Transient Ischaemic Attack (TIA)

Meet the patient

A 72-year-old diabetic man is brought by his wife. Twenty minutes ago his right face and arm went weak and he could not get the words out; the episode lasted 30 minutes and has now completely resolved. His blood pressure is 168/96, and when you feel his pulse it is irregularly irregular.^[2]

Two questions own the next hour, and they own every TIA: was this really a TIA, or a mimic? (check the glucose and scan the head first) and what is the mechanism — because the mechanism chooses the treatment. An irregular pulse points straight at atrial fibrillation, which means anticoagulation, not antiplatelets — and getting that single fork right is the difference between preventing a stroke and causing a bleed.^[1][2]

A warning shot, not a benign event — and why the clock was retired

In animal studies, cerebral blood flow thresholds separate tissue fate: about 20 mL per 100 g per minute defines the penumbra (electrically silent but viable neurons), and about 10 mL per 100 g per minute marks the infarct core. In human stroke the reported thresholds run far wider (penumbra 14 to 35, core below 9 mL per 100 g per minute), so treat the classic figures as teaching approximations.^[9] Duration matters as much as depth. Flow in a TIA is restored while the tissue is still viable, which is why most true TIAs last under one hour; the old 24-hour cut-off was retired because it misclassified patients whose symptoms outlasted the ischaemia but whose tissue never infarcted.^[1][10]

The modern tissue-based definition (endorsed by the AHA/ASA in 2009) is a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction. It deliberately retires the older time-based definition (symptoms resolving within 24 hours), because symptom duration is a poor discriminator of tissue fate — up to 30 percent of clinically diagnosed TIAs show infarction on diffusion-weighted MRI and are therefore reclassified as ischaemic stroke. The practical consequence: the boundary between TIA and minor stroke is set by imaging, not the clock.^[1]

The 5-10-20 numbers — and why urgent care pays

These are the numbers that win or lose a TIA stem, and they are non-negotiable.^[2]

The promise behind those numbers is the EXPRESS study: simply accelerating assessment and treatment reduced the 90-day stroke risk from 10.3 percent to 2.1 percent — an 80 percent relative reduction. That single finding is why "urgent" replaced "routine" in every modern guideline, and why a TIA clinic seen the same week is not optional.^[6]

Risk factors are the standard atherosclerotic and thromboembolic set, and they are also the targets of secondary prevention: hypertension (the single biggest modifiable factor), atrial fibrillation (the most important treatable cause — untreated AF carries an annual stroke risk of roughly 4 to 5 percent, rising with CHA2DS2-VASc factors), diabetes (a risk factor and, via hypoglycaemia, a dangerous mimic), dyslipidaemia, smoking, obesity, sedentary lifestyle, excessive alcohol, age, male sex, family history, prior TIA or stroke, and carotid or peripheral arterial disease. The factors predicting the highest early recurrence are atrial fibrillation, severe symptomatic carotid stenosis, crescendo events, and diabetes.^[1]

Why it resolves — recanalisation before the penumbra dies

A TIA shares the ischaemic cascade of a completed stroke; what differs is that cerebral blood flow is restored before the penumbra progresses to irreversible infarction. That single fact explains the duration, the recovery, and the urgency.^[1]

An embolus — from a ruptured carotid plaque, a left atrial thrombus in atrial fibrillation, or an aortic arch lesion — lodges in a cerebral or retinal artery, or a small penetrating artery transiently occludes. Downstream tissue becomes ischaemic: ATP depletion fails the sodium-potassium pump and drives cytotoxic oedema; glutamate release activates NMDA receptors and floods neurons with calcium. A central core of the most severely ischaemic tissue is surrounded by the penumbra — hypoperfused but salvageable, the target of all acute stroke therapy. In TIA the embolus fragments, lyses by endogenous fibrinolysis, or passes distally, and the collateral circulation restores perfusion before the penumbra infarcts.^[1]

In animal studies, cerebral blood flow thresholds separate tissue fate: flow of about 20 mL per 100 g per minute defines the penumbra (electrically silent but viable neurons), and about 10 mL per 100 g per minute marks the infarct core. A systematic review in human stroke found the reported thresholds far wider — penumbra 14 to 35 and core below 9 mL per 100 g per minute — so the classic numbers are teaching approximations, not bedside constants.^[9] Duration matters as much as depth. Flow in a TIA is restored while the tissue is still viable, which is why most true TIAs last under one hour; the old 24-hour cut-off was retired because it misclassified patients whose symptoms outlasted the ischaemia but whose tissue never infarcted.^[1][10]

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The three mechanisms — and the one that points to the retina

The TOAST classification drives the workup because the mechanism chooses the secondary prevention. Name the source, then treat it.^[1]

Read the deficit — anterior, posterior, lacunar

The cardinal feature is a sudden-onset focal deficit that is identical to stroke at onset, maximal immediately, and then resolves completely — usually within minutes, almost always within one hour. The territory tells you the artery.^[2]

Anterior (carotid) circulation — unilateral weakness or clumsiness of face, arm and/or leg (MCA affects face and arm more than leg; ACA affects the leg preferentially); dysphasia or aphasia (dominant hemisphere); neglect and visuospatial disturbance (non-dominant); homonymous hemianopia; and amaurosis fugax, the only TIA that produces monocular symptoms.^[1]

Posterior (vertebrobasilar) circulation — diplopia, vertigo, dysarthria, dysphagia; bilateral or alternating limb weakness; crossed sensory loss; ataxia; bilateral or isolated homonymous hemianopia; drop attacks; and crossed signs (ipsilateral cranial nerve palsy with contralateral motor or sensory deficit), the hallmark of a brainstem lesion.^[1]

Lacunar syndromes — pure motor hemiparesis, pure sensory stroke, ataxic hemiparesis, and the dysarthria-clumsy-hand syndrome — have a good short-term prognosis but a high lifetime vascular risk, because they signal systemic small-vessel disease.^[1]

Atypical presentations are deliberate examiner traps. Older patients may present with confusion or reduced consciousness rather than a clean focal deficit. Diabetic patients may have hypoglycaemia masquerading as a focal deficit — always check finger-prick glucose first. Isolated vertigo can be a posterior-circulation TIA; the HINTS examination (Head Impulse, Nystagmus, Test of Skew) is the bedside discriminator — a central, "bad" pattern (normal head-impulse test, direction-changing nystagmus, skew deviation) points to stroke, not benign vestibular neuritis.^[2]

Exclude the mimics — glucose first, always

TIA is a diagnosis of inclusion that requires exclusion of mimics, and the single most important mimic is the cheapest to reverse: hypoglycaemia. Check a finger-prick glucose in every patient before labelling the event a TIA.^[2]

The tempo discriminator, one line: a TIA is sudden, negative, and maximal at onset; a migraine aura is positive and marching; a postictal paresis follows a seizure and resolves more slowly; a tumour is progressive. Hypoglycaemia and a subdural can fool the unwary — glucose and CT close both traps.^[2]

The ABCD2 score — what it does, and what it cannot do

The ABCD2 score stratifies the two-day stroke risk after a suspected TIA and drives triage urgency. It does not diagnose TIA and it does not exclude mimics — it is purely a risk-prediction tool, derived and validated by Johnston and colleagues across four independent cohorts.^[3]

The total ranges from 0 to 7. The original validation reported the two-day stroke risks: high risk (6 to 7) — 8.1 percent; moderate (4 to 5) — 4.1 percent; low (0 to 3) — 1.0 percent.^[3]

The workup — exclude mimics, then find the mechanism

The workup serves two aims: exclude mimics and haemorrhage, and identify the mechanism that will direct secondary prevention. The minimum dataset is brain imaging, carotid imaging, ECG and cardiac monitoring, and baseline bloods.^[1]

1. Brain imaging — CT brain first to exclude haemorrhage and mass lesions; MRI with diffusion-weighted imaging is the most sensitive modality and confirms or excludes infarction. Infarction on MRI means the event is a stroke, not a TIA — which upstages both prognosis and management.
2. Carotid imaging within 24 hours for any anterior-circulation event — duplex Doppler ultrasound first-line to grade stenosis; CT or MR angiography confirms the degree (graded by the NASCET method) and maps the arch for surgery.
3. ECG to detect atrial fibrillation; if normal, prolonged monitoring (24-hour Holter, external loop recorder, or an implantable loop recorder) to catch paroxysmal AF — the commonest finding in cryptogenic TIA.
4. Echocardiography — transthoracic if a cardioembolic source is suspected; transoesophageal for valvular disease, left atrial thrombus, or a patent foramen ovale (especially in the young).
5. Bloods — glucose and HbA1c, fasting lipids, full blood count, urea and electrolytes, coagulation. In the young, add a thrombophilia screen, toxicology, autoimmune and vasculitic markers, and dedicated dissection imaging (fat-suppressed neck MRI or CTA).^[1]

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The immediate bundle — glucose, scan, twenty-one days

Admit any patient with an ABCD2 of 4 or higher, crescendo or recurrent events, diagnostic uncertainty, those unable to comply with outpatient care or living alone without support, and any patient with posterior-circulation symptoms or a positive DWI (which means stroke, not TIA). The public-facing message driving every downstream benefit is FAST — Face, Arm, Speech, Time.^[2]

Twenty-one days of dual — CHANCE and POINT

For a non-cardioembolic TIA, give dual antiplatelet therapy — aspirin plus clopidogrel — for 21 days, then step down to monotherapy. CHANCE used a clopidogrel 300 mg load, then 75 mg daily, on top of aspirin; POINT loaded with clopidogrel 600 mg. Neither trial fixed the aspirin dose (CHANCE left day-one aspirin at a clinician-determined 75 to 300 mg; POINT allowed 50 to 325 mg), so the common UK loading practice of aspirin 300 mg is guideline convention, not trial protocol.^[1][4][5]

The 21-day window rests on two landmark trials that every examiner expects you to name.^[1]

CHANCE showed the benefit; POINT and MATCH showed the bleeding cost of continuing. In MATCH, adding aspirin to long-term clopidogrel after a stroke or TIA doubled life-threatening bleeding over 18 months without a meaningful ischaemic gain — which is exactly why dual therapy is capped at 21 days before stepping down to monotherapy.^[4][5][11]

Cardioembolic TIA — anticoagulate, do not antiplatelet

If the mechanism is atrial fibrillation, give anticoagulation — not antiplatelets. A direct oral anticoagulant (apixaban, rivaroxaban, dabigatran, or edoxaban) is preferred over warfarin for non-valvular AF on the strength of the Ruff 2014 meta-analysis, which pooled the four pivotal DOAC trials (over 71,000 patients) and found DOACs reduced stroke or systemic embolism by 19 percent and intracranial haemorrhage by about half versus warfarin, with similar major bleeding.^[8]

Because a TIA by definition produces no infarct, anticoagulation can be started immediately — there is no haemorrhagic-transformation delay as there is after a completed cardioembolic stroke.^[1]

Carotid endarterectomy — the highest-NNT operation in stroke medicine

For symptomatic carotid stenosis, offer carotid endarterectomy for stenosis of 50 percent or more, with the greatest benefit and lowest NNT for stenosis over 70 percent (NNT about 3).^[7]

Timing is everything. The operation should be performed within 2 weeks of the event, because the benefit collapses with delay — the NNT rises from about 3 within 2 weeks to over 100 beyond 12 weeks. Carotid artery stenting is an alternative in selected patients (younger, high surgical risk, hostile neck) but carries a higher periprocedural stroke risk in older patients.^[7]

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The targets — and what the bundle delivers

Every TIA patient leaves on the same vascular-risk bundle, individualised to the mechanism.^[1]

• Blood pressure — lower it; in PROGRESS a perindopril-based regimen (perindopril plus indapamide where tolerated) cut recurrent stroke by 28 percent overall and by 43 percent with combination therapy.^[12]
• Lipids — a high-intensity statin: in SPARCL, atorvastatin 80 mg daily reduced fatal or nonfatal stroke over five years (hazard ratio 0.84).^[13]
• Glycaemic control — optimise diabetes (HbA1c target individualised).
• Smoking cessation and lifestyle — diet, weight, exercise, alcohol moderation. In INTERSTROKE, ten potentially modifiable risk factors accounted for about 90 percent of the population attributable risk of stroke, with hypertension alone at about 48 percent.^[14]

Modelled cumulatively, applying five proven strategies together — diet, exercise, an antiplatelet, a statin, and an antihypertensive — prevents about four-fifths of recurrent vascular events after stroke or TIA.^[15] EXPRESS showed what that looks like in practice: accelerating assessment and treatment cut the 90-day stroke risk from 10.3 percent to 2.1 percent.^[6]

The scenarios that change the answer

• Crescendo TIA (recurrent events clustering over hours to days) — a marker of very high imminent stroke risk. Admit, image urgently, expedite definitive therapy (CEA or anticoagulation) once the mechanism is found; pooled trial data show operative benefit is greatest within two weeks of the last event.^[16]
• Severe symptomatic carotid stenosis (over 70 percent) — CEA within 2 weeks plus best medical therapy; the highest-NNT intervention in stroke medicine.
• Cardioembolic TIA (atrial fibrillation) — anticoagulation with a DOAC replaces antiplatelets; start immediately as there is no infarct to transform.
• Posterior-circulation TIA — obtain urgent CT angiography of head and neck; if symptoms progress to basilar artery occlusion, this is a mechanical thrombectomy emergency.
• Young patient (under 45) — a different workup: carotid or vertebral dissection (fat-suppressed neck MRI or CTA), patent foramen ovale (bubble echo and TOE), thrombophilia, substance use, autoimmune vasculitis. ABCD2 underperforms here.^[2]

How TIA patients come to harm — the preventable list

• Labelling a mimic (hypoglycaemia, migraine aura, postictal paresis) as a TIA — or, conversely, dismissing a true TIA as trivial.^[2]
• Failing to exclude haemorrhage on imaging before starting antiplatelets — a microbleed or early intracerebral haemorrhage can present with a transient deficit.^[1]
• Over-relying on ABCD2 — it underestimates risk in the young and ignores carotid stenosis and atrial fibrillation.^[1]
• Delaying carotid endarterectomy beyond 2 weeks — the benefit collapses with delay.^[7]
• Giving antiplatelets instead of anticoagulants in atrial fibrillation.^[8]
• Continuing dual antiplatelet therapy well beyond 21 days into accumulating bleeding risk.^[5]
• Sending the patient home with a "come back if it happens again" and no booked review.^[2]

Prognosis, disposition, and driving

With urgent assessment and aggressive secondary prevention, the 90-day stroke risk can be reduced by up to 80 percent (EXPRESS: 10.3 percent to 2.1 percent). The highest-risk period is the first 48 hours, which is exactly why urgent rather than routine assessment is mandated. The features predicting the highest early stroke risk are an ABCD2 of 6 or higher, severe carotid stenosis, atrial fibrillation, crescendo events, and a positive DWI.^[6][1]

Long term, TIA patients have a reduced life expectancy, mostly from cardiovascular disease — which is why lifelong vascular risk reduction is essential rather than a finite course. Secondary prevention also reduces the risk of cognitive decline and vascular dementia.^[2]

A patient is safe for discharge from the TIA service once the workup is complete, secondary prevention is started, carotid imaging is arranged or performed, and follow-up is booked — with clear safety-net advice to return immediately if symptoms recur.^[1]

Driving advice (DVLA, UK): a patient must not drive for at least one month after a single TIA; after multiple TIAs within a short period, not until symptoms have been controlled for three months, and the DVLA must be notified. Regional rules differ — advise the patient to check their local licensing authority.^[2]

Special populations

• Atrial fibrillation — anticoagulation with a DOAC, not antiplatelets; start immediately as there is no infarct.
• Symptomatic carotid stenosis — endarterectomy within 2 weeks for stenosis over 50 percent; NNT about 3 for over 70 percent; benefit falls rapidly after 2 weeks.
• Crescendo TIA — very high stroke risk; admit, image, and consider urgent intervention.
• Pregnancy — a hypercoagulable state raising TIA and stroke risk; aspirin is safe, DOACs are avoided, and low-molecular-weight heparin is used if anticoagulation is required.
• Diabetic — higher risk and worse outcome; tight glucose and blood-pressure control; remember that hypoglycaemia is a mimic.
• Already on anticoagulants presenting with TIA — assess adherence and the INR or DOAC level; exclude intracranial bleed on imaging before continuing or escalating therapy.^[1][2][7][8]

The evidence and the regions

The AHA/ASA 2019 acute ischaemic stroke guideline (Powers et al.) codified the 21-day dual-antiplatelet window, the urgency of carotid intervention, and the requirement for 24-hour assessment; NICE NG128 sets the UK pathway (immediate aspirin, specialist assessment within 24 hours, no ABCD2-based triage); and the European Stroke Organisation guidelines agree on urgency and short-term dual therapy. EXPRESS established the benefit of urgent treatment; CHANCE and POINT underpin the 21-day window; Johnston 2007 validated ABCD2; and the Ruff 2014 meta-analysis made DOACs first-line for AF.^{[1][3][4][5][6][7][8][17]}

The mantra, and the mnemonic

The mantra: check the glucose, scan the head, twenty-one days of dual — then find the mechanism and treat it.^[1][2]

Ward-round test — three stems, thirty seconds each