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Painful HemipJegrc Shoulder'

Robert leasell MD

Sanjit Bhogal MSc

Norine Foley BASc

Mark Speechley PhD

From the Departments of Physical Medicine and Rehabilitation, S1. Joseph Health Care, London, Parkwood Hospital, London and Epidemiology and Biostatistics, University of Westem Ontario, London, Ontario. Canada

® Ontario

Canadian Stroke Network

Painful Hemiplegic Shoulder

Robert Teasell MD, Sanjit K. Bhogal MSc, Norine Foley BASe,

Mark Speeehley PhD

Last Updated May 9, 2005


Table of Contents

11.1 Causes of Hemiplegic Shoulder Pain............................................... 5

11.2 Shoulder Subluxation ........................................................................6

11.2.1 PATHOPHySiOLOGy................................................................................................. 6

11.2.2 SCAPULAR ROTATION .............................................................................................. 7

11.2.3 PAIN IN SHOULDER SUBLUXATION ............................................................................ 8

11.3 Spasticity, Contractures and Hemiplegic Shoulder

Pain (HSP) ........................................................................................10

11.3.1 SPASTIC MUSCLE IMBALANCE ................................................................................ 12

11.3.2 FROZEN OR CONTRACTED SHOULDER .................................................................... 14

11.4 Rotator Cuff Disorders ....................................................................16

11.5 Functional Impact of Painful Hemiplegic Shoulder ...................... 16

11.6 Management of the Painful Hemiplegic Shoulder......................... 17

11.6.1 POSITIONING OF THE HEMIPLEGIC SHOULDER ......................................................... 17

11.6.2 SLINGS AND OTHER AIDS ....................................................................................... 19

11.6.3 STRAPPING THE HEMIPLEGIC SHOULDER ................................................................ 21

11.6.4 ACTIVE THERAPIES IN THE HEMIPLEGIC SHOULDER. ................................................. 22

11.6.5 INJECTIONS IN THE HEMIPLEGIC SHOULDER ............................................................. 24


11.6.7 SURGERY AS TREATMENT FOR MUSCLE IMBALANCE ................................................. 29

11.6.8 MOTOR BLOCKS AS TREATMENT FOR MUSCLE IMBALANCE ....................................... 29

11.6.9 SUMMARY OF THE MANAGEMENT OF HEMIPLEGIC SHOULDER ................................... 30

11.7 Shoulder Hand Syndrome ...............................................................31

11.7.1 PATHOPHySiOLOGy............................................................................................... 32

11.7.2 CLINICAL PICTURE ................................................................................................ 32

11.7.3 DIAGNOSTIC TESTS ............................................................................................... 34

11.7.4 TREATMENT OF SHOULDER-HAND SYNDROME ......................................................... 34

11.7.5 CORTICOSTEROID TREATMENT OF SHOULDER-HAND SYNDROME ............................. 35

11.7 Summary .............................................................................................. 37

a ··


Key Points

Spasticity and hemiplegic shoulder pain are related. Further research is needed before conclusions regarding positioning of the hemiplegic shoulder can be made. There is limited evidence that shoulder slings influence clinical outcomes. Strapping the hemiplegic shoulder does not appear to influence clinical outcomes, including pain. Aggressive range of motion exercises (i.e. pullies) results in a markedly increased incidence of painful shoulder; a gentler range of motion program is preferred. Adding ultrasound treatments is not helpful while NSAIDs may be helpful. Corticosteroid injections do not improve hemiplegic shoulder pain or range of motion. A potentially new treatment of the painful hemiplegic shoulder that requires further research involves deinnervation of the subscapularis and pectoralis major muscles. Oral corticosteroids appear to improve shoulder-hand syndrome for at least the first 4 weeks.



11. Painful Hemiplegic Shoulder

Hemiplegia is a common clinical consequence of a focal cerebral insult resulting from a vascular lesion (ie. hemorrhagic or ischemic stroke). Good shoulder function is a prerequisite for successful transfers, maintaining balance, performing activities of daily living and for effective hand function (Risk et al. 1984). The incidence of shoulder pain varies between studies, with estimates which range from 48% to 84% (Najenson et al. 1971, Poulin de Courval et al. 1990). Shoulder pain can result in significant disability in and of itself (Najenson et al. 1971, Poduri 1993) and can occur as early as 2 weeks post stroke, but usually occurs 2-3 months post stroke onset (Poduri 1993). Although many etiologies have been proposed for hemiplegic shoulder pain, increasingly it appears to be a consequence ofspasticity and the sustained hemiplegic posture. Shoulder pain may be more common among patients with neglect following stroke (Kaplan 1995).

11.1 Causes of Hemiplegic Shoulder Pain

Possible sources of hemiplegic shoulder pain are listed in Table 11.1.

Factors most frequently associated with shoulder pain are shoulder (glenohumeral)

SUbluxation (Crossens-Sills and Schenkman 1985, Moskowitz et al. Table 11.1 Potential Causes of Hemiplegic shoulder 1969b, Savage and Robertson Pain Mechanism 1982, Shai et al. 1984), shoulder Anatomical Site Rotator Cuff Muscle contractures or restricted shoulder Muscle Imbalance range of motion (Bloch and Bayer Subscapularis Spasticity 1978, Braun et at 1981, Fugl-Meyer Pectoralis Spasticity et al. 1975, Crossens-Sills and Schenkman 1985, Hakuno et al. Humeral Fracture Bone 1984, Risk et al. 1984) and Glenohumeral Subluxation Joint spasticity, particularly of the subscapularis and pectoralis Bursitis Bursa muscles (Braun et al. 1981, Caldwell et al. 1969, Moskowitz Tendonitis Tendon 1969a, 1969b) .. Other suggested Frozen or Contracted Shoulder Joint Capsule causes of shoulder pain include (Adhensive Capsulitis) reflex sympathetic dystrophy (Chu et al. 1981, Davis et at. 1977, Shoulder-hand Syndrome Other Perr;got et al. 1975), or injury to the (Reflex Sympathetic Dystrophy) rotator cuff musculotendinous unit (Najenson et al. 1971, Nepomuceno et al. 1974).


11.2 Shoulder Subluxation

11.2.1 Pathophysiology

Shoulder subluxation is best defined as changes in the mechanical integrity of the glenohumeral joint causing a palpable gap between the acromion and humeral head. The most reliable clinical measurement of the subacromial space used in clinical research is calipers (Boyd 1992). The glenohumeral joint is multiaxial and has a range of motion, which exceeds that of other jOints in the body. To achieve this mobility the glenohumeral jOint must sacrifice stability. Stability is achieved through the rotator cuff, a musculotendinous sleeve which maintains the humeral head in the glenoid fossa, while at the same time allowing shoulder mobility. During the initial period following a stroke the hemiplegic arm is flaccid or hypotonic. 1herefore the shoulder musculature, in particular the rotator cuff musculotendinous sleeve, cannot perform its function of maintaining the humeral head in the glenoid fossa ~nd there is a high risk of shoulder I subluxation.


Shoulder subluxation is a very common problem inlhemiPlegiC patients. During the initial flaccid stage of hemiplegia the involved extremity must be adequately supported or the weight of the arm will result in shoulder sublJxation. Improper positioning in bed, lack of support while the patient is in the upright pO$ition or pulling on the hemiplegic arm when transferring the patient all contribute to gllenohumeral subluxation. Down and lateral subluxation commonly occur secondary to prolonged downward pull on the arm against which hypotoniC muscles offer little resistance (Chaco and Wolf 1971). The resulting mechanical effect is overstretching of the glenohumeral capsule (especially its superior aspect) and flaccid supraspinatus and del~oid muscles (Basmajian and Bazant 1959, Shahani et al. 1981) (Figure 11.1). i

Figure 11.1 A. Normal Shoulder. The humeral head is supraspinatus muscle.

ma~ntained in the glenoid fossa by the







Figure 11.1 B. Shoulder Subluxation. During the initial phase of hemiplegia, the supraspinatus muscle is flaccid. The weight of the unsupported arm can cause the humeral head to sublux downward out of the glenoid fossa.





11.2.2 Scapular Rotation

There appear to be other factors playing a role in subluxation of the glenohumeral joint. Basmajian and Bazant (1959) proposed that in the normal state, subluxation of the humeral head was prevented by upward angulation of the glenoid fossa and the upper part of the shoulder capsule, the coracohumeral ligament and supraspinatus muscle. After a hemiplegic stroke they hypothesized that the upward angulation of the scapula would be lost. Calliet (1980) added that in the flaccid stage, the scapula assumed a {jepr-essedanddownward rotated -position, as the paretic serratus anteriofand the upper part of the trapezius muscles no longer support the scapula. The combination of flaccid supportive musculature (in particular, the supraspinatus muscle) and a downward rotated scapula was presumed to predispose the head of the humerus to undergo inferior subluxation relative to the glenoid fossa.

Table 11.2 Scapular Rotation In the Hemiplegic Shoulder Author, Year Country Prevost et al. 1987 Canada Method Outcome

50 patients who had experienced a cerebrovascular accident, presenting with right hemiplegia. Inferior subluxation of the shoulder in hemiplegia was measured using a tridimensional (3-D) x-ray technique, giving true vertical distance

The angle of abduction of the arm of the affected side was significantly greater than on the non-affected side, p<0.05, but the relative abduction of the arm was on the same order of magnitude for both sides. There was no significant


Author, Year Country

Method separating the apex of the humeral head and the inferior margin of the glenoid cavity. Both shoulders were evaluated and the difference used as a measure of subluxation. The measure was then compared to the orientation of the scapula relative to the vertical and the abduction of the arm. 34 hemiplegic patients were divided into high-tone and low-tone groups according to Ashworth scoring of muscle tone.

Outcome relationship between the orientation of the scapula and the severity of the subluxation. The abduction of the humerus was weakly (r=.24) related to the subluxation, which partly explained the weak association found between the relative abduction of the arm and the SUbluxation. Scapula was significantly further from the midline and lower on the thorax on the affected side in the low-tone group. Glenohumeral subluxation was Significantly greater in the low-tone group. Scapular abduction angle was significantly greater on the non-affected side in the low-tone group. In the high-tone group, no differences were found between the affected and the non-affected side in either the angular or linear measures.

Cuiham et al. 1995 Canada

Prevost et al. (1987), using a 3-D x-ray technique, studied the movement of the scapLlla and humerus in stroke patients. They studied 50 stroke patients comparing the affected to the non-affected shoulder. They were able to demonstrate that there was a difference between the affected and non-affected shoulders in terms of the vertical position of the humerus (ie. degree of subluxation) in relation to the scapula. The orientation of the glenoid fossa was also different; however, they found that with the subluxed shoulder it was actually facing less downward. There was no Significant relationship noted between the orientation of the scapula and the severity of subluxation. They concluded that the scapular position was not an important factor in the occurrence of inferior subluxation in hemiplegia (Prevost et al. 1987). This finding was confirmed by Culham et al. (1995).

11.2.3 Pain in Shoulder Subluxation

Shoulder subluxation may be associated with several conditions including: shoulder pain (Crossens-Sills and Schenkman 1985, Mos.kowitz et a!. 1969b, Savage and Robertson 1982, Shai et al. 1984, Roy et al. 1994) and frozen shoulder or brachial plexus traction injury (Kingery et a/. 1993), although evidence for the latter is lacking (Kingery et al. 1993). It has long been assumed that if not corrected; a pattern of traction on the flaccid shoulder will result in pain, decreased range of motion and contracture. However, not aI/ patients with a subluxed hemiplegic shoulder experience shoulder pain and it remains controversial as to whether it causes hemiplegic shoulder pain (Fitzgerald-Finch and Gibson 1975, Moskowitz et al. 1969b, Shahani et al. 1981, Bender and McKenna 2001). The failure to conSistently report an association may be due, in part to a failure to examine the contribution of other probable etiological factors concurrently. Although several studies have reported an association, others have not


confirmed this finding. The reader is also reminded that statistical associations are also not evidence of causality. (see Table 11.3)

Table 11.3 Studies which Support or Fail to Report an Association between Shoulder Subluxation and Pain Studies Supporting the Role of Shoulder

Subluxation in Pain

Shai et al. 1984 Van Ouwenaller et al. 1986 Poulin de Courval et al. 1990 Roy et al. 1994 Chantraine et at 1999 Aras et al. 2004 Studies Which Fall to Support the Role of

Shoulder Subluxation in Pain

Peszczynski & Rardin 1965 Bohannon 1988 Vangenberge & Hogan 1988 Bohannon & Andrews 1990 Kumar et al. 1990 Arsenault et al. 1991 Joynt 1992 Zorowitz et at 1996 Ikai et al. 1998

Individual Studies

A selection of studies examining the relationship between shoulder subluxation and pain are presented in Table 11.4.

Table 11.4 Pain and Subluxation in the Hemiplegic Shoulder Author, Year Country Bohannon & Andrews 1990 USA Methods 28 consecutively admitted patients undergoing rehabilitation for their first stroke who could follow instructions, and were aware of the position of their paretic limb in space were included. Paretic shoulder SUbluxation and paretic shoulder pain were measured. Shoulder SUbluxation was measured while the patients sat on the edge of a mat table with their paretic upper extremity dependent and the examiner used his thumb to palpate the separation between the acromion and the head of the humerus. He then graded subluxation as none (0), minimal (1) or substantial (2). Shoulder pain was measured during slow lateral rotation of the joint while the patients were supine. All patients' shoulders were abducted about 45° and their elbows were held at 900 with their forearms pronated with measurements beginning from neutral shoulder rotation. Patients' responses were graded on a 3-point scale (Ritchie Index) of: no pain, complaint of pain and wince, complaintof pain, wince and withdrawal. SROMP measurements taken with patients' shoulders laterally rotated until they first expressed pain in the shoulder, at Main Outcome 70.8% of patients demonstrated enough shoulder pain to at least cause them to wince when their shoulders were rotated laterally 90°. The SROMP of the paretic side was measured as 64.50:!;.28.8° and 64.6°:!;.28.9°. A significant Pearson correlation (-77s, p<0.001) was observed between the Ritchie Index and SROMP indicating that patients with higher scores on the Ritchie Index had fewer degrees. of lateral rotation of the shoulder before pain was experienced.


Author, Year Country Joynt 1992 USA

Methods which point a fluid-filled gravity goniometer. was applied and read. A convenience sample of 97 patients suffering from pain in the upper extremity was examined. The interval from stroke onset to examination ranged from several days to a few years. 49 patients had specific complaints of shoulder pain.

Main Outcome

Zorowitz et al. 1996 USA

20 stroke patients with shoulder pain, admitted to a rehabilitation hospital within 6 weeks of their first stroke were studied.

Aras etal. 2004 Turkey

85 consecutive stroke patients admitted to one of the largest rehab facilities in Turkey were studied to identify the incidence of shoulder pain and the factors associated with it.

49 patients with specific shoulder pain were compared to 18 patients with pain, not localized to the shoulder. Patients complaining of shoulder pain did not exhibit sUbluxation more frequently than patients with general pain in the affected extremity. Shoulder pain after stroke was not correlated with age, vertical, horizontal, or total asymmetry, shoulder f1exion or abduction. or Fugl-Meyer scores. However, shoulder pain was strongly correlated with degree of shoulder extemal rotation 27 patients had glenohumeral joint subluxation and reported shoulder pain. compared to 5 patients with the same finding, but without pain.

Conclusions Regarding Shoulder Subluxation Post-Stroke Shoulder subluxation occurs early on in the hemiplegic arm due to flaccid supporting shoulder musculature and is not a result of downward scapular rotation. Shoulder subluxation may be a cause of shoulder pain; however, patients with shoulder subluxation do not necessarily experience pain and not all cases of hemiplegic shoulder pain suffer from subluxation. Although it has not been established that shoulder subluxation is the primary cause of hemiplegic shoulder pain it would still seem prudent to take care early on with the hemiplegic upper extremity to avoid subluxation.

11.3 Spasticity, Contractures and Hemiplegic Shoulder

Pain (HSP)

Abnormal muscle tone, including spasticity may be directly related to HSP. Spasticity is defined as a disorder of motor function characterized by a velocity-dependent increase in resistance to passive stretch of muscles accompanied by hyperactive muscle stretch reflexes and often associated with a clasp-knife phenomena. Spasticity is one component of the upper motor neuron (UMN) syndrome and is the inevitable accompaniment of hemiplegia and an incomplete motor recovery. Under normal


circumstances a delicate balance exists between facilitating and inhibiting influences upon both alpha and gamma motor neurons, which together maintain appropriate control of skeletal muscle length and strength of contraction at the spinal cord level. After a stroke, input from one or more of the supraspinal suppressor areas will decrease or stop entirely. The balance of control over the muscle tips in favour of facilitation and spasticity results. Spasticity develops only if there is loss of input from both pyramidal and extrapyramidal motor systems. Spasticity presents as increased tone and reflexes on the involved side of the body.

Individual Studies

Table 11.5 Spasticity and Hemiplegic Shoulder Pain Author, Year Country Bohannon et al. 1986 USA No score Methods 50 patients with hemiplegia was secondary to cerebrovascular accident, whose unaffected shoulders demonstrated normal and pain-free range of hemiplegia shoulder external rotation (ROSER. 90°); able to adequately follow instructions to allow testing of all variables pertinent to the study. Information was retrieved from patients' records concerning their initial physical therapy evaluation. Relationships between pain and other variables were determined. 219 hemiplegia patients were followed for 1 year after their stroke. Radiographic examinations were done for each patient. Outcome Of the 50 patients reviewed. 72% had shoulder pain. 20 had some pain while 16 had severe pain. Three zero-order correlations were significant: ROSER and shoulder pain (r=-0.061, p<0.001), time since onset of hemiplegia and shoulder pain (r=0.45, p<0.01). and time since onset of hemiplegia and ROSER (r=0.37, p<0.01). One-way ANOVA demonstrated that time since onset of hemiplegia (F=8.28, p<0.001) and the ROSER (F=18.44, p<0.001) were significantly different in patients with no pain, some pain, and pronounced/severe pain. 72% of patients had shoulder pain at least once during their recovery occurring most often in patients having spasticity (85%) than in patients which flaccidity (18%). Appearance of spasticity was evident in 80% of patients while 20% remained hypotonic.

Van Ouwenaller et al. 1986 Switzerland No score

Van Ouwenaller et al. (1986) looked at various factors in 219 patients followed for one year after a stroke and identified a much higher incidence of shoulder pain in spastic (85%) than in flaccid (18%) hemiplegics. They identified spasticity as "the prime factor and the one most frequently encountered in the genesis of shoulder pain in the hemiplegic patient." They were unsure of the etiology of the subsequent shoulder pain. Poulin de Courval et al. (1990) examined 94 hemiplegic subjects involved in a rehabilitation program after stroke and reported that subjects with shoulder pain had significantly more spasticity of the affected limb than those without pain. In contrast, Bohannon et al. (1986) conducted a statistical analysis of 50 consecutive hemiplegic patients (36 with shoulder pain) and asserted that "spasticity ... was unrelated to shoulder pain." Joynt (1992) also supported this finding after examining 67 patients with shoulder problems following stroke. Nevertheless, evidence for spasticity in particular hypertonic muscle imbalance, as a cause of hemiplegic shoulder pain is growing.


11.3.1 Spastic Muscle Imbalance

Hemiplegia following stroke is characterized by typical posturing reflecting hypertonic muscle patterns. Flexor tone predominates in the hemiplegic upper extremity and results in scapular retraction and depression as well as internal rotation and adduction of the shoulder. This posture is the consequence of ablation of higher centers and subsequent release of motor groups from pyramidal and extrapyramidal control. In stroke recovery, this "synergy pattern" of muscles is 'inevitable where recovery is incomplete. One consequence of this is the development of spastic muscle imbalance about the shoulder jOint. Clinically the internal rotators of the shoulder predominate after a stroke involving that arm and external rotation is one of the last areas of shoulder function to recover. Hence, during recovery motor units are not appropriately recruited or turned off; the result is simultaneous co-contraction of agonist and antagonist muscles. A shortened agonist in the synergy pattern becomes stronger and the constant tension of the agonist can become painful. Stretching of these tightened spastic muscles causes more pain. Shortened muscles inhibit movement, reduce range of motion, and prevent other movements especially at the shoulder where external rotation of the humerus is necessary for arm abduction greater than 90 degrees. Muscles that contribute to spastic internal rotation/adduction of the shoulder include the subscapularis, pectoralis major, teres major and latissimus dorsi muscles. However, two muscles in particular have been implicated as most often being spastic leading to muscle imbalance. These are the subscapularis and pectoralis major muscles.

Subscapularis Spasticity Disorder

The subscapularis muscle originates on the undersurface of the scapula and inserts on the lesser tuberosity of the humerus as well as the capsule of the shoulder joint (Figure 11.2). It is a major internal rotator of the shoulder (Hollinshead and Jenkins 1981). The subscapularis muscle also participates in arm abduction and extension from a flexed position (Cole and Tobis 1990). In normal, nerve impulses to the subscapularis are inhibited during arm abduction; the muscle then relaxes and allows the humerus to externally rotate, thus preventing impingement of the greater tuberosity on the acromion (Codman 1934). As part of the typical flexor synergy pattern in spastiC hemiplegics, internal rotators, including the subscapularis muscle, are tonically active. This limits shoulder abduction, flexion and external rotation. Bohannon et al. (1986) found limitation of external rotation of the hemiplegic shoulder was the factor which most correlated with hemiplegic shoulder pain. Zorowitz et al. (1996) also found that limitation in shoulder external rotation correlated strongly with pain. Hecht (1995) specifically linked this problem to the subscapularis muscle when he noted, "The subscapularis muscle is the primary cause of shoulder pain in spastic hemiplegia where external rotation is most limited. Although other muscles may contribute to spasticity, pain and functional contracture, the subscapularis is the keystone of the abnormal synergy pattern."


Figure 11.2 The Subscapularis Muscle. The subscapularis muscle is a major internal rotator ofthe shoulder. As part of the typical flexor synergy pattern in spastic hemiplegics, the subscapularis is tonically active limiting not only external rotation but also shoulder abduction and flexion.


The subscapularis spasticity disorder is characterized by motion being most limited and pain being reproduced on extemal rotation. A tight band of spastic muscle is palpated in the posterior axillary fold. In support of this, Inaba and Piorkowski (1972) reported external rotation was the most painful and limited movement of the hemiplegic shoulder.

Pectoralis Spasticity Disorder

The pectoralis major muscle serves to forward 'Hex, adduct and internally rotate the arm. Hecht (1995) has reported on a subset of hemiplegic patients with greater limitations in abduction (and flexion) than on external rotation. In these patients a spastic pectoralis major muscle appears to be problematic. This disorder is characterized by motion being most limited and pain produced on abduction. A tight band of spastic muscle can be palpated in the anterior axillary fold (Hecht 1995). It is also noteworthy that the pectoralis major muscle is a synergist of the subscapularis muscle.



Figure 11.3 The Pectoralis Major Muscle. The pectoralis major muscle serves to adduct, internally rotate and forward flex the arm at the shoulder.


Pecto#alis Majof (c:JavictJIar division)

Pec1ora1is MajOr

(slerna' di'llision)

11.3.2 Frozen or Contracted Shoulder

A frozen or contracted shoulder is a frequently identified source of pain in the spastic hemiplegic shoulder (Bohannon et al. 1986, Eto et al. 1980, Fugl-Meyer et al. 1975, Grossens-Sills and Schenkman 1985, Hakuno et al. 1984, Risk et al. 1984). Individual Studies

Table 11.6 Evidence of Frozen Shoulder Post Stroke Author, Year Country Hakuno et al. Methods 77 patients with hemiplegia caused by cerebrovascular accidents were randomly selected from all hemiplegic patients treated at rehab centre. Cases with dementia and verbal dysfunction were eliminated. Paralysis affected the right side in 35 patients and the left side in 42 patients. In 35 cases the affected arm was dominant whereas 42 cases had paralysis in nondominant arm. Positive contrast arthography was preformed on both shoulders of all patients. An anterior approach for injection of the jOint with contrast material was employed. The needle was inserted directly into the glenohumeral joint space under fluoroscopic control. Anteroposterior Outcome Contractures/adhesions were found in paralyzed shoulders at a statistically significant higher rate (54.6%) than in the non-paralysed side (32.5%). The occurrence rate of contrast leakage from a capsule tear on the subscapular bursa and the bicipital tendon sleeve was higher on the non-paralysed side than on the paralysed side. It was suggested that capsular contracture due to hemiplegia reduces capsular tearing during arthrographic maneuvers.




Author, Year Country Crossen-Sills & Schenkman 1985 USA

Methods radiographs were made in internal and external rotation. 21 male patients all received standard physical therapy treatment. Shoulder pain, range of motion and sUbluxation were assessed on admission, three weeks post admission and at discharge.


Rizketal. 1984 USA

Bohannon et at 1986 USA No Score

Study of 30 spastic hemiplegic (18 with left hemiplegia and 12 with right hemiplegia) patients with painful ipSilateral shoulders meeting the following criteria: maximum passive range of motion (ROM) of 600 abduction, 90° forward flexion, 150 external rotation, 45° extension; any stress at the limit of motion produced severe shoulder, with no improvement during the previous 2 weeks, no history of recent trauma to the affected shoulder during the previous 2 weeks, no history of seizures or anticonvuslant medications; no clinical signs suggesting shoulder-hand syndrome, no bone disease or polyarthritis or previous shoulder pain before stroke onset. All patients had shoulder arthrograms performed. Electromyographic studies were done on the deltoid, triceps, and biceps brachii muscles on the muscles on the involved side. 50 patients whose hemiplegia was secondary to a stroke, whose unaffected shoulders demonstrated normal and pain free range of hemipl~ia shoulder external rotation (ROSER, 900); able to adequately follow instructions to allow testing of all variables pertinent to the study. Information was retrieved from patients' records concerning their initial physical therapy evaluation. Relationships between pain and other variables were determined.

67% of the patients entered the rehab centre with Signs of shoulder pain. An additional 10% developed initial signs of shoulder pain by 3 weeks post·admission and another 5% developed signs of pain at time of discharge. Positive correlation noted between loss shoulder range and increase in pain and between subluxation and pain. There was no correlation between subluxation and range of motion. Suggestion that pain began in the acute cares facility and worsened while in rehab. 23 patients had capsular constriction typical of frozen shoulder (adhesive capsulitis). 7 patients had normal arthrograms. None showed rotator cuff of capsular tears. Electromyography revealed electrical silence in the shoulder musculature at rest.

Of the 50 patients reviewed, 72% had


shoulder pain. 20 had some pain while 16 had severe pain. Three zero-order correlations were Significant: ROSER and shoulder pain (r=-0.061, p<0.001); time since onset of hemiplegia and shoulder pain (r=0.45, p<0.01); and time since onset of hemiplegia and ROSER (r=0.37, p<O.01). One-way ANOVA demonstrated that time since onset of hemiplegia (F=8.28. p<0.001) and the ROSER (F=18.44, p<0.001) were significantly different in patients with no pain, some pain, and pronounced/severe pain.


In summary, while shoulder subluxation is not always associated with shoulder pain, spasticity generally is. The problem of hemiplegic shoulder pain appears to be due to a combination of spastic muscle imbalance and a frozen contracted shoulder. However, overaggressive stretching of the shoulder through an aggressive stretching program may simply aggravate pain (see Treatment), as it does not address the issue of spastic muscle imbalance.

Conclusions Regarding Spastic Hemiplegic Shoulder There is an association between spasticity and the development of hemiplegic shoulder pain. Spasticity and subsequent frozen shoulder are the most likely causes of hemiplegic shoulder pain. Spasticity and hemiplegic shoulder pain are related.

11.4 Rotator Cuff Disorders

Because shoulder pain is so often associated with rotator cuff disorder in a non-stroke population it should not be surprising that it would be seen as a potentially common cause of hemiplegic shoulder pain. However, Risk et al. (1984) failed to demonstrate any evidence of rotator cuff tears on arthrography in 30 patients with hemiplegic shoulder pain (Risk et al. 1984). A similar study (Nepomuceno and Miller 1974) reported a 33% incidence of rotator cuff tears in painful shoulders after strokes. Partial tears of the rotator cuff musculature are common and it is always difficult determining whether they were present premorbidly even in previously asymptomatic patients. Joynt (1992) diagnosed 67 stroke patients as having hemiplegic shoulder pain. 28 patients received a subacromial injection of 1% lidocaine; approximately half obtained moderate or marked relief of pain and improved range of motion. However, this provides only indirect evidence of rotator cuff disorders as a possible cause of hemiplegic shoulder pain. Generally, hemiplegic shoulder pain is not commonly associated with rotator cuff disorders.

11.5 Functional Impact of Painful Hemiplegic Shoulder

A painful hemiplegic shoulder can be very limiting. It has the potential to further add to the disability seen with hemiplegia.



Table 11.7 Impact of Painful Hemiplegic Shoulder on Function Author, Year Country Wankyln et at 1996 Methods 108 post stroke patients were studied. Patients were over the age of 60, about to be discharged home and had suffered stroke with persisting disability defined as a Barthellndex score less than 20. Outcomes 63.8% of all patients developed hemiplegic shoulder pain (HSP). HSP was associated with reduced shoulder shrug and reduced pinch grip. Patients who required assistance with transfer were more likely to suffer with HSP. Significantly more patients with Barthellndex scores less than 15 reported HSP compared to those with a score between 15~20 at both discharge (59% vs. 25%) and at 8 weeks (77% vs. 51O/~: 54 patients (63.5%) had shoulder pain. Shoulder pain was reported more frequently among patients with reflex sympathetic dystrophy, lower motor functional level of shoulder and hand, subluxation, and limitation of external rotation and flexion of shoulder. Age was also associated with.the development of shoulder pain. No relationships were found between shoulder pain and sex, time since onset of disease, hemiplegic side, pathogenesis, spasticity, neglect, and thalamic pain, or extension of hospital stay.


No Score

Aras et al. 2004 Turkey No Score

85 consecutive stroke patients admitted to one of the largest rehab facilities in Turkey were studied to identify the incidence of shoulder pain.

Wanklyn et al. (1996) and Roy et al. (1996) both demonstrated an association between hemiplegic shoulder pain and poor functional outcomes. However, a cause and effect relationship has not yet been established.

Conclusions Regarding Functional Impact of Hemiplegic Shoulder Pain The development of painful hemiplegic shoulder is associated with severe strokes and poorer functional outcome.

11.6 Management of the Painful Hemiplegic Shoulder

Management of the painful hemiplegic shoulder is difficult and response to treatment is frequently unsatisfactory (Risk et al. 1984). Early passive shoulder range of motion is an important prophylactic treatment. Supporting and protecting the involved shoulder in the initial flaccid stage is also regarded as important. Treatment involves analgesics, nonsteroidal anti-inflammatory medications, physical modalities (local heat and cold), transcutaneous electrical nerve stimulation, and local steroid injections. Surgical procedures are rarely utilized.

11.6.1 Positioning of the Hemiplegic Shoulder

The muscles around the hemiplegic shoulder are often paralyzed, initially with flaccid tone and later with associated spasticity. Careful positioning of the shoulder serves to


minimize subluxation and later contractures as well as possibly promote recovery. Bender and Mckenna (2001) have noted that a primary goal of early stroke management is to prevent the development of hypertonicitiy (Johnstone 1992) and to discourage inefficient patterns (Bobath 1990). Bender and McKenna (2001) noted that the "recommended position for the upper limb is towards abduction, external rotation and flexion of the shoulder," however, from Carr and Kenny (1992) review, Bender and McKenna cite that "most popular theories failed to yield consensus for exact degrees of the positioning."

Individual Studies

Table 11.8 Positioning ofthe Shoulder in Stroke Patients Author, Year Country PEDro Score Carr and Kenney 1992 No Score Methods Outcomes

Review of the literature.

Dean et al. 2000 Australia 5 (RCT)

Ada et al. 2005 Australia 6 (RCT)

23 patients were randomized to receive an experimental therapy or to a control group. Subjects in both groups participated in a multidisciplinary rehabilitation program and participated in active training of reaching and manipulation tasks. The experimental group received prolonged positioning to the affected shoulder each day, five days a week for six days (positionina). 36 stroke patients were randomized to an intervention or a control condition. Patients in the experimental group received two, 30-minute sessions of sustained shoulder positioning. Patients in both groups received 10 minutes of shoulder exercises and routine upper limb care. The treatment was provided for 4 weeks. Assessments of contracture were taken at weeks 2 and 6 after stroke.

General agreement about postures with the shoulder protracted. the arm brought forward, the spine straight and fingers extended. Still controversy regarding height of the arm in the forward position. Changes in active and passive range of motion were not Significant between the groups with the level of pain remaining unchanged.

Positioning the shoulder in maximal extemal rotation (position 1) significantly reduced the development of contractures, compared to the control group. In position 2 (where patients sat with the affected arm resting on a table with the shoulder at 90°, for 30 minutes daily), did not prevent the development of contractures.

Conclusions Regarding Positioning of the Hemiplegic Shoulder There is consensus (Level 3) opinion that proper positioning of the hemiplegic shoulder helps to avoid subluxation. However, there is conflicting (Level 4) evidence that prolonged positioning does not influence active and passive range of motion or level of pain. Given the small numbers of studies and the "fair" quality rating of the only RCT, further research is warranted.



Further research is needed before conclusions regarding positioning of the hemiplegic shoulder can be made.

11.6.2 Slings and Other Aids

Arm slings are often used in the initial stages following a stroke to support the affected arm. However, their use is controversial and they can have disadvantages in that they encourage flexor synergies, inhibit arm swing, contribute to contracture formation and decrease body image causing the patient to further avoid using that arm. However, a Sling remains the best method of supporting the tlaccid hemiplegic arm while the patient is standing or transferring. Ada et al (2005) conducted a systematic Cochrane review evaluating the benefit of shoulder slings and supports, and concluded that there is insufficient evidence that thj3se devices reduce or prevent shoulder subluxation following a stroke. The review included only four RCTs (Ancliffe et al. 1992, Griffin et al. 2003 [unpublished data]. Hanger et al. 2000 and Hurd et al. 1974). The results are presented in Table 11.9.

Table 11.9 Results from Systematic Review (Ada et al. 2005) Outcome Studies Included & Intervention Peto Odds ratio (95% Cl) or Weighted Mean Difference (WMD) (95% Cl) ORS.7(1.1,67.1) (Favours no slinQs) WMD 14 days (9.7, 17.8) (Favours slings) WMD 0.83 (-1.46,3.12) (No difference) WMD 0.8 (-1.5,3.1) (No difference) OR 1.00 (0.1, 9.3) (No difference) I WMD -1.4 degrees (-10.9,8.10) (No difference)

Proportion of patients with pain at follow up Number of days pain was delaved with treatment Pain scores on VAS (10 cm scale) Motor Assessment sub scores ! (0-18) . Proportion of patients with , contractures Range of shoulder external rotation at end of follow up

Hurd et a!. 1974 - hemisling Ancliffe et al. -strapping Griffin et a!. Hanger et al. 2000 - strapping Hanger et al. -strapping Hurd et al 1974- sling Hanger et al. 2000 - strapping

As tone returns to the shoulder muscles, the risk of shoulder subluxation decreases and slings can then be withdrawn. Slings tend to accentl!ate the adduction and internal rotation posture and may contribute to shortening of tonically active muscles. The best method to support the shoulder has yet to be determined. In the absence of empirical evidence of their efficacy, many devices are available and in common use, . including a variety of slings and lapboards.


Individual Studies

Table 11.10 Slings and Other Aids in Hemiplegic Shoulders Author, Year Country PEDro Score Hurd et al. 1974 USA No Score Moodie et al. 1986 Canada No Score Methods Outcomes

Williams et al. 1988 Canada No Score

BrooKe et al. 1991 USA No Score

14 patients were alternately assigned to be treated with a sling or without a sling, assessed 2 to 3 weeks and 3 to 7 months post stroke. Series of radiographs (anterior/posterior view) of 10 patients' affected and unaffected limbs in order to permit comparisons for degree of subluxation and the 5 aids to be evaluated were then applied to the patients' affected arm and an AlP view was taken of each: conventional sling; shoulder roll; Hook-Hemi Harness; arm trough; and plexiglass lap tray. Radiographs were taken of 26 hemiplegic patients with subluxated shoulders with two different supports-the Bobath shoulder roll and the Henderson shoulder sling. Radiographs of the unsupported affected shoulder were compared with radiographs of the same shoulder with each support applied. Radiographs of the unaffected shoulder were used as a comparison in determining the amount of subluxation. Three different shoulder supports were applied to 10 patients by their occupational and physical therapists: Hams hemi-sling, the Bobath sling and the arm trough or lapboard.

Of the 7 patients without slings, 5 had no pain, while 2 had little pain. Of the 7 patients treated with slings, 6 had little pain, while 1 had no pain.

Shoulder roll and Hook-Hemi Harness did not reduce SUbluxation to the same extent as the other 3 devices. Subluxation was reduced within 20% of the correct alignment in B out of 10 patients when treated with the sling; 6 of the 10 treated with the arm trough, and 7 of the 10 patients treated lap tray. Suggested that the sling, trough, and lap tray reduced the mean SUbluxation to within .56 cm of normal control while the roll and hook tended to under-correct the subluxation.

There was no significant difference in the reduction of inferior subluxation between the two types of shoulder supports. However, there were significant differences in subluxation between measurements of the unsupported affected shoulder and the unaffected shoulder and between measurements of the unsupported affected shoulder and the supported affected shoulder using both supportive devices.

Zorowitz et al. 1995 USA No Score

An occupational therapist applied each shoulder support to each of 20 patients in the following order: (1) single-strap hemisling; (2) Rolyan humeral cuff sling; (3) Bobath roll; and (4) Cavalier support.

Harris hem i-sling improved correction of the subluxation with mean vertical distance of 37.Bmm vs 3B.5mm compared to the uninvolved shoulder while the mean difference between Harris and Bobath sling was 5.5(2.9) mm, in favour of the Harris sling. For horizontal measurement, mean difference between Harris and Bobath slings was 8.3(6.3) mm, in favour of the Hams sling. The single-strap hemisling corrected vertical displacement, while the Roylan and Bobath roll significantly reduced vertical displacement. The Bobath roll and the Cavalier support produced a significant lateral displacement of the humeral head of the affected shoulder compared with the unaffected shoulder. The Roylan humeral cuff sling significantly decreased the total SUbluxation a~mme!!y.


Conclusions Regarding Slings in Hemiplegic Shoulder There is limited (Level 2) evidence that shoulder slings prevent subluxation associated with hemiplegic shoulder pain, although there is also limited (Level 2) evidence that one device or method is better than another. There is limited evidence that shoulder slings influence clinical outcomes.

11.6.3 Strapping the Hemiplegic Shoulder Individual Studies

Table 11.11 Strapping the Hemiplegic Shoulder Author, Year Country PEDroScore Ancliff et al. 1992 Australia No Score Methods Outcomes

Hanger et at 2000 New Zealand 7 (ReT)

A pilot study of 8 patients who were assigned to receive strapping of the shoulder with a 5 cm wide ixomull Stretch (BDF, Australia), applied by one physiotherapist and changed every 3 to 4 days as needed to the hemiplegic side or to receive no strapping. 98 patients were randomized to have their affected shoulder strapped for 6 weeks in addition to standard physiotherapy or to receive standard physiotherapy only.

Patients in the strapping group experienced a significantly longer pain free period than the patients who were not strapped

No significant differences were found between groups on measure of pain, range of movement and on functional outcome measures. There was a trend for less pain at 6 weeks and improved functional upper limb function for the strapping group.

Conclusions Regarding Strapping the Hemiplegic Shoulder There is moderate (LeveI1b) evidence that strapping the hemiplegic shoulder does not result in Significant reductions in pain or improve upper limb function or range of motion. Strapping the hemiplegic shoulder does not appear to influence clinical outcomes, including pain.


11.6.4 Active Therapies in the Hemiplegic Shoulder

The association of spasticity, muscle imbalance and a frozen shoulder with shoulder pain suggests that a therapeutic approach designed to improve range of motion ofthe hemiplegic shoulder will improve pain.

Individual Studies

Table 11.12 Active Therapies in Hemiplegic Shoulder Author, Year Country PEDro Score Inaba et al. 1972 USA 7 (RCT) Methods 33 patients with hemiplegia who experienced shoulder pain in the range of 0-90 degrees of flexion or abduction of the arm after stroke were treated. Patients were randomly assigned to 1 of 3 groups: Range of motion (ROM) exercises and positioning group; ROM exercises and ultrasound; or ROM exercises and mock ultrasound. All patients received ROM exercises for 4 weeks and given a minimum of 15 treatments. 28 patients were randomized to receive a rehabilitation program of range of motion by therapist (ROMT) once a day, 5 days a week; or a rehabilitation program with use of skate board once a day, 5 days a week; or a rehabilitation program with use of overhead pulley once a day, 5 days a week while an inpatient on a stroke rehabilitation unit. Outcomes No significant differences between the groups were observed in measures of ROM.

Kumaretal. 1990 USA 5 (quasi randomized controlled trial)

Patridge et al. 1990 UK 5 (RCT) Poduri etal. 1993 USA No Score

Tyson & Chissim

65 patients were randomized to receive cryotherapy or Bobath therapy daily for five days and then after at the therapist's discretion for a total of four additional weeks and assessed by a blinded investigator. Patients with stroke experiencing shoulder pain after completing outpatient therapy were studied. One group of patients received either a nonsteroidal anti-inflammatory drugs (Ibuprofen 400-800g tid, and Sulindac, 150 mg bid.) taken 30 to 60 minutes prior to occupational therapy. A second group of patients received only occupational therapy consisting of range of motion, active assistive and strengthening exercises and activities of daily living training. 22 stroke patients with consequential weakness of the arm instructed to hold the

Significant difference in the incidence of pain reported between the groups. Shoulder pain. was more common in the overhead pulley (63%) group than in the ROMT group (8%). ROM was Significantly reduced in those patients who developed shoulder pain when compared to those who did not develop shoulder pain motion abduction, forward flexion, internal rotation and external rotation. Shoulder subluxation was found in 46% of all patients with no significant difference between treatment groups. A greater proportion of patients treated by the Bobath method reported no pain or only occasional pain on exit of the study compared to those treated by the cryotherapy method. A Significantly greater proportion of patients receiving the treatment drug prior to therapy experienced pain relief. Flexion, abduction and functional recovery were significantly greater in those patients who were taking the nonsteriodal anti-inflammatory drug before therapy.

There was significant greater range of flexion for the axilla hold.


Author, Year Country PEOro Score 2002

Methods hemiplegic shoulder at: (1) an axilla hold involving shoulder support and (2) a distal hold without shoulder support. Each hold was repeated to obtain three measurements with order of testing randomized.


. UK

· 4 (RCn


Inaba et al. (1972) in a "good" (PEDro 7) study found no significant differences in the outcomes of patients who received: ROM exercises and positioning, ROM exercises and ultrasound or ROM exercises and mock ultrasound. Kumar et al. (1990) in a good (PEDro = 6) RCT found that overhead pullies caused dramatically higher levels of shoulder pain than more restrained ROM exercises.

Shoulder Pain in Hemiplegia: The Role of Exercise (Kumar et al. 1990) To assess the occurrence of pain in patients in patients undergoing rehabilitation of hemiplegia, 28 patients were aSSigned to one of three exercise programs commonly used in the rehabilitation of hemiplegia: 1) range of motion by the therapist (ROMn, 2) skate board on a table (SB) and 3) overhead pulley (OP). Pain Experience of Groups







c 60

40 20 0




. Comparing the number of patients who developed pain in each group, there were dramatically · more patients in the OP group experiencing pain after rehabilitation compared to the other two groups. Patients in the ROMT group experienced the least amount of pain after rehabilitation.

Partridge et al. (1990) found that treatments using Bobath therapy resulted in significantly less pain than cryotherapy. The general message that emerges from these three studies is that an active ROM exercise approach is preferable to more passive modalities but an overly aggressive approach (Le. overhead pullies) resulted in a very high incidence of hemiplegic shoulder pain when compared to a gentler approach.


Conclusions Regarding Active Therapies in the Hemiplegic Shoulder There is moderate (Level 1b) evidence that aggressive range of motion therapies, using overhead pullies results in increased rates of shoulder pain. There is moderate (LeveI1b) evidence that Bobath therapy for the hemiplegic shoulder is associated with greater pain reduction than passive cryotherapy (application of local cold therapy). There is moderate (Level 1b) evidence that gentle exercises to improve range of motion are the preferred approach. There is moderate (Level 1b) evidence that adding ultrasound therapy to range of motion exercises does not change outcomes. There is limited (Level 2) evidence that providing an oral nonsteriodal anti inflammatory drug leads to less pain, improved range of motion and improved functional recovery in stroke patients with shoulder pain receiving occupational therapy. Aggressive range of motion exercises (i.e. pullies) results in a markedly increased incidence ofpainful shoulder; a gentler range of motion program is preferred. Adding ultrasound treatments is not helpful while NSAIDs may be helpful.

11.6.5 Injections in the Hemiplegic Shoulder

Corticosteroid and/or local anesthetic injections are commonly used for shoulder pain, in particular rotator cuff tendinopathies. It is not surprising that there would be interest in this mode of treatment in hemiplegic shoulder pain.

Individual Studies

Table 11.13 Injections in Hemiplegic Shoulder Author, Year Country . PEDro Score Joynt 1992 USA No Score Dekkeret al. 1997 Netherlands No Score Methods Outcomes

A retrospective study following 67 stroke patients with hemiplegic shoulder pain. Twenty-eight patients received a subacromial injection of 1% lidocaine. 9 patients with a presence of shoulder pain in the paretic arm with disturbances of sleep and with the presence of ROM restriction of external rotation partook in a multiple-baseline (AB) stUdy of tramicinolone acetonide. The treatment condition (phase BJ was 4 weeks

50% of the 28 patients who underwent a subacromial injection of local anaesthetic obtained moderate or marked pain relief and improved ROM. Intra-articular injections of triamcinolone acetonide demonstrated a Significant reduction in pain with highly significant effect in 5 of the 9 patients. Range of motion improved in 4 out of 7 patients but improvement did


Author, Year Country PEDro Score ·



Outcomes not reach statistical significance at the group level. No significant improvement was observed for any of the primary outcome measures with triamicinolone acetonide treatment.

Snels et al. 2000 Netherlands 8 (ReT)

long, during which three intra-articular injections of triamcinolone acetonide were administered at day 1, 8 and 22. 35 patients demonstrating hemiplegia after stroke and pain in hemiplegic shoulder greater than 4 on the visual analogue scale CVAS) with limitation of passive external rotation of the hemiplegic shoulder were randomized to receiver either three injections with triamicinolone acetonide (40 mg Kenacrot A 40 in 1rnl) or three placebo injections (1 rnl saline solution).


One RCT (Snels et al. 2000), of "good" quality (PEDro 8), failed to show a benefit of corticosteriod injections. There is insufficient evidence to recommend this mode of treatment and one trial casting doubt on its efficacy.


Conclusions Regarding Injections in the Hemiplegic Shoulder


There is moderate (LeveI1b) evidence, based on one "good" RCT that corticosteroid injections do not improve shoulder pain or range of motion in patients with hemiplegia. Corticosteroid injections do not improve hemiplegic shoulder pain or range of motion.

11.6.6 Functional Electrical Stimulation (FES) in the Hemiplegic Shoulder

As cited by Gresham et al. (1995), the U.S. AHCPR Post Stroke Rehabilitation Guidelines defines FES as "bursts of electrical stimulation applied to the nerves or muscles affected by the stroke, with the goal of strengthening muscle contraction and improving motor control." Theoretically. FES should help to compensate or facilitate flaccid shoulder muscleswhichin turn should reduce the risk of shoulder subluxation. Price & Pandyan (2001) conducted a systematic review of all forms of electrical stimulation (ES) used in the prevention and treatment of post stroke shol.Jlder pain. The included studies and the results are presented in Tables 11.14(a) and 11.14(b). The authors concluded that there was insufficient evidence from which to draw conclusions.


Table 11.14(a) Studies Included in the Systematic Review authored by Price & Pandyan (2001) Study Faghri et al. 1994 Leandri et at 1990 Linn et al. 1999 Sonde et al. 1998 Intervention FES vs. no sham treatment Sham treatment vs. high intensity TENS vs. low intensity TENS No sham treatment vs. electrical stimulation (not FES or TENS) No sham treatment vs. Iow frequency TENS

Len~th of Treatment 6 weeks 4 weeks

4 weeks 3 months

Table 11.14(b) Results From Studies Evaluating Any form of ES in the Treatment and Prevention of Shoulder Pain Outcome Significant Result (Y/N) No No Yes No Yes No Odds Ratio'" or Weighted (or Standardized) Mean Difference and 95% Cl 0.64 0.19, 2.14) .. 0.13 (-1.00 1.25) 9.17 (1.43, 16.9) 0.24 -0.14,0.62) -1.13 !~1.66 -D.60} 0.05J-0.28,0.3711

New cases of shoulder pain Pain intensity rating change from baseline Passive humeral lateral rotation Motor score change from baseline Glenohumeral subluxation compared to baseline Spasticity score chanae from baseline

Individual Studies

Eleven studies specifically evaluated the effects of FES on the treatment of shoulder pain. (Table 11.15)

Table 11.15 FES in Hemiplegic Shoulder Author, Year Country PEDro Score Baker et al. 1986 USA 4RCT Methods Outcomes


63 patients with a minimum of 5 mm of shoulder subluxation in their involved upper extremity were randomized to a treatment or control group. Patients in the treatment group received neurosmuscular electrical stimulation (NMES) for 5 weeks, while patients in the controlgroup used conventional hemi-slings or wheelchair arm supports. 26 patients were randomized to receive either functional electrical stimulation (FES) in which two flaccid/paralyzed shoulder muscles (supraspinatus and posterior deltoid) were induced to contract repetitively up to 6 hours daily for six days in addition to conventional therapy (FES) or to receive conventional therapy (control). 26 patients received conventional physical At six weeks, the mean subluxation of the study group was significantly less compared to the control (8.6 vs. 13.3). Three- month radiographs demonstrated that patients in the treatment group had lost an average of 1-2 mm, which had been achieved during the study period. The authors did not demonstrate a causal relationship between subluxation and shoulder pain. After treatment, the FES group showed a significant increase in arm function, tone and EMG activity compared to control patients.

Faghri et al. 1994 USA 4 (RCT)

Faghri &

Weekly evaluation of arm and shoulder muscle


Author, Year Country PEDro Score Rodgers 1997 USA 4 (RCT) Chantraine et at 1999 Switzerland 4 (quasi randomized controlled trial) Kobayshi et al. 1999 Japan 5 (RCT)

Methods therapy with 13 patients randomized to the treatment group, which received additional functional neura-muscular stimulation (FNS) therapy for 6 weeks. 115 patients were alternately assigned to receive traditional Bobath treatment in addition to functional electrical stimUlation (FES) for 5 weeks or to receive traditional Bobath treatment for 5 weeks.

Outcomes function (range of motion), tone, and posterior deltoid muscle EMG activity showed significant improvement in the experimental group when compared to the control group over 6 weeks. AdVantage of treatment group was maintained 6 weeks after termination of the FNS. Significant motor recovery was noted in favour of FES treatment at three months and was maintained at 24 months. Significant reduction also noted in pain in favour of FES treatment at three months and again maintained at 24 months. Significant reduction in shoulder subluxation in favour of FES treatment was noted at three months and maintained 24 months post-treatment. Difference in subluxation in group S, 2.8(3.6) mm and group D, 2.8(2.5)mm was significantly greater than that of the control -1 (2.8)mm under the stress test. The mean abduction force tended to increase in group S and was significantly greater in group D. The treatment group had significantly less subluxation and pain after the treatment period, but at the end of the follow-up period there were no significant differences between the 2 groups.

17 patients were randomized to receive therapeutic electrical stimulation (lES) for 15 minutes twice a day to either the suprasupinatus muscle (group S) or middle deltoid muscle (group D) in conjunction with conventional therapy, or to receive conventional therapy only. Linn et al. 40 patients were randomly assigned to a 1999 control or treatment group. Patients in the Scotland treatment group received electrical 6 (RCT) stimulation (ES) 4 times daily, ranging from 30 minutes in week one to 60 minutes by week 4. Patients in both groups received daily occupational and physical therapy. Treatments lasted for four weeks. Assessments of shoulder subluxation, pain, and motor control. were carried out at 4 and 12 weeks after stroke Wang etal. 32 patients were involved in a randomized 2000 A-B-A trial of functional electrical stimUlation Taiwan therapy in which the supraspinatus and 5 (RCT) posterior deltoid were induced to contract repetitively up to 6 hr/day for 6 weeks (FES). Yu et al. 2001· 8 patients partiCipated in six weeks of USA percutaneous intramuscular electric No Score stimulation (per-NMES).

For patients with hemiplegia of short duration, FES treatments produced decreased shoulder subluxation after first and second FES treatment. At end of treatment, there was a significant improvement of shoulder subluxation, pain, shoulder pain-free rotation and in FIM scores. Further improvements were noted at the 3 month follow up in subluxation, pain, Fugl· Meyer, shoulder pain-free external rotation and in FIM scores. Pain scores were significantly lower for percNMES than trans-NMES as assessed by the VAS and the MPQ.

Yu et al. 2001 USA 6 (RCT)

10 hemiplegic stroke patients with at least 1 fingerbreadth of glenohumeral subluxation received 3 randomly ordered pairs of neuromuscular stimulation (NMES) to the suprasinatus and poterior deltoid muscles of the subluxated shoulder. The stimulation


Author, Year Country PEDro Score

Methods types were percutaneous-NMES (percNMES) and transcutaneous-NMES (transNMES). After each stimulation pain was evaluated with the visual analog scale NAS) and the McGiII Pain Questionnaire (MPQ). 15 stroke survivors with chronic (> six months) hemiplegia and a therapy-resistant painful shoulder with subluxation were studied. Shoulder subluxation was indicated by at least 1/2 fingetbreadth of glenohumeral separation on palpation. Patients received 6 hours of Percutaneous Neuromuscular electrical stimulation (P NMES) per day for a total of six weeks. 7 site, single-blinded, randomized clinical trial. 61 chronic stroke survivors with shoulder pain and subluxation volunteered to be randomized to receiVe intramuscular neuromuscular electric stimulation (NMES) to the supraspinatus. posterior deltoid, middle deltoid, and trapezius for 6 hours a day for 6 weeks or to the control condition of a cuff-type sling for 6 weeks. Main outcome measure Brief Pain Inventory question.


Renzenbrink & IJerman 2004 Netherlands No Score

Yu etal. 2004 USA 7 (RCT)

A significant reduction in pain was found on the Brief Pain Inventory. Pain reduction was still present at six months follow-up. All domains, in particular bodily pain, of the SF-36 showed improvement in the short term. After six months of follow-up, bodily pain was still strongly and significantly reduced, whereas social functioning and role physical demonstrated a nonsignificant improvement of more than 10% compared with baseline. The main outcome measure was the Pain outcome measure Brief Pain Inventory question 12 (BPI12), an 11-point numeric rating scale, assessed at the end of treatment, and at 3 and 6 months post treatment. Post stroke shoulder pain was significantly less in the NMES group compared to control at 3 and 6 months following treatment.


All of the RCTs reviewed reported a benefit associated with FES treatment, although there was variability in the outcomes assessed: range of motion, muscle tone, EMG activity, shoulder subluxation, shoulder pain and muscle function.

Conclusions Regarding FES in the Hemiplegic Shoulder There is strong (Level 1a) evidence that functional electrical stimulation improves

a number of clinical outcomes associated with the hemiplegic shoulder.

Significant improvements have been reported for muscle function, tone, EMG activity, pain, subluxation and range of motion. The improvement was maintained for up to 24 months follow-up. Functional electrical stimulation improves a number of hemiplegic shoulder clinical outcomes.



11.6.7 Surgery as Treatment for Muscle Imbalance

Given that spastic muscle imbalance has been identified as a cause of hemiplegic shoulder pain, treatment designed to reverse that imbalance could potentially relieve hemiplegic shoulder pain.

Table 11.16 Surgery for Muscle Imbalance In the Hemiplegic Shoulder , Author, Year Country PEDroScore Braun et al. 1971 USA No Score Methods Surgical procedure on 13 patients to release the insertion of the major muscle causing internal rotation and adduction of the shoulder. Gradual increase in range of motion was obtained by completing an intensive post-operative exercise therapy program involving passive range of motion, positioning of the shoulder, abduction while supine, through the use of reciprocal pulley exercises. Outcomes 10 of the 13 patients operated on regained 90 degrees of passive abduction and 20 degrees of external rotation within 2 months following surgery. However, 6 months later, all of the patients were complaining of pain and discomfort.

Conclusions Regarding Surgery as Treatment for Hemiplegic Shoulder Pain There is limited (Level 2) evIdence that surgically resecting the subscapularis and pectoraliS muscle tendons improves pain and range of motion in stroke patients with a painful hemiplegic shoulder. Further research is needed to confirm these findings.

11.6.8 Motor Blocks as Treatment For Muscle Imbalance

As discussed previously, subscapularis spastiCity is characterized by shoulder range of motion being most limited with pain being reproduced on external rotation. This appears to correlate well with hemiplegic shoulder pain that is now thought to be a consequence of spastic muscle imbalance about the shoulder in many cases. Pectoralis muscle spasticity, characterized by limitation of range and pain on shoulder abduction, is seen to a lesser extent, causing a similar muscle imbalance. Motor blocks for spastic muscle imbalance offers the ability to redress that imbalance and relieve hemiplegic shoulder pain.

Individual Studies

Table 11.17 Motor Block for Muscle Imbalance in Hemiplegic Shoulder Author, Year Country PEDro Score Hecht 1992 No Score



Outcomes Immediate and significant improvement in ROM observed in abduction, flexion and external rotation. Relief of pain was noted

A retrospective study of 13 patients with spastic hemiplegia, limited ROM and painful shoulder and with duration of



Author, Year Country PEDroScore

Methods hemiplegia for 2 to 13 months. Patients received percutaneous phenol nerve blocks to subscapularis muscle innervation. Prospective study of 20 patients receiving botulinum toxin muscle blocks to the subscapular and pectoralis major musculature.

Outcomes with previously painful movements.

Hecht 1995 No Score

85% benefited from subscapularis block, and 55% benefited from pectotalis major block and 45% showed improved active ROM.


Two small cohort studies examining deinnervating specific muscles, in particular the subscapularis and pectoralis major muscles, improved ROM and pain. This is a promising line of research that nevertheless requires a RCT to demonstrate its efficacy as a viable treatment before definitive conclusions can be drawn.

Conclusions Regarding Motor Block for Muscle Imbalance There is limited (Level 2) evidence that motor blocks of the subscapular and pectoralis muscles can be used to treat muscle imbalance, pain and decreased range of motion of the hemiplegic shoulder, although this new treatment requires further research. A potentially new treatment of the painful hemiplegic shoulder that requires further research involves deinnervation of the subscapularis and pectoralis major muscles.

11.6.9 Summary of the Management of Hemiplegic Shoulder

Despite the high prevalence of patients suffering from painful hemiplegic shoulders, the evidence for effective treatment is underwhelming. There is strong (Level 1a) evidence supporting functional electrical stimulation and moderate (Level 1b) evidence supporting an active therapy-oriented approach. There is also moderate (Level 1b) evidence that overaggressive therapies using pullies substantially increases pain when compared to gentler range of motion therapy approaches. There is moderate (Level 1b) evidence that positioning of the shoulder, shoulder strapping, local corticosteroid injections and adding local ultrasound therapy do not alter outcomes. There have been no RCTs conducted on the use of slings, motor blocks for spastic muscle imbalance or providing NSAID medications prior to therapy, although there is limited (Level 2) evidence of a benefit for all three of these treatment approaches.


There is consensus (Level 3) opinion that prevention and avoidance of overaggressive therapy is important. Those individuals caring for the stroke patient, particularly early on, should be aware of the potential for shoulder injury. The shoulder should be carefully positioned and supported against gravity while sitting or standing. Range of motion exercises should not carry the shoulder beyond 90 degrees of flexion and abduction unless there is upward rotation of the scapula and external rotation of the humeral head (~resham et al. 1995).

Table 11.18 Summary of RCTs for Management of Hemiplegic Shoulder Author, Year POSitioning of the Shoulder Dean et at 2000 Ada et al. 2005 Slings and other Aids No RCTS Strapping Han~er et al. 2000 Active Therapies Patridge et al. 1990 Kumar et al. 1990 PEDro Score 5 6 n 23 36 Outcomes





7 5 5

98 65 28


(for aggressive pullies) Injection Snels et al. 2000 Functional Electrical Stimulation Unn et al. 1999 Kobayshi et al. 1999 Chantraine et at 1999 . Faghri et al. 1994 i Faghri & Rogers 1997 Baker et al. 2004 Surgery for Muscle Imbalance No RCTs Motor Block for Muscle Imbalance No RCTs 7 6 5 4 4 4 4 35 40 17

+ -



26 26


+/ + + + + +

0 0







11.7 Shoulder Hand Syndrome

Shoulder hand syndrome is often regarded as a form of sympathetically mediated pain involving the hemiplegic upper extremity. Shoulder hand syndrome is characterized by hand pain and swelling, exquisite tenderness or hyperaesthesia, protective immobility, trophic skin changes and vasomotor instability of the involved upper extremity. The relationship between the sympathetic nervous system and pain remains hypothetical and has yet to be proven.


11.7.1 Pathophysiology

Shoulder hand syndrome has been associated with lesions of the pre-motor area of the brain. The etiology of shoulder hand syndrome is unknown; the sympathetic nervous system has often been implicated largely because of the associated vasomotor changes. Theoretical peripheral and central etiologies have been proposed. Peripheral etiological theories postulate a role for trauma to the peripheral nerves. One of these theories postulates ephaptic conduction between efferent sympathetic nerves and afferent somatic nerves with the latter depolarization being perceived as pain. Numerous central etiological theories have also been proposed. For instance, it has been postulated that there is a disruption of autonomic nervous control from higher CNS centres, which directly affects the internuncial pool of the spinal cord leading to decreased inhibition of the sympathetic neurons of the lateral horn. Pain, either from contractures or shoulder subluxation, may stimulate the internuncial pool of the spinal cord resulting in an abnormal sympathetic response. A linkage between the abnormal sympathetic nervous system and pain has also been postulated but never proven. Geurts et al. (2000) systematically reviewed the etiology and treatments of post stroke hand oedema and shoulder-hand syndrome. The authors identified 5 etiological studies and 6 therapeutic stUdies. The authors evaluated the stUdies based on 11 methodological criteria and by standardized effect sizes. Based on their systematic review of the literature, the authors concluded that the shoulder was involved in only half the cases with all of the cases characterized by painful swelling of the wrist and hand, thereby suggesting a "wrist-hand syndrome" in half the cases. Furthermore, they noted that the hand edema was not a lymphoedema and that shoulder hand syndrome usually coincided with increased arterial blood flow (Geurts et al. 2000).

11.7.2 Clinical Picture

Shoulder hand syndrome generally presents initially with pain in the shoulder followed by a painful, edematous hand and wrist. There is frequently decreased range of motion at the shoulder and hand while the elbow joint is spared (Oavis et al. 1977). Passive flexion of the wrist, MCP and PIP jOints is painful and limited due to edema over the dorsum of the fingers. As time progresses, the extensor tendons become elevated and the collateral ligaments shorten. If untreated it has long been thought that shoulder hand syndrome eventually progresses to a dry, cold, bluish and atrophied hand. However, experience would suggest that in most cases the pain and often the edema subsides spontaneously after a few weeks.

Table 11.19 Clinical Features of Shoulder-Hand Syndrome Author, Year Country PEDro Score Davis et al. 1977 USA No Score Methods Outcome

68 patients diagnosed with shoulder-hand syndrome; 41 had right hemiplegia. Eleven patients were in their 5th decade, 37 in their th 6 and 20 in their th decade. Patients

All 68 patients became pain free within 3 weeks; most were pain free within 4 to 6 days when subjected to passive stretching of the involved joints. No clear association


Author, Year Country PEDroScore


Outcome was found between SHS and co-existing medical conditions. The majority of patients had partial motor loss, moderate or severe sensory loss and varying degrees of spasticity and thus did not differ grossly from the rest of the thromoboembolic stroke population. None of the treated patients. including those who suffered recurrences, progressed to a frozen shoulder.

having hemiplegia from other causes such as hemorrhage and trauma were excluded from this study. All patients' charts were reviewed by a team composed of authors; information was abstracted with regard to I age, sex, handedness, side of hemiplegia. sensory and motor status, associated medical conditions. date of diagnosis of SHS and response to treatment. On day of diagnosis all patients were given 16 mg of triamcinolone diacetate (Aristocort) orally in four divided doses and treatment maintained for 14 to 21 days. All patients were provided with sling. Eto et al. 1980 7 autopsy cases of hemiplegia shoulderJapan hand syndrome from patients that had been No Score admitted to the University of Tokyo Hospital or an affiliated hospital. Observed over a6 year period, autopsy cases of hemiplegia shoulder-hand syndrome. Their clinical and post-mortem records were available in determining the cerebral localization of the syndrome and of unilateral longstanding autonomic dysfunction following hemiplegia.

Tepperman et al. 1984 Canada No Score

85 consecutive patients admitted to a rehabilitation unit with post-stroke hemiplegia. All had suffered a hemispheric stroke of thrombotic, embolic or hypertensive hemorrhagic etiology as determined by CT brain scan. Patients were assessed prospectively for radionuclide and clinical features of reflex sympathetic dystrophy (RSD). Each patient underwent a three-phase bone scan within 72 hours of admission. Delayed images of both wrists and hands as well as total body were obtained 2 to 4 hours after injection. 219 hemiplegic patients of whom 44 had flaccid paralysis and 175 evolved rapidly toward a spastic state. Stroke was the most frequent cause (79%). Spasticity was diagnosed on the basis of an increase of the myotatic reflex. The presence of subluxation was sought. Criteria for diagnosing the RSD syndrome were involvement of both the hand and shoulder and presence of the usual characteristic symptoms. Each shoulder was tested for

Van Ouwenaller et al. 1986 Switzerland No score

One of the cases showed an isolated brain lesion in the premotor area due to a metastasis from malignant melanoma. Four other cases with cerebral infarction and one with glioblastoma of the cortex in the area supplied by the middle cerebral artery. The seventh case showed a hemorrhagic cerebral lesion in the lentiform nucleus. The most common overlap area in the 6 of the 7 cases was located in the premotor region including the anterior part of the motor region. The shoulder-hand syndrome following hemiplegia always develops on the side contralateral to the brain lesion. 21 patients (25%) exhibited radionuclide evidence of RSD based on delayed scan criteria of increased uptake in the hemiplegic wrist, metacarpal-phalangeal (MCP) and interphalangeal (IP) joints. 8 of the scan-positive RSD patients presented a low soft tissue blood flow pattern identical to the non-RSD hemiplegic patients while the remaining 13 showed a high flow pattern. MCP tenderness to compression proved to be the most valuable clinical sign of RSD, with a predictive value, sensitivity, and specificity rates of 100%.85.7% and 100% respectively. The RSD syndrome was present in only 23% of all cases but was seen more often in spastic patients. 27% vs. 7%.



Author, Year Country PEDroScore



an isolated tendon lesion and for several contributing factors.

Shoulder hand syndrome develops in about one in four hemiplegics. It is associated with involvement of the premotor region and spasticity in the involved upper extremity. Diagnosis can be made clinically, with metacarpal phalangeal joint tenderness to compression the most consistent sign. The natural history appears to be a positive one, with most patients improving spontaneously.

11.7.3 Diagnostic Tests

Routine radiographs of the involved upper extremity may demonstrate a patchy, periarticular demineralization (Sudek's atrophy) as early as 3-6 months after the onset of clinical signs. The most sensitive diagnostic test is the technetium diphosphonate bone scan which demonstrates increased periarticular uptake (mostly at the shoulder and wrist) in the affected upper extremity. Bone scan abnormalities appear earlier than the x-ray changes. Tepperman et at (1984) found 25% of hemiplegic patients demonstrated evidence of reflex sympathetic dystropy in the involved upper extremity although only two~thirds went on to develop the clinical syndrome. Temporary resolution of symptoms with sympathetic blockade is considered diagnostic despite potential difficulties with the technique in terms of diagnostic validity. Thermography, in controlled studies, has failed to conSistently diagnose reflex sympathetic dystrophy and is not considered a valid test.

Conclusions Regarding Shoulder-Hand Syndrome Shoulder hand syndrome is a painful clinical entity, which is not understood from a pathophysiological standpoint. Diagnosis is made clinically. Most cases appear to improve with time.

11.7.4 Treatment of Shoulder-Hand Syndrome

Prevention of shoulder problems and aggressive early treatment are recommended to prevent the development of a non-functional painful upper extremity. The various treatment options are outlined in Table 11.20. Therapy consists of vigorous physiotherapy with a focus on range of motion exercises. A one to two week course of high dose corticosteroids and/or sympathetic blocks either in the form of stellate ganglion blocks or guanethedine local venous blocks may be tried in perSistent disabling cases. A surgical sympathectomy may be considered if stellate ganglion sympathetic blocks are consistently effective but symptoms recur. However, there is no evidence that surgical sympathectomy alter outcomes. There is no definitive therapeutic intervention for reflex sympathetic dystrophy, as reflected by the large



number of suggested treatments. Shoulder hand syndrome, which presents for greater than 6 months without appropriate treatment, has a poor prognosis (Lieberman 1986).

Table 11.20 Potential Treatments for Shoulder Hand Syndrome

Prevention · Extremely early ROM exercises · Avoid shoulder subluxation Exercise · Prevention and treatment of upper

extremity contractures

· Active exercise if possible · Frequent passive ROM Modalitles · Interferential deep heat · Heat/cold modalities especially contrast baths · Hand desensitization program · Transcutaneous electrical nerve stimulation

Splints · Resting splint of hand and wrist


Medication · Analgesics · NSAIDs · High dose oral corticosteroids (10 day course and then taper) Injections · Stellate ganglion sympathetic block · Guanethedine bier block Surgical · Sympathectomy


11.7.5 Corticosteroid Treatment of Shoulder-Hand Syndrome

One RCT examined the efficacy of an oral corticosteroid in the treatment of shoulder hand syndrome after stroke.

Table 11.21 Corticosteroid Treatment of Shoulder-Hand Syndrome

Author, Year Country PEDro Score Braus etal. 1994 Germany 5 (RCT) Methods Outcome

36 hemiplegic patients secondary to a stroke of the middle cerebral artery and exhibited definite shoulder-hand syndrome were studied. Patients were randomized to receive either 8 mg methylprednisolone or a placebo over 4 weeks. All patients received daily physical therapy. For patients in the placebo group, if no improvement was noted in shoulder·hand syndrome then they were given 4 weeks of corticosteroid treatment as per the experimental group .

No significant improvement was noted in shoulder-hand syndrome in the placebo group after 4 weeks at which time all patients switched over the corticosteroid protocol. Patients receiving the corticosteroid treatment demonstrated significant improvement in shoulder·hand syndrome that was maintained at 6 months. 31 of the 36 patients became almost symptom free within 10 days of treatment with low dose oral corticosteroids.




The study by Braus et al. (1994) was the only RCT exarnining a treatment for shoulder hand syndrome. Oral corticosteroids improved SHS for at least 4 weeks. Geurts et al. (2000) in their review concluded that oral corticosteroids were the most effective treatment for SHS.

Conclusion Regarding Oral Cortlcosteroids In SHS There is moderate (Level 1b) evidence that oral corticosteroids improves shoulder-hand syndrome for at least the first 4 weeks.

Oral cortlcosterolds appear to improve shoulder-hand syndrome for at least the first 4 weeks.


11.7 Summary

. 1. Shoulder sUbluxation occurs early following a stroke.

2. Hemiplegic shoulder pain is associated with shoulder subluxation and

spasticity, but not with scapular rotation.

3. There appears to be an important role for the subscapularis muscle and to a lesser extent pectoralis major musculature, which develop greater tonic activity on the hemiparetic side with subsequent muscle.imbalance about the shoulder. 4. The development of painful hemiplegic shoulder is associated with severe

strokes and poorer functional outcome.

5. There is moderate (LeveI1b) evidence that prolonged positioning does not

negatively influence shoulder range of motion or pain.

6. There is limited (Level 2) evidence that shoulder slings prevent sUbluxation associated with hemiplegic shoulder pain, although there is also limited (Level 2) evidence that one device or method is better than another. 7. There is moderate (Level 1b) evidence that strapping the hemiplegic shoulder does not result in significant differences in pain, range of motion or upper limb function. 8. There is moderate (Level 1b) evidence that the use of overhead pul/ies results in surprisingly high levels of hemiplegic shoulder pain and should be avoided. 9. There is moderate (LeveI1b) evidence that a gentle range of motion program

by a therapist results in less hemiplegic shoulder pain.

10. There is moderate (LeveI1b) evidence that corticosteroid injections do not improve shoulder pain or range of motion in hemiplegic patients. There is limited (Level 2) evidence that oral non-steroidal anti-inflammatories can reduce pain during therapy sessions. 11. There is strong (LeveI1a) evidence that functional electrical stimulation improves muscle function, pain, subluxation and range of motion of the hemiplegiC shoulder. 12. There is limited (Level 2) evidence that surgically resecting subscapularis and pectoralis tendons improves outcomes in stroke patients with painful hemiplegic shoulder.


13. There is limited (Level 2) evidence that motor blocks of the suprascapular and pectoralis muscles treat muscle imbalance, pain and decreased range of motion of the hemiplegic shoulder. 14. Shoulder hand syndrome is a poorly understood clinical entity. Most cases improve with time. 15. There is moderate (LeveI1b) evidence that oral corticosteroids improves shoulder hand syndrome for at least the first 4 weeks.



Ada L, Goddard E, McCully J, Stavrinos T, Bampton J. Thirty minutes of positioning reduces the development of shoulder external rotation contracture after stroke: A randomized controlled trial. Arch Phys Med Rehabil 2005;86:230-234. Ada L, Foongchomcheay A, Canning C. Supportive devices for preventing and treating subluxation of the shoulder after stroke. Cochrane Database Syst Rev 2005;CD003863. Ancliffe J. Strapping the shoulder in patients following a cerebrovascular accident (CVA): A pilot study. Australian Journal of Physiotherapy 1992;38:37-39. Aras MD, Gokkaya NK, Comert D, Kaya A, Cakci A. Shoulder pain in hemiplegia: results from a national rehabilitation hospital in Turkey. Am J Phys Med Rehabil2004;83:713-719 Arsenault AB, Silodean M, Duil E, Riley E. Clinical significance of the V-shaped space in the subluxed shoulder of hemiplegics. Stroke 1991 ;22:867-871. Baker LL, Parker K. Neuromuscular electrical stimulation of the muscles surrounding the shoulder. Phys Ther 1986;66:1930-1937. Basmajian JV, Bazant FJ. Factors preventing downward dislocation of adducted shoulder joint: electromyographic and morphological study. J Bone Joint Surg (Am) 1959;41: 1182-1186. Bender L, Mckenna K. Hemiplegic shoulder pain: Defining the problem and its management. Disability and Rehabilitation 2001;23(16):698-705. Bloch R, Bayer N. Prognosis in stroke. Cl Orthop Related Res 1978;131:10-14. Bohannon RW. Relationship between shoulder pain and selected variables in patients with hemiplegia. Clinical Rehabilitation 1988; 2: 111-117. Bohannon RW, Andrews AW. Shoulder subluxation and pain in stroke patients. American J Occup Therapy 1990; 44(6):507-509. Bohannon RW, Larkin PA, Smith MB, Horton MG. Shoulder pain in hemiplegia: statistical relationship with five variables. Arch Phys Med RehabIl1986;67:514-516. Boyd EA. Clinical measures of shoulder subluxation: their reliability. Can J Public Health 1992;83 Suppl 2:524-8. Braun RM, West F, 1VI00ney V, Nickel RL, Roper B, Caldwell C. Surgical treatment of the painful shoulder contracture in the stroke patient. J Bone Joint Surg (Am) 1971;53:1307-1312. Brooke MM, de Lateur BJ, Diana-Rigby GC, Questad KA. Shoulder subluxation in hemiplegia: effects of three different supports. Arch Phys Med Rehabil 1991 ;72:582-586. Cailliet R. The shoulder in hemiplegia. Philadelphia, PA, FA Davis Co., 1980. Caldwell CB, Wilson DJ, Brown RM. Evaluation and treatment of the upper extremity in the hemiplegic stroke patient. Clin Orthop 1969;63:69-93. Carr EK, Kenney FD. Positioning of the stroke patient: a review of the literature. Int J Nurs Stud 1992;29(4):355-369.


Chaco J, Wolf E. Subluxation of the glenohumeral joint in hemiplegia. Am J Phys Med 1971; 50:139 143. Chantraine A, Baribeault A, Uebelhart 0, Gremion G. Shoulder pain and dysfunction in hemiplegia: effects of functional electrical stimulation. Arch Phys Med RehabiI1999;80:328-331. Chu Os, Petrillo C, Oavis SW, Eichberg R. Shoulder-hand syndrome: Importance of early diagnosis and treatment. J Am Ger Soc 1981; 29:58-60. Codman EA. The Shoulder. Boston, Thomas Todd Co, 1934.

Cole TM, Tobis JS. Measurement of musculoskeletal function. In: Kottke FJ, Lehmann JF (eds).

Krusen's Handbook of Physical Medicine and Rehabilitation. Philadelphia, Saunders, p.25, 1990.

Crossens-Sills J. Schenkman M. Analysis of shoulder pain. range of motion, and subluxation in patients with hemiplegia. Phys Ther 1985; 65:731. Culham EG, Noce RR, Bagg SO. Shoulder complex position and glenohumeral subluxation in hemiplegia. Arch Phys Med Rehabil1995;76:857-64. Oavis SW, Pestrilio CR, Eischberg RD. Chu OS. Shoulder-hand syndrome in a hemiplegic population: a 5-year retrospective study. Arch Phys Med Rehab 1977;58:353-355. Dean CM. Mackey FH, Katrak P. Examination of shoulder positioning after stroke: A randomised controlled pilot trial. Australian Journal of Physiotherapy 2000;46:35-40. Oekker JH, Wagenaar RC, Lankhorst GJ, de Jong BA. The painful hemiplegic shoulder: effects of intra articular triamcinolone acetonide. Am J Phys Med Rehabil1997;76:43-48. Eto F, Yoshikawa M, Ueda S, Hirai S. Post-hemiplegic shoulder-hand syndrome with special reference to related cerebral localization. JAm Ger Soc 1980;28:13-17. Faghri PO, Rodgers MM, Glaser RM, Bors JG, Ho C, Akuthota P. The effects of functional electrical stimulation on shoulder subluxation, arm function recovery, and shoulder pain in hemiplegic stroke patients. Arch Phys Med Rehabil1994;75:73-79. Faghri PD. The effects of neuromuscular stimulation-induced muscle contraction versus elevation on hand edema in CVA patients. J Hand Ther 1997;10:29-34. Fitzgerald-Finch OPt Gibson 11: Subluxation of shoulder in hemiplegia. Age Ageing 1975;4:16-18. Fugl-Meyer AR, Jaasko L, Leyman I, Olsson S, Steglind S. Post-stroke hemiplegic patient: I. Method for evaluation of physical performance. Scand J Rehab Med 1975;7:13-31. Geurts A, Visschers B, van Limbeek J, Ribbers G. Systematic review of aetiology and treatment of post stroke hand oedema and shoulder-hand syndrome. Scan J Rehab Med 2000;32:4-10. Hakuno A, Sashika H, Ohkawa T, Itoh R. Arthrographic findings in hemiplegic shoulders. Arch Phys Med Rehab 1984; 65:706-711. Hanger HC, Whitewood P, Brown G, Ball MC, Harper J, Cox R, Sainsbury R. A randomized controlled trial of strapping to prevent post-stroke shoulder pain. Clin Rehabil2000;14:370-380. Hecht JS. Subscapular nerve block in the painful hemplegic shoulder. Arch Phys Med Rehabil 1992;73:1036-1039.




Hecht JS. The role of spasticity in hemiplegic shoulder pain and what to do about it. 57th Annual Assembly of American Academy of Physical Medicine and Rehabilitation, Orlando, Florida, November 17, 1995, pp. 248-255. Hollinshead WH, Jenkins OB. Functional anatomy of the limbs and back. Philadelphia, Saunders p.105, 1981. Hurd MM, Farrell KH, Waylonis Gw. Shoulder sling for hemiplegia: friend or foe? Arch Phys Med Rehabil 1974;55:519-522. Inaba MK, Piorkowski M. Ultrasound in treatment of painful shoulder in patients with hemiplegia. J Phys Ther 1972;52:737-741. Johnstone M. The stroke patient: Principles of rehabilitation. Churchill Livingstone, Edinburgh, 1982. Joynt RL. The source of shoulder pain in hemiplegia. Arch Phys Med Rehabil 1992;73:409-413. Kaplan M. Hemiplegic shoulder pain--early prevention and rehabilitation. West J Med. 1995 Feb;162(2):151-2. Kaplan PE, Meredith J, Taft G, Betts HB. Stroke and brachial plexus injury: A difficult problem. Arch Phys Med Rehab 1977;38:415-18. Kingery WS, Date ES, Bobobo CR. The absence of brachial plexus injury in stroke. AM J Phys Med Rehab 1993; 72:127-175. Kobayashi H, Onishi H, Ihashi K, Vagi R, Handa V. Reduction in SUbluxation and improved muscle function of the hemiplegic shoulder joint after therapeutic electrical stimulation. J Electromyogr Kinesiol 1999;9:327-336. Kozin F, McCarty D, Sims J. Genant H. Reflex sympathetic dystrophy: I. Clinical and histological studies: evidence for bilaterality, response to corticosteroids and articular involvement. Am J Med 1976;60:321-331 (a). Kozin F, Genant HK, Bekerrnan C, McCarty DJ. Reflex sympathetic dystrophy syndrome: 11. Roentgenographic and scintigraphic evidence of bilaterality and of periarticular accentuation. Am J Med 1976;60:332-338(b). Kozin F, Ryan LM, Carrera GF, Soin JS, Wortman RL. Reflex sympathetic dystrophy syndrome (RSOS): III SCintigraphic studies, further evidence for the therapeutic efficacy of systemic corticosteroids, and proposed diagnostic criteria. Am J Med 1981 ;70 23-30. Kozin F. Two unique shoulder disorders: Adhesive capsulitis and reflex sympathetic dystrophy syndrome. Postgrad Med 1983;73(5):207-216. Kumar R, Metter EJ, Mehta AJ, Chew T. Shoulder pain in hemiplegia. The role of exercise. Am J Phys Med Rehabil 1990; 69(4):205-208. Lieberrnan JS. Hemiplegia: Rehabilitation of the upper extremity. In: Kaplan PE, Cerullo LJ (eds.): Stroke Rehabilitation. Stoneman, MA, Butterworth Publishers, p.95-117, 1986. Linn SL, Granat MH, Lees KR. Prevention of shoulder subluxation after stroke with electrical stimulation. Stroke 1999;30:963-968. Moodie NB, Brisbin J, Morgan AM. Subluxation of the glenohumeral joint in hemiplegia: Evaluation of supportive devices. Physiotherapy Canada 1986;38:151-157.


Morin L, Braro G. Strapping the hemiplegic shoulder: A radiographic evaluation of its efficacy to reduce subluxation. Physiotherapy Canada 1997; 49:103-108. Moskowitz E. Complications in rehabilitation of hemiplegic patients. Med Cnn North Am 1969;53541 559(a). Moskowitz E, Goodman CR, Smith E, Balthazar E, Mellins HZ. Hemiplegic shoulder. NY State J Med 1969; 69:548-550(b). Najenson T, Yacubovich E, Pikelini S. Rotator cuff injury in hemiplegic patients. Scand J Rehab Med 1971; 3:131-137. Nepomuceno CS, Miller JM Ill. Shoulder arthrography in hemiplegic patients. Arch Phys Med Rehab 1974; 55:49-51. Partridge CJ, Edwards SM. Mee R, Van Langenberghe HV. Hemiplegic shouldar pain: a study of two methods of phsyiotherapy treatment. Clinical Rehabilitation 1990;4:43-49. Patterson JR, Zabransky R, Grabois M. Ferro P. Evaluation of the effectivenss of sling orthoses for the correction of glenhummeral subluxation in the hemiplegic. Archives Phys Med RehabiI1984;65:635. Perrigot M, Bussel B, Pierrot Oeseilligny E, Held JP. L'epaule de I'hemiplegique. Ann Med Phys 1975;18:175-187. Poduri KR. Shoulder pain in stroke patients and its effects on rehabilitation. J Stroke Cerebrovasc Ois 1993;3:261-266. Post MW, Vfsser-Meily JM, Boomkamp-Koppen HG, Prevo AJ. Assessment of oedema in stroke patients: comparison of visual inspection by therapists and volumetric assessment. Disabil Rehabil 2003;25: 1265 1270. Poulin de Courval L, Barsauskas A, Berenbaum B. Oehaut F, Oussault R, Fontaine FS, Labrecque R, Leclerc C. Giroux F. Painful shoulder in the hemiplegic and unilateral neglect. Arch Phys Med Rehabil. 1990 Aug;71 (9):673-6. Prevost R, Arsenault AB, Duti! E, Drouin G. Rotation of the scapular and shoulder subluxation in hemiplegia. Arch Phys Med Rehab 1987;68:786-790. Price Cl, Pandyan AD. Electrical stimulation tor preventing and treating post-stroke shoulder pain: a systematic Cochrane review. CUn Rehabil2001;15:5-19 Rizk TE, Christopher RP, Pinals RS, Salazar JE, Higgins C. Arthrographic studies in painful hemiplegic shoulders. Arch Phys Med Rehab 1984;65:254-55. Roper TA, Redford S, Tallis RC. Intermittent compression for the treatment ofthe oedematous hand in hemiplegic stroke: a randomized controlled trial. Age Ageing 1999;28:9-13. Roy CW, Sands MR, Hill LO. Shoulder pain in acutely admitted hemiplegics. Clinical Rehabilitation 1996;18:497-501. Renzenbrink GJ, IJzerman MJ. Percutaneous neuromuscular electrical stimulation (P-NIVIES) for treating shoulder pain in chronic hemiplegia. Effects on shoulder pain and quality of life. Clin Rehabil 2004; 16:359-365 Savage R, Robertson L. Relationship between adult hemiplegic shoulder pain and depression. Physiotherapy Can 1982;34:66-90.


Shahani BT, Kelly EB, Glasser S. Hemiplegic shoulder subluxation. Arch Phys Med Rehab 1981;62:519. Shai G, Ring H, Costeff Hr Solzi P. Glenohumeral malalignment in hemiplegic shoulder. Scan J Rehab Med 1984; 16:133-136. Snels lA, Beckerman H, Twisk JW, Oekker JH, Peter OK, Koppe PA, Lankhorst GJ, Bouter LM. Effect of triamcinolone acetonide injections on hemiplegic shoulder pain: A randomized clinical trial. Stroke 2000;31:2396-2401. Steinbrocker O. Shoulder-hand syndrome: present perspective. Arch Phys Med Rehab 1969;49:388 395. Tahmoush AJ. Causalgia: redefinition as a clinical pain syndrome. Pain 1981;10:187. Tepperman PS, Greyson NO, Hilbert L, et al. Reflex sympathetic dystrophy in hemiplegia. Arch Phys Med Rehab 1984;65(8):442-447. Tyson SF and Chissim C. The immediate effect of handling technique on range of movement in the hemiplegic shoulder. Clinical Rehabilitation 2002;16:137-140. Van Ouwenwaller C, Laplace PM, Chantraine A. Paniful shoulder in hemiplegia. Arch Phys Med Rehabil 1986; 67:23-26. Wang RY, Chan RC, Tsai MW. Functional electrical stimulation on chronic and acute hemiplegic shoulder subluxation. Am J Phys Med Rehabil 2000;79:385-390. Wanklyn P, Forester A, Young J. Hemiplegics houlder pain (HSP): natural history and investigation of associated features. Disability and Rehabilitation 1996; 18:497-501. Williams R, Tafts L, Minuk T. Evaluation of two support methods for the subluxated shoulder of hemiplegic patients. Phys Ther 1988;68:1209-1214. Yu OT, Chae J, Walker ME, Fang ZP. Percutaneous intramuscular neuromuscular electric stimulation for the treatment of shoulder subluxation and pain in patients with chronic hemiplegia: a pilot study. Arch Phys Med Rehabil 2001 ;82:20-25. Yu DT, Chae J, Walker ME, Hart RL, Petroski GF. Comparing stimulation-induced pain during percutaneous (intramuscular_ and transcutaneous neuromuscular electric stimulation for treatment shoulder subluxation in hemiplegia. Arch Phys Med Rehabil 2001 ;82:756-60. Zorowitz RD, Idank 0, Ikai T, Hughes MB, Johnston MV. Shoulder subluxation after stroke: A comparison of four supports. Arch Phys Med Rehabil1995;76:763-771. Zorowitz RD, Hughes MB, Idank 0, Ikai T, Johnston V. Shoulder pain and SUbluxation after stroke: Correlation or coincidence? American Journal of Occupational Therapy 1996;50: 194-201.



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