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Q1 LONG ANSWER 10M ★ High-yield

Discuss the aetiology, clinical features, investigations and management of ischaemic stroke.

General Medicine · Final Professional

Definition

Stroke is a sudden focal neurological deficit of vascular origin lasting more than 24 hours (or leading to death). Ischaemic stroke (80–85%) results from arterial occlusion; haemorrhagic stroke (15–20%) from vessel rupture. Stroke is a leading cause of death and the commonest cause of adult disability in India, occurring roughly a decade earlier than in Western populations.

Aetiology — Toast Classification

MechanismFeatures
Large artery atherosclerosisCarotid or vertebrobasilar stenosis; artery-to-artery embolism; often preceded by TIA
CardioembolismAtrial fibrillation (commonest), rheumatic mitral stenosis (important in India), prosthetic valves, recent MI with mural thrombus, infective endocarditis, cardiomyopathy, patent foramen ovale
Small vessel (lacunar)Lipohyalinosis of penetrating arteries from hypertension and diabetes; produces classic lacunar syndromes
Other determinedArterial dissection (young patients, neck trauma), vasculitis, antiphospholipid syndrome, hypercoagulable states, sickle cell disease, moyamoya
Undetermined (cryptogenic)No cause found despite full evaluation

Risk factors: hypertension is the single most important modifiable factor; also diabetes, smoking, dyslipidaemia, atrial fibrillation, obesity, physical inactivity, alcohol, and prior TIA or stroke.

Clinical Features BY Territory

TerritoryFeatures
Anterior cerebral arteryContralateral leg > arm weakness, urinary incontinence, abulia, grasp reflex
Middle cerebral arteryContralateral face and arm > leg weakness and sensory loss, homonymous hemianopia, gaze deviation towards the lesion; aphasia if dominant hemisphere, neglect if non-dominant
Posterior cerebral arteryHomonymous hemianopia with macular sparing, visual agnosia, memory disturbance
VertebrobasilarCrossed signs — ipsilateral cranial nerve palsy with contralateral limb weakness; vertigo, diplopia, dysarthria, dysphagia, ataxia; locked-in syndrome in basilar occlusion
LacunarPure motor hemiparesis, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis, dysarthria–clumsy hand. No cortical signs — no aphasia, neglect or visual field defect

Investigations

  • Non-contrast CT brain immediately — the first investigation, to exclude haemorrhage before thrombolysis. Early ischaemic changes may be subtle (loss of grey-white differentiation, hyperdense MCA sign, insular ribbon sign); infarct becomes clearly hypodense after 24–48 hours.
  • MRI with diffusion-weighted imaging — far more sensitive for early and posterior fossa infarction.
  • CT/MR angiography — to identify large vessel occlusion amenable to thrombectomy; CT perfusion to define salvageable penumbra in late-window patients.
  • Cardiac: ECG and prolonged rhythm monitoring for atrial fibrillation; echocardiography for cardiac source.
  • Vascular: carotid Doppler.
  • Bloods: glucose (check immediately — hypoglycaemia mimics stroke), CBC, coagulation profile, renal function, lipids, HbA1c; in the young add thrombophilia screen, antiphospholipid antibodies, homocysteine, vasculitis screen and HIV.
  • Swallow assessment before any oral intake — non-negotiable.

Management

1. Hyperacute — "time is brain"

  • Airway, breathing, circulation; oxygen only if hypoxic; correct hypoglycaemia.
  • Intravenous thrombolysis with alteplase or tenecteplase for eligible patients within the licensed window from symptom onset, after CT excludes haemorrhage. Absolute contraindications include intracranial haemorrhage, recent major surgery or trauma, active bleeding, and severe uncontrolled hypertension.
  • Mechanical thrombectomy for large vessel occlusion, in an extended window when perfusion imaging shows salvageable tissue. This has transformed outcomes for proximal occlusions.
  • Blood pressure: do not lower acutely in most ischaemic strokes — cerebral autoregulation is impaired and perfusion depends on systemic pressure. Lower only if extremely high, or if thrombolysis is planned (to below the required threshold), or if there is another indication such as aortic dissection or heart failure.
  • Aspirin started within 24–48 hours (and after 24 hours if thrombolysed); dual antiplatelet therapy for a short period in minor stroke and high-risk TIA.

2. Stroke unit care — the intervention with the broadest mortality benefit

Organised multidisciplinary stroke unit care reduces death and dependency more reliably than any single drug. It includes:

  • Nil by mouth until swallow assessed; nasogastric feeding if unsafe.
  • Glycaemic control, treatment of fever and infection, avoidance of hypoxia.
  • DVT prophylaxis with intermittent pneumatic compression; early mobilisation.
  • Pressure area care, bladder and bowel care, and prevention of aspiration pneumonia.
  • Early physiotherapy, occupational therapy and speech therapy.

3. Secondary prevention — begun before discharge

  • Antiplatelet therapy (aspirin, clopidogrel) for non-cardioembolic stroke.
  • Anticoagulation for atrial fibrillation — DOAC preferred over warfarin except in rheumatic mitral stenosis and mechanical valves, where warfarin is mandatory (a distinction of particular importance in India).
  • High-intensity statin; blood pressure control (the single most effective long-term measure); glycaemic control; smoking cessation; weight, diet and exercise.
  • Carotid endarterectomy or stenting for symptomatic high-grade carotid stenosis, performed early.

4. Rehabilitation and complications

Long-term rehabilitation with goal setting; management of spasticity (physiotherapy, botulinum toxin), post-stroke depression (common and under-treated), pain, seizures, contractures and caregiver support.

DANGER / REMEMBER

Check the capillary glucose in every suspected stroke before anything else. Hypoglycaemia produces focal deficits indistinguishable from stroke and is instantly reversible; thrombolysing a hypoglycaemic patient is a catastrophic error. Other stroke mimics to consider: seizure with Todd's paresis, migraine with aura, hypertensive encephalopathy, space-occupying lesion, and functional weakness.

NEEDS VERIFICATION

Thrombolysis and thrombectomy time windows, blood pressure thresholds, and antiplatelet regimens are guideline-specific and have changed with recent trials — confirm against current stroke guidelines before publication.

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