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Page 1: Painful Hemiplegic Shoulder

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Painful Hemiplegic Shoulder Robert Teasell MD, Sanjit K. Bhogal MSc, Norine Foley MSc

Last Updated June 1, 2006

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Table of Contents

11.1 CAUSES OF HEMIPLEGIC SHOULDER PAIN ..................................6

11.2 SHOULDER SUBLUXATION ..............................................................7

11.2.1 PATHOPHYSIOLOGY................................................................................................. 7 11.2.2 SCAPULAR ROTATION.............................................................................................. 9 11.2.3 PAIN IN SHOULDER SUBLUXATION .......................................................................... 10

11.3 SPASTICITY, CONTRACTURES AND HEMIPLEGIC SHOULDER PAIN (HSP)..................................................................13

11.3.1 SPASTIC MUSCLE IMBALANCE ................................................................................ 15 11.3.2 FROZEN OR CONTRACTED SHOULDER .................................................................... 17

11.4 ROTATOR CUFF DISORDERS .......................................................19

11.5 FUNCTIONAL IMPACT OF PAINFUL HEMIPLEGIC SHOULDER.....................................................................................20

11.6 MANAGEMENT OF THE PAINFUL HEMIPLEGIC SHOULDER......21

11.6.1 POSITIONING OF THE HEMIPLEGIC SHOULDER ......................................................... 21 11.6.2 SLINGS AND OTHER AIDS....................................................................................... 22 11.6.3 STRAPPING THE HEMIPLEGIC SHOULDER ................................................................ 24 11.6.4 ACTIVE THERAPIES IN THE HEMIPLEGIC SHOULDER.................................................. 26 11.6.5 INJECTIONS IN THE HEMIPLEGIC SHOULDER............................................................. 29 11.6.6 FUNCTIONAL ELECTRICAL STIMULATION (FES) IN THE HEMIPLEGIC SHOULDER.......... 31 11.6.7 SURGERY AS TREATMENT FOR MUSCLE IMBALANCE................................................. 35 11.6.8 MOTOR BLOCKS AS TREATMENT FOR MUSCLE IMBALANCE....................................... 35 11.6.9 SUMMARY OF THE MANAGEMENT OF HEMIPLEGIC SHOULDER ................................... 37

11.7 SHOULDER HAND SYNDROME (SHS) ...........................................38

11.7.1 STAGES AND SYMPTOMS ....................................................................................... 38 11.7.2 PATHOPHYSIOLOGY............................................................................................... 39 11.7.3 DIAGNOSTIC TESTS............................................................................................... 41 11.7.4 TREATMENT OF SHOULDER-HAND SYNDROME......................................................... 42 11.7.5 PHARMACOLOGICAL TREATMENT OF SHOULDER-HAND SYNDROME.......................... 43 11.7.6 GRADED MOTOR IMAGERY AS A TREATMENT FOR CRPS1....................................... 44

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11.8 SUMMARY.........................................................................................46

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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 improve upper limb function, but may reduce 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. A motor imagery program appears to improve shoulder-hand syndrome.

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11. Painful Hemiplegic Shoulder Shoulder pain resulting from hemiplegia is a common clinical consequence of a focal cerebral insult resulting from a vascular lesion (ie. hemorrhagic or ischemic stroke). 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, by itself, can result in significant disability (Najenson et al. 1971, Poduri 1993) and although it can occur as early as 2 weeks post stroke, an onset time of 2-3 months post stroke is more typical (Poduri 1993). In a recent prospective study, Gamble et al. (2002) reported that 52/152 (34%) developed shoulder pain following stroke, 28% by two weeks and 87% by two months. By 6 months, the pain had resolved in 80% of the patients. Shoulder pain can negatively affect rehabilitation outcomes as 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). Lo et al. (2005) catalogued the different types of shoulder dysfunction based on both clinical and arthrographic findings and reported that 16% of patients of a cohort of 32 patients with hemiplegic shoulder pain within one-year of stroke had shoulder-hand syndrome, 4% had rotator cuff tears and 50% suffered from frozen shoulder. 63% of patients had a single type of shoulder dysfunction while 34% had two types. 11.1 Causes of Hemiplegic Shoulder Pain Although many etiologies have been proposed for hemiplegic shoulder pain, increasingly it appears to be a consequence of spasticity and the sustained hemiplegic posture. Shoulder pain may be more common among patients with neglect following stroke (Kaplan 1995). 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. 1969b, Savage and Robertson 1982, Shai et al. 1984), shoulder contractures or restricted shoulder range of motion (Bloch and Bayer 1978, Braun et al. 1981, Fugl-Meyer et al. 1975, Crossens-Sills and Schenkman 1985, Hakuno et al. 1984, Risk et al. 1984) and spasticity, particularly of the subscapularis and pectoralis muscles (Braun et al. 1981, Caldwell et al. 1969,

Table 11.1 Potential Causes of Hemiplegic shoulder Pain

Anatomical Site Mechanism Muscle Bone Joint Bursa Tendon Joint Capsule Other

Rotator Cuff, Muscle Imbalance, Subscapularis Spasticity, Pectoralis Spasticity Humeral Fracture Glenohumeral Subluxation Bursitis Tendonitis Frozen or Contracted Shoulder (Adhensive Capsulitis) Shoulder-hand Syndrome (Reflex Sympathetic Dystrophy)

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Moskowitz 1969a, 1969b). Other suggested causes of shoulder pain include reflex sympathetic dystrophy (Chu et al. 1981, Davis et al. 1977, Perrigot et al. 1975), or injury to the rotator cuff musculotendinous unit (Najenson et al. 1971, Nepomuceno et al. 1974). The role of central post stroke pain in the etiology of shoulder pain is unclear (Walsh 2001). 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. Therefore the shoulder musculature, in particular the rotator cuff musculotendinous sleeve, cannot perform its function of maintaining the humeral head in the glenoid fossa and there is a high risk of shoulder subluxation. Shoulder subluxation is a very common problem in hemiplegic 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 subluxation. Improper positioning in bed, lack of support while the patient is in the upright position or pulling on the hemiplegic arm when transferring the patient all contribute to glenohumeral 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 deltoid muscles (Basmajian and Bazant 1959, Shahani et al. 1981) (Figure 11.1).

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Figure 11.1 A. Normal Shoulder. The humeral head is maintained in the glenoid fossa by the supraspinatus muscle.

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.

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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 depressed and downward rotated position, as the paretic serratus anterior and 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

Method Outcome

Prevost et al. 1987 Canada

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 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.

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 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.

Culham et al. 1995 Canada No Score

34 hemiplegic patients were divided into high-tone and low-tone groups according to Ashworth scoring of muscle tone. Low tone patients scored less than 4 and high tone patients had a score of 4 or greater on the MAS.

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.

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Author, Year Country

Method Outcome

Price et al. 2001 UK No Score

30 patients, 6 months post stroke received a standardized clinical assessment, whereby manual palpitation of the subacrimonial space was performed to identify those with subluxation. The Upper Limb Motricity Score (ULMS) was used to record arm strength. The degree of scapular downward tilt and dynamic scapular lateral rotation were assessed by a Scapula Locator System device to determine their association with subluxation.

24 patients had no shoulder subluxation, 6 patients suffered from shoulder subluxation. Among all patients, the average degree of scapular downward tilt was 10.04 for the unaffected side and 10.46 for the affected side (p=ns). There was no difference in the scapular downward tilt of the affected shoulder of subjects with and without subluxation.

Prevost et al. (1987), using a 3-D x-ray technique, studied the movement of the scapula 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). Culham et al. (1995) reported that while patients with low-tone had significantly greater subluxation compared to the high-tone group, (0.52 vs. 0.21) there was no correlation between the amount of subluxation and the scapular abduction angle or the humeral abduction angle. Price et al. (2001) compared patients with and without stroke (n=15) and reported that subluxation in stroke patients was unrelated to scapular resting position. These authors also reported that the normal scapula tilts downward to a greater degree found in other studies. 11.2.3 Pain in Shoulder Subluxation Shoulder subluxation may be associated with several conditions including: shoulder pain (Crossens-Sills and Schenkman 1985, Moskowitz et al. 1969b, Savage and Robertson 1982, Shai et al. 1984, Roy et al. 1994) and frozen shoulder or brachial plexus traction injury (Kingery et al. 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 all 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 and to account for the chronicity of stroke since there is a correlation between early signs of shoulder subluxation and the development of pain. Paci et al.

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(2005) suggested that pain associated with subluxation is probably present later after stroke since “fibrous changes or injury can occur in connective tissue of the ligaments and joint capsule due to incorrect alignment between the humerus and the scapula”. Although several studies have reported an association, others have not confirmed this finding. Heterogeneity of patient characteristics and timing and method of assessment (radiological vs. clinical examination) may account for the lack of consistency of findings. (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

Studies Which Fail to Support 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 al. 1999 Lo et al. 2003 Aras et al. 2004

Peszczynski & Rardin 1965 Bohannon 1988 Van Langenberghe & Hogan 1988 Bohannon & Andrews 1990 Kumar et al. 1990 Arsenault et al. 1991 Joynt 1992 Zorowitz et al. 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

Methods Main Outcome

Shai et al. 1984 Israel No Score

33 patients received at least a single radiograph early in their hospitalization. Clinical status was assessed 4 to 11 months after stroke.

There was a significant correlation between abnormal radiologic findings early in the course of stroke and the development of pain. 19/33 patients had evidence of subluxation on radiograph and 17/33 had shoulder pain. Of those with shoulder pain 14/17 (82%) had subluxed shoulders.

Bohannon 1988 USA No Score

30 patients admitted for inpatient rehabilitation as average of 31 days following stroke. A variety of tests were performed at admission and discharge to assess their correlation with shoulder pain. Subluxation was assessed by palpitation and observation (clearly subluxed vs. not clearly subluxed).

24 patients had shoulder pain on initial assessment and 27 on final assessment. 30% of shoulders were subluxed on initial assessment and 47% at final assessment. There was no statistical significant relationship between pain and subluxation.

Bohannon & 28 consecutively admitted patients undergoing 70.8% of patients demonstrated

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Author, Year Country

Methods Main Outcome

Andrews 1990 USA No Score

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 450 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, complaint of pain, wince and withdrawal. SROMP measurements taken with patients’ shoulders laterally rotated until they first expressed pain in the shoulder, at which point a fluid-filled gravity goniometer, was applied and read.

enough shoulder pain to at least cause them to wince when their shoulders were rotated laterally 900. The SROMP of the paretic side was measured as 64.50+28.80 and 64.60+28.90. 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.

Joynt 1992 USA No Score

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.

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.

Wanklyn et al. 1996 UK No Score

108 patients were assessed clinically, 3 times over a 6-month period following stroke. Subluxation was assessed clinically and graded in finer-breadths palpable below the acrimonion process.

Subluxation was detected clinically in 31 (29%) patients at hospital discharge and 27 (26%) at 26 weeks. Shoulder pain was not associated with subluxation at 2/3 assessment points. The authors do not provide details of the data.

Zorowitz et al. 1996 USA No Score

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

Shoulder pain after stroke was not correlated with age, vertical, horizontal, or total asymmetry, shoulder flexion or abduction, or Fugl-Meyer scores. However, shoulder pain was strongly correlated with degree of shoulder external rotation

Ikai et al. 1998 Japan No Score

75 patients with shoulder subluxation were assessed for pain using a visual analogue scale at rest and during passive range of movement. The degree of pain was expressed as nonexistent (0), mild (1-3), moderate (4-7), or severe (8-10) during passive movement.

At rest, 10 patients reported pain. During passive range of movement, 5 patients reported no pain, 25 reported mild pain, 36 reported moderate pain and 9 reported severe pain. Shoulder

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Author, Year Country

Methods Main Outcome

pain was not related to the degree of shoulder subluxation.

Lo et al. 2003 Taiwan No Score

32 consecutive patients with shoulder pain following stroke were assessed for shoulder subluxation, which was diagnosed by a gap of more than one finger breadth between the acrimonion and the head of the humeral bone on palpation.

14 (44%) of patients had clinically diagnosed shoulder subluxation.

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 and the factors associated with it.

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

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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 Methods Outcome

Bohannon et al. 1986 USA No score

50 patients with hemiplegia was secondary to cerebrovascular accident, whose unaffected shoulders demonstrated normal and pain-free range of hemiplegia 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.

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.

Van Ouwenaller et al. 1986 Switzerland No score

219 hemiplegia patients were followed for 1 year after their stroke. Radiographic examinations were done for each patient.

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.

Joynt 1992 USA No Score

97 patients were examined between 6-9 months post stroke for evidence of shoulder dysfunction and pain, based on clinical examination.

67 patients were diagnosed with a shoulder problem. 49% of patients reported shoulder pain. Shoulder pain was unrelated to spasticity, assessed by resistance to rapid stretch.

Aras et al. 2004 Turkey No Score

The association between spasticity measured by the Ashworth scale and shoulder pain was assessed in 85 consecutive stroke patients, who were grouped by the presence or absence of shoulder pain.

54 patients had shoulder pain and 31 did not. There was no association between spasticity and shoulder pain.

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

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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 individuals, 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

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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 of the 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 external 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 flex, 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.

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

11.3.2 Frozen or Contracted Shoulder A frozen or contracted shoulder (adhesive capsuluitis) is characterized clinically by limitations in range of movement, with a pattern of restriction. This condition 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

Methods Outcome

Hakuno et al. 1984 Japan

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 non-dominant arm. Positive contrast arthography was preformed on both shoulders of all patients. An anterior approach for injection of the joint with contrast material was

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.

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Author, Year Country

Methods Outcome

employed. The needle was inserted directly into the glenohumeral joint space under fluoroscopic control. Anteroposterior radiographs were made in internal and external rotation.

Crossen-Sills & Schenkman 1985 USA

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.

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.

Rizk et al. 1984 USA

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, 900 forward flexion, 150 external rotation, 450 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.

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.

Bohannon et al. 1986 USA No Score

50 patients whose hemiplegia was secondary to a stroke, whose unaffected shoulders demonstrated normal and pain-free range of hemiplegia 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.

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.

Lo et al. 2003 32 consecutive patients with shoulder pain 16 (54%) of patients had rotator cuff

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Author, Year Country

Methods Outcome

Taiwan No Score

following stroke were assessed for shoulder subluxation, which was diagnosed by a gap of more than one finger breadth between the acrimonion and the head of the humeral bone on palpation.

tears diagnosed by arthrograpy.

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. Najenson et al. (1971) reported that 13 of 32 (40%) patients with severe paralysis of the upper extremity were found to have a rupture of the rotator-cuff ligament based on arthrographic findings. 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

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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

Methods Outcomes

Wankyln et al. 1996 UK No Score

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 Barthel Index score less than 20.

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 Barthel Index 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. 51%).

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.

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.

Roy et al. 1995 UK No Score

76 patients suffering from a first stroke were studied. Separate regression equations were created for the outcomes of length of hospital stay (LOS), performance of ADL (Barthel Index), arm function (Frenchay arm function) and arm power (Motricity Index)

Shoulder pain on movement was associated with increased LOS, poorer performance on ADL, arm function and arm power. Shoulder pain was a statistically significant predictor of arm function.

Wanklyn et al. (1996) and Roy et al. (1995, 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.

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11.6 Management of the Painful Hemiplegic Shoulder Management of the painful hemiplegic shoulder, once the condition has developed, is difficult and response to treatment is frequently unsatisfactory (Risk et al. 1984). The best treatment approach has not been definitely established, in part, due to the uncertainty of the etiology of the pain. As a result, a wide variety of treatments have been used, with varying degrees of success (Snels et al. 2002). Ideally, measures should be taken immediately following stroke to minimize the potential for the development of shoulder pain. Early passive shoulder range of motion, and supporting and protecting the involved shoulder, in the initial flaccid stage are regarded as important steps to reduce the development of shoulder pain. 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, while poor positioning may adversely affect symmetry, balance and body image. As cited by Gilmore et al. (2004), Davies (2000) suggests that through careful and correct positioning, the development of shoulder pain can be prevented. 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 of the Shoulder in Stroke Patients Author, Year Country PEDro Score

Methods Outcomes

Carr and Kenney 1992 No Score

Review of the literature. 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.

Dean et al. 2000 Australia 5 (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

Changes in active and passive range of motion were not significant between the groups with the level of pain remaining unchanged.

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Author, Year Country PEDro Score

Methods Outcomes

a week for six days (positioning). Ada et al. 2005 Australia 6 (RCT)

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.

Positioning the shoulder in maximal external 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 900, 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.

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 flaccid 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 these 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.

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Table 11.9 Results from Systematic Review (Ada et al. 2005) Outcome Studies Included & Intervention Peto Odds ratio (95% CI) or

Weighted Mean Difference (WMD) (95% CI)

Proportion of patients with pain at follow up

Hurd et al. 1974 – hemisling OR 8.7 (1.1, 67.1) (Favours no slings)

Number of days pain was delayed with treatment

Ancliffe et al. 1992 -strapping Griffin et al. 2003

WMD 14 days (9.7, 17.8) (Favours slings)

Pain scores on VAS (10 cm scale)

Hanger et al. 2000 – strapping WMD 0.83 (-1.46, 3.12) (No difference)

Motor Assessment sub scores (0-18)

Hanger et al 2000. -strapping WMD 0.8 (-1.5, 3.1) (No difference)

Proportion of patients with contractures

Hurd et al 1974- sling OR 1.00 (0.1, 9.3) (No difference)

Range of shoulder external rotation at end of follow up

Hanger et al. 2000 - strapping WMD –1.4 degrees (-10.9, 8.10) (No difference)

As tone returns to the shoulder muscles, the risk of shoulder subluxation decreases and slings can then be withdrawn. Slings tend to hold the limb in a poor position, which may accentuate 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

Methods Outcomes

Hurd et al. 1974 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.

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.

Moodie et al. 1986 Canada No Score

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 A/P view was taken of each: conventional sling; shoulder roll; Hook-Hemi Harness; arm trough; and plexiglass lap tray.

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 8 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.

Williams et al. 1988 Canada No Score

Radiographs were taken of 26 hemiplegic patients with subluxated shoulders with two different supports-the Bobath

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

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Author, Year Country PEDro Score

Methods Outcomes

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.

affected shoulder and the unaffected shoulder and between measurements of the unsupported affected shoulder and the supported affected shoulder using both supportive devices.

Brooke et al. 1991 USA No Score

Three different shoulder supports were applied to 10 patients by their occupational and physical therapists: Harris hemi-sling, the Bobath sling and the arm trough or lapboard.

Harris hemi-sling improved correction of the subluxation with mean vertical distance of 37.8mm vs 38.5mm 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 Harris sling.

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.

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 asymmetry.

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 no better than another.

There is limited evidence that shoulder slings influence clinical outcomes. 11.6.3 Strapping the Hemiplegic Shoulder Strapping the hemiplegic shoulder is used as a method to prevent or reduce the severity of shoulder subluxation and may provide some sensory stimulation. There are three different forms of strapping the hemiplegic shoulder, which have been described previously: Ancliffe 1992: 5-cm wide lightweight adhesive tape (Fixomull Stretch), “the first length of tape was applied to the shoulder half way along the length of the clavicle, continued

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across the deltoid muscle in a diagonal direction... the tape was terminated approximately one-quarter of the way of the along the spine of the scapula. A second length of tape was applied in the same direction as the first but 2 cm below. A small length of tape was applied over the shoulder to secure the ends”. Morin & Bravo 1997: “A 10 cm-wide Elastoplast adhesive bandage was applied under tension from the forearm under the olecranon laterally to the top of the shoulder. Two other 7.5 cm-wide bandages were applied from the olecranon under the forearm to the forearm to the top of the shoulder, with one passing anteriorly over the clavicle and the other posteriorly covering the spine of the scapula. No free space was left between the bandages.” Hanger et al. 2000: Three lengths of nonstretch Elastoplast Sports tape were used. “The two main supporting tapes were applied first. Both were applied using a lifting action, starting 5 cm above the elbow, and moving up the arm front and back, crossing at the top of the shoulder. The posterior arm tape was then anchored down past the clavicle whereas the tape from the anterior aspect of the arm came across the shoulder and down past the spine of the scapula. They were both supported at the lower end by a short tape to prevent them peeling off”. Individual Studies Table 11.11 Strapping the Hemiplegic Shoulder Author, Year Country PEDro Score

Methods Outcomes

Ancliffe 1992 Australia No Score

A pilot study of 8 patients who were assigned to receive strapping of the shoulder applied by one physiotherapist and changed every 3 to 4 days as needed to the hemiplegic side or to receive no strapping. Treatment began within 48 hours of admission to hospital.

Patients in the strapping group experienced a significantly longer pain free period than the patients who were not strapped (21 vs. 5.5 days). However, all patients in the strapping group eventually did experience pain. The longest pain-free period was 25 days.

Hanger et al. 2000 New Zealand 7 (RCT)

98 patients were randomized to have their affected shoulder strapped for 6 weeks in addition to standard physiotherapy or to receive standard physiotherapy only 15 days following stroke.

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.

Griffin & Bernhardt 2006 Australia 7 (RCT)

33 patients at risk of developing hemiplegic shoulder pain were randomized to therapeutic shoulder (TS) strapping, sham shoulder (SS) strapping or to a no strapping (control) group 10 days post stroke. Lightweight adhesive tape was used and strapping continued for over 4 weeks. Primary outcome was the number of pain free days. Secondary outcomes included range of movement, Motor Assessment

One person in the TS group developed shoulder pain compared to 5 persons in the other 2 groups. Subjects in the TS group reported 26 pain-free days, compared to 19 days for SS subjects and 16 days for subjects in the control group. The difference was statistically significant for the comparison of TS and control group. There were no differences between groups on any of the secondary outcomes.

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Author, Year Country PEDro Score

Methods Outcomes

scale scores and Modified Ashworth scores.

Conclusions Regarding Strapping the Hemiplegic Shoulder There is conflicting (Level 4) evidence that strapping the hemiplegic shoulder reduces the development of pain. There is moderate (Level 1b) evidence that strapping does not improve upper limb function or range of motion.

Strapping the hemiplegic shoulder does not appear to improve upper limb function, but may reduce 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 of the hemiplegic shoulder will improve pain. Individual Studies Table 11.12 Active Therapies in Hemiplegic Shoulder Author, Year Country PEDro Score

Methods Outcomes

Inaba et al. 1972 USA 7 (RCT)

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.

No significant differences between the groups were observed in measures of ROM.

Kumar et al. 1990 USA 5 (quasi-randomized controlled trial)

28 patients were assigned 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.

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

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Author, Year Country PEDro Score

Methods Outcomes

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.

Patridge et al. 1990 UK 5 (RCT)

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.

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.

Poduri et al. 1993 USA No Score

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.

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.

Tyson & Chissim 2002 UK 4 (RCT)

22 stroke patients with consequential weakness of the arm instructed to hold the 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.

Mean shoulder flexion for the axilla hold was 115.2 degrees and 97.7 degrees for the distal hold (p < 0.001).

Lynch et al. 2005 USA 6 RCT

35 stroke patients with significant upper motor impairment were randomized to a control group (n=16), which received self-range of motion exercises under the supervision of a physiotherapist or to the experimental group (n=19) of continuous passive motion treatments with the use of a device (25 min sessions, 5 days/week until discharge). All patients received rehabilitation therapies for 3.5 hours per day.

There were no between group differences in changed scores between groups on any of the outcome measures assessed (joint stability, Modified Ashworth scale, Fugyl-Meyer (pain and self-care FIM scores).

Gustafson & McKenna 2006 Australia 6 (RCT)

34 patients with upper extremity hemiparesis admitted within 100 days of stroke were randomized to a participated in a programme of two static positional stretches, each held for 20 minutes, once daily or to a control condition where the affected arm was supported when seated in bed. Outcome measures included: pain-free passive range of motion, shoulder pain (Ritchie Articular Index), Motor recovery (Motor Assessment Scale) and functional independence (modified BI) measured at hospital admission and discharge.

There were no significant between group differences reported for any of the outcomes. Over time, all participants reported decreased range of motion, motor recovery and functional independence. The control group reported a decrease in pain while the treatment group reported an increase.

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Discussion 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) found that overhead pullies caused dramatically higher levels of shoulder pain than more restrained ROM exercises. Although there were no statistically significant differences in change scores between the control and the experimental group, Lynch et al. (2005) reported a trend towards improvement in the area of shoulder joint stability associated with continuous passive motion using the OrthoLogic Danniflex600 shoulder CPM system. A programme of positional static stretches was not only ineffective in reducing loss of range of motion into external rotation, but was also associated with increasing levels of pain (Gustafson & McKenna 2006). Counter to previous research, subjects in this study continued to improve functionally, despite a loss of range of motion and increasing pain, reported by subjects in the treatment group. 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 (ROMT), 2) skate board on a table (SB) and 3) overhead pulley (OP).

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.

Pain Experience of Groups

0

20

40

60

80

ROMT SB OP

% in

Pai

n

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 (i.e. overhead pullies) resulted in a very high incidence of hemiplegic shoulder pain when compared to a gentler approach.

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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 (Level 1b) 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. There is moderate (Level 1b) evidence that static positional stretches performed daily during rehabilitation are associated with increasing pain and decreasing range of motion.

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.

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

Methods Outcomes

Joynt 1992 USA No Score

A retrospective study following 67 stroke patients with hemiplegic shoulder pain. Twenty-eight patients received a subacromial injection of 1% lidocaine.

50% of the 28 patients who underwent a subacromial injection of local anaesthetic obtained moderate or marked pain relief and improved ROM.

Bhakta et al. 17 patients received a single course of Shoulder pain improved in 6 of 9

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Author, Year Country

PEDro Score

Methods Outcomes

1996 UK No Score

intramuscular injection of botulinum toxin to biceps brachii, flexor digitorum profundus, flexor digitorum superficialis and flexor carpi ulnaris an average of 1.5 years post stroke. Dosages of 400-1,000 MU of Dysport or 400 MU of Botox were administered.

patients. Pain resolved completely in two patients. Benefit lasted for up to 11 months.

Dekker et al. 1997 Netherlands No Score

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 B) was 4 weeks long, during which three intra-articular injections of triamcinolone acetonide were administered at day 1, 8 and 22.

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 not reach statistical significance at the group level.

Snels et al. 2000 Netherlands 8 (RCT)

35 patients demonstrating hemiplegia after stroke and pain in hemiplegic shoulder greater than 4 on the visual analogue scale (VAS) 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 1ml) or three placebo injections (1 ml saline solution).

No significant improvement was observed for any of the primary outcome measures with triamicinolone acetonide treatment.

Discussion 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. A single uncontrolled study by Bhakta et al. (1996) evaluated the use of botulinum toxin in the treatment of shoulder pain in an uncontrolled study. The majority of patients responded to treatment. Conclusions Regarding Injections in the Hemiplegic Shoulder There is moderate (Level 1b) evidence, based on one “good” RCT that corticosteroid injections do not improve shoulder pain or range of motion in patients with hemiplegia. There is limited (Level 2) evidence that botulinum toxin can reduce pain in the hemiplegic shoulder.

Corticosteroid injections do not improve hemiplegic shoulder pain or range of

motion.

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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.” The supraspintus and posterior deltoid muscles are most likely to be treated as they are important muscles in maintaining the correct alignment of the glenohumeral joint (Paci et al. 2005). Theoretically, FES should help to compensate or facilitate flaccid shoulder muscles, which in turn should reduce the risk of shoulder subluxation. The ideal intensity of treatment is thought to be 6 hours daily, five days a week for 6 weeks. FES is performed at frequencies of between 35 to 50 Hz (Paci et al. 2005). Price & Pandyan (2001) conducted a systematic review of all forms of electrical stimulation (ES) used in the prevention and treatment of post stroke shoulder 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. There was evidence that FES, in addition to conventional therapy, improves function but is not superior for preventing pain. Table 11.14(a) Studies included in the Systematic Review authored by Price & Pandyan (2001) Study Intervention Length of Treatment Faghri et al. 1994 FES vs. no sham treatment 6 weeks Leandri et al. 1990 Sham treatment vs. high intensity TENS vs.

low intensity TENS 4 weeks

Linn et al. 1999 No sham treatment vs. electrical stimulation (not FES or TENS)

4 weeks

Sonde et al. 1998 No sham treatment vs. low frequency TENS 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) Odds Ratio* or Weighted (or Standardized) Mean Difference and 95% CI

New cases of shoulder pain No 0.64 (0.19, 2.14) * Pain intensity rating change from baseline No 0.13 (-1.00, 1.25) Passive humeral lateral rotation Yes 9.17 (1.43, 16.9) Motor score change from baseline No 0.24 (-0.14, 0.62) Glenohumeral subluxation compared to baseline Yes -1.13 (-1.66 , -0.60) Spasticity score change from baseline No 0.05 (-0.28,0.371) Ada &Foongchomcheay (2002) also conducted a meta-analysis to examine the effect of electrical stimulation on shoulder subluxation following stroke. This review included the results from 6 RCTs (Baker & Parker 1986, Faghri et al. 1994, Kobayashi et al. 1999, Linn et al. 1999, Wang et al. 2000). The results, presented in Table 11.15 suggest that early treatment following stroke helps to prevent the development of hemiplegic shoulder while later treatment helps to reduce pain, in addition to conventional therapy.

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Table 11.15. Pooled Results from Ada & Foongchomcheay (2002) Outcome Intervention Significant Result

(Y/N) Weighted Mean

Difference and 95% CI Shoulder subluxation (mm)

Early ES + CT* vs. early CT

Yes 6.5 (4.4, 8.6)

Shoulder subluxation (mm) Late ES + CT vs. Late CT

No 1.9 (-2.3, 6.1)

Function (Bobath assessment chart, Motor assessment scale and Fugl-Meyer) expressed as a percentage

Early ES + CT vs. early CT

Yes 18.6 (0.4, 36.7)

Function (Bobath assessment chart, Motor assessment scale and Fugl-Meyer) expressed as a percentage

Early ES + CT vs. early CT

No 14.4 (-5.4, 34.2)

Pain (range of motion-degrees) Early ES + CT vs. early CT

No 3.7 (-1.2, 8.6)

Pain (Visual analogue scale-cm) Late ES + CT vs. Late CT

Yes 1.6 (0.1, 3.0)

* CT= conventional therapy; ES= electrical stimulation Individual Studies Eleven studies specifically evaluated the effects of FES on the treatment of shoulder pain. (Table 11.16). Table 11.16 FES in Hemiplegic Shoulder Author, Year

Country PEDro Score

Methods Outcomes

Baker & Parker 1986 USA 4 RCT

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 control group used conventional hemi-slings or wheelchair arm supports.

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.

Faghri et al. 1994 USA 4 (RCT)

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).

After treatment, the FES group showed a significant increase in arm function, tone and EMG activity compared to control patients.

Faghri & Rodgers 1997 USA 4 (RCT)

26 patients received conventional physical therapy with 13 patients randomized to the treatment group, which received additional functional neuro-muscular stimulation (FNS) therapy for 6 weeks.

Weekly evaluation of arm and shoulder muscle 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.

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Author, Year Country

PEDro Score

Methods Outcomes

Advantage of treatment group was maintained 6 weeks after termination of the FNS.

Chantraine et al. 1999 Switzerland 4 (quasi-randomized controlled trial)

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.

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.

Kobayshi et al. 1999 Japan 5 (RCT)

17 patients were randomized to receive therapeutic electrical stimulation (TES) 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.

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.

Linn et al. 1999 Scotland 6 (RCT)

40 patients were randomly assigned to a control or treatment group. Patients in the treatment group received electrical 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

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.

Wang et al. 2000 Taiwan 5 (RCT)

32 inpatient and outpatient rehabilitation patients with hemiplegia were assigned to one of two groups based on the duration of hemiplegia: the short and the long duration. Subjects in each group were randomly assigned to either a control subgroup or an experimental subgroup. Subjects in the experimental subgroups were treated in a type A-B-A study design, which consisted of an FES training (A), routine therapy or regular daily activity without FES training (B), and another FES training (A). Each period lasted for 6 wk. FES training program, consisted of five sessions/week.

The experimental subgroup of short duration showed significant improvements in reducing subluxation as indicated by x-ray compared with the control subgroup of short duration after the first FES treatment. The same effect was not shown for the experimental subgroup of long duration. The second FES treatment program only resulted in an insignificant change of shoulder subluxation for both the short- and long-duration subgroups.

Yu et al. 2001 USA No Score

8 patients participated in six weeks of percutaneous intramuscular electric stimulation (per-NMES).

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.

Yu et al. 2001 USA

10 hemiplegic stroke patients with at least 1 fingerbreadth of glenohumeral subluxation

Pain scores were significantly lower for perc-NMES than trans-NMES as assessed by the

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Author, Year Country

PEDro Score

Methods Outcomes

6 (RCT) received 3 randomly ordered pairs of neuromuscular stimulation (NMES) to the suprasinatus and poterior deltoid muscles of the subluxated shoulder. The stimulation types were percutaneous-NMES (perc-NMES) and transcutaneous-NMES (trans-NMES). After each stimulation pain was evaluated with the visual analog scale (VAS) and the McGill Pain Questionnaire (MPQ).

VAS and the MPQ.

Renzenbrink & Ijerman 2004 Netherlands No Score

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 fingerbreadth of glenohumeral separation on palpation. Patients received 6 hours of Percutaneous Neuromuscular electrical stimulation (P-NMES) per day for a total of six weeks.

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.

Yu et al. 2004 USA 7 (RCT)

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.

The main outcome measure was the Pain outcome measure Brief Pain Inventory question 12 (BPI 12), 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.

Chae et al. 2005 USA 7 (RCT)

12 month follow up from Yu et al. 2004. Treatment success was defined as a minimum 2-point reduction in Brief Pain Inventory question 12 at all post treatment assessments. Secondary measures included pain-related quality of life (Brief Pain Inventory question 23), subluxation, motor impairment, range of motion, spasticity, and activity limitation.

22 patients in the intervention group and 21 patients received 12-month assessments. The electrical stimulation group exhibited a significantly higher success rate than controls (63% vs. 21%). Repeated-measure analysis of variance revealed significant treatment effects on post treatment Brief Pain Inventory questions 12 and 23. There were no other significant between group differences.

Discussion 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. The results suggest that FES can reduce pain in the affected shoulder and also improve upper extremity function. Percutaneously placed devices may improve treatment compliance.

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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 11.17 Surgery for Muscle Imbalance in the Hemiplegic Shoulder Author, Year

Country PEDro Score

Methods Outcomes

Braun et al. 1971 USA No Score

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.

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

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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 11.18 Motor Block for Muscle Imbalance in Hemiplegic Shoulder Author, Year Country PEDro Score

Methods Outcomes

Hecht 1992 No Score

A retrospective study of 13 patients with spastic hemiplegia, limited ROM and painful shoulder and with duration of hemiplegia for 2 to 13 months. Patients received percutaneous phenol nerve blocks to subscapularis muscle innervation.

Immediate and significant improvement in ROM observed in abduction, flexion and external rotation. Relief of pain was noted with previously painful movements.

Hecht 1995 No Score

Prospective study of 20 patients receiving botulinum toxin muscle blocks to the subscapular and pectoralis major musculature.

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

Bhakta et al. 1996 UK No Score

17 patients received a single course of intramuscular botulinum toxin to biceps brachii, flexor digitorum profundus, flexor digitorum superficialis and flexor carpi ulnaris.

Shoulder pain improved in 6 of 9 patients with shoulder pain.

Discussion Three 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.

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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 insufficient evidence that positioning of the shoulder, shoulder strapping, local corticosteroid injections and adding local ultrasound therapy do not prevent subluxation, decrease pain or increase functionality. 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 (Gresham et al. 1995).

Table 11.19 Summary of RCTs for Management of

Hemiplegic Shoulder Author, Year PEDro Score n Outcomes Positioning of the Shoulder Dean et al. 2000 5 23 - Ada et al. 2005 6 36 +/- Slings and Other Aids No RCTS - - - Strapping Hanger et al. 2000 7 98 - Griffin & Bernhardt 2006 7 32 + Active Therapies Inaba et al. 1972 7 33 - Patridge et al. 1990 5 65 + Kumar et al. 1990 5 28 -

(for aggressive pullies)

Lynch et al. 2005 6 35 - Gustafson & McKenna 2006 6 34 - Injection Snels et al. 2000 8 35 - Functional Electrical Stimulation Baker et al. 1986 4 63 + Faghri et al. 1994 4 26 + Faghri & Rogers 1997 4 26 + Linn et al. 1999 6 40 +/-

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Table 11.19 Summary of RCTs for Management of

Hemiplegic Shoulder Kobayshi et al. 1999 5 17 + Chantraine et al. 1999 4 115 + Wang et al. 2000 5 32 + Yu et al. 2001 6 10 + Yu et al. 2004 & Chae et al. 2005 7 61 + Surgery for Muscle Imbalance No RCTs - - o Motor Block for Muscle Imbalance No RCTs - - o

11.7 Shoulder Hand Syndrome (SHS) 11.7.1 Stages and Symptoms Shoulder hand syndrome, also known as reflex sympathetic dystrophy (RSD) and complex regional pain syndrome (type 1) is characterized by numerous peripheral and central nervous system changes. Peripheral changes include vasomotor tone with associated hand pain and swelling, exquisite tenderness or hyperaesthesia, protective immobility, trophic skin changes and vasomotor instability of the involved upper extremity. Central changes include a disruption of sensory cortical processing, disinhibition of the motor cortex and disrupted body schema (Moseley et al. 2004). Iwata et al. (2002) empirically describe 3 stages of RSD (Table 11.20). Table 11.20 Stages and Characteristics of SHS

Stage Characteristics I Persistent pain, described as burning, or aching and aggravated by movement

The extremity is edematous, warm and hyperesthetic Lasting 3-6 months

2 Early dystrophic changes in the limb present Atrophy of the muscle and skin Vasospam with hyperhydrosis

3 Soft-tissue dystrophy Contractures which produce “frozen shoulder” Pain and vasomotor changes are infrequent

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 (Davis 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.

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Shoulder hand syndrome is often regarded as a form of sympathetically mediated pain involving the hemiplegic upper extremity. The relationship between the sympathetic nervous system and pain remains hypothetical and has yet to be proven. 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. While recovery is largely spontaneous, conditions which persists for greater than 6 months are often difficult to treat. 11.7.2 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 link 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. Iwata et al. (2002) suggested that SHS might be due to paresis following stroke, mediated by disruption of homeostasis and the balance between intracellular and extracellular fluid. Three possible mechanisms include: i) an increase in capillary blood pressure, caused by a decrease in peripheral venous return and lymph flow; ii) a drop in the colloidal osmotic pressure in the early stages of stroke due to an acute phase response; iii) enhanced permeability of capillary walls which may result from synovial inflammation, brought about by rough management of the affected arm and hand.

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11.7.2 Incidence Table 11.21 Incidence of Shoulder-Hand Syndrome Author, Year Country PEDro Score

Methods Outcome

Davis et al. 1977 USA No Score

540 rehabilitation inpatients with hemiplegia were evaluated with respect to side of hemiplegia, dates of onset of hemiplegia and of pain, age, sex, handedness, sensory losses, associated medical diseases and treatment response. All patients’ charts were reviewed by a team composed of authors

68 (12.5%) patients were diagnosed with RSD. Care was used to distinguish these patients from those with other shoulder pathologic conditions and pain syndromes.

Eto et al. 1980 Japan No Score

7 autopsy cases of hemiplegia shoulder-hand syndrome from patients that had been admitted to the University of Tokyo Hospital or an affiliated hospital. Observed over a 6 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.

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.

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.

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.

Van Ouwenaller et al. 1986 Switzerland No score

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 an isolated tendon lesion and for several

The RSD syndrome was present in only 23% of all cases but was seen more often in spastic patients, 27% vs. 7%.

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Author, Year Country PEDro Score

Methods Outcome

contributing factors. Kondo et al. 2001 Japan No Score

152 stroke patients admitted to a rehabilitation unit and followed for approx. 200 days were monitored for the development of RSD, assessed clinically by a physician. Half of the patients were treated with a protocol to prevent RSD, consisting of passive ROM exercises, performed by therapists and restrictions on passive movement by patients. The remaining patients received standard inpatient rehabilitation.

The incidences of RSD were 15/81 (18.5%) for patients receiving the protocol and 23/71 (32.4%) among patients who did not.

While the incidence of RSD appears to range between 12-32%, Petchkrua et al. (2000), suggested that the incidence of RSD is over-estimated and the results from previous studies were obtained before patients routinely received early intensive inpatient rehabilitation. At admission to hospital and once a week until discharge, patients admitted to an acute rehabilitation facility were evaluated for shoulder pain, decreased passive range of motion of the shoulder, wrist/hand pain, edema, and skin changes. If three of these five criteria were positive, patients underwent a triple-phase bone scan (TPBS). Bone scan findings consistent with CRPS type 1 were taken as confirming the diagnosis. Of 64 subjects, 13 underwent bone scans, with only one (1.56%) positive result. The authors noted it was possible that patients were discharged before they developed symptoms of RSD. Patients from a more recent study (Kondo et al. 2001) who received standard multidisciplinary rehabilitation had a much higher incidence of RSD (34%). Conclusions Regarding the Incidence of RSD Post Stroke The incidence of RSD post stroke ranges form 12-34% and may be influenced by the timing as well as the type of assessment. 11.7.3 Diagnostic Tests Several approaches to diagnose RSD have been used. 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 al. (1984) found 25% of hemiplegic patients demonstrated evidence of reflex sympathetic dystrophy 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

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to consistently diagnose reflex sympathetic dystrophy and is not considered a valid test. However, Kozin et al. (1981) suggested that that clinical measurements such as grip strength, tenderness and ring size were more accurate diagnostic indicator of RSD. Iwata et al. (2002) have suggested that a ratio of the circumference of the middle finger (affected:unaffected) greater than 1.06 at four weeks post stroke was predictive of RSD Conclusions Regarding Shoulder-Hand Syndrome Shoulder hand syndrome is a painful clinical entity, which is not understood from a pathophysiological basis. The 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 11.22. 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 11.22 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

Modalities

• Interferential deep heat • Heat/cold modalities especially contrast

baths • Hand desensitization program • Transcutaneous electrical nerve stimulation

Splints

• Resting splint of hand and wrist (controversial)

Medication

• Analgesics • NSAIDs • High dose oral corticosteroids (10 day

course and then taper) Injections

• Stellate ganglion sympathetic block • Guanethedine bier block

Surgical

• Sympathectomy

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11.7.5 Pharmacological Treatment of Shoulder-Hand Syndrome Three studies evaluated drug therapies for the treatment of SHS associated with stroke. The results are presented in table 11.23. Table 11.23 Corticosteroid Treatment of Shoulder-Hand Syndrome Author, Year

Country PEDro Score

Methods Outcome

Davis et al. 1977 New York No Score

A retrospective study of 68 patients suffering from hemiparesis and SHS resulting from stroke. All patients received 16 mg of an oral steroid (triamcinolone diacetate) daily for 14 to 21 days. Patients self-described their pain.

All patients became pain- free, when subjected to passive stretching of the involved joints, within 3 weeks. Six patients experienced a relapse of their pain, which resolved during a second course of treatment.

Braus et al. 1994 Germany 5 (RCT)

36 hemiplegic patients secondary to a stroke of the middle cerebral artery and exhibited definite shoulder-hand syndrome were studied. Patients were randomized to orally 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.

Hamamci et al.1996 Turkey No Score

A controlled trial of 41 hemiplegic patients with grades 1-2 of SHS. All patients received conventional physical therapy as part of inpatient rehabilitation. 25 patients received 1 x 100 IU salmon calcitonin daily for 4 weeks and 16 patients received a saline injection as a placebo. Pain was measured on a 7-point visual analogue scale at the beginning and end of treatment

By the end of the 4th week patients receiving calcitonin had significantly lower median pain scores compared to the controls (1 vs. 5). Patients receiving calcitonin treatments also reported less tenderness and improved range of motion. There was no difference in hand edema between groups.

Discussion The study by Braus et al. (1994) was the only RCT examining a treatment for shoulder-hand syndrome. Oral corticosteroids improved SHS for at least 4 weeks. Despite a limited number of trials, a review by Geurts et al. (2000) concluded that oral corticosteroids were the most effective treatment for SHS. While a single controlled trial found that calcitonin treatment effectively treated pain associated with SHS, it is not widely used clinically.

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Conclusions Regarding Oral Corticosteroids in SHS There is moderate (Level 1b) evidence that oral corticosteroids improves shoulder-hand syndrome for at least the first 4 weeks. There is limited (Level 2) evidence that calcitonin improves pain associated with SHS following stroke.

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

11.7.6 Graded Motor Imagery as a Treatment for CRPS1 Motor Imagery has been suggested as an alternative therapy to conventional medical management of SHS and involves activation of cortical networks without initially involving movement of the affected limb. A version of this strategy (mirror therapy) has been used successfully for patients suffering from phantom pain. There may be an association between CRPS and a neglect-like condition, such that patients may need to focus their attention to move the affected limb (Moseley et al. 2004). A single RCT evaluated the effectiveness of this treatment following stroke. Table 11.24 Studies Evaluating Motor Imagery Post Stroke Author, Year

Country PEDro Score

Methods Outcome

Moseley et al. 2004 Australia 6 (RCT)

13 chronic SHS patients were randomly allocated to a motor imagery program (MIP) or to ongoing management (usually pharmacological). The MIP consisted of two weeks each of a hand laterality recognition task, imagined hand movements and mirror therapy, each two weeks in duration. After 12 weeks, the control group was crossed-over to MIP.

There was a significant improvement in Neuropathic pain scale scores associated with MIP treatment which persisted at 6 weeks. The NNT to experience a > 50% reduction in pain was 3.

In the first phase of the treatment hand laterality recognition, avoidance of activation of the primary motor cortex was achieved by only initiating activation in the pre-motor cortices. In the second stage, patients were asked to imagine their own hand placed in the same position as a picture selected from 28 pictures chosen at random. In the final stage, pictures of the unaffected hand were placed into a cardboard mirror box. Patients were asked to adopt the posture in the picture (n=20) times with both hands, but to discontinue if they experienced pain.

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Moseley et al. (2004) reported that treatment with MIP was more effective than ongoing medical management of CRPS1. Patients experienced significant reductions in pain and swelling associated with treatment, which persisted for at least 6 weeks. The authors also noted that 6 weeks after completing the MIP program, approximately 50% of patients no longer fulfilled the diagnostic criteria for CRPS1. Conclusions Regarding Graded Motor Imagery There is moderate (Level 1b) evidence that a modified imagery program can reduce pain associated with shoulder-hand syndrome.

A motor imagery program appears to improve shoulder-hand syndrome.

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11.8 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 (Level 1b) 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 conflicting (Level 4) evidence that strapping the hemiplegic shoulder

reduces the development of pain. There is moderate (Level 1b) evidence that strapping the hemiplegic shoulder does not improve range of motion or upper limb function.

8. There is moderate (Level 1b) evidence that the use of overhead pullies results

in surprisingly high levels of hemiplegic shoulder pain and should be avoided. 9. There is moderate (Level 1b) evidence that a gentle range of motion program

by a therapist results in less hemiplegic shoulder pain. 10. There is moderate (Level 1b) 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. There is limited (Level 2) evidence that botulinum toxin can reduce pain in the hemiplegic shoulder.

11. There is strong (Level 1a) 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.

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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 (Level 1b) evidence that oral corticosteroids improves

shoulder hand syndrome for at least the first 4 weeks. 16. There is moderate (Level 1b) evidence that a modified imagery program can

reduce pain associated with shoulder-hand syndrome. There is limited (Level 2) evidence that calcitonin improves pain associated with SHS following stroke.

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