Ischaemic Stroke & TIA

Stroke

Three main mechanisms: single perforator/small vessel disease (lacunar syndrome — in situ small vessel disease); cardio-embolic (heart-to-artery embolism); large vessel artery-to-artery embolic infarcts.

Second most common cause of death in the Western world.

History

• FAST recognition: Face dropped, Arms — can they lift both, Speech slurred/understanding impaired, Time critical — call 000.
• Major risk factors: hypertension, smoking, cardiovascular disease, atrial fibrillation, diabetes.
• Other risk factors: cardiac failure, dyslipidaemia, obesity, alcohol excess, oral contraception, migraine, stress.
• Differential: syncope, seizure, migraine, cerebral tumour/other space-occupying lesion, hypoglycaemia, hyponatraemia, delirium, head injury, MELAS syndrome.

Examination

Vital signs (SpO₂, BP, pulse, temperature, BSL); full neurological exam (cranial nerves, upper/lower limbs).

Investigations

• Acute: immediate brain imaging (CT) if a reperfusion candidate, otherwise within 60 minutes. Vascular imaging (CTA or MRA, aortic arch to cerebral vertex) for potential thrombectomy candidates. ECG. Echocardiogram for thromboembolic source.
• Non-acute: carotid Doppler/CTA/MRA; echocardiogram; fasting glucose/HbA1c; fasting lipids. Careful evaluation and workup for an embolic source with a transthoracic or transoesophageal echocardiogram, Holter monitoring, and vascular imaging are mandatory to guide appropriate evidence-based treatment and prevent stroke recurrence.

Management

• Immediate ambulance transfer to hospital, notify the stroke team ahead of arrival.
• IV thrombolysis for eligible patients.
• Antiplatelet therapy as soon as imaging excludes haemorrhage, for patients not receiving reperfusion therapy.
• Management in a dedicated stroke centre is recommended; refer to rehabilitation after acute care.
• Driving: individualised assessment of residual deficit — minimum no driving for 4 weeks (private), 3 months (commercial), for everyone.
• Secondary prevention: smoking cessation, diet modification, regular physical activity, weight loss, reduced alcohol, BP <130/90; long-term antiplatelet (aspirin 100mg) for high-risk minor stroke/TIA — add clopidogrel to aspirin for the first 3 weeks to prevent early recurrence, then stop the dual therapy (long-term dual antiplatelets are not indicated for secondary cerebrovascular prevention without acute coronary disease/recent stent); anticoagulation for AF. The Stroke Foundation currently advises dual antiplatelet therapy for three weeks after a non-valvular, non-arrhythmic minor ischaemic stroke or high-risk TIA, then switching to monotherapy. High-dose statin (e.g. atorvastatin 80mg or rosuvastatin 40mg) is first-line for all patients after an ischaemic stroke, regardless of cholesterol level.

TIA

Focal neurological symptoms from focal ischaemia that have fully resolved.

History

Sudden onset, short duration (<60 min), usually complete recovery within 24h, consciousness usually preserved. 90% anterior circulation — carotid TIAs cause unilateral symptoms; vertebrobasilar TIAs often cause bilateral/crossed features.

Differential: classic or variant migraine with aura (hemiplegic, ophthalmoplegic, retinal), focal epileptic seizures, multiple sclerosis, transient global amnesia, syncope, intracranial structural lesion (AVM, tumour), vestibular disorders (labyrinthitis, BPPV, Meniere’s), hypoglycaemia, adverse drug/toxic reactions, peripheral nerve lesions (carpal tunnel, Bell’s palsy), psychological conditions (anxiety/hyperventilation, panic, somatisation).

Examination

Neurological exam (cranial nerves, limbs); BP and pulse.

Investigations

• Anterior circulation symptoms (cognitive impairment, weakness/ incoordination, numbness/sensory loss, dysarthria, visual loss): early carotid imaging (CTA aortic arch to cerebral vertex, carotid Doppler, or MRA) — do not delay beyond 2 days (strong recommendation).
• MRI brain to exclude stroke mimics and intracranial haemorrhage (weak recommendation).
• ECG for AF during initial assessment; consider prolonged cardiac monitoring.
• Echocardiogram for thromboembolic source.

Management

• Symptomatic patients should present to ED.
• High-risk indicators (crescendo TIA, current/suspected AF, current anticoagulant use, carotid stenosis, high ABCD² score) → urgent specialist referral.
• If AF is diagnosed, anticoagulate after brain imaging excludes ICH.
• Lifestyle modification: smoking cessation, exercise, optimise diabetes and dyslipidaemia.
• Driving: no driving for 2 weeks (private), 4 weeks (commercial).
• See Stroke section above for secondary prevention.

Carotid artery stenosis

Classified as symptomatic or asymptomatic — this distinction significantly alters management. Carotid artery stenosis is one of the major causes of acute ischaemic stroke (~20% of cases), typically affecting the anterior circulation (hemiplegia, dysphasia, monocular vision loss via the retinal artery) — not a differential for vertigo/cerebellar symptoms, since ICA emboli preferentially enter the anterior circulation.

• Symptomatic = a haemodynamically significant ICA stenosis (>50%) linked to a neurological ischaemic event in the preceding 6 months. Symptomatic plaques are considered “unstable,” similar to acute coronary syndrome pathophysiology.
  • >70–99% stenosis: carotid endarterectomy (CEA) — the gold standard, reducing recurrent stroke risk from >25% (medical therapy alone) to 9–15%. Ideally performed within 2 weeks of the event (risk of re-embolisation is highest in the first 2 weeks, remaining elevated to 6 weeks) — refer/admit promptly.
  • 50–69% stenosis: a “grey area” — refer for consideration.
  • ≤49% stenosis: surgery confers no benefit — observe.
• Asymptomatic — best medical therapy (BMT) is the mainstay: aspirin monotherapy, statin therapy, and cardiovascular risk modification (smoking cessation, BP control, dyslipidaemia treatment, diabetes screening/control — antiplatelet therapy, statin therapy and cardiovascular risk modification). There is no role for carotid stenting in asymptomatic disease.
  • Carotid endarterectomy for 70–99% stenosis (also refer for consideration at 50–69%).
  • >80% stenosis: refer for non-urgent vascular surgical review to consider surgery — benefit is greatest in younger patients with fewer comorbidities (more lifetime stroke-risk reduction to gain); older patients with more comorbidities benefit less and carry a higher surgical complication rate.
  • <80% stenosis: referral is not usually required — annual carotid Doppler surveillance to monitor progression (surveillance may reasonably stop in elderly patients with significant comorbidities).
• Carotid Doppler ultrasound is the first-line investigation (inexpensive, non-invasive, accurate vs angiography, but sonographer-dependent) — should be performed at an accredited vascular laboratory. CT angiography is a useful secondary modality, particularly for surgical planning.
• Carotid artery stenting carries a higher periprocedural stroke rate than CEA and is reserved for patients in whom CEA is contraindicated (prohibitive anaesthetic risk, “hostile neck” from prior surgery/radiotherapy).
• Post-CEA follow-up: carotid Doppler at ~4–6 weeks and 6 months to check for restenosis.