Background: Good shoulder function is a prerequisite for effective hand function, as well as for performing multiple tasks involving mobility, ambulation, and activities of daily living (ADL). 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.
Most studies have speculated about the etiology of shoulder pain in hemiplegia but have failed to establish a cause-and-effect relationship. 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). However, identifying the exact mechanism(s) of shoulder pain can be inherently difficult, with many of the current treatment regimens varying according to assumptions made about its cause. 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. Chae et al indicate that the amount of motor recovery is related to the degree of initial severity and the amount of time before voluntary movements are initiated. Numerous neurofacilitative treatments have been developed in hopes of improving the quality and decreasing the amount of time to recovery. Unfortunately, Chae et al have found that the length of stay at most acute inpatient rehabilitation facilities is shortening, with restoration of maximal function involving the use of compensatory strategies as the primary means for treatment rather than the restoration of motor control.
Pathophysiology: 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. The trapezius, serratus anterior, and rhomboids provide proper scapular alignment. The latissimus also works to depress the scapula. Erector spinae muscle tone, along with the righting reflex, maintains the vertebral column in an upright alignment. If any of these components are disrupted during the recovery process, then shoulder function may be compromised or a painful shoulder may result.
Following a stroke, the brain and body progress through the following series of stages, which are discussed in detail by Cailliet: (1) transischemic attack, (2) flaccidity, (3) spasticity, and (4) synergy. A gradual progression from one stage to the next usually occurs, but they are not mutually exclusive of one another, and they can occur simultaneously in the affected limb.
Once the inciting injury to the brain occurs, the flaccid stage evolves with a state of areflexia. This stage of areflexia includes loss of muscle tone and volitional motor activity, variable sensory loss, and loss of muscle stretch reflexes.
Muscular support of the humeral head in the glenoid fossa by the supraspinatus and deltoid muscles is lost. This leads to downward and outward subluxation of the humeral head, with the only support coming from the joint capsule. The shoulder capsule is thin and is composed of 2 tissue layers. The inner synovial layer, the stratum synovium, is highly vascular but poorly innervated, making it insensitive to pain but highly reactive to heat and cold. The outer layer, the stratum fibrosum, is poorly vascularized but richly innervated, predisposing it to pain from stretch. For this reason, Faghri et al suggest that added capsular stretch in a flaccid shoulder may predispose the capsule to irreversible damage and the shoulder to pain.
Flaccidity of the trapezius, rhomboids, and serratus anterior muscles leads to depression, protraction, and downward rotation of the scapula, which Cailliet believes leads to significant angular changes of the glenoid fossa, subsequently contributing to subluxation. Also, the spine begins to flex laterally toward the hemiparetic side because of the elimination of the righting reflex, further altering the scapulothoracic relationship.
However, Prevost et al compared the affected and unaffected shoulders by using a 3-dimensional radiographic technique that determines the true position of the humeral head in relation to the scapula. This technique revealed less downward rotation of the glenoid fossa than originally expected, and no significant relationship was found between the extent of scapular orientation and the severity of subluxation (Prevost, 1987; Culham, 1995). Subsequently, it was concluded that scapular position does not contribute as much to inferior subluxation as was originally thought. Teasell points out that this now appears to be the most widely accepted viewpoint.
As stroke recovery evolves, flaccidity may progress to spasticity. Cailliet explains that normally, the brainstem contains upper extremity (UE) flexor patterns and lower extremity (LE) extensor patterns that are refined and coordinated by the premotor and neocortexes. 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. When primitive tonic neck reflexes are present, the elbow extends when the head turns toward the affected side, and the elbow flexes when the head turns away. The presence of primitive tonic neck reflexes is considered prognostically unfavorable for motor recovery.
The first evidence of UE spasticity is internal rotation of the humerus from the subscapularis and pectoralis major, with a debate as to which muscle contributes stronger to this pattern. This pattern may then progress into the forearm pronators (ie, pronator quadratus, pronator teres, flexor carpi radialis). Spastic involvement of the rhomboids leads to scapular depression and downward rotation, while the latissimus dorsi contributes to adduction, extension, and internal rotation of the humerus. 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. For example, during internal rotation, excessive spasticity of the internal rotators of the humerus (ie, subscapularis, pectoralis major, latissimus, teres major) overwhelms the external rotators (ie, supraspinatus, infraspinatus, teres minor). 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.
If neurologic impairment of the completed stroke progresses, synergy patterns, which tend to worsen with initiated efforts, may emerge. Cailliet proposes that the synergy component that usually occurs first is spastic elbow flexion; the shoulder phase is weaker and usually requires a more reflexive status to occur. The restrictions created by the synergy patterns create therapeutic challenges to attaining meaningful UE function. Upper extremity flexor synergy patterns include (1) 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.”
Other clinical trials report a general incidence of shoulder pain in patients with hemiplegic stroke as 16-84% (Forster, 1994; Najenson, 1971), while that for shoulder subluxation has been found to be as high as 81% (Najenson, 1971).
Reflex sympathetic dystrophy (RSD) also appears to be a relatively common complication of hemiplegia, with Van Ouwenaller reporting an incidence of 27% in patients with spasticity versus 7% of those with flaccidity. Other sources report an incidence of 12.5-61%.
History: Obtaining an accurate and detailed history is an important part of the examination. For those patients who have difficulty with communication, the history may be provided by a family member. Common symptoms of the shoulder/UE reported by patients with hemiplegia may include the following:
Physical: The physical examination of a patient with shoulder dysfunction associated with hemiplegia is extensive, as the physician is required to assess the involved musculoskeletal and neurological conditions. Suggested clinical tests and evaluations include the following: