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1981; 61:1041-1045.PHYS THER.

Judy Griffin and Gay ReddinLiterature ReviewShoulder Pain in Patients with Hemiplegia : A

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Shou lde r Pa in in P a ti en t s w i t h H e m i p l e g i a

A Li teratu re Review

JUDY GRIFFIN, MS,and GAY REDDIN, BS

T h e p r i m a r y c a u s e o f h e m i p le g i c s h o u l d e r p a in r e m a i n s e l u s i v e , m a k in g p r e v e n

t i o n a n d e f fe c t i ve m a n a g e m e n t d i f fi c u l t . S e v er a l p o s s i b l e ca u s e s a r e d i s c u s s e d ,

s u c h a s p a s s i ve e x e r c i s e , s u b l u x a t io n , a n d s h o u l d e r -h a n d s y n d r o m e . Tr e a t m e n t

c o n s i d e r a ti o n s a n d s u g g e s t i o n s f o r c l in i c a l r es e a r ch a r e p r e s e n t e d .

K e y Wo r d s : Hemipleg ia , Shoulder joint, Pain.

Shoulder pain is a serious and frequent complica

tion in patients with hemiplegia. The incidence has

been reported as high as 70 percent1

and 84 percent2

in patients suffering from a cerebrovascular accident

(CVA). Complaints of pain usually occur when pas

sive m otion is attempted at the shoulder joint, but in

severe cases the patient has pain at rest. Painful,

limited joint range of motion (ROM) interferes with

use of the limb in functional activities and prevents

the patient's full participation in rehabilitation.3

Under normal circumstances, pain-sensitive soft

tissue surrounding the glenohumeral joint (GHJ)—rotator cuff, joint capsule, subacromial bursa, and

biceps brachii tendon—is subject to many stresses.

Gravity provides traction stress, and GHJ flexion and

abduction movements create friction-compression

stress between the humeral head and coracoacromial

liagment.4

Hemiplegia may produce additional

stresses of paralysis, sensory and perceptual deficits,

and abnormal tone. Cailliet has observed that latent

tendinitis and bursitis symptoms may become acti

vated during hemiplegia.5

The primary cause of hem iplegic shoulder pain hasnever been identified. H owever, a variety of causative

agents has been suggested by authorities, including

improper passive movement, spasticity, contractures,

GHJ subluxation, and shoulder-hand syndrome. The

purposes of this article are to review the literature

concerning possible causes of the pain, propose man

agement considerations, and identify areas needing

clinical research.

LITERATURE REVIEW

H a n d l i n g T e c h n i q u e s

Handling of the affected arm, during such activities

as exercise, positioning, and transfers, constitutes a

potential strain upon the GHJ. For complete GHJ

abduction to occur without compression of suprahu-

meral soft tissue, the scapula must upwardly rotateand the humeral head must depress and externally

rotate. During passive exercise, if abduction of the

paralyzed shoulder is performed without attention to

this fact, compression trauma to capsule, bursa, or

tendon may result.4

Persons changing position of the

unconscious patient may inadvertently apply traction

to the flaccid arm, traumatizing periarticular tissue.3

Also, sensory deficits may facilitate rough handling

of the paralyzed arm b y relatives, hospital p ersonnel,

or the patient himself.

Rotator cuff injury has been cited as a cause ofhemiplegic shoulder pain. Using arthrogram studies

with 32 hemiplegic patients, Najenson and associates

found that 40 percent had rupture of the rotator cuff

and that 10 of 11 patients with severe shoulder pain

had rupture of the rotator cuff.2

Non e of the patients

had a history of shoulder dysfunction prior to the

onset of hemiplegia. The precipitating cause of the

rotator cuff tear was identified as forced humeral

abduction without external rotation, although other

possible contributing causes such as subluxation and

aging changes in the rotator cuff were mentioned.

"Especially contraindicated, from our point of view,is the passive abd uction performed in the physiother

apy department by the patients themselves, using

M s. Griffin is Assistant Professor, The University of Tennessee

Center for the Health Sciences, Department of Physical Therapy,

M emphis , TN , and Research Coordinator for Physical Medicine and

Rehabil i tat ion, St . Francis Hospital , 5959 Park Ave, M emphis , T N

38117 (USA ).

M s. Reddin is Senior Physical Therapis t , Stroke Unit and Geri-

atrics , Baptis t M emorial Hosp ital—Lam ar Unit , 1025 E. H. Cru mpBlvd, M emphis , TN 38104.

This article was submitted May 26, 1980, and accepted December

9, 1980.

Volume 61 / Num ber 7, July 1981 1041







pulleys to produce abduction in the glenohumeraljoint through traction with the unaffected arm.

,,2Voss

has also stated that the use of overhead pulleys canproduce shoulder pain.6

Other investigators have implied that physical therapy may contribute to painful, limited shoulder motion. In a long-term study of 107 severely disabledhemiplegic patients receiving physical therapy,

Brocklehurst and associates found that stiff and painful shoulders were present in 21 patients by two weekspostonset and had developed in 37 additional patientsby one year postonset.7 "Disappointingly, painfullimitation of shoulder movement was not affected bythe amount of physiotherapy given or the time atwhich it was started."7 However, there was no controlgroup for comparison in that study, and the severityof joint pain and limitation of motion were not described.

S p a s t i c i t y , F l a c c i d i t y , a n d C o n t r a c t u r e s

Immediately following an upper motor neuron lesion such as a CVA, the affected extremities becomeflaccid in approximately 90 percent of cases.

8Flaccid

ity usually lasts a short time and is replaced by apredictable pattern of spasticity within 12 to 18months.9 In the shoulder girdle, spasticity develops inmuscle groups producing scapular retraction-depression and humeral adduction-internal rotation.9,10

There is wide agreement among experts that suchspasticity interferes with the normal scapulohumeralrhythm necessary during GHJ abduction; therefore,passive elevation of the spastic shoulder causes softtissue compression and pain if proper attention is notgiven to scapular mobilization and humeral externalrotation.9-11

The presence of spasticity increases the likelihoodof contractures.12 Once contractures develop, a cycleis established in which attempts to stretch the contracture cause pain, generating reflex protectivespasm of the contracted muscles and patient apprehension and hostility.11 Consequently, increasingly

greater limitations of passive ROM, reduced activemotion, disuse atrophy, and osteoporosis result.5

Flaccidity and spasticity have each been named asthe cause of hemiplegic shoulder pain. Tobis statesthat the typical clinical picture of hemiplegic shoulderpain includes flaccid, paralyzed, and atrophic shoulder musculature, with GHJ subluxation.13 Conversely, Bobath states that shoulder pain does notbecome a problem until spasticity develops.14 Otherinvestigators have noted that hemiplegic patients withspastic shoulder girdle musculature more frequently

complain of pain than do patients who have flaccidity.1, 15 The relative incidence of flaccidity versus spasticity in patients with hemiplegic shoulder pain is notwell documented in the literature.

S u b l u x a t i o n

The incidence of GHJ subluxation has been reported as high as 81 percent in patients with hemiplegia.2 Many authorities maintain that such GHJmalalignment is the main cause of shoulderpain.

12,13,16,17However, others discount any relation

ship between pain and subluxation. Johnstone states,

"The flaccid or hypotonic hanging shoulder will sublux but this is not a factor to which any undue concernought to be given.,,9 Bobath maintains that subluxation is not painful as long as the scapula is mobile,10

and Mossman suggests that subluxation is harmlessas long as passive ROM is not painful.12

Although several investigators have reported theincidence of GHJ subluxation, few have documentedthe relationship between pain and subluxation. Anexception is Najenson and associates' classical studyof associations among hemiplegic patients' shoulder

pain, rupture of the rotator cuff, and GHJ subluxation. In that study, 25 of the 26 patients with GHJsubluxation also had moderate or severe pain.2 Subluxation would therefore appear to be strongly associated with shoulder pain. According to Tobis, thetraction forces present in GHJ subluxation may contribute to rotator cuff tears.13 All of Najenson andassociates' 13 hemiplegic patients with documentedrupture of the rotator cuff had GHJ malalignment.2

The relationship between GHJ subluxation andabnormal tone is unclear. Miglietta and associates

reported finding no relationship between subluxationand spasticity.16 Many authorities suggest that subluxation is caused by spasticity in muscles that depressthe humerus and downwardly rotate the scapula.5,10

On the other hand, some evidence exists that spasticity may actually reduce subluxation; apparently, hyperactive stretch reflexes can be stimulated by theweight of the unsupported arm during ambulation,causing temporary reduction of subluxation.1819

However, flaccidity may be the characteristic stateduring the subluxation process. According to thisviewpoint, gravitational pull unopposed by flaccid

shoulder musculature produces painful and possiblyirreversible overstretching of superior joint capsuleand supraspinatus muscle.13,16

Subluxation appears to develop in the first fewweeks following hemiplegia. Investigating the relationship of supraspinatus muscle activity to the onsetof GHJ subluxation, Chaco and Wolf performedEMG studies on 40 patients at four- and eight-weekintervals after a CVA.20 All six patients who ultimately developed subluxation had done so withinfour weeks, when the affected arm was flaccid (no

supraspinatus EMG activity). Two of the patientslater developed spasticity but maintained their subluxation. These investigators concluded that the supraspinatus muscle began responding to "loading" of

1 0 4 2 PHYSICAL THERAPY







the dependent arm when spasticity appeared, and

subluxation did not occur. However, if the superior

capsule had been allowed to become overstretched

when the flaccid supraspinatus muscle could not re

spond to loading, the GHJ subluxation persisted,

even though spasticity and muscle activity later ap

peared. Chaco and Wolf recommended that "... to

avert subluxation of the glenohumeral joint, loading

on the joint should be avoided as long as the affected

limb is flaccid.,,20

Moskow itz and associates suggested

that support of the flaccid shoulder early in manag e

ment can reduce the incidence of subluxation to as

low as 2 to 5 percent.8

Active Motor Funct ion

Severity of motor disability in hemiplegia is appar

ently associated with shoulder pain and subluxation.

Fugl-Meyer and associates found that patients with

poor motor ability in the affected arm tended todevelop joint pain and limited passive motion,

whereas patients who quickly regained motor func

tion did not.21

In one study o f 222 hemiplegic patients,

the incidence of GHJ malalignment was 66 percent

in patients with com plete or severe paralysis but only

16 percent in patients with partial paralysis.17

Mig-

lietta and associates reported that 79% of hemiplegic

patients with subluxation had no active shoulder

motion, whereas only 9 percent of patients without

subluxation had such severe paralysis.16

Whether the

presence of subluxation can actually impede return

of active motion, as has been suggested by Miglietta

and associates,16

and whether shoulder subluxation

and pain can be reversed if active motion later im

proves, cannot be ascertained from available data.

Shoulder-Hand Syndrome

Pain in the hemiplegic arm may in some cases becaused by a reflex neurovascular disorder. A typicalconstellation of symptoms, often referred to as the"shoulder-hand syndrome" or "reflex sympathetic

dystrophy," may materialize after a CVA or a myocardial infarction and is also known to develop following external trauma such as peripheral nerve injury or fracture.

22The proportion of patients who

may be expected to develop the shoulder-hand syndrome following CVA has been estimated at 12.5percent, but the incidence of the undiagnosed condition may be much larger.

23The syndrome can occur

in patients whose upper limbs are flaccid and withoutcontractures.

12

Phases of progression in shoulder-hand syndromewere originally described by Steinbrocker.

24Initially,

the main signs are usually edema of wrist, metacarpophalangeal, and proximal interphalangeal jointsand hot, dry, and red or blotchy skin. The patient

complains of severe pain in the hand or shoulder, or

both, and protectively restricts any movem ent or sen

sory input to the limb. Gradually, muscle atrophy

and trophic changes in skin, connective tissue, and

joints become the major signs, and the hand becomes

cyanotic, cool, and damp. The typical deformity po

sition assumed by the hand is metacarpophalangeal

joint extension and interphalangeal joint flexion, re

sembling the "intrinsic minus hand. , ,5 Symptoms arepresumed to result from reflex stimulation of the

sympathetic nerve supply by an irritative focus or

from interference with autonomic nervous system

control by the cerebral lesion.25

Although the signs and symptoms of shoulder-hand

syndrome can develop suddenly, they may begin

slowly and insidiously, going unrecognized until

changes are irreversible. Early signs of joint swelling

may be dismissed as dependent edema. Complaints

of severe pain and hyperesthesia and the patient's

refusal to move the wrist, fingers, and shoulder maybe dismissed as emotional lability, depression, or

organic brain syndrome, when in fact the patient's

emotional disorder appeared after, not before, signs

of painful restricted motion.22

The existence of a

shoulder-hand syndrome in the upper limb is incom

patible with the rehabilitation goals of increased mo

bility and function of the upper limb.

Management Considerations

Vigorous painful stretching of the affected shoulder

should be avoided. All persons managing the patient

(including family) should be instructed in proper

handling techniques and in the dangers of pulling on

the affected arm. Prior to, and during, passive or

assistive elevation of the affected shoulder, methods

should be used to reduce spasticity, and attention

should b e directed toward scapular mobilization and

humeral external rotation during shoulder abduction.

Techniques for accomplishing such mobilization are

described by Bob ath,10

Johnstone,9

and Brunnstrom.11

Because traumatic soft tissue compression can occur

with passive humeral abduction, therapists shouldcaution against passive abduction greater than 90

degrees and shou ld direct treatment goals toward full

shoulder external rotation and flexion. Shoulder pu l

leys do not provide adequate scapular rotation and

humeral external rotation and should no t be used as

a means of passive elevation of the affected arm.

All possible efforts should be undertaken to prevent

GHJ subluxation in the first few weeks after onset of

hemiplegia, when the upper limb is flaccid. The most

effective w ay to prevent subluxation has not yet be en

established, although opinions abound in the litera

ture. Shoulder slings have been condem ned for inter

fering with body image, immobilizing the arm, rein

forcing flexor tone, impairing postural support, and

Volume 61 / Number 7, July 1981 1043







impeding normal gait.6

Many question whether slings

prevent subluxation: Friedland states that "there is

no need to support a painfree shoulder in order to

prevent or correct subluxation since the sling does n ot

prevent, improve, cure or reduce such a deformity."19

In one study comparing a small group of new hemi-

plegic patients using a sling with a control group, no

appreciable difference in GHJ subluxation was found

to exist.26 Slings other than the traditional type havebeen described and alternatives, such as lapboards

and arm rests fitted to the wheelchair, have been

used .10 ,12 ,27

How ever, the effectiveness o f any of these

methods in preventing subluxation has yet to be

established.

Inasmuch as degree of paralysis seems related to

GHJ subluxation and pain, therapists should vigor

ously employ methods to improve active motion in

the affected shoulder. Such methods are described by

several authorities.5,9-11

However, a causal relation

ship between use of these techniques and improve

ment in neuromuscular function has not been docu

mented, as observed by Friedland.19

Many authorities believe the most effective treat

ment of the shoulder-hand syndrome is a sympathetic

block followed by intensive physical therapy.22,28

Ap

parently, the decreased pain following interruption of

sympathetic function permits increased use of the

limb with resultant increased sensory input from mus

cle contraction and joint motion.28

Success has also

been reported using a combination of corticosteroids

and physical therapy. Davis and associates reported

complete resolution of symptoms within three weeks

in 68 hemiplegic patients with early signs of shou lder-

hand syndrome, using a combination of oral steroids,

a sling, and exercise preceded by heat or cold.23

All

authorities concur that the best response to treatment

occurs when symptoms are recognized and treated

early. The type o f physical therapy for shoulder-hand

syndrome described in the literature includes proce

dures to overload sensory input and to desensitize,

such as the application of continuous cold or heat

treatments (up to eight hours a day), deep strokingand kneading massage, and vigorous active and pas

sive exercise.29

Any procedures that increase the pa

tient's pain should be avoided, inasmuch as pain

encourages immobilization. The use of transcutane

ous electrical nerve stimulation has been reported

effective in the treatment of reflex sympathetic dys

trophy.30

'31

CONCLUSIONS

In patients with hem iplegia, pain and limited shou l

der joint ROM tend to occur together and constitute

a significant problem. Although a blend of factors,such as contracture, poor motor function, and im

mobilization, may be responsible, GHJ subluxation

seems highly suspect as a cause, and all possible

efforts should be made to prevent subluxation when

the limb is flaccid. Forced passive stretching of the

shoulder into abduction can traumatize the rotator

cuff and bursae and is contraindicated, especially if

external rotation is limited or if spasticity is present.

Improper exercise technique and subluxation may

both contribute to the apparently high incidence of

rotator cuff lesions in hemiplegic patients. Shoulder-hand syndrome is treatable if recognized early but

leads to irreversible pathophysiological changes if

unrecognized. Preventive management by therapists

aware of shoulder biomechanics and the deficits sus

tained by the hemiplegic patient should help elimi

nate the problem of the painful upper extremity.

When pain does occur, a thorough evaluation by the

therapist and early treatment are essential.

REFERENCES

1 . Caldwell CB , Wilson DJ, Braun R M: Evaluation and treatmentof the upper extremity in the hemiplegic stroke patient. ClinOrthop 63 :69 -93 , 1 969

2. Najenson T, Yacubovich E, Pikielini S: Rotator cuff injury inshoulder joints of hemiplegic patients. Scand J Rehabil Med3 : 1 3 1 - 1 3 7 , 1 9 7 1

3. Rusk H: Rehabilitation Medic ine. St. Louis, MO, C.V. MosbyCo , 1 9 7 7 , p p 6 0 1 - 6 2 0

4. Caill iet R: Shoulder Pain. Philadelphia, PA, F.A. Davis Co,1 9 6 6 , pp 3 3 - 5 8

5. Caill iet R: The Shoulder in Hemipleg ia. Philadelphia, PA, F.A.Dav is Co , 1980 , pp 8 9-1 20

6. Voss D: Should patients with hemiplegia wear a sl ing? PhysTher 49:1030, 1969

7. Brocklehurst JC, Andrews K, Richards B, et al : How muchphysical therapy for patients with stroke? Br Med J 1 :1 307-1 3 1 0 , 1 9 7 8

1 0 4 4 P H Y S I C A L T H E R A P Y

Longitudinal studies of patients with hemiplegia

are needed to document the relationship of such

factors as spasticity, GH J sub luxation, painful limited

shoulder ROM, and active motor ability in the af

fected upper extremity. Longitudinal studies might

also clarify under what circumstances subluxation

deve lops and w hether it ever resolves. Further clinical

research is need ed to identify the most effective mean s

of preventing GHJ subluxation. Clinical evidence is

needed concerning effectiveness of facilitation meth

ods in affecting return of active motion. Inasmuch as

some authorities have implied that physical therapy

may be ineffective in preventing and treating hemi

plegic shoulder pain, a controlled study concerning

this question seems indicated. Efforts should be madeto document signs of shoulder-hand syndrome in the

hemiplegic population, determine the real incidence

of this disorder, and identify the most effective early

therapy.







8. Moskowi tz H, Goodman CR, Smi th E, e t a l : Hemip leg icshou lder . NY Sta te J Med 69:548-550, 1969

9. Johns tone M: Resto ra t i on o f Moto r Funct ion i n the St rokePatien t. New York, NY, Church i l l Livings tone, Inc. 1978, pp1 5 - 1 7 7

10 . Bobath B: Adu l t Hem ip leg ia : Eva lua t i on and Trea tment . L on

d o n , Eng land , Wi ll iam H e inem ann, 1978, pp 58-1 34

11. Brunns t rom S: Movement Therapy in Hem ip leg ia . New York,NY, Harper & Row, Publ i shers , Inc. 1970, pp 64-99

12 . M o s s m a n P L : A P r o b le m - Ori e n ted Ap p r o a ch t o S t r o k e Re habi l i ta t i on . Spr ing f ie ld , IL , Char les C Thomas, Publ i sher ,1 9 7 6 , p p 1 4 5 - 1 5 2

13 . Tobis JS : Problems in rehabi li ta ti on o f the hem ip leg ic pa t i en t .

NY Sta te J Med 57:1377-1380, 1957

14. Bobath K: Le t te r to the ed i to r . Phys Ther 52 :44 4-44 5,197 2

15. Dard ie r E, Re id C: Hemip leg ia and pa in fu l shou lders ( l et te r

to the ed i to r ) . Phys Ther 52:1208, 1972

16 . Mig l i e t ta O, Lewi tan A, Rogof f JB : S u b l u xa t io n o f t h e s h o u l

der i n hemip leg ic pa t i en ts , NY Sta te J Med 59:457-460,

1959

17 . Najenson T, P ik ie lny S: Ma la l i gnment o f the g lenohumera l

jo in t fo l low ing hem ip leg ia : A rev iew o f 500 cases . Anna ls o f

Phys ica l Med ic ine 8:96-99, 1965

18 . Taketomi Y: Observa t ions on sub luxa t ion o f the shou lder

jo in t i n hemip leg ia . Phys Ther 55: 39-40, 1975

19 . Fr ied land F: Phys ica l the rapy. In L ich t S (ed) : S t roke and i tsRehabi l i ta t ion. Bal t imore, MD, Wi l l iams & Wil l iams Co, 1975,p p 2 4 6 - 2 4 8

20. Chaco J, Wol f E: Subluxa t ion o f the g lenohumera l jo in t i nh e m i p l e g i a. Am J P h y s M e d 5 0 : 1 3 9 - 1 4 3 , 1 9 71

2 1. Fug l -Meyer AR, Jaasko L, Nor l i n V: The pos t -s t roke hemi p leg ic pa t i en t . Scand J Rehabil Med 7:7 3-83, 1975

22. Moskow i tz E, B ishop H F, Pe H, e t a l : Pos t -hem ip leg ic re f l exsympathe t ic dys t rophy. JAMA 167:836-838, 1958

23. Davis SW, Petr i l lo CR, Eichberg RD, et a l : Shoulder-hands y n d r o m e in h e m i p l eg i c p o p u l a t io n : A 5-year re t rospect ives tud y. Arch Phys Med Rehabil 58:35 3-356, 1977

24. Ste inbrocker O: Shou lder -hand syn drom e: Asso c ia ted pa in fu l homo la te ra l d i sab i l i ty o f shou lder and hand w i th swe l l i nga n d a t ro p h y o f h a n d . Am J M e d 3 : 4 0 2 - 4 0 7 , 1 9 47

2 5 . S w a n DM : S h o u l d e r - h a n d s y n d r o m e f o l l o w i n g h e m i p l e g i a .Neuro logy 4:4 80-48 2, 1954

26. Hurd MM, Far re ll KH , Waylon is GW: Shou lder s l i ng fo r hem ip leg ia : Fr iend o r foe? Arch Phys Med Rehabi l 55:519-522,1974

27. Zanke l H T: St roke Rehabi l ita t i on . Spr in g f ie ld , IL , Char les CT h o m a s , P u b li s h e r, 1 9 7 1 , p p 1 3 8 - 1 4 0

28. Bon ica JJ: Causa lg ia and o ther re f l ex sympathe t ic dys t ro p h i e s . P o s tg r a d M e d 5 3 : 1 4 3 - 1 4 8 , 1 9 7 3

29. Johnson EW, Pannozzo AN: Management o f shou lder -handsyndrome. JAMA 195:152-154, 1966

30 . St i l z RJ, Car ron H , Sanders DB: Reflex sym pathe t ic dys t ro phy in a 6 year -o ld : Successfu l t rea tmen t by t ranscu taneo usnerve s t imu la t i on . Anes th Ana lg 56:438-443, 1977

31. Rich l i n DM, Car ron H, Rowl ingson JC, e t a l : Ref lex sympathe t ic dys t rophy: Successfu l t rea tment by t ranscu taneouss t imu la t i on . J Ped ia t r 93:84-86, 1978

Volume 61 / Number 7, July 1981 1 0 4 5







1981; 61:1041-1045.PHYS THER.

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