Residency · Residency · Physical Medicine Rehabilitation
Post-Stroke Shoulder Pain and Subluxation
Epidemiology and Significance
Hemiplegic shoulder pain (HSP) affects 22-72% of stroke survivors. Onset can be immediate or delayed weeks to months post-stroke. HSP is a major barrier to rehabilitation participation and functional recovery. Associated with longer hospital stays, poorer functional outcomes, and reduced quality of life.
Often multifactorial with more than one pain generator contributing simultaneously. Prevention is far more effective than treatment.
Etiology of Hemiplegic Shoulder Pain
Glenohumeral Subluxation
Inferior subluxation is most common; results from flaccid paralysis of the rotator cuff and deltoid. The weight of the flaccid arm creates a downward distraction force. Supraspinatus and posterior deltoid are the primary suspensory muscles. Subluxation develops in the early flaccid stage (days to weeks).
Measured clinically by finger-breadths between acromion and humeral head, or by radiograph. Subluxation itself may not be painful; the relationship between subluxation and pain is inconsistent. Subluxation may predispose to capsular stretching, brachial plexus traction, and rotator cuff injury.
Rotator Cuff Injury
Impingement syndromes are common due to altered scapulohumeral rhythm. Rotator cuff tears may result from improper handling and range of motion techniques. Supraspinatus and bicipital tendinopathy from repetitive overhead positioning during therapy. Ultrasound studies show high rates of rotator cuff pathology in hemiplegic shoulders.
Adhesive Capsulitis (Frozen Shoulder)
Develops from immobility and limited active ROM. Progressive capsular fibrosis and contracture. Loss of external rotation is the earliest and most prominent finding. More common in patients with prolonged flaccidity followed by spasticity. Prevention through early ROM exercises is critical.
Spasticity-Related Pain
Spastic internal rotators and adductors create abnormal shoulder positioning. Subscapularis, pectoralis major, and latissimus dorsi spasticity. Painful muscle spasms, particularly at night. Sustained abnormal posturing leads to soft tissue shortening.
Complex Regional Pain Syndrome (CRPS)
Previously termed "shoulder-hand syndrome". Type I CRPS can develop after stroke, affecting the shoulder, hand, or both. Features: burning pain, allodynia, edema, vasomotor changes, sudomotor changes, trophic changes. Incidence estimated at 10-30% of stroke survivors with shoulder pain. May be underdiagnosed; maintain high clinical suspicion.
Brachial Plexus Traction Injury
Stretching of the brachial plexus from glenohumeral subluxation or improper transfers. Flaccid arm without support is vulnerable to traction during transfers and repositioning. May cause neuropathic pain and additional weakness.
Central Post-Stroke Pain (Thalamic Pain)
Central neuropathic pain from stroke affecting the spinothalamocortical pathway. Burning, aching, or lancinating pain contralateral to the lesion. May include the shoulder but typically involves larger body regions. Allodynia and hyperalgesia are characteristic. Different mechanism from peripheral causes; requires neuropathic pain management.
| Etiology | Key Features | Timing | Primary Treatment |
|---|---|---|---|
| Subluxation | Inferior gap, flaccid stage | Days to weeks | Positioning, FES, sling |
| Rotator cuff injury | Impingement, improper handling | Weeks to months | ROM, injection, PT |
| Adhesive capsulitis | Loss of ER, immobility | Weeks to months | ROM, steroid injection |
| Spasticity | IR/adduction posturing, spasms | Weeks to months | Botulinum toxin, stretching |
| CRPS | Edema, allodynia, vasomotor changes | Variable | Graded motor imagery, steroids |
| Brachial plexus traction | Neuropathic pain, weakness | Early | Prevention, neuropathic agents |
| Central post-stroke pain | Burning, allodynia, large region | Variable | Gabapentinoids, TCA, SNRI |
<image>Illustration showing the multiple etiologies of hemiplegic shoulder pain including inferior glenohumeral subluxation with a gap between the acromion and humeral head, rotator cuff impingement from altered scapulohumeral mechanics, adhesive capsulitis with thickened capsule, and spastic muscle patterns causing internal rotation and adduction posturing</image>
Assessment
History
Timing of pain onset relative to stroke. Character of pain (nociceptive, neuropathic, mixed). Aggravating factors (ROM exercises, transfers, positioning). Impact on therapy participation and sleep. Previous shoulder pathology.
Physical Examination
Visual inspection: subluxation (sulcus sign), edema, atrophy, skin changes. Palpation: acromion-humeral head distance, tenderness over rotator cuff, bicipital groove. ROM: active and passive; note limitation pattern (capsular vs. non-capsular). Spasticity assessment: MAS of shoulder adductors, internal rotators, elbow flexors.
CRPS features: color changes, temperature asymmetry, edema, allodynia. Neurological examination: motor level, sensation, reflexes. Scapular position and mobility.
Imaging
Radiograph: quantify subluxation, exclude fracture, identify calcification. Ultrasound: rotator cuff integrity, bursal effusion, biceps tendon, dynamic assessment. MRI: rarely needed unless surgical pathology suspected; difficult to perform with hemiplegic positioning.
Electrodiagnosis
Consider if brachial plexus traction injury is suspected. Assess for axillary nerve injury (deltoid), suprascapular nerve injury (supraspinatus, infraspinatus). NCS and needle EMG of the affected upper extremity.
Prevention
Positioning
Support the affected arm at all times (lap tray, arm board, pillow). Shoulder in slight abduction, external rotation, and scapular protraction when supine. Avoid traction on the arm during transfers and repositioning. Proper wheelchair positioning: arm trough, lap tray, or hemi-sling during transport. Educate all nursing staff, therapists, and family members on proper handling.
Range of Motion
Gentle passive ROM beginning within the first few days post-stroke. Avoid aggressive overhead stretching (risk of impingement and rotator cuff injury). Scapulothoracic mobilization before glenohumeral ROM. Pain-free range only; never force ROM. Pulley exercises are contraindicated (inadequate scapular control, risk of impingement).
Sling Use
Indicated primarily for subluxation prevention during ambulation and transfers. Multiple sling types: hemisling, Bobath sling, GivMohr sling, shoulder orthosis. No single sling design has proven superior. Slings should NOT be worn during seated rest (promotes flexor synergy posturing).
Remove sling for therapy and ROM exercises. Evidence for sling use is limited; they address subluxation but may contribute to contracture if overused.
Electrical Stimulation for Subluxation Prevention
Surface or intramuscular electrical stimulation of the posterior deltoid and supraspinatus. Applied early in the flaccid stage to maintain muscle tone and prevent subluxation. Evidence supports reduction of subluxation and possibly pain when applied early. Optimal protocols: 4-6 hours/day for 4-6 weeks. FES may be more effective than slings for subluxation prevention.
<image>Demonstration of proper shoulder positioning and support strategies after stroke showing correct positioning in bed (slight abduction and external rotation with pillow support), in a wheelchair (arm trough with slight abduction), and during ambulation (appropriate sling type), contrasted with improper techniques that risk traction injury</image>
Treatment
Physical and Occupational Therapy
Active-assisted ROM progressing to active ROM as motor recovery allows. Scapular stabilization exercises. Therapeutic taping (kinesiotaping) for scapular repositioning. Neuromuscular re-education of rotator cuff and periscapular muscles.
Modalities: heat before stretching, ice after therapy, TENS for pain. Functional electrical stimulation integrated into task practice.
Pharmacologic Management
NSAIDs/acetaminophen: first-line for nociceptive pain. Neuropathic pain agents: gabapentin, pregabalin, duloxetine, amitriptyline (for CRPS or central pain). Muscle relaxants: tizanidine or baclofen if spasticity is a significant contributor. Topical agents: lidocaine patches, diclofenac gel.
Injection Therapies
Intra-articular corticosteroid injection: for adhesive capsulitis and glenohumeral synovitis. Subacromial-subdeltoid bursa injection: for impingement symptoms. Suprascapular nerve block: targets the primary sensory nerve of the shoulder (70% of shoulder joint innervation); effective for hemiplegic shoulder pain. Botulinum toxin injection: for spastic shoulder adductors and internal rotators (subscapularis, pectoralis major); reduces spasticity-related pain and improves ROM.
Management of Specific Etiologies
Adhesive Capsulitis
Aggressive but gentle ROM program. Intra-articular corticosteroid injection. Hydrodilatation (distension arthrography). Serial static stretching and joint mobilization. Consider manipulation under anesthesia for refractory cases (rarely needed).
CRPS Management
Graded motor imagery program. Mirror therapy. Desensitization techniques. Corticosteroid taper (short course, early CRPS).
Bisphosphonates (limited evidence). Stellate ganglion block (if sympathetically maintained pain). Aggressive physical and occupational therapy.
Spasticity Management
Botulinum toxin to spastic muscles (subscapularis, pectoralis major, biceps, brachialis). Oral antispasticity agents as adjuncts. Positioning and stretching programs. See Post-Stroke Spasticity Management topic for comprehensive approach.
Clinical Pearls
Prevention is the most important intervention: proper positioning, handling, and early ROM from day one. Pulley exercises are contraindicated in hemiplegic shoulder; they cause impingement without proper scapular control. Never pull on the hemiplegic arm during transfers; all staff and family must be trained. Subluxation and pain are NOT synonymous; treat pain generators individually.
Suprascapular nerve block is an underutilized and highly effective treatment for hemiplegic shoulder pain. Always assess for CRPS in a painful hemiplegic shoulder; hand edema, color changes, and allodynia are key clues. The hemiplegic shoulder often has multiple simultaneous pain generators; a comprehensive assessment and multimodal treatment plan are essential. Shoulder pain that limits therapy participation creates a vicious cycle of immobility, deconditioning, and further pain; aggressive pain management enables rehabilitation progress.
References
- Vasudevan JM, Browne BJ. Hemiplegic Shoulder Pain: An Approach to Diagnosis and Management. Phys Med Rehabil Clin N Am. 2014;25(2):411-437.
- Adey-Wakeling Z, Crotty M. Upper Limb Reduction of Subluxation and Pain After Stroke. Cochrane Database Syst Rev. 2013.
- Wilson RD, et al. Upper-Limb Recovery After Stroke: A Randomized Controlled Trial Comparing EMG-Triggered, Cyclic, and Sensory Electrical Stimulation. Neurorehabil Neural Repair. 2016;30(10):978-987.
- Winstein CJ, et al. Guidelines for Adult Stroke Rehabilitation and Recovery. Stroke. 2016;47(6):e98-e169.
- Snels IA, et al. Treating Patients with Hemiplegic Shoulder Pain. Am J Phys Med Rehabil. 2002;81(2):150-160.

