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and Treatment

by Manual Methods


Edited by
Warren 1. Hammer, MS, DC, DABCO
Private Practice
Norwalk, Connecticut


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This book is dedicated to the fantastic
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My wife, Martha, my daughters, Melodie and Deborah,

and my granddaughters Rosie, Abigail, and Danielle.

I am indeed blessed.


Contributors ............................................................
Preface .................................................................
INTRODUCTION ............................................ 1

Chapter 1 Basics of 50ft-Tissue Examination ............................... 3

Warren I. Hammer

Passive and Contractile Soft-Tissue Examination ... . ....... . ...... ... .. . . .. ...... . .
Capsular Pattern ... . ... . . . ..... . ....... .. . .. .. . . . . .... . . .. . . . .. . .. . . . ... . .. . 9

Tenderness and Palpation .. . . . ......... ... ....... . . . .. . .... . .... . . . . .. ....... . 10

Spinal Relation to Extremity Soft-Tissue Lesions . .. . . .... . ... . ..... .. .......... ... . 11

Anti-Inflammatory Therapy and Soft Tissue .. ... . . .............. . . . .... . . . . . . .. . . . 11

Chart Interpretation ... . . . . ........ . . ... ... . .... ... ....... . ....... . . . . ... ... . 12

Chapter 2 The Effect of Mechanical Load on 50ft Connective Tissues. . . . . . . . . . . . 15

Katie Lundon

Principles Underlying Soft-Tissue Response to Mechanical Loading. . . . . . . . . . . . . . . . . . . . . 15

Components of Connective Tissues: Roles and Responses to Mechanical Loading. . . . . . . . . . 16

The Strong Relationship between Structure and Function in Connective Tissues. . . . . . . . . . . 18

Connective Tissue Response to Immobility . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

Joint Hypomobility. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26

Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

vi Contents


Chapter 3 The Shoulder .............................................. . 33

Warren I. Hammer

Pertinent Functional Anatomy and Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

Scapulothoracic Motion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

Scapular Posterior Tilting. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

Role of the Scapula. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

Sternoclavicular-Acromioclavicular Motion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

Shoulder Muscle Group Actions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

Glenohumeral Motion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

Clinical Review of the Shoulder Muscles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

GlenohumeralJoint Stability. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

Functional Examination of the Shoulder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

Lesions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103

Soft Tissue Treatments for Adhesive Capsulitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125

Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153

Appendix 3-A Shoulder Functional Diagnosis Chart. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 162

Chapter 4 The Elbow and Forearm . ..................................... . 163

Warren I. Hammer

Functional Anatomy and Pertinent Biomechanics. . . . . . . . . . . . . . . . . . . . . . ..... ..... ... 163

Functional Examination of the Elbow. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..... ..... ... 168

Lesions of the Elbow. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..... ..... ... 175

Elbow Biomechanics in Other Throwing Motions . . . . . . . . . . . . . . . . . . . . . .......... ... 189

Elbow Injuries in Nonthrowing Sports. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..... ..... ... 189

Elbow Entrapment Neuropathies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..... ..... ... 190

Radial Nerve Course in Arm and Forearm. . . . . . . . . . . . . . . . . . . . . . . . . . . ..... ........ 190

Ulnar Nerve Course in the Arm and Forearm. . . . . . . . . . . . . . . . . . . . . . . . . ..... ..... ... 197

Median Nerve Course in the Arm and Forearm. . . . . . . . . . . . . . . . . . . . . . . ..... ........ 201

Appendix 4-A Elbow Functional Diagnosis Chart. . . . . . . . . . . . . . . . . . . . ............. 212

Chapter 5 The Wrist and Hand ......................................... . 213

Warren I. Hammer

Functional Anatomy and Pertinent Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213

Wrist Stability (Carpals and Ligaments) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215

Functional Examination of the Wrist. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 216

Wrist Lesions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220

The Hand. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241

Fingers: Functional Anatomy and Pertinent Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . 241

Thumb: Functional Anatomy and Pertinent Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . 243

Functional Examination of the Fingers .... . . .................................... 244

Hand Lesions Treated by Manual Methods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250

Appendix 5A-1 Wrist Functional Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 256

AppendiX 5A-2 Fingers and Thumb Functional Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . 257

Contents vii

Chapter 6 The Hip and Thigh .......................................... . 259

Warren 1. Hammer

Functional Anatomy and Pertinent Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 259

Functional Examination. ................. .... .... . . . . .... . .. .. ....... .. . ..... 266

Lesions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 6

Appendix 6-A Hip Functional Diagnosis Chart. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310

Chapter 7 The Knee and Leg . .......................................... . 311

Warren I. Hammer

Functional Anatomy and Pertinent Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 311

Knee Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 323

Functional Examination of the Tibiofemoral Joint. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332

Grading Sprains. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333

Lesions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 352

Appendix 7-A Knee Functional Diagnosis Chart. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 398

Chapter 8 The Foot: Hyperpronation and Hypopronation 399

Thomas C. Michaud

Ideal Foot Function ............... . .... . ..... .... ..... .... .. ... .. .... . ..... . 399

Abnormal Foot Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 404

Orthotics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 423

Chapter 9 Gait Analysis-Implications for Diagnosis, Treatment, and Rehabilitation. 427

Keith A. Innes, Steve Palazzo, Anthony Tortorella

Gait Analysis: Why Do It? What Does It Reveal? .. .. .. . .. .. ...... .. ... .. ...... . ... . 427

The Indistinguishable Division between Health and Disease ................. . ....... .


The Neurology of Gait ....... . ... .. . ... .. . ...... . .. . .... . . .. ............ . ... .

The Cerebral Cortex and Gait. ................. . .. . ......... ... .... .. . . ....... .

GTOs and Gait ................................... .. ........... . ........ ... .


The Brain Stem and Gait .... . ................................... . . .. . ....... .


The Cerebellum and Gait ............... . .. . .............. .... .. . . ........... .


The Basal Ganglia and Gait. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 432

The Cerebral Cortex and Gait. . . . . ............. .. . . .... .. . . ............ .. . . ... .


Lumbosacral Nociception and Gait ............................................ .


Gait and Life Experience ........................................... ... ...... .


The Challenge . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 436

The Relationship between the Upper Extremity and Gait .......... . . ....... . ....... . .

Rehabilitation protocols and Learning .... ...... .... . ......... . . . .... . ... ... .. . . .

Gracovetsky's Spinal Engine Theory .... . . .... . . .. . . ... ............... . ......... .


A Model of Theoretically Ideal Gait . . . . . .. . . ...... .. ......... . . . .. .... ......... .


The Components of the Gait Cycle ... ... .... . ... .. . . . . ............ . .. . . . . .. .... .


Tonic/Local, Phasic/Global, and Mobilizer/Stabilizer: What Do These Terms Have in Common? ..


The Feed-Forward/Anticipatory Event . . ......... . . . .... . ................. .


The Core (Inner Unit) ................................................. .. .


Gait ...... . . . . . . . ...... .. .......... . .... . . . ............................. .

viii Contents

Dynamic Gait Visualization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447

The Upper Extremity and Gait. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 449
Treatment: The Adjustments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 450

Chapter 10 Lumbar Spine Instability: Assessment and Exercise Based Restabilization 461
Stuart M. McGill

The Injury Process: Tissue Damage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 462

Summary of Specific Tissue Injury Mechanisms Relevant for Therapeutic Exercise . . . . . . . . . 462
The Injury Process-Motor Changes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 463
Instability as a Cause of Injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 464
On Stability: The Foundation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 464
How Is Instability Found? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465
A Philosophy of Low Back Exercise Prescription . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 466
The Stabilizers of the Lumbar Torso. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 467
Beginning a Stabilization Program . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 470
Looking Forward . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 472


Warren I. Hammer

Etiology of Tendinopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475

TendinopathyfTendinitisfTendinosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475
Manual Treatment Methods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 475

Chapter 11 Joint Mobilization . .......................................... . 481

Peter A. Gale

The Ankle and Foot Complex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 482

The Shoulder. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 486
The Elbow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 490
The Wrist. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 493
The Hip. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497
The Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 499
Sectional Drop Unit Manipulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 503

Chapter 12 Muscle Dysfunction and Muscle Energy Techniques . ............... . 507

Gary lerna

Muscle Hypertonicity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 507

Common Postural Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 509
Muscle Length Assessment. .. ... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 517
Muscle Energy Techniques. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 518
Conclusion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 547

Chapter 13 StrainiCounterstrain . ........................................ . 549

Edward K. Goering

History of Counterstrain Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 549

Physiology of Manipulation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 550
Contents ix

Counterstrain Systems. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 553

Manipulation of Specific Regions of the Spine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 554

Chapter 14 Combining Friction Massage with Neuromuscular Reeducation SM 563

Warren 1. Hammer; Peter J. Levy

Friction Anesthesia ..... . .. . ...... . .... .. ... . . . . . ... . . .. . . .. . . . ... . .......... 564

Friction Technique. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 564

Treatment Time . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 564

Number of Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 564

Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 564

Friction Massage for Chronic Bursitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 565

Neuromuscular Reeducation SM (NMR) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 565

Illustrations and Procedures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 565

Chapter 15 Graston Technique® ......................................... . 589

M. Terry Carey-Loghmani, Warren 1. Hammer

Tensegrity "The Architecture of Life" . . ... .. . . .. . . .. . . . . . . . . .. . . .... .. . . . .. . 590

Posterior Layer of Lumbar Fascia . . . ... . .. . ...... . .. .. . . . . .. ..... .. .... .. . . .... . 592

Testing for Shortened Lumbar Fascia .. .. . . . . .... ... . . . . ... .. . ... .. .. . . .. .... ... . 594

Graston Technique® Methods .. .... . . .. .. . .. .. ... .. .. . ... .. . . . .. . .... . . .... . . . . 596

CervicaVShoulder Fascia .. . .. ... . . . .. . . .. . . . . . .. . . . . .. .... .. ... ... . . . .... ... . 597

Use of GT for the Cervical Areas .... . ... .. . . . .. ... ... . ... .... . .. . . .. .... . ... .. . 598

Use of GT for the Upper Thoracic and Scapular Areas . ... . . ... .. . .... . .... . . . ...... . 600

Use of GT for the Shoulder . ... . .... . ... ... .. .. . . . . .... . . .. . . . . .. . .... . .. . . . . .

Elbow Areas ... . .. . ... .. ... . ... .. . ... .. . .... . . . ..... . . . . .. ... .. .. .. . . . . ... .

Entrapments .... . . . .. . .. . ... .. ... .. . . . . ... . .. .. . . . . .. . .... . .. . . . .. . . .. . . .. .


Wrist and Hand . .. . .... . . . .... . ......... .. ... . .. . .. .. . .... .. . .. .. . . .. . .. . . .


Hip and Thigh Fascia . .... . . ... . .. . . .. . ... ... .. . . .. .. .. .. ... . .. . ..... . .. ... . .

Adductors ..... . . . ...... . .... . ... .. . . . . .. . .... . .. . ... .. .. .. .. . .. . .. . .. ... .


Knee ... . .. . .. . .. . .. . ...... . ..... . .. . .. .. . ... . .. . .. . .. . . .. .. . .... . . . . .. . . .


Fascia of the Foot . . . . . .... . .. . . . .... . . . . .. . ..... .. ..... . ...... .. .. . ... . . . .. .


Achilles Tendinopathy . . . .... . . . .. . .. . . ... .. . . .... . ... .. .... ..... ... . . . .... . .

Ankle Ligamentous Sprains . . . . . . . .... .. ....... . . . ... . .... . . . .. . .. . . . . . .. . .. . .


Plantar Fasciitis ... .. . . . .. ... . .. . . .... . .. . .... . . ... . ........ . . . .. . . . .. . . . .. .


Research in Progress . . .... . . . . .. . . . .. . . .... . . . ....... . .... . . . .. . .. . . . .. . . .. . .


Acknowledgment . .. . . . . . . .. ... . . .. . . . .. ... . . .... . .. . . . .. . . . .. .. .. . . . .. . . . . . 624

Chapter 16
The Lower Cervical Spine: An Integrated Approach to Joints, Fascia,
and Muscles ............................................... .

Marc Heller


Assessment Tools . . . . . . . . . . . .. . . . ... . . . . . . . ... .. . . . . ..... . .. . ..... . . . . . .... .


Assessing and Treating the Lower Cervical Joints ... . . . ....... . . . .. . . .. . . .. ... .. . . . .


Muscle Energy (Postisometric Relaxation Applied to Joint Dysfunction) . . . . .. . .. . . .. ... . .


Anterior Cervical Fascial Structures ... . .. ... . .. . .. . ... .... .. ... . . . . . . . . . . . . .... .

Conclusion . ... . . . . . ... . .. . . . ... ..... . . . . . . .. .. .. ....... . . . ... . . . .. . .. .. .. .


Acknowledgment . . .. . .. .. . . . . . . ....... . . . . .. . . . . . . ... . .... . .... . . . .... . .. . .

x Contents

Chapter 17 Soft-Tissue Treatment of Temporomandibular Disorders . ........ . ... . 643

Darryl D. Curl

Relevant Anatomy and Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 644

Temporomandibular Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 650

Additional Interventions for TM Soft-Tissue Conditions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 661

Chapter 18 Mobilizations with Movement, "NAGS," "SNAGS ," and More 665

David Mikos

The GlenohumeralJoint. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 666

Acromioclavicular Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 667

Scapular MWM . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 668

The Hip . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 669

The Ankle. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 670

NAGs and SNAGs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 672

NAGs......... ............................... ............. . ....... ....... 672

SNAGs. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 673

Chapter 19 Integration of Taping Techniques with Myofascial Therapy . . ... ... .. . . 675

Vincent DeBono

The Role of Taping in Myofascial Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675

The Proprioceptive Effect of Taping. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 676

Introduction to Kinesio Taping Method . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 678

Illustrated Case Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 684

Chapter 20 ELDOA: Longitudinal Osteo-Articular De-coaptation Stretching . .... . . . 689

Guy Voyer, Robert Black

The Spine. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 689

Effects of ELDOA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 689

Technique. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 690

Chapter 21 Active Isolated Stretching . .................... .. .............. . 697

Aaron L. Mattes

Technique. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 698

Chapter 22 Active Release Techniques®: Long Tract Nerve Release . ............. . 713

P Michael Leahy

Median Nerve at the Pronator TeresIFlexor Digitorum Superficialis . . . . . . . . . . . . . . . . . . . . . 713

Saphenous Nerve at the Sartorius/Gracilis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 715

Meniscal Entrapment of the Knee. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 715

Contents xi

Chapter 23 Nutritional Considerations in the Treatment of Soft Tissue Injuries ..... 717
David R. Seaman

Inflammation-The Traditional View. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 717

Inflammation-A Contemporary View. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 719
A Dietary Approach to Normalize the Expression of Inflammation. . . . . . . . . . . . . . . . . . . . . . 726
Supplements to Normalize the Expression of Inflammation. . . . . . . . . . . . . . . . . . . . . . . . . . . 727
EPAlDHA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 728
Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 730
Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 731

Chapter 24 Conservative Treatment of Soft-Tissue Injuries .................... . 735

Mark De Carlo, Erin Baril!, Nick Cosgray, and Debbie Cyphers

Phases of Rehabilitation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 735

Upper Extremity: Specific Diagnoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 736
Lower Extremity: Specific Diagnoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 747

Index. .. . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . 759

Erin Barrill, PT, ATC Vincent DeBono, DC

Staff Physical Therapist/Athletic Trainer Dean
Methodist Sports Medicine Center National University of Health Sciences
Indianapolis, Indiana Lombard, Illinois
Director of Rehabilitation
Indianapolis Colts Mark De Carlo, PT, MHA, SCS, ATC
Indianapolis, Indiana Director of Physical Therapy
Chief Officer
Robert Black, RMT Methodist Sports Medicine Center
Private Practice Indianapolis, Indiana
Ontario, Canada
Peter A. Gale, DC, CCSP
M. Terry Carey-Loghmani, PT, MS
Private Practice
Associate Clinical Professor
Needham, Massachusetts
School of Health and Rehabilitation Sciences
Indiana University
Indianapolis, Indiana Edward K. Goering, DVM, DO, MSHPHE
Private Practice
Nick Cosgray, MS, PT, ATC Family Medical Associates
Staff Physical Therapist/Athletic Trainer Portland, Oregon
Methodist Sports Medicine Center Certified Counterstrain Instructor
Indianapolis, Indiana Jones Institute
Associate Professor
Darryl D. Curl, DDS, DC Family Practice
Norco , California Western University Health Sciences
Pomona, California
Debbie Cyphers, MPT
Staff Physical Therapist Marc Heller, DC
Methodist Sports Medicine Center Private Practice
Indianapolis, Indiana Ashland, Oregon

Contributors xiii

Gary lerna, DC Thomas C. Michaud, DC

Clinic Director Private Practice
Hartford Spine and Pain Center, Inc. Newton, Massachusetts
Farmington, Connecticut
David Mikos, DC, PT
Keith A. Innes, DC Montowese Chiropractic Center LLC
Professional Services Facilitator North Haven, Connecticut
Faculty Member
4KInstitute LLC Steve Palazzo, DC
Former Chair of Clinical Sciences Adjunct Professor
University of Bridgeport University of Bridgeport
College of Chiropractic College of Chiropractic
Bridgeport, Connecticut Faculty Member
P. Michael Leahy, DC Private Practice
Private Practice Port Jefferson, New York
Colorado Springs, Colorado
David R. Seaman, DC, MS
Peter J. Levy, DC Assistant Professor
Private Practice Palmer College of Chiropractic Florida
Santa Barbara, California Port Orange, Florida
Neuromuscular Reeducation sM
Anthony Tortorella, DC
Katie Lundon, BSc(PT), MSc, PhD, MCPA Adjunct Professor
Lundon Orthopaedic Physical Therapy Consulting University of Bridgeport
Ontario, Canada College of Chiropractic
Bridgeport, Connecticut
Aaron L. Mattes, MS, RKT, LMT Faculty Member
Kinesiotherapist K4Institute LLC
Aaron Mattes Therapy Private Practice
Medical Center of Sarasota Easton, Connecticut
Sarasota, Florida
Guy Voyer, Osteopathe DO
Stuart M. McGill, PhD
Professor of Spine Biomechanics
Department Chair
Department of Kinesiology
University of Waterloo
Ontario, Canada

It amazes some that a textbook about functional soft tis­ This edition has been thoroughly updated with essential
sue examination and manual methods of treatment requires information and includes 13 new chapters on the effects of
updating. MRI studies often disprove the validity of previous manual loading on soft tissue , lumbar stabilization, gait, tap­
tests. Almost every month, some publication produces evi­ ing methods, fascial release , treatment of the temporo­
dence that earlier testing methods we have taken for granted mandibular joint, Mulligan Technique, Graston Technique®,
are not necessarily as sensitive and specific as we thought, Active Release®, Neuromuscular Reeducation,SMActive Iso­
and new tests are developed to replace older, well estab­ lated Stretching, Longitudinal Osteo-Articular De-coarctation
lished tests. At times, just altering the position of a patient's Stretching (ELDOA), and nutrition for soft tissue.
extremity in testing reveals more or less information. As I enter my 47 th year of practice, I am wholly con­
The question of how we affect soft tissue when we touch, vinced of the old adage that the more tools we have in our
compress, or stretch tissue , either with our hands or special toolbox the more options we have to help our patients.
instruments, has produced new information at the cellular Every chapter in this text is based on successful clinical ex­
level. The idea that the effect of mechanical load on soft tis­ perience that has withstood the test of time. The more prac­
sue is capable of creating mechanical signal transduction re­ tical knowledge we can accumulate over time, the easier it
sulting in changes in gene expression and extracellular becomes to focus in with greater intensity on the source of
matrix composition literally sends chills through my spine. the patients' pain, and then hopefully, on the answer to
There is strong evidence that we are truly healing tissue by their problem.
human touch.

Warren 1. Hammer



Basics of Soft Tissue Examination

Warren I. Hammer

For practitioners who primarily use their hands to treat the thumb and first metacarpal joint represents only half of
the human structure, examination must include functional the examination. In this passive evaluation, we are also
tests to determine the type of soft tissue creating the pain. stressing the trapeziometacarpal joint, a common area of
Manual practitioners literally must use all their senses to de­ arthritis; the radio dorsal aspect of the wrist, where an inter­
cide where and how to treat the patient. By observation, section syndrome may be present; and the radial collateral
they can evaluate gait and stance and become aware of the ligament and other local areas that are in the vicinity. Al­
abnormal tensions emanating from the patient-the tight though the Finkelstein test may be positive-and crepitus
upper trapezius, the hypotonic gluteus maximus, the hy­ in the local tissues would be another confirming point-to
pertonic hamstring, the weak abdominals , and the fascial confirm this condition functionally, we must stress the con­
restrictions causing abnormal inclinations, such as tilted tractile tissue. Isometric testing of the extensor pollicis bre­
head, forward shoulders, or torsioned pelvis. Practitioners vis and abductor pollicis longus muscles provides essential
can then palpate all of the abnormal tensions they visualize information in this condition because the connective tissue
to confirm their presence. Palpation of soft tissue eventually portions of these particular muscles are also involved. The
becomes an art. All of us have heard patients state that the combination of passive and resistive testing corroborates
previous doctor "never even touched me" versus "doctor, each testing method and helps determine which particular
how did you know that area was painful?" An experienced tissue represents the primary lesion. Fortunately, more and
doctor should be able to literally "feel" the patient's pain. more practitioners are currently taking this information into
The inflamed warm tissue and the nodular, lumpy, leathery, account. One of the benefits of functional testing is the
doughy, springy, taut sensations all represent particular knowledge that if all of the tension tests are negative for a
manifestations of the soft tissue lesion. particular area there is a probability that the local pain is re­
Dr James Cyriax, an English orthopedic surgeon, was ferred although at times a localized tender boney lesion may
truly ahead of his time when he created a functional exami­ not respond to functional testing.
nation based on his differential analysis of passive and con­ Recently an intertester reliability study of the Cyriax
tractile tissue. Even to the present day, many practitioners evaluation was carried out on 21 shoulder cases,' and 19 of
are not truly familiar with this basic foundation of examina­ the 21 cases evaluated were put in the same diagnostic cate­
tion. The purpose of a soft tissue examination is to deter­ gory for a percentage agreement of 90.5 %. The kappa value
mine the source of the pain. of 0.875 indicated "almost perfect" agreement among the
We must question our established orthopedic tests to de­ examiners. In the March 2005 issue of the Journal of Or­
termine exactly what tissue or tissues are being stressed. In thopaedic and Sports PhYSical Therapy , a study was per­
the first and second editions of this text, I questioned the formed assessing the agreement between assessors on the
usefulness of Finkelstein's test, which is considered by diagnosis of shoulder pain with the use of Cyriax's selective
many to be pathognomonic of de Quervain's disease. The tissue tension tests. The investigators concluded that selec­
passive stretching of the extensor and abductor tissues of tive tissue tension tests in conjunction with a preliminary


clinical history enable good agreement between trained as­ used to evaluate joint play. If passive tissue involvement is
sessors 2 Even steroid injections were more effective in re­ still suspected, the joint can be examined during compres­
ducing shoulder pain when they were placed at anatomical sion (labral problems) or with added weight to stress the
sites determined by specific muscle testing than at painful passive tissue (acromioclavicular joint) further.
trigger points.) The shoulder chapter (see Chapter 3) con­ Because active motion stresses both the contractile and
tains more updated rotator cuff testing, which eliminates the passive tissue , active motion is best used as a guide to
some of the synergistic muscles that were involved in the the status of the patient with regard to the range of motion
original Cyriax method of evaluation. (ROM) and the patient's willingness to move rather than as
This text stresses the functional examination. It is as­ an assessment of tissue involvement. Although an active and
sumed that the practitioner will take an adequate history passive motion producing pain in the same direction refers
and perform an inspection of the whole body, with particu­ to passive tissue involvement, and although an active and
lar attention being paid to the areas of involvement. passive motion producing pain in the opposite direction
may refer to contractile tissue involvement, it is more sys­
tematic to perform all the passive motions together and then
all the contractile motions together. Normally, active motion
is always less than passive motion because of the limitation
created by the contracted muscle. The assessment of passive
Passive Testing testing is by evaluation of what is known as "end feel, " or
the feeling perceived by the examiner at the final stressed
Passive tissue refers to tissue that does not have its own (overpressure) range of passive motion. Cyriax6 distin­
contractile ability, such as joint capsules, bursae, fasciae, lig­ guished among six types of end feel:
aments, nerve root, and dura mater. Whereas passive testing
also stretches contractile tissue, which is incriminated by 1. Bone to bone: This is a hard end feel; it is normal in
isometric testing, passive movements apply tension to the elbow extension and abnormal in elbow flexion. The
noncontractile structures that normally limit and guide limiting factor may also be ligamentous (cruciates for the
movement and maintain joint integrity. Usually, if the pas­ knee) or bony (olecranon process to olecranon fossa).
sive movement at end range is painful, the associated 2. Soft tissue: There is normal tissue approximation
stretched muscles can be tested isometrically in the oppo­ with, for example, elbow, knee, or hip flexion ; this
site direction to determine whether the contractile tissue is approximation is abnormal if it is less soft as a result
the source of the pain. By definition, passive testing is nei­ of scar tissue, contracture, or arthrosis. The degree of
ther active nor spontaneous and requires an examiner to arthrosis or osteophyte formation allows the clinician
perform the movement. to distinguish the degree of hardness. Early arthrosis
Before passive motion testing is performed, it is impor­ would feel less hard.
tant to explain to the patient what you are attempting to 3. Spasm or "twang": This phenomenon results when
accomplish so that the patient will be in a relaxed, coopera­ passive movement stresses a fracture, inflamed joint,
tive state. In the case of a recent trauma, care must be taken or metastasis (i.e., the muscles have actively or reflex­
not to force movement passively of a joint with a restricted ively acted to end motion). This condition is always
range of motion. In a cervical spine trauma with restricted abnormal and should undergo further testing, such as
motion, it is wise not even to attempt passive motion until radiologic evaluation. Manipulation is contraindicated.
further tests are performed. After performing the passive 4. Capsular: This is normally the firm end feel of a nor­
motion tests, the examiner cannot definitely incriminate the mal shoulder, hip, or knee at the extreme end of rota­
passive tissue until the contractile tissue is tested. Passive tion. There is a hardlike stoppage of motion with a
movements stretch the muscular component at the end give to it, described as leather being stretched or two
range by applying force in a direction opposite to the mus­ pieces of tough rubber being squeezed together. It is
cle movement and may be used to corroborate irritated con­ abnormal if the capsular feeling is firmer than usual
tractile tissue. For example, the rotator cuff muscles are or associated with decreased ROM . In the absence of
stretched, especially at the end range of passive motion. For Significant inflammation or effusion, this firmer feel­
example, passive internal rotation of the shoulder stretches ing usually indicates a capsular fibrosis. 7The presence
the external rotators, that is, the infraspinatus, teres minor of inflammation or effusion with a firmer feeling may
muscles. Increased translation of the humeral head occurs indicate an acute phase of an adhesive capsulitis.
when the muscles are removed 1 .5 Passive motion also meas­ 5. Springy block: This is a hard rebound or relatively
ures the range of joint motion and muscle flexibility and is soft feeling indicating an intra-articular pathology,
Basics of Soft Tissue Examination 5

such as loss of knee extension due to a torn meniscus this reason, passive testing should always be performed first
or loose body, and is always abnormal. A spinal fixa­ to help rule out the passive joint structures.
tion would elicit a springy block; loss of movement When muscles are tested, the patient is asked to use
due to a muscular spasm may cause a springy bounce. maximum strength for at least 2 seconds. After a particular
6. Empty feeling: This phenomenon occurs when the muscle is incriminated, palpation of the muscle for areas of
examiner feels that more movement is possible, but tenderness and soft tissue abnormalities plus the effect of
the patient demands that the motion stop because of stretching the muscles on the passive examination helps
severe pain; it may indicate anything from an acute pinpoint the particular site of contractile tissue at fault.
bursitis to cancer and is always abnormal. The prob­ Kronberg et al. 10 showed by electromyographic recordings
lem is usually extra-articular. that in coronal abduction (Fig. 1-1) using reference voluntary
contraction (i.e., an isometric maximum voluntary contrac­
Hypermobility evaluation: Some patients have hyper­ tion), "there was no Significant difference between the supra­
mobile joints resulting in excessive motion; this condition and infraspinatus." Therefore, if abduction were tested in the
occurs in shoulder instability, patella dislocation, Ehlers­ coronal plane from 0 to 180 degrees, the supraspinatus mus­
Danlos syndrome, Marfan syndrome, rheumatoid arthritis, cle could not be distinguished from the infraspinatus muscle,
osteogenesis imperfecta, systemic lupus erythematosus, po­ which again negates the practice of always testing in a neutral
liomyelitiS, myotonia congenita, and some neurologiC con­ position. The anterior and middle deltoid would also enter
ditions. A hypermobile patient would exhibit three or more the picture; the middle and anterior deltoid would best be
of the following tests B: passive thumb apposition to touch tested around 120 degrees of coronal abduction. Figure 1-2
the forearm, passive little finger hyperextension of more depiCts electromyographic activity during external rotation of
than 90 degrees, elbow hyperextension of more than 10 the shoulder from the neutral position, at 45 degrees abduc­
degrees, knee hyperextension of more than 10 degrees, and tion, and at 90 degrees abduction. It is evident that although
forward flexion of the trunk with the knees straight and the the supraspinatus is active during external rotation, the infra­
palms of the hands resting flat on the floor. Some clinicians spinatus is significantly more active than the supraspinatus,
include excessive ankle dorsiflexion and foot eversion. except that at zero degrees of rotation at all three levels of ab­
duction, muscle testing could not distinguish between the
Contractile (Isometric) Testing supraspinatus and the infraspinatus. It is also interesting that
at 90 degrees of abduction, testing the infraspinatus while it is
Contractile tissue refers to the muscular component and rotated 40 to 60 degrees provides greater strength than test­
also to the tendon stressed by its contracting muscle. Ten­ ing it when it is rotated at 90 degrees.
dons are no longer regarded as inert tissue because they re­ Much of the muscle testing, especially for the rotator cuff
spond to elastic recoil and longitudinal movement. Tendons in this text, is based on an electromyographic analysis con­
can stretch up to 4% before damage occurs. 9 The muscle ducted by Kelly et al. II These investigators formulated their
belly, the musculotendinous junction, the body of the ten­ study to maximize the neural activation of the desired cuff
don, and the tendo periosteal junction are all included. Cyr­ muscle, Simultaneously to minimize the activation from in­
iax6 developed methods of testing that help pinpoint the volved synergistic muscles, to have good test-retest reliabil­
particular area that is involved. He emphasized testing the ity, and to minimize positional pain so that maximal effort
muscle to elicit maximum strength while the joint is in its can be exerted (see Chapter 3).
most relaxed, neutral pOSition to reduce joint compression.
A problem with neutral joint position muscle testing is that Interpretation of Muscle Testing
sometimes testing a muscle in a neutral position allows
extra activity from a synergistic muscle, which may mask • Muscle testing that responds without pain and nor­
the pain the practitioner is attempting to elicit. For exam­ mal strength usually indicates a normal muscle. How­
ple, testing the subscapularis muscle (a medial shoulder ro­ ever, in cases in which the patient may complain, for
tator) with the arm at the side with the forearm in a sagittal example, of pain only after 15 laps of swimming,
position (neutral shoulder joint position) allows the domi­ repetitive testing may be necessary to elicit the pain.
nant pectoralis major to be active. Internally rotating the Pain after repetitive testing sometimes indicates an ar­
shoulder behind the back (lift off test) enables the pectoralis terial blockage. For example, repetitive testing of the
major activity to be reduced, emphasizing more subscapu­ gluteus maximus eventually resulting in pain may be
laris activity. The isometric muscle testing used in this text due to intermittent claudication from blockage of the
takes these factors into consideration. It would seem that iliac arteries. Pain occurring soon after maximal con­
muscle testing creates some joint stress in any position. For traction rather than immediately after contraction is

100 , - - - - - - - - - -----, 100

-A- Subscapularis
..... Supraspinatus
-& Infraspinatus
. . ......
-. - PectoraNs major
1 50

-B- Deltoideus ant ..i

. •. Deltoideus mecI
; ..

Deltoideus post
* Latl..imus dorsi
o 30 eo 90 120 150 180 0 30 eo 90 120 150 180
Degrees Degr...
Figure 1-1 The recorded normalized EMG activity during shoulder abduction. Source: Reprinted with permission from M Kronberg, G
Nemeth, L Brostrom. Muscle activity and coordination in the normal shoulder: an electromyographic study. Clinical Orthopaedics and Related
Research, Vol. 257 , p. 79, © 1990,jB Lippincott Company.

considered a positive result. Corroboration of the iso­ • If resisted tests of two muscles surrounding the same
metric test result can be completed by eliciting pain joint are painful, it is possible that both muscles are
by passively stretching the muscle, although with involved or one of the muscles with two functions is
mild injury, the passive stretch may be negative. involved. For example, the supraspinatus and infra­
• Pain associated with normal strength may indicate spinatus both function as abductors and external ro­
minor involvement of a muscle or tendon (tendino­ tators (see Figs. 1-1 and 1- 2). The muscle that elicits
pathy). In this situation, the pain also may reflexly in­ the most pain with associated painful tenderness
hibit the muscle , creating minimal weakness, but the would probably be the most significant muscle. The
contractile tissue is strong. Because of the pain, the biceps brachii is also a supinator of the elbow, and
patient may not desire to produce a maximum effort. both elbow flexion and supination might be painful
(see Shoulder, Chapter 3). Because the supinator
• Contractile testing may aggravate passive (inert)
function of the biceps is strongest with elbow flexion,
tissue. For example , contraction of the gluteus me­
the supinator could be tested in shoulder extension
dius may aggravate (compress) a trochanteric bur­
with a straight arm to lessen the biceps input.
sitis, or resisting the pectoralis major may aggravate
a rib fracture or a metastatic lesion near a muscle • If more than two muscles are painful, the cause is
insertion. usually inflammatory or in rare cases even a metas­
tases. If all of the muscles in a tested area are painful,
• Pain and weakness must always be regarded as seri­
the pOSSibility of a musculotendinous lesion de­
ous, from a partial tear to a fracture to a metastatic le­
creases. There may even be a tumor or in some cases
sion. It usually requires additional evaluation, such as
a misinterpretation by the patient.
x-ray study or magnetic resonance imaging.
• Weakness without pain may refer to a neurologiC Grading of muscle strength is based on the amount of re­
problem or a complete muscle or full thickness ten­ sistance determined by the examiner. A practical method 12
don rupture . of gradation is based on the 5 to 0 deSCription, in which 5 is
• If there is pain on resisted testing, the clinician might "normal," with full ROM against gravity and full resistance;
be able to differentiate whether the lesion is within 4 is "good," with full ROM against gravity and some resist­
the tendon or the muscle belly. Tendon involvement ance; 3 is "fair," with full ROM against gravity, meaning that
usually allows a full range of motion, whereas muscle the patient can hold the muscle against gravity as long as
belly involvement, especially if it is ruptured, would there is no resistance; 2 is "poor," with full ROM with grav­
not allow full range of motion because of a possible ity eliminated; 1 is "trace," with slight contractility and no
protective spasm. ROM; and 0 is "zero," with no evidence of contractility.
Basics of Soft Tissue Examination 7

100 100
-A-- Subscapularis
(.) .. .&c.. Supraspinatus (.)
a: >
-B- Infraspinatus a:
.• . Pectoralis major !
)( 50
~ -e- Deltoideus ant
ae • Deltoideus mad ae
-+- Deltoideus post ........... ....
.. ­ - "

. _ . Latissimus dorsi ..... ~.~.~..

0 20 40 60 80 100
0 20 40 60 80 100
A % Rotation % Rotation
100 100
-A-- Subscapularis
.&c . Supraspinatus
(.) (.)
a: -e- Infraspinatus >
50 ......•............• ............•

. • . Pectoralis major

-e- Deltoideus ant



E . • Deltoideus mad
ae ae
~. --*- Deltoideus post

. - . Latissimus dorsi
0 0
0 20 40 60 80 100 0 20 40 60 80 100
B % Rotation % Rotation
100 100
-A-- Subscapularis
.&c . Supraspinatus
(.) (.)
-B- Infraspinatus
"i .•. Pectoralis major "i
~ 50

.• . . . . .•..
-e- Deltoideus ant
H.. Deltoideus mad
;:c 50

ae ae
-+- Deltoideus post

. _ . Latissimus dorsi
0 0
0 20 40 60 80 100
0 20 40 60 80 100
C % Rotation
% Rotation

Figure 1-2 The recorded normalized EMG activity during external rotation in (A) neutral pOSition, (B) at 45° abduction, and (C) at 90°
abduction; the arm was not supported. Source: Reprinted with permission from M Kronberg, G Nemeth, L Brostrom. Muscle activity and co­
ordination in the normal shoulder: an electromyographic study Clinical Orthopaedics and Related Research, Vol. 257 , p. 80, © 1990, JB lip·
pincott Company

The Guides to the Evaluation oj Permanent Impairment 13 gives The history of a patient may reveal that the pain does not
a grading scheme based on percentage of impairment, occur immediately after use of the extremity but possibly
which 5 is 0%, 4 is 5% to 20% , 3 is 25% to 50%, 2 is 55% during or at the end of activity. Often one or two resisted
to 75%, 1 is 80% to 90%, and 0 is 100% impairment. muscle tests may not elicit pain. Repetitive loading (i.e.,
Matsen et al. 14 differentiate the size of a cuff tear by iso­ testing 10-15 isometric contractions in a row) may be nec­
metric muscle testing. Partial tears usually create increased essary to create the pain of which the patient complains.
pain with minimal loss of strength. In the shoulder, for ex­ Sometimes, the patient must be examined during or after
ample, all of the cuff muscles blend together proximal to activity to find the source of the pain.
their insertions into the capsule, and as the tear progresses Although it is thought that testing a muscle in a
in size, the supraspinatus, the infraspinatus and finally the stretched position would create a weakened position for the
subscapularis become involved, and weakness increases on muscle in order to put a muscle at a disadvantage, if muscle
testing (see Chapter 3). testing is equivocal, it appears that a muscle may be in a
Isometric muscle testing is useful in emphasizing mus­ more weakened position if it is tested in a shortened posi­
cle atrophy (Fig. 1-3) and depicts how atrophy of the in­ tion. Isometric force generation is greatest at the end ROM,15
fraspinatus becomes more visible with resisted external in which passive tension is greatest when the muscle is
rotation. stretched beyond its resting length (at or near end ROM) .16

Figure 1-3 (A) Atrophy of the left infraspinatus is visible with the arm at rest, but becomes much more apparent (B and C) with resisted
external rotation of both shoulders. Fifteen months later (D), the bulk of the infraspinatus has improved significantly and appears near nor­
mal in size during manual muscle testing. Source: Reprinted with permission from KP Black, JA Lombardo. Suprascapular nerve injuries
with isolated paralysis of the infraspinatus. AmencanJoumal Sports Medicine, Vol. 18, No.3, p. 226, © 1990, American Orthopaedic Society.
Basics of Soft Tissue Examination 9

A functional examination attempts to examine the total tractile tissue certainly points the examiner in a more defi­
function of the involved tissue to pinpoint the source of the nite direction.
pain. Stressing just one motion (e.g., passive motion with­ Another obvious example of distinguishing between pas­
out resisted muscle testing) prevents complete differentia­ sive and contractile tissue in arriving at the source of pain is
tion of the tissues involved. a sprain of the acromioclavicular ligament. This structure is
It is probably impossible to test functionally a particular made up completely of passive ligamentous tissue; it is an
tissue without stressing some adjoining related tissue, but area not under muscular control. Passive testing, such as
most of the functional tests described are as specific as pos­ passive abduction and passive horizontal adduction, would
sible. The correlation of the positive and negative passive, create pain, whereas contractile testing of the shoulder cuff
resistive, and other additional tests allows the practitioner or adductor muscles would test painless except during the
to reach a more precise conclusion. acute case, which would be aggravated by resistive muscu­
It is difficult to imagine examining soft tissue without lar stress in the area. However, even in the acute case, the
first distinguishing whether the passive or the contractile passive findings would be more painful than the resistive
tissue (or both) is involved. Nevertheless, in the United testing.
States, even to this day, most practitioners do not con­
sciously attempt to make this distinction. Reports continue
to be published that attempt to distinguish, for example, be­
tween a "stiff and painful shoulder" and "adhesive capsuli­
tis. " The stiff and painful shoulder includes conditions such
as tendinopathy, rotator cuff tears, and arthrosis of the joint. One of Cyriax's6 great contributions to soft tissue analysis
The adhesive capsulitis is described as shOwing limited mo­ is his concept of the capsular and noncapsular patterns.
tion, both actively and passively. All the aforementioned Knowledge of the capsular pattern improves diagnostic abil­
could be distinguished simply by relating the examination ities. For example, every arthritic hip shows more of a limi­
to the differentiation of passive and contractile tissue. tation of medial rotation than other ranges followed by
Testing results for a chronic adhesive capsulitis of the limited hip flexion. The severity of the arthritis/arthrosis is
shoulder would probably show on examination a loss of determined by the amount of limitation. Many present-day
passive lateral rotation, glenohumeral abduction, and me­ orthopedists accept the fact that medial hip rotation less
dial rotation (see Capsular Pattern), with a harder end feel than 15 degrees and hip flexion less than 115 degrees rep­
than normal. Resistive testing of the associated shoulder resents an arthritis/arthrosis. 17 "Limited internal rotation of
muscles would probably test strong (unless there was atro­ the hip Significantly predicted the diagnOSiS of a disorder as
phy) and painless. Elimination of the contractile tissues by originating primarily from the hip, as opposed to originat­
resisted isometric muscle testing and the finding of pain ing from the spine." 18 A capsular pattern refers to a particu­
and limitation on passive testing would automatically point lar sequence of passive limitation of motion in a joint
to a capsular shoulder problem. Isometric muscle testing is controlled by muscles; this pattern affects the whole joint.
usually painless in a chronic adhesive capsule; however, it When the entire capsule is shortened or inflamed, or if the
must be understood that depending on the stage of the ad­ synovial membrane lining the capsule by itself is inflamed,
hesive capsulitis, the presence of inflammation would result as in an acute sprain, passive testing of the joint demon­
in painful isometric testing. An important sign in compar­ strates a proportional limitation of motion for that particu­
ing contractile and passive tissue with regard to an inflam­ lar joint. For example, conditions that shorten the capsule,
matory process is that in the inflammatory stage of adhesive such as arthrosis or any type of arthritis that affects the cap­
capsulitis or bursitis, the isometric testing would usually ex­ sule and synovium, express a capsular pattern. Even acute
press a muddled appearance of pain on two or three mus­ conditions affecting only the synovium (e.g. , ligamentous
cles rather than specifying a particular tendon. The knee injury) cause a capsular limitation of motion because
association of painful passive restrictions with an unex­ of the muscular spasm protecting the capsule. Why the pro­
plained variety of positive isometric muscle test results tective muscle spasm mimics the capsular pattern in the
would indicate an inflammatory problem, pOSSibly of the acute stage before capsular limitation is unknown. The cap­
bursa or the capsule. Tendinopathy and rotator cuff tears sular pattern in the knee and elbow is more limitation of
would be evaluated by isometric muscle testing, which flexion than extension, but a study challenges Cyriax's cap­
would indicate pain and relative strength (tendinopathy) or sular pattern with respect to osteoarthritis of the knee. 19 The
pain and weakness (tears). Of course, radiologic and other authors state that a pattern of a ROM loss may be useful,
tests may be necessary to confirm the functional examina­ but the quantitative definition (flexion loss always greater
tion, but the logical distinction between passive and con- than extension loss) does not hold true, at least with respect

to the knee. It is the author's experience that sometimes ex­ bursitis, or tumor (see Chapter 6 for noncapsular pattern
tension may be more limited than flexion in an arthritic and "sign of the buttock").
knee joint, but most of the time, flexion is more limited. In
an editorial by Richard M. Ellis20 commenting on this study, Summation of Capsular Patterns of Passive Limitation
"the authors still agreed that 76 (of 79) subjects . .. have
shown a capsular pattern. The capsular pattern has proven Shoulder: most limited external rotation; next gleno­
to be extremely useful in determining probable arthritis and humeral abduction, then internal rotation.
capsular involvement." Elbow: flexion usually more limited than extension; rota­

In most of cases, every arthritic shoulder or, more tions full and painless except in advanced conditions.

commonly, an adhesive capsulitis demonstrates more Wrist: equal limitation of flexion and extension; little limita­

limitation of lateral rotation, less limitation of gleno­ tion of ulnar and radial deviation.
humeral abduction, and least limitation of medial rota­ Trapezio metacarpal joint: only thumb abduction.
tion when compared with all the other motions. Every Hip: most limited is internal rotation followed by flexion.
joint has its own particular pattern of capsular limitation; Some limitation of abduction and little or no limitation
these are discussed separately in later chapters. If only a of adduction and lateral rotation.
portion of the capsule is involved (shortened), only Sign of the buttock: passive hip flexion more limited and
movements that stretch that portion of the capsule are more painful than straight-leg raise.
involved instead of a capsular pattern. Many clinicians Knee: more limitation of flexion than extension.
who may not be familiar with the capsular pattern con­ Ankle: more limitation of plantiflexion than of dorsiflexion.
firm Cyriax's concept. Neviaser and Neviaser21 describe Talocalcaneal joint: increasing limitation of varus until fixa­
shoulder limitation in adhesive capsulitis as restricted tion in valgus.
motion, both actively and paSSively, primarily in three Midtarsal joint: limitation of adduction and internal rota­
planes: abduction or elevation, internal rotation, and ex­ tion; other movements full.
ternal rotation. Mintz and Fraga n found the capsular pat­ Big toe: much more limitation of extension and slight limi­
tern in the elbow to be more limiting of flexion than tation of flexion.
extension in foundry workers with osteoarthritis of the Cervical spine: equal limitation in all directions except for
elbow. Fareed and Gallivan 23 mentioned that exquisite flexion, which is usually full.
pain on external rotation was the most sensitive indicator Thoracic spine: limitation of extension, side bending, and
of the presence of frozen shoulder syndrome. The earliest rotation; flexion is less limited.
sign of the shoulder capsular pattern is limitation of ex­ Lumbar spine: marked and equal limitation of side bending
ternal rotation by itself. with limitation of flexion and extension.
On more than one occasion, patients have been told that
they have an "arthritic elbow." However, the full range of
flexion and extension with bone-to-bone end feel on exten­
sion and soft-tissue end feel on flexion, with rare exceptions
eliminates the diagnOSiS of arthritis. Often, the same patient The preface to this text discusses the importance of func­
exhibits pain on resisted wrist extension; this phenomenon tional testing compared with treating the most tender area
helps confirm a lateral epicondylopathy. in regard to injection of shoulder lesions. Often, tissues that
The noncapsular pattern refers to conditions that do not are embryologically related refer to the same area; for exam­
primarily affect the capsule. For example, acute bursitis ple, the shoulder capsule, bursa, supraspinatus, and infra­
shows more limitation of abduction than external rotation. spinatus, which are supplied mainly by C-5, refer along the
A loose body in the elbow or knee usually reveals more lim­ same sclerotome or dermatome and can create similar ten­
itation of extension than flexion. In the hip with the capsu­ derness at the deltoid tubercle or beyond.
lar pattern, internal rotation would be the earliest passive As important as tenderness is, the clinician must rely
motion to become limited; in a noncapsular pattern, inter­ first on a complete functional extremity examination of all
nal rotation would rarely be limited. Conditions that do not the areas that can create the tenderness before tenderness
primarily affect the capsule and therefore exhibit a noncap­ can be accepted as the sine qua non. Anterior thigh pain de­
sular pattern should prompt the examiner to consider con­ mands at least a functional examination of the lumbar
ditions not necessarily related to arthrosis. In the hip, for spine, hip, knee, and related muscles and fasciae. On par­
example, the condition could be almost any other condi­ ticular occasions, tenderness may be the only symptom. For
tion, such as osteomyelitis of the femoral head, abscess, example, a chronic meniscus problem may not elicit pain
Basics of Soft Tissue Examination 11

on any of the meniscus stress tests , and the clinician may SPINAL RELATION TO EXTREMITY SOFT TISSUE
have to rely on the history and localized tenderness at the LESIONS
joint line. Localized tenderness of the joint line may be
more valid than most orthopedic tests for the meniscus (see
Although spinal lesions may be related to pain in the ex­
Chapter 7). Garrick and Webb" mentioned an apparent
tremities, a functional examination of both the spine and
peroneal tendinitis revealed by pain on isometric testing of
the distal extremities usually pinpoints the source of the
the peroneal muscles, but palpation of maximal tenderness
pain. Some research results have shown that spinal manip­
just medial to the tendons may indicate a posterior ankle
ulation is effective in radicular problems.25-27 Empirically,
impingement due to an enlarged posterior process of the
restoration of spinal mobility and function in itself is re­
talus. Besides a functional extremity examination, pressing
lated to improving the homeostasis of the surrounding ex­
on an active trigger point, performing a specific interseg­
tremity soft tissue.28--47 Interestingly, the relation of the spine
mental spinal or extremity joint play examination, or pal­
to the somatoautonomic and somaticosomatic components
pating soft tissue (i.e ., the fascia and tender points) in the
has recently been "discovered" by the medical profession:·
counterstrain technique helps in selecting more specific
but treatment of soft tissue adjacent to the spine, as de­
therapy Sometimes, friction can be used to anesthetize a
scribed in the chapters on the Graston technique, neuro­
doubtful area. If possible, a functional examination that ag­
muscular rehabilitation, friction massage, postisometric
gravates the tender spot should be performed before major
relaxation, and postfacilitation stretch in this text, acts as a
credence is attached to the tender area.
complement to the spinal component, often allowing easier
A common example of an incomplete nonfunctional ex­
spinal manipulation. In many cases, the adjacent soft tissue
amination is the use of "shoulder impingement" syndrome
component, such as fascial adhesion or chronic muscular
as a diagnostic entity Impingement, like whiplash, repre­
tightness, may be the underlying cause of the spinal block­
sents a mechanism of injury rather than a diagnosis. Various
age, which must be treated to prevent recidivism of spinal
shoulder impingement tests are used to determine that
fixation .
something is impinged upon. Some physicians inject lido­
caine into the subacromial area and , on finding less pain on
the previously painful impingement signs, decide that
something is being pinched. The patient may even be re­
lieved of symptoms, but a functional examination helps
evaluate the specific area of impingement and the possible It is very important for the drugless practitioner to be
causes of the impingement. Although a radiologic examina­ aware of the uses and effects of nonsteroidal anti-inflamma­
tion may incriminate an extrinsic cause, such as an acromial tory drugs (NSAIDs), because they are readily available over
spur, an enlarged coracoid process, an abnormally curved the counter, and there is an increasing tendency to recom­
or hooked acromion, acromioclavicular osteophytes, or ten­ mend them when the patient is in pain. In a recent experi­
don calcification, a functional examination can help incrim­ ment: 9 the use of NSAIDs for the treatment of tendon
inate the particular tissue that is being impinged. For inflammation might increase the levels of leukotriene B4 (an
example, isometric resistive testing might incriminate the inflammatory mediator) within the tendon, potentially con­
tenoperiosteal or musculotendinous portion of the tributing to the development of tendinopathy Leadbetter50
supraspinatus, the infraspinatus, the subscapularis, or the stated that treatment of persistent signs of inflammation by
long head of the biceps. The site of impingement may be repeated efforts to turn off the body's alarm is not a substi­
discovered by a functional examination for shoulder insta­ tute for finding the cause of the fire. NSAIDs are metabo­
bility or rotator cuff weakness. Practitioners who use man­ lized through the liver and affect prostaglandin-driven renal
ual therapy cannot be satisfied with a diagnOSiS of "shoulder functions ; therefore , NSAIDs are contraindicated with any
impingement syndrome," and efficacious manual therapy liver or renal disease. In addition , gastrointestinal toxicity
depends on pinpoint accuracy A complete functional exam­ and peptic ulcer history must be considered. The syndrome
ination often gives the practitioner a working diagnosis, of NSAID-associated gastropathy may be responsible for
such as supraspinatus tendinopathy of the musculotendi­ more than 2500 deaths per year among patients with
nous area. Of course, radiologic studies and tests (e.g. , mag­ rheumatoid arthritis. 51 Older patients have a greater ten­
netic resonance imaging, computed tomography, and dency for adverse reactions because a change in their drug
arthrography) may be needed if the patient does not show receptors occurs. Most important is the interaction of
early progress or if the interpretation of the functional ex­ NSAIDS with other medications often taken by the elderly,
amination is uncertain. especially diuretics, hypertenSive drugs , oral hypoglycemiC

drugs, anticoagulants, and renally metabolized medica­ denced by diminished joint swelling distant from the in­
tions. 50 NSAlDs may be clinically useful for the reduction of jected site, transient eosinopenia, and depression of plasma
synovitis Goint, tendon sheath, or bursa) , as an adjunctive cortisol levels reflecting hypothalamic-pituitary-adrenal axis
pain reliever for acute and chronic injury, and during a suppression. 53 Johnson63 stated that steroid injection at the
comprehensive rehabilitation program. Leadbetter50 cau­ wrist should be used only in the most select instances at the
tioned against the use of NSAlDs in the elderly for minor distal attachments of tendon to bone. Steroid injection into
conditions, and especially in the "at risk" patient with the the most tender spot may produce rupture of the tendon or
triad syndrome of nasal polyps, asthma, and aspirin intoler­ its insertion.
ance. Celecoxib (Celebrex) , a cyclooxygenase (COX)-2­ Because of the adverse effects of corticosteroids on soft
specific inhibitor, was developed to circumvent the gastro­ tissues and cartilage, it is important to know whether exer­
intestinal toxicity of nonspecific NSAlDs. Recently, there cise or manipulation will have an adverse effect during or
has been evidence that the use of COX-2 inhibitors may in­ immediately after steroid therapy64 Further studies are
crease the risk of serious cardiovascular events, such as my­ needed in this regard. Medical doctors differ in their opin­
ocardial infarction, stroke, and heart failure n ions about how often joints and soft tissue should receive
Some investigators believe that limited controlled studies steroids, from a maximum of once every 1 to 3 months to a
and extensive clinical experience support the efficacy of maximum of no more than once in the course of a treat­
corticosteroids in the palliation of rheumatoid arthritis and ment program.'··65 They also state that tendon injection
other inflammatory musculoskeletal conditions S3 NirschP' should be in the sheath and never into the tendon. 63
stated that "there are no scientific data to indicate that anti­ The realization that the diagnosis of "tendinitis" is a mis­
inflammatory medications have a biologiC healing stimu­ nomer and that most of the time the condition is a degener­
lus. " He separated pain relief from the promotion of ative "tendinosis" questions the use of anti-inflammatory
healing. Healing of tissue is accomplished by restoring nor­ medication (See section: Part III on Tendinopathy).
mal biomechanics through rehabilitation and the use of
manual techniques as explained in this text. NirschP' men­
tioned three concepts to initiate a healing stimulus: (1) en­
hancement of peripheral aerobics (oxygenation, nutrition,
and collateral circulation); (2) collagen induction, strength­ At the end of the chapters on extremity examination are
ening, and alignment; and (3) enhancement of biochemical functional diagnosis charts, which correlate the functional
changes associated with endurance training. tests with the lesions. Plus (+) means that pain will proba­
Corticosteroid injection is not effective in acute trauma, bly occur as a result of a speCific test. For example, lateral
injection into the tendon, immediately before competition, epicondyloathy can be diagnosed with pain on resisted
and in joint instability or malalignment. 5' Leadbetter'o rec­ wrist extension, and a diagnosis of supraspinatus tendinitis
ommended a 6-week preinjection trial of rest, adjusted level requires pain on resisted shoulder abduction.
of play, and conditioning and rest (protected activity) for 2 Plus/minus (+/-) , or possible pain, is used to indicate
to 6 weeks after injection. that either related or unrelated tests mayor may not aggra­
Some of the side effects of corticosteroids are avascular vate the involved tissue. Other tests not directly related to
necrosis, especially of the hip," which results from an ad­ the source of the pain may aggravate the tissue as well. Of
verse effect on lipid metabolism, causing fatty emboli; ten­ course, some of these tests may be related to the source of
don rupture due to the inhibition of the formation of the pain and also mayor may not be painful, depending on
healing adhesions, which results in weakening 56 ; alteration the severity of the condition. For example, an infraspinatus
of biomechanical ligamentous properties due to inhibition tendinopathy is painful on resisted lateral rotation (+) . De­
of the formation of granulation and connective tissue 57 •58 ; pending on the size of the lesion, passive medial rotation
arthropathy due to softening of the subchondral bone, (stretching of the infraspinatus) mayor may not be painful
delay in chondroitin synthesis, and inhibition of the forma­ (+/- ), and stressing the coracoacromial ligament by way of
tion of ground substance in mesenchymal tissue (articular the coracoacromial impingement test mayor may not al­
cartilage)59; vertebral osteoporosis60 ; infectious arthritis and ways aggravate the supraspinatus tendon.
bursitis" ; and depressed mental status due to decreased Possible limited ROM on passive testing is indicated by
corticoadrenal function. 61 Some of the articular damage has limitation (L); the limited movement has an abnormal end
been attributed to steroid analgesia, which results in micro­ feel. The term possible limited ROM is used because if L
trauma S3 due to painless overuse. refers to a capsular pattern, then all the ranges of limitation
Local injection of corticosteroids has proved to have a of the capsular pattern may not be present. In the knee,
systemic effect on remote collagenous structures ,62 as evi­ under meniscus, the top four passive motions may show an
Basics of Soft Tissue Examination 13

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41. lewitt K. Manipulative Therapy in Rehabilitation oj the Motor System. 55. Fisher DE, Bickel WH. Corticosteroid-induced avascular necrosis. A
london: Butterworth; 1985:25. clinical study of seventy-seven patients. ] Bone Joint Surg Am.
42. Cibulka MT, Rose Sj, Delitto A, et al. Hamstring muscle strain 1971;53:859-873.
treated by mobilizing the sacroiliac joint. Phys Ther. 1989;666: 56. Kapetanos G. The effect of the local corticosteroids on the healing
1220-1223. and biomechanical properties of the partially injured tendon. Clin
43. Muckle os. Associated factors in recurrent groin and hamstring in­ Orthop Relat Res. 1982;163:170-179.
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44. Gunn CC, Milbrandt WE. Tenderness at motor points: an aid in the 58. Behrens F, Shephard N, Mitchell N. Alteration of rabbit articular car­
diagnOSiS of pain in the shoulder referred from the cervical spine. ] tilage by intra-articular injection of glucocorticoids.] Bone Joint Surg
Am Osteopath Assoc. 1977;77:196-712. Am. 1975;57:70-76.
45. Kellgren jH. On the distribution of pain arising from deep so­ 59. Bentley G, Goodfellow jW Disorganisation of the knees follOWing
matic structures with charts of segmental pain areas. Clin Sci. intra-articular hydrocortisone injections. ] Bone JOint Surg Br.
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46. Korr 1M. Clinical significance of the facilitated state: symposium on 60. Sweetnam R. Corticosteroid arthropathy and tendon rupture [edito­
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Assoc. 1955;54:265-282. 61. Hench PS, Kendall El, Slocumb CH, et al. Effects of cortisone ac­
47. Wall P. The mechanisms of pain associated with cervical vertebral etate and pituitary ACTH on rheumatoid arthritis, rheumatic
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48. Arkuszewski Z. Editorial.] Man Med. 1989;4:42-43. 62. Melmed EP. Spontaneous bilateral rupture of the calcaneal tendon
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The Effect of Mechanical Load on

Soft Connective Tissues

Katie Lundon

Connective tissues are ubiquitous in the human body. tervertebral disc. The gross morphology as well as the inter­
Connective tissues encompass a broad and diverse range of nal remodeling of connective tissue-based structures is di­
tissues including the dense regular connective tissues, that rected in no small way by the physical forces that are
comprise tendons, ligaments, and articular cartilage, and imparted on them. Connective tissues must respond
dense irregular (fascia) connective tissues, such as the inter­ qUickly, robustly and reversibly to deformations caused by
stitial connective tissues separating and connecting muscles internal and external stresses 1 There is a differential
and surrounding all organs, nerves, and blood vessels. Con­ response of connective tissues to mechanical loading
nective tissues define the shape of the human body and in both within similar and between different connective tis­
this way must respond to internal and external stresses in sue-based structures. For instance, flexor tendons from
an expedient, strong, and for the most part, reversible man­ hindlimbs of canines present with much larger cross­
ner. Connective tissues are targeted by many therapies that sectional areas than other tendons from a similar region,
aim to improve posture and address movement patterns in such as the peroneus or extensor tendons; however, the
the human body. These therapeutic approaches are based stiffness of the flexor tendons was shown to be much lower
on physical or mechanical stretching of these soft connec­ than the other tendons throughout their stress-strain re­
tive tissues, which can, in health, also be achieved as a re­ sponses, identifying that the differences in the mechanical
sult of normal movement and exercise, or are used by response of tendons and other connective tissues contribute
necessity to achieve tissue "release" to ultimately allow in­ significantly to musculoskeletal performance. 2 Furthermore,
creased movement around contracted joints. Generally, an there is new information about the mechanical responses of
appropriate degree of mechanical loading is an important collagenous tissues, showing that responses to multiple
regulator of connective tissue homeostasis in health and cyclic loads at different points along the length of the same
during repair after injury to these tissues. tendon differ according to each site.) It was also found that
different sections of the same long tendons from the
hindlimbs of canines displayed different resistance to defor­
mation. In general, the bone-end sections were stiffer and
carried greater loads for a given strain than the muscle-end
sections; the mid portions were the least stiff and carried the
smallest loads for a given strain. 3
Gross Structural Effects Finally, there are differences in mechanical behaviors and
responses to loading between loose and high-Ioad-bearing
In health, mechanical loading is essential to the physical soft connective tissues. For instance, in a study aimed to de­
maintenance and management of both injured and unin­ termine elastic and viscoelastic mechanical properties of
jured connective tissue-based structures, including fascia, subcutaneous tissue in uniaxial tension with incremental
tendons, ligaments, capsules, articular cartilage, and the in­ stress relaxation, the elastic response of the loose connective


tissue was observed as linear, as opposed to the typical non­ commodate for both tensile strength if they are also associ­
linear response of dense regular connective tissues.· It has ated with large diameter fibrils and creep resistance.7 In
been suggested that loose connective tissues may function contrast, fibrils that have more spatial layout (as are found
to transmit mechanical signals to and from the abundant fi­ in nerve sheaths, blood vessels, and interstitial connective
broblasts and immune, vascular, and neural cells present tissues) have smaller, uniform fibrils ranging approximately
within these tissues.· In addition to the better-known me­ from 25 to 1000 nm and presenting with distinctive , uni­
chanical properties of the connective tissues, the mode of modal distribution. These fibrils typically run into small,
innervation of the dense irregular connective tissues (i.e., wavy bundles and often form three-dimensional isotropic
mechanoreceptors) also has recently received attention for networks, that as a result of soft highly compliant matrices,
their part in achieving the more immediate changes in vis­ are able to resist multidirectional stresses with high, cyclical
coelastic deformation of these fascial tissues after short-term deformations without permanent effects.7 Although gliding
loading. s freedom of individual collagen fibers in collagen-based tis­
sues varies with their configuration, this characteristic is
critical to the maintenance of normal connective tissue mo­
bility.9 In addition, the relative proportion of collagen and
other fibers plays a role in connective tissue biomechanics.
For instance, whereas collagenous fibers assist in the pro­
Extracellular Matrix Composition duction of force in structures such as the ligament and the
tendon, elastic fibers also contribute to the ability of tissues
Fibers and organs to regain their original form after mechanical
deformation. Elastin and collagen, as the main fibrillar con­
The mechanical (supportive and connective) behavior of stituents of connective tissue, display elastic behavior under
regular dense connective tissue is governed largely by tension that depends on both molecular and supramolecu­
fibers , most of which are collagen. The collagen family is a lar mechanisms.
diverse group of proteins distinguished by a native triple­
helical structure. The collagen triple-helix is important for Other Elements of the Extracellular Matrix
the integrity and underlying function of multiple connec­
tive tissue-based structures, including skin, bone, cartilage, Recent study has identified that as mechanical loading
tendon, and dentin. Most collagens assist in anchOring cells (tension) within the connective tissue matrix increases, the
to the extracellular matrix (ECM) and some function in cel­ mechanisms used by cells to remodel the matrix change. Fi­
lular regulation. 6 It is the characteristics of these fibers and broblasts in matrices that were held under tension or re­
their interaction with other components of the matrix that laxed respond differently to growth factor stimulation, and
determine overall soft tissue strength. Ligaments and ten­ switching between mechanically loaded and unloaded con­
dons present with a multimodal collagen fibril diameter dis­ ditions influences whether cells acquire proliferative!
tribution that endows them with optimal functional biosynthetic active or quiescent/resting phenotypes. 1O Func­
properties. In general, a fibril bundle can either fail by force tions of matrix components of connective tissues, such as
or load-dependent tearing, where collagen fibrils break as matrix hyaluronan and matrix proteoglycans, are related to
their tensile strength is exceeded, or by the time-dependent interactions with other matrix substances, such as collagen,
creep, which occurs when fibrils slide past each other and to provide scaffolding and shape. Their variable structures
the tissue they form disaggregates. 7 In addition to the phys­ provide speCifiCity of function for particular tissues and spe­
ical properties of collagen and the architectural arrangement cific aspects of interaction with other matrix molecules.11
of fibers (cross-helical, cross-ply, or quaSi-random net­ ECM composition appears to adapt speCifically to altered
work), mechanical properties of connective tissues, in terms loading conditions via two mechanisms: (1) stress regulates
of their measured tensile strength, are well correlated with the production of ECM proteins indirectly, by stimulating
the average diameter of their collagen fibrils. s The propor­ the release of a paracrine growth factor, or (2) directly, by
tion of collagen fibrils of different sizes, often reflecting col­ triggering an intracellular (fibroblast) Signaling pathway
lagen fiber maturity, largely contributes to soft connective that results in the potent activation of gene expression of
tissue mechanics. The benefit of tissues having a higher multiple cellular, and matrix-related elements.12 Proteogly­
fraction of small-diameter fibrils that would ultimately en­ cans (PGs) are believed to be primarily competent in ab­
sure a better interfibrillar binding by virtue of their higher sorbing compressive stresses, and PG interfibrillar bridges
surface/volume ratio, however, would be that they could ac­ ("shape modules") as supramolecular structures ubiqui­
The Effect of Mechanical Load on Soft Connective Tissues 17

tously distributed throughout connective tissue extracellu­ turn provide a high degree of specificity in function of dif­
lar matrices, have inherent elastic properties. 1 For instance, ferent soft connective tissues. 11 Articular cartilage is sub­
L-iduronate residues in shape module decoran PGs are sug­ jected to cycliC compressive stresses as the joints are loaded.
gested to be molecular springs, cycling through alternative Chondrocytes within articular cartilage respond to the me­
conformations and anionic glycosaminoglycan (AGAG) chanical stresses associated with normal joint loading via a
interfibrillar bridges. Shape modules are postulated to par­ series of signaling pathways. Chondrocytes rely on loading
ticipate in a sliding filament, process converting local com­ to maintain the functionality of the cartilage ECM. The inte­
pressions into disseminated tensile strains. 1 Therefore, the grin subunits alpha-Sand beta-1 form the receptor for fi­
elasticity of fibrils and AGAGs, manifest at molecular and bronectin, an ECM protein, and are believed to be involved
larger-scale levels, allows for a graduated and smooth re­ in mechanotransduction as well as in the regulation of cy­
sponse to variable stresses that occur in everyday move­ tokine production, thereby modulating chondrocyte cellu­
ment. lar physiology.22 Specific biomolecules, such as nitric oxide,
have also been implicated in these mechanotransduction
processes. For instance, synthesis of nitric oxide can be in­
Mechanisms Underlying Cell and Matrix Response to hibited by dynamic compressive strain of chondrocytes in
Mechanical Loading vitro, which, in turn leads to an up-regulation of speCific
metabolic parameters B
Connective tissues, when exposed to mechanical stress The positive effect of physical strain on tendon and other
or loading forces , be it either tension or compression, connective tissue-based structures is recognized; however,
demonstrate a strong relationship between mechanical little knowledge exists about how mechanical strain specifi­
stimulation and biochemical phenomena via the ultimate cally affects, for example, tendon cells H Although relatively
production of biochemical regulators of fibroblasts. Exter­ little is known about the mechanisms that occur between
nally applied mechanical loading leads to the rapid and mechanical stimulation and cellular (fibroblastic) responses,
sequential induction of distinct extracellular matrix compo­ studies from flow-mediated endothelial mechanotransduc­
nents through its effect on fibroblasts .12 Application of phys­ tion have showed that effects occur within seconds and in­
ical force through both stress and motion modulates the clude a variety of electrophysiologic and biochemical
synthesis of proteoglycans and collagen by the fibroblasts. 13 responses in the cells. 2s Based on the findings of Quinn et
Mechanical stretching of fibroblasts stimulates their prolif­ al,26 cell-matrix interactions may be an important aspect of
eration 1' and biochemically modifies their resident environ­ the chondrocyte/fibrocyte response to mechanical compres­
mentiS by affecting their synthesis of ECM proteins. 16 sion that might involve macromolecular transport limitations
Mechanical stimulation can alter cellular function, includ­ and morphologiC changes associated with fluid flow and
ing ion transport, such as an influx of extracellular Ca2+, 17 local compaction of the matrix around cells. Fibroblasts ap­
release of second messengers (activation of inositol triphos­ pear to sense force-induced deformations, such as strain, in
phate pathways involving cyclic adenosine monophosphate the surrounding ECM.12 There is further evidence that
and intracellular Ca2+) ,18 protein synthesis,16 and gene ex­ tenascin C, a large ECM glycoprotein modulator that is di­
pression. 19 Mechanical loading is a potent stimulator of gene rectly regulated by mechanical stress via the rapid induction
expression for a wide variety of cellular elements, such as of its messenger RNA in stretched fibroblasts under both in
cell receptors , protein kinases, cell growth/differentiation vivo and in vitro conditions, does not depend on prior pro­
factors, ECM proteins, lipid metabolism, protein metabo­ tein syntheSiS and is not mediated by factors released into the
lism, transcription factors, and binding proteins 20 Further­ medium. 12 Tenascin C plays a role in a variety of lesions and
more, the tensegrity model holds that the cytoskeleton may specifically appears to block adhesion of smooth muscle cells
function to transmit forces or messages of these forces from to fibronectin, an ECM protein that contributes to the struc­
cell surface structures to the nucleus of the cell. 21 Connec­ tural integrity of the ECM. Tenascin C has both adhesive and
tive tissue matrix contains the linear polysaccharide (gly­ antiadhesive properties, depending on the cell type to which
cosaminoglycan) hyaluronan, and the glycosaminoglycans it binds. Integrins are the prinCiple receptors for the ECM;
chondroitin-derma tan sulphate, and keratin sulphate cova­ they bind to tenascin C and serve as transmembrane linkages
lently linked to protein (proteoglycans) Hyaluronan is a between the ECM and the actin-cytoskeleton. lntegrins are
linear polymer consisting of alternating N-acetylglu­ composed of alpha (.) and beta (-,) subunits. Several studies
cos amine and glucuroniC acid residues. Modifications of support that integrins within cell-matrix adhesions act as
chondroitinldermatan and keratin by variable sulfations, for "strain gauges," triggering pathways in response to changes
example, provide for multiple structural variations that in in mechanical stress.27 .28 Mechanotransduction processes in

response to mechanical stresses share many common fea­ General Properties of Connective Tissue
tures with processes in cell adhesion, such as an increase in
tyrosine phosophorylation of proteins in the focal adhesion Connective tissues demonstrate properties of extensibil­
sites. In addition, other cell components, such as intermedi­ ity. The dense regular connective tissues are viscoelastic,
ate filaments, are directly implicated in providing cell re­ displaying both viscous and elastic rheologic properties
silience and in maintaining tissue integrity, each of which has with both time- and frequency-dependent properties. 30.l 1
direct implications for the soft connective tissues. By main­ Creep is demonstrated when the application of a fixed
taining the shape and plasticity of the cell, the intermediate extension to a connective tissue-based structure results in
filament network acts as an integrator within the cell space. the initial stress generated decreasing with time (stress­
The state of mechanical force imposed on the tissue or a cell relaxation), whereas with the application of a fixed stress,
can alter the shape of certain elements of the cytoskeleton the initial extension achieved in the tissue increases with
and thus participate in the control of cell functions 28 The time (load-deformation) (Fig. 2-1). Mechanical creep, de­
studies of Chiquet et aP2 support the idea that cytoskeletal fined as the elongation of tissue beyond its intrinsic exten­
"pre-stress" is necessary for mechanotransduction to work; Sibility resulting from a constant load applied over time, is
relaxation of the cytoskeleton for example by inhibiting Rho­ regarded to playa role in conventional tissue lengthening
dependent kinase suppresses the induction of the tenascin C as a result of a chronic stretching force 32 In creep, the con­
gene by cyclic stretch and hence desensitizes the fibroblasts tinued extension of the material under constant load
to mechanical signals. 12 At the level of the ECM genes, Chi­ means that reorientation due to increasing overall strain in
quet and colleagues l2 have shown that there are related en­ the specimen can occur, driven by the strain energy im­
hancer sequences that respond to static stretch in both the parted to the specimen, which increases with time. 33 Net­
tenascin C and the collagen XII promoter. In the case of the works of fibrous collagen and elastin within these tissues
tenascin C gene, different promoter elements might be in­ are clearly able to reorientate themselves after the applica­
volved in induction by cycliC stretch, identifying that differ­ tion of force. In health, a physiologic increase in stress lev­
ent mechanical signals may regulate distinct ECM genes in els increases collagen formation and content in tendon and
complex ways. 12 ligaments, 13 whereas deprivation of stress causes weakening

Toe region Linear region Yield and failure region
Mechanical loading of connective tissues induces the ex­
pression of ECM and cytoskeletal genes that are involved in
matrix remodeling.29 Fibrillar (elastin, collagen) elasticity 200
under tension forces depends on molecular-based mecha­
nisms. 1 It has been determined that the processes underly­
ing mechanical loading of connective tissues, in particular g
tensile forces, depend in part on force transmission through 'C

beta-1 and alpha-5 integrin subunits and actin filaments , as .3 100

well as the modulation thereof by micro tubules through
mechanotranscriptional coupling of filamin A.29 The elastic­
ity of collagen fibrils and anionic glycosaminoglycans al­ 50
lows for a graduated and smooth response to stresses of
varying degrees.I In contrast, compression stresses are ab­
sorbed via PGs and PG interfibrillar bridges that are also re­ o 1.0 2.0 3.0 4.0 5.0 6.0 7.0 8.0
ferred to as shape modules. Indeed, L-iduronate residues in Deformation (mm)
shape module decoran PGs have been referred to as molec­
ular springs cycling through alternative conformations. I Figure 2-1 Basic stress-strain or load-deformation curve for ten­
don. Source: Woo SL-Y et al. Anatomy, biology and biomechanics
of tendon, ligament and meniscus. In: Simon SR, ed . Orthopaedic
Basic Science. Rosemont, IL: American Academy of Orthopaedic
The Effect of Mechanical Load on Soft Connective Tissues 19

(e.g., disorganization of collagen fibers in tendon) of con­ tic), across which five distinct regions can be further distin­
nective tissue-based structures 34 guished.
The experimental application of stress or mechanical
load on tendon or ligament tissue has been used to observe The Elastic Range: Toe and Linear Regions
the overall gross tissue response of collagen to mechanical
elongation. The mechanical behavior of tendon or ligament The Toe Region
is studied by elongating the structure to the point of rup­
ture while measuring the associated increase in length and When low force loading results in approximately 1.2% to
tension. This phenomenon manifests in the nonlinear 1.5% strain, as occurs in the early elastic range, there is an
stress-strain curves (Fig. 2-2) that are typical of these tis­ initial, temporary straightening of collagen fibers attributed
sues.30 Applied force and resultant elongation are related as to the straightening of the crimp at the level of the collagen
stress and strain, respectively, on these curves. Stress is de­ fascicle 3s .36 This occurs in the toe-linear region of the stress­
fined as the amount of tension or load per unit cross­ strain curve, which is also the region within which physio­
sectional area that is placed on a specimen. Strain is the logic limits of elongation in tendon are defined. There is
elongation of a structure or material that occurs in response restoration of initial length, and the internal fibril crimp is
to stress. As a result one achieves a stress-strain curve that regained on release of stress in the toe region, demonstrating
depicts values of change in length and tension of this the elastic properties of the structure. As can be seen in the
structure. The stress-strain curve of most connective tis­ curve, the relationship between force and elongation in the
sue-based structures has two basic ranges (elastic and plas- toe region is nonlinear. Normal functional range for ligament
and capsules is hypotheSized to be within the toe region 37

The Linear Region

8 B The linear region of the stress-strain curve represents the

behavior of the collagen fibrils (parallel) after the crimp has
7 been removed. 3s .36 The lengthening of ligament or tendon in
this region is still within its phYSiologic limits, as full recovery
.-. 6 of the gross structure occurs on withdrawal of the loading.
Once a tendon reaches the linear region of the stress-strain

E 5

curve, the collagen can be permanently lengthened through
internal micro failure (denaturing and weakening the fibers),
which occurs when the tissue is subjected to excessive strain

and/or temperature. The crimp form is permanently lost
when strain (elongation) exceeds 3% or 4% of the original
length of the structure, where denaturation of collagen fibers
having lost their crimp can be visualized ultrastructurally
Any strain occurring in this region can be attributed to
stretching of the denatured fibers, based on observations
made on discrete collagen fibers taken from tendon and sub­
12.0 15.0 jected to stress. Because deformation to the end of the linear

range is completely reversible, elongation of connective tissue
Linear = ,...!­
into this range. does not cause gross injury, nor does it result
~ ' I' in any macroscopic length increase of the gross structure. 37
Physiologic range - - - - - - ' - - Ligament --1
The Plastic Range: Progressive Failure, Major and

Figure 2- 2 Normal stress-strain curve for ligament illustrating Complete Failure Regions

toe, elastic, and plastic regions. Source: Binkley J. Overview of liga­

ment and tendon structure and mechanics. Implications for clini­ There is a distinct increase in the slope of the curve in
cal practice. Physiother Can. 1989;41(1):24-30. the progressive failure region. There is extensive micro fail­
ure internally; however, the appearance of the tendonlliga­
ment at the gross level remains initially intact. Irreversi.ble

lengthening and failure of ligament or tendon occurs here. sues ranging from the perimysial connective tissue that sep­
It is represented by a decrease in slope of the curve as por­ arates muscle fascicles 33 to the annulus of the intervertebral
tions of the tissue collagen begin to fail, leading to the "yield disc: 2 where there is a cross-ply or cross-helical arrange­
point. " 38 As further stress is applied, a maximal load point is ment of collagen fibers with respect to the long axis of the
reached, whereupon complete failure occurs rapidly Elon­ muscle fiber or craniocaudal axis of the body, respectively
gation into the plastic range results in permanent gross tis­
sue lengthening or complete failure (macro failure), in
which actual rupture of the gross tissue is sustained. Mechanism(s) Underlying A Gain in Connective Tissue
Extensibility Following Loading
Structural Change with Mechanical Force
As stated before, reorientation of collagen fibers due to
If applied in a sufficient amount or for a sufficient length limited extension (force dependence) of connective tissues is
of time, mechanical forces can bring forth structural a well-documented phenomenon 43 Connective tissues also
changes equivalent to those produced by heat or chemical display time-dependent properties that may be more difficult
change. Beyond the more immediate neurobiologic re­ to explain in the acute sense. However, the immediate fas­
sponse of fascial tissues to stress, and under the aforemen­ cial responsiveness to physical pressure or manual therapy
tioned loading conditions, it has been proposed that techniques may be due to a process more likely related to
recovery of the connective tissue proper results from strain target tissue mechanoreceptors as opposed to a mechanical
occurring between collagen molecules (if less than 3%) and process involving more permanent disruption of connective
the minimal displacement of these collagen molecules per­ tissue fibers. It is clear, however, that in the case of abrupt,
mits associated bonds to reorganize. These events would short-term application or sustained long-term application of
not occur at higher strain levels (> 4% strain). stress, micro failure occurs as some individual collagen
When a load is imposed on a connective tissue-based fibers and fiber bundles break, ultimately resulting in more
structure but the stress is removed before rupture (see yield permanent (plastic) elongation of the connective tissue­
phase), the structure recovers its original length with rest or based structure (Fig. 2-3). However, a lack of obvious fiber
when no further load is applied. The structure returns to its reorientation was observed during the time course of either
original length and is said to have "recovered. " Further­ a strong stress-relaxation or a creep transient , indicating
more , it is important to understand that the term recovery that long-range reorientation of collagen fibers is not the
refers only to the return of the tendon or ligament to its only principal structural event associated with the viscoelas­
original length at a macroscopic level and does not rule out tic behavior of these extensible connective tissues." The
the presence of some internal microfailure, that is, in fact, a nonlinear (strain-dependent) nature of the stress-relaxation
clinically desirable effect to regain more permanent and response in these tissues suggests that relaxation processes
local mobility of the connective tissue. both within the collagen fibers themselves and/or at the
One property common to the extensible connective tis­ fiber-matrix (molecular relaxations within the proteoglycan
sues of the musculoskeletal system is that they become pro­ matrix surrounding the collagen fibers) interface may be, in
gressively stiffer as they become extended, and the collagen part, responsible for their viscoelastic nature 4l Therefore,
fibers become aligned with the direction of the stretching. viscoelastic properties of extensible connective tissues may
In order to achieve a permanent elongation of collagen be attributed to phenomena associated within the collagen
fibers, either an extremely forceful stretch of 3% to 8% fiber fibers as well as at the interface between fiber and matrix.
elongation (coincident with some tissue tearing and conse­
quent inflammation) or the imposition of a prolonged
stretch (load deformation) applying a lesser 1% to 1.5% Neurobiologic Response to Connective Tissue Loading: An
fiber elongation (and consequently no minimal inflamma­ Important Piece of the Puzzle
tion) must occur39 •40
Of further interest is the knowledge that collagen fibers Yahia et al44 demonstrated the viscoelastic properties
also present as cross-helical, cross-ply, or quasirandom net­ of lumbodorsal fascia , shOwing clear forces- and time­
works. It is plausible that the strain-induced reorientation dependent viscoelastic phenomena, such as creep, hystere­
of these networks gives rise to the different nonlinear me­ sis, and stress relaxation. It has remained a curiosity to
chanical properties of connective tissue at finite strains practitioners of manual therapy how mechanical loading of
within the extensible connective tissues 4 ! The clinical im­ the fascial tissues , for instance, can effect an immediate re­
plication of loading extensible connective tissue-based sponse that cannot be explained by mechanical properties
structures is thus reflected in the diverse presentation of tis­ of these tissues alone. Purely mechanical properties of con­
The Effect of Mechanical Load on Soft Connective Tissues 21

Loading cycle
Peak loads

1 2 3 4 ...



Figure 2-38 Effect of cyclic loading of tendon. Note that the

stress-strain curve gradually shifts to the right. Typically, after 10
cycles, the curves become quite repeatable and steady Source: Woo
SL-Y et al. Anatomy, biology and biomechanics of tendon, liga­
Elongation ment and meniscus. In: Simon SR, ed. Orthopaedic Basic Science.
Figure 2-3A A typical loading (top) and unloading (bottom) Rosemont, IL: American Academy of Orthopaedic Surgeons;
curve from cyclic tensile testing of knee ligaments. The two non­ 1994:52. ISBN: 0-89203-059-3
linear curves form anyone cycle for a hysteresis loop. The area be­
tween the curves is referred to as the area of hysteresis, and
represents the energy losses within the tissue. Source: Woo SL-Y et
al. Anatomy, biology and biomechanics of tendon, ligament and
sensory receptors are receptive to slow stretch by their in­
meniscus. In: Simon SR, ed. Orthopaedic Basic Science. Rosemont,
fluence on the alpha motor neurons via the spinal cord to
IL: American Academy of Orthopaedic Surgeons; 1994:62.
lower their firing rate and effect a tonus decrease in re­
lated striated motor fibers .45 An ultimate decrease in tonus
of targeted tissues, as might be experienced after deep,
nective tissue plasticity in the short term do not fully ex­ slow, but active stretching (e.g., in Hatha yoga postures),
plain the time-dependent phenomenon following mechani­ as well as other forms of active soft tissue stretching/mobi­
cal loading. Schlei p 45 postulated that there is, if not only in lization that occur when these Golgi receptors become
part, but perhaps an exclusive contribution via the stimula­ stimulated, results in a lowered firing rate of specific alpha
tion of sensory mechanoreceptors, which in turn alter tone motor neurons.· 5 However, passive stretching of myofascial
in motor units (via gamma motor tone) in targeted tissues, tissue does not affect the Golgi tendon organs," because
allowing the tangible sensation of immediate tissue release. the muscle fibers absorb the stretch, in contrast to the ef­
Therefore, the plasticity of connective tissues following fects of dynamic forces imposed on muscle fibers during a
mechanical loading likely encompasses a mechanism be­ contraction. 48
yond solely influencing the mechanical properties of the In addition to the Golgi receptors found in connective
connective tissue proper (Fig. 2-4). Fascia clearly con­ tissue-based structures, such as ligaments and joint cap­
tains a dense network of mechanoreceptors·...6 and, in sules, fascia from thoracolumbar fascia was shown to be
fact, is innervated by four different types of mechanore­ richly populated by mechanoreceptors encompassing large
ceptors that appear to play a role in responding to me­ Pacini's corpuscles and slightly smaller paciniform corpus­
chanical or manual loading techniques. Golgi receptors cles, the smaller and more longitudinal Ruffini's bodies, and
are ubiquitous in dense connective tissues, such as liga­ finally, some interstitial receptors (type III and IV receptors)
ments (Golgi end organs) and joint capsules, as well as at within muscles with their related fascia. 46 In fact, these in­
the myotendinous junctions (Golgi tendon organs). These trafascial mechanoreceptors have been observed in tissues

Tonus change Central

of related skeletal .....~----­ Nervous System
motor units

Proprioceptive function

Palpable tissue .1
Tissue manipulation -------l.~ Stimulation of
response,-. .

\ ~ Global muscle


Interstitial receptors
& Ruffini endings
Local fluid

Intrafascial Autonomic
smooth muscle cells .. Nervous System

Figure 2-4 Flow chart of several processes involved in the neural dynamics of immediate tissue plasticity in myofascial manipulation. The
practitioner's manipulation stimulates intrafascial mechanoreceptors, which are then processed by the central nervous system and the auto­
nomic nervous system. The response of the central nervous system changes the tonus of some related striated muscle fibers. The autonomic
nervous system response includes an altered global muscle tonus, a change in local vasodilation and tissue viSCOSity, and a lowered tonus of
intra fascial smooth muscle cells. Source: Schleip R. Fascial plasticity-a new neurobiological explanation. Journal of Bodywork and Movement
Therapies 2003; 7(2):lO4-116.

ranging from muscle fascia, tendons, ligaments, aponeu­ and IV) found in fascia can be stimulated and consequently
roses, and joint capsules.' Mechanical loading in the form trigger changes in the autonomic nervous system via
of manual touch or passive stretching can in this way changes to the local pressure in fascial arterioles and capil­
speCifically stimulate a connective tissue-based structure laries.'9 Pacinian receptors also seem to be involved in high­
via the alteration in tonus of motor units in muscle units in velOCity manipulation.' Ruffini's endings appear to be
the correspondingly attached muscle and can accomplish mostly stimulated by slow, deep pressure techniques, par­
the clinically reported release or measurable increase in ticularly when tangential force, such as lateral stretch, is
range of motion around a joint. It may be that Ruffini's or­ used. 'o
gans, known to be responsive to tangential pressure, partic­ In general, the viscoelastic material properties of connec­
ularly lateral stretch, and the interstitial receptors (types III tive tissue contribute to its behavior in that when loaded
The Effect of Mechanical Load on Soft Connective Tissues 23

more rapidly, it behaves more stiffly (the material deforms joint and Tissue Mobilization
less) than tissue that is loaded at a slower rate. 51 Sustained
stress is known to produce a higher strain than cyclic stress The repair and maintenance of connective tissues are the
in tendon tissue, with both recovering if the strain is below responsibility of the mesenchymally derived fibroblast,
4%.52 The presence of mechanoreceptors in fascia 44 .46 allows whose activity is regulated, in part, by the mechanical envi­
for a better understanding of why a conditioning stretch ap­ ronment in which it dwells. It is clear that dynamic strain is
plied before loading results in a tissue length increase of integral to cell stimulation and to the healthy organization
0.4% to 0.8% that does not immediately recover on re­ and overall strength of all components of the connective tis­
moval of the 10ad.'2 sue extracellular matrix. The purposes of therapeutic load­
ing of connective tissues are to immediately affect
neurobiologic receptors, in addition to the more long-term
Connective Tissue: Evidence for the Biologic Response syntheSiS of proteoglycans and collagen by fibroblasts; to
to Physical Activity, Exercise, and Joint Mobilization improve the motion of collagen fibers; and to prevent the
development of anomalous cross-links between fibers and
In health, it is clear that the formation and maintenance other macromolecular elements of the extracellular matrix.
of collagen in dense connective tissue is highly dependent As the role of proteoglycans is to attract and hold water
on stress as a physical stimulus. Normal cellular functions molecules, an increase in their syntheSiS theoretically acts to
as well as pathophysiologic changes in numerous condi­ lubricate the connective tissue fibers. It is a goal of thera­
tions in connective tissue-based structures rely on, or as it peutic loading of joints and fascial tissues to ultimately limit
may be, stem from, mechanical changes in the surround­ the number of cross-links formed between fibers and other
ing matrix environment. Consideration of the effects of elements of the extracellular matrix, particularly after tissue
immobilization and conditions of stress deprivation, par­ release techniques.
ticularly in association with trauma to the dense connec­
tive tissues, is of equal clinical significance. Even in the
Continuous Passive Motion on Tissues of Synovial joints
absence of trauma there are many negative effects of im­
mobilization and deprivation of stress on connective tissue
There has been significant effort to determine the ef­
integrity: fects of continuous passive motion on articular cartilage
healing and regeneration, and it is well regarded that the
immediate postoperative institution of a continuous pas­
Exercise sive motion (CPM) machine allows for accelerated heal­
ing of periarticular tissues and prevents adhesions and
In the longer term, mechanical loading of dense con­ joint stiffness in connective tissue-based structures, such
nective tissues, such as a tendon, is known to influence as tendons and ligaments after injury and surgical
local collagen synthesis, and micro dialysis studies have in­ repair. 55 The application of CPM during the early postop­
dicated that mechanical loading of human tendon during erative period was shown to be most beneficial when
exercise or training elevates tendinous type I collagen syn­ there was a slow rate of motion as opposed to a faster
thesis/production and degradation. 53 Degradation of colla­ rate, and 1 week of CPM begun immediately after injury
gen and other extracellular matrix proteins is controlled achieves the same benefits as 3 weeks of CPM, with
through interactivity between matrix metalloproteinases reparative tissue remaining intact at l-year, after surgery.5
and their tissue inhibitors. 54 Findings from one study The use of postoperatively CPM decreased the atrophiC
demonstrated enhanced interstitial amounts of MMPs and changes associated with immobilization and significantly
TIMPs after exercise in human peritendinous tissue in vivo, increased the strength of repair tissue at 6 and 12 weeks
and the magnitude and time pattern of these changes may relative to controls after a medial collateral ligament re­
indicate that MMPs and TIMPs playa role in ECM adapta­ placement using the semitendinosus tenodesis in the
tion to exercise in tendon tissue.54 In uphill running exer­ rabbit model,57
cise, an increased local production of type I collagen in
human peritendinous tissue was observed. 53 Transforming
growth factor-(3I, a potent stimulator of type I collagen Effect ofjoint Motion and Loading
synthesiS, is released from cultured tendon fibroblasts in
response to mechanical loading and is potentially how me­ Houlbrooke et al 58 sought to identify whether the loss of PG
chanical loading and collagen syntheSiS occur in tendon in immobilized nonweight-bearingjoints was due to a lack of
tissue during exercise. 53 compression, a lack of movement, or both. This study showed

that movement alone without weight bearing was in fact suffi­ Therapeutic pressure may provide the initial stimulus for
cient to maintain GAG content, as was weight bearing without the healing cascade, and the application of heavy pressure
movement during a period of immobilization; however, there appears to best promote fibroblast proliferation that may be
was a significant loss in articular cartilage GAG in immobilized of particular Significance for patients with cumulative
and non-weightbearingjoints. 58 Based on these findings, every trauma disorders, such as Achilles tendonitis, rotator cuff
effort to maximize range of motion across joints, even in the tendonitis , golfer's elbow, and tennis elbow. 64
absence of weight bearing, should be made to maintain articu­
lar cartilage matrix and, by extension, all connective tissue­ Joint Mobilization and Manipulation
based structures. In addition, this study identified that weight
bearing alone is equally beneficial in maintaining the integrity Therapeutic loading of connective tissues, in the form of
of articular cartilage matrix under conditions in which there is mobilization and manipulation, is used primarily to relieve
an immobilized joint (as in the case of a casted or splinted pain and increase mobility of joints. 66 .67 The application of
limb). mechanical loading through graded manual therapeutic
techniques is often directed toward restoring the subtle mo­
Passive Physical Tissue Mobilization tions between joint surfaces, including the arthrokinematic
motions of spin, glide, and roll."" Graded mobilizations are
Passive physical mobilization of specific connective small-amplitude passive movements that aim to accomplish
tissue structures, such as in deep friction massage, has a gliding or traction at or within a joint. 66 The effect of
been used in the management of soft tissue conditions, graded mobilizations applied at the end of the available
such as acute and chronic tendonitis. 59 Although deep arthrokinematic range of motion is to elongate connective
friction massage is used to augment ligament and tendon tissues, as opposed to those applied at the beginning of the
healing and repair,60 the underlying mechanisms are not available range, which intend to treat pain through activa­
well understood . Physiologic effects of soft tissue friction tion of neural structures."" The structures that tend to
techniques include local hyperemia, massage analgesia, shorten and in turn limit joint excursion include ligaments,
and reduction of adherent scar tissue 61; in the case of joint capsules, and periarticular fascia. The impact of repet­
acute tendonitis, the effects are to accelerate tendon heal­ itive, low-stress, small-amplitude movements that are com­
ing by propelling the inflammatory process to comple­ ponents of mobilization is that synOvial fluid may be
tion, which then encourages subsequent stages of healing distributed across articular cartilage and the intervertebral
to ensue. 62 The intent of friction massage is to obtain or disc , allowing joint lubrication, as well as the cell's experi­
restore mobility within speCific sites of connective tis­ ence of movement on the periarticular joint structures, such
sue-based structures and to prevent the formation of ad­ as ligaments and capsule.'5.68
hesions after injury to these structures. 59 The technique
requires the transverse application of deep localized mas­ Mobilization: The graded mobilizations applied in the
sage to speCific structures that varies in length and force, range of Maitland grades I and II are applied with the in­
depending on the acuteness of the injury and the phase tent to relieve pain but not to permanently elongate con­
of healing. 60 The impact of friction massage ranges from nective tissues M Mobilization of joints within this range
modulation of synthesis of matrix components of con­ are considered to work within the "toe region" of the struc­
nective tissues (inflammatory to repair phase) to alter­ ture's stress-strain curve and clinically may be referred to
ation of scar formation by influencing the laying down of as "taking out the slack," 67 because there is temporary re­
new collagen fibers and intermolecular cross-linking lief of the crimp within the structure itself. At higher
processes and encouragement of connective tissue lubri­ ranges of graded mobilizations (Maitland grades III and
cation (repair to remodeling phases). IV), loading affects the length of connective tissues
Augmented soft tissue mobilization techniques may fa­ through the process of internal microfailure mechanisms
cilitate tendon healing via the recruitment and activation of that result in a change in the resting length of connective
fibroblasts that ultimately promote healing and early recov­ tissue through plastiC deformation. Microfailure implies
ery of limb function 63 In one study in which augmented that there is physical disconnection of some of the individ­
soft tissue mobilization techniques were applied to inflamed ual collagen fibers and bundles as a result of progressive
tendons, stimulation of fibroblast proliferation was depend­ loading and ultimate tissue deformation that results in per­
ent on the magnitude of the pressure applied.64 Fibroblast manent lengthening of tissue. This corresponds to the lin­
proliferation and activation are key events in the tendon ear to end-linear phase of the structure's stress-strain
healing process and are responsible for the production of curve. This microfailure is considered a form of "therapeu­
cellular mediators of healing and synthesis of collagen. 65 tic damage" to the connective tissue that is necessary to ac­
The Effect of Mechanical Load on Soft Connective Tissues 25

complish permanent lengthening. This therapeutic damage Periarticular Tissues: Biologic Response to
affects physical relationships between collagen, associated Immobilization
macromolecules, and ground substance of the ECM and
subsequently results in a known cycle of tissue inflamma­ The biochemical composition of periarticular connective
tion, repair, remodeling, and consolidation. tissues follOwing periods of enforced joint immobilization
reveals a significant loss of water, hyaluronic acid, chon­
Manipulation: Both manipulation and mobilization of droitin-4 and chondroitin-6 sulfate. 73 .74 Immobilization of
joints entail passive joint movements, during which the the knee joint for 9 weeks resulted in a reduction of the me­
joint or joint complex is taken through a speCific range chanical properties of the lateral collateral ligament, with a
of motion. Although mobilization encompasses low­ specific reduction in ligament stiffness. 75 Furthermore, an
velocity movements within or up to the limit of the range increase in collagen turnover (synthesis and degradation)
of motion of a joint, manipulation involves a low­ was found in the immobilized medial collateral ligament
amplitude , high-velocity thrust at the limit of the joint and patellar tendon, with the associated reduced stiffness at­
range, with the intent to briefly move the joint beyond tributed to a change in ligament substance itself rather than
the point of restriction, and ultimately effecting connec­ to tissue atrophy 75
tive tissue micro failure in the late linear region of the These findings are relatively uniform across connective
stress-strain curve. tissue-based structures, such as tendon, capsule, ligament,
and fascia," and it has been demonstrated that collagen
mass may decline by 10% and collagen turnover increase
with accelerated processes of degradation and synthesis
under conditions of immobilization. 76 In tissues such as lig­
aments that are recognized for their relatively high order of
The adverse functional effect of prescribing immobi­ fibril arrays in health, any new fibrils formed under condi­
lization for musculoskeletal ailments was noted as early as tions of immobilization display a disordered arrangement,
the 19th century 69 The complete biologic basis for the link which results in a change in overall physical properties, in­
between application of load and the cellular and meta­ cluding a reduced ultimate load to failure of the tissue. 76 In
bolic response continues to remain open to investiga­ tissues such as synovium and capsule, which are inherently
tion H .53.54 Motion inflicted too early after injury or repair more extensible, the disordered deposition of fibrils appears
of connective tissues can have detrimental effects by exac­ to impede flexibility by prodUCing fiber-fiber gliding im­
erbating the inflammatory reaction and may even damage pediments at speCific points along the structure and is
repair tissue, leading to failure of the healing process. thought to occur because of the absence of the usual con­
However, when connective tissue-based structures are de­ trols on orientation of matrix imposed by physical forces. 76
prived of stress, significant morphologic, biochemical, and In addition, a Significant decrease in the proportion of
biomechanical changes occur. There are clinical circum­ smaller, cross-sectional area collagen fibrils as well as a sig­
stances that involve immobilization of joints and associ­ nificant increase in the proportion of larger-diameter colla­
ated periarticular connective tissue structures that are gen fibrils may occur after immobilization, findings
impossible to avoid (as in the case of casting and splinting attributed to decreased synthesis and degradation of colla­
of underlying injured sites) , with the natural consequence gen during immobilization." Collagen fibril size and den­
of a stiff joint with restricted motion. Even in cases of sity have been shown to be altered with increased levels of
short periods of immobilization, as might be indicated mechanical stress. After immobilization, ligaments reach
after a simple elbow dislocation, splintage of the reduced their linear and maximum stress at lower-than-normal lev­
elbow for 2 weeks was noted to enhance patient comfort els of applied forces, indicating that ligaments become more
and did not adversely affect the eventual outcome, compliant and ligament laxity and complete ligament fail­
whereas splintage for over 3 weeks resulted in worse func­ ure may occur with comparatively low levels of force. "·"·78
tion at 6-month follow-up .7o In extreme cases, alterations Noyes et al" were able to demonstrate the change in the re­
associated with prolonged immobilization of a joint may lationship between load and ligament elongation after im­
lead to full restriction of joint motion and subsequent mobilization measured in terms of a decrease in ligament
intra-articular ankylosis, typically occurring within a pe­ stiffness (slope of the load-deformation curve) or as an in­
riod of time in excess of 1 year. 71 Furthermore, contrac­ crease in ligament extenSibility (compliance or elongation
tures occur more frequently, after less trauma, and after per unit load) that was related to the degree of immobility
shorter periods of time in older individuals than in imposed. In fact, reduced load-to-failure to about one third
younger individuals n of that of normal controls is evident at the bone-ligament

bone complex after periods of immobilization. 76 •79 There­ The development of joint contractures is commonly ob­
fore, it is critical that sufficient time is permitted for the served after immobilization with splints or casts; however,
healing of soft tissues, that undue forces are avoided in the other mechanisms include neuromuscular disorders with
early phases of healing, particularly after removal of casts, muscle imbalance; disorders causing joint pain, such as
and that there is appropriate strengthening of supporting trauma, sepsis, inflammatory disorders, degenerative proces­
muscles after injury to allow the optimal healing and repair ses, and congenital disorders; as well as prolonged bed rest
of injured ligaments to occur. and a variety of disturbances that result in mechanical incon­
gruity of joint surfaces and shortening of soft tissues. 76 Neuro­
muscular conditions, immobilization, muscle weakness or
paralysis and spasticity are the three main factors leading to
the development of contractures variously affecting the joint
Contractu res itself, the contractile tissue, and/or the connective tissue. 8> A
general loss in lubricating and buffering volume of water and
Extended periods of immobilization negatively affect the glycosaminoglycans in concert with increased inter- and in­
health of joint complexes and ultimately manifest in functional tramolecular cross-links of collagen contribute to joint stiffness
limitations that are associated with joint contractures. The ex­ and a loss of viscoelastic properties of soft connective tissues. 9
cessive intermolecular cross-links interfere with joint extensi­ Therefore, both qualitative and quantitative changes in the pe­
bility and do not allow free gliding between fibers or between riarticular collagenous structures around a joint occur because
the fibers and other components of the ECM. Development of of a lack of mechanical loading and movement across the
joint contracture often results in loss of independence and ex­ joint. The deposition of collagen at focal points in relation to
tremity function , as well as impairment of gross motor tasks, the capsule and ligament structures may restrict joint motion
such as ambulation, seating, and ability to transfer. by not being properly aligned and may ultimately produce an
A number of periarticular structures are implicated when effective shortening of the connective tissue-based structures.
a joint is described as having a contracture, including the
joint capsule and ligaments, as well as the muscles and their Management of Soft Tissue Contractures: The Impact of
tendons that adapt to an altered joint position. It is appreci­ Mechanical Loading
ated clinically that connective tissue homeostasis is nega­
tively disrupted, resulting in changes in fibrous structures, The two main factors contributing to the development
when diarthrodial joints are subjected to prolonged periods of contractures are (1) the myogenic restriction caused
of immobilization. In particular, it has been shown that im­ by the muscle and its related tendon and fascia, and (2)
mobilization across joints following conditions of muscu­ the arthrogenic restriction caused by bone, cartilage,
loskeletal trauma causing inflammation triggers contracture synovium, capsule, and ligaments. 86 In a controlled
formation more rapidly and to a greater extent than that study, the components of arthrogenic versus myogenic
caused by immobilization without superimposed trauma. 79 impediments to range of motion at different times after
In contrast to conditions of immobilization alone, when joint immobilization pointed to an increased role of
there is trauma to connective tissue-based structures, fibro­ arthrogenic changes contributing to the limitations after
plasia and excessive scar formation contribute independ­ immobilization, especially as the period of immobility
ently to early contracture formation. There may be several extended beyond 2 weeks. 86 During immobilization, con­
mechanisms underlying the development of a contracture nective tissue is lost at a slower rate than contractile
and ultimate restriction in the range of motion of an af­ tissue ; therefore , there is a relative increase in the pro­
fected joint. Damage incurred at the synovium, capsule, portion of connective tissue in a muscle after a period of
cartilage and bone appear to greatly contribute to joint stiff­ immobilization B7 When joints are immobilized for any
ness after long-term immobilization. The proliferation of length of time , the connective tissue of joint structures
intra-articular connective tissue (pannus) and the associated loses its extenSibility, allowing the development of ab­
adhesions formed in its association with cartilage B0-82 ; an in­ normal cross-linking between connective tissue fibers.
crease in cross-linking between collagen fibrils, the ECM, or Forced motion of contractures causes physical disruption
lack of hydration between collagen fibers 83-<l5 ; as well as of the adhesions between gross structures, the intermole­
adaptive shortening of the joint capsule79 are all potential cular cross-linking, or both, between fibers in periarticu­
contributors to joint contracture. With prolonged immobi­ lar connective tissue. 13 In a classic experiment, when
lization of a joint, fibro-fatty connective tissue proliferates subjected to load and heat , the viscoelastic characteris­
and encroaches the joint space; these changes are first seen tics inherent to contracted connective tissue of tendon
by 2 weeks after immobilization. made it the most responsive to the combined application
The Effect of Mechanical Load on Soft Connective Tissues 27

of a sustained low load and high temperature within the toskeleton to transmit forces or messages of these
therapeutic range (up to 45°C) to achieve the greatest in­ forces from cell surface structures to the nucleus of
crease in length of the soft connective tissue. 88 the cell. 2! In this way, mechanical force imposed on
the tissue or a cell can alter the shape of certain ele­
ments of the cytoskeleton and thus participate in the
control of cell functions. 28 Different mechanical Signals
may regulate distinct ECM genes in complex waysl2
1. The impact of therapeutic physical loading on dense by inducing the expression of ECM and cytoskeletal
connective tissues results in both (a) immediate and genes that are involved in matrix remodeling. 29
(b) more long-term, sustained effects. 4. Mechanical stretching of fibroblasts stimulates their
• Stimulation of mechanoreceptors causes a more proliferation!4 and biochemically modifies their resi­
immediate change in viscoelastic deformation of dent environment!5 by affecting their syntheSiS of ECM
fascia via stimulation of sensory mechanoreceptors proteins. !6 Substances such as transforming growth
that in turn alter tone in motor units (via gamma factor-[31, a potent stimulator of type I collagen syn­
motor tone) in targeted tissues, allowing the tangi­ thesis, are released from cultured tendon fibroblasts in
ble sensation of immediate tissue release. s" s In fact, response to mechanical loading and may contribute,
fascia is innervated by four different types of in part, to the mechanism underlying how collagen
mechanoreceptors that appear to playa role in the syntheSiS occurs in tendon tissue during exercise. 53 Fi­
immediate response to mechanical or manual load­ broblasts appear to sense force-induced deformations,
ing techniques. Mechanical loading in the form of such as strain, in the surrounding ECM.!2 The mecha­
manual touch or passive stretching can in this way nism(s) underlying this speCifically involve:
specifically stimulate a connective tissue-based a. Altered cellular function, including ion transport!7
structure via the alteration in tonus of motor units b. Release of second messengers!8
in the correspondingly attached muscle and ac­ c. Protein synthesis!6
complish the clinically reported "release" or meas­ d. Gene expression!9
urable increase in range of motion around a joint. 5. Tenascin C is an ECM component (glycoprotein) di­
rectly regulated by mechanical stress via the rapid in­
• The aim of therapeutic deformation of collagen­
duction of its messenger RNA in stretched fibroblasts
based structures is to cause increased freedom of
under both in vivo and in vitro conditions. It has both
movement by affecting their ultrastructural charac­
adhesive and antiadhesive properties, depending on the
teristics between both collagen fibers and the ma­
cell type, and binds to fibronectin and integrins. Inte­
trix (ECM) in which they are embedded.
grins are the prinCiple receptors for the ECM and serve
• It is a goal of therapeutic loading of joints and fas­ as transmembrane linkages between the ECM and the
cial tissues to ultimately limit the number of cross­ actin cytoskeleton. Therefore, mechanical loading may
links formed between fibers and other elements of regulate the production of ECM proteins indirectly, by
the extracellular matrix to prevent the formation of stimulating the release of a paracrine growth factor, or
adhesions after injury to these structures,S9 particu­ directly, by triggering an intracellular (fibroblast) Signal­
larly after tissue release techniques. ing pathwai2 that activates gene expression for a spec­
2. The interrelationship of the cellular components (e.g., trum of cellular elements, including cell receptors,
fibroblast) and the ECM it manufactures is well recog­ protein kinases, cell growth/differentiation factors,
nized. loading of connective tissue cells maintains the ECM proteins, lipid metabolism, protein metabolism,
functionality of the matrix of the dense connective tissue tranSCription factors, and binding proteins 10
structure. It can modulate the syntheSiS of proteoglycans 6. Physiologic effects of soft tissue friction techniques (as
and collagen by the fibroblasts, and a phYSiolOgiC in­ a form of localized mechanical stimulation) include
crease in stress levels increases collagen formation and local hyperemia, massage analgeSia, and reduction of
content in tendon and ligaments.13 Fibroblast prolifera­ adherent scar tissue 6!; in the case of acute tendonitis,
tion and activation are key events in the healing process the effects are to accelerate tendon healing by pro­
of connective tissue-based structures and are responsi­ pelling the inflammatory process to completion,
ble for the gene expression and thereby production of which then encourages subsequent stages of healing
cellular mediators of healing and syntheSiS of collagen. 65 to ensue 62 The impact of friction massage ranges from
3. By way of the tensegrity model, mechanical loading modulation of syntheSiS of matrix components of
on the fibroblastlchondroblasts stimulates the cy- connective tissues (inflammatory to repair phase) to

alteration of scar formation by influencing the laying 12. Chiquet M, Renada AS , Huber F, Fluck M. How do fibroblasts trans­
down of new collagen fibers and intermolecular cross late mechanical signals into changes in extracellular matrix produc­
tion? Mallix Bio!. 2003;22:73-80.
linking processes and encouragement of connective
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Extremities & Lumbar Spine



The Shoulder
Warren 1. Hammer

To remain the most mobile joint in the body, the shoulder Coronal (Frontal) Plane
must sacrifice stability Except for the superior coracohumeral
ligament, the shoulder does not have the strong ligaments and Impure Swing: According to Kessler and Hertling,4 full
capsule that stabilize all other human jOints. l The muscles elevation of the humerus in sagittal flexion and coronal ab­
therefore have the dual function of providing mobility and sta­ duction is an impure swing because for full abduction, the
bilization. The shoulder has been likened to a golf ball sitting humerus must rotate approXimately 90 of external rotation
on a tee, necessitating a delicate interplay between capsu­ on its long axis. 5 It is impossible to elevate the arm fully in
loligamentous structures and the musculotendinous rotator this plane with the arm in internal rotation. During abduc­
CUff2 When we think of the shoulder, we must include, the tion in this plane at about 1200 , the arm automatically ro­
acromioclavicular joint, the sternoclavicular joint, and the tates externally A normal limitation of end-range elevation
scapulothoracic functional joint, in addition to the gleno­ is due to abutment of the undersurface of the supraspinatus
humeral joint. Some consider the extracapsular space between tendon against the superior glenOid fossa , limiting eleva­
the coracoacromial arch and the greater tuberosity another tion. l This is a reason why end-range pain of passive coro­
functional joint 3 Normal shoulder motion is dependent on nal abduction may indicate supraspinatus irritation at the
normal movement of these articulations. Synchronized move­ articular side rather than the bursal side (see Functional Ex­
ment also requires normal capsular and ligamentous flexibility, amination of the Shoulder, Passive Testing).
along with the balance of muscles. Scapular motion must also
be included in evaluation of the shoulder joint because scapu­ Lateral Rotation Mechanics of the Humerus in the Coro­
lar motion provides optimal muscle length-tension ratios and nal Plane of Abduction: During early abduction, the ante­
reduces the muscular energy requirements of the rotator cuff rior capsule is forced into a twisted position and exerts an
during arm motion. Of equal importance is the function of the external rotation moment. As abduction progresses, the ex­
scapula as part of the kinetic chain. Our examination therefore ternal rotation untwists the capsule and allows further abduc­
must include all the elements, not only pertaining to the tion.6 The twisting of the anterior capsule is associated with
scapulohumeral area but also the whole kinetic chain, such as tightening of the inferior glenohumeral ligament (IGHL) ,
the spine, hips, and trunk. which limits coronal elevation to 900 . Gagey et all stated that
to continue elevation beyond 90 the tension of the IGHL

PERTINENT FUNCTIONAL ANATOMY AND causes the humerus to move toward the scapular plane.
Reasons for Lateral Rotation in the Coronal Plane: It
Shoulder Elevation used to be thought that lateral rotation was necessary to
clear the greater tuberosity from the acromion and cora­
Shoulder elevation occurs in three major planes-coro­ co acromial ligament 8 Walker9 stated that this is not true,
nal, scapular, and sagittal (Fig. 3-1) because external rotation was really necessary for the greater


Figure 3-1 Planes of elevation. A) coronal; B) scapular; C) sagittal. Source: © 1990, David Bolinsky.

tuberosity to clear the glenoid to prevent impingement of 2. The length-tension relationships of the deltoid and
the humeral head on the glenoid rim. 10 Recent evidence!! of cuff muscles are optimal, thereby facilitating optimal
superior glenoid impingement agrees with Walker. muscle force.
3. Greater external rotatory force and less compressive
force are exerted because the scapular attachment of
Humeroscapular Motion: Humeroscapular motion
the infraspinatus and teres minor is more posterior
may also be limited in abduction because of bony contact of than normal to the glenohumeral joint axis in this
the proximal humeral shaft against the acromion.! plane. The lengths of these muscles are increased (op­
timal length-tenSion relationships) , increasing their
Scapular Plane: The arm is raised 30° to 45° anterior rotatory force.
to the coronal plane, which is the normal resting position of
the scapula. This is a most favorable range of motion be­ Patients with painful shoulders due to subacromial le­
cause (1) the mechanical axis of the humerus approximates sions (bursitis, rotator cuff, or biceps injury) automatically
the mechanical axis of the scapula l2 ; (2) the inferior part of elevate their arms in the scapular plane to reduce the stress
the capsule is lax, and no appreciable humeral rotation is of other elevating positions. R. f Warren , MD performs pas­
required as in the coronal plane, where the capsule is sive motion testing in this plane because it is the position of
twisted; and (3) the deltoid and supraspinatus are optimally maximum motion (personal communication, March 1995).
aligned for elevation of the arm,13 thereby avoiding sub­ The arm should be as close as possible in the plane of the
acromial impingement during arm abduction. scapula during the throwing motion.
This plane of motion is recommended in rehabilita­
tion 14 ,l 5 for these reasons:
Sagittal Plane (Forward Flexion)
1. In the coronal plane, the anterior capsular structures
are tensioned, which may complicate soft tissue heal­ In the sagittal plane, an impure swing is produced in
ing. Excessive motion in the coronal plane may put which the humerus must rotate medially on its long axis for
overload on the anterior cuff tendons. full elevation. The capsule is put under tension.
The Shoulder 35

Clinical: Because lateral rotation is necessary before Scapulohumeral Rhythm

full coronal abduction is attainable, in conditions involving
limited abduction due to adhesive capsulitis or muscle con­ Normal scapular motion consists of substantial rotations
tracture, stretching procedures initially should be directed around three axes, not simply upward rotation 17 (see
toward improving lateral rotation. The infraspinatus and Scapular Dyskinesis). The scapula hardly moves during the
teres minor should be checked for flexibility and strength first 30° of humerothoracic elevation. During the first 30° to
because they are also responsible for producing the neces­ 50° of humeral abduction or flexion , the scapula is in a set­
sary external rotation for arm elevation. ting phase but moves laterally. Motion is localized at the
glenohumeral joint, but after 50° of abduction, the scapula
True Glenohumeral Motion during Flexion and Extension: rotates about a fixed axis through an arc of approximately
If the scapula is anchored, true glenohumeral flexion is about 65° as the shoulder reaches full elevation. The exact ratio of
90° (Fig. 3-2A) and extension is about 45° (Fig. 3-2B). glenohumeral motion to scapulothoracic upward rotation
motion is debatable, depending on how the study was
measured. Jobe et aP8 stated that in the scapular plane, the
SCAPULOTHORACIC MOTION scapulohumeral movement totals 3:2 , with a 4:1 ratio dur­
ing the first 30° of humeral abduction and 5:4 during the
remaining abduction.
Scapular Instantaneous Center of Rotation
In a study by McQuade and Smidt 19 the above scapulo­
humeral rhythm ratios were found to be "overly simplistic"
Determining instantaneous center of rotation (ICR)
because the above ratios did not calculate the rhythm ratios
identifies the true actions of the scapular rotator muscles,
when the arm was loaded. "Light shoulder loads caused an
Figure 3-20 6 represents a model that varies somewhat
increase of the scapulohumeral rhythm (decreased scapular
between individuals. In Figure 3-2A, during the begin­
motion) from 3.1:1 to 4.3:1 as the arm was elevated. Heavy
ning phase of arm abduction , the upper trapezius and
shoulder loading resulted in an increasing scapulohumeral
lower serratus anterior are working harder than the mid­
rhythm from 1.9:1 to 4.5:1 as the arm was elevated. " 19
dle and lower trapezius because of their longer force arms
although in some people, the ICR shifts earlier, indicating
increased activity of the lower trapezius. In Figures 3-2B Scapular Rotation
and C, during the phase of arm abduction from about 82°
to 139°, the ICR migrates from the root of the scapular The greatest relative amount of scapular rotation occurs
spine toward the acromioclaricular joint with increased between 80° to 140° of arm abduction.16 The scapula dur­
activity of the lower trapezius because of the increased ing arm elevation tilts posteriorly and rotates medially (su­
length of its force arm, espeCially as the arm moves past perior angle) and upwardly McClure et apo found increased
90° abduction. At the end of phase C, there is more gleno­ scapular external rotation during humeral elevation, occur­
humeral motion occurring than scapular rotation . At the ring mostly beyond 90° elevation and increasing dramati­
end of phase C, the rotatory force of the upper trapezius cally at the end range . This concept of increased external
has diminished (shorter moment arm) while the force rotation of the scapula differs from the concept of the
arms of the lower trapezius and lower serratus anterior scapula protracting (internally rotating) during shoulder el­
have not decreased in length and are the main upward ro­ evation, as is usually taught. The authors believe that exter­
tatory force couples acting on the scapula. The middle nal rotation of the scapula may lessen the need for
trapezius acts as a stabilizer to retract the scapula. The glenohumeral rotation at end-range elevation. Scapular mo­
lower trapezius also retracts the scapula but at the same tion is important in reaching humeral end-range external
time creates a strong upward rotatory force. As the arm rotation in order to reduce stress on the glenohumeral joint
approaches the vertical position, phase three , (Fig. 3-2C) , capsule. Without this scapular motion, it is possible that
increased upper trapezius and levator scapulae activity there would be increased demands on the glenohumeral
prevents excess depression of the shoulder girdle and ro­ joint, leading to eventual capsular laxity and anterior insta­
tates the acromion , thereby creating more space in the bility They also think that the scapular external rotation is
subacromial space. Swimmers who use the butterfly stroke influenced by the contour of the ribs.
and have weak upper trapezius and/or lower serratus an­ Scapular rotation occurs through action at the acromio­
terior fail to get the acromion out of the way and create a clavicular and sternoclavicular joints (see Sternoclavicular­
repetitive impingement. During phase 3, there is increased Acromioclavicular Motion). Force couple (two forces of
activity of the lower serratus anterior and lower trapezius. equal magnitude in opposite directions that rotate a body)


Upper Trapezius

Middle Middle
Trapezius Trapezius

Lower Lower Lower Lower

(a) Trapezius Serratus Anterior (b) Trapezius Serratus Anterior

Upper Upper
Trapezius Trapezius Deltoid

Middle Middle
Trapezius Trapezius

Lower Lower Lower Lower

(e) Trapezius Serratus Anterior (d) Trapezius Serratus Anterior

Figure 3-2 A, True passive glenohumeral flexion (908) is determined with the scapula anchored. B, True passive glenohumeral ex­
tension (458) is determined with the scapula anchored. C , A biomechanical model of scapular rotation during beginning of first phase
of arm abjuction (a), beginning of second phase of arm abduction (b) , beginning of third phase of arm abduction (c) , and full arm ab­
duction (d). As arm abduction progresses, the scapular ICR (+ with circle around it) migrates from the root of the scapular spine to­
ward the acromioclavicular joint region and alters the length of the rotary force arms (broken lines) of the upper, middle, and lower
serratus anterior. Source: Bagg SD, Forrest W]. A biomechanical analysis of scapular rotation during arm abduction in the scapular
plane. AmericanJoumal of Physical Medicine and Rehabilitation. © 1988, vo!. 67, no. 6, pp. 238-245. Williams &: Wilkins, 1988.
The Shoulder 37

for elevating the scapula and allowing scapular stabilization trapezius , rhomboid, levator scapulae, and serratus ante­
are the upper and lower portions of the trapezius working rior. Group 2 includes the extrinsic muscles of the shoul­
together with the rhomboid muscles, paired with the serra­ der-the deltoid , biceps, and triceps . Group 3 consists of
tus anterior muscle. There is recent evidence that the upper the intrinsic muscles-the four muscles that make up the
trapezius does not elevate the scapula and may not act as a rotator cuff. In order for the above muscles to function ef­
force couple with the lower trapezius, because the upper fiCiently, both concentrically and eccentrically, the scapula
and lower fibers of the trapezius do not act in opposite di­ must be firmly anchored by the scapular (group 1) stabi­
rections (see Trapezius and Levator Scapulae under the lizer muscles. Acting as a stable anchor for the muscles
heading Clinical Review of the Shoulder Muscles) .21 Differ­ helps to maintain the normal resting length of the at­
ent force couples come into play, depending on the particu­ tached muscles (optimal muscle length/tension) , espe­
lar activity. cially the deltoid, by maintaining the muscle length of the
muscle origins from the approaching insertion. Maximum
tension in a muscle develops when the muscle's length
reaches 90% of its maximum length 23 Reduced tension of
SCAPULAR POSTERIOR TILTING the attached muscles causes them to work less effiCiently,
and all phases of the thrOWing motion are affected. Weak­
During humeral elevation, most of the posterior tilting ness of the parascapular muscles allows for increased lat­
occurs after 90° and sharply increases at the end range. Pos­ eral scapular motion. Weakness of cuff muscles results in a
terior tilting may be important in order to allow the lack of required humeral head depression during shoulder
humeral head and rotator cuff tendons to clear the anterior elevation by the subscapularis and infraspinatus and nec­
aspect of the acromion during elevation. Subjects with im­ essary abduction and external rotation created by the
pingement had about 10° less posterior tilting than asymp­ supraspinatus and deltoid. 22 Eventual functional shoulder
tomatic subjects. Posterior tilting of the scapula may also be impingement may result (see Impingement Syndrome,
related to the posterior rotation of the clavicle (40°) along Functional Causes).
its long axis, which occurs mostly after 90° of humeral ele­ "If the scapula is abnormally mobile , the origin and in­
vation (see Scapular Retraction Test)17 sertion points of the muscles may be reversed so that the
distal ends of the muscles are more stable and less force is
developed," 22 that is, for overhead thrOwing, tennis serve,
and the like. In this case, the scapula is pulled laterally by
ROLE OF THE SCAPULA the muscle, which would be contracting from the more sta­
ble distal end on the humerus rather than from the proxi­
Increases Joint Stability mal end on the scapula, resulting in scapular dyskinesis and
lateral scapular slideY The dysfunctional (less anchored)
The scapula, especially in the throwing shoulder,5,17,22 scapula tends to slide laterally and therefore reduces the
increases joint stability by plaCing the glenoid fossa under normal length/tension curve of the attached muscles (mus­
the humeral head , serving as a stable base for glenohumeral cle fibers shorten) , which results in decreased muscle effi­
function . Throughout shoulder movement, it is necessary ciency regarding eccentric and concentric contractions.
that the instant center of rotation is maintained between the Decreased muscle efficiency of the cuff and scapular mus­
glenOid and the humeral head, creating a congruency (see cles and lack of scapula stability may eventually be an im­
Mechanisms ResponSible for Concavity Compression) of portant dynamiC factor causing shoulder instability.
the glenohumeral articulation. Without the maintenance of
a congruent joint stability, there is an increased tensile stress Removes the Acromion from the Path of the Elevating
on the capsular ligaments, resulting in excessive stretch Humerus
during the throwing motion22 and eventual instability and
possible impingement syndrome. With maximum abduction, the acromion is elevated
about 36°24 The scapula must rotate in the cocking and ac­
Acts As a Base for Muscle Attachment celeration phases to clear the acromion from the rotator cuff
to decrease impingement and coracoacromial arch compres­
Kibler 17 divided the muscles attached to the scapula sion. Almost all thrOwing occurs between 85° and 100° of
into three groups. Group 1 consists of the muscles con­ abduction, where the acromion must be tilted up to prevent
cerned with stabilization and rotation of the scapula-the cuff impingement. 17

During the Throwing Motion Must Be Able To Retract

and Protract around the Thoracic Wall

During the windup and cocking phase of the throwing

motion, scapular retraction occurs to build up the stored en­
ergy in the anterior muscles to allow for a change of muscle
contraction from eccentric to concentric for the anterior mus­
cles and concentric to eccentric for the posterior muscles.
During the acceleration and follow-through phase, full Figure 3-3 Shock-absorbing function of the scapula. The recoil
scapular protraction is necessary to prevent excessive over­ mechanism of the scapula absorbs impacts of blows to the shoul­
load injury of the posterior structures that decelerate (ec­ der, a mechanism that the hip joint lacks. Source: Reprinted with
centrically contract) the anterior structures. During pennission from Clinical Orthopaedics (1961 ;20:41). © 1961 , JB
acceleration, the scapula protracts laterally and then anteri­ Lippincott Company
orly around the thoracic wall, thus allowing the scapula to
maintain a normal position with the humerus 17
Kibler l7 wrote that loss of coordinated retraction/pro­
traction during throwing causes a functional anteversion or clear the humeral head away from the inflammatory or de­
opening up of the anterior aspect of the glenohumeral joint generative lesion. Scapulothoracic motion can be evaluated
during external rotation, thereby removing the normal ante­ on shoulder inspection (see Scapular Dyskinesis).
rior bony buttress. This may result in stress to the anterior Scapular movement, which is responsible for one third
labrum and ligaments. of shoulder motion, must always be considered in every
shoulder problem. Electromyographic (EMG) analysis of
shoulder function in tennis players showed that in the
Acts As a Link in the Kinetic Chain of the Throw serve, forehand, and backhand strokes, the serratus anterior
was essential; because the serve in tennis is similar to the
The scapula acts as link in the kinetic chain of the throw overhand throw, this muscle is especially important for
that transfers large forces and energy from the legs , back, pitchers as well. Ryu and colleagues27 stated that efficient
and trunk to the arm and hand. In tennis players who serve serratus anterior function is essential in stabilizing the
with their feet and body off the ground, the entire base of scapula against the thoracic wall and in rotating the scapula
stability is transferred from the feet to the scapula 17 Scapu­ to form a stable platform against which the humeral head
lar dyskinesia prevents the normal transfer of energy, result­ can move. Fatigue of the serratus anterior muscle may en­
ing in a higher level of activity of the distal arm to danger scapulothoracic-glenohumeral synchrony and lead
compensate for the loss of proximal force and therefore in­ to abnormal compensatory biomechanics.
creased distal strain (see Scapular Dyskinesis). The most important upward rotators of the glenOid are
the trapezius and the serratus anterior. Perry28 explained
that although both these muscles are almost of equal size,
Acts As a Shock Absorber EMG analysis during swimming shows that the serratus
works at 75% of its maximum, whereas the trapezius works
The scapula acts as a shock absorber because of its abil­ from 34% to 42% of its maximum. She stated that a 75%
ity to recoil and absorb the impact when there are direct workload of the serratus during prolonged swimming can­
blows to the shoulder or indirect blows from the humerus not be maintained.
(Fig. 3_3) 25 Training and rehabilitation must include increased em­
Clinical: Of the 180° of abduction (the average person phaSiS on all the scapular muscles, especially the serratus.
does not reach 180°), the scapula moves approximately 60°. Swimmers often overdevelop their pectoral and anterior
In the absence of glenohumeral motion,26 scapulothoracic cervical muscles, resulting in slumping posture and weak
movement by itself can elevate the humerus approximately scapular retractors and adductors (rhomboids , middle
65° by the so-called shrugging mechanism. This mechanism trapezius, upper fibers of the latissimus dorsi) and lateral
can be noted on inspection as resulting from lesions (rup­ rotators (Figs. 3-4 to 3-8) . Although it is generally accepted
ture) of the deltoid or rotator cuff or acute and chronic in­ that the upper trapezius is a shoulder elevator, new infor­
flammatory and degenerative processes in the area. Often, mation disputes this concept (see Trapezius and Levator
with subacromial impingement and inflammation, asyn­ Scapulae under the heading of Clinical Review of the Shoul­
chronous scapulothoracic motion occurs in an attempt to der Muscles). Weak scapular musculature may result in fail­
The Shoulder 39

M iddle fibe rs
of Irapezius
mo jor

Upper fibe rs
of latissimus
dorsi '

Figure 3-4 Swimmer's posture. Sagittal posture analysis shows B

that this swimmer has forward shoulders and prominent lordosis.
Source: Reprinted with permission from Clinics in Sports Medicine Figure 3-5 Protractors (A) and retractors (B) of the scapula.
1986;5(1):11 © 1986, WB Saunders Company Source: Reprinted with permission from GP Bogumill, Functional
anatomy of the shoulder and elbow. In: Symposium on Upper Ex­
tremity Injuries in Athletes. p. 198, American Academy of Or­
thopaedic Surgeons, © 1986, The CV Mosby Co.
ure to position the glenoid in time under the humeral head
during the recovery phase (abduction and external rotation)
of swimming. This may result in acromial impingement of
the humeral head structures due to failure of the humeral these muscles may create inhibition and shutting down of
head to clear the acromion completely. The overdevelop­ the cuff muscles 29 Perry5 mentioned that slumping posture
ment of internal shoulder rotators compared with external also causes excessive stretch on the levator scapulae and
rotators is another cause of secondary impingement, result­ some stretch on the upper trapezius (Fig. 3-9). Increased
ing in "swimmer's shoulder." cervical lordosis and forward shoulders are related to the
It is essential to consider the relationship between the impingement syndrome (see Impingement Syndrome).
scapular and the glenohumeral joint in all shoulder prob­ Improved ergonomics and posture help prevent shoulder
lems. Because the rotator cuff muscles originate off the problems. Both the levator scapulae and the upper trapezius
scapula, inharmonious scapular movement due to fatigued may shorten and be responsible for cervical spine and
scapular muscles must put the cuff muscles at a disadvan­ shoulder involvement. The association of tight upper
tage. Rotator cuff muscles, which also function as dynamic trapezii and levator scapulae with weak lower trapezii and
stabilizers to the humeral head, when weakened would cre­ latissimus dorsi may result in an abnormal upward motion
ate added stress for the static shoulder stabilizers (capsule during shoulder elevation and eventual micro trauma and
and ligaments). cuff impingement. We must always ensure scapular mobil­
Abnormal scapulothoracic rhythm may stress the levator ity by ensuring flexibility and strength of the involved mus­
scapulae and upper trapezius, creating myofascial trigger cles. Often, the rotator cuff and midscapular muscles must
points and eventual adhesions. Overstretching of the scapu­ be strengthened while the upper trapezius, levator scapulae,
lar muscles and eventual tightening of the anterior (pectoral, and pectorals must be stretched. The lateral rotators should
subscapular, and scalene) muscles may occur. Facilitation of be strengthened to balance the excessively strong internal

Anterior deftoid

rere, major _ _---">_­

latissimus dorsi

Upper trapezius
Figure 3-7 Internal rotators of the arm. Source: Reprinted with
levator Kopuloe
permission from GP Bogumill, Functional anatomy of the shoulder
Rhomboideus minor
and elbow. In: Symposium on Upper Extremity Injuries in Athletes. p.
204, American Academy of Orthopaedic Surgeons, © 1986, The
Rhomboideus motor
CVMosby Co.

Upper Posterior deltoid

of trapezius ---...",.~""

Infraspinatus --4~~~

Teres minor ----"1-;...;...:;..;

Figure 3-6 Elevators (A and B) and upward rotators (C) of the

scapula. Source: Reprinted with permission from GP Bogumill,
Functional anatomy of the shoulder and elbow. In: Symposium on Figure 3-8 External rotators of the arm. Source: Reprinted with
Upper Extremity Injuries in Athletes. pp. 199-201, American Acad­ permission from GP Bogumill, Functional anatomy of the shoulder
emy of Orthopaedic Surgeons, © 1986, The CV Mosby Co. and elbow. In: Symposium on Upper Extremity Injuries in Athletes. p.
204, American Academy of Orthopaedic Surgeons, © 1986, The
CVMosby Co.
The Shoulder 41

the clavicle becomes an axis for upward rotation, occurring

at the SC]. Due to the S shape of the clavicle, the acromial
end becomes higher to allow further elevation and upward
rotation of the scapular32 If rotation of the clavicle is pre­
vented, elevation of the arm is limited to 110 0 The coraco­
clavicular ligaments therefore aid in coupling glenohumeral
abduction and flexion to scapular rotation on the thorax 33
The posterior sternoclavicular ligament and the costoclavic­
ular ligaments limit protraction, and the anterior stern­
oclavicular ligament limits retraction. 34 The sternoclavicular
joint moves anteriorly with horizontal flexion (adduction)
and posteriorly (horizontal extension), a total of 35 032

Acromioclavicular Joint

The acromioclavicular (AC) joint suspends the scapula

from the clavicle and supports the weight of the upper ex­
tremity Superior and inferior AC joint ligaments provide
horizontal stability The coracoclavicular ligaments, the
conoid and the trapezoid (sometimes separated by a bursa),
Figure 3- 9 Slumping posture causes excessive stress to the leva­ are suspensory ligaments that provide vertical stability Ro­
tor scapulae, parascapular muscles, capsule, and cuff. Eventual tation of the scapula about the acromioclavicular joint be­
shortening of the pectoral faSCia, myofascial trigger points, and fi­ gins between the 60 0 to 90 0 position and continues until
brosis may occur. Source: © 1990, David Bolinsky. maximal arm abduction has been completed. 16 The clavicle
retracts about 20 0 , indicating posterior (tilt) movement of
the scapula. This retraction occurs mostly from 130 0 to
150 0 of humeral elevation, beginning at about 25 0 of scapu­
lar plane elevation. I? It reaches the close-packed position
rotators. Subsequent chapters discuss direct treatment, between 90 0 and 1200 (i.e., locked so that the AC joint is
stretching, mobilization, and rehabilitation. unable to elevate further). Additional elevation of the
scapula after the close-packed AC position occurs because
STERNOCLAVICULAR-ACROMIOCLAVICULAR as the scapula rotates upward, the coracoid process rotates
MOTION downward, causing the coracoclavicular ligaments to pull
the clavicle into long-axis rotation 4 The trapezius muscle
reinforces the AC capsule and the superior AC ligament
The clavicular joints are synovial joints. The total range posterosuperiorly, while the clavicular head of the deltoid
available at the clavicular joints must of necessity equal the reinforces the capsule anteriorly These are important mus­
60 0 total range of the scapulothoracic joint 30 cles to rehabilitate in AC sprain (see Acromioclavicular
Sprain). The sum of the ranges of motion at the sternoclar­
Sternoclavicular Joint, Clavicular Motion icular and AC joints equals the range of motion of the
scapula. Neer and Rockwood 32 measured a maximum of 8
The clavicle elevates in total about 300 , reaching its max­ degrees of AC motion.
imum at about 130 0 of elevation 31 The sternoclavicular
joint (SC]) elevates 4 0 for every 100 of humeral elevation Clinical: The AC joint is more related to scapular mo­
(35 0 to 40 0), up to 90 0 , where it stops elevating. At this tion and clavicular rotation than the sternoclavicular joint,
point of about 90 0 of shoulder abduction or flexion, trans­ which acts as a lever arm and stabilizer. Turek26 stated that
verse axial rotation of the clavicle (up to 50 begins at the
if the clavicle is prevented from rotating by fixation of the
SC]. This posterior clavicular axial rotation is essential for outer or inner ends, abduction of the arm above 110 is
upward rotation of the scapula and shoulder flexion or ab­ prevented. This explains why an arthritic AC joint may
duction. The upward rotation of the clavicle is caused by limit shoulder elevation.
tightening of the coracoclavicular ligaments (trapezoid and Sports that emphasize excessive abduction and external
conoid). As these ligaments become taut, the attachment on rotation cause repetitive axial clavicle rotation, resulting in

abnormal sheer stress at the AC joint. Pain appearing at the

AC joint on active or passive abduction beginning at ap­
proximately 90° elevation and continuing to the 180° end
range may indicate an AC lesion. Pain occurs because AC
stress is provided by its close-packed position and long-axis
rotation. Horizontal adduction is another AC close-packed
position that creates pain when the joint is involved (see
Functional Examination of the Shoulder; Acromioclavicular
For complete forward flexion and abduction of the
shoulder, there is approximately 60° of scapula rotation and
90° to 105° of glenohumeral rotation. The remaining 10° to
15° of shoulder flexion or abduction is produced by spinal
extension or spinal lateral flexion. If only one arm is ab­
ducted or flexed, lateral displacement of the spinal column
produced by the contralateral spinal muscles is necessary Extensors:
When both arms are abducted or flexed, exaggeration of the long head
lumbar lordosis by the lumbar muscles is necessary. 35 It is of triceps

essential to restore normal joint play to both the AC and the Posterior
sternoclavicular joints (see chapter on Joint Play).
Teres min.,,-++---,


Shoulder Flexion (Anteversion) portian of
B mojor

Shoulder flexion (forward in the sagittal plane/antever­

Figure 3-lO Flexors and extensors of arm. Source: Reprinted
sion) in order of importance involves the clavicular and with permission from GP Bogumill, Functional anatomy of the
some of the acromial fibers of the deltoid, the biceps brachii, shoulder and elbow. In: Symposium on Upper Extremity Injuries in
pectoralis major, the coracobracialis, and the serratus ante­ Athletes. p. 201, American Academy of Orthopaedic Surgeons, ©
rior. The coracobrachialis and biceps brachii act mainly dur­ 1986, The CV Mosby Co.
ing the first 90° of flexion (Fig. 3-10). Shoulder flexion is
possible if the serratus anterior is paralyzed but the scapula
will be elevated from the thoracic wall (winged scapula).

External Rotation major, and latissimus dorsi. The subscapularis is the only
one that comes close to being a pure internal rotator. The
External rotation uses the infraspinatus, teres minor, pectoralis major combines internal rotation with adduction,
and posterior deltoid (Figs. 3-8 and 3-11). The infra­ the anterior (clavicular) deltoid flexes the shoulder as it ro­
spinatus performs more work than all the other external tates internally, and the latissimus dorsi and teres major
rotators combined. With lateral rotation, the scapula and combine internal rotation with adduction and extension.
clavicle are Simultaneously pulled backward by the
trapezius and rhomboid muscles, also creating movement
at the sternoclavicular and acromioclavicular joints 3 6 The Adduction
supraspinatus is also a weak lateral rotator and flexorY
Adduction (Fig. 3-12) in order of importance in­
Internal Rotation volves the lower portion of the pectoralis major, and the
clavicular and posterior portion of the deltoid. These are
Internal rotation (Figs. 3-7 and 3-11), in order of im­ the main muscles that act as the arm is brought down to
portance, involves the subscapularis, pectoralis major, long the side of the body from the overhead position against
head of the biceps, clavicular part of the deltoid, teres resistance.
The Shoulder 43

Extension (Retroversion)
External rotators:
Teres minor
The muscles involved in extension, in order of impor­
tance, are the teres major, the latissimus dorsi, the long
Inl.rnal rotatou:
head of the triceps brachii, and the deltoid. 36
latissimus dorsi
Teres major
Subscapularis Abduction
Anterior deltoid
Pectoralis major
Abduction involves principally the deltoid, supraspina­
tus , and long head of the biceps brachii. In the coronal
plane, the posterior deltoid is active, whereas in the scapu­
lar plane the middle and anterior deltoids are active. Mura
.... -~ . -~' .......
et aP8 found that "the entire infraspinatus contributes both
Figure 3-11 Rotators of arm from above . Source: Reprinted with to abduction torque at the glenohumeral joint and to con­
permission from GP Bogumill, Functional anatomy of the shoulder straining the humeral head against superior motion. "
and elbow. In: Symposium on Upper Extremity Injuries in Athletes. p.
203 , American Academy of Orthopaedic Surgeons, © 1986, The Clinical: Resistive muscle testing is used to determine,
CVMosby Co . among other things, whether the contractile unit elicits pain
and/or weakness. Pain and almost normal strength (mini­
mal weakness and muscle substitution) on testing indicate
that some part of the muscle and/or tendon is involved.
Learning the muscle action allows us to specify the involved
muscle. Examining a patient in the motion or position that
elicits pain also provides valuable information. Patients who
complain of pain later in their activity may require repeti­
tive muscle testing to elicit their pain and/or require the ex­
aminer to be present during the activity.

_____ .~n""'or deltoid


Force Couples

Force couples are defined as two equal forces that act in

opposite directions to rotate a segment around its axis of
motion.39 The scapulothoracic force couple was discussed
under Scapular Rotation. The glenohumeral force couple re­
quired to rotate (elevate) the arm is made up of the deltoid
and rotator cuff muscles.
Figure 3-12 Adductors of the arm. Source: Reprinted with per­ The dominant vector direction of the deltoid is superior,
mission from GP Bogumill, Functional anatomy of the shoulder providing 89% total force .4o The rotator cuff (Fig. 3-11)
and elbow. In: Symposium on Upper Extremity Injuries in Athletes. p . provides a compression and depression of the humeral
203 , American Academy of Orthopaedic Surgeons, © 1986, The head and the deltoid elevates the arm. The infraspinatus,
CV Mosby Co. teres'minor, and subscapulariS are major depressors (mean
vector direction is 50 inferior relative to the face of glenoid,
providing 80% total force) .4o This inferior force counteracts
the superior force of the deltoid . The compressive, stabiliz­
ing function of the supraspinatus is due to its vector dire~­
tion 70 angle of insertion relative to the face of the glenOld

(Fig. 3-13) 33 The dominant force of the supraspinatus is


Figure 3-l3 Angle of insertion of the supraspinatus, which al­

lows its compressive, stabilizing function. Source: Reprinted with
permission fromJC Delee and D Drez. Orthopaedic Sports Medicine
Principles & Practice. Vol. 1, p. 627, © 1994, WB Saunders

compression. A fixed fulcrum is created by the cuff muscles Figure 3-14A Compression by the infraspinatus and subscapu­
to prevent the deltoid from causing the arm to migrate up­ laris can help stabilize the humeral head in the absence of a
ward when shoulder abduction is below 90°. Compression supraspinatus, provided the glenoid concavity is intact. Source:
by the infraspinatus and subscapularis allowing elevation is Reprinted with permission from FA Matsen, SB Lippitt, JA Sidles,
possible, even in the absence of the supraspinatus (Fig. and DT Harryman. Practical Evaluation and Management of the
3-14A)1 Shoulder, with permission ofWB Saunders Company, 1994.
The main effect of force coupling is to keep the humeral
head centered on the glenoid ± 1 mm throughout the entire
range of motion. Matsen et all stated that the cuff muscles
provide stability primarily by acting as compressors of the
head into the glenoid concavity. The rotator cuff, which has
capsular insertions, also helps to stabilize the joint by ad­
justing tension in the capsuloligamentous system by a selec­
tive process of contraction. 41

Summary of Rotator Cuff Functions

The rotator cuff is a dynamic stabilizer of the humeral

head by way of force couple relationships. Important shoul­
der force couples are the deltoid counterbalanced by all of
the rotator cuff muscles, the subscapularis counterbalanced
by the infraspinatus/teres minor, and the anterior
deltoid/supraspinatus counterbalanced by the infraspina­
tus/teres minor. Primary stabilizers are those that steer the Figure 3-14B Independent deltoid muscle action. Dominant
humeral head and hold the humeral head centered in the force pattern is verticle shear. Impingement against acromion is in­
glenoid (humeral head compression) during the usual duced. Source: Reprinted with permission from CR Rowe. The
midrange daily functional positions. The rotator cuff is a Shoulder. p. 17, © 1988, Churchill Livingstone.
The Shoulder 45

humeral head depressor (subscapularis and infraspinatus!

teres minor). It balances the shearing forces applied by the
prime mover muscles, such as the deltoid and the pectoralis
major. The supraspinatus is primarily a humeral head com­
pressor and not a depressor.
The literature regarding the function of the cuff muscles,
especially the supraspinatus, has been contradictory. A
study by Howell et al42 on 10 normal volunteers was per­
formed, in which isolated paralysis of the suprascapular and
axillary nerves was induced, concluded that the supraspina­
tus and deltoid muscles are equally responsible for produc­
ing torque about the shoulder joint in the functional planes
of motion (forward flexion and elevation in the plane of the
scapula). A more recent study by Otis et al 43 disagreed with
Howell and found that the infraspinatus and subscapularis
also contribute to abduction of the shoulder in the plane of
the scapula. This study also showed that with internal rota­
tion, there was increased activity of the superior portion of
the infraspinatus to elevate the arm, and with external rota­
tion, there was increased activity of the superior portion of Figure 3-15 Erosion of the superior glenoid concavity compro­
the subscapulariS to elevate the arm. mises the concavity compression stability mechanism, allOwing
Perry28 stated that the supraspinatus is anatomically too upward translation. Source: Reprinted with permission from FA
small to lift the arm independently and that 98% maximum Matsen, SB Lippitt, JA Sidles, and DT Harryman. Practical Evalua­
effort of the supraspinatus can elevate the arm only 30°. She tion and Management of the Shoulder, with permission of WB Saun­
ders Company, 1994.
also stated that the supraspinatus does not initiate abduc­
tion by itself and that dynamiC EMG shows that the middle
and anterior deltoids and supraspinatus function synchro­
nously. It is questionable whether the arms can be abducted
without the use of the supraspinatus and the deltoid. thereby flattening the superior glenoid concavity (Fig. 3-15).
Lehmkuhl and Smith44 showed that the long head of the bi­ If this occurs, Matsen et all believe that repair of the cuff ten­
ceps with the arm in external rotation is able, although with dons or capsular reconstruction will never completely restore
poor leverage, to abduct the humerus. Basmajian and glenohumeral stability because of a permanent loss of an in­
Deluca 45 stated that the biceps brachii contributes in main­ tact concavity for compression. The compressive force on the
taining abduction while the arm is laterally rotated and the glenoid should always be equal to or greater than the vertical
forearm is supinated. shear force caused by the deltoid (a crucial reason why rota­
tor muscle strength should always be assessed). At 90° of ab­
Clinical: If rotator cuff function is impaired--even duction the shear and compressive forces should be equal.
slightly-for any reason, the corresponding normal fulcrum
of the humeral head is lost, and abnormal upward displace­ Sport-Specific Muscle Function: Originally, according
ment (deltoid shear) and impingement of the subacromial to Inman et al,16 muscular activity in the shoulder was
structures and humeral head against the undersurface of the based on an obligatory synergy between the deltoid and the
acromion are allowed (Fig. 3-14B) (see Impingement Syn­ superspinatus. They found that the supraspinatus, rather
drome).46 The posterior shoulder pain and weakness of the than being the initiator of abduction, worked together with
external rotators often found in athletes cause a loss of joint the deltoid progressively throughout the entire range of mo­
stability as a result of the imbalance created by the then­ tion. Although this may be true in ordinary shoulder ab­
stronger anterior cuff muscles. 47 The subscapularis, teres duction, in throwing or other sports dealing with shoulder
minor, and infraspinatus are important for shoulder abduc­ abduction and external rotation, sports EMG analysis has
tion, and strengthening of these muscles helps compensate shown that a more selective muscle action occurs that is as­
for an impaired supraspinatus. 48 sociated with specific periods of great intensity.49 During
If there is severe chronic rotator cuff deficiency, superior late cocking, for example, the supraspinatus is working
subluxation of the head of the humerus may occur, causing harder than the deltoid (see below). This type of informa­
erosion wear on the superior lip of the glenOid fossa and tion is extremely important in rehabilitation of the athletic

shoulder (see illustration of phases of pitching (Fig. thereby aggravating the impingement syndrome due to su­
3-111)) . perior deltoid shear. The deltoid normally decreases in ac­
tivity during late cocking, but with impingement, the
deltoid prolongs its increased activity:
CLINICAL REVIEW OF THE SHOULDER MUSCLES When normalized supraspinatus activity was compared
in control subjects and patients with rotator cuff tears , in­
Supraspinatus creased levels of activity occurred in patients with rotator
cuff tears for all ranges of motion. 53 The broad covering of
Function the trapezius may mask supraspinatus atrophy:

The supraspinatus acts primarily as a stabilizing com­

Palpating Supraspinatus Insertion
pressor of the glenohumeral joint, thereby creating a ful­
crum for the deltoid to act more efficiently (see also Force
Based on cadaver studies by Mattingly and Mackarey,54
Couples under Glenohumeral Motion)32 The muscle also ,
the best position of maximal exposure is with the patient
because it circumscribes the spheroid of the humeral head,
sitting with maximal hyperextension, adduction, and me­
provides a head depression force. 5o Its peak activity occurs
dial rotation (Fig. 3-16). The musculotendinous portion is
during the late cocking position (abduction/external rota­
best palpated with the arm abducted 90° (see Fig. 14-3).
tion) after abduction is completed, to prevent anterior sub­
The belly is best palpated in the supraclavicular fossa with
luxation by drawing the humeral head toward the
the head extended, contralaterally rotated, and ipsilaterally
glenoid 33 With a heavy load in the hand with the arm at
bent toward the shoulder to relax the overlying trapezius.
the side, muscles with a vertical pull, such as the deltoid,
The supraspinatus belly, musculotendinous portion, and
triceps, and biceps brachii, are electromyographically silent,
insertion respond exceedingly well to friction massage,
whereas the horizontally directed supraspinatus and infra­
Graston Technique®, and Active Release® techniques. See
spinatus are active. 45,46 At the initiation of abduction from
the neutral position, the supraspinatus is more important
than the deltoid, whereas the middle portion of the deltoid
is of greater importance for elevation of the arm at the
higher angles of abduction, such as 60°.43 During abduc­
tion, the middle portion of the deltoid was most active, and
during adduction, the posterior portion was more active
than the middle and anterior deltoid. The posterior portion
of the deltoid did not participate in abduction until the
shoulder was elevated 110° in a plane 45° anterior to the
coronal plane. 51

Activity During Throwing with Instability

The supraspinatus shows increased activity throughout

late cocking and acceleration. The rotator cuff muscles
work harder during instability as a compensation to in­
crease humeral compression. 52

Activity During Throwing with Impingement

The supraspinatus shows a lower level of activity during Figure 3-16 Position for palpating the supraspinatus insertion
late cocking. 52 The lower activity reduces tension on the (dots). The patient sits with maximal hyperextension, adduction, and
supraspinatus tendon. This provides less coupling with the medial rotation. Source: Reprinted from G Mattingly and PJ Mackarey
deltoid, resulting in an imbalance between the supraspina­ Optimal methods for shoulder tendon palpation: a cadaver study
tus and the deltoid. An imbalance prevents the supraspina­ Physical Therapy. Vol. 76, No.2, Alexandria, Virginia, APTA, 1996,
tus from compressing the humeral head into the glenoid, with permission of the American Physical Therapy Association.
The Shoulder 47

Chapter 15 on Graston Technique® for new information no role in the deceleration of the arm during the follow­
pertaining to the anatomy of rotator cuff insertions. through phase of pitching. 43
Tightness of the external rotators results in anterior
Infraspinatus and Teres Minor translation and superior migration of the humerus during
throwing 61 Inability to raise the hand superiorly with the
Function arm behind the back may be due to a tight infraspinatus.

The infraspinatus and teres minor muscles act as exter­

nal rotators along with the posterior deltoid. Mura et aP8 Activity During Throwing with Instability
found that "the entire infraspinatus contributes both to ab­
duction torque at the glenohumeral joint and to constrain­ The muscles show increased EMG activity during early
ing the humeral head against superior motion." Their peak cocking and acceleration, which theoretically may be hold­
EMG activity occurs in the late cocking (concentric) and ing the humeral head posteriorly to prevent the anterior
follow-through (deceleration/eccentric) phase 52 Eccentric humeral translation 52 that occurs with anterior instability.
activity of posterior muscles during deceleration must
counteract a glenohumeral distraction force equal to the
body weight. 55 Their activation temporarily lags behind the
Palpating Infraspinatus and Teres Minor Insertion
supraspinatus56 during throwing. During shoulder abduc­
tion from 120° to 150°, the infraspinatus is more active
The best position for palpation of the insertion of the in­
than the supraspinatus,57 which is a reason why the infra­
fraspinatus and teres minor 54 with the least amount of over­
spinatus is adversely affected in prolonged overhead activi­
lying tissue is with the patient sitting in a position of
ties. During coronal abduction, EMG activity between the
shoulder flexion to 90°, 10° of shoulder adduction, and 20°
supraspinatus and infraspinatus does not show a Significant
of shoulder lateral rotation (Fig. 3-17). The best position
difference (see Chapter 1), indicating that pain on muscle
for palpating in the prone position is demonstrated in the
testing for abduction in the coronal plane may also indicate
a painful infraspinatus.
The infraspinatus and teres minor muscles also act as a
dynamic stabilizer by compressing and depressing the
glenohumeral joint, creating a fulcrum for the deltoid dur­
ing arm elevation (see Force Couples) that limits both ante­
rior and posterior shoulder translation. This action prevents
posterior translation because of its posterior position,58 aid­
ing in posterior shoulder stability, especially in the
midrange (45° to 75°) of abduction.
In the cocking position, the infraspinatus and teres minor
cause the humeral head to displace 3 to 4 mm posteriorly in
the glenoid,59 thereby reducing strain on the anterior-inferior
glenohumeral ligaments by resisting anterior humeral head
translation, thereby preventing overstretch of these anterior
static structures. During the deceleration phase of throwing,
the infraspinatus and teres minor resist anterior humeral
head translation by creating a posterior shear force of 50% of
body weight. During the follow-through phase of throwing,
Figure 3-17 Position for palpating infraspinatus and teres
the teres minor is much more active than the infraspinatus: minor insertion. The patient sits with shoulder flexion to 90°, 10°
the teres minor contributes 84% maximum voluntary con­ of shoulder adduction, and 20° of shoulder lateral forearm rota­
traction (MVC) versus 37% MVC for the infraspinatus, and tion. The dots represent infraspinatus insertion, the lines represent
the supraspinatus is working at 39% MVC60 The infraspina­ teres minor insertion. Source: Reprinted from G Mattingly and PJ
tus and teres minor muscles must be strengthened for both Mackarey Optimal methods for shoulder tendon palpation: a ca­
anterior and posterior instability. With 60° of abduction, the daver study Physical Therapy. Vol. 76, No.2, Alexandria, Virginia,
infraspinatus undergoes a decrease in its rotational moment APTA, 1996, with permission of the American Physical Therapy
arm, making it less effective as an external rotator, and plays Association.

chapter dealing with neuromuscular reeducation and fric­ Activity During Throwing with Impingement
tion massage (see Chapter 14).
Postural standing evaluation may exhibit the hands in a With impingement, there is decreased activity of the
pronated position, which may indicate a weak infraspina­ subscapularis with other internal rotators (pectoralis major
tus/teres minor or an overactive latissimus dorsi, pectoralis and latissimus dorsi, plus the serratus anterior), which al­
major, or teres major. Atrophy of the infraspinatus is usually lows increased external rotation, superior humeral head mi­
apparent by a hollowness in the infraspinatus fossa because gration, and impaired scapular rotation. This results in
of disuse or suprascapular neuropathy aggravation of the impingement syndrome.52

Palpating SubscapulariS Insertion

The insertion is palpated at the lesser tuberosity (see Fig.
Function 14-7). The tendon can be palpated without the overlying
deltoid by positioning the shoulder adducted to the side of
The subscapularis acts as a dynamiC internal rotator, the thorax and in a neutral position regarding flexion/exten­
along with the other internal rotators (pectoralis major, sion and medialllateral rotation, deep to the deltopectoral tri­
latissimus dorsi, and teres major). It contracts eccentrically angle (Fig. 3-18). The deltopectoral triangle is bounded by
to protect the shoulder during external rotation, where it the medial deltoid muscle CD), the inferior clavicle (C), and
shows more EMG activity than the concentrically contract­ the lateral pectoralis major (P) muscle. The subscapulariS
ing infraspinatus 62 The subscapulariS also acts as a passive tendon is palpated deep in this triangle between the long and
restraint limiting excessive anterior translation during exter­ short heads of the biceps brachii muscle. The subscapulariS
nal rotation under 90° abduction. It is most effective as a
passive restraint between 0° and 45° and less effective be­
tween 45° and 75° of abduction 63--{i5 The subscapularis is a
dynamiC muscular restraint along with the passive static re­
straints (inferior glenohumeral ligament and anterior cap­
sule), limiting forward humeral head translation in the
forward thrOwing position. It also acts as a dynamic stabi­
lizer by compressing and depressing the glenohumeral
joint, creating a fulcrum for the deltoid during arm eleva­
tion (see Force Couples).

Activity During Throwing

During the acceleration phase of throwing, professional

pitchers fire the subscapularis selectively over the other ro­
tator cuff muscles, whereas amateurs depend more on rota­
tor cuff muscles and biceps brachii for power. 66 The
subscapulariS also acts as a steering mechanism to position
the humeral head preCisely in the glenoid and to protect the
head from levering out of the joint52 during the acceleration

Figure 3-18 Position for palpatating the subscapularis tendon.

Activity During Throwing with Instability The shoulder is adducted to the side of the thorax in a neutral po­
sition, the muscle is palpated deep to the deltopectoral triangle,
where D is the medial deltoid muscle, C is the inferior clavicle,
With instability, there is decreased activity in all phases and P is the lateral pectoralis major muscle. Source: Reprinted from
of throwing. The subscapularis functions in the late cocking G Mattingly and PJ Mackarey. Optimal methods for shoulder ten­
stage to eccentrically decelerate the external rotation of the don palpation: a cadaver study. Physical Therapy. Vol. 76, No.2,
shoulder. The increased external rotation would perpetuate Alexandria, Virginia, APTA, 1996, with permission of the Ameri­
chronic anterior instability 52 can Physical Therapy Association.
The Shoulder 49

has a varied insertion. It inserts into the lesser tuberosity, strated that the biceps muscle acts as a flexor and an abduc­
coracohumeral ligament and the anterior capsule. 42A The tor of the shoulder. Both heads of the biceps showed higher
subscapularis tendon joins the supraspinatus tendon be­ activities during external rotation than during internal rota­
neath the biceps (see Chapter 15, Graston Technique®). tion for most motions. Sakurai et al found that in maintain­
ing elevation of the arm, the long head of the biceps worked
much harder than the short head and the deltoid. This find­
Deltoid ing might explain a cause of tendinopathy or rupture of the
long head. The biceps brachii may be more important as a
The deltoid muscle makes up about 20% of the shoulder supinator than an elbow flexor (see Resisted Shoulder!
musculature 67 The deltoid has the largest moment arm of Elbow Flexion).
the shoulder muscles during arm elevation and the largest Other functions of the biceps brachii besides flexion of
cross-sectional area. It is the primary elevator of the shoul­ the elbow have to do with passive stabilization of the shoul­
der. The deltoid is also an anterior shoulder stabilizer and is der. The long head of the biceps brachii acts as a stabilizer of
important when the shoulder is unstable. Kido et al 68 the humeral head in the glenOid, preventing superior transla­
proved that each portion of the deltoid muscle acted as an tion during abduction of the shoulder in the scapular plane 70
anterior stabilizer with the arm in abduction and external Yamaguchi et aI,53 disagreed with this conclusion. The biceps
rotation. They found that when the arm was elevated, con­ brachii may act as a passive stabilizer of the shoulder with
traction of the deltoid muscle produced more compression anterior instability because it shows its highest activity dur­
force to the glenohumeral joint than with the arm at the ing the acceleration phase 71 The biceps may enhance stabil­
side. In external rotation, the deltoid muscle insertion was ity by stiffening the anterior capsule n The long head of the
located more posteriorly than with the arm in neutral rota­ biceps tendon (LHB) also significantly decreases both poste­
tion and therefore functions also as a passive tension mech­ rior and anterior translation with the humeral head in both
anism. They believed that for anterior shoulder instability, neutral and external rotation with abduction D The LHB also
besides exercising the biceps and rotator cuff, the deltoid acts as an anterior stabilizer of the glenohumeral joint during
muscle should also be included. rotation of the arm. 74 When the LHB subluxes, it loses its an­
terior stabilizing effect on the glenohumeral joint and allows
anterior humeral translation The biceps brachii in the ab­
Biceps ducted external rotated position may be lessening stress to
the inferior glenohumeralligament.7 5
Function In throwers with instability (subluxation), there is in­
creased activity during acceleration. The biceps therefore
There is ongoing controversy regarding the function of aids in humeral head stabilization. 52 Therefore, Significant
the biceps brachii muscle. Perry28 stated that the biceps in hypertrophy of the biceps is not necessarily the goal in
the throwing position is more important as an elbow muscle training. The biceps brachii should be trained for en­
than as a Significant stabilizing force at the glenohumeral durance, like the cuff muscles 75 A secondary function dur­
joint. During throwing, the biceps brachii is active as the ing throwing is to create humeral compression, thereby
elbow flexes in late cocking and acts as an eccentric deceler­ resisting humeral distraction during deceleration.7 5 The
ator of the forearm during follow-through. The tendon is ac­ long head of the biceps stabilizes the humeral head on the
tive during the cocking, acceleration, and follow-through glenoid during powerful elbow flexion and forearm supina­
phases and can result in tendinopathy or even avulsion. A tion,76 acting in effect as a humeral head depressor. The bi­
EMG study on biceps activity during shoulder motion53 ceps brachii functions as a shoulder abductor under certain
agreed with that of Perry28 This study examined biceps ac­ conditions (see Glenohumeral Motion).
The long head's attachment to the supraglenoid labral
tivity specifically to the shoulder by relaxing the elbow so
rim associates the biceps with superior labral tears because
that shoulder activity could be evaluated without elbow in­
of repetitive overhead activity or trauma n According to
fluence. Yamaguchi et aP3 concluded that there was no sig­
Mattingly and Mackarey,54 the best position for palpatmg
nificant biceps activity coordinated with shoulder motion or
the long head of the biceps brachii muscle with the least
significant increases in activity with rotator cuff tears where
amount of overlying deltoid tissue is shoulder adducnon
head depressor function had been compromised. They be­
(00), with approximately 20° of medial rotation. Use the
lieved that, contrary to other studies, the shoulder functlOn
deltopectoral triangle (see Fig. 3-18) as for the subscapu­
of the biceps is mainly passive and functions as a weak
laris to pinpoint the tendon (Fig. 3-19). Have the patlent
humeral head depressor only in full external rotation. Using
resist the biceps to confirm location.
surface electromyography, Sakurai et a1 69 recently demon­


Figure 3-19 The deltopectoral triangle (see Fig. 3-18) is used

to pinpoint the biceps tendon. Source: Reprinted from G Mattingly
and PJ Mackarey Optimal methods for shoulder tendon palpation:
a cadaver study Physical Therapy. Vol. 76, No.2, Alexandria, Vir­ Figure 3- 19A Scapular position on completion of shoulder
ginia, APTA, 1996, with permission of the American Physical flexion. A), With optimal abduction and upward rotation of the
Therapy Association. scapula during shoulder flexion , the inferior angle reaches the
midline of the lateral side of the thorax. B), If the serratus anterior
muscle does not exert optimal control of the scapula, the inferior
angle will be posterior to the midline of the thorax. Source:
Sahrmann SA. Diagnosis and Treatment of Movement Impairment
Syndromes. St Louis Mosby; 2002.

Serratus Anterior


The serratus anterior is the major scapular rotator along

with the upper, middle, and lower trapezius, rhomboids, allow the coracoacromial arch to shift posteriorly away from
and levator scapulae (see also under Scapulothoracic Mo­ the flexing shoulder, resulting in possible impingement. The
tion; Functional Evaluation of the Shoulder, Inspection) clinician can determine whether there is adequate abduc­
The main function of the serratus is to pull the scapula for­ tion and upward rotation of the scapula, observing whether
ward (protraction), keeping it stabilized against the thoracic there is optimal abduction and upward rotation of the
cage thereby helping the lower trapezius rotate the scapula scapula during shoulder flexion (Fig. 3-19A). If normal in
upward. It is considered a major stabilizer of the scapula A), the inferior angle of the scapula should reach the mid­
during elevation. The serratus anterior, along with the pec­ line of the lateral side of the thorax. If the serratus anterior is
toralis minor, is a chief protractor (advancement of the deficient, the inferior angle will be posterior to the midline
scapula to an anterior position on the thoracic cage, i.e., of the thorax B). At the completion of shoulder flexion the
scapular abduction). The upper fibers of the serratus ante­ scapula should rotate 60°78 The midtrapezius, the rhom­
rior, which insert onto the superior angle of the scapula, sta­ boideus major, and the rhomboideus minor are the chief re­
bilize the scapula during the initial stages of shoulder tractors (adductors) of the scapula and therefore antagonists
abduction. The middle fibers that insert onto the vertebral to the serratus anterior. The superior and inferior parts of
border of the scapula are most important in protraction of the serratus anterior can act as synergists with the rhom­
the scapula, and the lower fibers of the serratus anterior, boids; when together they press the scapula onto the thorax.
which insert onto the inferior angle of the scapula, act If the serratus anterior is tested with the patient's arm below
mostly as an upward rotator of the scapula during abduc­ the horizontal, the muscle is at a mechanical disadvantage
tion. Fatigue and weakness of the serratus anterior does not and is therefore easier to detect weakness (winging)79
The Shoulder 51

Figure 3- 19B Tracing of a radiograph of a normal subject

standing upright at rest, on which the disposition of the fibres of
trapezius has been depicted. The lines depicting the various fasci­
Figure 3-19C and D Length assessments of the pectoralis
cles have been drawn semi-quantitatively to depict their relative
major muscle. C), Shortness of the sternal portion of the pectoralis
size in terms of cross-sectional area. The orientations of the fasci­
major muscle, limits the range of shoulder motion in 15Y of ab­
cles are indicated in degrees from the horizontal. Source: Johnson
duction. D), The clavicular portion of the pectoralis major muscle
G, Bogduk N, Nowitzke A, House D. Anatomy & actions of the
is often excessively long, as indicated by the excessive horizontal
trapezius muscle. Clin Biomech. 1994;9:44-50 . abduction of the shoulder, even in individuals with shortness of
the sternal portion. Source: Sahrmann SA. Diagnosis and Treatment
of Movement Impairment Syndromes. St Louis Mosby; 2002.

Activity During Fatigue or Impingement

When the scapula rotators are fatigued, especially the in excess tension and eventual tendinopathy at the supero­
serratus anterior, during overhead arm motion, the scapula medial angle of the scapula, where the levator scapulae in­
does not rotate and protract enough to keep up with the ad­ serts (see Scapular Dyskinesis and Scapular Retraction
vancing humerus (flexing into external rotation) and allows Test). The upper trapezius acts more as a scapular rotator
excess anterior translation of the humeral head. This creates than a true levator of the scapula 21 It can raise the scapula
additional stress on the passive anterior stabilizers of the only by rotating the clavicle about the sternoclavicular
shoulder,80 as well as on the cuff muscles. In a shoulder joint. Figure 3-19B shows the individual fibers of the
with anterior instability, there is increased activity of the upper trapezius. The thicker lines from C6, C7, and Tl in­
serratus anterior. 71 Increased activity leads to eventual fa­ dicate the major fascicles of the upper trapezius muscle.
tigue and weakness. In a thrower with impingement, this The weaker thinner fibers from the superior nuchal line
muscle decreases in activity. cannot be considered strong scapular elevators. The thicker
stronger inferior fibers of the upper trapezius have a trans­
Trapezius and Levator Scapulae verse orientation on the scapular in neutral position and are
more prone to draw the clavicle backwards or medially, but
Function not upwards. At the onset of upward rotation of the scapu­
lar the C7 and Tl fibers of the trapezius lie very close to
The upper trapezius and the lower trapezius, coupled the axis of rotation of the scapular, and this short moment
with the serratus anterior, upwardly rotate the scapula. The arm does not allow very much power for generating up­
levator scapulae is also important for helping elevate and ward rotatory moment of the scapular. In the early upward
rotate the scapula to maintain a stable glenoid base for the rotation of the scapular, the serratus anterior would be
humeral head. Sometimes, a scapular dyskinesis may result more active while the contribution of the upper trapezius

the glenohumeral joint, creating stress to the rotator cuff82

This occurs as a result of an abnormal length/tension rela­
tionship of the rotator cuff and the deltoid (which originate
off the scapula) , causing a loss of dynamic stability.75 There
is also a loss of normal elevation of the acromium, resulting
in secondary impingement. The shoulder can be abducted
only 90° without the trapezius 83 Increased upper trapezius
activity may occur as a result of poor hip extension (V
Janda, personal communication, 1994). The upper trapez­
ius must be rehabilitated after AC sprains because it at­
taches close to the AC joint. These fiber attachments are
usually torn in grade II and III AC sprains (see Acromio­
clavicular Sprain).
The upper trapezius is minimally active during quiet
standing and is continually active during walking, acting as
a suspensory muscle of the scapula. 84 If the upper trapezius
is overstretched, as found in depressed shoulders, this mus­
cle could be activated by shoulder shrugging, starting at 90°
of sagittal flexion and continuing the shrug position as the
arms are brought overhead so that the scapula is in upward
rotation. 78

Figure 3-19E Top, Length assessment of the latissimus dorsi Activity of the Levator Scapulae
muscle. The flat lumbar spine and limited range of shoulder flex­
ion are indicative of shortness of the latissimus dorsi muscle. Bot­ The levator scapulae bilaterally acts as a checkrein to
tom, Shoulder flexion increased by extension of the lumbar spine. cervical flexion and can be related to cervical pain by way
When this patient allows his lumbar spine to extend (taking some of its attachment to the transverse processes of the upper
of the stretch off of the latissimus dorsi), the range of shoulder four cervical vertebrae and connecting fascia. The superior
flexion is increased. Source: Sahrmann SA. Diagnosis and Treatment medial border of the scapula is often found to be a location
of Movement Impairment Syndromes. St Louis Mosby; 2002. of chronic restrictive soft tissue. It elevates the scapula
while rotating the inferior angle medially. If it is short, the
shoulder may appear elevated. Unilaterally, it lowers the
would be minimal. Johnson et aP! believe that the in­
glenOid by lifting the superior medial scapular border. It
creased EMG activity of the upper trapezius during early el­
laterally bends and rotates the cervical vertebrae toward the
evation of the scapula is not related to pulling the scapula
same side.8! Chronic shortness of the levator scapulae can
upwards but is achieving scapular elevation by exerting an
limit the action of the upper trapezius in elevating the lat­
upward moment on the clavicle at the cost of compression
eral border of the scapula 85 The superior medial border of
loads at the sternoclavicular joint. As upward rotation of
the scapulae may be easily palpated by having the patient
the scapula raises the acromion and spine, the C7 and Tl
lean prone on the elbows, thereby elevating the scapulae off
upper trapezius fascicles moment arms would increase and
the thorax. Always compare both sides. Perry5 mentioned
then contribute more to the force couple that generates up­
that slumping posture also causes excessive stretch on the
ward rotation or resists downward rotation 21 of the scapula.
levator scapulae and some stretch on the upper trapezius
The lower trapezius pulls the medial border of the scapula
(see Fig. 3-9). This can result in eventual shortening, my­
downward, and the serratus anterior pulls the scapula anterior
ofascia1 restriction, and trigger points.
(see Fig. 3-6C). Unilaterally, the upper trapezius also extends
and ipsilaterally bends and rotates the face to the opposite
side. The upper trapezius bilaterally extends the neck. The Rhomboids
middle trapezius adducts the scapula, and the upper and
lower fibers also act as stabilizers. 8! Function

Weakness The rhomboid muscles adduct and downwardly (medi­

ally) rotate the scapula. They also medially stabilize the
If there is weakness of the trapeziusllevator scapulae scapula during the follow-through phase (eccentric contrac­
force couple, there is an alteration of the biomechanics of tion) and concentrically adduct (retract) the scapula toward
The Shoulder 53

the vertebral column and press the scapula onto the tho­ eccentric strain of the cuff muscles, helping prevent exces­
racic wall during external rotation or horizontal abduction sive anterior translation of the humeral head. 75 The attach­
of the shoulder. They also act as scapular elevators (see Fig. ment of the latissimus dorsi to the intertubercular groove of
3-6A). If tight, they can restrict upward rotation of the the arm is related to shoulder function. During the late arm
scapula. If the rhomboids are weak, a thrower is unable to cocking (eccentric) phase, the latissimus must be able to
retract the shoulder fully and may stress the anterior shoul­ generate over 150% of its maximal manual muscle activity
derB6 Dr M. Leahy (personal communication, February during the late arm cocking and 133% during acceleration,
1995) stated that a weak or lesioned infraspinatus may when it concentrically contracts as it internally rotates the
cause overworking of the rhomboids during backward humerus B8
shoulder motion. Sahrmann78 stated that the shoulder The pectoralis major and pectoralis minor and surround­
shrugging exercise with the arms at the side would reinforce ing fascia (see Chapter 15, Graston Technique®) tend to
the activity of the rhomboid and levator scapulae muscles. shorten and must be addressed in the treatment of forward
Weak rhomboids may be responsible for a winged scapula shoulders, slumping posture, and resultant posterior tho­
but would allow elevation of the arm and can be differenti­ racic pain. Permanent relief to the posterior thoracic areas is
ated from the serratus anterior, which would not allow ele­ dependent on releasing tight anterior chest fascia. Wilk89
vation of the arm beyond 90°35 stated that the accelerators, such as the pectoralis major,
latissimus dorsi, teres major, and long head of the triceps,
Pectoralis Major and Latissimus Dorsi should be trained primarily with concentric exercise,
whereas the decelerators of the shoulder, such as the infra­
Function spinatus, teres minor, and posterior fibers of the deltoid,
should be trained eccentrically with elastic tubing exercises
The pectoralis major, depending on its particular fiber to control and limit joint motion. Elastic tubing allows both
orientation, hOrizontally adducts (sternocostal), coronally a concentric and an eccentric contraction. Tightness of the
adducts (sternocostal horizontal and ascending fibers), in­ internal rotators causes a thrower to be "opening up early,"
ternally rotates the humerus (clavicular and sternal fibers), thereby leading with the shoulder and creating an anterior
and forwardly moves the extended arm (clavicular fibers).85 subluxation force on the shoulder90
The pectoralis major also assists the latissimus dorsi in
pulling the raised arm down forcefully and raising the body Proprioception
when the arms are fixed 85 During late cocking, along with
the subscapularis, the pectoralis major eccentrically stabi­ There is a proprioceptive interaction between the dy­
lizes the anterior glenohumeral joint. The two muscles then namic stabilizers (rotator cuff and scapular muscles) and
concentrically contract to start the acceleration phase. the capsuloligamentous tissues. Mechanoreceptors (type II
These two muscles are the main muscles that impart veloc­ Pacini's corpuscles, Ruffini's end organ receptors, and free
ity to the ball. It often happens that the fibers forming the nerve endings) have been found in the glenohumeral liga­
sternal portion of the pectoralis major muscle test short ments and capsules. The glenOid labrum had no
compared with the clavicular portion that tests long. 78 Fig­ mechanoreceptors but did show free nerve endings. 91 .92
ures 3-19C and 3-19D show a long clavicular portion of There are ligamentomuscular reflex arcs, and studies have
the pectoralis major. This could be responsible along with shown that stimulation of nerves to the shoulder capsule
the latissimus dorsi in restricting shoulder girdle elevation, caused EMG activity of the cuff muscles, biceps, and
which is necessary for proper shoulder flexion. Figure deltoid.9 3 .94 With capsuloligamentous injury and the micro­
3-19E shows how to test for shortening of the latissimus trauma that follows, there is damage to the mechano­
dorsi muscle. Bilaterally, the latissimus dorsi can aid in ex­ receptors, leading to deafferentation, which adversely alters
tending the spine and tilt the pelviS anteriorly: A shortened afferent transmission to the central nervous system. These
latissimus dorsi limits shoulder flexion/elevation. If in this neuromuscular deficits impair reflex muscular stabilization,
case if the patient increases extension of the spine, shoulder, which predisposes the shoulder to functional instability: A
flexion/elevation will increase.78 Another cause of lack of diminished sense of joint position, kinesthetic awareness,
shoulder flexion with associated coracoid pain can be due and abnormal humeral and scapular muscular firing pat­
to tightness of the pectoralis minor and coracoid malposi­ terns also occur.
tion. Use of the shoulder retraction test with the patient in Proprioceptive function is diminished in patients with a
the supine position would allow increased flexion of the history of repetitive dislocation of the shoulder. In patients
shoulder.87 with chronic anterior instability of the shoulder, there is di­
The latissimus dorsi is important in the deceleration of minished ability to reproduce joint position and joint mo­
the shoulder during overhead activities by decreasing the tion. Impairment of the proprioceptive reflex system

consisting of joint mechanoreceptors inhibits effective regu­ bilizing influence. The scapular muscles help in stabiliza­
lation of appropriate muscular activity of the shoulder. With tion by providing a stable base for the glenohumeral articu­
a loss of proprioception, there develops a loss of stability lation.
The capsulolabral ligaments, muscles, tendons, and skin of
the shoulder area contain mechanoreceptors that provide
cumulative neural input (proprioception) to the central Active Mechanisms of Stabilization
nervous system.95 ,96 The conscious awareness of joint posi­
tion and movement resulting from proprioceptive input to Glenoid Compression
the central nervous system is called kinesthesia.9 5 Individ­
ual awareness of these factors is important in the prevention Glenohumeral joint stability requires a net joint reaction
and treatment of shoulder problems, because we can con­ force close to coaxial with the glenOid center line (Fig.
tract a muscle or change a position to prevent excessive 3-20A). The rotator cuff and periscapular muscles help
humeral translations. 47 The receptors in the capsulolabral maintain the necessary compressive force 104 within the sta­
structures respond to tension, and Terry et a1 97 stated that ble arc of the concavity (Fig. 3-20B). The periscapular mus­
the glenohumeral ligaments may then heighten the stretch cles aid the compression mechanism by aligning the glenoid
receptor response of the rotator cuff in response to joint po­ with the joint reaction force. 104 Figures 3-20C and D illus­
sitions. In turn, the selective contraction of the cuff muscles trates the possible subluxation or dislocation that may
protects the ligaments at extremes of motion 98 The exis­ occur when the joint reaction force is not balanced within
tence of ligamentomuscular reflex arcs in the glenohumeral the stable arc. Causes of the unbalance in C and D could be
joint suggests that the ligaments and muscles function syn­ due to dynamic cuff muscle imbalance, or periscapular
ergistically in stabilizing the shoulder. 99 muscle imbalance resulting in abnormal glenohumeral posi­
Prominent causes of diminished proprioception: tioning during particular motions. 104
Achieving glenOid compression is a prime aim of shoul­
1. Increased joint laxity due to stretching or trauma der rehabilitation. Compression of the head of the humerus
damaging joint capsule mechanoreceptors. lOo into the concave glenOid cavity prevents abnormal transla­
2. People with general joint laxity alone were less sensi­ tion, which eventually stresses both the contractile and the
tive in detecting passive shoulder rotation than peo­ passive elements of the shoulder. Concavity compression
ple who had "tight" joints. lOl People with increased resists the upward pull of the deltoid on the humeral head
external rotation may have less proprioceptive feed­ during elevation.
back via mechanoreceptors sensitive to stretch. Weakness/fatigue of the cuff muscles and the periscapu­
3. Shoulder muscle fatigue. 102 lar muscles is an important cause of decreased humeral
4. Repetitive micro trauma to the dominant shoulder in compression and is an important factor in the etiology of
the overhead-sport athlete. 103 the impingement syndrome. The mechanisms that center
and stabilize the humeral head during motion create a true
ball-and-socket joint with minimal rolling action.
Mechanisms Responsible for Concavity Compression
Stabilization of the glenohumeral joint is based on dy­
namic active stabilizers (glenohumeral and periscapular Primary Stabilizers: Primary stabilizers (muscles) , as
muscles) and passive stabilizers (glenoid fossa, capsule, differentiated from secondary stabilizers (ligaments) , hold
labrum, and glenohumeral and coracohumeral ligaments). the humeral head centered in the glenOid in the usual
At midranges of motion, the passive capsular ligaments are midrange daily functional positions. These muscles stabilize
relatively lax, and the cuff muscles provide stability by com­ the humeral head during active arm movements. Secondary
pressing the humeral head into the glenOid (concavity com­ stabilizers are concerned with limiting and protecting at the
pression). Stabilization by the capsular-ligamentous tissues, end ranges of motion, which are not the typical everyday
while protecting the congruity of the shoulder joint struc­ movements.
tures at rest, are especially important in restricting the end The rotator cuff, the long head of the biceps, and the del­
ranges of motion. The major force couples of the shoulder, toid muscles on contraction compress the humeral head
the deltoid superiorly, opposed by the infraspinatus and into the glenOid and increase the load needed to translate
teres minor inferiorly, the subscapularis anteriorly opposed the head. l05 Concavity compression by these muscles is
by the infraspinatus and teres minor posteriorly, have a sta­ compromised by weakness and tears. Balanced periscapular
The Shoulder SS


AIr..• ••

Figure 3-20 A) , The glenoid center line is defined as a perpendicular line to the midpoint of the glenoid concavity B) , The glenohumeral
joint is stable in positions where the net joint reaction force is balanced within the glenoid concavity C), The glenohumeral joint is unstable
in positions where the net joint reaction force is not balanced within the glenoid concavity D) , Abnormal glenoid version (abnormal glenoid
center line in relation to the scapula body) can contribute to the net joint reaction force not being balanced within the glenoid concavity.
Source: Reprinted with permission from 5 Lippitt, F Matsen. Mechanisms of glenohumeral joint stability. Clinical Orthopaedics and Related Re­
search. Vol. 291 , p. 26, © 1993 , Lippincott-Raven Publishers.

muscles, along with the cuff muscles, allow the net joint re­ With adhesion-cohesion there is molecular attraction of
action force to pass through the fossa 104 (see Glenoid Com­ the joint fluid , which may be compromised by inflammation
pression above). Normal glenoid and glenoid labrum or articular fracture. Limited joint volume creates a negative
increase the depth of the fossa. A labral tear compromises intra-articular pressure that may be compromised by capsu­
the negative atmospheric pressure and vacuum effect, re­ lar defects, joint effusions, or an unstable shoulder with a
sulting in loss of glenohumeral joint stability. loose capsule (see Bankart's Lesion). Traction of the arm in a

normal shoulder increases the negative pressure but not in glenoid. The fossa tilts downward 5° and retroverts 6° with
an unstable shoulder, where the vacuum effect is lost. respect to the scapular plane,4 offering little anterior and no
inferior bony support.
Secondary Stabilizers: Matsen et all regard capsu­
The glenOid serves as an attachment for the glenoid
loligamentous restraints as secondary because they are not
labrum, capsule, triceps, and long head of the biceps. Be­
responsible for holding the humeral head centered in the
cause the articular cartilage of the glenoid fossa is thicker
glenoid in the everyday midrange functional positions.
on the periphery than in the center, the fossa is more con­
They act as check reins at the limits of glenohumeral mo­
cave than it appears.108 The shoulder is not a true ball-and­
tion by tightening, thereby exerting a force on the humeral
socket joint, because at the extreme ranges of motion,
head to normalize the joint reaction force. 104 This action ex­
rotation is coupled with translation (see below).
plains why a shoulder may test very lax and be completely
stable because of adequate primary stabilizers (see
Laxityllnstability) . Glenoid Labrum
Influence of the Primary Stabilizers (Rotator Cuff, Biceps,
and Para scapular Muscles) on the Secondary Stabilizers The glenoid labrum is a rim of fibrous and elastic tissue
The cuff tendons insert and blend into the shoulder cap­ attached to the margin of glenOid articular cartilage. Its
sule. Selective contraction of the rotator cuff muscles reduces outer surface attaches to the capsule. The superior portion
translations of the humeral head because attached ligaments has a loose attachment, whereas the inferior structure has a
and capsules are made taut by rotator muscle contraction. more firm, immobile attachment. Tendons of the triceps and
For example, when the supraspinatus acts as an external ro­ the long head of the biceps attach to and reinforce the
tator during shoulder elevation, it tightens the inferior liga­ labrum. The biceps fibers blend with the superior labrum,
ments of the shoulder.106 Loading any of the cuff tendons and the inferior glenohumeral ligamentous fibers blend with
significantly reduces anterior shoulder instability 107 During the inferior labrum.
the cocking phase of throwing, the infraspinatus and teres The glenoid labrum functions to deepen the glenoid cav­
minor reduce strain on the anterior inferior glenohumeral ity, adding to the stability of the humeral head in the
ligaments by pulling the humeral head posterior. By helping midranges of glenohumeral motion. It provides attachment
to maintain glenohumeral concavity compression, strain on for glenohumeral ligaments. 109 Labral detachment by itself
the secondary stabilizers is reduced. is not necessarily responsible for shoulder anterior instabil­
Both anterior and posterior translation of the humeral ity unless there is also disruption of the anterior capsule,llo
head is decreased when the long head of the biceps tendon although rarely are labral tears seen without the presence of
is loaded. 105 Therefore, strengthening of the rotator cuff and instabilitylll (see Instability, Glenoid Labum Tests).
biceps muscles acts as a barrier to pathological gleno­
humeral translations (instability) . Capsule
Fatigue of the scapular rotators, especially the serratus
anterior, during overhead throwing does not allow the The capsule surrounds the shoulder joint, attaching to
scapula to protract with the advancing humerus, allowing the circumference of the anatomic neck and extends 1/2
excess anterior translation of the humeral head and stress inch inferiorly to the shaft of the humerus. It is lined by a
on the anterior secondary ligamentous stabilizers (see Serra­ synOvial membrane. The posterior capsule is the thinnest
tus Anterior above). part of the capsule and is located posterior to the biceps,
above the posterior band of the inferior glenohumeralliga­
Passive Static Stabilizers ment in the 9-0'clock to the 12-0'clock area.
The capsule is so loose and lax that the bones may be
The passive static stabilizers consist of the articular separated from each other by 2 or 3 cm by a distractive
(bony) and capsular-ligamentous structures. They are the force. It is lax in midrange and tight at extreme ranges . By
glenoid fossa, the glenOid labrum, and the capsule. itself, the thin capsule contributes little to the stability of
the joint because the capsule's stabilizing effiCiency is re­
Glenoid Fossa lated to its attachment to the cuff muscles and ligaments 1l2
The capsule is reinforced by the anterior glenohumeral cap­
The glenOid fossa provides minimal bony contact (33% sular ligaments, which help protect the shoulder in the ex­
of the surface of the humeral head). During normal motion, treme ranges of motion. The capsule has a capsular collagen
only 25% to 30% of the humeral head is in contact with the structure that, when stretched, causes a constriction that
The Shoulder 57

helps compress the joint and aids in the negative intra­ capsule to muscles crossing the joint, confirming the con­
articular pressure. 113 cept of synergism between the passive (ligaments) and ac­
The rotator cuff muscles are intimately blended with the tive (muscles) restraints of the glenohumeral joint. The
fibrous capsule 1l4 Bland et al115 states that the capsule synergistic action demonstrates how muscles can reduce
should be thought of as a conjoined tendon containing the strain in ligaments. As the IGHL is stressed in abduction
insertions of the capsular (cuff) muscles. The inferior gleno­ and external rotation, there is a reflex recruitment of the bi­
humeral ligaments, although considered thickenings of the ceps, subscapularis, infraspinatus, and supraspinatus mus­
anterior capsule, have been found to be distinct anatomic cles to bring the joint into stability Therefore, the muscles
structures. 116 playa major role in maintaining active joint stability
When the arm is resting in neutral, the superior portion
of the capsule is taut, and the inferior portion lies in lax Clinical: It is important to realize that instability can be
folds; when the arm is fully abducted, the inferior part of due to abnormality of one or more of the stabilizers. A tight
the capsule is the least supported and is subjected to the posterior-inferior capsule (determined by limited horizontal
greatest strain because it is stretched tightly across the adduction or limited internal rotation of the elevated arm)
rounded head of the humerus1l4 Separate motions of full may be responSible for excessive humeral head translation
horizontal adduction or internal rotation of an elevated arm in an anterior-superior direction during shoulder flexion
tenses the posterior capsule, and external rotation tightens (this may be a cause of shoulder impingement-see Im­
the anterior capsule. pingement Syndrome). A tight anterior capsule would force
The capsule is responsible for normal humeral head the humeral head backward during external rotation, 1 possi­
obligatory translation: in external rotation at 90° abduction, bly causing posterior humeral subluxation with posterior
tightening of the anterior capsule and inferior glenohumeral glenOid wear, as seen in glenohumeral osteoarthritis. A pa­
ligament causes the humeral head to translate posterior "roll tient can be taught to adduct hOrizontally or internally rotate
back" several millimeters 1l7 This coupled motion is also his or her own shoulder to stretch a tight posterior capsule.
aided by contraction of the infraspinatus (see Clinical Re­ Manual techniques can be used to free both the anterior and
view of the Shoulder Muscles, Infraspinatus and Teres posterior capsules (Active Release®, Graston Technique®).
Minor above). The humeral head moves anteriorly with Capsular tightness may be localized or generalized. Lo­
flexion or horizontal adduction. With normal internal rota­ calized capsular contractures create predictable limitations
tion, there is a mean anterior translation of the humeral of shoulder motions,l whereas generalized capsular con­
head 5 mm. Therefore, it is evident that the capsuloliga­ tractures produce a capsular pattern used to diagnose adhe­
mentous complex is an important factor in determining the sive capsulitis or osteoarthritis of the glenohumeral joint
direction of the translation. The capsuloligamentous com­ (see Capsular Patterns and Adhesive Capsulitis). Throwers
plex not only restricts movement by acting as a passive re­ sometimes suffer from posterior capsular ossification. In Ki­
straint but also acts to reverse humeral head movement 47 bler 17 stated that with posterior shoulder tightness of the
(see Clinical, below, for abnormal obligatory translation). capsule or posterior shoulder muscles, an excessive amount
The anterior capsule also helps resist posterior instability, of scapular protraction during the throw may occur during
and the posterior capsule helps resist anterior instability liS the follow-through, resulting in impingement as the scapula
The posterior capsule is much thinner than the anterior rotates down and forward.
capsule. The anterior capsule is strengthened in front by ex­ Table 3-1 allows us to determine which particular part
tensions from the tendons of the pectoralis major and the of the anterior or posterior capsule is involved, and treat­
teres major. 119 ment could be directed toward that portion of the capsule
The circle concept 120 of the shoulder describes the de­ (see Adhesive Capsulitis).
gree of tissue damage necessary for glenohumeral joint dis­
location. Humeral head dislocation in one direction
requires damage to the capsule on the opposite side of the Glenohumeral Ligaments
joint. For example, a throwing athlete with recurrent poste­
rior subluxation also may have or be prone to developing The glenohumeral ligaments (Fig. 3-21) come under
anterosuperior labral injuries. R. F Warren, MD stated that tension when the shoulder joint is placed at the extremes of
opposite-side damage is not always necessary (personal motion, and they protect against instability when all other
communication, March 1995). mechanisms have been overwhelmed. 123 There are the three
Guanche et aP21 have demonstrated the existence of a anterior glenohumeral ligaments. There are no definite pos­
reflex arc from mechanoreceptors within the glenohumeral terior ligaments except for the posterior band of the inferior

Table 3-1 Effect of Localized Capsular Tightness of

Shoulder Motion

Location of


Tightness Motion(s) Limited

Posteroinferior Elevation in anterior planes

Internal rotation of the elevated arm
Cross-body adduction
Posterosuperior Reach up the back
Anterosuperior External rotation at the side
Anteroinferior External rotation of the elevated arm

Source: Reprinted with permission from FA Matsen. SB Lippitt. JA

Sidles and DT Harryman . Practical Evaluation and Management of
the Shoulder. p. 39. © .1994. WB Saunders Company.

Figure 3-22 Diagram of the functional anatomy of an adducted

shoulder in neutral rotation. The superior glenohumeral ligament
(SGHL) is the primary restraint to inferior translation. The anterior
Biceps and posterior bands of the inferior glenohumeral ligament playa
Superior glenohumeral lesser role. PB, posterior band; AB, anterior band; MGHL, middle
glenohumeral ligament. Source: Reprinted with permission from
Middle glenohumeral MK Bowen and RF Warren. Clinics in Sports Medicine. Vol. 10. No.
ligament 4, p. 769, © 1991, WB Saunders Company
Subscapularis tendon

Inferior glenohumeral

Figure 3-21 Inside view of the shoulder joint showing the rela­
tionship between the rotator cuff biceps tendon and the static sta­
bilizers. including the superior. middle. and inferior glenohumeral
ligaments. Source: Reprinted with permission from]C Delee and
D Drez. Orthopaedic Sports Medicine Principles & Practice. Vol. 1. p.
628. © 1994, WB Saunders Company

glenohumeral ligament (see below). The function of the lig­

aments depends on the position of the shoulder and the di­
rection of the translating force. They reinforce the capsule
(Figs. 3-22 to 3-28).

Superior Glenohumeral Ligament

The superior glenohumeral ligament (SGHL) originates Figure 3-23 Diagram of the functional anatomy of a 45° ab­
ducted shoulder in neutral rotation. The inferior glenohumerallig­
from the anterosuperior labrum anterior to the biceps ten­
ament is the primary restraint resisting inferior translation. PB,
don and inserts superior to the lesser tuberosity 124 The
posterior band; SGHl, superior glenohumeral ligament; MGHl,
SGHL fOnTIS the floor of the biceps pulley The anterior middle glenohumeral ligament; AB, anterior band. Source:
labrum is located at the medial margin of the glenOid cavity Reprinted with permission from MK Bowen and RF Warren. Clin­
In the adducted arm, the SGHL is important in limiting in­ ics in Sports Medicine. Vol. 10, No.4, p. 770, © 1991, WB Saun­
ferior translation; it also limits anterior translation below ders Company
The Shoulder 59

Figure 3-24 Diagram of the functional anatomy of a 45° ab­ Figure 3-25 Diagram of the functional anatomy of a 45° ab­
ducted shoulder in internal rotation. With internal rotation, the ducted shoulder in external rotation. With external rotation the
anterior inferior glenohumeral ligament moves underneath the posterior inferior glenohumeral ligament moves underneath the
humeral head and resists inferior translation. PB, posterior band; humeral head and resists inferior translation. PB, posterior band;
SGHL, superior glenohumeral ligament; MGHL, middle gleno­ SGHL, superior glenohumeral ligament; MGHL, middle gleno­
humeral ligament; AB, anterior band. Source: Reprinted with per­ humeral ligament; AB, anterior band. Source: Reprinted with per­
mission from MK Bowen and RF Warren. Clinics in Sports Medicine. mission from MK Bowen and RF Warren. Clinics in Sports Medicine.
Vol. 10, No.4, p. 771 , © 1991 , WB Saunders Company Vol. 10, No.4, p. 771 , © 1991 , WB Saunders Company

Figure 3-27 Diagram of the functional anatomy of a 90° ab­

Figure 3-26 Diagram of the functional anatomy of a 90° ab­ ducted shoulder in internal rotation. With internal rotation, the
ducted shoulder in neutral rotation. The inferior glenohumerallig­ inferior glenohumeral ligament tightens around the head, and the
ament supports the head and prevents inferior translation. PB, anterior band of the inferior glenohumeral ligament moves under­
posterior band; SGHL, superior glenohumeral ligament; MGHL, neath the head to resist inferior translation. PB, posterior band;
middle glenohumeral ligament; AB , anterior band. Source: SGHL, superior glenohumeral ligament; MGHL, middle gleno­
Reprinted with permission from MK Bowen and RF Warren. Clin­ humeral ligament; AB, anterior band. Source: Reprinted with per­
ics in Sports Medicine. Vol. 10, No. 4, p. 772 , © 1991 , WB Saun­ mission from MK Bowen and RF Warren. Clinics in Sports Medicine.
Vol. 10, No. 4, p. 773 , © 1991, WB Saunders Company.
ders Company


Figure 3-28 Diagram of the functional anatomy of a 90° ab­

ducted shoulder in external rotation. With external rotation, the
posterior band of the inferior glenohumeral ligament moves un­
derneath the head to resist inferior translation. PB, posterior band;
SGHL, superior glenohumeral ligament; MGHL, middle gleno­
humeral ligament. Source: Reprinted permission from MK
Bowen and RF Warren. Clinics in Sports Medicine. Vol. 10, No.4, p.
773 , © 1991 , WB Saunders Company

45° abduction 33 ,65 In a flexed, adducted, and internally ro­

tated shoulder, the SGHL has a secondary role in limiting Figure 3-29 Schematic of the shoulder capsule illus­
posterior translation 3 3 Werner et aP4 stated that the most trating the location and extent of the IGHLC. A, anterior; P, poste­
important fUnction of the SGHL is the stabilization of the rior; B, biceps tendon; SGHL, superior glenohumeral ligament;
long head of the biceps in its intra-articular course. MGHL, middle glenohumeral ligament; AB, anterior band; AP, ax­
illary pouch; PB, posterior band; PC, posterior capsule. Source:
Reprinted permission from SJ O'Brien et al. The anatomy and
Middle Glenohumeral Ligament histology of the inferior glenohumeral ligament complex of the
shoulder. American Journal of Sports Medicine. Vol. 18, No. 5, p.
The middle glenohumeral ligament (MGHL) originates 451 , © 1990, American Journal of Spons Medicine.
below the SGHL and inserts medially to the lesser tuberos­
ity. It is variable in size from being absent to being as large
as the biceps tendon. 85 The MGHL lies beneath and is at­
tached to the tendon of the subscapularis. The MGHL, the
subscapularis, and the superior part of the inferior gleno­ Inferior Glenohumeral Ligament Complex
humeral ligament limit anterior translation at 45° of abduc­
tion 63 and during lateral rotation from 0° to 75° of The inferior glenohumeral ligament complex (IGHLC)
abduction 65 (see Clinical Review of the Shoulder Muscles, (Fig. 3-29) is a ligamentous complex consisting of an ante­
Subscapularis). The MGHL is a secondary restraint to infe­ rior band, a posterior band , and an interposed axillary
rior translation with the shoulder adducted and externally pouch 1l6 In viewing the glenOid as the face of a clock, the
rotated. 125 bands originate from the glenoid, the labrum, or the neck of
The Shoulder 61

the glenoid, with the anterior band attaching between the

2-0'clock and 4-0'clock area and the posterior band attach­ At 90° abduction and external rotation, the anterior
ing between the 7-o'clock and 9-0'clock area 1l6 The bands band shifts anteriorly and the posterior band shifts inferi­
extend to the lower part of the anatomic neck of the orly At this point, the anterior band of the IGHl and axil­
humerus.119 lary pouch support the head anteriorly, and the posterior
The IGHlC functions as the most important stabilizer, band of the IGHl provides support inferiorly
especially in the overhead position, against anterior and At 90° abduction and internal rotation, the posterior
posterior translation, especially between 45° and 90° ab­ band shifts posteriorly, and the anterior band moves inferi­
duction. It also provides inferior support (Fig. 3-30). orly At this point, the anterior band of the IGHl provides

Figure 3-30 Schematic drawing showing how the IGHLC functions to support the humeral head both anteriorly and posteriorly with the
arm in abduction. The arm is abducted 90° and is in neutral rotation (a). As the arm is internally rotated (b, c), the posterior band of the
IGHLC fans out to support the humeral head posteriorly. When the arm is externally rotated (b, d) the anterior band of the IGHLC fans out
to support the humeral head anteriorly. Source: Reprinted with permission from SJ O'Brien et al. The anatomy and histology of the inferior
glenohumeral ligament complex of the shoulder. American Journal oj Sports Medicine. Vol. 18, No . 5, p. 455, © 1990, American Journal of
Sports Medicine.

A \
Figure 3-30A A and B, The coracohumeral ligament eCHL) is a strong bank originating from the base of the lateral border of the coracoid
process, just below the cocracoacrornial ligament, and merging with the capsule laterally to insert on the greater tuberosity. This ligament
may be important as a suspensory structure for the adducted arm. Source: Rockwood CA, Matson FA. The shoulder 2nd. devill . Philadelphia,
WB Saunders Company 1998: Fig. 1-34 A,B the coracohumeral ligament etc. p. 19.

support inferiorly, whereas the posterior band of the IGHL pouch of the inferior glenohumeral ligament, which is the
provides support posteriorly. longest and strongest of the three glenohumeral ligaments.
The ligament under the greatest amount of tension at the The MGHL is usually a mere thickening of the capsule. The
time of injury is most prone to injury. Evaluation of injury posterior stability of the humeral head is provided by the
to the shoulder with respect to the capsuloligamentous tendons of the infraspinatus and teres minor tendons. 46
structures is based on the position of the humerus at the Bigliani127 and Turkel et all28 stated that the IGHL is the
time of injury and the direction of the force. As the arm is most important structure in preventing anterior-inferior in­
abducted during external rotation, the stress on the anterior stability with shoulder elevation. With elevation, tension
capsuloligamentous complex shifts from superior to infe­ across the capsule shifts more inferiorly. Biglianjl27 stated
rior. The functional passive evaluation (see Passive Evalua­ that with the arm at the side in external rotation, the
tion of the Shoulder) stresses the humerus at particular MGHL is an important anterior stabilizer. Then with ab­
ranges to determine the structures involved (Table 3-2). duction, as the humeral head shifts inferior, the IGHL be­
Anterior stability is probably of the most concern be­ comes the chief stabilizer. The IGHL also acts as a posterior
cause 95% of glenohumeral subluxation or dislocation oc­ stabilizer because it is shaped like a hammock, extending
curs in an anterior-inferior direction. 126 Up to 45° of posteriorly behind the humeral head 1 29 Harryman et aP30
abduction, an important anterior stabilizer is the subscapu­ found that the rotator interval capsule, the interval between
laris tendon. This muscle must be taken into consideration the supraspinatus and the subscapulariS, prevented disloca­
in the treatment of adhesive capsulitis with limitation of ex­ tion of the glenohumeral joint inferiorly and posteriorly.
ternal rotation under 45°. As abduction approaches 90°, the
subscapulariS tendon does not cover the anterior-inferior Clinical: Repetitive activities, such as swimming,
portion of the humeral head, so that the superior band of throwing, and racket sports, creating high loads, plus the
the IGHL provides the main support. At the upper range of high loads of contact sports, are the chief causes of ligamen­
abduction, anterior stability is provided by the axillary tous problems in athletes. In the treatment of adhesive cap­
The Shoulder 63

Rotator Interval

An interesting area probably more pertinent for the sur­

geon provides a good anatomic review for manual thera­
pists who treat the area with regard to the rotator cuff. The
rotator interval (Fig. 3-30B) includes the space between the
supraspinatus (SSP) tendon and the subscapularis (SSC)
tendon and, besides power, contributes to stability of the
shoulder. The space includes the coracohumeral ligament,
the superior glenohumeral ligament, and parts of the joint
capsule.132 The interval is bridged by the rotator interval
capsule, which fuses with the coracohumeral ligament and
which together serve as a roof over the intrarticular bi­
ceps. l33 The superior glenohumeral ligament forms the
floor of the biceps pulley. Because the rotator interval limits
external rotation, it is possible that manual treatment over
this area may be helpful in redUCing adhesive capsulitis, in
which external rotation is usually the most limited motion.


None of the tests to be discussed is absolutely diagnostiC

for anyone pathological entity, each having varying sensitiv­
Figure 3-30B The rotator interval limits external rotation. ity and specificity. For example, the impingement tests are
Source: Jost B, Koch Pp, Gerber C. Anatomy and functional aspects reasonably sensitive but poorly specific.134 It is important
of the rotator interval. ] Shoulder Elbow Surg. 2000; 9(4):336-341. for the practitioner to be aware of a variety of both contrac­
tile and stability tests to form an educated decision based on
a complete hiStory. As stated in the preface, this text does
not discuss the taking of an adequate hiStory, which is ab­
solutely essential. In all of the follOwing functional tests , it is
sulitis and especially the early stages of the capsular pattern, essential to compare the lesioned side with the nonlesioned
the approach must be based on treating both the passive side, although it must be realized that in a thrower, for ex­
and the contractile tissues. Joint play techniques, stretching ample , the sides may be normally asymmetric. For example,
techniques, myofascial techniques , and all other treatments a dominant arm may exhibit hypertrophy, elbow flexion
must take into account all the viscoelastic elements in the contracture, increased external rotation, and decreased in­
connective tissue of ligamentous joint capsules, tendons, ternal rotation, which may be considered normal. 133 With
and muscles. Both muscle and joint tissues contribute to experience, an examiner can develop what is referred to as a
total stiffness, and neither is so dominant that alterations in "differential directed" diagnostic approach. Instead of pur­
the other are obscured. l3l More discussion is provided suing the same screening approach with each shoulder pa­
under Adhesive Capsulitis (see below) and in the sections tient, it is often possible, by taking into consideration the
on soft tissue treatment. age of the patient along with the chief complaint, to direct
the examination to the particular lesioned site. In a 20 year
old, we might expect to find instability, labral pathology, or
Coracohumeral Ligament impingement rather than a cuff tear or adhesive capsulitis,
as in a 60 year old. It is necessary to relate the chief com­
The coracohumeral ligament (CHL) originates from the plaint to the history to arrive at a differential diagnosis. 133 It
base of the lateral border of the coracoid process, just below is also necessary to have a complete understanding of the
the coracoacromial ligament, and merges with the capsule different functional tests to eliminate and be directed to the
laterally to insert on the lesser and greater tuberosities (Fig. problem. Some functional tests are more reliable than oth­
3-30A). The CHL becomes taut in external rotation and re­ ers, and just because they provoke symptoms, this does not
sists inferior subluxation of the joint. always indicate that the tissue tested is absolutely involved.

Table 3-2 Stabilizers of the Glenohumeral Joint Based on Position and Ranges of Motion

Anterior Translation Posterior Translation Inferior Translation

Dependent position (with Subscapularis (primary) Posterior capsule (primary) SGHL (primary restraint)
weight in hand-neutral SGHL SGHL Coracohumeral ligament
position, adducted 0° Middle glenohumeral Anterior superior capsule Supraspinatus, posterior
ligament Deltoid, levator scapula,
upper trapezius

Arm abduction, coronal Coracohumeral ligament Posterior capsule SGHL

plane, 0° to 45° SGHL Anterior superior capsule IGHL: primary restraint at
MGHL: secondary restraint Infraspinatus, teres minor 45°
at 45° Inferior glenohumeralliga­
IGHL: primary at 45° ment: primary at 45°

Arm abduction, coronal MGHL: primary restraint if IGHL: primary at 45° IGHL: primary restraint at
plane, 45° to 75° thick Posterior capsule 45°
Superior portion of IGHL: Infraspinatus, teres minor
primary restraint at 45° to Anterior superior capsule
Subscapularis: decreasing

Arm abduction, coronal IGHL: primary restraint at IGHL: primary restraint at IGHL: primary restraint at
plane, over 75° 45° to 90° 45° to 90° 45° to 90°
MGHL: secondary restraint Posterior inferior capsule
at 90° Anterior superior capsule

IGHL, inferior glenohumeral ligament; MGHL, middle glenohumeral ligament; SGHL, superior glenohumeral ligament.

With experience and a battery of tests, the clinician can usu­ Inspection
ally arrive at a predictable decision.
The patient's entire upper extremity should be viewed
because distal portions of the arm to hand may reveal atro­
Sensitivity, Specificity, Positive Predictive Value phy or vasomotor changes caused by the proximal shoul­
der. Inspection involves an overview of the patient
"Sensitivity" of a test is defined as the probability that pa­ regarding symmetry (bony and soft tissue contour), muscle
tients who truly should have the positive response have that atrophy or hypertrophy, postural attitude , deformities , dis­
response when the test is performed. When a test has a very colorations, scars, and swellings (see under Lesions for par­
high sensitivity, a negative clinical finding effectively rules ticular deformities, e.g. , dislocations) .
out the diagnosis.135 "Specificity" of a test is defined as the
probability that patients who should truly have a negative
response express a negative response when the test is per­ Anterior Shoulder
formed (true-negative rate). "Positive predictive value" is
defined as the probability that a patient who receives a pos­ Symmetry: Check for symmetry of the clavicle and AC
itive test result will truly have a positive response (the ac­ and SC joints. An abnormal clavicular contour may be due
tual pathology tested for) ,l36 but predictive values of to an old fracture . In a step-down deformity, the distal clav­
clinical tests vary with disease prevalence and are popula­ icle appears superior to the acromion because of a recent or
tion dependent; therefore, they are not good estimators of old AC sprain or dislocation. Prominence of the distal clavi­
test performance. l37 cle may be due to a distal clavicular fracture or osteoarthritis
The Shoulder 65

of the AC joint. Anterior prominence or depression of the with forward shoulders. The posterior spine and paraspinal
sternoclavicular joint could indicate a recent or old injury tissue are put under strain in their attempt to brace the for­
wardly bending structure. Treatment of the painful posterior
Muscle Atrophy: The symmetry of the trapezius and structures, although necessary, cannot solve the problem
deltoid muscles should be observed and compared bilat­ unless treatment is also directed to the anterior pectoral
erally Inspect for anterior deltoid wasting (flattening of muscles and fascia.
the muscle, squaring of the lateral acromion, prominence Check for muscle wasting, spasm, or hypertrophy by
of the acromion, and abnormal protrusion or flattening viewing the sternocleidomastoid (SCM), scalenes, upper
of the greater tuberosity, indicating dislocation or deltoid trapezii, deltoids, and supraspinatus. Weak or wasted
atrophy), possible axillary nerve damage, instability, or scalenes may appear as a depression behind the SCM. V
impingement. Check also for atrophy of coracobrachialis! Janda (personal communication, 1994) regards this as part
biceps brachii (musculocutaneous nerve damage). Proxi­ of the aging process. The scapular spine may appear promi­
mal swelling of the arm may be due to distal biceps rup­ nent as a result of atrophy of the supraspinatus in the
ture; distal arm swelling of the muscle mass may be due suprascapula fossa (also seen posteriorly).
to proximal biceps rupture.

Posterior Shoulder
Arm Position: Most acute conditions result in an ad­
ducted and internally rotated arm. A minimally abducted
Scapulae: The scapulae should be symmetric with the
and externally rotated arm occurs in anterior dislocation. In­
inferior angles equidistant from the spine. If one side is more
ternal rotation and full abduction would not be possible. An
lateral, it may represent a scoliosis or loss of scapular stabi­
acute posterior dislocation (rare) would present with an in­
lization-possible weakness of the rhomboids anclJor serra­
ternally rotated and adducted arm. In thin patients with pos­
tus anterior or tightness of the pectoral muscles. Sprengel's
terior dislocation, you may see posterior prominence of the
deformity presents as a congenitally high, undescended
humeral head and anterior prominence of the coracoid 33
scapula. Prominence of the scapular spine may be due to at­
rophy of the suprascapular ancl/or infrascapular muscles oc­
Shoulder Height: Low shoulder usually occurs on the curring as a result of suprascapular nerve entrapment or tear.
dominant side as a result of overstretch of muscles, liga­
ments, and capsule. Usually, there are more hypertrophic
muscles on the dominant side. A difference in height may Static Evaluation of Scapular Winging (see Scapular
be due to scoliosis. Dyskinesis): With weakness of the serratus anterior, the
scapula is in a more superior position away from the poste­
rior chest wall (proximal winging). The inferior angle will
Lateral Shoulder be in a medial position. The examiner will find that press­
ing into the medial border of the scapula will offer less re­
The humeral head should appear as a smooth, rounded sistance than found on the normal side. With weakness of
contour anterior to the acromion. Forward, internally ro­ the trapezius, the scapula shifts inferiorly and lateralward,
tated shoulders are usually associated with a forward head or the scapula body is held in position while its medial bor­
position, which adversely affects the biomechanics of the der becomes more prominent. 138 A common cause of the
shoulder because the anterior muscles are working from a lower border of the scapula'S flaring out is weakness of the
shortened position and the external rotators are under ten­ middle trapezius or rhomboids B 5
sion. Usually associated with forward shoulders are chroni­
cally shortened upper trapezii and levator scapulae
associated with weakened middle and lower trapezii, serra­ Palpation
tus anterior, and latissimus dorsi, creating an abnormal
force couple and predisposing to an impingement syn­ Although palpation is important for recent or past post­
drome. The upper trapezius may contract before the del­ traumatic anatomic deviations, muscle tone, tissue sensitiv­
toids , adversely affecting scapulohumeral rhythm. Also ity, warmth, and swelling, palpation is also very important if
associated with this posture are tight pectoral muscles functional testing leads you to the source of the pain (Le.,
anclJor shortened anterior chest fascia. pain on resistive testing of the infraspinatus/teres minor
Forward shoulders are often the cause of posterior tho­ would lead you to those particular muscles and tendons).
racic pain. Palpation of posterior parathoracic areas usually Always evaluate the superficial fascia by determining
reveals thickened and tender fascial bands in the patient whether the skin moves freely in all directions.

Anterior Shoulder Causes of Crepitus (A udible and/or Palpable) During

Shoulder Movement
Run your fingers over the sternoclavicular joint, feeling
for depression or protrusion (posttraumatic) and along the Crepitus can be elicited, with the patient sitting, by
clavicle to the AC joint (to pinpoint tenderness for a pos­ holding the acromion down while passively moving the
sible AC sprain). Check the supraclavicular region for shoulder in a total range of circumduction. Crepitus is
nodes or thickenings. Examine the anterior subacromial caused by any of the following:
bursa and supraspinatus insertion by extending the arm
and palpating these structures beneath the anterior • Scarring of the subacromial soft tissues, espeCially the
acromion (position for palpation is demonstrated in Fig. bursa (irritation of bursal side of rotator cufD or
3-57. Palpate the long head of the biceps and surrounding scapulothoracic bursa14l Continued crepitus after de­
greater and lesser tuberosities by flexing the elbow at 90° compression surgery may indicate the remains of
with the shoulder in neutral and internally and externally thickened bursa because of an incomplete bursec­
rotating the shoulder (demonstrated in Chapter 14, Fig. tomy.142 The subacromial bursa is probably the chief
14-9). Check for trigger points along the scalene, SCM, cause of crepitus.
and deep cervical flexors . Palpate the coracoid process and • Torn glenOid labrum
associated coracoid bursa, pectoralis minor, coraco­ • Osteoarthritis of the AC or glenohumeral joint
brachialis, short head of the biceps, and coracoacromial
ligament superior and lateral to the coracoid. The cora­ • Intra-articular loose bodies
coacromial ligament palpates tender if it is involved (see • Rotator cuff tears (Rotating the arm at 90° elevation
Chapter 14 for palpation of the ligament and a possible may create crepitus due to abrasion of torn tendon
treatment , Fig. 14-17). Palpate the cora co acromial and margins against the AC arch.l)
coracoclavicular ligaments for differentiation of grade I • (see Snapping Scapula)
and grade II AC sprains (see under Acromioclavicular
Sprain) . Evaluation of Shoulder Active Range of Motions
The anterior capsule may be palpated just lateral to the
coracoid process. Confirmation of capsular tenderness may Evaluation of both active and passive motion is best per­
be assumed if the tenderness remains under the finger dur­ formed with the patient supine to fix the scapulae and min­
ing internal and external shoulder rotation 139 Patients with imize misleading compensatory actions of the spine and
anterior subluxation and secondary impingement findings pelvis. Evaluation of the passive motion is also probably
usually have tenderness over the greater tuberoSity or bi­ more accurate in the sitting position than in the standing
ceps tendon, whereas patients with multidirectional insta­ position for the same reasons. Because active motions stress
bility often have diffuse tenderness along the anterior cuff both contractile and inert tissue, active testing is used as a
and occaSionally posterior cuff structures 140 baseline to assess the present status of the shoulder against
future progress. In this text, contractile and inert tissues are
evaluated separately (see Chapter 1), and the information is
Posterior Shoulder correlated to determine which particular tissue or tissues
are involved. A loss of active range of motion coupled with
Palpate the upper trapezius, levator scapulae (espeCially normal passive motion may indicate a muscular cause. Loss
the superior medial border of the scapula), infraspinatus, of active shoulder motion may be caused by pain inhibition,
teres minor, middle trapezius, and rhomboids for in­ muscle weakness, soft tissue impingement, bony blockage,
creased tension, adhesions, and trigger points. The infe­ ankylOSiS, or fusion.
rior medial angle of the scapula may reveal an inflamed Simple assessment of shoulder range of motion, as de­
bursa. The posterior capsule may be palpated laterally scribed by Matsen et ai, 1 uses four parameters:
under the deltoid at the 9-0'clock to 12-0'clock areas of
the posterior shoulder, with the patient prone and the arm 1. Figure 3-31 illustrates the maximal angle of humeral
hanging (see Fig. 14-5). The posterior deltoid reaches elevation in flexion. Only 4% of men and 28% of
over along the posterior acromion to the superior medial women actually reach 180°. In one study, the mean
border of the scapula and therefore covers the lateral por­ range for women was 171° and for men was 167°28
tion of the infraspinatus belly. Palpation of the infraspina­ Active tests that combine lateral rotation and abduc­
tus belly should therefore be more medial than usually tion (Fig. 3-32A) and medial rotation and adduction
thought. (Fig. 3-32B) may also be used .
The Shoulder 67

Humeral Elevation

Figure 3-31 Maximal elevation is measured with the patient

supine with the opposite arm assisting in elevation, if necessary, to
gain maximal range. Source: Reprinted with permission [rom FA
Matsen , SB Lippit, JA Sidles, and DT Harryman. Practical Evalua­
tion and Management of the Shoulder. Figure 2-1, © 1994, WE Saun­
ders Company.

2. Figure 3-33 illustrates the maximal angle of external

rotation with the arm at the side.
3. Figure 3-34 illustrates maximal internal rotation. The
evaluation of shoulder internal rotation, although rec­
ommended by the American Shoulder and Elbow
Surgeons, has been criticized because pure shoulder
internal rotation is not being measured. It is possible
that a pathological condition of the elbow, wrist, or
thumb might alter the range of motion being
tested. 143 It was found that measurement of internal
rotation by vertebral level is not readily reproducible
between observers 143 Mallon et aJl44 found that the
scapulothoracic articulation was more Significant in
placing the arm behind the back by extension and in­
ternal rotation of the scapula on the thorax, and limi­
tation of this motion may not be strictly due to a loss
of internal rotation at the glenohumeral joint. Internal
rotation assessment by the "thumb on the spine"
method has 6° of freedom inherent in the test and has
no correlation with goniometrically measured gleno­
humeral rotation,145 because only one motion is Figure 3-32 A), Active combined lateral rotation and abduc­
glenohumeral. Figure 3-35 illustrates maximal cross­ tion. B) , Active combined medial rotation and adduction.
body adduction.
4. Figure 3-36 illustrates humerothoracic elevation,
measuring the angle between the humeral shaft and
the thoracic axis. Because these motions are impor­
tant in the stiff shoulder, Matsen et all estimated the the pain arises (see Passive Abduction). Pain at the extreme
values of these ranges in a population of 81 normal range of motion and associated crepitus is almost always
subjects aged 60 to 70 years . soft tissue in nature 140 Matsen et aJl state that in partial­
thickness tearing of the cuff muscles (see Rotator Cuff Rup­
During the assessment of active motions, the examiner turesfTears), there may be development of scarring, which
should also be aware of the area of pain and at what range would limit the range of shoulder elevation, horizontal

Cross Body



Figure 3-33 Maximal external rotation is measured with the Figure 3-35 Maximal cross-body adduction is measured as the
arm at the side (0° being the position in which the forearm of the minimal distance from the antecubital fossa to the contralateral
flexed elbow points straight ahead). We prefer to make this meas­ acromion when the arm is adducted horizontally across the body.
urement with the patient supine to help fix the thorax. Source: Source: Reprinted with permission from FA Matsen, SB Lippitt, JA
Reprinted with permission from FA Matsen, SB Lippitt, JA Sidles, Sidles, and DT Harryman. Practical Evaluation and Management of
and DT Harryman. Practical Evaluation and Management of the the Shoulder. p. 21, © 1994, WE Saunders Company.
Shoulder. p. 21, © 1994, WB Saunders Company.


T3 ­


• • t •• '
L4-L5 , .... t'

Figure 3-36 Humerothoracic elevation. The angle of elevation

Figure 3-34 Maximal internal rotation is measured by the high­ is the angle between the humeral shaft axis and the thoracis axis.
est segment of posterior anatomy reached with the thumb, for ex­ The angle is measured in the plane that contains these two axes,
ample, L4-L5, T7, T3, or C7. Source: Reprinted with permission that is, the plane of humerothoracic elevation. Source: Reprinted
from FA Matsen, SB Lippitt, JA Sidles, and DT Harryman. Practical with permission from FA Matsen, SB Lippitt, JA Sidles, and DT
Evaluation and Management of the Shoulder. p. 21, © 1994, WE Harryman. Practical Evaluation and Management of the Shoulder. fig­
Saunders Company. ure 2-5 on page 39, © 1994, WE Saunders Company.
The Shoulder 69

adduction, and internal rotation. The evaluation of active anterior tilt and forward pull on the scapula and weakness
motions at a later date is one of the ways of determining pa­ in the upper and lower trapezius, rhomboids, serratus ante­
tient progress. rior, and levator scapulae,148,lS0 with the serratus anterior
Active elevation of the shoulder may be limited and pas­ and lower trapezius probably being the most important. 1S1
sive elevation may be normal. This condition usually refers Other possible causes are shortened clavicles due to frac­
to a contractile problem, possibly due to a neurologic prob­ tures, acromioclavicular arthrosis, and injuries resulting in
lem or a problem due to inert structures. Other possible acromioclavicular instability, all of which may alter scapular
causes, according to Ombregt et al,146 may be a stress frac­ kinematics.
ture of the first rib. In this case, active and passive move­
ment of the neck away from the pain side might pull on the Postural Causes: Scapular dyskinesis may be related
rib, causing pain, and scapular movements (active, passive, to posture, such as in excessive thoracic kyphosis and cervi­
and resisted) may be painful, but the patient may not be cal lordosis, which may cause excessive scapular protraction
able to elevate the arm beyond 90° Long thoracic nerve in­ and acromial depreSSion, resulting in impingement.
volvement causing scapular winging due to serratus ante­ Slumped posture with rounded shoulders stretches the an­
rior weakening would limit active arm elevation to 45° to terior capsule and tightens the posterior capsule (see Inter­
90° (normal passive elevation) and spinal accessory nerve pretation of Limited Passive Internal Rotation). With
involvement of the trapezius causing a painless limitation of slouching or thoracic kyphosis, there is less normal poste­
about 5° to 10° of active arm elevation with normal full­ rior tilting of the scapular, predisposing to an impingement
range passive elevation. In both of the above cases, the pain syndrome by narrowing of the subacromial space during
is acute during the first 3 weeks before the active weakness shoulder elevation 149 With drooping shoulders causing a
shows. Other possible causes of weakness of active eleva­ protracted scapula, shoulder abduction is limited compared
tion with normal passive elevation might be involvement of with shoulder abduction with a normal posture. Erect sit­
the C5 nerve root due to severe weakness of the supraspina­ ting posture allows an increase in active range of shoulder
tus and deltoids or total rupture of the supraspinatus when flexion in patients with an impingement syndrome (see
some associated weakness of the subscapularis and infra­ Muscular Weakness and Imbalance between Force Couples
spinatus is present. for contradictory evidence regarding postural causes and
shoulder impingement). lS2

Scapulohumeral Rhythm Dynamic Evaluation of the Scapula: The scapula moves

Simultaneously about 3 axes of rotation and translates. It
Normal Synchrony: During arm elevation, the scapula normally tilts posteriorly and rotates medially and upwardly
usually does not move until 30° of abduction. From this as the arm elevates. 1S3 Scapulothoracic instability is defined
point on, the scapula rotates 12° for every 30° of gleno­ by either winging of the scapula at rest or obvious asynchro­
humeral abduction (2:1 scapulohumeral ratio in the coronal nous motion after a few repetitions of abduction. 1s4 Evaluate
plane). In the scapular plane, the scapulohumeral ratio is scapulothoracic instability by observing scapulohumeral
3:2 (see Scapulothoracic Motion). Bagg and Forrest 147 rhythm. Stand behind the patient and have him or her re­
found complete arm abduction from 154.9° to 18l.3°, with peatedly and slowly elevate the arm in the scapular plane
the average at 168.1°. The scapular contributed on average and return to neutral three to five times. Muscle weakness
63.8° and glenohumeral motion on average 104.3°. and mild scapular dyskinesis are noted more frequently in
the descending phase of the arm movement 17 because both
Scapular Dyskinesis: This is an alteration in the nor­ the serratus anterior and the trapezius must function eccen­
mal position or motion of the scapula during coupled trically to stabilize the scapula against the chest wall during
scapulohumeral movements 148 Although no particular pat­ arm descent. Look for possible reversal of rhythm resulting
tern of abnormal scapular motion has been associated with in shrugging, in which case, the scapula moves first, and
a particular shoulder diagnosis, normal scapular motion more than the humerus. Grasp the inferior-lateral border of
and stabilization are essential for normal humeral motion the scapula and ask the patient to elevate the arm slowly
(see Role of the Scapula). Kibler and McMullen 148 stated The point at which the scapula moves in relation to gleno­
that alterations in the function of the muscles that control humeral motion is noted. Normally, the scapula does not ro­
scapular motion are the most common cause of scapular tate but moves laterally for the first 30° to 50° of humeral
dyskinesis. Scapular dyskinesis has been found in impinge­ abduction. Visualize the motion of the scapula and gleno­
ment syndrome and glenohumeral instabililty.1 49 It is im­ humeral joint, and notice whether there are any hesitancies
portant to evaluate for muscle tightness in the pectoralis or breaks in the usual smooth normal motion. This type of
minor and short head of the biceps, creating an abnormal asynchrony may be due to adhesive capsulitis, ruptures,

subacromial inflammatory conditions, or a chronically short­

ened upper trapezius, to name a few possibilities.
With loss of internal rotation there may be compensatory
excessive movement or asymmetric movement of the
scapula on the chest walL2 Loss of shoulder internal rota­
tion is often due to a tight posterior capsule.
If the scapula is found to shift laterally with arm eleva­
tion, it is necessary to test the scapular stabilizers, especially
the rhomboids, middle trapezius, and serratus anterior, for
Winging can be functionally tested by having the patient
push against a wall, especially with the shoulders flexed for­
ward 45° (Fig. 3-37). Paine84 developed a dynamiC scapu­
lar winging test whereby a patient forward flexes the
shoulders with resistance, using rubber tubing, from neu­
tral up to 90° (Fig. 3-37A and B). Winging will occur espe­
cially with up to 45° forward arm flexion because the
scapula is in a setting phase at this range just before it cou­
ples with the glenohumeral joint. Winging can also be de­
tected by resisting a patient's arm elevation during forward
flexion. Bilateral winging may be normal in the asympto­
matic hypermobile patient 84 Testing the serratus anterior
with the patient's hands below the horizontal causes this
muscle to be at a mechanical disadvantage and makes it
more sensitive to weakness.
To evaluate scapular muscle strength, have the patient
perform an isometric scapular retraction pinch. If there is a
burning pain in less than 15 seconds, there may be weak­ Figure 3-37 Position shows winging of the scapula by having
ness of the scapular adductors. Normally a patient can hold the patient push into the wall with the hands below the waist. The
serratus anterior contracts to prevent backward rotation of the
this position for 15 to 20 seconds with no burning or
scapula. If weakness is present unilaterally, winging will be ob­
weakness 17
served. Source: Reprinted with permission from JR Andrews and
KE Wilk. The Athlete's Shoulder. p. 496, © 1994, WE Saunders
Scapular Winging

The subscapularis and the serratus anterior muscles help

stabilize the scapular against the chest wall and thus pre­
vent scapular winging. 155
• Weak trapezius: the scapula shifts inferiorly and later­
alward, or the scapula body is held in position while
Causes of Scapular Winging
its medial border becomes more prominent. 138
• Involvement of the long thoracic nerve due to trauma, • Weak serratus anterior (A weak serratus anterior is
repetitive overuse, idiopathic conditions, virus, pro­ the Single most commonly affected muscle in a rare
longed bed rest, general anesthesia, and inocula­ cause of shoulder pain and weakness known as acute
tions 156 (see Long Thoracic Nerve Injury). brachial neuropathy. 159 This diagnosis is sometimes
used to describe an unexplained shoulder pain or
• Congenital deformity or scoliosis
weakness, or both 160 [see Brachial Neuropathy].)
• Paralysis of the trapezius results in an elevated
• Paralysis of the serratus anterior would not allow ele­
acromion and a protracted inferior scapular border. 157
vation of the arm beyond 90°. A weak or damaged
• Muscular imbalance with associated weak serratus rhomboid might also cause scapular winging but arm
anterior 158 elevation would be normaP6
The Shoulder 71

Figure 3-37A and B This technique allows the clinician to view scapular winging during the dynamic elevation of the arm. Resistance from the
rubber tubing forces maximum contraction of the serratus anterior to stabilize the scapula. Weakness will be observed unilaterally as scapular
winging. Source: Reprinted with permission from JR Andrews and KE Wilk. The Athletes Shoulder. p. 497, © 1994, WE Saunders Company.

• Pure serratus anterior weakness due to nerve palsy re­ ther studies were needed. Clinically, however, learning
sults in a prominent superior medial border and a de­ these abnormal scapular patterns and applying stretching
pressed acromion. 157 and strengthening to involved tissues and paying attention
• Multidirectional instability (especially posterior insta­ to the kinetic chain should provide a basis for restoring a
bility) normal functional scapular pattern.
The pattern should be viewed by using the scapular
• Painful shoulder conditions associated with splinting
landmarks, such as the inferior medial angle, the superior
of the glenohumeral joint 138
medial angle, and the posterior acromial edge. The patient
• Voluntary self-induction, without pathology is observed first with the arms at rest at the side, and then
• Lax shoulder (Scapular winging is often seen in a scapular motion is observed as the arms are elevated and
young athlete with no specific shoulder complaints lowered in the scapular plane. It is important at this point
who has a physiologically lax shoulder161 [see Adoles­ to observe the patient's posture (see Postural Causes of
cent Shoulder].) Scapular Dyskinesis). Figure 3-37C depicts the type I pat­
tern, where at rest (AI) the inferior medial border may be
Several weeks may be necessary after a trauma before prominent dorsally, and with motion (B2) , the inferior angle
scapula winging occurs, to allow an overlying contracted tilts dorsally and the acromion tilts anteriorly over the top
trapezius to stretch out. of the shoulder. This axis of rotation occurs in the trans­
verse plane (C). Figure 3-37D shows the prominence of the
Patterns of Scapular Dyshinesis inferior medial border in type I dyskinesis. Possible muscle
involvement in type I might be tightness of muscles (pec­
Kibler et aP48,162 performed a reliability study observing toralis minor, biceps short head) and fascia related to the
scapular dysfunction as it moves around three axes of mo­ coracoid process, weakness of the serratus anterior, and
tion and translation Simultaneously The patterns of motion lower trapezius. The tilting of the acromion ventrally can be
observed allows a rapid method of assessing different pat­ related to impingement syndrome, and the scapular retrac­
terns of scapular dyskinesis. The authors stated at the end tion and scapular assistance tests (see Scapular Retraction
of the study that they had not reached any conclusion as to and Scapular Assistance Test) would probably be positive.
guidelines for treatment, nor did they correlate any particu­ Burkhart et al 163 found a pattern similar to type I in patients
lar pattern with a specific shoulder diagnosis, because fur­ with posterosuperior labral lesion. The pattern consisted of

inferomedial scapular border prominence at rest, with in­ and during motion (B2), movement is initiated by a shrug
creasing prominence, lack of acromial elevation, and lack of with superior translation of the entire scapula. The patient
full retraction on cocking. This pattern was associated with may be relieving impingement by shrugging to lift acromion
inflexibility of the pectoralis major and minor and weakness from compression of the cuff. There is no significant wing­
of the lower trapezius and serratus anterior. Figure 3-37E ing. The axis of motion occurs in the sagittal plane (C). In
depicts the scapular dyskinesis type II pattern. The verte­ type III, both the scapular retraction and the assistance tests
bral border is dorsally prominent at rest (Al) and tilting off might be positive. Figure 3-37G shows the superior medial
the thorax with elevation in the scapular plane (B2). This border prominence (A) and the scapular superior transla­
represents the classical "winging of the scapula." This mo­ tion on the shoulder (B). This pattern may be due to a weak
tion occurs vertically in the frontal plane (C) (see Scapular serratus anterior. Also check the pectoralis minor and ante­
Winging). The scapular assistance test might be positive rior shoulder fascia. Burkhart et aP64 stated that the type III
(see Scapular Assistance Test). Burkhart et aP63 found a pattern is associated with impingement and rotator cuff le­
type II pattern again with posterosuperior labral lesions. sions rather than labrallesions.
They found the entire medial border of the scapula winging
at rest, which became more prominent with cocking or ele­
vation. In this case, there was weakness of the upper and Effects of Scapular Dyskinesis
lower trapezius and rhomboid. Figure 3-37F shows the
Type III dyskinetic scapular pattern, which at rest (Al) Kibler and McMullen 148 stated that with scapular dyski­
shows prominence of the superior medial scapular border, nesis, there is a loss of control of retraction and protraction

Figure 3-37D Shows the prominence of the inferior medial bor­

der of the scapula found in Type I dyskinesis.

Figure 3-37C Type I Diskinetic scalpular problem. A) at rest.

B) in motion. 1. Inferior med. border prominence dorsally 2. Infe­
rior angle tilts dorsally 3. Acromium tilts ventrally over the top
thorax. Source: Adapted from W Ben Kibler, et al. Qualitative clini­
cal evaluation of scalpular dusfunction: a reliability study Journal
of Shoulder and Elbow Surgery. Nov/Dec 2002, Vol. 11, No.6,
p. 550, Mosby
The Shoulder 73

;::::"~:e':~t::~ ',:

~ ®'\~


c. c.

Figure 3-37£ Type II dyskenetic scapular pattern. B2 with motion Figure 3-37F Type III dsykinetic scalpular pattern. Superior
emphasizes scalpular winging as shoulder elevates. Source: medial border elevated and slightly anteriorly displaced (promi­
Adapted from W Ben Kibler, et al. Qualitative clinical evaluation of nence of superior medial border). Source: Adapted from W Ben Ki­
scalpular dusfunction: a reliability study. Journal of Shoulder and bler, et al. Qualitative clinical evaluation of scalpular dusfunction:
Elbow Surgery. NovlDec 2002, Vol. 11, No.6, p. 550, Mosby. a reliability study. Journal of Shoulder and Elbow Surgery. NovlDec
2002, Vol. 11 , No.6, p. 550, Mosby.

Figure 3-37G Type III dyskinesis: shows the superior medial border prominence A) and the scapular superior translation on the thorax
B). Source: Adapted from W Ben Kibler, et al. Qualitative clinical evaluation of scalpular dusfunwon: a relIabllIty study. Journal of Shoulder
and Elbow Surgery. NovlDec 2002, Vol. 11, No.6, p. 550, Mosby.

of the scapular necessary for overhead shoulder function. The Scapular dyskinesis is detrimental to the function of the
scapula must move in relation to the moving humerus to scapula in the kinetic chain. The kinetic chain starts from
maintain a "safe zone" of glenohumeral angulation and avoid the ground through the legs to the trunk, which act as the
hyperangulation of the humerus on the glenoid. 163,165 In­ force generators, and the shoulder acts as a funnel and force
creased angulation can result in increased humeral external regulator and force transferer, while the arm acts as the
rotation in the cocking and acceleration phase, causing the force-delivery mechanism finally to the arm and hand. The
arm to lag behind the body, increasing what is known as the more disadvantaged the proximal structures, the more bur­
"peel-back effect." There is a dynamic peel-back sign (seen den is put on the distal structures. Burkhart et aP63 believe
anhroscopically) in patients with posterior superior labrum that the labrum is key in providing glenohumeral stability
anterior posterior (SLAP) lesions, where the biceps can pro­ and may be injured by excessive force transmitted to the
vide a torsion force to the posterior superior labrum, causing shoulder if local or distant parts of the kinetic chain are
it to rotate medially over the comer of the glenOid onto the su­ stressed. It is important to evaluate the links in the kinetic
perior scapular neck. The biceps superior labrum complex, chain, such as hip/trunk strength and flexibility, spinal flex­
instead of being pulled from bone, is probably "peeled" from ibility, and scapular position and motion.
the bone. 163 In the cocking phase, a lack of full scapular re­
traction results in increased glenohumeral angulation and loss Snapping Scapula
of the stable base in arm elevation (see Role of the Scapula).
The scapula must provide the stable base necessary for the ori­ Etiology: The etiology of snapping scapula may be id­
gin of the extrinsic and intrinsic muscles that control arm mo­ iopathiC. Skeletal abnormalities include changes in the bone
tion and provide glenohumeral compression. If the scapular structure of the scapula surface or of the ribs. A tumor, such
does not fully protract around the thoracic wall, there is an in­ as osteochondroma (most common of the scapula),
crease in the deceleration forces of the shoulder that abnor­ Luschka's tubercle (exostosis of superiomedial scapula) ,
mally affects the normal "safe zone" (excess angulation) as the may be associated with Sprengel's deformity, scapular frac­
arm moves through the acceleration phase into horizontal ad­ ture malunion, and abnormal anterior angulation of the su­
duction. Tightness of the anterior coracoid muscles or the perior angle of the scapula. 166 Soft tissue causes might be
posterior capsule may create excess protraction, resulting in soft tissue tumors, repetitive micro trauma causing pe­
impingement as the scapula rotates down and forward. Exces­ riosteal micro tears with scars, traction osteophytes and
sive protraction by increasing glenohumeral angulation out­ bone spur formation in the medial muscle attachment,167
side of the safe zone can be responsible for anterior tension inflammation of the subscapular bursae, between the serra­
and posterior compression. Ideal muscle activation occurs tus anterior and subscapularis or between the serratus ante­
when the angle between the glenoid and humeral head is less rior and the ribs of the lateral chest wall or at the inferior
than 30°. angle of the scapula. 168 Some other problems leading to this
Burkhart et aP63 stated that lower-trapezius weakness is condition are muscle atrophy from disuse or nerve injury
associated with major alterations in scapulohumeral rhythm leading to a diminished soft tissue interposition between
because' it is a major scapular retractor and upward rotator, the scapula and the rib cage, muscle fibrosis from a previ­
with its line of action at a maximum with arm elevations be­ ous traumatic event, scoliosis, and thoracic kyphosis. 169
tween 45° and 100°. They stated that "decreased retraction Rarely, espeCially in pitchers, a nonneoplastic soft tissue
increases posterior glenohumeral compression on the labrum growth due to repetitive microtrauma, called an elastofi­
and rotator cuff and decreases the scapular role as a stable broma,167 may be causative. Grunfeld 169 found that scapu­
base for muscle origin, thereby effectively decreasing mus­ lar crepitus was asymptomatic in 31 % of 100 asymptomatic
cle strength" (see Scapular Retraction Test). Weakness of the persons.
serratus anterior and lower trapezius results in diminished
acromial elevation, causing a secondary impingement and Symptoms and Signs: Patient describes an audible ,
eventual rotator cuff tendinopathy and shoulder instability. palpable crepitus, and snapping, associated sometimes with
Especially overhead athletes may develop tenderness at the pai.n in the scapulothoracic area with shoulder girdle move­
superomedial angle of the scapula at the insertion of the le­ ments, especially at the superior angle and medial border of
vator scapula and posterosuperior periscapular and lower the scapula. The patient usually can create the feeling vol­
para cervical pain, because as the dyskinetic scapula tilts untarily moving the scapula. Sometimes, the shoulder is de­
and rotates laterally, excess traction is created on the levator scribed as " out of place." 168 Check for a shortened
scapulae, causing pain and muscle spasm. This would be pectoralis minor by observing a supine patient where the af­
relieved by the Scapular Retraction Test. 87 fected shoulder's resting position is anterior or higher.169
The Shoulder 75

Differential diagnosis: anything that might cause poste­ The leg and trunk must provide a stable base for arm mo­
rior scapular pain, including neoplasm, myofibrositis and tion, provide rotational momentum for force generation,
referred pain from the glenohumeral joint, subacromial and in the tennis serve, generate 50% to 55% of the total
bursa, or cervical root compression. It may be difficult to force and kinetic energy. 163
discover the precise site of the snapping. A simple test to evaluate pelviC lower-extremity control
is to have the patient perform a one-legged squat and evalu­
Treatment: Check for tightness or weakness in the sur­ ate balance and stability in a normal squat (Fig. 3-38A)
rounding muscles, such as the trapezius, latissimus dorsi, compared with an abnormal squat (Fig. 3-38B). Failure in
subscapularis, serratus anterior, rhomboids, deltoids, and the one-legged stance or squat indicates that a stable post
levator scapulae. Rehabilitation should include correction of around which optimum trunk angular momentum does not
forward head and shoulder posture, strengthening, and exist. When the kinetic chain is unstable at this level, shoul­
stretching. Endurance training is important because many der rotation velOCity must increase by 15% to 40% to main­
of the scapular muscles function as static stabilizers of the tain the same hand kinetic energy 163 Young et al 88 stated
shoulder girdle. It is important to stretch the antagonist that inflexibility of the hip musculature and weakness of the
muscle that might be inhibiting the weak muscles. 169 Mose­ muscles attaching to the thoracolumbar fascia affect spinal
ley et all 70 recommended exercises, such as scaption (lifting function, which secondarily affects the glenohumeral joint
weights in the scapular plane), push-ups with a plus, press­ and rotator cuff muscles. Evaluation of the patient's lordosis
ups, and rowing exercises. Soft tissue methods may be may be significant because increased lumbar extension dur­
tried, especially ones that release the surrounding fascia. If ing shoulder external rotation could prove detrimental to
there is a structural cause, surgery may be necessary If the the kinetic chain if the muscles supporting the lumbar
patient complains of pain and popping, grinding sounds spine are fatigued, creating a "passive" lordotic motion.
being produced with voluntary motion, be sure to check Early spinal extension may prevent reaching of the 170 to
the opposite side, which may show a bilateral problem or a 175 of shoulder external rotation, causing the pitching
secondary litigation-type symptom. 168 Trigger point injec­
tions may be useful.

Scapula Rehabilitation

Cuff muscles require the stable base of the scapula for

optimal muscle length/tension ratios and preservation of ro­
tator cuff muscular energy within the kinetic chain. The ro­
tator cuff muscles of the shoulder are not considered arm
accelerators, but stabilizers whose primary function is
maintaining concavity compression (maintaining the
humeral head in the glenoid). Because the entire body
working in a proximal-to-distal sequence is necessary for
optimal function, McMullen and Uhl l7l emphaSized the use
of the entire kinetic chain for shoulder rehabilitation by ini­
tiating shoulder exercises through proximal segment move­
ment. Their program begins with trunk and scapular
control exercises, emphasizing the training of movement
patterns rather than isolated muscles. In their kinetic chain
shoulder rehabilitation, normalization of scapular move­
ment precedes rotator cuff exercising. With scapular dyski­
nesis, it is recommended that the scapula be rehabilitated
before the cuff muscles in order to prevent increased gleno­
humeral translation. Kiblerl72 stated that in athletes, before
formal shoulder rehabilitation, one must evaluate inflexibil­
ities of the hamstrings, hip, and trunk. Also strength, weak­
ness, or imbalances of the rotators of the trunk, flexors, and
extensors of the trunk and hip, and any subclinical adapta­ Figure 3-38A Normal one-legged knee squat to determine
tions of stance patterns or gait pattern must be evaluated. pelviC lower-extremity control.

Figure 3-38B Abnormal one-legged knee squat. Figure 3-38C Exercise integrating diagonal trunk rotation with
scapular retraction.

shoulder and arm to angulate out of the safe zone behind

the trunk in the cocking phase and in the acceleration
phase ("slow arm" theory). This might lead to a higher ball
release point and a loss of accuracy. With the assumption of
a passive lordotic posture instead of a controlled eccentri­
cally contracting hip, spinal flexors, and thoracolumbar fas­
cia, there will not be the required "preloading" of muscles
before the throw. 88 Tight external hip rotators may cause
painful hips on the throwing arm side and tight hip flexors,
causing anterior rotation of the pelvis that could create
poorly controlled lordosis as well as reduce stride length. 88
Normal extension of the thoracic spine in late cocking is
necessary to maximize shoulder external rotation. In a
study by Kebaetse et al,173 thoracic posture affected shoul­
der range of motion, strength, and three-dimensional
scapular kinematics. In a slouched (flexed) thoracic posi­
tion, there was decreased scapular upward rotation and
posterior tilting and increased superior translation. There
was also decreased muscle force and shoulder abduction
range of motion (ROM) in the slouched position, which
may be caused by altered scapular dyskinesia. It is therefore
necessary to evaluate the position of the thoracic spine at
Figure 3-38D "Low row" isometric exercise combining hip/ rest and in motion.
trunk extension, scapular retraction, and arm extension.
The Shoulder 77

Figure 3-38E Exercising the scapula in a closed-chain position

by sequentially elevating, depressing, retracting, and protracting.

It is important to integrate hip extension and trunk ex­

tension with scapular retraction, which occurs in activi­
ties/sports requiring shoulder external rotation. Full arm
elevation requires full scapular retraction, which requires
spinal extension and hip extension. Figure 3-38C integrates
diagonal trunk rotation with scapular retraction. Figure
3-38D is a "low row" isometric exercise combining
hip/trunk extension, scapular retraction, and arm extension
as the patient pushes against resistance in a posterior direc­
tion. This exercise can begin as an isometric exercise, pro­
gressing to an isotonic exercise. This exercise also activates
the serratus anterior and the lower trapezius 174 Closed­
chain exercises are ideal to use for the rotator cuff before
open-chain exercise. Closed-chain exercise promote co­
contraction of the cuff muscles and exercises them with
ghenohumeral compression that diminishes glenohumeral
translation. A closed-chain exercise for the scapula (Fig.
3-38E) consists of the patient leaning against the wall with
the arm straight in the scapular plane and sequentially ele­
vating, depressing, retracting, and protracting the scapula.
Figure 3-38F shows strengthening exercise for the paras­
capular muscles, using the letters "I," "Y," and 'T" The pa­
tient lies prone and raises arms up with a weight. Press-ups
leaning against a table or wall and push-ups with a plus are

Passive Testing

Passive testing of the shoulder is probably more accurate

with the patient supine, and next, sitting and the scapula
fixed to avoid synergistic scapulothoracic motion affecting Figure 3-38F Exercising the parascapular muscles: (a) patient
glenohumeral motion. prone with positions of letter "I," (b) letter "Y," and (c) letter "T."

Figure 3-40 Supine apprehension test.

Figure 3-39 Passive coronal abduction.

Passive Abduction

Passive abduction (Appendix 3-A) (see also Stability Test­

ing) in or slightly posterior to the coronal plane allows a
more reliable impression of the presence of a painful arc in
patients with an impingement syndrome, especially in
throwers and tennis players who complain of pain as they
abduct in the coronal plane during play 175 Range of motion
is near 180° (Fig. 3-39). For maximal motion of the joint
with the least capsuloligamentous stress, passive motion test­
ing should be performed in the scapular plane (R. f Warren,
MD, personal communication, March 1995) (Fig. 3-40).
A painful arc (Fig. 3-41) can occur with active or passive / "\ .
arm elevation and from the abducted to the adducted neu­
tral position in the coronal, scapular, and sagittal planes U
(forward flexion). It is defined as no pain to approximately
60° to 80°, pain to approximately 120°, and then no pain.
Painful arc represents a pinching in the subacromial space
caused by the follOwing:
• Inflammation and swelling of the superior portion of
the tenoperiosteal portion of the supraspinatus and .-~.

infraspinatus, subscapularis, biceps tendon, and sub­ Figure 3-41 Painful arc. Pain occurs approximately between
acromial bursa 60° and 130°. Pain beginning about 90° and continuing to end
• An osteophyte off the inferior acromioclavicular joint range may indicate an acromioclavicular problem. Source: © 1990,
or hypertrophiC inferior capsule of the AC joint David Bolinsky.
The Shoulder 79

• Enlargement of the outer end of the clavicle/AC joint;

• Hypertrophied coracoacromialligament
• Enlarged anterior-inferior surface of the acromion
(type 2 or 3).
A painful arc would negate deltoid or adductor muscle
involvement because these muscles are not subacromial. It
may represent an imbalance in the glenohumeral force cou­
ple,176 that is, a weak supraspinatus and a normal deltoid,
creating a deltoid superior shear of the humeral head dur­
ing abduction (Fig. 3-42).
Pain beginning from 90° of abduction to the end range
(180°) may indicate an AC involvement (see Fig. 3-41). Pain
at the end range of abduction, creating a pinching effect due
to abutment of the deep surface of tendon insertion against
the glenoid rim 1 (Fig. 3-43), could indicate involvement (de­
generation, inflammation, or partial tears) of the undersurface
of the tenoperiosteal portion of the supraspinatus and infra­
spinatus cuff insertions and the subacromial bursa.
Pain and limitation at the end range due to hard end feel
, .
may be due to loss of accessory joint play of the AC joint or ,,'
,, . ,f

the glenohumeral joint. During shoulder elevation, palpate

an inferior glide of the medial clavicle on the sternum and a
" . "

superior glide of AC motion 85 (see Chapter 11, Joint Mobi-

Figure 3-43 Abutment of the deep surface of cuff insertion
against the glenoid rim at the extremes of motion. Source:
Reprinted with permission from FA Matsen, SB Lippit, JA Sidles,
and DT Harryman. Practical Evaluation and Management of the
Shoulder. p. 117, © 1994, WB Saunders Company.

lization). The examiner must be aware of the varieties of

end feel i.n all passive testing. Pain and limi.tation at end
range may be due to scarred partial-thickness rupture of the
cuff. Pain also may be due to extrinsic causes, such as osteo­
phytes, hypertrophied coracoacromial ligaments, or ana­
tomic variations. Relief of pain at end range may indicate a
radicular cause because the nerve root stretch is reduced.
Patients may state that they feel relief at night sleeping with
the arm overhead.

Passive External Rotation

During the active motion of lateral rotation with the arm

abducted to 90°, full external abduction, and maximum
horizontal abduction, the humeral head normally moves 4
Figure 3-42 Abrasion of the superficial surface of the cuff by
the coracoacromial arch resulting from slight superior displace­
mm posteriorly because of normal tightening of the anterior
ment of the head relative to the glenOid. Source: Reprinted with band of the IGHL and contraction of the lateral rotators (see
permission from FA Matsen, SB Lippit, JA Sidles, and DT Harry­ also Stability Testing). If the patient has anterior instability,
man. Practical Evaluation and Management of the Shoulder. p. 117, © the humeral head during this active motion translates ante­
1994, WB Saunders Company. riorly and might create pain or apprehension 98 ,177 If the

Figure 3-44A Evaluating external rotation while stabilizing the Figure 3-44B Evaluating internal rotation while stabilizing the
scapula. scapula.

posterior capsule is contracted, the humeral head is pre­ goniometer can be used to the point where the scapula just
vented from shifting posteriorly and tends also to translate starts to move on the posterior chest wall.
more anteriorly (see under Capsule). Lateral rotation may
create posterior shoulder pain that may be related to inter­
nal impingement (see Internal Impingement) due to com­ Interpretation of Pain During Passive External Rotation
pression of the articular side of the supraspinatus and with Abduction and Extension
infraspinatus and greater tuberosity against the posterosu­
perior glenoid labrum, particularly in the overhead thrower. • Instability: Patients with recurrent anterior dislocation
Because different ligamentous structures act as stabilizers or severe subluxation may present with immediate ap­
at different levels of abduction and rotation, you can local­ prehension and pain or a sudden protective muscle
ize the areas of involvement, depending on the position contraction to prevent a possible dislocation. "Appre­
tested 17B Testing can be performed at 45°, 90°, and 135° hension" is described as a feeling that the shoulder is
abduction in external rotation in the scapular plane, with "coming out of joint" or "slipping," as well as associated
the patient sitting. The examiner places one hand on the facial grimacing. The apprehenSion sign is usually due
posterior-superior aspect of the upper humerus and pushes to a compromising of the anteroinferior capsule, infe­
from posterior-inferior to anterior-superior, while slowly in­ rior glenohumeral ligament, or glenoid labrum. With
creasing external rotation with the other hand. The exam­ anterior instability, there is often abnormal superior
iners fingers should be on the anterior portion of the translation of the humeral head during scapular plane
shoulder as a barrier in case of sudden anterior instability. abduction. Fifty percent of patients with subluxation
Testing with the arm at 45° abduction in the scapular plane may not respond with apprehension. 179 Patients with
stretches and may be limited by the subscapularis, coraco­ only anterior subluxation experience pain and possible
humeral ligament, superior and middle glenohumeral liga­ clicking, but not usually apprehension. IBO Without the
ments, and anteroinferior capsule. The subscapularis patient's experiencing apprehension, we cannot be sure
becomes less important as an anterior stabilizer after 45°. At that a subluxation exists with this test, because the pain
90°, the IGHL is primary and the MGHL is secondary, and may be due to cuff tendinopathy, disorders, and so on
at 135°, the IGHL complex is primary. The supine position (see Pain without Signs of Instability).
is the most accurate method of evaluating shoulder rotation • A sudden loss of external rotation and sharp paralyz­
because the scapula can be stabilized against the examina­ ing pain in full abduction may be due to anterior sub­
tion table by downward pressure applied by the examiner luxation or impending dislocation (dead arm
to the anterior shoulder. Figure 3-44A evaluates external syndrome 1BI ). If in a throwing athlete, pain is pro­
rotation, and Figure 3-44B evaluates internal rotation. A duced in the abduction, extension, and external rota­
The Shoulder 81

tion positions, an anterior subluxation is probable,

shoulder in 90° abduction in the scapular plane with
even in the absence of apprehension. 182
maximum external rotation creates pain in the posterior
• Impingement: Pain may be elicited in patients with im­ aspect of the shoulder. This finding may indicate (90%
pingement who may have an occult instability, which sensitivity) for the diagnosis of partial-thickness under­
can best be identified by the anterior release test (see surface tears of the rotator cuff or posterior superior
Anterior Release Test under Anterior Stability Tests). labrum 184 (see Relocation Test for Internal Impinge­
Impingement of the upper surface of the rotator cuff, bi­ ment and Mayo shear test for posterior labral tear).
ceps, and subacromial bursae occurs against the cora­ Painful isometric testing of the cuff muscles determines
coacromial arch. According to Matsen et al, 1 when the whether passive testing is stretching a lesioned
humerus is extended, abducted, and externally rotated, muscle/tendon.
the comer of the glenOid normally abuts against the in­
• Rupture: Pain may be due to deep surface tearing of
sertion of the cuff at the tuberosity, but if the anteroinfe­
the supraspinatus, where its tendon is trapped be­
rior capsule is stretched, allOwing the humerus to shift
tween the tuberosity and the superior glenoid rim (in­
anteriorly instead of the normal posterior direction,
ternal impingement)185 (see Rupture).
there is an increased posterior contact between the gle­
noid lip and the insertion of the cuff at the greater • Stretches the subscapularis (especially when exter­
tuberosity (Fig. 3~5). This contact may "challenge the nally rotated below 75° abduction) and the pectoral
integrity of the posterior cuff insertion and the tuberos­ muscles.
ity." 1 The impingement occurs between the undersur­ • Stresses the AC ligament.
face of the tendinous portions of the supraspinatus and • The end feel may reveal joint play restriction of AC
infraspinatus muscles and the posterosuperior border of joint or glenohumeral joint. Palpate the AC joint and
the glenoid rim, also called "secondary subacromial im­ test for normal joint play motion.
pingement," 183 or internal impingement. Internal im­
• Anterior shoulder pain may be due to compression in
pingement can be suspected in the overhead athlete the quadrangular space (rare),186 especially if the
when the athlete complains of pain in the posterior
shoulder is abducted and externally rotated for about
aspect of the shoulder in the late cocking and early ac­
a minute 187 (see Quadrilateral Space Syndrome).
celeration phases of throwing (see Impingement Syn­
drome). With internal impingement testing, the • External rotation is the most limited motion of the
capsular pattern (see Adhesive Capsulitis). There may
also be limitation of external rotation due to poste­
rior-superior labral tears, osteoarthritis of the gleno­
humeral joint, posterior dislocation, cuff tears,
subcoracoid bursitis, contracted pectoral muscles,
and reflex sympathetic dystrophy.
• Pain also may be due to a suprascapular nerve injury
(see Suprascapular Nerve Injury).

Reasons for Posterior Pain with Passive External

Contact Rotation

• Lateral rotation may create posterior shoulder pain that

Figure 3-45 Posterior contact between the glenoid lip and the may be related to internal impingement (see Internal
insertion of the cuff to the tuberoSity occurs in the "apprehension," Impingement) due to compression of the articular side
or fulcrum , position, especially if the anteroinferior capsule has of the supraspinatus and infraspinatus and greater
been stretched, allowing the humerus to extend to an unusually tuberOSity against the posterosuperior glenOid labrum,
posterior scapular plane. This contact can challenge the integrity
particularly in the overhead thrower.
of the posterior cuff insertion and the tuberoSity. Source: Reprinted
with permission from FA Matsen, SB Lippitt, JA Sidles, and DT • With passive external rotation and abduction at 90°,
Harryman. Practical Evaluation and Management of the Shoulder. FIg­ posterior pain may be due to overuse impingement ir­
ure 3-48 , © 1994, WB Saunders Company. ritation of the external rotator muscle/tendons (see

Clinical Review of the Shoulder Muscles, Infraspina­ (see Posterior Dislocation) or adhesive capsulitis (see Adhe­
tus and Teres Minor). sive Capsulitis) or a problem in the glenohumeral joint or
• Posterior shoulder pain during passive external rota­ subacromial space. Glenohumeral abduction is the second
tion at 90° with anterior subluxation or instability most limited motion of the capsular pattern, which is com­
may also be due to pain from the posterior capsule, mon in adhesive capsulitis or osteoarthritis of the gleno­
because as the shoulder moves anteriorly, it tractions humeral joint.
the posterior capsule. Normal passive glenohumeral abduction with a fixed
scapula associated with limited passive scapulohumeral ab­
• Posterior-superior labral tears, allowing the humeral
duction indicates that the glenohumeral joint is intact and
head to impinge on the superior labrum, also may
may indicate an extra-articular shoulder problem in the
cause pain (see internal impingement).
shoulder girdle region,146 espeCially if isometric cuff tests
• Tears at the undersurface of the rotator cuff, with im­ and other passive tests are normal. The patient may be com­
pingement of the cuff at the superior glenoid 188 or ir­ plaining of pain localized at the base of the neck, pectoro­
ritation of posterior cuff insertion to the greater clavicular area, or the upper or mid trapezius areas. Muscle
tuberosity may also cause pain (see Impingement testing of the rotator cuff muscles would probably be nega­
Syndrome; also see Interpretation of Pain under Pas­ tive. The pain may be related to scapular dyskinesis. Com­
sive External Rotation). mon areas of involvement may be the sternoclavicular,
• A suprascapular nerve injury could cause the pain acromioclavicular joint and ligaments, the upper trapezius,
(see Suprascapular Nerve Injury). levator scapulae, pectoralis major and minor, serratus ante­
• Quadrilateral space syndrome, which traps the axil­ rior, latissimus dorsi, subclavius, or rhomboids. Other
lary nerve espeCially in the late cocking position. causes of normal passive elevation with a fixed scapula and
limited passive glenohumeral motion are shortening of the
pectoral muscles due to scarring after a radical mastectomy,
Passive Glenohumeral Abduction with a Fixed Scapula muscle spasm of the pectoralis major due to an apical lung
tumor (Pancoast's), and shortening of the costocoracoid fas­
Scapular movement is eliminated by stabilizing the infe­ Cia146 In order to determine which muscles or areas are in­
rior lateral edge of the scapula while passively abducting the volved in the shoulder girdle, see Isometric Evaluation of
arm in the scapular plane until scapular movement is felt. the Shoulder Girdle.
The humerus should abduct from 90° to 105° before the
scapula moves (Fig. 3-46). This test assesses the restriction
Passive Internal Rotation
of the glenohumeral joint, subacromial space , and capsule.
If the scapula moves immediately with shoulder abduction,
Passive internal rotation can be tested in three ways:
think of the possibility of a chronic posterior dislocation 25

1. With the patient's arm at the side with the elbow

flexed 90° and the arm pointing forward, the fore­
arm is moved internally while the shoulder is stabi­
lized (average range , 55° to 80°). It is very
important to completely stabilize the shoulder while
2. Place the patient's arm in 90° of abduction with the
elbow flexed 90° and pointing forward (Fig. 3-47A),
then internally rotate the shoulder (average range,
70°). As above, it is important to stabilize the shoul­
der. The range is limited by tightness of the posteroin­
ferior capsule (see Treatment of Tight Posterior
Capsule). A tight posterior capsule may be associated
with anterior instability. 140
3. Figure 3-44B evaluates internal rotation in the
supine position (see Supine External Rotation
Figure 3-46 Passive glenohumeral abduction. above).
The Shoulder 83

Figure 3-47B a, The patient lies perpendicular to the table and

the clinician grasps the lateral border of the scapular and stabilizes
it in the retracted position. b, The clinician allows the humerus lO
lower until motion has SlOpped, indicating that the posterior cap­
sule is tensioned. Source: Recreated from figs in: Tyler TF, Nicholas
S], Roy T, Gleim GW Quantification of posterior capsule tightness
Figure 3-47A Passive shoulder medial rotation at 90 0 humeral and motion loss in patients with shoulder impingement. American
abduction. Journal Sports Medicine. 2000;28(5):668-673.

4. Tyler et aP89 devised an accurate method of evaluat­

ing the degree of posterior capsular shoulder tight­
ness (Fig. 3-47B a,b). The patient must be on the side
at a right angle to the table with no rotation at all for­
ward or backward. The clinician grasps the lateral
border of the scapula and stabilizes it in the retracted
position (Fig. 3-47Ba). While holding this position
with the patient's torso perpendicular to the examina­
tion table , the clinician allows the humerus to lower
until motion has stopped indicating that the posterior
capsule is tensioned. The posterior capsule is ten­
sioned in a direct line of pull, and the clinician is feel­
ing for a firm end feel (Fig. 3-47Bb).

Measurement can be taken from the medial epicondyle

to the table. It was found that for every 4 of internal rota­
Figure 3-47e Home stretching of posterior capsule and exter­
tion range of motion lost, posterior capsule tightness in­
nal shoulder rotators.
creases 1 cm. The posterior capsule is the primary restraint
to any posterior force when the arm is positioned at 90 of
abduction. 189
• Limited by old, scarred, partial-thickness cuff lesions
Interpretation of Limited Passive Internal Rotation
• Third most limited motion of capsular pattern (see
• Tightness of the posterior band of the IGHL and pos­ Capsular Pattern, Chapter 1)
terior capsule • Normally limited by the lesser tuberosity contacting
• Tightness of the infraspinatus and teres minor the glenoid 1

With loss of internal rotation, possible excessive

1800 Rule163 : A patient with GIRD is at risk if there is
movement or asymmetric movement of the scapula 0
less than a 180 arc of internal and external rotation. A patient
on the chest waIF
with limited internal rotation may have increased external ro­
tation. If the gain of external rotation equals the loss of inter­
According to Tyler et al,189 many impingement patients 0
nal rotation, allowing a 180 arc of motion, then the chance of
have posterior capsule tightness.
problems occurring is lessened. "Shoulders with a posteroinfe­
rior capsular contracture that restricts the total arc to less than
Glenohumeral Internal Rotation Deficit 1800 are 'shoulders at risk'."

Kibler l74 stated that glenohumeral internal rotation

deficit (GIRD) is the most common restriction in shoulder Passive Horizontal Adduction
flexibility: Some of the effects of this restriction are:
In testing passive horizontal adduction (Fig. 3-48), the
• With forward arm flexion, an increase in anterior/su­ patient's arm is pressed across the chest above the nipple
perior humeral translation occurs, causing an external 0
line (average range, 130 Horizontal adduction stresses an

impingement tendinopathy: injured AC joint, the posteroinferior capsule, and the ante­
• In arm external rotation at 90 0 abduction, a posteri­ rior labrum and may cause a grinding of the anterior
orly/superiorly-directed humeral-head translation oc­ labrum. The movement may aggravate an existing impinge­
curs, causing an overload of the posterosuperior ment of the coracoacromial arch. Horizontal adduction
labrum and the undersurface of the posterosuperior stretches the posterior deltoid, the infraspinatus, the teres
rotator cuff (see Internal Impingement). Tight pos­ minor, and the belly of the supraspinatus muscle. It also
teroinferior capsules tend to push the humeral head pinches the subscapularis, the coracoid process, and the
toward the posterosuperior quadrant of the glenoid as subcoracoid bursa.
the shoulder goes into full external rotation in the late Motion may be limited because of tightness of the pos­
cocking phase of throwing. 163 teroinferior capsule or old, scarred, partial-thickness cuff le­
• Creates excessive scapular protraction in arm-forward sions (ruptures). Posterior capsular pain is predominant on
flexion or follow-through, to allow "a complete arc of passive horizontal adduction and espeCially on internal ro­
motion in throwing or serving." Excessive protraction tation. Limited motion often is associated with anterior in­
can be responsible for external impingement due to stability: 140 The bony contact of the coracoid process
decreased acromial elevation. normally limits this range of motion. 1
Horizontal adduction with internal rotation of the arm
• A tight posteroinferior capsule probably initiates the
can aggravate (a form of internal impingement); this is
pathological cascade to a SLAP lesion, and after a
known as an internal anterosuperior impingement. This is a
SLAP repair, recurrence of tightness may place the re­
complicated impingement that may be due to repetitive,
pair at risk in a throwing athlete. 87 A major cause of a
tight posteroinferior capsule (thickening and contrac­
ture) is due to the loads that affect it during the fol­
low-through while the arm is internally rotated.
During this period, the inferior part of the posterior
capsule is forced to directly resist the distraction
force 87
• Internal rotator shoulder stretch (Fig. 3-47C) shows
an active home treatment for the patient. The patient
must lie on the side at a right angle to the table to
stabilize the scapula with the down-sided arm and
elbow at a 90 angle. The patient then internally ro­
tates the forearm and holds for 30 seconds. The pa­
tient can be taught to perform postfacilitation
stretch (see Chapter 12). This type of stretch is bet­
ter than the horizontal adduction stretch that creates
an impingement position, does not stretch rotation,
and increases scapular protraction 174 Figure 3-48 Passive shoulder horizontal adduction.
The Shoulder 85

forceful internal rotation above the horizontal plane, where

the biceps pulley system and subscapularis tendon impinge
against the anterosuperior glenoid rim.190

Isometric Testing

The isometric tests for the shoulder are based on the

EMG studies by Kelly et al,191 which are discussed in Chap­
ter 1 under contractile (isometric) testing. These tests mini­
mize the activation from synergistic muscles and have
proved to have good test-retest reliability

Resisted Testing of Supraspinatus Figure 3-49 Test for supraspinatus muscle. See Figure 3-55A
for adding scapular retraction.
The optimal test for the supraspinatus with the greatest
EMG activity, which most minimizes the synergistic infra­
spinatus activity, is to have the patient elevate the out­
stretched arm 90° in the scapular plane with a "full can"
thumb-up position. In the thumb-up position, compared
with the thumb-down position, there is slightly less activa­
tion from the infraspinatus and a lessened possibility of im­
pingement, which is more likely to occur in the internal
rotation (thumb-down) position, possibly decreasing the re­
liability of the test. Itoi et aP92 studied the differences be­
tween thumb up and thumb down and concluded that both
positions were equally accurate in detecting the torn
supraspinatus tendon, but that the thumb-up position pro­
voked less pain, which can be beneficial because increased
pain may affect the interpretation of muscle weakness. Fig­
ure 3-49 demonstrates the test for supraspinatus muscle.
Testing the supraspinatus may appear weak in the sympto­
matic patient and strong in the asymptomatic patient. If
testing with scapular retraction increases strength of the
supraspinatus, (Fig. 3-55A) the weakness in both the
symptomatic and normal patient may be due to factors be­
sides supraspinatus weakness, such as scapula dyskinesis or
a lack of a stable base in the kinetic chain, i.e., inadequate
core stabilization (see scapular retraction test)192a Rehabili­
tation of the supraspinatus is recommended in the scapular
plane with the thumbs up because in this position, the infe­ Figure 3-50 Resisted shoulder abduction. No longer considered
rior capsule is not twisted, diminishing stress on the ante­ an accurate test.
rior and posterior capsule and rotator cuff that occur in the
thumb-down position. 75
An alternative method of testing the supraspinatus if the terior and middle deltoid,193 and also the infraspinatus, and
patient is unable to elevate his or her arm close to 90° is is not considered an accurate test for the supraspinatus (see
testing resisted abduction (Fig. 3-50) with the patient's arm Chapter 1). The deltoid is seldom involved in most shoul­
at the side (neutral 0° position). The patient's shoulder is der problems unless there was an undue strain to these par­
stabilized with one of the examiner's hands; the other exam­ ticular muscles or an axillary nerve i.nvolvement. Kronberg
iner hand is held against the lateral epicondyle of the pa­ et aP94 (see Chapter 1), based on EMG, found that
tient's elbow, which is flexed to 90 The above test in the neutral 0° position, the supraspinatus and infraspina­
measures the strength of both the supraspinatus and the an- tus could not be differentiated.

The supraspinatus insertion is best palpated with the arm

in extension and medial rotation. The musculotendinous por­
tion is best palpated with the arm resting at 90° in the scapular
plane. The supraspinatus belly in the supraspinatus fossa may
be palpated during testing by having the patient extend and
ipSilaterally bend the head and neck with the face rotated to­
ward the opposite side. 195 This relaxes the overlying trapezius.
The fossa should be palpated for any tender nodular adhe­
sions that may be responsible for lack of proper motion of the
supraspinatus muscle and tendon. This area responds to treat­
ment by friction massage, fascial release, active release, or
Graston technique. New information about the additional in­
sertions pertaining to the supraspinatus, infraspinatus, and
subscapularis is discussed in the Graston Technique chapter
(see Chapter 15).
Garrick and Webb 196 stated that during the above
supraspinatus test, if there is weakness of the supraspinatus,
anterior deltoid, or even the other cuff muscles due to cuff le­
sions or shoulder instability, a pectoral substitution pattern
may be observed. On resistive testing, increased tone and size
of the clavicular part of the pectoralis major would be seen
(for palpation see Clinical Review of the Shoulder Muscles).

Resisted Adduction Figure 3-51 Resisted shoulder adduction.

Resisted adduction tests primarily the pectoralis major

The infraspinatus is involved more often than the teres
and the latissimus dorsi and secondarily the teres major and
minor in most shoulder complaints. Painful resisted abduc­
the anterior deltoid. With one hand, the examiner stabilizes
tion associated with painful resisted lateral rotation is usually
the anterior-inferior acromion (the tone of the pectoralis
due to supraspinatus involvement, espeCially if abduction is
major on contracting can be palpated) and resists against the
more painful, but it could also be due to a double lesion.
medial humeral epicondyle of the elbow in 90° of flexion
Because the teres minor is also a weak adductor, pain or
(Fig. 3-51). Pain results in the axillary or pectoral areas. It is
weakness on resisted adduction after positive testing in ex­
possible to distinguish an involved teres minor from an in­
ternal rotation might indicate that the principal problem is
fraspinatus because if there is pain or weakness on isometric
located in the teres minor 198 (for palpation see Clinical Re­
adduction coupled with pain on testing of lateral rotation,
view of the Shoulder Muscles).
the teres minor (which is a weak adductor) may be involved.

Resisted External Rotation

According to Kelly et al,191 in order to achieve maximum

activation of the infraspinatus and minimal activation of the
supraspinatus and posterior deltoid muscles, the infraspinatus
should be tested at 45° of internal rotation. The tester stabilizes
the patient's flexed elbow against the patient's waist (to prevent
abduction of the elbow). The patient's forearm is placed in 45°
of internal rotation. The examiner then resists against the distal
forearm. Resistance should not be directed against the patient's
hand or wrist, which tests the wrist extensors (Fig. 3-52).
It is difficult in lateral rotation muscle testing to dis tin­
gUish between the teres minor and the infraspinatus be­
cause both are active. EMG studies do not agree on whether
testing the lateral rotators in neutral (arm at side) or at 90°
abduction with the elbow flexed in the 90° position favors Figure 3-52 Resisted testing of the infraspinatus and teres
the infraspinatus or the teres minor197 minor with the forearm at 45' of internal rotation.
The Shoulder 87

Figure 3-53 Resisted medial rotation. No longer considered an

accurate test. Figure 3-54 Maximum internal rotation lift-off test. Left, Dor­
sum of hand is placed in midline of posterior thorax at level of in­
ferior aspect of the scapula. Right, Subject is asked to lift hand
away from the thorax. It is important during this test that the ex­
aminer holds the patient's elbow in place to prevent substitution of
the triceps. Source: Reprinted with permission from JM Stefko et
Resisted Internal Rotation
al. Electromyographic and nerve block analysis of the subscapu­
laris lift-off test; Journal of Shoulder & Elbow Surgery. Vol. 6, No.4,
The tester stabilizes the patient's flexed elbow against the p. 349, © Mosby-Year Book, Inc.
patient's waist (to prevent elbow abduction) and resists in­
ternal rotation against the volar side of the distal forearm
(Fig. 3-53). Because this test of internal rotation tests the
subscapularis along with the pectoralis major, latissimus
dorsi, and teres major, a more definitive test is what is called
the "lift-off' test 198 Stefko et al,199 through EMG testing, de­
termined that the best position for creating the most isola­
tion for testing the internal rotation of the subscapularis was
by raising the dorsum of the hand in the midline of the pos­
terior thorax at the level of the inferior aspect of the scapula.
At this point, the subject is asked to lift the hand away from
the thorax. In this position, even though the latissimus
dorsi, teres major, and rhomboids were active (as they are in
all positions of the lift-off test and capable of lifting the
hand off the thorax), with the hand up at the inferior aspect
of the scapula, the hand cannot be lifted off without the
subscapularis (Fig. 3-54). The patient places the back of the
hand behind the back and attempts to lift the forearm back­
ward, away from the body, against examiner resistance. It is
important during this test that the examiner holds the pa­
Figure 3-54A Normal belly-press test.
tient's elbow in place to prevent substitution of the triceps.
This test maximizes subscapularis muscle activation and
minimizes the activity of the pectoralis major and latissimus
dorsi that is activated by the above test with the elbow in
the sagittal position against the waist. The lift-off test was not evident with the elbow-against-the-waist test. In order
originally described by Gerber and Krushell 199 to determine to ensure a valid interpretation for the lift-off test, a patient
whether the subscapularis was ruptured, in which case must have full, passive, painless, internal rotation so that
there would be zero lift-off capability. The lift-off test often the arm can be placed in the desired position200 (for palpa­
reveals a subscapularis weakness or pain response that is tion see Clinical Review of the Shoulder Muscles and New

cles are activated with both tests, the belly-press test acti­
vated the upper subscapularis muscle significantly more
than the lift-off test, and the lift-off test affected the lower
subscapularis muscle more than the belly-press test.
A tear of the subscapularis is especially indicated if there is
an increased external rotation range of motion associated with
the internal rotation weakness. Walch202 found that the lift-off
test was not reliable for the diagnosis of incomplete tears of the
subscapularis muscle (59% sensitivity and 85% specificity).

Resisted Shoulder/Elbow Flexion

Speed's test 175 (Fig. 3-55A) is used to assess the biceps

brachii. The patient's arm is extended and in 90° of forward
flexion , and the hand is supinated. The tester resists against
the distal forearm. Janda 203 stated that when the elbow is
hyperextended, the biceps brachii must create immediate
activity at full strength. Resistance against the elbow in 75°
of flexion and next to the trunk can also be tested (Fig.
Figure 3-54B Abnormal belly-press test. 3-55B). To confirm involvement of the biceps, the exam­
iner should always test resisted supination (Fig. 3-56).
Buchanan et aP04 showed that the biceps was most active
for supination loads rather than resisted elbow flexion.
Sometimes, only resisted supination is positive in a biceps
Insertional Areas of Cuff muscles in the Graston Technique lesion 205 In testing muscles, the examiner should observe
chapter, Chapter 15). If the patient's arm is passively the contours of the muscle bellies, which have tendons that
brought behind the back in the maximal lift-off position are prone to rupture, such as the biceps and the pectoralis
and the examiner lets go of the hand, if the patient is able to major. According to Burkhart et al,s7 the Speed test was
maintain the original position, then it is considered a nor­ found to be highly specific for anterior type 2 SLAP lesions.
mal lift-off lag sign. Involuntary dropping of the hand The biceps is tested with the hand supinated, the brachialis
would indicate a probable rupture of the subscapularis. is tested with the forearm pronated, and the brachioradialis is
Belly-Press Test: is useful especially when the patient is tested with the forearm in midposition. Resistance can also be
unable to internally rotate the shoulder. The patient places applied against the patient's extended forearm with the shoul­
the palm of the hand against the upper abdomen, just der extended and the hand pronated (Fig. 3-57). This posi­
below the level of the xyphoid process and is asked to press tion, without resistance, is excellent for palpation of the
maximally into the abdomen by internally rotating the anterior subacromial bursa. If the bursa is inflamed, tender
shoulder. Figure 3-54A represents normal subscapularis boggy tissue might be palpated. During the above tests, pain
strength. The test is considered positive for subscapularis may be localized at the AC joint if the supraglenoid origin of
dysfunction if the patient demonstrates flexion at the wrist the biceps is involved, at the bicipital groove or biceps belly, or
and shoulder adduction and extension. The patient main­ at the musculotendinous portion or its insertion at the radial
tains pressure against the abdomen by dropping the elbow tuberoSity. Pain at the supraglenoid origin also may indicate a
behind the trunk and extending, rather than internally ro­ problem at the superior glenoid labrum, possibly due to a su­
tating the shoulder (Fig. 3-54B). This study201 compared perior labral tear from anterior to posterior (SLAP) lesion (see
the lift-off test with the belly-press test and found that the Glenoid Labrum Tears). (For palpation see Clinical Review of
next most active muscles for both tests were the teres major the Shoulder Muscles.)
and supraspinatus. Performance of the two tests elicited The palm-up test evaluating the long head of the biceps
muscle activity greater than 57% MVC for the upper and brachii may not be a valid test because of the lever arm po­
lower subscapularis muscles, whereas all the other associ­ sition reqUired, which would stimulate many of the sur­
ated muscles tested below 23% MVC, indicating that the rounding muscles. Leroux 206 believes that the best way to
subscapularis muscle was the primary muscle challenged. test the biceps is with the elbow in 90° flexion with the arm
Although both the upper and the lower subscapularis mus­ in supination held against the trunk.
The Shoulder 89

Figure 3-S6 Resisted supination.

Figure 3-SSA and B Resisted elbow flexion.

Figure 3-S7A Testing resisted shoulder girdle protraction.

Figure 3- S7 Resisted shoulder flexion.


Figure 3-57B Testing resisted shoulder girdle retraction. Figure 3-57C Testing resisted shoulder girdle elevation.

Isometric testing of shoulder flexion, which involves the

anterior deltoid, coracobrachialis, pectoralis major, and bi­
ceps, and resisted testing of shoulder extension involving
the latissimus dorsi, teres major, posterior deltoid, teres
minor, and triceps are not usually performed. These two
tests involve such a variety of muscles that relative muscle
interpretation is impossible.

Resisted Testing of the Shoulder Girdle 146

Figure 3-57A depicts testing for resisted shoulder girdle

protraction. The practitioner resists the patientS forward
movement of the shoulder. This test stresses the subclavius,
pectoralis major and minor, and the serratus anterior. Figure
3-57B depicts testing for shoulder girdle retraction. The
practitioner resists the patientS backward movement of the
shoulder. This test stresses the rhomboids, upper, middle,
and lower trapezius, and latissimus dorsi. Figure 3-57C de­
picts testing for shoulder girdle elevation. The practitioner re­
sists the patient's upward shrug. Depending on the patient,
the practitioner might have to resist with both hands. This
tests the levator scapulae, upper trapezius (elevates clavicle),
rhomboids (elevates scapula). Figure 3-57D depicts testing Figure 3-57D Testing resisted shoulder girdle depression.
The Shoulder 91

for shoulder girdle depression. The practitioner resists under Ciullo 209 described a subacromial spur test that causes
the elbow as the patient pushes downward. Sometimes, a severe pain when the patient's arm is forwardly flexed past
practitioner must resist with both hands. This tests the sub­ 180°, at the anterior-inferior edge of the acromion. This test
clavius, pectoralis major (lower), latissimus dorsi. These tests is specifically valid only if roentgenography reveals a spur (a
help localize sources of pain in the shoulder girdle area that 15° caudad view may be reqUired).
can be treated by manual methods.

Impingement Signs Hawkins's Sign

Neer's Impingement Sign In Hawkins's test,210 the patient's elbow is flexed to 90°,
and the shoulder is forwardly flexed to 90° The examiner
Neers impingement test (Fig. 3-58) has the patient sit­ maximally internally rotates the arm while stabilizing the
ting as the examiner stands behind the patient with one scapula (Fig. 3-59). This test causes the coracoacromiallig­
hand on the scapula with downward pressure to prevent ament to impinge on the supraspinatus insertion and
scapular rotation. The shoulder is brought up into maxi­ greater tuberosity (24 mm). In testing swimmers for im­
mum flexion. This causes anterior shoulder pain because pingement, it was found that the Hawkins's test was more
pressure of the greater tuberosity is being forced against the sensitive than the Neers test 211 The Hawkins sign was
anterior acromion or coracoacromial arch. This test aggra­ found to be more sensitive than the Neer sign for subacro­
vates an irritated bursa or supraspinatus tendon. The test is mial bursitis 212 It is thought that any shoulder impinge­
considered positive if there is pain in the last 10° to 15° of ment test that involves medial rotation lacks specificity
forward flexion 207 ,208 This test may also be indicative of a because they are positive in all conditions responsible for
coracoid impingement. pain during medial rotation. 206

Evaluation of Neer's and Hawkin's Impingement Signs

MacDonald et aF12 found that both signs are "sensitive

for appearances suggestive of subacromial bursitis and ro­
tator cuff partial or complete tearing with a high negative
predictive value," but "they lack specificity in comparison
with arthroscopic findings." Sensitivity represents the abil­
ity of a test to discover pathosis when it is present. Nega­
tive predictive value is a measure of the proportion of

Figure 3-58 Neer's impingement test. Figure 3-59 Coracoacromial impingement test (Hawkins's test).

patients with negative test results who are actually free of

disease or lesions. Specificity is a statistical measure of
whether a test is negative when there is no pathosis. The
authors concluded that these tests may be more valuable
as a negative test, indicating that there is no rotator cuff
tendinitis or tearing.

Scapular Assistance Test (Fig. 3-59A and B)

Kiblerl? uses a "muscle assistance" test to determine

whether impingement is due to a lack of active acromial el­
evation. The examiner pushes the inferior medial border of
the scapula laterally and upward while stabilizing the upper
medial border of the scapula to simulate the serratus ante­
riorllower trapezius muscle portion of the elevation force
couple as the patient elevates the arm. If the impingement is
related to inhibition of these muscles, the impingement
symptoms diminish or are abolished. The test may relieve
an anterior or abducted painful arc, rotator cuff weakness,
and symptoms of external impingement, such as a hooked
acromion. The test gets the acromion out of the way by
keeping the scapular back and down instead of allOwing it
to go over and up, causing pain.

Scapular Retraction Test (Fig. 3-59C)

The entire medial border of the scapula is manually held

down in the retracted and posterior tilt position. This posi­
tion creates a stable base of origin for the rotator cuff mus­
cles, and when held in this position, previously tested
Figure 3-59A and B Scapular assistance test. weakened rotator cuff muscles may now test strong. In­
creased rotator cuff strength may mean that the cuff muscle
is dysfacilitated due to scapular protraction and that the cuff
muscles are actually strong. This may indicate weakness of
the trapezius and rhomboid muscles. l63 This test reposi­
tions the scapula in retraction, thereby decreasing glenOid
antetilting and redUCing mechanical impingement and pain.
A secondary cause of impingement due to scapular protrac­
tion could now be distinguished from primary impinge­
ment (see impingement syndrome).
This test is also positive in patients with internal im­
pingement (see Internal Impingement) demonstrating that
the scapula is part of the problem. The retraction position
relieves a positive modified Jobe relocation test, which is
posterior shoulder pain without apprehension when a pa­
tient's arm is abducted 90° and externally rotated. The re­
traction test relieves the internal impingement by getting
the glenOid out of the way. This test may also relieve posi­
tions of posterior instability, again relating the scapula to
Figure 3-59C Scapular retraction test. the problem.
The Shoulder 93

Stability Testing Craig2 stated that although we tend to compartmentalize

shoulder problems into speCific conditions, such as instabil­
Grading of Laxity/Instability ity and tendinopathy, most shoulder injuries-espeCially in
the athlete-really represent a disease continuum or an
Anterior/Posterior: Normally, translation is equal ante­ overlapping of soft tissue injuries. An overhead player even­
riorly and posteriorly213 Subluxation is defined as excessive tually may overstretch the static stabilizers, creating micro­
symptomatic translation of the humeral head on the trauma to the glenohumeral ligaments that eventually
glenOid. 108 The follOwing grading system is from the Hospi­ results in excessive translation of the humerus on the gle­
tal for Special Surgery214: noid, usually in the anterosuperior direction. This excessive
static motion results in dynamic (cufflperiscapular) muscu­
0: No perceived movement of the humeral head lar fatigue and eventual inflammation. In this case, the sub­
+ 1: Humeral head shifts to glenoid rim further in an ante­ tle glenohumeral instability is the cause of the loss of
rior or posterior direction than the contralateral dynamic stability In another scenario, primary cuff weak­
shoulder without moving over its edge ness and fatigability may result in overstretching of the
+2: Head glides over the glenOid rim (subluxes) and static stabilizers, resulting in secondary shoulder instability
spontaneously reduces with release of pressure
+3: Dislocates without spontaneously redUCing (clinical Occult Instability/Subluxation
dislocation)21S (The examiner can lock the humeral
head over the glenoid rim.) Occult instability/subluxation is often present as the un­
derlying mechanism responSible for a broad spectrum of
Fowler216 stated that posterior translation of the humeral shoulder dysfunction, espeCially in the overhead athlete 218
head up to 50% of the glenOid width may be normal, There need not be a history of dislocation, and often an in­
whereas greater than 50% would stress the rotator cuff (see stability exists without the awareness of subluxation by the
Instability: Laxity Versus Instability). Speer217 stated that patient or the doctor. Manual treatment without this knowl­
measurement of translation is a measurement of laxity, edge often leads to relapse. Knowledge of occult instability
which has wide variation in the population. He has found requires a great effort of rehabilitation to reduce this prob­
up to +2 anterior and +2 posterior laxity that were not lem (see Anterior Release Test under Anterior Stability Tests
symptomatic, although he would interpret this as hyperlax­ below).
ity He stated that he has never found +3 laxity in an individ­ Posterior glenohumeral subluxation, which is often
ual without symptoms. associated with multidirectional instability in athletes , is
becoming more common. The patient complains of pain
in several possible locations, such as the posterior cuff,
Grading Inferior Translation of the Humeral Head the biceps tendon , and the superior rotator cuff, as in the
typical impingement syndrome (see Pathomechanics dur­
0: No inferior translation of humeral head ing Arm Deceleration). Pain typically is felt during the
+1: Less than 5-mm inferior translation of humeral head deceleration and follow-through phases of pitching or
+2: 5- to lO-mm inferior translation of humeral head racket swinging and during the ascent phase of the
+3: More than 10-mm inferior translation of humeral head bench press.
The following stability tests provoke the chief static sta­
Glenohumeral stability can be interpreted as stability dur­ bilizers, which are the glenohumeral ligaments and labrum
ing the midranges of motion or as stability at the end ranges (capsulolabral complex). These tests are of a provocative
of motion. Midrange motion is stabilized primarily by con­ nature and attempt to move the instant center of rotation of
cavity compression (see Mechanisms Responsible for Con­ the glenohumeral joint in order to create a reproduction of
cavity Compression), a normal rotator cuff, and the the clinical symptoms, such as pain, increased feeling of
periscapular muscles. Stability at the end ranges of motion is movement, feelings of apprehension, or a palpable or audi­
supported by the capsular ligamentous system. Stability in ble "clunk" or "pop." 178 The clicking sound that occurs
the most mobile joint of the body requires dynamiC stabiliz­ with subluxation of the shoulder is often due to a defect in
ing help. As stated previously, the rotator cuff muscles center the posterolateral humeral head's riding over a tom labrum
the humeral head throughout all of the ranges of motion, and/or the anterior glenoid rim.219
whereas the scapular muscles stabilize the scapula and rotate Provocation of the patient's symptoms is necessary before
the scapula during overhead motions. Aggravations of the we assume that a stability test is positive because hyperlaxity
dynamiC or static stabilizers directly influence each other. may be considered normal in a particular patient (see Instabil­

ity: Laxity Versus Instability). Stability tests are used to test for
occult and overt shoulder instabilities due to capsular and gle­
noid labrum ruptures (Bankarts lesion), excessive capsular
laxity, impacted compression fracture of the humeral head
(Hill-Sachs lesion), greater tuberosity avulsion, and attenuated
and ruptured cuff muscles (especially the subscapularis)26
Shoulder instability may occur anteriorly, posteriorly, in­
feriorly, or multidirectionally Always compare stability test
findings with those of the contralateral normal shoulder first.
If pain is produced, it is important that the nature of the test
be explained to the patient so that he or she will be in a re­
laxed state because there is good correlation between transla­
tion awake and translation under anesthesia 220 During
stability testing, the examiner is determining the amount of
passive translation of the humeral head in the glenOid fossa
and is looking for reproduction of the patient's symptoms.

Anterior Stability Tests

Use of the supine position for instability testing is rec­

ommended because the edge of the table can be used as a
fulcrum to lever the humeral head anteriorly and posteri­
orly, and the patient is better able to relax 220 Figure 3-60 Anterior drawer test.
Anterior Drawer Test (Fig. 3- 60): With the patient
supine, the examiner puts the patient's hand in his or her
medial axilla with patient's arm relaxed. The examiner then (see Interpretation of Pain during Passive Lateral Rotation
draws (using the outside hand) the patient's proximal arm with Abduction and Extension above). The presence of
into approximately 70° to 80° of abduction (Fig. 3-60) in crepitus or grinding while causing translation of the
the scapular plane and maintains neutral rotation 2 17 ,221 humeral head suggests anterior labral avulsion. 1
With the outside hand, the examiner exerts a compressive
axial load on the humerus to reduce the humeral head in Load and Shift Test: According to Conway,40 the load
the glenolabral socket. With the inside hand, the examiner and shift test, whereby the examiner is seated behind the
immobilizes the scapula with the thumb on the coracoid patient, grasps the humeral head, and applies force posteri­
and the hand on the scapular spine. The examiner then ap­ orly and anteriorly, is really testing only the superior gleno­
plies an anterior translation of the humeral head on the gle­ humeral ligament and posterior capsule and is not an
noid, noting the grade of instability (see Stability Testing). effective test for the IGHLC, which is the principal structure
The humeral head can also be tested for posterior instability that is compromised.
in the above position by pushing the head posteriorly (see
below). Anterior Release Test: This test218 was developed
Exerting a loaded state of the humeral head in the gleno­ principally to detect occult shoulder instability, espeCially
labral socket reduces any inherent subluxation 222 Loading when the relocation and apprehension tests are eqUivocal.
of the humeral head is necessary because, according to Silli­ This test demonstrated 91.9% sensitivity, 99.9% specificity,
man and Hawkins,140 multidirectional laxity or scarring 87.1 % predictive value, 93.0% negative predictive value,
from previous surgery may result in the patient's humeral and 90.2% accuracy
head resting in a nonconcentric location, that is, the head Procedure: The patient is in the supine position with the
may be sitting anterior, posterior, or inferior from the gle­ affected shoulder over the edge of the examining table, ab­
noid center. ducted 90 0 The examiner exerts a posterior force on the pa­
The scapular plane is recommended for testing and dur­ tient's humeral head, and while the posterior force is
ing exercise because the true plane of movement in the maintained, the patient's arm is brought into extreme exter­
glenohumeral joint plus maximum glenohumeral motion nal rotation (Fig. 3-61A). The humeral head is then released
occurs in this plane (see Shoulder Elevation, Scapular (Fig. 3-61B). In a series of 82 patients, the sensitivity was
Plane). Use of the anterior drawer test at different levels of 92 %, the specificity was 89%, the positive predictive value
abduction helps localize the particular level of instability was 87% , and the negative predictive value was 93% 134
The Shoulder 95

Figure 3-61B The humeral head is released. Source: Figure by

Figure 3-61A The humeral head is held in a reduced position
James Capizzulo. Reprinted with permission from ML Gross and
while the arm is abducted and brought into maximum external ro­
MC Distefano. Anterior release test. Clinical Orthopaedics and Re­
tation. Source: Figure by James Capizzulo. Reprinted permis­
lated Research. No. 339, p. 106, © 1997, Lippincott-Raven Pub­
sion from ML Gross and MC Distefano. Anterior release test. lishers.
Clinical Orthopaedics and Related Research. No. 339, p. 106, ©
1997, Lippincott-Raven Publishers.

Interpretation: For a positive result, a patient should ex­

perience both apprehension and pain. Another interpreta­
tion is that pain alone was suggestive of rotator cuff
abnormalities, whereas pain and apprehension suggested
instability. 134

Posterior Stability Tests

Posterior Drawer Test (Fig. 3-62): The posterior

drawer test has a setup similar to that for the anterior
drawer test. The examiner alongside the patient first flexes
the patient's elbow 120 0 , abducts the shoulder 800 to 120 0 ,
and flexes the shoulder 20 0 to 30 0 with the outside hand.
With the inside hand, the scapula is stabilized with the fin­
gers on the scapular spine and the thumb on the lateral bor­
der of the coracoid process. Next, the examiner internally
rotates the humerus and flexes the shoulder 60 0 to 80 0
while applying posterior pressure with the thumb. With
posterior instability, the thumb pushes the humeral head
posteriorly along the lateral border of the coracoid
process 221
Figure 3-62 Posterior drawer test.
Posterior-Inferior Pressure Test: Pressure can also be
directed in a posterior-inferior direction to check the in­
tegrity of the posterior portion of the inferior glenohumeral while maintaining anterior to posterior pressure on the pa­
ligament,223 Pollock and Bigliani224 described the follOwing tient's elbow. If there is instability, during shoulder adduc­
test: pressure is exerted anterior to posterior on a 90 flexed tion, a sudden jerk occurs as the humeral head slips off the
elbow and shoulder while the arm is internally rotated and posterior lip of the glenOid. A second jerk may appear on re­
horizontally adducted 40° The examiner stabilizes the turn of the arm toward horizontal abduction.
scapula (Fig. 3-63). Posterior pain or a palpable protrusion
is a positive sign. A jerk test225 can occur if the examiner first Posterior Subluxation Test: Posterior instability is al­
holds the arm in the sagittal plane and then adducts the arm most always a subluxation rather than a dislocation,226

Figure 3-63 Posterior-inferior pressure test.

1. Sometimes, patients can reproduce a painless posterior

subluxation that they can easily reduce themselves.
2. Posterior subluxation pain may occur during the fol­
low-through of a throw but is rare compared with an­
terior subluxation (increased anterior humeral head
translation in the glenoid).

Sulcus Sign for Inferior Stability

The sulcus sign for instability (Fig. 3-64) is primarily a

test for competence of the anterior superior capsular struc­ Figure 3-64 Sulcus sign for inferior stability Source: Reprinted
tures, espeCially the superior glenohumeral ligament. 225 with permission from ]C Delee and D Drez. Orthopaedic Sports
Grasp the distal humerus and pull down in an inferior di­ Medicine Principles & Practice. Vol. 1, Fig. 15D-21, © 1994, WB
Saunders Company
rection longitudinally to the long axis of the arm at 0° of ab­
duction and look for a sulcus inferior/anterior or
inferiorllateral to the acromion. A finger of the other hand
can be used to create pressure in the sulcus to feel the de­
pression of the humeral head. The sulcus sign can be
recorded in centimeters: 1+ is an acromiohumeral interval
this patient as having a unidirectional (anterior) instability
of 0.5 to 1.0 cm; 2+ is an interval of 1 to 2 cm; 3+ is greater
with inferior hyperlaxity A sulcus sign or any of the insta­
than 2 cm (see Grading Inferior Translation of the Humeral
bility tests should be considered pathological only if they
Head under Grading of Laxityllnstability). In order to re­
provoke the patient's symptoms (see Instability: Laxity Ver­
flect the status of the IGHLC during a sulcus test, the arm
sus Instability).
would have to be pulled down at an abduction angle greater
than 45° during inferior translation,217 where either the an­
terior or posterior portions of the IGHLC would become
Inferior Subluxation of the Humeral Head
the prime stabilizers, depending on whether the shoulder
was internally or externally rotated (see under Inferior
Inferior subluxation of the humeral head may appear after
Glenohumeral Ligament Complex).
trauma, surgery (rotator cuff repair), or fracture repair222
Inferior instability is usually associated with atraumatic
multidirectional instability (combination of anterior, poste­
rior, and inferior laxity). Speer,217 however, believes that a Examination: In a radiographic examination of an in­
patient may have true anterior instability and demonstrate ferior subluxation, the center of the humeral head is at the
an asymptomatic sulcus sign on the lesioned side. Instead level of the inferior lip of the glenoid. To differentiate from
of assuming multidirectional instability, he would claSSify an anterior dislocation, in an anterior dislocation, the
The Shoulder 97

humeral head appears medial to the glenoid. To differentiate five of the follOwing tests: O'Briens, anterior slide, biceps
an inferior subluxation from an anterior dislocation, sup­ external rotation, anterior load and shift, modified jobe re­
porting the arm during radiography, thereby eliminating the location and the mayo dynamic shear test. The other tests
effects of gravity, would in an inferior subluxation show the mentioned can also be used. McFarland et aP28 stated that
humeral head centered in the glenoid cavity. Eliminating the commonly used tests for the diagnosis of SLAP lesions
gravity in the shoulder would not reduce a true dislocation. are less accurate than originally reported, and the presence
of a click is not necessarily reliable. A problem with all SLAP
Treatment of Inferior Subluxation: Support the arm tests is that SLAP lesions rarely occur in isolation. They can
when not exercising. Use isometric exercises to restore mus­ be associated with partial rotator cuff tears, Bankart injuries,
cle tone, which causes a disappearance of the inferior sub­ subaacromial impingement, acromioclavicular arthrosis,
luxation. There is usually atony of the deltoid and rotator Hill-Sachs lesions, glenohumeral chondromalacia, and os­
cuff muscles. Recognizing this transient inferior subluxation teoarthritis.205 The decision to operate on a shoulder for a
(positive inferior sulcus test) avoids unnecessary and ex­ suspected SLAP lesion should not be made on the basis of
pensive diagnostiC evaluations. labral tests alone. Because of the association of other shoul­
der lesions with these tests, magnetic resonance imaging
Testingfor Glenoid Labral Tear (MRI) should be used as a final decision maker.

Important tests for determining instability, besides the O'Brien Sign (Anterior Type 2 SLAP Lesion): This
apprehension tests described above for anterior, posterior, active compression test (S.]. O'Brien, personal communi­
and inferior instability and the relocation test (see Reloca­ cation, May 1997) revealed a sensitivity of 100% and a
tion Test below), are tests that elicit audible "clicking" or speCificity of 98.5% for labral tears and a sensitivity of
"clunking" when the glenoid labrum is stressed. Kibler227 100% and a speCificity of 96.6% for AC joint pathology.
stated that no single test is diagnostic and recommended In Figure 3-65A the patient's arm is forwardly flexed to

Figure 3-65 O'Brien sign. A) , While in the same position, the arm is maximally supinated. B), The arm ,is forwardly flexed to 90°, ad­
ducted to 10° to 15°, and maximally internally rotated. Source: Reprinted wuh permlsslOn from Stephen]. 0 Bnen, A new and effecttvetest
for diagnOSing labral tears and A.C. jOint pathology American Joumal of Sports Medicine, Sept/Oct 1998, pp. 610-613 , © 1998, Amencan
Journal of Spons Medicine.

90°, adducted 10° to 15°, and maximally internally ro­

tated. The patient should resist the examiner's downward
force. The examiner should not resist the patient's attempt
to actively forward flex past 90°. In Figure 3-65B, the pa­
tient, in the same position, maximally supinates the arm
and the test is repeated. A positive O'Brien sign is present
when pain or painful clicking is elicited with the first ma­
neuver and reduced or eliminated by the second maneu­
ver. The patient is asked to determine whether the pain is
"on top" of the joint, indicating an AC problem, or "inside
the joint," indicating a labral disorder.
Parentis et aP29 performed an anatomic evaluation of
the O'Brien test and found that in the internally rotated
position, there was consistent contact between the lesser
tuberoSity and the superior labrum, as well as between Figure 3-66 Glenoid clunk test.
the supraspinatus tendon and the lateral acromion. In the
externally rotated position, these contacts were absent.
The pain therefore in the internally rotated position may
be due to contact of the supraspinatus tendon with the Anterior Slide Test (Anterior SLAP Lesions): Kibler82
acromion, indicating a possible acromioclavicular arthri­ devised a test to challenge the competence of the anterior­
tis, rotator cuff pathology, bursitis, impingement, and a superior glenOid labrum. He stated that this test does not
tight posterior capsule (see GIRD). The internally rotated require the presence of a mobile free fragment and may be
position would also increase the pressure in the subacro­ more sensitive for picking up early instabilities. With the
mial area from a type II or III acromion (primary im­ patient's hand on the hip, the examiner directs a force on
pingement). The contact between the lesser tuberosity the patient's elbow in an upward and forward movement
and the superior labrum could be positive with a SLAP (Fig. 3-67). If there is a superior labral tear, the humeral
lesion. The authors stated that patients have difficulty in head shifts over the torn labrum, causing anterosuperior
deciding whether the pain is superficial that is, indicating pain and/or a pop just inferior to the acromion. McFarland
AC pathology or deep, indicating labral pathology, and et aP28,230 disagreed with Kibler and found only 8% sensi­
that the test could also be positive with shoulder insta­ tivity instead of 78.4% , and specificity of 84% instead of
bility. 91.5%. McFarland also found lower positive and negative
Stetson and Templin 230 compared arthroscopy with the predictive values.
results of preoperative tests and MRI to determine the valid­
ity of some shoulder tests and could not recommend the
O'Brien test as a good screening test, because it detects
SLAP lesions in only 47% to 54% of cases, another reason
that a series of tests must be utilized for labral problems.

Glenoid Clunk Test (Fig. 3-66) (see Glenoid Labrum

Tears): The patient's arm is abducted 90° to 100° and ex­
ternally rotated while the examiner Simultaneously com­
presses (loads) the humeral head, which anteriorly stresses
the anterior labrum. The arm should then be circumducted
while loading, searching for anterior-superior or posterior­
superior labrum tears. An audible "clunk" or grinding is felt
if a detached labral piece is caught. Craig2 described this
test as similar to the McMurray test for the knee, whereby
the humeral head is rotated into the glenoid, creating a sub­
luxation of the labrum into the joint and reprodUCing the
pain or clicking. Figure 3-67 Anterior slide test.
The Shoulder 99

Crank Test: Liu et aP3! found a high sensitivity and labrum with or without a click. 134 This test can be positive
specificity for this test in labral tears, whereas Stetson and with a SLAP lesion.
Templin,230 as for the O'Brien test, did not find the crank Nakagawa et aP32 recently developed a forced abduction
test a reliable screening test for glenoid labral tears. They test relieved by elbow flexion , which they state showed a sen­
believe that diagnostic arthroscopy should be the standard sitivity of 67%, a specificity of 67% and an accuracy with MRI
procedure for detecting SLAP lesions and other pathological of 67%. In this test (see Fig. 3-10lB) (a) when the patient's
conditions of the labrum. In this test, the patient may be shoulder is maxi.mally abducted, if there is a superior labral
upright or supine with the ann elevated to 160 in the tear, pain is caused by a traction force creating tension on the
scapular plane. The practitioner loads the joint along the long head of the tendon of the biceps, which attaches to the
axi.s of the humerus and performs internal (Fig. 3-68A) and superior labrum. Forced shoulder abduction also causes the
external humeral rotation (Fig. 3-68B). A positive test is humeral head to externally rotate, thereby increasing the ten­
pain usually during external rotation affecting the anterior sion on the long head of the biceps by altering the direction of

A 8

c D

Figure 3-68 Crank test. A) , internal rotation of the humerus; B) , external rotation of the humerus; C) , internal rotation of the shoulder;
D) , external rotation of the shoulder.

the biceps tendon. The tension on the long head decreases

rapidly with elbow flexion in the same position (see Fig.

Relocation Test: This test can be used to determine an­

terior shoulder instability, posterosuperior impingement of
the rotator cuff, and possible subluxation of the posterosu­
perior labrum. The scapula and the shoulder should be on
the table, and the arm and forearm should be brought to ex­
treme shoulder external rotation at 90° abduction in the
coronal plane with the elbow flexed 90° (Fig. 3-69). This is
really a supine shoulder apprehension test, causing anterior
shoulder pain due to the humeral head projecting anteriorly
due to instability instead of posteriorly. If the humeral head
is now pushed posteriorly and the shoulder is again put
into external rotation, the pain will be relieved (Fig. 3-70).
It is thought that in the apprehension test position, the Figure 3- 70 Supine apprehension test.
humeral head is slightly subluxed anteriorly and the reloca­
tion test pushes the head posteriorly, redUCing the subluxa­
tion, or that the anterior to posterior pressure acts as a
supportive buttress to relieve the patient's apprehension.22o out a tendency to dislocation, he or she may experience
If a patient has a positive anterior instability test, especially only pain and not apprehension during external rotation.
with apprehension, and is relieved by the relocation test The relocation test that follows may bring relief in patients
(positive relocation test), instability is confirmed. These with instability/subluxation. Patients with secondary im­
cases often have a history of a traumatic subluxation or dis­ pingement may be relieved, whereas patients with primary
location. lso If the patient has an anterior subluxation with- impingement have no change in their pain. It is apparent
that a variety of disorders may be relieved by this test. The
relocation test is most accurate when apprehension is re­
lieved, and instability is the diagnosis 233
EspeCially in overhand-throwing athletes with occult in­
stability who have increased glenohumeral rotation, hyper­
angulation, and anterior translation, the posterior aspect of
the supraspinatus and superior aspect of the infraspinatus
can become pinched between the humerus and the postero­
superior glenOid rim 234 If the relocation test results in pos­
terior and/or superior joint line shoulder pain that is
relieved by a posteriorly directed force to the humeral head,
this may indicate a diagnosis of internal impingement 235
(see Internal Impingement).
The test has been modified 234 by positioning the shoulder
in maximal external rotation not only at 90° but also at 110°
and 120° (Fig. 3-71). It was found that more extensive pathol­
ogy could be realized at higher levels of abduction. When all
three levels of abduction were tested and compared arthro­
scopically, every patient with a positive test showed fraying of
the posterosuperior labrum or undersurface of the rotator cuff.
Also seen were SLAP lesions, complete rotator cuff tears, labral
fraying, and Bankart's lesions. At 1l0° and 120°, almost all of
the patients showed painful posterosuperior impingement of
the rotator cuff. The authors stated that the modified reloca­
tion test with the impingement signs may not be expected
with the older nonathletic population234 Burkhart et al87
found that in the abduction-external position of the relocation
Figure 3- 69 Relocation test. test, the posterosuperior labrum can be subluxed and the pos­
The Shoulder 101

~ ---------------­

Figure 3-71 A), Shoulder relocation test is performed with patient supine and positioned near edge. Test was performed at 90°, 110°,
and 120° of shoulder abduction. B), Examiner grasps humeral head posteriorly and pushes anteriorly; positive test results when this ma­
neuver elicits posterosuperior joint line pain. Pain is typically relieved when examiner grasps humeral head and pushes posteriorly. Source:
Hamner DL, Pink MM, Jobe FW A modification of the relocation test: arthroscopic findings associated with a pOSitive test. Journal Shoulder
Elbow Surgery 2000;9(4).

terioirly directed force reduces the labral subluxation and re­

lieve the pain. The modified relocation test is considered
highly specific for posterior SLAP lesions, what is called the
"thrower's SLAP" 87

Biceps Load Test II: Kim et al,236 (Fig. 3-72A) The test
is performed as follows: the supine patient's arm is elevated
to 120° and externally rotated to its maximal point, with the
elbow in the 90° flexed position and the forearm in the
supinated position. The patient is asked to flex the elbow,
which is resisted by the examiner. Figure 3-72B demon­
strates the test in the standing position. This is the position
that reproduces the mechanism in the development of type
II SLAP lesions. A forceful traction of the displaced biceps­
superior labral complex occurs during the active contrac­
tion of the biceps muscle against resistance. The authors
believe that the test position changes the relative direction Figure 3-72A Biceps load test supine.
of the biceps fiber in a position of an oblique angle to the
posterosuperior labrum, causing a peeling of the superior
labrum off the glenOid margin. The test is positive if the pa­ Resisted Supination External Rotation Test: Myers et
tient complains of pain during the resisted elbow flexion or aP05 developed the resisted supination external rotation test
if the patient complains of more pain from the test than the RSER test based on the idea that the principle reason for a
pain that was already present in the test position. The test is SLAP lesion in the overhead athlete was due to the peel­
negative if pain is not elicited by the resisted elbow flexion back mechanism. The peel-back mechanism is explained by
or if the preexisting pain is unchanged or diminished by the the cocking position, causing the biceps tendon to transfer
resisted flexion. a torsional force to the superior labrum. This torsional force

Figure 3-72B Biceps load test standing

Figure 3-72C The examiner supports the arm at the elbow and
hand with the shoulder abducted to 90 and the elbow flexed 6Y

to 70 with the forearm in neutral or slight pronation.

The examiner supports the arm at the elbow and hand

with the shoulder abducted to 90 0 and the elbow flexed
65 0 to 70 0 with the forearm in neutral or slight pronation
(Fig. 3-72 C). The patient is then asked to maximally
supinate the hand against resistance as the examiner gently
externally rotates the shoulder to maximal external rota­
tion (Fig. 3-72D). The test is considered positive if the pa­
tient complains of anterior or deep shoulder pain, clicking
or catching, or reproduction of symptoms that occurs dur­
ing throwing. The test is considered negative if the patient
complains of posterior shoulder pain, apprehension, or no
pain. If there is a complaint of apprehension, there may be
a possible anterior instability, and if there is posterior
shoulder pain, there may be a possibility of internal im­
The authors of this test stated that in the Biceps Load
Figure 3-72D Patient maximally supinates their hand against Test II above, where elbow flexion is 90 0 , there is not maxi­
resistance as the examiner externally rotates the shoulder to maxi­ mum contraction of the biceps. They stated that it is neces­
mal external rotation. sary to maXimally load the biceps anchor and reproduce the
torsional load on the superior labrum to reproduce "the
suspected mechanism of injury in throwers."
caused a rotation of the posterior superior labrum medially
off of the superior glenoid, creating a SLAP lesion. This test Mayo Dynamic Shear: This test aggravates the poste­
proved to be more accurate than the O'Brien and crank rior labrum. The examiner holds the standing patient's
tests. shoulder in maximal external rotation and moves the arm
The test is performed by placing the patient in the from 120 0 to 800 in order to elicit posterior shoulder pain
supine position with the scapula stabilized on the table. (Figs. 3-72E(a) and 3-72E(b)
The Shoulder 103

Figure 3-72E a, b Mayo shear test.

LESIONS Neer 242 believed that 90% of rotator cuff tears were due
to structural primary impingement on the supraspinatus
from the overlying coracoacromial arch. Unfortunately, for
Impingement Syndrome
many overhead throwers who underwent acromioplasty
with the diagnosis of a primary impingement rather than a
Impingement syndrome is defined 237 as compromise of
secondary cause of impingement such as instability, these
the space between the coracoacromial arch and the proxi­
operations often were not successfup43
mal humerus. The coracoacromial arch covers the anterior
Etiologies (Table 3-3) have been categorized as either
glenohumeral joint. It is made up of the coracoid, the cora­
primary/structural or secondary/functional. In young ath­
coacromial ligament, the AC joint, the acromion, and the
letes, it was realized that most impingements were second­
subacromial bursa, which make up the roof over the ante­
ary because the underside of the cuff was more involved
rior glenohumeral joint. Miniaci and Fowler 238 feel that the
than the superfiCial bursal side.
term impingement should be associated only with "actual
mechanical abutment of the rotator cuff." They differentiate
between the term rotator cuff tendinitis and actual impinge­ Direct Primary/Structural Primary Impingement
ment because there are other causes of rotator cuff inflam­
matory lesions besides direct mechanical impingement. Osteoarthritis of the Acromioclavicular Joint: This
Neer and Welsh239 divided tendinitis in athletes into condition can create impingement of the supraspinatus due
three stages. Stage I consists of edema and hemorrhage, to inferior osteophyte formation. If the problem persists due
usually up to age 25; stage 2 consists of fibrosis and ten­ to osteophytes, it is prudent to surgically do a clavicle exci­
dinitis between the ages of 25 and 40; and stage 3 consists sion rather than just shave off the spur because due to the
of severe degeneration and rupturing in patients older than progression of the AC arthritis, the spur will recur and
40. However, Uhthoff and Sarkar240 stated that there have reimpinge.t42
not been any adequate pathological studies to establish the
characteristic features of the first two stages because leuko­ Hooked Acromion Processes: Morrison and Bigliani244
cytes in the tendon are rarely found, there is not severe described three types of anterior lateral acromions: type I
scarring in chronic impingement, and most tears begin on (flat), type II (curved), and type III (hooked). They found
the articular side rather than the bursal side. The lack of that 80% of their patients' cuff tears on the bursal side were
leukocytes could be due to tendinosis/degeneration. Wright associated with the hooked type III acromion and none
and Cofield 241 believe that Neer's stage II should include with the flat type I acromion.
tendon damage in the form of partial-thickness tendon tear­
ing, and stage III would define full-thickness tendon tearing Other Structural Causes: Other structural causes be­
(see Rotator Cuff RuptureslTears). side those mentioned in Table 3-3 could be exostosis of the

Table 3-3 Factors That potentially increase Rotar Cuff Impinge­ greater tuberosity, congenital enlargement of the supratu­
ment bercular ridge, unstable os acromiale,245 bony narrowing of
the supraspinatus outlet, and calcific deposit.
Acromioclavicular joint
Coracoid Impingement Due to Excessively Long or Lat­
Congenital abnormality
Degenerative spurs
erally Displaced Coracoid: In Neer's impingement test,
Acromion pain is felt between 120° and 130° of forward flexion. You
Unfused (bipartite acromion) may find anterior shoulder pain on horizontal adduction.
Abnormal shape (flat or overhanging)
Degenerative spur Degenerative Cuff Tear: Enlargements of the under­
Nonunion of fracture surface of the anterior acromion (spurs) could be due to a
Malunion of fracture degenerative cuff tear, allowing the humeral head to shift
Coracoid superiorly and causing degenerative proliferation.
Congenital abnormality
Posttrauma or postsurgical change in shape or location
Functional (Secondary) Causes of Impingement
Primary inflammatory bursitis (eg, rheumatoid arthritis)
Chronic thickening from previous surgery or injection Macrotrauma or Repetitive, Intrinsic, Eccentric Over­
Pins, wires, sutures, and other foreign materials project­ load Creating Microtrauma to Cuff Musdes246 : Eccentric
ing into the bursal space loading is more likely to stress tendons than concentric ac­
Rotator cuff tivity because eccentric contraction creates more force pro­
Thickening related to chronic calcium deposits duction and therefore greater tendon stress 247 Overload
Thickening from retraction of partial-thickness tears affects the inherent avascularity of the supraspinatus and
Flaps and other irregularities of upper surface due to par­ the infraspinatus near its insertion and the biceps tendon as
tial or complete tearing it courses over the head of the humerus,248 which presum­
Postoperative or posttraumatic scarring
ably cause a wringing out of the vessels on adduction. How­
Congenital abnormalities or fracture mal unions producing
ever, Jobe l88 stated that diminished tendon vasculature is
relative or absolute prominence of the greater tuberosity unlikely in athletes, compared with the rest of the popula­
Abnormally inferior position of a humeral head prostheSiS tion. The hypovascular critical zone has been found to be
producing relative prominence of the greater tuberosity hypervascular in patients with impingement syndrome, and
hypervascularity or angiogenesis is associated with sympto­
Functional matic rotator cuff disease secondary to mechanical impinge­
Scalpula ment 249 The resultant micro tears and swelling of the
Abnormal position
tendon is pressured by the unyielding cora co acromial arch,
Thoratic kyphosis
resulting in impingement of the subacromial area.
Acromioclavicular separation
Sarkar et a12 50 found that thickening of the coracoacro­
Abnormal motion

mial ligament as a causation of impingement may be sec­

Paralysis (eg of trapezius muscle)

Fascioscapulohumeral muscular dystrophy

ondary to involvement of the subacromial tissues. Swelling
Restriction of motion at the scapulothoratic joint
and thickening of the bursa and supraspinatus strain the
Loss of normal head depression mechanism coracoacromial ligament from below, so that the impinge­
Rotator cuff weakness (eg., suprascapular nerve palsy ment process may actually precede the thickening of the lig­
or C5-C6 radiculopathy) ament. The lateral band of the coracoacromialligament may
Rotator cuff tear (partial or full thickness) become hypertrophied. 188 The developmental adhesions in
Constitutional or posttraumatic rotator cuff laxity the coracoacromial ligament as well as the cuff muscles can
Rupture of the long head of biceps tendon be reduced by both friction, Active Release®, and Graston
Tightness of posterior shoulder capsule forcing the technique®. Repetitive overload described above can be di­
humeral head to rise up against the acromion during
rectly responsible for the next functional causation of mus­
cular weakness and force couple imbalance.
Capsular laxity
Muscular Weakness and Imbalance Between Force Cou­
Source: Reprinted with permission from FA Matsen III, and CT
Arntz, Subacromial impingement. In : The Shoulder. CA Rockwood ples (see Glenohumeral Motion; Scapulothoradc Motion):
Jr. and FA Matsen III, eds., p. 718, © 1990, WB Saunders Muscle imbalance, such as that caused by strong internal
Company. rotators and weak external rotators, may result in transient
The Shoulder 105

anterior humeral head displacement (subluxation/excessive humerus, resulting in impingement of the suprahumeral
laxity) during forward shoulder flexion. The humeral head structures.
may translate anteriorly and impinge on the anterior Tightness of the pectoralis minor and the short head
labrum. Inflexibility of internal rotation, due to shortened of the biceps that insert on the coracoid process can re­
posterior shoulder muscles or posterior capsule (see Capsu­ sult in scaular protraction. In this situation, there may be
lar Hypomobility below), may force the humeral head to a decrease in the normal posterior scapular tilt and a
rise anteriorly and superiorly up against the acromion dur­ lessening of the subacromial space, creating an external
ing flexion. Rotator cuff impairment and fatigue, disallow­ impingement. 174
ing normal cuff depression, and compression of the Budoff et aP51 stressed the idea that impingement of the
humeral head may cause an upward shift of the humeral rotator cuff in most patients is primarily an intrinsic prob­
head toward the acromion (Fig. 3-73). The loss of strength lem, where trauma or eccentric tensile overload eventually
of any of the rotator cuff muscles and biceps tendon de­ fatigues and weakens the cuff, allOwing the superior pull of
creases the necessary stabilization of the humeral head. Ab­ the deltoid to create abnormal superior migration of the
duction of the arm in any plane would create abnormal humeral head with arm raising. This functionally narrows
upward excursion of the humeral head and a high-riding the subacromial space, and the continued superior migra­
tion of the humeral head allows it to abut against the
undersurface of the acromion and the coracoacromial liga­
ment. Eventually, osteophytiC spurring occurs on the un­
dersurface of the acromion, and degenerative changes may
also occur on the overhanging coracoacromial ligament, re­
sulting in traction spurs at the insertion of the coracoacro­
mial ligament at the acromion. These spurs may be
mistaken for the abnormal acromial type 3 hook and be op­
erated on by acromioplasty The authors stated that this
operation fails to address the primary problem, which is in­
tratendinous degeneration or tendinosis. They prefer de­
bridement because acromioplasy disrupts the periosteum
and cortical bone of the acromion, exposing a large surface
of raw cancellous bone that may predispose to extensive
scar formation and subsequent fibrosis. As Noah and Gidu­
maP52 explained, the deltoid's action, when unopposed,
leads to secondary impingement. Garrick and Webb 196
stated "that most cases of impingement syndrome are sim­
ply the result of insuffiCiency of the stabilizing muscles of
the shoulder, which permits the humeral head to be dis­
placed when the arm is moved."
Imbalance of the scapular rotators (see Scapular Dyski­
nesis) prevents the optimal alignment, stabilization, and
movement of the scapula on the chest wall. Inefficient
scapular motion and its associated improper scapulo­
humeral rhythm reduces the length/tenSion relationship of
the scapular stabilizers and rotator cuff. Eventual fatigue of
Figure 3-73 With progreSSive cuff fiber failure, the head moves the scapulothoracic muscles can result in loss of necessary
up against the coracoacromial arch. A) Normal relationships of the acromial elevation, resulting in impingement-especially
cuff and the coracoacromial arch. B) Upward displacement of the during the cocking and follow-through phases. Weakness of
head, squeezing the cuff against the acromion and the coracoacro­
the scapulothoracic muscles reduces scapular stabilization
mial ligament. C) Greater contact and abrasion, giving rise to a
and results in diminished scapular motion, allOwing abnor­
traction spur in the coracoacromialligament. D) Still greater up­
ward displacement, resulting in abrasion of the humeral articular mal upward excursion of the humeral head. Inferior im­
cartilage and cuff tear arthropathy Source: Reprinted with permis­ pingement is probable because tears tend to occur on the
sion from FA Matsen, SB Lippit, JA Sidles, and DT Harryman. underside of the cuff.2 53 It is therefore important to examine
Practical Evaluation and Management oj the Shoulder. p. 123, © selectively and to increase the strength of the rotator cuff
1994, WB Saunders Company. and scapulothoracic muscles after pain is relieved to protect

against recurrent deltoid shear and instability due to weak­ toralis major, resulting in tendinopathy. They used the ex­
ness of the dynamic shoulder stabilizers. If there is weak­ ample of power lifting (bench press) , wherein the weaker
ness of both the parascapular and the rotator cuff muscles , stabilizing muscles suffer at the expense of the stronger
it is prudent to first strengthen the para scapular muscles to prime movers (pectoralis major). Insufficiency of shoulder
have a stable origin (scapular) of the rotator cuff muscles. dynamic stabilizers can result in clinical and occult anterior
Overuse of the dynamic stabilizers resulting in cuff fa­ instability, causing increased traction stress of the cuff mus­
tigue (weakness) may aggravate the static stabilizers, just as cles and predisposing to rotator cuff injury. 255
instability of the static stabilizers may aggravate the dy­ As differentiated from the usual patients with rotator cuff
namic stabilizers. Weakness of the subscapularis may be al­ injury, throwing patients are usually younger and complain
lOwing a hyperangulation during the cocking stage of the of posterior shoulder pain along the joint line when the arm
throw, so that there is an angulation, instead of translation, is externally rotated in 90° abduction and then horizontally
which would place an uneven stretch on the capsule and extended. Early on, throwers (e.g., tennis players) may
thus lead to a serial failure of the adjacent capsular tissue. complain only of stiffness and a longer time to warm up; in
Repeated stretch of the anterior capsule would eventually the later stages, they complain of posterior shoulder pain
result not only in contact between the rotator cuff and the and demonstrate a positive relocation test (see Relocation
posterior superior labrum, but also would eventually lead Test under Testing for Glenoid labral Tear above). Accord­
to anterior translation sufficient for a thrower to experience ing to Jobe,188 if rehabilitation consisting of strengthening,
subluxation.253 restoring range of motion, stretching of shortened muscles
It has been accepted that muscle imbalance may be and capsule, and reestablishing scapulohumeral synchrony
caused by abnormal postures, such as forward shoulders does not improve the condition, there is probably an over­
and forward cervical spine. People with forward head tilt, stretched capsule that will respond to surgery.
slumping shoulder posture, thoracic kyphosis, or hemiple­
gia lose the support of the glenoid cavity, which now faces Glenohumeral Instability: Glenohumeral instability
increaSingly downward, all of which may be associated with may be traumatic or atraumatic hyperelasticity (see
supraspinatus weakness. The arm is caused to abduct below), resulting in excessive migration of the humeral
slightly, which relaxes the superior capsule and results in in­ head (subluxation)-especially during overhead activi­
creased tone to the rotator cuff muscles. The increased stress ties. Another example is static stabilizers that eventually
to the remaining capsule may cause increased collagen pro­ affect dynamic stabilizers, resulting in impingement syn­
duction and result in capsular fibrosis.4 Overstretching of drome (see Atraumatic Instability for criteria for general
the scapular muscles and eventual tightening of the anterior joint hypermobility).
(pectoral, subscapular, and scalene) muscles may occur. Fa­ During late cocking and early acceleration, normally the
cilitation of these muscles may create inhibition and shut­ anterior capsular tension aids in the posterior translation of
ting down of the cuff muscles 29 Although all of the above the humeral head. If the anterior capsule is lax, the humeral
appears plausible, lewis et aP54 found that the scientific ev­ head translates forward , resulting in impingement 1l7
idence to support these theories is limited and that there Garth et aP56 mentioned how repetitive throwing, with
was no correlation between forward head posture, forward its increased external rotation, may create capsular laxity
shoulder posture, thoracic kyphosis, scapular protraction, and , along with muscular imbalance, may eventually lead to
glenohumeral flexion and abduction range, and pain in the instability and impingement.
symptomatic subacromial impingement syndrome patient. A subacromial spur may be formed due to a traction
One of their conclusions was that posture may appear to be phenomenon created by the repetitive impingement of the
faulty, but the individual may be flexible and capable of greater tuberoSity on the coracoacromial ligament. The
large ranges of movement. They also stated as mentioned repetitive impingement of the greater tuberoSity might be
above, that the relation of the acromion and posture affect­ due to instability or chronic cuff fatigue.
ing the bursal side cuff fibers does not relate to the much
more common finding of a degenerative tendinosis com­ Capsular Hypomobility Causing Obligate Translation 1 :
monly found on the articular (nonacromial) side. Tightness of the posterior capsule causes obligate anterior­
Garrick and Webb 196 stated that the impingement syn­ superior translation of the humeral head with shoulder flex­
drome does not necessarily mean that the subacromial ion (Fig. 3-74) and during abduction with internal rotation.
space is decreased. They believed that overuse and insuffi­ This translation can press the cuff against the coracoacromial
ciency of the shoulder stabilizing (cufD muscles allow the arch, causing a subacromial impingement. A tight posterior
humeral head to be continually displaced by the more de­ glenohumeral capsule increases scapular protraction, result­
veloped prime movers, such as the deltoid and the pec­ ing in impingement as the scapula rotates down and forward
The Shoulder 107

during follow-through. 17 Adhesive capsulitis associated with The patient's complaint over age 35 is usually associated
a tight inferior capsule may force the humeral head upward with a degenerative process that compromises the subacro­
against the anterior arch of the acromion, resulting in im­ mial arch due to subacromial proliferation, leading also to
pingement (24 mm) (see section on Glenohumeral Internal an impingement followed by vascular insuffiCiency and
Rotation Deficit). Tyler et aP89 stated that three of the most eventual rotator cuff tear. Bony protrusion occurs due to an
common findings contributing to secondary shoulder im­ acromial spur or osteophytes from the acromioclavicular
pingement are posterior capsule tightness, external rotation joint's rubbing against the supraspinatus tendon 260
weakness in a position of 90° of shoulder abduction and 90°
of elbow flexion, and abnormal scapulohumeral rhythm. Other Causes

Neuromuscular Insufficiency of the Rotator Cuff: Ir­ • Systemic diseases due to metabolic, endocrine, and
rheumatic disorders 240
lenbusch and Gansen 257 found that muscle incoordination
and imbalance can result in a functional impingement • An autoimmune mechanism with antibodies pro­
based on the loss of fast-twitch fibers type II that produce duced against denatured collagen and other structural
rapid contractions for brief sequences of motion and fine proteins 1l5
motor control of the joint. They found the loss of fast­ • Overtraining, poor technique, and poor equipment
twitch fibers by biopsy in patients with a supraspinatus syn­ • An increase in the amount and duration of load may
drome and partial or complete rupture of the rotator cuff. result in activation of intracelluar stress-activated pro­
This type of insuffiCiency would reduce the ability of mus­ tein kinases, causing tendon cells to undergo apopto­
cles to compensate for some of the primary and secondary sis or programmed cell death. Increased cell death
etiologies. They recommend immediate rehabilitation in the results in a collagenous matrix that is weaker and
earliest stages of the impingement syndrome, such as train­ more prone to tearing and eventual rupture 261
ing of muscle coordination and proprioception.

Internal Impingement (Thrower's Shoulder)

Cervical Radiculopathy: Grieve and Newman 258 stated
that vertebral joint problems, especially C-5 and C-6, cause This type of impingement is usually seen only in pa­
spasm of the rotator cuff musculature and "hitch up" the tients who perform excessive (overuse syndrome) abduc­
head of the humerus in the glenoid, disturbing the coordi­ tion and external rotation of their shoulder joint, as in
nation of humeroscapular movement and eventually result­ overhead motion athletes. The symptoms seldom appear
ing in the impingement syndrome. during activities of daily living. Jobe 188 described a gle­
noid impingement in which the greater tuberosity and its
Aging: HistologiC studies have shown degenerative attached inferior side of the supraspinatus tendon presses
changes characterized by calcification, fibrovascular prolif­ against the posterior-superior labrum and glenoid that can
eration, and micro tears in elderly individuals but not in lead to undersurface rotator cuff tears. This is called a
younger subjects. Aging, with its associated tendon degen­ posterosuperior impingement or internal impingement 262
eration, can result in enthesopathy (insertional tendinopa­ This occurs especially in pitchers during a throw) (see
thy), causing tendiniopathy, spur formation, bursal Fig. 3-43) when there is 90° glenohumeral abduction
hypertrophy, fibrosis, and scarring. It is rare not to find with maximal external rotation and horizontal extension
thinning and fibrillation of the rotator cuff by the fifth (late cocking and early acceleration). This type of contact
decade. 259 The age of the patient is important regarding between the undersurface of the rotator cuff tendon and
the progression and pathology of shoulder complaints. In the posterosuperior glenOid can be nonpathological and
active patients, especially overhead athletes aged 18 to 35 can occur normally, but rotator cuff overuse, espeCially of
years, the shoulder pathology is usually due to repetitive the subscapularis, which provides a dynamiC restraint in
stresses, leading to cumulative micro trauma and progress­ the cocking position, results in increased force on the an­
ing to instability, which causes impingement and eventual teroinferior glenohumeral ligament and anterior capsule,
rotator cuff tear. Another scenario could be shoulder laxity resulting in instability. Instead of the humeral head mov­
associated with muscle imbalance, resulting in repeated ing posteriorly during cocking, there is increased anterior
subluxation, leading to rotator cuff inflammation. The in­ movement of the humeral head, which aggravates the
stability factor is a reason why acromioplasty in the contact between the posterosuperior glenOid and the rota­
younger age group was not adequate over the long tor cuff.263 The primary problem in internal impingement
term. 238 is often instability249 Jobe 188 also stated that increased


Figure 3-74 Normal capsular laxity allows the humeral head to remain centered during elevation. Tightness of the posterior capsule can
create obligate anterior-superior translation with anterior humeroscapular elevation. This may cause squeezing between the humerus and
the undersurface of the acromion. Source: Reprinted with permission from FA Matsen, SB Lippitt, JA Sidles, and DT Harryman. Practical
Evaluation and Management of the Shoulder. p. 39, © 1994, WB Saunders Company

cuff labrum contact by the greater tuberosity could be due Internal impingement usually creates posterior pain in the
to limited upward rotation of the scapula due to weakness apprehension test, which is then relieved by the relocation
of the scapular rotators. GIRD (see above) is also related test (see Relocation Test) . It is thought that the posterior force
as causative of internal impingement. Posterior tightness during the relocation test relieves the contact by preventing
due to a contracted posterior capsule and/or infraspinatus the infolding of tissue between the cuff and the labrum. 264
and/or teres minor contracture can result in a loss of pos­ Throwers have to learn to throw with the arm in the scapular
terior translation of the humeral head aggravating the plane and prevent any hyperangulation (Fig. 3-74A).
contact between the undersurface of the infraspinatus and
the posterosuperior glenoid. 264 With a posteroinferior
capsule contracture, the humeral head may create a pos­ Pathology of Impingement Syndrome
terosuperior subluxation during cocking, causing internal
impingement and rotator cuff failure. 264 Compensating for As the condition progresses, swelling, fibrosis , and thick­
decreased capsular function, the rotator cuff tendons ening of the cuff tissue may hypertrophy to the point of de­
overwork, and the internal impingement adversely affects creasing the subacromial space. Most of the above etiologies
the undersurface of the cuff. As the cuff weakens, more are responsible for creating what is known as an impingement
stress is put on the anterior static restraints further exac­ syndrome, which mechanically can cause subacromial bursitis,
erbating the internal impingement. rotator and biceps tendinopathy, and eventual tearing.


Figure 3-74A A), In normal shoulder, humerus is abducted in scapular plane during cocking phase of throwing. B), If there has been
stretching of anterior soft tissue constraints, humerus may be abducted in coronal plane; this is termed hyperangulation, as humeral shaft
forms acute angle to scapula. Source: Modified fromJobe CM , et al. Anterior shoulder instability, impingement, and rotator cuff tear: theories
and concepts. In: Jobe FW, ed. Operative Techniques in Upper Extremity Sports Injuries. St. Louis: Mosby Year-Book Inc; 1996, p 173.
The Shoulder 109

Clinical: Unless the movements that cause the instabil­ use. Depending on the severity of the inflammation, pain
ity are eliminated and a strengthening program to compen­ may be felt anywhere down the CS-C6 sclerotome, extend­
sate for the instability is developed, the benefits of manual ing from the shoulder to the wrist. Local tenderness may be
methods on areas of tendinopathy will not be long term. In­ palpated over particular cuff muscles, but if at all possible,
stability is considered the primary cause of rotator cuff findings should be based on speCific resisted muscle testing
tendinopathy in the majority of young athletic patients. because the most painful area is not always the source of
The principal diagnostic key for tendinopathy is pain on pain. For example, a large percentage of patients with in­
resisted muscle testing and/or stretching of that muscle to volvement of any of their cuff muscles localize their pain at
mimic the patients complaint. Weakness in the early stages, if the deltoid tubercle, which is rarely involved.
present, is caused by reflex inhibition due to pain or disuse. In general, the athlete with a painful shoulder often pres­
Atrophy is seldom present. Because more people are involved ents with a combination of dysfunctional factors, such as
in recreational sports, problems with the cuff in the 30- to 40­ signs of impingement, scapular dyskinesis, diminished inter­
year-old age groups are becoming more frequent. The associa­ nal rotation, tight posterior capsule, weakness of the external
tion of pain with activity has been used to determine the rotators and scapular stabilizers, and-in later stages-supe­
severity of the condition. In the early stages, there is pain only rior or anterior glenohumeral translation (instability)267
after activity; then minimal pain with activity; then pain inter­ An effective treatment for stretching a tight posterior
fering with activity; pain remaining between activity; and fi­ capsule is the use of an active-release technique, in which
nally pain interfering with activities of daily life 265 the practitioner brings the posterior capsule into a short­
Patients may complain of night pain, which is more ened position and contacts the capsule. The patient then
common in cuff tears, but the nocturnal pain may be due to stretches the capsule by actively either internally rotating or
the inflammation's forming minor, filmy adhesions that are horizontally adducting the arm while the practitioner main­
broken as the patient moves. 266 The type of pain in tains a firm contact on the capsule. Figure 3-7SA shows
tendinopathy is usually a progressive pain associated with the shortened position of the capsule in external rotation,

Figure 3-75 A), Shortened position of the capsule in external rotation. B), Stretched position of the capsule in internal rotation. C), Shortened
position of the capsule in horizontal abduction. D), Stretched position of the capsule in horizontal abduction. Source: Copyright © 1998, Warren I.

and Figure 3-7SB shows the stretched position of the cap­ bility and associated impingement (secondary impingement);
sule in internal rotation. Figure 3-7SC shows the shortened anterior instability and associated impingement due to hy­
position in the horizontal abduction, and Figure 3-7SD perelasticity, atraumatic instability, or general joint hypermo­
shows the stretched position of the capsule in horizontal bility; and pure anterior instability-traumatic or atraumatic.
abduction. See the chapter on Graston Technique (Chapter
IS) for another excellent method of capsular treatment.
Roentgenograms are usually negative, showing no cal­ TendinosislTendinitislTendinopathy
cium deposits. In chronic tendinopathy of the cuff, there
may be areas of sclerosis, erosion, or small cystic changes at These conditions are discussed in the Part III, Manual
the greater tuberosity 266 Methods Treatment Section. Rehabilitation of the rotator
Table 3-4 explains the probable symptoms and findings cuff muscles is discussed in the chapter Conservative Treat­
associated with pure impingement (primary); anterior insta­ ment of Soft Tissue Injuries (Chapter 24) .

Table 3-4 Classification of Glenohumeral Subluxation and Associated Subacromial Impingement

Group Symptoms and Findings

1: Pure impingement 1: Positive impingement sign

2: Negative apprehension sign
3: Grade 0 or 1 humeral head translation
4: Arthroscopic
(a) Stable examination
(b) Undersurface cuff tear, subacromial bursitis
(c) Labrum and glenohumeral ligaments normal

2: Anterior instability and associated 1: Positive impingement sign

impingement 2: Grade 2 or more humeral head translation
3: Possible apprehension and relocation
4: Arthroscopic
(a) Unstable examination
(b) Undersurface cuff tear
(c) Labral damage
(d) Humeral head chondromalacia
(e) Subluxation of humeral head

3: Anterior instability and associated 1: Positive impingement sign

impingement (hyperelasticity) 2: Grade 2 or more humeral head translation
3: Possible apprehension and relocation
4: General joint hypermobility
5: Arthroscopic
(a) Unstable examination
(b) Undersurface cuff tear
(c) Attenuated but intact labrum
(d) Glenohumeral ligament (capsular laxity)
(e) Subluxation of humeral head over labrum

4: Pure anterior instability 1: Negative impingement sign

2: Grade 2 or more humeral head translation
3: Possible apprehension and relocation
4: Arthroscopic
(a) Unstable examination
(b) Normal cuff
(c) Labral damage and capsular laxity
(d) Humeral head chondromalacia and sublaxation

Source: Reprinted with permission from K Bak and P Fauno. Clinical Findings in Competitive Swimmers with Shoulder Pain . American Jour­
nal of Sports Medicine. Vol. 25, No. 2, p. 257, © 1997, Ame rican Orthopaedic Society.
The Shoulder III

Supraspinatus Tendinopathy • As with all muscles with a positive resisted test, palpa­
tion of the most tender and restricted tissue areas
The cuff muscle most commonly involved in tendinopa­
thy is the supraspinatus as a result of eccentric overload af­
Subscapularis Tendinopathy
fecting its stabilizing function. The most common sites of
involvement are just before the insertion on the greater
Pain is usually located on the anterior shoulder, with lo­
tuberosity and at the musculotendinous junction. In assess­
calized pain over the lesser tuberoSity or on the anterior
ing this muscle for treatment, as with all muscles, it is im­
scapular wall palpated in the axillary area. In the younger
portant to palpate the whole muscle for abnormal tissue
patient with anterior shoulder pain, subtle instability must
signs because all of the muscle/tendon must be approached
be ruled out.
with soft tissue treatment. The superior portion of the
tenoperiosteal insertion may elicit a painful arc; the muscu­
lotendinous portion, which is not subacromial, does not Functional Tests
elicit a painful arc . Pain on full passive abduction to 180° or
passive lateral rotation at 90° may stress the underside of
the tenoperiosteal junction on the roof of the glenoid. 268 • Pain and strong or possible minimal weakness on iso­
metric lift -off test (see Isometric Testing)
Functional Tests: (See Chapter 1 for contractile tissue • Possible pain on active or passive horizontal adduction
interpretation of all the following muscle tests .) • Possible pain on active or passive lateral rotation
• Possible painful arc if the insertion at the upper por­
• Pain and strong or possible minimal weakness on iso­ tion of the lesser tuberosity is involved 255
metric abduction (see Isometric Testing)
• Pain and strong or possible minimal weakness on re­ Note: Anterior shoulder muscle pain may also be related
sisted lateral rotation to strain of the other cuff muscles, pectoralis major and latis­
• Possible painful arc if insertion area is involved simus dorsi at their insertions, biceps, and at the anterior
deltoid origin (see Shoulder Girdle Tests). Isometric testing
• Possible pain on active and passive abduction at 180°
and stretching of these muscles help localize the problem
• Probable positive impingement test area . Rarely, the subscapularis may be impinged as it passes
• Possible pain on shoulder abduction at n-range beneath the coracoid process (coracoid impingement). Also
check the subclavius for tenderness and adhesions.
Mattes 269 (see Chapter 21) uses an active isolated
Infraspinatus Tendinopathy
stretching method to stretch muscles. In order to stretch the
external shoulder rotators, the clinician maintains the pa­
The patient may feel pain at the anterior or posterior
tient's head of the humerus at 90° abduction while the pa­
shoulder area. Principal sites of involvement are at the in­
tient rests his or her elbow on the clinician. The clinician
sertion of the infraspinatus in the middle part of the greater
then tells the patient to actively drop the forearm , thereby
tuberosity, the musculotendinous portion, and anywhere in
causing the internal shoulder rotators to work, which re­
the belly of the muscle in the infraspinatus fossa. The teres
laxes the external rotators (Fig. 3-76A). After the patients
minor is not involved as often as the infraspinatus unless a
arm reaches the end-pOint of internal rotation , the clinician
thrower complains of pain during the deceleration phase
assists in gently increasing the motion to the passive end­
(see Throwing Shoulder).
range and holds for 2 seconds (Fig. 3-76B). This stretches
the posterior rotator cuff, including the supraspinatus, in­
Functional Tes ts fraspinatus, and teres minor muscles. This is repeated for
two sets of 10 repetitions. For stretching the internal rota­
• Pain and strong or possible minimal weakness on iso­ tors, the patient is asked to actively externally rotate the
metric lateral rotation (see Isometric Testing) shoulder beginning from the forearm sagitta,l position, 90°
shoulder abduction to the active end-range of external rota­
• Possible pain on passive medial rotation stretch
tion (Fig. 3-76C). At this point, the practitioner assists by
• Pain on isometric lateral rotation and adduction (incrim­ gently paSSively increasing the external rotation to its pas­
inates the teres minor, which is also a weak adductor) sive end-range and holding for 2 seconds (Fig. 3-76D).
• Possible painful arc if the superior surface of the in­ This stretches the pectoralis major, subscapularis, latissimus
sertion is involved dorsi, and teres major.

Figure 3-76 To stretch external rotators: A), The patient actively drops the forearm, thereby causing the internal shoulder rotators to
work, which relaxes the external rotators. B), The clinician assists in gently increasing the motion to the passive end-range and holds for 2
seconds. To stretch internal rotators: C), the patient is asked to actively externally rotate the shoulder beginning from the forearm sagittal
position, 90 shoulder abduction to the active end-range of external rotation. D), The practitioner assists by gently passively increasing the

external rotation to its passive end-range and holding for 2 seconds (also see Chapter 21).

Biceps Tendinopathy sults from overuse, a direct blow, laxity of the transverse
humeral ligament resulting in subluxation, chronic irrita­
The shoulder capsule is lined with synovium, and the tion, or anatomic reasons, such as a narrow or shallow
sheath of the biceps tendon is an extension of the shoulder bicipital groove or a rough supra tubercular area. Booth and
joint synovial lining, beginning at the glenoid labrum. MarveF71 stated that tendinitis resulting from acute trauma
Therefore, bicipital tendinitis often may be associated with is infrequent because of the greater osseous protection af­
tendinitis of the rotator cuff or pain at the anterior aspect of forded this tendon compared with the tendons of the rota­
the shoulder joint. The biceps tendon does not slide in the tor cuff. Tenosynovitis of the long head of the biceps brachii
groove, but the humerus moves on a fixed tendon for a dis­ is often associated with impingement of the supraspinatus
tance of about 1 inche 270 Tenosynovitis of the long head of and subscapularis. Clark and Harryman 272 stated that the
the biceps is invariably found under and just distal to the tendon of the long head of the biceps muscle was "en­
transverse humeral ligament. Biceps tendinitis usually re­ sheathed by interwoven fibers derived from the subscapu­
The Shoulder 113

laris and supraspinatus tendons." If a biceps tendinopathy reeducation exercise (see respective chapters). Palpation is
fails to improve, think of the possibility of an accompanying necessary, preferably after a positive functional test to pin­
superior labral tear. point the lesion and determine local and surrounding tissue
Bicipital tendinitis is not a common shoulder problem. integrity. Are there painful nodules, adhesions, "piano
Pure traction overload tendinitis of the biceps tendon has wires," or "leathery" tissue! Because eccentric muscle over­
not been identified 273 Pain in the bicipital area is more load is a frequent cause of tendinitis, rehabilitation can be
often due to and associated with cuff tendinitis, but this directed toward improving eccentric stress. Curwin and
area may be involved by itself. Rupture of the biceps rarely Stanish274 recommended stretching (because it increases
occurs in the throwing athlete unless there are predisposing the resting length of the tendon), which lessens strain; ec­
factors such as chronic inflammation, mechanical spur in centric progressive muscle strengthening (rubber tubing);
the bicipital groove, or use of steroids 2 Palpating the long and exercises that emphasize increasing the speed of muscle
head of the biceps for tenderness may be difficult if the an­ contraction, which may allow the tendon to accept more
terior and middle deltoid is overdeveloped. It may be neces­ load. Sport-specific analysis is recommended because the
sary for the examiner to palpate the biceps with the patient added resistance of the swimmer's stroke might call for em­
supine while the arm is held to relax the deltoid. (See Clini­ phasizing concentric exercise for the anterior muscles and
cal Review of the Shoulder Muscles, Biceps, for the best pal­ eccentric exercises for the scapular stabilizers. In the early
pation position.) stages of isometric or isotonic exercise, the arms should be
near the patient's side to prevent aggravation of static and
Functional Tests (see also Bicipital Ruptures) dynamic tissue. As pain subsides, exercises can progress up
to 180 0 Exercises and stretching may be used that cause
• Speed's test or the elbow flexion test is painful and slight discomfort, but not pain (see Chapter on Rehabilita­
minimally weak on resisted shoulder flexion. Resisted tion of Soft Tissue Injuries, Chapter 24).
testing of the biceps with the elbow flexed is not as Besides the cuff muscles, it is necessary to ensure the
reliable as testing with the elbow extended 266 strength and flexibility of the serratus, trapezius, levator
• There is pain on resisted supination (elbow flexed, scapulae, rhomboids, teres major, and latissimus dorsi mus­
pronated forearm supinated against resistance). At cles to ensure dynamic stability of the glenohumeral joint.
times for a patient with anterior shoulder pain in Other distant areas of the kinetic chain must be evaluated
whom a biceps problem is suspected, the resisted regarding changes in strength or biomechanics that the ath­
supination test is positive and Speed's test is negative. lete may have adapted to compensate for the local pain. Im­
• Straight-arm flexion test: The standing patient hyper­ proper use of distant structures may be responsible for the
extends a straight pronated arm and attempts flexion local pain, such as scapular dyskinesis or abnormal muscle
against resistance; the test may be painful on stretch firing patterns. In biceps tendinopathy, the use of a strap
without resistance (see Fig. 3-57). just distal to the long head irritation (Similarly used in lat­
eral epicondylopathy) may offer relief during use. The strap
• The patient holds the arm in 180 0 of abduction and
creates a new origin for the biceps tendon and helps to rest
lateral rotation and slowly brings the arm to the side.
the strained area.
Pain may occur as the tendon is forced against the
Triceps and pectoralis tendinopathy are rarely present,
lesser tubercle. An audible or palpable click may indi­
but resistive testing and stretching pinpoint the problem,
cate an elongated subluxating or dislocating biceps
which responds readily to manual treatment.
tendon (see below).
• There is a possible painful arc if the lesion is located
Calcifying Tendinitis (Must Differentiate from Dystrophic
at the intracapsular area (rare). A painful arc is not
present with the usual bicipital groove lesion 268
• A lesion at the glenoid origin may create pain over the Etiology: The etiology is unknown. Calcifying tendini­
AC joint. This pain may be elicited by testing resisted tis is not pathologically related to rotator cuff degenera­
adduction with the arm slightly extended. 268 tion,275 tendon tears,276 or trauma 277 It may be an auto­
immune disease278
Musde- Tendon Treatment: Treatment consists of ice
and various modalities in the acute stage and a variety of Pathology: Calcifying tendinitis is considered a pri­
manual methods, such as friction, active release, counter­ mary reactive tendinopathy that is self-healing rather than a
strain, myofascial release, mobilization, post isometric re­ progressive deterioration 240 Hypoperfusion of cuff tendons
laxation, post facilitation stretch, and neuromuscular results in tissue hypoxia and eventual calcification 279 The

calcium deposit is usually in the body of the tendon rather or elevated. An aching (twinge-like) shoulder pain is usu­
than the insertion or bone, as in the dystrophic type. It is ally created by one specific motion, such as abduction, flex­
located usually in the supraspinatus and sometimes in the ion, and extension,283 depending on the location of the
infraspinatus tendon. Subscapularis deposits are usually deposit. A painful arc may be the only positive functional
asymptomatic. test. It may be difficult to pinpoint a calcium deposit as the
There is a chronic phase followed by an acute phase. The underlying cause because typical signs of cuff impingement
patient may live with a chronic non painful deposit of intra­ may be present. If possible, direct pressure on the calcium
tendinous calcium. Trauma or overuse creates a hyperemia, elicits the most tenderness.
and the symptomless, dry-state calcium develops a tooth­
paste-like consistency, which irritates the overlying bursa Treatment: Treatment is conservative and comprises
and causes a secondary bursitis and excruciating pain while the use of an arm sling, ice, stretching, and various modali­
the calcium is being resorbed. The calcium may evacuate ties. Surgery is rarely necessary284
into the bursa and relieve the condition.
Dystrophic Calcification
Radiologic Interpretation
• Chronic phase: Tendon body (not insertion) deposit
appears with a uniform density and well-defined
DystrophiC calcification is associated with degenerative
peri phery. 280
conditions, such as acromioclavicular and glenohumeral
• Acute phase: There is a fluffy, poorly defined, milky arthritis and chronic rotator cuff tears. There is deteriora­
appearance 280 of calcium. tion in which there is calcification of necrotic tissue.
• The greater tuberosity maintains its normal shape.24o
Radiologic Interpretation
Clinical: Calcifying tendinitis is more common in middle
age, in females, and in those with sedentary occupations 280
Uhthoff and Sarkar240 distinguished a dystrophiC calcifi­
cation from a calcifying tendinitis by the appearance of stip­
Acute Phase and Functional Testing: The signs and
pled calcifications that overlie an irregularly shaped greater
symptoms are similar to those of an acute bursitis or an
tuberosity. An associated finding of degenerative osteo­
acute brachial neuritis, with a red-hot burning pain in
arthritis is common. Calcification is located at the tendon
which both practically all resistive and passive tests are pos­
insertion into the bone 280
itive. A calcium deposit may be suspected if there is severe
direct tenderness over the localized calcium besides the
general tenderness palpated around the bursa. Excruciating Bursitis
pain is elicited in almost all passive and resisted tests for 1
to 4 days. There may be a positive painful arc, producing Of the eight bursae around the shoulder, only the large
the "jag and wince" phenomenon described by Codman,281 subacromial bursa has clinical significance. 5 Codman281
especially if the calcium deposit is large. stated that such designations as subdeltoid, subcoracoid,
The condition is self-limited, and remission occurs in 6 and supraspinatus bursae describe extensions of the sub­
to 14 days.271 If the depOSit ruptures spontaneously, the pa­ acromial bursa or the glenohumeral capsule. The subacro­
tient experiences immediate relief. Patients can seldom mial bursa is bounded superiorly by the coracoacromial
wait, however, and usually require needling or aspiration. ligament and acromion and inferiorly by the rotator cuff
DiagnOSiS is confirmed by the presence of an amorphous, and capsule. The bursa extends over the proximal humerus
ill-defined, cloudy calcium denSity instead of the usual beneath the deltoid and beneath the coracoid process. The
asymptomatic deposit that is sharply defined with circum­ bursa is lined with a synovial membrane whose walls are
scribed borders on roentgenography. The size of the calcific closely connected, creating a "potential space. " 1 The bursa
deposit does not appear to be correlated with the severity of allows free, well-lubricated movement of the greater
the symptoms.282 tuberosity beneath the acromion in abduction of 60° to
130° and of the deltoid over the proximal humerus.
Chronic Phase: The chronic phase is usually asympto­ According to Bland et aP1 5 and others,271 virtually all
matic, but if the calcium is dehydrated (chalk-like), it may cases of subacromial bursitis have a preceding tendinitis or
pinch the subacromial tissue when the shoulder is rotated tenosynovitis in the rotator cuff or the biceps tendon and
The Shoulder 115

sheath or some inflammatory process in the bone or joint o There may be a painful arc.
about the shoulder; the spread of inflammation to the bursa o All passive tests mayor may not aggravate the pain.
is a secondary event. Neviaser 285 stated that primary shoul­
o Depending on the acuteness of the bursitis, isometric
der bursitis is seen only in gout, rheumatoid arthritis , pyo­
muscle testing of the cuff muscles may incriminate
genic infections, and tuberculosis. Most hip and shoulder
none to most of the muscles. Often, the diagnosis of
bursitis is associated with repeated micro trauma in middle­
chronic bursitis is one of exclusion.
aged individuals in whom there is some degeneration of
tendon, muscle, or fibrous tissue 2 86 By middle age, the bur­ o With the patient's arm extended and with the arm ad­
sal walls become thickened and the cavity filled with adhe­ ducted, the bursa may be palpated under the anterior
sions. ll5 Bursal thickening and loss of ability to glide acromion, at the lateral acromion, and at the posterior
perpetuate increased wearing and fraying of the cuff, also lateral portion of the acromion. Moving the arm into
resulting in tendinitis. extension helps reveal the anterior portion of the bursa.

C linical: . Acute bursitis may result with or without Subcoracoid Bursitis

calcific tendinitis. As with the latter, patient presentation is
that of excruciating pain without relief on repositioning; Subcoracoid bursitis is an uncommon condition. There
all active movements are painful. Heat or swelling may be is usually localized pain inferior to the tip of the coracoid
palpable. process. Patte287 stated that impingement may occur in the
coracohumeral space between the coracoid process and the
Functional Tes ting
lesser tuberoSity. Computed tomographic studies have
shown a decrease in the above space in shoulder flexion
o Passive: Bursitis is noncapsular because there is more
and medial rotation. 288 The tissues pinched under the hook
pain and limitation on passive abduction than on pas­
of the coracoid are the thickest part of the subscapularis
sive lateral rotation (see Chapter 1, Capsular Pattern).
tendon, the superior and middle parts of the glenohumeral
o Passive: There is an empty end feel (i.e., the examiner ligament, and the subcoracoid bursa. Patte287 stated that
feels that more movement is present, but the patient's protuberances of the lesser tuberoSity and the abnormal
pain prevents further movement). structure of the coracoid process can impinge, espeCially
o Isometric testing is usually painful in the acute stage when associated with overuse in flexion and internal rota­
in all directions because of tension on the inflamed tion, as in swimming and gymnastics. The coracohumeral
bursa. As the condition subsides, resisted cuff testing space can be decreased by an isolated traumatic tear of the
should become stronger and painless or may elicit subscapularis (usually associated with a dislocation of the
pain, incriminating a particular causative cuff that can long head of the biceps) , scarring after a traumatic tear of
be treated by manual methods. the coracohumeral ligament, functional disability due to
laxity of a partial supraspinatus tear in the anterior part,
Chronic Subacromial Bursitis and calcification of the subscapularis.

Symptoms of chronic subacromial bursitis are vague; the Functional Testing

patient may complain of pain only after excessive overhead
use or may complain of a dull , unlocalized ache. Night pain o There is pain on passive horizontal adduction.
is common. • There is pain on extreme passive lateral shoulder
Functional Testing: The condition presents a "mud­
o There is pain with the coracoacromial impingement test.
dled" appearance. Because of the inflammatory process, al­
most any combination of resistive and passive testing may o There is pinpoint tenderness at inferior tip of cora­
be positive. Because in most cases, there is an underlying coid process.
tendinitis, as the inflammatory process abates, isometric
testing may incriminate the particular tendon that is the Functional D ifferentiation Between Tendinitis and Bursitis
source of the pain. Manual treatment, such as friction mas­
sage, can be used on the chronic bursal thickening (see Tendinitis usually precedes bursitis, but they may be
Friction Massage, Graston Technique). Functional testing present simultaneously Every tendinitis condition is accom­
reveals the follOwing: panied by pain on one or two speCific isometric tests, with

probable pain on passive stretching of the involved tendon. player), rupture usually occurs during the eccentric deceler­
Because the joint is rarely involved, even if active range of ation phase. Tears are rare in swimmers due to lack of de­
movement is painful and limited, full passive movement in celeration forces 267
tendinitis is usually possible. The causes of ruptures are a combination of extrinsic the­
When a bursa becomes inflamed, there may be any com­ ory (impingement syndrome) and intrinsic theory of tendon
bination of positive resisted and passive tests that do not degeneration and associated hypovascularity 241 More often,
specifically identify a particular problem. This explains why there is a progressive deterioration due to the normal aging
the functional diagnostic chart (see Appendix 3-A) shows process, microtrauma, ischemia, or chronic impingement
numerous +/- signs for bursitis. A chronic subacromial bur­ (cuff tears have a 95% association with subacromial impinge­
sitis may present with only a painful arc and no pain or ment).267 These ruptures ll5 seldom occur before age 50 but
weakness on isometric testing. After the tendons, the main are relatively common after age 60. There is a history of pre­
structure left in the painful arc area is the bursa. Bursitis is vious steroid injections. "Pseudorupture" is due to fracture of
usually a secondary problem, so that other causes of the the body of the scapula, causing painful and weak rotator
painful arc would also have to be considered (e.g., chronic cuff function because of inhibition from intramuscular hem­
tendinopathy of a particular cuff tendon or tendons, tendi­ orrhage 33 The condition usually resolves within a few weeks.
nosis, osteophytes, spurring of the inferior AC joint, en­
largement of the outer anterior end of the clavicle, and other
Location of Tears
extrinsic and intrinsic possibilities previously discussed).
• Superficial bursal side: usually more painful than
Treatment of Bursitis deeper tears 267 ; irritates the bursal floor and almost
always associated with impingement or compression
All the factors in .rehabilitation relating to tendinopathy • Intratendinous
must be addressed in the treatment of chronic bursitis.
• Articular side: area where degenerative lesions begin,
Frictioning and Graston technique of the underlying ten­
especially at the deep surface of the anterior insertion
don and fibrotic bursa often eliminate chronic bursitis
of the supraspinatus near the long head of the biceps. 1
problems. Deep pressure on a chronic bursa often aggra­
vates the condition because the inflammatory process is
rekindled. This is necessary for eventual healing and re­ Effects of Ruptures 267
modeling of the tissue. When chronic bursitis (including
the hip) is treated, it is necessary to warn the patient that During shoulder elevation, there is a lessening of required
after manual therapy is applied that the condition may get humeral head depression and caudal glide , allowing the del­
worse for 3 or 4 days before the pain subsides. Patient toid to pull the humeral head upward freely This creates im­
could use ice for relief. If ice is used 5 minutes after treat­ pingement and increased cuff damage. There is a lessened
ment, it will not retard the necessary healing inflammatory ability to maintain loads, thereby increasing load on adjoin­
process. ing fibers, and a diminished local vascularity, compromising
strength and repair. Progressive interstitial tearing usually be­
gins with the supraspinatus and progresses to the infraspina­
Rotator Cuff RuptureslTears
tus, teres minor, and eventually the subscapularis. Often,
there is an associated rupture of the long head of the biceps. 1

Rotator cuff ruptures or tears are caused by acute macro­ Types of Rotator Cuff Tears
trauma due to humeral fractures or fracture/dislocation,
acute anterior glenohumeral dislocation, or supraphysio­ Partial-Thickness Tear (Fig. 3-77): A partial-thick­
logiC eccentric rotator cuff contraction. 73 In a healthy, ness tear is difficult to diagnose based solely on physical
young adult (usually the throwing athlete) , the rupture re­ findings. The lesion usually requires adjunctive imaging,
sults in an avulsion of the greater tuberosity rather than such as arthrography, MRI , and ultrasonography. MRI is
avulsion of the tendon itself or a partial tear. Younger peo­ considered the best means available, although it is not per­
ple require a greater injury than older ones and do not usu­ fect for partial tears 241 The tear usually occurs at 30 to 55
ally suffer with a full-thickness cuff tear. The most common years of age , associated with an unexpected eccentric load. 1
traumatic cause is falling on an outstretched arm, which This type of tear may not be evident on testing, and the pa­
creates a destructive impingement. In a thrower (e.g., tennis tient might be treated for an "impingement syndrome" or
The Shoulder 117

against the coracoacromial arch (abrasion sign). Ordinarily,

the chief cause of shoulder crepitus is a degenerated bursa.

Full- Thickness Tear: The defect extends all the way

through from the articular surface to the bursal surface of
the rotator cuff (Fig. 3-78). The patient usually is over 40
years of age. A partial-thickness tear may progress to a full­
thickness tear, especially in the older patient.

Symptoms: There mayor may not be a feeling of a

snap. A gradual attrition of the degenerated tendon occurs
(tendinosis), creating increased weakness so that the rup­
Figure 3-77 Rotator cuff defects usually begin at the deep sur­ ture "sneaks up" on the patient or is followed by a sudden
face of the supraspinatus, near the long head of the biceps. Source: unexpected loading. The patient is unable to elevate or ro­
Reprinted with permission from FA Matsen, SB Lippitt, JA Sidles, tate the arm externally He or she shrugs the shoulder to
and DT Harryman. Practical Evaluation and Management of the perform elevation 3 Active range of motion is seldom more
Shoulder. Figure 4-21, p. 121, © 1994, WB Saunders Company. than 30° of abduction, but patients may have large tears of
the rotator cuff and still retain full elevation as long as some
depressor action of the cuff remains. 29o Sleeping on the af­
fected side, placing the hand behind the head, and throw­
ing overhand were found to be the most common
"tendinitis." The patient's symptoms improve, and he or she
functional impairments in full-thickness tears 1
is left with a minor residual weakness of one of the cuff
muscles (usually supraspinatus).
Functional Testing The drop-arm test mostly assesses
There are symptoms of shoulder stiffness, associated
the supraspinatus for a significant tear. The examiner pas­
with rest pain and nocturnal pain. Surgical treatment
sively abducts the patient's arm to 90° and then releases the
should be considered only if symptoms are severe for a pe­
arm. The patient may be unable to lower the arm with con­
riod of 6 to 18 months or more 241
trol or may drop the arm to the side (Fig. 3-79). The drop­
arm test is seldom evident in the athletic population. A
Functional Testing Compared with full-thickness tears, "drop away" sign refers to inability to duplicate full passive
partial-thickness tears are more painful and show less loss
of strength on isometric testing. 1 Active range mayor may
not be complete (depends on the amount of pain and the
muscular development of the patient). 289 Passive range is
usually full and painless unless there is associated impinge­
ment (positive impingement sign). Matsen et al,l stated that
there is often a selective contracture of the posterior capsule
resulting in limitation of shoulder flexion, internal rotation,
and horizontal adduction, especially in partial-thickness
tears. If the patient is unable to abduct to 90°, injection of a
local anesthetic or numbing by friction massage (see Chap­
ter 14) may enable the patient to abduct weakly to about
150°. The drop-arm test may be positive (see below). There
is mild atrophy of the supraspinatus more often than the in­
fraspinatus, usually visible within 2 to 3 weeks.

Subacromial Crepitus: Palpating the supraspinatus in­

sertion and feeling crepitus while the shoulder is abducted
to 90° and rotated medially and laterally is a sign of Figure 3-78 Full-thickness defect in the supraspinatus tendon.
a supraspinatus tear in both partial-thickness and full­ Source: Reprinted with permission from FA Matsen, SB Lippitt, JA
thickness tears. Matsen et all stated that the crepitance on Sidles, and DT Harryman. Practical Evaluation and Management of
rotation is due to the abrasion of the tom tendon margins the Shoulder. © 1994, WB Saunders Company.

fibrous tissue may tend to fill this hiatus. 292 Full-thickness

tears often occur in tennis players older than 40 years of
age. 127
The amount of weakness on muscle testing and range of
active motion help distinguish between a partial tear and a
complete tear and the massiveness of the tear. Small tears
usually affect only the supraspinatus, and partial tears elicit
more pain than complete tears and show minimal loss of
strength on isometric testing. Larger tears show decreased
isometric strength for the supraspinatus and infraspinatus,
and massive tears affect the supraspinatus, infraspinatus,
and subcapularis, causing weakness on isometric internal
Subscapularis rupture may also occur as a complica­
Figure 3-79 Drop-arm test. tion of anterior capsule stress, espeCially in hard throwing.
The stress on the head of the humerus can loosen the
labrum and glenOid anchorage, allOWing head luxation.
Anterior stability testing reveals laxness and creates
painful patient apprehenSion. There is a positive lift-off
elevation or external rotation.291 A tear represents weakness test or internal rotation lag sign (see Isometric Testing of
in the absence of a neurologic deficit. Passive range is usu­ Subscapularis).
ally full unless the tear bunches up. The shoulder is re­
markably weak on isometric testing and may be painful.
There may be supraspinatus and possible infraspinatus at­ Treatment
rophy. If severe enough, it progresses to the subscapularis.
There may be subacromial crepitance as in partial tear. Patients who have had their rotator cuffs injected with
Crackling, popping, and palpable crepitus may be elicited cortisone are more prone to tears 293 Usually, a massive tear
on passive rotation at 90° shoulder abduction. A supra­ should be operated on, espeCially in a young individual, but
spinatus defect may be palpated at the anterior lateral por­ according to Leach and Schepsis,266 rotator cuff tears do not
tion of the acromion lateral to the bicipital groove and just require emergency surgery, as tears of ligaments around the
medial to the greater trochanter while the proximal hu­ knee do. Others 294 state that the main indications for surgi­
merus is rotated. Radiologically, there is a decreased width cal treatment are severe, unremitting pain after 3 months of
(5 mm or less) of the humeral acromial space due to up­ conservative treatment or increasing loss of shoulder func­
ward displacement of the humeral head, and probable acro­ tion. Table 3-5 lists prognostic factors in cuff surgery.
mial spurring and subacromial sclerosis. One study recommended double-contrast arthrograms
in patients over 40 years of age if their symptoms persist
Clinical: It is necessary to distinguish partial or in­ longer than 3 months. Partial-thickness tears are often asso­
complete tears from complete or full-thickness tears be­ ciated with anterior instability in young athletes. Therefore,
cause complete tears may require surgery. In the functional especially if instability exists, the dynamic shoulder stabiliz­
examination of a partial tear that may be increasing to a ers should be strengthened to compensate for the over­
complete tear, the findings might be similar to those for a stretched static stabilizers. This would still be the primary
tendinitis or a bursitis. The isometric testing may indicate treatment without the presence of instability. It is important
a minimal weakness that the examiner accepts as reflex in­ that the rotator cuff musculature be strengthened in the
hibition due to pain and not an actual tendon defiCiency. sub impingement range (below 90° elevation) in the early
Matsen et all stated that the patient may eventually be­ stages so as not to aggravate the lesion.
come asymptomatic with minimal weakness and live with MorphologiC evaluation of the rotator cuff has shown that
a large cuff defect as long as the humeral head remains a tear must be considered a disease of the whole muscle, not
centered. only a tendon disease. Goutallier et al,295 using computed
The healing process in the rotator cuff tear takes place tomography, and Nakagaki et aI,296 using MRI, described a
only when the torn edges are in contact. In a partial tear, correlation between fatty degeneration and atrophy of the
some bridging of the gap by normal tissue remains , and muscle bellies and the extent of the tear. Therefore, in man­
The Shoulder 119

Table 3-5 Prognostic Factors Related to the Durability of Cuff Bicipital Ruptures
Booth and Marvel 271 distinguished between two types of
Encouraging Discouraging
bicipital ruptures: involvement of the transverse humeral
History ligament and the intertubercular fibers of the biceps tendon
Age under 55 years Age over 65
(see Clinical Review of the Shoulder Muscles, Biceps).
Acute traumatic onset Insidious atraumatic onset
Short duration of weakness Weakness longer than 6
No history of smoking months Clinical: Bicipital ruptures are not common in the
No steroid injections Many smoking-pack years throwing athlete unless there is an accompanying chronic
No major medications Repeat steroid injections inflammation , mechanical spur in the bicipital groove, or
No concurrent disease Systemic steroids or an­ steroidal use 2 Older patients, because of degeneration of
No infections timetabolites tissues, may not recall any trauma. The problem is usually
No previous shoulder Inflammatory joint related to catching or lifting a weight with the arm held in
surgery disease, other chronic
abduction or external rotation. An abducted and externally
Benign surgical history illnesses
rotated arm causes the biceps tendon to displace medially
History of previous
shoulder infection Neviaser 284 stated that the biceps tendon always displaces
Previous cuff repair medially, never laterally. Patients may complain of their
attempts shoulder's "going out," and they may reduce the tendon
History of failed soft tissue themselves.
repairs (eg , dehiscence,
Physical Examination Functional Tests
Good nutrition Poor nutrition
Mild to moderate weak­ Severe weakness Rupture of Transverse Humeral Ligament or Subluxa­
nesses Severe spinatus atrophy tion of Tendon
No spinatus atrophy Anterior superior insta­
Stable shoulder bility
Intact acromion Previous acromial re­ • Weak and painful resisted biceps (Speed's) test.
No stiffness section • Transverse humeral test:284 The examiner subluxates
Stiffness the patient's biceps tendon from the biCipital groove
X-rays by abducting the arm 90°, flexing the elbow 90°, and
Normal radiographs Upward displacement of bringing the shoulder into external rotation (this
the humeral head moves the tendon medially) (Fig. 3-80A) . The exam­
against the coracoacro­
iner palpates the biceps tendon and internally rotates
mial arch
the shoulder, which replaces the biceps tendon in the
Cuff tear arthroplasty
groove (moves tendon laterally), creating an audible
Source: Reprinted with permission from FA Matsen, SB Lippitt, JA or palpable snap (Fig. 3- 80B) . According to Abbott
Sidles, and DT Harryman. Practical Evaluation and Management of and Saunders,298 most of the time when this test is
the Shoulder. © 1994, WB Saunders Company.
positive, the cause is injury to either the gleno­
humeral ligament or the subscapulariS and not the
transverse humeral ligament.
• Biceps tendon instability test:221 The patient is tested
with the arm at the side and the elbow flexed 90
ual treatment of cuff tears, it is important to treat the whole The examiner pulls down on the elbow and asks the
muscle and not concentrate solely on the insertion area . The patient to resist external rotation by the examiner.
use of active release, Graston technique protocol, and fric­ The tendon may displace, causing pain and popping
tion massage is of benefit fo r the increased realignment of (Fig. 3-80C).
cells and the increase in fibroblastic proliferation (see Chap­ • Positive Yergason's test: The patient stands with the
ter 2, Pathology of Musculoskeletal Soft Tissue) . Rotator cuff elbow flexed 90° at the side with the forearm
repair in the diabetic population may result in complications pronated . The examiner grasps the elbow and distal
such as infections and shoulder stiffness 297 forearm and resists active flexion and supination by


Figure 3-80 Transverse humeral test. A) External rotation; B)

internal rotation; C) biceps tendon instability test.

the patient. If positive, the tendon elicits tenderness the proximal humerus (see Chapter 4, The Elbow and
at the biCipital groove. Forearm).
• Patient's arm is held in 180° abduction and lateral ro­
tation and slowly brought to the side; pain may occur • Painful and extremely weak resisted biceps (Speed's)
as the tendon is forced against the lesser tuberosity A test in the acute condition; there may be minimal
palpable click may indicate an elongated or dislocat­ pain and weakness in the chronic condition.
ing biceps tendon. • The patient is still able to flex the elbow and supinate
the forearm due to preservation of the brachialis muscle.
Rupture of Proximal Long Head and Distal End: • Swelling, tenderness, and mild-to-moderate ecchy­
With rupture of the proximal long head, there is a possi­ mosis are present in the antecubital fossa .
ble history of a "snap" and a visible biceps lump at the • The Significance of a ruptured proximal biceps is that
distal humerus with acute pain in the antecubital fossa. it almost always means rotator cuff pathology (E.
Rupture at the distal end would create a biceps lump at Rashkoff, personal communication, 1990). Some­
The Shoulder 121

times in the presence of a cuff tear, the biceps tendon posttraumatic arthritis, osteonecrosis, infection, hyper­
may undergo compensatory enlargement and become parathyroidism, villonodular synovitis, seronegative spon­
more active in older athletes. 299 dyloarthropathies, and Lyme disease. Patients may have a
chronic complete cuff tear and eventually develop an arthri­
tis, referred to as cuff tear arthropathy

Rehabilitation may be all that is necessary because only Treatment

20% of elbow flexion power is lost 300 Minor disability re­
sults in the older patient. Athletes may require surgery for Treatment consists of caring for the inflammation, joint
optimum performance. play technique (see Chapter 10, Joint Mobilization),
strengthening and stretching exercises based on the evalua­
Glenohumeral Osteoarthritis tion, and use of friction massage and active release for
restoring normal surrounding tissue adhesions.
Recently, through the use of arthroscopy and biochemi­
cal markers from synOvial fluid, osteoarthritis of the shoul­
der was found to be one of the most prevalent pathologies Acromioclavicular Joint Osteoarthritis
of the glenohumeral joint 301 It was shown that primary os­
teoarthritis usually initiates on the glenoid and proceeds to Osteoarthritis in the AC joint may be related to a de­
the humeral head articular surface during a course of sev­ generative cuff and subsequent humeral head superior
eral or many years. Shoulder osteoarthritis of the early and subluxation (deltoid shear) because an AC osteophyte is
moderate type has been very difficult to diagnose, which usually on the inferior AC joint. Roentgenography helps
may be a reason why it was thought to be rare, especially confirm the diagnosis by showing diminished joint space
because it is a nonweight -bearing joint. and osteophytes (the best views are taken in the antero­
posterior plane with the arm abducted to 100° and exter­
nally rotated or 15° caudad with the shoulder in the
Signs and Symptoms neutral position). There is usually pinpoint pain over the
joint, and crepitus. The joint may appear bulbous. Infe­
Glenohumeral osteoarthritis manifests as progressive rior spurring from this joint is related to the impingement
shoulder pain starting at the shoulder joint and spreading syndrome.
to the forearm. It is aggravated by motion and relieved by
rest. The patient has sleep pain and difficulty in daily activi­
ties such as combing the hair or putting on a sweater. Functional Tests

• Passive pain during abduction from 90° to 180°

Functional Tests
• Pain on passive horizontal adduction
There is a capsular pattern (see Capsular Pattern) on pas­ • Negative resisted tests (unless area is inflamed)
sive testing. Loose bodies in the inferior capsule are some­ • Possible crepitus with passive dorsal-ventral AC
times palpable, causing a painful catch and/or crepitus on joint gliding
abduction and rotation. Roentgenography may show sclero­
• Possible painful arc if an inferior AC spur is present
sis, cysts, teardrop osteophytes on the inferior joint surface,
and joint space narrowing. If a chronic cuff tear precedes • Positive O'Brien test (see Testing for Glenoid Labral Tear)
the glenohumeral arthritis, a radiograph usually shows the
head of the humerus pressing superiorly against the under­
surface of the acromion.
Treatment consists of rest, ice, and mobilization of the
Differential Diagnosis AC, sternoclavicular, and glenohumeral joints (see Chapters
10 and 14). Because limited glenohumeral motion may cre­
Glenohumeral osteoarthritis must be differentially diag­ ate increased compensatory AC joint motion and degenera­
nosed from other lesions that cause diminished joint space, tion, AC joint arthritis may be relieved by glenohumeral
such as rheumatoid arthritis (involves multiple joints), joint mobilization. 302

Acromioclavicular Sprain tenderness at both the AC and coracoclavicular ligaments.

The lateral end of the clavicle mayor may not appear supe­
Mechanism of Injury rior to the acromion in the step-off test. A grasp of the cen­
tral clavicle can probably displace it anteriorly and posteri­
Acromioclavicular sprain can be caused by direct force orly. There may be a slight increase in the coracoclavicular
from a fall on the superior aspect of the shoulder in the ad­ interspace. A radiograph may show widening of the AC
ducted position or by direct trauma (see Acromioclavicular joint, compared with the opposite side. The distance be­
Joint). It also can be caused by indirect force from a fall on tween the clavicle and the coracoid process is normal. An
the outstretched hand, which would affect the AC ligaments athlete usually discontinues the activity.
rather than the coracoclavicular ligaments. In this type of
fall , the coracoclavicular ligaments would be compressed by Type III Injury: A type III injury is a complete AC dislo­
the closing of the coracoclavicular space J3 cation due to disruption of both the AC and the coracoclav­
icular ligaments. The distal clavicle is high riding and free
Functional Examination floating as the shoulder complex droops inferiorly and medi­
ally. The lateral clavicle is unstable both vertically and hori­
On inspection, especially in the type II and higher le­ zontally. The clavicle can be depressed like a piano key.
sions (see below), the scapula (acromion) is displaced Tenderness is present not only at the AC joint and coraco­
downward in relation to the clavicle, which remains in its clavicular interspace but also along the superolateral one
normal anatomic position. Evaluate in a weight-bearing, fourth of the clavicle due to detachment of the deltoid and
standing, or sitting position and observe the contour of the trapezius fibers. An athlete withdraws from competition. Ra­
shoulder; palpate the AC joint for tenderness; check for diographs show AC joint dislocation and, compared with the
possible clavicular fracture; assess the anterior, posterior, uninjured shoulder, greater than a 25% increase in the cora­
superior, and inferior mobility of the clavicle; and evaluate coclavicular distance, indicating coracoclavicular disruption.
neurovascular status.
Type IV to Type VI Injuries: A type IV injury has clini­
Functional Tests cal findings similar to those of a type III injury except that
the clavicle is dislocated posteriorly, usually embedded in
• Positive O'Brien test (see Testing for Glenoid Labral Tear) the trapezius, and tents the skin over the lateral aspect of
• Pain during passive abduction from 90° to 180° the shoulder. It requires surgical reduction.
• Pain on passive horizontal adduction A type V injury has clinical findings similar to those of a
type III injury, but there is more displacement between the
• Resisted tests negative in chronic AC problem distal clavicle and the acromion. There is Significant damage
to the deltoid and trapezius fascia that is not normally seen
Types of Injuries 7J ,JOJ.J04 in an athlete. The distance between the clavicle and the
coracoid process is increased more than 100% compared
Type I and type II injuries are considered subluxations, with the opposite shoulder.
whereas type III and higher are considered complete dislo­ A type VI injury requires Significant trauma, usually re­
cations (Fig. 3-81). lated to rib fracture, nerve injury, and vascular compromise.
The shoulder has a flat appearance. The clavicle is inferior
Type I Injury: Only the AC ligaments are sprained, to the acromion or the coracoid, decreasing the coracoclav­
with minimal-to-moderate tenderness and swelling without icular interspace.
displacement. Palpation of the coracoclavicular interspace
(coracoclavicular ligaments) is not painful. A lesioned liga­
ment is always tender on palpation. An athlete with a type I Treatment
injury might remain in the game. There is full ROM with
discomfort at end ranges. Radiographs are normal. Type I and II injuries are definitely treated conservatively,
whereas most type III injuries respond to conservative care
Type II Injury: A type II injury is defined as a second­ unless they are Significantly symptomatic several months
degree sprain with disruption of the AC ligament. Coraco­ after injury. The challenge is to be sure that a diagnosed
clavicular ligaments are also sprained. There is moderate-to­ type III injury is not an underdiagnosed type IV to VI in­
severe pain at both locations. Palpation reveals moderate jury, which would require surgery.
The Shoulder 123

Conjoined tendon of
biceps and coracobrachialis

Type V Type VI

Figure 3-81 Types of injuries to the acromioclavicular-coracoclavicular complex. Source: Reprinted with permission from CS Neer and CA
Rockwood. Fractures and dislocations of the shoulder. In: CA Rockwood an d DP Green, eds., Fractures in Adults. p. 126, © 1984, Lippin­
cott-Raven Publishers.

Type I: Type I responds to rest, ice, anti-inflammatory • Adhesion of subacromial bursa, limiting abduction3
medication, and immobilization if it relieves pain. Light • Progressive fibrous proliferation of the articular cap­
friction massage may be used over the AC ligament (see sule and the rotator cuff tendons, particularly the sub­
Chapter 14, Friction Massage). Symptoms resolve within 7 scapulariS and its extension to the coracohumeral
to 10 days, and the athlete can return to competition within ligament312
1 to 2 weeks or as soon as full ROM is achieved without
• Adhesions between the anterior capsule and the intra­
pain. The athlete needs full strength and flexibility, espe­
articular subscapulariS tendon 313
cially of the trapezius and deltoid muscles. Use of a sling is
advised until pain subsides.
Fareed and Gallivan314 noted that the area of initial and
primary involvement is a triangular anatomic synovial fold
Type II: Type II also is treated symptomatically, but tap­
between the long head of the biceps and the subscapularis
ing, bracing, a harness, or a Kenny-Howard sling for 1 to 2
weeks for up to 8 weeks is recommended to prevent the con­ tendons. This bare area of synOvial tissue is in contact with
the adjacent subscapulariS muscle and the tendon, the long
dition from advancing to type III and for ligamentous heal­
head of the biceps, the anterior glenoid, and the humerus ,
ing. The patient may return to activities whenever full ,
and adhesions eventually form between the capsule and
painless ROM returns. The patient will need full strength and
these structures. A thickness of the synovium and joint cap­
flexibility, especially of the trapezius and deltoid muscles.
sule greater than 4 mm was a speCific (95%) and sensitive
Type III: A type III injury definitely needs some support, (70%) criterion for the diagnosis of adhesive capsulitis 3 15
such as a Kenny-Howard sling, although some practitioners There may be trigger points in the subscapularis that cause
advocate "skillful neglect," using a standard sling.?3 Perform a reflex autonomic reaction.278
early ROM tests as pain decreases. Initiate a vigorous strength­
ening program. The conclusion of two studies 305 ,306 regarding Possible Phases of Adhesive Capsulitis
conservative care for a type III injury is that even if symptoms
persist with activity when the injury is treated conservatively, 1. Acute inflammatory phase similar to acute bursitis or
there will not be significant shoulder weakness or functional tendinitis lasting from 2 to 9 months
limitations-even with throwing. 2. Stiffening phase with progressive loss of passive motion
in the capsular pattern lasting from 4 to 12 months
3. Thawing phase lasting 6 to 9 months with decreasing
Adhesive Capsulitis
pain and increasing motion

Etiology Often, a patient presents with symptoms of the second

phase without any history of an inflammatory phase.
The primary cause of adhesive capsulitis is unknown. It
has been associated with diabetes,307 thyroid disorders,308 in­
trathoracic disorders, intracranial pathology, trauma, immobi­ Functional Examination
lization, and cervical disk disease. Adhesive capsulitis is rare
in patients younger than 40 years and is more common in In the acute phase, there is the typical muddled ap­
sedentary workers than in laborers.284 It is more common in pearance of pain on both contractile and passive testing,
women aged 40 to 65 years, in patients with clinical depres­ but the most persistent finding is a painful restriction of
sion, and in patients with insulin-dependent diabetes mellitus. passive and active lateral rotation with the arm at the side
Diabetic patients are resistant to all types of conservative treat­ or at 90 0 •
ment for this condition. It occurs after 5% of mastectomies In the stiffening phase, the capsular pattern is pathog­
rarely after defibrillator implantation, and with chest wali nomonic in adhesive capsulitis (see Capsular Pattern in
tumor (see under Functional Examination).309 Chapter 1). The most limited passive motion is almost al­
ways external rotation, with the next limited motion
being passive glenohumeral abduction , and finally, limita­
tion of internal rotation . Depending on the amount of
stiffening in the second stage, passive external rotation
Adhesive capsulitis is primarily due to thickened capsu­
may be the only limited passive motion. As the stiffening
lar contractures both anteriorly and posteriorly271 ,310,311
progresses , the other parts of the capsular pattern appear.
There is secondary involvement of other areas, including
At this stage , if the inflammation still persists , there may
the follOwing:
be some pain on isometric testing, but the isometric test­
• Contracture of the coracohumeral ligament, limiting ing is usually generalized, that is, instead of being able to
external rotation3 pinpoint a specific tendon or two as in a tendinitis , pain
The Shoulder 125

may be found on resisted abduction, adduction, and in­ peratures and subsequent cooling of the tissue before re­
ternal rotation together. Of course, it is possible that a leaSing the tension. An effective procedure that the patient
cuff tendinitis may also be associated with an adhesive could do at home is first to warm up the shoulder with
capsulitis. moist heat for 10 to 15 minutes and then to lie supine with
In the chronic stiffening and thawing phase, the pathog­ the shoulder in external rotation while holding a 1- to 2-lb
nomonic finding is Cyriax's capsular pattern, usually with weight and maintaining the stretched position for up to 45
no pain on isometric testing. Limited external rotation can minutes or more with the moist heat on the anterior shoul­
be primary in a patient with a history of and the presence of der. The patient may feel discomfort, but not pain. Moist
posterior dislocation, osteoarthritis of the glenohumeral heat packs may have to be replaced every 10 minutes to
joint, and reflex sympathetic dystrophy 85 Rowe 25 stated maintain heat. During the last 10 to 15 minutes, ice should
that a rotator cuff derangement or tear eventually can cause be applied. The patient should follow this procedure at least
restricted motion and mimic the frozen shoulder. 5 days per week. Increasing the ROM in external rotation
In patients who had a tumor with symptoms of frozen allows increased gain of motion in forward flexion because
shoulder, Robinson et aP09 found that discrete areas of these two motions are coupled. Painless joint mobilization
boney tenderness were a significant predictive sign of tumor. can be used for breaking adhesions (see Chapters 10, 13,
They used gentle tapping, which should be differentiated and 14). Joint mobilization that affects the elastic compo­
from the pain produced by firm pressure that may be com­ nent rather than the viscous component may aggravate the
mon in rotator cuff syndrome and primary frozen shoulder. condition if pain is produced.
The particular areas that should be gently tapped were the
clavicle, coracoid, humeral head (slightly harder taping in
stocky individuals), scapular spine, and scapular body In all Hjelm's Treatment: Manual and Decompression
patients in whom pain was elicited by gentle tapping, espe­ Techniques
Cially in the young, a bone scan should be performed. Rick Hjelm

Clinical: Overstretching of the shoulder may create Adhesive capsulitis is a difficult problem to resolve. Fac­
pain and paresthesia down the C-6 dermatome, mimicking tors such as speCific technique application, order of move­
a radiculopathy, but radiation of the pain from the shoulder ment restoration, need for self-care, and number of visits
is to all the fingers instead of to the C-6 distribution 26 Cer­ allowed in a managed-care environment all playa role in
vical stress tests do not create shoulder pain unless there is the outcomes for this problem.
an accompanying cervical problem. In the first two stages, My principal method of treatment for adhesive capsuli­
there may be intense night pain that affects sleep. The final tis is the use of manual decompression, which increases
stage is extreme limitation of motion in the capsular pat­ (decompresses) the suprahumeral space by stretching out
tern, with pain only when the tissue is stretched. Because of the inferior glenohumeral ligament complex. The manual
a limited capsular pattern, the patient may present with the decompression techniques move the humeral head away
arm in internal rotation and adduction. There may be mini­ from the suprahumeral space and into the capsular struc­
mal atrophy of the deltoid and supraspinatus muscles. tures. This type of joint mobilization uses joint play by
Rowe 25 stated that an unrecognized chronic posterior dislo­ using the humeral head to stretch a specific aspect of the
cation may present as a frozen shoulder. Arthrography can capsule through careful joint placement. Decompressing
finalize the diagnOSiS (see Posterior Dislocation). the suprahumeral space allows the clinician to perform
low-load, long-duration stretches that are tolerable for the
patient and effective in increasing the ROM. These tech­
SOFT TISSUE TREATMENTS FOR ADHESIVE niques allow the patient to perform home physiologic
CAPSUUTIS stretching with increased intensity and less pain, thus
opening the door for ROM gains from home treatment.
Hot Pack Treatment with Stretching Conversely, in my experience, using physiologic overpres­
sure to stretch the capsule increases pain as the supra­
Manipulation under general anesthesia should be re­ humeral space is compressed by the humeral head. As a
served for patients who do not make any progress with con­ result, the patient cannot tolerate the stretch for a duration
servative care within 6 months (E. Rashkoff, personal com­ adequate to achieve a plastic, more permanent deformation
munication, 1990). of the capsule, and little ROM is gained. Subsequently, the
Rizk et aP16 and Sapega et aP17 explained that the best patient is less compliant with the home program.
way to lengthen connective tissue structures permanently A preferred order of movement restoration is critical.
without compromising their structural integrity is to use Begin with sequential restoration of abduction, external rota­
prolonged, low-intensity stretching at elevated tissue tem- tion, and horizontal adduction, and finally progress to the

combined movements of extension, adduction, and internal Distraction techniques cause less discomfort and are less
rotation-functionally known as reaching behind the back. likely to inflame the joint. Glide techniques are more spe­
Beginning with abduction and external rotation restores mo­ cific and effective for stretching but can inflame the shoul­
tion with less pain and accomplishes more tangible clinical der joint. If less than 90° passive abduction in the
and functional changes than does horizontal adduction or glenohumeral joint is present with this quick assessment,
reaching behind the back. Stretching the anterior and poste­ then progressive distraction techniques are used until 90°
rior aspects of the capsule in the same treatment session may abduction is achieved (Fig. 3-83). A belted distraction tech­
nullify the effectiveness of the capsular stretching; therefore, nique allows the clinician to hold the stretch for a greater
I recommend focusing on only one aspect of the capsule at a duration, provides a better feel for joint play, is ergonomi­
time with both the clinical and the home stretching program. cally sound, and is more tolerable to the patient. Proceed to
I find that reaching behind the back is often the most lim­ a specific glide technique, such as the 90/90 supine to
ited motion, which does require adequate capsular ligament "bowstring" capsular structures, thus increasing their length
length in several areas of the capsule. Therefore, it is the slow­ (Fig. 3-84). This contact speCifically stretches the anterior
est, most difficult motion to be restored. Work abduction and aspect of the inferior glenohumeral ligament complex by
external rotation of the anterior capsule exclusively until contacting the proximal superior humerus and directing its
ROM is restored to the 150° to 160° flexion and 75° external force inferior-anterior. After 75° to 80° of external rotation
rotation, then proceed to the posterior capsule stretches. It is is restored, begin restoring the functional movement of
important to establish a baseline of the patient's active func­ reaching across the chest or horizontal adduction.
tional movements as well as passive ROM measurements The lateral distraction technique, used to restore horizontal
using a goniometer or inclinometer. This information is use­ adduction, affords excellent posterior capsule stretch with
ful for the continual reassessment process, which gives the minimal patient discomfort (Fig. 3-85). Work in this direction
clinician feedback and plays a role in encouraging the patient. until 40° to 60° of horizontal adduction is achieved or the pa­
Modalities such as ultrasound and short-wave diathermy tient has restored function.
are used to preheat capsular structures for prestretch prepa­ Reaching behind the back involves the combined move­
ration. It is valuable to have the patient stretching while the ment of extension, a slight amount of horizontal adduction,
modalities are applied (Fig. 3-82). An initial goniometric and internal rotation. I proceed to the 90/90 posterior cap­
measure and a postmodality measure are taken. With the sule technique, which is effective in stretching the posterior
patient in the supine position, the clinician assesses the aspect of the inferior glenohumeral ligament complex and
amount of abduction in the glenohumeral joint. If the pa­ the posterior capsule with technique modifications (Figs.
tient has 90° passive abduction in the glenohumeral joint 3-86 and 3-87). Try to work into tolerable or slight dis­
without any scapular movement, treatment is initiated with comfort for 5 to 10 minutes per technique, 30 minutes per
a brief distraction technique (approximately 2 minutes) and
progresses to glide techniques (see below).

Figure 3-83 Distraction in progressive positions. 0) With the

patient supine, make the belt into a figure-eight shape and slide
Figure 3-82 Ultrasound during supine flexion stretch. 0) Posi­ the distal loop over the patient's involved arm onto the upper arm.
tion the patient's shoulder close to or slightly into the motion bar­ (2) Take out the jOint slack gradually while moving into abduc­
rier. Support the humerus if necessary (2) Ultrasound is delivered tion, horizontal abduction, and external rotation. (3) Stabilize the
at maximal intenSity to heat the capsular tissue prior to stretching. patient with belt fixation if necessary.
The Shoulder 127

Figure 3-84 Supine 90/90. (1) Position the patient diagonally Figure 3-85 Lateral distraction. (1) With the patient supine,
across the plinth with the involved shoulder near the edge . (2) place the patient's arm in the vertical position, allowing flexion
Take up the available motion by externally rotating, elevating, and and the hand to rest on the patient's chest. (2) Loop the belt
horizontally abducting the humerus. (3) Back off slightly and glide around the humerus while placing one hand between the belt and
the humeral head inferior-anterior by using the web space of your the humerus. Use the opposite hand to counter the pressure on
hand and plaCing it just off the edge of the acromion process. (4) the patient's elbow. (3) Lean back, pulling the humeral head
Assess the amount of glide of jOint play while positioning the straight laterally while maintaining the counterpressure at the
humerus in selective amounts of external rotation, horizontal ab­ elbow. (4) To increase the stretch, place the humerus into increas­
duction, and flexion. Combine these positions for most effective ing amounts of glenohumeral adduction while laterally distracting.
mobilization. (5) The belt technique can be used, but it is not as
versatile as variations in position and cannot be adjusted to maxi­
mize stretch.

Figure 3-86 Posterior capsule stretch. (1) With the patient Figure 3-87 Posterior capsule (modified). (1) Position the pa­
supine, abduct the humerus to 90' . Internally rotate the humerus tient supine. (2) Abduct the humerus to approximately 45". Inter­
until the anterior shoulder begins to move anteriorly into the sup­ nally rotate the humerus and place the patient's hand under the
poning hand. Measure this angle with a goniometer or an angle patient's buttock or lumbar spine until the anterior shoulder be­
finder. (2) Mobilize by placing one hand in the lumbrical position gins to move anteriorly into the supporting hand. (3) Mobilize by
over the anterior shoulder. Be careful not to irritate the anterior placing one hand in the lumbrical position over the anterior
shoulder structures. Push the anterior shoulder posteriorly while shoulder. Be careful not to irritate the anterior shoulder structures.
maintaining internal rotation with the other hand. Push the anterior shoulder posteriorly while maintaining internal
rotation with the other hand.

treatment session. Reassess often with active movement and

goniometric measures. The patient will be more compliant
at home if he or she is involved in the process. A treatment
can be finished with modalities such as ice and electrical
stimulation with the patient's arm held comfortably near
end-range flexion (Fig. 3-88). Expect the patient to experi­
ence some discomfort for 2 to 4 hours. Pain lasting longer
than that suggests that the treatment sessions were overly
aggressive or that additional pathology may exist.
The patient's effort in performing a home exercise pro­
gram is critical to maintaining clinically achieved ROM in­
creases and is necessary to increase ROM after the door has
been opened. Eventually, the patient will tolerate increased­
load and longer-duration stretches. Home phYSiologic
stretches into flexion are also more tolerable and do not Figure 3-89 Supine flexion stretch. The patient is positioned
compromise the suprahumeral space. I advocate long­ supine, and physiologic stretching is performed in flexion to avoid
duration, intensity-to-toleration stretches as the ideal but excessive suprahumeral jOint compression leading to increased
encourage frequent and brief self-stretching bouts to main­ pain and discomfort. Weight can be added to the wand to increase
tain capsular extensibility. Setting up strict home exercise stretch intensity Long duration is preferred over increased stretch
gUidelines, such as holding stretches for 2 to 3 minutes, can intensity.
inhibit the patient with a busy schedule. Demonstrate con­
venient stretches that can be performed across a desk or in a
doorway whenever and as often as possible to facilitate
compliance. I inform the patient that the amount of time a
joint is held at end range, not the load on the joint, is the
most important aspect of gaining ROM. The home stretches
correspond with the manual stretches being performed in
the clinic. For example, if abduction-external rotation is
being restored clinically, the same physiologic movement is
given for the home program.
To restore abduction-external rotation with home exer­
cises, I use supine tabletop flexion (Fig. 3-89), tabletop

Figure 3-90 Tabletop flexion stretch. A seated physiologic

stretch into flexion allows the patient to stretch frequently
throughout the day at home or at the office. The patient is in­
structed to support the arm on the work surface and to move the
body to gain motion in the glenohumeral joint.

flexion (Fig. 3-90), tabletop external rotation (Fig. 3-91),

pulleys (Fig. 3-92), sit and supine, and doorway flexion
(Fig. 3-93) exercises. Supine positioning can prevent tho­
racic spine compensation, but inevitably, the scapula will
continue to abduct prematurely. An inferior glide technique
using a belt can be used at home after the patient has
greater than 90° passive abduction at the glenohumeral
Figure 3-88 Posttreatment supine flexion stretch. Position and joint (Fig. 3-94). Horizontal adduction is restored with
support the shoulder comfortably near end range while applying across-the-chest overpressure (Fig. 3-95). Modifications of
ice anc\Jor electrical stimulation. this type of stretch can be made by increasing the amount
The Shoulder 129

Figure 3-91 Tabletop external rotation.

Figure 3-93 Doorway stretch. Although it is not possible to iso­

late the glenohumeral joint without .scapular compensation, this
doorway stretch provides a convenient way to stretch frequently
throughout the day.

Figure 3-92 Pulley stretch. Pulleys are used to stretch into end­
range flexion. Patients are encouraged to hold the stretch for as
long as possible. Figure 3-94 Self-belt manual decompression. A belt or luggage
strap 72 inches long is looped distal to the acromion and around
of internal rotation during horizontal adduction (Fig. the patient's foot. Ensure that the shoulder is abducted to 90'. Use
3-96). This becomes an effective stretch for the throwing the leg to push the humeral head inferiorly. One may need to alter
athlete. the leg position to maximize stretch. The patient needs to have 90'
Restore the reaching-behind-the-back movement with a passive abduction at the glenohumeral joint to perform this tech­
progression of stretches using a counter or table top. The nique.
extension component stretch involves sitting faCing away
from a table, placing the shoulder in extension, and extend­
ing the trunk (Fig. 3-97). Next, the thorax is side bent to­
ward the involved arm to stretch the adduction component

Figure 3-97 Reaching-behind-the-back stretch: extension. (1)

The patient is seated facing away from a table or counter top. (2)
The patient places the involved arm on the surface in a position of
extension. (3) The patient controls the amount of stretch on the
superior-anterior capsular structures by extending the trunk in a
Figure 3-95 Horizontal adduction stretch. The patient provides more extended position, stretching the superior-anterior capsular
physiologic overpressure into horizontal adduction. This .tech­ structures.
nique increases the functional movement of reaching across the
chest, which stretches the middle posterior capsule.

(Fig. 3-98). Finally, varying amounts of internal rotation are

added while the trunk is straightened to increase the exten­
sion angle (Fig. 3-99). With adequate clinical manual de­
compression, a compliant home program should cause the
patient to actually increase ROM between clinical visits.
Deciding how many treatments a patient may require to
restore motion to a painful, stiff shoulder is not an easy
task. The amount of limitation, compliance with the home
program, and state of the shoulder influence the required
number of treatments. In general, if the passive supine
flexion goniometric measure is less than 100°, up to 18
sessions may be reqUired. If the passive supine flexion
measure is less than 130°, 12 sessions may be required. If
the flexion measure is less than 150°, six to nine sessions
may be reqUired. If the patient has an acute presentation
and end-range stretching is not tolerated, more visits are
reqUired to accomplish the functional goals. If the clini­
cian has the opinion that the joint has not been decom­
pressed enough to allow the patient to be successful with
independent stretching at home, more clinical visits
Figure 3-96 Horizontal adduction with internal rotation
should be requested. Usually in a managed-care environ­
stretch. The patient positions the arm into horizontal adduction
ment, 100% of the motion is not restored during the clini­
and then uses the noninvolved arm to move the humerus into in­
ternal rotation to stretch the posterior capsule. This stretch helps cal time frames. Patients are encouraged to continue their
throwers in the follow-through phase of throwing. efforts at home.
Restoring function to a stiff, painful shoulder is never an
easy process, but use of these gUidelines and encouraging
patient compliance make a more enjoyable experience for
the clinician and the patient.
The Shoulder 131

Figure 3-98 Reaching-behind-the-back stretch: extension and Figure 3-99 Reaching-behind-the-back stretch: extension, ad­
adduction. (1) The patient is seated facing away from a table or duction, and internal rotation. (1) The patient is seated facing
counter top. (2) The patient places the involved arm on the sur­ away from a table or counter top. (2) The patient places the in­
face in a position of extension and adduction. (3) The patient con­ volved arm on the surface in a position of extension, adduction,
trols the amount of stretch on the anterior and posterior capsular and internal rotation. (3) The patient controls the amount of
structures by extending the trunk in a more extended position. stretch on the anterior and posterior capsular structures by ex­
tending the trunk in a more extended position.

Active Release Treatment

Leah y318 has devised a direct method for releasing the

anterior capsule of the shoulder in adhesive capsulitis. The free, continue to move the extremity at its end-feel position
practitioner first paSSively slightly abducts the supine pa­ until a barrier is felt. At this point, hold the end-feel posi­
tient's humerus (Fig. 3-100A) and places the flat of his or tion until a fascial release is felt, at which time, the pre­
her thumb on the coracobrachialis, following it just before scribed range of motion for the joint is continued.
the coracoid process. At this point, the practitioner slides The patient lies supine with arms down at the sides. The
off the tendon medially onto the anterior capsule. A firm therapist takes one upper extremity into external rotation
tension is maintained on the capsule as the humerus is and applies very gentle traction through the length of the
slowly abducted and externally rotated (Fig. 3-100B). If no limb (Fig. 3-100C ). Throughout the technique the thera­
spasm is created, the patient can actively abduct and exter­ pist should be tuning into subtle barriers, felt as slight re­
nally rotate the shoulder while the practitioner maintains sistance, at which point the limb is held until the barrier is
the tension. Graston technique instruments have also been released.
successfully used on the anterior capsule. Taking the arm through the arc of abduction over the
patient's head, and into adduction (extension) with trunk
Arm Pull rotation (Figs. 3-100D and 3-100E), apply lateral pull to
the medial border of the scapula while maintaining traction
John F. Barnes319 developed an arm-pull fascial release and rotation in the upper extremity. Return the upper ex­
method that can be very effective with patients who have tremity through the arc, maintaining traction and reversing
finger, wrist, elbow, and shoulder dysfunction. When the the rotation. During this technique, stretch can be applied
practitioner exerts a pull, the pull is stretched only to its to the fasciae over the carpal tunnel and through the fingers
end-feel. Extra force is contraindicated. If the end-feel feels and thumbs.

Figure 3-100A and B Releasing the anterior capsule in adhesive capsulitis. A) The humerus is passively slightly abducted while the prac­
titioner's thumb is on the anterior capsule; B) the humerus is slowly abducted and externally rotated. Source: © 1998, Active Release Tech­
niques, LLP

Instability: Laxity Versus Instability stated that laxity may be normal but is also a predisposition
to instability, which is a clinical entity
Laxity (see Stability Testing)217 is defined as a physio­
logic parameter that has a wide spectrum of variability in Instability (see Stability Testing)217 is defined as the in­
the human population. It is a hyperlaxity that is nonsymp­ ability to maintain the humeral head centered in the glenoid
tomatic. Speer217 stated that he has examined shoulders fossa. Stability testing reproduces the patient's symptoms of
with posterior and anterior grade 2+ without symptoms but apprehension, grinding, or popping. If the instability is
has never found a 3+ without symptoms. O'Brien et aP16 classified as "atraumatic," tests may reveal midrange gleno­
humeral instability (see Traumatic Instability; Atraumatic
Instability). It is important to rule out subtle, occult insta­
bility in the young patient with anterior shoulder pain, be­
cause all soft tissue treatments will fail if instability persists.
Sports such as throwing, swimming, or tennis , which re­
quire abduction and overextension, may cause sudden pain,
weakness ("slipping out"), a clicking sensation, or a general
ache after use.

Major Types of Instability

The diagnosis of instability is made not on a measure­

ment of laxity based on stability testing but on a careful
history and physical examination that creates the unsta­
ble symptoms for that patient. 1 Major laxity could be
Figure 3-100C Light tractioning with external rotation of the normal, and minor laxity could represent an unstable
upper extremity Source: Copyright © MFR Seminars. shoulder.
The Shoulder 133

Figure 3-100D The arm is slowly taked through a 3600 are, waiting at areas of tightness for the release to occur. Source: © MFR Seminars.

The most common injury is avulsion of the anteroinfe­

rior capsule and ligaments from the glenoid rim, 1 called a
Bankart lesion (Fig. 3-101). A Hill-Sachs lesion may de­
velop, which is an osseous grooved defect found on the
posterolateral portion of the humeral head, allOwing the
humeral head to sublux over the glenoid rim 320 A reverse
Hill-Sachs lesion is an ante rome dial lesion that is associated
with recurrent posterior instability In order for a Hill-Sachs
lesion to cause an anterior dislocation, a capsular lesion
must also be present. 321 Under age 35, most major injuries
cause avulsion of the glenoid labrum and glenoid rim frac­
tures; over age 35, the traumatic instability is usually due to
fracture of greater tuberosity and rotator cuff tears.l TUB is
the acronym for this lesion: trauma during abduction, ex­
ternal rotation, and extension of the arm in the coronal
plane; unidirectional in an anterior-inferior direction (95%
of all shoulder dislocations), causing a Bankart lesion.

Functional Examination for Traumatic Instability

• The apprehension test is positive (usually anterior,
Figure 3-100E Maintaining traction throughout, roll the pa­ less often posterior or inferior).
tient's body and pull the medial border of the scapula laterally.
• The relocation test is positive (see Relocation Test
After the release occurs, slowly reverse the direction to the starting
point. Source: © MFR Seminars. under Testing for Glenoid Labral Tear).
• Crepitance or grinding is present during the anterior
drawer test (anterior labral avulsion).
• The practitioner must check for other intra-articular
Traumatic Instability (History of Trauma) pathology or complications, such as labral lesions,
cuff tears, or fractures.
Etiology: Traumatic instability is caused by a force strong • Radiographs may indicate a Hill-Sachs lesion (see
enough to tear the glenohumeral capsule, ligaments, or rotator Fig. 3-101), which is a defect in the posterolateral part of
cuff, or a fracture of the humerus or glenoid. Falling on an out­ the humeral head that is due to a traumatic impacted
stretched, externally rotated and abducted arm or direct poste­ compression fracture, characteristic calcification, or dam­
rior pressure causes anterior instability Falling on a forwardly age to the anterior inferior glenoid lipl (Bankart's lesion).
flexed and adducted arm or a direct posterior blow with the • Check the degree of instability (see Grading Anterior
arm at shoulder level causes posterior instability and Posterior Instability).

"Reverse" Hill-Sachs
(posterior dislocation)

Hill-Sachs lesion
dislocation) ----,fI-~J

U !
Fracture of
glenoid rim
Anatomic variations

of the glenOid(

Figure 3-101 Outline of the anatomic lesions producing insta­

bility of the shoulder. Source: Reprinted with permission from CR
Rowe, ed. The Shoulder. p. 165, © 1988, WE Saunders Company.

Figure 3-101A Classification of SLAP lesions. A. Type I has de­

generative superior labrum tearing but attached biceps. B. Type II
has detachment of the superior labrum/biceps tendon complex
from the superior glenoid. C. Type III has a bucket handle tear of a
meniscoid superior larum but attached biceps. D. Type IV has lear­
ing of the superior labrum up into the biceps tendon. Source: Sny­ Figure 3-10lB (a) Pain occurs at the posterosuperior portion of
der Sj, Karzel RP, Del Pizzo W, et at. SLAP lesions of the shoulder. lhe shoulder with passive forced maximal abduclion. (b) Pain is
Arthroscopy. 6:274-279. relieved or diminished by elbow flexion, indicating a posilive leSl
for a superior labrallear.
The Shoulder 135

Atraumatic Instability allow increased humeral head translation, stressing the

static stabilizers. 22o Often in the throwing athlete, the use of
Whereas traumatic instability is usually demonstrated at the dominant arm overstretches the static stabilizers, creat­
the end ROM, atraumatic instability reveals itself in the ing the subtle instability
mid-ROM and usually in a multidirection over the usual
unidirection of the TUB syndrome. It occurs mostly in pa­ Clinical: Although an athlete may complain of pain,
tients under age 30 with a history of the shoulder's feeling clicking, and apprehension, shoulder instability may be an
"loose" or slipping out and "clunking" back into place dur­ occult, subtle finding for which the complaint may be only
ing everyday midrange activities with the arm out in front a sense of looseness or excessive movement with particular
of the body during lifting or reaching. 1 movements. Patients with anterior instability may complain
The diagnosis of atraumatic instability is based on failure of either anterior or posterior pain. Posterior pain may be
of factors responsible for maintaining midrange (see Mecha­ due to traction on the posterior capsule or the resistance of­
nisms Responsible for Concavity Compression; Dynamic fered by the posterior cuff tendons, which resist outward
Rotator Cuff Muscles, and Biceps Influence: The Secondary and anterior translation. 2
Stabilizers). AMBRII is the acronym used to describe this Bigliani127 stated that individuals younger than 30 years
syndrome: atraumatic instability, usually with multidirec­ who have anterior shoulder pain probably have instability
tionallaxity, bilateral findings, treated primarily by rehabili­ Muscle lesions are also responsible, although (contrary to cur­
tation; if surgery is necessary the rotator interval capsule rent thought) Rowe 25 found that in 158 shoulders operated
and coracohumeral ligament is reconstructed with tighten­ on for recurrent anterior dislocation, the subscapulariS muscle
ing of the inferior capsule. was normal in 83%. O'Brien et aP23 stated that repetitive trac­
tion and compression of the rotator cuff during subluxation
Functional Examination for A traumatic Instability may cause a patient to present with symptoms and signs of an
impingement syndrome (painful arc, positive isometric test­
• Stability testing is usually symptomatic in more than ing, and positive coracoacromialligament impingement test) .
one direction: anterior, posterior, sulcus test for infe­ Even minimal instability can increase the traction stress on the
rior instability cuff and result in fatigue and injury to the rotator cuff. Treat­
• Generalized joint hypermobility may be present: 322 ment for impingement will probably fail if an underlying
cause of instability is not corrected.
1. Hyperextension of the elbow> 10°
A functional examination for repetitive micro trauma re­
2. Hyperextension of the knee> 10°
sulting in occult instability may elicit pain or minimal ap­
3. Passive apposition of the thumb to the volar aspect
prehenSion on testing of the supine or standing patient for
of the forearm « 0.5 cm)
shoulder anterior, posterior, or inferior stability Isometric
4. Passive hyperextension of the second to fifth fin­
testing may reveal loss of strength of rotator muscles (espe­
gers > 90° or parallel to the forearm
cially external rotators), deltoids, and scapular stabilizers. If
5. Dorsiflexion of the ankle> 45°
there is weakness of the rotator cuff and anterior deltoid
General hypermobility is assumed if more than three of
muscles, resistive testing of these muscles (espeCially the
the above are met. If all five are positive, then general hy­
supraspinatus) may reveal pectoral substitution, causing ex­
permobility is considered severe.
cessive shoulder protraction and observable increased pec­
• The patient may be able to reproduce and reduce ab­ toral tone on the weak side. 196
normal translations voluntarily
Treatment of Instability: If the anterior instability is
• Radiographs are usually negative regarding past trauma.
acute, immobilization in internal rotation for up to 6 weeks
• Check the degree of instability (see Grading Anterior, may be needed. If it is subacute or chronic, less immobiliza­
Posterior, and Inferior Instability). tion is reqUired. (Painless motion is encouraged as soon as
possible.) It is extremely important to strengthen the rotator
Repetitive Microtrauma cuff muscles for instability problems, but in the early stages of
strengthening for anterior instability, there should be no
Repetitive microtrauma is due to cumulative forces over weight work with the shoulder in positions of abduction, ex­
a period of time, as in throwing or racquet sports. Cumula­ ternal rotation, or extension. In anterior instability, the adduc­
tive forces stress the static restraints, increasing over time tors and internal rotators (subscapulariS) are especially
the anterior translation of the humeral head, which in tum important. For posterior instability, it is essential to strengthen
becomes a predisposing factor to rotator cuff involve­ the external rotators and the posterior deltoid. If impingement
ment. 255 Weakness of dynamic stabilizers may eventually signs are present, exercises should not be performed with the

shoulder in the 90 abducted position, which causes en­ surfaces.231 Surgery may be needed. Tearing of the labrum,
croachment of the subacromial space. It is also important to which is attached to the glenoid, is an indicator that the
check the scapular rotators for strength and flexibility. The capsule is not attached. The labrum itself does not have to
scapular rotators may be strengthened by shoulder shrugs be the primary structures relating to the instability.
(upper trapezius), push-ups with a plus for the serratus ante­ SLAP (superior labrum tear that is anterior to posterior
rior, and chin-ups or pull-downs for the latissimus dorsi. 180 in direction) is the most common labral injury found al­
All manual methods applicable for stretching, joint play, trig­ most exclusively in throwers. The lesion is located in the
ger points, active release, and friction should be included to superior labrum, which begins posteriorly and extends an­
restore optimum soft tissue phYSiology teriorly. The nearby biceps exerts large tensile forces on the
superior labrum and is usually involved. SLAP may occur as
a result of a fall onto an outstretched arm with the shoulder
Glenoid Labrum Tears
in abduction and slight forward flexion, or in throwers who
complain of "catching" or "popping" with overhead activ­
The glenoid labrum composition differs according to dif­
ity.328 Examination may reveal a mild-to-moderate multidi­
ferent clinicians. Some believe that it is composed primarily of
rectional instability, espeCially in the lower to midposition
fibrous tissue with some elastic fibers324.325 located at the cir­
of arm elevation only.213 Symptoms of pain and instability
cumference of the glenoid cavity, whereas other studies l27 in­
may therefore occur when the patient reaches to the side.
dicate that it is more a redundant fold of capsular tissue than
The definitive diagnosis is provided by MRI and
fibrocartilage. The glenoid labrum is the attachment point of
arthroscopy. The association of the pain and clicking related
the capsule, and anchOring of the capsule to the glenoid rim is
to a labral injury may point to the superior labrum. A posi­
important for glenohumeral stability.128 The labrum is not as
tive Speed's may incriminate the superior labrum from
significant as the entire capsule in acting as a barrier against
which the long head of the biceps (superior glenoid tuber­
instability.127.l28 According to Leach and Schepsis,266 a glenoid
cle) originates.
labrum tear is a difficult condition to diagnose and is usually
associated with recurrent shoulder subluxation or dislocation.
Functional Testing (see Testingfor Glenoid Labral Tear)
Although labrum tears could be isolated, they are rarely seen
without the presence of instability. Figure 3-101A depicts
some of the main varieties of labral injuries. Type II, which is Shoulder Dislocations
the most common, is the only one in which there is an actual
detachment of the biceps insertion. If a biceps tendinopathy With regard to shoulder dislocations,25.33.85 less force is
fails to improve, think of the possibility of an accompanying reqUired to dislocate a shoulder under 20 years of age and
superior labral tear. over 40 years of age. 47 Barring a distinct trauma, the devel­
opment of a dislocation may occur over time, because the
Clinical (see glenoid clunk and grind test): According IGHL can undergo substantial plastic deformation (up to
to Liu et al,23I physical examination was more accurate in 24%) before a complete dislocation can occur. 223
predicting glenoid labral tears than MRl. Glenoid labral
tears are related to overhead thrOwing, trauma, and shoul­ Anterior Dislocation
der instability. Examination usually demonstrates objective
instability with or without clicking, or catching during In anterior dislocation (the most common), the humeral
glenohumeral rotation. Liu et aID I recommended stress head is usually displaced subacromially, and rarely beneath
testing the labrum, the load-and-shift and crank tests for the clavicle or within the thorax.
clicking, and the apprehension, relocation, crank, and sul­
cus tests for instability. The patient may present with recur­ Mechanism of Injury: Anterior dislocation is caused by
rent pain and "catching" or "snapping'" in the anterior or falling in a position of extreme external rotation with ab­
posterior shoulder. Andrews et aP26 found that the majority duction or hyperextension or by posterior force on the pos­
of patients demonstrated a catch or a pop, especially on full terior or posterolateral shoulder.
abduction or flexion, although others stated that the catch
or pop is not necessarily present. 327 Rotation of an ab­ Physical Examination: The arm is held in a slightly
ducted shoulder might cause the snapping over the anterior abducted and externally rotated position, resulting in re­
or posterior glenoid rim. Some shoulders are defined as striction of internal rotation. external rotation, adduction,
functionally unstable because the physical examination and full abduction. The humeral head may be palpated eas­
does not show gross instability but rather a subtle instabil­ ily with a prominent acromion and loss of shoulder contour
ity, especially in the athletic population, and during use, the due to a flat deltoid (Fig. 3-102). The posterior shoulder
shoulder may at times subluxate, allowing partially attached appears to be hollow. The patient is unable to reach across
labral fragments to become interposed between the joint the body anteriorly (positive Dugas sign) or posteriorly.
The Shoulder 137

Figure 3-102 An unreduced anterior dislocation of the right

shoulder. Note that the arm is locked in external rotation. Source:
Reprinted with permission from CR Rowe. The Shoulder. p. 245, ©
1988, WB Saunders Company.

Always evaluate the neurovascular status by checking

distal pulses, brachial plexus nerves, and-particularly in
Figure 3-103 The snowbird reduction technique. Source:
an anterior dislocation-the axillary nerve. The motor por­ Reprinted with permission from CD Westin et al. Anterior shoul­
tion of the deltoid is tested by isometric testing of the del­ der dislocation: a simple and rapid method for reduction. Ameri­
toid, and sensory testing is performed over the middle can Journal of Sports Medicine. Vol. 23, No.3, pp. 369-371,
portion of the deltoid. The sensory test may prove more © 1995, American Orthopaedic Society.
practical because there may be too much pain for deltoid
testing. 329

Treatment: Treatment of shoulder dislocations is beyond

the scope of this text, although the follOwing may apply. apply rotation or pressure as needed. After successful
reduction, a sling and a swath are applied .
• Delee and Drez 33 recommended, in a healthy athlete • Aronen self-reduction technique for an anterior
on the playing field before muscular spasm sets in, shoulder dislocation (Fig. 3-104): The patient sits on
manipulation in slight abduction, forward flexion, the ground and interlocks all fingers around the knee
and gentle internal rotation. on the side of the dislocated shoulder. Next, the pa­
• A new method of reducing anterior dislocation that tient applies a steady, linear traction by leaning back­
patients tolerate extremely welP30 is the snowbird ward and extending the hip. If the technique is
technique, in which the patient is seated, and a 3-foot performed within 10 minutes of the dislocation, there
loop of 4-inch-wide cast stockinette is placed around is less spasm, although the technique can be per­
the proximal forearm of the involved extremity with formed with the patient in spasm.
the elbow flexed 90° (Fig. 3-103). The patient sits as
straight as possible while the assistant stands on the Postreduction Treatment: Recheck the neurovascular
unaffected side, clasping his or her hands around the status and put the arm in a sling. Test axillary nerve sensation
chest in the axilla of the affected side. The doctor (lateral deltoid area) before and after reduction. Take postre­
places a foot in the stockinette loop, providing a firm duction radiographs. Fractures of the greater tuberosity may
downward traction. The doctor's hands are free to occur but usually reduce with the shoulder reduction. If the

• An indirect force (more common) due to a seizure or

electrical shock whereby the internal rotators force
the humeral head posteriorly
• A fall on the outstretched hand with the arm in an ad­
ducted position

Physical Examination-Acute Posterior Dislocation

• The patient presents with the arm adducted and in­

ternally rotated. There is limitation of external rota­
tion and abduction.
• The patient may be able to elevate the arm above the
head by using scapular rotation.
Figure 3-104 To perform the Aronen self-reduction technique • The best view for posterior bulge is from above a sit­
for an anterior shoulder dislocation, the patient sits on the ground ting patient.
and firmly interlocks all fingers in front of the knee on the same
side as the dislocated shoulder. He or she then applies steady trac­ • In a thin patient, the coracoid process may be prom­
tion by leaning backward and extending the hip. The patient must inent.
maintain full elbow extension and relax the shoulder muscles for
this technique to result in a successful reduction. Source: Reprinted Physical Examination-Chronic Posterior Dislocation
with permission from JG Aronen and RD Chronister. Anterior
shoulder dislocations. The PhYSician and Sports Medicine. Vol. 23, • The patient may have a history of a traumatic or an
No. 10, pp. 65-69, © 1995, McGraw-Hill, Inc. atraumatic instability. Testing may reveal increased
posterior translation or posterior apprehension.
• Inspection may reveal an abnormal posterior promi­
nence of the humeral head.

During functional examination of passive gleno­

humeral abduction with a fixed scapula, the scapula

fragment is displaced more than 1 cm after the reduction, the

moves immediately after the arm is abducted 25 (see

patient should be referred to an orthopedist. 329

Passive Shoulder Evaluation).

Immobilize for 4 to 6 weeks to allow capsular healing33

in the young. If the patient is over the age of 40, immobilize • The patient is unable to supinate the forearm fully
only until pain subsides because there is less tendency of re­ with the arm forwardly flexed (Fig. 3-105).
currence. In anterior dislocations, strengthen the rotator • An axillary shoulder radiograph is usually diagnostic. 33
cuff (especially the infraspinatus and subscapularis) and • Because of delay in diagnOSiS, the tendency of degener­
scapular muscles at 2 to 3 weeks in the older patient (older ative arthritis of the glenohumeral joint increases. 332
than 30 years) and at 6 weeks in the younger patient
• In comparing posterior dislocation with adhesive cap­
(younger than 30 years). Increase shoulder external rotation
sulitis, differentiate by the initial stages of adhesive
to 30° or 40° and shoulder flexion to 140°. Avoid extreme
capsulitis not present in posterior dislocation.
abduction and external rotation for 3 months after removal
of the sling.
Treatment: A radiograph is essential to rule out frac­
ture (often of the lesser tuberoSity). Neurovascular examina­
tion is necessary with all shoulder dislocations. As in most
Posterior Dislocation
dislocations, referral to an orthopedist is necessary. In an
Posterior dislocation is rare and usually subacromial. Di­ older patient, an arm in the unreduced posterior dislocation
position is more functional than that in a patient with ante­
agnosis initially is missed 50% to 80% of the time 331
rior dislocation, and the patient may prefer to get along
without reduction 25 Note: Because this diagnosis is fre­
Mechanism of Injury quently missed and there is a loss of external rotation and
abduction, a chronic fixed posterior dislocation may be di­
• Direct trauma to anterior sh'o ulder agnosed as an adhesive capsulitis.
The Shoulder 139

Figure 3-105 The Rowe sign. The patient with a posterior dislocation has limited external rotation and restricted supination with the arm
forward flexed . Source: Reprinted with permission from E Schwartz et al. Posterior shoulder instability Orthopaedic Clinics oj North America.
Vol. 18, No.3, pp. 409-419, © 1987, WB Saunders Company

Inferior Dislocation Weakness and No Pain-Differential Diagnosis

Inferior dislocation is uncommon. 333 Although the response of weakness and no pain on mus­
cle testing may indicate a chronic rupture , the usual cause is
neurologic. The following are some of th