4.2 Stroke Motor Recovery & Hemiplegic Complications

ABPMR Physical Medicine and Rehabilitation Board Exam Study Guide Exam

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1 Chapter 1: Introduction & Exam Overview

1.1 ABPMR Part I Exam Overview & Format 1.2 Board Review Strategy & Content Blueprint Breakdown

2 Chapter 2: Musculoskeletal Medicine

2.1 Shoulder & Upper Extremity Diagnostics 2.2 Knee, Hip & Lower Extremity Conditions 2.3 Spine Pathology, Radiculopathy & Myelopathy 2.4 Inflammatory Arthritis, Tendinopathies & Concussion 2.5 Bone Health, Osteoporosis & Metabolic Bone Disease 2.6 Thoracic Outlet Syndrome & Peripheral Nerve Entrapment 2.7 Fracture Rehabilitation & Immobilization Complications 2.8 Overuse Tendinopathies & Regenerative Medicine 2.9 Gait Analysis & Abnormal Gait Patterns

3 Chapter 3: Spinal Cord Injury Rehabilitation

3.1 ASIA Examination & Impairment Scale 3.2 Spinal Cord Injury Syndromes 3.3 Autonomic Dysreflexia & Acute Complications 3.4 Neurogenic Bladder, Bowel & Secondary Complications

4 Chapter 4: Stroke & Neuromuscular Rehabilitation

4.1 Stroke Vascular Syndromes & Acute Assessment 4.2 Stroke Motor Recovery & Hemiplegic Complications 4.3 Spasticity Assessment & Multimodal Management 4.4 ALS, GBS, CIDP & Neuromuscular Disease Rehab 4.5 Multiple Sclerosis & Demyelinating Disease Rehabilitation 4.6 Parkinsonism, Movement Disorders & Functional Neurologic Disorder

5 Chapter 5: Electrodiagnostics (EMG/NCS)

5.1 Nerve Conduction Studies Principles & Physics 5.2 Needle Electromyography & MUAP Analysis 5.3 Mononeuropathies & Radiculopathy Patterns 5.4 Neuromuscular Junction Disorders & Myopathies

6 Chapter 6: Traumatic Brain Injury

6.1 TBI Severity Classification, Glasgow Coma Scale, and Pathophysiology 6.2 Rancho Los Amigos Levels of Cognitive Functioning and Disability Rating Scale 6.3 Neurobehavioral Sequelae and Agitation Management 6.4 Concussion Evaluation, Vestibular-Ocular Dysfunction, and Return-to-Play/Work Protocols

7 Chapter 7: Chronic Pain & Interventional Spine

7.1 Fluoroscopic Spine Interventions 7.2 Opioid Stewardship & Controlled Substance Compliance 7.3 Complex Regional Pain Syndrome, Fibromyalgia & Myofascial Pain 7.4 Spinal Cord Stimulation & Intrathecal Therapy

8 Chapter 8: Amputee Rehabilitation & Prosthetics

8.1 Amputation Surgical Levels & Medicare K-Levels 8.2 Socket Designs & Suspension Systems 8.3 Prosthetic Feet & Microprocessor Knee Mechanisms 8.4 Post-Amputation Care, Residual Limb & Phantom Pain

9 Chapter 9: Pediatric Rehabilitation

9.1 Cerebral Palsy Classification & GMFCS 9.2 Spina Bifida & Myelomeningocele Management 9.3 Muscular Dystrophies & Neuromuscular Disease in Children 9.4 Pediatric Brachial Plexopathy & Congenital Disorders

10 Chapter 10: Prosthetics, Orthotics & Assistive Technology

10.1 Lower Limb Orthoses — AFOs & KAFOs 10.2 Spinal & Upper Extremity Orthoses 10.3 Upper Limb Prosthetics — Body-Powered vs Myoelectric 10.4 Wheelchairs, Seating Systems & Pressure Mapping

11 Chapter 11: Medical Rehabilitation & Outcomes

11.1 Dysphagia Assessment & Management 11.2 Neurogenic Bladder & Bowel Management 11.3 Pressure Injuries & Wound Management 11.4 Outcome Measures & Medical Complications 11.5 Cancer Rehabilitation & Oncologic Rehabilitation 11.6 Burns, Endocrine/Metabolic & Medical Complications Rehabilitation

12 Chapter 12: Cardiopulmonary Rehabilitation

12.1 Cardiac Rehabilitation Phases & Metabolic Equivalents 12.2 Pulmonary Rehabilitation & COPD Management

13 Chapter 13: Foundational Rehabilitation Concepts

13.1 Kinesiology, Biomechanics & Functional Anatomy 13.2 Rehabilitation Pharmacology & Medication Management 13.3 Research Methodology, Biostatistics & Evidence-Based Practice 13.4 Nutrition, Metabolism & Energy Expenditure in Rehabilitation 13.5 Diagnostic Procedures: Imaging, MSK Ultrasound, Urodynamics & Neuropsych Assessment

4.2 Stroke Motor Recovery & Hemiplegic Complications

Key Takeaways Explain This Topic AI

Motor recovery following stroke follows predictable sequential stages described by Brunnstrom (Stages I-VI), progressing from initial flaccidity (Stage I), appearance of spasticity and obligatory basic limb synergies (Stage II-III), voluntary movement breaking out of synergy (Stage IV-V), to isolated joint movement with normal coordination (Stage VI).

Hemiplegic shoulder subluxation occurs primarily in the flaccid stage (Brunnstrom I-II) due to paralysis of key shoulder stabilizers—specifically the supraspinatus and anterior deltoid muscles—allowing gravitational inferior displacement of the humeral head from the glenoid fossa.

Neuromuscular Electrical Stimulation (NMES) targeting the supraspinatus and posterior deltoid muscles is an evidence-based intervention to prevent and reduce shoulder subluxation during early rehabilitation, whereas lapboards and specialized shoulder slings provide passive joint support during upright transfers.

Complex Regional Pain Syndrome (CRPS) Type I (Shoulder-Hand Syndrome) after stroke manifests in three classic phases: Phase 1 (acute hyperemic/edematous, burning pain, allodynia), Phase 2 (dystrophic, skin thickening, cold cyanotic limb), and Phase 3 (atrophic, severe contractures, irreversible trophic changes).

Diagnosis of CRPS is established clinically using the Budapest Criteria and supported by a 3-phase bone scan showing diffuse periarticular increased uptake; primary acute management includes high-dose systemic corticosteroid tapers (prednisone), bisphosphonates, stellate ganglion blocks, and aggressive physical therapy.

Last updated: July 2026

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.

Brunnstrom Stage Spasticity Severity Synergy Status Motor Control & Functional Movement Capabilities
Stage I Absent (Flaccid) No synergies present Complete flaccidity; no voluntary or reflex movement
Stage II Developing Synergies first appear Minimal voluntary contraction; spasticity starts
Stage III Peak Spasticity Obligatory synergies Voluntary movement only within flexor/extensor synergy
Stage IV Declining Deviating from synergy Hand behind back; arm elevation to 90° with elbow straight
Stage V Minimal Independent of synergy Arm abduction to 90° with elbow straight; overhead reach
Stage VI Absent Normal isolation Isolated joint movement; normal speed and coordination
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).