Shoulder Pain in Patients with Hemiplegia

Transcription

1 Shoulder Pain in Patients with Hemiplegia A Literature Review JUDY GRIFFIN, MS, and GAY REDDIN, BS The primary cause of hemiplegic shoulder pain remains elusive, making prevention and effective management difficult. Several possible causes are discussed, such as passive exercise, subluxation, and shoulder-hand syndrome. Treatment considerations and suggestions for clinical research are presented. Key Words: Hemiplegia, Shoulder joint, Pain. Ms. Griffin is Assistant Professor, The University of Tennessee Center for the Health Sciences, Department of Physical Therapy, Memphis, TN, and Research Coordinator for Physical Medicine and Rehabilitation, St. Francis Hospital, 5959 Park Ave, Memphis, TN (USA). Ms. Reddin is Senior Physical Therapist, Stroke Unit and Geriatrics, Baptist Memorial Hospital Lamar Unit, 1025 E. H. Crump Blvd, Memphis, TN This article was submitted May 26, 1980, and accepted December 9, Shoulder pain is a serious and frequent complication in patients with hemiplegia. The incidence has been reported as high as 70 percent 1 and 84 percent 2 in patients suffering from a cerebrovascular accident (CVA). Complaints of pain usually occur when passive motion is attempted at the shoulder joint, but in severe cases the patient has pain at rest. Painful, limited joint range of motion (ROM) interferes with use of the limb in functional activities and prevents the patient's full participation in rehabilitation. 3 Under normal circumstances, pain-sensitive soft tissue surrounding the glenohumeral joint (GHJ) rotator cuff, joint capsule, subacromial bursa, and biceps brachii tendon is subject to many stresses. Gravity provides traction stress, and GHJ flexion and abduction movements create friction-compression stress between the humeral head and coracoacromial liagment. 4 Hemiplegia may produce additional stresses of paralysis, sensory and perceptual deficits, and abnormal tone. Cailliet has observed that latent tendinitis and bursitis symptoms may become activated during hemiplegia. 5 The primary cause of hemiplegic shoulder pain has never been identified. However, a variety of causative agents has been suggested by authorities, including improper passive movement, spasticity, contractures, GHJ subluxation, and shoulder-hand syndrome. The purposes of this article are to review the literature concerning possible causes of the pain, propose management considerations, and identify areas needing clinical research. LITERATURE REVIEW Handling Techniques Handling of the affected arm, during such activities as exercise, positioning, and transfers, constitutes a potential strain upon the GHJ. For complete GHJ abduction to occur without compression of suprahumeral soft tissue, the scapula must upwardly rotate and the humeral head must depress and externally rotate. During passive exercise, if abduction of the paralyzed shoulder is performed without attention to this fact, compression trauma to capsule, bursa, or tendon may result. 4 Persons changing position of the unconscious patient may inadvertently apply traction to the flaccid arm, traumatizing periarticular tissue. 3 Also, sensory deficits may facilitate rough handling of the paralyzed arm by relatives, hospital personnel, or the patient himself. Rotator cuff injury has been cited as a cause of hemiplegic shoulder pain. Using arthrogram studies with 32 hemiplegic patients, Najenson and associates found that 40 percent had rupture of the rotator cuff and that 10 of 11 patients with severe shoulder pain had rupture of the rotator cuff. 2 None of the patients had a history of shoulder dysfunction prior to the onset of hemiplegia. The precipitating cause of the rotator cuff tear was identified as forced humeral abduction without external rotation, although other possible contributing causes such as subluxation and aging changes in the rotator cuff were mentioned. "Especially contraindicated, from our point of view, is the passive abduction performed in the physiotherapy department by the patients themselves, using Volume 61 / Number 7, July

2 pulleys to produce abduction in the glenohumeral joint through traction with the unaffected arm.,,2 Voss has also stated that the use of overhead pulleys can produce shoulder pain. 6 Other investigators have implied that physical therapy may contribute to painful, limited shoulder motion. In a long-term study of 107 severely disabled hemiplegic patients receiving physical therapy, Brocklehurst and associates found that stiff and painful shoulders were present in 21 patients by two weeks postonset and had developed in 37 additional patients by one year postonset. 7 "Disappointingly, painful limitation of shoulder movement was not affected by the amount of physiotherapy given or the time at which it was started." 7 However, there was no control group for comparison in that study, and the severity of joint pain and limitation of motion were not described. Spasticity, Flaccidity, and Contractures Immediately following an upper motor neuron lesion such as a CVA, the affected extremities become flaccid in approximately 90 percent of cases. 8 Flaccidity usually lasts a short time and is replaced by a predictable pattern of spasticity within 12 to 18 months. 9 In the shoulder girdle, spasticity develops in muscle groups producing scapular retraction-depression and humeral adduction-internal rotation. 9,10 There is wide agreement among experts that such spasticity interferes with the normal scapulohumeral rhythm necessary during GHJ abduction; therefore, passive elevation of the spastic shoulder causes soft tissue compression and pain if proper attention is not given to scapular mobilization and humeral external rotation The presence of spasticity increases the likelihood of contractures. 12 Once contractures develop, a cycle is established in which attempts to stretch the contracture cause pain, generating reflex protective spasm of the contracted muscles and patient apprehension and hostility. 11 Consequently, increasingly greater limitations of passive ROM, reduced active motion, disuse atrophy, and osteoporosis result. 5 Flaccidity and spasticity have each been named as the cause of hemiplegic shoulder pain. Tobis states that the typical clinical picture of hemiplegic shoulder pain includes flaccid, paralyzed, and atrophic shoulder musculature, with GHJ subluxation. 13 Conversely, Bobath states that shoulder pain does not become a problem until spasticity develops. 14 Other investigators have noted that hemiplegic patients with spastic shoulder girdle musculature more frequently complain of pain than do patients who have flaccidity. 1, 15 The relative incidence of flaccidity versus spasticity in patients with hemiplegic shoulder pain is not well documented in the literature. Subluxation The incidence of GHJ subluxation has been reported as high as 81 percent in patients with hemiplegia. 2 Many authorities maintain that such GHJ malalignment is the main cause of shoulder pain. 12,13,16,17 However, others discount any relationship between pain and subluxation. Johnstone states, "The flaccid or hypotonic hanging shoulder will sublux but this is not a factor to which any undue concern ought to be given.,,9 Bobath maintains that subluxation is not painful as long as the scapula is mobile, 10 and Mossman suggests that subluxation is harmless as long as passive ROM is not painful. 12 Although several investigators have reported the incidence of GHJ subluxation, few have documented the relationship between pain and subluxation. An exception is Najenson and associates' classical study of associations among hemiplegic patients' shoulder pain, rupture of the rotator cuff, and GHJ subluxation. In that study, 25 of the 26 patients with GHJ subluxation also had moderate or severe pain. 2 Subluxation would therefore appear to be strongly associated with shoulder pain. According to Tobis, the traction forces present in GHJ subluxation may contribute to rotator cuff tears. 13 All of Najenson and associates' 13 hemiplegic patients with documented rupture of the rotator cuff had GHJ malalignment. 2 The relationship between GHJ subluxation and abnormal tone is unclear. Miglietta and associates reported finding no relationship between subluxation and spasticity. 16 Many authorities suggest that subluxation is caused by spasticity in muscles that depress the humerus and downwardly rotate the scapula. 5,10 On the other hand, some evidence exists that spasticity may actually reduce subluxation; apparently, hyperactive stretch reflexes can be stimulated by the weight of the unsupported arm during ambulation, causing temporary reduction of subluxation However, flaccidity may be the characteristic state during the subluxation process. According to this viewpoint, gravitational pull unopposed by flaccid shoulder musculature produces painful and possibly irreversible overstretching of superior joint capsule and supraspinatus muscle. 13,16 Subluxation appears to develop in the first few weeks following hemiplegia. Investigating the relationship of supraspinatus muscle activity to the onset of GHJ subluxation, Chaco and Wolf performed EMG studies on 40 patients at four- and eight-week intervals after a CVA. 20 All six patients who ultimately developed subluxation had done so within four weeks, when the affected arm was flaccid (no supraspinatus EMG activity). Two of the patients later developed spasticity but maintained their subluxation. These investigators concluded that the supraspinatus muscle began responding to "loading" of 1042 PHYSICAL THERAPY

3 the dependent arm when spasticity appeared, and subluxation did not occur. However, if the superior capsule had been allowed to become overstretched when the flaccid supraspinatus muscle could not respond to loading, the GHJ subluxation persisted, even though spasticity and muscle activity later appeared. Chaco and Wolf recommended that "... to avert subluxation of the glenohumeral joint, loading on the joint should be avoided as long as the affected limb is flaccid.,,20 Moskowitz and associates suggested that support of the flaccid shoulder early in management can reduce the incidence of subluxation to as low as 2 to 5 percent. 8 Active Motor Function Severity of motor disability in hemiplegia is apparently associated with shoulder pain and subluxation. Fugl-Meyer and associates found that patients with poor motor ability in the affected arm tended to develop joint pain and limited passive motion, whereas patients who quickly regained motor function did not. 21 In one study of 222 hemiplegic patients, the incidence of GHJ malalignment was 66 percent in patients with complete or severe paralysis but only 16 percent in patients with partial paralysis. 17 Miglietta and associates reported that 79% of hemiplegic patients with subluxation had no active shoulder motion, whereas only 9 percent of patients without subluxation had such severe paralysis. 16 Whether the presence of subluxation can actually impede return of active motion, as has been suggested by Miglietta and associates, 16 and whether shoulder subluxation and pain can be reversed if active motion later improves, cannot be ascertained from available data. Shoulder-Hand Syndrome Pain in the hemiplegic arm may in some cases be caused by a reflex neurovascular disorder. A typical constellation of symptoms, often referred to as the "shoulder-hand syndrome" or "reflex sympathetic dystrophy," may materialize after a CVA or a myocardial infarction and is also known to develop following external trauma such as peripheral nerve injury or fracture. 22 The proportion of patients who may be expected to develop the shoulder-hand syndrome following CVA has been estimated at 12.5 percent, but the incidence of the undiagnosed condition may be much larger. 23 The syndrome can occur in patients whose upper limbs areflaccidand without contractures. 12 Phases of progression in shoulder-hand syndrome were originally described by Steinbrocker. 24 Initially, the main signs are usually edema of wrist, metacarpophalangeal, and proximal interphalangeal joints and hot, dry, and red or blotchy skin. The patient complains of severe pain in the hand or shoulder, or both, and protectively restricts any movement or sensory input to the limb. Gradually, muscle atrophy and trophic changes in skin, connective tissue, and joints become the major signs, and the hand becomes cyanotic, cool, and damp. The typical deformity position assumed by the hand is metacarpophalangeal joint extension and interphalangeal joint flexion, resembling the "intrinsic minus hand.,,5 Symptoms are presumed to result from reflex stimulation of the sympathetic nerve supply by an irritative focus or from interference with autonomic nervous system control by the cerebral lesion. 25 Although the signs and symptoms of shoulder-hand syndrome can develop suddenly, they may begin slowly and insidiously, going unrecognized until changes are irreversible. Early signs of joint swelling may be dismissed as dependent edema. Complaints of severe pain and hyperesthesia and the patient's refusal to move the wrist, fingers, and shoulder may be dismissed as emotional lability, depression, or organic brain syndrome, when in fact the patient's emotional disorder appeared after, not before, signs of painful restricted motion. 22 The existence of a shoulder-hand syndrome in the upper limb is incompatible with the rehabilitation goals of increased mobility and function of the upper limb. Management Considerations Vigorous painful stretching of the affected shoulder should be avoided. All persons managing the patient (including family) should be instructed in proper handling techniques and in the dangers of pulling on the affected arm. Prior to, and during, passive or assistive elevation of the affected shoulder, methods should be used to reduce spasticity, and attention should be directed toward scapular mobilization and humeral external rotation during shoulder abduction. Techniques for accomplishing such mobilization are described by Bobath, 10 Johnstone, 9 and Brunnstrom. 11 Because traumatic soft tissue compression can occur with passive humeral abduction, therapists should caution against passive abduction greater than 90 degrees and should direct treatment goals toward full shoulder external rotation and flexion. Shoulder pulleys do not provide adequate scapular rotation and humeral external rotation and should not be used as a means of passive elevation of the affected arm. All possible efforts should be undertaken to prevent GHJ subluxation in the first few weeks after onset of hemiplegia, when the upper limb is flaccid. The most effective way to prevent subluxation has not yet been established, although opinions abound in the literature. Shoulder slings have been condemned for interfering with body image, immobilizing the arm, reinforcing flexor tone, impairing postural support, and Volume 61 / Number 7, July

4 impeding normal gait. 6 Many question whether slings prevent subluxation: Friedland states that "there is no need to support a painfree shoulder in order to prevent or correct subluxation since the sling does not prevent, improve, cure or reduce such a deformity." 19 In one study comparing a small group of new hemiplegic patients using a sling with a control group, no appreciable difference in GHJ subluxation was found to exist. 26 Slings other than the traditional type have been described and alternatives, such as lapboards and arm rests fitted to the wheelchair, have been used. 10,12,27 However, the effectiveness of any of these methods in preventing subluxation has yet to be established. Inasmuch as degree of paralysis seems related to GHJ subluxation and pain, therapists should vigorously employ methods to improve active motion in the affected shoulder. Such methods are described by several authorities. 5,9-11 However, a causal relationship between use of these techniques and improvement in neuromuscular function has not been documented, as observed by Friedland. 19 Many authorities believe the most effective treatment of the shoulder-hand syndrome is a sympathetic block followed by intensive physical therapy. 22,28 Apparently, the decreased pain following interruption of sympathetic function permits increased use of the limb with resultant increased sensory input from muscle contraction and joint motion. 28 Success has also been reported using a combination of corticosteroids and physical therapy. Davis and associates reported complete resolution of symptoms within three weeks in 68 hemiplegic patients with early signs of shoulderhand syndrome, using a combination of oral steroids, a sling, and exercise preceded by heat or cold. 23 All authorities concur that the best response to treatment occurs when symptoms are recognized and treated early. The type of physical therapy for shoulder-hand syndrome described in the literature includes procedures to overload sensory input and to desensitize, such as the application of continuous cold or heat treatments (up to eight hours a day), deep stroking and kneading massage, and vigorous active and passive exercise. 29 Any procedures that increase the patient's pain should be avoided, inasmuch as pain encourages immobilization. The use of transcutaneous electrical nerve stimulation has been reported effective in the treatment of reflex sympathetic dystrophy. 30 ' 31 CONCLUSIONS In patients with hemiplegia, pain and limited shoulder joint ROM tend to occur together and constitute a significant problem. Although a blend of factors, such as contracture, poor motor function, and immobilization, may be responsible, GHJ subluxation seems highly suspect as a cause, and all possible efforts should be made to prevent subluxation when the limb is flaccid. Forced passive stretching of the shoulder into abduction can traumatize the rotator cuff and bursae and is contraindicated, especially if external rotation is limited or if spasticity is present. Improper exercise technique and subluxation may both contribute to the apparently high incidence of rotator cuff lesions in hemiplegic patients. Shoulderhand syndrome is treatable if recognized early but leads to irreversible pathophysiological changes if unrecognized. Preventive management by therapists aware of shoulder biomechanics and the deficits sustained by the hemiplegic patient should help eliminate the problem of the painful upper extremity. When pain does occur, a thorough evaluation by the therapist and early treatment are essential. Longitudinal studies of patients with hemiplegia are needed to document the relationship of such factors as spasticity, GHJ subluxation, painful limited shoulder ROM, and active motor ability in the affected upper extremity. Longitudinal studies might also clarify under what circumstances subluxation develops and whether it ever resolves. Further clinical research is needed to identify the most effective means of preventing GHJ subluxation. Clinical evidence is needed concerning effectiveness of facilitation methods in affecting return of active motion. Inasmuch as some authorities have implied that physical therapy may be ineffective in preventing and treating hemiplegic shoulder pain, a controlled study concerning this question seems indicated. Efforts should be made to document signs of shoulder-hand syndrome in the hemiplegic population, determine the real incidence of this disorder, and identify the most effective early therapy. REFERENCES 1. Caldwell CB, Wilson DJ, Braun RM: Evaluation and treatment of the upper extremity in the hemiplegic stroke patient. Clin Orthop 63:69-93, Najenson T, Yacubovich E, Pikielini S: Rotator cuff injury in shoulder joints of hemiplegic patients. Scand J Rehabil Med 3: , Rusk H: Rehabilitation Medicine. St. Louis, MO, C.V. Mosby Co, 1977, pp Cailliet R: Shoulder Pain. Philadelphia, PA, F.A. Davis Co, 1966, pp Cailliet R: The Shoulder in Hemiplegia. Philadelphia, PA, F.A. Davis Co, 1980, pp Voss D: Should patients with hemiplegia wear a sling? 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5 8. Moskowitz H, Goodman CR, Smith E, et al: Hemiplegic shoulder. NY State J Med 69: , Johnstone M: Restoration of Motor Function in the Stroke Patient. New York, NY, Churchill Livingstone, Inc. 1978, pp Bobath B: Adult Hemiplegia: Evaluation and Treatment. London, England, William Heinemann, 1978, pp Brunnstrom S: Movement Therapy in Hemiplegia. New York, NY, Harper & Row, Publishers, Inc. 1970, pp Mossman PL: A Problem-Oriented Approach to Stroke Rehabilitation. Springfield, IL, Charles C Thomas, Publisher, 1976, pp Tobis JS: Problems in rehabilitation of the hemiplegic patient. NY State J Med 57: , Bobath K: Letter to the editor. Phys Ther 52: , Dardier E, Reid C: Hemiplegia and painful shoulders (letter to the editor). Phys Ther 52:1208, Miglietta O, Lewitan A, Rogoff JB: Subluxation of the shoulder in hemiplegic patients, NY State J Med 59: , Najenson T, Pikielny S: Malalignment of the glenohumeral joint following hemiplegia: A review of 500 cases. Annals of Physical Medicine 8:96-99, Taketomi Y: Observations on subluxation of the shoulder joint in hemiplegia. Phys Ther 55:39-40, Friedland F: Physical therapy. In Licht S (ed): Stroke and its Rehabilitation. Baltimore, MD, Williams & Williams Co, 1975, pp Chaco J, Wolf E: Subluxation of the glenohumeral joint in hemiplegia. Am J Phys Med 50: , Fugl-Meyer AR, Jaasko L, Norlin V: The post-stroke hemiplegic patient. Scand J Rehabil Med 7:73-83, Moskowitz E, Bishop HF, Pe H, et al: Post-hemiplegic reflex sympathetic dystrophy. JAMA 167: , Davis SW, Petrillo CR, Eichberg RD, et al: Shoulder-hand syndrome in hemiplegic population: A 5-year retrospective study. Arch Phys Med Rehabil 58: , Steinbrocker O: Shoulder-hand syndrome: Associated painful homolateral disability of shoulder and hand with swelling and atrophy of hand. Am J Med 3: , Swan DM: Shoulder-hand syndrome following hemiplegia. Neurology 4: , Hurd MM, Farrell KH, Waylonis GW: Shoulder sling for hemiplegia: Friend or foe? Arch Phys Med Rehabil 55: , Zankel HT: Stroke Rehabilitation. Springfield, IL, Charles C Thomas, Publisher, 1971, pp Bonica JJ: Causalgia and other reflex sympathetic dystrophies. Postgrad Med 53: , Johnson EW, Pannozzo AN: Management of shoulder-hand syndrome. JAMA 195: , Stilz RJ, Carron H, Sanders DB: Reflex sympathetic dystrophy in a 6 year-old: Successful treatment by transcutaneous nerve stimulation. Anesth Analg 56: , Richlin DM, Carron H, Rowlingson JC, et al: Reflex sympathetic dystrophy: Successful treatment by transcutaneous stimulation. J Pediatr 93:84-86, 1978 Volume 61 / Number 7, July