NeurologyTier 1Disease (DEADMAN)

Transient ischaemic attack

Description

Transient episode of focal neurological dysfunction from focal brain, spinal cord or retinal ischaemia, without acute infarction (tissue-based, not time-based, modern definition)
*A medical emergency, not a benign warning* - highest stroke risk is in the first 48 hours

Same mechanisms as ischaemic stroke, without permanent infarct

Large artery atherosclerosis - carotid stenosis, artery-to-artery embolism
Cardioembolic - AF (commonest cardiac source), valvular disease, recent MI, LV thrombus
Small vessel disease - lacunar TIA
Other: dissection (younger patients, neck pain/trauma), hypercoagulable states, vasculitis

Mimics to actively exclude

Hypoglycaemia, focal seizure with Todd's paresis, migraine with aura, syncope, functional/psychogenic, peripheral vestibular disease, transient global amnesia

A. Clinical

Sudden-onset focal negative neurological symptoms (weakness, sensory loss, dysphasia, visual loss/field defect, ataxia, diplopia) fully resolving, classically within an hour, always <24h
No modern imaging-independent time cutoff defines TIA - if diffusion-weighted MRI shows infarct, it is a stroke regardless of symptom duration

B. Risk stratification

ABCD2 score (Age, BP, Clinical features, Duration, Diabetes) - stratifies early stroke risk but no longer used alone to determine whether specialist review is urgent; guidelines now recommend urgent specialist assessment for all suspected TIA regardless of score
High-risk features requiring same-day work-up: crescendo TIA (>=2 in a week), AF, carotid territory symptoms, on anticoagulation

C. Investigations - all done urgently (same day where possible)

CT brain (exclude haemorrhage/mimic) +/- MRI with DWI (defines true TIA vs stroke, more sensitive)
Carotid imaging (duplex ultrasound, CTA, or MRA) - for anterior circulation symptoms, to identify stenosis amenable to endarterectomy
ECG and prolonged cardiac monitoring (24-72h Holter, or longer if cryptogenic) - detect paroxysmal AF
Echocardiogram if cardioembolic source suspected
Bloods: FBE, UEC, glucose, lipids, coagulation

A. Immediate - treat as a stroke emergency, not routine outpatient referral

All suspected TIA reviewed by a specialist/stroke service within 24 hours
Start antiplatelet immediately unless haemorrhage excluded is pending or anticoagulation already indicated

B. Antiplatelet therapy

High-risk TIA (ABCD2 >=4) or minor stroke: short-term dual antiplatelet therapy - aspirin + clopidogrel (or aspirin + ticagrelor), started within 24 hours, continued 21-30 days, then monotherapy (usually clopidogrel) long-term
Lower-risk or later presentation: aspirin monotherapy, transitioning to clopidogrel for long-term secondary prevention
*Do not continue DAPT long-term* - bleeding risk exceeds benefit beyond the short window

C. Anticoagulation

AF-associated TIA: anticoagulate (DOAC preferred) - typically after excluding haemorrhage and per bleeding-risk-adjusted timing (no infarct present, so earlier initiation than post-stroke is generally reasonable)

D. Carotid revascularisation

Symptomatic carotid stenosis >=70% (or 50-69% in selected patients): carotid endarterectomy, ideally within 2 weeks of the event - benefit falls rapidly with delay

E. Risk factor modification (same as ischaemic stroke)

Atrial fibrillation, carotid stenosis, hypertension, diabetes, hyperlipidaemia, smoking
Prior stroke/TIA, peripheral vascular disease, ischaemic heart disease
Obstructive sleep apnoea

Stroke risk after TIA: ~5% at 2 days without treatment, ~10% at 7 days, ~10-20% at 90 days
Early specialist assessment and treatment reduces subsequent stroke risk by up to ~80%
Crescendo TIA and high-grade carotid stenosis carry the highest short-term risk
Long-term prognosis mirrors ischaemic stroke risk factor burden if not modified

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