🧠 Master Stroke Management: The Student's Neuro-Physio Exam Guide
Stroke (Cerebrovascular Accident - CVA) is a critical neurological condition. This comprehensive guide covers the essentials for physiotherapy students, focusing on classification, pathophysiology, clinical presentation by vascular territory, and evidence-based rehabilitation strategies required for academic exams and clinical practice.
1. 🚨 Acute Cerebrovascular Events: Stroke, TIA, and RIND
Distinguishing between these terms is vital in the acute setting, especially for timely intervention.
| Condition | Definition | Duration | Outcome (Tissue Damage) |
|---|---|---|---|
| Stroke (CVA) | Brain tissue death (infarction or hemorrhage). | Permanent deficit (symptoms $>24$ hrs). | Irreversible damage on imaging. |
| Transient Ischemic Attack (TIA) | Temporary cerebral ischemia. | Symptoms resolve in $<24$ hours (typically minutes). | No permanent damage (high risk of future stroke). |
| RIND | Reversible Ischemic Neurological Deficit. | Symptoms resolve in $>24$ hrs but $<3$ weeks. | Minimal or no permanent damage. |
Pathophysiology Overview
A stroke occurs when blood flow to a part of the brain is interrupted, leading to cellular oxygen and glucose deprivation, resulting in neuronal injury and death.
[Image of Circle of Willis and Major Brain Arteries]2. 📊 Stroke Classification for Academics
A. Ischemic Stroke (85% of cases) - Blockage
- Thrombotic: Clot forms within an artery supplying the brain (often at atherosclerotic plaques).
- Embolic: Clot travels from another part of the body (e.g., from the heart due to Atrial Fibrillation) and lodges in a cerebral artery.
- Systemic Hypoperfusion: Global reduction in cerebral blood flow (e.g., severe hypotension/cardiac arrest).
- Watershed Infarct: Damage in border zones between major arterial territories (e.g., between MCA and ACA), highly sensitive to hypoperfusion.
B. Hemorrhagic Stroke (15% of cases) - Bleeding
- Intracerebral Hemorrhage (ICH): Bleeding directly into the brain tissue (commonly caused by chronic Hypertension leading to vessel rupture).
- Subarachnoid Hemorrhage (SAH): Bleeding into the subarachnoid space (typically from a ruptured aneurysm or Arteriovenous Malformation - AVM).
C. Classification Based on Vascular Territory (Key for Physio Diagnosis)
| Artery Affected | Clinical Features (Contralateral Deficits) |
|---|---|
| Middle Cerebral Artery (MCA) | Hemiplegia/paresis (Face & Arm > Leg), Sensory loss, Aphasia (L-hemisphere), Neglect/Apraxia (R-hemisphere). |
| Anterior Cerebral Artery (ACA) | Hemiplegia/paresis (Leg > Arm), Sensory loss in leg, Abulia (lack of will/motivation). |
| Posterior Cerebral Artery (PCA) | Homonymous Hemianopia (vision loss on one side of the visual field), Memory impairment. |
| Vertebrobasilar (Brainstem) | Ipsilateral cranial nerve deficits with contralateral body weakness/sensory loss (Crossed Signs), Ataxia, Dysphagia, Diplopia, Locked-in syndrome. |
3. 🛑 Risk Factors: Primary and Secondary Prevention
Modifiable Factors (Focus for Primary Prevention)
- Hypertension (Most significant controllable risk).
- Atrial Fibrillation (Requires anticoagulation).
- Diabetes Mellitus & Dyslipidemia.
- Smoking & Excessive Alcohol intake.
- Obesity & Sedentary lifestyle.
- Carotid artery stenosis (Surgical target).
Non-Modifiable Factors
- Age, Gender, Family History, Previous stroke/TIA.
4. 🔬 Pathophysiology: Targets for Recovery
Understanding these concepts is key to justifying acute medical treatment (tPA) and rehabilitation (Physio).
- Ischemic Cascade: The sequence of biochemical events following vessel occlusion, leading to neuronal cell death. This cascade includes energy failure and release of toxins.
- Excitotoxicity: Excess release of neurotransmitters (like glutamate) which overstimulate adjacent neurons, leading to massive $\text{Ca}^{2+}$ influx and subsequent cell death.
- Ischemic Penumbra: The area of tissue surrounding the core infarct that is functionally impaired but potentially salvageable by timely medical intervention.
- Neuroplasticity: The brain's inherent ability to rewire and reorganize surviving neural pathways. This mechanism underpins all effective physiotherapy treatment.
- Diaschisis: A temporary loss of function and electrical activity in brain areas remote from the lesion site, but functionally connected to it. Recovery from this can account for rapid early functional gains.
5. ⚠️ Clinical Presentation: UMN Signs and Synergies
High-Yield Motor Signs (Upper Motor Neuron - UMN Lesion)
The stroke lesion occurs in the corticospinal tract, resulting in UMN signs on the contralateral side of the body.- Spasticity: Velocity-dependent increase in muscle tone. Assessed using the Modified Ashworth Scale (MAS).
- Clonus: Rhythmic, involuntary muscle contractions.
- Hyperreflexia: Exaggerated Deep Tendon Reflexes (DTRs). Use the Reflex Grading Tool.
- Positive Babinski Sign: Dorsiflexion of the great toe and fanning of other toes when the sole is stroked.
- Synergies (Brunnstrom Stages): Stereotypical, involuntary movement patterns (flexion or extension) that the patient cannot break out of. Recovery often progresses through these stages.
6. 🩺 Diagnosis and Assessment Tools
A. Imaging (The First Step)
- CT Scan (First Line): Fast; used to rule out hemorrhage immediately. Ischemic stroke may not be visible for 6-12 hours.
- MRI (Gold Standard): Especially Diffusion-Weighted Imaging (DWI), which detects ischemic changes within minutes.
B. Clinical Scales (Physio Important)
These scales are crucial for measuring severity, prognosis, and functional outcome.- NIHSS (National Institutes of Health Stroke Scale): Measures severity of neurological deficits (motor, language, consciousness).
- Berg Balance Scale (BBS): Standard measure for balance assessment.
- Modified Rankin Scale (mRS): Measures degree of disability/dependence (0 = no symptoms, 6 = death).
- Fugl-Meyer Assessment (FMA): Highly reliable measure of motor impairment and recovery after stroke.
- Barthel Index: Measures functional independence in ADLs.
7. 📉 Common Complications
- Shoulder Subluxation & Pain: Due to flaccidity and pull of gravity on the limb.
- Deep Vein Thrombosis (DVT): Due to immobility (risk of Pulmonary Embolism).
- Contractures & Deformity: Often due to uncontrolled spasticity and poor positioning.
- Central Post-Stroke Pain (CPSP): Chronic pain due to damage to the central sensory pathways (Thalamus).
- Dysphagia: Difficulty swallowing, leading to high risk of aspiration pneumonia.
- Cognitive impairment (memory, attention) and Emotional changes (Post-stroke depression).
8. 📋 Physiotherapy Assessment Essentials
A structured approach is vital for accurate goal setting.
- Subjective: Onset, risk factor history, prior functional status.
- Objective: Motor & Tone
- Tone: Modified Ashworth Scale (MAS).
- Strength: Medical Research Council (MRC) / Oxford Scale or FMA.
- Reflexes: DTRs and pathological reflexes (Babinski).
- Coordination: Finger-Nose, Heel-Shin.
- Objective: Functional
- Balance: Berg Balance Scale, TUG, Sitting/Standing Balance.
- Gait: Gait analysis for common deviations (e.g., circumduction, foot drop).
- ADLs: Barthel Index.
9. 🏃 Physiotherapy Management: Stage-Specific Interventions
A. Acute Stage (0–48 hours) - Prevention and Positioning
- Positioning: Correct positioning to prevent contractures and pressure sores.
- Early Mobilization: As soon as medically stable (e.g., sitting up, short transfers) to prevent DVT.
- Passive ROM: Maintains joint integrity and prevents contractures.
- Chest Physiotherapy: To prevent aspiration/pneumonia.
B. Subacute Stage (Weeks 1–6) - Motor Re-learning
The goal is intensive, task-specific training utilizing neuroplasticity.- Task-Specific Training (TST): Repetitive practice of functional tasks (e.g., reaching, standing).
- Facilitation Techniques: PNF (Proprioceptive Neuromuscular Facilitation), Bobath/NDT, Rood Approach.
- Constraint-Induced Movement Therapy (CIMT): Restricting the non-affected arm to force use of the affected arm (only for patients with minimal wrist/finger extension).
- Weight-Bearing: Promotes motor control and muscle activation.
- Technology: FES (Functional Electrical Stimulation) for dorsiflexors (foot drop) or wrist extensors.
C. Chronic Stage (>6 weeks) - Optimization and Community Reintegration
- Strength & Endurance: Focused strengthening and aerobic training.
- Community Integration: Training for outdoor mobility, public transport.
- Home Exercise Program: Education for sustained recovery.
10. 🎯 Specialized Neuro-Rehabilitation
A. Gait & Balance Rehabilitation
- Balance: Balance board training, Tai Chi, Virtual Reality (VR) training.
- Gait: Body Weight Supported Treadmill Training (BWSTT), appropriate use of walking aids (e.g., AFO for foot drop).
B. Shoulder Pain & Subluxation
- Management: Proper positioning (support under the arm), NMES (Neuromuscular Electrical Stimulation) for deltoid/supraspinatus, Scapular stability exercises. Avoidance of traction/pulling on the flaccid arm.
11. 💊 Medical & Surgical Management (For Context)
- Thrombolysis (tPA): IV clot-busting drug for ischemic stroke, effective only if given within a narrow time window (typically 4.5 hours of symptom onset).
- Mechanical Thrombectomy: Surgical removal of a large clot, typically within 6-24 hours.
- Long-Term Meds: Antiplatelets (Aspirin, Clopidogrel), Anticoagulants (for AF), Statins (Cholesterol control), Antihypertensives.
- Surgical: Decompressive Hemicraniectomy (to relieve severe brain edema/pressure).
12. 📈 Prognosis and Prevention
Factors Affecting Prognosis
- Favorable: Younger age, TIA/small stroke, early recovery in first 2 weeks, high initial NIHSS score improvement.
- Unfavorable: Advanced age, large stroke size, hemorrhagic stroke, associated cognitive/perceptual deficits.
Prevention Measures
- Primary: Aggressive control of hypertension, diabetes, smoking cessation.
- Secondary: Strict compliance with antiplatelet/anticoagulant therapy and lifestyle modification post-stroke/TIA.
🎓 High-Yield Viva Questions (Exam Prep)
1. Explain MCA Stroke Syndrome: Contralateral hemiplegia (face and arm severely affected), hemianesthesia, aphasia (if dominant side), and neglect (if non-dominant side).
2. What is Spasticity? Velocity-dependent increase in the tonic stretch reflex. It is a sign of an Upper Motor Neuron (UMN) lesion.
3. Name the UMN Lesion Signs: Spasticity, Clonus, Hyperreflexia, Babinski sign, Pathological Synergies.
4. Define Constraint-Induced Movement Therapy (CIMT): Restraining the unaffected upper limb for 90% of waking hours over 2-3 weeks to "force" the use and improve function of the affected upper limb. Based on overcoming learned non-use.
5. What are the Brunnstrom Stages of Recovery? A sequence of 6-7 stages describing motor recovery from flaccidity (Stage 1) through development of synergies, to movement outside of synergy, and finally normal movement (Stage 7).
❓ Frequently Asked Questions (FAQs)
🎯 10 Practice MCQs for Neuro Exam
📚 Important Academic References
- O’Sullivan, S. B., & Schmitz, T. J. (2019). Physical Rehabilitation (7th ed.). F.A. Davis Company. (For comprehensive Physiotherapy Assessment and Management techniques like PNF, NDT, etc.)
- Lindsay, K. W., & Bone, I. (2016). Neurology and Neurosurgery Illustrated (5th ed.). Churchill Livingstone. (For Stroke Classification and Clinical Features by Vascular Territory)
- American Heart Association/American Stroke Association Guidelines for the Early Management of Patients with Acute Ischemic Stroke. (Current Year). (For acute medical management, tPA windows).
- Carr, J. H., & Shepherd, R. B. (2010). Motor Relearning Programme for Stroke. Butterworth-Heinemann. (Foundation for Task-Specific Training and Motor Relearning Principles).
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