Painful Shoulder in Hemiplegia C. Van Ouwenaller, MD, P.M. Laplace, MD, A. Chantraine, MD, PhD Hopital cantonal universitaire of Geneva, Switzerland ABSTRACT. Van Ouwenaller C, Laplace PM, Chantraine A: Painful shoulder in hemiplegia. Arch Phys Med Rehahil 6:23-36, 1986. @Shoulder pain is probably the most frequent complication of hemiplegia. In this study 219 hemiplegia patients were regularly followed up after their cerebrovascular accident (CVA) for one year (166 men, 53 women, with a mean age of 47 years). Criteria and parameters for evaluation of these shoulders were established at the outset. Distinction was made between tlaccid and spastic hemiplegia. Other influencing factors were subluxation reflex sympathetic dystrophy syndrome (RSD), isolated tendon lesion cuff rotator tear or association of some of these. Roentgen examinations were done for each patient. In our series of patients, 72% had shoulder pain at least once during the course of their recovery. This problem occurred more often in patients having spasticity (85%) than in those with flaccidity (18%). An evolution towards spasticity was noted in 80% of the patients in this series, whereas 20% remained hypotonic. Among the other possible causes of shoulder pain, anteroinferior subluxation was incontrovertibly the most frequently cited. The RSD syndrome was present in only 23% of all cases but was seen more often in spastic patients, that is 27% compared to 7% among flaccid patients. Whatever the cause, the subluxation with flaccid paralysis should be corrected and spasticity should be combatted as early and as vigorously as possible. KEY WORDS: Hemiplegia: Reflex sympathetic dystroph_v; Shoulder pain: Shoulder subluxation; Spastic& Shoulder pain is probably the most frequent complication of hemiplegia. Its repercussions on motor rehabilitation and the psychologic equilibrium of the patient make it all the more redoubtable. It can delay rehabilitation and functional recu- peration as the painful joint may mask improvement of motor function. The shoulder joint is a poorly balanced joint, having sac- rificed sturdiness to mobility. Its functional amplitude and flexibility depend less on the movement of humeral head in the glenoid cavity than on the musculotendinous sleeve which surrounds it and which blends with the joint capsule and lig- aments. The fibrous capsule and the ligaments of the glenohumeral joint are covered by a superficial osteoarticular layer composed of the acromion and the deltoid muscle. The subacromial and subdeltoid bursae run between this layer and the layer formed by the external rotators. This anatomic and functional unit corresponds to the sum of the humeroglenoidal, stemoclavic- ular, acromioclavicular and scapulothoracic movements. It is the most mobile joint in the human body. Many of the factors contributing to the occurrence of shoul- der pain in hemiplegia as cited in published reports seem to be contradictory. de SCze and associates’3 have shown that the lesions of the rotator cuff tendon or the tendon of the long head of the biceps brachii may cause shoulder pain. According to these authors, the frequency of rupture of the rotator cuff tendon increases with age (reaching 60% after age 50 years) and represents a determining factor. Moskovitz and associates,6 as well as Najenson and Pi- kielny,7 claim that anteroinferior subluxation of the humeral head can constitute a triggering factor in the hemiplegic pa- tient, especially in hypotonic paralysis. Spasticity also is men- tioned as a possible cause. ‘$ In our experience, the latter has always seemed to play a prominent role and we were partic- ularly attentive to this problem. Spasticity can cause irritation of soft tissues, notably various ligaments and muscles of the shoulder girdle, which are particularly prone to pain in view of the high concentration of neuroreceptors in this region.5 The reflex sympathetic dystrophy (RSD) syndrome or shoul- der-hand syndrome is cited by several authors as being re- sponsible for pain in the hemiplegic shoulder. Statistics on this subject, however, are conflicting. According to Perrigot and associates,’ ’ 70% of hemiplegic patients have RSD of the paralyzed shoulder, whereas Davis and associates3 found only 12.5% of hemiplegic shoulders with this syndrome among the 540 cases they studied. Finally, it should be remembered that a metastasis in the humerus or the glenoid cavity, especially in the early stages, is a possible cause of isolated pain, with or without other signs. OBSERVATIONS AND METHODOLOGY From January 1, 1979, to July 31, 1982, we treated 345 patients with hemiplegia in the physical medicine and reha- bilitation division of the University Hospital in Geneva. Of these, 219 were followed up regularly during their hospital stay as well as during their rehabilitation program carried out on an ambulatory basis after discharge. All were treated from the onset of their paralysis. Follow-up was at least six months or longer during rehabilitation ( 11 months average). Among these patients, 166 were men aged 19 to 78 years (mean 47 years) of whom 33 had flaccid paralysis and 133 evolved rapidly towards a spastic state. Of the 53 women, age 18 to 74 years (mean 46 years), 11 had flaccid paralysis whereas 42 had spasticity. The causes of hemiplegia were classic, with cerebrovascular accident (CVA) being the most frequent cause Presented at the 61st Annual Session of the American Congress of Rehabilitation Medicine. Boston, October 26, 1984. Submitted for publication November 24, 1984. and accepted in revised form April 24. 1985. Arch Phys Med Rehabil Vol67, January 1966
Painful Shoulder in Hemiplegia
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PII: 0003-9993(86)90489-2Painful Shoulder in Hemiplegia C. Van Ouwenaller, MD, P.M. Laplace, MD, A. Chantraine, MD, PhD
Hopital cantonal universitaire of Geneva, Switzerland
ABSTRACT. Van Ouwenaller C, Laplace PM, Chantraine A: Painful shoulder in hemiplegia. Arch Phys Med Rehahil 6:23-36, 1986. @Shoulder pain is probably the most frequent complication of hemiplegia. In this study 219 hemiplegia patients were regularly followed up after their cerebrovascular accident (CVA) for one year (166 men, 53 women, with a mean age of 47 years). Criteria and parameters for evaluation of these shoulders were established at the outset. Distinction was made between tlaccid and spastic hemiplegia. Other influencing factors were subluxation reflex sympathetic dystrophy syndrome (RSD), isolated tendon lesion cuff rotator tear or association of some of these. Roentgen examinations were done for each patient. In our series of patients, 72% had shoulder pain at least once during the course of their recovery. This problem occurred more often in patients having spasticity (85%) than in those with flaccidity (18%). An evolution towards spasticity was noted in 80% of the patients in this series, whereas 20% remained hypotonic. Among the other possible causes of shoulder pain, anteroinferior subluxation was incontrovertibly the most frequently cited. The RSD syndrome was present in only 23% of all cases but was seen more often in spastic patients, that is 27% compared to 7% among flaccid patients. Whatever the cause, the subluxation with flaccid paralysis should be corrected and spasticity should be combatted as early and as vigorously as possible.
KEY WORDS: Hemiplegia: Reflex sympathetic dystroph_v; Shoulder pain: Shoulder subluxation; Spastic&
Shoulder pain is probably the most frequent complication of hemiplegia. Its repercussions on motor rehabilitation and the psychologic equilibrium of the patient make it all the more redoubtable. It can delay rehabilitation and functional recu- peration as the painful joint may mask improvement of motor function.
The shoulder joint is a poorly balanced joint, having sac- rificed sturdiness to mobility. Its functional amplitude and flexibility depend less on the movement of humeral head in the glenoid cavity than on the musculotendinous sleeve which surrounds it and which blends with the joint capsule and lig- aments.
The fibrous capsule and the ligaments of the glenohumeral joint are covered by a superficial osteoarticular layer composed of the acromion and the deltoid muscle. The subacromial and subdeltoid bursae run between this layer and the layer formed by the external rotators. This anatomic and functional unit corresponds to the sum of the humeroglenoidal, stemoclavic- ular, acromioclavicular and scapulothoracic movements. It is the most mobile joint in the human body.
Many of the factors contributing to the occurrence of shoul- der pain in hemiplegia as cited in published reports seem to be contradictory. de SCze and associates’3 have shown that the lesions of the rotator cuff tendon or the tendon of the long head of the biceps brachii may cause shoulder pain. According to these authors, the frequency of rupture of the rotator cuff tendon increases with age (reaching 60% after age 50 years) and represents a determining factor.
Moskovitz and associates,6 as well as Najenson and Pi- kielny,7 claim that anteroinferior subluxation of the humeral head can constitute a triggering factor in the hemiplegic pa- tient, especially in hypotonic paralysis. Spasticity also is men- tioned as a possible cause. ‘$ In our experience, the latter has always seemed to play a prominent role and we were partic- ularly attentive to this problem. Spasticity can cause irritation
of soft tissues, notably various ligaments and muscles of the shoulder girdle, which are particularly prone to pain in view of the high concentration of neuroreceptors in this region.5
The reflex sympathetic dystrophy (RSD) syndrome or shoul- der-hand syndrome is cited by several authors as being re- sponsible for pain in the hemiplegic shoulder. Statistics on this subject, however, are conflicting. According to Perrigot and associates,’ ’ 70% of hemiplegic patients have RSD of the paralyzed shoulder, whereas Davis and associates3 found only 12.5% of hemiplegic shoulders with this syndrome among the 540 cases they studied.
Finally, it should be remembered that a metastasis in the humerus or the glenoid cavity, especially in the early stages, is a possible cause of isolated pain, with or without other signs.
OBSERVATIONS AND METHODOLOGY
From January 1, 1979, to July 31, 1982, we treated 345 patients with hemiplegia in the physical medicine and reha- bilitation division of the University Hospital in Geneva. Of these, 219 were followed up regularly during their hospital stay as well as during their rehabilitation program carried out on an ambulatory basis after discharge. All were treated from the onset of their paralysis. Follow-up was at least six months or longer during rehabilitation ( 11 months average).
Among these patients, 166 were men aged 19 to 78 years (mean 47 years) of whom 33 had flaccid paralysis and 133 evolved rapidly towards a spastic state. Of the 53 women, age 18 to 74 years (mean 46 years), 11 had flaccid paralysis whereas 42 had spasticity. The causes of hemiplegia were classic, with cerebrovascular accident (CVA) being the most frequent cause
Presented at the 61st Annual Session of the American Congress of Rehabilitation Medicine. Boston, October 26, 1984.
Submitted for publication November 24, 1984. and accepted in revised form April 24. 1985.
Arch Phys Med Rehabil Vol67, January 1966
24 PAINFUL SHOULDER IN HEMIPLEGIA, Van Ouwenaller
Painful Shoulder in Hemiplegia (n = 219) DISCUSSION
Pain
dystrophy (RSD)
RSD + SL
8 18% 149 85% 157 72%
8 18% 101 58% 109 50% 3 7% 52 30% 55 25%
3 7% 47 27% 50 23%
3 7% 43 25% 46 21%
(79%), followed by much lower percentages of head injury (14%), and tumors (7%).
Criteria and parameters for evaluation of these shoulders were established at the outset. The first distinction was be- tween flaccid and spastic hemiplegia. Spasticity was diagnosed on the basis of an increase of the myotatic reflex. Presence of subluxation was always sought. Criteria for the RSD syndrome were involvement of both the hand and shoulder and presence of the usual characteristic symptoms (edema, pain at rest and on passive motion of the different joints, and bone pain). Each shoulder was tested for an isolated tendon lesion and for an association of several contributing factors. Roentgenograms were done for each patient. Patients were observed daily both by attending physician as well as by the physical therapists and occupational therapists actually responsible for treatment.
The most notable result of this study is the close correlation between shoulder pain and spasticity in the hemiplegic patient. The group of hemiplegic patients with spasticity had a much higher proportion of shoulder pain than the group of patients with flaccidity. The effect of treatment of spasticity provides a supplementary argument in favor of the spasticity factor as an important element in the occurrence of shoulder pain. All inhibition and muscle relaxation techniques applied to the shoulder girdle muscles brought about clear-cut reduction of pain when applied judiciously and for long durations. Anti- spastic drugs also help to reduce spasticity. When rehabilita- tion with these techniques was not followed by complete joint improvement, injection of lidocaine into particularly tense muscles, for example, a spastic trapezius followed, if neces- sary, by an alcohol injection (which causes no harm to alpha fibers and muscle fibers as phenol does),14 resulted in remis- sion .
The role of spasticity is predominant, but the hemiplegic shoulder may also have a lesion of the rotator cuff tendon. de SCze and associates” and Olssonr” clearly showed the rela- tionship between age and wear and tear of the rotator cuff: after age 50 years the percentage of lesions increases, reaching 60% after age 60 years. However, Nepomuceno and Miller,’
They were able to note any modification concerning the condition of the patients’ shoulders. Patients followed a re- habilitation program based on mobilization using inhibition techniques such as those of Bobath. Certain physical agents were associated with pharmacologic treatment for pain relief.
RESULTS
The table shows details of the various possible causes of shoulder pain in the hemiplegic patient with respect to flac- cidity or spasticity of the shoulder girdle muscles. In general, in our series of patients, 72% had shoulder pain at least once during the course of their treatment. This problem occurred much more often (85%) in those patients with spastic hemi- plegia than in those with flaccid hemiplegia (18%). We also noted an evolution towards spasticity in 80% of the patients in our series, whereas 20% remained hypotonic. From the point of view of the pathogenesis of the hemiplegia, head injury patients with hemiplegia who remained flaccid showed no occurrence of shoulder pain. However, 50% of the cranial trauma patients with spasticity had pain. Follow-up of patients with brain tumor sequelae showed that each time there was a spastic evolution, it was accompanied by pain in the shoulder, while the four patients with flaccid hemiplegia in the same group had no shoulder complication. Among the patients with CVA, shoulder problems occurred in 24% of the patients with hypotonic hemiplegia compared with 88% among the patients with spasticity. The table shows that subluxation seems to be responsible for the greatest number of painful complications of the shoulder, both in spastic and flaccid hemiplegic patjents. Percentages are not significantly different for the RSD syn- drome, tenosynovitis, or RSD associated with subluxation.
Fig I-X-rays showing subluxation of the left shoulder
(bottom) and the clinical correspondence (top).
Arch Phys Med Rehabil Vol67, January 1666
PAINFUL SHOULDER IN HEMIPLEGIA, Van Ouwenaller 25
Fig 2-X-rays showing correction of the subluxation by a bem- isling (bottom) and the clinical correspondence (top).
in an arthrographic study of 24 hemiplegic patients with a mean age of 55 years. showed that 33% had a rupture of the rotator cuff. In a similar study of 32 hemiplegic patients with a mean age of 55 years, Najenson, Yacubovich, and Pikielni# showed that 40% of this population had a rotator cuff tear. These studies show that the incidence of cuff rupture is no greater in hemiplegic patients than in age-matched controls. Some authors have suggested that the hyperlaxity of the artic- ular capsule, combined with modification of muscle tonus and at times with peripheral neurologic lesions, would tend to in- crease the proportion of cuff tear. This cause can be neglected if one considers that the age of our population was clearly younger than that of other studies. Recently, another arthro- graphic study in painful hemiplegic shoulders failed to show any tendon lesion, but demonstrated in 23 of 30 patients, signs of adhesive capsulitis. ‘* This is in fact a supplementary ar- gument in favor of spasticity as an etiopathogenetic factor in the shoulder problem.
Among the other possible causes of shoulder pain, antero- inferior subluxation is incontrovertibly the most frequently cited (table). Although more frequent among flaccid than among spastic patients. among the latter it is more often associated with pain. All such diastases were confirmed by roentgenol- ogic examination (fig 1, top and bottom). There is a close
relationship between clinical findings and the x-ray finding of interruption of the scapulohumeral continuity. The RSD syn- drome was present in only 23% of all cases. If all too often shoulder pain of the hemiplegic patient carries the diagnosis of RSD syndrome, this prevalence has not been confirmed by our study or by Teppermann and associates,‘5 who recently observed 25% of RSD in a series of 85 hemiplegic patients. However. in our group of patients, this syndrome was seen in a proportion considerably higher among spastic patients (27%) as compared to 7% among patients with flaccidity. The as- sociation of RSD and subluxation did not increase this per- centage. Isolated tenosynovitis of the long head of the biceps brachii or the supraspinatus muscles was observed in 30% of the patients with spasticity. Contrary to the problems of a purely spastic origin, the RSD syndrome and the tenosynovitis respond reasonably well to medical treatment. However, with the exception of physical therapy and certain special tech- niques, spasticity has a tendency to sustain shoulder pain and to render it chronic.
CONCLUSION
The results of our study seem to principally support the close association of shoulder pain with spasticity. However, from our observation as well as the experience of previous authors, it seems clear that pain in the hemiplegic shoulder should be reduced by combating the spasticity as soon as pos- sible. Strategies to reduce pain from spasticity should start from the onset of paralysis and eventually would play a role in prevention.4 Certain recommendations might be useful. For example, it would be useful to instruct nursing personnel to this possible complication of the shoulder, underlining the pre- cautions to be taken when this joint is positioned or mobilized. The position of the shoulder in abduction while the patient is lying in bed with external rotation of the arm, forearm, and hand is important. The physical therapist must supervise the postures and start gentle range of motion. At the flaccid stage, occupational therapists play a prime role. An axillary cushion, attached to the trunk with a hamass bandage, a hemisling or an arm brace for wheelchairs will allow the patient to maintain a subluxated shoulder in the proper position (figs 1 and 3),
Fig 3-Subaxillary cushion used to correct the subluxation.
Arch Phys Med Rehabil Vol67, January 1996
26 PAINFUL SHOULDER IN HEMIPLEGIA, Van Ouwenaller
which should be constantly observed. An anteroinferior sub- luxation with flaccid paralysis should be corrected with a sling which does not interfere with possible neuro-orthopedic prob- lems. Any material used should be easily manipulated by the patient with the unaffected hand.
When spasticity appears, each case must be judged sepa- rately. Some patients will respond well to an antispastic drug (such as Tizanidine, 12 mg/day).2 Others will need treatment with diazepam. Mobilization and mostly techniques of inhi- bition or neuroproprioceptive facilitation should be applied as soon as possible. If the rehabilitation program, including ap- plication of physical agents (heat or cold) associated with administration of antispastic drugs, does not produce the an- ticipated results, it can be combined with lidocaine injections, supplemented by alcohol injections, for shoulder girdle mus- cles. This latter measure does not paralyze the treated muscle, as does phenol injection. Alcohol injection acts on the y fibers and in no instance does it produce necrosis of the muscle fibers.14 Hemisling or axillary cushion may also correct sub- luxation present in the patient with sbasticity and helps to reduce the pain. However, these devices might increase the spasticity or give an elbow flexion deformity.
In conclusion, spasticity, which is an inevitable complica- tion of hemiplegia, is the prime factor and the one most fre- quently encountered in the genesis of shoulder pain in the hemiplegic patient. It should be combatted as early and as vigorously as possible.
ADDRESS REPRINT REQUESTS TO: A. Chantraine, MD, PhD Division de medecine physique Hospital cantonal unversitaire 121 I GENEVE 4 Switzerland
References
1. Braun RM, West F, Mooney V, Nickel VL, Roper B, Caldwell
2.
3.
8.
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15.
C: Surgical treatment of painful shoulder contracture in stroke patient. J Bone Joint Surg [Am] 53:1301-1312, 1911 Chantraine A, van Ouwenaller C: New drug treatment of spas- ticity in hemiplegia. Excerpta Medica International Congress Se- ries 548:241-242, 1981 Davis SW, Petri110 CR, Eichberg RD, Chu DS: Shoulder-hand syndrome in hemiplegic population: 5-year retrospective study. Arch Phys Med Rehabil 58:353-356, 1911 Jensen EM: Hemiplegic shoulder. Stand J Rehabil Med [Suppl] 7:113-l 19, 1980 Kioresku MA: Innervation of shoulder joint in man. Arkh Anat Gist01 Embriol 66: l&15, 1914 Moskowitz E, Goodman CR, Smith E, Balthazar E, Mellins HZ: Hemiplegic shoulder. NY State J Med 69548-550, 1969 Najenson T, Pikielny SS: Malalignment of gleno-humeral joint following hemiplegia: review of 500 cases. Ann Phys Med 8:9& 99. 1965 Najenson T, Yacubovich E, Pikielni SS: Rotator cuff injury in shoulder joints of hemiplegic patients. Stand J Rehabil Med 3:131-131, 1911 Nepomuceno CS, Miller JM III: Shoulder arthrography in hemi- plegic patients. Arch Phys Med Rehabil 55:49-51, 1914 Olsson 0: Degenerative changes of shoulder joint and their con- nection with shoulder pain: morphological and clinical investi- gation with special attention to cuff and biceps tendon. Acta Chir Stand [Suppl] 181:1-130, 1953 Perrigot M, Bussel B, Pierrot Deseilligny E, Held JP: L’Cpaule de I’hCmiplCgique. Ann Mtd Phys 18:116181, 1915 Rizk TE. Christopher RP, Pinals RS, Salazar JE, Higgins C: Arthrographic studies in painful hemiplegic shoulders. Arch Phys Med Rehabil 65254-256, 1984 de S&e S, Ryckewaert A, Welfling J. Hubault A, Renier JC. Caroit M, Poinsard G: L’Cpaule sCnile: Ctude anatomique. Sem Hop Paris 37:18X-1883, 1961 Tardieu G, Got C. Lespargot A: Indications d’un nouveau type d’infiltrations au point moteur (alcool a 96”). Ann Med Phys l&539-551. 1915 Teppermann PS, Greyson ND. Hilbert L. Williams JI: Reflex sympathetic dystrophy in hemiplegia. Arch Phys Med Rehabil 651442441, 1984
ABSTRACTS of selected literature
Hagerman FC, Hikida RS, Staron RS, Sherman WM, Costill DL: Muscle damage in marathon runners. Physician Sportsmed 121 11:39-48, 1984. 0 Healthy people as well as highly trained athletes commonly ex- perience muscle soreness after severe exercise. Although many the- ories have been advanced, the pathophysiological basis for delayed muscle soreness is not known. The authors studied muscle biopsy samples from ten male runners immediately before and after a mar- athon and at one, three, five and seven days after the marathon. Results showed muscle degeneration after training and after the mar- athon, and there was a significant inflammatory response throughout the week of recovery after the marathon. Therefore, the authors sug- gest that anyone experiencing postexercise delayed soreness is prob- ably suffering from some degree of acute inflammation.
Shields RW: Alcoholic polyneuropathy. Muscle & Nerve 8:183- 187, 1985. 0 Alcoholic polyneuropathy is a common disorder. characterized by nonspecific clinical, electromyographic. and pathologic features. Nerve conduction studies and needle electromyography disclose finding:, consistent with a generalized, sensorimotor. axonal degenerative, po- lyneuropathy. Alcoholic polyneuropathy may be suspected when such findings occur in the setting of long-standing alcoholism and mal- nutrition. The lack of specific diagnostic criteria for alcoholic poly- neuropathy requires that other potential etiologies be excluded before that diagnosis is made. The institution of a nutritionally-balanced diet constitutes the principal therapy for alcoholic polyneuropathy, how- ever. significant improvement following such therapy is not fre- quently seen.
Arch Phys Med Rehabll Vol67, January 1966
Hopital cantonal universitaire of Geneva, Switzerland
ABSTRACT. Van Ouwenaller C, Laplace PM, Chantraine A: Painful shoulder in hemiplegia. Arch Phys Med Rehahil 6:23-36, 1986. @Shoulder pain is probably the most frequent complication of hemiplegia. In this study 219 hemiplegia patients were regularly followed up after their cerebrovascular accident (CVA) for one year (166 men, 53 women, with a mean age of 47 years). Criteria and parameters for evaluation of these shoulders were established at the outset. Distinction was made between tlaccid and spastic hemiplegia. Other influencing factors were subluxation reflex sympathetic dystrophy syndrome (RSD), isolated tendon lesion cuff rotator tear or association of some of these. Roentgen examinations were done for each patient. In our series of patients, 72% had shoulder pain at least once during the course of their recovery. This problem occurred more often in patients having spasticity (85%) than in those with flaccidity (18%). An evolution towards spasticity was noted in 80% of the patients in this series, whereas 20% remained hypotonic. Among the other possible causes of shoulder pain, anteroinferior subluxation was incontrovertibly the most frequently cited. The RSD syndrome was present in only 23% of all cases but was seen more often in spastic patients, that is 27% compared to 7% among flaccid patients. Whatever the cause, the subluxation with flaccid paralysis should be corrected and spasticity should be combatted as early and as vigorously as possible.
KEY WORDS: Hemiplegia: Reflex sympathetic dystroph_v; Shoulder pain: Shoulder subluxation; Spastic&
Shoulder pain is probably the most frequent complication of hemiplegia. Its repercussions on motor rehabilitation and the psychologic equilibrium of the patient make it all the more redoubtable. It can delay rehabilitation and functional recu- peration as the painful joint may mask improvement of motor function.
The shoulder joint is a poorly balanced joint, having sac- rificed sturdiness to mobility. Its functional amplitude and flexibility depend less on the movement of humeral head in the glenoid cavity than on the musculotendinous sleeve which surrounds it and which blends with the joint capsule and lig- aments.
The fibrous capsule and the ligaments of the glenohumeral joint are covered by a superficial osteoarticular layer composed of the acromion and the deltoid muscle. The subacromial and subdeltoid bursae run between this layer and the layer formed by the external rotators. This anatomic and functional unit corresponds to the sum of the humeroglenoidal, stemoclavic- ular, acromioclavicular and scapulothoracic movements. It is the most mobile joint in the human body.
Many of the factors contributing to the occurrence of shoul- der pain in hemiplegia as cited in published reports seem to be contradictory. de SCze and associates’3 have shown that the lesions of the rotator cuff tendon or the tendon of the long head of the biceps brachii may cause shoulder pain. According to these authors, the frequency of rupture of the rotator cuff tendon increases with age (reaching 60% after age 50 years) and represents a determining factor.
Moskovitz and associates,6 as well as Najenson and Pi- kielny,7 claim that anteroinferior subluxation of the humeral head can constitute a triggering factor in the hemiplegic pa- tient, especially in hypotonic paralysis. Spasticity also is men- tioned as a possible cause. ‘$ In our experience, the latter has always seemed to play a prominent role and we were partic- ularly attentive to this problem. Spasticity can cause irritation
of soft tissues, notably various ligaments and muscles of the shoulder girdle, which are particularly prone to pain in view of the high concentration of neuroreceptors in this region.5
The reflex sympathetic dystrophy (RSD) syndrome or shoul- der-hand syndrome is cited by several authors as being re- sponsible for pain in the hemiplegic shoulder. Statistics on this subject, however, are conflicting. According to Perrigot and associates,’ ’ 70% of hemiplegic patients have RSD of the paralyzed shoulder, whereas Davis and associates3 found only 12.5% of hemiplegic shoulders with this syndrome among the 540 cases they studied.
Finally, it should be remembered that a metastasis in the humerus or the glenoid cavity, especially in the early stages, is a possible cause of isolated pain, with or without other signs.
OBSERVATIONS AND METHODOLOGY
From January 1, 1979, to July 31, 1982, we treated 345 patients with hemiplegia in the physical medicine and reha- bilitation division of the University Hospital in Geneva. Of these, 219 were followed up regularly during their hospital stay as well as during their rehabilitation program carried out on an ambulatory basis after discharge. All were treated from the onset of their paralysis. Follow-up was at least six months or longer during rehabilitation ( 11 months average).
Among these patients, 166 were men aged 19 to 78 years (mean 47 years) of whom 33 had flaccid paralysis and 133 evolved rapidly towards a spastic state. Of the 53 women, age 18 to 74 years (mean 46 years), 11 had flaccid paralysis whereas 42 had spasticity. The causes of hemiplegia were classic, with cerebrovascular accident (CVA) being the most frequent cause
Presented at the 61st Annual Session of the American Congress of Rehabilitation Medicine. Boston, October 26, 1984.
Submitted for publication November 24, 1984. and accepted in revised form April 24. 1985.
Arch Phys Med Rehabil Vol67, January 1966
24 PAINFUL SHOULDER IN HEMIPLEGIA, Van Ouwenaller
Painful Shoulder in Hemiplegia (n = 219) DISCUSSION
Pain
dystrophy (RSD)
RSD + SL
8 18% 149 85% 157 72%
8 18% 101 58% 109 50% 3 7% 52 30% 55 25%
3 7% 47 27% 50 23%
3 7% 43 25% 46 21%
(79%), followed by much lower percentages of head injury (14%), and tumors (7%).
Criteria and parameters for evaluation of these shoulders were established at the outset. The first distinction was be- tween flaccid and spastic hemiplegia. Spasticity was diagnosed on the basis of an increase of the myotatic reflex. Presence of subluxation was always sought. Criteria for the RSD syndrome were involvement of both the hand and shoulder and presence of the usual characteristic symptoms (edema, pain at rest and on passive motion of the different joints, and bone pain). Each shoulder was tested for an isolated tendon lesion and for an association of several contributing factors. Roentgenograms were done for each patient. Patients were observed daily both by attending physician as well as by the physical therapists and occupational therapists actually responsible for treatment.
The most notable result of this study is the close correlation between shoulder pain and spasticity in the hemiplegic patient. The group of hemiplegic patients with spasticity had a much higher proportion of shoulder pain than the group of patients with flaccidity. The effect of treatment of spasticity provides a supplementary argument in favor of the spasticity factor as an important element in the occurrence of shoulder pain. All inhibition and muscle relaxation techniques applied to the shoulder girdle muscles brought about clear-cut reduction of pain when applied judiciously and for long durations. Anti- spastic drugs also help to reduce spasticity. When rehabilita- tion with these techniques was not followed by complete joint improvement, injection of lidocaine into particularly tense muscles, for example, a spastic trapezius followed, if neces- sary, by an alcohol injection (which causes no harm to alpha fibers and muscle fibers as phenol does),14 resulted in remis- sion .
The role of spasticity is predominant, but the hemiplegic shoulder may also have a lesion of the rotator cuff tendon. de SCze and associates” and Olssonr” clearly showed the rela- tionship between age and wear and tear of the rotator cuff: after age 50 years the percentage of lesions increases, reaching 60% after age 60 years. However, Nepomuceno and Miller,’
They were able to note any modification concerning the condition of the patients’ shoulders. Patients followed a re- habilitation program based on mobilization using inhibition techniques such as those of Bobath. Certain physical agents were associated with pharmacologic treatment for pain relief.
RESULTS
The table shows details of the various possible causes of shoulder pain in the hemiplegic patient with respect to flac- cidity or spasticity of the shoulder girdle muscles. In general, in our series of patients, 72% had shoulder pain at least once during the course of their treatment. This problem occurred much more often (85%) in those patients with spastic hemi- plegia than in those with flaccid hemiplegia (18%). We also noted an evolution towards spasticity in 80% of the patients in our series, whereas 20% remained hypotonic. From the point of view of the pathogenesis of the hemiplegia, head injury patients with hemiplegia who remained flaccid showed no occurrence of shoulder pain. However, 50% of the cranial trauma patients with spasticity had pain. Follow-up of patients with brain tumor sequelae showed that each time there was a spastic evolution, it was accompanied by pain in the shoulder, while the four patients with flaccid hemiplegia in the same group had no shoulder complication. Among the patients with CVA, shoulder problems occurred in 24% of the patients with hypotonic hemiplegia compared with 88% among the patients with spasticity. The table shows that subluxation seems to be responsible for the greatest number of painful complications of the shoulder, both in spastic and flaccid hemiplegic patjents. Percentages are not significantly different for the RSD syn- drome, tenosynovitis, or RSD associated with subluxation.
Fig I-X-rays showing subluxation of the left shoulder
(bottom) and the clinical correspondence (top).
Arch Phys Med Rehabil Vol67, January 1666
PAINFUL SHOULDER IN HEMIPLEGIA, Van Ouwenaller 25
Fig 2-X-rays showing correction of the subluxation by a bem- isling (bottom) and the clinical correspondence (top).
in an arthrographic study of 24 hemiplegic patients with a mean age of 55 years. showed that 33% had a rupture of the rotator cuff. In a similar study of 32 hemiplegic patients with a mean age of 55 years, Najenson, Yacubovich, and Pikielni# showed that 40% of this population had a rotator cuff tear. These studies show that the incidence of cuff rupture is no greater in hemiplegic patients than in age-matched controls. Some authors have suggested that the hyperlaxity of the artic- ular capsule, combined with modification of muscle tonus and at times with peripheral neurologic lesions, would tend to in- crease the proportion of cuff tear. This cause can be neglected if one considers that the age of our population was clearly younger than that of other studies. Recently, another arthro- graphic study in painful hemiplegic shoulders failed to show any tendon lesion, but demonstrated in 23 of 30 patients, signs of adhesive capsulitis. ‘* This is in fact a supplementary ar- gument in favor of spasticity as an etiopathogenetic factor in the shoulder problem.
Among the other possible causes of shoulder pain, antero- inferior subluxation is incontrovertibly the most frequently cited (table). Although more frequent among flaccid than among spastic patients. among the latter it is more often associated with pain. All such diastases were confirmed by roentgenol- ogic examination (fig 1, top and bottom). There is a close
relationship between clinical findings and the x-ray finding of interruption of the scapulohumeral continuity. The RSD syn- drome was present in only 23% of all cases. If all too often shoulder pain of the hemiplegic patient carries the diagnosis of RSD syndrome, this prevalence has not been confirmed by our study or by Teppermann and associates,‘5 who recently observed 25% of RSD in a series of 85 hemiplegic patients. However. in our group of patients, this syndrome was seen in a proportion considerably higher among spastic patients (27%) as compared to 7% among patients with flaccidity. The as- sociation of RSD and subluxation did not increase this per- centage. Isolated tenosynovitis of the long head of the biceps brachii or the supraspinatus muscles was observed in 30% of the patients with spasticity. Contrary to the problems of a purely spastic origin, the RSD syndrome and the tenosynovitis respond reasonably well to medical treatment. However, with the exception of physical therapy and certain special tech- niques, spasticity has a tendency to sustain shoulder pain and to render it chronic.
CONCLUSION
The results of our study seem to principally support the close association of shoulder pain with spasticity. However, from our observation as well as the experience of previous authors, it seems clear that pain in the hemiplegic shoulder should be reduced by combating the spasticity as soon as pos- sible. Strategies to reduce pain from spasticity should start from the onset of paralysis and eventually would play a role in prevention.4 Certain recommendations might be useful. For example, it would be useful to instruct nursing personnel to this possible complication of the shoulder, underlining the pre- cautions to be taken when this joint is positioned or mobilized. The position of the shoulder in abduction while the patient is lying in bed with external rotation of the arm, forearm, and hand is important. The physical therapist must supervise the postures and start gentle range of motion. At the flaccid stage, occupational therapists play a prime role. An axillary cushion, attached to the trunk with a hamass bandage, a hemisling or an arm brace for wheelchairs will allow the patient to maintain a subluxated shoulder in the proper position (figs 1 and 3),
Fig 3-Subaxillary cushion used to correct the subluxation.
Arch Phys Med Rehabil Vol67, January 1996
26 PAINFUL SHOULDER IN HEMIPLEGIA, Van Ouwenaller
which should be constantly observed. An anteroinferior sub- luxation with flaccid paralysis should be corrected with a sling which does not interfere with possible neuro-orthopedic prob- lems. Any material used should be easily manipulated by the patient with the unaffected hand.
When spasticity appears, each case must be judged sepa- rately. Some patients will respond well to an antispastic drug (such as Tizanidine, 12 mg/day).2 Others will need treatment with diazepam. Mobilization and mostly techniques of inhi- bition or neuroproprioceptive facilitation should be applied as soon as possible. If the rehabilitation program, including ap- plication of physical agents (heat or cold) associated with administration of antispastic drugs, does not produce the an- ticipated results, it can be combined with lidocaine injections, supplemented by alcohol injections, for shoulder girdle mus- cles. This latter measure does not paralyze the treated muscle, as does phenol injection. Alcohol injection acts on the y fibers and in no instance does it produce necrosis of the muscle fibers.14 Hemisling or axillary cushion may also correct sub- luxation present in the patient with sbasticity and helps to reduce the pain. However, these devices might increase the spasticity or give an elbow flexion deformity.
In conclusion, spasticity, which is an inevitable complica- tion of hemiplegia, is the prime factor and the one most fre- quently encountered in the genesis of shoulder pain in the hemiplegic patient. It should be combatted as early and as vigorously as possible.
ADDRESS REPRINT REQUESTS TO: A. Chantraine, MD, PhD Division de medecine physique Hospital cantonal unversitaire 121 I GENEVE 4 Switzerland
References
1. Braun RM, West F, Mooney V, Nickel VL, Roper B, Caldwell
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ABSTRACTS of selected literature
Hagerman FC, Hikida RS, Staron RS, Sherman WM, Costill DL: Muscle damage in marathon runners. Physician Sportsmed 121 11:39-48, 1984. 0 Healthy people as well as highly trained athletes commonly ex- perience muscle soreness after severe exercise. Although many the- ories have been advanced, the pathophysiological basis for delayed muscle soreness is not known. The authors studied muscle biopsy samples from ten male runners immediately before and after a mar- athon and at one, three, five and seven days after the marathon. Results showed muscle degeneration after training and after the mar- athon, and there was a significant inflammatory response throughout the week of recovery after the marathon. Therefore, the authors sug- gest that anyone experiencing postexercise delayed soreness is prob- ably suffering from some degree of acute inflammation.
Shields RW: Alcoholic polyneuropathy. Muscle & Nerve 8:183- 187, 1985. 0 Alcoholic polyneuropathy is a common disorder. characterized by nonspecific clinical, electromyographic. and pathologic features. Nerve conduction studies and needle electromyography disclose finding:, consistent with a generalized, sensorimotor. axonal degenerative, po- lyneuropathy. Alcoholic polyneuropathy may be suspected when such findings occur in the setting of long-standing alcoholism and mal- nutrition. The lack of specific diagnostic criteria for alcoholic poly- neuropathy requires that other potential etiologies be excluded before that diagnosis is made. The institution of a nutritionally-balanced diet constitutes the principal therapy for alcoholic polyneuropathy, how- ever. significant improvement following such therapy is not fre- quently seen.
Arch Phys Med Rehabll Vol67, January 1966
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