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Stroke - General Medicine (MBBS)

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Classification

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1. Ischemic Stroke

Definition

Vascular Anatomy (Circle of Willis)

• Anterior circulation: ICA → MCA + ACA (supplies most of cerebral hemispheres)
• Posterior circulation: Vertebral arteries → Basilar artery → PCA (supplies brainstem, cerebellum, occipital & medial temporal lobes)
• The Circle of Willis provides an anastomosis allowing collateral flow when one system is compromised.

Subtypes of Ischemic Stroke

• Atherosclerotic plaques in large vessels (ICA, MCA, vertebral/basilar arteries) rupture and cause local thrombus formation
• Gradual onset, often with preceding TIA ("stuttering" course)
• TOAST classification category: Large artery atherosclerosis

• Cardioembolic (most common embolic cause): Atrial fibrillation, mural thrombus (post-MI), dilated cardiomyopathy, valvular disease (mitral stenosis), infective endocarditis
• Artery-to-artery embolism: Atherosclerotic plaque fragments travel distally
• Paradoxical embolism: Venous thrombus crosses a patent foramen ovale (PFO) to enter arterial circulation
• Clinical clue: Multiple vascular territory involvement; sudden onset with maximum deficit at onset

• Affects penetrating arteries (<1.5 mm diameter) supplying basal ganglia, thalamus, internal capsule, pons
• Caused by lipohyalinosis (fibrinoid/lipid deposition causing luminal obliteration) or microatheroma - both linked to chronic hypertension
• Pure motor, pure sensory, sensorimotor, ataxic hemiparesis, clumsy-hand dysarthria syndromes
• Normal cortex (no aphasia, no neglect, no visual field defects)

• Occurs at junctions between major vascular territories during systemic hypotension or severe ICA stenosis
• Most often subcortical watershed ("man-in-a-barrel" syndrome when bilateral)

• Cervical artery dissection (~20% of strokes in young/middle-aged adults)
• Hypercoagulable states (antiphospholipid syndrome, protein C/S deficiency, polycythemia vera)
• Vasculitis, fibromuscular dysplasia, Moyamoya disease

TOAST Classification Summary

Clinical Features by Artery

TIA (Transient Ischemic Attack)

• Same mechanism as ischemic stroke but symptoms resolve within 24 hours (classically; newer tissue-based definition: no infarct on MRI)
• High short-term stroke risk: 10-15% within 3 months, with greatest risk in first 48 hours
• ABCD2 score (Age, Blood pressure, Clinical features, Duration, Diabetes) guides urgency of workup

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2. Hemorrhagic Stroke

A. Intracerebral Hemorrhage (ICH)

• Hypertensive vasculopathy (lipohyalinosis of deep penetrating arteries)
• Cerebral amyloid angiopathy (CAA): Amyloid deposition in leptomeningeal/cortical vessels → lobar hemorrhages in elderly
• AVM, cavernous malformation
• Coagulopathy, anticoagulant use
• Trauma (ICH in ~50% of traumatic brain injury patients)
• Hemorrhagic transformation of ischemic stroke (spontaneous: ~2nd week; with thrombolytics: earlier)

• Hypertension: Putamen/internal capsule (most common), thalamus, pons, cerebellum
• CAA: Lobar (cortical/subcortical)
• CVT: Adjacent to affected vein; hyperattenuating cortical/deep vein on CT is a clue

• Hyperattenuating (bright) round/oval lesion on non-contrast CT
• Early: 40-60 HU (heterogeneous) → 60-80 HU within hours/days → 80-100 HU over days (homogeneous hyperdense clot)
• Surrounding hypodense edema ring

• Sudden onset headache + focal neurological deficits + nausea/vomiting + elevated BP
• Consciousness impairment depends on size and location

B. Subarachnoid Hemorrhage (SAH)

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3. Diagnosis

Initial Assessment - Imaging

• Non-contrast CT brain: First-line, immediate - rules out hemorrhage, guides tPA eligibility
  • Ischemic: May be normal in first hours; early signs: loss of gray-white differentiation at insular cortex, sulcal effacement, hypodense basal ganglia, "dense MCA sign" (hyperdense clot in proximal MCA)
  • Hemorrhagic: Hyperattenuating lesion
• CT Angiography (CTA): Identifies vessel occlusion and stenosis (sensitivity ~97%, specificity ~99.5% for >50% stenosis)
• MRI DWI (Diffusion-Weighted Imaging): Most sensitive for acute ischemia (detects within minutes of onset); restriction of diffusion = cytotoxic edema
• CT Perfusion / MR Perfusion: Identifies ischemic penumbra (tissue at risk); used for extended thrombolysis/thrombectomy window decisions
• ASPECTS score: Summarizes early CT ischemic changes in MCA territory (max 10 = normal; <7 = poor prognosis)

Workup (after stabilization)

• ECG and cardiac monitoring: Look for AF
• Echocardiography: Mural thrombus, valvular disease, PFO
• Carotid Doppler ultrasound / CTA neck: Carotid stenosis, dissection
• Lipid profile, fasting glucose, HbA1c
• CBC, coagulation studies
• In young patients: Thrombophilia screen, homocysteine, antiphospholipid antibodies

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4. Treatment

Acute Ischemic Stroke

IV Thrombolysis (tPA)

• Drug: Alteplase (recombinant tPA), 0.9 mg/kg IV (max 90 mg), 10% as bolus + 90% over 1 hour
• Window: Up to 4.5 hours from symptom onset
• Key contraindications: Active bleeding, recent surgery, prior ICH, platelets <100,000, INR >1.7, systolic BP >185 mmHg (uncontrolled), blood glucose <50 or >400
• Main risk: Symptomatic intracranial hemorrhage in ~6% (NINDS trial)
• Hemorrhagic conversion risk factors: Older age, higher NIHSS (worse deficit), early infarct signs on CT, dense MCA sign, hyperglycemia, hypertension, longer time to treatment
• Patients benefitting from 3-4.5 hour window: Age <80, NIHSS ≤25, no prior stroke + diabetes combined, not on anticoagulation
• Tenecteplase is emerging as an alternative (single bolus, recent meta-analyses [PMID 39413337] show non-inferiority to alteplase within 4.5 hours)

Mechanical Thrombectomy

• Endovascular removal of clot using stent-retriever or aspiration device
• For large vessel occlusion (ICA, M1-MCA, basilar)
• Traditional window: up to 6 hours; can extend to 24 hours with favorable perfusion imaging (penumbra present)
• Landmark trials: MR CLEAN, EXTEND-IA, SWIFT PRIME
• Can be combined with tPA or used alone if tPA contraindicated

Blood Pressure Management (Acute)

• If tPA given: Maintain BP <180/105 mmHg
• If tPA not given: Permissive hypertension (allow up to 220/120 mmHg) - avoid aggressive lowering as it reduces perfusion to ischemic penumbra
• Exceptions: Hypertensive emergency with end-organ damage

Antiplatelet Therapy

• Aspirin 300 mg oral ASAP (if no hemorrhage and not thrombolysed, or 24 hours after tPA)
• For secondary prevention: Aspirin 75-100 mg daily; or clopidogrel; or aspirin + dipyridamole
• Dual antiplatelet (aspirin + clopidogrel) for 21 days after minor stroke/TIA reduces early recurrence (POINT/CHANCE trials)

Anticoagulation

• For AF-associated stroke: Start anticoagulation to prevent recurrence; timing optimized by stroke size (CATALYST meta-analysis, Lancet 2025 [PMID 40570866] - IPD meta-analysis of RCTs guiding early vs delayed anticoagulation)
• Acute anticoagulation with heparin for stroke-in-evolution or cervical artery dissection in selected cases

Statin Therapy

• Start high-intensity statin regardless of baseline LDL (reduces recurrence)

Glucose and Temperature Control

• Treat hyperglycemia (worsens infarct)
• Treat fever aggressively (increases metabolic demand in penumbra)

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Hemorrhagic Stroke Management

Intracerebral Hemorrhage

• Reverse anticoagulation immediately (Vitamin K + PCC/FFP for warfarin; specific antidotes for NOACs)
• Blood pressure lowering: Target SBP <140 mmHg (reduces hematoma expansion)
• No role for tPA (contraindicated)
• Surgical evacuation: For cerebellar hemorrhage >3 cm with deterioration, or superficial lobar hemorrhage with mass effect
• ICP management if indicated

Subarachnoid Hemorrhage

• Neurosurgical/interventional referral (clipping vs. coiling of aneurysm)
• Nimodipine 60 mg q4h for 21 days (prevents cerebral vasospasm)
• Avoid hypovolemia; monitor for delayed cerebral ischemia (Days 4-14)
• Watch for hydrocephalus (CSF obstruction by blood)

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5. Complications of Stroke

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6. Secondary Prevention

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7. NIHSS (National Institutes of Health Stroke Scale)

• Scores 0-42 (higher = worse deficit)
• Assesses: Level of consciousness, gaze, visual fields, facial palsy, arm/leg motor, limb ataxia, sensory, language, dysarthria, extinction/neglect
• Used to guide tPA eligibility and predict outcomes

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8. Prognosis

• Ischemic stroke: 30-day mortality ~10-20%; functional outcome depends on stroke size, location, NIHSS, age, comorbidities
• ICH: Higher acute mortality (~40% at 30 days); long-term functional status similar to ischemic stroke survivors
• SAH: ~50% mortality overall; good prognosis for perimesencephalic non-aneurysmal SAH

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Recent Evidence (2024-2026)

• Tenecteplase vs alteplase within 4.5h: Systematic review (Neurology, 2024) - tenecteplase is non-inferior and has practical advantages (single bolus)
• Anticoagulation timing post-stroke with AF: CATALYST IPD meta-analysis (Lancet, 2025) - provides individualized timing guidance
• Thrombolysis beyond 4.5h window: Meta-analysis (Stroke, 2025) - benefit in extended window with imaging selection

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