 605t Prone horizontal abduction with full glenohumeral external rotation, 598–599 at 90 degrees of abduction with external rotation, scapular muscle activity during, 609t at 90 degrees of abduction with internal rotation glenohumeral muscle activity during, 608t scapular muscle activity during, 609t at 90-135 degrees of abduction with external rotation, 614f in thrower’s 10 program, 845 Prone press-ups for golf, 483, 484f Prone rowing exercise, 841 into external rotation, in thrower’s 10 program, 845 in thrower’s 10 program, 845 Proprioception alterations in, with shoulder injury, 659 definition of, 661 joint position sense and, 661, 662f kinesthesia and, 661, 661f plyometrics and. See Plyometric exercise(s); Plyometrics. restoration of, 660–661 sensation of force and, 661–662 stability of shoulder and, 655–656 Proprioceptive awareness training, 660–661 Proprioceptive neuromuscular facilitation patterns approximation and, 641 case study of, 651–653 closed chain kinetic exercises compared with, 640 effectiveness of, 640 for female shoulder injuries, 576 for gymnastic injuries, 497 irradiation and, 641 isokinetic exercise and, 739, 741f manual contacts for, 640 for motion restriction, 692 open chain kinetic exercises compared with, 640 quick stretch and, 641, 649f resistance and, 640–641 strategies to optimize performance of, 642, 642t techniques and progressions for, 643–644, 646, 648–651 adjunctive procedures and, 651, 652f for shoulder impairments and functional losses, 644, 646, 648f–651f, 648–651 trunk and neck patterns and, 651
867
Proprioceptive neuromuscular facilitation patterns (Continued) theoretical basis for, 639–640 traction and, 641 for upper extremities, 641–643, 642t, 643f–647f, 643t, 648b combination of isotonics and, 642 relaxation techniques and, 643 repeated quick stretch and, 642 reversal of antagonists and, 642–643 rhythmic initiation and, 642 rhythmic stabilization and, 643 verbal commands and, 641 visual stimuli and, 641 Protective equipment, 805–807 equipment manager and, 806–807 football shoulder pads as, fitting of, 805–806, 806f historical background of, 805 legal and ethical considerations with, 815–816 maintenance of, 806 purpose of, 805 Protective padding materials, 808–809 rigid, 808, 809f soft, 809 Protraction clavicular, 23, 23f closed-chain, in prone plank position, 630f sternoclavicular joint and, 4 supine, 633f Protrusion, sternoclavicular joint and, 3, 4, 4f Provocative testing, 70, 70f. See also specific tests. in posterior instability, 212–214, 213f Proximal humeral epiphysiolysis, 508–510, 509f Proximal-to-distal muscle activation pattern for scapular dyskinesia, 677 Psychometrics, outcomes measure selection and, 822, 823t–824t, 824–825 Pulley maneuver for impingement, 535 Pull-through phase of front crawl stroke, 450, 452t Push and pull exercise, 617f Push-up exercise(s) deltoid activity and, 621 with feet elevated, glenohumeral muscle activity during, 607t glenohumeral muscle activity during, 607t with hands apart electromyographic analysis of scapulothoracic musculature during, 598t scapular muscle activity during, 609t one-arm, glenohumeral muscle activity during, 607t piked handstand, for gymnastic injuries, 501b, 502f with plus, 614f electromyographic analysis of scapulothoracic musculature during, 598t glenohumeral muscle activity during, 604t for scapular dyskinesia, 682t plyometric, on Swiss ball, 632f Swiss ball, for gymnastic injuries, 503b, 503f in thrower’s 10 program, 846 wall, in scapular dyskinesis assessment, 674
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868
INDEX
Putti-Platt procedure, 262 glenohumeral arthritis following, 315 scapulohumeral rhythm and, 23
Q Quadrilateral space syndrome, 290–291, 332f, 332–333, 333f, 354 diagnosis of, 332 treatment of, 332–333 Quadruped exercise, glenohumeral muscle activity during, 607t Quadruped rocking exercise, thoracic, 766, 766f Quick stretch in proprioceptive neuromuscular facilitation, 641, 649f repeated, 642
R Racquet preparation phase of tennis volley, electromyography during, 395, 396t Radial deviation for warm-up for golf, 475, 478t Radiculopathy cervical, shoulder pain caused by, 352–353 pain resulting from, 352 Radiography. See Conventional radiography. Range of motion, 111 active as body function measure, 819–820 in scapular dyskinesis assessment, 673b, 673–674, 674f following arthroplasty of the shoulder, 318 assessment of, 58–59, 59f, 60f as body function measure, 819–820 evaluation of, for conditioning program for shoulders, 778 normalization of, in impingement, 537, 538f restriction of. See Arthrofibrosis; specific conditions. short-arc exercises and, 734, 735f of shoulder complex, 3 in tennis players, 435t, 435–436 Range-of-motion assessment, 58–59, 59f, 60f Range-of-motion exercise(s), 839 active-assisted for impingement, 535 for instability, 551, 552 following posterior instability repair, 222–223 for superior labral anterior-posterior lesions, 138 internal, for superior labral anterior-posterior lesions, type II, 139 internal rotation, for superior labral anteriorposterior lesions, type II, 139 passive for instability, 551, 552 for superior labral anterior-posterior lesions, 138 for posterior instability, 215–216, 216f Reaching too short in front crawl stroke, 452–453, 453f, 454f Reciprocal innervation, law of, 776 Recoil action of elastic tissues, plyometrics and, 751–752 Recovery in conditioning program for shoulders, 778 Recovery phase of front crawl stroke, 450, 452t
Index_849-876-F06701.indd 868
Referred pain, 352 Reflexes monosynaptic, 656 muscle, dynamic stability of shoulder and, 658–660 Rehabilitation. See also Exercise(s). for acromioclavicular joint injuries, 311–312 for adhesive capsulitis, 295b, 295–296, 296f–298f following anterior capsular shift procedure, 138 following anterior stabilization, 205 following arthroplasty of the shoulder, 317–322, 318t capsular relationship optimization and, 318 range of motion and, 318 rotator cuff and scapular exercise progression for, 320–322, 321f strengthening and, 319–320, 320f subscapularis precautions for, 318, 319b following Bankart repair, 263–264 for baseball injuries, 413–414, 414f–415f, 416 biomechanics of exercises for, 589–600 effects of shoulder pathology and, 599, 600t electromyographic analysis of exercises and, 589, 590t–591t, 591–596 lower trapezius and, 597b, 598–599 scapulothoracic joint and, 596–599, 597t–598t serratus anterior and, 597–598, 598f, 598t, 599f following capsular plication, 137 for cervicogenic injuries, 357–359, 358f, 359f for female shoulder injuries. See Female shoulder injuries, rehabilitation for. for golf injuries. See Golf injuries, rehabilitation for. for gymnastic injuries, 497f, 497–504 flexibility and, 504, 504f phases of, 497–504, 498f for impingement, 532–539 stage I (acute inflammatory stage) of, 532–536 stage II (subacute state) of, 536–537, 537f stage III (progressive exercise stage) of, 537–539 stage IV (return to activity stage) of, 539 for instability. See Instability, rehabilitation for. for internal impingement, 128–130, 129f–136f following mini-open rotator cuff repair, 171–172 following open repair of rotator cuff tears, 161–162 for posterior instability, 215–217 phases of, 215f–217f, 215–217, 217t following posterior instability repair, 222–225 acute phase of physical therapy in, 222–223 advanced strengthening phase of, 223, 224f intermediate phase of physical therapy in, 223, 223f return to activity phase of, 224–225, 225f for scapular dyskinesis, 675–682 overhead elevation progression and, 678, 680f, 681 posture and, 675f–677f, 675–677 proximal stability and, 677–678, 678b, 678f–680f strengthening progression and, 681t, 682
Rehabilitation. See also Exercise(s). (Continued) for sensorimotor restoration, 660 following superior labral surgery, 138–139 for swimmer’s shoulder, 455–456 following thermal capsular shrinkage, 137 Relaxation techniques in proprioceptive neuromuscular facilitation, 644 Reliability of clinical outcomes measures, 824–825 Relocation test(s), 46, 68, 68f in instability, 408, 408f in multidirectional instability, 229, 231t in PASTA lesions, 144 in tensile failure of rotator cuff, 113 Repetitions, optimal number of, for short-arc exercises, 734 Repetitive microtrauma, acquired, 401 Resistance in conditioning program for shoulders, 781–782, 782b manual, for proprioceptive neuromuscular facilitation, 640–641 Resistance training for cervicogenic injuries, 356, 357f, 358f Resistance-tubing exercises, muscle activation of, 662f–664f, 662–664 Resistive-exercise progression continuum, 733–736, 734b Responsiveness of clinical outcome scores, 825 Rest, active, for impingement, 534 Rest intervals for isokinetic testing, 724 for short-arc exercises, 734–735 Resting position, biomechanics of, 17 Retraction clavicular, 23, 23f sternoclavicular joint and, 3, 4, 4f Retroversion, glenohumeral joint motion and, 6 Return to activity following brachial plexus injuries, 342 with female shoulder injuries, 578, 578b–586b gymnastics and, template for, 504–505 impingement and, 539 instability and, 550b–551b, 555–556, 556f following internal impingement, 130, 139 following posterior instability, 217 following posterior instability repair, 224–225, 225f for swimmers, 460–461 following tennis injuries, 440–441 Reversal of antagonists for scapular dyskinesia, 678 Reverse wrist flips in conditioning program for shoulder, 784f Rhomboid muscle(s) activity of exercises eliciting, 623 in shoulder exercises, 609t, 611t in baseball pitching, 386t exercise of electromyographic analysis of, 597t eliciting activity, 623 in front crawl, 454, 455 in golf swing, 398t, 466 major, scapulothoracic joint motion and, 11 minor, scapulothoracic joint motion and, 11
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INDEX Rhythmic initiation in proprioceptive neuromuscular facilitation, 642 for scapular dyskinesia, 678 Rhythmic stabilization exercises for instability, 557, 560f for internal impingement, 129, 129f in proprioceptive neuromuscular facilitation, 643, 650f Rib resection of cervical rib for axillary artery compression and aneurysm, 330 Roll of glenohumeral joint, 24–25, 26f Roll-gliding of glenohumeral joint, 24–25 Roos test, 70, 70f in thoracic outlet syndrome, 327, 328f Root avulsions, 338–339 Rotary drill swing plane, for warm-up, 475t, 476f transverse, for warm-up, 475t, 476f Rotation clavicular, 23 conoid ligament and, 5 deviating patterns of, scapulohumeral rhythm and, 23 downward, scapular, 19f, 20, 20f external. See External rotation; Prone external rotation; Side-lying external rotation; Standing external rotation. glenohumeral capsule and, 8 of glenohumeral joint, 24, 25f internal. See Internal rotation. scapular, clinical assessment of, 20 thoracic, 766, 766f trunk, in conditioning program for shoulder, 783f of trunk, in plyometric program, 753, 754f upward, scapular, 19f, 20, 20f Rotational stress fracture of the proximal humeral epiphyseal plate, 508–510, 509f Rotator cuff abnormalities of, imaging of, 81–85, 82f–85f anatomy of, 10–12, 11t, 116 variations of, 116–117, 117f in baseball pitching, 388 biomechanics of, 36, 603, 605–620 of infraspinatus and teres minor, 607, 612–619 of subscapularis, 617, 619–620 of supraspinatus, 603, 605–607 calcific tendinitis of. See Calcific tendinitis. compressive disease of, operative arthroscopy for, 99–100 examination in disorders of, 60–63, 61f–63f function of, 603, 605–620 of infraspinatus and teres minor, 607, 612–619 of subscapularis, 617, 619–620 of supraspinatus, 603, 605–607 impingement and. See Impingement. inflammation of, 685 injuries of. See Rotator cuff injuries; Rotator cuff tears. input to, increasing, in proprioceptive neuromuscular facilitation, 648–649, 650f isotonic exercises for, tennis injuries and, 438, 439f
Index_849-876-F06701.indd 869
Rotator cuff (Continued) muscles of, 10, 11t. See also Infraspinatus muscle; Subscapularis muscle; Supraspinatus muscle; Teres minor muscle. in football throwing, 389, 390 in front crawl stroke, 454 in golf swing, 466, 467t strengthening exercises for, 458, 458b, 459f in tennis serve, 395 normal anatomy of, arthroscopic, 94, 95f repetitive trauma of, restriction of motion due to, 686 rupture of, 11 strengthening of, for female shoulder injuries, 574f, 574–575, 575f tears of. See Rotator cuff tears. tendons of, 10 impingement and, 530 tensile failure of, 111–114 diagnosis of, 112–113 forces and muscle activity and, 111–112 pathogenesis of, 112 treatment of, 113 tensile lesions of, baseball and, 403–404, 405f vascular supply of, 13 Rotator cuff exercise(s) following arthroplasty of the shoulder, 320–322, 321f isotonic, in conditioning program for shoulder, 782b Rotator cuff injuries in baseball, 401–406 compressive, 404 internal impingement as, 402–403, 403f overuse tendinitis as, 403, 403f, 404f pitching and, 372 subacromial impingement as, 404–405, 405f tears as, 406 tensile lesions as, 403–404, 405f in children, 510–511 in football, 425–426 tears as. See Rotator cuff tears. tendinitis as, eccentric exercise for, 699–700, 703b, 703f, 703–704 Rotator cuff tears, 11 arthroscopic repair of, 100, 101 of L-shaped tears, 186 mini-open repair versus, 165–167, 173–174 baseball and, 406 classification of, 177, 178f contracted, 177 crescenteric, 177 arthroscopic repair of, 182–184, 183f–185f full-thickness, 143 imaging of, 83–85, 84f, 85f immobile, 177 impingement and, 527 L-shaped, 177 arthroscopic repair of, 186 massive, 177 open repair of, 159–162 mini-open. See Mini-open rotator cuff repair. mini-open repair versus, 165 operative procedure for, 159–161, 160f–162f rehabilitation following, 161–162 standard, 159–161, 162f
869
Rotator cuff tears (Continued) partial, partial articular tears with intratendinous extension lesions as, 146 partial articular supraspinatus tendon avulsion lesions as. See PASTA lesions. partial-thickness, 143. See also PASTA lesions. reverse L-shaped, 177 U-shaped, 177 arthroscopic repair of, 184–186, 185f, 186f Rotator cuff tendinitis, eccentric exercise for, 699–700, 703b, 703f, 703–704 Rotator interval, 11 closure of for anterior dislocation of shoulder, 249–250, 250f for anterior instability, 201, 201f glenohumeral stability and, 29 instability and anterior, 196f, 196–197 posterior, 210 normal anatomy of, arthroscopic, 94 Rowe Scale, 823t, 830t Rowing exercise(s), 614f compound, as eccentric exercise, 703, 703f with elastic tubing, for scapular dyskinesia, 681t electromyographic analysis of scapulothoracic musculature during, 597t prone, 841 into external rotation, in thrower’s 10 program, 845 glenohumeral muscle activity during, 608t scapular muscle activity during, 609t in thrower’s 10 program, 845 trapezius and serratus anterior activity during, 606t standing, with rotation, for golf, 480, 480f unilateral, for scapular dyskinesia, 681t RTV-11, 809 Ruffini endings, proprioception and, 655
S SADS repair for type II SLAP lesions, 276f–282f, 276–279 SAID principle, 629–630, 775–776 Salter-Harris fractures type I, 513 Little Leaguer’s shoulder compared with, 509 type II, 513, 514f type III, 513 Saphenous vein bypass grafting for axillary artery compression and aneurysm, 330 Sawa Shoulder Orthosis, 813, 813f Scaption exercise(s) below 80 degrees with external rotation, trapezius and serratus anterior activity during, 606t electromyographic analysis of scapulothoracic musculature during, 597t, 598t with external rotation, 614f in thrower’s 10 program, 844 more than 80 degrees, for scapular dyskinesia, 682t more than 120 degrees, for scapular dyskinesia, 682t
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870
INDEX
Scaption exercise(s) (Continued) with neutral rotation and increasing load using dumbbells, glenohumeral muscle activity during, 612t above 120 degrees with external rotation glenohumeral muscle activity during, 608t scapular muscle activity during, 609t trapezius and serratus anterior activity during, 606t above 120 degrees with internal rotation, glenohumeral muscle activity during, 608t teres minor muscle and, 617, 619 Scaption plane, isokinetic exercises and, 736 Scapula. See also Scapulohumeral entries. abnormal motion of, categorization of, 673, 673b biomechanics of, 671–672, 672f depression of, 632f, 634f anterior, 645f posterior, 644f dysfunction of, in female athletes, rehabilitation for, 575f, 575–576, 576f elevation of anterior, 643f posterior, 644f fractures of, in football, 426 glenoid fossa of. See Glenoid fossa of scapula; Glenoid labrum. lateral rotation of, neurodynamic testing in, 713 medial rotation of, neurodynamic testing in, 712 motion of glenohumeral stability and, 27 impairments in timing and control of, proprioceptive neuromuscular facilitation for, 646 position of, range of motion and, 127 resting position of, 7 assessment of, 673 shoulder function and, 11–12 SICK, 17 skin sensors attached to, for biomechanical assessment, 672, 672f snapping, 289–290 baseball and, 412–413 clinical presentation of, 289 treatment of, 290 stability of biomechanics of, 33–34 dynamic, 33 stabilization of, lateral, inferior capsule stretch with, 636f in subacromial impingement, 118 Scapular adduction exercise(s) prone, 646, 648f sitting, 646, 648f Scapular assistance test, 673–674, 674f in scapular dyskinesis assessment, 675 Scapular dynamic hug, standing, 615f glenohumeral muscle activity during, 604t Scapular dyskinesis assessment of, 672–675 active range of motion and, 673b, 673–674, 674f posture and, 672–673 proximal stability and, 674, 674f strength and, 674–675
Index_849-876-F06701.indd 870
Scapular dyskinesis (Continued) inferior angle pattern (type I) of, 673b medial border pattern (type II) of, 673b rehabilitation of, 675–682 overhead elevation progression and, 678, 680f, 681 posture and, 675f–677f, 675–677 proximal stability and, 677–678, 678b, 678f–680f strengthening progression and, 681t, 682 superior border pattern (type III) of, 673b symmetrical scapulohumeral pattern (type IV) of, 673b Scapular exercise(s) following arthroplasty of the shoulder, 320–322, 321f for internal impingement, 130, 135f Scapular lift, neurodynamic testing in, 713 Scapular ligament, transverse, suprascapular nerve entrapment and, 344 Scapular plane, 7 elevation in, 633f with internal rotation. See Empty can exercise. infraspinatus as shoulder abductor in, 614–615 joint stability and, 628, 629f L-bar external rotation exercise and, 839 L-bar internal rotation exercise and, 839 manual perturbation in, 635f motion in, 17–18, 18f, 19f Scapular protraction isokinetic exercise and, 738–739, 739f isometric, rhythmic stabilization with, 650f quick stretch for initiating, 649f supine, with shoulders horizontally flexed 45 degrees and elbows flexed 45 degrees, trapezius and serratus anterior activity during, 606t Scapular punch exercise forward, 615f forward, standing glenohumeral and scapular muscle activity during, 611t glenohumeral muscle activity during, 604t rotator cuff and deltoid muscle activity during, 610t upward, supine, trapezius and serratus anterior activity during, 606t Scapular retraction exercise(s), 632f on ball, for scapular dyskinesia, 678b, 680f with external rotation, 633f isokinetic exercise and, 739, 740f prone on Swiss ball, lower trapezius sequence and, 633f resisted, 634f for scapular dyskinesia, 678, 678b, 678f–680f with trunk extension, for scapular dyskinesis, 675, 675f, 676 Scapular row exercise(s) muscle activation of, 664f standing, high, at 135 degrees of flexion glenohumeral and scapular muscle activity during, 611t rotator cuff and deltoid muscle activity during, 610t standing, low at 45 degrees of flexion, glenohumeral and scapular muscle activity during, 611t
Scapular row exercise(s) (Continued) at 135 degrees of flexion, rotator cuff and deltoid muscle activity during, 610t standing, mid, at 90 degrees of flexion, glenohumeral and scapular muscle activity during, 611t Scapular slide, lateral, 673 Scapular taping, 815, 815f in female athletes, 575, 575f for scapular dyskinesis, 676, 677f Scapular winging, 56, 56f Scapulohumeral muscles, biomechanics of, 35–36, 36f Scapulohumeral rhythm, 20–23, 21t, 622 posture and, 22–23 shoulder pathology and, 22, 22f Scapulothoracic bursitis, baseball and, 413 Scapulothoracic control in swimmers, interventions for, 456 Scapulothoracic joint biomechanics of. See Biomechanics, of scapulothoracic joint. during exercise, electromyographic analysis of, 596–599, 597t–598t in front crawl, 454–455 motion and rhythm of, 11–12. See also Scapulohumeral rhythm. neuromuscular control and, 627–628, 628f Scapulothoracic mechanics, rehabilitation and, 497 Scapulothoracic muscle(s) in front crawl, 454 imbalances of, swimming and, 456 recruitment and endurance and, in swimmers, 456, 458 strengthening of, for swimmers, 456, 457f Scapulothoracic patterns, isokinetic exercise and, 738–739 Scapulothoracic rehabilitation, isokinetic exercise and, 731 SCOI rotator cuff classification, 177 SDQ, 823t Segmental resection with patching or primary anastomosis, for axillary artery compression and aneurysm, 330 Self-capsule stretches for impingement, 537, 538f Self-stretches for golf injuries, 471–472, 472f, 473f Sensation of force, 655, 661–662 Sensorimotor system, 655–665 alterations in, with shoulder injury, 659f, 659–660 neuromuscular, 659–660 proprioceptive, 659 assessment of, 661f–664f, 661–665 components of shoulder stability and, 655–659, 656f central nervous system processing as, 656–657 neuromuscular control as, 657–659 proprioception as, 655–656 restoration of, 660–661 Sensory examination, dermatomal, 69 Serratus anterior muscle activity of exercises eliciting, 622–623 in shoulder exercises, 606t, 611t
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INDEX Serratus anterior muscle (Continued) in baseball pitching, 386t, 387 exercise of electromyographic analysis of, 597–598, 598f, 599f eliciting activity, 622–623 exercise progression for, 681t–682t in front crawl stroke, 454, 455 in golf swing, 398t, 399, 466, 467 lower, in golf swing, 398t middle, 394t activity of, in shoulder exercises, 609t proprioceptive neuromuscular facilitation for, 646, 648, 648f scapular biomechanics and, 35 scapulothoracic joint motion and, 11–12 in tennis volley, 395, 396t upper, in golf swing, 398t in windmill pitching, 391, 391t Serve(s) tennis biomechanics of, 378–380, 379t electromyography during, 394t, 394–395 kinetic-chain concept applied to, 432f, 432–433 muscular activity patterns in, 430–431 volleyball, electromyography during, 392–394, 393t Setting phase of plyometric exercise, 752 Set-up phase of golf swing, pathomechanical analysis of, 467–468 Sex. See Boys; Female shoulder injuries; Girls; Men; Women. SF-36, 821 Shells for sternoclavicular joint protection, 812 Shift test in posterior instability, 212 Short-arc exercises, 733, 734f, 735 Shoulder Disability Questionnaire, 823t Shoulder dump exercise for scapular dyskinesia, 678b Shoulder extension exercise, muscle activation of, 664f Shoulder flexion exercise, muscle activation of, 664f Shoulder girdle oscillation techniques, neurodynamic testing and, 714–715, 715f Shoulder injury pads, 809, 810f Shoulder pads for football, fitting of, 805–806, 806f Shoulder Pain and Disability Index, 820, 822, 823t Shoulder press, unilateral, supine, with plus, for scapular dyskinesia, 682t Shoulder pull-down into extension for gymnastic injuries, 497, 499f Shoulder shrug exercise in scapular dyskinesis assessment, 674 trapezius and serratus anterior activity during, 606t Shoulder stability brace for instability, 556, 556f Shoulder Subluxation Inhibitor, 813, 813f Shoulder-grinding factor, baseball pitching and, 372 Shrug exercise, electromyographic analysis of scapulothoracic musculature during, 597t SICK scapula, 17 Side bend(s), trunk, in plyometric program, 753, 754f
Index_849-876-F06701.indd 871
Side bend and reach stretch for warm-up, 475t, 476f Side throw in plyometric program, 753, 756f Side-lying external rotation exercise(s), 841 electromyographic analysis of, 592, 593t in thrower’s 10 program, 844 at 0 degrees of abduction, 615f glenohumeral muscle activity during, 608t rotator cuff and deltoid activity during, 605t Side-lying gluteal series exercises, 769 Side-lying neuromuscular control drills for internal impingement, 130, 136f Side-on bowlers, 377 Side-to-side throws in conditioning program for shoulder, 783f in plyometric program, 757, 759f two-hand, in plyometric program, 757, 759f Simple Shoulder Test, 820–821, 824t, 829t Simply Stable Shoulder Stabilizer, 813–814, 814f Single leg squat in scapular dyskinesis assessment, 673, 674, 674f Single-anchor, double-suture repair for type II SLAP lesions, 276f–282f, 276–279 Single-plane movements for motion restriction, 689–690 Sit-ups using medicine ball in plyometric program, 757, 758f Skill development as exercise in conditioning program for shoulders, 785–786 Skill movements in conditioning program for shoulders, 778 Skin sensors for biomechanical assessment of scapula, 672, 672f Skybox view, 218, 218f SLAC lesions, dislocation and, 240 SLAP lesions, 31, 269–282 anatomy of, 269, 270f, 271f assessment for, 63–65, 64f, 65f baseball and, 409, 409f baseball pitching and, 372–373 biceps tendon attachment involved in, 91, 92f classification of, 269–271, 271f–273f complex, 271 treatment of, 276 diagnosis of, 272–275, 273f–275f dislocation and, 240, 240f examination in, 63–65, 64f, 65f in football, 425 historical background of, 269 imaging of, 79–80, 80f postoperative care for, 279, 281 single-anchor, double-suture repair for, for type II lesions, 276f–282f, 276–279 tennis and, 430 testing for, 127 treatment of, 275–279 type I, 269–270, 271f, 409 débridement of, 138–139 treatment of, 275 type II, 270, 272f, 409, 409f débridement of, 138–139 repair of, 139 treatment of, 275, 276f–282f, 276–279 type III, 270–271, 272f, 409 treatment of, 275 type IV, 271, 273f, 409 treatment of, 275–276 type V, rehabilitation for, 548
871
SLAP-prehension test in multidirectional instability, 232t Sleeper stretch for golf injuries, 472, 473f for internal impingement, 128, 129f for posterior capsule, 636f Sliders biomechanics of, 370t, 370–371, 371t for neurodynamic treatment, 715 Slings, postoperative, 814, 814f Snapping scapula, 289–290 baseball and, 412–413 clinical presentation of, 289 treatment of, 290 Soccer throw overhead, two-hand, in plyometric program, 753, 756f, 757, 759f two-hand, in plyometric program, 755, 758f Soccer throw exercise in conditioning program for shoulder, 783f Soft tissue injuries, 283–291 bursitis as, 283. See also specific bursae. tendinitis as, 283. See also specific tendons. Soft tissue mobilization for motion restriction, 692 Softball catching, interval sport program for, 581b–582b Softball infielding, interval sport program for, 582b Softball outfielding, interval sport program for, 583b for female athletes, 583b Softball pitching biomechanics of, 374–376, 375t electromyography during, 390–392, 391t interval sport program for, 578b–580b overhand pitching compared with, 374–376, 375t Softball throwing interval program, 796, 797b Somatosensory evoked potentials, afferent pathway assessment using, 662 Sonography. See Ultrasonography. Soreness rules for female athletes, 586b Southern California Orthopaedic Institute rotator cuff classification, 177 SPADI, 820, 822, 823t Specific adaptation to imposed demand principle, 629–630, 775–776 Speed’s test, 63, 64, 64f in biceps pain, 410 in biceps tendinitis, 284 in multidirectional instability, 232t Spider pads, 809, 810f Spike, volleyball, electromyography during, 392–394, 393t Spinal accessory nerve injuries, 354 in football, 423 Spinal accessory nerve palsy, 35 Spinal cord, processing at level of, shoulder stability and, 656 Spine, cervical. See Cervical entries; Cervicogenic shoulder disease. Spine and scapula stabilizing brace for scapular dyskinesis, 676–677, 677f Spinocerebellar tract, afferent information processing and, 657 Spinocerebellum, 657
9/19/08 7:17:26 PM
872
INDEX
Spinoglenoid notch, suprascapular nerve entrapment at, 343–344 treatment of, 347 Sport-specific drills in conditioning program for shoulder, 784, 784b, 786f Spurling test, 69, 69f, 354 in cervicogenic injuries, 357, 358f in neck and shoulder pain, 352–353 Stability core. See also Core stabilization. in swimmers, 459 dynamic, co-activation of rotator cuff muscles at humeral head and, 657–658 Stability exercises, 630, 630f–635f for core stabilization, 766–767 Stability of shoulder, 9, 9t, 26–33, 239. See also Instability of shoulder. adhesion-cohesion mechanism and, 33 articular surfaces and, 26–27 assessment of, 65–68, 66f–69f atmospheric pressure and, 33 capsuloligamentous capsule and, 28–31, 29f components of, 655–659, 656f central nervous system processing as, 656–657 neuromuscular control as, 657–659. See also Neuromuscular control. proprioception as, 655–656 dynamic, 31f, 31–33 dynamic restraint in, 655 functional, restoration of, 660–661 glenoid labrum and, 27–28, 28f mechanical restraint in, 655 proximal rehabilitation of scapular dyskinesis and, 677–678, 678b, 678f–680f in scapular dyskinesis assessment, 674, 674f rotator cuff muscles and, 719 Stability of trunk, screening of, in scapular dyskinesia, 677 Stability training for golf, 479–480 Stabilization exercises closed-chain on Fitter, 631f lateral, 631f in conditioning program for shoulder, 782, 784 dynamic, 551, 551f, 634f for instability, 551 progressions for, 630, 630f–632f in push-up position catch and toss with soccer ball, 632f wall dribble and, 634f rhythmic for instability, 557, 560f for internal impingement, 129, 129f in proprioceptive neuromuscular facilitation, 643, 650f scapular, lateral, inferior capsule stretch with, 636f Standard error of the mean, 826 Standardized response mean, 822 Standing chest press with rotation for golf, 480, 480f Standing external rotation electromyographic analysis of, 592 at 15 degrees of abduction with towel roll, rotator cuff and deltoid activity during, 605t
Index_849-876-F06701.indd 872
Standing external rotation (Continued) at 90 degrees of abduction rotator cuff and deltoid activity during, 605t rotator cuff and deltoid muscle activity during, 610t in scapular plane administration route for 45 degrees of abduction and 30 degrees of horizontal adduction, rotator cuff and deltoid activity during, 605t at 0 degrees of abduction glenohumeral and scapular muscle activity during, 611t rotator cuff and deltoid muscle activity during, 610t at 0 degrees of abduction without towel roll, rotator cuff and deltoid activity during, 605t Standing internal rotation at 45 degrees of abduction, glenohumeral muscle activity during, 604t at 90 degrees of abduction glenohumeral and scapular muscle activity during, 611t glenohumeral muscle activity during, 604t at 0 degrees of abduction glenohumeral and scapular muscle activity during, 611t glenohumeral muscle activity during, 604t rotator cuff and deltoid muscle activity during, 610t Standing row with rotation for golf, 480, 480f Standing stability chop exercise, 769, 771f Standing stability lift exercise, 769, 771f Step and pass in plyometric program, 753, 756f Sternoclavicular joint anatomy of, 3–4, 4f articular disc of, 3–4, 4f depression of, 3, 4f elevation of, 3, 4f protrusion of, 3, 4f retraction of, 3, 4f biomechanics of, 23, 23f costoclavicular ligament and, 3, 4, 4f protecting, 810, 812, 812f Sternoclavicular ligaments, anatomy of, 4 Steroid injections to reduce inflammatory process, in impingement, 533 for subacromial impingement, 120 Still rings, shoulder mechanics and, 495, 495f, 496f Stingers, 339–341 Straight-arm pulls, overhead, for gymnastic injuries, 497, 499f Strength. See also Weakness. assessment of, 49, 52, 59–60, 60t balance of, tennis injuries and, 438–440, 439f–441f in conditioning program for shoulders, 776–777 isometric, in swimmers, 449–450 in scapular dyskinesis assessment, 674–675 of shoulder, in tennis players, 436–437, 437t trunk, screening of, in scapular dyskinesia, 677 Strength training, 563–567. See also Strengthening exercises. for golf injuries, 474–478, 479t, 480b, 480f
Strength training (Continued) warm-up and, 474–475, 475t, 476f–478f, 478t for preadolescent and adolescent athletes, 563–567 age-specific guidelines for, 566f, 566–567, 567f benefits of, 564–565 efficacy of, 563–564 guidelines for, 565, 565t Strengthening exercises, 840–841. See also Strength training. following arthroplasty of the shoulder, 319–320, 320f for core stabilization, 767f, 767–769 for impingement, 537–539, 538b, 538t for instability, 550b, 551, 551f, 552, 555, 556f for internal impingement, 128–129 isotonic, for instability, 552, 553b–554b progression and, rehabilitation of scapular dyskinesis and, 681t, 682 for rotator cuff, in female athletes, 574f, 574–575, 575f for scapular dyskinesis, 676 for swimmers, 456, 457f, 458 for upper body, for instability, 552 Stress fractures of proximal humeral epiphyseal plate, 508–510, 509f Stretches biceps, for scapular dyskinesis, 676, 676f capsule inferior, with lateral scapula stabilization, 636f posterior, 636f cross-body, for golf injuries, 472, 472f external rotation, supine, with wand, 637f genie, for golf injuries, 472f for golf injuries, 471–472, 472f, 473f hamstring, for golf, 483, 483f hip, for golf, 483, 484f hip-gluteal, for golf, 483, 484f horizontal adduction, for posterior capsule, 636f iliotibial band, for golf, 483, 483f for internal impingement, 128, 129f internal rotation side-lying, for golf injuries, 472, 473f with wand, 637f latissimus dorsi active, 766, 766f for golf injuries, 474, 474f opposite pocket, for golf injuries, 472, 473f passive range of motion into internal rotation, for internal impingement, 128, 129f pectoralis minor, for golf injuries, 473f, 473–474 plyometrics and. See Plyometric exercise(s); Plyometrics. quick, in proprioceptive neuromuscular facilitation, 641, 642, 649f for scapular dyskinesis, 676, 676f self-capsule, for impingement, 537, 538f self-stretches, for golf injuries, 471–472, 472f, 473f side bend and reach, for warm-up, 475t, 476f sleeper for golf injuries, 472, 473f for internal impingement, 128, 129f for posterior capsule, 636f
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INDEX Stretches (Continued) supine horizontal adduction for internal impingement, 128, 129f with internal rotation, for internal impingement, 128, 129f supine hyperflexion, for gymnastic injuries, 504, 504f Stretch-shortening cycle, 750 Stride phase in baseball pitching biomechanics of, 365–366, 367f electromyography during, 385, 386t Stride-length stance exercise, 767 Strokes, tennis ground, 433, 433f muscular activity in, 433, 433f Subacromial arch, palpation of, 58 Subacromial bursa anatomy of, 12–13, 13f distention of, imaging of, 83 inflammation of, imaging of, 83 in rotator cuff disorders, 117 Subacromial decompression arthroscopic, for rotator cuff tears, 159 for PASTA lesions, with arthroscopic débridement, 146–147 to restore proprioception, 660 for rotator cuff tears, 182 Subacromial impingement. See Impingement, subacromial. Subacromial portal for operative arthroscopy, 107–108, 108f Subacromial space anatomy of, 527, 528f arthroscopic decompression of, 99 inadequate, eccentric exercise for, 699–700 normal anatomy of, arthroscopic, 95f, 95–96, 96f vascularity of, impingement and, 530–531, 531f Subclavian arteriography in quadrilateral space syndrome, 332, 333f Subclavius muscle, scapulothoracic joint motion and, 12 Subdeltoid bursitis, obliterative. See Adhesive capsulitis. Subdeltoid stabilization, arthroscopic, for anterior instability, 204f, 204–205 Subluxation of shoulder anterior, braces to prevent, 813, 813f frequency of, instability and, 545–546 instability and, 545 operative arthroscopy for, 101–102 posterior, 212 recurrent, 210 Subscapular bursa, anatomy of, 10, 12, 13, 13f arthroscopic, 93, 94f Subscapular nerve, anatomy of, 13 Subscapularis muscle abduction and, 620 activity of exercises eliciting, 619–620 in shoulder exercises, 604t, 608t, 610t, 612t in throwing, 112 alteration of, for anterior instability, 201, 202, 202f attachment to capsule, 10 in baseball pitching, 386t, 387 biomechanics of, 617, 619–620
Index_849-876-F06701.indd 873
Subscapularis muscle (Continued) cross-sectional area of, 11t dynamic stability and, 32 exercise of electromyographic analysis of, 589, 590b, 595–596, 596f eliciting activity, 619–620 in football throwing, 390t in front crawl stroke, 454, 455 function of, 617, 619–620 Gerber lift-off exercise (test) and, 620 in golf swing, 397t, 398, 399, 466 middle, 394t precautions for, following arthroplasty of the shoulder, 318 rupture of, with Bankart repair, 265 in tennis volley, 395, 396t testing of, 62f, 62–63 in volleyball serve and spike, 392, 393t in windmill pitching, 391, 391t Subscapularis tendon anatomy of, arthroscopic, 93, 94f injuries of, imaging of, 85 Sulcus sign, 46 in multidirectional instability, 65–66, 66f, 229, 231t in posterior instability, 212 in tensile failure of rotator cuff, 113 Sully Shoulder Stabilizer, 813 Superior labral anterior-posterior lesions. See SLAP lesions. Superior labrum, anterior cuff lesions, dislocation and, 240 Superior recess, anatomy of, arthroscopic, 94, 95f Supination external rotation, resisted (O’Brien test), 47 in labral pathology, 64, 65f in multidirectional instability, 232t in SLAP lesions, 127, 409 in tensile failure of rotator cuff, 113 of forearm, neurodynamic testing in, 711 in thrower’s 10 program, 847 Supine horizontal adduction stretch for internal impingement, 128, 129f Supine horizontal adduction with internal rotation stretch for internal impingement, 128, 129f Supine hyperflexion shoulder stretch for gymnastic injuries, 504, 504f Supraclavicular nerves, anatomy of, 13 Suprascapular nerve(s) anatomy of, 13–14, 343–344f, 708–709, 709f entrapment of, 343–348 baseball and, 411–412, 412f compression injuries and, 412 electromyography, 346–347 history in, 345 imaging in, 345–346, 346f nerve conduction studies in, 346–347 pathophysiology of, 343–345 physical examination in, 345 traction injuries and, 411–412 treatment of, 347–348 injuries of, in football, 423 neurodynamic testing of, 712, 712f Suprascapular notch, suprascapular nerve entrapment at, 343–344 treatment of, 347
873
Supraspinatus muscle activity of, in shoulder exercises, 604t, 605t, 607t, 608t, 610t, 612t anatomy of, 12 assessment of, 48–49 attachment to capsule, 10 in baseball pitching, 386t biomechanics of, 36, 603, 605–607 cross-sectional area of, 11t exercise of electromyographic analysis of, 589, 592, 593t, 594f, 594–595, 596f external rotation, peak muscle activity during, 593t exercise progression for, 681t–682t in football throwing, 390t in front crawl, 455 function of, 603, 605–607 in golf swing, 397t, 397–398, 466, 467 pathology of, coracohumeral ligament and, 29–30 in tennis serve, 394, 394t in tennis volley, 395, 396t testing of, 61, 62f in volleyball serve and spike, 392, 393t wasting of, conditions associated with, 56, 56f in windmill pitching, 390, 391t Supraspinatus tendon, anatomy of, 12, 12f Supraspinatus test, 61, 62f Surgery for acromioclavicular joint injuries, 308–311 procedure for, 309f–311f, 309–311 for adhesive capsulitis, capsular release as, 300–301 for anterior instability, 198–205 nonanatomic reconstructions as, 201–202, 202f open repair techniques for, 198–199, 199f open versus arthroscopic stabilization and, 202–204 for axillary artery compression and aneurysm, 330 for biceps long head ruptures, 287 for calcific tendinitis, 157 for impingement in female athletes, 520–521 internal, 130–131, 135–137 postoperative rehabilitation and, 137–139 for instability, in children, 512 for internal impingement, postoperative rehabilitation and, 137–139 motion restriction following, 687 for multidirectional instability, 233–236 anterior approach for, 233, 234f posterior approach for, 233–234, 234f for osteochondritis dissecans of glenoid, 410 for Paget-Schroetter syndrome, 332 for posterior instability, 217–222, 218f arthroscopic, 220–222, 221f, 222f open, 218–220, 219f previous, evaluation of, for conditioning program for shoulders, 778 for quadrilateral space syndrome, 333 to restore mechanical stability of shoulder, 660 for root avulsions, 338–339 for rotator cuff tears, PASTA lesions as, 146–152, 147f–151f
9/19/08 7:17:27 PM
874
INDEX
Surgery (Continued) shoulder bracing following, 814f, 814–815 for snapping scapula syndrome, 290 for suprascapular nerve entrapment, 347–348 suture techniques for for anterior dislocation of shoulder, 253, 253f for arthroscopic rotator cuff repairs, 179, 184, 184f, 185f, 185–186, 186f for mini-open rotator cuff repair, 166–167, 170–171, 172f for PASTA lesions, 148–150, 150f for posterior instability, 220–221, 221f for tensile failure of rotator cuff, 113 for thoracic outlet syndrome, 328–329 Suspensory procedures for anterior instability, 201, 202 Suture technique(s) for anterior dislocation of shoulder, 253, 253f for arthroscopic rotator cuff repairs, 179, 184, 184f, 185f, 185–186, 186f for mini-open rotator cuff repair, 166–167, 170–171, 172f for PASTA lesions, 148–150, 150f for posterior instability, 220–221, 221f Swimmer’s shoulder, 445–461 causes of, 447–448 definition of, 446–447 diagnosis of, 449 epidemiology of, 445–446 evaluation of, 449 examination in, 449 exercise progression continuum for, 456–459 core stability in, 459 emphasis on total arm strength, power, and endurance in, 459 glenohumeral joint muscle strengthening in, 458 glenohumeral muscle endurance in, 458–459 neuromuscular re-education of glenohumeral muscle recruitment in, 459 rotator cuff strengthening exercises in, 458, 458f, 459f scapulothoracic muscle recruitment and endurance in, 456, 458 scapulothoracic muscle strengthening in, 456, 457f functional specificity training for, 459 interval training programs for, 460–461 muscle activity with shoulder pain and, 454–455 prevention of, 461 prognosis of, 460 rehabilitation for, 455–456 technique and, 460 return to swimming and, 460–461 signs and symptoms of, 448–449, 449b Swimming biomechanics of, 381t, 381–382, 382t, 450f, 450–451, 451f, 452t front crawl stroke in biomechanics of, 450f, 450–451, 451f, 452t historical background of, 445 muscle activity with shoulder pain and, 454–455 normal muscle activity of, 453–454 pathomechanics of, 451–453, 452f–454f
Index_849-876-F06701.indd 874
Swimming (Continued) injuries in. See Swimmer’s shoulder. isokinetic shoulder strength and, 449–450 pathomechanics of, 447 phases of front crawl and, 450 Swing. See Baseball swing; Golf swing. Swiss ball cable chop exercise using, 769, 770f for gymnastic injuries, 498, 500f lift exercise using, 769, 770f plate crunch exercise using, 769, 769f plyometric push-ups on, 632f prone on elbows on, 631f scapular retraction and, lower trapezius sequence and, 633f push-ups using, for gymnastic injuries, 503b, 503f scapular retraction and, for scapular dyskinesia, 678b, 680f Sympathectomy, cervical, transthoracic, for axillary artery compression and aneurysm, 330
T T exercise, 767, 768f, 769 Take-away phase of golf swing electromyographic and kinematic analysis of, 465–466, 467t electromyography during, 397t, 397–398, 398t pathomechanical analysis of, 467–468 Tanner stages, 565, 565t Tape removal, 808 Taping, 807–808 of acromioclavicular joint, 809–810, 811f materials for, 807 principles of, 807–808 for rehabilitative purposes, 814, 815f for gymnasts, 497, 497f scapular, 815, 815f for scapular dyskinesis, 676, 677f T-bar exercise for impingement, 535–536, 536f Temporal recruitment in front crawl, 454–455 Tendinitis, 283 biceps. See Biceps tendinitis. calcific. See Calcific tendinitis. in female athletes, 569–570 overuse, baseball and, 403, 403f, 404f rotator cuff, eccentric exercise for, 699–700, 703b, 703f, 703–704 Tendinopathy of rotator cuff tendons, imaging of, 83, 83f Tendinosis, 282 of rotator cuff tendons, imaging of, 83, 83f Tennis anatomic adaptations of dominant shoulder and, 434–437 anthropometric, 434f, 434–445 postural, 435 range of motion and, 435t, 435–436 strength and, 436–437, 437t ground strokes in, 433, 433f humeral rotation and, 435, 435t injuries in. See Tennis injuries. interval program in, 796, 798, 799t joint kinematics and, 433–434
Tennis (Continued) muscular activity patterns in, 430–432 open stance in, 433, 433f serve in biomechanics of, 378–380, 379t electromyography during, 394t, 394–395 kinetic-chain concept applied to, 432f, 432–433 muscular activity patterns in, 430–431 strokes in ground, 433, 433f muscular activity in, 433, 433f volleys in, electromyography during, 395, 396t Tennis injuries, 429–441 epidemiology and cause of, 429–430, 432t injuries in. See Tennis injuries. return to functional activity following, 440–441 treatment of, 438–441 joint kinematics protection and restoration in, 438 to reduce overuse, 438 total arm rehabilitation in, 438 for upper extremity strength balance and local muscular endurance, 438–440, 439f–441f Tennis serve biomechanics of, 378–380, 379t electromyography during, 394t, 394–395 kinetic-chain concept applied to, 432f, 432–433 muscular activity patterns in, 430–431 Tensile lesions. See also Rotator cuff, tensile failure of. operative arthroscopy for, 100f, 100–101, 101f Tensioners for neurodynamic treatment, 715 Teres major muscle abnormalities of, imaging of, 85, 85f activity of, in shoulder exercises, 604t, 605t cross-sectional area of, 11t in volleyball serve and spike, 392, 393t Teres minor muscle abduction and, 617, 619 activity of exercises eliciting, 607, 612, 613, 616, 619 in throwing, 112 adduction and, 616–617 attachment to capsule, 10 in baseball pitching, 386t biomechanics of, 36, 607, 612–619 cross-sectional area of, 11t dynamic stability and, 33 exercise of electromyographic analysis of, 589, 591, 591b, 592 eliciting activity, 607, 612, 613, 616, 619 external rotation, peak muscle activity during, 593t external rotation and, 612–613 flexion and, 617, 619 function of, 607, 612–619 maximum predicted isometric force for, 612–613 scaption and, 617, 619 in volleyball serve and spike, 392, 393t in windmill pitching, 391, 391t Test-to-test reliability of clinical outcomes measures, 824–825
9/19/08 7:17:27 PM
INDEX Theraband, flexion and abduction pattern with, 652f Thermal capsular shrinkage for instability, in female athletes, 521 for internal impingement, postoperative rehabilitation following, 137 Thermal capsulorrhaphy for multidirectional instability, 235–236, 236f Thermoforming plastics for padding, 809 Thermoplaster acrylic for padding, 809 Thermoplastic foams for padding, 809 Thermosetting plastics for padding, 809 Ther-o-foam, 809 Thoracic kyphosis rehabilitation of scapular dyskinesis and, 675f–677f, 675–677 scapulohumeral rhythm and, 22 Thoracic nerve, long anatomy of, 708, 709f injuries of, in football, 422–423 neurodynamic testing of, 712–713, 713f palsy of, 35 Thoracic outlet syndrome, 325–329, 326f–328f anatomy and, 325–326, 326f baseball and, 411 clinical presentation of, 326–327 diagnosis of, 328, 328f neurovascular examination in, 327, 327f, 328f nonoperative treatment of, 328 surgical treatment of, 328–329 Thoracic outlet tests, 69–70, 70f Thoracic rotation exercise, 766, 766f Thrombolysis therapy for Paget-Schroetter syndrome, 332 Thrombosis of axillary artery, 329 effort, 330–332, 331f Thrower’s exostosis, 214 baseball and, 409, 410f imaging of, 77, 77f operative arthroscopy for, 102–103 Thrower’s series for isokinetic testing, 722 Thrower’s 10 program, 843–847 for adolescents, 567 for baseball injuries, 413–414, 414f–415f, 416 for instability, 556 for internal impingement, 130, 131f–135f Throwing in baseball. See Baseball pitching; Baseball throwing; Softball pitching. baseball pitch as model for, 111 in children, 507–508, 508b cricket, biomechanics of, 376–377 eccentric versus concentric external rotation and, 701, 701f electromyography data collected during, 111–112 end range of extension and abduction resisted in upright position and, with trunk rotation, 651 flat ground, biomechanics of, 371 in football biomechanics of, 373–374, 374t interval program in, 796, 798b overhead, electromyography during, 389–390, 390t javelin, biomechanics of, 376 neuromuscular control in, 671–672
Index_849-876-F06701.indd 875
Throwing (Continued) in plyometric program, 753, 755, 756f–758f proprioceptive neuromuscular facilitation and, 640 quadrilateral space syndrome and, 354 rotator cuff tears and, operative arthroscopy for, 101 scapular biomechanics in, 671–672, 672f skill development for, in conditioning program for shoulder, 785–786 tensile lesions and, operative arthroscopy for, 100f, 100–101, 101f windmill biomechanics of, 374–376, 375t electromyography during, 390–392, 391t interval sport program for, 578b–580b overhand pitching compared with, 374–376, 375t Throwing acceleration exercise, muscle activation of, 663f Throwing deceleration exercise, muscle activation of, 663f Thumbs up test, 61, 62f Thumb-to-forearm examination, 56, 57f Tilt anterior, scapular, 20, 20f posterior, scapular, 20, 20f Time rate to torque development in isokinetic testing, 726 Torque in isokinetic testing, interpretation of, 725–726 joint stability and, 628, 628f peak, 725–726 mean, 726 ratio to body weight, in isokinetic testing, 727, 732t, 733t Total body rehabilitation, isokinetic exercise and, 731 Total work in isokinetic testing, 726 Traction for cervicogenic injuries, 356, 357f for proprioceptive neuromuscular facilitation, 641 Trailing arm follow-through reach for warm-up for golf, 475t, 477 Training cardiovascular, for golf, 482–483 core, for golf, 480–481, 482f errors in, female shoulder injuries and, 570 functional specificity, for swimmers, 459 interval. See Interval sport programs. jump. See Plyometric exercise(s). neuromuscular, for golf injuries, 474–478 overuse of equipment in, swimmer’s shoulder and, 448 proprioceptive awareness, 660–661 stability, for golf, 479–480 strength. See Strength training. Training age, conditioning program for shoulders and, 778 Transcutaneous electrical nerve stimulation for female shoulder injuries, 573, 573t to reduce inflammatory process, in impingement, 533, 533f Translation of glenohumeral joint, 24–26, 26f Transtendon repair technique for PASTA lesions, 147–152, 148f–152f
875
Trapezius muscle(s) exercises eliciting activity of, 623 in golf swing, 466 lower activity of, in shoulder exercises, 606t, 609t, 611t in baseball pitching, 386t, 387 exercise of, electromyographic analysis of, 597t, 598–599 exercise progression for, 681t–682t in golf swing, 398t middle activity of, in shoulder exercises, 609t in baseball pitching, 386t, 387 exercise of, electromyographic analysis of, 597t in golf swing, 398t scapular biomechanics and, 34–35 scapulothoracic joint motion and, 11 upper activity of, in shoulder exercises, 606t, 609t in baseball pitching, 383, 386t exercise of, electromyographic analysis of, 597t exercise progression for, 681t–682t in front crawl, 454, 455 in golf swing, 398t Trapezius palsy, 35, 35f Trapezoid ligament, anatomy of, 5 Triceps brachii muscle activity of, in shoulder exercises, 611t in baseball pitching, 386t, 387, 388 biomechanics of, 37 cross-sectional area of, 11t in tennis volley, 395, 396t Tripod exercise, glenohumeral muscle activity during, 607t Trunk core stabilization and, 764 exercises for, 766, 766f, 767, 767f, 769, 769f extension of, in plyometric program, 757, 758f flexion of, in plyometric program, 757, 759f in proprioceptive neuromuscular facilitation, 651 stability of, screening of, in scapular dyskinesia, 677 strength of, screening of, in scapular dyskinesia, 677 Trunk rotation exercise in conditioning program for shoulder, 783f for golf, 483, 484f in plyometric program, 753, 754f Trunk side bend exercise in plyometric program, 753, 754f Trunk wood chop exercise in plyometric program, 753, 755f Tumbling, shoulder mechanics and, 493–494, 494f Twist exercise, low to high, 617f Two-hand chest pass in plyometric program, 753, 756f, 757, 759f Two-hand overhead soccer throw in plyometric program, 753, 756f, 757, 759f Two-hand side-to-side throws in plyometric program, 757, 759f Two-hand soccer throw in plyometric program, 755, 758f
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876
INDEX
U UCLA Shoulder Score, 824t, 831t Ulnar deviation neurodynamic testing in, 711, 712f for warm-up, for golf, 475, 478t Ultrasonography, 74 in multidirectional instability, 230 in PASTA lesions, 145 in posterior instability, 214 in suprascapular nerve entrapment, 345–346 in tensile failure of rotator cuff, 113 Underhand pitching, biomechanics of, 374–376, 375t Uneven bars, shoulder mechanics and, 494 Unilateral breathing, swimmer’s shoulder and, 447–448 Unilateral muscle ratios in isokinetic testing, 726–727, 728t–731t University of California Los Angeles Shoulder Score, 824t, 831t University of Connecticut protocol for anterior-inferior shoulder instability, 251–252 Upper cross syndrome, 780, 780f, 781b Upper limb neurodynamic testing, 710f, 710–711 Upper limb tension test in neck and shoulder pain, 352–353 Upper-extremity plyometrics for gymnastic injuries, 502–504, 503b, 504f
V Validity of clinical outcomes measures, 822, 824 Vascular examination, 69–70, 70f Vascular supply of shoulder, 13. See also specific blood vessels. Vaulting, shoulder mechanics and, 494–495 Velocities concentric versus eccentric muscle action and, 697t for isokinetic testing, 724, 724b Velocity spectrum overflow, short-arc exercises and, 734 Venography in Paget-Schroetter syndrome, 331, 331f Verbal commands for isokinetic testing, 724 for proprioceptive neuromuscular facilitation, 641 Vertical elevation in golf swing, 465 Vestibulocerebellum, 657 Viscoelastic polyurethane foam for padding, 809 Visual feedback for isokinetic testing, 724
Index_849-876-F06701.indd 876
Visual stimuli for proprioceptive neuromuscular facilitation, 641 Volley(s), in tennis, electromyography during, 395, 396t Volleyball middle attacker program for female athletes, 585b Volleyball outside attacker hitting program for female athletes, 583b–584b Volleyball right side attacker program for female athletes, 585b–586b Volleyball serve and spike, electromyography during, 392–394, 393t Volleyball setter and defensive specialist, hitting program for, for female athletes, 584b
W W exercise, 767, 768f, 769 Wall dribbling dynamic stabilization, 634f using plyoball, in plyometric program, 757, 760f Wall press-out exercise for gymnastic injuries, 500b, 501f Wall walk exercise, 766, 767f Wallerian degeneration, 337 Warm-up exercises for golf injuries, 474–475, 475t, 476f–478f, 478t for isokinetic testing, 723–724 muscle activation of, 662, 662f for plyometric program, 753, 754f, 755f Weakness. See also Strength. in brachial neuropathy, 341 with burners (stingers), 340 monitoring of, in cervicogenic injuries, 359, 359f in suprascapular nerve entrapment, 412 Wear patterns in shoulder, 315, 316f Weaver-Dunn technique for acromioclavicular joint injuries, 308 Weed-pull theory of SLAP lesions, 373 Western Ontario Rotator Cuff Index, 822, 824t Whole-body band exercise for gymnastic injuries, 497, 499f Windmill pitching biomechanics of, 374–376, 375t electromyography during, 390–392, 391t interval sport program for, 578b–580b overhand pitching compared with, 374–376, 375t Wind-up phase of baseball batting, 395 of baseball pitching biomechanics of, 365, 367f electromyography during, 385, 386t
Wind-up phase (Continued) of tennis serve electromyography during, 394t muscular activity patterns in, 430 of volleyball serve and spike, electromyography during, 392, 393t of windmill throw, electromyography during, 391t Wobble board for gymnastic injuries, 500, 502b, 502f, 503f twist exercise using, 769, 770f Women. See also Female shoulder injuries. gymnastic training and progression for, 491–492 Wood chops, trunk, in plyometric program, 753, 755f WORC Index, 822, 824t Work capacity, in conditioning program for shoulders, 777 World Health Organization International Classification of Impairments, Disabilities and Handicaps of, 818, 818t Wright maneuver in thoracic outlet syndrome, 327, 327f Wrist extension of neurodynamic testing in, 711 in thrower’s 10 program, 846 flexion of, in thrower’s 10 program, 846 proprioceptive neuromuscular facilitation pattern for, 642t supination and pronation of, for warm-up, for golf, 475, 478t ulnar deviation of, neurodynamic testing in, 711, 712f Wrist flips in conditioning program for shoulder, 784f reverse, in conditioning program for shoulder, 784f
X X-rays. See Conventional radiography.
Y Y exercise, 767, 768f, 769 Yergasson’s test, 63, 64f in biceps pain, 410 in biceps tendinitis, 284 in multidirectional instability, 232t
Z Zaslav test in multidirectional instability, 231t
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