Hemiplegic shoulder pain is a common complaint for stroke survivors. Many pathologies are included in the diagnosis of hemiplegic shoulder pain, and many with shoulder pain have a multifactorial cause. This article provides rehabilitation specialists with an approach to evaluation and management of those with hemiplegic shoulder pain.
Key points
- •
Hemiplegic shoulder pain (HSP): Shoulder pain is common after stroke, and it interferes with recovery and lowers quality of life. Multiple causes may contribute, with many experiencing multiple concurrent pathologies.
- •
Diagnosis: Careful history taking, musculoskeletal examination, and neurologic examinations must be performed. Imaging may aid in diagnosing some causes, although asymptomatic anatomic abnormalities may lead to misdiagnosis.
- •
Treatment: Conservative treatments should be attempted first, with emphasis on improving the biomechanics of the shoulder and function. Pain should be controlled with both nonpharmacologic and pharmacologic approaches. Some may benefit from more invasive treatments.
Introduction
The prevalence of HSP among stroke survivors is as high as 84%, although estimates vary depending on study methods. Shoulder pain may develop early in the course of recovery, with an estimated prevalence of 17% in the first week, and remains elevated throughout recovery with 20% to 24% experiencing it from 1 to 16 months after stroke. The prevalence in rehabilitation settings may be higher because this population has a greater number of associated risk factors for shoulder pain. Early diagnosis and appropriate treatment lead to resolution of symptoms in most patients; however, up to 32% of moderate to severely impaired stroke survivors have shoulder pain many years after their stroke.
Shoulder pain after stroke is not limited to a single pathology, and many will be affected by more than one pathologic condition, creating a multifactorial pain syndrome. The myriad of causes that have been reported includes impingement syndrome, rotator cuff dysfunction, tendinopathy, bursitis, adhesive capsulitis, peripheral nerve injuries, complex regional pain syndrome (CRPS), spasticity, central hypersensitivity, and contractures. Similarly, many different risk factors for shoulder pain have also been reported in the literature. The severity of motor impairment is one of the most frequently reported risk factors and also underlies other risks. The literature has also identified the duration of motor impairment, sensory impairment, reduced range of motion, spasticity, central sensitization, soft tissue injuries, and comorbidities such as diabetes mellitus as increasing the risk of shoulder pain. Shoulder pain is also common among those without neurologic injury, which makes it likely that stroke survivors may experience shoulder pain that is not related to their stroke.
Introduction
The prevalence of HSP among stroke survivors is as high as 84%, although estimates vary depending on study methods. Shoulder pain may develop early in the course of recovery, with an estimated prevalence of 17% in the first week, and remains elevated throughout recovery with 20% to 24% experiencing it from 1 to 16 months after stroke. The prevalence in rehabilitation settings may be higher because this population has a greater number of associated risk factors for shoulder pain. Early diagnosis and appropriate treatment lead to resolution of symptoms in most patients; however, up to 32% of moderate to severely impaired stroke survivors have shoulder pain many years after their stroke.
Shoulder pain after stroke is not limited to a single pathology, and many will be affected by more than one pathologic condition, creating a multifactorial pain syndrome. The myriad of causes that have been reported includes impingement syndrome, rotator cuff dysfunction, tendinopathy, bursitis, adhesive capsulitis, peripheral nerve injuries, complex regional pain syndrome (CRPS), spasticity, central hypersensitivity, and contractures. Similarly, many different risk factors for shoulder pain have also been reported in the literature. The severity of motor impairment is one of the most frequently reported risk factors and also underlies other risks. The literature has also identified the duration of motor impairment, sensory impairment, reduced range of motion, spasticity, central sensitization, soft tissue injuries, and comorbidities such as diabetes mellitus as increasing the risk of shoulder pain. Shoulder pain is also common among those without neurologic injury, which makes it likely that stroke survivors may experience shoulder pain that is not related to their stroke.
Patient evaluation overview
The approach to evaluation of a painful hemiplegic shoulder should begin with a history and physical examination, including neurologic examination of the central and peripheral nervous system of the upper limbs, active and passive range of motion, scapular motion, and careful palpation of potential anatomic structures that might generate pain. It is important to gather information from the patient or caregiver regarding prior injuries to the shoulder or premorbid symptoms that might have worsened. Salient features of the examination are described in the following sections relative to specific causes. HSP has neither a standard clinical definition nor a validated clinical examination. Providers need to be aware that many with HSP may have multiple underlying pathologies, may have noncontributory anatomic abnormalities, or may have overriding stroke-related symptoms that make precise diagnosis impossible. It may be helpful to consider the following systematic approach to integrating potential underlying pathologies in HSP: (1) impaired motor control, (2) soft tissue lesions, and (3) altered peripheral and central nervous activity ( Box 1 ).
Impaired motor control and tone changes
Flaccidity
Spasticity
Loss of motor function
Glenohumeral subluxation
Scapular dyskinesis
Spasticity of shoulder muscles
Soft tissue lesions
Impingement syndrome, rotator cuff tendinopathy
Bicipital tendinopathy
Adhesive capsulitis
Myofascial pain
Altered peripheral and central nervous activity
Peripheral nerve entrapment
Complex regional pain syndrome
Central poststroke pain
Central hypersensitivity
Impaired Motor Control and Tone Changes
Glenohumeral subluxation
Glenohumeral subluxation has been reported to occur in up to 81% of stroke survivors. Subluxation can be measured with the patient seated and the arm in a dependent position allowing the weight of the limb to distract the humeral head from the glenoid fossa. Subluxation can be measured by the number of fingerbreadths between the acromion and humeral head, or by radiographs, computed tomography, ultrasonography, and MRI. The fingerbreadth measurement is adequate in clinical practice because the relationship between subluxation and pain remains controversial. Some studies show an association between subluxation and pain, whereas others have demonstrated no association. It is likely that subluxation predisposes the shoulder to other types of painful pathologies such as CRPS, peripheral neuropathies, and rotator cuff injury.
Scapular dyskinesis
The impaired strength, unbalanced tone, and lack of control of the hemiplegic shoulder can disrupt the timed and coordinated movements known as scapulohumeral rhythm that can increase the risk for HSP. Aberrant recruitment of the infraspinatus muscle, serratus anterior muscle, and inferior trapezius muscles that stabilize the scapula during humeral movement have been found in those with HSP compared with pain-free stroke survivors, and the aberrant patterns are similar to recruitment patterns seen in nonstroke impingement syndrome of the shoulder. Evidence of impaired shoulder control can be detected with observation of scapular movement, with comparison with the unaffected shoulder, during a clinical examination and characterized into specific patterns ( Table 1 ), although the reliability in stroke survivors is unknown. Further evidence for scapular dyskinesis can be detected with improvement in symptoms during range of motion with the scapular repositioning test and the scapular assistance test.
| Inferior angle (type I) | At rest: prominence of inferior medial scapular border During arm motion: dorsal tilt of inferior angle, ventral tilt of acromion Axis of the rotation: horizontal plane |
| Medial border (type II) | At rest: prominence of entire medial border During arm motion: dorsal tilt of medial scapular border Axis of rotation: vertical in the frontal plane |
| Superior border (type III) | At rest: elevation of superior border with possible anterior displacement During arm motion: shoulder shrug initiates movement without significant winging Axis of rotation: sagittal plane |
Spastic shoulder muscles
Upper motor neuron lesions can result in a movement disorder characterized by a velocity-dependent resistance to passive stretching known as spasticity. The spasticity affects not only muscles at the shoulder but also the scapular stabilizers. The typical pattern of spasticity of the upper limb after stroke is internal rotation and adduction of the shoulder with flexion at the elbow, the wrist, and the fingers. The result is impairment in active and passive movement to varying degrees and impaired control of shoulder motion that can cause injury. The adducted humerus coupled with an increase in tone in the trapezius and rhomboids that impairs scapular elevation increases the risk of shoulder impingement and can lead to pain. Constant pull of adductors can also increase the strain of muscles on their attachment sites to bone, also causing pain. It is common for spasticity to lead to contractures of the shoulder that can be associated with pain during movement, although the pain might also be due to spasticity resulting from stretch.
Clinical evaluation of spasticity can be performed with the use of a descriptive scale. The Modified Ashworth Scale is frequently used and qualitatively describes the increase in resistance encountered during passive stretch. The Modified Ashworth Scale is an efficient, reliable, and simple measurement scale, although it has the downside of not ascribing a reason for any increase in resistance around a joint. For example, the scale does not discern between spasticity and other causes of increased resistance to passive stretch, such as contractures and rigidity.
Soft Tissue Lesions
The evaluation of a patient with shoulder pain should include provocative maneuvers in addition to a standard physical examination that includes range of motion and neurologic evaluation of the upper limb ( Table 2 ). Many causes of shoulder pain overlap, and imaging or other diagnostic studies may be beneficial.
| Impingement Syndrome/Rotator Cuff Tendinopathy | Bicipital Tendinopathy | Adhesive Capsulitis | Myofascial Pain | |
|---|---|---|---|---|
| Examination | Positive result of abduction test Positive result of drop arm test Presence of Neer sign Positive result of Hawkin test | Positive result of Yergason test Positive result of Speed test | External rotation <15° Early scapular motion | Palpation of shoulder and scapular muscles |
| Diagnostic test | Subacromial lidocaine injection MRI Ultrasonography | Tendon sheath injection of lidocaine | MRI Arthrogram | None |
Impingement syndrome and rotator cuff injury
Impingement syndrome is often thought of as an injury to the supraspinatus muscle or tendon resulting from repetitive compression between the inferior border of the acromion and the greater tuberosity of the humerus, although it encompasses many injuries of the shoulder including rotator cuff tendinopathy, rotator cuff tears, and bursitis. Although not extensively studied as a cause for HSP, one cross-sectional study has found that half of those with chronic HSP have evidence of impingement syndrome. Biomechanical changes after stroke such as laxity of passive restraints due to subluxation, weakness of muscles that stabilize the joint, abnormal muscle tone, and motor recovery in a proximal to distal gradient may place stroke survivors at greater risk for impingement syndrome and rotator cuff injury.
Imaging studies may be particularly helpful in identifying anatomic abnormality of the shoulder in those with HSP, although the presence of a tear or a tendinopathy is not related to the severity of pain. Recent MRI studies comparing those with shoulder pain with a pain-free group did not find differences in the prevalence of rotator cuff pathology or subacromial bursitis. Impingement syndrome and rotator cuff injuries may be common in those with stroke because they are common in the general population and the incidence increases with age. The high prevalence of rotator cuff pathology in asymptomatic patients increases the risk of misdiagnosis in those with shoulder pain after stroke.
Bicipital tendinopathy
The prevalence of bicipital tendinopathy in those with HSP is estimated between 7% and 54%. Bicepital tendinopathy is more likely in those with spasticity or movement synergies that result in greater activation of the biceps as an elbow flexor or a forearm supinator. The diagnosis is suggested when there is greater tenderness to palpation of the long head of the biceps at the anterior shoulder compared with the unaffected side. Provocative maneuvers, such as Yergason test that provokes pain at the anterior shoulder with resisted forearm supination, can be useful when the patient is able to participate. Imaging may also identify abnormalities of the long head of the biceps, although the findings may not correlate with pain in the acute phase of recovery in spite of the prevalence approaching 40%. Injection of an anesthetic agent at the point that is most painful over the bicipital groove can also provide evidence of the diagnosis if resulting in pain relief.
Adhesive capsulitis
Adhesive capsulitis is characterized by shoulder pain with gradual loss of range of motion because of shortening and thickening of the glenohumeral joint capsule along with adhesions of the capsule. In addition to shoulder pain with range of motion testing, the primary physical finding is a reduction in external rotation. Unfortunately, pain and reduced range of motion are also found with other pathologies in those with HSP, such as pain with spasticity. The prevalence of thickening and synovial membrane contrast enhancement on MRI is higher in those with HSP than in pain-free controls ; however, adhesive changes have been found in over 30% of stroke survivors in the contralateral shoulders when evaluated with arthography.
Myofascial pain
Myofascial pain is commonly associated with shoulder pain in those with HSP and nonstroke shoulder pain. Precipitating factors of myofascial pain, such as trauma, poor posture, muscle imbalance, degenerative changes, and stress, are common in those with stroke. Myofascial pain may be secondary to another condition, but the muscles may be pain generators contributing to the overall condition. Typical findings are hyperalgesic muscles around the shoulder, neck, and scapular stabilizers that exhibit taught bands, tender points, and trigger points that may result in referred pain.
Altered Peripheral and Central Nervous Activity
Peripheral nerve entrapment
Brachial plexus injury and other peripheral nerve injuries in HSP are difficult to diagnose because of the overlap with prominent symptoms due to the central nervous system (CNS) damage from the stroke, as well as because of limitations of electrodiagnostic studies in diagnosing proximal lesions. It has been hypothesized that injury to peripheral nerves may occur because of traction caused by inferior subluxation, trauma incurred as a result of hemiplegia, or trauma incurred through incorrect transfers. To date, electrophysiologic studies have been mixed in support of peripheral nerve injury as the cause of HSP, although it should be considered if a mechanism for injury is present or with findings of lower motor neuron injury in the setting of shoulder subluxation.
Complex regional pain syndrome
CRPS after stroke generally refers to CRPS type I because it follows CNS injury rather than damage to a peripheral nerve. The prevalence of CRPS type I in hemiplegia ranges from 12.5% to 70%, reflecting differences in study design and inclusion of study cohorts before routine treatment in rehabilitation centers. Risk factors for CRPS type I include motor impairment and trauma related to altered shoulder biomechanics. Other risk factors might exist and are not yet known because the pathophysiology of CRPS type I has not yet been elucidated. The diagnosis of CRPS type I is based on clinical examination and can be aided by standardized criteria ( Box 2 ). Triple-phase bone scan has been recommended as an adjunct diagnostic tool, although the highest sensitivity may be during the acute phase of CRPS type I.
- 1.
Continuing pain, which is disproportionate to any inciting event
- 2.
Must report at least 1 symptom in 3 of the 4 following categories:
- •
Sensory: Reports of hyperalgesia and/or allodynia
- •
Vasomotor: Reports of temperature asymmetry, skin color changes, and/or skin color asymmetry
- •
Sudomotor/edema: Reports of edema, sweating changes, and/or sweating asymmetry
- •
Motor/trophic: Reports of decreased range of motion, motor dysfunction (weakness, tremor, dystonia), and/or trophic changes (hair, nail, skin)
- •
- 3.
Must display at least 1 sign a at the time of evaluation in 2 or more of the following categories:
- •
Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch, deep somatic pressure, and/or joint movement).
- •
Vasomotor: Evidence of temperature asymmetry, skin color changes, and/or asymmetry
- •
Sudomotor/edema: Evidence of edema, sweating changes, and/or sweating asymmetry
- •
Motor/trophic: Evidence of decreased range of motion, motor dysfunction (weakness, tremor, dystonia), and/or trophic changes (hair, nail, skin)
- •
- 4.
There is no other diagnosis that better explains the signs and symptoms
a A sign is counted only if it is observed at the time of diagnosis.
Central poststroke pain
Formerly known as thalamic pain syndrome, central poststroke pain (CPSP) is a neuropathic pain syndrome that can arise from a stroke within the spinothalamocortical pathway, and most with CPSP have multiple lesions on MRI. The pain may be due to the lesion, although it might also be caused by neuroplasticity that occurs after the stroke. Typically the pain arises gradually, within the first month after stroke, although it may arise many months later. If pain arises more than 12 months after stroke, it might be reasonable to look for a new cause, including a new stroke. The clinical presentation of CPSP can be variable, including multiple sensations within a single individual, making diagnosis difficult. An algorithm to improve the diagnosis has been proposed ( Box 3 ), although standard diagnostic criteria for CPSP have not been established.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
