Hemiplegic Shoulder Pain - Physical Therapy

Hemiplegic Shoulder Pain 

Judy W Griffin 

PHYS THER. 1986; 66:1884-1893. 

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JUDY W. GRIFFIN 

Shoulder pain and stiffness.are, unfortunately, 

frequent complications in 

hemiplegia. The following clinical picture 

of hemiplegic shoulder pain (HSP) 

has been described by several authorities. 

1-3 The patient frequently has severe 

paralysis; glenohumeral joint (GHJ) 

subluxation or edema of the wrist and 

hand also may exist. Pain may be localized 

to the shoulder or can radiate to 

include the elbow and hand. Localized 

tenderness over the biceps brachii and 

supraspinatus tendons frequently is 

present. Although pain may be present 

at rest, the patient complains of increased 

pain with attempted passive motion 

or with a dependent position of the 

arm. The most painful and limited 

shoulder movement is usually lateral 

(external) rotation, which is followed in 

severity by abduction. 4-6 Pain may intensify 

at night, interfering with sleep. 

Many authorities believe spasticity is 

characteristic of the HSP syndrome, 7-9 

although flaccidity also has been described 

as the associated state of tone. 1 

No significant relationship between sex 

or hemiplegic side appears to exist. 4,10 

Duration of hemiplegia appears to be 

significantly related to HSP, although 

HSP can develop in the early weeks after 

stroke. In a longitudinal study of 135 

patients, Brocklehurst et al noted that 

pain and stiffness were present in 16% 

of the patients two weeks after the stroke 

and had developed in an additional 27% 

Ms. Griffin is Associate Professor, Department of 

Rehabilitation Sciences, University of Tennessee, 

Memphis, 800 Madison Ave, Memphis, TN 38163 

(USA). 

This article reviews the literature relevant to the possible causes, prevention, 

and treatment of hemiplegic shoulder pain. Shoulder pain and stiffness impede 

the rehabilitation of patients with hemiplegia. The cause of this complication is 

unknown, but it may be related to the severity of neurological deficits, preexisting 

or posthemiplegic soft tissue injury, subluxation, brachial plexus injury, or shoulder-hand 

syndrome. Shoulder pain may be preventable if risk factors can be 

identified and appropriate prophylaxis applied. Resolution of the condition depends 

on diagnosis and effective treatment at the onset of the symptoms. More 

clinical research is needed to clarify the cause of hemiplegic shoulder pain and 

to document the efficacy of prophylactic and treatment methods. 

Key Words: Cerebrovascular disorders, Hemiplegia, Pain, Physical therapy, 

Shoulder. 

after one year. 11 Liao et al noted a significant 

correlation between HSP and 

the duration of hemiplegia before physical 

therapy was begun. 4 Studies of patients 

with HSP have reported an average 

onset time after the stroke to be two 

to three months. 4,10,12 

Hemiplegic shoulder pain impedes 

and prolongs rehabilitation. Pain and 

limited shoulder range of motion interfere 

with self-care activities, impede balance, 

and create difficulty with transfers 

and ambulation. Liao et al found that 

patients with HSP demonstrated significantly 

less motor recovery in the upper 

limb and achieved less ambulatory success 

than comparable patients without 

HSP. 4 Shoulder pain limits patient ability 

and desire to participate in social as 

well as physical activities, and it contributes 

to anxiety, frustration, and discouragement. 

According to Braun et al, 

the patient who has pain when he 

moves will remain immobile. If he 

also has pain at rest, he usually withdraws 

from any rehabilitation program. 

13 

DEFINITION OF THE PROBLEM 

Epidemiological data concerning 

HSP have been gathered from patients 

enrolled in outpatient or inpatient rehabilitation 

programs; these patients 

inevitably are the most severely physically 

disabled. 11 Thus, the incidence of 

HSP essentially is unknown in patients 

not participating in rehabilitation programs, 

in patients with mild physical 

disability, or in patients after discharge 

from rehabilitation. In the general population 

of hemiplegic patients enrolled 

in rehabilitation programs, incidences of 

HSP have been reported at 38% 14 and 

70%. 15 Incidences at the time of patient 

admission into rehabilitation programs 

have varied from 28% 4 to 67%. 5 Development 

of HSP during the rehabilitation 

phase has been reported, 4,5 and one 

group of investigators noted that 72% 

of their patients developed HSP during 

rehabilitation. 16 Variability in reported 

incidences may be a result of patient 

differences in duration of hemiplegia 

and severity of paralysis, in addition to 

differences among investigators in defining 

HSP. 

A major obstacle to determining the 

magnitude of the problem is a lack of 

an accepted set of diagnostic criteria. 

Hemiplegic shoulder pain remains a 

nebulous clinical entity, defined differently 

by each investigator. Pain is an 

elusive symptom, defying quantitative 

measurement even in patients with intact 

sensorimotor, cognitive, and communicative 

faculties. The presence of 

pain in hemiplegic patients has been 

defined variously as discomfort with 

pressure over the supraspinatus or biceps 

brachii tendons 14 or shoulder joint 1 

and complaint of pain at rest or with 

movement. 17 Pain has been graded from 

moderate to severe, based on its radiation 

or location. 17 Several investigators 

reporting on HSP have not defined pain 

at all. 11,16,18-21 

A reduced amplitude of passive shoulder 

ROM frequently is included as part 

of the definition of HSP. Improvement 

or worsening of the pain is considered 

to be reflected by an increase or decrease 

of passive ROM. 4-6,22 Differences exist, 

however, among investigators in their 

descriptions of ROM. Examples include 

1884 PHYSICAL THERAPY 



percentage of patients who could not 

tolerate passive flexion to 90 degrees, 14 

description of ROM as limited or not 

limited, 1 and present or absent limitations 

of passive ROM. 11 Some investigators 

used a rating scale, combining 

percentage of limited ROM with the 

amount of associated pain. 5,6 A few research 

studies have reported direct goniometric 

measurements of each shoulder 

motion. 4,22 

Diagnosis of HSP typically is accomplished 

clinically, based on a combination 

of signs and symptoms. A need 

exists, however, for commonly agreed 

on diagnostic criteria and methods for 

measuring pain and ROM. Otherwise, 

the findings of different investigators are 

not comparable concerning either the 

incidence of HSP or the efficacy of prophylaxis 

and treatment. 

The pathogenesis of HSP remains unclear. 

Etiologic agents most commonly 

mentioned in the literature are subluxation, 

rotator cuff tears, severe paralysis, 

brachial plexus injuries, exacerbation of 

preexisting pathological conditions, and 

improper exercise or handling of the 

paralyzed arm. In more severe cases, a 

shoulder-hand syndrome (SHS) may exist. 

Chronic frozen shoulder also has 

been reported as the associated state of 

patients with HSP. Comprehensive 

long-range studies to identify the cause 

of HSP have not been conducted yet. 

Many investigators have sought to determine 

the incidence of single factors 

such as subluxation or rotator cuff tears; 

some have studied only patients with 

HSP, and others have studied the incidence 

of single factors in a general hemiplegic 

population. 

Purpose of Paper 

A single cause of HSP probably does 

not exist; the pathogenesis no doubt is a 

complex series of interrelated factors. 

Prospective, controlled research is lacking 

concerning the causes of HSP and 

efficacy of treatment. Several studies, 

however, have examined the association 

of HSP with one or more of the above 

potential etiologic factors. One purpose 

of this article is to review those studies. 

The ultimate value of such a review 

would be 1) to identify early after the 

stroke the patients who might be at risk 

and 2) to describe prophylaxis. Hemiplegic 

shoulder pain should be viewed 

as a largely preventable complication 

after stroke. Additional purposes of this 

article are to discuss the management of 

HSP and to summarize general approaches 

for further study of HSP. 

POSSIBLE CAUSES 

Neurological Deficits 

The reported positive association between 

HSP and loss of motor functions 

is impressive. Patients with slight paresis 

rarely complain of shoulder pain, 

whereas patients having severe paralysis 

frequently develop shoulder problems 

during rehabilitation. 3 Najenson et al 

noted 84% of hemiplegic patients with 

severe paralysis had moderate or severe 

shoulder pain. 17 In a prospective study 

of hemiplegic patients, Fugl-Meyer et al 

noted joint pain and limited ROM that 

developed in patients who initially had 

poor motor function. 18 In patients having 

had neurosurgery, the development 

of a stiff painful shoulder was found to 

be correlated significantly with both the 

extent of hemiparesis and impairment 

of consciousness. 10 

The trauma that may be associated 

with handling a paralyzed upper limb 

can aggravate preexisting conditions 

such as arthritis or tendinitis. 23 Paralysis 

imposes a condition of immobility that 

may contribute to the development of 

GHJ stiffness. Paralysis also may predispose 

the affected shoulder to subluxation 

or traction injury, which secondarily 

may cause pain. 

Abnormal tone—either flaccidity or 

spasticity—has been mentioned as an 

etiological factor in HSP. Because abnormal 

tone coexists with deficits in 

voluntary motor function, shoulder immobility 

and, therefore, danger of contractures 

result. Spasticity tends to be 

mentioned more frequently as being associated 

with HSP, perhaps because 

spasticity is the predominant condition 

over time in chronic hemiplegia. In a 

recent study of patients with cerebrovascular 

accidents (CVAs) with HSP, 88% 

were classified as spastic and 24% flaccid. 

16 Flaccidity and spasticity will be 

included in further sections as they 

relate to other possible causative agents. 

Other neurological deficits such as 

sensory loss, visual field deficits, communication 

disorders, loss of body image, 

and sensory-integrative disorders 

affect the prognosis for upper limb function. 

24 These deficits in combination 

with motor loss and abnormal muscle 

tone may increase the risk of HSP. 

Soft Tissue Injury 

Influence of preexisting pathological 

conditions. The painless excursions of 

shoulder flexion and abduction normally 

decrease with age. 25 One factor 

contributing to this decreased range is 

that of postural changes. The elderly 

individual develops increased dorsal kyphosis 

with resultant downward scapular 

rotation. 25 This position lowers the 

coracoacromial arch, causing impingement 

early in the range of GHJ flexion 

or abduction. 26 Also contributing to decreased 

shoulder ROM are the many 

degenerative changes in articular surfaces 

and soft tissue that occur with age. 

Such degenerative changes may or may 

not have been asymptomatic before the 

onset of the hemiplegia. 

Degenerative changes of the acromioclavicular 

joint, glenoid labrum, and articular 

cartilage of the glenoid fossa appear 

after the second decade of life, 27,28 

and hypertrophy of synovial tissue develops 

by age 30 years. 27 Between the 

fourth and fifth decades of life, and increasing 

with age, significant degenerative 

changes occur in the periarticular 

soft tissue: The biceps brachii tendon 

thickens and shreds; the rotator cuff, 

particularly the supraspinatus muscle, 

thins and frays; calcific deposits may 

appear in the rotator cuff tendons. 27 The 

most severe tears in the rotator cuff 

occur from ages 60 to 70 years. 27 With 

the wear and tear of normal use, degenerated 

areas of the rotator cuff and the 

biceps brachii tendon become edematous, 

and adjacent bursae thicken. The 

significant result is reduced space under 

the coracoacromial arch, with an increased 

likelihood of impingement and 

pain. Although extensive degenerative 

changes can be present without symptoms 

or an impairment of function, the 

additional stress of paralysis can activate 

previously asymptomatic abnormalities. 

2327 

Impingement during passive shoulder 

flexion and abduction. Impingement of 

soft tissue may occur during shoulder 

flexion or abduction if the humerus is 

compressed against the coracoacromial 

arch. Severe impingement can cause rotator 

cuff ischemia, 23 soft tissue injury, 

and pain. 3 Impingement usually is minimized 

by two mechanisms: upward rotation 

of the scapula, which elevates the 

coracoacromial arch, and humeral rotation, 

which alters the position of humeral 

tubercles in relation to the arch. 

Medial rotation must accompany flexion, 

and lateral rotation must accompany 

abduction to avoid impingement. 

2729 

In the flaccid paralytic state, the 

weight of the unsupported arm can 

lower the coracoacromial arch, increasing 

the danger of impingement during 

Volume 66 / Number 12, December 1986 1885 



passive elevation of the arm. Spasticity 

may increase the likelihood of impingement 

during GHJ abduction, because 

spastic rhomboid muscles fix the scapula 

in downward rotation, and spastic 

adductor-medial rotator muscles prevent 

lateral humeral rotation. 8,23 Spasticity, 

thus, might contribute to impingement 

during active and passive GHJ 

abduction. Several authorities in stroke 

rehabilitation have discussed the importance 

of reducing tone and adhering to 

biomechanical principles during passive 

elevation of the spastic shoulder. 30-32 

Improper passive exercise by health 

care professionals, family, or patients 

themselves may be a major cause of 

shoulder pain in hemiplegic patients. 

3,8,11,33 Failure to provide upward 

scapular rotation and lateral humeral 

rotation during passive abduction are 

the most frequently mentioned mechanisms 

of pain. Use of overhead pulleys, 

furthermore, has been cited as a cause 

of impingement pain 17,34 and even rotator 

cuff rupture. 17 No controlled studies, 

however, have been conducted in this 

area. 

Rotator cuff rupture. Partial tears of 

the rotator cuff are common after 50 or 

60 years of age. 27-28 Wear that is secondary 

to impingement has been cited as a 

major contributing factor in rotator cuff 

tears. 35 A fall or stress causing forcible 

abduction without lateral rotation can 

convert a partial tear to a complete rupture. 

36 Degenerative changes, however, 

can be so severe that even minor injuries 

in nonhemiplegic patients can precipitate 

a complete tear. 27 Patients with rotator 

cuff rupture have symptoms of 

severe pain, especially with passive flexion 

or abduction; tenderness with palpation 

at the rupture site; and atrophy 

and weakness of the lateral rotator and 

the deltoid muscles. 27,37 

Several arthrographic studies in hemiplegic 

patients have revealed a high incidence 

of rotator cuff tears. Ruptures 

were found in 33% of hemiplegic patients 

with painful, stiff shoulders; none 

of the patients had a premorbid history 

of pathological conditions of the shoulder. 

38 Examining only patients with severe 

paralysis, Najenson et al found a 

40% incidence of rotator cuff rupture 

on the affected side compared with a 

16% incidence on the nonaffected 

side. 17 Najenson et al further associated 

pain with rotator cuff rupture and subluxation; 

all of the 11 patients with severe 

pain had subluxation, and 10 had 

rupture of the rotator cuff. 17 

The cause of rotator cuff rupture in 

hemiplegia has been identified as impingement 

during passive abduction 

above 90 degrees 3 and as forced abduction 

without lateral rotation, especially 

with the use of overhead pulleys. 17 Rotator 

cuff rupture also may be facilitated 

by prior degenerative changes and by 

subluxation, 17 trauma during falls, 38 and 

repeated small traction injuries. 39 

Adhesive capsulitis. Conversely, 

other investigators have noted that adhesive 

capsular changes, not rotator cuff 

ruptures, are the predominant findings 

during arthrography of hemiplegic 

shoulders. Rizk et al performed arthrographic 

studies of 30 patients with stiff, 

painful shoulders and reported a 77% 

incidence of adhesive capsulitis; they 

saw no evidence of rotator cuff rupture. 

12 Hakuno et al, performing arthrography 

on both affected and unaffected 

shoulders in 77 randomly selected 

hemiplegic patients, found an equal incidence 

of rotator cuff rupture on affected 

and unaffected sides (22% and 

24%, respectively). 40 Hakuno et al further 

reported that adhesive changes were 

noted the most frequently during arthrography. 

Although adhesive changes 

were noted in both paralyzed and nonparalyzed 

shoulders, 55% of the paralyzed 

shoulders with adhesions had multiple 

adhesion sites compared with 4% 

of nonparalyzed shoulders. Adhesions 

in the GHJ and the subscapularis bursae 

were associated significantly with limited 

GHJ motion; adhesions in the bicipital 

tendon sleeve were associated significantly 

with subluxation but not with 

ROM restriction. 40 

The classical clinical picture for adhesive 

capsulitis 41 is strikingly similar to 

that described previously for HSP. The 

cause of adhesive capsulitis even in nonhemiplegic 

patients is unknown. 27 The 

most significantly related factors in development 

seem to be prolonged immobilization 

secondary to pain and age 

greater than 40 years. 27,28,41,42 Pain secondary 

to impingement may be a precipitating 

factor. 41 DePalma has noted 

that the ages of the greatest incidence of 

adhesive capsulitis and the most degenerative 

soft tissue changes are the same 

(40 to 60 years). 27 Suprascapular neuropathy 

also has been associated with 

frozen shoulder. 43 

In hemiplegic patients, the development 

of adhesive capsulitis has been 

related to paralysis, 10,40 unconsciousness, 

10 impingement pain, 3 and subluxation. 

20 The precise cause, however, remains 

obscure. 

Glenohumeral joint malalignment. Inferior 

subluxation of the GHJ appears 

more frequently in patients with hemiplegia 

than in other geriatric patients. 

Reviewing radiographs of 300 geriatric 

patients, Carpenter and Millard reported 

a 5% incidence of subluxation; 

80% of the subluxations were superior 

in the nonhemiplegic patients. 44 All 5 of 

the hemiplegic patients had inferior subluxation, 

and 4 of these had bilateral 

subluxation. The magnitude of inferior 

subluxation on the affected side, however, 

was much greater than on the unaffected 

side. Radiographic studies by 

other investigators have not demonstrated 

subluxation on the unaffected 

side. 245 

In hemiplegic patients, without regard 

to severity of paralysis or time since the 

onset of the hemiplegia, the incidence 

of inferior subluxation has been reported 

variously as 30%, 2,40 56%, 14 and 

64%. 20 In patients with severe paralysis, 

the reported incidences of subluxation 

usually are substantially higher: 66%, 2 

81%, 17 and 92%. 46 

Subluxation appears to develop during 

the several weeks immediately after 

the stroke, when flaccid paralysis prevents 

normal muscle response to loading. 

47 Using radiological examinations 

of stroke patients within 24 hours of 

their admission to the hospital, Smith et 

al found 60% of their patients with complete 

paralysis had GHJ malalignment. 

48 

Some evidence exists that subluxation 

may be irreversible after a certain period 

of time, regardless of return of active 

motion or spasticity in the deltoid and 

supraspinatus muscles. Longitudinal 

electromyographic studies demonstrated 

that subluxation developed during 

the flaccid period and did not occur 

after the supraspinatus muscle demonstrated 

EMG activity in response to 

loading. Having developed, however, 

the subluxation did not reverse even 

when supraspinatus muscle EMG activity 

became evident. 17 Some anecdotal 

reports indicate that, in many patients 

who have chronic subluxation at rest, 

temporary reduction of the subluxation 

can occur during ambulation 9 or during 

voluntary effort. 14 

Removal of the usual glenohumeral 

stabilizing mechanisms described by 

Basmajian and Bazant 49 permits inferior 

displacement of the humeral head in 

relation to the glenoid fossa: Specifically, 

superior tilting of the glenoid fossa 

is reversed secondarily to paralysis of 

the muscles that rotate the scapula up- 




ward and secondarily to the weight of 

the unsupported arm; the normal passive 

restraint mechanism from the 

superior capsule and coracohumeral ligament 

is ineffective secondarily to scapular 

downward rotation; and the normal 

active restraint mechanism of the posterior 

deltoid and supraspinatus muscle 

contractions is inactive secondarily to 

the upper motor neuron paralysis. The 

gravitational pull on the arm when the 

patient is upright creates an unopposed 

distracting force with resulting inferior 

subluxation of the humeral head 23 (Figure). 

Although the cause of inferior subluxation 

usually is attributed to paralysis 

resulting from CVA, other possible 

causes are rotator cuff tear 17 and brachial 

plexus upper trunk injury. 23,50 

Spasticity also has been mentioned as 

contributing to subluxation by positioning 

the scapula in downward rotation. 

23,30 The real association between 

subluxation and spasticity, however, is 

unclear. 

How dangerous is subluxation? Several 

authorities in rehabilitation discount 

any importance of subluxation, 

30,32,51 although they offer little 

evidence to support their view. Others 

believe that subluxation may be a major 

cause of HSP because of the resulting 

overstretching of the GHJ soft tissue. 

1,20,46 Passive dependence of the unsupported 

arm, even in an uninvolved 

shoulder, elongates the rotator cuff and 

creates ischemia in the biceps brachii 

tendon and in the "critical zone" of the 

rotator cuff. 26,28 Hakuno et al found a 

significant correlation between subluxation 

and arthrographically demonstrated 

adhesive changes in the bicipital 

tendon sleeve. 40 Subluxation may cause 

traction injury to the upper trunk of the 

brachial plexus. 50 Ring et al reported 

EMG evidence of axillary nerve dysfunction 

in patients with GHJ subluxation 

and hypothesized that initial stages 

of subluxation may cause axillary nerve 

compression. 52 

The relationship of pain to subluxation 

is unclear. Some investigators have 

reported no correlation between incidences 

of subluxation and pain. 12,14 Najenson 

et al, however, found 93% of 

their hemiplegic patients with severe paralysis 

that was accompanied by moderate 

or severe pain had subluxation. 17 

Although subluxation may not be associated 

with pain in the early stage of 

hemiplegia, if subluxation continues 

into the chronic spastic stage, the association 

of pain and limited motion may 

be higher. 13 A recent study found sub 

luxation was associated frequently with 

HSP; 85% of the patients with spasticity 

had HSP, and subluxation was present 

in 67% of these patients. 16 

Brachial plexus and peripheral nerve 

injuries. Electromyographic evidence of 

lower motor neuron involvement has 

been reported in hemiplegic patients 

and is found twice as frequently in the 

upper as in the lower limb. 23 Brachial 

plexus injury may be a source of shoulder 

pain and a cause of subluxation. 

Chino reported 75% of his hemiplegic 

patients with subluxation demonstrated 

Figure. Basmajian's principle. A) The normal 

position of the shoulder prevents subluxation 

because the humeral head cannot 

displace laterally out of the upwardly tilted 

glenoid fossa (dotted arrow). B) Drooping of 

the shoulder in some hemiplegic patients permits 

subluxation of the humeral head out of 

the downwardly tilted glenoid fossa (dotted 

arrow). (Reprinted by permission of W. B. 

Saunders Co. 92 ) 

neuropathic responses in the deltoid and 

supraspinatus muscles. 50 Kaplan et al 

found EMG changes consistent with injury 

of the upper trunk of the brachial 

plexus in five hemiplegic patients with 

flaccid paralysis and atrophy of the 

shoulder musculature. 53 Electromyographic 

evidence of pressure neuropathy 

of the ulnar nerve and brachial plexus 

neuropathies was reported by Moskowitz 

and Porter in eight hemiplegic patients. 

54 Other investigators have found 

no electrophysiological evidence of brachial 

plexus injuries in hemiplegic patients. 

12,19,46,47,55 

Signs of neuropathy are superimposed 

on the hemiplegic paresis. They include 

extensive segmental atrophy, an atypical 

pattern of return of motor function (ie, 

distal before proximal return), and electrophysiological 

signs. 54 

All investigators reporting brachial 

plexus injuries in hemiplegic patients 

identify the probable mechanism of injury 

as a combination of flaccid paralysis 

and traction injury. Traction stress is 

caused by either lack of support of the 

paralyzed flaccid shoulder 50,52-54 or pulls 

on the flaccid arm by personnel who 

move the patient. 54,56 Patients who are 

unconscious are at the greatest risk of 

having traction and pressure neuropathies. 

56 

The occurrence of a brachial plexus 

injury can increase rehabilitation time 

greatly. The superimposition of a lower 

motor neuron injury on the upper motor 

neuron lesion increases the likelihood 

for the development of painful 

contractures. 54 A brachial plexus injury 

constitutes a major setback for recovery 

of active motion; because of the slow 

rate of nerve regeneration, functional 

recovery of shoulder movement may be 

delayed by 8 to 12 months. 53 

Shoulder-hand syndrome. This reflex 

neurovascular disorder is characterized 

by pain and hyperesthesia, edema, 

trophic changes, and vasomotor instability. 

Signs and symptoms vary among 

patients, and onset may be dramatic. 57 

The temporal sequence of signs has been 

described by many authorities. 58-60 Early 

manifestations include pain and limited 

motion in the shoulder, wrist, and hand; 

the most restricted motions are shoulder 

lateral rotation and abduction, wrist 

dorsiflexion, and flexion of the metacarpophalangeal 

and proximal interphalangeal 

joints. Edema is evident in the wrist 

and finger joints, with increased skin 

temperature, rubor, and hyperhidrosis 

or hypohidrosis. As the condition progresses, 

pain decreases and stiffness predominates. 

The skin becomes shiny, cyanotic, 

and hyperhidrotic. Intrinsic 

muscle atrophy, nail changes, and thickening 

of subcutaneous tissue in the finger 

joints and palmar fascia develop. 

Osteoporosis is demonstrable radiographically. 

The syndrome may last 

from months to years. 61 

Shoulder-hand syndrome is known to 

develop after internal lesions such as 

CVA, myocardial infarction, cervical osteoarthritis, 

or spondylosis. The syndrome 

also develops often after trauma 

such as peripheral nerve injury, fracture, 

or spinal cord injury. 58,59,62 The precise 




mechanisms triggering SHS are unknown. 

Tissue injury may serve as a 

focus of noxious stimuli, altering central 

control of the sympathetic nervous system. 

58 Immobilization of the limb because 

of injury, debility, pain, or paralysis 

may result in decreased sensory input 

from the limb to the central nervous 

system, causing an imbalance in the central 

neural control of the sympathetic 

nervous system. 58 Inactivity of muscles 

that perform pumping actions in the 

hand and the axilla (secondary to paralysis 

or immobilization) may cause altered 

circulation and edema. 23,27,63,64 

In hemiplegia, however, vasomotor 

changes may not be related necessarily 

to paralysis. 51,65 The cerebrovascular lesion 

may disturb central vasomotor regulation, 

resulting in arteriolar vasodilation 

of the upper limb. 65 Lesion of the 

premotor and anterior motor cortical 

regions may cause SHS after a stroke. 66 

The incidence of SHS among hemiplegic 

patients is unclear. Ring et al 

found no cases in 24 patients followed 

one year after a stroke. 52 In a retrospective 

study of 540 hemiplegic patients, 

Davis et al reported a 12.5% incidence 

of SHS. 57 Van Ouwenaller et al found 

the incidence of SHS in 215 hemiplegic 

patients was 28%. 16 Finch and Harvey, 

in a prospective study of 20 patients 

hospitalized after stroke, reported 50% 

developed signs of SHS. 67 Of hemiplegic 

patients with shoulder pain, the percentage 

of patients with signs of SHS 

has been cited as 36% 6 and 32%. 16 

Davis et al reported that most of their 

patients who developed SHS did so two 

to four months after the stroke, and they 

hypothesized that the incidence was the 

least in patients with mild involvement. 

57 Mossman also reported that the 

syndrome was more typical of patients 

with little or no voluntary motor ability. 

51 Two studies comparing hemiplegic 

patients with and without SHS, however, 

reported no difference between 

groups in active motor ability or muscle 

tone. 6,67 Van Ouwenaller et al found a 

higher incidence of SHS in patients with 

spasticity than in those without. 16 

Hemiplegic patients with SHS have 

been found to be significantly more confused 

and have greater sensory loss than 

other hemiplegic patients; they also have 

a higher incidence of subluxation than 

other hemiplegic patients. 67 Weiss and 

Ellis stated that hemiplegic patients with 

prior myocardial infarction may be at 

special risk for developing SHS. 65 Confirming 

this finding, Finch and Harvey 

reported that half of the patients devel 

oping the syndrome had a history of 

cardiac abnormalities. 67 

Thalamic pain. A burning, excruciating 

pain may involve the face, tongue, 

and thorax as well as the affected 

limbs. 68 Marked proprioceptive loss 

usually is present, 68 and the patient may 

neglect the paretic side except during a 

painful episode. 69 Peculiar sensations relating 

to the limb, feelings such as absence, 

twisting, or changes in size, may 

be present. The pain may be constant 

but is exacerbated by changes in emotional 

states, visual or auditory stimuli, 

temperature, or cutaneous stimuli. 68,69 

Vasomotor disturbances may be present 

on the affected side, characterized by 

cycles of skin coolness, pallor, and hyperhidrosis, 

alternating with warmth, 

rubor, and edema. 

A lesion of the lateral thalamus, the 

posterior limb of the internal capsule, or 

the parietal lobe is believed to be responsible. 

68,69 The incidence is unknown. 

Thalamic pain responds poorly to treatment. 

70 

PROPHYLAXIS AND 

TREATMENT 

Although cases of HSP may result 

directly from CNS lesions, many may 

be caused by faulty treatment after the 

stroke. 71 Careless handling of the paralyzed 

upper limb at any time after the 

onset of hemiplegia can precipitate 

shoulder injury and pain. For prophylaxis 

to be effective, however, it must 

begin immediately after the stroke. After 

the pain cycle has begun, resultant anxiety, 

overprotection, and disuse inevitably 

produce decreased ROM and contractures. 

23 

Treatment of the many varieties of 

HSP represents a complex and difficult 

problem. The ideal treatment is prevention; 

the next best management is to 

implement a treatment program immediately 

when the first painful symptoms 

appear. 

Positioning and Handling of the 

Dependent Patient 

Education of the patient and everyone 

associated with the care of the patient in 

the acute period after the stroke is critical 

to the success of a positioning and 

handling program. According to Mulley, 

pain in the shoulder is a complex subject 

that has not yet been approached 

systematically, but even in our present 

state of ignorance we can prevent 

much pain and limitation of movement 

in the shoulder by careful positioning 

and handling. 33 

Adequate support and protection of 

the flaccid arm are essential when the 

patient is lifted or moved in bed. 48,71,72 

All persons moving the dependent patient 

must be instructed concerning the 

hazards of pulling on the affected arm. 

Methods of upper limb handling when 

the patient is moved in bed or is assisted 

to a sitting position have been described. 

30 ' 32 ' 72 " 74 

Positioning for the flaccid limb in bed 

also is important, and protocols are discussed 

in several sources. 23,30,32,72,74,75 

The typical spasticity pattern of scapular 

retraction, neck flexion to the affected 

side, shoulder medial rotation and adduction, 

and elbow-wrist flexion should 

be avoided. Pillows can be used to support 

and elevate the limb to lessen dependent 

edema of the hand. 74,76,77 When 

the patient is in the supine position, the 

shoulder should be supported in a flexion-abduction-lateral 

rotation position. 

71,72 Bohannon et al have described 

a method of shoulder positioning in bed 

using a device made of foam and Velcro. 

78 Chino recommended overhead 

suspension of the arm in bed. 50 When 

the patient is sidelying, the affected arm 

should be flexed and rotated laterally 

with the shoulder girdle protracted. 71 

Limited sidelying on the affected side 

sometimes is recommended. 77 When the 

patient is sidelying on the unaffected 

side, the affected shoulder should be 

supported on pillows and not allowed to 

lie in horizontal adduction. A horizontally 

adducted position may exert traction 

of the suprascapular nerve and 

cause HSP. 43 

Facilitation of Active Motion 

Early facilitation of activity in muscle 

groups producing protraction and upward 

rotation of the scapula and flexionabduction 

of the shoulder is essential. 

Methods to inhibit spasticity contributing 

to scapular retraction and shoulder 

adduction and medial rotation likewise 

are essential if spasticity is present. A 

discussion of these methods is beyond 

the scope of this article; descriptions of 

facilitation-inhibition programs may be 

found in several sources. 23,30-32,74,75,79,80 

Unfortunately, little controlled research 

is available documenting the relative efficacy 

of these methods. 

Electrical stimulation and EMG biofeedback, 

alone or in combination, have 

emerged as promising therapeutic adjuncts 

in the facilitation of voluntary 

motion and the inhibition of spasticity. 

81-85 Most studies relating to the efficacy 

of these methods, however, have 




een of distal extremity function, that 

is, facilitation of ankle dorsiflexion and 

wrist-finger extension. Few studies have 

been published relating to the effect of 

biofeedback on proximal muscle function. 

Lee et al found no difference in 

the deltoid muscle EMG activity between 

patients receiving biofeedback 

and patients in conventional physical 

therapy and placebo groups. 86 Inglis et 

al, however, found that hemiplegic patients 

receiving EMG biofeedback and 

physical therapy improved more in 

shoulder strength and ROM than patients 

receiving physical therapy alone. 87 

Patients with proprioceptive impairment 

may have limited success with biofeedback 

training, 88 although some evidence 

indicates sensory loss may not 

preclude improvement with biofeedback. 

89 Electrical stimulation and biofeedback 

may be effective in preventing 

or reducing GHJ subluxation, as will be 

discussed in the next section. 

Subluxation 

Prevention of subluxation requires 

the institution of prophylactic methods 

in the first few weeks of flaccid paralysis. 

46,50 After spasticity or active shoulder 

motion, or both, appear, subluxation 

seems unlikely to develop. 47 

Objective documentation of subluxation 

requires radiographs with the patient 

in the upright, not supine, position. 

17,20,46,48 Likewise, the efficacy of 

methods for preventing or reducing subluxation 

should be demonstrated radiographically. 

Shai et al hypothesized 

that earlier radiologic diagnosis of subluxation 

(ie, before grade I or II changes 

are demonstrated) might enable more 

effective prevention than if it is delayed. 

21 In their study, 12 of 14 patients 

showing early, positive radiologic signs 

of subluxation subsequently developed 

a painful shoulder, and 4 developed subluxation. 

Shai et al suggested that patients 

showing early radiologic signs of 

subluxation might be most likely to benefit 

from early orthotic intervention. 

When the patient is upright, the arm 

should be supported and positioned to 

prevent unopposed gravitational stress 

on the soft tissue of the GHJ. Various 

methods have been described for upper 

limb positioning in the wheelchair: pillows, 

a padded arm trough attached to 

the wheelchair arm or a lapboard, 30,72 or 

an overhead wheelchair sling. 15,23,72,90 

None of these methods has been proven 

to be more effective than others in preventing 

or reducing subluxation. 

Some support of the flaccid arm is 

necessary when the patient is ambulating. 

The patient with severe perceptual 

deficits and denial may need a sling for 

protecting the arm against trauma. 74 A 

multitude of sling types have been described. 

30,91-96 Elements to be considered 

in the choice of slings for particular 

patient problems have been summarized. 

95,96 External support can be discontinued 

when muscle tone around the 

GHJ is adequate to prevent subluxation. 

91 If needed, a sling should be used 

only during ambulation; the sling cannot 

be allowed to contribute to shoulder 

immobilization. An exercise program 

always should accompany the use of a 

sling. 24 

Controversy abounds concerning the 

use of slings; disadvantages to their use 

have been enumerated by many authorities. 

34,71,94,97 The major purpose of a 

sling is to provide an upward force to 

maintain the humeral head in the glenoid 

fossa. Unfortunately, little documentation 

exists in the form of radiological 

evidence to indicate which of the 

plethora of sling types produces the 

most effective reduction. In the only 

controlled, longitudinal study on sling 

efficacy, Hurd et al found one type of 

sling ineffective in preventing subluxation. 

19 Sodring 94 and Rajaram and 

Holta 98 reported radiographic evidence 

of GHJ reduction with two types of 

slings; however, no controlled research 

study was conducted to demonstrate the 

efficacy of subluxation in prophylaxis. 

In circumstances when the presence 

of subluxation has been determined to 

be the primary cause of HSP, use of a 

Varney brace has been reported to be 

successful; patients became asymptomatic 

in five to seven days. 99 After the 

subluxation is reduced and the shoulder 

is asymptomatic, an active and passive 

exercise program is important to improve 

and maintain ROM. 99 

Electrical stimulation of the supraspinatus 

and deltoid muscles can be used 

as an "electrical orthosis" for maintaining 

the alignment of the GHJ and has 

been recommended as an effective substitute 

for a sling. 83 Studies conducted at 

Rancho Los Amigos Rehabilitation 

Engineering Center reported that patients 

who were receiving electrical stimulation 

to the posterior deltoid and 

supraspinatus muscles demonstrated radiological 

evidence of reduced subluxation. 

100,101 Some evidence existed that 

the reduction was maintained after the 

stimulation was discontinued. 100 No 

prospective longitudinal studies could 

be located, however, documenting the 

efficacy of electrical stimulation for the 

treatment of subluxation. (See the article 

by L. Baker in this issue.) 

Electromyographic biofeedback has 

been reported to be successful in reducing 

subluxation, 82,85 although little prospective 

research seems to exist. In a 

controlled study on hemiplegic patients 

with subluxation, Shahani et al noted 

equal effectiveness of an EMG biofeedback 

program and a "conventional" 

physical therapy program in reducing 

subluxation; a correlation existed between 

the decrease in subluxation and 

the increase in strength and tone in the 

shoulder muscles. 102 

In a clinical report, Burstein recommended 

weight bearing on the affected 

arm and manual reduction of the subluxation 

during exercise as effective 

methods in relieving HSP. 103 Smith presented 

two case reports describing the 

reduction of subluxation and the increase 

of active abduction using an intensive 

facilitation program for the supraspinatus, 

deltoid, and serratus anterior 

muscles. 104 

Avoidance of Impingement 

During Passive Exercise 

Immobilization contributes to loss of 

motion, and passive ROM is an essential 

prophylactic measure to prevent joint 

stiffness and soft tissue contractures. 

The effectiveness of passive ROM, however, 

does not necessarily indicate that 

all types of shoulder exercise are beneficial 

or that a patient who begins to 

complain of pain during exercise requires 

more aggressive exercise therapy. 

11 Improperly administered passive 

exercise can cause impingement, resulting 

in soft tissue trauma, inflammation, 

and pain. 3,8,17,34,50 Increased exercise of 

the wrong type can contribute to the 

development of a stiff, painful shoulder. 

All persons performing passive exercise 

to the flaccid or spastic arm, from 

professional staff to family and the patient 

himself, must be taught the correct 

exercise techniques. Certainly, manual 

reduction of subluxation, if it exists, 

should be accomplished before passively 

elevating the arm. Medial or lateral rotation 

must accompany flexion or abduction, 

and scapular upward rotation 

must accompany either rotation to 

avoid soft tissue impingement. Spasticity 

must be reduced before elevating 

the arm more than 90 degrees. Overhead 

pulleys provide neither correct humeral 

nor correct scapular rotation during pas- 




sive elevation and are a likely cause of 

impingement. 

An important question to be addressed 

is how much ROM is "enough." 

All medical professionals seem "programmed" 

to take each joint through its 

full ROM. As previously noted, complete 

ROM to a young physical therapist 

is not necessarily complete ROM to a 

geriatric stroke patient. Perhaps a more 

realistic goal is the maintenance of painfree 

functional ROM in the shoulder. 

The affected arm must be pain free to 

serve even in an assistive role. 38 Functional 

ROM has been defined as flexion 

to 100 degrees, abduction to 90 degrees, 

lateral rotation to 30 degrees, and medial 

rotation to 70 degrees. 90 

Another aspect to be considered is 

whether abduction should be included 

in passive exercise, in view of its tendency 

to cause soft tissue impingement. 

Some authorities recommend that abduction 

should be performed only in the 

scapular plane, that is, 30 degrees to 40 

degrees from the frontal plane, 3,34 because 

lateral rotation is not required to 

prevent impingement. 27 Curtailing the 

amplitude of passive abduction in exercise 

programs might preserve functional 

ROM and minimize impingement pain. 

If impingement during ROM is determined 

to be the etiological factor in 

pain, then the amplitude of passive motion 

should be kept within the pain-free 

range. 15 Caldwell et al reported that pain 

subsided in 43% of their patients with 

HSP when the amplitude of passive 

ROM was limited. 15 

Should the patient begin to complain 

of pain during passive ROM, a thorough 

evaluation to assess the cause of pain 

should be conducted before pain and 

stiffness become established. 

Diagnosis of Established Painful 

Conditions 

If a patient has an established painful, 

stiff shoulder, the first step in treatment 

is the identification of the cause. A carefully 

detailed medical history is important 

to determine the prestroke history 

of any shoulder pathological conditions 

and to identify any known trauma that 

occurred after the stroke, such as 

falls. 23,27 A correct diagnosis of the cause 

is essential if the patient is to be helped." 

A thorough diagnostic examination of 

the neck and shoulder should be conducted 

to identify cervical spine pathological 

factors, rotator cuff or biceps 

brachii tendinitis, or GHJ or acromioclavicular 

joint arthritis. 42,99 Confirmatory 

evidence of rotator cuff tears and 

adhesive capsulitis can be obtained with 

arthrography. Radiographs can rule out 

humeral fracture 3 and ectopic ossification. 

105 Electrophysiological studies can 

be used to identify brachial plexus injurv. 

Shoulder-hand syndrome may be 

confirmed by a positive response to stellate 

ganglion block. 58 

Conservative Management 

If subluxation is identified as the causative 

agent, several treatment methods 

exist. Pain and stiffness in a subluxated 

shoulder, however, are not necessarily a 

result of subluxation. 15,102 Krempen et al 

examined 37 patients with pain and subluxation 

and found 16 patients had 

other, orthopedic causes for the pain." 

Conservative orthopedic management 

of patients with diagnoses of tendinitis, 

bursitis, and rotator cuff tears is 

similar. The goals of treatment are pain 

reduction and improvement of ROM. 

Symptoms may be reduced with oral 

anti-inflammatory agents and analgesics 

and injections of lidocaine and steroids 

into trigger points, the subacromial bursae, 

or the joint space. 27,28,42,106 As pain 

decreases, active, passive, and assistive 

exercises are used to improve ROM. 

Applications of heat, cold, phonophoresis, 

and transcutaneous electrical 

nerve stimulation may be effective in 

relieving pain and encouraging motion. 

106 Applications of heat, however, 

have not been proven to be of particular 

benefit in the treatment of HSP. Liao et 

al found no significant difference in the 

amount of improvement in ROM between 

patients treated with exercise only 

versus those treated with a combination 

of heat and exercise therapy; exercise 

appeared to be the most effective treatment. 

4 Thus far, in studies of hemiplegic 

patients with unstated etiologic factors 

of pain, ultrasound 22 and TENS 6 have 

not been found to decrease pain or to 

contribute to increased range of shoulder 

motion. 

If an injury to the upper trunk has 

been diagnosed, the brachial plexus 

must be protected until regeneration can 

occur. 53 The shoulder should be splinted 

in 45 degrees of abduction, a treatment 

similar to that of postsurgical repair of 

the upper trunk. 107 Care must be taken 

to prevent further traction injury until 

regeneration occurs. The prognosis for 

recovery of function varies widely. 23 

Although evidence exists that adhesive 

capsulitis in nonhemiplegic patients 

is a self-limited disease resolving in one 

to three years, (see the article by C. T. 

Wadsworth in this issue), the same does 

not appear to be true of hemiplegic adhesive 

capsulitis. 12,42 A vigorous program 

of ice or heat applications and 

active and passive exercises can be combined 

with anti-inflammatory and analgesic 

medications, oral corticosteroids, 

and muscle relaxants. 41 Suprascapular 

nerve blocks, 108 corticosteroid injections 

into trigger points, and stellate ganglion 

blocks have been reported to be beneficial. 

23 

Antispasmodic medications may supplement 

inhibition and relaxation techniques. 

16 Motor-point blocks of the 

trapezius 16 and pectoralis major 109,110 

muscles may aid in controlling spasticity. 

In the management of SHS, early recognition 

is the key to a favorable prognosis; 

prompt treatment is essential to 

prevent permanent disability. 58,60,111 An 

aggressive exercise program is an essential 

component of treatment. 27,59 Active 

muscle contraction and joint movements 

are important, as are light weightbearing 

activities. Exercise must be performed 

within the pain-free range and 

frequently for short periods during the 

day. Modalities such as heat or ice treatments 

or TENS may be used to increase 

sensory input and reduce pain. 28,71,112 

Although TENS has been reported as 

helpful in the management of reflex 

sympathetic dystrophies, no research results 

appear to be reported on the effectiveness 

of TENS in hemiplegic SHS. 

Aggressive and prompt management 

of hand edema is important, because 

prolonged edema will precipitate perhaps 

irreversible hand stiffness. 27 Dependent 

positions of the hand should be 

avoided; an elevated position is preferable. 

Intermittent pneumatic compression 

may be of value in reducing hand 

edeipa, 23,90,113 and an elastic glove is 

helpful also in controlling edema. 71 

Systemic administration of corticosteroids 

for two to three weeks is recommended 

by several authorities for the 

management of SHS. 27,59,71 Davis et al 

reported a complete resolution of symptoms 

in 68 hemiplegic patients using 

oral steroids in combination with an 

intensive rehabilitation program. 57 A 

sympathetic block followed by intensive 

rehabilitation is cited as the most effective 

treatrnent by Some researchers. 

58,61,111 Sympathectomy is suggested 

in refractory cases. 58,59,111 

The emotional state of patients with 

severe HSP has been described as tense, 

hyperresponsive to pain, overemotional, 

apathetic, and emotionally dependent. 23 

Whether such emotional states contrib- 




ute to the development of HSP or 

emerge as a result of the pain is unknown. 

111 In any event, appropriate psychological 

management is important for 

successful treatment. 23 

Surgical Management 

Surgical release of soft tissue may be 

of value if conservative methods have 

failed and if shoulder motion has become 

severely limited and painful. 112 

Recent improvements in rehabilitation 

techniques have decreased the need for 

surgical intervention. 75 The most frequently 

described surgical management 

involves resection of the subscapularis 

and pectoralis major tendons 15,114 and 

release of the capsule 115 ; insertions of 

the latissimus dorsi and teres major 

muscles also may be necessary. 116,117 Surgical 

release does not result in improved 

ROM without an intensive postoperative 

program of exercise and splinting to 

maintain and increase abduction and 

external rotation. 15,117 

The indications for surgery include 

ROM limitation to the point of functional 

impairment (ie, abduction to 45 

degrees and lateral rotation to 15 degrees 

or less 15 ), pain of such intensity that it 

interferes with skin hygiene 114 or prevents 

participation in rehabilitation, 15 

and progressively decreasing ROM resulting 

from increased internal rotator 

muscle spasticity. 15,109,117 Factors affecting 

the patient's rehabilitation potential, 

such as cognitive awareness, sensory and 

perceptual deficits, and communication 

disorders, also should be considered. 15 

Surgery usually is delayed until at least 

six months after the stroke when spontaneous 

recovery is fairly complete. 114 

Surgery is contraindicated in the presence 

of etiological factors other than soft 

tissue contracture or if postoperative 

therapy is unavailable. 15 Surgery for 

thalamic pain is not indicated. 15,118 

The reported magnitude of an increase 

in ROM after surgery is not great. 

Caldwell et al reported that the lateral 

rotation range was poor, although most 

patients regained 90 degrees of abduction; 

some patients developed active abduction 

postoperatively that had not 

been observed preoperatively. 15 

CONCLUSIONS 

Patients at highest risk for developing 

HSP seem to be those with severe upper 

limb paralysis, particularly if sensory 

loss and mental confusion also exist. 

Such a combination of factors not only 

immobilizes the limb but increases the 

likelihood for traction injury because 

the patient cannot protect himself. Increasing 

age may increase the risk also. 

Most patients over 50 years of age have 

significant degenerative changes around 

the GHJ. Such soft tissue pathological 

factors can be exacerbated only by 

events accompanying flaccid paralysis. 

The acute period after a stroke appears 

to be a critical time for the prevention 

of GHJ soft tissue injuries such as 

rotator cuff tears or brachial plexus injuries. 

Such trauma, which may go unnoticed 

in the acute period after a 

stroke, may cause significant HSP or 

functional impairment later in rehabilitation. 

Education of all personnel handling 

the flaccid arm is imperative if 

prophylaxis of shoulder injury is to be 

effective. 

Failure to provide support for the flaccid 

arm when the patient is upright may 

allow shoulder subluxation and consequent 

painful overstretching of soft tissue 

or nerve injury or both. The deleterious 

effects of subluxation may be 

cumulative. Effective methods for the 

prevention of subluxation remain to be 

established in a controlled clinical trial, 

but electrical stimulation appears 

promising. 

Immobilization is a key factor contributing 

to shoulder stiffness in elderly 

patients. In patients with hemiplegia, 

immobilization is promoted by paralysis, 

spasticity, and, sometimes, brachial 

plexus injury. Pain is another wellknown 

immobilizing influence. Lack of 

passive exercise for the paralyzed shoulder 

certainly will result in painful contractures. 

Careless passive exercise techniques 

without regard to biomechanical 

principles may cause impingement. 

Thus, improperly administered exercise 

may be a cause of trauma, pain, and 

further immobilization. 

When pain and stiffness begin to develop, 

a thorough evaluation of the 

cause is essential. Conservative management 

methods may be effective if the 

treatment is appropriate for the cause. 

Surgical intervention may be indicated 

in extreme cases. Early preventive measures, 

however, remain the key to minimizing 

the complication of shoulder 

pain in patients with hemiplegia. 

Need for Clinical Research 

Longitudinal studies are needed concerning 

developments in the shoulder 

after hemiplegia. Periodic assessments 

of shoulder status, from the onset until 

at least one year after the onset of hemiplegia, 

would add greatly to present 

knowledge concerning the evolution of 

HSP. Pertinent aspects to be included 

in such assessments are active motor 

function, sensory status, passive ROM, 

amount of pain associated with passive 

motion, spasticity, subluxation, and 

functional ability of the upper limb. 

Cognitive status and age also should be 

included. If HSP and limited ROM develop 

during the longitudinal study, 

prompt diagnostic steps to identify the 

cause should be instituted. When etiologic 

factors of the pain can be established, 

controlled studies of the relative 

effectiveness of various treatment methods 

are essential. The optimum treatment 

for hemiplegic patients with established 

diagnoses such as SHS or adhesive 

capsulitis currently is unknown. 

Knowledge of the effectiveness of 

methods for preventing subluxation (ie, 

electrical stimulation vs positioning 

alone) would be helpful in determining 

prophylaxis. Also of clinical importance 

are controlled studies to establish the 

relative efficacy of methods such as biofeedback, 

electrical stimulation, and exercise 

alone in improving proximal control 

in the hemiplegic shoulder. 

The obstacles to clinical research in 

the area of HSP may seem formidable: 

Hemiplegic patients admitted to rehabilitation 

settings differ widely in medical 

history and prestroke shoulder dysfunction; 

the time since the stroke varies 

among patients; and the history of 

shoulder trauma after the stroke often is 

impossible to ascertain. Such variables 

may account for the different responses 

to treatment and may make the original 

causes of HSP difficult to determine. 

Such difficulties might be overcome partially 

by beginning a longitudinal study 

immediately after the stroke and by including 

significant numbers of patients 

in the study. The HSP syndrome represents 

such a major obstacle to rehabilitation 

that systematic studies of the 

problem are imperative. Controlled research 

is needed to determine effective 

prophylaxis and to document the therapeutic 

efficacy of treatment. 

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Judy W Griffin 

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Hemiplegic Shoulder Pain - Physical Therapy

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