EBRSR [Evidence-Based Review of Stroke Rehabilitation]
11 Painful Hemiplegic Shoulder
Swati Mehta PhD (cand.), Robert Teasell MD, Norine Foley MSc (We gratefully acknowledge the contribution of Sanjit Bhogal PhD)
Last Updated: September 2013
Abstract 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). Painful hemiplegic shoulder can occur as early as 2 weeks post stroke but an onset time of 2-3 months post stroke is more typical. 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. Similarly, shoulder hand syndrome is pervasive in hemiplegic patients and can lead to significant medical complications. This review summarizes the existing literature with regard to hemiplegic shoulder pain after stroke. Topics include causes and management of hemiplegic shoulder pain with in-depth discussion of shoulder subluxation, spasticity, contractures, and rotator cuff disorders. Management techniques including shoulder positioning, slings and aids, surgical interventions, injections, and electrical stimulation along with other miscellaneous treatments are addressed. Finally, a full discussion of the physiology, incidence, and treatment of shoulder hand syndrome is included.
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Key Points
Causes of Hemiplegic Shoulder Pain
Spasticity and hemiplegic shoulder pain are related.
It is uncertain whether shoulder subluxation causes hemiplegic shoulder pain.
Interventions
It is uncertain if prolonged positioning or strapping helps to prevent or reduce hemiplegic shoulder pain.
There is limited evidence that shoulder slings prevent the development of subluxation.
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.
It is unclear whether injections with botulinum toxin reduce pain or improve passive range of motion. Corticosteroid injections do not appear to improve hemiplegic shoulder pain or range of motion.
Functional electrical stimulation may help to reduce or prevent shoulder subluxation, but does not appear to reduce pain.
Denervation of the subscapularis muscle may reduce shoulder pain and improve passive range of motion, more so than denervation of the pectoralis major muscle.
There is some evidence that alternative therapies such as massage, massage with acupuncture, and aromatherapy combined with acupressure can reduce shoulder pain.
Oral corticosteroids appear to improve shoulder-hand syndrome for at least the first 4 weeks.
Mirror therapy can reduce pain associated with shoulder hand syndrome.
Dr. Robert Teasell 801 Commissioners Road East, London, Ontario, Canada, N6C 5J1 Phone: 519.685.4000 ● Web: www.ebrsr.com ● Email: [email protected]
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Table of Contents Abstract ...... 1
Key Points ...... 2
Table of Contents ...... 3
11. Painful Hemiplegic Shoulder ...... 4
11.1 Incidence of Hemiplegic Shoulder Pain ...... 4 11.2 Causes of Hemiplegic Shoulder Pain ...... 5 11.3 Shoulder Subluxation ...... 6 11.3.1 Pathophysiology ...... 6 11.2.2 Scapular Rotation ...... 7 11.3.3 Pain in Shoulder Subluxation ...... 8 11.4 Spasticity, Contractures and Hemiplegic Shoulder Pain (HSP) ...... 11 11.4.1 Spastic Muscle Imbalance ...... 12 11.4.2 Frozen or Contracted Shoulder ...... 15 11.5 Rotator Cuff Disorders ...... 16 11.6 Functional Impact of Painful Hemiplegic Shoulder ...... 17 11.7 Management of the Painful Hemiplegic Shoulder ...... 18 11.7.1 Positioning of the Hemiplegic Shoulder ...... 18 11.7.2 Slings and Other Aids ...... 20 11.7.3 Strapping the Hemiplegic Shoulder ...... 22 11.7.4 Active Therapies in the Hemiplegic Shoulder ...... 24 11.7.5 Electrical Stimulation in the Hemiplegic Shoulder ...... 26 11.7.6 Surgery as Treatment for Muscle Imbalance ...... 32 11.7.7 Botulinum Toxin Injections as Treatment for HSP ...... 32 11.7.8 Steroid Injections as Treatment for HSP ...... 35 11.7.9 Aromatherapy/Acupressure Treatment for Shoulder Pain ...... 37 11.7.11 Subscapular Nerve Block for the Treatment for Shoulder Pain ...... 39 11.7.12 Segmental Neuromyotherapy for the Treatment for Shoulder Pain ...... 40 11.7.13 Summary of the Management of Hemiplegic Shoulder ...... 40 11.8 Complex Regional Pain Syndrome (CRPS) ...... 42 11.8.1 Stages and Symptoms of CRPS ...... 42 11.8.2 Pathophysiology of CRPS ...... 43 11.8.3 Incidence of CRPS ...... 44 11.8.4 Diagnostic Tests of CRPS ...... 46 11.8.5 Treatment of CRPS ...... 47 11.8.6 Pharmacological Treatment of CRPS ...... 47 11.8.7 Mirror Imagery as a Treatment for CRPS ...... 48 11.8.8 Passive Range of Motion Exercises for the Prevention of CRPS ...... 50 11.8.9 Calcitonin for the Prevention of CRPS...... 51 11.9 Summary ...... 52 References ...... 54
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11. Painful Hemiplegic Shoulder
11.1 Incidence of Hemiplegic Shoulder Pain Shoulder pain resulting from hemiplegia is a common clinical consequence of a focal cerebral insult resulting from a vascular lesion (i.e. 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 et al. 1990). The results of several studies reporting on the incidence of HSP are presented in Table 11.1
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 prospective study, Gamble et al. (2000) 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. Lindgren et al. (2007) reported that 74 (24%) of 305 patients with first ever stroke, who remained from an original cohort of 416 patients, experienced shoulder pain by month 16. Approximately half of these patients developed pain between stroke onset and 4 months. Rajaratnam et al. (2007) identified three factors that predict, with 98% accuracy, the development of hemiplegic shoulder pain following acute stroke: a positive Neer test, moderate or greater shoulder pain during the performance of the hand behind the neck manoeuvre and a difference of greater than 10 degrees of passive external rotation at the shoulder joint. Depression, reduction to light touch and reduction to temperature sensation have also been associated with shoulder pain (Gamble et al. 2000).
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 (Rizk et al. 1984). Lo et al. (2003) 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 adhesive capsulitis (frozen shoulder). Sixty-three percent of patients had a single type of shoulder dysfunction while 34% had two types.
Table 11.1 Incidence of Hemiplegic Shoulder Pain Author, Year Incidence Bohannon et al. (1986) The charts of 50 patients with hemiplegia secondary to stroke admitted for inpatient rehabilitation were reviewed. Pain, assessed during passive shoulder external rotation, was reported by 36 (73%) patients van Ouwenaller et al. 219 stroke patients initially hospitalized for stroke were assessed and followed up for an average of 11 (1986) months, were studied. 157 (72%) reported experiencing shoulder pain on at least one occasion during the study period. Jespersen et al. (1995) Retrospective chart review of 173 admissions for inpatient stroke rehabilitation. Self-reported shoulder pain was reported by 38 (22%) patients. 27 patients developed pain during rehabilitation while 11 patients developed pain following discharge during the 6 month follow-up period. Zorowitz et al. (1996) 20 patients with clinical evidence of subluxation, admitted within 6 weeks of stroke were assessed for pain using a 0-10 visual analog scale. Pain scores of 4-10 were reported by 9 (45%) patients. The remainder had no, or minimal pain. Gamble et al. (2000) 182 unselected, consecutive patients admitted to hospital and assessed for pain within 2 weeks of stroke. Pain was assessed using a visual analog scale. 31(25%) reported shoulder pain. Langhorne et al. (2000) 311 acute, consecutive stroke patients admitted to hospital were assessed for the presence of pain. Shoulder pain was reported in 9% of patients during hospitalization, 15% (from discharge-6 months), 11% (from 6-18 months) and 12% (18-30 months)
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Ratnasabapathy et al. Self-reported shoulder pain among survivors of a population based sample of 1,761 stroke survivors (2003) from New Zealand. One week after stroke painful shoulder was reported by 256/1474 (17%), 261/1,336 (20%) at one month and 284/1,201 (23%) at six months. Lindgren et al. (2007) Population-based cohort of 416 first-ever stroke patients were assessed for shoulder pain using a 0-100 mm visual analog scale. Shoulder pain was initially reported by 71 (22%) patients. At 4 months, 71/327 (22%) of the remaining patients reported shoulder pain by 16 months, 74/305 (24%) reported pain. Dromerick et al. (2008) 46 consecutive stroke rehabilitation inpatients were examined prospectively within 2 weeks of admission. Pain was self-reported in 17 (37%), 7 with pre-existing pain. Sackley et al. (2008) 600 hospitalized stroke survivors were followed over a one-year period to assess the incidence of various complications, including shoulder pain. At 3 months, 44/122 (36%) reported shoulder pain. At 6 and 12 months, 37/89 (42%) and 34/73 (47%) reported shoulder pain. Klit et al. (2011) 15.1% of 608 stroke survivors who responded to a postal questionnaire indicated that they experienced new onset of shoulder pain within 2 years of stroke. Hansen et al. (2012) 299 acute stroke patients were interviewed at 4 days following stroke onset and at 3 and 6 months by telephone to determine the incidence of post-stroke pain Newly developed shoulder pain was present at stroke onset (1.5%), 3 months (13.1%) and 6 months (16.1%)
The incidence of HSP varied greatly among the studies we reviewed. The variability was likely influenced by the timing of assessment and by the patient characteristics. The development of shoulder pain appears to increase over time following stroke.
Conclusions Regarding the Incidence of Hemiplegic Shoulder Pain Following Stroke
The incidence of post stroke shoulder pain varies from 9% to 73%
11.2 Causes of Hemiplegic Shoulder Pain
Although many etiologies have been proposed for Table 11.2 Potential Causes of Hemiplegic hemiplegic shoulder pain, increasingly it appears to be a shoulder Pain consequence of spasticity and the sustained hemiplegic posture. Shoulder pain may be more common among Anatomical Site Mechanism patients with neglect following stroke (Kaplan 1995). Muscle Rotator Cuff, Muscle Imbalance, Possible sources of hemiplegic shoulder pain are listed Subscapularis Spasticity, Pectoralis Spasticity in Table 11.2. Factors most frequently associated with shoulder pain are shoulder (glenohumeral) subluxation Bone Humeral Fracture (Grossens-Sills & Schenkman 1985; Moskowitz et al. 1969; Savage & Robertson 1982; Shai et al. 1984), Joint Glenohumeral Subluxation shoulder contractures or restricted shoulder range of motion (Bloch & Bayer 1978; Braun et al. 1971; Fugl- Bursa Bursitis Meyer et al. 1974; Grossens-Sills & Schenkman 1985; Hakuno et al. 1984; Rizk et al. 1984) and spasticity, Tendon Tendonitis particularly of the subscapularis and pectoralis muscles (Caldwell et al. 1969; Moskowitz 1969; Moskowitz et al. Joint Capsule Frozen or Contracted Shoulder (Adhesive Capsulitis) 1969) suggested causes of shoulder pain include reflex sympathetic dystrophy (Chu et al. 1981; Davis et al. Other Shoulder-hand Syndrome 1977; Perrigot et al. 1975), or injury to the rotator cuff (Reflex Sympathetic Dystrophy) musculotendinous unit (Najenson et al. 1971; Nepomuceno & Miller 1974). The role of central post stroke pain in the etiology of shoulder pain is unclear (Walsh 2001).
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In a recent study, the first of its kind, MRI was used to examine a potential association between structural changes in hemiplegic shoulder and pain (Shah et al. 2008). In a series of 89 patients with shoulder pain, 35% of subjects exhibited a tear of at least one rotator cuff, biceps or deltoid muscle and 53% exhibited tendinopathy of at least one rotator cuff, bicep or deltoid muscle, rotator cuff tears and rotator cuff and deltoid tendinopathies. These changes were not related to severity of shoulder pain.
11.3 Shoulder Subluxation
11.3.1 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 callipers (Boyd & Torrance 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 & Wolf 1971). The resulting mechanical effect is overstretching of the glenohumeral capsule (especially its superior aspect) and flaccid supraspinatus and deltoid muscles (Basmajian & Bazant 1959; Shahani et al. 1981) (Figure 11.1).
Figure 11.1 A. Normal Shoulder. The humeral head is maintained in the glenoid fossa by the supraspinatus muscle.
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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 in the glenoid fossa.
11.2.2 Scapular Rotation
There appear to be other factors playing a role in subluxation of the glenohumeral joint. Basmajian and Bazant (1959) proposed that in the normal state, subluxation of the humeral head was prevented by upward angulation of the glenoid fossa and the upper part of the shoulder capsule, the coracohumeral ligament and supraspinatus muscle. After a hemiplegic stroke they hypothesized that the upward angulation of the scapula would be lost. Cailliet (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 11.3 Scapular Rotation in the Hemiplegic Shoulder Author, Year Country Methods Outcomes PEDro Score Prévost et al. 50 patients who had experienced a cerebrovascular The angle of abduction of the arm of the (1987) accident, presenting with right hemiplegia. Inferior affected side was significantly greater than on Canada subluxation of the shoulder in hemiplegia was the non-affected side, p<0.05, but the relative measured using a tridimensional (3-D) x-ray technique, abduction of the arm was on the same order of giving true vertical distance separating the apex of the magnitude for both sides. There was no humeral head and the inferior margin of the glenoid significant relationship between the orientation cavity. Both shoulders were evaluated and the of the scapula and the severity of the difference used as a measure of subluxation. The subluxation. The abduction of the humerus was measure was then compared to the orientation of the weakly (r=.24) related to the subluxation, which scapula relative to the vertical and the abduction of the partly explained the weak association found arm. between the relative abduction of the arm and the subluxation.
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Culham et al. 34 hemiplegic patients were divided into high-tone and Scapula was significantly further from the (1995) low-tone groups according to Ashworth scoring of midline and lower on the thorax on the affected Canada muscle tone. Low tone patients scored less than 4 and side in the low-tone group. Glenohumeral No Score high tone patients had a score of 4 or greater on the subluxation was significantly greater in the low- MAS. 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.
Price et al. (2001) 30 patients, 6 months post stroke received a 24 patients had no shoulder subluxation, 6 UK standardized clinical assessment, whereby manual patients suffered from shoulder subluxation. No Score palpitation of the subacrimonial space was performed Among all patients, the average degree of to identify those with subluxation. The Upper Limb scapular downward tilt was 10.04 for the Motricity Score (ULMS) was used to record arm unaffected side and 10.46 for the affected side strength. The degree of scapular downward tilt and (p=ns). There was no difference in the scapular dynamic scapular lateral rotation were assessed by a downward tilt of the affected shoulder of Scapula Locator System device to determine their subjects with and without subluxation. association with subluxation.
Prévost 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 (i.e. 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 (Prévost 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. compared patients with and without stroke (n=15) and reported that subluxation in stroke patients was unrelated to scapular resting position (Price & Pandyan 2001). These authors also reported that the normal scapula tilts downward to a greater degree found in other studies.
11.3.3 Pain in Shoulder Subluxation
Shoulder subluxation may be associated with several conditions including: shoulder pain (Grossens-Sills & Schenkman 1985; Moskowitz et al. 1969; Roy et al. 1994; Savage & Robertson 1982; Shai et al. 1984) 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 (Bender & McKenna 2001; Fitzgerald-Finch & Gibson 1975; Moskowitz et al. 1969; Shahani et al. 1981). 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. (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
11. Painful Hemiplegic Shoulder pg. 8 of 66 www.ebrsr.com 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 11.4).
Table 11.4 Studies which Support or Fail to Report an Association between Shoulder Subluxation and Pain Studies Supporting the Role of Studies Which Fail to Support the Shoulder Subluxation in Pain Role of Shoulder Subluxation in Pain Shai et al. 1984 Peszczynski & Rardin 1965 Van Ouwenaller et al. 1986 Bohannon 1988 Poulin de Courval et al. 1990 Van Langenberghe & Hogan 1988 Roy et al. 1994 Bohannon & Andrews 1990 Chantraine et al. 1999 Kumar et al. 1990 Lo et al. 2003 Arsenault et al. 1991 Aras et al. 2004 Joynt 1992 Suethanapornkul et al. 2008 Zorowitz et al. 1996 Ikai et al. 1998 Huang et al. 2010 Barlak et al. 2009
A selection of studies examining the relationship between shoulder subluxation and pain are presented in Table 11.5.
Table 11.5 Pain and Subluxation in the Hemiplegic Shoulder Author, Year Country Methods Outcomes PEDro Score Shai et al. (1984) 33 patients received at least a single radiograph early in There was a significant correlation between Israel their hospitalization. Clinical status was assessed 4 to 11 abnormal radiologic findings early in the course No Score months after stroke. 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 30 patients admitted for inpatient rehabilitation as 24 patients had shoulder pain on initial (1988) average of 31 days following stroke. A variety of tests assessment and 27 on final assessment. 30% of USA were performed at admission and discharge to assess shoulders were subluxed on initial assessment No Score their correlation with shoulder pain. Subluxation was and 47% at final assessment. There was no assessed by palpitation and observation (clearly statistical significant relationship between pain subluxed vs. not clearly subluxed). and subluxation. Bohannon & 28 consecutively admitted patients undergoing 70.8% of patients demonstrated enough Andrews (1990) rehabilitation for their first stroke who could follow shoulder pain to at least cause them to wince USA instructions, and were aware of the position of their when their shoulders were rotated laterally 900. No Score paretic limb in space were included. Paretic shoulder The SROMP of the paretic side was measured subluxation and paretic shoulder pain were measured. as 64.50+28.80 and 64.60+28.90. A significant Shoulder subluxation was measured while the patients Pearson correlation (-77s, p<0.001) was sat on the edge of a mat table with their paretic upper observed between the Ritchie Index and extremity dependent and the examiner used his thumb SROMP indicating that patients with higher to palpate the separation between the acromion and the scores on the Ritchie Index had fewer degrees head of the humerus. He then graded subluxation as of lateral rotation of the shoulder before pain none (0), minimal (1) or substantial (2). Shoulder pain was experienced.
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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. Joynt (1992) A convenience sample of 97 patients suffering from pain 49 patients with specific shoulder pain were USA in the upper extremity was examined. The interval from compared to 18 patients with pain, not No Score stroke onset to examination ranged from several days to localized to the shoulder. Patients complaining a few years. 49 patients had specific complaints of of shoulder pain did not exhibit subluxation shoulder pain. more frequently than patients with general pain in the affected extremity. Wanklyn et al. 108 patients were assessed clinically, 3 times over a 6- Subluxation was detected clinically in 31 (29%) (1996) month period following stroke. Subluxation was patients at hospital discharge and 27 (26%) at UK assessed clinically and graded in finer-breadths palpable 26 weeks. Shoulder pain was not associated No Score below the acrimonion process. with subluxation at 2/3 assessment points. The authors do not provide details of the data. Zorowitz et al. 20 stroke patients with shoulder pain, admitted to a Shoulder pain after stroke was not correlated (1996) rehabilitation hospital within 6 weeks of their first stroke with age, vertical, horizontal, or total USA were studied. asymmetry, shoulder flexion or abduction, or No Score Fugl-Meyer scores. However, shoulder pain was strongly correlated with degree of shoulder external rotation. Ikai et al. (1998) 75 patients with shoulder subluxation were assessed for At rest, 10 patients reported pain. During Japan pain using a visual analogue scale at rest and during passive range of movement, 5 patients No Score passive range of movement. The degree of pain was reported no pain, 25 reported mild pain, 36 expressed as nonexistent (0), mild (1-3), moderate (4-7), reported moderate pain and 9 reported severe or severe (8-10) during passive movement. pain. Shoulder pain was not related to the degree of shoulder subluxation. Lo et al. (2003) 32 consecutive patients with shoulder pain following 14 (44%) of patients had clinically diagnosed Taiwan stroke were assessed for shoulder subluxation, which shoulder subluxation. No Score was diagnosed by a gap of more than one finger breadth between the acrimonion and the head of the humeral bone on palpation.
Aras et al. (2004) 85 consecutive stroke patients admitted to one of the 27 patients had glenohumeral joint subluxation Turkey largest rehab facilities in Turkey were studied to identify and reported shoulder pain, compared to 5 No Score the incidence of shoulder pain and the factors patients with the same finding, but without associated with it. pain. Suethanapornkul 327 patients from 9 rehabilitation centres were assessed 62 patients (19%) were found to have shoulder et al. (2008) weekly during inpatient rehabilitation for the presence pain and 122 (37%) patients had shoulder Thailand of pain and subluxation. (Neither the criteria used to subluxation. Shoulder pain was significantly No Score measure subluxation, nor the scale used to assess pain is more frequent in subjects with shoulder described). subluxation (odds ratio (OR) 2.48, and at 2-6 months after stroke onset (OR 4.0). Shoulder subluxation was significantly associated with hemorrhagic stroke, loss of proprioceptive sensation and was negatively associated with
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Brunnstrom's stage of arm recovery. Barlak et al. 187 consecutive stroke patients admitted for inpatient Shoulder pain was present in 114 (61%) (2009) rehabilitation were evaluated for the presence of HSP. patients. Of the 114 patients with pain, 71 Turkey Each patient was evaluated by clinical, radiographic, and patients showed various grades of No Score ultrasonographic examination. Daily living activities were glenohumeral joint subluxation. There was no assessed using the FIM at admission and at discharge. association between pain and degree of Patients were divided into two groups, one comprising subluxation. The group without HSP showed patients with shoulder pain and the other comprising significantly more improvement than the group patients without shoulder pain. They were then with HSP in functional outcomes (P=0.01) and compared with respect to clinical characteristics, the hospitalization period was significantly radiologic findings, and FIM scores. shorter (P=0.03). The mean discharge FIM score was higher among patients without HSP (93 vs. 82, p<0.001)
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.
It is uncertain whether shoulder subluxation causes hemiplegic shoulder pain.
11.4 Spasticity, Contractures and Hemiplegic Shoulder Pain (HSP)
Abnormal muscle tone, including spasticity may be directly related to HSP. Spasticity is defined as a disorder of motor function characterized by a velocity-dependent increase in resistance to passive stretch of muscles accompanied by hyperactive muscle stretch reflexes and often associated with a clasp-knife phenomena. Spasticity is one component of the upper motor neuron (UMN) syndrome and is the inevitable accompaniment of hemiplegia and an incomplete motor recovery. Under normal circumstances a delicate balance exists between facilitating and inhibiting influences upon both alpha and gamma motor neurons, which together maintain appropriate control of skeletal muscle length and strength of contraction at the spinal cord level. After a stroke, input from one or more of the supraspinal suppressor areas will decrease or stop entirely. The balance of control over the muscle tips in favour of facilitation and spasticity results. Spasticity develops only if there is loss of input from both pyramidal and extrapyramidal motor systems. Spasticity presents as increased tone and reflexes on the involved side of the body.
Table 11.6 Spasticity and Hemiplegic Shoulder Pain Author, Year Country Methods Outcomes PEDro Score Bohannon et al. 50 patients with hemiplegia was secondary to Of the 50 patients reviewed, 72% had shoulder
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(1986) cerebrovascular accident, whose unaffected shoulders pain. 20 had some pain while 16 had severe USA demonstrated normal and pain-free range of hemiplegia pain. Three zero-order correlations were No score shoulder external rotation (ROSER, 900); able to significant: ROSER and shoulder pain (r=-0.061, adequately follow instructions to allow testing of all p<0.001), time since onset of hemiplegia and variables pertinent to the study. Information was shoulder pain (r=0.45, p<0.01), and time since retrieved from patients’ records concerning their initial onset of hemiplegia and ROSER (r=0.37, p<0.01). physical therapy evaluation. Relationships between pain One-way ANOVA demonstrated that time since and other variables were determined. 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 219 hemiplegia patients were followed for 1 year after 72% of patients had shoulder pain at least once et al. (1986) their stroke. Radiographic examinations were done for during their recovery occurring most often in Switzerland each patient. patients having spasticity (85%) than in patients No score which flaccidity (18%). Appearance of spasticity was evident in 80% of patients while 20% remained hypotonic. Joynt (1992) 97 patients were examined between 6-9 months post 67 patients were diagnosed with a shoulder USA stroke for evidence of shoulder dysfunction and pain, problem. 49% of patients reported shoulder No Score based on clinical examination. pain. Shoulder pain was unrelated to spasticity, assessed by resistance to rapid stretch. Aras et al. (2004) The association between spasticity measured by the 54 patients had shoulder pain and 31 did not. Turkey Ashworth scale and shoulder pain was assessed in 85 There was no association between spasticity and No Score consecutive stroke patients, who were grouped by the shoulder pain. presence or absence of 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 shoulder problems following stroke. Nevertheless, evidence for spasticity in particular hypertonic muscle imbalance, as a cause of hemiplegic shoulder pain is growing.
11.4.1 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
11. Painful Hemiplegic Shoulder pg. 12 of 66 www.ebrsr.com 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 & Jenkins 1981). The subscapularis muscle also participates in arm adduction and extension from a flexed position (Cole & 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 specifically linked this problem to the subscapularis muscle when he noted, "The subscapularis muscle is the primary cause of shoulder pain in spastic hemiplegia where external rotation is most limited. Although other muscles may contribute to spasticity, pain and functional contracture, the subscapularis is the keystone of the abnormal synergy pattern,"(Hecht 1995).
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 11.2 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.
Figure 11.3 The Pectoralis Major Muscle. The pectoralis major muscle serves to adduct, internally rotate and forward flex the arm at the shoulder.
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11.4.2 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. 1974; Grossens-Sills & Schenkman 1985; Hakuno et al. 1984; Rizk et al. 1984).
Table 11.7 Evidence of Frozen Shoulder Post Stroke Author, Year Country Methods Outcomes PEDro Score Hakuno et al. 77 patients with hemiplegia caused by cerebrovascular Contractures/adhesions were found in paralyzed (1984) accidents were randomly selected from all hemiplegic shoulders at a statistically significant higher rate Japan patients treated at rehab centre. Cases with dementia (54.6%) than in the non-paralysed side (32.5%). and verbal dysfunction were eliminated. Paralysis The occurrence rate of contrast leakage from a affected the right side in 35 patients and the left side in capsule tear on the subscapular bursa and the 42 patients. In 35 cases the affected arm was dominant bicipital tendon sleeve was higher on the non- whereas 42 cases had paralysis in non-dominant arm. paralysed side than on the paralysed side. It was Positive contrast arthography was performed on both suggested that capsular contracture due to shoulders of all patients. An anterior approach for hemiplegia reduces capsular tearing during injection of the joint with contrast material was arthrographic manoeuvres. employed. The needle was inserted directly into the glenohumeral joint space under fluoroscopic control. Anteroposterior radiographs were made in internal and external rotation. Grossen-Sills & 21 male patients all received standard physical therapy 67% of the patients entered the rehab centre with Schenkman treatment. Shoulder pain, range of motion and signs of shoulder pain. An additional 10% (1985) subluxation were assessed on admission, three weeks developed initial signs of shoulder pain by 3 weeks USA post admission and at discharge. 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) Study of 30 spastic hemiplegic (18 with left hemiplegia 23 patients had capsular constriction typical of USA and 12 with right hemiplegia) patients with painful frozen shoulder (adhesive capsulitis). 7 patients ipsilateral shoulders meeting the following criteria: had normal arthrograms. None showed rotator cuff maximum passive range of motion (ROM) of 600 of capsular tears. Electromyography revealed abduction, 900 forward flexion, 150 external rotation, electrical silence in the shoulder musculature at 450 extension; any stress at the limit of motion rest. 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 anticonvulsant 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. Bohannon et al. 50 patients whose hemiplegia was secondary to a Of the 50 patients reviewed, 72% had shoulder
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(1986) stroke, whose unaffected shoulders demonstrated pain. 20 had some pain while 16 had severe pain. USA normal and pain-free range of hemiplegia shoulder Three zero-order correlations were significant: No Score external rotation (ROSER, 900); able to adequately ROSER and shoulder pain (r=-0.061, p<0.001); time follow instructions to allow testing of all variables since onset of hemiplegia and shoulder pain pertinent to the study. Information was retrieved from (r=0.45, p<0.01); and time since onset of patients’ records concerning their initial physical hemiplegia and ROSER (r=0.37, p<0.01). One-way therapy evaluation. Relationships between pain and ANOVA demonstrated that time since onset of other variables were determined. 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 following 16 (54%) of patients had rotator cuff tears Taiwan stroke were assessed for shoulder subluxation, which diagnosed by arthrography. No Score was diagnosed by a gap of more than one finger breadth between the acromion and the head of the humeral bone on palpation.
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.
11.5 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, Rizk et al. (1984) failed to demonstrate any evidence of rotator cuff tears on arthrography in 30 patients with hemiplegic shoulder pain. A similar study reported a 33% incidence of rotator cuff tears in painful shoulders after strokes (Nepomuceno & Miller 1974). 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. Twenty-eight patients received a subacromial injection of 1% lidocaine; approximately half obtained moderate or marked relief of pain and improved range of motion. However, this provides only indirect evidence of rotator cuff disorders as a possible cause of hemiplegic shoulder pain. Generally, hemiplegic shoulder pain is not commonly associated with rotator cuff disorders.
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11.6 Functional Impact of Painful Hemiplegic Shoulder
A painful hemiplegic shoulder can be very limiting and has the potential to further add to the disability seen with hemiplegia. However, a clear relationship between post-stroke shoulder pain and motor recovery has not been shown. The results from several studies have been conflicting.
Table 11.8 Impact of Painful Hemiplegic Shoulder on Function Author, Year Country Methods Outcomes PEDro Score Wanklyn et al. 108 post stroke patients were studied. Patients were 63.8% of all patients developed hemiplegic (1996) over the age of 60, about to be discharged home and shoulder pain (HSP). HSP was associated with UK had suffered stroke with persisting disability defined as reduced shoulder shrug and reduced pinch grip. No Score a Barthel Index score less than 20. 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) 85 consecutive stroke patients admitted to one of the 54 patients (63.5%) had shoulder pain. Shoulder Turkey largest rehab facilities in Turkey were studied to identify pain was reported more frequently among No Score the incidence of shoulder pain. 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) 76 patients suffering from a first stroke were studied. Shoulder pain on movement was associated UK Separate regression equations were created for the with increased LOS, poorer performance on No Score outcomes of length of hospital stay (LOS), performance ADL, arm function and arm power. Shoulder of ADL (Barthel Index), arm function (Frenchay arm pain was a statistically significant predictor of function) and arm power (Motricity Index) arm function. Ratnasabapathy A population based study of 1,761 stroke survivors. Shoulder pain was positively associated with et al.(2003) Predictors of shoulder pain were identified using motor deficit, side of deficit and severity of No Score multiple regression. deficit. In those surviving to six months after New Zealand stroke, the risk of shoulder pain increased with severity of upper limb motor deficit; mild (OR 2.46), moderate (OR 3.64) and severe (OR 4.94). Diabetes was also a predictor of shoulder pain (OR 1.57). Chae et al.(2007) In a cross-sectional study, using baseline data, the 4 models were presented-all included shoulder USA relationship between post-stroke shoulder pain, upper- pain and a series of potential covariates. No Score limb motor impairment, activity limitation, and pain- Model 1 identified 2 variables of FMA scores- related quality of life (QOL), was examined using subluxation and external rotation ROM. multiple regression. 61 chronic (> 12 weeks stroke Model 2 found there were no predictors of FIM onset) stroke survivors with post-stroke shoulder pain self-care. and glenohumeral subluxation were included. Shoulder Model 3 found FMA and stroke type were pain was assessed with the Brief Pain Inventory question predictors of AMAT function.
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12 (BPI 12), a self-reported 11-point numeric rating scale Model 4 found pain was a predictor of QoL (pain (NRS) that assesses "worst pain" in the last 7 days. was not a predictor of function in any of the Motor impairment was measured with the Fugl-Meyer other 3 models). Assessment (FMA). Activity limitation was measured with the Arm Motor Ability Test (AMAT) and the FIM instrument. Pain-related QOL was measured with BPI question 23, which assesses pain interference with general activity, mood, walking ability, normal work, interpersonal relationships, sleep, and enjoyment of life. Lee et al. (2009) 71 consecutive stroke patients with hemiplegic shoulder SA-SD bursal effusion was noted in 36 (51%) of Korea pain underwent shoulder sonography to establish patients and was the most common abnormality No Score whether a correlation existed between the sonographic seen on sonography. Tendinosis of the findings and the motor recovery, assessed using the supraspinatus tendon was found in 7 (10%), Brunnstrom stages (1-6). Sonographic findings were partial-thickness tear of the supraspinatus classified into 5 grades: 1) normal, or effusion of the tendon in 6 (9%), and full-thickness tear of the biceps tendon sheath; 2) tendinosis of the supraspinatus tendon in 2 (<1%) patients) No supraspinatus; 3) subacromonial subdeltoid (SA-SD) statistically significant correlation was found bursitis; 4) a partial-thickness tear of the rotator cuff; 5) between the grade of sonographic findings and full thickness tear of the rotator cuff. Brunnstrom stage (p = 0.183). Hemiplegic shoulder was associated with a higher number of abnormal sonographic findings than a noninvolved shoulder (p = 0.007).
While motor deficit has been associated with shoulder pain, a cause and effect relationship has not yet been established. In the present review, an association was demonstrated in 4 of the trials. The results from 2 newer studies (Chae et al. 2007; Lee et al. 2009) have not supported such a relationship.
Conclusions Regarding Functional Impact of Hemiplegic Shoulder Pain
The development of painful hemiplegic shoulder is associated with severe strokes and poorer functional outcome.
11.7 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 (Rizk 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.
11.7.1 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.
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As cited by Gilmore et al. (2004) Davies 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 1982) 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”.
A meta-analysis (Borisova & Bohannon 2009), which included the results from 5 RCT, representing 126 subjects, reported that shoulder positioning programs were not effective in preventing or reducing the loss of shoulder external rotation range of motion. Interventions assessed in the 5 trials included both positioning and stretching programs. In order to prevent contraction, the authors speculated that the duration of stretching may have been insufficient. While 2 hours of stretch was provided in the 2 trials that assessed this form of treatment, the authors speculated that at least 6 hours of stretching a day was required to prevent contracture formation in the soleus muscle of children with cerebral palsy. The authors also suggest that the treatment may have been initiated too late following stroke to be effective.
Table 11.9 Positioning of the Shoulder in Stroke Patients Author, Year Country Methods Outcomes PEDro Score Dean et al. (2000) 23 patients were randomized to receive an experimental Changes in active and passive range of motion Australia therapy or to a control group. Subjects in both groups were not significant between the groups with 5 (RCT) participated in a multidisciplinary rehabilitation program the level of pain remaining unchanged. and participated in active training of reaching and manipulation tasks. The experimental group received prolonged positioning to the affected shoulder each day, five days a week for six days (positioning). Ada et al. (2005) 36 stroke patients were randomized to an intervention Positioning the shoulder in maximal external Australia or a control condition. Patients in the experimental rotation (position 1) significantly reduced the 6 (RCT) group received two, 30-minute sessions of sustained development of contractures, compared to the shoulder positioning. Patients in both groups received control group. In position 2 (where patients sat 10 minutes of shoulder exercises and routine upper limb with the affected arm resting on a table with the care. The treatment was provided for 4 weeks. shoulder at 900, for 30 minutes daily), did not Assessments of contracture were taken at weeks 2 and prevent the development of contractures. 6 after stroke. Gustafsson & 34 patients with upper extremity hemiparesis admitted There were no significant between group McKenna (2006) within 100 days of stroke were randomized to a differences reported for any of the outcomes. Australia participated in a programme of two static positional Subjects in both groups demonstrated a 6 (RCT) stretches, each held for 20 minutes, once daily or to a reduction in mean pain-free passive range of control condition where the affected arm was supported motion into external rotation. All participants when seated in bed. Outcome measures included: pain- reported increased motor recovery and free passive range of motion, shoulder pain (Ritchie functional independence. There was a non Articular Index), Motor recovery (Motor Assessment significant increase in pain with movement Scale) and functional independence (modified BI) among subjects in the treatment group and a measured at hospital admission and discharge. decrease among subjects in the control group. There was a non significant decrease in pain at rest among subjects in both the treatment and control groups. de Jong et al. 19 patients with stroke onset no greater than 12 weeks At 5 weeks, there was a loss of passive range of
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(2006) post stroke with severe arm paresis were randomized to motion in both groups, although the losses were Netherlands receive routine inpatient rehabilitation (n=10) or less pronounced in the experimental group for 6 (RCT) rehabilitation + a prescribed positioning procedure for 5 3/5 measurements--shoulder external rotation weeks, twice daily for a ½ hour (n=9). The arm was (-19 vs.-18, p=0.37), shoulder flexion (-23 vs. - positioned with as much shoulder abduction, shoulder 29, p=0.29), shoulder abduction (-5.3 vs. –23, external rotation, elbow extension and supination of the p=0.042), elbow extension (0.6 vs. –4, p=0.84), forearm as the patient could endure. Passive range of forearm supination (-11 vs. –3, p=0.69). There motion, Ashworth scale scores, Pain (yes/no) Fugl- were no significant differences between the Meyer Assessment scores and BI scores were assessed groups on any of the other outcomes. No at baseline, 5 and 10 weeks following treatment. statistical tests were carried out at week 10 due to dropouts.
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 prevents loss of active or passive range of motion, or reduces pain.
Further research is needed before conclusions regarding positioning of the hemiplegic shoulder can be made.
11.7.2 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 1992; Hanger et al. 2000; Hurd et al. 1974), one presenting unpublished data (Griffin et al. 2003). The results are presented in Table 11.10.
Table 11.10 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 Hurd et al. 1974 – hemisling OR 8.7 (1.1, 67.1) follow up (Favours no slings) Number of days pain was delayed Ancliffe et al. 1992 -strapping WMD 14 days (9.7, 17.8) with treatment Griffin et al. 2003 (Favours slings) Pain scores on VAS Hanger et al. 2000 – strapping WMD 0.83 (-1.46, 3.12) (10 cm scale) (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 Hurd et al. 1974- sling OR 1.00 (0.1, 9.3) contractures (No difference) Range of shoulder external rotation Hanger et al. 2000 - strapping WMD –1.4 degrees (-10.9, 8.10) at end of follow up (No difference)
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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.
Table 11.11 Slings and Other Aids in Hemiplegic Shoulders Author, Year Country Methods Outcomes PEDro Score Hurd et al. (1974) 14 patients were alternately assigned to be treated with Of the 7 patients without slings, 5 had no pain, USA a sling or without a sling, assessed 2 to 3 weeks and 3 to while 2 had little pain. Of the 7 patients treated No Score 7 months post stroke. with slings, 6 had little pain, while 1 had no pain. Moodie et al. Series of radiographs (anterior/posterior view) of 10 Shoulder roll and Hook-Hemi Harness did not (1986) patients’ affected and unaffected limbs in order to reduce subluxation to the same extent as the Canada permit comparisons for degree of subluxation and the 5 other 3 devices. Subluxation was reduced within No Score aids to be evaluated were then applied to the patients’ 20% of the correct alignment in 8 out of 10 affected arm and an A/P view was taken of each: patients when treated with the sling; 6 of the 10 conventional sling; shoulder roll; Hook-Hemi Harness; treated with the arm trough, and 7 of the 10 arm trough; and plexiglas lap tray. 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. Radiographs were taken of 26 hemiplegic patients with There was no significant difference in the (1988) subluxated shoulders with two different supports-the reduction of inferior subluxation between the Canada Bobath shoulder roll and the Henderson shoulder sling. two types of shoulder supports. However, there No Score Radiographs of the unsupported affected shoulder were were significant differences in subluxation compared with radiographs of the same shoulder with between measurements of the unsupported each support applied. Radiographs of the unaffected affected shoulder and the unaffected shoulder shoulder were used as a comparison in determining the and between measurements of the unsupported amount of subluxation. affected shoulder and the supported affected shoulder using both supportive devices. Brooke et al. Three different shoulder supports were applied to 10 Harris hemi-sling improved correction of the (1991) patients by their occupational and physical therapists: subluxation with mean vertical distance of USA Harris hemi-sling, the Bobath sling and the arm trough 37.8mm vs. 38.5mm compared to the No Score or lapboard. 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. An occupational therapist applied each shoulder support The single-strap hemisling corrected vertical (1995) to each of 20 patients in the following order: (1) single- displacement, while the Roylan and Bobath roll USA strap hemisling; (2) Rolyan humeral cuff sling; (3) Bobath significantly reduced vertical displacement. The No Score roll; and (4) Cavalier support. 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. Hartwig et al. 41 patients admitted for inpatient stroke rehabilitation After adjusting for baseline differences, the
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(2012) with caudal subluxation of the glenohumeral joint and mean shoulder-hand syndrome score was Germany hemiparesis of the upper extremity after ischemic injury significantly lower by 3.1 points in the 7 (RCT) were randomized to 2 groups. Patients in the intervention compared to the control subjects. intervention group received usual care and wore a Marginal or no discomfort from treatment with functional orthosis (Neuro-Lux) for 10 hours each day the orthosis was reported in 15 patients (75%), designed to reduce subluxation. Patients in the control and only a single patient (5%) felt severe group received usual care only. The primary outcome discomfort during the entire treatment. was the average shoulder-hand syndrome score on days Compliance with the use of the orthosis during 14, 21 and 28 (scores range from 0-14). the prescribed time was 89%.
The majority of the trials assessed used a crossover design whereby patients served as their own control as they tried more than one type of sling for a period of time. In none of these trials was the order of slings randomized. It is also difficult to eliminate the effect of carry-over in this type of design; therefore, it is difficult to formulate conclusions. A single RCT examined the use of a supportive orthosis for the prevention and treatment of shoulder-hand syndrome (Hartwig et al. 2012).
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 moderate (Level 1b) evidence that a supportive orthotic device can prevent and treat symptoms of shoulder –hand syndrome.
There is limited evidence that shoulder slings influence clinical outcomes.
11.7.3 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 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 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
11. Painful Hemiplegic Shoulder pg. 22 of 66 www.ebrsr.com 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”.
Table 11.12 Strapping the Hemiplegic Shoulder Author, Year Country Methods Outcomes PEDro Score Ancliffe (1992) A pilot study of 8 patients who were assigned to receive Patients in the strapping group experienced a Australia strapping of the shoulder applied by one physiotherapist significantly longer pain free period than the No Score and changed every 3 to 4 days as needed to the patients who were not strapped (21 vs. 5.5 days). hemiplegic side or to receive no strapping. Treatment However, all patients in the strapping group began within 48 hours of admission to hospital. eventually did experience pain. The longest pain- free period was 25 days. Hanger et al. 98 patients were randomized to have their affected No significant differences were found between (2000) shoulder strapped for 6 weeks in addition to standard groups on measure of pain, range of movement New Zealand physiotherapy or to receive standard physiotherapy only and on functional outcome measures. There was 7 (RCT) 15 days following stroke. a trend for less pain at 6 weeks and improved functional upper limb function for the strapping group. Griffin & 33 patients at risk of developing hemiplegic shoulder One person in the TS group developed shoulder Bernhardt (2006) pain were randomized to therapeutic shoulder (TS) pain compared to 5 persons in the other 2 Australia strapping, sham shoulder (SS) strapping or to a no groups. Subjects in the TS group reported 26 7 (RCT) strapping (control) group 10 days post stroke. pain-free days, compared to 19 days for SS Lightweight adhesive tape was used and strapping subjects and 16 days for subjects in the control continued for over 4 weeks. Primary outcome was the group. The difference was statistically significant number of pain free days. Secondary outcomes included for the comparison of TS and control group. range of movement, Motor Assessment scale scores and There were no differences between groups on Modified Ashworth scores. any of the secondary outcomes. Appel et al. 14 patients with mild to moderate hemiparesis following From baseline to 5 weeks, patients in the control (2011) an acute stroke were randomized to receive a program group gained more MAS points on average UK of shoulder stapping in addition to inpatient compared with the intervention group (9.8 to 6 (RCT) rehabilitation or to rehabilitation only. One of 5 stapping 15.0 vs. 10.7 to 15.2). Patients in the control techniques was used depending on the patient. The group gained more FMA points on average stapping was maintained for 4 weeks (and changed compared with the intervention group (50.7 to every 3 days). The primary outcome was the Motor 60.4 vs. 51.8 to 60.6). Patients in the intervention Assessment Scale, assessed at baseline and at 1,2,3 and group took less time to complete the 9HPT 5 weeks. Additional outcomes were the Fugl-Meyer compared with those in the control group (94.8 Assessment (FMA) and the 9-Hole peg Test (9HPT). to 37.8 vs. 63.5 to 30.4). Results of between group tests of significance were not reported. Pandian et al. 162 individuals were randomized to a receive shoulder Significant improvement in both VAS scores were (2013) taping and conventional treatment or sham taping and seen on day 30 post treatment between the India conventional treatment. Visual Analogue Scale (VAS) treatment group compared to the control with 8 (RCT) and Shoulder Pain and Disability Index (SPADI) scores mean difference of 11.9mm (p=0.03). No were collected at 14 and 30 days post intervention. significant difference in SPADI scores were seen between the two groups.
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.
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Strapping the hemiplegic shoulder does not appear to improve upper limb function, but may reduce pain.
11.7.4 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.
Table 11.13 Active Therapies in Hemiplegic Shoulder Author, Year Country Methods Outcomes PEDro Score Inaba & 33 patients with hemiplegia who experienced shoulder No significant differences between the groups Piorkowski (1972) pain in the range of 0-90 degrees of flexion or were observed in measures of ROM. USA abduction of the arm after stroke were treated. 7 (RCT) 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. Kumar et al. 28 patients were assigned to receive a rehabilitation Significant difference in the incidence of pain (1990) program of range of motion by therapist (ROMT) once a reported between the groups. Shoulder pain was USA day, 5 days a week; or a rehabilitation program with use more common in the overhead pulley (63%) 5 of skate board once a day, 5 days a week; or a group than in the ROMT group (8%). ROM was (quasi- rehabilitation program with use of overhead pulley significantly reduced in those patients who randomized once a day, 5 days a week while an inpatient on a developed shoulder pain when compared to controlled trial) stroke rehabilitation unit. those who did not develop shoulder pain motion abduction, forward flexion, internal rotation and external rotation. Shoulder subluxation was found in 46% of all patients with no significant difference between treatment groups. Partridge et al. 65 patients were randomized to receive cryotherapy or A greater proportion of patients treated by the (1990) Bobath therapy daily for five days and then after at the Bobath method reported no pain or only UK therapist’s discretion for a total of four additional occasional pain on exit of the study compared to 5 (RCT) weeks and assessed by a blinded investigator. those treated by the cryotherapy method. Poduri et al. Patients with stroke experiencing shoulder pain after A significantly greater proportion of patients (1993) completing outpatient therapy were studied. One group receiving the treatment drug prior to therapy USA of patients received either a nonsteroidal anti- experienced pain relief. Flexion, abduction and No Score inflammatory drugs (Ibuprofen 400-800g tid, and functional recovery were significantly greater in Sulindac, 150 mg bid.) taken 30 to 60 minutes prior to those patients who were taking the nonsteriodal occupational therapy. A second group of patients anti-inflammatory drug before therapy. received only occupational therapy consisting of range of motion, active assistive and strengthening exercises and activities of daily living training. Tyson & Chissim 22 stroke patients with consequential weakness of the Mean shoulder flexion for the axilla hold was (2002) arm instructed to hold the hemiplegic shoulder at: (1) 115.2 degrees and 97.7 degrees for the distal UK an axilla hold involving shoulder support and (2) a distal hold (p < 0.001). 4 (RCT) hold without shoulder support. Each hold was repeated to obtain three measurements with order of testing randomized.
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Lynch et al. 35 stroke patients with significant upper motor There were no between group differences in (2005) impairment were randomized to a control group (n=16), changed scores between groups on any of the USA which received self-range of motion exercises under the outcome measures assessed (joint stability, 6 RCT supervision of a physiotherapist or to the experimental Modified Ashworth scale, Fugl-Meyer (pain and group (n=19) of continuous passive motion treatments self-care FIM scores). 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.
Discussion
Inaba & Piorkowski (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. 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.
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 nonsteroidal 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.
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11.7.5 Electrical Stimulation in the Hemiplegic Shoulder
Electrical neuromuscular stimulation is a term used to describe the application of electrical current to the skin, or directly into muscle that stimulates motor nerves and muscle fibres resulting in improved contractility and greater muscle bulk. The treatment can be used to improve muscle strength, joint misalignment, muscle tone, sensory deficits and self-reported pain intensity (Price & Pandyan 2001). Electrical stimulation is typically administered by two methods, functional electrical stimulation (FES) or transcutaneous electrical nerve stimulation (TENS). The distinction that is usually made between these two forms of treatment is that lower intensity, higher frequency stimulation is associated with TENS. It is more commonly used to treat pain. Patients usually describe a “pins-and-needles sensation.” FES has been described 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,” (Gresham et al. 1995).
The supraspinatus 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 and 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 4 weeks intensity TENS Linn et al. 1999 No sham treatment vs. electrical stimulation (not FES 4 weeks or TENS) 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 Odds Ratio* or Weighted (or (Y/N) 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)
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Ada and 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.
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 Yes 6.5 (4.4, 8.6) CT Shoulder subluxation (mm) Late ES + CT vs. Late No 1.9 (-2.3, 6.1) CT Function (Bobath assessment chart, Motor Early ES + CT vs. early Yes 18.6 (0.4, 36.7) assessment scale and Fugl-Meyer) CT expressed as a percentage Function (Bobath assessment chart, Motor Early ES + CT vs. early No 14.4 (-5.4, 34.2) assessment scale and Fugl-Meyer) CT expressed as a percentage Pain (range of motion-degrees) Early ES + CT vs. early No 3.7 (-1.2, 8.6) CT Pain (Visual analogue scale-cm) Late ES + CT vs. Late Yes 1.6 (0.1, 3.0) CT * CT= conventional therapy; ES= electrical stimulation
Fourteen RCTs specifically evaluated the effects of electrical stimulation on the treatment of shoulder pain (Table 11.16).
Table 11.16 Surface Electrical Stimulation in Hemiplegic Shoulder Author, Year Country Methods Outcomes PEDro Score Leandri et al. 60 patients with chronic hemiplegia shoulder pain Significant improvements in passive range of (1990) randomized to one of three groups. Group A received motion (PROM) were recorded for group A but Italy high intensity TENS plus basic physical treatment. Group not for the other groups. No between group 5 (RCT) B received low intensity TENS plus basic physical comparisons were made. treatment. Group C received sham intensity TENS plus basic physical treatment. Faghri et al. 26 patients were randomized to receive either After treatment, the FES group showed a (1994) functional electrical stimulation (FES) in which two significant increase in arm function, tone and USA flaccid/paralyzed shoulder muscles (supraspinatus and EMG activity compared to control patients. 4 (RCT) 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). Chantraine et al. 115 patients were alternately assigned to receive Significant motor recovery was noted in favour (1999) traditional Bobath treatment in addition to functional of FES treatment at three months and was Switzerland electrical stimulation (FES) for 5 weeks or to receive maintained at 24 months. Significant reduction 4 traditional Bobath treatment for 5 weeks. also noted in pain in favour of FES treatment at
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(quasi- three months and again maintained at 24 randomized months. Significant reduction in shoulder controlled trial) subluxation in favour of FES treatment was noted at three months and maintained 24 months post-treatment. Kobayashi et al. 17 patients with chronic shoulder subluxation were Difference in subluxation in group S, 2.8(3.6) (1999) randomized to receive therapeutic electrical stimulation mm and group D, 2.8(2.5) mm was significantly Japan (TES) for 15 minutes twice a day to either the greater than that of the control –1(2.8) mm 5 (RCT) suprasupinatus muscle (group S) or middle deltoid under the stress test. The mean abduction force muscle (group D) in conjunction with conventional tended to increase in group S and was therapy, or to receive conventional therapy only. significantly greater in group D. Linn et al. 40 patients were randomly assigned to a control or The treatment group had significantly less (1999) treatment group. Patients in the treatment group subluxation and pain after the treatment period, Scotland received electrical stimulation (ES) 4 times daily, ranging but at the end of the follow-up period there 6 (RCT) from 30 minutes in week one to 60 minutes by week 4. were no significant differences between the 2 Patients in both groups received daily occupational and groups. physical therapy. Treatments lasted for four weeks. Assessments of shoulder subluxation, pain, and motor control. were carried out at 4 and 12 weeks after stroke Wang et al. 32 inpatient and outpatient rehabilitation patients with The experimental subgroup of short duration (2000) hemiplegia were assigned to one of two groups based showed significant improvements in reducing Taiwan on the duration of hemiplegia: the short and the long subluxation as indicated by x-ray compared with 5 (RCT) duration. Subjects in each group were randomly the control subgroup of short duration after the assigned to either a control subgroup or an first FES treatment. The same effect was not experimental subgroup. Subjects in the experimental shown for the experimental subgroup of long subgroups were treated in a type A-B-A study design, duration. The second FES treatment program which consisted of an FES training (A), routine therapy only resulted in an insignificant change of or regular daily activity without FES training (B), and shoulder subluxation for both the short- and another FES training (A). Each period lasted for 6 wk. FES long-duration subgroups. training program, consisted of five sessions/week. Church et al. 176 stroke patients (≤10 days post-stroke) were There was no significant difference in the ARAT (2006) randomly assigned to receive surface neuromuscular scores, the primary outcome, between groups. UK electrical stimulation (sNMES) or placebo with a sham There were no other significant differences 9 (RCT) stimulator for 4 weeks. Both groups received standard between the groups with the exception of: the stroke unit care. One and 3-month assessments included gross and grasp subsections of the ARAT, the Action Research Arm Test (ARAT), Frenchay Arm Test, arm section of the MI and the Frenchay Arm Motricity Index (MI), Star Cancellation Test, pain scales, Test, where the control group fared better at 3 disability, global health status, and Oxford Handicap months. Scale. Koyuncu et al. 50 rehabilitation inpatients with shoulder subluxation There were no significant between group (2010) and shoulder pain were randomized to receive a 4-week differences in terms of pain, PROM or AROM. Turkey treatment of conventional rehab or conventional rehab However, there was a significant difference 4 (RCT) + 20 sessions of FES (1 hr/day x 5 days/wk, frequency 36 between the two groups for the amount of Hz) to the supraspinatus and posterior deltoid muscles. change in shoulder subluxation in favor of the The shoulder pain of all patients during resting, passive study group. range of motion (PROM) and active range of motion (AROM) was measured with the visual analog scale (VAS) while the shoulder subluxation levels were evaluated with the classification developed by Van Langenberghe and by using the millimetric measurements on anteroposterior shoulder X-ray before and after the physical treatment and rehabilitation program and compared.
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Fil et al. (2011) 48 patients admitted to hospital within 2 days of acute Patients remained in hospital and received Turkey stroke were randomized to receive either rehabilitation treatment for an average of 12 days. Shoulder 5 (RCT) according to Bobath concepts or Bobath-based therapy subluxation occurred in 9 (37.5%) subjects in the + high-voltage pulsed galvanic stimulation of the control group, whereas it was not observed in supraspinatus and deltoid muscles for 10 min, 2 x/day the study group. All shoulder joint displacement for the duration of the hospital stay. Outcomes were values were higher in the control group than in assessed before and after treatment. Two radiological the study group (horizontal asymmetry P = methods were used to measure the horizontal, vertical 0.0001, vertical asymmetry P = 0.0001, total and total asymmetry and vertical distance values of the asymmetry P = 0.0001, vertical range P = 0.002. shoulder joint. Motor functions of the arm were MAS scores were not significantly different evaluated with the Motor Assessment Scale. between groups at d/c from hospital.
Table 11.17: Intramuscular Electrical Stimulation Author, Year Country Methods Outcomes PEDro Score Baker & Parker 63 patients with chronic stroke and a minimum of 5 mm At six weeks, the mean subluxation of the study (1986) of shoulder subluxation in their involved upper group was significantly less compared to the USA extremity were randomized to a treatment or control control (8.6 vs. 13.3). Three- month radiographs 4 RCT group. Patients in the treatment group received demonstrated that patients in the treatment neuromuscular electrical stimulation (NMES) for 5 group had lost an average of 1-2 mm, which had weeks, while patients in the control group used been achieved during the study period. The conventional hemi-slings or wheelchair arm supports. authors did not demonstrate a causal relationship between subluxation and shoulder pain. Faghri (1997) 26 patients received conventional physical therapy with Weekly evaluation of arm and shoulder muscle USA 13 patients randomized to the treatment group, which function (range of motion), tone, and posterior 4 (RCT) received additional functional neuro-muscular deltoid muscle EMG activity showed significant stimulation (FNS) therapy for 6 weeks. improvement in the experimental group when compared to the control group over 6 weeks. Advantage of treatment group was maintained 6 weeks after termination of the FNS. Yu et al. (2001) 10 hemiplegic stroke patients with at least 1 Pain scores were significantly lower for perc- USA fingerbreadth of glenohumeral subluxation received 3 NMES than trans-NMES as assessed by the VAS 6 (RCT) randomly ordered pairs of neuromuscular stimulation and the MPQ. (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). Renzenbrink & 15 stroke survivors with chronic (> six months) A significant reduction in pain was found on the Ijerman (2004) hemiplegia and a therapy-resistant painful shoulder with Brief Pain Inventory. Pain reduction was still Netherlands subluxation were studied. Shoulder subluxation was present at six months follow-up. All domains, in No Score indicated by at least 1/2 fingerbreadth of glenohumeral particular bodily pain, of the SF-36 showed separation on palpation. Patients received 6 hours of improvement in the short term. After six months Percutaneous Neuromuscular electrical stimulation (P- of follow-up, bodily pain was still strongly and NMES) per day for a total of six weeks. significantly reduced, whereas social functioning and role physical demonstrated a nonsignificant improvement of more than 10% compared with baseline. Yu et al. 7 site, single-blinded, randomized clinical trial. 61 The main outcome measure was the Pain (2004) chronic stroke survivors with shoulder pain and outcome measure Brief Pain Inventory question
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USA subluxation volunteered to be randomized to receive 12 (BPI 12), an 11-point numeric rating scale, 7 (RCT) intramuscular neuromuscular electric stimulation assessed at the end of treatment, and at 3 and 6 (NMES) to the supraspinatus, posterior deltoid, middle months post treatment. Post stroke shoulder deltoid, and trapezius for 6 hours a day for 6 weeks or to pain was significantly less in the NMES group the control condition of a cuff-type sling for 6 weeks. compared to control at 3 and 6 months Main outcome measure Brief Pain Inventory question. following treatment. Chae et al. (2005) 12 month follow up from Yu et al. 2004. Treatment 22 patients in the intervention group and 21 USA success was defined as a minimum 2-point reduction in patients received 12-month assessments. The 7 (RCT) Brief Pain Inventory question 12 at all post treatment electrical stimulation group exhibited a assessments. Secondary measures included pain-related significantly higher success rate than controls quality of life (Brief Pain Inventory question 23), (63% vs. 21%). Repeated-measure analysis of subluxation, motor impairment, range of motion, variance revealed significant treatment effects spasticity, and activity limitation. on post treatment Brief Pain Inventory questions 12 and 23. There were no other significant between group differences. Chae et al. (2007) Secondary analyses from Yu et al. 2004 & Chae et al. Time from stroke onset was most predictive of USA 2005. Forward stepwise regression was used to identify treatment success. Subjects were divided 7 (RCT) factors predictive of treatment success among according to the median value of stroke onset: participants assigned to the electrical stimulation group. early (<77 weeks) versus late (> 77 weeks). Treatment success was defined as at least a 2-point Electrical stimulation was effective in reducing reduction on the Brief Pain Inventory Question 12 at 12 poststroke shoulder pain for the early group months following treatment. (94% vs. 7%, p < .001) but not for the late group (31% vs. 33%). FIM score was the second strongest predictor. Factors which were not predictive included age, stroke type, gender, Fugl-Meyer score and side of hemiplegia. Chae et al. (2013) 8 individuals from a stroke rehabilitation clinic were All 8 participants reported a 2 point pain USA recruited. Two monopolar needle electrodes were reduction. At 12 weeks, 6 out of 8 participants No score (Case inserted perpendicular to the skin surface at the motor maintained pain reduction. Significant series) points of the middle and posterior deltoids. The improvement in sleep was also seen. Rehabilicare NT2000 external stimulator was used to provide biphase waveform with current amplitude of 20mA at 12 Hz on the middle and posterior deltoids. Participants received therapy for 6 hours per day for 3 weeks. Outcome measures including Brief Pain Inventory 13 were measured at 4 and 12 weeks after treatment. Wilson et al. 25 individuals were randomized to receive either Significant reduction in pain intensity was seen (2014) peripheral nerve stimulation or usual care for chronic between the two groups at 10 weeks (2.9, 95% USA hemiplegic shoulder pain. Outcomes including: Brief CI 0.8-5.0) and 16 weeks (3.1 95% CI 1-5.2). No 8 (RCT) Pain Inventory and Short Form 36 were assessed at significant difference in SF-36 was seen between baseline, weeks 1, 4, 12, and 16. the two groups.
Discussion
Most of the RCTs reviewed reported a benefit associated with electrical stimulation, although there was variability in the outcomes assessed: range of motion, muscle tone, EMG activity, shoulder subluxation, shoulder pain and muscle function.
Electrical stimulation was found to be effective in the prevention of the development of shoulder subluxation when initiated acutely following stroke (Faghri et al. 1994; Fil et al. 2011; Koyuncu et al.
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2010) and also in reducing the vertical distance between the acromion and the humeral head in the chronic stage of stroke (Baker & Parker 1986; Kobayashi et al. 1999).
The majority of trials evaluated surface FES while Yu et al. (2001)and Chae et al. (2005; 2007) evaluated intramuscular devices. The studies demonstrated that intramuscular electrical stimulation demonstrated significant improvement in shoulder pain up to 6 months post intervention. One trial evaluated treatment with TENS. 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, since surface FES can be painful. However, the results from the largest and most methodologically rigorous trial (Church et al. 2006) suggest that FES treatment might actually be associated with harm and may worsen arm function, especially among those with severe paresis. The authors proposed several mechanisms to potentially explain this finding including over-use and over stimulation of the affected arm and the possibility that stimulation interfered with the motor re-learning processes, influencing and impeding upper limb recovery even after treatment ceased. These authors did not evaluate the benefit of FES with respect to reducing shoulder subluxation or spasticity, while noting that there is evidence that FES treatment has been shown to improve these parameters. A summary of the RCTs reviewed is presented in Table 11.17.
Table 11.18 Summary of RCTs Evaluating Electrical Stimulation for the Treatment of Hemiplegic Shoulder Author, Year N Intervention Main Outcome(s) PEDro Score Result Church et al. 2006 176 Surface FES vs. sham FES Action Research Arm Test (-) 9 Pain (-) Yu et al. 2004 61 Intramuscular FES vs. sling Pain (-) Chae et al. 2007, 2007 Yu et al. 2001 10 Intramuscular FES vs. surface FES Pain (intramuscular FES +) Linn et al. 1999 40 Surface FES vs. no FES Subluxation (-) Pain (-) Kobayashi et al. 1999 17 Surface FES vs. no FES Subluxation (+) 5 Pain (-) Leandri et al. 1990 60 High-intensity TENS + Physical Passive range of motion (+ high-intensity TENS) 5 therapy vs. low-intensity TENS vs. PT vs. sham TENS + PT Wang et al. 2000 32 Surface FES vs. no FES Subluxation (+ acute – chronic) 5 Passive range of motion (-) Fugl-Meyer (+ acute – chronic)
Fil et al. 2011 48 High-voltage pulsed galvanic Subluxation (+) 5 stimulation Motor Assessment Scale (-) Koyuncu et al. 2010 50 Surface FES vs. no FES Subluxation (+) 4 Pain (-) Baker & Parker 1986 63 Surface FES vs. sling or wheelchair Subluxation (+) 4 arm support Faghri et al. 1994 26 Surface FES vs. therapy Subluxation (+) 4 Pain (-)
Conclusions Regarding Electrical Stimulation in the Hemiplegic Shoulder
There is strong (Level 1a) evidence that that electrical stimulation helps to prevent the development of shoulder subluxation.
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There is strong (Level 1a) evidence that electrical stimulation does not reduce hemiplegic shoulder pain following stroke.
There is strong (Level 1a) evidence that FES does reduce shoulder subluxation.
Functional electrical stimulation may improve shoulder subluxation, but does not reduce pain in the hemiparetic shoulder.
11.7.6 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 11.19 Surgery for Muscle Imbalance in the Hemiplegic Shoulder Author, Year Country Methods Outcomes PEDro Score Braun et al. Surgical procedure on 13 patients to release the 10 of the 13 patients operated on regained 90 (1971) insertion of the major muscle causing internal rotation degrees of passive abduction and 20 degrees of USA and adduction of the shoulder. Gradual increase in external rotation within 2 months following No Score range of motion was obtained by completing an surgery. However, 6 months later, all of the intensive post-operative exercise therapy program patients were complaining of pain and involving passive range of motion, positioning of the discomfort. shoulder, abduction while supine, through the use of reciprocal pulley exercises.
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.
11.7.7 Botulinum Toxin Injections as Treatment for HSP
As discussed previously, subscapularis spasticity is characterized by shoulder range of motion being most limited with pain being reproduced on external rotation. This appears to correlate well with hemiplegic shoulder pain that is now thought to be a consequence of spastic muscle imbalance about the shoulder in many cases. Pectoralis muscle spasticity, characterized by limitation of range and pain on shoulder abduction, is seen to a lesser extent, causing a similar muscle imbalance. Intra-articular injections of steroids, botulinum toxin and other agents have been used in an effort to treat spastic muscles, reduce the imbalance and to relieve hemiplegic shoulder pain.
A Cochrane review (Singh & Fitzgerald 2010) examined the efficacy of the use of botulinum toxin in the treatment of shoulder pain. Six RCTs were included, five of which included patients with post-stroke shoulder pain. The sixth study included patients with shoulder pain resulting from osteoarthritis and rheumatoid arthritis. Treatment with BT was associated with reductions in pain at 3 and 6 months, but not at 1 month following injection.
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Table 11.19 Botulinum Toxin for Hemiplegic Shoulder Pain Author, Year Country Methods Outcomes PEDro Score Hecht (1992) A retrospective study of 13 patients with spastic Immediate and significant improvement in ROM No Score hemiplegia, limited ROM and painful shoulder and with observed in abduction, flexion and external duration of hemiplegia for 2 to 13 months. Patients rotation. Relief of pain was noted with received percutaneous phenol nerve blocks to previously painful movements. subscapularis muscle innervation. Hecht (1995) Prospective study of 20 patients receiving botulinum 85% benefited from subscapularis block, and No Score toxin muscle blocks to the subscapular and pectoralis 55% benefited from pectoralis major block and major musculature. 45% showed improved active ROM. Bhakta et al. 17 patients received a single course of intramuscular Shoulder pain improved in 6 of 9 patients with (1996) botulinum toxin to biceps brachii, flexor digitorum shoulder pain. UK profundus, flexor digitorum superficialis and flexor No Score carpi ulnaris. Yelnik et al. (2007) 20 hemiplegic patients with upper limb spasticity due Pain decreased from 7.5 to 1.5 by week 4 in the France to stroke were randomly assigned to receive either one treatment group and from 5.5 to 4 in the control 7 (RCT) injection of Botulinum toxin A (BT-A; 500 units) (n=10) group (p=0.025). There was also significant or placebo (n=10) in the subcapularis muscle. Non- improvement in lateral rotation (mean 12.5% vs. standardized physical therapy was given to both -2.5%, p=0.018), but not for change in abduction groups on weekdays. Pain was measured using a 10- (shoulder range of motion observed in the point visual analogue scale. treatment group (70% vs. 72.5%). Kong et al. (2007) 17 patients recruited from an outpatient clinic with At week 4 there was no significant difference in Singapore spastic shoulder pain resulting from a stroke that the resolution of shoulder pain between the 8 (RCT) occurred more than 3 months later were randomized groups. (Dysport: median VAS decreased from 6 to receive a single injection of 500 U of Dysport (n=8) to 4, placebo: decreased from 6 to 3). Subjects or saline placebo (n=9), injected into the pectoralis who received Dysport showed significantly major and biceps brachii. Pain was the primary greater improvements in median shoulder outcome assessed on a 10 point VAS at 4 weeks adductor and elbow flexor Ashworth Scale following treatment. Muscle tone and passive range of scores than placebo at week 4 but not at week 8 shoulder abduction were also assessed at weeks 4, 8 and 12. and 12. Marco et al. (2007) 31 patients with moderate to severe spastic shoulder Pain was reduced significantly more among Spain pain, 3 or more months post stroke, admitted for patients in the treatment group by the end of 6 8 (RCT) inpatient rehabilitation were randomized to receive moths (76.4 to 30.1 vs. 70.1 to 48.3, time x treatment with either TENS (short pulses of high treatment interaction p = 0.035). The degree of frequency and low intensity for 6 weeks) + 500 U of external rotation was also increased significantly Dysport injected into 4 sites of the pectoralis major more among patients in the treatment group muscle of the paretic side under EMG guidance (n=16), (7.9 to 38.9 vs. 6.7 to 19.3, group x time or TENS + placebo (n=15). Pain was assessed on a 100 interaction, p=0.041). There were no other point VAS at 1 week, 1,3 and 6 months. Other statistically significant differences between the outcomes assessed included spasticity (MAS) and groups. shoulder range of motion (flexion, abduction, and external rotation) de Boer et al. 22 stroke patients with spastic hemiplegia, substantial While pain decreased over time in both groups, (2008) shoulder pain and reduced external rotation of the there was no significant treatment effect of BT- The Netherlands humerus were randomized to receive a single injection A. Similarly, external rotation improved 6 (RCT) of either botulinum toxin A BT-A (2x50 units) or significantly over time with no between group placebo applied to the subscapularis muscle at two difference. locations. Pain was scored on a 100 mm vertical Visual
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Analogue Scale (VAS); external rotation was recorded by means of electronic goniometry. Assessments were carried out at 0 (baseline), 6 and 12 weeks Pedreira et al. In an open label study, 15 patients with spastic The mean pain score was reduced non- (2008) hemiparesis secondary to stroke received a single significantly over the study period (from 8 to 6); Brazil injection of BT-A (average dose 280 IU). Assessments however, there was a significant improvement No Score were performed at 1, 2 and 4 months after treatments in flexion and rotation. and included pain (0-10 visual analog scale) and goniometry (abduction, extension, flexion and rotation). All subjects received physical therapy. Ashford & Turner- 16 rehabilitation outpatients participated in a The mean time since injury was 15.7 months. Stokes (2009) prospective observational cohort study. Patients Sixteen weeks post-injection, significant UK received an individualized dose of BoNT-A (Dysport) improvements were identified in spasticity No Score (100-500U) injection and concurrent therapy for (p<0.001) and passive function (p=0.002), but spasticity of the shoulder girdle or proximal upper limb not pain (p=0.052). GAS scores had improved in following stroke/other acquired brain injury. Functional all but one subject, with goals either achieved or goals for intervention were determined through over-achieved. agreement with the patient or their carers using Goal Attainment Scaling (GAS). Evaluation of spasticity (Modified Ashworth Scale), pain (numbered graphic rating scale) and three standard passive function tasks (washing, dressing and positioning) were also undertaken. Marciniak et al. In a double blind RCT, 21 participants were placed in Significant improvement in worst pain and pain (2012) the BT-A group (100-150units) or placebo saline (40-60 with upper body dressing was seen, p<0.001 and USA units) control group. Assessments of shoulder ROM, p=0.03 respectively, for time but not based on 10 (RCT) McGill Pain Questionnaire-short form (MPQSF), group allocation. There was significant Functional Independence Measure (FIM), Visual reduction in spasticity and range of motion, Analogue Scale (VAS), and Disability Assessment Scale however this was based on time, p<0.001. No (DAS) were conducted at 12 week follow-up. significant group or time effect was seen in DAS or FIM.
Discussion
Five RCTs, all of good quality assessed the efficacy of botulinum toxin in the treatment of hemiplegic shoulder. The subscapularis muscle was the most common injection site. The inclusion criteria were generally strict which resulted in small sample sizes, and suggests that the trials may not have been adequately powered. The heterogeneity of treatments and doses hinder the process of formulating conclusions. The two trials that demonstrated a benefit of treatment in terms of pain reduction (Marco et al. 2007; Yelnik et al. 2007) used either a higher dose of Botox or added treatment with TENS. One study found reduction in pain, however this was due to time effects rather than group effects of being in the botulinum group (Marciniak et al. 2012). The results from these trials are summarized below.
Table 11.20 Summary of RCTs Evaluating Botulinum Toxin Author, Year N Intervention Main Outcome(s) PEDro Score Result Kong et al. 2007 17 500 U Dysport vs. placebo Pain (-) 8 Modified Ashworth Score (-) Range of motion (-) Marco et al. 2007 31 TENS + 500 U Dysport vs. TENS Pain (+) 8 + placebo Modified Ashworth Score (-)
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Range of Motion (+/-) Yelnik et al. 2007 20 500 U Botox vs. placebo Pain (+) 7 Range of Motion (+/-) De Boer et al. 2008 22 100 U Botox vs. placebo Pain (-) 6 Range of motion (-) Marciniak et al. 2012 21 100-150 U Botox vs. placebo Pain (-) 10 Range of motion (-) Spasticity (-)
Conclusions Regarding Botulinum Toxin for Shoulder Pain
There is conflicting (Level 4) evidence that botulinum toxin injected into the subscapularis muscle reduces spastic shoulder pain or improves passive range of motion of the hemiplegic shoulder. It is uncertain whether botulinum toxin reduces hemiplegic shoulder pain
11.7.8 Steroid Injections as Treatment for HSP
The use of a triamcinolone acetonide injection into the glenohumeral joint has also been examined as a means to relieve shoulder pain in patients with hemiplegia. Five trials were identified which examined the use of steroids following stroke.
Table 11.21 Steroid Injections for Hemiplegic Shoulder Pain Author, Year Country Methods Outcomes PEDro Score Dekker et al. 9 patients with a presence of shoulder pain in the Intra-articular injections of triamcinolone (1997) paretic arm with disturbances of sleep and with the acetonide demonstrated a significant reduction Netherlands presence of ROM restriction of external rotation in pain with highly significant effect in 5 of the 9 No Score partook in a multiple-baseline (AB) study of patients. Range of motion improved in 4 out of 7 tramicinolone acetonide. The treatment condition patients but improvement did not reach (phase B) was 4 weeks long, during which three intra- statistical significance at the group level. articular injections of triamcinolone acetonide were administered at day 1, 8 and 22. Snels et al. (2000) 35 patients demonstrating hemiplegia after stroke and No significant improvement was observed for Netherlands pain in hemiplegic shoulder greater than 4 on the any of the primary outcome measures with 8 (RCT) visual analogue scale (VAS) with limitation of passive triamicinolone acetonide treatment. external rotation of the hemiplegic shoulder were randomized to receive either three injections with triamcinolone acetonide (40 mg Kenacrot A-40 in 1ml) or three placebo injections (1 ml saline solution). Lim et al. (2008) 29 stroke patients with shoulder pain were randomized At 12 weeks after treatment mean decrease in South Korea to receive intramuscular injections of i) Botulinum pain was 4.2 in the BT-A group and 2.5 in the TA- 9 (RCT) toxin (BT-A) (100 U total) during one session to the treated group (p=0.051), and improvements in infraspinatus, pectoralis and subscapularis muscles in overall ROM were 82.9 degrees versus 51.8 conjunction with an intraarticular injection of normal degrees in these groups (p=0.059). There were saline to painful shoulder joint (n=16), or an no significant differences between the 2 groups intraarticular injection of triamcinolone acetonide (TA) in terms of improvement in physician global (40 mg) and an intramuscular injection of normal saline rating, Fugl-Meyer score or modified Ashworth to the same muscles. Outcome measures were pain scales. (measured using a numeric rating scale), physician's global rating scale, shoulder range of motion (ROM) in
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4 directions, arm function measured using Fugl-Meyer score, and spasticity measured using the modified Ashworth scale. Measurements were made at baseline and 2, 6, and 12 weeks after injection. Chae & Jedlicka 10 stroke patients from an outpatient clinic with pain The mean BP1 I2 score before treatment was (2009) in the hemiparetic shoulder received a single 7.8. Mean scores declined significantly over the USA subacromial injection of 60 mg triamcinolone study period. The mean BPI 12 score was 3.8 at No Score acetonide + 2.5 mL of 1% lidocaine. The primary week 12. The greatest decrease was seen at the outcome measure was the Brief Pain Inventory (BPI) end of week 2. Repeated measure analysis of question 12 (BPI 12), which assesses "worst pain" in variance revealed significant within group x time the previous 7 days. Secondary measures included BPI effect. question 15, which assesses present pain and BPI question 23 (BPI 23), which assesses pain interference with 7 daily activities. Outcomes were assessed at baseline, weekly for the first 4 weeks and then at 8 and 12 weeks post injection. Lakse et al. (2009) 38 stroke patients with hemiplegic shoulder (etiology Compared with baseline, patients who received Turkey either frozen shoulder or impingement syndrome) a steroid injection had significantly greater 4 (RCT) were admitted to an inpatient rehabilitation unit. All improvement in pain (at rest, at night and patients received conventional therapy including 5 during activity) and shoulder range of motion. sessions of transcutaneous electrical stimulation over 3 There were no significant differences between weeks. Patients were randomized to receive no groups on any of the secondary outcomes additional treatment, or a single injection of assessed. triamcinolone acetonide. Patients in the injection group received either intra-articular or subacromial injections of corticosteroid and local anaesthetic according to their pathology. The evaluations were performed before treatment and at the first and fourth weeks of treatment. Primary outcome measures were passive shoulder range of motion and verbal analog scale for shoulder pain. Additional outcomes included BI, Brunnstrom upper-extremity score, and modified Ashworth scale. Yasar et al. (2011) 26 patients with hemiplegic shoulder pain lasting an Intra-articular steroid injection was performed Turkey average of 8 months were randomized to receive a in 11 (42 %) patients, and suprascapular nerve 5 (RCT) single injection of intra-articular steroid (40 mg block in 15 (57%) patients. Pain was reduced triamcinolone acetonide) or suprascapular nerve block among patients in both groups over the study (2% Citanest) in an outpatient setting. Shoulder pain period. There were no differences in pain scores was measured using a visual analogue scale during between groups flexion, abduction, internal and external rotation at the moment the pain the point that pain started and at passive maximum range of motion values. Evaluations were made before the injection, and 1 hour, one week and one month after the injection. Rah et al. (2012) 58 subjects with chronic HSP (at least 3/10 on a VAS) There was significantly greater improvement Korea and evidence of rotator cuff disorder were randomly favouring the treatment group in VAS day and 9 (RCT) assigned to receive a single ultrasound-guided night scores, SDQ scores, flexion, external subacromial injection with triamcinolone acetonide rotation and internal rotation. 40mg (treatment group, n=29), or lidocaine (placebo group, n=29). All subjects participated in an exercise program. Main outcome, assessed at 2, 4, and 8 weeks, was the average shoulder pain level at day and night (VAS-day/nigh). Other outcomes included Modified
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Barthel Index, Shoulder Disability Questionnaire (SDQ), and angles of shoulder active range of motion (flexion, abduction, external rotation, and internal rotation).
Discussion
Five RCTs examined the potential benefit of steroid injection in the treatment of HSP; however, only one included a true placebo. The results from three trials suggested no benefit, while two were positive. One trial reported a benefit when steroid injection was added to a conventional rehabilitation program which also included treatment with TENS. In the single trial that compared triamcinolone acetonide with botulinum toxin the results are more difficult interpret since subjects in each group improved (Lim et al. 2008). Despite a lack of statistical significance, the authors of this trial suggested that treatment with Botox was still superior and the effects longer lasting.
Table 11.22 Summary of RCTs Evaluating Triamcinolone Acetonide Author, Year N Intervention Main Outcome(s) PEDro Score Result Rah et al. 2012 58 triamcinolone acetonide (40 mg) Pain (+) vs. lidocaine Lim et al. 2008 29 triamcinolone acetonide (40 mg) Pain (-) 9 vs. Range of Motion (-) 100 Botox-A Snels et al. 2000 35 triamcinolone acetonide (40 mg) Pain (-) 8 vs. placebo Action Research Arm Test (-) Fugl-Meyer (-) Yasar et al. 2011 26 triamcinolone acetonide (40 mg) Pain (-) 5 vs. subscapular nerve block Laske et al. 2009 38 triamcinolone acetonide vs. no Pain (+) 4 injection Range of Motion (+) Brunnstrom, BI (-)
Conclusions Regarding Steroid Injections for Shoulder Pain
There is conflicting (Level 4) evidence that intra-articular steroid injections improve pain associated with hemiplegic shoulder compared with placebo or no treatment.
Steroid injections do not help to reduce hemiplegic shoulder pain
11.7.9 Aromatherapy/Acupressure Treatment for Shoulder Pain
Aromatherapy has been shown to help reduce pain and anxiety associated with chronic pain conditions (Buckle 1999). The use of aromatherapy plus acupressure in the treatment of hemiplegic shoulder pain has been investigated in a single RCT.
Table 11.23 Aromatherapy Acupressure in the Treatment of Hemiplegic Shoulder Pain Author, Year Country Methods Outcomes PEDro Score Shin & Lee (2007) 30 patients with stroke of onset less than 30 days Before treatment median pain scores were similar
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Korea with hemiplegic shoulder pain were randomized to between groups (6 vs. 6). At the end of treatment 6 RCT either dry acupressure (n=15) or acupressure there was significantly greater pain reduction in the combined with 3 essential oils (rosemary, lavender aromatherapy group (2 vs. 4, p=0.001). and peppermint) (n=15). Treatment was provided twice daily (20 min sessions) for 2 weeks. A 7-point VAS was used to assess pain before and after treatment.
The authors speculated that the improvement in shoulder pain might result from an enhancement of the parasympathetic response through the effects of smell and touch that encourage relaxation. Relaxation has been shown previously to alter the perception of pain.
Conclusions Regarding Aromatherapy Acupressure
There is moderate (Level 1b) evidence that aromatherapy combing with acupressure can reduce pain associated with painful hemiplegic shoulder
11.7.10 Massage Therapy
Massage therapy has also been examined as a treatment for HSP. There are numerous theories about how massage therapy may affect the body. For example, the "gate control theory" suggests that massage may provide stimulation that helps to block pain signals sent to the brain. Other theories suggest that massage might stimulate the release of certain chemicals in the body, such as serotonin or endorphins, or cause beneficial mechanical changes in the body.
Table 11.24 Studies Assessing Massage Therapy For HSP Following Stroke Author, Year Country Methods Outcomes PEDro Score Mok & Woo 102 stroke patients were randomly allocated to a Significant improvements in all 5 variables at (2004) massage group or a control group. The treatment group post-test and 3-days post-test were seen for the Hong Kong receives 10-minutes of slow-stroke back massage (SSBM) massage group compared to the control group 5 (RCT) for seven successive evenings. 5 variables were evaluated (p<0.05). in the study: anxiety level, heart rate, systolic blood pressure (BP), diastolic BP and pain score. Li et al. (2012) 120 participants with hemiplegia stage 1 shoulder hand Individuals in the treatment group had China syndrome were randomly allocated to a 6 week significantly lower NPRS scores than those in the 6 (RCT) treatment group receiving massage and electric rehabilitation only group post treatment acupuncture or a control group receiving rehabilitation (p<0.05). The reduction in NPRS scores was therapy which involved pose training and bobath maintained up to 12 week follow up (p<0.05). exercise. Outcomes including numeric pain rating scale Significantly lower number of participants in the (NPRS), stage of shoulder-hand syndrome, Fugl-Meyer acupuncture/massage group developed stage II evaluation of upper limb and band were measured at end or III shoulder syndrome compared to those in of the 6 week treatment and at 12 week follow-up. the rehabilitation group post treatment and at 12 weeks follow-up (p<0.05). The Fugl-Meyer functional activity of upper limb was significantly higher among treatment group vs control group post treatment (p=0.02); however, this improvement was not maintained at 12 week follow-up. No significant difference in functional hand activity level was seen among
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the two different groups.
Discussion
Two RCTs examined the use of massage in improving should pain post stroke. Mok and Woo (2004)conducted a RCT evaluating the healing effects of slow-stroke back massage for elderly stroke patients with shoulder pain and anxiety. All the participants reported beneficial effects from the massage intervention, which included relief of pain, relaxation and ability to sleep better. Also, massage therapy patients had significantly lower blood pressure, lower levels of anxiety, lower pain and heart rate scores when compared with the control group. In the second RCT, Li et al. (2012) provided patients in the treatment group with combined acupuncture and massage therapy. The study found significantly lower pain among individuals receiving treatment compared to those in the standard treatment group for up to 12 weeks post treatment, however it is unknown whether the benefits were a result of the acupuncture, the massage or the combination. Function also improved post treatment; however it was not maintained over the 12 week period. More frequent therapy times may be required to maintain improved outcomes.
Conclusions Regarding Massage Therapy
There is moderate (Level 1b) evidence that massage therapy reduces pain and anxiety levels post- stroke.
There is moderate (Level 1b) evidence that massage therapy with acupuncture reduces pain post stroke.
11.7.11 Subscapular Nerve Block for the Treatment for Shoulder Pain
While suprascapular nerve block has been used to treat shoulder pain and improve range of motion in a variety of conditions including rotator cuff tendonitis, rheumatoid arthritis and frozen shoulder, it had not been evaluated specifically for used for hemiplegic shoulder pain previously. One small RCT has been published recently evaluating this treatment for post-stroke shoulder pain, compared with usual care, which was, in this case, ultrasound.
Table 11.25 Studies Assessing Nerve Block For HSP Author, Year Country Methods Outcomes PEDro Score Boonsong et al. 10 stroke patients with hemiplegic shoulder pain were At baseline, pain scores were similar between (2009) randomized to receive suprascapular nerve block (SSNB) groups (71 and 72). At week 4, the pain scores Thailand with 2 separate injections of 10 mL of 1% lidocaine or were significantly reduced in the nerve block 4 (RCT) ultrasound therapy 5 days a week for 4 weeks. During the group (20 vs. 50, p=0.004). There were no study period all of the patients were given the same significant differences between groups on ROM program of range of motion exercise. Outcomes were measures in either flexion and abduction at any assessed at baseline and 2 and 4 weeks and included pain time point. (0-100 VAS) and range of motion (ROM). Yasar et al. 26 patients with hemiplegic shoulder pain lasting an Intra-articular steroid injection was performed (2011) average of 8 months were randomized to receive a single in 11 (42 %) patients, and suprascapular nerve Turkey injection of intra-articular steroid (40 mg triamcinolone block in 15 (57%) patients. Pain was reduced 5 (RCT) acetonide) or suprascapular nerve block (2% Citanest) in among patients in both groups over the study an outpatient setting. Shoulder pain was measured using period. There were no differences in pain scores
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a visual analogue scale during flexion, abduction, internal between groups and external rotation at the moment the pain the point that pain started and at passive maximum range of motion values. Evaluations were made before the injection, and 1 hour, one week and one month after the injection.
It is difficult to comment on the efficacy of subscapular nerve block in the treatment of hemiplegic shoulder pain since only 2 small, underpowered studies have been conducted and in neither, was a placebo used for comparison.
Conclusions Regarding Subscapular Nerve Block
There is moderate (Level 1b) evidence that subscapular nerve block reduces hemiplegic shoulder pain compared with ultrasound therapy.
11.7.12 Segmental Neuromyotherapy for the Treatment for Shoulder Pain
SNMT is based on the principle that chronic pain, including shoulder pain, “Involves sensitization of nociceptive neurons in the segments of the spinal cord receiving their afferent sensory input from the affected part of the body…” The SNMT approach aims at diagnosing the precise segments involved in the sensitization process. The treatment includes a combination of treatment modalities including therapy, injections with local anaesthetics, the application of heat and electrical stimulation. Table 11.26 Studies Assessing Segmental Neuromyotherapy Nerve Block For HSP Author, Year Country Methods Outcomes PEDro Score Ratmansky et al. 24 patients (<3 months following stroke) with positive At the end of treatment and follow-up, pain (2012) Neer's and hand-behind-neck tests were randomized to scores in both groups had improved. The Israel receive standard hospital therapy for shoulder pain (1-2 decrease in the SNMT group was non- 7(RCT) hrs/day x 5 days/week x 4 weeks) with oral pain significantly greater (-4.1 vs. -2.9 and -3.2 vs. - medication, if required or standard therapy plus 12 1.4). Improvement in median FMA scores was additional treatments of segmental neuromyotherapy greater for patients in the SNMT group at the (SNMT), which included subcutaneous injections of end of treatment (median score =2.5 vs. -0.5, lidocaine, heat application, TENS treatment and passive p=0.02). Significantly greater improvement was stretching. Outcomes were assessed at baseline, the also shown in the Neer's test at the end of middle and end of treatment and at follow-up (2 months treatment p=0.014). post treatment) and included pain severity (measured using a VAS), Fugl-Meyer Assessment (FMA) arm score, and the Ashworth scale.
Conclusions Regarding Segmental Neuromyotherapy
There is moderate (Level 1b) evidence that Segmental Neuromyotherapy improves hemiplegic shoulder pain.
11.7.13 Summary of the Management of Hemiplegic Shoulder
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Despite the high prevalence of patients suffering from painful hemiplegic shoulders, the evidence for effective treatment is underwhelming and no particular intervention appears superior. A recent systematic review and meta-analysis, limited to the inclusion of 8 RCTs (Koog et al. 2010) reported that aromatherapy/acupressure, slow back massage and intramuscular neuromuscular electrical stimulation were more effective than the placebo condition. However, only electrical stimulation was assessed and found to be effect long-term (3 months). The effect size associated with treatment was -1.173 (95% CI - 1.943 to -0.403). The authors also reported there was no association between spasticity and HSP.
There is conflicting evidence that electrical stimulation helps to reduce pain and subluxation, and conflicting evidence that botulinum toxin can help to reduce pain or spasticity. There is moderate evidence supporting an active therapy-oriented approach, although 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 or shoulder strapping 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 evidence of a benefit for all three of these treatment approaches.
There is consensus 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 11.27 Summary of RCTs for Management of Hemiplegic Shoulder Author, Year PEDro Score n Outcomes Positioning of the Shoulder Ada et al. 2005 6 36 +/- Gustafson & McKenna 2005 6 32 - DeJong et al. 2006 6 19 - Dean et al. 2000 5 23 - 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 - Lynch et al. 2005 6 35 - Patridge et al. 1990 5 65 + Kumar et al. 1990 5 28 - Electrical Stimulation Church et al. 2006 (FES vs. sham FES) 9 106 - Yu et al. 2004 & Chae et al. 2005 & Chae et al. 2007 7 61 + (Intramuscular FES vs. sling) Yu et al. 2001 (Intramuscular FES vs. surface FES) 6 10 +
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Linn et al. 1999 (FES vs. no FES) 6 40 +/- Fil et al. 2011 5 48 + Kobayshi et al. 1999 (FES vs. no FES) 5 17 + Leandri et al. 1990 (TENS vs. sham TENS) 5 60 + Wang et al. 2000 (FES vs. no FES) 5 32 + Baker et al. 1986 (FES vs. sling) 4 63 + Faghri et al. 1994 (FES vs. therapy) 4 26 + Surgery for Muscle Imbalance No RCTs - 0 - Injections of Steroid or Botulinum toxin Rah et al. 2012 (steroid vs. lidociane) 9 58 + Kong et al. 2007 (botulinum toxin vs. placebo) 8 17 - Marco et al. 2007 8 31 +/- (TENS + botulinum toxin vs. TENS + placebo) Snels et al. 2000 (steroid vs. placebo) 8 35 - Lim et al. 2008 (botulinum toxin vs. steroid) 8 29 - Yelnik et al. 2007(botulinum toxin vs. placebo) 7 20 + DeBoer et al. 2008 (botulinum toxin vs. placebo) 6 22 - Yaser et al. 2011 (triamcinolone acetonide vs. subscapular nerve 5 26 - block) Laske et al. 2009 (steroid vs. no injection) 4 38 +/- Boonsong et al. 2009 (steroid vs. ultrasound) 4 10 +/- Massage/Other Ratmansky et al. 2012 (segmental neuromyotherapy) 7 24 + Shin & Lee. 2007 6 30 + Mok & Woo (slow back massage) 5 102 +
11.8 Complex Regional Pain Syndrome (CRPS)
11.8.1 Stages and Symptoms of CRPS
CRPS can be of type I or II. Type I is more common and is associated with hemiplegia. It is also referred to as shoulder hand syndrome or reflex sympathetic dystrophy. Type II CRPS is also referred to causalgia, is less common and is associated with traumatic injury. CRPS-1 is characterized by numerous peripheral and central nervous system changes in the absence of obvious nerve injury. 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 2004; Moseley 2006).
The condition is not unique to patients recovering from stroke, but is also associated with phantom limb pain, and is prevalent among patients with head injury, spinal cord injury and even mild injury to the extremities. Iwata et al. (2002) empirically describe 3 stages of CRPS (Table 11.28).
Table 11.28 Stages and Characteristics of CRPS Stage Characteristics Persistent pain, described as burning, or aching and aggravated by movement
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I The extremity is edematous, warm and hyperesthetic Lasting 3-6 months Early dystrophic changes in the limb present 2 Atrophy of the muscle and skin Vasospasm with hyperhidrosis Soft-tissue dystrophy 3 Contractures which produce “frozen shoulder” Pain and vasomotor changes are infrequent
CRPS 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 the condition 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.
CRPS 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. The incidence of HSP is known to be higher among patients with spasticity (Wanklyn 1994). CRPS develops in about one in four hemiplegics. It is associated with involvement of the premotor region and spasticity in the involved upper extremity. Typically patients with post stroke CRPS present with pain, hyperalgesia, joint stiffness and swelling and autonomic abnormalities. While recovery is largely spontaneous, conditions that persist for greater than 6 months are often difficult to treat.
11.8.2 Pathophysiology of CRPS
CRPS has been associated with lesions of the pre-motor area of the brain. The etiology of CRPS 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 although all of the cases were 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 CRPS usually coincided with increased arterial blood flow.
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Iwata et al. (2002) suggested that CRPS 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.
11.8.3 Incidence of CRPS
Several studies have examined the frequency of the development of CRPS following stroke. The results are reported in Table 11.29.
Table 11.29 Incidence of CRPS Author, Year Country Methods Outcomes PEDro Score Davis et al. 540 rehabilitation inpatients with hemiplegia were 68 (12.5%) patients were diagnosed with RSD. (1977) evaluated with respect to side of hemiplegia, dates of Care was used to distinguish these patients from USA onset of hemiplegia and of pain, age, sex, those with other shoulder pathologic conditions No Score handedness, sensory losses, associated medical and pain syndromes. diseases and treatment response. All patients’ charts were reviewed by a team composed of authors Eto et al. (1980) 7 autopsy cases of hemiplegia shoulder-hand One of the cases showed an isolated brain lesion Japan syndrome from patients that had been admitted to in the premotor area due to a metastasis from No Score the University of Tokyo Hospital or an affiliated malignant melanoma. Four other cases with hospital. Observed over a 6 year period, autopsy cases cerebral infarction and one with glioblastoma of of hemiplegia shoulder-hand syndrome. Their clinical the cortex in the area supplied by the middle and post-mortem records were available in cerebral artery. The seventh case showed a determining the cerebral localization of the syndrome hemorrhagic cerebral lesion in the lentiform and of unilateral longstanding autonomic dysfunction nucleus. The most common overlap area in the 6 following hemiplegia. 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. 85 consecutive patients admitted to a rehabilitation 21 patients (25%) exhibited radionuclide evidence (1984) unit with post-stroke hemiplegia. All had suffered a of RSD based on delayed scan criteria of Canada hemispheric stroke of thrombotic, embolic or increased uptake in the hemiplegic wrist, No Score hypertensive hemorrhagic etiology as determined by metacarpal-phalangeal (MCP) and CT brain scan. Patients were assessed prospectively interphalangeal (IP) joints. 8 of the scan-positive for radionuclide and clinical features of reflex RSD patients presented a low soft tissue blood sympathetic dystrophy (RSD). Each patient underwent flow pattern identical to the non-RSD hemiplegic a three-phase bone scan within 72 hours of patients while the remaining 13 showed a high admission. Delayed images of wrists and hands as well flow pattern. MCP tenderness to compression as total body were obtained 2 to 4 hours after proved to be the most valuable clinical sign of injection. RSD, with a predictive value, sensitivity, and specificity rates of 100%, 85.7% and 100% respectively. van Ouwenaller et 219 hemiplegic patients of whom 44 had flaccid The RSD syndrome was present in only 23% of all al. (1986) paralysis and 175 evolved rapidly toward a spastic cases but was seen more often in spastic patients, Switzerland state. Stroke was the most frequent cause (79%). 27% vs. 7%.
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No score 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 contributing factors. Daviet et al. (2002) 69 subjects recruited within 1 month of stroke and Between admission to rehabilitation and 3 weeks France who were referred for inpatient rehabilitation were 7 (10.1%) developed CRPS, at 3 months, the No Score prospectively assessed for the development of, and number had increased 24 (34.8%). The 5 main predictors of, CRPS-1. CRPS-1 was evaluated using the clinical predictors were motor deficit, spasticity, Labrousse severity scale (pain:0-3, vasomotor and sensory deficits, and initial coma. trophic changes: 0-3, restriction of joint movement:0- 4). Diagnosis was based on > 2 symptoms + severity >2. Petchkrua et al. 64 consecutive patients admitted for inpatient 13 (20.3%) developed clinical symptoms of CRPS- (2000) rehabilitation with upper extremity impairments 1 during rehabilitation based on at least 3 of the USA associated with first stroke were examined on a following 5 signs were present: shoulder pain, No Score weekly basis for the development of CRPS-1. decreased passive range of motion of the Diagnosis was confirmed using triple-phase bone scan shoulder, wrist/hand pain, edema, and skin (TPBS). changes. Only 1 case of CRPS-1 was confirmed using TPBS. Gokkaya et al. A cohort of 95 stroke patients admitted for inpatient 29 patients (30.5%) developed RSD. Their (2006) rehabilitation, which usually occurred 4 to 6 weeks rehabilitation stays were, on average, 10 days Turkey post stroke, were evaluated for the presence of RSD longer compared with patients without RSD. No Score and glenohumerol joint subluxation at admission. Patients in the lower categories of Brunnstrom scores tended to develop RSD more frequently. The presence of shoulder subluxation was also more frequent among patients with RSD (72.4% vs. 24.2%, p<0.001). Kocabas et al. 82 patients were evaluated for the presence of CRPS- The incidence of CRPS-I was 48.8% in the first 28 (2007) 1 weeks 2, 6, 14 and 28 after suffering a stroke. weeks. During the 6th, 14th and 28th week, it was Turkey Diagnosis was based on the presence of pain, edema present in 12%, 30% and 40% subjects, No Score of the wrist and fingers, change in respectively. colour/temperature of the hand and limited ROM of the shoulder and hand. Barlak et al. (2009) 187 consecutive stroke patients admitted for Shoulder pain was present in 114 (61%) patients. Turkey inpatient rehabilitation were evaluated for the 70 patients had complex regional pain syndrome- No Score presence of HSP. Each patient was evaluated by type I. There was no correlation between clinical, radiographic, and ultrasonographic presence or absence of CPRS-1 and degree of examination. Daily living activities were assessed subluxation. A significantly higher percentage of using the FIM at admission and at discharge. Patients patients with CPRS-1 were either in Brunnstrom were divided into two groups, one comprising recovery stage I or II patients with shoulder pain and the other comprising patients without shoulder pain. They were then compared with respect to clinical characteristics, radiologic findings, and FIM scores.
There is a wide range of reported prevalence of CRPS following stroke. Part of variability can be attributed to timing and form of assessment used. 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
11. Painful Hemiplegic Shoulder pg. 45 of 66 www.ebrsr.com 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. However, the results from several newer studies suggest the incidence is higher. Since both of these studies originated in the same country, the results may not be generalizable. The authors themselves speculate that the poor economic conditions with limited patient care capabilities likely contributed to the high prevalence (Kocabas et al. 2007).
Conclusions Regarding the Incidence of CRPS Post Stroke
The incidence of CRPS post stroke ranges from 12%-48% and may be influenced by the timing as well as the type of assessment.
11.8.4 Diagnostic Tests of CRPS
Several approaches to diagnose CRPS have been used, although no one single test will identify all persons with SHS. Three sets of criteria are used routinely: International Association for the Study of Pain (IASP) 1994 consensus criteria (Stanton-Hicks et al. 1995), Bruehl’s (1999) criteria and Veldman’s (1993) criteria. The sensitivities and specificities of these sets of criteria range from 70% to 100% and 36% to 94%, respectively. Common features among these criteria include: pain, allodynia, hyperalgesia, edema, sweating changes, and limitations in range of motion. Quisel et al. (2005) have suggested that although diagnosis through instrumentation, bone scans (scintigraphy) and radiography are common, there is limited evidence that these techniques add to the accuracy of the diagnosis.
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. The accuracy of these blocks, however, has improved with image guided injections (e.g. ultrasound guided stellate block). Thermography, in controlled studies, has failed to consistently diagnose reflex sympathetic dystrophy and is not considered a valid test. However, Kozin et al. (1981) suggested 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 CRPS
CRPS 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.
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11.8.5 Treatment of CRPS
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 11.30.
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. Constraint-induced movement therapy and sensory discrimination training have also been proposed as possible treatments for SHS (Acerra et al. 2007). 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. In fact, it is widely accepted that there is little evidence that many of the commonly-used treatments associated by SHS are effective (Pertoldi & Di Benedetto 2005; Quisel et al. 2005). CRPS, which presents for greater than 6 months without appropriate treatment, has a poor prognosis (Lieberman 1986).
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.
Table 11.30 Potential Treatments for CRPS Prevention Splints Extremely early ROM exercises Resting splint of hand and wrist (controversial) Avoid shoulder subluxation Medication Exercise Analgesics Prevention and treatment of upper extremity contractures NSAIDs Active exercise if possible High dose oral corticosteroids (10 day course and then Frequent passive ROM taper) Antidepressants Modalities Interferential deep heat Injections Heat/cold modalities especially contrast baths Stellate ganglion sympathetic block Hand desensitization program Guanethedine bier block Transcutaneous electrical nerve stimulation Surgical Sympathectomy
11.8.6 Pharmacological Treatment of CRPS
Four studies evaluated the use of corticosteroids for the treatment of SHS associated with stroke. The results are presented in table 11.31.
Table 11.31 Corticosteroid Treatment of CRPS Author, Year Country Methods Outcomes
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PEDro Score Davis et al. (1977) A retrospective study of 68 patients suffering from All patients became pain- free, when subjected to USA hemiparesis and SHS resulting from stroke. All passive stretching of the involved joints, within 3 No Score patients received 16 mg of an oral steroid weeks. Six patients experienced a relapse of their (triamcinolone diacetate) daily for 14 to 21 days. pain, which resolved during a second course of Patients self-described their pain. treatment. Braus et al. (1994) 36 hemiplegic patients secondary to a stroke of the No significant improvement was noted in Germany middle cerebral artery and exhibited definite shoulder-hand syndrome in the placebo group 5 (RCT) shoulder-hand syndrome were studied. Patients were after 4 weeks at which time all patients switched randomized to orally receive either 8 mg over the corticosteroid protocol. Patients methylprednisolone or a placebo over 4 weeks. All receiving the corticosteroid treatment patients received daily physical therapy. For patients demonstrated significant improvement in in the placebo group, if no improvement was noted shoulder-hand syndrome that was maintained at in shoulder-hand syndrome then they were given 4 6 months. 31 of the 36 patients became almost weeks of corticosteroid treatment as per the symptom free within 10 days of treatment with experimental group. low dose oral corticosteroids. Kalita et al. (2006) 60 patients who developed CRPS-I following stroke Symptoms of CRPS developed a median of 28 days India were randomly assigned to receive 40 mg post stroke. In the prednisolone group, 83.3% 7 (RCT) prednisolone or 20 mg piroxicam (NSAID) daily. CRPS- patients showed significant improvement, I was assessed at 1 month using a 0-14 point scale. compared to 16.7% in the piroxicam group. The The primary end point was a 2 or more point mean change in CRPS score in prednisolone group reduction in CRPS score. was 6.47 (95%CI 4.37-7.36), whereas in piroxicam group it was only 0.47. Rah et al. (2012) 58 individuals with post stroke hemiplegic shoulder Significant improvement in VAS day and SDQ Korea pain were randomized to a treatment group receiving scores were seen among individuals in the Score (RCT) triamcinolone 40mg or lidocaine placebo group. treatment group compared to placebo at week 4 Visual analog scale (VAS), Modified Barthel Index, and 8 (p<0.05); while night scores improved at Shoulder Disability Questionnaire (SDQ) were week 2, 4, and 8 (p<0.05). measured at 2, 4, and 8 weeks post treatment.
Discussion
The efficacy of corticosteroids for the treatment of CRPS-1 has not been well-studied. In only three RCTs identified, two in which placebo was used and one in which a NSAID was used as the alternative treatment. Steroids were demonstrated to be of benefit. Braus et al. (1994) reported that oral corticosteroids improved CRPS-1 symptoms for at least 4 weeks. Kalita et al. (2006) also reported a significant decrease in symptoms with steroids. Rah et al. (2012) found improvements in both pain and disability measures up to 8 weeks post treatment.
Conclusions Regarding Oral Corticosteroids in CRPS
There is moderate (Level 1b) evidence that oral corticosteroids improve CRPS for at least the first 4 weeks.
Oral corticosteroids appear to improve CRPS for at least the first 4 weeks.
11.8.7 Mirror Imagery as a Treatment for CRPS
Mirror therapy is a technique that uses visual feedback about motor performance to improve rehabilitation outcomes. It can be used to improve motor performance, which is discussed in other chapters. Although it is more commonly associated with the treatment of phantom limb pain it may also
11. Painful Hemiplegic Shoulder pg. 48 of 66 www.ebrsr.com be useful in the treatment of CRPS-1 post stroke. It is believed that mirror imagery helps to create a movement illusion of the affected arm with the brain. These mirror illusions are believed to compensate for a reduced or absent proprioceptive input and to re-establish the normal pain free relationship between sensory feedback and motor intention, resolving the pain state. The patient is seated in such a manner so that the unaffected limb may be viewed in the mirror (or mirror box), while the affected limb is concealed behind the mirror while performing a variety of movements with the upper limb.
Three RCTs examining the use of mirror therapy following stroke have been assessed.
Table 11.32 Studies Evaluating Mirror Therapy Post Stroke Author, Year Country Methods Outcomes PEDro Score Moseley 51 patients with phantom limb pain or CRPS1 (37 The mean decrease in pain between pre- and (2006) with stroke) were randomly allocated to motor post-treatment was 23.4 mm (95% CI 16.2 to 30.4 Australia imagery, consisting of 2 weeks each of limb laterality mm) for the motor imagery group and 10.5 mm 6 (RCT) recognition, imagined movements, and mirror (95% CI 1.9 to 19.2 mm) for the control group. The movements, or to physical therapy and ongoing improvement in pain was maintained at 6-month medical care. Pain was assessed before and after follow-up (32.1 vs. 11.6 mm). treatment and again at 6 months using a 100 mm visual analogue scale) Cacchio et al. 48 patients admitted for inpatient rehabilitation with The mean scores of both the primary and (2009) evidence of CRPS-1 of the hemiplegic upper limb secondary end points significantly improved in the Italy received a 4-week conventional rehabilitation mirror group (P < .001). No statistically significant 7 (RCT) program and were randomized to receive mirror improvement was observed in any of the control therapy or to a control condition. All patients group values. Moreover, statistically significant received 2-3 hours of therapies daily, 5 days/week. differences after treatment (P < .001) and at the Patients in the intervention group were seated with 6-month follow-up were found between the 2 the arms perpendicular to the mirror board. Patients groups. At 6-months follow up, the mean pain observed the reflection of their unaffected arm while scale score at rest (0-10) was 4.7 vs. 8.1. performing movements with their affected arm. Patients in the control group performed the same movements, but the mirror was covered. The primary end points were a reduction in the visual analogue scale score of pain at rest, on movement, and brush- induced tactile allodynia. The secondary end points were improvement in motor function as assessed by the Wolf Motor Function Test and Motor Activity Log. Assessments were conducted before/after treatment and at 6 months. Cacchio et al. 24 stroke patients were randomized to one of three The mean VAS pain scores at baseline ranged (2009) treatment groups: active mirror group as described from 62-64 at baseline across groups. After 4 Italy above, a covered mirror group and a mental imagery weeks, patients in the active mirror therapy group (RCT) group. In the 2 mirror groups, patients performed a had the lowest pain scores (5) vs. 80 (mental variety of movements with the upper limb for 30 min imagery group) vs. 72 (covered mirror group). At Letter–insufficient per daily. Following 4 weeks of treatment, subjects in the end of 8 weeks, following crossover to active info to enable the 2 non-active mirror therapy groups were crossed therapy the mean VAS pain scores were 10 or scoring over to the active mirror therapy group. Outcome lower. measures, assessed at baseline and 8 weeks included pain on a VAS scale (0-100) and the Wolf-motor function test.
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Among the three studies described above, the one authored by Moseley (2006) included mirror therapy as one component of the three-part treatment Motor Imagery Program (MIP). The mechanisms underlying motor imagery remain unclear, although it is known that both real and imagined movements activate similar cortical networks. Proposed mechanisms include reconciliation of motor output and sensory feedback, activation of mirror neurons and graded activation of cortical motor networks (Acerra et al. 2007).
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.
Mirror therapy, when provided as a single intervention was found to be more effective in reducing pain than either sham mirror therapy or mental practice. The effects were also reported to be long lasting. (Cacchio et al. 2009).
Conclusions Regarding Mirror Therapy Post Stroke
There is strong (Level 1a) evidence that mirror therapy can reduce pain associated with shoulder- hand syndrome.
A mirror therapy program appears to improve shoulder-hand syndrome.
11.8.8 Passive Range of Motion Exercises for the Prevention of CRPS
In addition to treatment of CRPS-1, there are also strategies to prevent its development. Although physiotherapy is regarded as the cornerstone of integrated treatment, no controlled trials have been conducted to evaluate its effect in preventing the development of CRPS. A single trial using historical controls evaluated the benefit of an exercise program to reduce the development of CRPS following stroke (Table 11.33).
Table 11.33 Physical Therapy to Prevent CRPS Author, Year Country Methods Outcomes PEDro Score Kondo et al. (2001) 152 stroke patients admitted to a rehabilitation unit The incidences of RSD were 15/81 (18.5%) for Japan and followed for approx. 200 days were monitored for patients receiving the protocol and 23/71 (32.4%) No Score the development of RSD, assessed clinically by a among patients who did not. 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 set protocol developed by the authors was in response to the observation that patients were inappropriately performing excessive passive range of motion exercises, which may have contributed to
11. Painful Hemiplegic Shoulder pg. 50 of 66 www.ebrsr.com the development of CRPS. They hypothesized that by limiting inappropriate exercise and replacing it with a set protocol performed by therapists that they could reduce the incidence of CRPS.
Conclusions Regarding Physical Therapy to Prevent CRPS
There is limited (Level 2) evidence that passive range of motion exercises can prevent the development of CRPS
11.8.9 Calcitonin for the Prevention of CRPS
Although calcitonin has been used successfully to treat osteoporosis, as well as a variety of pain conditions following surgery and trauma, its use in the treatment of CRPS-1 following stroke has not been examined previously. Its mechanism of action is not well-understood and no site of action has been identified. A single historically controlled trial was identified examining the benefit of intramuscular injections of calcitonin, in addition to regular rehabilitation.
Table 11.34 Calcitonin to Prevent CRPS Author, Year Country Methods Outcomes PEDro Score Matayoshi et al. 24 hemiplegic patients admitted for inpatient The incidence of CRPS in all patients with post- (2009) rehabilitation with severe stroke and with any upper stroke hemiplegia during the control period was Japan limb or finger graded as Brunnstrom stage (BrST) III or 8.2%. Among patients with severe stroke who No Score below received conventional therapies plus a once- received calcitonin, the incidence of CRPS was weekly intramuscular injection of 20 U of calcitonin. significantly lower compared with the control This group of patients was compared with a historical group (12.5% vs. 57.1%, p<0.001). CRPS was cohort of 35 that received rehabilitation therapy only. completely prevented when calcitonin was Patients were observed during the in-hospital started 4 weeks or earlier after stroke, but rehabilitation period. The main outcome measure was prophylactic effects were weak when calcitonin onset of CRPS. was started >6 weeks after stroke.
Conclusions Regarding Calcitonin to Prevent CRPS
There is limited (Level 2) evidence that intramuscular injections of calcitonin can prevent the development of CRPS.
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11.9 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 conflicting (Level 4) evidence that prolonged positioning prevents loss of active or passive range of motion, or reduces pain.
6. There is limited (Level 2) evidence that shoulder slings prevent subluxation associated with hemiplegic shoulder pain.
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 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 helps reduce hemiplegic shoulder pain.
10. There is moderate (Level 1b) evidence that a supportive orthotic device can prevent and treat symptoms of shoulder –hand syndrome.
11. 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.
12. There is limited (Level 2) evidence that oral non-steroidal anti-inflammatories can reduce pain during therapy sessions.
13. There is strong (Level 1a) evidence that that functional electrical stimulation does not reduce hemiplegic shoulder pain following stroke, but does prevent the development of shoulder subluxation.
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14. There is conflicting (Level 4) evidence that botulinum toxin injected into the subscapularis muscle reduces spastic shoulder pain and improves passive range of motion of the hemiplegic shoulder.
15. There is conflicting (Level 4) evidence that intra-articular steroid injections improve pain associated with hemiplegic shoulder. There is strong (Level 1a) evidence intra- articular steroid injections do not improve arm function compared with either botulinum toxin or placebo.
16. There is moderate (Level 1b) evidence that subscapular nerve block reduces hemiplegic shoulder pain compared with ultrasound therapy.
17. There is moderate (Level 1b) evidence that Segmental Neuromyotherapy improves hemiplegic shoulder pain.
18. There is moderate (Level 1b) evidence that aromatherapy combing with acupressure can reduce pain associated with painful hemiplegic shoulder.
19. There is moderate (Level 1b) evidence that massage therapy reduces pain and anxiety levels post-stroke.
20. There is moderate (Level 1b) evidence that massage therapy with acupuncture reduces pain post stroke.
21. CRPS is a poorly understood clinical entity. Most cases improve with time.
22. There is moderate (Level 1b) evidence that oral corticosteroids improve CRPS for at least the first 4 weeks.
23. There is moderate (Level 1b) evidence that a modified imagery program can reduce pain associated with shoulder-hand syndrome.
24. There is limited (Level 2) evidence that passive range of motion exercises can prevent the development of CRPS-1.
25. There is strong (Level 1a) evidence that mirror therapy can reduce pain associated with shoulder-hand syndrome.
26. There is limited (Level 2) evidence that intramuscular injections of calcitonin can prevent the development of CRPS.
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