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🧠 COMPLETE ORAL SURVEY GUIDE: STROKE, TIA & SUBARACHNOID HAEMORRHAGE

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PART 1 - STROKE I: Definition, Epidemiology & Pathogenesis

What is a Stroke?

Epidemiology (Numbers to Remember)

• 3rd most common cause of death in developed countries
• Incidence of first stroke: 2 per 1000 per year
• Rare below age 45; rises to 30 per 1000/year in those over 80
• 25% die within 6 months (most within 1 month)
• 40% of survivors are dependent at 6 months

Types of Stroke (The 80-15-5 Rule)

Causes of Cerebral Infarction

Atheroma - The Key Villain

1. Stenosis not compensated by anastomoses
2. Plaque ulcerates → fragments become emboli
3. Ulcerated base acts as focus for thrombus

Risk Factors for Atheroma (Relative Risk of Stroke)

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Embolic Strokes - Sources

• Atrial fibrillation (most common cardiac source)
• Mural thrombus post-MI
• Left ventricular dilatation
• Rare: bacterial endocarditis vegetations, atrial myxoma

Thrombotic Strokes - 3 Mechanisms

1. Vessel wall abnormality - atheroma causes irregular surface → thrombus
2. Hypercoagulable states - polycythaemia, sickle cell, protein C/S deficiency, antiphospholipid syndrome
3. Stasis - severe stenosis or arterial dissection (commonest identifiable cause in young adults)

Small Vessel Disease (Lacunar strokes)

• Process of lipohyalinosis / microatheroma in small penetrating arteries
• Leads to occlusion → lacunar infarcts

Intracerebral Haemorrhage

• Usually due to hypertension
• Mechanism: Charcot-Bouchard microaneurysms rupture
• Locations: Basal ganglia 50%, Lobar white matter 20%, Pons 10%, Cerebellum 10%
• Other causes: AVM, anticoagulants, ruptured saccular aneurysm

Ischaemic Penumbra (Important Concept!)

• After infarction, the core dies but the penumbra (surrounding area) may be saved
• Cytotoxic oedema peaks at 5 days then gradually clears
• By 3 weeks: gliosis begins, infarct shrinks
• In small vessel strokes: gliosis creates fluid-filled pockets called "lacunes"

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PART 2 - STROKE II: Clinical Features & Classification

Key Clinical Feature: ONSET

• Space-occupying lesions: weeks to months
• MS plaques: days to weeks

Stroke Classification (TACS/PACS/POCS/Lacunar)

1. Total Anterior Circulation Stroke (TACS)

• Dense flaccid hemiparesis (arm + face + leg)
• Homonymous hemianopia
• Higher cortical dysfunction (aphasia if dominant, neglect if non-dominant)
• Eyes deviate away from hemiparetic side
• High mortality, severe morbidity

2. Partial Anterior Circulation Stroke (PACS)

• Only some features of TACS
• Depends on which MCA branch:
  • Inferior MCA: Hemianopia + Wernicke's aphasia (or constructional apraxia)
  • Superior MCA: Hemiparesis + Broca's aphasia (or neglect)
  • ACA infarct: Leg > arm weakness + apathy + incontinence

3. Posterior Circulation Stroke (POCS)

• PCA: Contralateral homonymous hemianopia + hemisensory loss + cortical blindness
• Basilar occlusion: "Locked-in syndrome" - conscious but can't move (only eye movements may remain)
• Lateral Medullary Syndrome (Wallenberg's):
  • Ipsilateral: facial pain/temp loss, Horner's, cerebellar ataxia, vocal cord paralysis
  • Contralateral: body pain/temp loss
  • Note: crossed signs = brain stem lesion

4. Lacunar Strokes (5 Pure Syndromes to Remember)

Differential Diagnosis of Stroke (Box 1)

• Space-occupying lesion (tumour, abscess, bleed into tumour)
• Subdural haematoma (slower onset, confused patient)
• Multiple sclerosis (younger patients)
• Head injury
• Hypoglycaemia (always check BSL first!)
• Todd's paralysis (post-seizure weakness mimicking stroke)

Important Clinical Pearls

• Infarction vs haemorrhage CANNOT be distinguished clinically - need CT/MRI
• Haemorrhage more likely if: severe headache + coma at onset
• Horner's syndrome + anterior circulation stroke = think carotid dissection
• Multi-infarct dementia: multiple small deep infarcts → dementia + small-stepped gait

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PART 3 - STROKE III: Investigations & Treatment

Investigations - Answer 4 Questions

1. Is it a stroke? → CT/MRI (DWI MRI best for early ischaemia)
2. What type? → Imaging differentiates haemorrhagic from ischaemic
3. Why did it occur? → Risk factor screen, cardiac workup, vascular imaging
4. What could make it worse? → Metabolic screen (glucose, electrolytes, O2)

Tests Done in EVERY Patient (*)

• BP, blood glucose*, cholesterol*, thyroid function*, ECG*, full blood count*, ESR/plasma viscosity*

Additional Tests Based on Clinical Picture

• Cardiac source suspected: Echo, 24h tape, blood cultures
• Young patient, no atheroma risk factors: Thrombophilia screen (protein C/S, lupus anticoagulant), ANA, anticardiolipin Ab, syphilis serology, temporal artery biopsy
• Anterior circulation stroke: Carotid Doppler (looking for operable stenosis)
• Haemorrhagic, young, non-hypertensive: Cerebral angiography (AVM/aneurysm)

Treatment Goals (5 Aims)

1. General medical support
2. Minimize stroke size
3. Prevent complications
4. Optimize recovery
5. Prevent recurrence

Key Treatments

• Given within 3 hours of onset
• Must do CT first to exclude haemorrhage
• Reduces stroke size and improves outcome
• Contraindications: no motor deficit, onset >3h, impaired consciousness, recent seizure, ICH history, pregnancy, recent surgery, BP >185/110, coagulopathy (INR >1.5)

• Elevated in >80% of acute strokes
• Usually manage conservatively (don't lower aggressively - cerebral perfusion at risk)
• Only treat if diastolic >120 or hypertensive encephalopathy

• Acute: Raised ICP + herniation, aspiration pneumonia
• Immobility: DVT, pneumonia, contractures, bed sores, UTI, constipation
• Later: Depression (50%!), epilepsy (5%), thalamic pain, social problems

• Nurses, physiotherapists, OT, speech therapist, dietician, psychologist, social worker
• Stroke unit care reduces mortality by 25% and improves functional recovery

Prognosis

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PART 4 - TIA AND PREVENTION OF STROKE

What is a TIA?

• Acute loss of neurological function due to ischaemia lasting less than 24 hours, with complete recovery
• Occurs in 10% of patients prior to a stroke
• Annual incidence: 30 per 100,000
• Cause: artery-to-artery emboli or cardiac emboli (same as embolic stroke)

Clinical Features by Circulation

• Amaurosis fugax - fleeting monocular blindness ("like a shutter coming down") - classic!
• Aphasia, dyslexia, dysgraphia

• Homonymous visual field loss
• Dysarthria
• Vertigo + diplopia + dysphagia (only TIA if combined, not in isolation)
• Bilateral weakness/sensory loss

• Unilateral weakness (face/arm/leg)
• Unilateral sensory loss

TIA vs Mimics

Secondary Prevention of Stroke

• For AF - reduces risk from 12% to 4%/year (INR 2-3)
• Also in mural thrombus, LV dilatation

• For symptomatic stenosis >70% (especially >80%)
• Reduces recurrent stroke risk significantly (NASCET/ECST trials)
• Requires surgical morbidity/mortality <7% to be worthwhile
• Occluded carotid = no further embolic risk, so surgery not indicated

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PART 5 - SUBARACHNOID HAEMORRHAGE (SAH)

What is SAH?

Pathology

• Most SAH = ruptured intracranial aneurysm (usually saccular/berry aneurysm on Circle of Willis)
• 5% caused by AVM (arteriovenous malformation)
• Aneurysm distribution (where they occur most):
  • Anterior communicating artery: 40%
  • Posterior communicating artery: 30%
  • Middle cerebral artery: 20%
  • Basilar artery: 10%

Classical Presentation (4 Features)

1. Sudden severe headache - "thunderclap", "worst headache of my life", "as if hit by a bat"
2. Transient loss of consciousness
3. Vomiting
4. Neck stiffness + sometimes focal neurological signs

Key point: A 3rd nerve palsy with pupillary involvement = posterior communicating artery aneurysm - urgent neurosurgical referral!

Important Clinical Alert

• 1/6 patients die before reaching hospital
• On arrival: 1/3 drowsy, 20% stuporous or in coma
• 50% are initially misdiagnosed - always think SAH in sudden severe headache
• About 1/3 have had a warning "sentinel headache" in the weeks before - a smaller bleed they recovered from

Investigations

• CT brain: positive in 95% within 24h, only 67% by 3 days
• If CT negative: Lumbar puncture (wait at least 6 hours after onset) - look for xanthochromia (yellow CSF = blood breakdown products - confirmed by spectrophotometry)

• Four-vessel cerebral angiogram (gold standard) - Fig 4a in images
• CT angiography increasingly used, less invasive - Fig 4b
• 1 in 10 patients with definite SAH will have no source found (low recurrence risk)

Complications (The Big 3)

1. Rebleeding from ruptured aneurysm
2. Cerebral vasospasm → ischaemia (reduced by nimodipine + hypervolaemia)
3. Hydrocephalus (CSF reabsorption blocked → needs drainage)

Treatment

• Transfer to neurosurgical centre
• Monitor: pulse, BP, Glasgow Coma Scale
• Prevent rebleeding: Coiling (endovascular - preferred if technically possible) or surgical clipping
• Reduce vasospasm: Nimodipine (calcium antagonist) + sustained hypervolaemia (3 litres saline/day)
• Avoid antihypertensives (worsen vasospasm/ischaemia)
• Treat hydrocephalus with drainage

Prognosis

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QUICK REVISION CHEAT-SHEET FOR YOUR ORAL

• Stroke types: 80% infarction / 15% ICH / 5% SAH
• Infarction causes: Emboli 30% / Thrombosis 30% / Small vessel 20%
• Hypertension = relative risk 5x for stroke (biggest modifiable risk factor)
• TIA precedes 10% of strokes; risk highest immediately after TIA
• rTPA window: 3 hours from onset
• SAH CT: positive 95% in 24h; LP if CT negative (after 6h)
• SAH aneurysm sites: Anterior comm 40%, Post comm 30%, MCA 20%, Basilar 10%
• Carotid endarterectomy: indicated for symptomatic stenosis >70%
• Aspirin reduces recurrence from 10% → 8%/year
• Anticoagulation in AF: reduces stroke risk from 12% → 4%/year

• Infarct vs haemorrhage: cannot be distinguished clinically - need CT
• TACS vs PACS: TACS has all 3 features (hemiparesis + hemianopia + cortical dysfunction)
• Lacunar vs cortical: Lacunar has NO cortical features (no aphasia, no neglect, no hemianopia)
• Wallenberg's (lateral medullary): crossed signs - ipsilateral face + contralateral body
• Locked-in syndrome: basilar artery occlusion - conscious but paralysed, only eye movement preserved
• SAH headache vs migraine: SAH is instantaneous "thunderclap"; migraine builds up over 15-30 min

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