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Shoulder and Hemiplegia

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A common sequela of stroke is hemiplegic shoulder pain that can hamper functional recovery and subsequently lead to disability. Poduri et al report that hemiplegic shoulder pain can begin as early as 2 weeks poststroke but typically occurs within 2-3 months poststroke. Some of the most frequently suspected factors contributing to shoulder pain include subluxation, contractures, complex regional pain syndrome (CRPS), rotator cuff injury, and spastic muscle imbalance of the glenohumeral joint (Teasell, 1998). Hanger et al suggest that it is highly probable that the cause is multifactorial with different factors contributing at different stages of recovery (ie, flaccidity contributing to subluxation and subsequent capsular stretch, abnormal tonal and synergy patterns contributing to rotator cuff or scapular instability). Because of the difficulty in treating shoulder pain once established, initiate treatment early. For individuals who have had strokes with resultant hemiplegia, motor and functional recovery also are important steps in the treatment process. In order to understand the pathologic processes and changes that occur in the hemiplegic shoulder, the factors that contribute to normal shoulder position need to be understood. As proposed by Cailliet, normal anatomic position involves a well-approximated glenohumeral joint, proper glenoid fossa angle (forward and upward), and proper scapular alignment with the vertebral column. The joint is stabilized by musculature (ie, supraspinatus, deltoid, latissimus) and, to a smaller degree, the shoulder capsule, which supports the humerus. If any of these components are disrupted during the recovery process, then shoulder function may be compromised or a painful shoulder may result. Flaccid stage This stage of areflexia includes loss of muscle tone and volitional motor activity, variable sensory loss, and loss of muscle stretch reflexes. The shoulder capsule is thin and is composed of 2 tissue layers. Spastic stage As stroke recovery evolves, flaccidity may progress to spasticity. Following a stroke, the connections that control these reflexes can be interrupted, resulting in the release of these basic patterns and the evolution of spasticity and synergy patterns. If the neurologic deficits become severe enough, primitive tonic neck reflexes may develop. Biceps brachii spasticity further depresses the head of the humerus and flexes the elbow. As spasticity and synergy evolve, Teasell notes there is a failure of the antagonist muscles to relax when the agonist muscles contract, thus creating cocontraction. The muscles causing downward and outward rotation of the scapula, the rhomboids, overwhelm the trapezius and serratus anterior muscles. Spastic unilateral paraspinal muscles overwhelm those on the contralateral side, causing lateral flexion of the spine toward the affected side. Synergy stage If neurologic impairment of the completed stroke progresses, synergy patterns, which tend to worsen with initiated efforts, may emerge. The restrictions created by the synergy patterns create therapeutic challenges to attaining meaningful UE function. Upper extremity flexor synergy patterns include (1)

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shoulder/scapular depression (downward rotation and retraction), (2) humeral adduction/internal rotation, (3) elbow flexion, (4) forearm pronation (rarely supination), and (5) wrist/finger flexion (thumb-in-hand position). When treating patients in flexion synergy, aim therapy at retraining the overwhelmed agonists, stressing the desired components of function, and releasing the uninhibited flexion patterns by initiating opposite movements at the "key points of control." Clinical History Common symptoms of the shoulder/UE reported by patients with hemiplegia may include the following: Reduced mobility of the shoulder Tenderness Swelling/edema Pain with movement Decreased coordination Physical o Pain with motion o Decreased range of motion (ROM) o Decreased reflexes o External and clinical methods for measuring subluxation (Boyd, 1992) include the following: Assess arm function - Action Research Arm Test Evaluation of shoulder pain o Shoulder lateral rotation ROM to the point of pain (SROMP) Evaluate for complex regional pain syndrome (CRPS) Neurologic examination o Manual muscle testing Assess strength and tone Evaluate spasticity (Modified Ashworth scale) o Sensory evaluation

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Vibration o Reflexes o Fugl-Meyer index to test motor performance Causes Glenohumeral subluxation

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Subluxation is a common problem in patients with hemiplegia, especially during the flaccid stage, and often occurs within 3 weeks poststroke. o Subluxation appears to be caused by the weight of the flaccid arm applying direct mechanical stretch to the joint capsule as well as traction to unsupportive muscles of the shoulder. Teasell suggests that other factors contributing to subluxation include improper positioning, lack of support in the upright position, and pulling on the hemiplegic arm when transferring the patient. o Controversy exists as to an association between shoulder subluxation and pain. Subluxation has been a commonly sited cause of shoulder pain and disability, with Yu et al reporting that longitudinal data suggests a correlation between early subluxation and shoulder pain. However, Bohannon et al have found no significant correlation between the presence of subluxation and the occurrence of pain, while Wanklyn et al have found no association between the severity of subluxation and the degree of pain. Numerous cases of subluxation without pain have been documented, as well as cases of a painful shoulder without subluxation. o A correlation between subluxation and RSD also has been studied. Dursun et al found that subluxation was present in 74.3% of patients with RSD and 40% of patients without RSD; of these same patients, 78.6% with subluxation and 38.1% without subluxation reported shoulder pain. Dursun concluded that shoulder subluxation might be a causative factor of RSD as well as shoulder pain. Bohannon et al found that performing shoulder palpation to help diagnose subluxation can be reliably graded, with good interrater reliability and good correlation with more precise radiographic measurements. o Treatment of subluxation by reduction remains a controversial means of controlling shoulder pain. Sling use also may cause lateral subluxation, impair proprioception, interfere with functional activities, or promote undesirable synergy patterns; furthermore, sling use may not prove beneficial in preventing shoulder subluxation. Even though sling use and other supportive devices remain controversial, Yu et al report that treatment of shoulder subluxation continues to be the standard of care for several reasons, including the following: Painful shoulder subluxation most commonly is present when the UE is in a dependent position. Painful shoulder subluxation improves with joint reduction. Early prevention is warranted since chronic shoulder pain often is refractory to treatment. Subluxation may inhibit functional recovery by limiting shoulder ROM. Yu et al demonstrated substantial reduction in subluxation, and possibly enhancement of motor recovery

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and reduction of shoulder pain. o Spasticity is defined as a velocity-sensitive disorder of motor function causing increased resistance to passive stretch of muscles and hyperactive muscle stretch reflexes. o Van Ouwenaller identified spasticity as a prime factor and one of the most common causes of shoulder pain in patients with hemiplegia. Compared to patients with flaccidity, patients with spasticity seem to experience a much higher incidence of shoulder pain, which is thought to be the result of muscle imbalance. The muscles found to predominate the synergy pattern in the shoulder include the adductors (ie, teres major, latissimus dorsi), and to a greater extent, the internal rotators (ie, subscapularis, pectoralis major). Bohannon et al reports finding external rotation to correlate most with hemiplegic shoulder pain. o The mainstay of treatment for spasticity begins with physical therapy and the use of ROM and stretching exercises, although overly aggressive stretching should be avoided. If conservative treatment fails, then the use of motor point blocks have been advocated as an effective means for improving pain, ROM, and possibly function. Complex regional pain syndrome (shoulder-hand syndrome, RSD, causalgia, sympathetically maintained pain, Sudeck atrophy, minor dystrophy) o The International Association for the Study of Pain has advocated using the terms complex regional pain syndromes (CRPS) type 1 (RSD) and type 2 (causalgia). Davis et al report that CRPS occurs in 12.5% of patients who have had a stroke, while Chalsen et al report the incidence as 61%. Davis et al demonstrated that of those patients developing CRPS, 65% had done so by 3 months poststroke, and 98% had done so by 5 months poststroke. Snider reports that about 5-8% of patients have an incomplete nerve injury. Other factors may include UE immobilization, myocardial infarction, stroke, rotator cuff tear, shoulder spasticity, and glenohumeral joint subluxation. o For the best prognosis, early recognition and prompt treatment are essential for patients with CRPS. Treatment options are numerous, with physical therapy as the cornerstone. ROM exercises, optimal positioning of the limb, and avoiding painful stimuli are all suggested. Kingery reports that the prognosis for resolution with preserved ROM is better in patients with some voluntary movements, with less spasticity, and without significant sensory loss. Nearly 35% of patients with CRPS type 1 have symptom resolution in one year. Adhesive capsulitis o Glenohumeral capsulitis is postulated to play an important role in hemiplegic shoulder pain. Patients usually present with pain and limited passive movement of the shoulder, especially external rotation and abduction. o Joynt et al report that adhesive changes may reflect a later stage in the recovery process when chronic irritation or injury, inflammation, or lack of movement eventually results in adhesions. o When Rizk et al performed shoulder arthrography in 30 patients with hemiplegic shoulder pain, they found changes consistent only with capsular restriction typical of adhesive capsulitis in 77% of subjects. This finding suggests an association between adhesive changes and shoulder pain.

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o A study by Wanklyn et al also found an association between reduced ROM (specifically external rotation) and hemiplegic shoulder pain, with an incidence as high as 66%. Because diminished ROM of shoulder spasticity and adhesive capsulitis present similarly, it is often difficult to distinguish between pain in the limited hemiplegic shoulder based on capsulitis, spasticity, or a combination. Subacromial bursitis o Some patients with hemiplegia complain of lateral shoulder pain that radiates down the arm when moved. o Joynt et al demonstrated that injecting 10 mL of 1% lidocaine into the subjective pain sites related to at least moderate pain relief at the subacromial injection site and improved ROM in 50% of the patients. Brachial plexus traction neuropathies/injury o Wanklyn et al reported a 27% increased incidence of shoulder pain in dependent patients after discharge, which may reflect improper handling at home by caregivers. Kaplan suggests that plexus injury should be considered in a patient who has atypical return of distal function. Neglect Snels et al have found that on numerous occasions, patients with sensory deficits, visual field deficits, or neglect more commonly experience recurrent injuries of the shoulder, possibly contributing to capsulitis. o Treatment options suggested by Lorish et al include caloric stimulation, prism glasses, visuospatial cueing, computer-assisted training, and compensatory strategies. Thalamic syndrome (central poststroke pain, analgesia dolorosa, Dejerine-Roussy syndrome) Patients describe the pain as burning, tingling ("pins and needles"), sharp, shooting, stabbing, gnawing, dull, or achy. This pain often is refractory to treatment. o The patient also relates experiencing hyperpathia (an exaggerated pain reaction to mild external cutaneous stimulation). Other treatment alternatives include sympathetic blockade, guanethidine block, as well as psychological evaluation and treatment. Soft tissue injury/trauma o Soft tissue trauma often is a result of uncontrolled ROM exercises, poor positioning of the hemiplegic patient, or improper transfer technique. o Kumar et al showed that 62% of their patients using an overhead pulley system for therapy and performing ROM exercises experienced shoulder pain irrespective of other pathology, thus demonstrating that overaggressive stretching or ROM should be avoided during the rehabilitation process. o Patients with poor cognition, neglect, and other sensory deficits tend to be predisposed to traumatic injuries to the affected extremity. o Through the use of shoulder arthrography, Najenson et al demonstrated an incidence of rotator cuff tear in patients who were poststroke and were experiencing shoulder pain to be as high as 40% on the affected side, compared to only 16% on the unaffected side. o Other studies, including one by Joynt et al, have revealed no incidence of rotator cuff tear with

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Treatment Physical Therapy Therapy during the flaccid stage

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hemiplegic shoulder pain. Teasell reports that hemiplegic shoulder pain is not commonly associated with a rotator cuff disorder.

Arm support and preservation of joint ROM is performed through early passive motion. Before active rehabilitation exercises of the extremities are started, Cailliet suggests initiating trunk motions with sideto-side rolling. As the patient progresses from the supine to the prone position, attempt to maintain the patient in reflex-inhibiting positions. Upon regaining the seated position, the patient begins gentle weight-bearing exercises through the impaired arm with the elbow and wrist extended, causing glenohumeral joint reduction and proprioceptive stimulation to the shoulder. Sensory stimulation, as well as NMES, can be used to initiate sensory-motor reeducation. Therapy during the spastic stage A major goal of early stroke management is the prevention of muscle spasticity that could interfere with the patient's potential for regaining function. As muscle tone returns to the hemiplegic limb, spasticity may progressively increase. Development of motor control The recruitment patterns of individual motor units in these affected muscles are slow and inconsistent. More conventional rehabilitation methods involve reeducating weak muscles by strengthening and stretching. Neurodevelopmental technique Developed by the Bobaths for the treatment of cerebral palsy, the neurodevelopmental technique (NDT) is probably the most widely accepted method used in the development of motor control in patients with hemiplegia. Brennan relates that exercises that promote normal muscle tone and diminish excessive spasticity through the use of reflex-inhibiting postures are performed and allow the patient to feel normal movements while preventing the use of compensatory motions. Sensorimotor integration So theoretically, if motor recovery does in fact depend on motor relearning, then optimal therapies can be tailored for individual patient needs through treatments performed by robotic devices. Overall, Volpe believes that "focused sensorimotor exercise appears to produce better motor outcome." Functional utilization of evolving synergies Assuming normal stages of recovery following stroke, Brunnstrom encouraged reflex tensing in order to develop flexor and extensor synergies during early recovery. Functional utilization uses techniques such as tonic stretches and voice commands to elicit muscle contractions. Motor relearning program Developed by Carr and Shephard, this practical method emphasizes motor relearning by practicing taskspecific motor activities while sitting, standing, or walking. Therapists analyze each task, determine which components the patient cannot perform or has difficulty performing, trains the patient in those components of the task, and ensures carryover of this training during daily activities. Brennan has maintained that ultimately, treatment focuses on eliminating unnecessary muscle activity, subsequently expediting skilled motor activities. Biofeedback

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Proprioceptive neuromuscular facilitation

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Developed by Kabat, Knott, and Voss, proprioceptive neuromuscular facilitation (PNF) involves repeated muscle activation of the limbs by quick stretching, traction, approximation, and maximal manual resistance in functional directions (ie, spiral and diagonal patterns) to assist with motor relearning and increasing sensory input. Brennan asserts that it is based on the principles of normal human development (ie, mass movements precede individual movements, reflexive movements precede volitional movements, developments occur cephalically to caudally, control is gained proximally prior to distally, the timing of normal movements is distal to proximal). Lorish and coauthors have considered it to be an optimal method of stretching in patients with hemiplegia. In an attempt to relax spastic antagonist muscle groups, rhythmic stabilization can be used, which involves alternating voluntary contractions of agonist and antagonist muscles. However, Brandstater revealed PNF to be more effective when muscle weakness is not due to upper motor neuron lesions. Active repetition Parry and coworkers found that stroke patients who were less severely impaired (ie, possessed some early volitional arm movement) prior to treatment benefited from the use of early additional therapies that involved repetitive movements and functional tasks. However, patients with severe arm impairment showed very little improvement in function irrespective of receiving additional therapies. This data supports previous clinical trials that suggest there is no current physical therapy approach that results in sustained improvements of upper limb function in patients who are severely impaired. Patient should visualize (ie, mirror) specific movements. Position the UE to decrease scapular depression and retraction. Apply sensory stimulation simultaneously to movements. Use prone exercises to stimulate righting reflexes that tend to imitate primitive motor function. Start seated and standing stimulation exercises to help decrease subluxation and modify synergy patterns. Avoid vigorous traction on the arm when stretching connective tissue around the spastic joint. Use of electric stimulation can enhance muscle relaxation. Use the functional arm to simultaneously train the paretic arm to improve ROM and proprioceptive stimulation. Use modalities (eg, ice, transcutaneous electrical nerve stimulation [TENS], vibration) to diminish spasticity.

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