Summarise in detail
Acute Cerebrovascular Accident (Stroke) — Detailed Summary
1. Definition and Significance
A stroke (ACVA) is the sudden interruption of cerebral blood flow causing neural tissue damage. It is a leading global cause of death and long-term disability. Early diagnosis and treatment are critical to reducing mortality and improving functional outcomes.
2. Classification
2.1 Ischemic Stroke (80–85% of cases)
| Subtype | Mechanism |
|---|---|
| Thrombotic | Local thrombus at an atherosclerotic plaque |
| Embolic | Embolus from heart or large arteries occludes a cerebral artery |
| Lacunar | Small deep infarcts from hypertensive damage to perforating arteries |
| Hemodynamic | Sharp BP drop (heart failure, hypovolemia) reduces cerebral perfusion |
2.2 Hemorrhagic Stroke (15–20% of cases)
- Intracerebral hemorrhage (ICH): Bleeding into brain parenchyma, often from hypertension or aneurysm rupture
- Subarachnoid hemorrhage (SAH): Bleeding between arachnoid and pia mater, usually from aneurysm rupture
2.3 Transient Ischemic Attack (TIA)
Temporary neurological deficit (typically <1 hour, always <24 hours) with no infarction on MRI. Considered a warning sign of impending stroke.
3. Etiology and Risk Factors
Modifiable
- Arterial hypertension — most important (~50% of ischemic, ~70% of hemorrhagic strokes)
- Diabetes mellitus
- Dyslipidemia (high LDL, low HDL)
- Atrial fibrillation — leading cause of embolic stroke in the elderly
- Smoking, obesity, physical inactivity
- Alcohol abuse (particularly for hemorrhagic stroke)
Non-Modifiable
- Age (risk sharply rises after 55)
- Sex (men at higher risk; women have worse outcomes)
- Race/ethnicity (higher in African Americans and Asians)
- Genetics (family history of stroke or aneurysm)
4. Pathogenesis
Ischemic Stroke
Blood flow stops → oxygen/glucose deprivation → energy deficit → membrane depolarization → glutamate release → intracellular Ca²⁺ accumulation → oxidative stress → mitochondrial damage → apoptosis and necrosis
Ischemic penumbra: A salvageable zone surrounding the irreversibly damaged core. This is the target of reperfusion therapy (thrombolysis, thrombectomy).
Hemorrhagic Stroke
Vessel rupture → blood extravasation → mechanical brain damage + raised intracranial pressure → toxic effects of blood breakdown products → vasospasm (especially in SAH)
5. Clinical Presentation
General Signs (All Types)
- Hemiparesis / hemiplegia (one-sided weakness or numbness)
- Aphasia or dysarthria (speech disturbance)
- Visual disturbance (monocular blindness, diplopia, field loss)
- Dizziness, ataxia, gait disturbance
- Severe headache (hallmark of hemorrhagic stroke)
- Reduced consciousness
Vascular Territory-Specific Symptoms
| Territory | Key Features |
|---|---|
| MCA (most common) | Contralateral hemiparesis (face + arm > leg), hemihypesthesia, global aphasia (left), neglect (right) |
| ACA | Contralateral hemiparesis (leg > arm), personality changes, abulia |
| PCA | Homonymous hemianopia, visual agnosia, memory impairment |
| Vertebrobasilar | Dizziness, nausea/vomiting, diplopia, dysarthria, dysphagia, ataxia, alternating syndromes (Wallenberg, Weber) |
Subarachnoid Hemorrhage Features
- "Worst headache of life" (thunderclap onset)
- Vomiting, photophobia, neck stiffness (meningismus)
- Loss of consciousness in 30–50% of cases
6. Diagnosis
Clinical Tools
- FAST scale: Face asymmetry, Arm weakness, Speech disturbance, Time to call emergency
- NIHSS (0–42 points): Quantitative severity scoring
Imaging
| Modality | Role |
|---|---|
| Non-contrast CT (NCCT) | First-line; normal in early ischemia (<6 hrs); hyperdense foci in hemorrhage/SAH |
| Brain MRI (DWI/ADC) | Most sensitive for early ischemic changes |
| CT angiography | Detects thrombus and vascular anomalies |
| MR angiography | No radiation; less available |
| Duplex ultrasound | Assesses carotid atherosclerosis |
Laboratory
- CBC, coagulation (INR, APTT), glucose, lipids, electrolytes, creatinine
- Cardiac enzymes (if cardioembolism suspected)
- Toxicology screen if indicated
Cardiac Evaluation
- ECG — atrial fibrillation, MI
- Holter monitoring — paroxysmal arrhythmias
- Echocardiography — thrombi, vegetations, patent foramen ovale
7. Differential Diagnosis
Conditions mimicking stroke:
- Hypoglycemia
- Epileptic seizure (Todd's paralysis)
- Migraine aura
- Brain tumour
- Acute metabolic encephalopathy
- Meningitis / encephalitis
8. Treatment
8.1 Prehospital Phase
- ABCDE approach (airway, breathing, circulation)
- O₂ if SpO₂ <94%
- Do not lower BP unless dangerously elevated (exception: hemorrhagic stroke)
- Correct hypoglycemia
- "Time is brain" — rapid transfer to stroke centre
8.2 Acute In-Hospital Management
General Measures
- Stroke unit / ICU admission
- Head elevation 30° (if ICP not raised)
- Temperature control (hyperthermia worsens outcome)
- Dysphagia screening (aspiration prevention)
- Subcutaneous heparin (DVT prophylaxis in immobile patients)
Ischemic Stroke — Specific Treatments
-
Thrombolysis (alteplase / rt-PA)
- Indication: symptom onset ≤4.5 hours, no hemorrhage on CT
- Dose: 0.9 mg/kg (10% IV bolus + 90% infusion over 60 min)
- Contraindications: recent stroke (<3 months), prior ICH, BP >185/110, recent surgery (<14 days), platelets <100,000, INR >1.7, active bleeding
-
Mechanical Thrombectomy
- Indication: large vessel occlusion (ICA, MCA-M1), onset ≤6 hours (up to 24 hours in selected cases)
- Catheter-based clot retrieval
-
Antiplatelet Therapy
- Aspirin 160–325 mg loading → 75–100 mg/day (started 24–48 hrs after onset; 24 hrs post-thrombolysis)
- Clopidogrel 75 mg/day for aspirin allergy, or dual antiplatelet therapy for 21 days in minor stroke
Hemorrhagic Stroke — Specific Treatments
- Aggressive BP reduction (target <140/90; IV labetalol or nicardipine)
- Reverse anticoagulation (vitamin K, prothrombin complex concentrate, tranexamic acid)
- ICP management (mannitol, hypertonic saline, decompressive hemicraniectomy)
- Surgery: haematoma evacuation (large cerebellar bleeds); aneurysm clipping or endovascular coiling (SAH)
8.3 Secondary Prevention
- Antihypertensives (target BP <130/80)
- Statins (atorvastatin 40–80 mg/day regardless of LDL)
- Antiplatelet or anticoagulant therapy (warfarin, apixaban, rivaroxaban for AF)
- Lifestyle modification (smoking cessation, diet, exercise)
- Carotid endarterectomy or stenting (stenosis >70%)
8.4 Rehabilitation
- Begin within 24–48 hours
- Multidisciplinary team: physiotherapy, occupational therapy, speech therapy, psychology
- Targets: speech recovery, motor function, ADL skills
- Manage complications: depression, spasticity, pain, post-stroke epilepsy
9. Symptom Localisation Reference Table
| Symptom | Stroke Type | Localisation | Key Feature |
|---|---|---|---|
| Hemiparesis | Ischemic (MCA/ACA) | Contralateral motor cortex | Face+arm>leg (MCA); leg>arm (ACA) |
| Aphasia | Ischemic (left MCA) | Dominant hemisphere | Non-fluent / fluent / global |
| Dysarthria | Any (lacunar/brainstem) | Motor speech apparatus | Slurred speech, no language errors |
| Homonymous hemianopia | Ischemic (PCA) | Occipital lobe | Same visual field lost bilaterally |
| Diplopia | Posterior circulation | CN III/IV/VI or MLF | Vertical or horizontal double vision |
| Ataxia/vertigo | Posterior circulation | Cerebellum/brainstem | Nystagmus, dysmetria, gait instability |
| Thunderclap headache | Hemorrhagic (SAH/ICH) | Meninges/parenchyma | Worst-ever headache + meningismus |
| Decreased consciousness | Hemorrhagic/massive ischemic | Brainstem/bilateral hemispheres | Poor prognosis, herniation risk |
10. Clinical Case (Illustrative)
A 67-year-old woman with hypertension and atrial fibrillation presents with sudden right hemiparesis, global aphasia, and NIHSS of 14 — 2 hours after onset. NCCT shows early left MCA territory ischemia with no hemorrhage; CT angiography confirms M1 occlusion. Alteplase 0.9 mg/kg is given within the treatment window. Follow-up CT at 24 hours shows a small infarct without hemorrhagic transformation. Aspirin 100 mg/day is initiated and the patient is transferred to rehabilitation.
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