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.
References 1. Kelley DL: Kinesiological Fundamentals of Motion Description. Englewood Cliffs, NJ, Prentice-Hall, 1971. 2. Dempster WT: Mechanisms of shoulder movement. Arch Phys Med Rehabil 46:49, 1965. 3. DePalma AF: Surgery of the Shoulder, 2nd ed. Philadelphia, JB Lippincott, 1973. 4. Warwick R, Williams P (eds): Gray’s Anatomy, 35th ed. London, Longman, 1973. 5. Bateman JE: The Shoulder and Neck. Philadelphia, WB Saunders, 1971. 6. Brantigan OC: Clinical Anatomy. New York, McGraw-Hill, 1963. 7. Bechtol CO: Biomechanics of the shoulder. Clin Orthop 146:37, 1980. 8. Inman VT, Saunders JB, Abbott LC: Observations on the function of the shoulder joint. J Bone Joint Surg 26:1, 1944. 9. Moore KL: Clinically Oriented Anatomy. Baltimore, Williams & Wilkins, 1980. 10. Perry J: Normal upper extremity kinesiology. Phys Ther 58:265, 1978.
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11. Abbott LC, Lucas DB: The function of the clavicle: Its surgical significance. Ann Surg 140:583, 1954. 12. Ljungren AE: Clavicular function. Acta Orthop Scand 50:261, 1979. 13. Bearn JG: Direct observations on the function of the capsule of the sternoclavicular joint in clavicular support. J Anat 101:159, 1967. 14. Moseley HF: The clavicle: Its anatomy and function. Clin Orthop 58:17, 1968. 15. Kent BE: Functional anatomy of the shoulder complex. Phys Ther 51:867, 1971. 16. Frankel VH, Nordin M: Basic Biomechanics of the Skeletal System. Philadelphia, Lea & Febiger, 1980. 17. Kessler RM, Hertling D: Management of Common Musculoskeletal Disorders: Physical Therapy Principles and Methods. New York, Harper & Row, 1983. 18. Dvir Z, Berme N: The shoulder complex in elevation of the arm: Mechanism approach. J Biomech 11:219, 1978. 19. Bost FC, Inman VTG: The pathological changes in recurrent dislocations of the shoulder. J Bone Joint Surg 24:595, 1942. 20. Codman EA: The Shoulder. Boston, Thomas Todd, 1934. 21. Steindler A: Kinesiology of Human Body Under Normal and Pathological Conditions. Springfield, Ill, Charles C Thomas, 1955. 22. Gagey O, Bonfait H, Gillot C, et al: Anatomic basis of ligamentous control of elevation of the shoulder (reference position of the shoulder joint). Surg Radiol Anat 9:19, 1987. 23. Johnston TB: The movements of the shoulder-joint: A plea for the use of the “plane of the scapula” as the plane of reference for movements occurring at the humeroscapular joint. Br J Surg 25:252, 1937. 24. Norkin C, Levangie P: Joint Structure and Function: A Comprehensive Analysis. Philadelphia, FA Davis, 1983. 25. Sarrafian SK: Gross and functional anatomy of the shoulder. Clin Orthop 173:11, 1983. 26. 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, 2002. 27. 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, 2002. 28. Osbahr DC, Cannon DL, Speer KP: Retroversion of the humerus in the throwing shoulder of college baseball players. Am J Sports Med 3:347, 2002. 29. Pieper HG: Humeral torsion in the throwing arm of handball players. Am J Sports Med 26:247-253, 1998. 30. Saha AK: Dynamic stability of the glenohumeral joint. Acta Orthop Scand 42:491, 1971. 31. Saha AK: Mechanics of elevation of glenohumeral joint: Its application in rehabilitation of flail shoulder in upper brachial plexus injuries and poliomyelitis and in replacement of the upper humerus by prosthesis. Acta Orthop Scand 44:668, 1973. 32. Basmajian JV, Bazant FJ: Factors preventing downward dislocation of the adducted shoulder joint. J Bone Joint Surg Am 4:1182, 1959. 33. Cyprien JM, Vasey HM, Burdet A, et al: Humeral retrotorsion and glenohumeral relationship in the normal shoulder and in recurrent anterior dislocation (scapulometry). Clin Orthop 175:8, 1983. 34. Randelli M, Gambrioli PL: Glenohumeral osteometry by computed tomography in normal and unstable shoulders. Clin Orthop 208:151, 1986.
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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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15
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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38
33.
34.
35. 36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
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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.
9/19/08 7:06:00 PM
CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
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.
Ch02_017-042-F06701.indd 39
39
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.
9/19/08 7:06:00 PM
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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.
9/19/08 7:06:01 PM
CLINICAL BIOMECHANICS OF THE SHOULDER COMPLEX
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.
Ch02_017-042-F06701.indd 41
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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.
Ch06_089-098-F06701.indd 97
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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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OPERATIVE ARTHROSCOPY OF THE SHOULDER
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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OPERATIVE
