Physical Therapy of the Shoulder (Clinics in Physical Therapy) (3rd Edition)

Physical Therapy of the

THIRD

EDITION

Edited by

Robert A. Donatelli, Ph.D., P.T., O.CS. I nsLruclor Divisioll oj Physical T herapy Departmellt oj Rehabilitatioll Medicille EmOlY Ulliversity School oj Medicille At/alita, Georgia Natiollal Director oj Sports Rehabilitatioll Physiotherapy Associates Memphis, Tellllesse

CHURCHILL LIVINGSTON'

,-I-JJ

New York, Edinburgh, london, Madrid, Melbourne, San Francisco, Tokyo

Library of Congress Cataloging-in-Publication Data Physical therapy of the shoulder I edited by Robert A. Donatelli.3rd ed. p.

em. - (Clinics in physical therapy)

Includes bibliographical references and index. ISBN 0-443-07591-3 (alk. paper) I. Shoulder-Wounds and injuries. 2. Shoulder-Wounds and injurics-Treatment. 3. Shoulder-Wounds and injuries-Physical therapy. I. Donatelli, Robert. IT. Series. [DNLM: I. Shoulder-injuries. 2. Shoulder Joinl-injul"ies. 3. Physical Therapy-methods.

WE 810 P578 1997)

R0557.5.P48 1997 617.5' 72062-de20 DNLM/DLC for Library of Congress

96-29475 CIP

€:I

Churchill Livingstone Inc_ 1997, 1991,1987

All rights reserved. No pal1 of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying. recording, or otherwise. without prior pennis­ sion of the publisher (Churchill Livingstone, 650 Avenue of the Americas, New York, NY 10011). Distributed in theUnited Kingdom by Churchill Livingstone. Rober1 Steven­ son House, 1-3 Baxter's Place, Leith Walk, Edinburgh EHI 3AF, and by associated companies, branches, and representatives throughout the world. M edical kn owledge is constantly changing. As new infollnation becomes available, changes in treatment, procedures, equipment and the use of drugs become necessary. The editors/authors/contributors and the publishers have, as far as it is possible, taken care to e nsure that the information given in this text is accurate and up to date. However, readers are strongly advised

to confirm that the infolmation, especially with regard to drug usage, com­ plies with the latest legislation and standards of practice.

The Publishers have made every eFronto trace the eopytight holders for bor­ ,'owed material. If they have inadvertently overlooked any, they will be pleased to make the necessal)' 31T3ngements at the fil'St oppol1unity.

Acquisitions Editor: Carol Bader Production Editor: Palll Bemsteill Production Supervisor: Kathleell R. Smith Cover Design: Jeannette Jacobs Printed in the United States of America First published in 1997

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I would like 10 dedicate this book to my late father, Revy Donatelli,

and 10 my mother, Rose Donatelli. They provided the guidance, motivation, and love 10 help me through my college years, enabling me to pursue a career in physical therapy. I would also like to dedicate the book to my sistel; Linda Schultheiss, and to my brothel; Jerry DonatelliJor their friendship, love, and support.

Contributors Robert A. Dotlatelli, Ph.D., P.T., O.e.S.

Mark S. Albert, M.Ed., P.T., A.T.C, S.e.S. Part-time

InstmctOl;

Department

of

Physical

Therapy, College of Health Sciences, Georgia State University;

Clinical

Specialist,

Physiotherapy

instructor,

Division

of

Physical

Therapy,

Depal·tment of Rehabilitation Medicine, EmOlY University School of Medicine, Atlanta, Geor­ gia; National Director of Sports Rehabilitation,

Associates, Atlanta, Georgia

Physiotherapy Associates, Memphis, Tennessee

Robert Catltll, M.M.Sc., P.T., M.S.e. Assistant Professor, Institute of Physical Therapy,

Peter 1. Edgelow, M.A., P. T.

SI. Augustine, Florida; Clinical Director, PhYSiO­

Senior Staff Therapist, Physiotherapy Associates; Graduate

therapy Associates, Atlanta, Georgia

Residency

in

Orthopaedic

Physical

Therapy, Kaiser Permanente, Hayward, Califoll1ia

Deborah Seidel Cobb, M.S. P.T. Physical

Therapist,

Physiotherapy

Associates,

Atlanta, Georgia

Clinical

Pl'OfessOl;

Depal1ment

of

Orthopaedics, West Virginia College of Osteo­ pathic Medicine, Lewisburg, West Virginia; Hon­ oralY Clinical Lnstmctor, Graduate Pl'Ogram in Physical Therapy, Division of Allied Heath Pl'Ofes­ sions, Department of Rehabilitation Medicine, EmOlY University School of Medicine; Past Chair­ man, Department of Surgery, Medical

Centel�

Staff

orthlake Regional

Orthopaedic

Surgeon,

Dekalb Medical Centel; Northlake Regional Med­ ical Center, Georgia;

Eastside

Medical Center, Atlanta,

Orthopaedic

Surgeon,

Killian

Hill

Orthopaedic and Sports Medicine Clinic, Lilbull1, Georgia

PhYSiotherapy

Associates·

Robert L. Elvtry, P.T. Senior

Lecturer,

School

of

PhYSiotherapy,

Curtin University of Technology, Perth, Western Australia, Australia

Blanca Zita Gotlw!ez-Kitlg, P. T., e.H.T. Clinic

Director,

Physiotherapy

Associates,

Jonesboro, Georgia

Jolm e. Gray, P.T. Assistant Clinical

InstmctOl; Specialist,

Ola

Grimsby

Department

of

Institute; Physical

Therapy, Sharp Rees-Stealy, San Diego, Califor­ nia; Fellow, American Academy of Orthopaedic Manual Physical Therapists

Jeff Cooper, M.S., A.T.e. Athletic Trainel; The Phillies, Philadelphia, Penn­ sylvania; Consultant, Physiotherapy Associates, Atlanta, Georgia

Therapist,

Jonesbol'O, Georgia

Bntce H. Greenfield, M.M.Sc., P.T., O.e.S. Instmctor, Division of PhYSical Therapy, Depart­ ment of Rehabilitation Medicine, Emory Uni­ versity School of Medicine, Atlanta, Georgia

Ola Grimsby, P.T.

Karetl E. Dallis, M.P.T., A.T.C. Physical

Director,

Scottsdale Sports Clinic, Scottsdale, Alizona

David J. Conaway, D.O. Associate

Todd S. Ellet!becker, M.S., P.T., S.C.S., e.S.e.S. Clinic

Physiotherapy

Associates,

Chailman of the Board, Ola Grimsby institute, San Diego, Califoll1ia vii

viii

CONTRIBUTORS

Susan Ryerson, P.T.

Toby Hall, P.T. Physiotherapy,

Pal1.ner, Making Progress, Alexandda, Virginia;

Curun University of Technology, Perth, Western

Adjunct Clinical Faculty, Massachusetts General

Clinical

Consultant, School

of

Hospital Institute of Health Professions, Boston,

Australia, Australia

Massachusetts, CoordinatorlInstmctOJ; NeUl'ode­ velopmental

Mari" A. Johanson, M.S., P.T., O.e.S. Clinic

Director,

Physiotherapy

Associates,

Peachtree City, Georgia

Rehabilitation

Partnel; Making Progress, Alexandria, Virginia; Adjunct Clinical Faculty, Massachusetts General Hospital Institute of Health Professions, Boston, Massachusetts; CoordinatorlInstructor, Neurode­ velopmental Treatment Association, Inc., Chicago, illinois

lnc.,

Projects

Coordinator,

Georgia

Baptist Medical Center, Atlanta, Georgia

LoriA. I1lein, M.S., P.T., S.e.S., A.T.e. Associate Lecturer, Depaltment of Kinesiology, University of Wisconsin School of Educalion; Senior Clinical Therapist, SPOl1S Medicine Center, University of Wisconsin Clinics Research Park, Madison, Wisconsin

Angelo J. Mattalino, M.D. Medical Director, Southwest Sports Medicine and Orthopaedic Surgery Clinic, Ltd., Scottsdale, Medical Director, Baseball Research

and Rehabilitation Center/Physiotherapy, Tempe, Adzona

Staff Orthopaedic Surgeon, The Hughston Clinic; Orthopaedic

Surgeon,

Hughston

Timothy Uhl, M.S., P.T., A.T.e. Director of Physical Therapy, Human Perfor­ mance and Rehabililation Center, Columbus, Georgia

Joseph S. Wilkes, M.D.

George M. McCluskey III, M.D. Staff

Association,

Dorie B. Syen, M.S., O.T.R., e.H.T.

Kathryn L£vil, M.Ed., O.T.R.

Adzona;

Treatment

Chicago, Winois

Sports

Medicine Hospital, Columbus, Georgia

Associate

Clinical

Professor,

Depru1ment

of

Orthopaedics, Emory University School of Medi­ cine; Orthopedist, The Hughston Clinic; Medical Director,

Piedmont

Hospital Sports

Medicine

Institute, Allanta, Georgia; Orthopedic Consul­

Timothy J. McMaJwn, P. T.

tant, United Stales Luge Association, Lake Placid,

Clinical Instmctor, Division of Physical Therapy,

New York

Department of Medicine, Emory UniverSity School of Medicine, Atlanta, Georgia; Assistant DirectOJ; Physiotherapy Associates, Lilburn, Georgia

Michael J. Wooden, M.S., P.T., O.e.S. [nstmctor, Division of Physical Therapy, DepaJ1ment of Rehabilitation Medicine, Emory Uni­

Helen Owens, M.S., P.T.

versity School of Medicine; National Director,

Owner, Orthopedics Physical Therapy Services,

Clinical

Lockport, illinois

Memphis, Tennessee

Research,

Physiotherapy

Associates,

Preface N0n11al function of the shoulder is cdtical for

I am honored to include Ola Gdmsby, John Gray,

performance,

Robcl� Elvey, Toby Hall, and Peler Edgelow as chapler

and activities of daily living. Given the impot1ance of

authors in the third edition. Their contributions to the

recreational activities,

occupational

normal shoulder biomechanics, it is not sUI-prising

Neurologic Considerations section are excellenl. The

that changes in shoulder mechanics, altered kinemat­

chaplers on Inten'c1ationship of Ihe Spine and Shoul­

ics, and anatomic deficits contribute to shoulder

der Girdle, Neural Tissue Evaluation and Treatment,

pathomechanics. Our role as physical therapists is to

and

assess the intricate shoulder mechanics to determine

Trauma

NeurovascuJal"

abnormal movement pancrns before we begin our

demonstrate the importance of understanding the

treatment program.

intcn"elationship between the musculoskeletal and

Disorders

Consequenses Affecting

the

of

Cumulative

Thoracic

Outlet

Many rehabilitation students and clinicians are

neurologic systems. Chapter 7 was completely rewl'it­

uncertain in assessing shoulder pathomcchanics and

ten with a more clinical approach 10 brachial plexus

in

lesions.

establishing treatment protocols for different

shoulder pathologies. This Shol1coming is due to the

The Special Considerations section l1!views the

vadcLY of treatment appI'oachcs to the shoulder and

most common pathologies and dysfunctions of the

the complexity of the shoulder and upper quarter

shoulde.: In Chapter 12 John Gray demonst.-ales Ihe

inten"elationships.

importance of understanding how other systems in

In keeping up to date with new and innovative

the body can refer pain to the shoulder. MobiIi7..ation,

treatment techniques, surgical procedures, and evalu­

strengthening exercises (including isokinetics), and

ation methods for the shoulder, this third edition of

myofascial techniques are discussed in the Treatment

Physical Therapy of Ihe Shoulder has become a LOtally

Approaches section. All four chapters in this section

new book. We have expanded the third edition to 20

include figures accurately demonstrating treatment

chapters from 16. There are 18 new authors and 10

techniques. The Surgical Considerations section fea­ tures new infol"mation on the most common surgical

new chapters. The third edition has been divided into five sec­ tions; Mechanics of Movement and Evaluation, Neu-

procedures for shoulder instabilities, rotator cuff repairs, and total joint replacements.

1"Oiogic Considerations, Special Considerations, Tt1!at­

Any rehabilitation professional entrusted with

ment Approaches, and Surgical Considerations. Case

the care and treatment of mechanical and patho­

studies are presented thT"OUghout the text.

logic shoulder dysfunclion will benefit from this

Chapter t emphasizes the clinical mechanics of

book. We trust that the third edition of Physical

shoulder movement. The mechanical components of

Therapy of Ihe Shoulder will meel the reader's expec­

shoulder elevation arc descdbed and divided into

lation of comprehensive, clinically relevant presen­

phases. Jeff Cooper, a new author for this edition who

tations that are well documented, contemporar)"

is Ihe alhlelic Irainer for Ihe Philadelphia Phillies,

and personally challenging to the student and clini­

does an excellent job in descdbing the mechanics of

cian alike.

pitching and injudes related to the sport.

Chapter 3

reviews the traditional approach of Cyriax's differen­ tial soft tissue evaluation of the shoulder and all the special tests.

Roberl A. DOl/alel/i, Ph.D., P.T., o.c.s.

ix

Contents MECH A N IC S

OF

CHAPTER 8

M OV E ME NT

The Shoulder in Hemiplegia I 205

A N D EV A LU AT I O N

Susan Ryerson and Kathryn Levit

CHAPTER

1

Functional Anatomy and Mechanics I t Robert A. Donatelli CHAPTER 2

Throwing Injuries I t 9 Jef{Cooper CHAPTER

3

S PEC I AL C O N S I DE R AT I O N S CHAPTER

9

Impingement Syndrome and Impingement-Related Instability I 229 Lori A. Theill and Bruce H. Greenfield

Differential Sofl Tissue Diagnosis I 57 Marie A. Joha>lson and Blal1ca Zita Gonzalez-Killg

NEU R OL O G IC C O N S I DE R AT I O N S

CHAPTER

10

Frozen Shoulder I 257 Helen Dwel1s CHAPTER

1 I

Etiology and Evaluation of Rotator Cuff Pathology and Rehabilitation I 279

CHAPTER 4

IntelTelatiollship of the Spine to Ihe Shoulder Girdle I 95 Dla Grimsby GIld John C. Gray CHAPTER 5

Neural Tissue Evaluation and Treatment I t 3 t

Todd S. Ellellbecker CHAPTER

12

Visceral Pathology Referring Pain to the Shoulder I 299 John C. Gray

Robert L. Elvey alUl Toby Hall CHAPTER

6

Neurovascular Consequences of Cumulative

T R E AT M E NT A P P R O AC HE S

Trauma Disorders Affecting the Thoracic Outlet: A Patient-Centered Treatment

CHAPTER

13

Approach I t 53

Manual Therapy Techniques I 335

Peter I. EdgelolV

Robert A. Do/lOtelli and Timothy 1. McMahon

CHAPTER

7

Evalualion and Trcalment of Brachial

CHAPTER

Plexus Lesions I t 79

Strengthening Exercises I 365

Bruce H. Greenfield and Dorie B. Syen

Korell E. Davis and Robert A. Donatelli

14

XL�

CONTRIBUTORS

CHAPTER

15

Myofascial Treatment I 383 Deborah Seidel Cobb and Robert Call1L1 CHAPTER

16

Isokinetic Evaluation and Treatment I 401 Mark S. Albert al1d Michael 1. Wooden

SUR G IC AL C O N S ID E R AT I O N S

CHAPTER

19

Shoulder Girdle Fractures I 447 Michael J. Wooden al1d David J. CO//aIVay CHAPTER

20

Total Shoulder Replacement I 459 George M. McClLlskey III al1d Timothy Uhl

I NDE X

477

Color insert follows page 117. CHAPTER

17

Instabilities I 421 Al1gelo J. Mallalil10 CHAPTER

18

Rotator Cuff Repairs I 435 Joseph S. Wilkes

Functional Anatomy and Mechanics ROB E R T

A .

DONATELLI

One of the most common peripheral joints to be treated in the physical therapy clinic is the shoul­ der joint. The physical therapist must under­ stand the anatomy and mechanics of this joint to most effectively evaluate and design a treatment program for the patient with shoulder dysfunc­ tion. This chapter will describe the pertinent functional anatomy of the shoulder complex and relate this anatomy to the h.lBctional move­ ments, stability, and muscle activity. The shoulder joint is beller termed the shoulder complex, because a series of articula­ tions are necessary to position the humerus in space (Fig. 1. 1). Most authors, when describing the shoulder joint, discuss the acromioclavicu­ lar joint, sternoclavicular joint, scapuloLhoracic articulation, and glenohumeral joint.'- 4 Demps­ ter relates all of these areas by using a concept of links. The integrated and harmonious roles of all of the links are necessary for full normal mobilityS The glenohumeral joint sacrifices stability for mobility. The shoulder is capable of moving in over 16,000 positions, which can be differen­ tiated by I' in the normal person 6 The mobility of the shoulder is dependent upon proximal sta­ bility of the humerus and scapula. The position of the humerus and scapula must change throughout each movement in order to maintain stability6

Osteokinematic and Arthrokinematic Movement Analysis of shoulder movement emphasizes the synchronized movement of four joints: the gle­ nohumeral, scapulothoracic, sternoclavicular, and acromioclavicular joints.,,,·7 rus moves into elevation, movement must OCClIr at all four joints. Elevation of the arm can be observed in three planes: the h'ontal plane (ab­ duction), sagittal plane (flexion), and plane of the scapula (scaption)8,9 Movement of the long bones of the arm into elevation is refen'ed to as osteokinematics. Arthrokinematics describes the intricate movement of joint surfaces: rolling, spinning, and sliding.lo

OSTEOKINEMATIC MOVEMENT

Scaplion-Abduclion

Abduction of the shoulder in the fTontal or coronal plane has been extensively re­ searched.4,•. 11-1 7 Poppen and Walker1 5 and Johnston,' suggest that the true plane of move­ ment in the shoulder joint occurs in the plane of the scapula. The scapula plane (scaption) is defined as elevation of the shoulder in a range 1

2

PHY S I CAL

THERAPY

OF

THE

SHOUL DER

7

3"-_----�

,.

FIGURE 1. 1 The componenls o( Ihe shoulder joinl cOlI/plex. ( 1) Glenohllmeral joilll. (2) SlIbdeltoid joil/I. (3) Actol11ioc/avicultlr joilll. (4) Scapulolhoracic joi11l. (5 ) Slemoc/avicular joi/lI. (6) Firsl coslOslemal joinI. (7) Firsl costovertebral joinf,

between 30' and 45' anterior to the frontal plane (Figs. I.2 and 1.3).15 Kondo et al. IS devised a new method for tak­ ing radiographs to define scaption during eleva­ tion. The medial tilting angle was used to de­ scribe scaption. Medial tilting angle refers to the tilting of the scapula toward the sagillal plane. As the medial tilting angle increases. there is a movement of the scapula around the thoracic cage. Kondo et ailS demonstrated that the me· dial tilting angle was constant at 40' anterior to the fTontal plane throughout the range of 15 0' of elevation. Several authors believe that the plane o[ the scapula is clinically significant because the length·tension relationship of the shoulder ab­ ductors and rotators are optimum in this plane of elevations.15 Research has demonstrated that the length of the muscle detelmines the amount of stretch applied to the individual sarcomeres. enabling them to exert maximum tension,I9 The length-tension curves obtained from nOtmal muscle' show that maximum tension is dcvel-

FIGURE 1.2

Elevatiol'l ill the plalle o( the scapula.

oped when the muscle length is approximatel} 90% of its maximum length. I. Convel ely. when the muscle is fully shortened. the tension devel· oped is minimal.2o.2I Therefore. the optimal lengthened position of the muscle tendon will fa­ cilitate optimal muscle contraclion. 22 Several studies have compared the torque production of different shoulder muscle groups when tested in scaption versus other body planesn.27 Soderberg and Blaschak23 and Hell· wig and Perrin24 demonstrated no significant differences in the peak IOt'que of the glenohu. meral rotators between scaption and other body planes. These studies used 45' and 40' anterior to the frontal plane. respectively. for the scaption test position. Greenfield et al." reported greater torque production of the external rotators when tested in scaption versus the coronal plane. Fur-

FUNCTIONAL

ANATOMY

AND

MECHANICS

3

Plane of the scapula

, I

,

,

,

I I , ,, I , I , I , , , I , , , , III ." ,,( w

FIGURE 1.3 Abduction in t"e plane of the scapula.

thermore, Tata et a1.'6 reported higher ratios of abduction to adduction and external to internal torque when tested in the scapular plane at 30· and 35· anterior to the frontal plane, respec­ tively. Whitcomb et al.l? found no significant dif­ ference between torque produced by the shoul­ der abductors in the coronal and scapular planes, using a scaption position 35 · anterior to the frontal plane. The studies cited indicate that the external rotators are the only muscle group that demon­ strated a significant increase in torque produc­ tion in the scaption plane 30· anterior to the fron­ tal plane. The pectoralis major and the latissimus muscles groups are not attached to the scapula. Therefore, it would seen reasonable that when comparing the torque output of the internal rota­ tors, the change in position of the scapula should not effect the optimal length-tension relation­ ship. Thus, the internal rotators exhibit no change in the torque output when testing in dif­ ferent planes of movement. In addition to optimal muscle length-tension relationship in the plane of the scapula, the cap­ sular fibers of the glenohumeral joint are re­ laxeds Poppen and Walkeri' demonstrated that in scaption there is an increase in joint congru­ ity, allowing for greater joint stability. Therefore, for reasons of glenohumeral stability, avoidance of impingement, and balance of muscle action, scaption may be the plane in which shoulder

trauma is minimal, and the most advantageous plane for strength trainjng programs. Flexiol1

The movement of flexion has been less thor­ oughly investigated. Flexion is movement in the sagittal plane. Full nexion from 162· to 18 0· is possible only with synchronous motion in the glenohumeral, acromioclavicular, sternoclavic­ ular, and scapulothoracic joints. " The move­ ment is similar to that of abduction.

ARTHROKINEMATIC MOVEMENT

The motion OCCUlTing at Jomt surfaces is arthrokinematic motion, of which there are three types: rolling, gliding, and rotation (Fig. 1.4) Rolling occurs when various points on a moving surface contact various points on a sta­ tionary surface. Gliding occurs when one point on a moving surface contacts multiple points on a stationary surface. When rolling or gliding occur, there is a Significant change in the contact area between the two joint surfaces. The third type of arthrokinematic movement, rotation, oc­ curs when one or more points on a moving sur­ face contact one point on a stationary surface. There is little displacement between the two joint surfaces in rotation. All three arthrokinematic movements can

4

PHYSICAL

THERAPY

OF

THE

Gleno-Humeral

SHOULDER

Jt.

Rotation

Gliding FIGURE 1.4

Arthrokinematic molion occurr;'1g at the glenohumeral joint: rolling, rolation, and

gliding.

occur at the glenohumeral joint, but they do not occur in equal proportions. These motions are necessary for the large humeral head to take ad­ vantage of the small glenoid articulating sur­ face.'• Saha investigated the contact area be­ tween the head of the humems and the glenoid with abduction in the plane of the scapula 14 and found that the contact area on the head of the humerus shifted up and forward while the con­ tact area on the glenoid remained relatively con­ stant, indicating a rotation movement. Poppen and Walker measured the instant centers of rota­ tion for the same movement. in the first 30°, and often between 30° and 60°, the head of the humems moved superiorly in the glenoid by 3 mm, indicating rolling or gliding. At more than 60°, there was minimal movement of the humems, indicating almost pure rota­ tion. 15 Normal arthrokinematic movements occur only in the presence of normal periarticular con­ nective tissue, extensibility, and integrity and muscle function. A stiff shoulder has limited cap­ sular nexibility and altered muscle function. In

order to reestablish harmonious movement within the shoulder complex the therapist must rehabilitate the connective tissue by restoring its extensibility, and restore the normal balance of muscles. Rotations of the HumerLis

Concomitant external rotation of the hume­ rus is necessary for abduction in the coronal plane.4.8,IO.1 4.17 Some investigators have postu­ lated that this motion is necessary for the greater tuberosity to clear the acromion and the cora­ coacromial ligament.,·2.' 7 Saha reports that there is sufficient room between the greater tu­ berosity and the acromion to prevent bone im­ pingement. External rotation also remains nec­ essary for full coronal abduction even after the acromion and the coracoacromial ligament are surgically removed. Saha has reasoned that ex­ ternal rotation is necessary to prevent the hu­ meral head from impinging on the glenoid rim.16 Rajendran,28 using cadaveric glenohumeral joints. demonstrated automatic external rotation

FUNCTIONAL

of the humerus is an essential component of ac­ tive as well as passive elevation of the arm through abduction. Even in the absence of extra­ articular influences such as the coracoacromial arch and glenohumeral muscles, external rota­ tion of the humerus was spontaneous. An Kn et al.29 used a magnetic tracking system to monitor the three-dimensional orientation of the hume­ rus with respect to the scapula. Appropriate co­ ordinate transformations were then performed for the calculation of glenohumeral joint rota­ tion. Maximum elevation in all planes anterior to the scapular plane required external axial ro­ tation of the humerus. Furthermore, Oti et al. 30 demonstrated that external rotation of the humerus allows the in­ sertion of the subscapularis tendon to move lat­ erally, resulting in an increase in the distance from the axis of elevation in the scapula plane. An increase in the moment arm enhances the ability of the superior fibers of the subscapularis to participate in scaption. Conversely, internal rotation of the humerus increases the moment a,m of the superior fibers of the infraspinatus, enhancing the ability of the muscle to participate in scaption. Flatow et al.3I reported that acro­ mial undersurface and rotator cuff tendons are in closest proximity between 60· and 120· of ele­ vation. Conditions limiting external rotation or elevation may increase rotator cuff compression. Rajendran and Kwek" described how the course of the long head of the biceps will influence ex­ ternal rotation of the humen,s, which in turn prevents tendon impingement between the greater tuberosity and the glenoid labrum, and allows glenohumeral elevation to move to com­ pletion. Brems" repo'is that external rotation is possibly the most impo'iant functional motion that the shoulder complex allows. Loss of exter­ nal rotation could result in significant functional disability.

Static SWiJilizers of the Glerwhumeral Joint The stability of the glenohumeral joint is depen­ dent on the integrity of soft tissue and bony structures such as the labrum, glenohumeral lig-

ANATOMY

AND

MECHANICS

5

aments, capsular ligaments, and the bony gle­ noid.34 The glenohumeral joint contributes the greatest amount of motion to the shoulder be­ cause of its ball and socket configuration. Saha35 confirmed the ball and socket joint of the gleno­ humeral articulation in 70 percent of his speci­ mens. In the remaining 30 percent, the radius of curvature of the humeral head was greater than the radius of curvature of the glenoid. Thus, the joint was not a true enarthrosis.'· Saha'· further described the joint surfaces, especially on the head of the humerus, to be very i'Tegular and to demonstrate a great amount of individual va,-ia­ tion. The head of the humerus is a hemispherical convex articular surface that faces superior, me­ dial, and posterior. This articular surface is in­ clined 130· to ISO· to the shaft of the humerus and is retroverted 20· to 30.3 The retroversion, and the poste,;or tilt of the head of the humerus and the glenoid, cultivate joint stability (Fig. 1 . 5 ) . This retroversion of the head of the humerus cor­ responds to the forward inclination of the sca­ pula, so that fTee pendulum movements of the arm do not occur in a straight sagittal plane but at an angle of 30· across the body.'· This CO'Te­ sponds to the natural arm swing evident in am­ bulation. The head of the humerus is large in relation to the glenoid fossa; therefore only one-third of the humeral head can contact the glenoid Fossa at a given time.'·3. The glenoid fossa is a shallow structure deepened by the glenoid labrum. The lab,um is wedgeshaped when the glenohumeral joint is in a resting position, and changes shape with various movements.37 The glenoid and the labrum combine to form a socket with a depth up to 9 mm in the superior-inferior direction and 5 mm in the anteroposterior direction.3• The functional Significance of the lab,um is ques­ tionable. Most authors agree that the labrum is a weak supporting structure.37 .39 The function of the labrum has also been described as a "chock block" preventing humeral head translation.3• Moseley and Overgaard37 considered the labrum a redundant fold of the capsule composed of dense fibrous connective tissue but generally de-

6

PHYSICAL

THERAPY

OF

THE

SHOULDER

A

B

FIGURE 1.5 (A) Rumenls with marker through the head-I1eck al1d a secol1d marker through the epicol1dyies. (B) Retroversion of the hUl11erus as seen frol11 above.

void of cartilage except in a small zone near its osseous attachment. The glenohumeral joint has been described by Matsen et al40 as a "suction cup" because of the seal of the labrum and glenoid to the humeral head. This phenomenon is caused by the gradu­ ated flexibility of the glenoid surface, which per­ mits the glenoid to conform and seal to the hu­ meral head. Compression of the head into the socket expels the synovial fluid to create a suc­ tion that resists distraction. A negative intra-ar­ ticular joint pressure is produced by the limited joint volume,,1 Matson et al. portance of an intact glenoid labrum in estab­ lishing a concavity compression stabilization.

The compressive load is provided by dynamic muscle contraction. The glenoid fossa faces laterally. and Munro" found that the glenoid faced down­ ward in 80.8 percent of the shoulders that they studied with radiographs. Saha" found a 7. 4° retrotilt of the glenoid in 73.5 percent of nOlmal subjects. The retrotilt is a stabilizing factor to the glenohumeral joint. Both the humeral and glenOid articular surfaces are lined with alticular cartilage. The cartilage is the thickest at the pe­ riphery on the glenoid fossa and at the center of the humeral head.'6 The capsule and ligaments reinforce the gle­ nohumeral joint. The capsule attaches around the glenoid rim and forms a sleeve around the head of the humerus, attaching on the anatomi­ cal neck. The capsule is a lax structure; the head of the humerus can be distracted one-half inch when the shoulder is in a relaxed position." The capsule is reinforced anteriorly and postetiorly by ligaments and muscles. There is no additional support inferiorly, causing weakness of this por­ tion of the capsule. This inferior pOltion of the capsule lies in folds when the arm is adducted. The redundant portion of the capsule adheres to itself and limits motion in adhesive capsulitisJ6 The anterior capsule is reinforced by the gle­ nohumeral ligaments. The sUPPOtt that these lig­ aments lend to the capsule is insignificant 44 Also, these ligaments are not consistently present in each individual. Turkel et al.45 described the inferior gleno­ humeral ligament as the thickest and most con­ sistent structure. The inferior glenohumeral liga­ ment attaches to the glenOid labrum. Turkel ct al.45 determined the relative contribution to an­ terior stability by testing external rotation in dif­ ferent positions. The subscapularis resisted pas­ sive external rotation in the adducted position more than any other anterior structure (Fig. J .6) In patients with internal rotation contracture and pain after anterior repair for recurrent dislo­ cation of the shoulder, surgical release of the subscapularis increased the external rotation range of motion an average of 27046 Turkel et al.45 demonstrated at 45° abduction that external rotation was resisted by the subscapularis, mid-

FUNCTIONAL

ANATOMY

ANO

MECHAN I C S

7

FIGURE 1.6 Exlernal rolalion of the humerus in Ihe adducled posilion. The mosl stabilizing structure 10 this movement is the subscapularis muscle.

FIGURE 1.7 Exlernal rOlaliol1 o f Ihe humerus al 45°abduclion. The mosl slabilizing struclLlres for Ihis movemel11 are Ihe middle alld il1(erior Iigamel1ls and subscapularis muscle.

die glenohumeral ligament. and superior fibers of the inferior ligament (Fig. J . 7). At 90° of ab­ duction. external rotation was restricted by the inferior glenohumeral ligament (Fig. J .8). Hoi et al. the biceps (LI-lB) and short head of the biceps (SH B) have similar [unctions as anterior stabiliz­ ers of the glenohumeral joint with the arm in abduction and external rotation. Furthermore. the role of the L H B and S H B increased with shoulder instability. Warner et aJ48 studied the capsuloligamentous restraints to superior and inferior translation o[ the glenohumeral joint. The primary restraint to inferior translation of the adducted shoulder was the superior glenohu-

meral ligament. The coracohumeral ligament appeared to have no significant suspensory role. Abduction to 45° and 90° demon trated the ante­ rior and posterior portions. respectively. of the glenohumeral ligament to be the main static sta­ bilizers resisting infel'ior translation. Guanche et al49 studied the synergistic ac­ tion of the capsule and the shoulder muscles. A renex arch from mechanoreceptol"S within the glenohumeral capsule to muscles crossing the joint was identified. Stimulation of the anterior and the inferior axillary articular nerves elicited electromyographic (EMG) activity in the biceps. subscapularis. supraspinatus. and infraspinatus muscles. Stimulation of the posterior axillary ar-

8

PHYSICAL

THERAPY

OF

THE

SHOULDER

communicates with the shoulder joint. The infe­ rior recess is referred to as the axillary pouch, and the middle synovial recess lies posterior to the subscapularis tendon. Arthrograms of frozen shoulders in relatively early stages, before gleno­ humeral abduction is completely restricted, show obliteration of the anterior glenoidal bursa.5I

Dtfnamic Stabilizers of the Glenohumeral JCJint

Extemai rotatio" of the humerus at 90·abduction. The most stabilizing structure for this movement is the inferior ligamem. FIGURE 1.8

ticular nerve elicited EMG activity in the acromi­ odeltoid muscle. The coracohumeral ligament is the strongest supporting ligament of the glenohumeral joint. Fibers of the capsule and coracohumeral liga­ ment blend together and insert into the borders of the supraspinatus and subscapularis.'o The coracohumeral ligament limits external rotation and elevation of the humerus.'o Release of the coracohumeral ligament increased external rota­ tion both with the arm held in adduction and at 90' of abduction.'o Between the supporting ligaments and mus­ cles lie synovial bursa or recesses. Anteriorly there are three distinct recesses.5I The superior recess is the subscapular bursa, which normally

The major muscles that act on the glenohumeral and scapulothoracic joints may be grouped into the scapulohumeral, axiohumeral, and axiosca­ pular muscles. The muscles of the scapulohum­ eral group, which include the rotator cuff mus­ cles, originate on the scapula and insert on the humerus. The rotator cuff muscles insert on the tuberosities and along the upper two-thirds of the humeral anatomic neck.10 The subscapularis muscle is often overlooked in shoulder dysfunc­ tion. It has the largest amount of muscle mass of the four rotator cuff muscles4 As previously noted, passive external rotation range of motion with the ann neutral (adducted) is resisted by the subscapularis muscle. Many times trigger points develop within the subscapularis muscle second­ ary to trauma or microtrauma, resulting in re­ strictions in external rotation in neutral and lim­ ited glenohumeral elevation. Travell and Simons" believe that a trigger point within the subscapularis may sensitize the other shoulder girdle musculature into developing secondary and satellite trigger points, leading to major re­ strictions in glenohumeral jointmotion. The rotator cuff muscles have been de­ scribed as steerers of the head of the humeills on the glenoid. 1 6 The subscapularis, latissimus dorsi, teres major, and teres minor act as hu­ meral depressors. 165. 3 The arthrokinematics (rolling, spinning, and sliding) of the glenohu­ meral joint result from the action of the steerers and the depressors of the humeral head. Transla­ tion of the humeral head is of clinical interest in most shoulder disorders. At the glenohumeral joint, the amount and direction of translation de-

FUNCTIONAL

fine the type of instability. Wuelker et al.54 dem­ onstrated that translation of the humeral head during elevation of the glenohumeral joint be­ tween 20' and 90' averaged 9 mm supel;orly and 4.4 mm anteriorly. Translation of the humeral head during active elevation may be diminished by the coordinated activity of the rotator cuff mu c1es. Thi active control of the translation forces provides dynamic stability to the glenohu­ meral joint. Perry55 describe 17 muscle groups providing a dynamic interactive stabilization of the composite movement of the thoraco-scapu­ lar-humeral articulation. Abnormal glenohumeral translation is ob­ served most often in overhead throwing athletes. Loss of coordinated balance between accelerat­ ing, decelerating, and stabilizing muscle function may produce microtraumatic injuries and possi­ bly instability of the glenohumeral joint. Further examination of the dynamic stabilizers in the throwing athlete will be discussed in Chapter 2. The deltoid muscle makes up 41 % of the scapulohumeral muscle mass.4 This muscle, in addition to its proximal attachment on the acro­ mion process and the spine of the scapula, also arises from the clavicle. The distal insertion is on the shaft of the humenrs at the deltoid tuber­ cle. The mechanical advantage of the deltoid is enhanced by the distal insertion and the evolu­ tion of a larger acromion process.4 The deltoid is a multipennate and fatigue-resistant muscle. This may explain its rare involvement in shoul­ der pathology.56 The deltoid and the clavicular head of the pectoralis major muscles have been described as prime movers of the glenohumeral joint because of their large mechanical advan­ tage.4 Michiels and Bodem57 demonstrated that deltoid muscle action is not restricted to the gen­ eration of an abducting moment in the shoulder joint. The clavicular and scapular regions of the deltoid muscle group afford stability to the gle­ nohumeral joint. Itoi et al47 reported that the biceps muscle group becomes more important than the rotator cuff muscles as stability from the capsuloliga­ mentous stnrcture decrease . The anterior dis­ placement of the humeral head under 1.5 kg force was significantly decreased by both the

ANATOMY

AND

MECHANICS

9

long and short head of the biceps loading in all capsular conditions when the arm was in 60' or 90' of external rotation and abduction.

Sternoclnivicular JrJint The sternoclavicular (SC) joint is the only articu­ lation that binds the shoulder girdle to the axial skeleton (Fig. 1. 9). This is a sellar joint, with the sternal articulating surface greater than the cla­ vicular surface, providing stability to the joint. 10 The joint is also stabilized by its articular disc, joint capsule, ligaments, and reinforcing mus­ c1es.5 . SS The disc binds the joint together and di­ vides the joint into two cavities. The capsule sur­ rounds the joint and is thickest on the anterior and posterior aspects. The section of the capsule from the disc to the clavicle is more lax, therefore allowing more mobility here than between the disc, sternum, and first rib. 10 The interclavicular ligament reinforces the capsule anteriorly and infel;orly. The costoclavicular ligament con­ nectS the clavicle to the first rib. 10 The SC joint gains increased stability fTom muscles, espe­ cially the sternoclydomastoid, sternohyoid, and sternothyroid.'8

Acromioclavicular JrJint At the other end of the clavicle is the acromioclav­ icular (AC) joint. This articulation is character­ ized byvariability in size and shape of the c1avicu-

FIGURE 1.9 The upper and lower allachmel1ls or the lII.eI1iscus and upper and lower ligaments or the sternoclavicular joint.

10

PHYSICAL

THERAPY

OF

THE

SHOULDER

b

a FIGURE 1.10 Axes o( l11otio/1 o( the clavicle. (a) Lon gitudinal axis o( rotatioYl. (h) Vertical axis (or protraction and retraction. (c) HoriZOl1lal axis (or elevatiol1 and depression. The stemal end o( the scapula is on the le(t. (From Schenkmal1 and Ru go de Cartaya!S with permissiol7.)

lar facets and the presence of an intra-articular meniscus.5 8 The AC joint capsule is more lax than the sternoclavicular joint; thus a greater degree of movement occun; at the AC joint. contributing to the increased incidence of dislocations.5 8 There are three major supporting ligaments to the AC joint. The conoid and trapezoid ligaments are col­ lectively called the coracoclavicular ligament and the acromioclavicular ligament. It is through the conoid and trapezoid ligaments that scapula mo­ tion is translated to the clavicleS Rotation of the clavicle is the major move­ ment at the AC joint. Steindlel.59 joint rotation occun'ing around three axes. Lon­ gitudinal axial rotation. vertical axis for protrac­ tion and retraction. and horizontal axis for eleva­ tion and depression (Fig. 1. 10) are all controlled and facilitated by the conoid. trapezoid. and acromioclavicular ligaments.

ScapukJtJwracic Jaint The scapulothoracic joint is not an anatomic joint. but it is an important physiologic joint that adds considerably to motion of the shoulder gir­ dle. The scapula is concave. articulating with a convex girdle.1.55 The scapula is without bony

or ligamentous connections to the thorax. except for its attachments at the acromioclavicular joint and coracoacromial ligament. The scapula is pri­ marily stabilized by muscles. The importance of the scapula rotators has been established as an essential ingredient to glenohumeral mobility and stability (Fig. 1. 1 1). The stable base. and therefore the mobility of the glenohumeral joint. is largely dependent on the relationship of the scapula and the humerus. The scapula and hu­ merus must accommodate the ever-changing po­ sitions during shoulder movement in order to maintain stability6

Punctional Bimnechanics As previously noted. shoulder elevation is de­ fined as the movement of the humerus away from the side. and it can occur in an infinite number of body planes.41 Shoulder elevation can be divided into three phases. The initial phase of elevation is 0' to 60' degrees. The middle or "critical phase" is 60' to 140'. The final phase of elevation is 140' to 180'. Specific to each phase of movement. precise muscle function and joint kinematics allow nor­ mal pain-free motion. Analysis of the precise

FUNC TIONAL

A

ANATOMY

AND

MECH ANICS

11

B

Force couple o{ /IIuscles aClillg 01 scapula (A) Axis o{ scaplliar rotalioll {rol1l 0°10 30� (8) Axis o{ scapular rOlalion {rol1l 30°10 60° (FUT' (orce o{ upper lrapezius; FLT, force of lower lrapezius; F SA force o{ serralus anlerior.) (Modified (rol11 Schel1kl11al1 al1d Ruga de Cartaya,65 wilh perl11issiol1.) FIGURE 1. 1 1

components critical for each phase of shoulder elevation will determine the success of clinical management of shoulder dysfunction. ° ° INITIAL PHASE OF ELEVATION: 0 TO 60

All three arthrokinematic movements occur at the glenohumeral joint, but they do not occur in equal proportions. These movements-roll, spin, and glide-are necessary for the large hu­ meral head to take advantage of the small gle­ noid articulating surface.'· Saha·o and Sharkey and Marder·' investigated the contact area be­ tween the head of the humerus and the glenoid with elevaLion in abduction and in scaption. The studies found that the contact area on the head of the humerus was centered at 30· and shifted superiorly 1.5 mm by 120°. Poppen and Walker14 also studied the instant centers of rotation for abduction. They reported that in the first 30· and orten between 30· 60· of abduction, the head of the humerus moved superiorly in the glenoid by 3 mm, indicating that rolling or gliding of the head had occUlTed. The EMG activity of the su-

praspinatus muscle indicates an early rise in ten­ sion, producing a compressive force to the gleno­ humeral joint surface. The deltoid muscle also demonstrates EMG activity in the initial phase of elevation. The sub­ scapularis, infraspinatus. and teres minor mus­ cles are important stabilizers of the humerus in the initial phase of elevation.' Kadaba et al.SJ re­ port EMG activity of the upper and lower por­ tions of the subscapularis muscle recorded by intramuscular wire electrodes. During the initial phase of elevation, EMG activity of the upper subscapularis was greater at the beginning of the range, while that in the lower subscapularis in­ creased as the elevation reached 90·." A signifi­ cant amount of force is generated at the glenohu­ meral joint during abduction4.15 In the early stages of abduction, the loading vector is beyond the upper edge of the glenoid.·2 During the initial stage of elevation, the pull of the deltoid muscle produces an upward shear of the humeral head.' This shearing force peaks at 60· o[ abducLion and is counteracted by the transverse compressive [orees of the rotator cuff

12

PHY S I CAL

THERAPY

OF

THE

SHOULDER

muscles.3.1S The primary function of the sub­ scapularis muscle is to depress the humeral head, counteracting the superior migrating force of the deltoid.53 At 60° (abduction), the down­ ward (short rotator) force was maximal at 9.6 times the limb weight or 0.42 times the body weight. 2 .15 The subscapularis, infraspinatus, and latissimus dorsi muscle have small lever arms that form 90° angles to the glenoid face, produc­ ing compressive forces to the joint. Movement of the scapula is permitted by movement in the AC and SC joints. Shoulder ab­ duction is accompanied by clavicular elevation. Sternoclavicular elevation is most evident dur­ ing the initial phase of aim elevation. There are 4° SC movement for each 10° of shoulder abduc­ tion' The acromioclavicular joint moves pri­ marily before 30° and after 135°.4 The instantaneous center of rotation (lCR) of the scapula during the initial phase of eleva­ tion is located at or near the root of the scapula spine in line with the SC joint."3 The initial phase of arm elevation is refelTed to by Poppen and Walkerls as the selling phase; scapula rotation occurs about the lower midportion. The relative contribution fTom scapular rotation dUl;ng the initial phase of elevation is considerably less than from glenohumeral motion. Bagg and For­ est"3 estimated a 3.29 to I ratio of glenohumeral to scapulothoracic mobility during the initial phase of elevation. The upper trapezius and lower serratus antedor muscles provide the nec­ es ary rotatory force couple to produce upward scapular rotation during the early phase of arm abduction."3 MIDDLE OR CRITICAL PHASE OF ELEVATION:

60° TO 1000

The middle or critical phase of elevation is initi­ ated by excessive force at the glenohumeral joint. As previously noted, the shearing force of the del­ toid muscle is maximum at 60° elevation (Fig. 1.12). Wuelker et al.54 simulated muscle forces under the coracoacromial vault. The forces at the glenohumeral joint were recorded and applied to the shoulder muscles at a constant ratio ap­ proximating physiologic conditions of shouldel-

..,"

FIGURE 1.12 [" the early stages of glenohumeral abduction, the deltoid reactive force (D) is localed outside the glel10id fossa. This force is counteracted by (he transverse compressive forces of the supraspinatus (S) and infraspi"atus (I) lIIuscies. The resu/talll reactive force (R) is therefore 1II0re favorably placed within the glenoid fossa for joint stability.

elevation: deltoid, 43 percent supraspinatus, 9 percent; subscapularis, 26 percent; and infra­ spinatus/teres minor, 22 percent (Fig. 1.13). Peak forces under the coracoacromical vault OCCUlTed between 51° and 82° of glenohumeral joint eleva­ tion. These force values may represent the patho­ mechanics of shoulder impingement. The resultant acting forces, which are stabi­ lizing to the joint, are maximum at 90° of eleva­ tion,3 with shear and compressive forces equal"' As the arm reaches the end of the critical phase, the resultant force and the shearing forces of the deltoid are almost zero.'·1S Dynamic stability of the glenohumeral joint is established by the balance of shearing and compressive forces. In the early part of the criti­ cal phase, dynamic stability must be initiated be­ fore further progression of pain-fTee movement can occur. As previously noted, the lower fibers of the subscapularis muscle showed more activ­ ity at 90° of abduction.53 The deltoid muscle reaches maximum EMG activity at about 110° of abduction and maintains a plateau level of activ­ ity.3 Supraspinatus EMG activity peaks at 100° of elevation and rapidly diminishes thereafter.' The subscapularis activity decreases substan-

FUNCTIONAL

FIGURE 1.13 Force cOl/pie o( deltoid al1d rotalor cuff muscles. ROlalory (orces, aClirlg all Opposile sides o( axis o( malian, combine 10 produce upward rOlaliol1. Trallslalory (orces cancel each olher auI. ( FRR rolalOlY (orce o( rolator cuff; FTR, translatory force of rotator cuff; FRO, rolalory (orce o( delloid; FTO, lrallslatory (orce o( deltoid.) {Modified (rom Schenkmal1 and de Carlaya,65 wilh pemlissioll.)

tially after 130° of elevation, supporting the con­ cept that antelior ligament stability is critical be­ yond 130° of elevation.' The head of the humerus demonstrates an excursion of I to 2 mm of a superior and inferior glide on the glenoid surface. I' The movement of the humeral head in a superior and inferior di­ rection after 60' of elevation indicates that a roll and glide is occun·ing in opposite directions, re­ sulting in a spin of the bone. As previously noted, external rotation of the humerus is critical for elevation (abduction) of the arm. 8agg and Fon·est63 evaluated 20 subjects and found three distinctive patterns of scapulohum­ eral movement. Each pattern had three phases with varying ratios of humeral to scapular move­ ment. The most common paltern had 3.29' of

ANATOMY

AND

MECHANICS

13

humeral motion to every degree of scapular mo­ tion from 20.8' to 8 1.8' scaption. The humeral component decreased to 0.71' for scaption be­ tween 81.8° and 139.1°. Therefore, the greatest relative amount of scapular rotation occurs be­ tween 80° and 140' of arm abduction63 The ratio of glenohumeral to scapulothoracic motion has been calculated to be 0.71 to I during the middle phase of elevation.64 Doody et al.,'2 along with Freedman and Munro," proposed that the sig­ nificant role of the scapular rotators during the critical phase of elevation is secondary to the rel­ atively long moment arms of the upper trapezius, lower trapezius, and lower serratus anterior muscles. Therefore, during the middle phase of elevation, the scapula rotators provide an impor­ tant contribution to elevation of the humerus in the plane of the scapula. Movement of the scapula is permitted by movement of the acromioclavicular and sterno­ clavicular joints. The relative contribution of these two joints changes throughout the range of motion depending on where the instant center of rotation (ICR) lies.63 DUling the middle phase of abduction, the ICR of the scapula begins to migrate towards the AC joint. Clavicular eleva­ tion about the SC joint, coupled with scapular rotation about the AC joint, facilitates normal scapular mobility. Motion can occur at the AC joint with less movement occuning at the SC joint, because of the clavicular rotation around its long axis.' The double-curved clavicle acts like a crankshaft permitting elevation and rota­ tion at the AC end. The rotation of the scapula about the AC joint is initiated between 60° and 90' of elevation63 Clavicular elevation is com­ pleted between 120° and 150° of humeral abduc­ tion63 Clavicular elevation at the AC joint per­ mits maximum scapular rotation. At approximately ISO' of elevation the ICR of the scapula is in line with the AC joint.63 0 0 FINAL PHASE OF ELEVATION: 140 TO 180

During the final phase of elevation, the ratio of glenohumeral to scapulothoracic motion is 3.49 to I, indicating relatively more glenohumeral motion63 The ICR of the scapula has relocated

14

PHYS I CA L

THERAPY

OF

THE

S H OULDER

upward and laterally. The rotatory force arm of the upper trapezius muscle has reduced in length, and the role of this muscle is now suppor­ tive to the scapula64 The new location of the ICR of the scapula allows the middle trapezius to be­ come a prime mover for downward scapular 1'0· tation64 The lower trapezius and the serratus an­ terior muscles continue to increase in activity during the final phase of elevation, acting as an upward rotator and opposing the forces of the upper and middle trapezius.63 As the humerus elevates towards the end of the elevation range of motion, it must disengage itself fTom the scapula. As previously noted, the ratio of glenohu meral to scapulothoracic motion is 3.49 to I . Good extensibility of the latissimus, pectoralis major, teres major, teres minor, infra­ spinatus. and subscapularis muscles is impor­ tant in order to allow the humerus to disasso­ ciate itself from the scapula. Often with passive humeral elevation, a bulge of the scapula is noted laterally. The bulge is usually the inferior angle, secondary to increased protraction of the sca­ pula. Lack of elongation of these muscles pre­ vents the normally dominant movement of the humerus at the end of the elevation range. l often observe tightness of the subscapularis muscle, teres major muscle, or both. Furthermore, observation of limited passive humeral elevation may exhibit elevation of the chest cavity. If muscles connecting the humerus and rib cage are not Ilexible enough, movement will occur at both ends. The latissimus and pec­ toralis major muscles connect the humerus to the rib cage. Lack of dissociation of the rib cage from the humerus will result in excessive rib cage mobility in passive terminal elevation.

Summary oj SIuruJJJ.er Phases oj Mavenumt The initial phase of elevation occurs predomi­ nantly at the glenohumeral joint. A 3-mm supe­ rior glide of the humeral head has been observed in the initial phase of elevation. The activity of the deltoid muscle produces this superior shear-

ing force at the glenohumeral joint. The activity of the supraspinatus, infraspinatus, teres minor, and subscapularis muscles counteract the forces of the deltoid muscle, creating a resultant force that is stabilizing to the joint and necessary for full pain-free movement to continue. The result­ ant force in the nOlmal glenohumeral joint is maximum at 90° of elevation. The early phase of scapula movement is described as the selling phase, with the majority of movement OCCUlTing at the glenohumeral joint. The middle phase of elevation is referred to as the critical phase. At the beginning of the criti­ cal phase, maxjmum shearing forces of the del­ toid muscle occur. The ratio of glenohumeral to scapulothoracic movement shifts, emphasizing the laller. The increased scapula movement is established by the activity of the upper and lower trapezius and lower anterior en-alus mll des. The arthrokinematic movement of the head of the humerus on the glenoid has been observed as an inferior and superior glide of 1.5 mm. During the final phase of elevation, the movement is once again dominated by the gleno­ humeral joint. Good extensibility of the latissi­ mus, pectoralis major, teres major, teres minor, and subscapularis muscles is necessary to allow the increased and unconstrained movement of the humerus away fTom the scapula.

Summary Patients with shoulder dysfunction are routinely treated in the physical therapy clinic. An under­ standing of the anatomy and biomechanics of this joint can help provide the physical therapist with a rationale for evaluation and treatment. Most studies involving shoulder anatomy and bi­ omechanics reveal a common pallem along with a wide variation among subjects. The physical therapist should keep this variation in mind when treating an individual patient. Treatment may be directed toward restoring mobility, providing stability, or a combination of the two. The shoulder is an inherently mobile complex, with various joint surfaces adding to

FUNCTION A L

the freedom of movement. The shallow glenoid with its flexible labrum and large humeral head provides mobility. At times, this vast mobility oc­ curs at the expense of stability. The shoulder re­ lies on various stabilizing mechanisms, includ­ ing shapes of joint surfaces, ligaments, and muscles to prevent excessive motion. Nearly 20 muscles act on this joint complex in some man­ ner, and at variolls limes can be both prime mov­ ers and stabilizers. Harmonious actions of these muscles are necessary for the full function of this joint.

ANA TOMY

AND

M E C H A N I CS

15

I I . Calliet R: Shoulder Pain. FA Davis, Philadelphia, 1 966 1 2 . Doody SG, Freedman L, Waterland JC: Shoulder movements during abduction in the scapular plane. Arch Phys Med Rehabil 5 1 d : 595, 1 970 1 3 . Saha AK: Mechanics of elevation or glenohumeral joint. Acta Orthop Scand 44: 6688, 1 973 1 4. Poppen NK, Walker PS: Forces at the glenohu­ meral joint in abduction. Clin Ol1hop 1 35: 1 65 , 1 978 1 5 . Poppen NK, Walker PS: Normal and abnormal motion or the shoulder. J Bone Joint Surg 58A: 1 95 , 1 976 1 6 . Saha AK: TheOl)' of Shoulder Mechanism: De­ scriptive and Applied. Charles C Thomas, Spring­ field, I L , 1 96 1 1 7. Codman EA: The Shoulder. Thomas Dodd, Bos­ 'on. 1 934

We give special thanks to Martha Kaput Frame for her contributions to this chapter.

1 8. Kondo M, Tazoe S, Yamada M: Changes of the tilting angle of the scapula rollowing elevation of the arm. In Ga.eman JE, Welsh RP (eds): Surgery of the Shoulder. Philadelphia. CV Mosby. 1 984 1 9. Williams PE, Goldspink G: Changes in sarcomere

References

Icngth and physiological propcl-tics in immobi­ lized muscle. J Ana. 1 27 : 459, 1 978 20. Tabu.), JC, Taba.), C. Tardieu C et al: Physiologi­

I . Kent BE: Functional anatomy of the shoulder complex. A review. Phys Ther 5 I :867. 1 97 1 2 . Lucas 0: Biomechanics orthe shoulder joint. Arch Surg 1 07:425, 1 973 3. SalTafian SK: Gross and functional anatomy of the shoulder. Clin Orthop Rei Res 1 73 : II , 1 983 4. Inman VT. Saunders M , Abbotl LC: Observations on the function of the shouldcrjoinl. J Bone Joint Surg 26A: 1 , 1 944 5. Dempster Wf: Mechanism of shoulder move­ ment. Arch Phys Med Rehabil 46A:49, 1 965 6. Moseley JB et al: EMG analysis of the scapular muscles dllling a shoulder rehabilitation pro­ gram. Am J Spo.1S Med 20: 1 28, 1 992 7. Bechtol C: Biomechanics of the shoulder. Clin Or­

thop 1 46:37, 1 980 8. JohnsLOn TB: Movements or the shoulder joint: plea ror use of "plane of the scapula" as plane or

cal and structural changes in the cat's soleus mus­ cle due (0 immobilization at di fferent lengths by plaste.· casts. J Physiol 224:23 1 , 1 972 2 1 . Tardieu C , Huet E, BreL M D et a l : Muscle hypoex­ tensibility in children with cerebral palsy, I . Clini­ cal and experimental observations. Arch Phys Med Rehabil 63:97, 1 982 22. Lucas 0: Biomechanics o f the shoulderjoint. Arch Surg 1 07:425, 1 973 23. Soderberg GJ. Blaschak MJ: Shoulder in.ernal and external rotation peak torque production through a velocity spcCl!um in di ffering positions. J Orthop Sports Phys Ther 8:5 1 8 , 1 987 24. Hellwig EV, Perrin DH: A comparison of two posi­ tions for assessing shoulder rotator peak torque: the traditional frontal plane versus the plane o f .he scapula. [sokin Exerc Sci 1 : 202. 1 99 1 25. Greenfield BH, Dona.elli R , Wooden MJ, Wilkes

reference for movements occUlTing at humero­

J: lsokinetic evaluation of shoulder rotational

scapula joint. Br J Surg 25:252, 1 937

strength between the plane of the scapula and the

9. Townsend H . Jobe F, Pink M , Pen), J : Electromyo­

fTontal plane. Am J SpO.1S Med 1 8: 1 24. 1 990

graphic analysis of the glenohumeral muscles

26. Tata EG, Ng L, Kramer IF: Shoulder antagonistic

during a baseball rehabilitation program. Am J

strength I"alios dudng concentric and eccentric

Sports Med 1 9:264, 1 99 1 1 0. Wa.wick R, Williams P (eds): Gray's Anatomy. 35.h British Ed. WB Saunders. Philadelphia. 1 973

muscle actions in the scapular plane. J Orthop Sports Phys Ther 1 8:654, 1 993 27. Whitcomb W. Kelley MJ. Leiper CI: A comparison

16

PHYSICAL

THERAPY

O F

THE

S H O UL D E R

o f torque production during dynamic strength

42. Fl'eedman L, Munro Rl-I: Abduction of the arm

testing of shoulder abduction in the coronal plane

in the scapular plane: scapular and glenohumeral

and the plane or the scapula. I Ol1hop SpOl<S Phys

movements, A roentgenographic study. J Bone Joint Surg 48A: 1 503, 1 966

Ther 2 1 :227, 1 995 28. Rajendran K: The rotary innucnce of articular

43. Kapanji [A: The Physiology or the Joints- Upper

contours during passive glenohumeral abduction.

Limb, Vol 1 . Churchill Livingstone, New York,

Singapore Med J 33:493, 1 992 29. An KN, Browne AO, Korinek S et al: Three-dimen­ sional kinematics of glenohumeral elevation. J Or­ thop Res 9: 1 43 , 1 9 9 1 3 0 . Oti

J C , liang CC, Wickiewicz TL e l a l : Changes

in the momcnt arms of the l"otatorcufr and deltoid muscles with abduction and rotation. J Boneloint Surg 76-A:667, 1 994 3 1 . Flatow EL, Soslowsky U, Ticker J8: Excursion or the rotator cuff under the acromion: patterns of subacromial contact. Am J Spons Med 22:779, 1 994 32. Rajendran K, Kwek BH: glenohumeral abduction and the long head or the biceps. Singapore Med 1 32:242, 1 99 1 33. Brems JJ: Rehabilitation following lOlal shoulder arthroplasty. Clin Ol1hop 307:70, 1 994 34. TefT), GC, Hammon D, France P et al. The stabiliz­ ing function of passive shoulder restraints. Am J Sports Med 1 99 1 ; 1 9:26-34

1 970 44. Basmajian J : The surgical anatomy and function of the aml-tnmk mechanism. Surg Clin North Am 43 : 1 475, 1 963 45. Turkel SI, Panio MW, Marshall JL, Girgis FG: Sta­ bilizing mechanisms preventing anledor disloca­ tion of the glenohumeral jOint. J Bone Joint Surg 63A: 1 208, 1 98 1 46. MacDonald PS, Hawkins RJ, Fowler PJ, Miniaci A: Release of the subscapularis for intemal rota­ tion contracture and pain after antel-ior repair for ,'ccun'cm antedor dislocation of the shoulder. J Bone Ioint Surg 74A:734, 1 992 47. Itoi E, Kuechle DK, Newman SR, MUlTey BF, Am Koy et al: Stabilizing function of the biceps in sta­ ble and unstable shoulders. J Bone Joint SlIrg Br 75:546, 1 993 48. Warner JJ, Deng XH, WalTen RF, Torzilli PA: Static capsuloligamentolls dor-infel-ior

translation

rcstraints to supc­

of the

glenohu meral

joint. Am J SpOJ<S Med 20:675, 1 992

35. Saha AK: Dynamic stability of the glenohumeral joint. Acta 011hop Scand 42:49 1 , 1 97 1 36. Kessell L: Clinical Disocders or t h e Shoulder. 2nd Ed. Churchill Livingstone, Edinburgh, 1 986 37. Moseley I-IP. Overgaard B: The anterior capsular

49. Guanche C, Knatt T, Solomonow M et al: The syn­ ergistic action of the capsule and the shoulder muscles. Am J Sports Med 23: 1 995 SO. Hanyman DT, Sidles JA, Han-is SL, Matsen FA: The role of rotator interval capsule in passivc mo�

mechanism in reCUITent anterior dislocations of

tion and stability of the shoulder. J Bone Joint

the shouJder: mm'phological and clinical studies

Surg 74A:53, 1 992

with special reference to the glenoid labrum and glenohumeral ligaments. J Bone Joint Surg 448: 9 1 3 , 1 962 38. Bowen MK. Russell FW: Ligamentous control of shoulder stability based on selective CUlling and static translation experiments. Clin Sports Med 1 0:757, 1 9 9 1 39. Reeves B : Expcdmcnts i n t h e tensile strength o f the an terior capsular structures o f t h e shoulder i n man. J Bone Joint Surg 50B:858, 1 968 40. Matsen FA, Lippitt SB, Slidies IA et al: Stability. In Matson FA, Lippitt SB, Slides JA et al. (eds): Practical

Evaluation and

Management of the

Shoulder. WB Saunders, Philadelphia, 1 993 4 1 . Pagnani MJ, Galinat BJ, Warren RF. Glenohu­

5 1 . KlImmeil BM: Spectrum of lesions of the anterior capsular mechanism of the shoulder. Am J Sports Med 7 : 1 1 1 , 1 979 52. Travel l I, Simons D: Myorascial Pain and Dys­ function. Thc T';gger Point Manual. Williams & Wilkins, Baltimore, 1 993 53. Kadaba M P , Cole MF, Wooten P et al: [ntramus­ cular wire electromyography of the subscapularis. I OJ L. Extension: Full range. Pulls anterior cervical spine.

176

PHYS I CAL

THERAPY

OF

THE SHO U LDER

Rotation: (R): Full range. Pulls L supraclavicular region. Rotation: (L): 80°. Pulls right cervical spine and pain left trap. S H O U L D E R F L E X I O N

(R) (with elbow extension): 1 35° pulling whole arm to thumb. (R) (with elbow flexion): 1 80°. (L) (with elbow extension): 1 1 0° pulling whole arm to thumb. (L) (with elbow flexion): 1 35° pulling into the upper arm. U P P E R L I M B T E N S I O N T EST

Recorded in sequence of examination to tension point. (R): I/wnl; 2/80°; 3/45°; 4/wnl; 5/wnl; 6/1 20° with pull in right thumb. (L): I /wnl; 2/60°; 3/30°; 4/wnl; 5/wnl; 61 1 50° with pull in left arm. B R E A T H I N G PATT E R N

Paradoxical with early scalene contraction on quiet inspiration, right more than left. PALPATION

Sensitive scalenes on right compared to the left. S T R E N G T H

Flexor carpi ulnaris: (R) 4/5, (L) 515. Adductor pollicis: (R) 4/5, (L) 515. E F F E C T O F T R I A L S E L F C E RVICAL T R A C T I O N (KABAT)

Results in increase strength of right thumb and ulnar wrist flexion. Testing reveals that the me­ chanical sensitivity is from compression through the top of the head." Thoracic spine, cervical spine, and rib cage: Pos­ tural dysfunction in flexion with elevated first rib bilateral.

ASSESSMENT

.I. C37 motor root irritability on the right.

2. Findings suggestive of plexus irritability bi­ laterally, right greater than left, with ele­ vated first rib on the right and left ancl para­ doxical breathing pattern. 3. Postural factors influencing the problem. 4. Cervical and upper thoracic dysfunction in flexion. TREATMENT PLAN

I . Instruct in "what is wrong" and use home kit for treating upper quarter neurovascular entrapments.

2. Progress through the home program ap­ proach to dealing with these dysfunctions beginning with the Kabat protocol and pro­ gressing through the diaphragmatic brealh­ ing, thoracic and rib mobilization. 3. Restoration of the relaxation and warming response during repeated movements of the upper extremity. 4. Train in protective body mechanics to mini­ mize stress from work. 5. lnitial modification of work sched ule; no overtime; no lifting; awareness of posture; no sitting with legs crossed; feet flat on noor. Posture instruction. RESULTS AND DISCUSSION

This case history was chosen to illustrate that findings present in severe cases of neurovascular entrapment are evident early in the history. The problem is that if they are not looked for they will often be missed. I f addressed early, they dis­ appear rapidly, and one has a clear picture of the relevance of these findings. When the patient can also see the relationship between the findings and their ability to change those findings, this reinforces the issues they need to address to gel well and stay well. There is much yet to learn with these problems. For example: Was this an example of a progression of a problem that clearly involved the cervical

TR A U M A

D ISOR D ERS

spine following the auto accidents but now was involving other tunnels as well? The initial treatment involved self cervical traction (Fig. 6.6) and breathing. The result in 24 hours was to abolish the right wrist pain, but now she complained of left wrist pain due to using the leFt wrist and hand for self-traction. Examination of the left wrist uncovered slight carpal dysfunction secondary to the recent rollerblade Fall on the wrists. Self-mobilization of the left wrist cleared that complaint in 24 hours and it did not return. Progression of treatment through the foam rollers and selF-mobilization of the neural tissues cleared all symptoms, and she has re­ mained free of any arm symptoms For 6 months. Slight ongoing neck discomfort associated with stress from data entry is relieved with the home program.

A F F EC T I N G

THE

T H OR A C I C

O U T LET

177

4. Sanders RJ, Ratzin Jackson CG, Banchero N, Pearce WH: Scalene muscle abnolmalities i n trau­ matic lhoracic outlet syndrome. 1 59:23 I , 1 990

5. Kandel ER, Schwal1 z J H : Plinciples of Neural Sci­ ence, Edward Arnold, London, 1 98 I

6, Phillips H, Grieve GP: The thoracic outlet syn­ drome. p. 359. In Grieve G (cd): Modern Manual Therapy of Ihe Vel1ebral Column. Churchill Liv­ ingslone, New York, 1986

7, Sanders J, Haug CE: Thoracic OUllet Syndrome. Philadelphia, JB Lippincott, 1 99 I

8. Pratt NE: Neurovascular entrapment in the re­ gions of the shoulder and postel;or triangle of the neck, Phys Ther 48: I 894, 1 986

9. Karas S: Thoracic outlet syndrome. Clin SPOlts Med 9:297, 1 990

1 0. Lord !W, Rosati LM: Thoracic-outlet syndromes. Clinical Symposia, CrnA Pharmaceutical Com­ pany, Summit, N, 1 97 I

1 J . Edgelmv Pl: Thoracic oUllet syndrome: a patient centered

treatment

approach.

p.

1 32.

In

Shackloch MO (cd): Moving in on Pain. Butter­ worth-Heinemann, Sydney, 1 995

1 2 . Butler 0: Mobilisation of the Nervous System, Churchill Livingstone, London, 1 99 1

1 3 . Gi fford L : Fluid movement may partially account

Summary

for the behaviorof symptoms associated with noc­ iceplion in disc injury and disease. In ShackJock M (ed): Moving in on Pain. Butterworth-Heine­

Even though diagnostic procedures are more thorough and treatment is growing more sophis­ ticated, much additional research is needed to aid in devising improved evaluation and treat­ ment procedures for the TOS patient. The ability to change symptoms and signs early in the cOurse of the condition needs to be followed over time to see if early intervention will have a long­ term afFect on the course of the pathology.

man, Sydney, 1 995

1 4 . Nichols H M : Anatomic slnlct ures of the thoracic outlet. Clin Ol'lhop 207: I 3, 1986

1 5. Peet RM, Hemiksen ro, Anderson TP, Mal1in G M : Thoracic outlet syndrome. Mayo Clinic Proc 3 1 :

2 8 1 , 1 956 1 6. Lindgren KA, Leino E: Subluxation of the first l'ib: A possible thoracic outlet syndrome mechanism. Arch Phys Med Rehabil 68:692, 1988

1 7. Celcgin Z: Thoracic outlet syndrome: What does it mean for physiotherapists? p. 825. In Proceed­ ings of IXth Congress World Confederation for

References

Physical Therapy, Stockholm, 1 982 1 8. Elvey RL: The investigation of arm pain. p. 530. I n Gl'ieve G (ed): Modem Manual Therapy of the

1 . Sunderland S: Sixth biennial conference proceed­ ings, Manipulative Therapists Association of Aus­ tralia. Adelaide, t 989

Vertebral Column. Churchill Livingstone, New York, 1 986

1 9 . Sallstrom J, Schmidt H: Cervicobrachial disor­

2. Roos DB: New concepts of thoracic olltlet syn­

ders in cCl1ain occupations with special reference

drome that explain etiology, symptoms, diagnosis

to compression in the thoracic oUllet. Am J Ind

and treatment. Vase Surg 1 3 :3 1 3 , 1 979

3. Telford ED. Mottershead S: The "costoclavicular syndrome." 1 :325, 1 947

Med 6:45, 1 984

20. Hursh LF, Thanki A: The thoracic outlet syn­ drome. PosIgrad Med 77: 1 97, 1 985

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2 1 . Crawford FA: Thoracic outlet syndrome. Surg Clin NOI�h Am 60:947, 1 980 22. Kabat H : Low Back and Leg Pain from Herniated CClvical Disc. St. Louis, Warren H. Green, 1 980

23. Adson AW: Surgical treatment for symptoms produccd by cervical ribs and the scalenus anticus muscle. Surg Gynecol 85:687, 1 947 Reprinted in Clin Orthop 207:3, 1 986

24. Wood VE. Twito R. Verska JM: Thoracic outlet syndrome. The results of first db resection in 1 00 patients. Ol1hop Clin North Am 1 9 : t 3 I , 1 988 25. Narakas A, Bonnard C, Egloff DV: The ceravico thoracic ouLlet compression syndrome. Analysis of surgical treatment. Ann Chir Main 5 : I 95, 1986

26. Upton ARM, McComas AJ: The double crush in nerve enlrapment syndromes. Lancet 2:359, 1 973

27. Osterman AL: The double crush syndrome. 01'thop Clin North Am 1 9: 1 47 , 1988

28. Liebenson CS: Thoracic outlet syndrome: Diagnosis and conselvative management. J Manipulative Physiol Ther I I :493, 1 988

29. Young HA, Hardy DG: Thor'acic outlct syndrome. Br J Hosp Med 29:457, 1 983

30. Roos DB, Owens JC: Thoracic outlet syndrome. Arch Surg 93:7 I , 1 966

3 1 . Et heredge S, Wilbur B, Stoney RJ : Thoracic outlet syndrome. Am J SUl'g 1 3 8 : I 75, 1 979

32. Karas S: Thoracic outlet syndrome. Clin Sports Med 9:297, 1 990

33. Riddell 0 1-1 , Smith 8M: Thoracic and vascular aspeeLs of thoracic outlet syndrome. Clin 011hop 207:3 I , 1 986 34. Machleder H I : Thoracic olltlet syndromes: New concepts f rom a century of discovery. Cardiovasc Surg 2 : 1 37 , 1 994

35. Pascarelli E, Quilter 0 : Repetitive Strain Injury: A Computer User's Guide. John Wiley & Sons, New York, 1 994

36. Baxter BT, Blackburn 0 , Payne K, Pcarche WH, Vao JST: Noninvasive evaluation of the upper extrcmity. Surg Clin North Am 70:87. 1 990 37. Sucher 8M: Thoracic outlet syndrome-A myofascial variant, 1. Pathology and diagnosis. JAOA 90:686, 1 990 38. Dawson OM, Hallett M, Millender LH: Thoracic oUllet syndromes i n Entrapment Neuropathies. LiLLIe, Brown, BaSion, 1983 39. Chodo.-off G, Dong WLG, Honet JC: Dynamic approach in the diagnosis of thoracic Olillet syndrome using somatosensory evoked responses. Arch Phys Med Rehabil 66:3, 1985 40. Pavot AP, Ignacio DR: Value of in frared imaging in the diagnosis of thoracic outlet syndrome. Thcm1ology 1 : 1 42 , 1 986

4 1 . McNair JFS, Maitland GD: Manipulative therapy technique in the management of some thoracic syndromes. In Grant R (cd). Physical Therapy of the Celvical and Thoracic Spine. Churchill Livingstone, New York, 1988

Evaluation and Treatment of Brachial Plexus Lesions B Rue E D 0 R I E

H . B

•

GREENFIELD 5 YEN

The brachial plexus supplies both motor and sen5011' innervation to the upper extremities and re­ lated shoulder girdle structures. Lesions to the brachial plexus compromise the neurologic in­ tegrity, and hence the function, of the shoulder and related upper extremity. Evaluation ofshoul­ der dysfunction should include an assessment of the integrity and functional status of the brachial plexus. The complex structure of the brachial plexus requires a thorough understanding of the multiple i nnervation patterns to the various mus­ cles. An understanding of the mechanisms of in­ juries to the brachial plexus, pathophysiologic changes of nerve fibers and nerve roots, and po­ tential for recovery is essential for proper and ef­ fective clinical management. Therefore, this chapter provides a review of the anatomy of the brachial plexus, classification of brachial plexus injuries, description of pathomechanical and pathologic changes to the specific nerve fibers and nerve roots, and a reviewof a c1arifying evalu­ ation to assess the nature and extent of brachial plexus lesions. Clinical case studies offer a com­ bined physical and occupational therapy man­ agement ofa patient with a brachial plexus injury.

ArwJmny oj the Brachial Plexus The anatomy of the brachial plexus is divided into a review of the gross anatomy of the plexus and its relationship to surrounding structures,

as well as a review of the microscopic anatomy of the nerve and nerve trunks. SUPERFICIAL ANATOMY

The brachial plexus comprises the anterior pli­ mary divisions of spinal segments C5, C6, C7, C8, and TI, as shown in Figure 7.1. The components of the brachial plexus include the following: 1. Undivided anterior primary rami 2. Trunks-upper, middle, lower 3. Divisions of the trunks-anterior and poste­ rior 4. Cords-lateral, posterior, and medial 5. Branches-peripheral nerves derived fTom the cords The segmental motor innervation of the brachial plexus to the muscles of the shoulder is shown in Figure 7.2. The anatomy of the plexus has been previously descl·ibed. I The fourth celvical nerve usually gives a branch to the fifth cervical, and the first thoracic nelve frequently receives one [Tom the second thoracic. When the branch from C4 is large, the branch from T2 is frequently ab­ sent and the branch fTOm T I is reduced in size. This constitutes the prefixed type of plexus. Con­ versely, when the branch fTom C4 is small or ab179

180

P H Y S I C A L

T H E R A P Y

Sponal nervez C·�

O F

T H E

Trunk3

tr_-:-12 Lesions may be described as preganglionic or postgangli­ onic. Preganglionic avulsion injuries indicate that the nerve root has been torn from the spinal cord and preclude the possibility of recovery. Post ganglionic lesions may be either in continu-

TABLE 7.1.

Etiologic classificatiol1 of brachial

plexus il1juries as related to the shoulder and cervical spine Traumatic Open injuries Fractures Closed injuries Fractures Obstetric Postnatal exogenous Sports injuries (e.g. 'bumer' syndrome, shoulder dislocations) Compression Exogenous (sometimes isolated branches) Anatomic predisposition (sometimes isolated branches) Genetically determined (sometimes isolated branches) Posture (muscle imbalances/spasms) Tumors Primory tumors of brachial plexus Secondary involvement of plexus by tumors of surrounding tissues Vascular local vascular processes or lesions Participation in generalized vasculopothies (e.g., polyarteritis no· doso and lupus erythematosus) Physical fadars Radiotherapy Electric shock Infectious, inAammatory, and toxic processes Involvement of local sepsis Viral or infectious Cryptogenic (neuralgic amyotrophy) Para infectious Related to serum therapy Genetic predisposition Cryptogenic (Modified (rom Mwuellflwier el al,9 with penuissioll.)

ity (root and sheath intact) or IUptured (root in­ tact and nerve sheath IUptured).4 Spontaneous recovery may occur with the first injury; but without surgical repair of the IUpture, no recov­ ery will occur i n the second lesion. Finally, the postganglionic avulsion is classi­ fied as either supraclavicular, which involves Ihe tlUnks and divisions of the plexus, or infraclavic­ ular, which involves the cords and branches'> [n a se,-ies of 420 brachial plexus cases that under­ went operations, Alnot reported that 75 percent were supraclavicular lesions and 25 percent were infTaclavicular lesions.' SUPRACLAVICULAR LESION

Isolated supraclavicular lesions affect the upper, middle, or lower llUnks of the brachial plexus. However, according to Alnot, in his series of pa­ tients, 15 percent of the supraclavicular lesions were double level, affecting two Uunks, or com­ bined supraclavicular and infraclavicular le­ sions. These lesions occur when the arm is forced violently into abduction and the middle part of the plexus is blocked temporarily in the coracoid region. Terminal branches are torn away and concomitant supraclavicular lesions occur when Ihe head is jerked violently to the opposite side. Lower down in the plexus, the musculocuta­ neous nerve (which is tightly attached near the origin of the coracobrachialis muscle), the axil­ lary nerve in the quadrilateral space behind the shoulder, or the suprascapular nerve in the su­ prascapular notch of the scapula is entrapped and torn .>-6 UPPER TRUNK LESION

Palsy of the C5 and C6 roots of the brachial plexus is known as Erb's palsy or Duchenne-Erb paralysis.' The muscles affecled include the del­ toid, biceps, brachia lis, infraspinatus, supraspi­ natus, and serratus anterior. Also usually in­ volved are the rhomboids, levator scapula, and supinator muscles. Therefore, this injury causes severe restriction of movement at the shoulder and elbow joints. The patient is unable to abduct or externally rotate the shoulder. The patient

E V A L U AT I O N

A N D

T R E AT M E N T

cannot supinate the forearm because of weak­ ness of the supinator muscle. Sensory involve­ ment is usually confined along the deltoid mus­ cle and along the distribution of the musculocutaneous nerve. According to Comtet et al.7 partial or total spontaneous recovery of traumatic Duchenne-Erb paralysis is a frequent occurrence. The delay between the injury and re­ innervation of the con'esponding muscle varies From 3 to 24 months. Therefore, long.term reha­ bilitation with periods of reevaluations is imper­ ative. MIDDLE TRUNK LESION

The middle trunk receives innervation from the C7 nerve root and courses distally to form a major portion of the posterior cord" The middle trunk offers a major neural contribution to the radial nerve. Therefore, a lesion affecting the middle trunk of the brachial plexus weakens the extensor muscles of the arm and forearm, ex­ cluding the brachioradialis, which receives pri­ mary innervation from the C6 nerve rool. Sen­ sory deficit occurs along the radial d istribution of the posterior arm and forearm and along the dorsal radial aspect of the hand. Brunelli and Brunelli found I 1 percent of a total series of bra­ chial plexus injuries were isolated lesions to the middle trtlOk 8 Middle trunk lesions were pro­ duced by trauma to the shoulder in an anteropos­ terior direction. LOWER TRUNK LESION

The lower trunk of the brachial plexus receives innervation from nerve roots C7 and Tl. There­ fore, injury to the lower trunk known as Dejerine KJumpke, affects motor control in the fingers and wrisl. The extent of disability is determined by whether the plexus is prefixed or postfixed. The intrinsic muscles of the hand are only slightly affected in a lesion involving a prefixed plexus, whereas paralysis of the flexors of the hand and forearm occur in a lesion to a post fixed plexus'" Sensory deficit is present along the ulnar border of the arm, forearm, and hand. Hor­ ner's syndrome occurs if the sympathetic fibers

O F

B R A C H I A L

P L E X U S

L ES I O N S

185

contained within the anterior primary ramus of TI are injured.' The sympathetic fibers of Tl provide motor control to the eye. INFRACLAVICULAR LESION

Infraclavicular lesions include injuries to the cords or the individual peripheral nerves of the brachial plexus. In Alnot's series of 105 patients with infTaclavicular brachial plexus injuries, 90 percent of the cases were seen in young people (15 to 30 years of age) after car or motorcycle accidents.' The causes included (l) anteromed­ ial shoulder dislocation, which caused most of the isolated lesions of the axillary nerve and the posterior cord; (2) violent downward and back­ ward movement of the shoulder, which caused stretching of the plexus; and (3) complex trauma with multiple fractures of the clavicle, scapula, or upper extremity of the humerus, which caused more diffused lesions affecting multiple cords and terminal branches. LATERAL CORD LESION

According to Alnot.' injury to the lateral cord is rare. Because the musculocutaneous nerve and the lateral head of the median nerve are affected, motor deficit consists of palsy of elbow flexion, associated with a deficit of muscle pronators of the foreal'm and wrist and finger flexors. When the lesion is proximal, the lateral pectoral nerve is injured, resulting in partial or total palsy of the upper portion of the pectoralis major muscle. Sensory deficit is localized at the foreann and at the thumb level. MEDIAL CORD LESION

Isolated injury to the medial cord is also rare. Upper medio-ulnar palsy results in injury that is total in the distribution of the ulnar nerve and only partial in the distribution of the median nerve, the flexor pollicis longus muscle, and the flexor digitorum profundus muscle of the index finger. Partial palsy of the lower portion of the pectoralis muscle results in injury to the medial pectoral nerve.s

186

P H Y S I C A L

T HE R A P Y

OF

T HE

S H O U L DE R

POSTERIOR CORO LESION

A posterior cord lesion involves the areas of dis­ tribution of the radial, axillary, subscapular, and thoracodorsal nerves. The lesion results in weak­ ness of the extensors in the arm, with impair­ ment of medial rotation and elevation of the arm at the shoulder.

PERIPHERAL NERVE LESION

Common peripheral nerve or branch injuries in­ clude, but are not limited to, lesions of the long thoracic nerve, axillary nerve, dorsal scapular nerve, and suprascapular nerve. I njuries to the dorsal scapular and suprascapular nerves are re­ viewed in Chapter 4

LONG THORACIC NERVE LESION

The long thoracic nerve originates from the ante­ rior primary rami of C5, C6, and C7 nerve roots after these nerves emerge from their respective intervertebral foramen. The nerve reaches the serratus anterior muscle by traversing the neck behind the brachial plexus cords, entering the medial aspect of the axilla, and continuing down­ ward along the lateral wall of the thorax.I Al­ though isolated injuries to the long thoracic nerve are rare, traumatic wounds or traction in­ juries to the neck that result in isolated weakness of the selTatus anterior muscle with winging of the medial border of the scapula are presumptive evidence of a long thoracic nerve lesion.2 Normal shoulder abduction and flexion results from a synchronized pattern of movements between scapula rotation and humeral bone elevation. Variations in the scapulohumeral rhythm in the l iterature have been repOl·ted.IJ-16 For every 15° of abduction of the arm, 10° occurs at the gleno­ humeral joint and 5° occurs from rotation of the scapula along the posterior thoracic wall. 13 The rotation of the scapula results from a force cou­ ple mechanism combining the upward pull of the upper trapezius muscle, the downward pull of the lower trapezius muscle, and the outward pull of the serratus anterior muscle.'6 Therefore, palsy of the serratus anterior muscle in the pres-

ence of a long thoracic nerve injury, during ab­ duction or flexion of the arm, results in partial loss of scapular rotation. The ability of the upper and lower trapezius muscles to temporarily com­ pen ate the loss of the serratus anterior muscle to externally rotate the scapula allows For close to full range (180°) flexion and abduction of the arm.17 However, these muscles quickly fatigue after four or five repetitions, resulting in signifi­ cant loss of full active shoulder flexion and ab­ duction range of motion.

AXILLARY NERVE LESION

The axillary nerve originates from spinal seg­ ments C5 and C6, travels to the distal aspect of the posterior cord of the brachial plexus, and ad­ vances laterally through the axilla. I The nerve bends around the posterior aspect of the surgical neck of the humerus to innervate the deltoid muscle and the overlying skin, as well as the teres minor muscle. The most frequent cause of isolated axillary nerve lesion is anteromedial shoulder d isloca­ tion.5.7 In 80 percent of cases, anteromedial dis­ location results in a neuropraxia of the axillary nerve, with total recovery in 4 to 6 months.5 Complete lesion to the axillary nerve results in loss of active shoulder abduction. Sensory changes include an area of anesthesia along the deltoid muscle. However, even in the presence of a total axillary nerve lesion, some active shoulder abduction and external rotation is possible. Re­ sidual shoulder abduction results from the ac­ tions of the supraspinatus and infraspinatus muscles, as well as the biceps muscle. The stabili­ zation of the humeral head by the supraspinatus muscle combined with the action of the long head of the biceps muscle allows, in some cases, full overhead abduction. SpeCifically, by exter­ nally rotating the aim, the patient places the long head of the biceps muscle in the line of abduction pull. However, the strength of abduction under these conditions is poor, and loss of muscle power occurs quickly with repetitive move­ ments.

E V A L U A T I O N

A N D

T R E A TM E N T

PaIlwrnechanics oj TraurrwJ:ic Injuries to the NfmJes According to Stevens, the majority of traumatic injuries to the brachial plexus results in traclion or tensile strains. I. The brachial plexus is stretched between twO firm points of allach­ ment, the transverse processes proximally and the c1avopectoral fascial junction distally, in the upper axilla. Stevens compares the cords of the plexus as a traction apparatus with a neutral axis at the C7 vertebra, when the arm is at the hori­ zontal position. Specifically, he compares the brachial plexus as a single cord with five separate points of auachment firmly snubbed al the trans­ verse processes, as shown in Figure 7.6. Accord­ ing to Stevens, a traclion apparatus mUSl have a neutral axis and a line of resistance. When lhe force of traction falls through this neutral center of axis at the C7 vertebra, the traction is equally borne by all part of the apparatus, represented

Fig. A

A and

C

I'l�"",,",----�-�� Pulley centered on its base to show that its purpose is

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by nelve roOts C5 through T I. A slight deviation ["om this neutral axis creates an unequal pull to one side or the other of the apparatus. That is, if the line of traclion falls outside the neutral axis of C7, the entire force is transmitted fyom the neulral axis and all tension is released on lhe cords on the other side. Therefore, if tension is imparted to an alTn elevated above the hOl-izon­ tal, slress is increased to the lower rools of lhe brachial plexus. Conversely, if tension is im­ parted to an arm depressed below the horizontal, slress is increased to the upper roots of the bra­ chial plexus (Fig. 7.6) '· Therefore, the relative posilion of the shoulder and neck at the time of injury, as well as the magnitude of the forces, diclateS the area and extenl of injUl)' to the bra­ chial plexus.

Musculoskeletal Injuries As previously mentioned, a majority of brachial plexus injuries result from trauma, and occur as a complication of musculoskeletal injuries. Ex­ amples of these injuries include the so-called "burner syndrome," shoulder dislocalions, and fractures.

only to change the direction of application of tension-but must

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"BURNER" SYNDROME

The "burner" or "stinger" syndrome i one of the most common type of sports injuries lhat occur to the upper trunk of lhe brachial plexus··lo-I> This injury often has been thought to occur sec­ ondary to traction 10 the brachial plexus when an athlele sustains a laleral flexion injury to lhe neck. Specifically, the syndrome is an abrupt change in the neck and shoulder angle, as experi­ enced by football players making a tackle, with depression of the shoulder and rotation of the neck to the contralateral shouder.6. 10-1 1 Markey et al reported another common mechanism of injUl)' due to compression of the fixed brachial plexus between the shoulder pad and the supe­ rior medial scapula when the pad is pushed into the area of Erb's point. 10 Regardless of the mech­ anism of injury, at the time of injury the athlete

188

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relates a stinging or buming pain, radiating from the shoulder into the arm. '0- 12 Location of the lesion varies, and cervical rool avulsion has been seen in severe cases. Most "bumer" injuries are self-limiting and resolve within minutes of insult. Potential prob­ lems include persistent neck tenderness and upper extremity weakness. [f these problems persist, electromyography should be performed at 3 to 4 weeks to assess for seriolls nelV'e damageW-1l DISLOCATIONS

Injuries to the brachial plexus can occur as a re­ sult of shoulder dislocation. The incidence of secondary brachial plexus injury after shoulder dislocation ranges from 2 to 35 percent in the li terature. Guven et al. reported the "unhappy triad" at the shoulder that included concomitant shoulder dislocation, rotator cuff tear, and bra­ chja] plexus injury.'9 Axillary nerve injury some­ times occurs with acute anterior dislocation of the humeral head. Wang et al. presented a case with concomitant mixed brachial plexus injury in the presence of infel;or dislocation of the gle­ nohumeral joint.2o Travlos et al. classified bra­ chial plexus lexions due to shoulder dislocation into diffuse infraclavicular, posterior cord, lat­ eral cord, and medial cord injuries.21 The type of injury partly depends on the mechanism of injury and the direction of dislocation of the hu­ meral head. FRACTURES

Traumatic injuries associated with fractures in the shoulder girdle and humerus bones have been associated with brachial plexus injuries. Della Santa et al. found sixteen cases of costocla­ vicular syndrome related to compression of the subclavian artery and brachial plexus were due to callous and scar formation as a result of fTac­ tures of the c1avicieH Stromquist et al. reported three cases of injury to the axillary artery and brachial plexus complicating a displaced proxi­ mal fracture of the humerus." Blom and Dahl­ back found two cases in a series of 31 cases of

proximal humeral fTaclures with associates bra­ chial plexu injuries.'4 Silliman and Dean report that an associated complication of scapular frac­ tures around the scapular spine is suprascapular nerve injury.6

Palhophysiolo{Jy of Injury The extent of injury to the nerve trunk, ranging [Tom a nondegenerative nCUI"opraxia to a sever­ ance of the nerve or plexus (neurotmesis), will dictate the course of treatment (surgical versus nonsurgical) and the prognosis and relative time frames for full recovery. Five major degrees of injury are described by Sunderland"; 1. First-degree l1erve il1jury. This injury is char­

acterized by interruption of conduction at the site of injury with preservation of the an­ atomic continuity of all components com­ prising the nerve trunk, including the axon. Clinical features include temporal), loss of motor function to the affected muscles, but the presence of electric potential due to axo­ nal continuity is retained. Cutaneolls sen­ SOl)' loss may occur, but will recover in ad­ vance of motor function. Most patients recover spontaneously within 6 weeks after injury. 2 . Second-degree nerve illjllry. In this injul)', the axon is severed and fails to survive below the level of injlll)' and, for a variable but shon distance, the axon degenerates proximal to the point of the lesion. How­ ever, the endoneurium is presclved within the endoneurial tube. Histologic changes to the nerve include breakdown of the myelin sheath, Schwann cell degeneration, and phagocytic activity with eventual fibrosis. Clinical features include temporal)' com­ plete loss of motor, sensOl)" and sympa­ thetic functions in the autonomous distribu­ tion of the injured nerve. Several months will pass before recovel), begins, with proxi-

EVA L U A T I O N

A N D

TRE A T M E N T

mal reinnervation occurring before distal re­ innervation to the involved muscles. 3. Third-degree l1ellle injury. This condition is characterized by axonal disintegration, Wal­ lerian degeneration both distal and proxi­ mal to the site of the lesion, and disorgani­ zation of the internal structure of the endoneural fasciculi. The general fascicular pattern of the nerve trunk is retained with minimal damage to both the perineurium and epineurium. Because the endoneural tube is destroyed, intrafascicular fibrosis may obviate axonal regeneration. Many axons fail to reach their original or function­ ally related endoneurial tubes, and are in­ stead misdirected into foreign endoneurial tubes. Clinically, motor, sensory, and sympa­ thetic functions of the related nerves are lost. The recovery is long, up to 2 to 3 years, with a chance of significant residual dys­ function.

4. Fourth-degree l1elve il1jury. This type of in­ jury is similar to third-degree nerve injury, but the perineurium is disrupted. Therefore, the chance for a residual dysfunction due to fibrosis and mixing of regenerating fibers at the site of injury, which may distort the nor­ mal pattern of innervation, is high. 5. Fifth-degree IlelVe injwy. In this injury, the entire nerve trunk is severed, with resultant complete loss of function to the affected structures. Obviously, without surgical graft­ ing, recovery is negligible.

CIi1:rifying Eval:uation A thorough and systematic clarifying evaluation is essential for the clinician to accurately assess the nature and extent of the brachial plexus le­ sion and to develop an appropriate and effective treatment plan. Because most brachial plexus le­ sions slowly improve over a long period of time, the clinician must maintain and update accurate records concerning the progress of the patient.

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The clinician should use any one of a number of charts for recording results of the physical exam­ ination, as shown in Figure 7.7. Evaluation and treatment is a conjoint effort by a physical and an occupational therapist who specializes in the treatment of hand and upper extremity injuries. Knowledge of hand management and rehabilita­ tion is particularly important in lower trunk inju­ ries to the brachial plexus. Additionally, in the presence of fourth-and fifth-degree nerve inju­ ries to the brachial plexus, occupational therapy offers strategies for splinting as well as equip­ ment modification or assurance to assist perma­ nently dysfunctional individuals.

Histmy MECHANISMS OF INJURY

Because mo t brachial plexus injul'ies result from trauma, a thorough history should include questions concerning the nature and mecha­ nisms of injury. According to Stevens, the dif­ ferent varieties of sU'ess, and the relative posi­ tion of the arm and head at the time of the stress, make tremendous differences in the kinds of lesions suffered, in the locality of the lesion, and in prognosis. I S The magnitude of forces, that is, high-speed versus slow-speed in­ juries, is important to ascertain. According to Frampton, high-speed, large-impact accidents are commonly associated with preganglionic plexus injuries, while slow-speed, small-impact accidents are commonly associated with post­ ganglionic injul-ies.4 Examples of high-velocity injuries are those resulting from falls from speeding motorcycles, while examples of low­ velocity injuries are those resulting from a fall down a stairway. PAIN

The area and nature of pain should be docu­ mented. Pain, described as a constant burning, crushing pain with sudden shoots of paroxysms of pain, is central in nature. This pain occurs as a result of deafferentation of the spinal cord

190

P H Y S I C A L

THE R A P Y

OF

THE

S H O U L D E R

BRACHIAL PLEXUS �E

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at the damaged root level, leading to undamp­ ened excitation of the cells in the dorsal horn of the spinal cord. The confused barrage of abnormal firings is received and interpreted centrally as pain and is eventually felt in the derma tomes of the nerve root that is avulsed.2• In a series of 188 patients with post-traumatic brachial plexus lesions, Bruxelle et al found that 91 percent experienced pain at least 3 years after injury'>· Pain may also result from second­ ary injuries to bones or related soft tissues. The report of any anesthesias or paresthesias should be noted and documented. The presence of Hor­ ner's syndrome, which is characterized by en-

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results o( physical examil1atiol1 (or brachial plexus il1jury. (Frolll Leffert2, with permission.)

ophthalmos, myosis, and ptosis, along wilh a deficit of facial sweating on the affected side, reOects damage to the TI nerve root. Questions concerning the course of events since injury or a change in the severity of the symptoms estab­ lish an indication of an improving or worsening lesion. A condition that is resolving sponta­ neously may indicate first- or second-degree nerve injuries, while a condition that has not changed across the course of 6 weeks may indi­ cate at least a third-degree nerve injury, accord­ ing to Sunderland's classification. Finally, the clinician should document the patient's occupation, handedness, and previous

E V A L U A T I O N

A N D

T R E A T M E NT

state of health to assist in establishing feasible goals for retum to the patient's premorbid activ­ ity level.

Physical. FJval.uat:ion The components of the physical evaluation in­ clude: ( I) posture; (2) passive range of motion of the cervical spine, shoulder, and upper extrem­ ity; ( 3 ) motor strength; (4) sensation; (5) palpa­ tion; and (6) special tests. The occupational ther­ apy evaluation includes assessment for ( I ) edema; (2) coordination; ( 3 ) activities of daily living; and (4) vocational and avocational pur­ suits. The physical evaluation should be repeated frequently during the process of rehabilitation to carefully assess subtle signs of nerve reinnerva­ tion.

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cian should obselve the attitude or position of the upper extremity and hand. An ann position of adduction and intemal rotation can result from Duchenne-Erb pa"llysis. Pronation of the forearm with flexion at lhe wrist and metacarpo­ phalangeal and proximal i nterphalangeal joints can result from injury to the lower trunk of the brachial plexus.' External deformities along the clavicle, which may indicate fracture, should be noted. Both nonunions and malunions of the clavicle can result in significant compression of the brachial plexus. The supraclavicular fossa is inspected for the presence of swelling or ecchy­ mosis in those patients with recent injury and for nodularity and induration in the brachial plexus where the injury is 0ld 4 The eyes are obselved for constriction of the pupils or ptosis of the eye­ lids, which can indicate the presence of Horner's syndrome.2 PASSIVE RANGE OF MOTION

POSTURE

The patient is obselved from the front, side, and behind. From behind, the clinician observes for muscle atrophy as well as winging of the scapula. Winging of the scapula signifies weak.ness of the serratus anterior muscle, which may indicate a lesion of the long thoracic nerve. Ipsilateral atro­ phy of the supraspinatus or infraspinatus mus­ cles can signify suprascapular nelve entrapment. Atrophy of the deltoid muscle, in addition to the supraspinatus and infraspinatus muscles, can indicate an upper trunk plexus lesion, such as Duchenne-Erb Paralysis of the C5 and C6 nerve trunks. Isolated atrophy of the deltoid muscle in­ dicates an isolated axillary nelve lesion. From the side, the clinician should obselve for changes consistent with a forward head posture: accentu­ ated upper thoracic spine kyphosis, protraction and elevation of the scapulae, increased cervical spine inclination, and backward bending at the atlanto-occipital junction. The forward head posture results in muscle imbalances that can further result in entrapment of various nerves of the brachial plexus in the area of the thoracic outlet. 21 Thoracic outlet syndrome is discussed in detail in Chapter 16. From the front, the clini-

The passive range of motion of all joints of the shoulder girdle and upper limb must be assessed and recordecl using a standard goniometer. Defi­ cits of joint motion from immobility result in contractures of joint capsule, adhesions in the joints, and shortening of both muscle and ten­ dons above the affected joints. The classic stud­ ies of Akeson et al demonstrated the deleterious effects of 9 weeks of immobilization on peria.-ti­ cular structures, including the loss of water and glycoaminoglycans, randomization and abnor­ mal cross-linking of newly synthesized collagen, and infi ltration in the joint spaces of fatty fibrous materials.28 MOTOR STRENGTH

Several manuals are available that review proper isolation, stabilization, and grading procedures for manual muscle testing.29.3o Most grading sys­ tems grade muscle for 0 to 5, with 0 being a flac­ cid muscle and 5 representing normal muscle strength.29 A complete upper extremity test should be perfonned initially to provide the clini­ cian a data base from which to measure improve­ ment. Therefore, retests should be performed pe-

192

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riodically. A thorough manual muscle test assists the clinician in pinpointing the site and extent of the plexus lesion. Establishing an appropriate strengthening program is based on isolating and grading involved muscles. lsokinetic testing can also assist clinicians in measuring muscle strength deficits, usually for peak torque, power, and work, compared with the uninvolved upper extremity. Refer to Chapter 16 for a review of isokinetic testing protocols in the shoulder. SENSATION

Assessment of sensory loss assists in the diagno­ sis of the level and extent of the plexus lesion. Total avulsion of the plexus results in total anes­ thesia of the related areas. However, in a mixed lesion, and when recovery is OCCUlTing, the sen­ sory pattern may vary in the arm. The sensory evaluation may include deep pressure, light touch, temperature, stereognosis, and two-point discrimination, depending on the patient's sta­ tus.4 Sensory changes are documented along dermatomes, as illustrated in Figure 7.7. COORDINATION

Loss of sensation and muscle control in the pres­ ence of a brachial plexus injury results in a loss of gross and fine motor coordination in the affected upper extremity. There are numerous tests on the market designed to assess an individual's co­ ordination. Each requires varying amounts of fine and/or gross motor coordination. The Pur­ due pegboard (Lafayette Instructional Co .. La­ fayette, I N ) , for example, assists the clinician in assessing the patient's manual dexterity. Patients are requested to place pegs with both the right and left hands, singularly and in tandem, and to perform a speCific assembly task using pins, collars and washers. These tests are timed and compared with normative values " The thera­ pist should determine the most appropriate tests based on the patient's level of functioning. VASCULAR

In the presence of severe brachial plexus injuries, particularly with associated fractures of the clav­ icle, disruption of the subclavian or axillary ar-

teries may occur. Additionally, all patients who have had a significant nerve injury will have evi­ dence of vasomotor changes.' Assessment of the brachial and radial pulses and inspection for dusky, cool skin indicating venous insufficiency should be performed by the clinician. EDEMA

Edema must be assessed and treated to prevent stiffness in the joints. The concept of volumetrics to measure upper extremity edema is well estab­ lished. The patient's hand is submerged in a lu­ cite container (Volumeter, Volumeters Unlim­ ited, Idyllwild, CAl, and the amount of water displaced is measured using a 500-ml graduated cylinder. Both extremities should be measured and the results recorded. Circumferential mea­ surements of the hand and forealm are another method of measuring edema. However, this technique is best suited for individual digit swell­ ing or in the case of open wounds, which may preclude the patient getting the extremity weI. Manual palpation is also used to measure edema. The severity of the edema is usually rated from I to 3, with I being minimal and 3 being severe or pitting edema. PALPATION

Manual palpation is used to assess for myofas­ cial trigger points about the affected shoulder girdle and upper extremity musculature. Trigger points result from tight and contracted muscles or from partially denenlated muscles exhibiting poor muscle control and altered movement pat­ terns. Active trigger points refer pain into the af­ fected upper extremity, as well as the shoulder girdle, neck, and head.3, .33 SPECIAL TESTS

The presence of Tinel's sign, demonstrated by tapping over the brachial plexus above the clavi­ cle, can be quite useful in distinguishing rupture from a lesion in continuity '.4 A distal Tinel's sign indicates a lesion in continuity whet'e the axonal connections within the ner've trunk are intact.

EV A L U A T I O N

A N D

T R EA T M E N T

This may con'espond to a first-degree nerve in­ jury or a regenerating second- or third-degree nerve injury, as described by Sunderland. Con­ versely, the presence of a localized tenderness to tapping above the clavicle indicates a possible neuroma resulting fTom disruption of part of the plexus. This type of injury would correspond to a fourth- or firth-degree nerve injury. ACTIVITIES OF DAILY LIVING

The patient is questioned regarding all aspects of self-care to identify those specific tasks he or she is not able to perform owing to the extent of the brachial plexus injury. Such areas include self-care skills such as feeding, bathing, groom­ ing, and dressing, Based on the specific limita­ tions of the patient, the occupational therapist then determines whether to provide the patient with specific adaptive equipment or to instruct the patient in one-handed techniques. ASSESSMENT FOR SPLINTING

In the case of a complete brachial plexus injury, the patient is fitted with a nail arm splint that allows the patient to use the extremity at home and at work. The splint is fitted early, to prevent the patient from relying on one-handed methods as a means of performing specific activities.' In the case of a CS-7 injury, the patient might re­ quire a long wrist and finger extension assist splint (Fig. 7.8). The patient may also be fitted with a resting hand splint (Fig. 7.9) to wear at night to help maintain the wrist and fingers in a balanced position. VOCATIONAL

A detailed job description is obtained to assess the patient's potential to return to work. In addi­ tion, a functional capacity evaluation can be per­ fOimed later in the rehabilitation process to as­ sess the patient's physical demand level. AVOCATIONAl

Because the brachial plexus-injured patient is unable to work , avocational pursuits are often an important source of much-needed diversional activity. The occupational therapist questions

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the patient closely as to premorbid hobbies or potential areas of interests. Activities of interest are developed that encourage use of the affected extremity.

Lahoratory FJual:uJL/:i.ons oj Brachial Plecus LesWns Also included in the overall evaluation of a pa­ tient with a brachial plexus injury are laboratory evaluations involving electrodiagnostic testing, myelography, and radiographic assessment. These evaluations help the clinician diagnose the area and extent of the Ie ion and provide baseline measurements to help evaluate progress. RADIOGRAPHIC ASSESSMENT

Every patient who has sustained a significant in­ jury to the brachial plexus should have a com­ plete radiographic series done of the cervical spine and involved shoulder grid Ie, including the c1avicle.2 Fractures of the clavicle with callus, which can impinge on the nerve trunks along the costoclavicular juncture, or fractures of the cer­ vical transverse processes, which can indicate a root avulsion, must be ruled out.2,4 Magnetic resonance imaging (MRJ) has been used to detect injuries to the brachial plexus. Bil­ bey et al evaluated 64 consecutive patients with suspected brahial plexus abnormalities of di­ verse causes with MRJ.34 MRJ was found to be 63 percent sensitive, 100 percent specific, and 73 percent accurate in demonstrating the abnor­ mality in a diverse patient population with multi­ ple etiologies of brachial plexus injuries. MYELOGRAPHY

Myelography is used to indicate the status of the nerve roots in the presence of traction injuries to the brachial plexus. According to Leffert, root avulsion can occur in the presence of a normal myelogram.2 However, a well-documented study by Yeoman indicates the efficacy of myelogra­ phy as a valuable adjunct to the diagnosis of bra­ chial plexus root lesions ]5

194

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FIGURE 7.8

A lOl!g

melacarpophaiQ/lgeal extension splint used 1-VEtil a patient who has weak wrist extension and trace {iflger extension.

ELECTROMYOGRAPHY

Because the loss of axonal continuity results in predictable, time-related electric charges, knowledge and assessment of these electric charges can be used to provide information con­ cerning muscle denelvation and reinnelvation.2 For example, while normally innelvated

muscle exhibits no spontaneous electric activity at rest when examined with needle electrodes, denervated muscle produces readily recogniz­ able small potentials ( fibrillations) or large po­ tentials (sharp waves), which are the hallmark of denervation. These electric discharges usually appear 3 weeks following injury to the plexus and signal the onset of Wallel-ian degeneration of a

FIGURE

7.9 A resling hand

sp/il!! used rol/oIVil1g a brachial plexus lesiol! 10 prevel1l overslre!c/ling or weak and {tl!ger exl€/1sor lIluscies by lIlail1laillil1g Ihe l-vrist in approximately 20" or dorsif/exiol!.

E V A L U A T I O N

A N D

TR E A T M E N T

specific nerve. The clinician is able to localize the lesion by sampling muscles innervated by dif­ ferent nerves and root levels. Additionally, when a root avulsion is sus­ pected in a patient who has sustained a traction injury of the brachial plexus, the clinician should also peform an electromyographic eval­ uation of the po terior cervical musculature. The posterior cervical muscles are segmentally innervated by the posterior primary rami of the spinal nerves that provide the anterior primary rami to form the plexus. Denervation of the deep posterior cervical muscles is highly corre­ lated with root avulsion. Conversely, if the elec­ tromyogram is positive for the muscles inner­ vated by the anterior primary rami but not for the posterior cervical muscles, whatever possi­ ble damage exists is presumed to be infragangli­ onic in nature.36

Nerve Coruiucl:ii.m Stuilies Nerve conduction velocity tests may be used to help distinguish muscular weakness in the af­ fected upper extremity from cervical interverte­ bral disc protrusion, antel;or horn cell disease, or a brachial plexus lesion. Because anterior horn cell diseases and intervertebral disc protru­ sions do not in(]uence nerve conduction latency, the clinician can be certain that a proximal nelve conduction delay is a result of a brachial plexus lesion 37 Another type of electrodiagnostic testing is the F response, an outgrowth of the measure­ ment of velocity of conduction; this is a late reaction that potentially results from the back­ firing of antidromically activated anterior horn cells. Electrical stimulation of motor points as­ sesses the strength-duration cUlves of affected muscles.J8 A denervated or partially denervated muscle requires more time and current than a normally innervated muscle. Serial strength­ duration testing therefore allows the clinician to assess neuromuscular recovery.38

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Rehabil:itation Goals and Treatment The approach to rehabilitation for brachial plexus lesions is directed at maintaining or im­ proving soft tissue mobility, muscle strength and function within the constraint of the nerve in­ jury, and function. Because regeneration is ex­ cruciatingly slow, rehabilitation in severe cases is a long-term process, lasting as long as 3 years. Therefore, patient and family education, as well as home exercise programs, are an integral com­ ponent of treatment. Surgical grafting in the presence of fourth­ and fifth-degree nerve injuries necessitates, on the pal-t of the therapist, knowledge of soft tissue healing constraints. The relatively high chance of residual upper extremity dysfunction in some cases requires vocational and avocational re­ training, as well as occupational therapy inter­ vention for assistance-providing devices and splints. According to Framptom: rehabilitation falls into three stages: the early stage, consisting of diagnosis, neurovascular repair, and education concerning passive movement and self-care of the affected extremity; the middle stage, when recovery is occun-ing and intensive reeducation may be indicated; and the late stage, when no future recovery is expected and assessment for reconstructive surgery can take place. The time frames and extent of each phase are predicted based on the extent of the lesion and the individ­ ual's own motivation and recuperative capabili­ ties. Goals, treatments, and rationales for the treatments for each stage of rehabilitation are exemplified in the case study presented below.

CASE STUDY 1 This case study presents a typical brachial plexus injury affecting the shoulder and upper extrem­ ity function. Initial findings are delineated in the clarifying evaluation. The goals and phases of treatment are presented as a combined physical and occupational therapy approach. Rationales

196

P H Y S I CA L

T H E R A P Y

O F

T H E

S H O U L D E R

for specific treatments are presented, when relevant.

30°, and supination measured 50°. The patient had full pronation and wrist and finger Oexion and extension.

HISTORY

A 25-year-old right-handed man was involved in a motor vehicle accident and suffered a traction

MOTOR STRENGTH

Motor strength was graded as follows:

lesion to his brachial plexus. Electrodiagnostic testing indicated an infTaganglionic lesion to his

Grade 0

left brachial plexus at Erb's joint, that portion of

Grade I

the brachial plexus where C5 and C6 unite to join the upper trunk. Radiologic studies indicated no

=

no contraction trace

Grade 2

=

poor

Grade 3

=

fair

tient was referred to physical and occupational

Grade 4

=

good

therapy 4 weeks after the initial injury.

Grade 5

=

nOI111al

fTactures at the cervical spine or clavicle. The pa­

The patient reported numbness and tingling along the lateral aspect of his left shoulder, in

The patient's muscles were graded as fol­

the area of the deltoid muscle, and weakness in his left shoulder, elbow, wrist, and hand. He re­

lows: deltoid

ports intermillent pain in his left shoulder and

natus

neck made worse with attempted elevation of his left arm. He reported less numbness and in­

brachialis 2, serratus anterior 5, subscapu­ laris 3, extensor carpi radialis longus and bre­

creased strength in his left arm since the initial

vis

injury.

was 88 Ib on the right and 1 0 Ib on the left.

VOCATION

SENSATION

The patient works as a carpenter.

=

=

2, supraspinatus

3, teres minor

=

=

3, in fraspi­

2, biceps brachii

=

=

2,

=

=

=

3 , and supinator

=

3. His grip strength

Sensation was impaired to light touch and to sharp/dull along the lateral aspect of the left

POSTURAUVISUAL INSPECTION

shoulder, in the area of the deltoid muscle, and

Atrophy was observed in the deltoid, supraspi­

along the radial side of the forearm.

natus, and infTaspinalUs muscles on the left com­ pared with the right side. His left arm was held in internal rotation along his lateral tnmk, with

COORDINATION

Coordination was assessed using the Purdue

his forearm pronated and his wrist and fingers

pegboard and rated as follows: right hand, 14;

in slight Oexion.

left hand, 2; both hands, 4; assembly task, 6.

PASSIVE RANGE OF MOTION

EDEMA

Elevation in the plane of scapula measured 1 20°,

The patient had 2 + edema palpated along the

external rotation in adduction measured 30°, ex­

dorsum of the left fingers at the proximal inter­

ternal rotation in 45° abduction measured 60°,

phalangeal joints and metacarpal joints and

and external rotation in 90° abduction measured

along the dorsum of the left hand. His volumetric

70°. His elbow, forearm, wrist, and hand passive

measurements were 482 cc on the right and 525

range of motion were all within normal limits.

cc on the left.

ACTIVE RANGE OF MOTION

PALPATION

Elevation in the plane of scapula measured 60°, external rotation in adduction from full internal

Trigger points were palpated in muscle bellies of

rotation measured 20°, elbow Oexion measured

subscapularis muscles.

the left upper trapezius, left rhomboid, and left

EVALUATION

A N D

T R E A T M E N T

ACTIVITIES OF DAILY LIVING IADL)

The patient was unable to perform the following self-care activities: Feeding-unable to cut his food. Bathil1g-unable to wash his right shoulder and upper ann. Groollling-unable to apply deodorant to his right underarm. Dressing-unable to tie shoes, bulton shirt, zip pants or jacket, or buckle belt. ASSESSMENT

This is a patient whose history revealed a trac­ tion injury to the upper trunk of the brachial plexus involving nerve trunks C5 and C6. Be­ cause he demonstrated at least poor muscle con­ trol of the affected muscles, which is sponta­ neously improving since the initial injury, the extent of the injury is classified as between a first- and second-degree injury, according to Sunderland's c1assification.25 Therefore, one can expect combined resolution of nerve function, with full return of function of the left upper ex­ tremity. Passive range of motion is moderately lim­ ited in the affected shoulder with restrictions of the related joint capsule, fascia, tendon, and muscle. Soft tissue limitations are consistent with the findings of Akeson et al..'8 Tabary et al.,39 and Cooper" a who studied the affects of immobilization on periarticular capsule, tendon, and muscle, respectively. The loss of motor con­ trol results in altered scapulohumeral rhythm. The rotator cuff muscles, particularly the supra­ spinatus. infraspinatus, and teres minor mus­ cles, are unable to adequately control gliding of the humeral head during elevation of the shoul­ der. The resultant weakness, even in the presence of a weak deltoid muscle, results in impingement of the suprahumeral soft tissues underneath the unyielding corocoacromial ligament. Chronic impingement results in inflammation and de­ generation of the rotator cuff tendons. Compensation of the scapula muscles to ele­ vate the arm in the presence of weakness of the

O F

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L E S I O N S

197

rotator cuff and deltoid muscles results in in-ita­ tion and trigger points in both the left upper tra­ pezius and left rhomboid muscles. A trigger point palpated in the subscapularis muscle is the result of the shoulder and arm positioned in in­ ternal rotation and along the lateral trunk wall, which maintained the subscapularis muscle in a shortened position. The contracted subscapu­ laris muscle resulted in the greater limitation of passive external rotation with the ann adducted along the lateral trunk wall, as opposed to exter­ nal rotation with the arm abducted to 45° or 90°. (R. Donatelli, personal communication.) The weakness in the left upper extremity and hand resul t in a loss of normal muscle pumping activity to remove interstitial fluid. In addition, the patient tended to keep his arm down at his side. These two factors result in increased edema in the left upper extremity, especially the left fin­ gers and hand, compared with the right. The weakness in the left upper extremity, a well as the patient's decreased manual dexterity, inter­ fered with some self-care activities. Fortunately, the patient is right-handed, which will expedite his return to employment as a cm-penter. REHABILITATION GOALS AND TREATMENT

E A R L Y STAGE FIRST GOAL

The first goal is to reduce pain. T R E A T M E N T . Heat, low-voltage surge stimulation, and spray and stretch (see Ch. 1 2) were applied to the active trigger points in the lefI upper trape­ zius and left rhomboid muscles in our patient. Transcutaneous neuromuscular stimulation, using a high-rate, low-intensity conventional set­ ting with dual channels and four electrodes, was applied around the left shoulder. The transcuta­ neous neuromuscular stimulation device was worn 8 hours per day.

RATIONALE. According to Travell and Simons, my­ ofascia I trigger points in the shoulder girdle muscles refer pain into the left shoulder and arm in a consistent paltern." Therefore, reduction of trigger point tenderness in the left upper trape­ zius and left rhomboid muscles will alleviate part

198

P H Y S I CA L

T H E RAPY

OF

T H E

S H O U L D E R

of this patient's pain. The conventional transcu­

ments,

taneous

selling

indicates no optimum time frames for applying

stimulates large A-beta sensory fibers that modu­

grade IV manual stretching to the perialticular

late impulses from the small A-delta and C fibers

capsule. Clinically, we use three sets of I -minute

in the dorsal horn of the spinal cord.·, ·42 Pain impulses along the A-delta and C fibers in this

grade IV oscillations into the restricted tissue

neuromuscular

stimulation

respectively. The

scientific

literature

preceded by heat and followed by ice.

patient resulted from irritation of nociceptor endings in the connective tissue sheaths sur­

THIRD GOAL

rounding the nerve fibers and trunks, due to the

The third goal is to avoid neural dissociation to

traction injury.42

the reinnervating muscles.

SECOND GOAL

TREATMENT.

The second goal is to restore full passive range

stimulation with a pulse duration of 30 msec was

of motion and soft tissue mobility. TREATMENT.

1n our patient, low-voltage surge

stimulation followed by spray and stretch tech­ niques were applied to the active trigger points in the muscle belly of the subscapulruis. Mobili­ zation techniques, in the grades III and IV range according to Maitland's classification, were ap­ plied to the various joints in the left upper ex­ t remity ·J Special attention was directed at man­ ual distraction of the specific details concerning mobilization techniques at the shoulder com­ plex. Patients with this condition are given a pro­ gram of range of motion self-exercises in order to preserve the range of motion at those joints where there is no, or only limited, active range of motion. Each patient is given an active range of motion exercise program for the uninvolved

High-frequency

low-volt

muscle

applied to the partially denervated muscles. The preferred duty cycle was 1 0 seconds on and 20 seconds off, for a period of 30 minutes. The pa­ tient was instructed to use a home stimulator three to four times daily. RATIONALE.

According to strength-duration stud­

ies, muscle stimulation to a partially denervated muscle requires a higher CLuTent and longer pulse duration than does stimulation to a nor­ mally innervated muscle.J• In addition to main­ taining reinnelvating muscle tissue viability, electrically i nduced mu cle contractions facili­ tate normal circulation, decrease edema, and present

potential

null-itional

or tropic skin

changes."·45 FOURTH GOAL

Reducing edema is the fourth goal.

joints so that these joints do not become re­ stricted due to disuse of the extremity in general.

TREATMENT.

The patient's family should be fam i l iar with the

the hand from a distal to proximal direction,

Retrograde massage was applied to

exercise program so that they can encourage the

with the patient's hand and forearm elevated

patient to follow through and become active par­

above his healt.'· In addition, the patient and

ticipants in the patient's rehabilitation.

his wife were provided with wrillen instructions

RATIONALE.

In our patient, the painful limitation

of external rotation with the shoulder adducted along the lateral trunk wall results from a con­ tracted subscapularis muscle. Therefore, spray

regarding elevation of the arnl, retrograde mas­ sage, and first

pumping to activate muscle

pumping action in the hand and forearm. Coban (3M Medical-Surgical, St Paul, M N )

and stretch, followed by distraction of the medial scapula border, elongates the subscapularis

i s a gentle elastic wrap used for edema control.

muscle and improves external rotation with the

proximally and should overlap approximately

shoulder in the adducted position. Mobilization

in. The advantages of Coban are thaI it is reusa­

It is wrapped diagonally from the fingertips

t

techniques at the shoulder are d i rected at the in­

ble (thus reducing costs), may be worn for pro­

ferior and anterior capsules, respectively, to pro­

longed periods, and allows for full range of mo­

mote abduction and external rotation move-

tion.47

E V A L U A T I O N

A N D

T R E A T M E N T

R A T I O N A L E . Retrograde massage, in a gravity-as­ sisted position, facilitates the reabsorption of in­ terstitial fluids into the lymphatic system. Fist pumping, resulting in alternate contraction and relaxation of the musculature in the hand and forearm, promotes venous blood return to the heart.

FIFTH GOAL

The fifth goal is to increase the patient's ADL independence. T R E A T M E N T . The patient was issued adaptive equipment to increase his self-care independ­ ence until he exhibited a greater degree of motor control. For example, he was issued a rocker knife to help him cut his meat and a button hook to help him button his shirt. In addition, he was instructed in specific one-handed methods of performing certain tasks, such as tying his shoe laces.

SIXTH GOAL

Providing emotional support education is the sixth goal. TREATMENT. Patient and family education and psychological referral were used to accomplish the sixth goal. In certain instances, the therapist must help the patient through the initial stages of denial, anger, and depression associated with a severe brachial plexus injury. A patient's emotional state will affect his or her pelformance in ther­ apy. The therapist should be an active listener and recognize the normal process of emotional recovery in patients with severe disability. Fear is a major component and compounds a patient's anxiety. This anxiety can often be reduced if the patient is educated as to the nature and extent of the injury, the course of recovery, the course of therapy, and the prognosis for recovery. One cannot stress enough the importance of involv­ ing the patient's family in the rehabilitation pro­ cess. Family relationships often become strained as a result of serious injury. Financial issues may become a source of wony and concern for all involved. The family members may need as much SUpp0l1 as the patient and will also benefit from the education process.

O F

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199

M I D D L E STA G E FIRST GOAL

The first goal in the middle stage is to reeducate reinnervating muscles. Manual proprioceptive neuromus­ cular facilitation techniques emphasizing diago­ nal patterns, with the patient supine, were begun at approximately 3 weeks after the initial evalua­ tion. Light-weight isotonic strengthening was added to the program , using adjustable-weight cuffs. Initial isotonic strengthening emphasized external rotation movement patterns at the shoulder as well as flexion and extension move­ ments at the elbow and pronation and supina­ tion at the forearm. As strength improved, the patient was progressed to isokinetic strengthen­ ing at slow speeds of approximately 600/s, em­ phasizing rotational movement palterns in the shoulder. The patient was progressed to isoki­ netic diagonal movement patterns in the supine position when isokinetic testing indicated a dif­ ference of left to light external rotation strength, as measured in peak torque, and power was within 20 percent. Refer to Chapter 3 for isoki­ netic testing and strengthening strategies for the shoulder. Modalities such as vibration and tapping are used while the patient is exercising or perform­ ing functional activities. Appropriate sensory stimuli can evoke desired muscular responses, and this stimulation must be followed by pur­ poseful activities if motor learning is to take place '· Biofeedback and neuromuscular electri­ cal stimulation are used on selected weak mus­ cles to facililate muscle reeducational strength. TREATMENT.

Manual proprioceptive neuromuscu­ lar facilitation diagonals allow the clinician to assess early subtle strength changes across treat­ ments. Early isotonic strengthening is directed at restoring strength in the shoulder rotator cuff muscles, specifically the supraspinatus, infraspi­ natus, and teres minor muscles. The goal is to restore, during elevation of the shoulder, the dy­ namic steering mechanism of the rotator cuff muscles on the humeral head 49 The restoration of rotator cuff muscle strength reestablishes the normal balance between these muscles and the RATIONALE.

200

P H Y S I C A L

T H E R APY

O F

T H E

S H O U L D E R

upward pull of the deltoid muscle. Isokinetic strengthening is instituted as soon as the patient is actively exercising with \ - or 2-lb weights. Isokinetic contraction offers the advantage of ac­ commodating resistance to maximally load a contracting muscle throughout the range of mo­ tion SO The patient exercises at preselected speeds, beginning with slower speeds, so that he or she can consistently "catch" and maintain the speed of the dynamometer. External rotational strengthening is emphasized early, as previously mentioned, to restore the dynamic glide of the humeral head along the glenoid [ossa by reestab­ lishing strength in the supraspinatus, infraspi­ natus, and teres minor muscles. Isokinetic test­ i ng is performed every 2 to 3 weeks to assess peak torque and power values of the involved com­ pared with the uninvolved upper extremity. Iso­ kinetic diagonal strengthening patterns are per­ fanned initially supine, to eliminate the affect of the muscles working directly against gravity. Diagonal patterns are eventually performed with the patient sitting or standing, after bilateral strength deficits between the left and light shoul­ der rotators are within 20 percenl. Although not scientifically substantiated, we have obselved that when bilateral shoulder rotational strength deficits are greater than 20 percent, impinge­ ment of the suprahumeral soft tissues and pain, du.-ing active shoulder elevation, occurs. In occupational therapy. our patient worked on tabletop activities with his left upper extremity supported. The activities were directed toward strengthening his elbow, forearm, and wrist musculatul·e. For example, he transferred pegs from one bucket placed in fTont of him to a bucket placed to his far left. This activity required active elbow flexion and exten­ sion in a gravity-eliminated position. As his shoulder strength improved, he was able to per­ form this same activity unsupported. Addition­ ally, he was able to stack cones, which required active shoulder abduction against gravity. He used light weights to strengthen WTist flexion and extension, supination, and pronation. Elastic I'lIbber tubing, such as Theraband ( Hygenic, Akron, OH), was used at home to improve elbow OCCUPATIONAL T HERAPY.

and wrist strength. He was issued therapeutic putty and instl'llcted in hand-strengthening exer­ cises. SECOND GOAL

The second goal is to continue mobilization to the restricted joints. Low-load prolonged stretching using surgical tubing was applied to the restricted peri­ articular capsules, especially the anterior aspect of the glenohumeral capsule, to promote exter­ nal rotation. The patient was positioned with his shoulder in 45° of abduction and his elbow in 90° flexion. Surgical tubing attached to his wrist provided a 30-minute low-load stretch into exter­ nal rotation. T R EA T M E N T .

R A T I O N A L E . Using rat tail tendons, Lehman et al demonstrated that the optimum method to stretch pericapsular tissue is to use low-load pro­ longed stretch.5I According to Lehman et al the prolonged stretching allows the viscoelastic ma­ teral in the capsular tissue, including the water and glycoaminoglycans, to creep or to elongate with the tissue.

THIRD GOAL

If necessary, continue the third goal for edema control. FOURTH GOAL

The fourth goal is to reevaluate the use of assis­ tance-providing devices and to modify the use of these devices. F1FfH GOAL

Increasing coordination is the fifth goal. As our patient's motor performance improved, coordination activities became an in­ tegral part of his treatment program. Initially, the activities focus on such gross motor skills as placing large pegs into a bucket while being timed and, later, placing those same pegs into a pegboard. As he continued to improve, the activi­ ties required more fine motor skills, such as ma­ nipulating nuts and bolts (graded from large to small), practicing on an ADL board, turning coins and so forth. All activities were timed to document progress. Trombly and Scott state that TREATMENT.

E V A L U A T I O N

A N D

T R E A T M E N T

in order to increase coordination, activities

OF

B R A C H I A L

P L E X U S

L E S I O N S

201

safely and accurately perform his job. At that

should be graded along a continuum rTom gross

time,

to rine and that as the patient's coordination im­

projects that required minimal rine motor tasks

the

patient

started

on

woodworking

proves, the activities should require faster speeds

sanding, staining. At 1 5 months, he progressed

and more accuracy.52

to work.ing on more intricate projects and, at 1 8 months, he returned to work.

LATE STAG E FIRST GOAL

The flrst goal in the late stage is to optimize mus­ cle strengthening within the constraints of rein­ nervation. Isokinetic strengthening is contin­

TREATMENT.

ued to all major arrected muscle groups in the left upper extremity. Rotational and diagonal strengthening at the shoulder is continued. Fast­ speed training, at 1 80·/s, is added when bilateral slow-speed dericits, at 60·,s, are within 20 per­ cent. The patient is instructed in an aggressive

CASE STUDY 2 The second case study presents a pattern or in­ jury that occured to the lower portion or the bra­ chial plexus K\umpke. lnitial rindi ngs are deline­ ated in the clarifying evaluation and should be compared and contrasted to the findings in Case Study I . Goals, phases or treatment, and princi­ ples of treatment are similar to Case Study I and have been omitted to avoid redundancy. HISTORY A

home strengthening program using adjustable

42-year-old male construction worker was work­

curf weights. Functional training, including l i rt­

ing on a scafrold, slipped, and grabbed a ra iling

ing, carrying various-size weights, hammering,

with his right hand. The result was a forcer·tli upward pull or the arm. This injury occured ap­

and sawing activities, is instituted. RATIONALE.

Strengthening in the clinic is contin­

ued ir the patient continues to exhibit strength gains with periodic isokinetic strength retests. Fast-speed training is instituted to improve mus­ cular endurance. Fast-speed training is not insti­ tuted until

slow-speed

bilateral

deficits are

within 20 percent. We have observed clinically that, in the presence or slow-speed, bilateral defi­ cits greater than 20 percen t, the patient cannot consistently "catch" and maintain the faster speeds or the dynamometer. Functional training ror this particular patient is designed to simulate the working conditions and motor requirements or carpentry. SECOND GOAL

Optimizing joint and soft tissue mobility is the second goal.

proximately 7 weeks ago. The patient reports numbness and tingling along the ulnar border or his right arm into the fourth and fifth ringers. He reports occasional burning pain along the same distribution as well as along the lower portion of his right neck. He l·epol·ts weak.ness in his right grip. He also has slight "drooping" of his right eyelid. A neurologist perrOlmed an EMG last week that indicated increased insertional activ­ ity within the medial finger and wrist flexors and intrinsic hand muscles. A diagnosis or a second­ degree/third-degree lower trunk brachial plexus injury was made. The patient was given nonsteri­ odal anti-inflammatory medication and refelTed to a program

of physical and occupational

therapy. VOCATION

The patient is a construction worker and is right­

THtRD GOAL

The third goal is to help the patient return to work.

hand dominant. POSTURAL!VISUAL INSPECTION

At I year postinjury, a job analysis

Mild atrophy was observed in the intrinsic mus­

was done to identify those tasks the patient

cles of the right hand. A mild c1awhand deror­

would need to perrorm in order to be able to

mity was observed and characterized by hyper-

TREATMENT.

202

P H Y S I C A L

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O F

T H E

S H O U L D E R

extension of the fourth and fifth digits at the

eyelid indicated a potential sympathetic compo­

metatarsal-phalangeal joints and flexion of the

nent

interphalangeal joints.

physical/occupational therapist should monitor

(Homer's

syndrome)

and

the

the condition carefully for sympathetic dystro­ ACTIVE AND PASSIVE RANGE OF MOTION

Mild to moderate restriction in flexion of fourth and fifth metatarsal-phalangeal joints and exten­ sion of fourth and fifth interphalangeal joints.

EMG examination combined with clinical test­ ing that produced a minimum strength grade of

3 in all affected muscle groups indicated a proba­ ble partial denervation of muscles affected by C8 and T 1 nerve roots. The extent of the injury was

MOTOR STRENGTH

The patient's muscles were graded as follows:

3 + , medial half of flexor digitorum profundus 3, opponens digiti min­ imi 3, abductor digiti minimi 3, flexor digiti minimi 3, interossei muscles 3, medial lum­ bricales (fourth and fifth digits) 3, flexor pol­ Iicis brevis 3 + , and adductor pollicis brevis 3. flexor carpi ulnaris

phy in the right hand. Fibrillation potentials with

=

=

=

=

=

=

=

=

=

therefore diagnosed as a second degree (rule out third degree) [axonotmesisl with Wallerian deg­ neration of some muscle fibers but probable preservation of the endoneurial tube. Sponta­ neous recovery will occur in case ofaxonotmesis, but axonal outgrowth takes a long time in these cases (at least a year) due to the limited growth rate and the long distance to their target muscles.

A comprehensive program of both physical and

SENSATION

occupational therapy based on a phased ap­ proach outlined in the initial case is indicated;

Sensation was impaired to light touch and

as with all lower trunk brachial plexus injuries,

sharp/dull along the ulnar side of the arm, fore­ arm, and hand. Special tests: Froment's sign was equivocal; the patient was asked to grasp a piece of paper between the thumb and index finger. With full paralysis of the adductor pollicis brevis, the thumb would flex; however, only slight flex­ ion was produced when the paper was pulled away. EDEMA

1 + edema along the dorsum of right hand; the hand was slightly cool to palpation, but no trophic changes were noted. The Purdue peg board indicated coordination deficits in the right hand; ADL assessment indi­ cated d i fficulties in self-care similar to those out­ lined in Case Study I . ASSESSMENT

a comprehensive hand therapy program should be designed by a certified hand therapiSt. Peri­ odic electromyographic evaluations should be performed to check for reinneravation charac­ terized by pol phasic action potentials. If signs of recovery fail to appear after 1 year, surgical exploration should be performed.

Summary The case studies illustrate the problem-solving approach to patient treatment. Signs and symp­ toms evaluated during the c1a" ifying evaluation are prioritized in order of their clinical signifi­ cance. Treatment is divided into three phases to allow the clinician to establish appropriate goals within the constraints of nerve reinnervation. The patient is progressed through each phase based on continued re-evaluation of signs and

The pathomechanics of injury involved an up­

symptoms. The patient is discharged when clini­

ward traction injury of the right limb that af­

cal tests and evaluation indicate no further im­

fected the lower portion of the brachial plexus, as desc,-ibed by Stevens. Lower plexus injuries

discharged on a home program and is periodi­

affect nerve roots C8 and T I . Ptosis of the right

cally reevaluated. Treatment is resumed if re-

provement in motor capabilities. The patient is

E V A L U A T I O N

A N O

T R E A T M E N T

evaluation confirms additional signs of mOlOr re­ innervation.

A

combined

physical

and

occupational therapy approach recognizes the potential of significant long-term dysfunction of the patient's upper extremity.

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L E S I O N S

movements. A roentgenographic study. J Bone

Joint Surg 48A: I 503, 1 966

I S . Poppen NK, Walker PS: Normal and abnOlmal mOlion of the shoulder. J Bone Joint Surg 58A: 1 95, 1 976

1 6. Inman VT, Ralston HJ, Saunders J B et al: Relation of human electromyograms to muscular tension. Electroencephalogr

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1 9 . Guven 0, Akbar Z, Yalcin S, Gundes H: Concomi, tant rotator cuff tear and brachial plexus injury in association with anterior shoulder dislocation:

unhappy triad of the shoulder. J Ol'lhop Trauma 8:429, 1 994

20. Wang KC, Hsa KY, Shik CH: Brachial plexus in, jury with erect dislocation of the shoulder. 011hop Rev 2 1 : 1 345, 1 992 2 1 . Travlos J, Goldberg I, Boorne RS: Brachial plexus lesions associated with dislocated shoulder. J Bone Joint Surg 72B: 68, 1 990 22. Della Santa D, Narakos A, Bonnard C: Late lesions of the brachial plexus after fracture of the clavicle. Ann Chir Main Memb Supcr ( France) 1 0:53 1 , 1 99 1

23. Stromquist Lidgren L, Norgren L , Odenberg S: Neurovascular

injury

complicating

displaced

proximal fractures of the humerus. injury 1 8:423, 1 989 24. Blom S, Dahlback LO: Nelve injuries i n disloca­ tion or the shoulder joint and rractures or the neck of the humelus. Acta ChiI' Scand 1 36:46 1 , 1 970 25. Sunderland S: Nerves and Nerve Injuries. 2nd Ed. Churchill Livi ngstone, Edinburgh, 1 978

1 0 . Markey KL, DiBendello M. Curl WW: Upper llunk

26. Bruxelle J, Travers V , Thiebaut JB: Occun'ence

brachial plexopathy. The sti nger syndrome. Am J

and treatment of pain arter brachial plexus injury.

SP0l1S Med 2 1 :650, 1 993

I I . Hershman EB, Wilbourn AJ. Bergfeld JA: Acute

Clin 011hop ReI Res 237:87, 1 988 27. Janda V: Muscles, central nervous motor regula·

brachial neuropathy in athletes. Am J Sports Med

tion and back problems. p. 29. In KOIT 1M (cd):

1 7:655, 1 989

The Neurobiologic Mechanisms i n Manipulat ive

1 2. Speer KP, Bassett FH [ 1 1 : The prolonged burner syndrome. Am J Spol1S Med 1 8:59 1 , 1 990

1 3 . Inman VT, Saunders M , Abbot LC: Observations on the function of the shoulder joint. J Bone Joint Surg 26A: I , 1 944

1 4. Freedman L, Munro RR: Abduction of the arm in the scapulat· plane: scapular and glenohumeral

Therapy. Plenum, New York, 1 978 28. Akeson WH, Amiel D, Mechanis GI et al: Collagen cross-linking alterations in joint contractu res: changes in the reducible cross-links in pcTiar1icu· lar connective tissue collagen arter nine weeks or immobilization. Connect Tissue Res 5: 1 5, 1 977 29. Highet WB: Grading or motOI- and sensory recov·

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ery i n nelVe injuries. p. 356. In Seddon HJ (ed):

4 t . Lampe GN, Mannheimer JS: Stimulation Charac­

Research

teristics of T.E.N.S. FA Davis, Phi ladelphia, 1 984

Council Rep0l1 Sel'ies T2 282. Her Majesty's Sta·

42. Guyton AC: Organ Physiology: Structure and

Peripheral

Nerve

Injuries.

Medical

tion..,), Office, London, 1 954 30. Daniels L, W0I1 hingham C: Muscle Testing. Tech· niques of Manual Examination. 4th Ed. WB Saun­ ders, Philadelphia, 1 980 3 1 . Hamm NH, Curtis D: Nonnative data for the Pur­ due pegboard on a sample of adult candidates for vocational rehabilitation. Percept MOl Skills 50: 309, 1980 32. Travell JG, Simons DG: Myofascial Pain and Dys· function. The Tr;gger Point Manual. Williams &

Wilkins, Baltimore, 1 984

33. Janda V: Some aspects of extracranial causes of facial pain. J Prosthet Dent 56:4, 1 986

34. Bil bey JH, Lamond RG, MaLLrey RF: MR imaging of disorders of the brachial plexus. J Magn Reson Imaging 4 : 1 3 , 1 994 35. Yeoman PM: Cervical myelography i n traction in­ juries of the brachial plexus. J Bone loint Surg 50B:25, 1 968 36. Bufalini C, Pesalori G: Posterior cervical electro­ myography in the diagnosis and prognosis of bra­ chial plexus injuries. J Bone Joint Surg 5 1 B:627, 1 969 37. Bonney G, Gilliat RW: Sensory nerve conduction after t1-aClion lesion of the brachial plexus. PI-OC R Soc Med 5 1 :365, 1 95 8 38. SCOll P M : Clayton's Electrotherapy a n d Actino· t herapy. 7th Ed. Ball iere Tindall, London, 1 975 39. Tabary JC, Tardieu C, Tardieu G, Tabary C: Exper· imental rapid sarcomere loss with concom itant hypoextensibility. Muscle Nerve 4: 1 98 , 1 9 8 1

Function of the Nervous System. 2nd Ed. WB Saunders, Philadelphia, 1 976 43. Maitland GD: Peripheral Manipulation. 2nd Ed. ButienvOl1hs, London, 1 977 44. Gutman E, Guttman L: Effects of electrotherapy on denclvatcd muscles i n rabbits. Lancet t : 169, 1 942 45. Hatano E et al: Electrical stimulation on dener­ vated skeletal muscles. p. 469. In Goria A (cd): Posttraumatic Pel-ipheral

NClvc Regcneration:

Expedmental Basis and Clinical Implications. Raven PI"CSS, New York, 1 98 1 46. Reynold C: The stiff hand. p . 95. In Malick H , Kasch M (cds): Manual o n Management o f Spe­ cific Hand Problems. AREN Publication, Pitts­ burgh, 1 984 47. Enos L, Lane K, MacDougal B: Brief or new: the use of self-adherent wrap in hand rehabi litalion. Am J Occup Ther 38:265, 1 984 48. Trombly C, SCOll A: Occupational Therapy for Physical Dysfunction. Williams & Wilkins. Balti­ more, 1 977, p. 7 1 49. Saha AK: Dynamic stability o f the glenohumeral joint. Acta Ol1hop Scand 42:49 1 , 1 97 1 50. Hislop HJ, Pen;ne JJ: The isokinetic concept of exercise. Phys Ther 47: 1 1 4, 1 967 5 1 . Lehman JF, Masock AJ, WalTen CG, Koblanski IN: Effect of therapeutic temperaturc on tcndon extensibility. Arch Phys Med Rehabil 5 1 :48, 1 970 52. Trombly C, SCOll A: Occupational Therapy for Physical Dysfunction. Williams & Wilkins, Balti­

more, 1 984

40. Cooper RR: Alterations during immobilization

53. Hollinshead W: Functional Anatomy of the Limbs

and regeneration of skeletal muscles i n cats. J

and Back. 4th Ed. WB Saunders, Philadelphia,

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1 976.

The Shoulder in Hemiplegia SUSAN

RYE R SON

KATHRYN

LEV J T

Hemiplegia, a paralysis of one side of the body, occurs with strokes or cerebrovascular accidents involving the cerebral hemisphere or brain stem. Although hemiplegia is Lhe classic and most ob­ vious sign of neurovascular disease of the brain, it can also occur as a result of cerebral tumor or trauma. I One of the most worrisome physical prob­ lems for clients with hemiplegia is the shoulder. 2 Shoulder pain, subluxation, loss of muscular ac­ tivity, and loss of functional use are the most common complainLs. These problems can be avoided with proper assessment and treatment and can be ameliorated if they already exist. This chapter reviews biomechanical and motor con­ trol impairments and presents a fTamework for the clinical management of Lhese shoulder prob­ lems in hemiplegia.

Normal, SIuru.lder Girdi£ Mechanics Before beginning a study of the shoulder girdle in hemiplegia, it is important to review the nor­ mal mechanics of the shoulder (see eh. I). Three areas of normal shoulder mechanics should be emphasized: (I) the mobility of the scapula on the thorax,' (2) scapulohumeral rhythm and the

faclOrs influencing both humeral mobility and humeral stability in the glenoid fossa:·5 and (3) the muscular attachments of the shoulder-girdle complex."· Because muscles that move the sca­ pula and humerus have attachments to the cervi­ cal, thoracic, and lumbar spine, and to Lhe rib cage, a loss of motor control and alignment will have multiple effects on the shoulder girdle.

Abrwrmal Bimnechanics The loss of motor conLrol of the shoulder in pa­ tients with a hemiplegia affects the operation of normal biomechanical principles. In hemiplegia, three factors prevent normal shoulder biome­ chanical patterns from occurring: loss of muscu­ lar control and the development of abnormal movement patterns; secondary soft tissue changes that block motion; and glenohumeral joint subluxations. These Lhree factors combine to allow at least three distinct types of shoulder and arm dysfunction. LOSS OF MUSCULAR CONTROL AND DEVELOPMENT OF ABNORMAL MOVEMENT

Following the onset of a cerebrovascular acci­ dent with hemiplegia, a low tone or flaccid state is present. The length of the lower tone state var205

206

PHYSICAL

THERA PY

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SHOULDER

ies from a short period of hours or days to a pe­ riod of weeks or months. This state is character­ ized by a decrease in active postural tone and a loss of motor control in the musculature of the head, neck, trunk, and extremities. Initially, no movement i s possible. As motor return occurs, individual muscles gradually become stronger. In other patients, as motor return occurs, the pattern of control is imbalanced; not all muscles around a joint retum at the same strength. Spinal extensor control becomes more evident than spinal flexor control. Early patterns of motor return pull the scapula and arm into ab­ normal postures. When the scapula and hume­ 'us are pulled severely out of alignment, certain muscle groups are positioned in shortened ranges. This results in lengthening or mechani­ cal disadvantage in opposing muscle groups. Be­ cause the shortened muscles are available to the patient to use actively, muscle activity in these shortened groups is reinforced cortically with the attempt to move the aml. Muscle firing in these groups may also be reinforced by associ­ ated movements7 Thus, "functional spasticity" can develop when muscles of the upper extrem­ ity are maintained in an almost constant state of excitation. A third pattem of motor dysfunction in pa­ tients is characterized by abnormal coactivation of limb or trunk muscles. These patients get re­ turn in both flexor and extensor muscle groups, but have difficulty integrating the firing pattems to produce lateral or rotational movement pat­ terns. These patients also have the ability to re­ cruit distal muscle groups. However, these distal muscle groups are recruited abnormally in what appears to be an attempt to substitute for proxi­ mal weakness. As an example, the biceps and wrist flexors may be recruited to help lift the weight of the arm during shoulder flexion while no contraction of the deltoid can be palpated (Fig. 8.1). Over time, a more constant state of excitation develops in the biceps and wrist flexor muscles, leading to muscle shortening. The con­ stant muscle firing in these shortened groups can quickly pull the carpal bones out of alignment, leading to deformities in the forearm, wrist, and hand. The emergence of spasticity will pe'-petu-

F'GURE 8.1 Left hemiplegia: biceps a17d wrist flexors recruited to help move shoLilder.

ate abnormal alignment. However, inhibition of spasticity alone will not produce a functional arm. Motor reeducation must be directed toward both the recruitment or strengthening of absent or weak muscle groups and the retraining of available muscles to fire appropriately. Thus, treatment must address the abnormal tonal state, abnormal movement components, and ab­ normal joint alignment to restore normal move­ ment. To restore the normal mechanical rela­ tionships of the bones, soft tissue stretching may be necessa ry.

Soft TissLie Blocks to Motio17 Soft tissue blocks to motion can be catego­ rized as loss of scapular mobility, loss of gleno­ humeral mobility, and loss of the ability to disso­ ciate the scapula and hume,us. The loss of scapular stability on the thorax occurs in all but the most minor slrokes, and is influenced ini­ tially by such factors as the pull of the arm into gravity, the development of postural asymmetry, and the influence of pattems of motor retum and treatment. As the scapula assumes a position that combines elements of elevation, downward rotation, and abduction, the position of the sca­ pula prevents forward flexion of the arm past 60' to 80'. Because upward rotation is not available

THE

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HEMIPL EGIA

207

for the scapula, glenohumeral movement greater than 60· is not possible. Without treatment, the scapula loses its mo­ bility on the thorax and becomes fixed, thus eliminating the scapular component of scapulo­ humeral rhythm. The loss of this scapular com­ ponent, consisting of scapular abduction and up­ ward rotation, results in the substitution of scapula elevation. The loss of scapula upward rotation and protraction is important f1Jnction­ ally because it is necessary for reach and pain­ fTee elevation of the arm. However, loss of scapu­ lar adduction and depression has equal func­ tional importance for resistive tasks such as lift­ ing, pushing, carrying, and upper extremity weight-bearing. The goal in treatment is to re­ store the normal resting position of the scapula on the thorax and to regain mobility and motor control in all planes of motion. Changes in scapula position will alter the ori-

FtGURE 8.3 Left hemiplegia: impingement of humeral greater tuberosity beneath acromion.

FtGURE 8.2

Left hemiplegia: inferior subluxation.

entation of the glenoid fossa and affect the rest­ ing position of the humerus. In cases of chronic hemiplegia, the humerus is always positioned in some degree of intemal rotation, but its position relative to the glenoid fossa will depend on the alignment of the scapula. With a downward-ro­ tated and depressed scapula, inferior subluxa­ tion and internal rotation result (Fig. 8.2). In pa­ tients with an elevated, abducted scapula and a hyperextended humerus, the humeral head will be positioned anteriorly in the fossa. In patients with an elevated, abducted scapula and a hume­ rus that postures in abduction and intemal rota­ Lion, the humeral greater tubercle will impinge under the coracoid process (Fig. 8.3). Loss of dissociation of the humerus from the scapula is the third block to nOlmal movement. [n this case, the scapula has mobility on the thorax and the humerus retains mobility in the glenoid fossa, but any movement of the humerus

208

P H Y 5 IC A L

THER A P Y

�

0F

THE

5 H 0 UL 0 ER

�

J..

!J

~ �: \

,

\

A

�

\

,

\

� B

o

c

(A) Nonnal glel10humeral aligl1mel1t. (B) II1{eriol' glel10humeral joil1t sublllxatiol1. (C) Al1Ierior glel10humeral joint subluxation. (D) Superior glenohumeral joint subluxatioll.

FIGURE 8.4

THE

into nexion or abduction results in simultaneous scapular abduction. SHOULDER SUBLUXATION

Shoulder subluxation occurs in hemiplegia when any of the biomechanical factors contrib­ uting to glenohumeral stability are disturbed. The most important factor is the position of the scapula on the thorax. The scapula is nOl-mally held on the thorax at an angle 3D· from the fTon­ tal plane.' When the slope of the glenOid fossa becomes less oblique and no longer faces up­ ward, the humerus "slides down" the slope of the fossa, and inferior subluxation, the subluxation most fTequently mentioned, occurs'·6 Two other forms of subluxation exist in the hemiplegic shoulder: anterior and superior sub­ luxation. Each of these subluxations have down­ ward-rotated scapulae, as does the inferior sub­ luxation, but the other scapula and humeral planes of movement vary (Fig. 8.4). These sub­ luxations are discussed in detail in the next sec­ tion. Subluxation is not painful as long as the sca­ pula is mobile.7 However, the subluxed shoulder should not be allowed to progress into a painful shoulder with loss of passive range of motion (ROM).

SHOULDER

IN

HEMIPLEGIA

209

humerus in relative abduction. With humeral ab­ duction, the shoulder capsule is lax superiorly, and the head of the humerus can slide down the glenoid fossa4 With scapular downward rotation, the gle­ noid fossa orients downward and the passive locking mechanism of the shoulder joint, as de­ scribed by Basmajian,6 is los!. The loss of this mechanism, the loss of postural tone, and the loss of tension of the shoulder capsule result in an inferior humeral subluxation of the hemiple­ gic shoulder. When the body is in an upright position, the weight of the paretic arm and upper trunk will cause the spine to curve with the concavity to the hemiplegic side or to Oex forward (Fig. 8.5). This laterally flexed position of the spine places the scapula lower on the thorax, with inferior angle winging. As motion return occurs and the upper trapezius and levator scapular become ac­ tive, an inferior subluxation may be found with an elevated scapula. In either case, the humerus

Type 1 Ann With a severe loss of muscular activity, head and trunk control are virtually absent. This loss of trunk control results in increased lateral trunk Oexion on the hemiplegia side. The scapula in these patients is downwardly rotated for one or more of the following reasons. First, the loss of scapular muscle activity allows the scapula to lose its normal orientation on the thorax and rotate downward (the superolateral angle moves inferiorly). Second, loss of trunk control results in increased lateral trunk Oexion. The scapula, moving on this laterally Oexed trunk, becomes relatively downward rotated, and the glenoid fossa faces inferiorly.3.4 Third, the weight of the arm, if not supported, will pull the weakened scapula downward and place the

FIGURE 8.5 Type I, left hemiplegia: fonvard flexiol1 of IrLlI1k with flaccid aI'''' influencing scapLlla position.

210

PHYSICAL

THERAPY

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THE

SHOULDER

FIGURE B.6 (A) Type I, left hemiplegia: left side o( body (allil7g laterally into gravity, scapula lower 01'1 thorax. (B) Type I, left hemiplegia: humerus hangs by the side in il'llemal rotatiol7, elbow extension, and (oreann prO/1Qtiol7.

will hang by the side in internal rotation, the elbow will extend passively, and the forearm will pronate (Fig. 8.6). With an inferior subluxation, the humeral head is located below the inferior lip of the gle­ noid [ossa. As subluxation occurs, the shoulder capsule is vulnerable to stretch, especially when the humerus is hanging by the side of the body. In this position, the superior portion of the cap­ sule is taut.' The weight of the dependent hume­ rus will place an immediate stretch on the taut capsule. Over time, the superior portion of the capsule will become permanently lax." When subluxation occurs, the movement possibilities are limited owing to the mechanical position of the humeral head. Any movement that occurs will not follow the rules of scapulo­ humeral rhythm. With an inferior subluxation of

long standing, scapular elevation with humeral internal rotation may be the only movement available. Soft tissue tightness is found in both sections of the pectoral muscles, and posteriorly in the rotator cuff and the insertion of the latissimus dorsi muscle. To re­ duce an inferior subluxation, the scapula must first be upwardly rotated to neutral and moved to its normal position in the frontal plane (ele­ vated if low on the rib cage and depressed if high on the rib cage). The humerus is then moved to neutral fTom internal rotation and lifted up into the fossa. Care must be given to keep the spine aligned vertically during the subluxation reduc­ tion. R E DUCTION OF INFERIOR SU B L UXATION.

THE

Biochemical shoulder problems resulting from this type of arm include I. Downward rotation of the scapula

2. Vertebral border and/or inferior angle wing­ ing of the scapula 3. Inferior glenohumeral joint subluxation 4. Humeral internal rotation

Type /I Ann The second pattern develops as the trunk gains more extension control than flexion con­ trol. An increase in cervical and lumbar exten­ sion is evident. The head and neck assume a posi­ tion of ipsilateral flexion and contralateral rotation. At the thoracic level, this imbalance re­ sults in a unilateral loss of control of the abdomi­ nals. Therefore, the rib cage loses its abdominal "anchor" and will flare laterally and/or rotate (Fig. 8.7). The scapula and humerus are strongly

SHOULDER

IN

H E MIPLEGIA

211

influenced mechanically by this db cage devia­ tion. The downward-rotated scapula begins to move superiorly on the thorax, and the humerus hyperextends with internal rotation. The gleno­ humeral joint will sublux anteriorly. With an an­ terior subluxation, the humerus is internally ro­ tated and positioned inferior to and forward of the glenoid fossa (Fig. 8.4B). The humeral head appears aJigned with the acromion in the sagittal plane, resulting in an apparent shortening of the length of the clavicle. As the humeral head moves forward out of the socket, the distal end of the humerus moves into hyperextension. Infel-ior angle or vertebral border winging of the scapula will occur. This combination of lib cage rotation and humeral hyperextension allows the elbow to flex and the forearm to pronate (Fig. 8.8). As the sca­ pula continues to elevate on the thorax, and the subluxed, internally rotated humerus moves into stronger hyperextension, the humeral head pro­ trudes forward against the proximal end of the

FIGURE 8.7 (A & B) Type II, left hemiplegia: loss of rib cage al1chor with rib cage rotated bachvard and humeral hyperextension with internal rotalion.

212

PHYSICAL

THERAPY

OF

THE

SHOULDER

FIGURE 8.9 Type II, right hemiplegia: ,,,tllieral hyperextension with (orearm S«pilwtioll.

FIGURE 8.8 Type II, left hemiplegia: h«meral hyperextensiol7 with (oreann pronatiol7.

biceps tendon. This forward pressure of the hu­ ments against the already shortened biceps ten­ don will mechanically move the forearm into a supinated position (Fig. 8.9). The wrist may ap­ pear to be less flexed as the carpals move dorso­ laterally. This anterior subluxation will limit move­ ments that require the huments and hand to be in front of the body. If the patient is asked to lift the arm, shoulder elevation with humeral inter­ nal rotation, hyperextension, and elbow f1ex;on will be the movement pattern available. Soft tissue tightness will be present in the pectoral muscle groups, rotator cuff, biceps, forearm, and hand. To con'ect this subluxation, the rib cage is derotated and spinal alignment is cOiTected; the scapula R E D UCTION OF

ANTERIOR

SUBLUXATION.

can then be realigned on the rib cage. To realign the scapula on the rib cage, it must be moved down from its elevated position and upwardly rotated to neutral. While stabilizing the scapula in its corrected position, the huments is moved from internal rotation to neutral. The humeral head can then be moved back as the distal end of the huments is brought forward out of hyper­ extension, and then lifted up into the fossa. Biomechanical shoulder problems resulting from this type of arm include I. Downward rotation and elevation of the sca­ pula

2. Scapular inferior angle andior vertebral bor­ der winging 3. Anterior subluxation 4. Humeral internal rotation

In chronic cases of anterior subluxation, elbow flexion becomes more dominant and the forealTn adducts across the abdomen. Shorten­ ing and spasticity in pectoral and biceps groups

THE

SHOULDER

IN

HEMIPLEGIA

213

may develop, and the scapula loses mobility in the direction of depression and upward rotation.

Type /II Ann The third type of arm pattern is character­ ized by abnormal coactivation of the limb mus­ cles. This gives an appearance of "mass" flexion in the hemiplegic upper extremity. The neck and tnmk control in clients with this upper extremity pattern contain elements of both flexion and ex­ tension. The control patterns are not sufficiently integrated to allow selective combinations of movement, and rib cage f1airing accompanies ac­ tive movement of the hemiplegic arm. The sca­ pula is usually elevated and abducted on the thorax. The scapula moves superiorly and tilts anteriorly, causing the humerus to lie under the coracoid process in a superior subluxation. The humerus is tightly held in internal rotation and abduction, so that the elbow joint lies directly below the shoulder in the frontal plane but is abducted away from the rib cage. Passive motion of the glenohumeral joint is severely limited because the humeral head is lodged under the coracoid process. Although the deltoid and biceps attempt to initiate humeral motion, no dissociation occurs between the hu­ merus and scapula. During attempts to move, these patients typically "fire" strongly in this ele­ vation-abduction-internal rotation pattern, with elbow and wrist flexion (Fig. 8.10). By in­ creasing humeral internal rotation, patients can "lock" their elbows into elbow extension. When distal movement exists, it is used to reinforce the active shoulder pattern. The wrist assumes a flexed and radially deviated position. This moves the forearm from pronation in the direction of supination. Soft tissue tightness in the deltoids, pector­ als, and rotator cuff are frequent secondary com­ plications. Soft tissue tightness in these groups is often mistaken for atrophy from brachial plexus injury. The superior subluxation is the most difficult to re­ duce. The scapula is returned to a neutral posi-

R E D UCTION OF SUPERIOR SUBLUXATION.

FIGURE 8.10 Type If{, left hem.iplegia: active 1110tion available in shoulder elevation, I",meral abduction, internal rotation, al1d elbow flexion.

tion; it must be lowered, rotated upward, and adducted. The humerus is externally rotated to neutral, using slight traction if necessary. Exter­ nal rotation of the humerus is then combined with horizontal adduction of the distal humerus as the humeral head is brought back into the fossa. Biomechanical shoulder problems resulting from this type of arm include I. Scapula elevation and abduction with vertebral border winging

2. Superior subluxation 3. Humeral internal roLation 4. Lack of dissociation between scapula and humerus, and between scapula and rib cage

Relatiol1ship of Subluxatiol1 to COl1lrol The type of shoulder subluxation and the mOlOr control available affect the hemiplegic pa­ tient's ability to move the arm functionally in three ways. First, the loss of antigravity postural

214

PHY SICAL

THERAPY

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THE

SHOULDER

tone ;lnd the subsequent pallerns of moLion re­ turn will change the relationship of the scapula to the trunk and the relationship of the distal arm to the scapula. This change in position will alter the anatomic relationship of the jOinls. Sec­ ond, the changes in bony alignment will change the resting length and direction of pull of the major muscle groups of the shoulder and arm. Biomechanically, this will lead to muscle imbal­ ance and problems of motor control. Third , changes in muscle excitation and recruitment pallerns may occur in these muscles, in which resting lengths have been altered. Pallerns of spasticity or abnormal coaclivation of muscles may result in problems in any or all of these areas and will contribute to the abnormal and ineffi­ cient motor pallerns associated with hemiplegia. Clinically, it is necessary to analyze the patient's motor patterns to identify the segments of abnor­ mal motion. This will facilitate more effective treatment.

ance or improper movement pallerns. When the joint is improperly aligned, passive or active mo­ tion either with or without weight-bearing will result in joint pain. This pain is sharp and stab­ bing in nature. It is relieved immediately when joint alignment is corrected. At the shoulder, joint pain occurs when glenohumeral alignment and rhythm is not maintained. The most fre­ quent reasons for poor al ignment are (t) lack of appropriate humeral rotation during forward flexion and (2) improper placement of the hu­ meral head in the glenOid fossa. Treatment for this type of pain begins with immediate cessation of the movement pattern. Forced motion with pain must never be allowed. The movement should STOP; the limb should be lowered, and the bones must be cOITectly re­ aligned before treatment begins again. If soft tis­ sue orjoint tightness exists, realignment may not be possible unless soft tissue or joint mobility is improved or increased.

MuscuWskeletal C011Si.derations SHOULDER PAIN

Shoulder pain is one of the major problem areas in hemiplegia.' Pain occurs in the hemiplegic shoulder as a result of muscle imbalance with 10 s of joint range, impingement of the shoulder capsule during improper ROM, improper mus­ cle stretching, tendinitis, hypersensitivity, or hy­ posensitivity; pain also is caused by sympathetic changes. To plan a treatment program, the nature of the pain, the precise anatomic location of the pain, the duration of the pain, and the body posi­ tion during the movement that causes the pain must be assessed. Four categories of shoulder pain can be identified: joint pain, muscle pain, pain from altered sensitivity, and shoulder-hand pain syndrome.

Join' Pain Joint pain in hemiplegia occurs when a joint is placed in a biomechanically compromised po­ sition as a result of either shoulder muscle imbal-

FIGURE 8.1 I Left hemiplegia: body moving 0/1 weight-bearing upper extremity.

THE

Muscle Pain Muscle pain occurs as a shortened or spastic muscle is lengthened too fast or lengthened be­ yond the range to which the shortened muscle is "accustomed." Often, this type of pain occurs when the upper extremity is in a weight-bearing position and the patient is asked to move the body on the limb (Fig. 8.11). Muscle pain is per­ ceived as a "pulling" sensation and is localized to the region or the muscle belly that is being stretched. The pain is immediately relieved if the amount or severe stretch is decreased a few de­ grees. Because lengthening shortened muscles is a goal or treatment, the muscle is not allowed to move back to the shortened range, but is allowed to shorten until the pain is relieved. Treatment can proceed with careful attention given to speed and progression or movement. The pain that accompanies tendinitis is re­ lated to muscle pain , [or it is caused by the same mechanisms. Overstretching or a limb muscle rollowed by overaggressive weight-bearing with poor jOint alignment results in tendinitis. The pain is described as aching or sharp, remains arter the weight-bearing is stopped, and is re­ rerred to other locations. In the hemiplegic upper

FIGURE 8.12

SHOULDER

IN

HEMIPLEGIA

215

extremity, the two most common types are bicip­ ital groove tendinitis with pain referred down into the muscle belly, and bicipital tendinitis across the elbow with pain referred down the volar aspect of the forearm. The inappropriate weight-bearing pattern that leads to tendinitis in these cases is severe humeral internal rotation with forced elbow extension, along with an inac­ tive trunk and "leaning" on a weak scapula (Fig. 8.12). The weight-bearing extended arm activity should be stopped until the pain subsides. When weight-beru;ng treatment is resumed, particular care should be given to proper joint alignment and active trunk scapular pattern (Fig. 8.13).

Altered Sensitivity The pain that occurs because or altered sen­ sitivity of the central nervous system (eNS) to sensory input is found at the acute stage of recov­ ery following an insult. This pain occurs in the upper extremity, and is described as both diffuse and aching and local­ ized to the shoulder and sharp. It typically occurs during the middle or a treatment session that has included tactile , sensory, kinesthetic, and propri-

Le(t hemiplegia: weight-bearing with improper alignment.

216

PHY SICAL

THER APY

FIGURE 8.1 3

OF

THE

SHOULDER

Left hemiplegia: weight-bearil1g with proper alignment.

oceptive stimuli. One explanation for its occur­ rence is that the levels of "tolerance" of the im­ paired eNS have been reached. The treatment should stop for that session, and the duration of treatment and the nature of the treatment should be noted. Subsequent treatment should be graded to allow movement to continue but not to exceed the patient's sensory tolerance. If treat­ ment is stopped completely, these patients may proceed to shoulder-hand syndrome.

Shoulder-Halld Syndrome Shoulder-hand syndrome begins with dif­ fuse "aching pain" in the shoulder and entire arm. Because this pain interferes with the desire to move the arm, the hand soon becomes swollen and tender. If passive motion is forced on a swol­ len wrist and hand, the joints will become sharply painful. The second stage is characterized by de­ creased ROM of the shoulder girdle, hand, and fingers. Skin changes are also present because of the lack of motion and loss of tactile input. The syndrome culminates with presence of atrophied bone and severe soft tissue deformity

and joint contractures. Shoulder-hand syn­ drome can be prevented by a program that I. Grades the motor program in stages with in­ creasing sensitivity to movement

2. Gradually but consistently uses weight-bear­ ing activities for the entire shoulder girdle and upper extremity 3. Reeducates open-ended activities (non­ weight-bearing) with appropriate scapulo­ humeral rhythm 4. Prevents edema 5. Teaches patients how to care for their arm

Treat:rnent

Pln.nning

The treatment of the deficits in motor control in the patient with hemiplegia focuses on the im­ provement of function and the prevention of fur­ ther disability from secondary complications. In this section, treatment objectives for the hemi-

THE

plegic shoulder will be presented in three major categories. The first category of objectives is de­ signed to help the patient releam basic postural control. The second set of objectives focuses on the neuromuscular deficits of hemiplegia: loss of extremity motor control and function. In the third category, the objectives for the secondary complications of hemiplegia-subluxation, pain, loss of motion, and spasticity-will be dis­ cussed.

SHOULDER

IN

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217

non-weight-bearing palterns, and (4) reeducat­ ing distal movement for functional skills.

Reestablishing Nonnal Alignlllent It is necessary to reestablish normal align­ ment before attempting to reeducate motor con­ trol. The shoulder girdle must be properly aligned either by lengthening shortened or spas­ tic muscles or by supporting body parts that do not have sufficient muscular activity.

REESTABLISHMENT OF POSTURAL CONTROL

The objectives for establishing postural control include (I) facilitating righting reactions, equi­ librium reactions, and protective reactions; and (2) providing normal tactile, proprioceptive, and kinesthetic input. Before specific retraining of the shoulder in patients with hemiplegia can begin, postural control of the head, neck, and trunk must be present. This postural trunk con­ trol provides the body with the ability to shift weight. The ability of the body to shift and bear weight to one side fTees the opposite extremity for the functions of reaching, grasping, and re­ leasing. Along with sensory feedback (tactile, proprioceptive, kinesthetic, visual, and vestibu­ lar), movement requires a base of stability or base of support, a point of mobility, and a weight shift. Weight shift, either anterior, posterior, lat­ eral, or diagonal, is followed by one or more of the following: righting reactions, equilibrium re­ actions, protective reactions, or falling. The es­ tablishment of head and neck control allows the shoulder girdle to dissociate or move freely from the thorax and the humerus to dissociate from the scapula. To establish good motor control, the body (trunk) must be able to adjust posture auto­ matically so that an upper extremity movement may achieve its purpose. NEUROMUSCULAR DEFICITS

Objectives for reestablishing motor control and function of the hemiplegic arm include (I) rees­ tablishing normal alignment, (2) establishing normal weight-beal;ng patterns in the upper ex­ tremity, (3) initiating and "holding" proximal

Establishing Weight-Bearing The ability to accept and bear weight on the affected aIm following a stroke is one of the most important goals of a therapeutic program. Active weight-bearing on either a partially flexed or ex­ tended upper extremity is used as a means of increasing mobility; increasing postural control of the trunk.; improving motor control of the af­ fected arm; introducing and grading tactile pro­ prioceptive, and kinesthetic stimulation; and preventing edema and pain. Positions that pro­ vide weight-bearing for a hemiplegia shoulder and arm include (I) rolling onto the affected side in preparation for getting out of bed (Fig. 8.14A and B), (2) supporting the forearm on a pillow placed in the lap or on a lap board or on a table when silting (Fig. 8.14C), and (3) extending the weight-bearing arm down onto a countertop while standing. An active weight-bearing program for the pa­ retic arm stresses "active" pattems in the trunk and does not allow the patient to lean or "hang" on the ligaments of the affected extremity (Fig. 8.1SA and B). This active participation of the trunk. is accomplished by plaCing the upper ex­ tremity in an aligned weight-bearing position and asking the trunk or "body" to move on the stable arm in anterioposterior, lateral, and rota­ tional directions (Fig. 8-1SC to H). In the acute stage of hemiplegia, when very little postural control is present, upper extremity weight-bearing is used to facilitate proximal motor control. When the upper extremities are "fixed" onto the supporting surface through fore­ arm weight-bearing activities, the arm becomes

218

PHYSICAL

THERAPY

OF

THE

SHOULDER

FIGURE 8.14

Weight-bearing positions (or the LIpper extremity.

(A) Left hemiplegia: rolling onto afef cted

hemiplegia: //loving onto affected sLlpporting (oreann 011 table.

a point or stability ror movements of the trunk and pelvis. As the body moves away from the arm, scapular protraction and upward rotation, humeral nexion, and upper trunk nexion are en­ couraged (Fig. 8.16A). As the body moves toward the arm, scapular adduction and trunk extension are encouraged as the humerus moves into more extension (Fig. 8.16B). When the pelvis and trunk move laterally, the scapulae move in oppo­ site directions. one into more abduction and one into more adduction. The humerus on the side or the lateral weight shirt becomes more externally

rotated, while the other humerus becomes more internally rotated (Fig. 8.17). For patients with available but synergistic movement patlerns, upper extremity weight­ bearing can be used to lengthen or inhibit tight or spastic muscles while simultaneously racili­ tating muscles that are not active. When the person sits with hands down and open, a rota­ tional movement of the body toward the ar­ fected upper extremity will lengthen tight shoul­ der depressors and downward rotators, tight humeral internal rolatOl-S, and elbow nexors,

THE

while simultaneously activating the opposing groups (Fig. 8.18A & B).

iI,itiatil1g and "Holdil1g" Proximal Non-Weight-Bearing Paltems When the hand or arm is placed in a position of weight-bearing, the motions of the shoulder girdle occur as a reaction to the body's move­ ment over the rixed extremity. When the arm is

SHOULDER

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219

taken out or weight-bearing and is asked to move in space, the demands on the shoulder girdle are dirferent from weight-bearing demands. The motor demands on the shoulder for non-weight­ bearing (open-ended) activities can be divided into (I) the ability to hold the weight of the limb against gravity; (2) the ability to initiate antigrav­ ity movement paUerns, including the ability to switch from glenohumeral to scapulohumeral movement as needed; and (3) the ability to recip-

•

J A

D

/. ur..o:...____ . �l.,

B

c

E

FIGURE B. t 5 (A) Right hemiplegia: improper lI'eight­ bearil1g 011 extended anl1-"hal1gil1g" 011 shoulder a l1d mechal1ically 10ckil1g elbow. (8) Right hemiplegia: extended arm weight-bearing. (C-H) Establishing extended­ arm weight-bearing il1 silting. Therapist aligl?S palients left shoulder while she practices combining trunk and arm nlovements. (Figure continues)

220

PHYSICAL

THERAPY

F

H FIGURE S.15

(Conril1ued)

OF

THE

SHOULDER

rocate and coordinate the combinations of mo­ bility and stability needed for reaching, grasping, carrying, and releasing. Motor reeducation aimed at training the hemiplegic arm to move against gravity will vary according to the patterns of return present and variables such as pain, spasticity, or malalign­ ment. Techniques for managing pain and spas­ ticity are discussed under ''Treatment of Second­ my Complications" later in the chapter and should be used before treatment of motor con­ trol proceeds. Orthopedic changes, particularly those that are long standing, represent a particu­ lar treatment challenge because although ortho­ paedic malalignment at the shoulder will neces­ sitale compensation or abnormal movement, it is frequently impossible within a treatment ses­ sion to reposition the scapula or humerus in nor­ mal alignment before proceeding with move­ ment reeducation. In these cases, the goal is to gain some increase in mobility in the direction of normal alignment, followed immediately by a movement pattern that uses this new mobility. Over successive treatments, as soh tissue mobil­ ity is increased and passive resting positions be­ come closer to normal alignment, the types and combinations of movement can be increased. When pain, spasticity, and malalignment of the shoulder joints are not problems, treatment can be directed immediately to improving motor control. in the acute stage, in which muscle tone is low and little motion is present, teaching the patient to manage the weight of the arm against gravity is the first stage of motor control to be introduced. This is done by teaching the patient to "hold" the scapula and humerus in an anti­ gravity position (Fig. 8. 19A).7.9 "Place and hold" activities are practiced in supine and, later, in sitting positions until the patient develops con­ trol of the arm in various combinations of sca­ pula and humeral patterns (Fig. 8.19B and C). The patient is then taught to move actively within his or her range of control. When the con­ cept of holding has been achieved, the patient is asked to initiate patterns at the shoulder. This is done by moving the hemiplegic ann in many functional patterns combined with strong sen­ sory stimulation during each treatment session.

THE

SHOULDER

I N

HEMIP L E G I A

221

•

B FIGURE B . 1 6 Right hemiplegia: (A) moving body away from weight-bearing ann; (8) moving body toward weight-bearing arm.

Muscle groups that are unable to contract after the joint has been realigned need to be stimu­ lated. The techniques of stimulation have been described by Bobath and others. The techniques are the same, although they have been ascribed different names, including joint compression (pressure tapping, joint approximation); resis­ tance with proper alignment maintained; quick stretch (inhibitory tapping, "pull-push"); sweep tapping (bmshing, icing); and repetition. When the patient has movement available,

FIGURE B. 1 7 Right hemiplegia: weight shifting to right moves right humerus into more external rOlalion while left htllnerus begins /0 move into Ihe direClion of inlernal rOlalion.

but efforts to move the ann produce abnormal pallerns, treatment is directed toward establish­ ing more normal coordination. This may involve both inhibiting the abnormal way in which mus­ cles are recmited and retraining in the COITect pallern of motor recmitment. Problems in motor recmitment can best be addressed by teaching the patient to identify and quiet muscles that are firing inappropriately through techniques of in­ hibition or biofeedback. The patient is then taught to allow passive motion of the arm with­ out firing muscles inappropriately or allowing muscle tone in the ann to increase. The patient is then encouraged to try to "follow" the movement and finally to perform it actively with less assis­ tance from the therapist. Place and hold exer­ cises are useful in helping the patient use the correct muscles at the shoulder girdle without inappropliately firing distal muscle groups. While new recmitment pallerns are being estab­ lished, the patient is also taught appropriate con­ trol of the previously "overused" muscles. Thus, the patient learns to inhibit biceps activity when reaching, but to use the biceps appropriately to bling the hand to the mouth. Patients who have less spasticity or more complete motor return have fewer problems with abnormal recmitment but more problems with motor control. This category of patients has missing components of motor activity. Compen­ satol), motions resembling an abnormal pattern result. For example, lack of active external rota-

222

PHY SICAL

T H ERAPY

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FIGURE B. I B (A & B ) urt hemiplegia: rotational body movements over a weigh/­ bearing upper exrremity.

B

A

tion of the humenls will lead to a substitution pattern of abduction, internal rotation of the hu­ menlS, and scapula elevation (Fig. 8.20). If this motor pattern is being used because the patient cannot actively externally rotate the humenls, the goal of treatment must be to make external rotation available during active shoulder move­ ment and to establish the ability to hold the hu­ merus in external rotation while moving distally. Similarly, other patients may have difficulties with protraction and upward rotation of the sca­ pula. In this case, the therapist must control the motion of the scapula proximally to facilitate the correct motion of the scapula while the patient works on upper extremity placing or movement sequences.

position the hand appropriately for grasp by se­ lecting appropriate forearm and wrist positions, hold the hand in position while the fingers move, and sustain grasp while moving proximally. Problems in any of these areas may inlerfere with adaptive grasp. As shoulder girdle control builds, the posi­ tions and movements of the distal segments must be added in treatment so that various distal posi­ tions are available to the patient to use function­ ally. As new combinations of motor behavior are learned, the patient should be taught a fllllc­ tional task using this pattern to ensure carry-over from exercise into everyday life.

Reedllcating Distal Movemel1lS Distal motor control, to be accurate, must be based on normal patterns of mobility and stabil­ ity in the scapula and glenohumeral joint. Once the patient can initiate normal motion at the gle­ nohumeral and scapulothoracic joints and can maintain the shoulder in positions against grav­ ity, the patient must learn to add combinations of elbow position and forearm rotation to the control established at the shoulder. To use the hand functionally for grasping, carrying, and re­ Ip:;'I Walch et al. 3J arthroscopically evaluated 1 7 throwing athletes with shoulder pain during

PATHOLOGY

FIGURE 11.1

AND

REHAB I LITAT I ON

283

Schematic representation of

posterosuperior glenoid impingement between the posterior edge of the glenoid and the deep surface tendollS. (From Walch et al.,33 with permission.)

throwing and found undersurface impingement that resulted in 8 partial-thickness rotator cuff tears and 12 lesions in the posterosuperior la­ bn.lm. Impingement of the undersurface of the rotator cuff on the posterosuperior glenoid la­ bnlm may be a cause of painf'ul structural dis­ ease in the overhead athlete. One final type or classification of rotator cuff tear is the intratendinous or interstitial rotator cuff tear. This tear develops between the bursal and articular side layers of the degenerated ten­ don. 34 Shear within the tendon appears to be re­ sponsible in the pathogenesis of this rotator cuff tear. Rotator cuff pathology has several underly­ ing etiologic factors, as evidenced by the classifi­ cation schemes and scientific research in the lit­ erature. Although it is imperative to understand the common causes and classifications of rotator cuff pathology and types of rotator cuff tears, it is of paramount imponance that a stnlctured, SCientifically based evaluation procedure is used not only to identify rotator cuff pathology but to ultimately identify the cause.

284

PHYSICAL

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OF

THE

SHOULDER

Clinical, Evaluation of the Shoulder for Rotator Cuff Patlwwgy It is beyond the scope of this chapter to com­ pletely cover a comprehensive evaluation of the shoulder; this is provided in Chapter 3. A brief discussion of specific aspects of the evaluation process that are of critica1 impOI·tance in identifi­ cation and delineation of rotator cuff pathology, however, is wan-anted. The multiple etiologies and specific types of rotator cuff pathology are reflected in the types of clinical tests routinely employed. During the subjective exam, specific ques­ tioning, particularly for the overhead athlete, can greatly assist in understanding the probable cause and type of rotator cuff injury. Merely es­ tablishing that the patient has pain with over­ head throwing or during the tennis serve does not provide the optimal level of information that more speCific questioning aimed at identifying what stage or phase of the overhead activity would. Specific muscular activity patterns and joint kinetics inherent in each stage of these sport activities can assist in the identification of compressive disease or tensile type injuries. The presence of instability, however subtle, during the cocking phase of overhead activities can pro­ duce impingement or compressive symp­ toms,9.32.33 whereas a feeling of instability or loss of control during the follow-through phase dur­ ing predominantly eccentric loading can indi­ cate a tensile rotator cuff injury'" Additional questions regarding a change in sport equip­ ment, ergonomic environment, and training his­ tory provide information that is imperative in understanding the stresses leading to injury. Objective evaluation of the patient with rota­ tor cuff pathology must include postural testing and observation. 35 Tests to identify scapular winging in multiple positions (waist level, and 90' of flexion or greater) with an axial load via the arms are indicated. Testing for scapular dys­ kinesia can be performed using the Kibler scapu­ lar slide test in both neutral and 90' elevated po­ silions. 3 6 A tape measure is lIsed to measure the

distance from a thoracic spinous process to the infe,-ior angle of the scapula. A difference of more than I cm is considered abnormal, and may indicate scapular muscular weakness and poor overall stabilization of the scapulothoracic joint.36 A detailed, isolated assessment of glenohu­ meral joint range of motion is a key ingredient to a thorough evaluation. Identification of selective internaJ rotation range of motion loss on the dominant extremity was consistently reported in elite tennis players3 7.3 8 and professional baseball pitchers. (Ellenbecker TS: unpublished data, 1 99 1). A goniometric method using an anterior containment force by the examiner ( Fig. 1 1 .2) to minimize the scapulothoracic contribution and or substitution is recommended by this author. The loss of internal rotation range of motion is significant for two reasons. The relationship be­ tween internal rotation range of motion loss (lightness in the posterior capsule of the shoul­ der) and increased anterior humeral head trans­ lation has been scientifically identified. The in­ crease in anterior humeral shear force reported by Han-yman et al. 39 was manifested by a hori­ zontal adduction cross-body maneuver, similar to that incurred during the follow-through of the throwing motion or tennis serve. Tightness of the posterior capsule has also been linked to in­ creased superior migration of the humeral head during shoulder elevation 40 Anterior translation of the humeral head and superior migration are two key factors indicated in rotator cuff pathol­ ogy. 8.9Internal rotation range of motion loss has also been consistently identified in a population of patients with glenohumeral joint impinge­ ment.4 1 Measurement of active and passive internal and external rotation at 90' of abduction along with scapular plane elevation, forward flexion, and abduction are performed during the evalua­ tion of the patient with rotator cuff injury. Docu­ mentation of combined functional movement patterns (Apley's scratch test),·2 such as internal rotation with extension, and abduction and ex­ ternal rotation, is important, but specific, iso­ lated testing of glenohumeral joint motion is a

R OTATOR

FIGURE 11.2

CUFF

PATHOLOGY

AND

R EHAB I L I TAT I ON

285

Goniometric

measurement of ;ntenw/ rota/ion range o( motio17.

necessary requirement to identify important gle­ nohumeral joint motion restrictions.) 7 Detelmination of isolated and gross muscu­ lar strength during the evaluation of the patient with rotator cuff pathology not only has a major impact on the determination of the underlying cause. but assists in the formulation of a specific. objectively based rehabilitation program. Iso­ lated testing in the "empty can" position for the supraspinatus is performed in the scapular plane. 30° anterior to the coronal plane (Fig. 4 J J . 3 ) . 3 .44 Testing for the infraspinatus and teres minor is done with resisting external rotation in both the neutral adducted and 90° abducted posi­ tion. Resisted internal rotation in the neutral ad­ ducted position is generally recommended for the subscapularis. 44 Care must be taken when interpreting normal grade static manual muscle tests of the internal and external rotators. Nor­ mal grade % muscular strength has shown large variability when compared to isokinetic testing in patients with rotator cuff pathology. and in normal controls. 4S Regardless of this repOl-ted variability. the consistent application of manual muscle testing for the rotator cuff. deltoid. scap­ ular stabilizers. and distal upper extremity mus­ cle groups is highly recommended. For the pa­ tient with subtle symptoms and apparently

FIGURE 11.3

Supraspinatus MMT POSiTiol1.

286

PHYSICAL

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nOl-mal muscular strength, more specific, dy­ namic, isokinetic testing is indicated to better identify muscular weakness or u nilateral strength imbalances··

Special Tests The classic tests for evaluation of a patient with rotator cuff pathology are the impingement tests. The impingement test reported by Neerlo.11 places the shoulder in full forward flexion with overpressure. This places the su­ praspinatus under the coracoacromial arch, and can compress the tendon and reproduce the patient's symptoms. A second impingement test, reported by Hawkins and Kennedy, 47 in­ volves 90° of forward flexion with full internal rotation. This test passes the rotator cuff under the coracoacromial arch, with pain and a facial grimace being indicative of a positive test. A final impingement test is the crossed arm ad­ duction test, which involves horizontally ad­ ducting the humerus starting in 90° of elevation. These impingement tests primarily indicate the presence of rotator cuff injury from compres­ sive or impingement etiology.10.48 Tests to de­ termine the i ntegrity of the static stabilizers of the glenohumeral joint are a vital part of the comprehensive evaluation. 8.9 Rotator cuff in­ jury caused by instability of the glenohumeral joint is a common occurrence in younger indi­ viduals and in overhead athletes. 8.9 Clinical tests for instability must be routinely performed on the patient with rotator cuff pa­ thology, to determine the underlying mobility status and/or degree of instability in the glenohu­ meral joint. Clinical tests for instability of the glenohumeral joint include the apprehension and M D I sulcus signs, as well as the fulcrum, load and shift, and subluxation relocation tests. ( Further discription of these clinical tests can be found in Chapter 3). The subluxation relocation test popularized by Jobe8.32 is performed with the patient supine, with 90° of glenohumeral joint abduction and 90° of external rotation. The examiner pushes the humeral head forward,

using one hand on the posterior aspect of the patient's shoulder. This places tension on the an­ terior capsule and can produce a subtle anterior subluxation of the humeral head, often repro­ ducing the patient's shoulder pain. 8 The reloca­ tion portion of the test consists of a posteriorly directed force produced by the examiner, by placing the heel of the hand over the humeral head anteriorly. This posterior force centralizes the humeral head in the glenoid fossa. A positive subluxation/relocation sign consists of provoca­ tion of the patient's symptoms, with the anterior translation in the position of 90° of abduction and external rotation, with cessation of the symptoms with the relocation (posterior central­ ization force). Capsular mobility testing with the patient su­ pine at 30°, 60°, and 90° of abduction is also per­ formed with both anterior and posterior stresses imparted. The anterior stress applied at 30°, 60°, and 90° tests the integrity of the superior, middle, and inferior glenohumeral ligaments, respec­ tively·8 The degree of translation of the humeral head relative to the glenOid, as well as endfeel, are bilaterally compared and recorded ·"9 Cap­ sular mobility testing with the shoulder in 90° of abduction is particularly important, due to the important hammock-like stabilizing function of the inferior glenohumeral ligament complex. The anterior band of the inferior glenohumeral ligament provides critical reinforcement against anterior translation of the humeral head (sublux­ ation) with the arm in a position of 90° of abduc­ tion and 90° of external rotation 48 An additional test to determine the degree of anterior capsular laxity is the Lachman test of the shoulder· With the patient supine and the shoulder abducted 90° with 45° of external rota­ tion, an anterior force is applied to the humeral head to assess anterior translation of the gleno­ humeral joint and note the end point of the ante­ rior capsule· The consistent use of these instability tests will provide the clinician with greater insight re­ garding the relationship, if any, between the pa­ tient's rotator cuff pathology and glenohumeral joint instability. The identification of either ante­ rior or multidirectional glenohumeral joint lax-

R OTATOR

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ity should lead to the formulation of a treatment plan addressing the instability 9 The special tests listed above are by no means comprehensive, with many other areas of significant emphasis, such as tests to determine the integrity of the biceps and glenoid labrum, being of paramount importance. Interpretation of the results of a comprehensive evaluation will allow the clini­ cian to develop an objectively based rehabilita­ tion program for rotator cuff pathology.

Biomechani.cal Concepts Jor Rehalril.itati<m oj Rotator Cuff PaIlwliJgy Several biomechanical concepts have significant applications in the fOlmulation and application of rehabilitative exercise for the patient with ro­ tator cuff pathology. One important concept is the force couple. A force couple consists of a pair of forces acting on an object that tends to pro­ duce rotation, even though the forces may act in opposing directionsSO An example of a force couple in the shoulder is the deltoid-rotator cuff force couple outlined by [nOlan et al. 5J The force vector of the deltoid, if contracting unopposed, is superior. which would create superior migra­ tion of the humeral head. 52 The supraspinatus muscle has a compressive [unction when con­ tracting, creatingan approximation of the hume­ rus into the glenoid (Fig. 1 1 .4). The infraspi­ natus, teres minor, and subscapularis produce a caudal rorce that resists the superior migration of the humeral head. One factor of key impor­ tance when clinically interpreting the force cou­ ple concept is the muscle's force potential in rela­ tion to its physiologic cross-sectional areaso Research shows the subcapularis to have the greatest force potential, followed closely by the infraspinatus-teres minor groupSO The smallest physiologic cross-sectional area is exhibited by the supraspinatus. These small rotator cuff cross-sectional areas paJe in comparison to the larger force-generating capacities of the deltoid muscle. The presence of a force couple imbal-

FIGURE 11.4

Deltoid-rotator Cliff (orce callpie.

ance is often identified on initial evaluation of the patient with rotator cuff pathology. 3S . ! Weakness of the rotator cuff, coupled with hy­ pertrophy or training enhancement of the del­ toid through uneducated exercise prescription by the patient using traditional "large shoulder muscle group dominant" resistive training exer­ cises, further perpetuates this force couple im­ balance. The coordinated interplay between the rota­ tor cuff and deltoid musculature ic f,!rther dem­ onstrated in EMG analysis by Kronberg et al. 2 .

This study illustrates that all of the rotator cuff muscles are involved, to some extent, with basic shoulder movements, acting to assist in the movement and counterbalance the micromo­ tions of the humeral head to keep it stable within the glenoid. Additional force couples described in the lit­ eratureS .50 are the serratus anterior-trapezius and internal-external rotator couples. The serra­ tus anterior-trapezius force couple is also impor­ tant in rotator cuff pathology, as it produces up­ ward rotation of the scapula, ' moving the overlying acromion superiorly out of the path of the elevating proximal humerus. The internal-ex­ ternal rotator force couple is another commonly imbalanced pair in the overhead athlete, due to

288

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selective development of internal rotation strength, which overpowers the controlling and decelerative influence of the external rota­ tors.50,53,54 Further evidence of the rotator cuffs vital function in glenohumeral joint arthrokinematics has been demonstrated by Cain et al.55 and Blaiser' in cadaveric studies. These studies have shown the rotator cuffs ability to reduce the strain on the anterior capsule (inferior glenohu­ meral ligament) with the shoulder in 90° of ab­ duction and external rotation. This important stabilizing function to resist anterior translation demonstrates the rotator cuff's critical contribu­ tion to joint stability. Additional biomechanical research by Clark et al.'6 identifies the int imate, adherent association of the rotator cuff to the capsuloligamentous structures, and the ability of rotator curr muscular contraction to create ten­ sion and effect orientation of the capsuloliga­ mentous complex. Muscular force vectors have been studied with the shoulder in the functional position of 90° of abduction and external rota­ tion.57 In this abducted position, the subscapu­ laris functions as a flexor and internal rotator, the supraspinatus as an extensor, and the infra­ spinatllS as an adductor. This study demon­ strates the importance of working the dynamic stabilizers of the shoulder in both neutral and functional positions to most closely simulate the actual muscular length, tension, and contraction specificity incun·ed in ADL and overhead sport movement patterns.

RehabilitaJ:Wn of Rotatnr Cuff Patlwlogy Both nonoperative and postoperative rehabilita­ tion of the rotatorcuff involve the following prin­ ciples. REDUCTION OF OVERLOAD AND TOTAL ARM REHABILITATION

The initial goal of any treatment program in­ cludes the reduction of pain and inflammation by protection of the extremity from stress, but

not complete function.2o Application of modali­ ties and modification of, or complete cessation of, sport and ergonomic movement patterns is often required. Care should be taken to identify the presence of any compensatory actions in the upper extremity kinetic chain, such as excessive scapular movement andior elbow kinematics.'8 Early use of distal strengthening of the elbow, forearm, and wrist is indicated, pat1.icularly in postoperative cases where the degree and length of immobilization is greater. Mobilization of the scapulothoracic joint and submaximal strength­ ening of the scapular stabilizers is indicated, tak­ ing great care not to impart inappropriate stresses or loads to the injured tissues.

RESTORATION OF NORMAL JOINT ARTHROKINEMATICS

Thorough evaluation to determine the degree of hyper or hypomobility of the glenohumeral joint, coupled with isolated joint range of motion mea­ surements, predicates the progression of and in­ clusion of stretching and joint mobilization in treatmenl . The presence of increased anterior capsular laxity and underlying instability of the glenohumeral joint, a finding conSistently found in overhead athletes, contraindicates the appli­ cation of joint accessory mobilization and stretching techniques that attenuate the anterior capsule. Posterior capsular mobilization and stretching techniques to improve internal rota­ tion range of motion are often indicated and ap­ plied. The consequences of posterior capsular tightness have been outlined earlier in the chapter. In postoperative rehabilitation of rotator cuff repairs, the use of joint mobilization tech­ niques to both retard and address the effects of immobilization is recommended. In addition to the posterior capsular mobilization described, specific emphasis on the caudal glide in varying positions of abduction is applied assertively, to stress the inferior capsule and prevent both ad­ hesions and functional elevation range of motion loss.

R O T A T OR

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289

PROMOTION OF MUSCULAR STRENGTH BALANCE AND LOCAL MUSCULAR ENDURANCE

The addition of resistive exercise is begun as in­ nammation and pain levels allow. Early submax­ imal resistive exercise in the rotator cuff and scapular muscles is initiated in the form of multi­ ple-angie isometrics, progressing rapidly to sub­ maximal isotonic exercises, because of their in­ herent dynamic characteristics ·6 The pl·esence or lack of pain over the joint or affected ten­ don(s) determines the speed of progression and intensity of exercise. Resistive exercises that em­ phasize concentric and eccentric muscular con­ tributions from the key dynamic stabilizers of the shoulder are used. Movement patterns re­ quiring high activation levels from the rotator cuff based on EMG confirmation via biomechan­ ical study are applied '9- 61 The proper use of these patterns using a low-I·esistance ( never greater than 5 pounds and typically initiated with either no weight or as little as I pound) high-repetition format is recommended to en­ hance local muscular endurance62 of the rotator cuff musculature. The movement patterns pic­ tured in Figure I 1 .5 have been biomechanically studied, and produce high levels of rotator cuff activation. These positions also do not place the shoulder in a potential position of impingement, nor do they place excessive stress to the often attenuated anterior capsuloligamentous com­ plex. The movement patterns recommended for strengthening the rotator cuff do not place the shoulder in elevation beyond 90° or posterior to the coronal plane. Similar positional limitations are applied in this stage of rehabilitation for strengthening the scapular stabilizers. Pallerns resisting scapular protraction and retraction, elevation and depres­ sion produce considerable muscular activity in the serratus anterior, trapezius, and rhom­ boids 6J Use of closed-chain exercise, which ap­ proximates the glenohumeral joint and produces co-contraction of the proximal stabilizing mus­ culature of the scapulothoracic joint, is also rec­ ommended in both non- and postoperative reha­ bilitation of the rotator cuff. Progression to advanced-level plyometric exercises for the

FIGURE 1 1.5

ROlalor cuff exercises predicated 011

eieclromyographic research.

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upper exlremily is also indicated. Commonly ap­ plied are medicine balls and therapeutic Swiss balls in exercise pallems that utilize the stretch­ shortening cycle of the scapulolhoracic muscu­ lature, such as chest passes, and various throw and catch maneuvers that alter the position of the glenohumeral joint 6' Resistive exercises with emphasis on the bi­ ceps muscle are recommended in rotator cuff re­ habilitation, due to the glenohumeral joint stabi­ lizing and humeral head depression actions.65- 67 Strengthening of the biceps in neutral and 90· of shoulder flexion is recommended, with concen­ tric and eccentric contractions implemented. The use of isokinelic exercise is warranled in later stages of both non- and postoperative re­ habililation. As patients lolerate medium-resis­ lance surgical tubing exercise and can perform isolated rolalor cuFf exercise wilh a 3-pound weight, they are considered for this progression.

A FIGURE 1 ( ,6

plane.

The Davies modified base pOSItIOn is initially used for all patients for internal and exlernal ro­ lation. 3 5.46 Submaximal intensities at speeds ranging from 2 1 0· 10 300·/sec are used, wilh spe­ cific emphasis on the external rolators because of their important role in funclional activilies3 .'.7 and in the mainlenance of dynamic glenohu­ meral joint slability.' ·56 Progression from lhe modified position in palients who will reLUm to aggressive overhead activity is followed, using tissue tolerance as the guide. lsokjnetic internal and external rotation in lhe scapular plane, with 80· to 90· of abduc­ tion using fasl conlraclile velocilies, has been successf�llly used as an end-slage rota lor cuff ex­ ercise, to prepare lhe rolator cuff musculalure for the demands of overhead activily (Fig. I 1 .6). Interprelation of isokinetic tesl dala lypi­ cally focuses on bilaleral comparisons and uni­ lateral strength raoos. 46 Unilaterally dominant

B

(A & B) /sokillelic illlemaliexlenwl rolalion wilh 90·of abdtlClioll il1 l"e scaplllar

R OTATOR

C U FF

upper extremity sport athletes often demon­ strate I S to 30 percent greater internal rotation strength on the dominant arm, with bilaterally symmetrical external rotation strength. 35 .46.53.5 4 Although bilateral comparison does provide im­ portant baseline comparison for the individual, the unilateral strength ratio may be o[ even greater importance. J5 ,41,46 The unilateral externaliinternal rotation ratio in healthy shoul­ de, has been reported at 66% throughout the velocity spectrum ·6 Patients with rotator cuff impingement and glenohumeral joint instability have significant alterations o[ this normal 66 percent ratio ' ! The unilateral strength ratio is also altered « 66 percent) in the dominant atom in overhead throwing and racquet sport athletes due to the selective internal rotation strength de­ velopment. 3 5.46.53 .54 Isokinetic exercise and iso­ lated joint testing is an objectively quantifiable method to address the force couple imbalances often inherent in the shoulder with rotator cuff pathology.

Specijic Factors Influencing the RehabiJ,ilaticm oj Rotator Cuff Tears SURGICAL APPROACH

The type of surgical approach used during open repairs of rotator cuff tears has a considerable innuence on several aspects of the rehabilitative process. Two surgical approaches commonly seen in rehabilitation will be briefly discussed. The "deltopectoral approach" consists of an an­ terolateral incision beginning JUSt below the middle one third of the clavicle, crosses the cora­ coid tip, and continues distally in an oblique lat­ eral fashion to the anterior aspect of the hume­ rus "" Nearly all anterior surgical procedures can be accomplished using this surgical exposure, in­ cluding open rotator cuff tears. In some cases, anterior surgical exposure of the shoulder requires detachment of the deltoid origin from the anterior aspect of the acro­ mion "9 This is particularly common i[ an open subacromial decompression is performed. The

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subacromial decompression is used to remove a portion o[ the overlying offending structure, and provide both protection for the rotator cuff and prevention of further disease progression follow­ ing its repair.69 Another commonly used surgical exposure for rotator cuff repair is the lateral "deltoid-split­ t i ng" approach. This surgical approach begins with a transverse incision through the skin, 4 to 6 cm in length, beginning at the anterolateral corner of the acromion and continuing poste­ riorly to the posterolateral corner 70 A straight longitudinal incision based off the lateral aspect of the acromion, along the line of the deltoid fi­ bers, is also frequently used. Regardless of the orientation of the skin incision, the deltoid is then split in line with its fibers near the antero­ lateral corner of the acromion. The deltoid's ori­ gin is protected and not detached. The deltoid is not split further distally than 5 cm to avoid dam­ age to the axillary nerve. 70 The type of surgical approach used in an open rotator cuff repair dictates the progression of both range of motion and resistance exercise following surgery. With the anterior deltopect­ oral approach ( where the deltoid can be de­ tached from its origin), restrictions regarding the application of active OJ' resistive exercise are nor­ mally given, to allow the deltoid's origin to heal and become viable before the larger stresses in­ cUl'red with active or resistive movements are ap­ plied. Active-assistive movement following sur­ gery with the m ini-arthrotomy technique, using the lateral deltoid splitting approach, can nor­ mally commence on the first postoperative day. 7o Preservation of the deltoid's origin allows more aggressive range of motion and earlier ap­ plication of strengthening exercises during the rehabilitation process. This author's protocol for rehabilitation following open rotator cuff repair with a deltoid splitting surgical approach is given in Case Study I later in the chapter. Progression of both range of motion and re­ sistive exercise is much [aster following arthro­ scopic rotator cuff debridement (Case Study 2). Active, active-assistive, and passive range of mo­ tion all commence on the first postoperative day following artlu'oscoPY unless associated surgical procedures were performed such as anterior

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capsulorrhaphy, repair of a Bankart lesion with suture tacks, laser capsulorrhaphy, or extensive subacromial decompression. Submaximal inten­ sity resistive exercise is also initiated rapidly, fol­ lowing debridement of pa.-tial rotator cuff tears. Because arthroscopic approaches to the shoul­ der do not disturb the deltoid origin or the tra­ pezo-deltoid fascia, resistive exercise using a low-resistance, high-repetition format is recom­ mended early, to retard atrophy and begin to normalize muscular strength imbalances. 7o LENGTH OF IMMOBILIZATION

The degree and length of immobilization of the shoulder following rotator cuff repair can greatly affect early rehabilitation emphasis. Traditional immobilization in a sling or sling and swathe for up to 6 weeks following open rotator cuff repairs results in a capsular pattern of range of motion limitation that requires extensive joint mobiliza­ tion and passive stretching. Extensive limitation in active and passive elevation, as well as external rotation of the shoulder, are commonly present following this degree and length of immobiliza­ tion. Patients seen following arthroscopic de­ bridement of partial rotator cuff tears often re­ ceive no immobilization other than a sling for one to two postoperative days, and hence often require minimal accessory mobilization to re­ store normal joint arthrokinematics. The com­ mon finding of associated instability and capsu­ lar laxity in the overhead athlete with partial undersurface rotator cuff tears, coupled with minimal immobilization time following arthro­ scopic debridement, often deemphasize the im­ portance of accessory joint mobilization, espe­ cially to the anterior capsule. As stated earlier, the loss of internal rotation range of motion does indicate the application of posterior capsular mobilization and passive stretching techniques in this population. 39.40 SURGICAL PROCEDURE

Debate in the literature regarding the surgical management of rotator cuff tears exists. Open repair of the tom rotator cuff tendon versus ar-

throscopic debridement and subacromial de­ compression are two options frequently dis­ cussed. 7 ' - 73 Rockwood and Burkhead7 ' followed 93 patients who underwent open debridement and subacromial decompression for irreparable rotator cuff tears. Minimal deterioration in func­ tion and no degenerative changes were repOl�ed with an 8-year average follow-up evaluation. Burkhart 73 studied 25 patients who undelwent a1�hroscopic debridement and subacromial de­ compression of massive rotator cuff tears with an average 30 monlh follow-up. Eighty-eight per­ cent of the patients in this series were found to have good or excellent results, with no deteriora­ tion of results over time. Finally, Montgomery et al. 72 compared the results of open surgical repair to a.�hroscopic debridement in 87 consecutive patients with full-thickness rotator cuff tears. A 2- to 5-year follow-up revealed that the open sur­ gical repair group had superior results as com­ pared to the arthroscopic group. The literature contains an extensive an-ay of research demon­ strating the efficacy of various surgical proce­ dures for rotator cuff pathology which is far be­ yond the scope of discussion of this chapter. One consistent finding is the important role of physi­ cal therapy in both the conservative treat­ ment 74 , 75 as well as postoperative management of rotator cuff disease.

Fa.ctms IrIjl'l.lffl1.(Jing tIw Results oj NO'Yl(J[Jerativ e RehahUitation oj Rotatm Cuff Tears Several factors are consistently rep0l1ed in the literature as having a significant relationship to the outcome of nonoperative treatment of rota­ tor cuff disease. Clinical findings and prognostic factors associated with unfavorable clinical out­ comes in a sample of 1 36 patients with impinge­ ment syndrome and rotator cuff disease were ( I ) rotator cuff tear greater in size than 1 .0 cm' , (2) a history of pretreatment symptoms greater than 1 year, and (3) Significant functional impairment at initial evaluation. 7 5 Itoi and Tabata74 repo.�ed on the clinical outcome of conservative treat-

ROTATOR

CUFF

ment of 1 24 shoulders with a full-thickness rota­ tor cuff tear with a follow-up of 3 years. The pri­ mary factors relating to an unsatisfactory result were identified in their sample as limited abduc­ tion range of motion and significant abduction muscular weakness on initial evaluation of the patient. Factors not associated with clinical out­ come included patient age, gender, occupation, associated instability, dominance, and chronic­ ity of onset.

Summary Rehabilitation of rotator cuff pathology requires an extensive, objectively based evaluation and thorough understanding of the complex bio­ mechanical principles and etiologic factors associated with rotator cuff injury. A rehabil­ itation program aimed at restoring nOlmal joint arthrokinematics and normal muscular strength, endurance, and balance is supported by the scientific principles currently present i n th e literature. Isolated treatment and evaluative focus on the rotator cuff and glenohumeral joint must be combined with a more global upper ex­ tremity kinetic chain approach to comprehen­ sively address rotator cuff pathology.

CASE STUDY 1 REHABILITATION FOILOWING ARTHROSCOPIC ROTATOR CUFF DEBRIDEMENT OF AN UNDERSURFACE TEAR OF THE SUPRASPINATUS

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ing follow-through of his pitching motion. In ad­ dition to localized anterior left shoulder pain, the patient complained of weakness, loss of velocity in his throwing performance, and eventually an inability to tolerate repeated repetitions of over­ head activity. His pertinent history includes pre­ vious bouts of what he calls impingement dating back to his high school and collegiate baseball years. He denies any dislocations of his left shoulder. After 2 months of nonoperative treat­ ment, including nonsteroidal anti-inflammatory medication and physical therapy for rotator cuff and general upper extremity strengthening, he was scheduled for further diagnostic testing. Diagnostic testing revealed an undersurface (articular side) tear in the supraspinatus tendon. He underwent an arthroscopic procedure to de­ bride the margins of the partial-thickness tear. He is referred to physical therapy one day follow­ ing arthroscopic surgel)'. INITIAL FINDINGS

Examination of the patient postop reveals no ob­ vious atrophy with the exception of a hollowing in the infraspinous fossa on the left. Passive mo­ tion on the second day postop is 1 20· in forward flexion, 1 00· of abduction, 75· of external rota­ tion, and 20· of internal rotation. Good distal strength is present, and intact neurologic status is confirmed. Passive accessory mobility of the patient's left shoulder reveals a 2 + anterior translation at 60· and 90· of abduction, as com­ pared to a 1 + on the right uninjured shoulder. Posterior and caudal mobility are equal bilater­ ally. Additional special tests such as labral and impingement test are defelTed due to the pa­ tients acute postoperative nature. TREATMENT

SUBJECTIVE INFORMATION

WEEK I

The patient is a 27-year-old professional baseball pitcher who started having left anterior shoulder pain in early April following a normal, unevent­ ful spring training. Although the patient denies any particular incident of i njury, he reported ini­ tially decreased recovery following pitching and pain in the anterior aspect of his shoulder dUl;ng the acceleration phase and continued pain dur-

Modalities are applied (electric stimulation and ice) to decrease pain and swelling, with a pri­ mary goal initially of restoring normal joint mo­ tion. Passive, active assistive and active ROM are used to telminal ranges as tolerated. Accessory mobilization is applied in the posterior and cau­ dal directions to facilitate the return of flexion, abduction, and internal rotation ROM. Anterior

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glides are not indicated due to the hypelmobility assessed on initial evaluation. Application of iso­ metric and manually resisted rotator cuff strengthenjng is initiated along with scapular stabilization techniques (rhythmic stabilization, manual protraction/retraction). At the end of the rirst postoperative week, the patient has 1 75° of forward Oexion and abduction, 90° of external rotation, and 35° of internal rotation measured with 90° of abduction. WEEKS 2

4

Continued use of ROM techniques at telminal ranges of motion are indicated, with posterior glides and emphasis on stretching of the poste­ rior musculature to increase internal rotation. Progression of the patient's rotator cufr strength­ ening program includes concentric and eccentric isotonic exercise using the pallerns with high levels of scientirically documented rotator cuff activation. Initially a I -pound weight is tolerated with progression to 3 pounds by 3 weeks postop. Advancement of the patient's scapular strength­ ening program includes the use of closed-chain Swiss ball exercise, seated rows, shrugs, and ser­ ratus anterior dominant activities including a protraction punch movement pattern with tub­ ing and manual resistance. Distal strengthening is of key importance, and bicep/tricep and forealm/wrist isotonics are perfOlmed both in the clinic and in the home program. Continued progress of this patient is documented with AROM of the left shoulder a t 1 75° of forward Oexion and abduction, 95° of external rotation, and 40° of internal rotation.

plied during thi> time frame. Results of the pa­ tients initial isokinetic test show 1 0 to 1 5 percent greater internal rotation strength when com­ pared to the uninjured extremity and 5 to 1 0 per­ cent weaker external strength at 5 weeks postop. External/internal rotation ratios range between 45 and 50 percent, revealing a relative weakness or imbalance of external rotation strength on the dominant extremity. A plyomctric program with medicine balls to simulate functional muscular contractions and facilitate scapulothoracic strength is initiated dUI-ing this stage. WEEKS 8- 1 2

Continued mobilization and PROM to normalize glenohumeral joint motion are performed, with continued emphasis on the posterior capsule and posterior musculature. Isotonic rotalor cuff ex­ ercise is progressed to not more than 5 pounds, and advancement of the scapular programs in isotonic, closed-chain . and plyometric venues continues. Isokinetic testing at 8 to 9 weeks postop shows 25 percent greater internal rota­ tion strength, and equal external rotation strength measured in the modiried position. At this time the patient is progressed to an interval Ihrowing program , carried out at the clinic on alternate days beginning with tossing at a 30-foot distance, progressing over the next 3 to 4 weeks to 60, 90, and 1 20-foot stages. Once the patient tolerates 1 20 feet with as many as 75 10 1 00 repe­ titions, he is progressed to throwing off the mound at 50 percent intensities. The isokinetic strengthening is progressed to a more functional 90° abducted position in the scapular plane. The continuation of a lotal arm strength program both in-clinic and at home is followed.

WEEKS 4-8

Addition of isokinetic exercise in the modified base position is warranted with this patient. Tol­ erance of a minimum of 3-pound isolated rotator cuff exercises, negative impingement tests, and functional range of motion make him a candi­ date between 4 to 6 weeks postop. A submaximal introduction to the isokinetic fOl-m of resistance is recommended, with an isokinetic test to docu­ ment internal and external rotation strength ap-

CASE STUDY 2 OPEN ROTATOR CUFF REPAIR (DELTOID SPll1TING APPROACH) SUBJECTIVE HISTORY

The patient is a 5 1 -year-old male competitive tennis player with a I year history of shoulder tendonitis/impingement symptoms reported as

ROTATOR

CUFF

intelmittent based on his level of activity. One month ago the patient was hitting a serve early in a match with minimal warm-up and felt a deep, sharp pain in the anterolateral aspect of his shoulder as his arm was accelerating forward just prior to impacting the ball. He was unable to continue playing, and following the match was unable abduct or flex his arm more than 90°. Continuous pain was reported, even with rest and sleeping, and he was evaluated by an or­ thopedic surgeon 2 days later. An M R l was scheduled, which revealed a full-thickness tear of the supraspinatus tendon. He subsequently underwent an open surgical repair using a del­ toid splitting approach, and is refelTed for post­ operative rehabilitation 2 days following sur­ gery. INITIAL FINDINGS

The patient presents with his right arm immobi­ lized in a sling. Initial orders are for passive range of motion for the initial 2 weeks within the limitations of 100° of flexion and abduction, 30° to 40° external rotation. The patient has no distal radiation of symptoms and full light touch sensa­ tion and strong distal grip. The initial exam con­ sists primarily of a neurologic screening and pas­ sive range of motion measurement. The patient's contralateral extremity has a 1 ° load and shift and anterior translation. The patient expressly denies any instability in either shoulder prior to this injury. Instability or impingement tests are not performed on the postop shoulder at this time. INITIAL PHASE

(lVeeks 0-6)

Modalities consisting of electric stimulation and ice are applied as needed to control pain and in­ crease local blood now. Passive range of motion is performed using the above guidelines as maxi­ mal ranges. Evaluation of the patient's accessory movement reveals a decreased caudal glide and posterior glide relative to the contralateral ex­ tremity. Accessory mobilizations are applied using the caudal and posterior directions along with passive stretching. Mobilization of the sca­ pulothoracicjoint is also used. Passive stretching

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of the elbow, particularly into extension because of the continued use a sling for immobilization, is i ndicated, as well as the use of grip putty to prevent disuse atrophy of the forearm and wrist musculature during the immobilization period. The patients initial range of motion at 1 week status post open rotator cuff repair is 90° of flex­ ion and abduction, 50° of internal rotation, and 30° of external rotation. During the third postop­ erative week, passive range of motion is pro­ gressed to active-assistive range of motion. The use of overhead pulleys and the upper body er­ gometer are added within the range of motion restrictions listed. Submaximal multiple angle isometrics are performed for shoulder IRIER, as well as manual resistance exercise for the biceps and triceps, scapular protractors/retractors, and elevators, and distal forearm and wrist muscula­ ture. PHASE II: TOTAL ARM STRENGTH

(WEEKS 6-12)

The patient's range of motion is advanced from active assistive to active, and terminal ranges of flexion, abduction, and internal and external ro­ tation are included. CLm-ent range of motion of the patient is 1 20° of flexion, 1 05° of abduction, 60° of external rotation, and 60° of internal rota­ tion. Continued mobilization of the glenohu­ meral joint is combined with end-range passive stretching techniques to restore normal joint arlhrokinematics. Initiation of resistive exercise in the form of isotonic internal and external rota­ tion, prone extension, horizontal abduction, and eventually scaption are performed with no resis­ tance, progressing the resistance level as toler­ ated. Advancement of the scapular strengthening program to include plyometrics with a Swiss ball and eventually a medicine ball are included dur­ ing this time frame. Concentric and eccentric muscular work are performed using surgical tub­ ing and controlled execution of the resistive exer­ cise patterns with isotonic resistance. At 1 0 days po top this patient has 1 55° of forward flexion, 1 45° of abduction, and 85° of external rotation with 90° of abduction. Sixty degrees of internal rotation is present with 90° of abduction. Toler­ ance of 3-pound isolated rotator cuff exercises (ment ioned earlier) is demonstrated. The patient

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is progressed to isokinetic internal and external rotation in the modified base position for a trial of submaximal isokinetic exercise. Continued use of home exercise for the rotator cuff using tubing as well as the use of tubing and a counter­ balanced weight for a forearm and wrist pro­ gram, to begin to prepare the distal upper ex­ tremity for the return to tennis play in the later stages of rehab.

charge of the patient from formal physical therapy.

Referenc es I . Blaiser RB, Guldberg RE, ROlhman ED: Anterior stability: Contributions of rotator cuff forces and the capsular ligaments in a cadaver model. J Shoulder Elbow SlIrg 1 : 1 40, 1 992 2. Kronberg M, Nemeth F, Brostrom LA: Muscle ac­

RETURN TO ACTIVITY PHASE

(WEEKS /2-/6)

Continued accessory mobilization to achieve full ranges of elevation is applied to this patient, as well as passive stretching in physiologic range of motion patterns. An isokinetic test is performed in the modified base position, revealing equal in­ ternal rotation strength bilaterally, with a 35 per­ cent external rotalion deficit identified. The pa­ tient's ERlIR ratio is 54 percent, well below the desired 66 percent balance. Range of motion for this patient has continued to improve to 1 75° of flexion and 1 60° of abduction, 95° of external ro­ tation, and 60° of internal rotation. Advancement of the patient's strengthening program includes the 90° abducted position for both isokinetic lRlER and surgical tubing strengthening. Plyo­ metric exercise with medicine balls intensifies, as does the entire scapular program, including the use of closed chain push-ups and step-ups with emphasis on protraction for serratus strengthening. The patient conlinues with reha­ bilitative exercise and close adherence to a home program to reinforce the concepts of total arm strength in preparalion for the interval return to tennis play. Achievement of greater external ro­ talion muscular strength and endurance is rec­ ommended before this patient begins the inter­ val tennis program. The guided return to tennis will include groundstroke activity initially, with progression to volleys and serving based on toler­ ance to the forehand and backhand groundstrokes. Typically the interval program following an open repajr of a full-thickness rota­ tor cuff tear takes up to 6 to 8 weeks before pro­ tected match play can resume. Emphasis on con­ tinued use a rotator cuff and scapular strength maintenance program is followed upon dis-

tivity and coordination in the nannal shoulder: An electromyographic sJUdy. Clin Olihop 257:76, 1 990 3. Rhll KN, McCormick J, Jobe FW et al: An electro­ myographic analysis of shoulder fllnction in ten­ nis players. Am 1 SPOliS Med 1 6:48 1 , 1988 4. Vangheluwe B, Hebbelinck M : Muscle actions and ground reaction forces in tennis. lnt J Sports Bio­ mechan 2:88, 1 986 5. Miyashita M . Tsunoda T, Sakurai S ct al: MusclI­ lar activities in the Lennis serve and overhead throwing. Scand 1 SPOlis Sci 2:52, 1 980 6. lobe FW, Maynes DR, Tibone lE et al: An EMG analysis of the shoulder in pitching. Am J Sports Med 1 2 :2 1 8, 1 984 7. Fleisig GS, Andrews JR, Dillman Cl, Escamilla RF: Kinetics of baseball pitching with impl ica­ tions about injury mechanisms. Am J Sports Mcd 23:233, 1995 8 . lobe FW, Kivitne RS: Shoulder pain in the over­ hand or throwing athlete: The relationship of an­ terior instability and l"Otator cuff impingement. Orthop Rev 28:963, 1989 9. Andrews JR, Alexander EJ: Rotator cuff injury i n throwing and racquet sports. Spor1s Med Ar1hros­ cop Rev 3:30, 1 995 1 0. Neer CS: Anterior acromioplasty for the chronic impingement syndrome in the shoulder. A pre­ li monary repoli. 1 Bone Joint Surg 54A:4 1 , 1972 I I . Neer CS: Impingement lesions. Clin Orthop 1 73: 70, 1983 12. Golding FC: The shoulder: Theforgol lenjoinl. Br J Radio1 35: 1 49, 1 962 1 3 . COllon RE, Rideoul OF: Tears or the humeral ro­ tator cuff: a radiological and pathological ne­ cropsy survey. 1 Bone Joint Surg 46B:314, 1 964 1 4. Poppen NK, Walker PS: Forces at the glenohu­ meral joint in abduction. Clin Olihop 1 35 : 1 65 , 1 978 1 5 . Lucas DB: Biomechanics of the shoulder jOint. Arch Surg 1 07:425, 1 973

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1 6 . Wuelker N, Plil' W, Roelman B: Biomechanical data conccming thc shoulder impingement syn­ drome. Clin O'1hop 303:242, 1 994 1 7 . Elliol B, Marsh T, Blanksby B: A Ihree dimen­ sional ci ncmatographic analysis of the tennis se"'e. Inl J SPO'1S Biomechan 2:260, 1 986 1 8. Bigliani LU, Ticker IB, Flalow EL el al: The rcla­ tionship of acromial architecture to rOlalor cuff disease. Clin Sporls Med 1 0:823, 1 99 1 1 9. Zuckerman JO, Kummer FJ, Cuomo et al: The in­ nuence of coracoacromial arch analOmy on rota­ lor cuff Icars. J Shoulde,- Elbow Surg 1 :4 , 1992 20. Nirschl RP: Shoulder lendonilis. In Pelll'onc FP (cd): Upper Extremity InjUlies in Athletes. Ameri­ can Academy of 011hopaedic Surgeons Sympo­ sium. Mosby, Washinglon, DC, 1 988 2 1 . Cofield R: Current concepts review of rotator cuff diseasc of Ihc shoulde,-. J Bone Joim Surg 67A: 974, 1985 22. Codman EA: The Shoulde,·. 2nd Ed. Thomas Todd, Boslon, 1934 23. Chansky HA, lannolli JP: The vascularilY of Ihe rolalor cuff. Clin SPO'1S Med 1 0:807, 1 99 1 24. Ralhbull1 JB, MacNab I : The microvascular pal­ lem of Ihe rolalor cuff. J Bone Joinl Surg 52B: 540, 1970 25. Brooks CH, Revell WJ, Headey FW: A quamilalive histological study of the vascularity of the rotator cuff tendon. J Bone Joinl Surg 74B: l S I , 1 992 26. Swiontowski MF, Iannotti IP, Boulas HJ et al: In­ traoperative assessment of rotator cuff vascularity using laser doppler Oowmelry. p. 208. In Post M , Mon'ey BF, Hawkins R J (eds): Surgery o f the Shoulder. St. Louis, Mosby Vear Book, 1990 27. lannolli JP: Lesions of the rotalor cuff: Pathology and Pathogenesis. In Matsen FA, Fu Fl-!, Hawkins RJ (eds): The Shou lder: A Balance of Mobility and Siabilily. American Academy of Orthopaedic Sur­ geons, Rosemonl, IL, 1 993 28. Loehr JF, Helmig P, Sojbjerg JO, JungA: Shoulder instability caused by I'olator cuff lesions: An in vitro sludy. Clin O'1hop 303:84, 1 994 29. Miller C, Savoie FH: Glenohumeral abnormalilies associated with full-thickness tears of the rotator cuff. O,1hop Rev 23: February 1 994, 1 59 30. Fukada H, Hamada K, Vamanaka K: Pathology

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supraspinatus tcndon: Reference to rotatOI' cuff tearing. J Shou lde,- Elbow Surg 3:79, 1 994 32. Jobe FW, Pink M: The alhlete's shoulder. J Hand Ther April-June 1994, 1 07 33. Walch G, Boileau P, Noel E, Donell ST: Impinge­ ment of the deep surface of the supraspinatus tcn­ don on the posterosuperior glenoid l"im: An ar­ throscopic slUdy. J Shoulder Elbow Surg 1 :238, 1 992 34. Fukuda H, Hamada K, Nakajima T, Tomonaga A: Pathology and pathogenesis of the intratendinous teadng of the rotator cuff viewed from en bloc h istologic sections. Clin O'1hop 304:60, 1 994 35. Ellenbecker TS: Rehabililation of shoulder and elbow injudes in tennis players. Clin Sports Med 14:87, 1 995 36. Kibler WB: Role of the scapula i n the overhead Ihrowing mOlion. Comemp O'1hop 22:525, 1 99 1 37. ElienbeckerTS, Roelert E P , Piorkowski P : Shoul­ der intel-nal and eXlernal rotation range of motion of elite junior tennis players: a comparison of two protocols, abstracled. J Orthop Spo'1S Phys The,-, 1 7 :65, 1 993 38. Chandler n, Kibler WB, U h l TL el al: Flexibilily comparisons of elite junior tennis players to other ath leles. Am J Sports Med 1 8 : 1 34 , 1 990 39. Harryman DT, Sidles lA, Clark 1M, et al: Transla­ tion of the hu meral head on the glenoid with pas­ sive glcnohumcral joint motion. J Bone Joint Surg 72A:1 334, 1 990 40. Matscn FA Ill, Artnz CT: Subacromial impi nge­ ment. p. 623. In Rockwood CA Jr, Malsen FA I I I (eds): T h e Shoulder. W B Saunders, Philadelphia, 1990 4 1 . Warner JJP, Micheli LJ, Arslanian LE, el al: Pal­ lems of nexibility, laxity, and strength in normal shoulders and shou lders with instability and im­ pingement. Am J Sports Med 1 8:366, 1 990 42. Hoppenfeld S: Physical examination of the spine and extremities. Prentice-Hall, Norwalk, CT, 1 976 43. Saha AK: Mechanism of shoulder movements and a plea for the recognition of "zero position" of gle­ nohumeral joint (rep,-inled). Clin Orthop 1 73:3, 1983 44. Daniels L, Wort hingham C: Muscle Testing: Tech­ niques of Manual Examination. 5th Ed. WB Saun­ ders, Philadelphia, 1 986

and pathogenesis of bursal side rotator cuff tears

45. Ellenbecker TS: Muscular slrength relalionship

viewed from en bloc h istologic sections. Clin Or­

between nOlmal grade manual muscle testing and

thop 254:75, 1 990 3 1 . Nakajima-T, Rokumma N, Kazuloshi H et at: His­ tologic and biomechanical characteristics of the

isokinctic measurement of the shoulder intemal and extcmal rotators, abstracted. J Ol-lhop Sports Phys Ther 1 9:72, 1 994

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THE

SHOULDER

46. Davies GJ: A compendium of isokjneLics in c1ini· cal usage. 4th Ed. S & S Publishers, LaCrosse,

WI.

1 992

during a baseball rehabilitation program. Am J SPOl1S Med 1 9:264, 1 99 1 6 2 . Fleck 5, Kraemer W: Oesigning Resistance Train­

47. Hawkins RJ,

Kennedy JC:

Impingement syn­

drome in athletes. Am J SP0l1S Med 8: 1 5 1 , 1 980 48. Obrien SJ, Neves MC, Arnoczky SJ et al: The anat­

ing Programs. Human Kinetics, Champaign, IL. 1987 63. Moesley JB, Jobe FW, Pink M : EMG analysis of

omy and histology of the inferior glenohu meral

thc scapular muscles dud ng a shoulder rehabi lita­

ligament complex of the shoulder. Am J Sports

tion program. Am J SpOl·ts Med 20: 1 28, 1 992

Med 1 8 :449, 1 990

64. Wilk KE, Voight ML, Keirns MA et al: Stretch·

49. Altchek OW, Skyhar MJ, WalTen RF: Shoulder ar­

shortening drills for the upper extremities: theOl),

throscopy fOl' shoulder instability. p. 1 87. In: In·

and clinical application. J Ol1hop Sports Phys

structional Course Lectures. The Shoulder. Amer­ ican

Academy

of

Orthopaedic

Surgeons,

Rosemont, I l l inois

,

cJectromyographic

50. Dillman CJ: Biomechanics of the rotator cuff. Sports Med Arthroscop Rev 3:2, 1 995

analysis

of

the

throwing

shoulder with glenohumeral joint instability. J Bone Joint Surg 70A:220, 1988

5 1 . Inman VT, Saunders ill , de C M Abbot LC: Obser­

66. Itoi E , Kuechle OK, Newman SR et al: Stabilising

vations on the function of the shoulder joint. J

function of the biceps in stable and unstable

Bone Joint Surg 26A: I , 1 994

shoulders. J Bone Joint Surg 75B:546, 1 993

52. Weiner OS, MacNab I: Superior migration of the hu meral head. J Bone Joint Surg 52B:524, 1 970 53. Ellenbecker TS: Shoulder internal and external rOlation stl-englh and range of molion of highly skilled junior tennis players. Isokinci Exercise Sci 2 : 1 , 1 992

54.

Ther 1 7:225, 1 993 65. Glousman R, Jobe FW Tibone JE et al: Dynamic

67. Rodosky MW, Hamer CO, Fu FH: The role of the long head of the biceps muscle and superior gle­ noid labium in antcl;or stability of the shoulder. Am J SPOl1 Med 22: 1 2 1 . 1 994 68. Harryman DT: Common approaches to the shoul­ der. p. 3. I n : Instructional Course Lectures. Upper

Ellenbecker TS, Maltalino AI: Concentric isoki­

Extremity. American Academy of Ol1hopaedic

netic shoulder internal

Surgeons, Rosemont, Illinois

and external

rotation

strength in professional baseball pitchers. J Or­ thop SP0l1S Phys Ther (submilled) 55. Cain PR, M u tschler TA, Fu F et al: Anteriol- stabil­ ity of the glenohu meral joint. A dynamic model. Am J Sports Med 1 5 : 1 44 , 1 987 56. Clarke J, Sidles JA, Matsen FA: The relationship of the glenohumeral joint capsule to the rotator cuff. Clin Orlhop 254:29, 1990

69. Kunkel 55, Hawkins RJ: Open Repairofthc rotator cuff. I n Andrews JR, Wilk KE (eds): The Athlete's Shoulder. Churchill Livi ngstone,

ew York, 1994

70. Tim merman LA, Andrews JR, Wilk KE: Mini­ open repair of the rotator cuff. In Andrews JR, Wilk KE (cds): The Athlete's Shoulder. Churchill Livingstone, New York, 1 994 7 1 . Rockwood CA Jr, Burkhead WZ: Management of

57. Bassell RW, Browne AO, MOITCY BF, An KN : Gle·

patients wilh massive rotator cuff defects by

nohumeral muscle force and moment mechanics

acromioplasty and rotator cuff debridement. 01'­

in a position of shoulder instability. J Biomecha­ nics 23:405, 1 990

thop Trans 1 2 : 1 90, 1 988 72. Montgomery TJ, Yerger B, Savoie FH: Manage­

58. Cooper IE, Shwedyk E, Quanbury AO et al: Elbow

ment of rotator cuff tears: a comparison of arthro­

joint restriction: effect on functional upper limb

scopic debridement and surgical repair. J Shoul­

motion dUI-ing performance of three feeding ac­ tivities. Arch Phys Med Rehabil 74:805, 1 993

der Elbow Surg 3:70, 1 994 73. Burkhart 55: AI1hroscopic debridement and de­

59. Ballantyne BT, O'Hare SJ, Paschall I L et al: Elec·

compression for selected rotator cuff tears. Clini­

lromyographic activity of selected shoulder mus­

cal results, pathomechanics, and patient selection

cles in commonly used therapeutic exercises.

based on biomechanical parameters, Orthop Clin

Phys Ther 73:668, 1 993 60. Blackbum TA, McLeod WO, White B et al: E M G analysis o f posterior rotator cuff exercises. Ath­ letic Training 25:40, 1 990 6 1 . Townsend H, Jobe FW Pink M et al: Electromyo· ,

graphic analysis of the glenohu meral muscles

NOl1h Am 24: 1 1 1 , 1 993 74. Itoi E , Tabata 5: Conservative treatment of rotator cuff tears. Clin O.1hop 275: 1 65 , 1 992 75. Bal1olozzi A, Andreychik D. Ahmad 5: Determi­ nants of outcome in the treatment of rotator cuff disease. Clin Orthop 308:90, 1 994

Visceral Pathology Referring Pain to the Shoulder J 0 H N

c .

G RAY

An important component of the inilial or­ thopedic evaluation is to differentiate the etiol­ ogy of a patient's pain complaints as neuromus­ culoskeletal in origin versus visceral pathology or disease. Screening for visceral disease is im­ portant for several reasons: ( I ) many diseases mimic orthopedic pain and symptoms, and a subsequent delay in diagnosis and treatment may lead to severe morbidity or death; (2) there is a significant increase in the number of patients over the age of 60 seeking orthopedic medical care; and (3) there is an increase in the managed care environment that encourages fewer refer­ rals to specialists, fewer referrals for diagnostic testing, and less time given to plimary care phy­ sicians to make an accurate diagnosis of every patient complaining of musculoskeletal pain. Consequently, the physical therapist in an outpa­ tient orthopedic selling is evaluating and lreat­ ing patients who have greater morbidity and are more acutely ill than the patients who presented for therapy 1 0 or 1 5 years ago. Recent research has found that approximately 50 percent of all the patients refen'ed for outpatient orthopedic physical therapy have at least one of the follow­ ing diagnoses: high blood pressure, depression, asthma, chemical dependency, anemia, thyroid

problems, cancer, diabetes, rheumatoid arthri­ tis, kidney problems, hepatitis, or heart attack . I Two imp0l1ant aspects of the orthopedic evaluation that will help detect visceral pathol­ ogy or disease are a careful history and palpa­ tion. A sampling of important questions related to the history-taking portion of the evaluation is listed below2: I . Describe the first and last time you experi­ enced these same complaints . 2. Are your symptoms the result of a trauma, or are they of a gradual or insidious onset?

3. Was it a macrotrauma (motor vehicle acci­

dent, fall, sports injury) or repeated micro­ trauma (overuse injury, cumulative trauma disorder)?

4. What was the mechanism of injury? 5. Do you have any other complaints of pain throughout the rest of your body-head, neck, chest, back, abdomen, arms, or legs? 6. Do you have any other symptoms through­ out the rest of your body-headaches, nau­ sea, vomiting, dizziness, shortness of breath, weakness, fatigue, fever, bowel or bladder changes, numbness, tingling, pins or needles? 299

300

P H Y SI C A L

T H E R A P Y

OF

T H E

S H O U L D E R

7. Is your pain worse at night?

8. Are there positions or activities that change your pain, either aggravating or re­ lieving your symptoms? 9. Does eating or digesting a meal affect your pain? 1 0. Does bowel or bladder activity affect your pain? I I. Does coughing, laughing, or deep breath­ ing affect your pain? 1 2 . Does your shoulder pain get worse with ex­ el1ional activities (climbing stairs) that don't directly involve your shoulder? The following are some warning signs, gath­ ered during the history and interview, that may indicate possible visceral pathology or disease. 3.4 t.

Pain is constant.

2. The onset of pain is not related to trauma or overuse. 3. Pain is described as throbbing, pulsating, deep aching, knifelike, or colicky.

4. There is no relief of pain or symptoms with rest. 5. Symptoms are bilateral. 6. Constitutional symptoms are present: fever, night sweats, nausea, vomiting, pale skin, dizziness, fatigue, or unexplained weight loss . 7. Pain is worse at night.

8. Pain does not change with body position or activity. 9. Extraordinary relief of pain is obtained with aspirin (bone cancer). 1 0. Pain changes in relation to organ function (eating, bowel or bladder activity, cough­ ing or deep breathing, menstrual cycle). I I . Indigestion, diarrhea, constipation, or rec­ tal bleeding are present . 1 2 . Shoulder pain increases with exel1ion that does not stress the shoulder (walking or climbing stairs) .

A self-administered patient questionnaire (Fig. 1 2. 1 ) is useful as a screen for possible vis­ ceral pathology or disease. For example, if a pa­ tient has a few checks under the "yes" column for pulmonary, then refer to the section below titled "lung." In this way you can analyze the pa­ tient's signs and symptoms to see if they con'e­ late with a Pancoast tumor or a pulmonary in­ farct . The idea is not to diagnose visceral pathology, which should be left to the physician, but to assess whether or not the patient's symp­ toms are 0I1hopedic in origin. The second important aspect of the evalua­ tion is palpation. Palpation should include the lymph nodes (for infection or neoplasm), which are normally up to I to 2 cm, in the cervical (me­ dial border of sternocleidomastoid, anterior to upper trapezius muscle), supraclavicular, axilla, and femoral triangle regions.3. , Abnormal find­ ings are swollen, tender, or immovable lymph nodes'> Palpate the abdomen for muscle rigidity and significant local tenderness (possible vis­ ceral disease), or a large pulsatile mass (indica­ tive of an aortic aneurysm).'·5 Palpation i n the right upper abdominal quadrant will reveal the l iver, gallbladder, and portions of the small and large intestines (Plate 1 2. 1 ) . The left upper ab­ dominal quadrant will reveal the stomach, spleen, tail of the pancreas, and portions of the small and large intestines (Plate 12. 1 )· The kid­ neys lie deep posteriorly in the left and right upper abdominal quadrants . " The appendix and large intestine are found in the right lower quad­ rant, and other p0l1ions of the large intestine may be found in the left lower quadrant · A tender mass in the femoral triangle or groin area may indicate a hernia · A pulsating mass in the midline may indicate an aortic aneurysm · When evaluating abdominal tenderness it is important to differentiate the source as originating from the superficial myofascial wall or from the deep viscera . If palpable tenderness is again elicited with the abdominal wall contracted and the head and neck flexed off the table, then the symptoms are originating from the myofascial abdominal wall." If, however, the palpable tenderness disap­ pears in the above situation, then you should sus­ pect deep visceral pathology. " The ability to palpate and interpret peri ph-

VI S C E R A L

P A T H O L O G Y

eral pulses is another important diagnostic tool for the orthopedic manual therapist. When pal­ pating a pulse, the therapist needs to compare the amplitude and force of pulsations in one ar­ tery with those in the cO'Tesponding vessel on the opposite side.7 Palpation of the artery should be performed with a light pressure and a sensi­ tive touch. If the pressure is firm, then there is a risk of not being able lO perceive a weak pulse or misinte'-prcting your own pulse as that of the patient's 7 Pulsations may be recorded as normal (4), slightly (3), moderately (2), or markedly re­ duced ( 1 ), or absent (0).7 Palpate the arterial pulses for cardiovascular and peripheral vascu­ lar disease . The arterial pulses may be palpated in the upper extremity (axillary 3I1ery in the ax­ illa, brachial artery in the cubital fossa, ulnar and radial arteries at the wrist) and lower extremity (femoral artery at femoral triangle, popliteal ar­ tery at popliteal fossa, posterior tibialis artery posterior to medial malleolus, and dorsal pedis arte,), at the base of the first and second metatar­ sal bones).'. s·7 • Be aware of the easy and common diagnoses of osteoarthritis, degenerative joint or disc dis­ ease, and spondylosis in the elderly population. Many asymptomatic elderly persons have posi­ tive radiographs for these diseases. Also, the el­ derly in our society are at a greater risk for vis­ ceral pathology and disease. In addition, old asymptomatic orthopedic injuries may become symptomatic due to facilitation from a segmen­ tally related visceral organ in a diseased state"" o Pain may be defined as an unpleasant sen­ so,) , and emotional experience associated with actual or potential tissue damage" . True visceral pain can be experienced within the involved vis­ cuS.'·'2 and poorly localized.3.121. 3 There is also a strong autonomic reflex phenomenon, including sudo­ motor (i ncreased sweating) changes, vasomotor (blood vessel) responses, changes in arterial pressure and heart rate, and an intense psychic alarm reaction. I 1 . 12,1 4 Viscera are innervated by . These free nerve end­ nociceptors (Plate 1 2 . 2)3" ings are found in the loose connective tissue walls of the viscus, including the epithelial and serous linings, as well as the walls of the local blood vessels in the viscus . 3 After activation of .

R E F E R R I N G

P A I N

TO

T H E

S H O UL D E R

301

these nociceptors by sufficient chemical or me­ chanical stimulation, neural information is transmitted along small unmyelinated type C ne,ve fibers within sympathetic and parasympa­ thetic nerves . 3. 1 5- 17 This information is subsequently relayed to the mixed spinal nerve, dorsal root, and into the dorsal horn of the spinal cord (Plate 1 2 .2) . Sec­ ond-order neurons in the dorsal horn project in the anterolateral system." Within the anterolat­ eral system, nociceptive impulses ascend in the spinothalamic, spinoreticular, and spinomes­ encephalic tracts." The targets in the brain for these tracts are the thalamus, recticular forma­ tion, and midbrain, respectively." Chemical stimulation of nociceptors may re­ sult from a buildup of metabolic end products, such as bradykinins or proteolytic enzymes, sec­ ondary to ischemia of the viscus.3 Prolonged spasm or distension of the smooth muscle wall of viscera can cause ischemia secondary to a col­ lapse of the microvascular network within the viscus.' Chemicals, such as acidk gastric fluid, can leak through a gastric or duodenal ulcer into the peritoneal cavity, resulting in local abdomi­ nal pain . 3.,s Mechanical stimulation of visceral nocicep­ tors can occur secondary to torsion and traction of the mesentery, distention of a hollow viscus, or impaction.J , I I - 14 Distention may result from a local obstruction such as a kidney stone or from local edema due to infection or innammation .' Spasm of visceral smooth muscle may also be a sufficient mechanical stimulus to activate the nociceptors of the involved \�SCUS. 3.13 . '8 Visceral pain is not uncommon in patients suffering from neoplastic disease. Pain com­ plaints from cancer patients have several origins. Somatic pain occurs as a result of activation of nociceptors in cutaneous and deep tissues (tumor metastasis to bone) and is usually con­ stant and localized." Visceral pain results from stretching and distending or from the produc­ tion of an innammatOl), response and the release of algesic chemicals in the vicinity of nocicep­ tors .' "'. ' 2 Metastatic tumor infiltration of bone and gastrointestinal and genitourinal), tumors that invade abdominal and pelvic viscera are ve,), common causes of pain in the cancer pa-

302

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PATIENT QUESTIONNAIRE DATE

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FAMILY HISTORY OF CANCER RECENT SURGERY

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COLOR CHANGE OF VAGINAL DISCHARGE INCREASED FREQUENCY OF URINATION

FIGURE 1 2. 1

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INCREASED AMOUNT OF VAGINAL DISCHARGE INCREASED

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(A & B) A self-administered patiellt qLlestiol1lwire. (Figllre cOlitilll/es.)

V I S C E R A L

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PAIN CHANGES IN RELATION TO MENSTRUAL CYCLE

GASTROINTESTINAL DIFFICULTY IN SWALLOWING NAUSEA

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HEARTBURN VOMITING

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FOOD INTOLERANCES CONSTIPATION DIARRHEA

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.................... CHANGE IN COLOR OF STOOLS RECTAL BLEEDING ..............................

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HISTORY OF LIVER OR GALLBLADDER PROBLEMS ............ HISTORY OF STOMACH OR GI PROBLEMS

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INDIGESTION

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LOSS OF APETITE

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PAIN WORSE WHEN LYING ON YOUR BACK

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PAIN CHANGE DUE TO BOWEL/BLADDER ACTIVITY PAIN CHANGE DURING OR AFTER MEALS

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MALE UROGENITAL SYSTEM PAINFUL URINATION BLOOD IN URINE

(MEN ONLY)

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DIFFICULTY CONTROLLING URINATION

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CHANGE IN FREQUENCY OF URINATION

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INCREASE IN URINARY URGENCY

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DECREASED FORCE OF URINARY FLOW URETHRAL DISCHARGE

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HISTORY OF URINARY INFECTION HISTORY OF VENEREAL DISEASE IMPOTENCE

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PAIN WITH EJACULATION HISTORY OF SWOLLEN TESTES .

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....................

FIGURE 1 2 . 1

(Col1linuedj. (B).

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llQ

303

304

P H Y SI C A L

T H E R A P Y

OF

T H E

S H O U L D E R

tienl." Deafferentation pain results fTom injury to the peripheral and/or central nervous system as a result of tumor compression or infiltration of peripheral nerve or the spinal cord, or injury to peripheral nerve as a result of surgery, chemo­ therapy, or radiation t herapy for canceL" Ex­ amples are metastatic or radiation-induced bra­ chial or lumbosacral plexopathies, epidural spinal cord and/or cauda equina compression, and postherpetic neuralgia. I I Somatic, visceral, and deafferentation pain may be complicated by sympathetically main­ tained pain, in which efferent sympathetic activ­ ity promotes persistent pain, hyperpathia, and vasomotor and sudomotor changes . I I Also, noci­ ceptors may be facilitated following injury, lead­ ing to lower threshold of activation, greater in­ tensity of response to injury, and the emergence of spontaneous activity within the interneuron 9 pool of the dorsal horn . I 1.1

The obselvation has been made that visceral disease produces not only orthopedic pain, but . I For example, true orthopedic dysfunction.2o2 pain referred to the T4 spinal segment fTom car­ diac t issue (angina) may cause renex muscle guarding of the muscles supplied by T4, which will interfere with the normal mobility of that segment of the spine. This may then produce movement around a nonphysiologic axis at that segment and subsequently lead to joint injury, locking, or hypomobility.

Theories on Visceral

Referred Pain I. Referred pain is pain experienced in tissues that are not the site of tissue damage, and whose afferent or efferent neurones are not physically involved in any way."

Cerebral Cortex Thalamus

Spinothalamic Tract

Cervical Segment of the Spinal

Viscera

fiGURE 12.2 Schematic drawing ora single afe f r nerve fiber receiving input {i'olll bOlh skin and viscera.

V I S C E R A L

P A T H OLOGY

2. Pain happens within the central nervous sys­ tem, not in the damaged tissue itself. Pains do not really happen in hands or feet or heads; they happen in the images of heads and feet and hands.22 3. Referred pain fTom deep somatic structures is often indistinguishable fTom visceral re­ ferred pain.2J

4. Visceral pain fibers constitute less than 1 0 percent of the total afferent input to the lower thoracic segments of the spinal cord and are rarely activated. I S In this way, a vis­ ceral stimulus may be mistaken for the more familiar somatic pain. IS 5 . Visceral referred pain may be due to misin­ terpretation by the sensory cortex 24 Over the years, specific cortical cells are repeat­ edly stimulated by nociceptive activity fTom a speci fic area of the skin. When nocicep-

R EfE R R I N G

P AI N

TO

T H E

S H O U LD E R

305

tors of a viscus are eventually stimulated, chemically or mechanically, these same sen­ sory cortex cells may become stimulated with the cortex interpreting the origin of this sensory input based on past experience. The pain, therefore, is perceived to arise fTom the area of skin that has repeatedly stimulated these cOl-tical cells in the past. The referred pain may lie within the der­ matome of those spinaJ segments that re­ ceive sensory information from the visceral organ.2 4 6. Sensory fibers dichotomize as they "leave" the spinal cord, one branch passing to a vis­ ceral organ as the other branch travels to a site of reference in muscle or skin (Fig. 1 2. 2 ).2 5.2 . 7. Visceral nociceptor activity converges with input from somatic nociceptors into com-

Cerebral Cortex Thalamus

Spinothalamic Tract

Afferent Nerves

Viscera

FIGURE 1 2.3 Schematic drawing of a visceral afe f r afferem l7erve converging onto the same spil70thalamic tract cell il7 the dorsal hom of the spil7ai cord.

306

P H Y S I C AL

T H E R A P Y

OF

T H E

S H O UL D E R

mon pools of spinothalamic tract cells i n th e dorsal horn of t he spinal cord. Visceral pain is then referred to remote cutaneous sites because the brain "misinterprets" the input as coming from a peripheral cuta­ neous source. which normally bombards the central nervous system with sensory stimuli (Fig. 1 2.3).6.11 - 1 5 .2 3.2 7 29

esophagus. stomach and pancreas) can refer pain to the shoulder through contact with the diaphragm (Plates 1 2. 1 . 1 2.3. and Fig. 1 2.4)J [n the rat. cervical (C3. C4) dorsal root ganglion cells were seen that had collateral nerve fibers that emanated fTom both the diagphragm and the skin of the shoulder (Fig. 1 2.2)." Symploms

Viscera Capahle oj ReJerring Pain to the Shoulder DIAPHRAGM

The central portion of the diaphragm. which is segmentally innervated by cervical nerves C3 to CS via the phrenic nerve/ 30 can refer pain to the shoulder.25 .29- 34 Although the diaphragm is a musculotendinous strllctUl'e and not a viscus, it is i nteresting in tel·ms of the distance it refers its pain to the shoulder. Also. many viscera (liver.

Pain in the shoulder is most often felt at the supel·ior angle of the scapula. in the suprascapu­ lar region. and in the upper trapezius mus­ c1e Jo. 3I NOImally there are no complaints of pain in the region of the diaphragm. unless the patient suffered trauma or a musculoskeletal strain to the surrounding tissues. Diagnosis

Local tenderness or shoulder pain during palpation of the diaphragm. Full active and pas­ sive shoulder girdle elevation may cause pain.

Cerebral Lortex ---t ThalaIIT US ----fj

C4 Seg m en t the Sp ina l Cord ��=-C4 Affe rent Nerve

+--·PflTenic Nerve

FIGURE 1 2.4 Schematic drawillg o( all a(e ( renl nen'e (rom Ihe diaphragm converging onto the same Spil1ol/llIlamic lracl cell as is a somatic afe f rent (rolll Ihe skill o( Ihe shol.llder.

V I S C E R A L

PATHOLOGY

because this motion changes the shape of the thoracic cage and subsequently puts tension on the diaphragm." Shoulder pain is reproduced or exacerbated by deep breathing, coughing, or sneezing,32,

CASE STUDY 1 HISTORY

A 24-year-old right-handed male presented to physical therapy (February 1 992) with a diagno­ sis of "left shoulder pain." His only complaint was periodic, and severe, localized left shoulder pain at the acromioclavicular joint (Fig. 1 2.5). He denied neck pain, headaches, weakness, arm pain, or paresthesias. The patient denied any other complaints or symptoms throughout the

R E F E R R I N G

P A I N

TO

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S H O UL D E R

307

rest of his body. He reported he was a competi­ tive racquetball and volleyball player. He played either sport three to four times a week. The pa­ tient reported pain for the 6 days prior to presen­ tation, but denied any trauma. Nine days prior to evaluation he participated in a 2-day walleyball (volleyball on a racquetball court) tournament. Six days prior to presentation the patient was involved in two competitive racquetball league matches . He reported a constant low-intensity ache that never went away, regardless of what he did. He was able, however, to produce a sudden and sharp pain with certain movements. He was able to sleep on his left side without much difficulty. Eating and bowel or bladder activity had no af­ fect on his symptoms. Coughing, laughing, and deep inhalation did, however, produce a sudden sharp pain in the shoulder. PAST MEDICAL HISTORY

1 99 1 : Muscle strain on left side of rib cage 1 990: Muscle strain on left side of rib cage 1 987: Low back i njury-sprain/strain

J l

PHYSICIAN-ORDERED TESTS

No radiographs were ordered. GENERAL HEALTH

The patient questionnaire (Fig. 1 2.6) did not pro­ duce any significant "red flags" to indicate vis­ ceral involvement. The patient was young and appeared fit and healthy. CERVICAL SCREEN

Active and passive ROM was WNL and painless. Cervical axial compression (see Fig. 4 . 1 4) and Spurling's quadrant compression tests (see Fig. 4. 1 6 ) were negative. SHOULDER AROM AND PROM FIGURE t 2.5 Paill diagram from a 24 year-old righl-hQ/1ded l1Iale wilh a presellling diagnosis of "Ief l shollider pail1. "

Left shoulder active and passive ROM was WN L with minimal discomfort and no reproduction of symptoms.

308

P H Y S I C A L

T H E R A PY

OF

T H E

S H O U L D E R

PATIENT QUESTIONNAIRE DATE 02/15/92 NAME Case S tudy 1!1 AGE ....................................... HEIGHT WEIGHT (Ibe) FEVER AND/OR CHILLS UNEXPLAINED WEIGHT CHANGE NIGHT PAIN/DISTURBED SLEEP ................... ..................•.......• EPISODE OF FAINTING DRY MOUTH (DIFFICULTY SWALLOWING) DRY EYES (RED, ITCHY, SANDY) HISTORY OF ILLNESS PRIOR TO ONSET OF PAIN HISTORY OF CANCER FAMILY HISTORY OF CANCER RECENT SURGERY (DENTAL ALSO) DO YOU SELF INJECT MEDICINES/DRUGS DIABETIC PAIN OF GRADUAL ONSET (NO TRAUMA) ......lI...CONSTANT PAIN x PAIN WORSE AT NIGHT PAIN RELIEVED BY REST ........................ .

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X

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--X-

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PULMONARY HISTORY OF SMOKING ........................... SHORTNESS OF BREATH ...................................... FATIGUE WHEEZING OR PROLONGED COUGH ......... HISTORY OF ASTHMA, EMPHYSEMA OR COPD HISTORY OF PNEUMONIA OR TUBERCULOSIS .

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CARDIOVASCULAR HEART MURMUR/HEART VALVE PROBLEM ............. HISTORY OF HEART PROBLEMS .................... SWEATING WITH PAIN ........................... RAPID THROBBING OR FLUTTERING OF HEART HIGH BLOOD PRESSURE DIZZINESS (SIT TO STAND) SWELLING IN EXTREMITIES ................... HISTORY OF RHEUMATIC FEVER ................... ELEVATED CHOLESTEROL LEVEL FAMILY HISTORY OF HEART DISEASE PAIN/SYMPTOMS INCREASE WITH WALKING OR STAIR .............. CLIMBING AND RELIEVED WITH REST .

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PREGNANT WOMEN ONLY CONSTANT BACKACHE ............................ INCREASED UTERINE CONTRACTIONS ............................. MENSTRUAL CRAMPS CONSTANT PELVIC PRESSURE ..................... INCREASED AMOUNT OF VAGINAL DISCHARGE ......... INCREASED CONSISTENCY OF VAGINAL DISCHARGE COLOR CHANGE OF VAGINAL DISCHARGE ............ ............. INCREASED FREQUENCY OF URINATION .

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FIGURE 12.6

--X­ X X

Patient questionnaire (or Case Swdy I.

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x

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V I S C E R A L

P A T H O L O G Y

RESISTED TESTING

There was no reproduction of symptoms. THORACIC SPINE AROM AND PROM

Thoracic motion was minimally limited in flex­ ion and extension. Sharp leFt shoulder pain, how­ ever, was noted with movement into the end range of flexion or extension. RESISTED TESTING

There was no reproduction of symptom PALPATION

There was no tenderness or reproduction of symptoms with palpation of musculoskeletal structures throughout the celvical spine, chest, and shoulder. Palpation of the lymph nodes and arterial pulses in the cervical spine and upper extremities was negative. Palpation of the abdo­ men revealed local pain and tenderness along the left anterolateral border of the diaphragm and costal margin, just under the rib cage. Palpation of this peripheral portion of the diaphragm did not reproduce shoulder pain. RIB AROM AND PROM

Active deep inhalation and passive lower rib cage compression reproduced left shoulder pain. RESISTED TESTING

There was no reproduction of symptoms. NEUROLOGIC EXAMINATION

Sensation, deep tendon reflexes and strength testing of the upper extremities was WNL. SPECIAL TESTS

Passive nexion with humeral internal rotation ( I R) or external rotation (ER) was negative; gle­ nohumeral, sternoclavicular, and acromioclavi­ cular joint compression and distraction were negative; upper limb nerve tension tests were negative. Immediate and sharp left shoulder

R E F E R R I N G

P A I N

TO

T H E

S H O U L D E R

309

pain, however, was reproduced with deep inhala­ tion, coughing, or laughing. JOINT MOBILITY

Glenohumeral, scapulothoracic, sternoclavicu­ lar, and acromioclavicular joint mobility were all WNL, gTade 3, with no symptom reproduction. ASSESSMENT

The patient's signs and symptoms were consis­ tent with an extrinsic source of shoulder pain. This extrinsic source appeared to be from an irri­ tation of the central left hemidiaphragm with subsequent referred pain to the left shoulder. PNEUMOPERITONEUM

Pneumoperitoneum, or air in the peritoneal cav­ ity, can refer pain to the shoulder due to pressure on the central por-tion of the diaphragm (Plate 1 2.3 and Fig. 12.4).30 -32. Air may become trapped within the peritoneal cavity in a number of different ways. Perforation of an abdominal viscus can re­ lease air into the peritoneum.30.38 .42 Examples of this are a peptic ulcer, acute pancreatitis, perfo­ rated appendix, and a splenic infarct or rup­ lure, 32,38A 2 Symptoms

The patient may complain of acute or spas­ modic shoulder and/or abdominal pain . In the case of a splenic inFarct or rupture, the pain will be in the left shoulder." There will be a variety of symptoms depending on which viscus is perfo­ rated. See the associated symptoms under "Dia­ phragm" earlier in the chapter. Diagl10sis

Pain and/or rigidity will be noted with ab­ dominal palpation. An upright plain anterior­ posterior radiograph will demonstrate free intra­ peritoneal air under one or both hemidi­ aphragms 36 See the associated diagnostic clues under "Diaphragm" earlier in the chapter.

310

P H Y S I C A L

T H E R A P Y

OF

T H E

S H O U L D E R

Abdominal or vaginal surgery that allows op­ erative free air to enter and become trapped within the peritoneal cavity, is another source of refen-ed pain to the shoulder. Symptoms

Pain in the shoulder. See the associated symptoms under "Diaphragm."

activItIes can be fatal due to an air embo­ Iism.36.37.39- 4 1 To create pneumoperitoneum, air must first enter the vagina before it passes through a patent os cervix to enter the body cav­ ity of the cervix and subsequently travel through the uterine tube prior to escaping into the perito­ neal cavity (Fig. 12.7). SYl1lptOlltS

Pain in the shoulder. See the associated symptoms under "Diaphragm."

Diagnosis

There will be a history of recent abdominal or vaginal surgery. The abdomen is not tender to palpation and rigidity is absent . An upright plain anterior-posterior radiograph will demon­ strate free intraperitoneal air under the dia­ phragm.3. See the associated diagnostic clues under "Diaphragm." For females, certain activities during preg­ nancy, within 6 weeks postpartum, or follOWing abdominal or vaginal surgery, can lead to pneu­ moperitoneum. These include menstruation, ef­ fervescent vaginal douching, vigorous sexual in­ tercourse, orogenital insufflation, and knee to chest stretching exercises.>··37. 39 .0 The last three .

Diagnosis

There will be a history of current or recent pregnancy or recent abdominal or vaginal sur­ gery. The abdomen is not tender to palpation and rigidity is absent. An upright plain anterior-pos­ terior radiograph will demonstrate free intraper­ itoneal air under the diaphragm. 3• See the asso­ ciated diagnostic clues under "Diaphragm." LUNG

The lung, which is innervated by thoracic nerves TS to T6,3 is capable of referring pain from two distinct diseases to the shoulder. 3o . 32 . 33 .35,43- 4.

Diaphragm

Peritoneal Cavity

'------ Body Cavity '----- Uterine Wall '------05

Cervix

�L------ Vagina

FIGURE 1 2.7 Schel1latic drawing of the pathway (hat air mllst travel in order /0 create a pneumoperitoneum.

V I S C E R A L

P A T H O L O GY

The first is pulmonary infarction that is often secondary to a pulmonary embolism.32 ... The second is a Pancoast tumor. The most common cause of pulmonary embolism is a deep venous thrombosis (DVT) originating in the proximal deep venous system of the lower legs 46 Risk fac­ tors for DVT include blood stasis due to bed rest, endothelial (blood vessel) injury from surge.), or trauma, and a state of hypercoagulation 46 Other ri k factors include congestive heart failure, trauma, surgery (especially of the hip, knee, and prostate), more than 50 years of age, infection, diabetes, obesity, pregnancy, and oral contracep­ tive use 46 Pain is refen'ed to the shoulder due to contact with the central portion of the dia­ phragm (Plate 1 2.3 and Fig. 1 2.4). 30-32 SYlllptOI11S

Pain in the shoulder is most often felt at the superior angle of the scapula, in the supraclavic­ ular region, and in the upper trapezius mus­ c1e.30 .3I Patients will usually report the relief of pain when lying on the involved shoulder" Symptoms related directly to the pulmona.) , em­ bolism may include swollen and painful legs with walking, acute dyspnea or tachypnea, chest pain, tachycardia, low-grade fever, rales, diffuse wheezing, decreased breath sounds, persistent cough, restlessness, and acute anxiety.46- 48 See the associated symptoms under "Diaphragm" earlier in the chapter. Diagnos;s

There is a history of recent surge.)'. Chest radiographs, arterial blood gas studies, pulmo­ nary angiography, and ventilation-perfusion (V/O) scintigraphy are diagnostic tools available for the physician.4' Plain radiographs may not demonstrate the infarct, however, which may be hidden by the dome of the diaphragm.32 This is a potentially fatal condition that needs rapid re­ fen'al for emergency medical attention. See the associated diagnostic clues under "Diaphragm." The second disease state is a Pancoast tumor that occurs in the apical portion of the lung (Pla te 1 2.4 ) 30 .32. 35.43. 45.46.50 .51 Lung cancer is the

R E F E R R I N G

P A I N

TO

T H E

S H O U L D E R

311

most common fatal cancer in both men and womenso It commonly refers pain to the supra­ clavicular fossa, usually on the right siden Pain from a Pancoast tumor may be referred to the shoulder due to the involvement of the upper ribs. 5 1 Shoulder and arm pain may also occur secondary to contact between the cancerous lobes of the lung with the eighth cervical (C8) and first thoracic ( T I ) nerves, resulting in shoul­ der and upper extremity symptoms similar to thoracic outlet syndrome or a C8 radiculopa­ thy 35. 43 .45. The chest wall and subpleural lymphatiCS are often invaded by the tumor. 5 1 Other structures that may be involved include the subclavian artery and vein, inte.-nal jugular vein, phrenic nerve, vagus nerve, common ca­ rotid artery, recurrent laryngeal nerve, sympa­ thetic chain, and stellate ganglion.43. 45. 5 1 Cancer can metastasize to the lungs fTom carcinomas in the kidney, breast, pancreas, colon, or uterus 46 The lung itself is a common source of meta­ static cancer to bone, the liver, adrenal glands, and the brain' 6.50 Symptoms associated with cancer of the spine include a deep, dull ache that may be unrel ieved by rest. so Pain often precedes a pathologic fracture.so I f a fracture is present, then the pain may be sharp, localized, and asso­ ciated with swelling S O Pain will be reproduced with mechanical stress, thereby simulating a pure musculoskeletal dysfunction. Neurologic signs and symptoms will be present in some pa­ tients due to compression of the spinal cord. Pain is exacerbated by percussion of the spinous pro­ cess, with a reflex hammer, of the involved verte­ brae so Symptoms

Shoulder pain is the presenting symptom in over 90 percent of patients with a Pancoast tumor.43.46 A.m pain is common, often involving the medial aspect of the forearm and hand, in­ cluding the fourth and fifth digits.43.4S• thesias may be felt in the arm and hand due to compression of the subclavian artery and vein." Patients will often report relief of pain when lying on the i nvolved shoulder.2 Associated symptoms include Horner syndrome (contrac-

312

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tion of the pupil, partial ptosis of the eyelid, and sometimes a loss of sweating over the affected side of the face; Plate 1 2 .4), supraclavicular full­ ness, hand intrinsic atrophy, and discoloration or edema of the arm. 32 .. 3,, 5 . .6.5 1 Also, some patients will complain of a sore throat, fe­ ver, hoarseness, bloody sputum, u nexplained weight loss, chronic cough, dyspnea, ancIJor wheezing. 3 5 .4S-47

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Diagnosis

Smoking is a risk factor.35"6 Peak incidence occurs in smokers around 60 years of age.3S Refer the patient for a chest radiograph (Plate 1 2 .4). However, bone lesion of the spine may be detected before lung lesion on plain radiograph, because lung cancer metastasizes to bone early.46.S0

CASE STUDY 2 HtSTORY

A 66-year-old right-handed female presented to physical therapy (May 1 994) with complaints of severe WIO) right shoulder pain that radiated down her arm and along the ulnar border of her forearm and hand to include the third through fifth digits (Fig. 1 2 .8). The patient presented with a diagnosis of "frozen shoulder." She denied neck pain, headaches, or chest pain. About 6 weeks prior to her evaluation she reported an episode in which it felt like her whole right arm went numb. This symptom did not return. She did, however, report periodic mild numbness along the ulnar border of her right hand. On fur­ ther discussion she admitted that she forgot to tell her physician about the numbness. The pa­ tient stated that her shoulder pain started gradu­ ally sometime in January 1 994. Her pain was ag­ gravated by reaching into the back seat of her car from the driver's seat. Relief of pain occurred when she lay down on her right side. The patient denied that there was any change in her symptoms following stair climbing, a greasy meal, or a bowel movement. Except for what she described on the patient questionnaire,

FtGURE 1 2.8 Pain diagrarn (1'01'11 a 66-year-old right-/zGl,ded (elllale IVith a presel1tillg diagnosis o( "(rozell shoulder. "

the patient denied any other complaints or symp­ toms throughout her body. PAST MEDICAL HISTORY

1 994: Surgery to R. TMJ (2 months ago) for a malignant melanoma. 1 99 1 : Fell on right shoulder, no fracture, re­ solved in 4 months. 1 975: Lumbar disc surgery. PHYSICIAN-ORDERED TESTS

Cervical spine and right shoulder radiographs were negative per physician. GENERAL HEALTH

The patient questionnaire (Fig. 1 2 .9) revealed a family history of cancer. Her grandmother had throat cancer, her father had prostate cancer,

VISC E R A L

P A T H O L O GY

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PATIENT QUESTIONNAIRE Case S tudy lI2

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H ISTORY OF ILLNESS H ISTORY OF CANCER

DO YOU SELF DIABETIC .

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INCREASED CONS ISTENCY OF VAGINAL D I SCHARGE COLOR CHANGE OF VAGINAL D ISCHARGE INCREASED FREQUENCY OF URINATION

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Patient questiol1l1aire (or Case SlLIdy 2.

313

314

P H Y S I C A L

T H E R A P Y

OF

T H E

S H OUL D E R

and her sister had pancreatic cancer. It also re­ vealed that she is a 1 00 pack-year smoker (packs per day X number of years she smoked). The pulmonary part of the questionnaire was signifi­ canl. CERVICAL SCREEN

Active and passive extension and, separately, right rotation reproduced shoulder pain. Cervi­ cal axial compression testing was positive only in extension (see Fig. 4 . 1 4). Valsalva was negative. Spurling's quadrant compression test was posi­ tive on the right for reproduction of right arm pain (see Fig. 4. 1 6). SHOULDER AROM AND PROM

Active and passive ROM were equally limited. Abduction and ER were moderately limited with minimal limitations in lR and flexion. Minimal shoulder pain and no arm pain was reproduced. RESISTED TESTING

The shoulder girdle muscles tested strong and painless in the three muscle lengths tested. PALPATION

Swelling and tenderness were noted in the supra­ clavicular fossa. There was no edema or skin dis­ coloration noted in the extremities. PalpaLion of the lymph nodes, arterial pulses, and the abdo­ men was negative. NEUROLOGIC EXAMINATION

Sensation to light touch and pinprick was de­ creased in the right C8 and T I dermatome. Deep tendon reflexes were (2 + ) and equal at the bi­ ceps, brachioradialis, and tdceps tendons. The dght abductor digiti minimi tendon reflex was ( I + ) . Strength was decreased as follows: right triceps ('JIs ), wrist flexion and extension ('Ys), and the intrinsics of the hand were Ws ). SPECIAL TESTS

Glenohumeral joint compression and distraction were negative. Passive shoulder flexion with I R or E R was minimally painful a t the shoulder in

both cases. Passive right shoulder girdle depres­ sion with cervical left sidebending produced shoulder and arm pain; brachial plexus tension stretch also reproduced the symptoms. Thoracic outlet tests were negative. JOINT MOBILITY

The acromioclavicular, sternoclaviculal', and scapuloLhoracic joint mobility was WNL, grade 3. The glenohumeral joint was minimally re­ stricted, grade 2, i n distraction only. This was mostly due to muscle guarding. ASSESSMENT

The patient's signs and symptoms appeared to be consisted with a right C8 radiculopathy. A brachial plexus lesion could not be ruled out . Suspicions were raised with respect to the insidious onset of symptoms, age of the patient, constant pain, night pain, family history of can­ cer, patient history of cancer, pulmonary symp­ toms, and a 1 00 pack-year smoking history. The patient was refen'ed back to her physician dur­ ing Lhe initial course of physical therapy, during which minimal progress was made. Following a chest radiograph the patient was diagnosed with a Pancoast tumor in her right lung.

ESOPHAGUS

The esophagus, which is segmentally innervated by thoracic nerves T4 to T6, is able to refer pain to the shoulder Lhrough contact with the central portion of the diaphragm (Fig. 1 2.4) -'·6, 5 2 Esoph­ ageal pain is Lransmitted via afferents in the splanchnic and thoracic sympaLheLic nelves. 1 S The pdmary afferent fibers, both A-delta and C fiber neurons, pass through the paravertebral sympathetic chain and Lhe rami communicans to join the spinal nelve and enter the dorsal root ganglia before entering the dorsal horn of the spinal cord (Plate 1 2.2).I S RefelTed pain is thought to occur through convergence of visceral (cardiac and esophageal ) and somatic afferents onto the same dorsal horn neurons (Fig. 1 2.3)I . S,5 3

V I S C E R A L

P A T H O L O GY

R E F E R R I N G

Symptol1ls

Pain in the shoulder that may be exacerbated during or following meals J There may be subst­ ernal chest, neck, or back pain 47 Other symp­ toms include difficulty swallowing, weight loss, and (in the late stages) drooling 47 Symptoms as­ sociated with cancer are bloody cough, hoarse­ ness, sore throat, nausea, vomiting, fever, hic­ cups, and bad breath 47 Symptoms associated with renux esophagitis are regurgitation, fTe­ quent vomiting, and a dry nocturnal cough ·7 The patient will complain of heartburn that is aggravated by strenuous exercise, or by bending over or lying down, and is relieved by sitting up or taking antacids ·7 See the associated symp­ toms under "Diaphragm" earlier in the chapter. Diagnosis

Positive 24-hour intraesophageal p H and pressure recordings, acid perfusion, edropho­ nium stimulation, balloon distension, and ergo-

P A I N

TO

T H E

S H O U L O E R

315

novine slimulation.3 .5 4 .55 See the associated di­ agnostic clues u nder "Diaphragm." HEART

The heart, which is innervated by thoracic nerves T I to TS,3 is capable of referring pain to the shoulder.30-33 .52 .56 Cardiac afferen t fibers have shown evidence of convergence with esophageal afferents and somatic afferents in the upper tho­ racic spinal cord B I n fact, esophageal chest pain is known to mimic angina pectoris. 54 In addition, convergence has been demonstrated between cardiac afferents, abdominal viscera (gallblad­ der, for example) afferents, and somatic affer­ ents in the lower thoracic spinal cordY·53 Con­ vergence has also been noted with proximal somatic afferents (shoulder), phrenic (dia­ phragm), and cardiopulmonary spinal afferents onto the cetvical spinothalamic tract neurons (Fig. 1 2 . 1 0).'9 This explains how diaphragmatic disease and cardiac disease are both able to refer

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Cerebral Cortex Thalamus

Spinothalamic Tract Afferent Nerves

Cervical Segn)ent of the Spinal Cord

FIGURE 1 2 . 1 0 Schematic drawing or a somatic afferent nerve (shoulder), a phrenic nerve (diaphragm), and a cardiopulmollGry afferent nerve converging onto the same spinothalamic tract neuron.

(::::hr

agm

316

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pain to the shoulder and other cervically related derma tomes. Symptoms

The patient may complain of pain in the left shoulder that is often associated with reports of numbness and tingling in the left hand s .3 I ,47.57 Pain may also be felt in the chest, neck, arm (usu­ ally the left and a C8 and TI distribution), jaw, posterior thorax, or epigastrium 8•J5.47. s7 The pa­ tient may describe tightness, pressure sensa­ tions, throbbing, cramping, or aching in the above areas s,,, Other symptoms include exer­ tion and nocturnal dyspnea, ankle edema, palpi­ tations, easy fatigability, syncope, weakness, anxiety, prOrl.lse sweating, nausea, vomiling, .• tachycardia, or bradycardia . 8. J s 7 Diagnosis

A history of shoulder or chest pain (angina) on effort or exercise, such as a brisk walk, not associated with movements of the shoulder. 8 Re­ lief of symptoms with rest.8 There may be a rest­ ing pulse greater than 1 00 or less than 50 beats per minute." Blood pressure consistently higher than 1 60/90 is a positive sign . " Nitroglycerin will provide immediate relief of symptoms. Refer for ECG, blood test (increased CPK), treadmill with echocardiogram, and/or angiography. Heart dis­ ease is most common in men over 40 and is asso­ ciated with smoking, obesity, high blood pres­ sure, diabetes, and physical inactivity."·5 7 Timely recognition of a cardiac problem cannot be overstated; coronary anery d isease presents as angina, myocardial infarction, hean failure, and sudden death."

CASE STUDY 3 HISTORY

A 48-year-old obese left-handed male presented to physical therapy ( December 1 994) with a diag­ nosis of "shoulder pain-bursitis," and complain­ ing of moderate (0/10) pain in his left shoulder

FIGURE 1 2. 1 1 Pain diagram (rolll a 48-year-old le{l-handed male with a presenting diagllosis o( "shoulder pain-bllrsitis. "

(Fig. 1 2. 1 I ). He reponed the pain was not con­ stant and did not radiate down his arm. He de­ nied neck pain or upper extremity numbness. He did admit that his left hand "tingled" evel), once in a while. His shoulder pain started 2 months ago. The patient reponed that his symptoms started 2 days after an afternoon of throwing and catching a football with his son. His shoulder pain was aggravated by activities of waxing his car, carrying groceries, or climbing stairs. He re­ ported relief of symptoms with rest. The patient denied a change in symptoms after eating a greasy meal, bowel movement, coughing, laughing, or deep inhalation. Other than what he reported on the patient question­ naire, he denied any other complaints or symp­ toms throughout his body.

V I S C E R A L

P A T H O L O GY

R E F E R R I N G

P A I N

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317

PAST MEDICAL HISTORY

JOINT MOBILITY

1 993: Arthroscopic surgery to the right knee . 1 993: Fell onto left shoulder, sprained, resolved in 3 months. 1 985: Lumbar disc surgery.

No restrictions or hypermobilities were found in any of the joints in the shoulder girdle.

PHYSICIAN-ORDERED TESTS

No radiographs or special lab tests ordered. GENERAL HEALTH

The patient questionnaire (Fig. 1 2. 1 2 ) was signif­ icant for the pulmonary and cardiovascular sec­ tions . At the time of evaluation he was a 35 pack­ year smoker, had a history of heart problems (palpitations and tachycardia), and both his fa­ ther and grandfather died prematurely of heart allacks . CERVICAL SCREEN

Active and passive ROM was WNL and painless. Cervical axial compression and Spurling's quad­ rant compression tests (see Fig. 4 . 1 6) were nega­ live.

ASSESSMENT

The patient's symptoms were not reproduced dudng a thorough neuromusculoskeletal exami­ nation, and therefore his complaints were not consistent with an orthopedic dysfunction or in­ jury. A return to the interview process revealed that the patient periodically felt a tightness or pressure on his chest at the same time he felt the shoulder pain. Both symptoms rapidly went away when he sat down and relaxed. The symp­ toms were reproduced when he climbed a hill behind his house. Subsequently the patient was referred back to the physician for follow-up to mle out cardio­ pulmonary disease. He was subsequently diag­ nosed with myocardial ischemia with associated angina pectoralis. His symptoms disappeared with nitroglycerin.

SHOULDER AROM AND PROM

PERICARDITIS

Active and passive ROM were WNL and painless.

The heart, which is innervated by thoracic nerves T 1 to T5, is capable of refelTing pain to the shoul­ der in cases of pericarditis . 3 .35 .5 7 Pericarditis is an inflammation of the sac sUITounding the heart. 35 , 5 7

RESISTED TESTING

Shoulder girdle muscles were strong 'Ys and pain­ less. PALPATION

No Significant musculoskeletal tenderness was found throughout the shoulder girdle. Palpation of the lymph nodes and the abdomen was nega­ tive . Palpation of the arterial pulses in the left upper extremity revealed that they were of nor­ mal (grade 4) strength. NEUROLOGIC EXAMINATION

Sensation, deep tendon reOexes, and strength testing of the upper extremities was WNL.

Symptoms

There is usually a sharp burning pain in the chest or left shoulder.35 .47• 57 Pain may be aggra­ vated by deep breathing, coughing, or lying Oat; and relieved by sitting up and leaning for­ ward s .3 s.. ,.s, Other symptoms include fever, tachycardia, and dyspnea.47 Symptoms of chronic pericarditis include pitting edema of the arms and legs, serous fluid in the pedtoneal cav­ ity, enlarged liver, distended veins in the neck, and a decrease in muscle mass . 47

SPECIAL TESTS

Passive Oexion with humeral I R or E R was nega­ tive; glenohumeral compression and distraction were negative; upper limb nerve tension tests were negative.

Diag'lOsis

There will often be a pel-icardial friction rub, which has different characteristics than a heart murmur, noted during auscultations of the

318

P H Y S I CAL

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S H O U L D E R

PATIENT QUESTIONNAIRE Case Study *3

NAME AGE

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PRIOR TO ONSET OF PAIN

HI STORY OF CANCER RECENT SURGERY

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HI STORY OF ASTHMA ,

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WHEEZING OR PROLONGED COUGH

EMPHYSEMA OR COPD

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INCREASE WITH WALKING OR STAIR

CLIMBING AND RELIEVED WITH REST

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PREGNANT WOMEN ONLY CONSTANT BACKACHE

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INCREASED UTERINE CONTRACTIONS MENSTRUAL CRAMPS

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INCREASED CONSI STENCY OF VAG INAL DISCHARGE COLOR CHANGE OF VAGINAL DISCHARGE INCREASED FREQUENCY OF URINATION

FIGURE 1 2 . 1 2

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Patiel1l questiOn/wire {or Case Study 3.

_x_ _x_ _x_ � _x_

V I S C E R A L

P A T H O LO G Y

thorax ·.47 Patients with chronic pericarditis will demonstrate pulsus paradoxus, which is an exag­ gerated decline in blood pressure during inspim­ tion.47 There are a variety of etiologies including viral and bacterial infection, trauma, cancer, col­ lagen vascular disease, uremia, postcardiac sur­ gery, myocardial infarction, radiation therapy, and aortic dissection.s . 3s . 57 BACTERIAL ENDOCARDITIS

Bacterial endocarditis is another source of pain in the region of the shoulder girdle. 57-59 I t is an inflammation of the cardiac endothelium overly­ ing a heart valve due to a bacterial infection s .57 If left undiagnosed and untreated, bacterial en­ docarditis can be fataI.5 • .59 Risk groups for this i1lnes include patients with abnormal cardiac valves, congenital heart disease, or degenerative heart disease (calcific a0l1ic stenosis); parenteral drug abusers; and those with a history of bacter­ emia.57- 59 Treatment is with antibiotics,57-59 History will often reveal no trauma or previ­ ous occun'ence of these symptoms . Plain radio­ graph may show destructive changes indicative of an infection .'··59 Symptoms are not due to re­ fen'ed pain; therefore the patient will have a posi­ tive musculoskeletal examination of the involved joint. Monarticular involvement is thought to be secondary to deposition of large particulate masses (emboli) that contain immune com­ plexes.57-59 SYlIlptoms

Pain is most common in the glenohumeral, sternoclavicular. or acromioclavicular joints. and is usually monarticular. 57-59 Low back pain, which may mimic a hemiated disc, and sacroil­ iac joint pain are often reported.57 In approxi­ mately 25 to 27 percent of patients, musculoskel­ etal complaints are the first symptoms of this disease . 57 - 59 There may be an abrupt onset of intermittent shaking chills with fevery,57 The patient may also complain of dyspnea and chest pain with cold and painful extremities.57 Other symptoms include pale skin, weakness, fatigue, night sweats , tachycardia , and weight IOSS 8.47,57

R E F E R R I N G

P A I N

TO

T H E

S H O U L D E R

319

Diagnosis

Palpation of the i nvolved joint will reveal warmth, redness and tenderness. 57-59 An acute synovitis in a single joint, especially the metacar­ palphalangeal, sternoclavicular, or acromioclav­ icular joints-which are not commonly involved in other diseases-should raise suspicions of bacterial endocarditis .'··59 There is a heart mur­ mur, positive blood test for anemia, elevated erythrocyte sedimentation rate (ESR), decrease in serum albumin levels, increase in serum glob­ ulin concentration, and microhemaluria.58.59 There is relief of symptoms with antibiotics. Fever will be present at some time during the iIIness .'7-59 Associated signs are dyspnea, pe­ ripheral edema, fingernail clubbing, enlarged spleen, anorexia, Roth's spots (small white spots in the retina, usually surrounded by areas of hemorrhage), petechiae (small purplish hemor­ rhagic spots on the skin), and Janeway lesion (small red-blue macular lesions) on the palm of the hands or the soles of the feet.47 Diagnosis may be difficult in elderly patients who have a higher frequency of non pathologic hear1 mur­ murs and are less likely to develop a fever in re­ sponse to infection.57-59

CASE STUDY 4 HISTORY

A 64-year-old right-handed female presented to physical therapy (September 1 993) with a diag­ nosis of "right shoulder pain." She reported the sudden onset, without trauma, of right shoulder and upper trapezius pain approximately I month prior to presentation (Fig. 1 2 . 1 3). She denied neck pain, headaches, arm pain, or numbness and tingling. The patient also stated that her low back had been stiff during the week prior to pre­ sentation. The patient denied a change in her symp­ toms after eating a greasy meal, bowel move­ ment, coughing, laughing, or deep inhalation. Other than what she repor1ed on the patient questionnaire, she denied any other complaints or symptoms throughout her body .

320

P HY S I C A L

T H E R A PY

OF

T H E

S H O U L D E R

CERVICAL SCREEN

Active and passive ROM into flexion or left side­ bending produced a "stretching ache" in the right upper trapezius. Cervical spine axial compres­ sion was negative in the flexed, neutral, and ex­ tended postures (see Fig. 4. 1 4). Spurling's quad­ rant compression test was also negative (see Fig. 4. 1 6). SHOULDER AROM AND PROM

Active and passive flexion, extension, abduction, horizontal adduction, and horizontal abduction reproduced pain . In addition, specific active and passive scapular motions of elevation, depres­ sion. protraction, and relraction were also repro­ ductive of the patient's pain. RESISTED TESTING

There was no muscle or group of muscles that reproduced pain in all three muscle lengths (shortened, mid, and lengthened). PALPATION FIGURE 1 2 . 1 3 Pain diagram (rom a 64-year-old right-hal1ded (emale with a presel1ling diagl10sis o( "right shoulder pain. "

PAST MEDICAL HISTORY

1 993: Root canal, 6 weeks ago . 1 993: Surgery (March) to implant a prosthetic heart valve. 1 975: Hysterectomy. PHYSICIAN-ORDERED TESTS

No imaging studies were ordered. GENERAL HEALTH

The patient questionnaire (Fig. 1 2 . 1 4) revealed recent surgery, fever, shortness of breath, and a prosthetic cardiac valve. On further questioning the patient admitted to an episode of chest pain 2 weeks ago, but she related this to muscle sore­ ness from washing her windows.

The right sternoclavicular joint was slightly warm and red, with exquisite tenderness noted. A palpable band of tender tissue was noted in the right upper trapezius muscle. There was no tenderness or enlargement noted with palpation of the lymph nodes. Palpation of the abdomen did not reveal rigidity or viscus enlargement. Pal­ pation of the arterial pulses in the right upper extremity revealed that they were of normal (grade 4) strength. There were no petechia or Janeway lesions on her skin. Ankle edema was noted bilaterally. NEUROLOGIC EXAMINATION

Upper extremity sensation, DTR, and strength were all WNL. SPECIAL TESTS

Glenohumeral compression and distraction were negative; passive flexion with IR or ER were equally painful; the empty can sign was also neg­ ative.

V I S C E R A L

PATHOLOGY

R E F E R R I N G

P A I N

TO

T H E

S H O U L D E R

PATIENT QUESTIONNAIRE Case S tudy .4

NAME AGE

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EPI SODE O F FAINTING

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DRY MOUTH

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FEVER AND/OR CHILLS

UNEXPLAINED WEIGHT CHANGE NIGHT PAIN/DI STURBED SLEEP

DRY EYES

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H I STORY OF ILLNESS H I STORY OF CANCER

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PAIN RELI EVED BY REST

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CONSTANT PAIN

PAIN WORSE AT NIGHT

x x X

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DO YOU SELF INJECT MEDICINES /DRUGS . . . . . . . . . . . DIABETIC . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . sudden onset PAIN OF GRADUAL ONSET (NO TRAUMAl .

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(DENTAL ALSO)

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PAIN

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FAMILY H I STORY OF CANCER RECENT SURGERY

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PRIOR TO ONSET OF

X

� � ...liL

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--1L--1L-

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--1L--1L-

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PULMONARY H I STORY OF SMOKING

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EMPHYSEMA OR COPD

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HI STORY OF PNEUMONIA OR TUBERCULOSIS

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CARDIOVASCULAR HEART MURMUR/HEART VALVE PROBLEM . . . . . . . . . . . . . HI STORY OF HEART PROBLEMS . . . . . . . . . . . . . . . . . . . . SWEATING WITH

PAIN

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DIZZ INESS SWELLING

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FAM ILY H I STORY OF HEART D ISEASE

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PAIN/SYMPTOMS INCREASE WITH WALKING OR STAIR CLIMBING AND RELI EVED WITH REST

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INCREASED UTERINE CONTRACTIONS . . . . . . . . . . . . . . . MENSTRUAL CRAMPS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CONSTANT PELVIC PRESSURE . . . . . . . . . . . . . . . . . . . . . INCREASED AMOUNT OF VAGINAL DISCHARGE

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INCREASED CONS ISTENCY OF VAGINAL D I SCHARGE COLOR CHANGE OF VAGINAL D ISCHARGE INCREASED FREQUENCY OF URINATION FIGURE 1 2. 1 4

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--1L-

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-lI..--1L-

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Patient qLlesti0l1l1aire (or Case Study 4.

-lI..-

321

322

P H Y S I C A L

T H E R A PY

OF

T H E

S H O U L D E R

JOINT MOBILITY

The mobility of the glenohumeral, acromioclavi­ cular, and scapulothoracic joints was graded WNL, grade 3. The right sternoclavicular joint was graded hypomobile, grade 2, in all direc­ tions. Pain was reproduced with both compres­ sion and distraction of the sternoclavicular joint. ASSESSMENT

The patient's signs and symptoms were consis­ tent with an irritable right sternoclavicular joint with capsular and articular cartilage or meniscus involvement. The patient's history of prosthetic valve surgery, recent surger)" shortness of breath, fever, chest pain, and sudden onset of pain without trauma were of concern. She was referred back to her primary care physician in order to rule out cardiac disease. The patient was subsequently diagnosed with bacterial endocar­ ditis. After a week on antibiotics her shoulder pain disappeared. VASCULAR

An aneurysm within a subclavian vessel, or an aortic orifice of a subclavian vessel. can result in pain at the shoulder -'D- 32 .47 .52 This is a poten­ tially dangerous arterial condition.3S An aneu­ rysm is an abnormal widening of the arterial wall caused by the destruction of the elastic fibers of the middle layer of that wall or due to a tear in the inner lining of the arterial wall that allows blood to flow directly into the wall and subse­ quently widen it." Aortic aneurysms can enlarge and compress pain-sensitive stnlctures in the upper mediastinum, leading to shoulder pain . 3D They generally occur in the elderly and slowly enlarge over a period of many years . " Rapid morbidity or mortality is expected if an aneu­ rysm ruptures,35 SY"lploms

Pain in the shoulder that may include throb­ bing and cramping. The patient may also repo.1 paresthesias, neck pain, and/or chest pain.47 Other symptoms include night sweats, pallor,

nausea, weight loss, Raynaud's phenomenon, di­ plopia, dizziness, and syncope ·7 Symptoms may be aggravated by an increase in activity level (climbing stairs, fast walk, or upper extremity repetitive motions), and relieved by rest .32 Diagnosis

There will be a prolonged capillar)' refill time for the fingers, systemic hypotension, and a weak or absent distal pulse . 47 Bilateral dilation of the pupils will occur late.47 A chest radiograph may or may not allow visualization of the aneu,),sm. Arterial occlusion, usually due to atheroscle­ rosis or compression of the subclavian artery, as in thoracic outlet syndrome, of the shoulder can present as a deep constant pain or lead to is­ chemic pain with exercise . JO.60 SYlllptoms

Patients will complain of pain in the region of the shoulder girdle that may mimic a nerve root compression 6' Other symptoms include paresthesias, coldness, weakness, and fatigue in the involved extremity . 47.6 . Diagnosis

Systolic blood pressure will be higher while diastolic blood pressure remains unchanged in the involved extremity.47 Claudication will be noted with a distal pulse that is weak or ab­ senl.47 .6• The extremity will be cool, cyanotic, and demonstrate a prolonged capillar), refill time ·7 Tachycardia and angina pectoris may also be present . 47 Contrast angiography will demonstrate arterial occlusion that is best seen with the extremity elevated.6 ' In the case of tho­ racic outlet syndrome, one of the following tests will be positive: Adson's, costoclavicular, hyper­ abduction, pectoralis minor, or the 3-minutc flap-arm test 60-62 Thrombophlebitis of the axillary and subcla­ vian veins can also cause shoulder pain (Fig. 1 2 . 1 5).30. '2 .63 Thrombophlebitis is an inflamma­ tion of a vein in the presence of a blood clot. This is a Se,"iOllS situation, because an emboli may

V I S C E R A L

PATHOLOGY

R E F E R R I N G

P A I N

TO

T H E

S H O U L D E R

323

Thrombosis or the subclavian vein at the level or the thoracic outlet. (From Rohrer:' with pem7ission.) FIGURE 1 2. 1 5

break free and travel to the lung, a potentially fatal condition. The risk of pulmonary emboliza­ tion for persons wilh a subclavian thrombosis is approximately 1 2 percent ·3 Deep vein thrombo­ sis of the upper extremity is often due to venous trauma from repetitive motions of the shoulder, which is refen'ed to as effort thrombosis, in per­ sons with an abnonnal thoracic outlet ·3 Other causes of venous thrombosis include the pres­ ence of indwelling venous catheters (central lines or pacemaker leads), local compression, ra­ diation, or hypercoagulability ·3 Symptoll1s

There will be pain in the region of the shoul­ der girdle. Fever and chills may be presenL47 The patient may complai n of cold and swollen fin­ gers " Patients with effort thrombosis complain of the sudden onset of swelling and cyanosis in­ volving the entire arm ·' These patients will often report a history of upper extremity exertion

such as weightlifting ·3 Symptoms of shol'tness of breath, pleuritic chest pain, hemoptysis, or a new nonproductive cough are suggestive of a pulmonary embolus ·3 Diagnosis

Edema, coldness, and cyanosis will be noted in the fingers, hand, and upper alm,"··3 .•4 Dis­ tension of the superficial veins is usually seen in the hand, upper arm, shoulder, or anterior chest wall.·3 .M Effort thrombosis is usually seen in young, healthy individuals with an athletic phy­ sique,·3 I t is also seen frequently in hikers who carry backpacks ·3 Exertion of the involved ex­ tremity will lead to a significant exacerbation of the pain and swelling,,3 PhYSician-ordered tests include duplex ultrasound scanning and venog­ raphy. The shoulder-hand syndrome, also known as reflex sympathetic dystrophy or minor causal­ gia, is another source of shoulder pain and dys-

324

P H Y S I C A L

T H E R A P Y

O F

T H E

S H O U L D E R

function from a vascular diso;·der.60 This syn­ drome is precipitated by trauma to the upper extremity (sprain, laceration, fracture, or rotator cuff tear), cervical disc disease, cervical spon­ dylosis, hemiplegia, herpes zoster, and cardio­ vascular disease ·o These disorders are responsi­ ble for a reflex stimulation of the sympathetic nerve supply to the extremity with a resultant increase in vasomotor tone.60

Fig. 1 2 .4).3.•.32.52.•5 Cancer of the liver is more common in men and women over the age of 50 3 The liver is one of the mo t common ites of me­ tastasis from primary cancers elsewhere in the body (colorectal, stomach, pancreas, esophagus, lung, and breast cancers) ·' Hepatitis, or inflam­ mation of the liver, can range from the subclini­ cai to the rapidly progressive and fatal stage ···5 Symptoms

Symptoms

Patients will complain of shoulder pain and tenderness in conjunction with aching, paresthe­ sias, swelling, coldness, and stiffness in the hand and fingers ·o The symptoms are constant, even at resl.60 Diagnosis

Limited mobility (active and passive) of the shoulder, wrist, hand, and fingers will be noted in association with cyanosis, coldness, non pit­ ting edema, and hyperhidrosis in the hand and fingers ·o Eventually the fingers will demon­ strate stiffness, weakness, muscular atrophy, flexion deformity, and trophic changes of the nails . ·o After 6 months, plain radiographs will show spoLly osteoporosis of the head of the hu­ merus, carpus, and sometimes the phalanges ·o After 9 months, the skin of the hand becomes smooth and glossy, and there is atrophy of the subclItaneolls tissue and intrinsic muscles. flex­ ion contractu res of the fingers, and osteoporosis of the entire extremity . ·o Additional diagnostic tests that may be indi­ cated for a variety of vascular disorders include Allen's test, Doppler ultrasonic flow detector, systolic blood pressure, pulse volume recording, angiography, and auscultation of the major ar­ teries.7,62 LIVER

The liver, which is segmentally innervated by thoracic nerves T7 to T9, is able to refer pain to the right shoulder through its contact with the central portion of the diaphragm (Plate 1 2 . 1 and

Right shoulder pain may be acute or spas­ modic in nature.3 The patient may also complain of headache, myalgias, and arthralgias " Other symptoms include indigestion, nausea, vomit­ ing, unexplained weight loss, and fatigue.3,.,,7 .•5 Pain fyom cancer of the liver may be described as deep, gnawing, and poorly localized to the upper abdomen or back 3 See the associated symptoms u nder " Diaphragm" earlier in the chapter. Diagnosis

There may be an upper abdominal mass, an enlarged liver, or tenderness in the right upper quadrant of the abdomen.3 .•.•7.•5 Associated signs are jaundice, pale skin, purpura, ecchymo­ sis, spider angiomas, palmar erythema, an­ orexia, and the accumulation of serous fluid in th e peritoneal cavity.···7 .•5 Refer the patient for radiograph, diagnostic ultrasound, CT scan, or M R I of the abdomen.·5 See the associated diag­ nostic clues under "Diaphragm." PANCREAS

The pancreas, which is segmentally innervated by thoracic nerves T6 to T I 0, can refer pain to the left shoulder through contact with the central portion of the diaphragm (Plate 1 2 . 1 and Fig. 1 2.4) 3 .•. 30. 52 Shoulder pain is usually at the left scapula or supraspinous area " Cancer of the pancreas is more common in men and women over 50 years of age 3 Pancreatic cancer has been linked to diabetes, alcohol use, a history of pan­ creatitis, and a high-fat die! . 42 Pancreatitis, or inflammation of the pancreas, may be caused by heavy alcohol use, gallstones, viral infection, or

V I 5C E R A l

PAT H 0lOG V

blunt trauma . ···2 Acute pancreatitis can be rata1." Symptoms

Pain in the left shoulder, mid epigastrium, andior back "··2 Patients with a pancreatic ab­ scess, cancer, or pancreatitis may complain of rever, weight loss, jaundice, tachycardia, nausea, andior vomiting..,··7 In addition, patients with a pancreatic abscess may also report an abrupt rise in temperature, dialThea, and hypoten­ sion ·7 Patients with pancreatic cancer may also complain or ratigue, weakness, and gastrointesti­ nal bleeding.47 A patient with pancreatitis will often bend rorward or bring the knees to the chest in order to relieve the pain . .,·47 These pa­ tients will report an exacerbation of pain with walking or lying supine." In addition, these lat­ ter patients will complain of a waxing and wan­ ing pain in the epigastric and left upper quadrant or the abdomen " Pain will be exacerbated byeat­ ing, alcohol intake, or vomiting.· See the associ­ ated symptoms under "Diaphragm" earlier in the chapter. Diagnosis

There may be an abdominal mass, enlarged liver or spleen, or tenderness in the epigastric area.3.6,47 Diagnostic ultrasound, CT scan, or MRI may be necessary for an accurate diagnosis . See the associated diagnostic clues under "Dia­ phragm." GALLBLADDER

The gallbladder (Plate 1 2. 1 ), which is i nnervated by thoracic nerves T7 to T9, is capable Dr rerer­ ring pain to the right shoulder.3 .6·30-32 .47 . 52 .• 5 Af­ rerent fibers (T6 to T i l ) from the gallbladder pass into hepatic and coeliac plexuses and then enter the major splanchnic nerves, through which they pass to the sympathetic chain into the spinal cord 27 Common diseases of the gall­ bladder include cholecystitis (inflammation) and cholelithiasis (stones).3 Risk factors ror the latter include age (increases with age), sex (more

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common in women), pregnancy, oral contracep­ tive use, obesity, diabetes, a high-cholesterol diet, and liver disease "S Gallbladder cancer is more commOn in men and women over the age or 50 ]

Symptoms

Cramping pain or a deep, gnawing, poorly localized pain in the back or right shoulder may be the first symptoms ]··,47.•S Pain is usually re­ ferred to the right scapula.J .6··s Other symptoms include chronic epigastric or right upper abdom­ inal pain after meals. nausea, vomiting, and rever ",47 .•S Patients surfering with cholelithiasis, the passage of a stone through the bile or cystic duct, will complain of udden and severe parox­ ysmal pain in addition to chills and restless­ ness.47

Diagnosis

Gallbladder cancer is characterized by weight loss, anorexia, andior jaundice.47 .•s Pa­ tients with cholecystitis will have a fever, jaun­ dice, tenderness over the gallbladder, and ab­ dominal rigidity.·7.•s Cholelithiasis will produce a low-grade fever in the patient "··7 Fatty or greasy roods will exacerbate the symptoms or gallbladder disease ]··s There will be tenderness, and occasionally a palpable mass, in the right upper abdominal quadrant.· Rerer ror radio­ graph, diagnostic ultrasound, and/or CT scan . ·s These disorders are more common in obese women over 40 years of age.3 .•

CASE STUDY 5 HISTORY

A 5 1 -year-old right-handed obese female pre­ sented to physical therapy (May 1 995) with a di­ agnosis of "right shoulder strain." She com­ plained of a periodic severe, deep, and generalized ache across the back of her right

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The patient denied having more shoulder pain during prolonged walks or climbing stairs. Ac­ cording to the patient, coughing, laughing, or deep breathing did not increase her symptoms. Other than the information she provided on the questionnaire, the patient denied any other com­ plaints or symptoms throughout her body. PAST MEDICAL HISTORY

1 994: Arthroscopic decompression of right shoulder (August). 1 993: Diagnosis of hepatitis. 1 990: MVA with diagnosis of cervical sprain/strain, whiplash. 1 983: Diagnosis of diabetes. PHYSICIAN-ORDERED TESTS

Cervical spine radiographs demonstrated mild to moderate spondylosis throughout the cervical spine; dght shoulder radiographs were negative. GENERAL HEALTH

FIGURE 1 2 . 1 6 Pail1 diagram (rom a 51-year-old right-hal1ded (emale with a presel11il1g diagnosis o( "righ t shoulder strain. "

shoulder (Fig. 1 2. 1 6). The patient reported the sudden onset of a severe ache in her t;ght shoul­ der after a day of housecleaning 2 weeks ago. She admilled to a chronic history (5 years) of headaches, neck pain, and left shoulder pain with tingling in her left hand. The symptoms in her neck and left shoulder did not change after cleaning her house, and they remained mild in intensity. She stated t ha t she had never had sig­ nificant pain in the dght shoulder prior to the 2 weeks before her evaluation. She did admit that there was an occasional ache in her right shoul­ der blade over the past 2 months before presenta­ tion to physical therapy. The pain in her left shoulder was not the same as the pain in the right. The left shoulder pain was sharp, shooting, and localized. She reported her pain was worse at night.

The patient questionnaire (Fig. 1 2. 1 7) was signif­ icant for gastrointestinal symptoms. Further questioning revealed that she had a low-level fever for the 3 weeks prior to the evaluation. She also admilled having upper abdominal pain after greasy meals. The patient also stated that her right shoulder pain was worse following a large meal. CERVICAL SCREEN

Active and passive cervical extension, lefl side­ bending, or left rotation reproduced neck and lefl shoulder pain. Cervical spine axial compres­ sion was negative in flexion and neutral; there was reproduction of left shoulder pain in exten­ sion. Spurling's quadrant compression was neg­ ative on the right; left sided testing was positive for left shoulder pain and tingling in the left hand (see Fig. 4. 1 6). None of the cervical provoca­ tional tests reproduced dght shoulder pain. SHOULDER AROM AND PROM

Active and passive ROM testing of the right shoulder did not reproduce pain, although mild restrictions were noted with flexion, abduction, and extemal rotation.

V I S C E R A L

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PATIENT QUESTIONNAIRE Case S tudy '5

NAME AGE

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( D I F F I CULTY SWALLOWING) (RED,

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HISTORY OF ILLNESS HI STORY OF CANCER

SANDY )

DO YOU SELF DIABETIC

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PAIN WORSE AT NIGHT

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PAIN OF GRADUAL ONSET CONSTANT PAIN

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FAMILY HI STORY OF CANCER RECENT SURGERY

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HEARTBURN VOMITING FOOD

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PAIN CHANGE DUE TO BOWEL/BLADDER ACTIVITY PAIN CHANGE DURING OR AFTER MEALS FIGURE 1 2. 1 7

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HI STORY OF LIVER OR GALLBLADDER PROBLEMS HI STORY OF STOMACH OR GI INDIGESTION

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Patiel1t questionnaire (01' Case Study 5, 11l0di{ied to show signi{ical1l portions o(

both pages.

RESISTED TESTING

Resistive testing of the muscles throughout the right shoulder girdJe did not reproduce pain.

nodes and arterial pulses in the neck and upper extremity were WNL. Palpation of the abdomen revealed rigidity and exquisite tenderness in the right upper abdominal quadrant.

PALPATION

Mild tenderness, without reproduction of signifi­ cant shoulder pain, was noted in the left upper trapezius, left middle trapezius and rhomboids, and the right infTaspinatus muscle belly. Lymph

NEUROLOGIC EXAMINATION

Increased sensitivity to light touch and pin.prick was noted in the left C6 dermatome. Hyperre· flexia (3 + ) was noted for the left brachioradialis

328

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DTR. Isometric manual muscle testing of the upper extremities was WNL. SPECIAL TESTS

Right glenohumeral compression and distrac­ tion tests were negative; passive flexion with I R or E R was negative; the empty can sign was also negative. JOINT MOBILITY

The right acromioclavicular and scapulothoracic joints were graded 3, WNL, in mobility. The right sternoclavicular joint was hypomobile, grade 2, in distraction and inferior gliding. The right gle­ nohumeral joint was hypomobile, grade 2, in all directions, probably due to muscle guarding . ASSESSMENT

The patient's signs and symptoms were i nconsis­ tent with an active orthopedic injury of the right shoulder. Chronic joint dysfunction was noted in the right shoulder girdle. The left shoulder and hand symptoms were thought to be secondal), to a mild and chronic left cervical radiculopathy. The cervical spine did not appear to be a source of right shoulder symptoms . Of concern was the patient's history of diabetes, hepatitis, fever, shoulder pain associated with greasy meals, and the exquisite tenderness in the right upper ab­ dominal quadrant. The patient was refen-ed back to her pl-imary care phYSician to 11.1 Ie out any gas­ trointestinal problems. The patient was subse­ quently diagnosed with cholecystitis.

KIDNEY

The k.idney (Plate 1 2- 1 ) , which is innelvated by thoracic nerves T I 0 to L 1 .3 may refer pain to the shoulder girdle region.32.66 There are several pa­ thologies to consider with respect to the kidney, including cancer, perinephriC abscess, and other disease processes such as kidney stones. Associ­ ated disorders are pyelonephritis, nephritis, ne­ phropathy, nephrotic syndrome, renal artery oc­ clusion, renal failure, renal infarction, and renal tuberculosis.47

Symptoms

Some of the following complaints may be noted: acute or spasmodic ipsilateral shoulder, lower abdominal, groin, low back, or nank pain; weakness, fatigue, or generalized myalgia; unex­ plained weight loss; nausea, vomiting, or chills; or painf"ul, frequent. or urgent urination or he­ maturia.3,47 .66.67 Diagnosis

Tenderness will be noted at the costoverte­ bral angle and, in the case of innammation, there will be a fever.47.66 Musculoskeletal pain is rarely the primary complaint. Cancer of the kidney is most common between the ages of 55 and 60 s0 It can metastasize to the lung, brain, or liver so Metastasis to bone occurs late in the disease pro­ cess. so In patients with a pel-inephl-ic abscess, there is no tenderness over the renal areas of the back, and only mild distension is noted during abdom­ inal palpation . 67 There will be an elevated ESR, white cell count, and fever 67 A plain anteropos­ terior KUB (view of the kidney, ureters, and blad­ der) radiograph will demonstrate the following: ( 1 ) difficulty identifying the psoas stripe, (2) ab­ sence of the renal outline, and (3) curvature of the spine towards the side of the disease.67 Refer for an intravenous pyelogram and/or CT scan. Kidney stones may produce a severe cramping pain .' Chronic kidney disease may be associated with poor calcium deposits in bone, which will lead to a weak bone structure .' For all of the diseases of the kidney that have been discussed, patients may benefit by refelTals for diagnostic ultrasound, CT scan, or MRJ . STOMACH

The stomach, which is segmentally innelvated by thoracic nelves T6 to T I O, can refer pain to the shoulder through contact with the central portion of the diaphragm (Plate 1 2. 1 .2 and Fig. 1 2.4).3.30 Cancer of the stomach is more common in men and women over 50 years of age .' Risk factors for an ulcer or gastritis include heavy al-

V I S C E R A L

PATHOLOGY

cohol use, smoking, and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) 6.42 Symptollls

Pain is most often described in the right shoulder." The patient may also complain of epigastric or right upper abdominal quadrant pain.6,42 Patients with cancer, an ulcer, or gastri­ tis may complain of weight loss, night pain, or chronic dyspepsia-painful digestion, a sense of fullness after eating, heartburn, nausea, vomit­ ing, and a loss of appetite.··42•47 Patients with stomach cancer may complain of a deep, gnaw­ ing and poorly localized pain in the upper abdo­ men or back J Persons with an ulcer may also complain of gastrointestinal bleeding and epi­ gastric pain I to 2 hours after a meal, which oc­ curs with vomiting, fullness, or abdominal dis­ tention.42 .47 Patients with gastritis may also report belching, fever, malaise, anorexia, or bloody vomi!.47 See the associated symptoms under "Diaphragm" earlier in the chapter. Diagl10sis

There may be an abdominal mass or tender­ ness J .47 Abdominal CT scan or MRl may be nec­ essary for an accurate diagnosis. See the associ­ ated diagnostic clues under "Diaphragm." COLON AND LARGE INTESTINE

The colon and large intestine, which is inner­ vated by thoracic and lumbar nerves T i l to L t ,3 is capable of refelTing pain to the right shoulder (Plate 1 2 . 1 ) 68 The gastrointestinal tract (GI) has dual innervation (Plate 12.2). There are afferent fibers that join sympathetic nerves and afferent fibers that join parasympathetic nerves.·9 Pain from the GI is predominately mediated by affer­ ent activity in sympathetic nerves such as the splanchnic and hypogasuic nerves 69 These af­ ferent nerve fibers have theircell bodies in thora­ columbar spinal ganglia and their central projec­ tions enter the spinal cord at levels between T2 and L3 69 Disorders relevant to thi region in­ clude ulcerative colitis, irritable bowel syn-

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drome, spastic colon, obstructive bowel disease, diverticulitis, and cancer. Colon cancer is the most frequently diagnosed cancer in the Uni ted States 6 Cancer in this region is most common in men and women over the age of 50 J·50 Metas­ tasis to the spine, liver, and lung are common 6. 50 Smoking, alcohol, NSAIDs, and caffeine may in­ crease the risk of disease. 3 The NSAIDs may also mask the symptoms J Other dsk factors include a prior history of inflammatory bowel disease, prior·cancer ofanother organ, and benign polyps of the colon 6 Symptoms

Pain is referred to the right shoulder from the hepatic flexure of the colon (Plate 1 2 . 1 ) 68 A cramping pain is often described in the lower midabdominal region 6A2A7 There may also be a fluctuation of pain with eating habits, painful bowel movements, diarrhea, indigestion, nau­ sea, vomiting, change in bowel habits, bloody stools, jaundice, and weight loss J ,,7 Irritable bowel syndrome is the most common gastroin­ testinal disorder in Western society.42 Symptoms are aggravated or precipitated by emotional stress, fatigue, or alcohol, or by eating a large meal with fruit, roughage, or a high fat content ·2 I n addition to the above symptoms there may be constipation, foul breath, and flatulence.42 The predominant symptom with ulcerative colitis is rectal bleeding and dian·hea ·2 With obstructive bowel disease the patient will complain ofconsti­ pation, rapid heart rate, and short episodes of intense cramping pain.47 Diverticulitis, an in­ flammation in the wall of the colon, will produce constant left lower abdominal pain with radia­ tion commonly to the low back, pelvis, or left leg 6 [n cases of cancer, there may be a change in the frequency of bowel movement, a sense of incomplete evacuation, bloody stools, unex­ plained weight loss, weakness, fatigue, exer­ tional dyspnea, and vertig0 6A7 .50 Diagnosis

Patients may exhibit abdominal distension, abdominal tenderness, rectal bleeding, anorexia, and abnOlTnal bowel sounds ·7 Diagnosis is con­ firmed by a positive colonscopy.

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POSTVIRAL FATIGUE SYNDROME

Postviral fatigue syndrome (PFS) is yet another source of pain in the region of the shoulder gir­ dle.30.70-77 Recent research has suggested a rela­ tionship between PFS and fibromyalgia.72 .7' The criteria for a diagnosis of fibromyalgia syndrome includes neck and shoulder pain as well as a specific tender point in the supraspinatus muscle.78-8 1 There appears to be an association between PFS and the abnormal early onset of i ntracellu­ lar acidosis during exercise.7 1 .75.7. This is thought to represent excessive lactic acid pro­ duction secondary to a problem with metabolic regulation 7 1 .75-7. It also appears to be a problem with muscle metabolism.7o.7 ' . 75.77 There is spec­ ulation that this d isease is related to destruction of the mitochondria within the cell.7I •7' This sub­ sequently leads to an inability to perform aerobic glycolysis, so that the patient is stuck in perpet­ ual anaerobic glycolysis, which results in a build­ up of lactic acid leading to early fatigue and com­ plaints of muscle soreness.7I·7•.7• M itochondrial damage and fibromyalgia have been associated with the in'itable bowel or "leaky gut" syn­ drome.7•.' 1 .'2 A healthy intestinal wall is coated with hundreds of different species of microorga­ nisms. This protective coating of microorga­ nisms acts in concert with the physical ban'ier provided by the cells lining the intestinal tract to provide the body with important filter-like pro­ tection. Damaging substances like unhealthy bacteria, toxins, chemicals, and wastes are fil­ tered out and eliminated. Persons with "leaky gut" syndrome, however, are not able to filter out all of the damaging substances. Subsequently, unhealthy bacteria, toxins, chemicals, and wastes leak through the intestinal wall and into the bloodstream. One very well known risk factor for the development of intestinal mucosal dam­ age is the use of nonsteroidal anti-inflammatory drugs (NSAlDs). 83-.9 Persons with PFS are more susceptible to vi­ ruses and have a harder time fighting viruses due to their inability to metabolize essential fatty acids.7• The essential fatty acids are proposed to have a strong antiviral effect.74 I n addition,

omega-3 fatty acids have successfully been used to treat ulcerative colitis.90 Postviral fatigue syn­ drome is also known as myalgic encephalomyeli­ tis; Epstein-Ba'T virus syndrome; chronic fatigue syndrome; and Iceland, Akureyri, or royal free disease. Symptoms

Insidious onset of severe muscle fatigue and myalgia, exacerbated by exercise, ,7.7o Most com­ mon in cervical, thoracic, and shoulder re­ gions.7o There may be associated headaches, diz­ ziness, cognitive dysfunction, sore throat, andJor disturbed sleep ·7.70 Diagl10sis

Postviral fatigue syndrome is most common in young and middle-aged adults, especially women. It always follows a viral infection (cox­ sackie, Epstein-Barr, rubella, or varicella) and primarily affects skeletal muscle. There is usu­ ally mild lymphadenopathy and fever.47 Plain ra­ diographs and laboratory studies, such as ESR, are not helpful. Range of motion in the spine or extremities is usually within normal limits. Mus­ cle biopsies are not diagnostic, but abnormalities in fatty acid metabolism have been noted 7o.H Single-fiber EMG studies have demonstrated prolonged jitter values.7o There may be associ­ ated psychological problems, such as depres­ sion, in patients with chronic complaints.7 1 -73 Note: The case studies used in this chapter have been modified for instructional purposes.

Summary The best way to determine if a patient has vis­ ceral pathology is to first eliminate all possible neuromusculoskeletal tissues as a source of the symptoms. This requires skill, confidence, and experience in pel·forming your own orthopedic evaluation. If you cannot reproduce a patient's symptoms or have difficulty identifying a tissue in lesion, or if a patient does not respond to treat-

V I S C E R A L

PATHOLOGY

ment, then ruling out visceral pathology be­ comes imperative. An orthopedic patient who demonstrates signs and symptoms of visceral pa­ thology can be saved from severe morbidity or death by early referral to the appropriate physi­ cian.

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(cd): Examination in Physical Therapy Practice: Screening for Medical Disease. 2nd Ed. Churchill Livi ngstone, New York, 1 995 9. Natkin E, HarTington G, Mandel M : Anginal pain referred to the teeth: report of a case. Oral Surg 40:678, 1 975 1 0. Henry J, Montuschi E: Cardiac pain refen'ed to site of previously experienced somatic pain. BI' Med J 9: 1 605, 1978 I I . Payne R: Cancer pain: anatomy, physiology, and

Acknowledgernent.s

pharmacology. Cancel' 63:2266, 1 989

I wish to thank Ola Grimsby and Jim Rivard for their contribulions and hard work on Ihe illus­ trations for this chapter.

1 2 . Procacci P, Maresca M: Clinical aspects of visceral pain. Funct NeuroI 4 : 1 9 . 1 989 1 3 . Cervero F: Mechanisms of acute visceral pain. Br Med Bull 47:549, 1 9 9 1 1 4 . Gebhart G, Ness T : Central mechanisms o f vis­ ceral pain. Can J Physiol PharmacoI 69:627, 1 99 1 1 5. Lynn R: Mechanisms o f esophageal pain. Am J

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Manual Therapy Techniques ROBERT TIMOTHY

A

DONATELLI J

M cMAHON

The p,;mary goal of the clinician is to optimize function, decrease pain, restore proper mechan­ ics, facilitate healing, and assist regeneration of tissues. Manual therapy has been demonstrated clinically to be an important part of rehabilita­ tion and assessmenl of restricted joint move­ ment. Clinical application of manual techniques is based on an understanding of joint mechanics, tissue histology, and muscle function. Signifi­ cant advancement has been made in describing the benefits of passive movement by such re­ searchers as Akeson, Woo, Mathews, Amie!, and Peacock. 1-3 With this knowledge in hand the cli­ nician can apply manual therapy techniques dur­ ing critical stages of wound healing to influence extensibility of scar lissue, reduce the develop­ ment of restrictive adhesions, and provide foun­ dations of neuromuscular mechanisms to re­ store homeostasis. I Through an understanding of the effects of immobilization and sort tissue healing constraints we can establish criteria for phases of manual therapy techniques. This chapter will focus on manual therapy for the shoulder complex from a basic science and problem-solving approach. Manual therapy will be discussed in relation to soft tissue and joint mobilization and muscle reeducation. Management of the shoulder patient will be dis­ cussed from a perspective of protective versus nonprotective injuries.

Normal joint function includes a dynamic combination of arthrokinematics (intimate me­ chanics of joint surfaces), osteokinematics (the movement of bones), muscle function, fascial ex­ tensibility, and neurobiomechanics (addressed in Chap. 6). Dysfunction and pain of the shoulder can result from altered function of any or all of these systems. A detailed sequential evaluation that hypothesizes particular impairments dic­ tates which particular manual therapy strategies are appropriate. Please refer to Chapter 3 for shoulder evaluation procedures. Clearing the cervical and thoracic spine and brachial plexus is reviewed in Chapter 4 and 5. Manual techniques discussed wiu focus on the shoulder complex. DEFINITIONS

Several terms must be defined when mobiliza­ tion is discussed. Articulation, oscillation, dis­ tractions, manipulation and mobilization all de­ scribe a specialized type of passive movement. Articulatory techniques are derived [rom the osteopathic l iterature. They are defined as pas­ sive movement applied in a smooth rhythmic fashion to stretch contracted muscles, ligaments, and capsules gradually." They include gentle techniques designed to stretch the joint in each of the planes of movement inherent to the joint.' The force used during articular techniques is 835

336

P H YSI C AL

T H E RAP Y

OF

T H E

SH OU LDE R

usually a prolonged stretch into the restriction or lissue limitation. Oscillatory techniques are best defined by Maitland, who describes oscillations as passive movements to the joint, which can be a small or large amplitude and applied anywhere in a range of movement, and which can be performed while the joint surfaces are held distracted or com­ pressed'- There are four grades of oscillations. Grade I is a small-amplitude movement per­ formed at the beginning of range. Grade 2 is a large-amplitude movement performed within the range, but not reaching the limit ohhe range. Grade 3 is a large-amplitude movement up to the limit of range. Grade 4 is a small-amplitude movement performed at the limit of range'­ Grades I and 2 are used primarily for neurophys­ iologic effects and do not engage detectable re­ sistance. Grades 3 and 4 are designed to initiate mechanical changes i n the tissue and do engage tissue resistance. Distraction is defined as "separation of sur­ faces of a joint by extension without injul)' or dislocation of the parts. " 6 Distraction techniques are designed to separate the joint surface at­ tempting to stress the capsule. Manipulation is defined by Dorland's Illus­ trated Medical Dictionary as "skillful or dexterous treatment by the hand. In phYSical therapy, the forceful passive movement of a joint beyond its active limit of motion."7 Maitland describes two manipulative procedures. Manipulation is a sud­ den movement or thrust, of small amplitude, performed at a speed that renders the patient powerless to prevent itS Manipulation under an­ esthesia is a medical procedure used to restore normal joint movement by breaking adhesions. Mobilization is defined as "the making of a fixed or ankylosed part movable. Restoration of motion to ajoint."6 To the clinician, mobilization is passive movement that is designed to improve soft tissue and joint mobility. I t can include oscil­ lations, articulations, distractions, and thrust techniques. Mobilization, in this chapter, is defined as a specialized passive movement, attempting to restore the arthrokinematics and osteokinema­ tics of joint movement. Mobilization includes ar­ ticulations, oscillations, distractions, and thrust

techniques. The techniques are built on active and passive joint mechanics and are directed at the periarticular structures that have become re­ stricted secondary to trauma and immobiliza­ tion. These same techniques can be effective tools i n assessment of specific joint impair­ ments. Soft tissue mobilization (STM) for purposes of this chapter will be as defined by 10hnson: "STM is the treatment of soft tissue with consid­ eration of layers and depth by initially evaluating and treating superficially proceeding to bony prominence, muscle, tendon, and ligament.'"

Effects ojPassive Movmrumt em Scar Tissue: Indications and Contraindications Jor Mobilization Research indicates that mobilization is most ef­ fective in reversing the changes that occur in connective tissue following immobilization. I Ad­ ditionally, mobilization after trauma must be carefully analyzed. When is it safe to apply stress to scar tissue? How much stress should be ap­ plied to the scar in order to promote remodeling? What djrection should stress be applied? These important questions must be answered before we can determine the indications for mobiliza­ tion of scar tissue. Indications for mobilization will be discussed in regards to protective and non protective categories of shoulder injuries. A case study EOImat will be used for each categol), to illustrate changes in treatment and discuss the rationale of each phase.

CASE STUDY 1 PROTECTIVE INJURY

Protective injuries are £i'om surgery and/or trauma with significant soft tissue damage or re­ pair. Examples of protective injuries include an­ terior capsular shift, Bankart repair, rotator cuff repair, and shoulder dislocation. Rehabilitation for patients with protective injuries is divided

M A N U A L

into six phases: maximum protection, protected mobilization, moderate protection, late moder­ ate protection, minimum protection, and return to function. This case study will illustrate the concepts of phased rehabilitation in a patient with a protective shoulder injury. H ISTORY

A 16-year-old female basketball player was re­ fen'ed for postoperative rehabilitation of a right anterior capsulolabral reconstruction. The pro­ cedure performed was a mini-open procedure that include a rotator cuff interval reduction and anterior capsular shift with labra! cartilage re­ pair. Prior to surgery the patient had recurrent anterior dislocations for the past 3 years. Func­ tional limitations included weakness and insta­ bility, especially with basketball activities, and difficulty sleeping on the effected side. Additional past medical history includes previous arthro­ scopic surgery to repair torn cartilage to the same shoulder 2 years prior with little change in symp­ toms. The patient presented 2 weeks postopera­ tively with stiffness, weakness, and some mild pain.

T E C H N I Q U E S

337

Palpable tenderness and trigger points on subscapularis, selTatus anterior, levator sca­ pula, pectoralis minor, and lower portions of longus colli muscles. Scapular gliding revealed pectoralis major and minor tightness, and excessive mobility of the scapula in an anterior direction. Hypermobility of wrist, knee bilaterally, and left shoulder joints. ASSESSMENT

Adolescent female athlete with a protective shoulder injury and reconstructive surgery. Pa­ tient is cUITently in the protective mobilization phase. Patient appears to have anterior pectoral tightness and middle trapezious stretch weak­ ness. Inherent ligament laxity throughout other joints. PHASE I : MAXIMUM PROTECTION PHASE

Postwoulld)

(I 1010 Days

TREATMENT

SUMMARY OF I N ITIAL FINDtNGS

See Table 1 3 . 1 for ROM measurements. Slightly elevated and protracted scapula R Decreased fascial mobility of suture, and along fascia of inferior clavicle. TABLE t3. 1

TH E R A PY

Patient was immobilized in a sling postopera­ tively for the first 5 to 7 days. AAROM and PROM in the following protected ranges: Up to 90° of flexion, 45° of internal rotation, 90· of abduction, and neutral external rotation to be started 1 to

Protective injury case study I: Summarizariol1 o( ROM measuremel1ls WEEKS P OSTO PER A T IVELY 2

4

•

•

I.

PROM (degrees) Flexion

80

130

140

165

176

Abduction

58

90

102

160

170

-5

14

25

45

64

-10

18

30

53

75

NT

NT

38

56

80

Internal rototion, 450 obd. position

43

63

63

65

70

Extension

NT

NT

60

69

78

Flexion

NT

NT

125

160

170

Scaption

NT

NT

130

165

175

External rototion, neutrol position Extemol rototion, �5° abd. position External rototion, 90" abd. position

AROM (degrees)

Abbreviatioll: NT.

nOI

rested.

338

PH Y S I C A L

T H E R A PY

OF

T H E

S H OULDE R

2 weeks postoperatively. Ice and rest with al-m supported for pain reduction. RATIONALE

Immobilization during the first 3 to 5 days is crit­ ical to allow the inflammatory and proliferation stages to proceed. The inflammatory stage be­ gins I hour postwound and continues for 72 hours, during which vasodilation, edema, and phagocytosis of debris in and around the wound are occurring.9 The matrix and cellular prolifera­ tive stage begins 24 hours postwound and is characterized by endothelial capillary buds, with fibroblasts synthesizing extracellular matrix." , IO The scar is still quite cellular with presence of macrophages, mast cells, and fibroblasts. Little to no motion should occur dUling the first 3 to 5 days in order to protect the newly forming net­ work of capillaries.' Excessive motion too early can result in a prolonged inflammatory stage and excessive scarring. Heat should also be avoided secondary to vascular stress on capillary bud­ ding. Ice can be used to control swelling and pain. By the 7th to IDth day postwound gentle stress to the tissues is initiated. The fibroblastic stage of healing has already begun with presence of fibroblasts in the wound.9. lo Gentle early mo­ tion, such as with grades I and 2 joint mobiliza­ tion and PROM in protected positions, helps to faci litate aligning of newly forming collagen fi­ bers, aid muscle relaxation, and prevent adhe­ sion formation. In protected injuries with surgi­ cal involvement, it is helpful to have an operative report to inform the therapist of the specific tis­ sues involved in the procedure. For this case study, the anterior capsule, a small portion of the subscapularis, and the labrum were primar­ ily involved. (10 Days 10 3 Weeks) See Table 13.1 {or current ROM measures. PHASE 2: PROTECTED MOBILIZATION

TREATMENT

Continued grades I and 2 joint mobilization pro­ gressing toward grades 3 and 4 by 3 weeks. Scap­ ular gliding passive and active assistive. Strain

counterstrain an indirect positional release tech­ nique" to spinal and rib dysfunctions. PROM and AAROM in protected positions described in the previous phase. RATIONALE

The goal of this phase is to promote a functional scar and attempt to decrease other compensa­ tDly or contributing dysfunctions. Early mobili­ zation is critical in effecting scar tissue length, glide, and tensile strength. As the infiammatolY phase ends, the fibroplasia stage of healing has already begun. The production of scar tissue be­ gins on the fourth day of wound healing and in­ creases rapidly during the first 3 weeks.'·12 Pea­ cock has substantiated this peak production of scar by the increased quantities of hydrxypro­ line.' Hydryxyproline is a byproduct of collagen synthesis.'·13 Collagen production begins and continues to increase For up to 6 weeks. 2 .9.IO The newly syntheSized collagen fibrils are weak against tensile force. Intramolecular and intermolecular cross-linking of collagen de­ velopS, designed to resist tensile forces.'·13 The first peak in tensile strength occurs around the 2 1 st day postwound.' Gentle mobilization techniques can be effec­ tive during early fibroplasia due to the immatu­ I-ity of the collagen tissue. Arem and Madden demonstrated that after 1 4 weeks of scar matura­ tion, elongation of scar was no longer possible. I. I n contrast, the 3-week-old scar was significantly . lengthened when subject to the same tenSIOn. " Peacock hypothesizes that the mechanism by which the length of the scar is i ncreased becomes critical for the restoration of the gliding mecha­ nism.' Stretching, or an increase in length of the scar, is a result of straightening or reorientation of the collagen fibers, without a change in their dimensions.' For this to occur, the collagen fi­ bers must glide on each other. The gliding mech­ anism is hampered in unstressed scar tissue by the development of abnormally placed cross­ links and a random orientation of the newly syn­ thesized collagen fibrils. " Early gentle passive molion starting around the I Dth day and pro­ gressing to the 2 1 st day facilitates the develop-

M AN U AL

ment of tissue tensile strength by helping align newly synthesized collagen. Additionally, im­ proved tensile strength allows for early AROM in the next phase. PHASE 3: MODERATE PROTECTION PHASE

Weeks)

(3 '0 6

REEVALUATION

See Table \3.2 [or PROM measures. Continued muscle guarding of subscapularis. Serratus ante­ rior, first rib, longus colli, and scalenes with lillie to no tenderness. Subjective reports of decreas­ ing soreness and pain of GH joint at rest. Sutures have been removed and superficial closure com­ plete. Patient continues with anterior chest mus­ cle tightness and decreased scapular excursion.

T H E R AP Y

T E C HN I Q UE S

339

tween collagen fibers. Tensile strength has reached its first peak, allowing gentle AROM as early as 3 weeksz i n protected positions (rotation before elevation especially in contractile compo­ nent i njuries). STM to sutures and sUI1'ounding fascial planes facilitates suture scar extensibility and proper muscle function, and decreases pain. An additional goal of rehabilitation for this phase is to prevent muscle atrophy, inhibition, and effects of immobilization. PNF scapular pat­ terns with a progression towards resisted pat­ terns during this phase foster activation and res­ toration of scapular muscle activity, providing dynamic proximal stability. Progressive isomet­ ric exercises in protected posi tions can be used around 5 weeks by the patient at home or work to stimulate inhibited muscle and provide dynamic tension to healing soft tissue.

TREATMENT

PROM stretching and physiologic oscillations to 30' of external rotation in neutral and 45' ab­ ducted positions, joint mobilization G H joint with grades 3 and 4 in a posteroanterior (PA) direction and gentle posterior capsule stretch­ ing. STM to superficial scar (suture), inferior clavicle, fascial restricitons between pectoralis major and minor and between rib cage and pec­ toralis minor. Muscle reeducation initiated with proprioceptive neuromuscular facilitation PNF scapular techniques with active, eccentric, and concentric pallerns (primarily posterior eleva­ tion and depression). Gentle AAROM and AROM initiated but continuing to avoid combination of external rotation and abduction. At 5 weeks iso­ metrics begun in the Plane of the Scapula (30' to 45' a'1erior to frontal plane) for internal and external rotation, extension, and abduction.

RATIONALE

The moderate protection phase allows for more AAROM progressing toward AROM by the 4th week. Collagen production continues to be high until the 6th week.z.o,lo The goal of rehabilitation at this stage is to fu,-ther facilitate extensibility of newly synthesized collagen, realign randomly oriented collagen, and enhance fiber glide be-

PHASE 4: LATE MODERATE PROTECTION (61012 Weeks)

REASSESSMENT

Decreased tenderness and improved fascial glide of suture scar and sU'Tounding superficial fas­ cia. Scapular mobility within normal limits. Refer to Table 1 3.\ for ROM measures.

TREATMENT

Six to eight weeks PROM stretching with empha­ sis on external ROM in the plane of the scapular and 45' abducted position. Continuing PNF scapular pallerns working on any areas of weak­ ness. AROM PNF pallerns for upper extremity initiated with some resistance in weak aspects of the pallern. Active scapular stabilization and movement pallerns incorporating closed kinetic chain exercises. At 8 to \ 2 weeks, AROM exercises begun in unrestricted ROM (no loadjngofjoint in external and abduction). ( Progressive resistive exercises) (PREs) in protected ROM with emphasis on rota­ tor cuff strengthening. progressing to overhead exercises. Submax isokinetic internallexternal rotation in the plane of the scapula (limited ex­ ternal rotation to 45').

340

P H Y S I C AL

TABLE 13.2

T H E R AP Y

OF

T H E

S H O U L DE R

Summarization of phases of rehabilitation for protective shoulder il1juries M AXIMUM PROTE CT ION

P HASES

Time

1-10

day,

PROTE CTE D MO BILI ZAT ION

10 day, to 3

MO DE R ATE PROT E CTION

LATE MO DER ATE PROT E CT ION

MIN M I UM PROT ECTION

R ETURN TO FUN CT O I N

3-6 week,

6-12 weeks

12-16 weeks

+ 16 weeks

weeks Stage of heeling

InAommotory, proliferative early fibroplasia

Eorly nbroplo,io

Fibroplasia, maturation

Maturation

Maturation

AIIoturotion

GooI,

Protect newly formed scor

Facilitate functional $Cor, aligning new collogen fibers; dear $pinal and rib dysfunction

Enhonce tensile strength of seer

Stress scar; restore force couples; proximol, di,tol

Some as previous phose; increase strength rototor cuff, poroscopulor muscles

Retum to function progressively

Monual therapy techniques

7-10 day,

Joint mobsgrades 1 end 2 progress ta 3,4; STM surrounding tissue; PNF scapular pottems; protected PROM

As previous, STM to suture, scapular release tech.; PNF scapular pottems

Scopular release tech.; PNF UE pottems; Iow-lood prolonged streich

PNF UE patterns with signi�cant resistance; low-food prolonged stretch if needed

A, needed for any deficits

Other theropeutic interventions

Position education; ontiinAommotory modolities; ice

Home program of PROM in protected ranges

(odmon exercises, T-bar, Swiss boll, foam roller; AAROM and AROM exercises

lsokinetics in protected ROMsubmax; octive scopular stabilization exercises; PRE,

Some os previous, increasing effort and ROM; plyoboll throwing

Progressive retum to sport drill" ligh. recreational activities

postwound, grades 1 and 2 joint mob,

RATIONALE

At 6 weeks collagen production tapers off. The maturation or remodeling phase of healing be­ gins around 3 weeks and continues for up to 12 to 1 8 months." Maximizing scar extensibility is essential, because by 1 4 weeks scar deformabil­ ity may be greatly decreased. 13 Strengthening is emphasized more during this phase_ Some strengthening has already begun using

PNF scapular pallerning to reestablish balance of function of the parascapular muscles in the previous phase. During the firsl 2 to 3 weeks of this phase, active and reactive scapular stabiliza­ tion activities are initiated. These exercises help to restore force couples around the scapula and usually involve some co-contraction or synergy pallerns of the rotator cuff. During the last 3 to 4 weeks of this pha e , emphasis shifts toward

M A N U A L

strengthening the rotator cuff throughout the full range of movement. Through the progres­ sions described, proximal stability and force couples are established before distal force cou­ ples. Low-level weights or theraband resistance for this case study for internal and external rota­ tion effected healing subscapularis tendon and enhanced dynamic GH joint stability. PHASE 5: M I N I MAL PROTECTION

T E C H N I Q U E S

341

TREATMENT

Patient began progressive basketball shooting and drill activities at 1 8 weeks. Patient was in­ structed not to begin team play until 22 weeks postoperatively. Patient was discharged at 1 8 weeks with an extensive program of rotator cuff strengthening and scapular stabilization exer­ cises.

(12/016 Weeks)

REEVALUATION

RATIONALE

See Table 1 3 . 1 for ROM measurements. Patient demonstrating some elevation of scapula with late elevation phase; excessive scapula elevation increased with resistance. Activities of daily liv­ ing within normal limits. No pain with most ac­ tivities and exercises.

TREATMENT

Continued progression of weights and reps of previous phase of exercises. Chest pass throwing against plyoLrampoline with 2.5-1 b, ball. STM performed to apparent remaining fascial restric­ tions along the inferior clavicle followed by man­ ual and PRE strengthening of lower trapezious and sen-atus anterior. PNF resistive patterns per­ formed close to end-range abduction and exter­ nal rotation.

RATIONALE

Multiple repetitions in unresLricted ROM con­ tinue to provide sLress to the maturing scar. Man­ ual techniques during this phase are used to fur­ ther fine-tune function and clear any remaining restrictions. Neuromuscular control at end­ range abduction and external rotation is essen­ tial to help protect capsular reconstruction and return to sport. PHASE 6: RETURN TO FUNCTION

T H E R A P Y

(16 Weeks +)

REEVALUATION

Isokinetic testing reveals externaVinternal rota­ tors ratio at 8 1 percent and 20 percent stronger than uninvolved side.

The return to function phase begins usually around 1 6 weeks if elements of movement are free of abnormal patterns and pain. This phase happens sooner based on patient response, spe­ cific trauma, and level of function requ ired. Ex­ ercises are more functionally based and maximal efforts are used. lsokinetic testing of rotator cuff muscles infOlm the therapist of any deficits in particular internal External ratio's, that may in­ dicate increased hazard for return to function. Currently reimbursement issues and managed care policies may not allow physical therapists to follow a patient completely through all phases of rehabilitation. In summary, protected shoulder injuries can be safely progressed through a phased program of rehabilitation based on stages of sofl tissue healing. Table 1 3.2 summarizes the various stages. Manual therapy techniques used at spe­ cific stages of healing can enhance the strength and extensibility of scar, reestablish force cou­ ples, and restore functional movement patterns.

CASE STUDY 2 NON PROTECTIVE INJURY

Nonprotective shoulder IIlJuries are primaJ;ly shoulder dysfunctions that have no significant soft tissue healing constraints. Examples of non­ protective injuries include postacromioplasty, prolonged immobilization, adhesive capsulitis, and impingement syndromes. Often these pa­ tients present with pain, stiffness, and limited function. This case study will illustrate the con-

342

PH Y S I C A L

T H ER A P Y

OF

T H E

S H O U L DE R

cepts O r rehabilitation ror a patient with a non­ protective injury.

along longus colli muscles at C5-6 L, Poste­ rior aspects or ribs 2-4 L, L subscapula,-;s, supraspinatus, infraspinatlls, teres minor, and levator scapula

HISTORY

A 46-year-old remale homemaker presents with lert shoulder pain and stirfness. Patient was re­ rerred 5 days postarthroscopic surgery and closed manipulation. Patient began having pain and stirfness several months prior possibly due to overworking in her yard. Lert L shoulder be­ came increasingly stiff and painful the 5 to 6 weeks prior to surgery. Diagnosis given was ad­ hesive capsulitis. Past medical history: "stirr neck" 2 to 3 years ago.

Capsular testing revealed restricted motion in all dil'ections

ASSESSMENT

Patient with nonprotective shoulder injury, Ad­ hesive capsulitis with strong muscle guarding and possible adaptive shortening or subscapu­ laris. Unable to fully assess capsular restrictions secondary to muscle guarding or rotator curr and subscapularis muscles.

SUMMARY OF I N I T I A L FINOINGS

I N ITIAL PHASE

See Table \ 3.3 ror initial ROM measurements.

TREATMENT

Functionally, patient is unable to reach over­ head, fasten bra. Moderate difficulty with dressing, placing hand behind back, and washing opposite axilla Upper quarter screening: Extension and si­ debending L or cervical spine were limited by 50 percent and painrul actively and pas­ sively with over pressure. L scapula protracted, downwardly rotated, and winging Tenderness and muscle spasm: Posterior cervical spine C 1-2, ante,-;or cervical spine

TABLE 13.3

Indirect techniques such as strain and counterstrain used on cervical, rib, and shoulder musculature, PROM stretching to tolerance in external and internal rotation, flexion and ab­ duction with scapula stabilized. Joint mobiliza­ tion or grades I and 2. Patient instructed in posi­ tioning comrort ror L shoulder and cervical spine. RATIONALE

The initial phase or rehabilitation ror nonpro­ lected injuries primarily rocuses on anti-inflam­ matory modalities, grades I and 2 joint mobiliza-

NO'lprOleCl;ve inju,y case slLldy 2: Summarizatiol1 or ROM measurements T IME

4 WEEKS

6 WEEKS

10 WEEKS

112

140

150

174

80

120

150

170

-20

5

30

36

62

10

20

45

56

70

INITI A L

2 WEE KS

102 70

PROM Idegree,1 flexion Abduction External rotation, neutral position External rotation, 450 abet position External rototion, 900 abel position

NT

40

46

75

Internol rolotion, 450 abd. position

NT 52

54

52

53

71

Hyperextension

48

50

53

53

71

70

90

112

132

155

AROM (degree'l Scoption Abbre";(lIio,,;

NT, I/ot tested.

M A N UA L

tion, and education. Patients often will perform habitual patterns of movement, maintaining cur­ rent state of dysfunction. Correction, modifica­ tion, or cessation of predisposing activities is es­ sential. Goals of rehabilitation during this phase are to reduce inOammation and pain, restore proximal stability spine, scapula muscle activity, and avoid painful positions. Clearing spinal and rib dysfunctions that contribute or are source problems for shoulder signs and symptoms is es­ sential during this phase for an optimal func­ tional outcome. INTERMEDIATE PHASE

T H E R A P Y

T E C H N I Q U E S

343

pula using theraband and a I -lb weight ini tially for 1 0 minutes progressing to 20 minutes over a series of 4 to 5 treatment sessions. High-speed (2000/s) isokinetics were initiated for internal and external rotation in the plane of the scapula in the available ROM. Scapular release tech­ niques used to mobilize fascial restrictions within subscapularis, se'Tatus anterior, and leva­ tor scapula. Joint mobilization, myofascial re­ lease techniques used to address facet joint irri­ tation C5-6 and suboccipitally. PNF scapular patterns progressing from passive to resistive movements with emphasis on posterior depres­ sion, as illustrated in Figure 1 3 . 1 .

REEVALUATION

By the third treatment, patient repons decreased soreness of the L shoulder at rest. Still experienc­ ing pain with reaching and overhead activities. See Table 13.3 for ROM measurements. De­ creased pain and stiffness of cervical spine but ROM still restricted. Continued abnormal posi­ tion of L scapula. TREATMENT

Continued PROM stretching, joint mobilization as previous. Patient staned on low-load pro­ longed stretch with heat in the plane of the sca-

RATIONALE

The intermediate phase of rehabilitation begins when patient reactivity allows for more aggres­ sive progression of techniques. Goals of this phase are to maximize ROM of all components of shoulder movement and normalize force cou­ ples of scapula and GH joint. Emphasi is placed on restoring rotation at the GH joint and then on elevat ion. Traditional manual therapy techniques used to treat limited shoulder ROM have followed the arthokinemalic movements of joint surfaces oc-

FIGURE 1 3.1

344

P H Y S ICAL

T H E R A P Y

OF

T H E

S H O U L DE R

curring at the glenohumeral. Kaltenbom deter­ mined the appropriate method of applying a glid­ ing mobilization technique by the convex concave mle. 15 Forexample, slidingofthe convex humeral head an a concave glenoid surface occurs in the opposite direction of the humems. Therefore, during elevation of the shoulder, the humeral is sliding inferiorly as the bone moves superiorly. However, data are now available that challenge the concave-convex mle of arthrokinematic mo­ tion. Poppen and Walkeri. report a movement of the humeral head in a superior and inferior di­ rection during elevation of the shoulder. Howell et al. demonstrated translatory motion of head of the humems to be opposite of that predicted by the concave-convex mle. Only patients with instability demonstrated translation in the direc­ tion predicted by the concave-convex mle.17 Soft tissue tension capsular, ligament rather than joint surface geometry may be a greater determi­ nant of the arthrokinematics of the GH joint. The type and fTequency of force used to mobi­ lize depends on the implicated tissue. In this case study, the implicated tissue of restriction is the anterior and inferior capsule, GH ligaments, and subscapularis. The authors advocate the use of low-load prolonged stretch in addition to oscilla­ tion techniques ror more signiricant soft tissue re­ strictions. Connective tissue structures such as ligaments, tendons and capsules respond to me­ chanical stress in a time-dependent or viseoelas­ tic manner. ' 8-21 Viscoelasticity is a mechanical property of materials that describes the tendency of a substance to deform at a constant rate. The rate of deformation is not dependent on speed of the external force applied. If the amount of defor­ mation does not exceed the elastic range, the structure can return to the original resting length after the load is removed. If loading is continued into the plastic range, passing the yield point, fail­ ure of the tissue will occur. Failure is thought to be a function of breaking intermolecular cross­ links rather than mpture of the collagen tissue. 22 If pel-manent increase in ROM is a goal of treatment, then manual therapy should be aimed at producing plastic defOl·mation. Taylor et al. 23

showed that there is a increased risk of tissue trauma and injury with rapid stretch rates. Rap­ idly applied forces will cause material to react i n a stiff, brittle fashion, causing tissue tearing. Gradually applied loads result in tissue respond­ ing i n a more yielding manner with plastic defor­ mation. If the tissue is held under a constant ex­ ternal load and at a constant length, force relaxation occurs. 24 In addition to increasing extensibility of GH capsular and ligamentous stmctures, muscle ex­ tensibility must also be addressed. Clinically the authors have found subscapularis to be com­ monly restricted in shoulder dysfunction. Sub­ scapularis is the most stablizing factor during external rotation of the glenohumeral joint in 0° of abduction. " Additionally, most patients tend to guard or immobilize a painful shoulder by ad­ ducting and intemally rotating the GH joint, thus shortening subscapulmis. In prolonged immobilization and dysfunc­ tions such as adhesive capsulitis, subscapularis may accommodate to a shorten position. Mus­ cles respond to immobilization by degeneration of myofilaments, change in sacromere alignment and configuration, decrease in mitochondria, and decreased ability to generate tension. 2• Mus­ cles accommodate to immobilization in a short­ ened position by losing sarcomeres. Tabary et al. found that muscles immobilized in a shortened position for 4 weeks had a 40 percent decrease in total sacromeres and displayed an increased resistance to passive movement. 27 Muscles im­ mobilized in a lengthened position had 20 per­ cent more sacromeres and demonstrated no change in resislance to passive motion. Functionally, limited subscapularis extensi­ bility may effect functional elevation. Otis et al. 28 have recently documented the importance of re­ storing rotation to the glenohumeral joint in order to facilitate elevation. It was demonstrated that the contribution of infraspinatus moment arm to abduction is enhanced with internal rota­ tion while that of subscapulmis is enhanced with external rotation. 28 Low-load prolonged stretch and rotational exercises in the plane of the sca­ pula in our case study are an atlempt to reverse

M A N U AL

the effects of immobility, increasing the extensi­ bility and strength of the subscapularis muscle. Restrictions of subscapularis tend to also affect parascapular muscles secondary to the altered scapulohumeral rhythm. Scapular release techniques and STM (de­ sc,ibed later in the chapter) can be used to re­ lease fascial restrictions that have developed as a result of abnormal movement paLlerns. In this particular case, the patient had excessive pro­ traction and downward rotation of the scapula with trigger points in the levator scapula, serra­ tus antedor, and pectoralis minor. Warwick and Williams29 report a possible fusion of the sen·a­ tus anterior and levator by their fascial connec­ tion. Excessive tone of pectoralis minor effectly depresses the scapula and restricts the scapular rotation necessary for proper elevation. Further­ more, the se'Tatus anterior and levator scapula work as a force couple to rotate the scapula. In­ creasing the extensibility of the fascia of these three muscles would allow proper functioning of parascapular force couples during elevation. RETURN TO FUNCTION PHASE

REEVALUAT t O N

See Table 1 3.3 for I O-week ROM measurements. All ADLs without pain and patient has started working in the yard without limitations. Patient

TABLE t 3.4

T H E R A P Y

T E C H N I Q U E S

345

without cervical pain but ROM ce,vical spine 3/4 normal SB L and R.

TREATMENT

Patient instructed in exercise progressions for next 2 months with emphasis on rotator cuff and parascapular muscle exercises. Patient allowed to progress back to swimming and gardening ac­ tivities to tolerance.

RAT t O N A L E

Once ROM and strength are optimized, a home program is finalized to further facilitate physio­ logic changes such as increased sacromeres and remodeling of periarticular tissues. In the com­ petitive and industdal athlete, fonn, technique, and training error cOITecUon is essential to pre­ vent recurrence of dysfunction. In summary, rehabilitation of nonprotective injUlies depends on the implicated tissues or sys­ tems in dysfunction or restriction. Table 1 3.4 summarizes the phases of rehabilitation. G H joint arthrokinematics may be strongly inOu­ enced by periarticular tissue extensibility and muscle function rather than pure joint geometry. Manual techniques must comply with the type of tissue or system response desired. Continual

Summary o( phased rehabilitation (or nonprotective shoLilder injuries

PHASES

Signs and

IN T I A I L

INTERMEDIATE

RETURN TO FUNCTION

Pain at rest; difficulty

No poin at rest; poin with resistance; moderate

ROM maximized; functional

symptoms

sleeping; poin

reactivity; limited rot, and elevation;

movement poin free;

(reactivity)

before

weakness of rolator cuff and/or

muscle imbalances

resistance

poroscopulor muscles

Gools

Decrease poin

Restore rotation ROM and strength of

Monuol theropy

Grocles 1 and 2

Grades 3 and .4 ioint mobs; STM; scopular

resolving Retum to Fundion

poroscopulor muscles and rotator cuff techniques

joint mobs

release techniques; PNF scapular and UE

Fine-tuning of functional pottems with PNF

patterns; Iow·1oad prolonged stretch Other therapeutic interventions

Anti-inRammatory

Heat with stretch; isokinetic and isotonics

Home program, correct

modalities;

working ratation before elevation in POS;

technique and training

positioning and

isometrics; AAROM with T bars, Swiss

errors

activity

bolls, loom rollers; GH io;n' ond scopulor

education

toping techniques

346

P H Y S ICAL

T H E R A P Y

OF

T H E

S H O U L DE R

reassessment of subjective, functional, and ob­ jective measures assists the therapist in evaluat­ ing treatment effectiveness.

Role of Mobil:ization The primary role ofjoint mobilization is to restore joint mobility and facilitate proper biomechanics of involved structures. Joint mobilization has two proposed rationales-neurophysiologic and bio­ mechanical. The neurophysiologic effect is based on the stimulation of peripheral mechanoreceptors and the inhibition of nociceptors (pain fibers). Noci­ ceptors are unmylelinated nerve fibers that have a higher threshold of stimulation than mechano­ receptors ]o.3 I There is evidence that stimulation of peripheral mechanoreceptors blocks the trans­ mission of pain to the eNS,3o Wyke postulates that this phenomenon is due to a direct release of inhibitory transmitters within the basal spinal nucleus, inhibiting the onward flow of incoming nociceptive afferent activity. Joint mobilization is one method of enhancing the fTequency of dis­ charge fTom the mechanoreceptors, thereby di­ mi nishing the intensity of many types of pain. The biomechanical effect of joint mobiliza­ tion is focused on the direct tension of periarticu­ lar tissues to prevent complications resulting from immobilization and trauma. The lack of stress to connective tissue results in changes in normal joint mobility. The periarticular tissue and muscles sur­ rounding the joint demonstrate significant changes after periods of immobilization. Akeson et al. have substantiated a decrease in water and glycosaminoglycans (GAG, the fibrous tissue lu­ bricant), an increase in fatty fibrous infiltrates (which may form adhesions as they mature into scar), an increase in abnormally placed collagen cross-links (which may contribute to the inhibi­ lion of collagen fiber gliding), and the loss of fiber orientation within ligaments (which significantly reduces their strength). ' ·3 Passive movement or stress to the tissues can help to prevent theses changes by maintaining tissue homeostasis. 2 The exact mechanisms of prevention are uncertain.

CONTRAINOICATIONS

We can understand contraindications to Jomt mobilization by becoming aware of the common abuses of passive movement. The abuses of pas­ sive movement can be broken down into two categories: creation of excessive trauma to the tissues and causing undesired or abnormal mo­ bility. ' I mproper techniques, such as extreme force, poor direction of stress, and excessive velocity, may result in serious secondary i njury. In addi­ lion, mobilization to joints that are moving nor­ mally or that are hypermobile can create or in­ crease joint instabilities. Ultimately, selection of a specific technique will determine contraindications. For example, the very gentle gradc I oscillations, as described by Maitland, rarely have contraindications. These techniques are mainly used to block pain. They are of small amplitude and controlled ve­ locity. In contrast, manipulative techniques have many contraindications. Haldeman describes the following conditions as major contraindica­ tions for thrust techniques: arthrides, disloca­ tion, hypelmobility, trauma of recent occur­ rence, bone weakness and destructive disease, circulatOlY disturbances, neurologic dysfunc­ tion, and infectious disease.32

PRINCIPLES OF JOINT MOBI LIZATION TECHNIQUES

The mobilization techniques are designed to re­ store intimate joint mechanics. Several general principles should be remembered during appli­ cation of the techniques. Hand Position The mobilization hand should be placed as close as possible to the joint surface, and the forces applied should be directed at the periarti­ cular tissues. The stabilization hand counteracts the movement of the mobilizing hand by apply­ ing an equal but opposite force or by supporting or preventing movement at sUITounding joints. Excessive tension in the therapist's hands during

M A N U A L

JOint mobilization can result in the patient guarding against the mobilization. Direction of Movement The direction of movement of mobilization should take in account the mechanics of the joint mobilized, the aI1hrokinematic and osteokinem­ atic impairments of the dysfunction, and the cur­ rent reactivity of the tissues involved. The direction of forces to the joint is also de­ termined based on the response desired. Neuro­ muscular relaxation and pain modulation effects will be appreciated if the direction of force is op­ posite pain. Biomechanical effects will be appre­ ciated if forces are directed towards resist but to patient tolerance. The resistance represents the direction of capsular or joint limitation. Move­ ment into the restriction is an attempt to make mechanical changes within the capsule and the surTounding tissue. The mechanical changes may include breaking up of adhesions, realignment of collagen, or increasing fiber glide. Certain move­ ments stress specific parts of the capsule. For ex­ ample, arthrogram studies demonstrated that ex­ ternal rotation of the glenohumeral joint stresses the anterior recess of the capsule.33 Body Mechal1ics Proper body mechanics are essential in ap­ plication of mobilization techniques. The thera­ pist is able to impart desire direction and force of movement if working from a position of stability. The therapist should stand close to the area being mobilized and use weight shifting through legs and trunk to assist movement in the vector of mobilization. The therapists hands and arms should be positioned to act as fulcrums and le­ vers to fine-tune mobilization.

T H E R A P Y

T E C H N I Q U E S

347

demonstrate the elongation of tissue under var­ ied loads. A high-load, shon-duration treatment ( l OS g to 1 65 g for 5 minutes) and a low-load, long-duration treatment (5 g for 1 5 minutes) were compared.34.35 The results indicated that low-load, long-duration stretch was more effec­ tive in obtaining a permanent elongation of the tissue. In humans, Bonutti et al.36 determined that the optimal method to obtain plastic defor­ mation and reestablish ROM is static progressive stretch (SPS). One to two 3D-minute sessions per day of SPS for I to 3 months produced an overall average i ncrease in motion of elbow con­ tractures of 69 percent, with exceUent compli­ ance by the patients. As previously noted, the au­ thors advocate the use of low-load prolonged stretch with heat to facilitate plastic deformation of shoulder capsular restrictions. Figure 1 3.2 de­ picts one method of low-load prolonged stretch for external rotation. The patient needs to be in a subacute stage of reactivity and the stretch is to patient tolerance. Heat used in conjunction with the stretch has been found to be more effec­ tive than stretch alone.37•3• The patient's shoul­ der is placed in the plane of the scapula with a wedge or tack of towels. The stretch is per­ formed by theraband resistance to assist with po­ sitioning and the use of a hand weight and grav­ ity to stretch anterior periarticular Slnlctures. Duration of stretch can be from 20 to 30 minutes. Little research has been performed on joint mobilization to determine the optimum dura­ tion of oscillation. Often the duration is deter­ mined by the change desired by the therapist. For example, GH joint mobilization of grades I or 2 performed to facilitate neuromuscular relax­ ation could be performed until muscle guarding was reduced and ROM increased.

Gherwhurneral Joint Techniqu£s FIGURE 1 3.3: I N FERIOR GLIDE OF THE

Duratiol1 (Illd Al1IplilLlde Several animal model studies have been per­ formed to determine the most effective tech­ nique for obtaining permanent elongation of col­ lagenous tissue, using different loads and loading time. The studies used rat tendons to

HUMERUS

Patiem Positiol1 Supine, with the involved extremity close to the edge of the table. A strap may be used to stabilize the scapula. The extremity is abducted to the desired range.

348

P H Y S I C A L

T HERAP Y

O F

T H E

S H O U LDE R

FIGURE 1 3.2

Therapist Pos;t;OI1 Facing the lateral aspect of the upper arm. Cephalad hand web space is placed on superior ghenohumeral i nferior to acromion. Assisting hand supports the weight of the arm by holding

the distal upper arm superior to epicondyles and bracing patient's arm against therapist. As­ sisting hand/arm can also impart distractive force and change amount of rotation. The mobi­ lizing hand glides the head of the humerus inferiorly, allempting to stress the axillary

FIGURE 1 3.3

M A N U A L

T H E R A P Y

349

T E C H N I Q U E S

FIGURE 1 3.4

pouch or inferior portion of the glenohumeral capsule.

/

FIGURE 1 3.4: LONGITUDINAL DISTRACTION-I NfERIOR GLIDE Of THE HUMERUS

I

Patielll Position

/

Supine, with the involved extremity as close as possible to the edge of the table. Therapist Position Facing the joint, with inner hand up into the axilla pressing against scapulaghenoid. The outer mobilizing hand grips the epicondyles of the humerus and imparts a distractive force stressing the inferior capsule. To increase the ef­ ficiency of the pull, the therapist can weight shift and rotate the body slightly away from the pa­ tient. A prolonged stretch is often eFFective with this technique.

fiGURE 1 3.5: POSTERIOR GLIDE Of THE HUMERUS

Patient Position Supine, with arm slightly abducted and flexed into plane of the scapula and resting on the therapist's thigh.

fiGURE 1 3.5

350

P H Y S I CA L

T H E R A P Y

OF

T H E

SHOULDER

Therapisl POSilioll

Opposite side of patient's shoulder. Mobiliz­ ing hand is same is i nvolved shoulder. Therapist cups patient's elbow in mobilizing hand and as­ sists mobilization with therapist sternum. Assist­ ing hand stabilizes the scapula under patient. Mobilization movement is along 35° of glenOid tilt. The level of flexion can be changed to work the most restl;cted part of the capsule. This tech­ nique is useful with subacute and chronic poste­ rior capsule tightness. FIGURE 1 3.7: LATERAL DI STRACTION OF THE HUMERUS

Paliel1l Posilion

Supine, close to edge of table, with the in­ volved extremity flexed at the elbow and gleno­ humeral joint. The extremity rests on the thera­ pist's shoulder. A strap and the table stabilize the scapula. Therapist Posiliol1

FIGURE 1 3.6

Therapisl Posil iOI1

Sitting on treatment table at 45° tum from sagittal plane. Mobilizing hand is placed on ante­ rior humeral head, with a wedge or rolled towel under lateral scapula. Assisting hand supports distal extremity to facilitate relaxation. The mo­ bilization is directed posterior along the plane of the glenoid. This technique is useful for reactive shoulders with posterior capsule tightness. FIGURE 1 3.6: POSTERIOR GLIDE OF

Facing laterally, both hands grasp the hume­ rus as close as pO sible to the joint. The therapist should assess which vector of movement is most restricted by staJiing laterally with mobilization and proceeding caudally. To improve delivery of oscillation or stretch, therapist should align his or her trunk along vector of mobilization. FIGURE 1 3.8: ANTERIOR GLIDE OF THE HEAD OF THE HUMERUS

Paliel1l Position

Prone, with the involved extremity as close as possible to the edge of the table. The head of the humerus must be off the table. A wedge or towel roll is placed just medial to joint line under the coracoid process. The extremity is abducted and flexed into the plane of the scapula.

HUMERUS

Therapisl Positiol1 Paliel1l POSi/iol1

Supine with involved shoulder flexed 90° and horizontal adducted to first tissue resistance.

Distal to the abducted shoulder facing ceph­ alad. The outer hand applies slight distraction force while the i n ner mobilizing hand glides

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FIGURE 1 3.7

Therapist Position

the head of the humerus anteriorly, stressing the anterior capsule. The tendon of the subscap­ ularis is also stressed with this technique. The mobilization can be fine-tuned by changing the angle of the anterior force to the area most restricted.

FIGURE 1 3.9: ANTERIOR/POSTERIOR GLIDE OF THE HEAD OF THE HUMERUS

Patient Position

Facing laterally in a silting position, with the forearm of the involved extremity held between the therapist's knees. Both hands grasp the head of the humerus and apply anteroposterior move­ ment oscillating the head of the humerus. Grades I and 2 are mainly used with this tech­ nique to stimulate mechanoreceptor activity. FIGURE 1 3. 1 0: ANTERIOR/POSTERIOR GLIDE OF THE HEAD OF THE H U M ERUS

Patient Position

Prone, with the involved extremity over the edge of the table abducted to the desired range. A strap may be used to stabilize the scapula.

FIGURE 1 3.8

Supine with the involved extremity supported by the table. A towel roll, pillow, or wedge is placed under the elbow to hold the arm in the POS.

352

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FIGURE Therapist Positiol1

Therapist Position

Facing laterally in a sitting posItion. The fingertips hold the head of the humerus while a gentle up-and-down movement is applied. This technique is used with grades 1 and 2 oscilla­ lions. FIGURE 1 3. 1 1 : EXTERNAL ROTATION OF

1 3.9

THE

HUMERUS

Facing laterally with caudal mobilizing hand grasping the distal humerus. the heel ohhe ceph­ alad mobilizing hand over the lateral aspect of the head of the humerus. Force is applied through both hands. The caudal hand rDiates the humerus extemally and provides long-axis dis­ traction while the cephalad hand pushes the head of the humerus in a posterior direction.

Patient Position

Supine with the involved extremity sup­ ported by the table. The arm is held in the plane of the scapula.

FIGURE

13.10

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353

FIGURE 1 3 . 1 1

FIGURE 1 3 . 1 2: EXTERNAL ROTATION! ABDUCTION/INFERIOR GLIDE OF THE HUMERUS

Patient Position

Supine with the involved extremity sup­ ported by the table. The arm is abducted in the plane of the scapula.

FIGURE 1 3 . 1 2

Therapist Position

Facing laterally with the caudal hand hold­ ing the distal humerus and the heel of the cepha­ lad hand over the head of the humerus. The cau­ dal hand abducts the arm and externally rotates the humerus while maintaining the POS. The cephalad hand simultaneously pushes the head of the humerus into extemal rotation and slight

354

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FIGURE 1 3 . 1 3

infelior glide. The force can be oscillated, thrusted, or a prolonged stretch.

Sternocla:vwular and Acromiocla'lli.cular Techniques FIGURE 1 3. 1 3: SUPERIOR GLIDE OF THE STERNOCLAVICULAR JOINT

Palienl Position

Supine with the involved extremity close to the edge of the table. Therapist Position

Facing cranially. The volar sUiface left thumb pad is placed over the infelior surface of the most medial aspect of the clavicle. The right thumb reinforces the dorsal aspect of the left thumb. Both thumbs mobilize the clavicle supe­ riorly. Graded oscillations are most successful with this technique. FIGURE 1 3. 1 4: INFERIOR/POSTERIOR GLIDE OF THE STERNOCLAVICULAR JOINT

Pat;el1l Position

Supine with the patient's head supported on a pillow. The patient's cel-vical spine sidebent to­ ward and rotated away from involved side 20' to 30'.

Therap;st POS;/;o/l

At the head of the patient, using thumb pad or pisiform contact on the most medial pOl1ion of the clavicle. Mobilization is performed in a inferior/posteriorflateral direction parallel to the joint line. Elevating the involved shoulder to a position of restriction and then performing mo­ bilization the SC joint may assist the rotational component of clavicle motion joint.

FIGURE 1 3. 1 5: ANTERIOR GLIDE OF THE ACROMIOCLAVICULAR JOINT

Patient Pos;tioll

Supine at a diagonal to allow the involved acromioclavicular joint to be over the edge of the table.

Therapisl Position

Mobilizing force is perfol'med with both thumbs (dorsal surfaces together). The therapist places the distal tips of the thumbs posteriorly to the most lateral edge of the clavicle. Both thumbs push the clavicle anteriorly. Graded oscillations are mainly used with this technique,

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355

FIGURE 1 3 . 1 4

The force is applied simultaneously. Both hands push the bones in opposite directions, obtainjng a general stretch to the capsular structures of the acromioclavicular joint. Oscillations or a pro­ longed stretch are used with this technique.

Soft Tissue MolJi1izatWn and Scapulotlwradc Release Techniql.ws

FIGURE 1 3 . 1 5

FIGURE 1 3. 1 6: GAPPING OF THE ACROMIOCLAVICULAR JOINT

Patient Positiol1 Silling close to the edge of the table Therapist Posit;oll Facing laterally with the heel of the left hand over the spine of the scapula and the thenar em­ inence to the right hand over the distal clavicle.

Soft tissue mobilization for purposes of this chapter will be as defined by Johnson: "STM is the treatment of soft tissue with consideration of layers and depth by initially evaluating and treating superficially proceeding to bony promi­ nence, muscle, tendon, ligament etc." · The goals of STM in the patient are similar to those of joint mobilization: development of functional scar, elongation of collagen tissue, increase in GAGs, and facilitatation of lymphatic drainage .'9 In overuse syndromes, trauma, postsurgical conditions, and abnormal movement patterns of the shoulder, areas of tenderness and restricted extensibility of connective tissue may develop. Adhesions within the fascia may reduce the mus­ cles' ability to broaden during contraction and

356

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FIGURE 1 3 . 1 6

lengthen during passive elongation .'9 Abnormal compensations may occur, possibly leading to breakdown of compensating tissues. Within the shoulder complex several areas are importanl to evaluate for fascial restrictions. Scapulothoracic releasing techniques will also be described due to the musculotendious and fascial characteristics of this articulation. The following is a descl-iption by muscle(s) or space between structures to evaluate and mobilize. Table 1 3.5 defines the types of techniques re­ ferred to in the figure legends.

TABLE 1 3.5

Treatment hand tecimiq"es

Susloined pressure: Pressure applied directly to restricted tissue at the desired depth and direction of maximol restriction Directoscillations: Repeoted oscillations on and off a restriction with uptake of slack as restriction resolves Perpendicular mobilization: Direct oscillations and/or sustained pressure techniques performed perpendicular to muscle fiber or soft ti nue play Parallel mobilization: Pressure applied longitudinally to restrictions along Ihe edge of Ihe muscle belly '" along bony conlou" Perpendiculor (transverse) strumming: Repealed

mylhmicol defor­

mations of a muscle belly to improve muscle play and reduce tone

FIGURE 1 3 . 1 7 SUBSCAPULARIS

(Adapted (rom 1011"S0I1, J9 wi/It penniss;oll.)

Patiel1l Position

Supine with the shoulder abducted to tolerance Therapist Position

Facing axilla with mobilizing fingers on muscle belly of subscapularis. Parallel mobiliza­ tion or perpendicular strumming or direct oscil­ lation may be used. Assistive techniques are sus­ taining pressure while elevating and adducting the shoulder as in Figure 1 3 . 1 7B.

F I G U R E 1 3 . I B: SUBSCAPULARIS ARC STRETCH

Patient Position

Supine Therapist Position

Cephalad hand simultaneously elevates, ex­ ternally rotates, and distracts the involved shoulder, while the caudal hand (thenar side)

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357

A FIGURE 1 3. 1 7

B

stabilizes the lateral border o f the scapula. Both movements occur simultaneously in a slight arcing fashion. FIGURE 1 3. 1 9: PECTORALIS MINOR

Patient Positio/1 Supine or sidclying with aim slightly ab­ ducted and Oexed. Therapist Position Mobilizing fingers glide along in a superfi­ cial vector along ribs 3 to 5 lateral to medial un­ derneath pectoralis major. Often pectoralis minor is bound down and tender in shoulder dys­ function. STM techniques used: direct oscilla­ tion, sustained pressure , perpendicular and par­ allel deformations. Assistive techniques are inhalation, contract relax with shoulder protrac­ tion. FIGURE 1 3.20: SERRATUS ANTERIOR-UPPER PORTION

Patient Position Side\ying with involved side up.

Therapist Positiol1 Standing posterior to patient's shoulder. Caudal hand elevates the scapula in an cephalad and anterior direction off the rib cage. The thera­ pist can use the fingers of top hand to roll over and palpate the superior fibers of the serratus anterior that attach to the 1 st and 2nd ribs as well as the fascial attachments between levator scapularis and serratus anterior.29 STM tech­ niques: sustained pressure, direct oscillation. As­ sistive techniques: resistive PNF djagonal con­ tract relax, deep breath.

FIGURE 1 3. 2 1 : SERRATUS ANTERIOR -LOWER PORTION

Patient Position Sidelying. Therapist Position Place mobilizing fingers along an interspace of ribs 2 to 8 on interdjgitations of serratus ante­ rior. STM techniques used: parallel techniques

358

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FIGURE 1 3. I 8

FIGURE 1 3 . 1 9

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359

FIGURE 1 3.20

FIGURE 1 3.2 1

along rib contours medial to lateral or lateral to medial. Assistive techniques: deep breath, con­ tract relax with scapular depression, rotation of the thoracic pine to the same side. Restrictions may be evident with previous history of rib frac­ ture or abdominal surge.),.

FIGURE 1 3.22: INFERIOR CLAVICLE

Patient Position

Supine with involved extremity supported by a pillow.

360

P H Y S I C A L

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THE

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FIGURE 1 3.22

Therapist Position

Same side as involved shoulder. Palpating medial to lateral or vice versa along inferior clav­ icle, look for fascial restrictions and tenderness especially at the costoclavicular ligament, sub­ clavius muscle, and the conoid and trapezoid lig­ aments. This region is important to evaluate and treat in shoulder patients who have protracted and externally rotated scapula with adaptive shortening of anterior chest musculature. FIGURE 1 3.23: SCAPULAR DISTRACTION

Patient Positim,

Sidelying close to the edge of the table with the involved extremity accessible to the thera­ pist. A pillow may be placed against the patient's chest to provide anterior support.

FIGURE 1 3.24: SCAPULAR DISTRACTION, POSTER I O R APPROACH

Patient Position

Sidelying as previous bUI closer to posterior edge of table. Therapist Position

Posterior to patient with therapist's hips in perpendicular orientation to patient's trunk. Therapist's adjacent leg on the treatment table with knee bent and placed along midthoracic spine. Outer mobilizing hand grasps the verte­ bral border of the scapula. Inner hand supports the anterior GH joint. Once hand placement is achieved, the therapist leans back, distracting the scapula away from the thoracic wall. Sus­ tained stretch most effective with this technique.

Therapist Positiol1

Facing the patient with caudal hand under­ neath inferior angle of the scapula and the ceph­ alad hand grasping the vertebral border of the scapula. Both hands tilt the scapula away from the thoracic wall along with the distraction of the scapula by the therapist leaning backward.

FIGURE 1 3.25: SCAPULAR EXTERNAL ROTATION

Patient Position

Sidelying with the involved extremity acces­ sible to the therapist.

M A N U AL

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361

FIGURE 1 3.23

FIGURE 1 3.24

Therapist Positiol1

Facing the patient with the caudal hand under the extremity through the axillary area. The cephalad hand grasps the superior aspect of the scapula while the caudal hand grasps the inferior angle. The force is applied simultane­ ously, producing an external rotation of the sca-

pula. Figure \ 3 .26 demonstrates external rota­ tion of the scapula with soft tissue technique using the therapist's elbow to mobilize upper trapezious and levator scapula. Assistive tech­ niques include patient actively rotating cervical spine toward and away from involved side, and spray and stretch to upper trapezious trigger points.

362

P H Y S I C A L

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OF

T H E

S H O U L D E R

FIGURE 1 3.25

FIGURE 1 3.26

FIGURE 1 3.27: SCAPULA DISTRACTION, PRONE

Patient Position

Prone with the involved extremity supported by the table. Therapist Positiol1

Facing cephalad. outer hand under the head of the humerus and the adjacent mobilizing

hand web space under the inferior angle of the scapula. The forces are applied simultaneously. The outer hand lifts the G H joint while the adja­ cent hand lifts the inferior angle of the scapula.

Summary Rehabilitation of shoulder injUlies using manual techniques is based on an understanding of

M A N U A L

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363

T E C H N I Q U E S

FIGURE 1 3.27

stages of sort tissue healing, normal and abnor­ mal arthrokinematics and osteokinematics of the shoulder complex, effects of biomechanical stress on various tissues, and muscle function. The application of manual techniques for the shoulder is dependent on a thorough sequential evaluation and continual reassessment. Indica­ tions and contraindictions for mobilization are based on an understanding of the histology of immobilized and traumatized tissues. Clinical management o[ shoulder i njuries has been dis­ cussed from a perspective of protective versus nonprotective injuries, and phased programs of rehabilitation have been presented. Research on the efficacy of manual therapy must be advanced and traditional concepts and techniques should comply with current and future discoveries.

Ackrwwledgements We would like to Ihank Jill Heinzmann, R.P.T. and John Zubal, A.T.C. for their assistance with the manual technique piclures.

References I . Frank C, Akeson WH, Woo S el al: Physiology and therapeutic value of passive joint motion. Clin Or­ Ihop 1 85: 1 1 3 , 1984

2. Peacock EE II': Wound Repair. 3rd Ed. WB Saun­ ders, Philadelphia, 1984 3. Akeson WH, Amici D, Woo SLY: Immobility ef­ fects on synovial joints. The pathomechanics of joint contracture. Biorheology 1 7:95, J 980 4. Stoddard A: Manual of Osteopathic Technique. HUlchinson, London, 1959 5. Maitland GD: Pedpheral Manipulation. Butter· worth Publishers, London, J 970 6. Clayton L (cd): Taber's Cyclopedic Medical Dic­ lional),. FA Davis, Philadelphia, 1 977 7. Friel I (cd): Dorland's Ill ustrated Medical Diction­ al)'. 25th Ed. WB Saundel'S, Philadelphia, 1 974 8. Johnson

GS:

Course

notes,

Functional

Or·

thopedic 1 , institute for Physical Art, San Fran­ cisco, Mal'eh 1 99 1 9 . Andriacchi T e t al: Ligament: InjlllY and repair. In Woo SLY, Buckwalter J (eds): InjUJ)' and Re­ pair of the Musculoskeletal Soft Tissues. Ameri· can Academy of Orthopaedic Surgeons, 1 99 1 t o. Kellet J : Acute ST injuries, a review o f the litera· ture. Med Sci SPOI'ts Exel'c 1 8 :5, 1 986 J 1 . Jones LH: Strain and Counterstrain. American Academy of Osteopathy, Colorado Spl'ings, 1 9 8 1 1 2 . Kelly M , Madden JW: Hand surgel), and wound healing. p. 49. In Wolf011 FG (ed): Acute Hand Injuries:

A

MulLispeciaJty

Approach.

LillIe,

Brown, Boston, 1 980 1 3 . Cohen KI, McCoy BJ, Dicgclmann RF: An update on wound healing. Ann Plast Surg 3:264, 1 979 1 4 . Arem Al, Madden JW: Effects of stress on healing

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wounds: intermittent noncyclical tension. J Surg

cal and structural changes on the cat soleus mus­

Res 20:93, 1 976

cle due to immobili7.ation at di fferent Icngths by

1 5. Kaltenbom FM: Mobilization of the Extremity Joints. Olaf Norris Bokhandel. Oslo, Norway, 1980 1 6. Poppen NK, Walter PS: Normal and abnormal motion of the shoulder. J. Bone Joint Surg 58: 1 95 , 1 976 1 7 . Howell SM, Galinat BJ et al: NOImal and abnor­ mal mechanics of the glenohumeral joint in the hOlizontal plane. J Bone Joint Surg 70:227, 1 98 8 1 8. Vidik A : O n t h e rheology and morphology of soft collagenous tissue. J Anat 1 05 : 1 84, 1 969 1 9, Reigger LL: Mechanical properties of bone. I n Davis GJ, Gould JA (eds): Orthopaedic a n d SPOI�S Physical Therapy. CV Mosby, Sl. Louis, 1 985 20. Betsch OF, Bauer E: Structure and mechanical propel�ies of rat tail tendon. Biorheology 1 7:84, 1 980 2 1 . Butler DL, Grood ES, Noyes FR et al: Biomecha­ nics of ligament and tendons. Exer SPOl1 Sci Rev 6 : 1 26, 1 979 22. Hirsh G: Tensile properties during tendon heal­ ing. Acta Orthop Scand, suppJ. 1 53: I , 1 974 23. Taylor DC, Dalton 10, Seaber AV et al: Viscoelas­ tic properties of musculotendon units: The biome­ chanical effects of stretching. Am J Sports Med 1 8:300, 1 990 24. Van Brockl in JD, Follis DG: A study of the me­ chanical behavior of loe extenSOl' tendons uncleI' applied stress. Arch Phys Med 46:369, 1965 25. Turkel SJ, Panio MW, Marshall n, Girgis FG: Sta­

plaster casts. J Physiol 224:23 1 , 1 972 28. Otis JC, Jiang CC, Wickicwicz TL et al: Changes in the movement alms of the rotator cuff and deltoid muscles with abduction and rotation. J Bone Joint Surg 76:667, 1 994 29. Wanvick R, Williams P (eds): Gray's Anatomy, 35th Blitish Ed. WB Saunders, Philadelphia, 1973 30. Wyke BD: The neurology of joints. Ann R Coli Surg Engl 4 1 :25, 1 966 3 1 . Wyke BD: Neurological aspects of pain therapy: a review of some cun-cnt concepts. p. I . In Swer­ dlow M (ed): The Therapy of Pain. MTP Press, Lancaster, England, 1 98 1 32. Haldeman S: Modern Developments in the Pdnci­ pies and Practice of Chiropractic. Appleton-Cen­ tury-Crofts, East Norwalk, CT, 1 980 33. Kummel BM: Spectrum of lesion of the antedor capsulc mechanism of the shoulder. Am J Sports Med 7: 1 1 1 , 1 979 34. WalTen CG, Lehman IF, Koblanski NJ: Elonga­ tion of rat tail tendon: effects of load and tempera­ ture. Arch Phys Med Rehabil 52:465, 1 9 7 1 3 5 . Warren C G , Lehman JF, Koblanski N J : Heat and stretch tech-procedure:

an

evaluation using rat

tail tendon. Arch Phys Med Rehabil 57: 1 22, 1 976 36. Bonutti PM, Windau BS et al: Stalic progressive stretch to ,-eestablish elbow range of motion. Clin Ol�hop 303: 1 28, 1 994 37. Lehman IF, Masock AJ , WalTen CG, Koblanski IN: Effects of therapeutic temperatures on tendon extensibility. Arch Phys Med Rehabil 5 1 :48 1 , 1 970

bilizing mechanisms preventing anledor d isloca­

38. Lentell G, Hetherington T, Eag n J , Morgan M: The

tion of glenohumeral joint. J Bone Joint Surg 63:

use of thermal agents to innuence the effective­

1 208, 1 98 1 26. COOpel' RR: Alterations during immobilization and regeneration of skeletal muscle i n cats. J Bone Joint Surg 54:9 1 9, 1 972 27. Tabary JC, Tabary C, Tardieu C et al: Physiologi-

ness or a low load prolonged stretch. Ol�hop Sports Phys Ther 1 7:200, 1 992 39. Johnson GS: Soft tissue mobilization. In Donatelli R, Wooden MJ (cds): Ol�hopaedic Physical Ther­ apy, Churchill Livi ngstone, New York, 1 994

Strengthening Exercises KAREN ROBERT

E

DAVIS A

DONATELLI

Strengthening is one of the most vital compo­ nents of shoulder rehabilitation. Once sufficient healing occurs and adequate range of motion i s obtained, strengthening often becomes the main focus of treatment. As the effects of prolonged immobilization are becoming more apparent, early mobilization and strengthening are gaining in popularity. The present chapter defines strength, strength training principles, and exercise pre­ scription. Muscles essential to shoulder mobility and stability are discussed along with specific strengthening exercises for the shoulder. The case studies present treatment programs for two shoulder patients. These cases apply strengthening principles to the rehabilitation plans. Incorporating strengthening exercises and exercise prescription appropriately to each patient is as important as any other component of treatment. This chapter will provide some guidelines to follow when designing your own strengthening regime.

Strength Strength is defined as the ability to produce force and is often used as a measure of ability.' Strength is important in both health and perfor­ mance.' Strength training can positively effect the entire musculoskeletal system as bone, mus­ cle, and associated connective tissue adapt ac-

cordingly-' Strength training i ncreases the maxi­ mum strength of tendons and ligaments while stronger muscles reduce the relative daily stress placed upon joints throughout the body.' Strength training i ncreases skeletal muscle mass, force-generating capability, and metabolic capacity. Strength training also increases nexi­ bility, possibly increasing performance and re­ ducing the potential for injury both with work­ related and athletic activities.3

Muscular Endurance "Absolute muscular endurance (AME) i the abil­ ity to maintain a given fixed submaximal force output during work relying prima,;ly on anaero­ bic metabolism until exhaustion."" Factors that conu;bute to AM E or anaerobic capacity include (1) biochemical adaptations, (2) maximal strength level , (3) neural adaptations, and (4) muscle hypertrophy." Muscle endurance has been described as performing work using mod­ erate to heavy loads over a period of time.' Most clinicians are familiar with the cardiovascular factors contributing to overall endurance or aer­ obic capacity. Cardiovascular factors may con­ tdbute to muscle endurance; however, increases in adenosine triphosphate (ATP), creatinine phosphokinase (CP), glycogen stores, myokinase activity, and maximum strength largely com­ prise anaerobic capacity.' Concentrations of 365

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SH OULDER

ATP-CP and glycogen in skeletal muscle are im­ portant in maintaining high-intensity work loads and work rates.· Observations of increased ATP­ CP and glycogen stores have been found after strength training.

Power and A[!ility Power is the rate at which work is performed. I An i ncrease in power allows the athlete to per­ form at higher work rates. Increasing maximum power would enable an athlete or patient to work at a smaller percentage of maximum and there­ fore endure longer work periods. The speed at which a skill is performed can be expressed in terms of Newton's second law, "force equals mass times acceleration." The velocity of a move­ ment may be enhanced by increasing the force. Strength-speed training and speed training in­ crease the speed of movement by general strengthening of the appropriate muscles, mak­ ing movements raster,' Agility, the ability to rapidly change the di­ rection of the body, is strongly related to strength and power. Studies have shown that significant increases in the strength of the legs accompanies increases in power and velocity or movemenl.! General performance may be increased by in­ creasing maximal strength through resistive training.

Muscle Piher Types The two basic fiber types found in human muscle are slow or type I muscle fibers and fast or type Il muscle fibers.s Type 1 fibers are able to maintain muscle contractions for extended periods of time, deriving their energy by oxidative metabo­ lism, aerobically. Type II fibers produce more force than type I fibers, deriving their energy fTom nonoxidative metabolism, anaerobically. Adenosine l1-iphosphate is required for energy to create and maintain muscle contraclions. 6 Cre­ atinine phosphokinase and myosin kinase are re­ quired for anaerobic metabolism.

Strm1{/th Training Strength training results in the interaction of neural, muscular, and mechanical factors7 .• Neural factors include motor unit activity, 1..,­ cruitment of motor units, and modulation of the fTequency of motor unit firing. Muscular factors include the cross-sectional area of a muscle and the length-tension relationship at the time of contraction7 The moment arm identified and the force generated by the muscle comprise the mechanical factors. At very short and very long lengths, muscle generates low tension'" There is an optimal length at which a muscle is able to generate the most tension. The most consistent finding after resistance training is an increase in the cross-sectional area of the muscle.lo Lncreased cross-sectional area is a major contributor to muscle strength; how­ ever, initial gains in muscle strength are not due to this increase. During the first few weeks, neu­ ral adaptations are thought to mediate the initial strength improvements. Several of the mecha­ nisms contributing to this initial increase in force production include (I) an increase in motor neuron excitability, (2) better co-contrac­ tion of synergists, (3) inhibition of neural protec­ tive mechanisms, and (4) an increase inhibition of antagonists'O Muscle fiber size does not change until approximately 8 to 1 2 weeks of training. The actual muscle fiber size increase is secondary to the addition of myofiblil proteins to the muscle fibers. 10 Strength training improves the strength of each motor unit, and thus fewer motor units are required at a given submaximal workload. 10 After strength training, more motor unit reserves are available for continuation of work. Pure aerobic training will likely reduce the ability of strength-power athletes to perform. I I Andersen and Kearney" demonstrate that a so­ called repetItion continuum exists. When strength and endurance training al'" performed in excess, maximal strength performance can be blunted possibly secondaty to the transforma­ tion of fast twitch to slow twitch muscle fi­ bers,ll.1 2

S T R ENGTHENING EXER CI SES

Exercise Types The three basic methods used in strengthening in­ clude isometrics, isotonics, and isokinetics. An isomeldc, or static, contraction is a muscular contraction where there is no change in the angle of the involved joint(s) and little or no change in the length of the contracting muscle. " Isometrics produce strength gains specific to the joint angle performed.'4 Isometric training is not effective throughout the range of motion unless many joint angles are trained. Isometric and dynamic mea­ sures of strength are not strongly related; there­ fore, training with isometrics ror sports or activi­ ties that require dynamic strength is not recommended. Combination training, including isometrics and dynamic training, would provide the benefits of both types of strengthening. In rehabi litation, isometric and multiangle isometrics are advantageous with protective in­ juries were wound healing is present. There is an approximate 20' physiologic strengthening overflow with isometrics, allowing pain-free strengthening with possible strength improve­ ments in the affected range. 15 An isotonic contraction is a muscular con­ traction where a constant load is moved through a range of motion of the involved joint(s)." Iso­ tonics include conccntric (shortening) and ec­ centric (lengthening) muscle contractions. Iso­ tonics mimic many functional activities and, be­ cause the resistance is preset, are appropriate to use when a predetermined amount of work is to be performed. Maximal eccentric contractions produce higher tension levels than concentric conlraclions. Eccentric training requires longer recovery periods and alone has not been shown to be superior to concentric training. 1 6 An isokinetic contraction i s a muscular con­ traction through a range of motion at a constant velocity." Isokinetics are discussed in detail in Chapter 16.

367

eccentric contraction, of a mass is followed by a rapid acceleration, concentric contraction. The stretch reflex, or stretch-shortening cycle, is evoked by the rapid eccentric contraction, result­ ing in a grealer concentric contraction. 1 7 The ec­ centric, amortization, and concentric phases comprise a plyometric exercise. Amortization occurs following the eccentric phase, prior to the active concentric or push-off phase of the activ­ ity. The shorter and quicker the amortization phase, the more power will be developed. 17 Because plyometrics are a high-intensity type of training, adequate strength is a prerequi­ site. Drills should progress from basic to ad­ vanced with intensity progressing from low to high.'7 Adequate recovery time must be allowed because plyomet,;cs incorporate maximal-erfort multijoint movements. Two to four days of re­ covery is suggested depending on the SPOil and time of year. Recommendations for frequency range from one to three days per week, with 1 5 to 20 minutes per session depending on the sport. It is recommended that a training schedule with alternating days of heavy lifti ng and plyometric training be constructed to provide sufficient re­ covery periods. The types of contractions used in strength training may vary; however, the principles of strength training must be considered for all pro­ grams to improve strength, power, endurance, and overall function. The principles of strength training, intensity, frequency, duration, and specificity will be discussed in the following sec­ tion.

Exercise Presr:riptiun The basic principles of training include intcnsity, frequency, duration, and specificity.' WaI-m-up, rest periods, periodization and maintenance must also be incorporated into a complete exer­ cise prescription.

Plyometrics

INT

Plyometrics are high-intensity training bridging the gap between speed and strength.'7 Plyome­ trics are exercises in which a rapid deceleration,

Intensity or volume is den pendent on the num­ ber of sets and repetitions, rest between sets, du­ ration of workout, and the amount of weight or

368

PHYSICAL

THERAPY

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THE

SH O U LDER

load used." Paulello describes repetitions (reps) as "the number of times an exercise is done with­ out resting during one set." The completion of one exercise performed consecutively without rest is known as a set. The maximal load lifted over a given number of repetitions before fatigu­ ing is a repetition maximum. abbreviated RM. Determining 1 RM may be feasible when the athlete is healthy. I n a clinical selling. however. using a predicted RM to determine a load to be used is more appropriate and safe. Determining a 1 0 RM. and then calculating or using a stan­ dard chart to derive 1 RM. is a more feasible method. Once 1 RM is established. the desired percentage. usually 80 percent. may be obtained. To determine 1 0 RM the patient performs 1 0 rep­ etitions with a weight. After a 2- to 4-minute rest period. more weight is added and additional sets of 1 0 repetitions are performed until a weight . . . only al Iowing 1 0 repeltltons IS performed . 20 I t is known that high-intensity load training or high volume (sets and reps) will result in mus­ cular adaptations and strength gains. '9 The spe­ cific amount of resistance required for these strength gains varies. 19 Novice trainees can in­ crease strength with a load of 35 percent of iso­ metric J RM and 45 percent of J RM in circuit training. Eighty percent of I RM is more com­ monly used with athletes. The I RM is tested weekly. and during the other training days work­ outs are performed at 50 to 90 percent of 1 RM. depending upon the goals of training. Six or fewer repetitions. with weight based on a low RM (I to 5 RM). provide the most strength and power benefits.20 Weight based on 6 RM to 1 2 RM provides moderate gains. and weight based on 20 RM and above provides mus­ clllar endurance gains without strength gains. The intensity of training is categorized as high. moderate or low with corresponding RMs of 90 percent. 70 to 90 percent and below 70 percent. 20 Moderate workloads and moderate volumes of work are suggested for athletes retraining after injury. prepubescent athletes. and hypertensive populations. The intensity of training in rehabili­ tation must consider tissue healing and prior physical activity of the patient and be directed towards rehabilitation goals. •

FREQUENCY AND DURATI O N

Recommendations on training are based on ex­ periments varying sels, repetitions, exercises, and frequency or days per week.' Generally. training 3 days per week is recommended. This will vary according to the muscle groups trained and the desired outcome. Lower body and larger muscle groups will require more time for recov­ ery. whereas upper body training may be per­ formed more often withoul overtraining. Dudng the first few weeks of training. the frequency should be less. Also. eccentric loading causes more muscle damage. and the frequency of train­ ing should be less to avoid injury and over­ training. It is recommended that athletes re­ covering from injury should resume training at 50 to 60 percent of preinjury status and increase 1 0 percent per week.'o Athletes recover faster from Single-joint exercises than from multiple­ joint exercises.2o I n rehabilitation. multiple-joint exercises requiring more energy should be per­ formed plior to single-joint exercises requiring less energy. An example of this principle includes performance of multiplane PNF diagonal pat­ terns for the shoulder prior to perfOimance of single-plane internal-external rotation exercises of the shoulder. when both exercises are to be performed during the same workout. SP

Specificity of trammg is the most important principle in strength training. The rehabilitation goals will determine the specificity of training and dictate the intensity. frequency. and dura­ tion of the program. The SAID (specific adapta­ tions to imposed demands) principle indicates that the body will gradually adapt to the specific demands imposed upon it. '4 Thus. the demands must be specific to the desired goals and con­ stantly change for continual adaptations and re­ sultant increases in strength. WARM- U P

General and specific warm-up methods have been demonstrated to improve performance as well as reduce the ,-isk of injury from training.'

S T R E N G T H E N ING EX ER C I S ES

General warm-up should include stretching of all muscles crossing all joints. Specific warm-up includes light to moderate sets performed for each exercise. It is our experience that specific warm-up also allows for the observation of the proper technique for the exercise performed. REST

PERIO DS

Rest periods are dependent upon the volumes and loads. They should be designed with the strengthening goals in mind. When training for absolute strength, longer rest periods ( 3 to 5 min­ utes) are used between heavy, near-maximal rep­ etitions.'9 Brief rest periods of 30 to 60 seconds are used with higher volumes of exercise, more exercises, and moderate loads (8 RM to 12 RM).

369

M AIN TEN ANCE

Maintenance programs i n rehabilitation must be developed to maintain reasonable strength, power, and endurance levels to prevent reinjury. Rehabilitation maintenance programs are simi­ lar to in-season programs used in atheletics where competitive seasons are of considerable length. The volume and intensity must be suffi­ cient enough to maintain strength, power, and or endurance levels but not producing an overload when combined with work or sport activities. Stone and O'Bryant I recommend using three sets of 2 to 3 reps with moderate to heavy weight for major exercises, and 3 to 5 reps with resistive exercises. We have found success in mainte­ nance programs that comprise three sets of 8 to

PERIOOIZA ION T

The periodization system is used to prevent over­ training while optimizing peak performance.2i Peliodization is a systematized and organized method of [raining to "peak" at the right time. With event sports, periodization is geared for peaking on a given day. With team sports, such as basketball, baseball, or football where all the games are important, periodization is geared for peaking for an entire season. Periodization in­ volves not only in-season but also off-season and preseason. Variation in training is important in break­ ing up the monotony that occurs when the body adapts to imposed demands. Overload and change in stimulus are required to optimize training. A macrocycie in peliodization refers to the overall training period.2 i Two or more meso­ cycles can occur in a macrocycie, consisting of weeks to months in length. These mesocycles comprise the distinct periods of preseason, in­ season, and off-season or transition peliods. Mesocycles begin with high-volume, low-inten­ sity training, and progress to low-volume, high­ intensity training just prior to competition. The type of transition period, length, and number of mesocycles are sport or activity dependent. We believe rehabilitation goals and discharge main­ tenance plans can also be designed using the pe­ riodization principles.

13 FIGURE 14.1 Elevation in the plane of the scapula with internal rotation.

370

PHYSIC A L T H E R APY

OF

THE

SH O U L D E R

FIGURE 14.2

Prolle

horizontal abdLlctiol1 at

100°\\1;117 extenw! rOlatio1l.

10 repetitions pel-formed 2 or 3 days per week with moderate weights.

Strengthening Exercises for the Shoulder The muscles of the glenohumeral joint have been grollped inLO three functional categories by Saha." The first group, prime movers, include the deltoid and clavicular head of the pectoralis major. The second group, steering muscles, in­ clude the supraspinatus, subscapularis, and in­ fraspinatus. This group majntains the humeral head in the glenoid. Finally, the latissimus dorsi, teres major and minor, and sternal head of the pectoralis major are collectively the third group, the depressors. Dynamic glenohumeral stability is provided by the rotaLOr cuff. The rotator cuff muscles are important providers of joint stability as they ap­ proximate the humeral head in the glenoid fossa.>' The importance of force coupling be­ tween the rotator cuff and the deltoid is best de­ scribed by Inman et al.24 The sheer forces across the joint from the deltoids' upward pull are bal-

anced by the [iring of the rotator cuff dUl;ng ele­ vation. Townsend et al.25 performed an electromyo­ graphic (EMG) analysis of the glenohumeral muscles. The four rotator cuff muscles and other positioners of the humerus were studied using common shoulder exercises from rehabilitation programs used by professional baseball clubs. Four exercises were found to be the most chal­ lenging for every muscle. These exercises were ( I ) elevation in the plane of the scapula with in­ ternal rotation (Fig. 1 4 . 1 ) (2) Oexion, (3) prone horizontal abduction with the arm externally ro­ tated ( Fig. 1 4.2), and (4) press-up (Fig. 1 4.3). The plane of the scapula is fun her defined in Chapter I. The supraspinatus has been identified as the most frequently injured muscle of the rotator cuff group.2. Jobe and Moynes2• also support that the rotator cuff muscles should be evaluated and strengthened individually. They report max­ imal supraspinatus muscle activity at 90' of arm abduction, 30' of ho.-izontal Oexion, and full in­ ternal rotation in the upright position. Black­ burn et al.27 duplicated this test position de­ scribed by Jobe and Moynes2• and analyzed vm·iolls other exercise positions, reporting the

S T RENG THENING

FIGURE 14.3

Press-lip.

greatest supraspinatus EMG activity in the prone position with the humerus horizontally ab­ ducted I DO· and externally rotated to thumb-up position (Fig. 1 4.2). The EMG activities of the inrTaspinallis and teres minor were maximized wit h (prone) external rotation with 90· of abduc­ tion at the glenohumeral joint and 90· of Ilexion at the elbow joint (Fig. 1 4.4). Won-ell et al.'· compared the supraspinatus EMG activity during the two previously de­ scribed test positions for the supraspinatus, re­ vealing the prone position superior to standing for EMG activity. The prone position is advo­ cated in strengthening the supraspinatus to pro­ mote more supraspinatus muscle activity. How­ ever, we suggest that the patient remain pain fTee while perfolming this or any exercise in the prone position.

E X ERCIS E S

371

The scapular rotator muscles are essential to glenohumeral mobility and stability.29 These muscles include the upper trapezius, lower tra­ pezius, levator scapulae, rhomboids, middle and lov.rer serratus anterior, and pectoralis minor. The scapular rotator muscles stabilize the gle­ noid fossa as the humeral head al"liculates. Dy­ namic balance and coordination are provided at the scapulothoracic joint. Many force couples exist around the shoulder complex, most impor­ tantly the serratus anterior, upper trapezius, and lower trapezius at the scapulothoracic joint. These muscle act synchronously on the scapula to upwardly rotate and position the glenoid dur­ ing full elevation of the humerus.,o.3o Moseley et al.'9 examined and identified four exercises that best strengthen the scapular rotators. These ex­ ercises include (I) elevation in the plane of the scapula with internal rotation (Fig. 14. 1 ), (2) rowing (Fig. 1 4.5) (3) push-up with a plus (Fig. 1 4.6), and (4) press-up (Fig. 1 4.3). The roles of these muscles and exercises are further dis­ cussed in detail in Chapter 2. Strengthening o f th e biceps brachii i s an im­ portant component of the shoulder rehabilita­ tion program (Fig. 1 4.7). The anatomic align­ ment of the biceps brachii allows it to function, assisting the rotator cuff, as a compressor of the humeral head." As the scapula upwardly ro­ tates, the rotator cuff and biceps brachii depress the humeral head, redUCing shear forces from the deltoidJI.32 Rodosky et al.'2 investigated the effects of tension on the long head of the biceps ,,�th the arm abducted and externally rotated. Tension in the long head of the biceps increased torsional rigidity to external rotation, increasing anterior stability of the glenohumeral joint. This increased stability is greatest during the middle ranges of elevation.

Does Strength Equal FUnction? Few studies exist involving strength training spe­ cific to the shoulder and consequent improve­ ments in f"lll1ction.33-35 Wooden et al.33 demon­ strated strength gains and improvement in

372

PHYSIC A L

THERAPY

OF

THE

SH O U LD E R

FIGURE 14.4 Prolle extemal rotatiol1 with 90·of abductiol1 at the shoulder and 90·offlexiol1 at the elbow.

f,mction training baseball pitchers. Isotonic con­ centdc exercises were used on an isokinetic de­ vice. The results indicated statistically signifi­ cant increases in throwing velocity and an increase in external rotator torque. Ellenbecker et al." compared the effects of concentric isokinetic versus eccentric isokinetic exercise on rotator cuff strength and power and on tennis serve velocity. Concentric strength was significantly improved in both groups after 6 weeks of training. Improvements in eccentric strength and serve velocity were only found with the concentric training group; however, not using a controlled group weakened the results of this study. Mont et al.37 performed a study similar to Ellenbecker's examining strength training isold­ netically and functional outcomes using tennis serve velocity. Mont et al. compared isokinetic training of the shoulder internal and external ro­ tators using concentrically trained, eccentrically trained, and control groups. Slatistically signifi­ cant concentric and eccentric gains were ob­ tained with both training groups when com­ pared to the control. The increase in serve velocity was greater than I I percent. All three studies illustrate sport-specific

funcUonal improvements through strength training. Several other studies have shown in­ creases i n power and velocity of movement with significant increases in the strength of the legs. I Extensive reviews of the physiologic effects of resislance and endurance training illustrate the effects on performance.36-39 Muscle strength, endurance, verticle jump, and sprint speed are just a few of the va,;ables increased with resis­ tance and endurance training.

Summary Strength is a measure of human performance. Strength is a result of the interaction of neural, muscular, and mechanical factors. Initial gains in muscular strength during the first few weeks are secondary to neural adaptations. Increases in cross-sectional area of muscle contdbute to strength gains after the first few weeks of train­ ing. The plimary cellular effects of strength training occur in the fast, type II, muscle fibers. The type II fibers are responsible for muscle strength and power and must be recruited dur­ ing training to be hypertrophied. Training with

STREN GTH E NI N G EXERCISES

373

A

FIGURE 14.5 (A) Sealed rowing. (B) One-anu ro\.vil'1g.

B

low or moderate weight will not provide this stimulus. Strength training must also be specifi­ cally designed to meet the rehabilitation goals. lncreases in maximum strength allow the athlete or worker to perform at a smaller per­ centage of their maximum effort and thus en­ dure longer work rates. This ability represents an overall increase in muscular endurance. Ade­ quate muscle strength and endurance at the shoulder complex is necessary to maintain ade­ quate physiologic and accessory motion, and thus normal scapulohumeral rhythm. The muscles at the shoulder complex must work together to provide adequate stability and

mobility. This is achieved by synchronous activ­ ity of the rotator cuff. long head of the biceps, rotators of the scapula, and the deltoid. Fatigue or weakness of any of these muscle can lead to abnOlmal translation of the humeral head." Weakness of the rotator cuff is also thought to trigger glenohumeral instability.'9 Scapular ro­ tator muscle weakness allows excessive scapular movement, contdbuting to poor scapulohum­ eral rhythm. Abnormal humeral head transla­ tion of the humeral head, or altered scapulohum­ eral rhythm, can contribute to initation of adjacent tissues and shoulder pathology." Proprioceptive exercises and eventually plyo-

374

PHYSICAL

FIGURE 14.6

THERAPY

Push-up with

a

OF

THE

SHO U L D ER

plus.

metrics must be applied to enhance neuromuscu­ lar control. All types of strengthening must coin­ cide with the stage of rehabilitation appropriate for that patient. Progression of the strengthening program must be sequential while working to meet the patient's goals. Criteria for reduction in pain and improvement in ROM and strength must be met before the patient is progressed. Fi­ nally, to complete a rehabilitation program, some form of f�mctional training must be incorporated prior to the return to work or sport. The next two cases discuss two common pa­ tient types. The first case illustrates a work injury that demonstrates the importance of strength at the shoulder joint in providing stability to avoid impingement. The second case, involving an overhead athlete, demonstrates the need for

FIGURE 14.7

Biceps curls.

strengthening to provide dynamic stability to avoid instability and overuse.

CASE STUDY 1: IMPINGEMENT SYNDROME

The focus of this case was to restore soft tissue mobility and muscular strength and endurance to the shoulder complex and educate the patient in a maintenance program specific to his job­ related tasks. HISTORY

This case presents a 45-year-old airplane me­ chanic. This patient repOJ1s his job tasks require working on airplanes from supine, kneeling, and

STRENGTHENING

standing positions, with most activities requir­ ing reaching in front and/or overhead. He has been performing these job duties for 1 5 years. He reports intermillent shoulder pain during the last 3 to 4 years that has progressively worsened over the last 3 to 4 months. He has been referred to physical therapy with a diagnosis of "impinge­ ment syndrome." INITIAL EVALUATION

Radiographic findings did not reveal an abnor­ mal shaped acromion; however, mild bone spur­ ring was present on the underlying surface of the AC joint. Visual inspection revealed gross atro­ phy of the right shoulder complex. Gross pos­ tural changes including an increased thoracic kyphosis, forward head, and rotated humerus were apparent. Active elevation of the humerus in the plane of the scapula was approximately 80· and limited by pain. The lateral border of the scapula protracted excessively during active elevation. Passive extel11al rotation was limited to 5· at O· of abduction and 20· at 90· of abduc­ tion. Accessory glenohumeral motion testing re­ vealed moderate capsular restrictions in anterior and posterior directions for the involved extrem­ ity. Overall passive scapular mobility was limited in rotation and distraction from the lib cage. Isokinetic assessment of the rotator cuff was deferred at this point due to limited ROM for rotation; however, gross manual muscle tests re­ vealed 4/5 intel11al rotator and 3/5 extel11al rota­ tor strength. The patient was not able to assume the prone test position for the supraspinatus. Su­ praspinatus testing standing revealed pain and weakness. Strength assessments revealed 3 + 15 muscle grades for the scapular rotators, serratus anterior, middle and lower trapezius, rhom­ boids, and extel11al glenohumeral rotators. Im­ pingement testing was positive (see Chapter 3). Neurologic testing was normal. Palpation re­ vealed trigger points within the subscapularis, levator scapulae, and pectoralis major muscles. N I

Apparent muscle atrophy and postural and ra­ diographic changes may be attlibuted to disuse and age-related changes of the glenohumeral

EXERCISES

375

joint. Limits in passive range of motion demon­ strate limits in mobility of the subscapularis and capsular structures.40.4I Limits in the scapuloth­ oracic articulations were also identified. Limits i n active elevation correspond to the passive findings. During this middle phase of elevation (60· to 1 40·), there is an i ncrease in scapulothor­ acic movement.42 Adequate glenohumeral and scapular rotator strength is critical, because maximum shearing forces of the deltoid occur at this phase. This middle range is also the range in which this patient performs the majority of his work-related tasks. The presence of trigger points i n the muscle and shoulder complex cor­ respond to overactivity of these muscles com­ pensating for the reduced scapular motion.43 All of this patient's findings are contributors to a reduced suprahumeral space leading to im­ pingement. TREATMENT PLAN AND RATIONALE

I N I T IAL P H AS E ( W E E K I)

This patient was placed on light duty at work and his overhead activities were limited during his rehabilitation. This patient was seen three times per week during the first 1 2 weeks of physical therapy. Initial treatments focused on restoring soft tissue mobility. Heat in conjunction with a low load prolonged stretch into external rotation was applied to the shoulder (Fig. 1 4.8). The hu­ merus was positioned 30· anterior to the frontal plane and 1- to 3-pound weights were progres­ sively added to patient tolerance for 1 0, 20, and 30 minutes in consecutive treatment sessions. Elevating tissue temperatures with superficial moist heat in conjunction with a low load pro­ longed stretch are thought to cause plastic defor­ mation in connective tissues.44 Soft tissue tech­ niques to reduce trigger points followed by glenohumeral and scapular mobilizations were then performed. Active stretching of the antagonistic mus­ cles, pectoralis major, upper trapezius, and leva­ ERPRETATION OF FINDINGS tor scapulae was performedTprior to strengthen­ ing of the agonistic scapular rotators. Janda (49) describes muscle imbalances occurring from tight muscles inhibiting its antagonist. Janda45

376

PHYSICAL

T HERA P Y

OF

THE

SHOULDER

FtGURE t4.8 Moisl heal wilh a low load prolollged wilh 2 Ib weighI slreleh into extenwl rotQtim1.

stresses the importance of stretching the antago­ nists prior to strengthening the agonists. After two visits, improvement in external ro­ tation reached 45· at O· of abduction and 60· at 90· of abduction. Scapulothoracic rhythm was improved, and excessive protrusion of the sca­ pula with active movements was reduced. Active elevation was full; however, a painful arc was present, implicating impingement of subacro­ mial tissues. All strengthening movements and daily tasks were limited to 90· of elevation during this phase. A 5- minute general warm-up using an upper body ergometer was used prior to active stretch­ ing and strengthening exercises (Fig. 1 4.9). Stretches for both the inferior and posterior rota­ tor cuff were incorporated with 30-second holds, repeated five times. Isotonic strengthening exercises included the following.

I. Elevation in the plane of the scapula with 2. 3. 4. 5.

the arm internally rotated (Fig. 1 4. 1 ) Prone horizontal abduction at 1 00· with arm externally rotated Press-up (Fig. 1 4.3) Seated rowing (Fig. 1 4.5a) Biceps curls (Fig. 1 4.7)

6. Prone extension with internal rotation (Fig. 1 4. 1 0) Eighty percent of an estimated I RM was used as the load for all i otonic scapular rotator exer­ cises. Three sets of 1 0 repetitions was preceded by a specific warm-up of the exercise without weight. At this time the patient's ability to per­ form the exercise through pain-free ROM was assessed. Isok.inetic testing of the glenohumeral rota­ tors was performed in the plane of the scapula. Test results indicated a 45 percent deficit of the extemal rotators and a 22 percent deficit of the internal rotators. During the next visit, isokinelic strengthening of the rotators was begun u ing speeds of 90· and 1 20· per second for 3 sets of 1 0 repetitions (Fig. 1 4.1 I) Each physical therapy session concluded with ice to the shoulder for 1 0 minutes. lee was applied t o prevent any adverse inOammatory responses secondary to stretching, to maintain the plastic deformation gained with treatment, and to reduce delayed-onset muscle soreness.46 M t D DL E PHAS E ( W E E K S 3 TO

5)

During the following 3 weeks of physical ther­ apy, this patient was seen three times per week. Heat with stretch and soft tissue manipulation

S T RENG THENING

FIGURE 14.9

Upper body ergometer.

EXERCI S E S

377

FIGURE 14. 1 1 Isokil1etics (or internal and extemal rotation o( the shoulder il1 the plane o( t"e scapula (30 "anterior to (rol1tal plal1e).

continued prior to strengthening until active and passive mobility testing was within normal lim­ its (at the end of week 3). Isotonic and isokinetic strengthening were continued. A new I RM was established at the beginning of each week with the load increasing accordingly. A set of 1 0 repe­ titions was added to the isokinetic strengthening weekly, progressing to six sets of 1 0 repetitions by the fourth week of treatment.

FINAL PHASE ( W E E K 6)

FIGURE 14.10

rotation.

Prone extension with inlernal

Prior to discharge, manual muscle testing re­ vealed 4/5 strength of the scapular rotators. Iso­ kinetic reassessment demonstrated a 1 5 percent

378

PHY SICA L

THERAPY

OF

THE

SH O U LD ER

external rotator deficit and a 1 0 percent increase in internal rotator strength. A majntenance program was reviewed prior to discharge. This program incorporated all of the isotonic strengthening exercises performed during therapy. with sidelying internal and ex­ ternal rotation exercises replacing the isokinet­ ics for the glenohumeral rotators. The patient was instructed to perform three sets of 1 0 repe­ titions for each exercise 3 days a week for 6 weeks. A continued program of three sets of 1 0 repetitions for each exercise was recom­ mended to be performed 2 days per week indefi­ nitely provided this patient was performing the same job tasks.

CASE STUDY 2: ROTATOR CUFF AND BICIPITAL TENDONITIS The focus of the case is to identify the contribut­ ing factors to rotator cuff and bicipital tendonitis. initiate the appropriate strengthening program. and return this athlete to competitive sports. HISTORY

This case presents a 2 1 -year-old collegiate female tennis player with a complaint of chronic right shoulder pain. Her prior history for this shoulder includes similar painful episodes. usually occur­ ring mid to late season. during the past 3 years. Previous treatments include the use of oral anti­ inflammatories and modality treatments admin­ istered in the athletic training facility on campus. Her CUITent complaints have not subsided with these types of conservative treatment and she has been referred for physical therapy evaluation and treatment. Her CUITent medical diagnosis is "ro­ tator cuff and bicipital tendonitis." INITIAL EVALUATION

Radiographic Findings were normal. Visual in­ spection revealed moderate right scapular eleva­ tion. protraction. and atrophy of the posterior rotator cuff muscles. External rotation was lim­ ited by 30' in the adducted position. when com­ pared to the uninvolved side. She presented with

pos i tive impingement sign. Apprehension and relocation tests were positive. Biceps brachialis testing was positive for Speed's test. Posteriorly. li mited capsular mobility was detected. Manual muscle testing demonstrated pain and weakness of the supraspinatus. subscapularis. and infra­ spinatus/teres minor (315 muscle grades). The scapular rotators (serratus anterior. upper. mid­ dle. and lower trapezius. and rhomboids) dem­ onstrated fair plus (3 + 15 muscle grades) strength. but fatigued quickly with repetitive testing. Overall this athlete reported her current shoulder pain had progressed from intermittent to constant. and was significantly aggravated by most activities using the right arm over 90' of elevation. Isokinetic testing of the glenohumeral rota­ tors was performed in the plane of the scapula. Test results i ndicated peak torque. power. and total work deficits of greater than 40 percent for the external rotators and greater than 20 percent for the internal rotators when compared to the uninvolved side. The peak torque of the external rotators was 50 percent of the internal rotators. Palpation revealed trigger points within the subscapularis muscle belly and tenderness along the anteriosuperior aspect of the right shoulder. INTERPRETATION OF FINDINGS

Signs and symptoms indicate a possible second­ ary impingement and tendonitis as a result of abnormal anterior translation of the humeral head. The abnormal or excessive translation may be secondary andlor contributing to the loss of dynamic stability from the rotator cuff and bi­ ceps tendon. evident by the tendonitis.2) The scapular rotator weakness and posterior capsu­ lar tightness are also predisposing andlor precip­ itating factors. TREATMENT PLAN AND RATIONALE I NITIAL PHASE (WEEK I )

This athlete was restricted from tennis activities during the initial phase of treatment. She did. however. independently perform lower body and conditioning workouts. She was seen for

^1

S TR E N G TH E N I N G EXERCI SE S

5 consecutive days during this initial phase. Treatment focused on decreasing the reactivity of the inflamed tissue and restoring normal soft tissue mobility within the shoulder complex. Heat was applied to the shoulder joint in conjunction with low-voltage surged electrical stimulation to the subscapularis trigger points to begin treatment. Soft tissue and joint mobili­ zations were applied to the glenohumeral and scapulothoracic joints to further reduce the trigger points and improve posterior capsular mobility. Low-voltage medium-frequency electrical simulation was applied to the supraspinatus and posterior rotator cuff while isometric were performed for external rotation in the plane of the scapula for 1 5 minutes. All treatments dur­ ing this initial phase of treatment commenced with an iontophoresis treatment at the rotator cuff insertion site using dexamethasone sodium phosphate followed by a l a-minute application of ice. Overall tissue reactivity and subjective re­ port of pain were reduced by the fourth day

A

FIGURE 14.1 z

(A & B) SerratLls press.

B

379

of treatment, and the use of the upper-body ergometer (UBE) was initiated in an attempt to begin general muscular endurance training. Rhythmic stabilization exercises for the gleno­ humeral and scapulothoracic joints were also initiated at this point in treatment, manually performed by the therapist. M I DDLE PHASE (WEEKS 2 TO 6)

During week 5-minute warm-up was perfOlmed on the UBE prior to active stretching and iso­ tonic strengthening exercises as in Case I. Iso­ tonic exercises included the following.

I. Elevation in the plane of the scapula (Fig.

1 4. 1 ) 2 . Prone horizontal abduction at 1 00° with extemal rotation (Fig. 1 4.2) 3. Seated rowing (Fig. 1 4.5a) 4. Biceps curls (Fig. 14.7) 5. Sen'atus press (Fig. 1 4 . 1 2 ) 6 . Prone extension with internal rotation (Fig. 1 4. 1 0)

380

P H Y SI C A L

TH ERA P Y

OF

THE

SH OU LDER

rest periods between sets. A I O-minute applica­ tion of ice terminated each session. Proprioceptive training progressed to in­ clude the following closed kinetic chain activi­ ties.

I. Balancing on 2 . BalanCing on ance board 3. Balancing on tramp 4. Balancing on cise ball

hands and knees hands and knees on the bal­ hands and knees on the mini­ hands and knees on an exer­

FI N A L P H A S E ( W E E K S 7 A N D 8 )

FIGURE 14.13

Plyoball sil1gle-arl7l baseball {hrolV.

Three sets of 1 0 repet i tions were perfornled using a weight equal to 80 percent of I RM, by the calculated 1 0-RM method, detel-mined dur­ ing the first session each week. An additional set for each isotonic exercise was added each week, progressing to seven sets by week 6. Thirty-sec­ ond rest periods between sets and 60-second rests periods between exercises were incorpo­ rated. Submaximal concentric training of the gle­ nohumeral rotators was initiated during week 2 using a velocity spectrum from 1 200 to 3000 per second (Fig. J 4. 1 I). As the athelete tolerated, isokinetics were progressed to a maximal effort level by week 3 . Isokinetic training began with 8 repetitions during weeks 2 and 3, increasing to 1 0 repetitions during weeks 4 and 5, and to 1 2 repet itions during week 6, allowing I S-second

A reassessment of the glenohumeral rotators re­ vealed a 5 percent deficit of external rotator strength, a t 5 percent increase in internal rotator strength, and a 75 percent external to internal rotalDr value. Scapular rotator strength assessed by manual muscle tests were 515. The upper body ergometer warm-up, three sets of 1 0 repetitions of isotonic exercises and the isokinetic velOCity spectrum, one set of 1 0 repetitions at each speed, began each treatment session during the final phase. Based on the strength improvements, functional drills were safely incorporated. These drills were perfornled evel), other day, totaling 3 days per week, and included the following activities. Drills with surgical tubing I . PNF diagonals for 0 I and 02 2. Internal and external rotation at 900 of eleva­ tion in the plane of the scapula Modification of these exercises included adding a brief hold and vaL)'ing the speed of arm move­ ment. Orilla with PlyobalVminitramp (beginning with 1 0 throws, increasing by 1 0 each session):

.I . Overhead soccer pass with two hands 2. Chest pass 3. Single-arm baseball throw (Fig. 1 4. 1 3) 4. Tn.ll1 k rotations mirroring ground strokes (forehand and backhand)

381

S T REN G THENI N G EXER CI SE S

S. Sit-ups with a ball toss/catch using a slanted minitramp 6. Prone trunk extension with the plyoball overhead

Two-minute rest periods were allowed between each exercise. Prior to discharge a program was developed with the athlete and her coach. Using periodiza­ tion principles, this program encompassed year­ round training with in-season, off-season, and preseason guidelines.

and absolute and relative cndurance. Res

Q

Exer

Sport 53: I , 1 982 1 2 . Kraemer WJ: Exercise physiology comer: the dy­ namics of muscular stnlcturc and function. NSCA J 4:46, 1 983 1 3 . Lamb DR: Physiology of Exercise: Response and Adaptations. 2nd Ed. Macmillan, New York, 1 984 1 4. Amheim Dd, Prentice WE: Principles of Athletic Training. 8th Ed. Mosby Year Book, SI. LOllis, 1 993 t S. Atha J: Strengthening muscle. Exel' SP0l1S Sci Rev 9: 1 , 1 9 8 1 1 6. El lcnbeckerTS, Davies GJ, Rowinski MJ: Concen­ lIic versus eccen tric isokinetic strengthening of the rotator cuff. Am J SP0l1S Med 1 6 :64, 1988 1 7. Allcrheilgn WB: Speed development and plyomc­

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I. Stone MH, O'Bryant H : Weight Training: A Scien­ tine Approach. Burgess International, 1 987 2. Kraemer WJ: General adaptations La resistance and endurance training programs. In Baechle TR (cd): Essentials of Strength Training and Condi­ tioning/National Strength and Conditioning Asso­ ciation. Human Kinetics. Champaign, I L , 1 994 3. lobe FW, Moyers DR: Delineation of diagnostic crileria and rehabilitation program for rotator cuff injuries. Am J SP0l1S Mcd 1 0:336, 1 982 4. Stone MH, Wilson D, Rozenek R et al: BJ"idging the gap: anaerobic capacity physiological basis. NSCA J 5:40, 1 984 5. Flcck 5J, Kraemer WJ:

Designing Resistance

Training Programs. Human Kinetics. Champaign, lL, 1 987 6. Tesch PA, Colliander EB, Kaiser P: Muscle metab­ olism during intcnsc, hcaVY-I'csistance exercise. ElIr J Appl Physiol 55:362, 1 986 7. Enoka RM: Muscle strength and its development: new perpectives. Spotts Med 6: 1 46, 1 988 8. Rut herford OM, Jones DA: The role of learning and coordination in strength training. Eur J Appl Physiol 55: 1 00, 1 986 9. Lieber RL, Bodine-Fowler SC: Skeletal mllscle mcchanics: implications for rehabilitation. Phys Thel' 73:844, 1 993 1 0. Dudley GA, Harris RT: Neummuscular adapta­

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and

Conditioni ng/National

Strength and Conditioning Association. Human Kinetics, Champaign, lL, 1 994 1 8. Pauletto B: Let's talk training #2: intensity. NSCA J 8:33, 1 986 1 9. Wathen D: Training volume. In Baechle (cd): Es­ sentials of Strength Training and Conditioni ng/ National Strength and Conditioning Association. I-Iuman Kinetics, Champaign, lL, 1 994 20. Wathen, D: Load assignmenl. In Baechle (ed): Es­ sentials of Strength Training and Conditioni ng! National Strength and Conditioning Association. Human Kinetics, Champaign, IL, 1 994 2 1 . Wathen 0: Periodizalion: Concepts and Applica­ tions. In Baechle (cd): Essentials of Strength Training and Conditioning/National Strength and Conditioning

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Champaign, IL, 1 994 2 2 . Saha

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Charles C Thomas, Springfield, l L, 1 96 1 23. Pappas A , Goss T, Kleinman P : Symptomatic shoulder instability due to lesions of the glenoid labrlllll. Am J SPOl-tS Med 9: I I , 1 9 8 1 24. Inman VT , Saunders M , Abbot LC: Observations on the function of the shoulder joint. J Bone Joint Surg 26: I , 1 994 "25. Townsend H, Jobe FW, Pink M, Pen,), J: EMG analysis of the glenohumeral muscles during a

tions to conditioning. In Baechle, TR (cd): Essen­

baseball rehabilitation program. Am J Sports Med

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20:264, 1 99 1

tional Strength and Conditioning Association. Human Kinetics, Champaign, lL, 1 994 I I . Andersen T, Kearney JT: Effects of three resis­ tance training programs on muscular slrength

26. Jobe FW. Moynes DR: Delineation o f diagnostic criteria and a rehabilitation program for rotator cuff injuries. Am J Spotts Med 1 0:336, 1 982 27. Blackbul11 TA, McLeod WD, White B Wofford L:

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training. p. 29. In Bernhardt DB cd: Sports Physi­

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28. Worrell TW, Corey BJ, York Sl, Santiestaban J:

Livingston, New York,

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38. Kraemer W1, Deschenes MR, Fleck S1: Physiolog­

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Sports Exer 24:744, 1 992

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1 988 39. Stone MH, Fleck SJ, Triplett NT, Kraemer WJ: Health-and pelformance-related potential of re­ sistancetraining. Spor1s Med 1 1 :2 1 0, 1991

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40. Turkel SJ, Panio MW, Marshall Jl, Grigis FG: Sta­

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32. Rodosky MW, Hamer CD, Fu FH: The role of the

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Joint Surg 74A:53, 1 992 42. Bagg SD, Forest WI: Eleclromyographic study of

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the scapular rotators during ann abduction in the

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34. ElienbeckerTS, Davies GJ, Rowinski MJ: Concen­ tric

VCI"SliS

eccentric isokinetic strengthening of

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tr-aining of

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43. Travell IG, Simons DG: Myofascial Pain and Dys­ function. The Trigger Point Manual. Williams Wilkins, Balt imore, 1 984. 44. WatTen G, lehman JF, Koblanski IN: Heat and stretch procedures: an evaluation using rat tail lendon. Ach Phys Med Rehab 57: 1 22 , 1 976 45. Janda V: Central nelvous motor regulation and back problems. In Korr 1 M (ed): The Neurobiolo­ gic

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37. Kraemer WJ, Daniels Wl: Physiological effecls of

adelphia, 1 986

Myojascial Treatment DEB 0 RA H ROB E R T

SEIDEL

COB B

CAN T U

Introduct:ion The complexity of the shoulder joint ohen makes it a difficult joint for a physical therapist to evalu­ ate and treat. The biomechanical complexity of the shoulder is a function of an interrelationship between bony structures and myofascia. Evalua­ tion and treatment of the shoulder must there­ fore address both of these components. Two highly inten'elated approaches to treat­ ing the shoulder are joint manipulation and my­ ofascia I manipulation (Fig. 15.1). All of the myo­ fascial tissues including capsule, ligament, and sUITounding fascia are categorized as soh tis­ sues. The question is, when is one performing joint mobilization and when is one performing myofascial manipulation? What is the difference between the two? Both joint mobilization and myofascial manipulation have their effects upon connective tissue. Joint manipulation has been defined as "the skilled passive movement of a joint.'" This move­ ment is gained pIimarily by following the rules of arthrokinematics. This makes joint mobilization easier to understand and use. Myofascial mobili­ zation, on the other hand, is not as clear-cut. Many myofascial lesions do not follow any arthrokinematic rules. The basis for myofascial mobilization is more intuitive, relying on palpa­ tion rather than arthrokinematics. By definition, myofascial manipulation is defined as "the forceful, passive movement of

musculofascial elements through its restrictive directions, beginning with its most superficial layer and progressing into depth, while taking into account its relationship to the joints con­ cerned.'" This definition contains several key elements: I. Myofascial manipulation as defined [or this chapter is direct technique. (Find the lesion and treat in the direction of the restriction.)

2. Awareness of the 3-dimensionality of myo­ fascia is key to its successful implementa­ tion. 3. A strong interrelationship exists between joint mobilization and myofascial manipula­ tion. The pIimary focus of this chapter is the treat­ ment of the myofascial tissues significant to the shoulder joint.

HistoliJrJy of Connective 'fli.ss'tw Connective tissue comprises 16 percent of a per­ son's body and stores 23 percent of the body's total water content! Skin, muscle, tendon, liga­ ments, joint capsule, periosteum, aponeuroses, and blood vessel walls all contain connective tis­ sue. Bone, cartilage, and adipose tissue can also 383

384

PHYSICAL

THERAPY

OF

THE

SHOULDER

Connective Tissue Mobilization

J oint

Myofascial

Mobil ization

Manipulation

·

FIGURE 15.1

to treatil1g the shoulder.

histologically be considered connective tissue but are not relevant to our discussion of myofas­ cia.'5 Connective tissue is comprised of cells, ground substance, and three fiber types: Colla­ gen, elastin, and retinaculin (Table 15.1 ) 5.6 As therapists, we are concemed with the ordinary connective tissue that compdses the superficial

TABLE 15.1.

Components of connective (issue

Collagen: Mo�1 tensile of connective tissue fibers Type I collagen: Ordinary connective tissue (loose and dense) Type II collagen: Hyaline cartli oge Type III collogen: lining of arteries and fetal dermis Type IV collagen: Basemenl membranes Elastin: More elastic then collogen. lining of arteries and ligamen­ tum flovum Reticulin: Most elastic fiber. Framework of lymph nodes and glands Ground substance: Viscous medium in which cells and connective tissue lie Mechanical barrier against foreign matter Medium for nutrient ond waste diffusion Maintains spacing between adjacent collagen fibers (interfiber distance) to prevent cross-links

and deep fascia as well as the nerve and muscle sheaths, ligaments, and tendons. CLASSIFICATION OF CONNECTIVE TISSUE

Connective tissue can be divided into three types based on fiber density and arrangement: dense regular, dense irregular, and loose regular. Ten­ dons and ligaments are comprised primarily of dense regular connective tissue, which is charac­ terized by a high proportion of collagen fibers to ground substance, and a parallel arrangement of fibers. These characteristics allow for high ten­ sile strength with low extensibility. Dense regu­ lar connective tissue has poor vascularity due to its compactness. Healing time is therefore signif­ icantly increased after any trauma (see Fig. 15.4). Dense irregular connective tissue is found in joint capsule, periosteum, dermis of skin, fascial sheaths, and aponeuroses. A dense multidirec­ tional fiber atTangement is charactetistic of this type of connective tissue. Due to the structure it is able to limit forces in a three-dimensional manner. As compared to dense regular connec-

Int

MYOFASCIAL

tive tissue, it possesses a higher proportion of ground substance as well as increased vascu­ larity. Loose regular connective tissue is found in the superficial and deep fascia as well as nerve and muscle sheath, endomysium, and the sup­ portive structure of the lymph system. This tis­ sue is the most easily mobilized with myofascial techniques .3-5.7

Effects oj immofliJ:ization and MolJilization on Connective Tissue With an understanding of the normal biomecha­ nics and histology of the myofascial tissue, it is now important to see how these tissues are af­ fected by immobilization, trauma, and remobili­ zation. This is essential so that realistic goals can be set in the clinic. [t is important to remember that most of the available information on the ef­ fects of immobilization of connective tissue has come from research done on animals, most of which were normal and nontraumatized. This is fundamentally different from patients typically seen in a orthopedic clinic. I Amiel et al. performed extensive animal studies on the immobilzation of connective tis­ sue dut;ng the 1960s and I 970S8-13 Their studies typically involved immobilizing a normal animal knee then analyzing the histologic effects on con­ nective tissue. The authors found fibrofatty infil­ trates, primarily in the areas of capsular folds. With longer periods of immobilization greater amounts of infiltrate developed and adhesions began to form in the connective tissue. Under histologic examination, no significant loss of collagen was found-only loss of ground substance (glycosaminoglycans and water). With the loss of ground substance came a de­ creased fiber distance, leading to cross-link de­ velopment between collagen fibers. Immobiliza­ tion leads to a lack of stress being applied to the collagen fibers, causing them to align in a hap­ hazard fashionu This alignment leads to a de­ creased tissue extensibility·-13 When immobili­ zation occurs for less than 12 weeks, the rate of

TREATMENT

385

collagen synthesis and degradation are the same. After 12 weeks of immobilization, collagen deg­ radation exceeds collagen synthesis, resulting in a net collagen 10ss. 14 In a study by Evans et ai, it was found that if rat knees were experimentally immobilized, then manipulated under high velocity, pal·tial joint mobility could be restored. If these joints were allowed to move prior to manipulation, full mo­ bility could then be restored. This held true for immobilization of less than 30 days. Longer pe­ riods of immobilization result in less optimal re­ turn of mobility.13

Other Physiologic Resprmses To MyojasciaJ, Manipulation Soft tissue mobilization and massage are com­ monly used interchangeably. Additional effects of massage on the body have been well docu­ mented in the literature. Three secondary effects are on blood now, the basal metabolism, and the autonomic system. Massage has been shown to increase blood now to the extremities. Deep massage strokes in­ crease total blood now in both animal and human subjects. Massage causes capillaries to dilate in the region of the stroking, resulting in increased blood volume and now. Of signifi­ cance is the fact that milder massage does not produce the same effect. The type and depth of the myofascial technique may alter the effect produced on the body. IS-17 The autonomic system has also been shown to be effected by massage. Ebner reported that connective tissue massage stimulates circulation in a region of the body, which in turn opens up increased circulatory pathways to other body re­ gions. The mechanical friction created by mas­ sage stimulates the mast cells in connective tis­ sue to produce histamine. Histamine causes vasodilation, resulting in increased blood now " around the body. IS,19,

386

PHYSICAL

THERAPY

OF

THE

SHOULDER

MyoJascial EJuai:uation oj the Shoulder When evaluating the shoulder, the physical ther­ apist is looking for acorrelatiol1 of (indil1gs that might be indicative or a dysfunction. History, as well as the results from visual, movement, and palpatory exams, should be considered. II is im­ portant to remember that connective tissue changes, in the absence or other objective find­ ings, are not necessarily dysr"lmctional. Several consistent findings are a beller indicator of a problem. For example, consider a patient who presents with a stiff and painrul shoulder. Exter­ nal rotation and abduction are most limited. Physical evaluation reveals tightness of the inter­ nal rotators and adductors, especially pectoralis major, latissimus dorsi, and teres major. Postur­ ally, this patient assumes a protracted position. This combination of rindings is indicative of a shoulder dysfunction possibly related to postural abnormalities. The individual findings of pos­ ture or tightness were not significant until they con'elated with pain and loss or motion. Treat­ ment must then address all the significant com­ ponents contributing to the dysfunction. HISTORY

History gives valuable insight into patient condi­ tions before a hand ever touches them. For exam­ ple, myorascial pain of nonmechanical origin is usually dull and nonspecific. Myorascial pain or mechanical origin is more specific, If a patient reports specific sharp pain that is easily repro­ duced, a more specific pathology may be present. By knowing the behavior of the patient's pain, we can begin to isolate the nature of the problem. We then move on to try to correlate the history with objective findings.

For the shoulder, we must consider the trunk and neck positions in both silling and standing as well as the relationship of the scapulae relative to the trunk. The evaluator should be looking for areas of muscle or connective tissue asymmetry as well as increased muscle activity. Because fas­ cial planes can be restricted over large areas of the body, a head to foot evaluation may be needed. If a leg length discrepancy exists, a pa­ tient may develop muscle asymmetry due to pro­ longed shortening or lengthening or a muscle or group of muscles. Vladamir Janda helped demonstrate the er­ fects of myofascial imbalances on postural im­ balances. He looked extenSively at how muscles respond to dysfunction. Janda observed that changes in muscle function play an important role on the pathogenesis of many painful condi­ tions. Janda defined a poslLlral muscle as one that responds to dysfunction by lightening and a pha­ sic muscle as one that responds to dysfunction by weakening. In the upper extremity we see a typical patlem of tightening of the upper trape­ zius, levator scapulae, and pectoralis with weak­ ening of the deep neck flexors and lower scapular stabilizers. All or these contribute to the typical kyphotic, protracted posture often seen in the clinic, (Table 15.2).20.21 Tight muscles tend to act in an inhibitory way on their antagonist muscles. It does not seem reasonable to start a strengthening pro­ gram for the weakened antagonist as the first step in a rehabilitation program. After stretching of the tightened muscles, the strength of the in­ hibited muscles may retum without any rurther treatment. In the case of a fTozen shoulder pa­ tient, it would make sense to first stretch out the

J. p

phasic muscles of TABLE 15.2. Postural vers the shoulder girdle and LIp eI' thoracic regiol1 POSTURAL

POSTURAL EVALUATION

Body posture can give us clues as to the area of movement disturbance or where the body may have excessive stress placed upon it. The impor­ tance of posture is in how it relates to runction.

PHASIC

Upper trapezius

latissimus dorsi

levator scapulae

lower trapezius

Pectoralis minor

Middle traps

Pectoralis major (upper portion)

Rhomboids

Cervicol erector spinae

Anterior cervical musculature

MYOFASCIAL TREAT MENT

shortened internal rotators and adductors like the subscapulal;s before allempting to strengthen the weakened external rotators and abductors. MOVEMENT ANALYSIS

l

Active movement testi may provide further in­ formation with which correlate postural find­ ings. It is important to onsider what is happen­ ing to the entire body when looking at active shoulder motion. Quality as well as quantity should be considered. Do limitations in range con·e1ate to postural findings? For example, if on postural evaluation the patient was found to have a forward head position with pectoralis major and minor shortening, we may expect to see limited forward elevation of the shoulder. Passive range of motion should also be for both quality and quantity of movement as well as for endfeel. Is the endfeel capsular,or is there limitation by soft tissue? Proper stabilization is necessary to achieve true range of motion and proper endfeel. See Chapter 3 for a detailed eval­ uation sequence.

387

the layers of tissue perpendicular to the tissues as well as moving the perpendicular tissues. The examiner should be able to palpate the tendons, muscle bellies, muscle sheath, myotendinous junctions, joint capsule, tenoperiosteal junc­ tions, and deep periosteal layers of tissue. To as­ sess mobility of muscle, a technique called trans­ verse muscle play may be used. This involves bending of th� muscle to assess its transverse flexibility, (see Figs. 15.3 and 15.4). Palpatory findings will change with treatment, so it is im­ portant to be constantly reassessing.

Myof(J$ciaJ. Techniqu£s for the Shoul.der The following therapeutic techniques are just a few of many available treatments for the shoul­ der. These techniques have been chosen because of their effectiveness in the clinic as witnessed by the authors. It is important to remember that any technique can be modified to suit the patient problem or needs of the clinician. POSITIONING OF THE PATIENT AND

PALPATORY EXAM

Now that posture and movement have been as­ sessed, the examiner can begin to palpate for the location of the dysfunction. As previously men­ tioned, palpatOlY findings must also correlate with postural and movement findings to be of any significance. The palpatory exam includes the myofascial structures by layer and palpation of the joint structures. Palpation of the shoulder must include the scapular, cervical, thoracic, and anterior chest wall regions. Superficial palpation is performed on the skin and superfiCial connective tissues. The ex­ aminer should be assessing for temperature, moisture,and light touch to determine the exten­ sibility of the connective tissues. Tissue rolling is one way to check the extensibility of these Sl!llctures. It involves the lifting away of the su­ perficial connective tissue and skin fTom the un­ derlying structures. Deep palpation involves palpation through

THERAPIST

Maximum effectiveness cannot be achieved if the technique is not efficiently executed. If a therapist is not properly positioned, the patient may not be able to relax, or the therapist may be pUlling undue stress on the patient's body. Remember to avoid needless body contact with the patient. A pillow between the patient and therapist can provide a mechanical baiTier as needed. JOINT PROTECTION

Because the hands are the primary tool of the manual therapist, it is essential to protect them. Here are a few general suggestions on how a manual therapist can protect the hands: J. Avoid hyperflexion or hyperextension of the joints. This will decrease the problems of hyperrnobility and early arthritis.

388

PHYSICAL

THERA PY

OF

THE

SHOULDER

Palient Position

Supine with the head in a neutral position on the treatment table. Therapist Position

Seated near the patients' head at a 45° angle to the shoulder girdle. Procedure

Begin stroking with the fingertips in a medial to lateral position. Once the glenohumeral joint is reached, replace the hands in the original posi­ tion and repeat the stroke. The strokes may be­ come progressively deeper. TRANSVERSE MUSCLE PLAY OF THE PECTORALS (FIGS. 15.3, 15.4)

Ratior/ale FIGURE 15.2

2. Use elbows, pisiforms, or fists on patients who are too large to safely use your fingers on. Be creative. 3. During off hours from work, try to rest your hands and protect them h'om excessive strain. 4. Use cold water rinses or short ice massage on your joints if innammation occurs h-om vigorous treatment of a patient.

Tightening of the pectorals is a common problem found in shoulder patients, especially those with the forward head posture. I n order to achieve full shoulder range of motion and pos­ tural correction, the extensibility of these mus­ cles must be restored. Patienl Position

Supine with the shoulder abducted to 90° to 120° (less nexion with h-ozen shoulders). Therapist Position

ANTEROPOSTERIOR LATERAL ELONGATION Of THE UPPER THORACIC REGION (FIG. 15.2)

Alongside the patient at a 45° angle to the shoulder girdle. The patient may rest the arm on the therapist's knee to � hieve beller relaxation. The thumbs are place Funderneath the muscle and the fingers grasp f": above.

?!

Rationale

This technique is used for relaxing and lengthening the myofascia in the upper thoracic region and the shoulder girdle. This technique is of great value to patients who have protracted shoulder girdles. I t should be used before trying to teach postural correction or strengthening.

Procedure

Gently lift and bend the pectoral muscle away [Tom the anterior chest wall. Small oscilla­ tions can be performed as well as a static hold. Be careful to not contact breast tissue.

MYOFASCIAL

FIGURE 15.3

FIGURE 15.4

TREATMENT

389

390

PHYSICAL

THERAPY

OF

THE

SHOULDER

FIGURE 15.5

FIGURE 15.6

MVOFASCIAl

SUBSCAPULARIS TECHNIQUES (FIGS. 15.5, 15.6)

Rationale

The subscapularis muscle is often found to have significant restrictions in patients with de­ creased shoulder range of motion due to poor posture or immobilization. When [·ull shoulder motion cannot be achieved, the therapist should recheck the subscapularis and the surrounding myofascia for trigger points or restrictions. Patient Position

Supine with the arm abducted 30' to 60'. The arm may rest against the therapist for relaxation. Therapist Positiol7

Standing alongside the patient. One hand is placed from above into the belly of the subscapu­ laris. The other hand may be used to stabilize the patient's arm, or it may be used to assist the upper hand in doing the mobilization. Proced"re I

Small oscillations or sustained pressure can be used as a therapist applies moderate pressure into the subscapularis. The bottom hand may grasp from beneath to per[olm a muscle play technique. Procedure 2

The patient's arm is elevated into flexion and gently distracted. The therapist places the palm of the hand along the lateral border of the sca­ pula. Gentle stroking in a caudal direction is ap­ plied with the palm. If more specific fascial re­ strictions exist, the fingertips may be used to provide a static or oscillatory pressure. ANTEROLATERAL FASCIAL ELONGATION (FIG.

TREATMENT

391

Patient Position

Supine with the shoulder elevated 120' to 160' depending on the area of restriction. Therapist Position

At the top of the bed, grasping the patient's arm and providing a gentle upward distraction. The palm of the upper arm is placed just below the breast line. Be sure of proper draping and appropriate hand placement when performing this technique. Procedure

The therapist applies a stronger tractioning force on the flexed arm while the lower arm trac­ tions in the direction of the umbilicus. The direc­ tion of force may be changed to accommodate the existing restrictions. Lubricants should not be used to prevent shear force. ROTATIONAL THORACIC LAMINAR RELEASE (FIG. 15.8)

RatiO/wle

To mobilize the paravertebral and perisca­ pular muscles into rotation. This is a deeper tech­ nique than those already described. Patient Position

Sidelying with the head suppolied and the upper arm resting on the side of the body. Therapist PositiOI1

Directly facing the patient with a pillow fit snugly between therapist and patient. The lower hand is placed along the paravertebral muscles near the medial border of the scapula. The upper hand rests on the glenohumeral joint.

15.7)

Rationale

This technique elongates the superficial an­ terior fascia, which is often restricted in patients with a protracted shoulder girdle position.

Procedure

The fingers of the lower hand apply a deep pressure in a sweeping downward motion, while the upper hand retracts the shoulder girdle and

392

PHYSICAL

THERAPY

OF

THE

SHOULDER

FIGURE 15.7

FIGURE 15.8

MYOFASCIAL

TREATMENT

393

FIGURE 15.9

applies a rotational force through the thoracic spine. SCAPULAR FRAMING (FIGS. 15.9 TO 15. 11)

Rariol1ale

A commonly performed technique that de­ creases tone in the periscapular muscles and pre­ pares the scapulothOiacic tissues for aggressive stretching. Parienr Posiriol1

Lying on the side faCing the therapist, with a pillow separating the two. The patient's arm should be resting comfortably on the pillow. Therapisr Posiriol1

Standing Facing the patient with the upper hand placed on the anterior acromion.

then stroke in a downward direction along the border of the scapula with the lower hand. Procedure for Lareral Border

Place the palm of the lower hand over the acromion to stabilize the joint. The palm of the upper hand is placed over the lateral border of the scapula, and then strokes caudally with a Firm pressure down the length of the border. Procedure for Superior Border

Place the fingertips of both hands medial to the cervicothoracic junction over the upper tra­ pezius. Stroke outward toward the acromion with a film pressure. If needed, a gentle stretch performed with the palm of the hand can be given at the end of the stroke. SCAPULAR MOBILIZATION (FIG. 15.12)

Ratiol1ale Procedure for Medial Border

Place the fingers of the lower hand gently along the medial border of the scapula. Gently retract the shoulder with the upper hand, and

To mobilize the scapula off the rib cage in order to stretch the surrounding myofascia. This technique should be done after there has been preparation of the tissues by scapular flaming.

394

PHYSICAL

THERAPY

OF

THE

SHOULDER

FIGURE 15. I 0

FIGURE 15. 1 I

MYOFASCIAL

TREATMENT

395

fiGURE 15. 12

Patie'1t Position

The patient is lying on the side facing the therapist, with a pillow separating the two.

muscles to allow for better posture and improved shoulder range of motion. Patient Position

Therapist Position

Standing directly in front of the patient with the top hand placed on the anterior shoulder joint. The fingers of the bottom hand lightly grasp the medial border of the scapula. Procedure

Lift the scapula and shoulder girdle complex off of the thoracic rib cage. If the patient is larger, two hands may be needed.

Seated with the hands behjnd the head. Therapist Position

Standing directly behind the patient with either the knee or rup stabilizing the thoracic re­ gion. As previously mentioned, a pillow should be placed between therapist and patient. The therapist grasps the patient just below the el­ bows. Procedure 1

SEATED PECTORAL AND ANTERIOR fASCIAL STRETCHES (FIGS. 15.13 TO 15.15)

Rationale

Sometimes patients are better able to relax in the seated position. These stretches can be used to elongate the anterior fascia and pectoral

A posterior force towards the patient's head is applied while the patient takes deep breaths to improve anterior elongation. To incorporate the lateral fascia and muscles, the patient can be asked to lean or rotate to one side while the same force is applied. The patient's arms may also be fully extended for this technique.

396

PHYSICAL

FIGURE 15.13

THERAPY

OF

THE

SHOULDER

FIGURE 15.15

Proced"re 2

The patient may have only one arm extended upwards. while the therapist places one hand along the lateral I-ib cage and the olher just below the elbow. A traction rorce is then applied in op­ posite directions. A rotary component can also be added using the technique stated above. CROSS-FRICTION OF SUPRASPINATUS AND BICEPS TENDON (FIG. 15.16)

RatiO/wle

Cross-friction is used to increase local blood now to enhance the rate or healing. It is vel)' effective in treating tendonitis or the biceps or supraspinatus. Patiel1t Positiol1

Supine with the arm abducted 30· and the elbow bent. FIGURE 15.14

Tilerapisl POSiliol1

At the patient's side supporting the arm with the bottom hand. The thumb or the top hand is in the bicipital groove.

MYOFASCIAL

TREA TMENT

397

FIGURE 15.16

Procedure

The therapist may alternately laterally and medially rotate the shoulder to create some gentle friction. Direct fl-iction over the bicipital groove is applied with the thumb. The second and third fingers with slight flexion at the distal interphalangeal joints may also be used if the patient is less acute. To friction the supraspi­ natus, the therapist abducts the shoulder 80° to 90° and palpates the notch fOI-med by the acro­ mion spine and the clavicle. The musculotendi­ nous junction lies here. Use the same technique as described earlier.

in the upper trapezius,levator scapulae, and pec­ toral muscles. Cervical range of motion is limited by 25 percent into rotation and sidebending to the right. Left shoulder active range of motion is 100° of flexion, 90° of abduction, and 45° of external rotation. Passive range of motion is 100° of flexion, 90° of abduction, and 55° of external rotation with pain before end-range. There are multiple tender spots in the upper thoracic, sca­ pulothoracic, and anterior chest wall regions. The acromioclavicular joint is painful to palpa­ tion and to internal rotation and adduction movements. PATIENT PROBLEMS

CASE STUDY A 34-year-old female patient presents at our clinic with an 8-week history of left shoulder pain following a fall. She has a history of a Bank­ art repair to the same shoulder in 1990 after an injury sustained in a motor vehicle accident. The 0I1hopedist has I1.Iled out injury to the prior re­ pair as cause for her pain. On evaluation she pre­ sents with atrophy of the rhomboids and lower trapezius. Significant increase in tone is present

I.

Increased tone in the upper trapezius

2. Increased tone in the rhomboids 3. Increased tone in the levator scapulae 4. Increased tone in the pectorals 5. Decreased range of motion of the left shoulder 6. AC joint pain 7.

Trigger points in the UIT and scapulothora­ dc regions

398

PHYSICAL

THERAPY

OF

THE

SHOULDER

8. Restrictions in the anterior chest wall myo­ fascia 9. Decreased cervical range of motion From a myofascial standpoint, a good way to begin treatment of this patient would be to address these components prior to range of mo­ tion or strength. The previously discussed tech­ niques might be incorporated into treatment of this patient in the following way. I.

Increased pectoral tone: pectoral muscle play

2. Restricted anterior chest wall: anterior fas­ cial elongation with or without a rotary componenl 3. Peliscapular restlictions: scapular framing, scapular mobilization, subscapularis release

4. Increased tone in upper thoracic region/upper trapezius: anterior/posterior lateral elongation of upper thoracic region 5. Increased tone in paravertebral muscles: ro­ tational thoracic laminar release

After performing each myofascial technique, reassess the patient's range of motion to see what effect the treatment has made. Large increa es in range can be achieved through the perfor­ mance of myofascial techniques without ever performing true range of motion or joint mobili­ zation of the glenohumeral joint. Once the myo­ fascial restrictions are eliminated and the range of motion is improved, begin strengthening exer­ cises if they are still required. Consider each pa­ tient's problems individually, continually reas­ sessing the causes of limitation. Use these findings to guide your choice of treatment ap­ proach. If one approach is not working, consider a change in technique. Remember that the afore­ mentioned techniques are only a small sample of available treatments. In the case of this patient, myofascial treat­ ment assisted in the ability to isolate the primary problem. On initial evaluation there was too much muscle guarding and myofascial restric­ tions to identify the cause of this patient's pain. After 4 treatment sessions using the discussed techniques, this patients pain centralized to the

A

34-year-old palienl who preseJ1led wilh al1 8-week hislory o( le(1 shoulder pain (allowing a (all. (A & B) PreseJ1lalion o( Ihe palieJ1l after Ihe (irsl (our IrealllleJ1l sessions. FIGURE 15.17 A

B

MYOFASCIAL

acromioclavicular joint. This problem could not have been easily identified early on due to the protective muscular responses of the body. Once those protective mechanisms were removed, the problem became obvious. Figure 15.17 show, the presentation of the patient afler the first 4 treat­ ment sessions. At this point, the positions of the scapula and clavicle have moved closer to nor­ mal and the prominence of the acromioclavicu­ lar joint has become more obvious. The patient was refen'ed back to the orthopedist for closer examination of the AC joint.

References J. 2.

3. 4.

5. 6. 7.

8.

9.

10.

399

nective tissue response to immobilitiy: an acceler­ ated aging response. Exp Gerontol 3:289, 1968 II. Akeson WH, Amial 0, MechanicGL et al: Collagen cross-linking alterations in joint contr-acturcs. Connective Tissue Res 5:15, 1977 12. Akeson WH, Amial 0: Immobility effects of syno· vial joints: the pathomechanics of joint con· tracture. Biorheology 17:95, 1980 13. Evans E, Eggers G, Butler JK et al: Experimental immobilization and mobilization of rat knee joints. J Bone Joint Surg 42A:737, 1960 14. Amial 0, Akeson WH, Woo S et al: Stress dep,·iva. lion effect on metabolic turnover of medial collat· eral ligament collagen. Clin O.1hop 172:265, 1983 J 5. Laban MM: Collagen tissue: implications of its re· sponse to stress in vitro. Arch Phys Med Rehabil 43:461, 1962 16.

Cantu R. Grodin A: Myofascial Manipulation. Aspen Publishing, Gaithersburg, UD, 1992 Dicke E, Schliack H, wolrr A: A Manual or ReOex· ive Therapy. S Simon Publishing, Scarsdale, NY,

17.

1978

18.

Ham AW, Cormack DH: Histology. JB Lippincott, Philadelphia, 1979 Copenhaver WM, Bunge RP, Runge R et al: Bai· ley's Textbook of Histology. Williams & Wilkins, Baltimore, 1975 Warwick R, Williams PL: Gray's Anatomy. p. 32. 3rd Bdtish Ed. WE Saunders, Philadelphia, 1973 Cummings G: Soft Tissue Changes in Con­ tracture. Stokesville Publishing, Atlanta. 1985 Grodin A, Cantu R: MyofasciaJ Manipulation: Theory and Clinical Management. Forum Med­ icum, Berryville, VA, 1989 Woo S, Matthews N, Akason WH et al: Connec­ tive Tissue Response to Immobility. AI1hdtis Rheum 18:257, 1975 Akeson WH, Woo SL, Amial 0 et al: The connec­ tive tissue response to immobilization: biomc­ chanical changes in pedarticular connective tis­ sue of the rabbit knee. Clin Orthop 93:356, 1973 Akeson WH, Amial 0, LaViolette 0 et al: The con-

TREATMENT

19.

20.

21. 22. 23.

24.

Neuberger A, Slack H: The metabolism of collagen fTom liver, bones, skin and tendon in nOlmal l"31s. Biochem J 53:47, 1953 Frankel VH, Nordin M. Basic Biomechanics of the Skeletal System. p. 90. Lea and Febinger, Phila· delphia, 1980 Wakim KG: The effects of massage on the circula· lion of nonnal and paralyzed extremities. Arch Phys Med Rehabil 30:135, 1949 Wolfson H: Studies on the effect of physical thera­ peutic procedures on function and structure. JAMA 96:2020, 1931 Martin GM, Roth GM, Elkins C, KlUsen F: Cuta· neous temperature of the extremities of nOlmal subjects and paticnts with rhcumatoid arthritis. Arch Phys Med Rehabil 27:665, 1946 Cuthbenson DP: Effects of massage on metabo· lism. Glasgow Med J 2:200, 1933 Ebner M: Connective Tissue Manipulation. Kreiger Publishing, Malabar, FL, 1985 Janda B: Central nervous motor regulation and back problems. p. 28. In 1M Korr (cd): The Neuro· biologic Mechanisms in Manipulative Therapy. Plenum Press, New York, 1978 Donatelli R, Wooden M: Orthopaedic Physical Therapy. p. 151. Churchill Livingstone, New York, 1989

Isokinetic Evaluation and Treatment MAR K

5 .

MICHAEL

ALBERT J .

WOODEN

Isokinelic exercise has become a popular form of resislive exercise in the physical therapy clinic. Since the late I960s, the literature has consisted primarily of research data and clinical infonna­ tion relaling to the knee. However, recenl ad­ vances in equipment have made it possible to use positioning to apply isokinetics effectively to most other extremity joints, including the shoul­ der complex. The purposes of this chapter are to list some advantages of isokinetics in shoulder evaluation and treatment, to describe the adapt­ ability of several dynamometers to shoulder di­ agonal patterns, to discuss principles of isoki­ netic testing and training with emphasis on shoulder positioning, and to describe considera­ tions of test data interpretation.

Practical Advantages oj Isokinetics lsokinelic exercise, unlike isotonic exercise, of­ fers totally accommodating resistance to a mus­ cular contraction.'-3 Because the speed of move­ ment is constant, resistance to the movement varies according to the amount of force applied to the resistance arm. Therefore. in a maxirnum­ effort isokinetic contraction, the muscle is loaded maximally at each point in the range of motion (ROM).'-3

With isotonic equipment or free weights, be­ cause the speed of movement is not preset, resis­ tance to muscle contraction will vary according to gravity, positioning, lever aI-m lengths (in the equipment and in the patient's limbs), and cam sizes.3 If, because of these factors, effective resis­ tance occurs only at a certain point in the range, it is possible that the muscle is being strength­ ened only at that point. Consequently, isokinetic exercise offers the advantage of loading a muscle effectively throughout its ROM by fixing the speed of movement. [sokinetics offers several other clinical ad­ vantages, such as the capacity for a wide range of speeds, both for testing muscle function and for rehabilitation or strength training ' This al­ lows the clinician to determine at what velocities muscle torque deficits occur: at low speeds (so­ called "strength" deficits), or high speeds ("power" and "endurance" deficits).2 Testing and training at higher speed attempts to simulate normal activities in which angular velocities (as in walking, nmning, swimming, Ihrowing, and other activities) are far in excess of most isotonic speeds.3 Even the highest speeds of the MERAC (Universal Corp., Cedar Rapids, LA), at 500"/s, are not fast enough to ·match many activities, espe­ cially sports activities. However, exercising at different speeds may cause quantitative and qualitative recruitment of different muscle fiber

401

402

P H Y SIC A L

THERA P Y

OF

T H E

S HO U LD E R

types: therefore, most or all of the muscle can be loadeds-s Increases in speed of isokinetic concentric contraction are associated with decreases in both torque output and electromyographic activ­ ity of the muscle.'·s-s Therefore, compressive re­ action forces at the joint should also decrease. In joints that exhibit an inflamed or painful re­ sponse to exercise, increasing the speed may temporarily "spare the joint" by redUCing joint reaction forces. Whether training solely at high speeds contributes to an increase of strength at low speeds is controversial, however4.s Never­ theless, the use of higher speeds is an important safety factor in reactive joint conditions, pro­ vided that concentric isokinetic contraction is used. Whether at fast or slow speeds, isokinetic re­ sistance will accommodate to pain levels, further ensuring safety, because if the patient needs to decrease or stop the contraction suddenly be­ cause of pain, the resistance will decrease imme­ diately, because resistance will never exceed the amount of force applied] Unlike isotonic exer­ cise, miminal momentum is produced with isok­ inetics. The use of submaximal effort isokinetics also enhances safety in cases of patient pain or reactive joint inflammation. Decreasing the force used in isokinetic resistance exercise will, in turn, decrease joint reaction forces as pro­ duced in submaximal eff0l1. Submaximal effort training may also produce pain reduction selec­ tive recruitment of muscle fiber type (slow twitch or type I), and improved joint lubrication. In ad­ dition to the advantages already discussed, Dav­ ies3 cites many other physiologic and clinical ad­ vantages of isokinetics. As with all types (or modes) of clinical muscle training, isokinetics possesses several disadvantages or precautions, which will be discussed in the next section. For example, a major physiologic limitation of Cybex systems prior to the 6000 model was an inability to exercise and measure muscle eccentrically. Because muscle generates the most amount of tension eccentrically9 and because much of func­ tional movement requires eccentric contraction, rehabilitation and testing of the glenohumeral joint in an eccentric mode have important appli­ cations and have received increasing emphasis

from clinicians and investigators. 10-1J Isotonic exercise inco'lJorates eccentric muscle loading; however, for reasons previously stated, it does not fully accommodate for length-tension changes nor does it adequately control momen­ llIm or force vector problems. With the advent of recent technology in dynamometry, inSlluments such as the Kincom (Chattanooga CO'lJ., Chatta­ nooga, TN), Biodex (Biodex, Shirley, NY), and Lido (Loredan Biomedical, Davi , CAl have the capability of applying eccentric isokinetic load­ ing with the inherent length-tension accommo­ dation. Controversy exists as to the safety of ro­ botic instruments when applied to human subjects, and continued research is needed to clarify this issue. A key concept to robotic testing and training involves thorough understanding of the alterations in the force-velocity curve th . at are produced by robotics. Another consideration is that the resistance mechanism, at least on Cybex equipment, is uni­ axial. Extremity joints, of course, are multiaxial, as their instantaneous centers of rotation change constantly through movement.'O-'4 The exten­ sive mobility of the shoulder and the multiple articulations within the shoulder complex fur­ ther complicate the appropriate alignment of the machine axis with the changing, compromised axis of the patient's shoulder. Other practical disadvantages of isokinetics in the clinic include the high cost of equipment, the amount of floor space required, and the time required to change positions and attachments to test the different movements. The latter is a par­ ticular problem with shoulder evaluation, be­ cause so many positions and motions are recom­ mended. Testing of diagonal pallerns reduces the time required for multiple dynamometer po­ sition changes, while assessing multiple muscle groups. The testing and training protocols imple­ mented before readiness for diagonal patterns require decisions about the positioning of the glenohumeral joint. To protect injured tissues while maintaining effective strengthening tech­ niques, several important biomechanical princi­ ples warrant consideration. The 900 abducted po­ sition (900 AP) as described in the Cybex manual4 can produce optimal external rotation torque

I SOKI N E T I C

and work values.'2. 1S In addition, the proximity of the position may risk glenohumeral joint im­ pingemenl.'5-'8 The 90' AP also involves long­ lever arm forces that are contraindicated in cases of joint instability and Significant rotator cuff weakness.'9 The 90' AP is deleterious when re­ stricted internal rotation ROM is present!O as torsion forces are transmilled from the scapula through the coracoclavicular ligaments into the acromioclavicular joint. In contrast, the neutral position (elbow ad­ dueted close to the patient's chest wall) produces the optimal internal rotation torque values as well as high external rotation values. Two nega­ tive considerations of this position are the micro­ vascular wringing out effect,3,2 1 which deprives the active supraspinatus of necessary blood flow, and stress on the anterior capsular mechanism with forced stretching of the often inflexible sub­ scapularis muscle (more often a significant prob­ lem in males). Both Hinton 12 and Soderberg and Blaschak lS suggest the need for multiple posi­ tions for testing and training and, not surpris­ ingly, that no Single patient or glenohumeral po­ sition is optimal for all clinical purposes, However, a compromise position that is safe frOI'll both vascular and biomechanical perspec­ tives is the intermediate, or 45', abducted posi­ tion. Although Hageman et al.22 found high con­ centric and eccentric torque values for both external and internal rotation at 45' AP, appro­ priate protection for both the anterior and poste­ rior capsular and labral mechanisms also was found to exist. Interestingly, the 45' AP closely simulates the modified base position advocated by Davies3 and can be readily adapted to con­ form to the plane of the scapula, which creates low capsular stress and produces peak isokinetic rotator cuff torque?3.2. The 45' AP is also simply applied to all dynamometer setup capacities, with minor patient position or machine adjust­ ment . Finally, the 45' AP positions conform closely to the natural. functional plane of motion (the plane of the scapula), and consequently pro­ vide a comfortable training position for most pa­ tients with pain, restl;ctions, and/or rotator cuff suppression.

E V A L U A T ION

EvaJ.uatiJm

A ND

T RE A T M EN T

403

oj SlurukJer IMg()'l'l()./$

The Cybex II manual contains detailed informa­ tion on testing all the cardinal plane movements of the shoulder.· Photographs and descriptions of positioning and machine settings allow for isolated testing of abduction, adduction, flexion, extension, and internal and external rotation. These procedures provide excellent information on speci(;c muscles or muscle groups and are indicated for certain pathologies. The process of testing all of these movements as part of a com­ prehensive shoulder evaluation is quite time­ consuming, however, and can be clinically un­ manageable. Excessively high charges and ques­ tionable validity of multiple glenohumeral mus­ cle measurement pose further arguments against multiple movement testing. The time manage­ ment problem can be solved by evaluating over­ all muscle function with two diagonal move­ ments, thus eliminating several lengthy steps. In addition to its practical benefits, diagonal movement testing may also be more functional than cardinal plane movements, which fail to isolate and measure motion of the acromioclavi­ cular, sternoclavicular, and scapulothoracic joints ' Of course, movement of these joints oc­ curs throughout the range of glenohumeral mo­ tion. Resisted diagonal movement will load muscles that effect movement at all joints in ' the shoulder girdle. KnOll and V oss, 25 pioneers in proprioceptive neuromuscular facilitation (PNF), first described "mass movement patterns" as being inherently diagonal in nature. These di­ agonals are dictated by anatomy-shapes of joints, lines of muscle pull, and soft tissue restric­ tions-and are those movements observed to be most used in everyday activities.25 The move­ ments to be described in this chapter are similar to the classic upper extremity PNF pallerns,

Testing Procedure The first diagonal movement described is the combination of extension, abduction, internal rotation (ExlfAbdJIR) and flexion, adduction, ex-

404

PHY S I C A L

FIGURE

T H E R A PY

16.1

O F

T H E

S H O U L D E R

(A) Initiation of the

diagonallllovel1lellt ExtlAbdJIR.

(B) End of diagonal move/1/em ExtlAbdJIR. (C) El1d of diagolwl 1Il0Velllel1t FlexlAddJER.

temal

rotation (FlexlAddlER).

Figure

16. 1A

shows the initiation of the ExtlAbdIlR move­ ment. and Figure 16. 1 B shows the end of that same diagonal. blocked manually to prevent hy­ perextension. Figure 16.1 C illustrates the end po­ sitions for the FlexlAddlER movement. For both movements. the patient is in-

structed to try to keep the elbow Slraight and to rotate the arm intemally or eXlemally. depend­ ing on which movement is being performed. To allow for rotation. a swivel handle is used. It should be pointed out. however. that the rota­ tional component cannot be resisted by the appa­ ratus. as would be the case if manual J'esistance

I S O KI N E T I C

:'1"

E V A L U AT I O N

A N D

T RE A T M E N T

405

,'

,

Ii '

·1· . '"

A

B

FIGURE 16.2

(A)

To rqLle CLlrve s o { uninvo lved shoLllder {o r E xllAbdllR and Fle xJAddlER. (B)

Torque curves o { invo lved sho ulde r {or E xllAbdllR and FlexJAddlER.

were used in PNF,2 5 The dynamometer is tipped forward 15° to account for trunk movement and the forward-inclined plane of the scapula. 23.26 Figure 16.2A is the normal torque curve for the diagonal ExtlAbdJIR and FlexlAddlER in a postanterior dislocation patient who has re­ covered most of her ROM. The shoulder is tested at 600/s (low speed) and 1800/s (high speed), the speeds recommended by Cybex for flexion and extension.' An athlete or unusually strong per-

son can also be tested at higher speeds as long as measurable torque is being produced. Figure 16.2B represents the torque curve for the injured side in the same patient. The lower root-pound readings for the "left involved shoulder" indicate strength deficits, at low and high speeds, ranging from 33 to 77 percent. Table 16. 1 gives a sum­ mary of the torque measurements taken [Tom Figure 16.2, Not only can strength deficits be computed,

406

P HY S ICAL

TABLE 16.1 DIAGO NAL

T H ERA P Y

Flex/Acid/ER

TH E

SHO ULD E R

Summary o( peak lorque de(icils SPEED

RIGHT UNINVO L VE D (FT -L 8

Ext/Abd/IR

O F

60'/. 1 80"/. 60'/. 1 80"/.

(D(lw (rom Figure

L EFT UNINVO L VE D

24

16 6 10

18

12

30 26

DE FICIT

,'lb,

(FT -L B

47 77

58 33

16.2)

FIGURE 16.3 (A) fnilialion o( diagonal movel1lel1f ExIIAdd/fR. (B) End o( diagol7all1lovel1lenl ExtIAdd/fR. (C) h,ilialion o( diagol7all1lovel11el1f Flex/AbdIER.

but the shapes of the torque curves in Figure 16.2 can also be compared. The low-speed curves (600/s) for the involved shoulder show a slower "rate of ,;se" than [or the nOlmal )side. That is, the weaker side took longer to reach its peak torque. In addition, the duration o[ each ExliAbdlIR and FlexiAddlER contraction at low and high speed is shorter, as compared with the opposite side, indicating the inability to sustain tension. These variations in curve shape are further indications o[ mu cle weak-

I S OK I N E T IC

E V A L U A T I O N

A NO

TR E A T M E N T

407

A

MERAC iso kil1etic diago.-wl pallems. (A) fl1itiatiol1 o f diagol1al movement £ttlAeldifR. (B) E .-,eI of diagOlwl movel11el1f ExtlAddlfR. FIGURE 16.4

B

ness that should improve after appropriate isok­ inetic training. Last, a comparison of the lower "position angle" scale indicates limitations at the extremes of ROM, although in this case the differences are slight. This evaluation procedure can also be done [or a second diagonal, the combination of Ext! AddnR and FlexlAbdJER. The sequence of these movements is illustrated in Figure 16.3. The start

and finish positions for Ext!AddJIR are shown in Figure J 6.3A and B, and Figure J 6.4A and B, and initiation of FlexiAbd/ER is shown in Figure J 6.3C. ln this diagonal, the extreme of the Oexion movement was blocked either manually or, as shown, using UBXT (Cybex, Ronkonkoma, NY) atlachments. Torque deficit computation and shape of curve comparisons were done as previ­ ously described.

408

P H Y S I C A L

T H ERA P Y

OF

T H E

S H O U L D ER

/nterpretat:inn of /sokinetic Test Parameters Traditional clinical practice with isokinetics has focused on the knee, with consideration of a spe­ cific agonjst to antagonist torque ratio (ham­ string to quadriceps) as a key clinical parameter. Similarly, the glenohumeral joint presents a key clinical parameter with external rotation to in­ ternal rotation (ERIIR) torque ratios expressed as a percentage. Two studies,,·2. have reported ERIIR ratios of 80 percent or greater; however, most studies3 , J 2, 13, J 5, J 8,29,33 have consistently demonstrated normative ratios of 60 percent to 70 percent Table 16.2. Consequently, the ERIIR ratio of 60 percent to 70 percent provides a basis for clinical description of normal force couple synergy and muscular tension capacity. The pa­ rameters of total work and endurance should also be examined, as they provide an additional perspective for clinical decision maIUng and dis­ charge status, and perhaps have greater func­ tional significance than peak torque values.'9

TABLE 16.2

Because the upper extremity muscles are smaller in cross-sectional area than most lower extremity muscles, they tend to demonstrate smaller normative peak torque to body weight (PTIBW) relationships. The strongest muscle groups of the upper extremity also produce the highest PTIBW ratios: 45 percent to 56 percent for adductors and 25 to 26 percent for abductors, as consistently reponed by Davies3 and Alderink and Kuck. 13 No consensus regarding external ro­ tation and internal rotation PTIBW ratios has been reported, with external rotation values ranging from 8 percent to 16 percent and inter­ nal rotation values ranging fTom 13 to 22 per­ cent. 3,13,18 The limited number of studies regarding shoulder isokinetic parameters and normative data have been performed with a variety of pa­ tient populations (mostly small numbers), differ­ ing test speeds and dynamometers, inconsistent methodology, and varied patient positions. Con­ sequently, applying the normative data to a given population or to predicting functional progress or discharge status must be done \vith caution,

Comparisons of upper-extremity 11lUsc!e torque

STUDY

Cook et 01.27

Soderberg and Blaschak" Dovie,'(Ch. 1 2) Ivey et 01.29

Alderink and Kuck'J

Hinton12 Connelly·Moddux et 01.18

SUBJE CTS

Mole pitchers and nonpitchers Moles, nonothletes 20 Mole, and femole, 31 Normals, mixed activity 24 Mole" high school and college pitchers 26 Pitchers, high school 21 Male,, 20 females

SPEEDS

FLEXION! E XTENSION

ABDUCTORSf ADDUCTORS

70-8 1 % 76-99%

NA

70-8 1 % 8 1 %°

NA

NA

57-69%

60% Mole" 48% females 66% Mole" 73% females

66% Mole" 52% females 61 % Mole" 57% females

64%°

90°, 1 20°, 1 80°, and 300"/,

48-55%

50-57%

66-76%°

90" and 240°/,

NA

NA

56-62%°

600/,

NA

NA

63% Mole" 7 1 % females

1 800/,

600, 1 800, 300"/, 600 and 300°/, 600 and 1 80°/,

NA, /tOI available, " Data (rom 90" shoulder abducted posirioll.

EXTERNAL ROTATI ONI INTERNAL ROTATION

67%°

I S O K I N E TIC

However, userul and consistent concepts have emerged from available isokinetic normative shoulder studies that provide general guidelines for clinical decision making. Bilateral compa,;son testing, in which peak torque at the injured joint is expressed as a per­ centage of deficit compared with the uninvolved ("normal") side, is one method of interpretation of isokinetic test data commonly used in the clin­ ical setting. Unfortunately, this method fails to account for differences in strength that may arise from hand dominance, sports activity, occupa­ tional demands, and preexisting injury. Com­ mon disagreements on whether strenglh differ­ ences occur between the dominant and nondominant sides provide a dilemma for clini­ cal consideration. lvey et al.,29 Connelly-maddux et al.,'8 and Reid et al.28 found no statislical dif­ ference between dominant and nondominant sides, ,while Alderinck and Kuck 13 concun'ed with the exception of shoulder adductors and ex­ tensors. In contrast, Cook et al.27 and Coleman3o described strength differences between sides in baseball throwers, and Davies3 determined 10 to 25 percent differences between nondominant and dominant extremities. Perhaps, then, a small strength difference should be expected in a pa­ tient with vigorous and repetitive occupational or sports use of the dominant arm, but normal use in activities of daily living (ADLs) does not produce an expectation for greater peak torque of the dominant side. When possible, industrial or sports pre­ screening with isokinetic testing provides an ideal situation to establish "normal" values for a given individual that are useful if injury or dys­ function occurs.

Treatment Protocol$ In general, isokinetic rehabilitation of the shoul­ der can be initiated when the joint complex has progressed to tolerance of resisted exercise through a given ROM. Fractures, dislocations, muscle tears, and other soft tissue injuries should be well healed, stable, and past the acute

E VA L UA T I O N

AN D

TRE A T M E N T

409

Exercise progress iol1 bas e d on the time/healil1g stages (earliest to latest)

TABLE 16.3

Multiple-angle isometrics (submoximal effort) MultipJe·ongle isometrics (maximol). inertial Short·orc concentric isokinetics Isubmoximal), inertial Short-arc isotonics Short·arc concentric isokinetics (maximal) Full ROM concentric isokinetics {submaximal) Full ROM isotonics Full ROM concentric isokinetics (maximal)

(Adapted (rom Davies, j with permiss;oll.)

stage. Although full active ROM is not required, it should be painless at its extremes. [n postsurgi­ cal cases, knowledge of the surgical procedure (review of the dictated surgical report is ex­ tremely helpful) is essential in determining di­ rection of resisted movement. Table 16.3 reviews resistive exercise progressions that are effective preparatory stages for isokinetics and indicates the appropriate timing of isokinetic resistance modes. Isokinetic training should be applied after consideration of patient position, dynamometer position, and attachments. In addition, the pa­ tient's scapular control, parameters of repeti­ tion, rest periods, speeds, allowable ROM for the particular pathology, and stage of healing should be considered. Despite careful clinical planning with isoki­ netics, some patients will respond negatively with val"ied inOammatory responses of the ten­ don, capsule, and synovium, requiring immedi­ ate treatment. The use of cryotherapy postisoki­ netics is useful to prevent such symptomatic responses. Our clinical expel"ience, in agreement with Engle and Canner.'9 indicates that each isokinetic training session should be followed by continual reassessment of program tolerance and results, and progression to more challenging training should be preceded by two or three trial sessions of fixed intensity. [n all cases of painful arc, joint restriction, and instability, approptiate use of SlOps to block movement is necessary, especially when using faster speeds in excess of 1800/s. Blocking may

410

PHY S I C AL

T H E R A PY

OF

T H E

S H O UL D E R

be produced manually or as a function of the dynamometer with mechanical or electronic technology. Each patient problem dictates indi­ vidualized blocking; however, anterior glenohu­ meral instability problems require restriction of external rotation with abduction, while posterior instability requires restriction of internal rota­ tion with Oexion. In choosing which speed to use in isokinetic rehabilitation, several criteria are used. The most simple determination is based on the evalu­ ation. For the most part, low-speed torque defi­ cits require low-speed training, whereas faster speeds are used for high-speed deficits. Often, however, deficits occur at both testing speeds, as the curves in Figure 16.2 indicate. In this case, a helpful guideline is the "25 percent rule." That is, if the strength deficit at the 60'/s testing speed is greater than 25 percent, rehabilitation at that speed is indicated. If the deficit is less than 25 percent at the lower testing speed, training should be at 180'/s or faster. There are several exceptions to this rule. As mentioned previously, the need to reduce joint reaction forces may necessitate high-speed train­ ing even though major deficits at the low testing speed are found. The same is true for a painful joint when the patient will not tolerate move­ ment at the indicated speed. Contractile pain is usually less at faster speeds, although occasion­ ally slow-speed exercise is tolerated belter. Other ways of lessening pain include submaximum ef­ fort and short-arc contraction, which avoids pain localized to a portion of the ROM. Some general guidelines for selecting speeds and pain­ reducing protocols are listed in Table 16.4. Sub­ maximum effort training is sometimes done for a few treatment sessions prior to actual testing of a patient who is not yet ready for the maxi­ mum effort contractions that are necessary for bilateral strength comparisons. Eccentric isoki­ netics also present a major contrast to concentric speed selection. Because of inherent force-ve­ lOCity curve differences between eccentric and concentrics, eccentrics speeds for the shoulder must be much slower for both early and ad­ vanced applications. A useful clinical speed spec­ trum for a variety of diagnostic and patient con-

TABLE 16.4 Guidelil1e s {or isokine tic spe e d {lI1d pro to col sele ctio n il1 shoulder re habilitatio n 150KN I ETIC SP EED

P R OT O C O L.

t . Strength de�cit > 25% 2. Potient too weak to generate torque at higher speeds J. High-speed mevement toe painfvll t. Strength de�cit < 25

60"/s

180"/s

Velocity spectrum protocol Short-orc contraction Submoximum effort contraction

2. low-speed controction too painfvl 3. Decrease joint reaction forces Trein at several speeds; simulate speeds used in normal activities To ovoid painful ranges; possible instability at end range 1. Not ready for maximum effort at ony speed due 10 poin, inAammation, incomplete healing, etc. 2. Poor tolerance to initiol test done ot maximum effort

siderations is 30'/s to 180'/s with common starting speeds of 60'/s to 120'/s.

General.

Test and Warm-Up

CO'fISiileratWns Before maximal-effort isokinetic tesiing, it is im­ portant to provide a warm-up stimulus to in­ crease intra-articular temperature and influence the viscoelastic properties of collagenous tissues to reduce strain potential. Warm-up sessions can consist of upper extremity repetitive, low-load isolonics, and/or submaximal aerobics for up to 5 minutes' duration, avoiding muscular fatique. Apparatuses such as the Schwinn AirDyne (Schwinn Bicycle Co., Chicago, IL), UBE (Cybex, Ronkonkoma, NY), or the pulley mechanism of the Nordic Trak (Chaska, MN) can all provide the aerobic component. Warm-up repetitions are then provided on the dynamometer with 5 to 10 graduated efforts at 120'/s and five warm-ups at each test speed. As a general rule, test speeds will vary fTom

I S O KI N E T I C

600/s to 3000/S.27 Based on clinical expe.-ience, 600/s is excessively slow for initial training and test speeds because of the production of large shear forces that are contraindicated in cases of acute injury, capsular sprains, and joint instabil­ S ity. Davies3 and Soderberg and BlaschakI sup­ port early clinical training with intermediate speeds (1200/s to 1800/s) and gradual change to velocity spectrum rehabilitation protocol (VSRP) with increased velocities up to 3000/s and, finally, incorporating slow speeds 600/s to 900/s) du.-ing late-stage rehabilitation. As de­ scribed by Wallace et al.,31 1200/s is easily con­ trolled and tolerated by most individuals and provides the basis for our preferred initial wal-m­ up speed. Maximal effort testing of the glenohumeral joint after most traumatic injuries, arthroscopy, rotator cuff pathology, or arthrotomy should not be instituted until good tolerance of submaximal work has been demonstrated, at least 1 month after the procedure. Retest sessions should be scheduled at I-month intervals to avoid negative reinforcement to the patient, owing to the pre­ dicted gradual changes in muscle physiology and force development that may manifest only 5 per­ cent increases per week.32 Questions regarding numbers of repetitions and frequency of training sessions are difficult to answer because there is great variability among patients and the conditions requiring rehabilita­ tion. A recommended starting protocol for low speed diagonal training is 60 repetitions (e.g., six sets of 10 repetitions) at 1200/s. To avoid overuse, patients work out no more than three times a week at regular intervals, with repetitions added depending on tolerance, until 90 repetitions are pelformed. High-speed training can be progressed in a similar way at 1800/s, although Davies3 recom­ mends the use of several speeds at each session, using the VSRP-' Patients may build up to three sets of 10 at three different training speeds. Table 16.5 is an example of VSRP. in general, when retesting shows strength deficits to be reduced to 10 percent or less, isoki­ netic training is discontinued. It is important to emphasize functional activities and ongoing

EV A L U A T I ON

TABLE 16.5

AND

T R E A T M EN T

411

Velocity spectnllll re habilitatiol1

protocol REPETITIONS PER SPEED

10

60-90-120-150-180-210-180-150-120-90-60

(Adapled (rom Davies,J wil" penllissioll.)

home exercises at this stage to promote full re­ covery.

Updn.ted NorrJULtive and Punctinnal CO'I1Si.derations Updated literature provides a clear consensus on isokinetic torque normative data trends, but, it remains difficult to make precise comparisons of isokinetic norms due to large methodologic variations in test devices, patient populations, patient test positions, and test speeds used. This section will review several areas of data impor­ tant in clinical judgement and patient program management with respect to normative data for speCific sports, sport-specific torque shifts ex­ pected as a result of training, limited perspec­ tives on functional inferences (validity), and ec­ centric Lo concentlic ratios for individual muscles.

SPORT-SPECIFIC NORMATIVE DATA

Although exact etiology is not yet proven, many studies concur that the propulsive phase (power or accelerative phase) of overhead upper extrem­ ity and shoulder motions produce a clear torque ratio shifts in many athletes, specifically in base­ ball, tennis, and swimming.34-37 Athletic torque ratio shifts are most apparent for the external to interna1 rotation ratios and fOl- the abduction to adduction ratios. Possible training induced changes create disproportionate increases in the torque levels of the propulsive muscles, the ad­ ductors, and internal rotators, without concomi­ tant increases of external rotation or abduc­ tion.13.34-36 McMaster et aP4 found 52 percent

412

P H Y S I C AL

TABLE 16.6

T H ERA P Y

O F

T HE

S H O ULDER

Sport-specific 170mwlive torque ratios

STU OY

Beach et 01. 37 (hondler el 01." McMoster et 01.3'4 McMaster el 01.38 Ng and Kromer39 Wilk et ol."'o wilk el 01:" wilk et ol."2

POSITION

POPULATION

28 OJ,,. 1 swimmers 24 College tennis players 27 College swimmers 15 Olympic-level water polo players 20 Female college tennis players 83 Pro baseball players 150 Pro baseball p;lchers 50 Pro baseball pitchers

ABO/ADD

Prone 900 oW. Supine 90" abel. 45" obd

56% NA Men 48% Women 48% 65-68% NA 78-84% NA NW 93-72% W 77-89%

NA Scapular plane Sitting, frontal plane Sitting, 90° abd. Sitting, frontal plane

ERlIR

70% 60-70% 45-57% 57-74% 67-75% 78% 65-75% 61-65% NA

Abbrev;aliotts: NW. llOl1willdowed data; W, windowed data.

greater torque ror intemal rotation and 43 per­ cent greater torque ror the adductors in compar­ ing swimmers to nonswimmers, while Alderink and Kuck round similiar increases of 50 percent greater adduction in the throwing side for base­ baJJ players compared to nonthrowers.13 Both Chandler et aL 35 and Brown et al.36 demon­ strated ERIIR ratios in the nondominant side of tennis and baseball players despite no dirfer­ ences in the extemal rotation torque between sides, which ful"lher demonstrates the torque shifts from increased internal rotation/adduc­ tion torque. Table 16.6 reviews sport-specific normative torque ratios and pertinent informa­ tion on the tested populations and patient posi­ tions used in data sampling. Although few stud­ ies have reported on horizontal abduction to horizontal adduction, Weir et aL 4 3 established a 100 percent ratio in high school-aged wrestlers. In addition, Weir et al. demonstrated a signifi­ cant increase in torque for both motions at slow speed as wrestlers aged from freshmen to senior years. This trend of increased tOt-que as ages change from 14 to 18 is worthy or further study ror other sports and certainly would be benericial information for other muscle group torque ra­ tios. TORQUE RATIOS IN NORMALS

Normative data for athletes is important, but in most orthopedic/sports clinical settings, pa­ tients with shoulder complaints are not highly

trained athletes, and expected torque ratios will more closely conform to predicted levels ror nonnals. Tala et al 4 4 demonstrated abduction/ adduction ratios of 100 percent to 102 percent and external/internal rotation ratios or 78 per­ cent to 87 percent for healthy males and re­ males. Joy's found external/internal rotation ra­ tios of 65 percent and abduction/adduction ratios of 70 percent to 81 percent for college­ aged females. Although the variations in exter­ nal rotation may be explained by the use of different dynamometers (Tata et aI., Kincom, Joy, Biodex), the large variability between ab­ duction/adduction ratios may be explained by the test positions used. Tata et al. used plane of scapular position, while Joy used a [Tontal plane position. Tata et al.'s study rurther sug­ gested that the scapular plane is more clinically appropriate for testing and training, a view­ point shared by the first author or this chapter for nonathletic patient cases. Finally, McMaster et al.34 round externallinternal rotation ratios of 65 to 78 percent and 58 to 74 percent for healthy

males

and

females,

respectively.

McMaster's abduction/adduction ratios were 65 to 72 percent and 62 percent ror males and females, respectively. This inrormation, coupled with the data outlined in Tables 16.2 and 16.6, provides a comprehensive overview of male and remale nonathletic and athletic norms for the agonist/antagonist ratios that are important pa-

I SO K I N E T I C

rameters of muscle synergy in the shoulder complex.

ECCENTRIC TO CONCENTRIC TORQUE COMPARISONS

Although important clinical information is man­ isfested by the agonist/antagonist ratios, another isokinetic measurement parameter, the eccen­ tric/concentric torque ratio [rom a single muscle, may provide guidelines regarding normal mus­ cle function versus injury or dysfunction. Al­ though extensive additional literature on this CUITent topic is walTanted, it appears that the relationship of eccentric and concentric function is important to injury prevention, assessment, and rehabilitation issues '· Generally, eccentric torque potentials exceed concent';c torque lev­ els in any given muscle, speed, or position con­ sideration.46 Therefore, the eccentric to concen­ tric ratio will be expected to be minimally 100 percent. Ng and Kramer'9 found ratios of 1 19 percent and 127 percent for internal and exter­ nal rotation, while Joy45 found similiar levels of 129 percent and 123 percent, respectively. In addition, Joy delineated ratio of 1 3 1 percent and 1 1 7 percent for abduction and adduction, respectively. The actual peak performance of eccentric torque may not be sampled accurately at speeds of 180°/5 or slower as in the above studies, but due to intrinsic characteristics of the isokinetic-eccentric loading, patient safety may preclude testing speeds above 1800/s. Mont et al.4 7 determined tennis players' isokinetic perfOlmance for both external to internal rota­ tion ratio and eccentric to concentric force ratio that appears widely variant h·om all other sam­ pled studies and the first author's clinical expe­ rience.

FUNCTIONAL INFERENCES AND RELATIONSHIPS

Although controversy exists about functional in­ ferences (or validity) from isokinetic measure­ ments, much of the criticism of isokinetics re­ lates to the common use of peak torque measurements in predi The dry form resembles osteoarthritis in that sclerosis, rimming osteo­ phytes, and loss of joint space occur. 1l is some­ times referred to as "mixed arthritis." The wet and resorptive forms are characterized by severe bone loss, bone erosion secondary to pannus, and central glenoid wear with "centralization" of the humeral head (Fig. 20.2). Synovial prolifera­ tion and hypertrophy can be marked, requiring aggressive synovectomy as part of the operative procedure. In rheumatoid shoulders, contracture and

FIGURE 20.11 Gravity-elilllil1ated f/exiol1 i/1 the sidelyi/1g positio/1. A hardside suitcase with a towel draped over it works well to sLipport the ann.

shortening of ante,-ior soft tissues is rare, and external rotation is easily achieved without sub­ scapularis lengthening. Rotator cuff defects are usually repairable, and acromioplasty is seldom indicated. Occasionally, severe bone 10 s, ero­ sion, and centralization of the humeral head make glenoid replacement and cuff repair inad­ visable. These patients are placed in a "limited goals" rehabilitation program, which will be dis­ cussed later.

I I I /

/

/

ARTHRITIS OF DISLOCATION

Degenerative arthritis that is the result of recur­ rent dislocations of the glenohumeral joint or of a surgical procedure for anterior or posterior dis­ locations that displaces the humeral head to a po­ sition opposite the surgical approach is referred to as arthritis of dislocation. In most shoulders, the head subluxates posterioriy following an an­

Active assisted elevation with a stick in the plane of the scapLila. FIGURE 20.10

terior approach for a procedure to correct recur­ rent anterior dislocations. In others, a unidirec­ tional

surgical

approach

was

used

for

a

TOTAL

SHOULDER

467

R EPLACEMENT

I

FIGURE20.12 Beginning inlenw/ rOlalioll and extension exercise using a stick.

\ \ \ \ \ \ I I I I I I

(�:C�-_-�:-::"-_I

P,

, '

, I , ,

L.I

multidirectional instability problem with resid­ ual inferior instability causing persistent symp­ toms. Most patients in this group are under the age of 4S at the time of the shoulder replacement. Special problems encountered duringarthro­ plasty in patients with arthritis of dislocation are often related to the initial procedure for instabil­ ity. These problems include previous surgical scars associated with cutaneous neuromas, scar­

changes in the version of the humeral and gle­ noid prosthetic components. Modifications in the rehabilitation program are made depending on the degree and direction of instability noted preoperatively and intraoperatively. Retained hardwal'e is common in shoulders that have had previous surgery. Any intra-articu­ lar hardware, including any previously placed screws or staples, should be removed.

ring and atrophy of the anterior deltoid, and sub­ scapularis contracture that severely restricts ex­

OSTEONECROSIS

ternal rotalion.

Osteonecrosis or avascular necrosis can be the result of trauma, steroid use for systemic disease, alcohol abuse, or other causes. Only the femoral

Glenoid wear is usually pronounced when the humeral head is located eccentrically in the glenoid. Altering the version of the glenoid com­ ponent is preferable to glenoid bone grafting in most shoulders. Stretching of soft tissues to ac­ commodate a chronically subluxating or dislo­ cating humeral head must be addressed with a capsulon'haphy to balance soft tissues and to sta­ bilize the prosthesis along with cOlTesponding

head has a higher incidence of nontraumatic os­ teonecrosis than the humeral head. Neer2 and others"·l2 have divided osteonecrosis into four stages. Stages 3 and 4 of osteonecrosis usually require prosthetic replacement. In stage 3, the humeral head displays collapse of subchondral bone with a normal glenoid articular surface

468

PHYSICAL

THERAPY

OF

THE SHOULDER

� --....\

--,'

)

(

/

�

"

../

B

A FIGURE20.13

(A) Ten'llil1al stretching (or elevatiOll. (8) External rotation tvith a Ivall.

(Fig. 20.3). In these patients with an intact gle­ noid, humeral head replacement alone is indi­ cated. Total shoulder replacement is reserved for patients with stage 4 osteonecrosis, with marked degenerative changes of the humeral head and glenoid al1.icular surfaces (Fig. 20.4). The rotator cuff and biceps tendon are usually intact in these patients. CUFF TEAR ARTHROPATHY

mechanical factors contribute to this degenera­ tive process. Gross instability of the glenohu­ meral joint develops, and the humeral head mi­ grates cephalad causing wear into the acromion, acromioclavicular joint, and coracoid process. All patients treated with humeral head replace­ ment or total shoulder replacement along with rotator cuff repair are placed in a limited goals rehabilitation program postoperatively with em­ phasis on pain reduction and stability instead of function.

Neer described cuff tear arthropathy in 1975 as severe destruction of the glenohumeral joint

POST-TRAUMATIC ARTHRITIS

with humeral head collapse and a massive rota­

Arthritis related to previous fractures or frac­ ture-dislocations of the proximal humerus or glenoid is treated with prosthetic replacement in

tor cuff tear in the absence of other known etio­ logic factorsS A combination of nutritional and

) ,f , '" " " '

,

:

1-/ v

,,

,

/'

"

FIGURE 20.14 Elastic resistive exercises {or 'he glenohumeral joil1f. ElbolV is flexed 10 900'° decrease lever arm slress.

469

470

PHYSICAL

THE RAPY

OF

THE

SHOULDE R

Postoperative rehabilitation must be individ­ ualized for these patients, with close communi­ cation between the surgeon and therapist. Early restoration of passive motion prevents reforma­ tion of unwanted scar tissue that blocks motion. Patients with preoperative instability and dislo­ cation must restrict motion in provocative posi­ tions to avoid prosthetic dislocation . One year of exercise is required to regain full motion and strength in these patients.

RelwhiJ:itatUm The rehabiliation of a patient who has had a total shoulder replacement should be like that of any other total joint replacement rehabilitation pro­ gram. The primary reason for undergOing the surgery is pain relief, and the secondary goal is improvement of function. In our attempts to as­ sist these patients in recovery, we must keep these goals in the con'ect order. It is velY easy for the therapist to focus on the functional as· pects too intently and sacrifice the primalY goal of decreasing pain. This is not to say patients will not have any discomfort as they rehabilitate their

Assisled elevation wilh slick (allowed by isomelric hold al end rQl'ge independelllly, (allowed by aClive eccenlric lowering as loleraled {shown above}. II is usually reconlllle"ded 10 Ihe palielll 10 keep Ihe slick close 10 Ihe ann 10 aid ill support in lowering, especially i( Ihe palielll has a pai"(1I1 or iveak arc. FIGURE 20.15

some patients. The procedure can be compli­ cated by soft tissue scatTing, bone loss, retracted

shoulders; however, it should be monitored and minimized. Along with these goals, the immedi­ ate postoperative goals for rehabilitation are to prevent glenohumeral contracture while simul­ taneously protecting the prosthesis, rotator cuff, and deltoid. It is critical for the therapist, doctor, and patient to have reasonable and clear goals going into surgery.

CATEGORIES OF REHABILITATION

julies. Retained hardware and deltoid deficiency

Rehabilitation after shoulder replacement should be individualized to the needs of the pa­

from previous failed surgeries often complicate

tient and related to the goals of the procedure.

tuberosities, malunion, nonunion, and nerve in­

the situation further and elevate the risk for in­

J n general, however, there are three categories

fection with subsequent procedures.

of rehabilitation programs: (A) programs for pa­

Special attention should be given to the re­

tients with a good rotator cuff and deltoid, (B)

pair of a torn, retracted, and scarred rotator cuff

programs for patients with a poor rotator cuff

to maintain proper deltoid tension and restore

and deltoid, and (e) limited goals programs.

normal humeral length and glenohumeral ver­ sion.

The first two categories are designed to acco­ modate the patient's rotator cuff status and del-

TOTAL

SHOULDE R

R E PLACE ME NT

471

FIGURE 20.16 Scapliol1 is elevaliol1 of Ihe ami il1 lite scapular plal1e 10 slrenglhel1 Ihe deltoid, supraspinarLls, and lrapel.ius.

toid integrity. The third category is included for those patients who have one or a combination of the following pathologies that leads to total shoulder arthroplasty: rheumatoid arthdtis, pre­ viously failed rotator cuff repair, rotator cuff arthropathy, Erb's palsy, or previously failed total shoulder arthroplasty. The following guidelines can be used by the clinician to develop an individualized rehabilita­ tion program based on the status of the rotator cuff and deltoid musculature. It is important to listen to the patient's comments, as this will guide the rehabilitation progress. The time lines in Appendix 20. 1 A-C are merely sugges­ tions for rehabilitation progress. It is more im­ portant to listen to patients regarding their progress.

Sidelyil1g exlerrlal rolalion 10 slrel1glhel1 Ihe infraspil1alus is usually per{onued wilh a small pillow under Ihe elbow. FIGURE 20.17

Patients in the limited goals program are placed in this category based on the recommen­ dation of their surgeon. Pain relief is the primary goal of surgery for these patients. Full return of

472

PHYSICAL

THERAPY

OF

THE SHOULDER

Lifting the Arm The initial treatment session is by far the most impOliant step in any shoulder rehabilita­ tion program, because it sets the stage for the rest of the process. If this session is good, the patient develops trust and confidence in the ther­

"

I I

I

,

I

, ,

}

\

I I

I

\ \ \

I

�

1

Within the first minute or two, the therapist

knowledge of the surgical procedure and its post­

,

-.:,1...

,

throughout the healing process.

dividual patient. Here is where the therapist's

\, r\ \ I

patient resists the passive motion or has pain, the patient will associate pain with rehabilitation

must dete,-mine the best way to approach each in­

, ' \

,

apist. However, if the session is bad because the

t\

�,�

F I GURE 20.18 Prone extension is used /0 strengthen the teres minor and posterior de/wid. I( the patient is LIIwble to lie prone, he or she can simply lean (onvard 10 a com(0I1able positiol7 al7d lean 017 the ,ma((ected arm (or support.

function is not an objective. Frequent communi­ cation between the surgeon and therapist is needed to determine the appropriate time for re­ habilitation to begin. The time frame described in Appendix 20.1 C is very conservative and should be modified according to individual needs and re­ sponse to the rehabilitation program. CRITICAL POINTS AND TECHNIQUES

C0I1I111UnicQlion Communication between surgeon and thera­ pist, whether wrillen or oral, is c,itical. The sur­ geon's opinion regarding the status of the re­ paired tissues and the prosthetic components guides the therapist in choosing a protocol and selling realistic goals for the patient. For exam­ ple, if the surgeon had to antevert the glenoid component more than normal, the amount of ex­ ternal rotation the patient could expect to re­ cover would be lessened. If full external rotation is forced in such a patient, the 'isk of shoulder dislocation would be high.

operative progress is needed. Having this knowl­ edge gives the patient confidence in the thera­ pist's expertise. From a technical standpoint, the therapist and the patient should be in a comfortable posi­ tion before performing the passive range of mo­ tion. Hand placement is also very important. In general, the more proximal placement of the ther­ apist's hand on the patient's arm, the beller. The patient will sense the therapist has beller control of his or her arm and will not have a tendency to actively move it (see Fig. 20.6).

Per(onning Extemal Rota/iol1 When externally rotating the patient's arm, watch the position of the humerus. If the hume­ rus is posterior to the midline of the body, the amount of external rotation will be lessened and more painful to achieve. In extension, stress will be placed on the sutures in the anterior struc­ tures.

Exercise Prescription Most patients who have a total shoulder re­ placement are elderly and may have other medi­ cal problems; therefore, the volume of exercises should be kept at a reasonable level. Patients are generally very compliant in the early stages of rehabilitation because they do not want to jeop­ ardize the results of their surgery and they want to get the arm moving again. Keep the number of repetitions low-in the 5 to 10 range-and the frequency at 2 to 4times each day. Some patients

TOTAL

I I I I

I I

FIGURE20.19 Prone horizolllal abductioll is used 10 strengthen the supraspilwtus. Watch (or scapular subs/ilution when supraspillatus is weak.

I I , I I \ I I I

'

I I

SHOULDER

R EPL ACEMENT

473

I I I

r'

I I I I I I I I ,

\

Ii �, �/ h r\

���

will want to do more, but it is very easy to i'Titate

elastic resistance exercises, or both. On the other

the rotator cuff tendons when initiating passive

hand, if a patient is having pain with isometrics,

range of motion, active assisted range of motion, and light resistive exercises. The patient's re­ sponse after the first 2 to 3 days of new activities

reduce the pain and still accomplish the goal of

should serve as a guide for modifying the pro­ gram to reach the patient's goals with minimal discomfort.

Resistive Exercise Progression Resistive exercises typically follow this pro­

switching to gravity eliminated activities might increasing strength and active range of motion.

Special COl1sideratiol1s When osteoarthritis is the disorder necessi­ tating total shoulder replacement, posterior gle­ noid wear and acromioclavicular joint involve­ ment is common. From a rehabilitation

gression: isometric, gravity eliminated molion .

standpoint, glenohumeral elevation in the pure

active assisted range of motion, isometric hold at end range of active assisted range of motion

frontal plane (Oexion) is contraindicated be­

with eccenlric lowering, active range of malian,

cation. Therefore, elevation activities for these

cause of the chance of posterior shoulder dislo­

light elastic resistance below shoulder level, light

patients are best perfomled in the plane of the

dumbbell resistance, modified activities, and full

scapula. Early in the rehabilitation process, ex­

relurn to activities. Again, the patient's response to the exercises

to the freshly shaved ends of the acromion and

cessive horizontal adduction can cause pain due

determines the progression of the program. For example, if a patient is moving the arm actively,

clavicle.

comfortably, and biomechanically correctly, it would not be inappropriate to move directly

much slower to recover than osteoarthritis pa­ tients. Because of the systemic nature of the dis­

from isometrics to active range of motion or light

ease process, other joints, such as wrist, hand,

Rheumatoid arthritis patients are generally

474

PHYSICAL

THE RAPY

OF

THE SHOUL DE R

and neck, are involved. Typical exercises for

their total shoulder arthroplasty patients. Before

these patients must be modified to avoid aggra­

such a program can be developed, however, a

vating these other joints. Osteopenia is often

thorough understanding of the surgery and the

present, and many patients have rotator cuff

purpose of the surgery is needed. Each surgeon

tears.

will have his or her own philosophy, and the re­

In these

patients, rehabilitation must

progress slowly and without force. [f the patient

habilitation program should reflect that. It is a

is nonambulatory when undergoing total shoul­ der arthroplasty, transfers should not be done

team approach that benefits the patient the most.

independently for approximately 5 to 6 months. Avascular

necrosis

patients

who

often

undergo a humeral head replacement only, are typically younger than the average total shoulder patient, and their musculotendinous structures are not involved. For these reasons, these pa­ tients often progress rapidly through the rehabil­ itation process as long as they are motivated and no complications arise. Patients who develop arthritis after disloca­ tion also have need of a modified postoperative program. By the time total shoulder arthroplasty is indicated in these patients, they have usually had I or 2 previous operations. They have shoul­ der stiffness and are apprehensive about un­ stable positions of the arm. The deltoid and sub­ scapularis

muscles

of

their

shoulder

References I. Pean IE, Bick EM (trans): The classic on pros­ thetic methods intended to rcpair bone frag­ ments. Clin Ol�hop 54:4, 1973 2. Neer CS: Glenohumeral al�hroplasty. p. 143. In: Shoulder Reconstruction. WB Saunders. Phila­ delphia, 1990 3. Neer CS: Replacement arthroplasty for glenohu­ meral osteoarthritis. J Bone Joint Surg 56A:1, 1974 4. Corield RH: Unconstrained total shoulder pros­ thesis. Clin Orthop 173:97, 1983 5. Neer CS, Craig EV, Fukuda H: Cuff-tear arthro­ pathy. I Bone Joint Surg 65A:1232, 1983

are

6. Post M, Gdnblat E: Preoperative clinical evalua­

predisposed to retears because of the previous

tion. p. 41. In Friedman RI (ed): Arthroplasty of

surgery. The surgeon's recommendation that these structures be protected for a longer period can delay rehabilitation. Cuff tear arthropathy patients have massive rotator cuff tears and severe deterioration of the glenoid and humeral head. Surgeons often have to modify the version of the prosthesis and split the subscapularis muscle to obtain closure of the rotator cuff. These patients almost always are placed in the limited goals program.

the Shoulder. Thieme, New York, 1994 7. Neer CS, Kirby RM: Revision of the humeral head and total shoulder arthroplasties. Clin Ol�hop 170:189,1982 8. Nee,- CS. Welson KC, Stanton FJ: Recent experi. ence in total shoulder replacement. J Bone Joinl Surg 64A:319, 1982 9. Friedman RJ: Total shoulder al�hoplasty in rheu­ matoid arthritis. p. 158. In: Shoulder Reconstruc­ tion. WB Saunders, Philadelphia. 1990 10. Friedman RI, Thornhill TS, Thomas WH, Sledge CB: Nonconstrained lotal shoulder replacement in patients who have rheumatoid arthritis and class TV function. J Bone Ioint Surg 71A:494, 1979

Summary The purpose of this chapter is to provide sugges­ tions and guidelines for clinicians who are estab­ lishing individual rehabilitation programs for

II. Ficat P, Arlet J: Necrosis or the remonll head. p. 53. In: Ischemia and Bone Necrosis. Williams & Wilkins, Baltimore, 1980 12. Springfield OS, Enneking WJ: SurgelY of aseptic necrosis ofLhe femoral head. Clin Ol�hop 130:175, 1978

APPENDIX 20. 1

Rehabilitation Programs Following Total Shoulder Replacement CATEGORY A Postoperative Rehabilitatiol1 Program (or Total Shoulder Arthroplasty-Good RotGtor Cuff and Deltoid

Day 1

Days 2-3

Home Program Precautions Weeks 1-2

Arm is pos in c sling. Out of bed. into choir and ambulating. Elbow, wrist, ond hand active range of motion. Possive external rotation with 0 slick to poin tolerance and not beyond 30" (Fig. 20.5). Possive pendulum motions by therapist. Family members ore instructed in technique of passive forward elevation fOr rehabilitation at home (Fig. 20.6). Passive forward elevation in the plene of the scopula. When 1200 of elevation is possible, the patient begins using 0 rope ond pulley to elevate the arm (Fig. 20.7). Instruct patient in odivities of doily living. Discharge from hospitol. Passive external rotation with stick to 300. Passive forward elevation with family member; progression to use of rope and pulley. Elbow, wrist, and hand active range of motion. No lifting with involved orm. Shoulder extension is limited. Elbow not 10 go behind midline of the body. Review home program and modify as appropriate. Begin scapular stabilizing exercises within pain toleronce (Fig. 20.8). Retraction and Elevation and f ressian Begin glenahumera jaint isometrics with elbow Aexed (Fig. 20.9). Flexion, extensian, abduction Internal and external rotation Begin active assisted elevation (Fig. 20.10) or gravity-eliminated active range of motion in elevation and external rototion (Fig.

Weeks 4-6

Weeks 10-12

20.17).

£

Weeks 2-4

20.11).

Correct scopulohumerol rhythm should be maintained during these exercises. Activities of doily living to tolerance keeping the arm below shOulder level.

Begin extension and internal rotation stretches (Fi g. 20.12). Terminal stretching for elevation and external rototion (Fig. 20.13). Light elastic resistance exercises replace isometrics performed with elbOw Rexed to 90" and below shoulder level (Fig. 20.14). Flexion, extension, and abdudion in the p)one of the scapula (scoption) Internal and external rotation Assisted elevation of arm with stick, wall, or rope and pulley with isometric hold at end range followed by active eccentric Iowe.-ing to poin toIeronce (Fig . 20.15). light dumbbell program replaces elastic resistance. $caption-elevation in the plane of the scapula (Fig. 20.16). Sidelying or prone external rotation (Fig.

Months 5-6

Prone extension (Fig. 20.18). Prone horizontol obduction (Fig. 20.19). Upon obtaining 85 percent of normal adive range of motion of the shoulder and 0 manual muscle testing score of ot leost four out of a possible five for anterior deltoid, internal, and external rotators, modified sport odivities are allowed; short irons and pu�ing for golf, and groond strokes in tennis. Full return to sport with full odive and passive rang e of motion. Modified weighrlihing program (elbow does not pass midline of body). Continue stretching and strengthening program independenrly. lsokinetic testing is allowed, if necessary.

475

476

PHY SIC AL

THE RAPY

OF

THE

S H OUL D E R

CATEGORY B Postoperative Rehabilitation Program (or Total Shoulder Arthroplasty-Poor Rotator Cuff and Deltoid

CATEGORY C

In Hospital

Lill1ited Goals Program In sling with obduction pillow. Elbow, wrist, and hond active range of

Day I

In a sling with obduction pillow of varying size, or airplane splint. Out of

molion. Weeks 2-3

f.Aay or may nol begin passive forward

bed into choir and ambulating.

elevation in the plane of scopula with

Elbow, wrist, and hand active range of motion. Day. 2-3

Passive pendulum with therapist to tolerance. Family member is instructed in technique

ossistonce of family member. Week 6

Remain in sling for another 3 to 6 weeks for

rehabilitation at home.

activities of doily living.

May or may not begin passive external rotation

Begin passive external rotation in limited

with stick, to pain tolerance.

range 10" to 20",

Discharge from hospital. Program Precautions

Begin scopular stabilizing exercises in poin

Passive pendulum. Elbow, wrist, and hand active range of motion. Passive external rotation with stick.

tolerance. Weeks 12-14

If in obduction pillow sling, do not let arm

tolerance. Months 4-5

rolation. Passive forword elevation in the plane of the scapula. Instruct family member to 120"; progress to rope and pulley. Passive external rotation with stick to 30°. Week. 4-6

Begin scapular stabilizing exercises within pain tolerance. Begin glenohumeral joint isometrics with elbow Rexecl within pain tolerance.

Week. 6-8

Begin active assisted range of motion exercises or gravity eliminated exercises for elevation and external rotation exercises with appropriate scapulohumeral rhythm as available. Begin terminal stretching for elevation and external rotation. Begin gen�e internal rotation stretches.

Week. 8-10

Replace isometric exercises with light elastic bond exercises below shoulder level. Assisted elevation of arm with stick, wall, or rope and pulley with isometric hold at end range and active eccentric lowering.

Week. 1 2-14

Replace light elastic bond exercises with light dumbbell exercises. Focus on correct scapulahumeral rhythm with active range of motion of shoulder.

Begin light elastic resistance exercises. Progress to active elevation activities as poin

come into adduction, extension, or internal Week. 1 -2

Begin isometrics. Begin gravity eliminated activities within pain

No active range of motion activities for the shoulder.

Begin passive forward elevation iF nol started previously.

of passive forward elevation for

Home

Sutures removed.

allow•. Reasonable Outcomes

Active elevation to 1200. Active external rotation to 30". Goal of pain-free use of arm belaw shoulder level.

Months 5-6

When 85 percent of available active range of motion is possible and anterior deltoid and internal and external rolator cuff strength reach four (out of a possible five) on manual muscle testing, modified sport and weightlifting activities are allowed as tolerated. Continue terminal stretching in elevation and in external and internal rotation.

Index Page numbers rollowed by r indicate figures; those followed by t indicate tables.

Abduction of !>houldcr. See {lisa Eleva­ tion of !>houldc,in active range of

11101 ion

in total shouldcn-epiacement, 462,

assess­

ment,63-65.64f, 136-137 biol11cchanic.!. of,3-5, 4f,99-100, 100f

with extcnsionJintcmaJ rotation

arthrokinemmics in.3-5, 4f

Acromioclavicular ligament.10 in elevation of �houidcr. 280 f,.aclures of. 449. 451 f impingement of humeral grealer tuberosity undel� in hemiple­

muscles in,S,6,7. I tr-13f,

gia, 207,207f

II 14 ostcokinematics in, 1-3. 2f, 3f in exercise program for throwing injuries of shoulder,29,29(, 30. 30r. 32,32f, 36-37,37f,38r. 49f,51 in isokinctic exercise with cxtensionlinternal rotation movements,403-407,404f, 405f,406f with nexionlcxtcrnal rotation movement!.,40M, 407 in scnpulm" plane. 1-2.2[, 3f in Mrcnglhening c.'(crciscs, 249f, 251r. 252f,370f,372f. 473f lesling or, 691, 72.171 Absolute muscular endurance. 365-366,373 AccessorV' motion in joint mobility,68. 72 Acromidchoid mu�clc, in gleno­ humeral �tability,8 Acromioclavicular joint, I. 2r

in impingement syndrome

shape of, 234f. 235,235f. 238, 280 Acromioplasly e.xacerbation of instability in, 243 239 Aclive motion

case �tud.v on, 397-398, 398f in range of motion a�scssmcnl,63

ADL. See Daily living activities Adson's test in thoracic outlet svn­ drome,170 Aerobic training.366 Age

in brachial plexus inju1'ies, 196.198

in frozen shouldcl-, 262

evaluation of,62-65,64[, 136-137,

in impingement syndrome,235, 2361

387 posture in, 387 in fractures of shoulder girdle, 448 of clavicle. 448 of humerus. 450,45 I of scapula, 449 in frozen shoulder. 260.265-266 in exercise program,269-270,272

torque and. 412 Agility,relationship to power and strength, 366 Akureyn disease, referred pain from, 330 Anaerobic capacity. 365-366. 373 Anatomy of shoulder complex, I, 5-10 acromioclavicular joint in.9-10

limitations in.reasons for. 62

brachial plexus in,179-184

in postoperative management of

glenohumeral joint in, I, 5-6,6f

instability,430. 431,432

in thoracic outlet syndrome. 169,

gapping in. 355, 356f

258,270,346 manipulation techniques in.270

in impingement syndrome. 232,

in protective injuries, 339

antedOI- glide in, 354-355,355f

arthrography in,262f and frozen shouldel� 258,259

analomy of,9-10

mobili/..3tion techniques involving

365-366 Adhesions,capsula,", 258

in immobilization,formation of,

arthritis of.464,473

innervation of,59

Adenosine triphosphate (ATP).

role of,231-232,232f

predictive value of. 63

in nexion of �hould(.'r, 3

movement, 406f testing of, 69t,72

position of,230f,23lf

in abduction of shoulder,12, 13

in frozen shoulder,265

movement,406[. 407, 40?r with flexionlextel11al rotation

Acromion

forces in.11-14.12f. 13r.99

refcn-cd pain to. 319

in isokinetic excl-cbe

464,473

175-176 in total shoulder replacement, 466f, 473

relationship to spine,95-96 scapulothoracic jOint in.10 slcl11oclavicuial- joint in,9,9f Anesthesia.myofascial mobili7 ..ation under,273.336 in fTozen shoulder, 273 Aneurysms,rcfen-ed pain from, 322

Acupuncture in frozen shoulder, 268

Angiofibroblastic hyperplasia. 281

Adduction of shoulder

Anti-inflammatory agents, nons-

in exercise program for throwing injuries of shoulder,41 ,41f hypov3scuial-ily of rotator cuff dur­ ing,281-282

teroidal in impingement syndrome,236 postviral fatigue syndrome (PFS) and,330

477

478

IN 0 E X

Aplcy'� :,cratch test, 284

in throwing injuries or shoulder. 23, 24

Appcndh:, perforated, pneumoperi· loneum from, 309 Apprehension lest in instability of .houldcl·, 22, 75r, 76-77, 286,

AI1ificial shouldcl' joints, 459-476 Assessmenl pnx:edul'CS, See Evaluation procedures 322

spec/lie sporl

nonopcralivc treatment options for.

60

oSlcoarthdlis, 460f, 463, 464, 473

237, 240-253

Arthrography

4 1 1 -4 1 2 , 412t

in frozen shoulder. 259-260, 26 1 . 262, 262r. 264

peripheral nerve entrnpments in. 1 17

in instabilities of shoulder, 423

rotator curr pathology in, 240-242 strength training improvements in. 37 1-372

concave--convex mlc of. 344

instabilities in, 424. 429

of glenohumeral joint

thmwing injuries or shoulder in.

in abduction of shoulder, 4f 8-9

training principles rO I� 368, 369 Autonomic nervOllS system

in rOlation of shoulder. 3, 4f. 4-5.

impact or myorascial mobili7..3tion

I I , J3

on, 385

in scaption or shoulder, 4 Iypes or motion. 3 or, 266

tion or, 270, 27 1

47 1 , 474

tenodesis or. 439, 443r

joint, 7, 9, 23, 37 1 , 422 strengthening c'\:cl'-cises ror. 37 1 , 374r tendinitis or case study on. 378-380. 379r. 380r

Axillary nerve injury or. 1 84, 185, 1 86, 1 88 ncumpraxia in, 1 86

�UrgCI)', 424

396-397, 397r in rotalOr curr pathology. 282, 290

in stabilization or glenohumeral

l'Cren'cd pain rmm, 322-323

compared to open reconstructive

myorascial mobili7..ation or,

total shoulder replacement in. 459,

injury or. 192

Arthroscopy

joint, 422 in musculocutaneous ncn'c palsy,

short head or. 7

A:dll3ry artcf), and vein

.!>houldcr replaccmcnl in, 463.

in stabilizalion of glenohumeral

etiology or. 467 46Ir, 462r, 463, 467-468, 474

Ar1hropmhv. posHraumatic, tOlal

231

in scaption-abduction or shoulder. 5

Avascular necrosis

mobili7..31ion techniques in rcstora·

in impingement syndrome. 81 r. 82.

arthroscopic debridement or, 439

vasoconstl"iction renex or, 162

joint play techniques in assessment

2 1 2-2 1 3

1 1 7-1 1 8

1 9-55

role of steerer'S and depressors in.

shonening and spa�ticily in.

long head or, 7, 2 3 . BOr

�ul'gicaJ techniques ror shouldcr

definition of. I

in hemiplegia

hypovascularilv or, 2 8 1 -282

in rotator cuff tcal'S. 437r. 437-438 Arthrokinematics

Biceps brachii muscle and tendon

inappropriate u�e or. 206, 20M

predictive value or, 4 1 3

for �tcroid injections, 272-273

371 -372

in frozen shoulder, 258-259

isokinetic IOrque ratios ror. 4081,

in adhesive capsulitis, 262r

muscle activity studies in. 245

Bench PI'CSS exercise, 41. 42r

impingement syndrome in. 232.

post-traumatic, 468, 470

isokinetic torque ratios for, 4081.

results or slI'CngLh training in.

evaluation or shoulder' problems in,

462-463

der in. 1 9-55 Baseball players

4 1 1 -4 1 2 , 4 1 21, 4 1 3

Athletes. See a/so Overhand athletes;

glenohumeral. 461 -462. 463

Baseball. throwing injuries or shoul­

impingement and instability in, 232

Atherosclerosis. rdelTed pain rrom,

Arthritis in 10la1 shoulder rcplacemcni after dblocalion, 463. 466-467, 474

ing, 250

AI1icuiation techniques, 335-336

423 AI1criai pulses, palpation of , 300-301

Basal ganglia. in nClIf'Omuscular train­

myorascial mobili7.ation in. 396-397 . 397r

physical c'\:amination in. 1 9 1

in rrozcn shoulder, 273

muscles innen·atcd by, 99

in instabilities or shoulder

palsy or. I 1 7

te�ts in evaluation or. 82. 8U, 83. 83r. 85r. 86 working posture and, 104

as diagnostic tool, 427

Axillary pouch or n.'Ccss. 8

tenosynovitis or, 258

indications ror, 424

Axillary region, pillpation or, 741. 75

lests in evaluation or. 81 [-83r.

laser capsulolT'Uphy in, 424.

A.'\:iohumeral and axioscapular mus-

428-430

c1cs, response to dysrunction,

po�topcr'3live management in,

in injured athletes, 2 1

69t, 7 3

injur)' or, 23

430-431 preoperative steps in, 427-428. 428r

in prorcssionals versus amateurs, 21

B

strengthening exercise ror. 50r. 5 1

as stabilization technique. 427-428, 428r-430r in I'olator cuff tears. 29 1-292 a� diagnostic tool, 438. 438r. 443, 443r. 444, 444r as surgical treatment. 293-294, 439. 439r, 440r. 444. 445r

82-83, 85r. 86 in throwing movements. 20, 2 1

Bacterial endocarditis, referred pain from,319 case study on. 3 1 9-322. 320r. 32 1 r Bankhar1lesion. detection or, 423 Bankhal1

l"Cconstru cl ion,

425r

i n lotal shoulder replacement. 464 Biceps curl exercise. 50r, 5 1 . 374r

424-426.

Biceps labral comple'\:. in throwing injUlics or shoulder, 22-23 Biorccdback techniques in hemiplegia, 221

479

tN0EX Biomechanics of shouldcl'

motor strength in. 191-192,

in abduction. 3-5.4f.10f-13f.10-14

194-195.196.202

in brachial plexus injuries. 187.187f

myelography in, 193

in flexion.3

nClve conduction velocity tests in.

in glenohumeral stability. 5-9. ?r. 8f.287-288 in hemiplegia.205-214 in type I ann. 211

109

occupationallherapy in, 189. 193. 195.200

c

pain in. 189-191.196.197 palpation in.192.196

in type III aim, 213

passive range of motion in. 191,

in rotation.12, 13

injuries, 187-188 Bursitis, cervical spine pathology in.

195

in type II ann. 212 relationship to spinc.99-100

Bumcl' syndrome in bl-:lchial plexus

196.198. 202

Cancer causes of pain in. 301,304 rcfCITCd pain from

patholllechanics of. 187. 187f

colon. 329

Body Blade. 25

pathophysiology of. 188-189

gallbladder. 325

Brace�.in clavicle fractures.448

peripheral nerve, 186

kidney.328

Brachialis muscles. in rnu�culocuta-

physical e x amination in.

liver, 324

neous nerve palsy. I 17-118 Brachial plexus.179-203 anatomy of.99.179-184 in relationship to other structUl'es, 181-182 in axilla.181-182 components of.179

191-193.196-197.201-202

lung.3 1 1-314

posterior cord, 186. 188

pancreas, 324-325

posture in. 105.191.196,

stomach, 328

201-202 radiography in, 193 rchabilitation in. 193.195. 197-201

of spine. symptoms of.31 1 Capsular fibrosis, in impingement �yndmmc, 237 Capsular laxitv tests, 286

sensory loss in. 192. 196.202

Capsular lesions. stages of. 264

in shoulder dysfunction , 109-110

Capsular mobility tests, 286

divisions of. 179.180

special tests in. 192-193

Capsula!' pattem, limitation of gleno-

injury of.116. 184-189

splinting in.189. 193.194f

humeral movement� in. 67�8.

supraclavicular.184

260-261.452

conis of. 179.180 injury of. 185-186

active range of motion in, 196.202 anatomic features in protection

tests in. 192-193

Capsule

Tinel's sign in, 192-193

of acromioclavicular joint, 10

case study on. 195-203

tdggerpoints in, 192, 197-198

of glcnohumeral joint

chan on results of evaluation in,

uppenrunk, 184, 187-188.191

anatomy of. 6

vascular injuries in, 192

in cClvical ncrve root iiTitation.

from, 182-183

189.190f c1a))sification of,184, 184t comparison to hemiplegia, 213 as complication of musculoskcle-

ud injuries, 187-188

vocational assessment in.193, 196.201 in neck.181 neuralgia of.radicular pain in.134

coordination in.192.196.200.202

palpation of nerve trunks and neu-

daily living activities in.193.196.

rovascular bundle of, 140

199 degrees of severity.188-189 in droopy shoulder syndrome, 105

roots of. anatomic features provid­ ing protection from injuries. 183.183f in segmental innelvation of shoul­

edema in. 192. 196. 198.202

der muscles, 179.180.180f,

electromyography in, 188.

181f

194-195 emotional SUpp0l1 in,199 evaluation of. 189-195. 196-197, 201-202 history of patient in. 189-191. 196.201 hobby and leisun! activities in. 193 infraclavicular. 184. 185. 188 laboratory cvaluation of, 193-195 latcral cord,185.188 lower trunk. 185.191

tests in evaluation of,192-193 in frol-cn shoulder. 264-265 in thoracic outlet syndrome. 157, 161 trunks of.179,180 ana,omy of. 182f. 182-183. 183f. 191 injury of. 183f. 184-185.191 Brachial pulse, in br achial plexu� injuries.192 Breathing pattems in thoracic outlet syndrome

mechanisms of.189

evaluation of,170, 176

medial cord, 185, 188

as risk factor. 157. 159, 162-163

middle trunk.185

treatmcnt of,172f.172-173

108 in frol-en shoulder, 258. 259.270.

&e. {lisa FI'Ol-en shoulder in impingement syndrome.237. 238.241 laxity of.in throwing movements, 21 mobili7..ation techniques involv­ ing.344 in range of motion lests.65, 66f. 68.68f in stabili7..ation of joint, 7-8.422 stress on, 347 in throwing movemelllS, 22 of sternoclavicular jOint, 9 Capsule-labrum complex. in anhro­ scopic stabilization of shoul­ der. 427-428. 428f Capsulitis. adhesive, 6. &e also Fl'Olen shoulder; Nonprotective inj uries glenohumeral joint in. 67-68. 238 fibrotic changes in, 109 impingement syndromc in, 238 rehabilitation for.case 342-346 use of telm. 258

study

on,

480

IN 0 E X

Capsulolabral reconstruction, 24. 424 antcr;or. 426,426f rehabilitation in. 426,431-433 poslcdor, 426-427 rehabilitation in. 427 Cardiac disease, refcrTcd pain fTom, 58,58t, 136,315-322 case studies on,31 M. 316-317, 318r, 319-322, 320f, 321 f diagnosis of, 316,317,318 Cardinal plane in isokinetic exercise. 417 range of motion tests in,63 Cardiovasculal'conditioning, in throw­ ing injuries of shoulder, 26 Carpal tunncl syndrome fluid dynamics in, 154,161 pressure gradient research on, 163,164f nerve compression in, 167 shoulder' pain 311d. 118 in thoracic oULlet syndrome. inci­ dence of. 167 Cartilage of glenohumeral joint. anatomy of, 6 Causalgia. active movement dysftlnc­ lion in,136,137 Cerebellum. in neuromuscular train­ ing. 250 Cervical disc disease chronic. intrinsic shoulder pathology from, I 10 compl'es�ion testing in. 110. 11 l f cvaluation of. l lO-IIL I l l f frozcn shouldcl' and. 109 refen-cd pain in, 110 shouldel'-hand Ccrvical faceljoint itTitation ca::;c study on. IIS-124 ccrvical disc disease and, 112 distraction techniqucs in, 121. 122f. l23f evaluation of, 112f. 112-113, 118-120,119f fncc! joint blocks in, 113 posture in. 100-101. 10If

Cervical ncrvc root it,-itation evaluation of. 113f,113-116, 114f-115f referred pain in. 113 Cervical nelves. 179. ISO

compression test. 110. II If. 121 Spurling's test, 112. I 12f

10If injury of. splinting in. IS9 initation of in reflex sympathetic dystrophy. 108 in shoulder pathologies,IDS palsy of, 184 Cervical plexus,anatomy of, 99 Cervical quadrant tesL. 265 Cervical radiculopathy. See also Cervi­ cobrachial pain syndrome case study on. 143-150. 146f-147f effect of sensitizcd neurai tissue in, 138f EMG rcsponscs lO nervc trunk stim­

ulation in. 141. 146f,147f frozen shoulder and. 109 myofascial neck and shoulder pain in, 105, 105f pain and paresthesia in, 134 Celvical region

drome. 159, 161 Cervical lateral glide technique, in treatment of neural tissue. 14Sf Cervical muscles cieclronlVographv of, in brachial plexus injuries. 195 response to dv�function,69t, 73

in thoracic outlct syndromt'. 174, 174f vasoconstriction of shoulder tissue initiated by, 108 whiplts, 64

i n !teapula fractures, 449

retroversion of. 5, 6f

in throwing injuries of shoulder. 25

rolling motion of, in abduction of

Hooked (or tvpe I I I ) acromion proces!o>. predi�po!o>ition to trauma from, 58 Ilornel'\ syndrome. 1 8 1 . 1 8 5 , 190, 1 9 1 . 201

der, 2 6 1 , 270 I-I"\'perabduction of a11m., in thoracic outlet syndrome. 170- 1 7 1 Hvpere1asticity with impingement position in instability continuum. 243 i n throwing injlllies of shoulder', 22 Hvperextcnsion of humeru�, in hemi· plcgia and tvpe II arm. 207, 2 1 1r. 2 1 1 -2 1 2, 2 1 2 f Hypermobility o f shoulder, 6 8 , 72 1I)'pomobilitv of shoulder. 68, 72

radiography of, 452f-456f

impingement undcl' acromion. i n

Ilome exercise programs

in throwing movements. 20, 2 1 Ilvaluronic acid levels i n frolen shoul,

rehabilitation in. 4 1 4- 4 1 5 .

195, 198, 201

428-430

glenoid

i n neck, 450-45 I , 45 I f, 452f

fractul-cs of. 450, 451 f. 452f

instabilitie� of shoulder.

10

fossa, 5

45lr

brachial plcxu� injudes, 193. Holmium VAG laser cap�ulorraph". i n

size of head i n relation

4&5

shoulder. 4, 4f. I I . 1 3 rotation of i n abduction of shoulder. 4-5, 6-7, 7f, 8, 8f in hemiplegia, 2 1 8. 2 2 1 f

Icc applications following isokinetic c'\:crc isc. 409 in frozen shoulder, 267, 269 in impingement 'iyndrome. 236. 239, 240, 376 i n rotator cuff rehabilitation. 293, 295 in tendinitis, 379 in throwing injulies of shoulder, 24 Iceland di!>e3SC, refen-ed pain from. 330 Immobilization collagen changes in, 258. 270, 338, 339, 385 complications from, 344-345, 448 in fractures of shoulder girdle. 447-448, 453 of clavicle, 448 of humerus. 450, 45 1 , 452 of scapula, 448. 449 frolcn shoulder i n , 258, 2 6 1 , 270 glycosaminoglycan levels in, 346. 385 impact on myofascial tissue, 385 passive mo\'cment following, 336. 338-339 periarticular tissue and muscles in. 447-448 i n rotator cuff rehabilitation. 292 I m pingement-in�tabilitv complex. See

also Stability of �houlder classification scheme i n , 240, 242-243 in throwing injuries of shoulder, 22 Impingement syndrome. See also Non­ protective i njuries acromion i n . 230f-232f, 2 3 1 -232. 234f-235r. 235, 238 age relationships in

in brachial plc'\:u� injur-les, J 1 6

i n rotator' cuff pathology. 284

in rotutor cuff degeneration, 235

i n Pancoast tumor, 3 1 1-3 1 2

and scapulohumeral rhythm, 1 0

stages of pathology, 2361

486

IN 0 E X

Impingement syndrome (COIl/iuued)

in tensile overload, 241 -242

in athletes. 232, 237, 240-253

tests in evaluation of, 242, 286-287

case study on, 374-378

in throwing injudes of shoulder,

diagnosis of

22, 26-27

painful arcs in, 63, 64, 236, 239

treatment of. 252-253

size of subcoracoid space in, 230

underlying instability in.

with underlying instabili ty, 243 evaluation of, 235-236, 2361, 237, 238, 238f, 239, 243-244, 252-253, 286-287, 375 glenohumeral joint in

242-243, 28 1 undersurface rotator cuff tears and, 282-283 spasticity of muscles in, 236. 237 stretching and strengthening exer­

Lnhibition technique� in hemiplegia, 221 Innervation o f shoulder muscles, brachial plexus in, 99, 1 79. 1 80, 1 80f, 1 8 H Instability continuum. See a/�o Stabil· ity of shoulder classification scheme in, 240. 242-243 in throwing injuries of shotlldel� 22 Instability-related impingement. See

3lt hrokincmatics. 23 1 , 2 3 1 f

cises in, 237. 237r. 239, 240,

force couple at, 232-233, 233f, 237

243, 245f-249f, 245-248, 369f,

lnterclavicular ligament. anatomy of. 9

rehabiliLation of stabilizing mus·

3 7 1 f, 373f-374f, 375-378,

Intel-rcrential stimulation, in impinge­

cles in, 244-245, 249-250. 2 5 1 f, 252f, 253, 288-293

376f-377f subacromial space in, 229-230, 230f

in hemiplegia. 207. 2 1 4

subcoracoid, diagnosis of. 230

inside o r undcrsUiface tears in, 283f

surgical options in. 239

muscle imbalances in, 73. 232-233,

tests in evaluation of. 24, 77, 80f,

236, 287 posture and. 233 neuromuscular retraining in. 249-25 1 pain in, reproduction of. 436f pathology of cxtdnsic factors, 2 3 1 -234 inldnsic factors, 234-235 slages of, 235-239

8 1 f, 8 1 -82, 2 3 1 -232, 232f, 242 in throwing injmies of shoulder, 22 tests in evaluation of, 24

ogy, 280, 435 evaluation of. 286 position in instability continuum, 242 .Iage I, 236-237, 239-240, 280 S1age II, 237-238, 280 S1age III, 238-239, 280 in throwing injuries of shoulder; 22 treatment of. 236t, 236-237. 237f. 2371, 238, 280-281 upper surface rotator cuff teaf'S

anatomy of, 97, 97f. 98, 1 60f, 1 6 1 doorbell test of, 1 1 3

Lnitability le\'els

461 -462 treatment of, 236t, 236-237, 237f. 2371, 238, 243-250, 2 5 1 -253 I mpingement tests Hawkins and Kennedy, 81 f. 82, 286

in etiology of rotator cuff pathol­

183f Im'el1.ebral foramina

i n total shoulder replacement,

precipitating factors in, 233-234

case study on, 239-240

rOOI S aI, 1 49r. 149-150, 183,

posture and, 1 0 1 Iontophoresis treatment, 379

crossed

pl'imary, 235-239. 236t

ment syndrome, 236 Intervertebral forumen, injmv of nClve

throwing movements in, 2 1

pol:llure in, 233 predisposition to, 6 1 , 234-235

Impingement. secondal),

illm

adduction, 286

Neer, 8 1 r, 82, 23 1-232, 232[, 286 Impulse Inertial Exercise System, 250, 252f InOammatory stage in healing of shoulder ginilc fractures, 447 Infraclavicular brachial plexus injulies, 184, 1 85. 188 Infrahyoid muscles, anatomy and function of. 96 Infraspinatus muscle nnd tendon in abduction of shoulder, 5, 1 1 . 1 2 , 1 2 f, 1 4

in passive range of motion lests, 65-66 predictive value of. 57, 59 Irritable bowel syndrome, refcn-ed pain from , 329 Isokinetic exercise, 401-417 abduction/adduction ratio in, 4081, 4 1 1 - 4 1 3, 4 1 2 1 advantages and disadvantage� of, 401-403 blocking of movements in, 409-4 1 0 i n brachial plexus injUl;es, 192, 1 99-200, 201 case studies on, 4 1 4-4 1 7 compared to isotonic excrcise, 40 I , 402 concentric training in, 372

in brachial plexus injuries, 197. 200

cryotherapy following, 409

manual muscle testing of, 285

diagonal movement pallel1lS in,

in scaption of shoulder, S

368, 402, 403-407, 404-405f,

and, 435, 437f

in stabili7.ation of shoulder, 7, 1 1 .

407f, 4 1 7

243-244

strengthening exercises for. 29. 29[,

primal"V versus secondal),. 229, secondal)'

14, 370, 422 30r. 369f-37 I f, 370, 47H

case study on. 25 1-253

in suprascapular nerve palsy, 1 J 7

classification of. 240

tears in, anatomic description of, 282

diagno�lic difficulties related to.

in tensile overload, 24 1 , 242

243 in etiology of rotator cuff pathol­ ogy, 2 8 1 , 435 evaluation of. 243-244. 252-253. 286-287 rehabilitation issues in, 243-250 surgery in. 242-243

in throwing movements, 20, 2 1 in injured athletes, 2 1 injury of, 22 in professionals versus amateurs, 21 strengthening cxercises for. 29, 29f, 30f

in brachial plexus injuries. 192, 1 99-200, 201 eccentric tmining in, 372 equipment used in, 40 1 . 402. 403, 410 extemaVinternal rotation ralio in. 408, 4081 , 4 1 7 normative data on, 408, 4081, 4 1 1 - 4 1 3, 4 1 2 1 , 4 1 7 i n fracture!lo of shoulder girdle, 453, 455 frequency of. 411 general considerntions in. 4 1 0-41 1

IN 0 E X in impingement :-.yndmmc. 376.

concentric and eccentric training in.

377, 377[

Lateral glide technique, in t1-eatmcnt of neural tissue. 142. 1-I8f

367, 380

maximal crrol1 in. 40 1 . 4 1 1

in impingement syndrome. 369f.

mu�le loading in. 40 1 . 402

Lateral slide test. 70f-7 1 f. 73. 75. 232

37 I f. 373[-374[, 376, 377, 377[.

eccentric. 368. 402. 4 1 0

378

i n assessment of scapular posilion, 61 Latissimu:, dorsi muscle, 3

in pobloperative management of

rrequency o f training and. 368 negative respon!>C to. 409

in abduction of shoulder. 1 2. 1 4

inblability. 43 1 . 432. 433

in nonprotcctive injuries, 343

anatomy and function of. 95-96

in rotator cufr rehabilitation. 289.

po�itioning of glenohumeral joint

in stabilization of shoulder. 8. 370

294, 295

in. 402-403, 4 1 0, 4 1 7

strengthening exercises for,

in strength training, 367. 372

369[-37 1 [. 370

in tendinitis. 369f. 370r, 373f-374f.

i n po�lopcrative managemenl of in�tabililv, 43 1 , 432-433

in throwing movements. 20, 2 1

377[, 379[, 379-380

i n injured athletes, 2 1

in throwing injuries of !;houlder. 25.

progression of. 409, 4 1 1 propriocepti\'e neuromuscular faeil·

i n profeSSionals versus amateurs,

29[-36[, 29-5 1

21

L .. : lxitv of capsule. 6. 1 0

italion in, 403 repetitions in. 4 1 1 . 4 1 1 t in rotalol' cuff reh� , bilitalion, 290.

tests i n evalualion of. 286

J

in throwing movements. 2 1 . 22

290[, 294, 296 'p'->ed 0[, 401-402, 4 1 01, 4 1 0-4 1 1 ,

Leisure activitie� in brachial plexus Jobe subluxation relocation lcst. 7M.

41 11,413 in blrenglh training. 367. 372. 401

77, 77[, 423

in lendinitis, 380 as tc�ting procedure. 75. 34 1 , 40 I .

anatomy and function of. 96

lion techniques; Myofascial

spasms i n , 236

mobili7..ation

strengthening exercises for. 369£.

in cervical spine disorders. 1 2 1 .

402, 403-407

122[, 123[

bilateral and unilateral compar·

definition of. 383

isons in. 409

3 7 1 , 3 7 1 [, 373[, 374[ Levator scapula s.vndromc. 104 Lifestyle. daily living activities in

intcn-elationship with myofascial

interpretation of, 408t, 408-409. 413 predictive value of. 4 1 3

in brachial ple.xus injuries, 193. 1 96,

lllobiJi7..ation. 383. 384f

199

in postoperati,·c management of

limitations in.

instability. 43 1 , 432

i n preM:reening. 409

i n rotalol' cuff rehabilitation. 288

for alhletcs. 4 1 1 - 4 1 2 . 4 1 2t. 4 1 3

cine ligament anatomy of. 6

266

capsular mobility teslS for. 286

in frozen shoulder. 266

i n impingement syndrome. 2 4 1

in manipulalion technique. 270.

eccentlic/concentric. 4 1 3 for nonnals. 4 1 2-413

271

pred icti,'e value of. 4 1 3

a n d stabilitv o f joint. 6-7, 7f. Bf. 1 3 Links. i n shoulder complex, 1 Lippman test, 8S£. 86

torque relat ionship!oo i n

Livel� refen'ed pain from, 1 35. 324 K

Load and shift test, 286. 42 1 -422

Kabat\ self ceryicle traction protocol,

Locking test, 80£. 82

body weight. 408. 4 1 7 'p'-'ed, 401-402

grading system i n , 422

in treatment prolocols, 40 1 . 4091. 409-4 1 0, 4 1 1 warm·up in, 4 1 � l l I...omctlic exercbe

indication for IotaI

LigamcnlS of shoulder, See also spe·

in evaluation of shoulder problems.

dominantlnondominant side, 409

as

shoulder replacement. 461

Joint play motion:,

torque ratios III

age. 4 1 2

injuries. 1 9 3 J..c,'ator scapula mUM:le

Joint mobilization. See also Mobili7..a­

submaximal cffon in. 40 I. 4 1 0. 4 1 1

time required for. 402. 403

487

1 70, 1 70[, 176

Long thoracic nerve palsy. 1 1 7

Kibler scapular slide test. 284

Ludington's lest. 83. 83f

Kidney. refelTed pain from . 328

Lung. referred pain from. 3 1 0-314.

Kinesthesia

i n fraclUres of -"houlder girdle. 453

dc,,'elopment of, 250

in postoperat ive management of

testing of. 75-76

3 1 2[, 3 1 3 [ caM'SS­ ment of. 69f-70f. 7 1 1-72t.

evaluation of. 342, 342t. 343, 345

pain in. lOS. 1 05f. 386

examples of, 3 4 1

three-dimensionalil".v of, 383

rehabilitation for

Mvokinase. anaerobic capacity and,

M\'elograph\ in cervical !'opine dbol'­ dCI";. 1 1 1 . 1 1 6

outlet syndr'Ome. 169-1 70, 1 7 6 Ncurologic dbeases. i n shoulder dvs­

immobilization affect i ng.

in 'itrcngth training. adaptations of.

case study on. 3 4 1 -346. 342t, 343f phases of. 345t

365. 366 Mvopathies in shoulder dysfl.lnction.

Nonsteroidal anti-innammatorv drugs

1 10

Mvocardial b.chcmia. rdcn"t.'CI. pain

(NSAIDs)

from. 3 1 M. 3 1 6-317. 3 1 8f

in impi ngement syndrome. 236

Mvofascial dysfunction in brachial plcxu'i injuries, 192. 197

po!oo tviral fatigue syndrome (PFS) N

and. 330

in workel'"!.,;-friclion . of 'iupraspinalus and bicep!Cle

shouldcr replacement, 463.

structural features of, 182f

in stabilization of .!.houlder. 9. 370 369f-37 I f. 370

470-474, 475-476 Post-traumatic anhropathy, in total

sensitized, 136, 1 37, I 38f, 149-150

strengthening exerci.!.es for. in thl'Owing movements, 20. 2 1

in lotal shouldcl' replacement.

dysesthetic and nerve lrunk pain from, 134, 1 34f

Physical examination

in dorsal scapular nerve palsv. 1 1 6-1 1 7 i n elevation of 3rm, 99-100. 1 00f ergonomics and. 1 0 1 f. 103f. 1 0 3 - 1 04

in brachial plexu� injulics. 1 9 1 - 1 93. 196-197, 20 1-202 in lotal shoulder replacement,

cvaluation of. 60-6 1 . 62f in brachial plexus injuries, 1 9 1 .

461-463 Pillow �uceze. in excrcise program for throwing injuries. 50f. 5 1 Pitchers, See Baseball players Pilching, See Overhand throwing; Throwing movements Plastic deformation mobili7.ation tcchniques in, 344, 347, 348f stretching tcchniqucs in. 375 Platysma, anatomy and function of, 96 Plyometlic excrcise in postoperative managemcnt of instability, 43 1 , 432 in rotator cuff I'chabililation, 289-290, 294, 295, 296 in strength training. 367. 373-374. 380[, 380-381 Pneumoperitoneum

491

1 96 myofascial, 386-387 in rotator cuff pathology, 284 in thoracic outlet syndrome, 1 9 1 in frozen shoulder, 264 headache and, 100 head position in, 60--6 1 fOlWard, 100-102, 1 0 I f i n hcmiplegia. 206. 2 1 7 i n type I arm. 209. 209f in

twe

II aim, 2 1 1 f. 2 1 1-2 1 2 .

2 1 2f in type lIJ arm, 2 1 3 . 2 1 3f in impingement syndrome. 233 myofascial imbalances and. 386 nOlmal, alignment of spine in. 1 00, 10If i n peripheral nerve entrapments. 1 17

creation of. 3 1 0f

predisposition to lrauma and. 58

in referred pain to shoulder. 309-3 1 0

sustained, in cumulative trauma

Position of thcrnpist during elevation of shoulder, 472 duling mobilization, 387 Postfixcd plexus, in thoracic oUllet syndrome, 1 6 1 Postoperative peliod in an hroscopy. 430-43 1 in dislocation of shouldcr, 337-341 isokinetic exercise in, 409 in open capsular shift surgery. 43 1 -433 in rotalor cuff l"Chabililation, 288. 29 1 , 292, 295-296, 439, 443, 444-445 in throwing injuries of shouldel� 24

disorder. 103 in thoracic outlel syndrome cvaluation of. 1 69. 1 75, 1 9 1 as risk factor, 1 57. 1 59. 1 6 1 . 1 65. 166 Postvin:d fatigue !'.yndrome refcrred pain fTom. 330 relationship with fibromyalgia, 330 Power, in speed and sll-cngth training, 366 Pregnancy, activities during, pneu� moperitoneum from, 3 1 0 Preoperative evaluation i n 10lal shoulder rcplacement. 459. 461 -463

492

IN 0 E X

Pres��lIp exercise

Provocation tests

in impingement syndrome, 245, 247, 247f,248f. 249f for scapular rotatOl' muscles.245.

active. 62-65, 64f

neural tissue, 138-1 40, 1 45f

goniomelric.284-285.285f

Psychological factors in brachial plexus injuries, 1 99

247f sitting.72f,75.37 1 f fOI-thmwing injuries. 32,44, 46f

in frozen shoulder, 26 1 Pulley exercises in frozen shoulder.2 7 1

Pressure glddienl research, in carpal

i n tOlal shoulder l'Cplaccmelll, 463f

tunnel syndrome. 163, 164f

tests for

in frozen shouldel� 265

passive,65-68,6M-68f Recruitment of muscles, abnormal.in hcmiplegia,206, 20M treatment of, 221 Recun'cnl meningeal nl'l"ve,anatom.v of.97f,98

Pressure techniques.in soft tissue mobili:t.alion,3561

Pulmonary disease. rcfelTcd pain

Primal''\' impingement syndrome. See

Pulses, aJ1erial, palpation of, 300-30 1

in fl'ozen shoulder.272

Purdue pegboard test of coordination

in hl!miplcgia, 206, 2 1 6. 220-223,

Impingement syndl·ome.

from, 58. 58t. 311

pdmary

in brachial plexus injul'ies, 1 92, 1 96,201

Pdmar:v tensile overload, 240, 241 Proprioception.testing of.75-76

Push-up exercise, 71f.75.374f

Proprioceptive exercise cognitive role in, 250 muhilevcl nervous system retrain­

from cervical region, 59,bOt, 105.108

for scapular rotator muscles, 245, 24M

tion (PNF), 339, 343, 343f

fol' throwing injuries.48. 48f

equipment used in, 250, 251f, 252f in impingement syndrome.250 in Ihl'Owing injuries of shoulder. 24-25 Proslhc�i:;.glenohumeral.459-475

clinic�ll considerations in. 459-463 constrnined

01'

fixed fulcnJm type.

464 cady dc�igns of, 459 indications

fOl',

459, 463-470

in o.sleoarthrili�. 463, 464. 473 patient profile in, 459, 461 postoperative management in, 470-474, 475-476 preoperative evaluation in, 459, 461 -463 revision of previous operalive pro­ ccdun:s in.462. 466--467.47 1 in rheumatoid at1hritis.459.460f. 464, 466, 47 1 , 473-474 in rotator cuff tears.46 1 .462, 464, 466,468, 474

compared to local pain, 58, 1 34-- 1 35, 1 4 8

dysesthetic. 1 34, 1 34f

Quadranl lest (Maitland), 1 38 Questions,in assessment of pain, 58-59

from esophc .study on, 307- 3 1 0

Q

in chronic dislocation. 463, 466-467

in disc disease. 1 1 0 in facet joinl inilation, 1 1 1 - 1 1 2,

from diaphragm, 306-310,30n.3 1Of

in fractures o f humerus.454 in isokinclic exercise. 403

to arm and hand,311

for throwing injul'ies. 32, 47f. 48

24M, 247

in strength training.373-374, 380

222f-223f, 225, 226 Refen'cd pain in brachial plexus injuries, 1 92,197

in impingement syndrome,245,

Proprioceptive neuromuscular facilita-

in brachial plexus injuries, 1 99-200

in impingement syndl'Ome,247. 247f Pu.sh-up plus exerci.se

ing in, 249-250

Reeducation of muscles

provocation teM via, 1 39 Radial pulse.in brachial plexus injuric:" 1 92 Radiculopathy, 1 3 1 - 1 32, See also Cer­ vical radiculopathy Radiographv in arthritis of glenohumeral joint. 460f.464 in brachial plexus injUlies, 1 93 in cervical spine disorders, I I I. 1 1 3, 1 16 in clavicle fnlclurcs, 449[, 4S0f

from livel� 324 From lung, 3 1 0-314, 3 1 2f.3 1 3f case �tud:v on, 3 1 2-3 1 4 from nerve trunk, 1 34, 134f fTom pancreas.324-325 patterns in, 1 33 physiology of. 133f, 1 33-134, 1 34f from postviral fatigue syndl'Ollle. 330 radicular. 132-133, 134, 134f somatic, 132,133.133f from stomach, 328-329 in thoracic oUllet wndrome.322 underlying medical conditions in. 58, 58t

in defining scaption, 2

in vascular di.se.t:sc,322-324,323f

in fro7.en shouldel� 261, 262,262f,267

in vi.sccral disea�c, 132. 1 33, 133f,

in humerlls fracture!), 452-456f

1 35-1 36, 299-331

in trauma. 462, 463. 467

in instabilities of shoulder, 423

comp�lJ'ed to sOl1l. 21 strengthening exercises for. 29, 29f, 30f Tests. See also specific lest in brachial plexus injuries, 192-193 of cOOl-dination, J 9 1 - 1 92, 1 96.

202

muscle guarding in. 109

abdominal or vaginal, pneumoperi-

in throwing movements, 20, 2 1

caution during, 57-58

scopic stabilization of shoul­ SurgelY

in tensile overload. 24 1 , 242

202

in throwing movcmcnts, 1 9. 20. 2 1 in injured athlt.!les, 2 1

tears i n , 282

of muscle strenglh. 194-195. 196.

tests in L'valuation of. 73, 80f, 8 1 r. 82-83, 83f-85r. 84

calci.hc. 435. 436f chronic, 435, 438 Tennis players isokinetic torque !"atios for, 4 ) I , 4 1 2 , 4 1 21, 4 1 3

in cClvical spine screening. 59, 60t in frozen shoulder, 260. 264-265 impingement crossed arm adduction. 286 Hawkins and Kennedy, 81 f, 82. 286 Neer, 8 l f, 82. 2 3 1 -232, 232f, 286 in instability of shoulder. 75f-79f, 76-78, 8 1 , 286-287,422-423 isokinetic exercise in. 40 I . 402. 403-407 passive range of motion. caution duting, 57-58 in thoracic outlet syndrome. 168. 1 69- 1 7 1 i n throwing injuries of shoulder, 22, 23 Thoracic nerves, 1 79. 180

in humerus fractures. 449. 450

muscle activity in, 279

injury of, 185, 186, 1 9 1

in impingement :syndroml.!, 239.

results of isokinetic slrength train�

palsy in, 1 1 7

242-243, 280-2 8 1 i n instabilities o f shoulder arthroscopic, 427-428. 428f-430f controversy over, 424 laser, 428-430 open reconstruct in" 24, 424-427, 425r. 426f in rotator cuff tears. 241 approaches to. 291 artlu"Oscopically a:.:siSied repair. 439, 440r. 444, 445f arthroscopic debridement, 291-292, 293-294, 439, 439f coracoacromial decompression, 439 indication:. for. 438 open repail� 29 1 . 292, 294-296,

ing in. 372 Tenosynovilis. bicipital. fTozen shoul­ der in, 258 Tensile overload in etiology of rotator cuff pathology. 281

Thoracic outlct anatomyof. 1 5M. 1 57-1 6 1 , 1 58f. 1 60f dysfunctional reflexes in. 162-163 examination of. 60 Thoracic outlet syndrome

pathology or. 240

analogy of lake in. 163-164. 165f

primary, 240, 2 4 1

analogy of orthodontist in. 155. 164

secondary. 240. 24 1-242

brachial plexus in, 157. 1 6 1

undersurface rotator cuff tears and,

breathing pallems in

282-283 Teres major muscle and tendon in abduction of shoulder. 1 4 i n stabilization o f shoulder, 8, 370 strengthening exercises COI-, 369f-37 1 r. 370, 472f Teres minor muscle and tendon

evaluation 0[, 1 70, 176 as risk factor, 1 57. 1 59. 1 62-163 treatment of, 1 72f, 1 72-173 case study on, 174-177 differential diagnosis of. 166-167 dysfunctional reflexes in. 162-163 treatmenL of, 1 72, 1 76

in abduction of shouldel� I I . 1 2 . 1 4

early intelvenlion in, 176-177

i n axillary nelve paby, I 1 7

err0l1 thrombosis in, 323

rehabilitation after, 291-292

i n brachial plexus injuries, 197. 200

evaluation of, 167- 1 7 1

results of. 439. 441

in impingement syndrome, 244. 245

objective, 168- 1 7 1 , 1 75-176

manual muscle testing or. 285

subjective, 167-168. 1 75

439, 44 1 , 44 1 f-443f, 443

in temile overload. 242

497

in throwing injuries of shoulder, 24

in slabili7.3tion of shoulder, 8. 1 I . 1 4

exercises i n , 1 72f-174f, 1 72-174

tOlal shoulder replacement in.

strengthening exercises for.

fluid dynamics in, 154, 1 6 1 . 1 63r.

459-476

283f-285r. 284, 472f

1 63-164, 164f

498

IN 0 E X

Thoracic outlet syndl"Ome (Continued)

of infraspinatus muscle and tendon.

functional profile in. 167. 1 75

22

gendel' iss-ues in, 1 6 6

instability continuum in. 22

hislOry o f patient i n , 167-1 68. 1 75

muscle activity in. 2 1 -22. 245

multiple entrapment sites in, 1 53,

in musculocutaneous nerve palsy. 1 1 8

1 66-167 nCUI"Ovascular consequences of, 1 53-177 occupational and ADL issues in, 164-166 pain in

body's

prevention of. 24 rehabilitation goals in. 24 of rotator cuff. 240 location or. 2 4 1 pl'imary tensile overload i n . 2 4 1 o f serratus nntel'ior muscle, 2 1 . 2 2

response lO, 1 55. 1 57

o f supraspinatus muscle and ten� don, 22, 23

evalualion of, 167, 1 75 during treatment, 1 72. 174

surgery in. 24, 424, 429

predictive value of. 4 1 3 relationship t o body \",'eight, 408. 4 1 7 relationship 1 0 speed. 401 -402. 4 1 3 Total shoulder replacement. 459-476 communication between surgeon and therapist in, 472 glenohumeral joint in clastic resistive exercises for, 469f, 473 isometric cxerci�es for. 465f, 470f hislOry taking in, 459. 460 indications fOI� 463-470 physical examination in, 461 -463 rehabilitation in

Panco�,sl lumor in, 1 36, 1 3 7

lests in, 22

catcgories of. 470

posture in

throwing programs in. 25-26. 53-55

critical points and techniques in.

evaluation of, 169. 1 75. 1 9 1 as risk factor, 1 57, 1 59, 1 6 1 , 1 65. 166

Throwing movements acceleration, 20 in injured throwers, 22

rcfen-cd pain in, 322

muscles active during, 2 1 , 22

fisk factors for. 1 57, 1 59. 1 6 1

in professional venous amateur

scalene muscles in, 1 59 in shouldcr dvsfunction, 1 1 0

pitchers. 2 1 stabilization o f glenohumeral

.!ttenosis in, 1 54- 1 6 1 . 1 57 symptom control in, 155. t 57 teMs in, 168, 1 6 9- 1 7 1 r3lse�positive results of, 1 7 1

joint duting. 23 cocking, 1 9-20 in injured throwers. 2 1 . 22 l11uscles active during, 2 1 , 22,

tissue repair in, 1 64 treatment of

241 stabilization o f glenohumeral

case slUcly on, 1 76-177 dcconditioning renexes, 162, 1 72, 1 76 Edgclow protocol fOI� 1 7 1 - 1 72

joint during. 23 deceleration. 20-21 repetitive microtrauma during. 241 throwing injuries in. 2 1 -22

goals in, 1 7 1

exercise programs for, 25-26. 53-55

methods to "ell-Olin swamp", 174,

follO\v·through, 20-2 1

1 74f

stabilization of glenohumeral

method!> to "open tunnels", l 72f- 1 73f, 1 72-174

joint during, 23 in professionals versus amateurs,

patienl comrol in, 1 54-- 1 55, 1 57, 1 7 1 - 1 72 Thoracic region, mobilization or. 388,

2 1 . 241 Windup, 1 9 Thrust techniques. See Manipulation

388f, 3 9 1 -393, 392f Thoracic spine, segmemaJ mobility or. 99 Thoracodol"'Sal nerve, muscles inner· vated by, 99 Thrombophlebitis. referred pain from.

322-32 3, 323f Throwing injudes. 1 9-55 a!,throscopy in, 23, 24, 293-294 of biceps muscle and tendon, 23 biomechanics or, 22-23 clas.