4.2 Stroke Motor Recovery & Hemiplegic Complications

Stroke Motor Recovery & Hemiplegic Complications

Motor recovery following stroke follows a predictable sequence of neuromuscular changes. Physiatrists must understand motor recovery stages to select appropriate therapeutic interventions, manage hemiplegic shoulder pain, and treat post-stroke complications such as Complex Regional Pain Syndrome (CRPS).

Brunnstrom Stages of Motor Recovery

Signe Brunnstrom defined six distinct sequential stages of motor recovery following stroke. Recovery can plateau at any stage, but patients typically progress sequentially through these stages without skipping steps.

• Stage I: Flaccidity:
  • Immediately following acute stroke (diaschisis phase), affected limbs exhibit total flaccidity.
  • Complete absence of voluntary movement, muscle tone, or reflex activity.
• Stage II: Appearance of Synergies and Spasticity:
  • Minimal voluntary muscle contraction begins to return.
  • Basic limb synergies (obligatory mass movement patterns) or components of synergies appear as weak voluntary movements or involuntary associated reactions.
  • Spasticity begins to develop, manifesting as increased muscle tone in synergy muscles.
• Stage III: Peak Spasticity and Voluntary Synergy Control:
  • Voluntary control of basic movement synergies is achieved. Patients can voluntarily initiate mass flexor or extensor movement patterns.
  • Spasticity reaches its peak severity. Patients cannot perform isolated joint movements outside the obligatory synergy patterns.
  • Upper Extremity Flexor Synergy: Scapular retraction and elevation, shoulder abduction and external rotation, elbow flexion (strongest component), forearm supination, and wrist/finger flexion.
  • Upper Extremity Extensor Synergy: Scapular protraction, shoulder adduction and internal rotation (strongest component), elbow extension, forearm pronation, and wrist/finger flexion.
  • Lower Extremity Extensor Synergy: Hip extension, adduction, and internal rotation, knee extension (strongest component), and ankle plantarflexion with inversion (equinovarus).
• Stage IV: Movement Deviating from Synergy:
  • Spasticity begins to decline. Voluntary movement patterns that deviate from basic limb synergies emerge.
  • Representative movements include placing the hand behind the lumbar spine, elevating the arm to 90° forward flexion with the elbow extended, and performing forearm pronation/supination with the elbow flexed to 90°.
• Stage V: Complex Combinations Outside Synergy:
  • Basic synergies lose their dominance. Spasticity becomes minimal.
  • Patients master increasingly complex movement combinations outside of synergy, such as arm abduction to 90° with elbow extended, overhead arm elevation, and forearm pronation/supination with elbow extended.
• Stage VI: Isolated Movement and Normal Coordination:
  • Spasticity disappears completely.
  • Individual joint movements are fully isolated and well-coordinated. Movement speed and motor control approach normal levels.

Hemiplegic Shoulder Subluxation

Shoulder pain affects up to 70% of stroke survivors. Hemiplegic shoulder subluxation occurs primarily during the flaccid stage (Brunnstrom Stages I and II) and significantly contributes to painful soft tissue trauma.

Pathomechanics and Assessment

In healthy individuals, Glenohumeral stability relies on the muscular tone of the rotator cuff—specifically the supraspinatus muscle—which holds the humeral head securely within the shallow glenoid fossa, against the downward pull of gravity.

• Etiology: Flaccid paralysis of the supraspinatus and anterior/posterior deltoid muscles, combined with scapular downward rotation and capsular stretching, permits the humeral head to slip downward out of the glenoid cavity (inferior subluxation).
• Clinical Exam: Palpable gap between the acromion process and the top of the humeral head, quantified by finger-breadths (e.g., 1-finger or 2-finger subluxation).
• Clinical Complications: While subluxation itself is not inherently painful, the lack of joint support causes chronic traction on the glenohumeral capsule, brachial plexus, and rotator cuff tendons, predisposing the patient to impingement, bicipital tendinitis, and Complex Regional Pain Syndrome.

Rehabilitation Interventions

• Neuromuscular Electrical Stimulation (NMES): High-level evidence supports surface NMES applied to the supraspinatus and posterior deltoid muscles during early flaccid recovery. Cyclic electrical stimulation induces muscle contractions, reduces subluxation distance, restores joint alignment, and prevents capsular stretching.
• Postural Support and Slings:
  • Wheelchair Support: Lapboards, hemiplegic trough armrests, and supportive cushions provide passive joint realignment while seated.
  • Ambulatory Slings: Specialized functional slings (such as the GivMohr sling) support the humeral head while keeping the forearm extended, reducing subluxation during gait without promoting hypertonicity. Traditional triangular arm slings should be avoided because they hold the arm immobilized in internal rotation and elbow flexion, reinforcing upper extremity flexor synergy.

Complex Regional Pain Syndrome (CRPS Type I / Shoulder-Hand Syndrome)

Post-stroke Complex Regional Pain Syndrome (CRPS) Type I, historically termed Shoulder-Hand Syndrome, is a painful neuroinflammatory condition triggered by autonomic dysregulation, peripheral neurogenic inflammation, and prolonged limb immobilization.

Classic Three Clinical Phases

• Phase I (Acute / Hyperemic Phase, Months 1–3):
  • Characterized by severe, burning pain in the hemiplegic shoulder, wrist, and hand.
  • Marked hyperalgesia and allodynia (pain elicited by non-painful light touch).
  • Prominent non-pitting edema of the wrist and hand, local warmth, hyperhidrosis (increased sweating), and skin erythema.
• Phase II (Dystrophic Phase, Months 3–6):
  • Pain persists; skin becomes cool, cyanotic, pale, and indurated (brawny edema).
  • Loss of skin turgor, brittle nails, and muscle atrophy of the intrinsic hand muscles.
  • Marked range-of-motion restriction and stiffness of the shoulder and finger joints.
• Phase III (Atrophic Phase, Months 6+):
  • Severe irreversible skin atrophy, glossy skin appearance, and joint capsule contractures ("claw hand" deformity).
  • Severe diffuse periarticular osteoporosis on imaging; pain may decrease, but motor loss and flexion contractures are fixed.

Diagnostic Evaluation

• Budapest Criteria: Clinical diagnosis requiring presence of continuing pain disproportionate to any inciting event, plus at least one symptom in three of four categories (Sensory, Vasomotor, Sudomotor/Edema, Motor/Trophic).
• Triple-Phase Bone Scan: The most sensitive diagnostic imaging study. Shows increased diffuse periarticular radiotracer uptake (technetium-99m MDP) in the affected hand and wrist joints during Phase 3 (delayed bone phase).

Multimodal Management

• Systemic Corticosteroids: Short-course, high-dose oral corticosteroids (prednisone 40–60 mg daily tapered over 2–4 weeks) represent the gold standard acute medical treatment, producing dramatic reduction in neurogenic inflammation, hand edema, and pain.
• Bisphosphonates: Intravenous pamidronate or oral alendronate reduces bone turnover and provides significant pain relief in CRPS.
• Interventional and Physical Therapies: Stellate ganglion sympathetic blocks provide pain relief for sympathetically maintained pain. Physical and occupational therapy emphasize desensitization, early aggressive active-assisted ROM, mirror therapy, and edema control (compression garments).