Transient Ischaemic Attack: Diagnosis and Management

Introduction

A transient ischaemic attack (TIA) is an episode of neurological dysfunction caused by focal ischaemia of the brain, spinal cord or retina, without evidence of acute infarction on imaging.¹ The older, purely clinical definition - symptoms resolving within 24 hours - has been superseded by this tissue-based one, because imaging shows that many patients with rapidly resolving symptoms already have a small infarct, meaning they have had a stroke, not a TIA, however briefly the deficit lasted.

In practice, most true TIAs resolve within an hour, and a deficit lasting several hours is more likely to reflect infarction that has simply improved than resolving ischaemia. The label matters less than the response: a suspected TIA is managed with the same urgency as a stroke, because it is often the only warning a patient gets before a completed stroke.

TIA is common - lifetime prevalence is around 2% - and it is one of the highest-yield topics in finals because the entire management algorithm hinges on risk stratification and speed.

A practical difficulty worth anticipating is that the diagnosis rests entirely on a history of symptoms that have already resolved, often described by a patient who was frightened at the time and may not recall the sequence precisely. Establishing whether the deficit was focal and negative, whether it was maximal at onset, and how long it truly lasted, is what separates a TIA from its mimics - and a collateral account from anyone who witnessed the event is as valuable here as it is in suspected seizure.

Aetiology

The mechanisms are identical to those of ischaemic stroke, because a TIA and an ischaemic stroke sit on the same spectrum of the same underlying disease process - the difference is simply whether the ischaemia was brief enough, and collateral supply good enough, to avoid infarction.

• Artery-to-artery embolism from an atherosclerotic plaque, most importantly at the carotid bifurcation - the single most important cause to identify, because it is surgically treatable
• Cardioembolism - atrial fibrillation, recent myocardial infarction, valvular disease, patent foramen ovale (particularly in younger patients with no other risk factors)
• Small vessel (lacunar) disease - related to chronic hypertension and diabetes
• Hyperviscosity and haematological causes - polycythaemia, thrombocythaemia, sickle cell disease
• Hypoperfusion - severe carotid or vertebrobasilar stenosis with a systemic drop in blood pressure, producing watershed ischaemia rather than embolism

Risk factors

• Hypertension
• Atrial fibrillation and other cardioembolic sources
• Smoking
• Diabetes mellitus
• Dyslipidaemia
• Carotid artery stenosis
• Increasing age
• Previous TIA or stroke - by far the strongest predictor of a further event

Clinical features

Symptoms are focal, negative (loss of function rather than positive phenomena like jerking or shimmering lights, which point instead towards seizure or migraine), and of sudden onset, mirroring the territory involved:

• Amaurosis fugax - transient monocular visual loss, classically described as a curtain descending over one eye, caused by retinal artery ischaemia from an ipsilateral carotid source
• Unilateral weakness or sensory disturbance of the face, arm or leg
• Dysphasia if the dominant hemisphere is involved
• Homonymous hemianopia
• Ataxia, vertigo, diplopia or dysarthria if the posterior circulation is involved - often occurring in combination rather than alone, since an isolated one of these is more likely to be a peripheral or non-vascular cause
• Transient global amnesia is a distinct entity, not usually vascular, and should not be labelled a TIA

Risk stratification

The ABCD2 score was historically used to stratify short-term stroke risk after a suspected TIA, but current UK guidance has moved away from using it to determine urgency: NICE now recommends that all patients with a suspected TIA are treated as at high risk of stroke and are assessed by a specialist within 24 hours, regardless of score, because relying on a low score was found to miss patients who went on to have a stroke.² You should still recognise it, since it remains widely referenced and useful as a prognostic descriptor.

Clinical examination

• By definition, the focal neurological examination has often normalised by the time of assessment - document this explicitly rather than assuming no examination is needed
• Cardiovascular: pulse for atrial fibrillation, blood pressure in both arms, carotid bruits, murmurs
• Fundoscopy: retinal artery occlusion or embolic plaques (Hollenhorst plaques) if amaurosis fugax is described
• Visual fields, speech and limb examination to confirm resolution and document a baseline
• Cognitive screen if there is diagnostic uncertainty with transient global amnesia or a functional presentation

Differential diagnosis

• Migraine with aura - positive visual symptoms spreading over 20-30 minutes, followed by headache, in a younger patient with a similar previous history
• Focal (partial) seizure or Todd's paresis - positive motor phenomena, or post-ictal weakness following an unwitnessed seizure
• Hypoglycaemia - always check capillary glucose
• Peripheral vestibular disorders (BPPV, vestibular neuritis) - isolated vertigo without other focal signs
• Transient global amnesia - sudden, isolated anterograde amnesia lasting hours, with preserved personal identity and no other focal deficit
• Functional neurological disorder
• Structural lesion - subdural haematoma or tumour can produce transient, fluctuating focal symptoms
• Multiple sclerosis relapse - in a younger patient, especially with optic neuritis or other demyelinating features

Investigations

Every patient with a suspected TIA needs urgent brain and vascular imaging, arranged the same day wherever possible, since the diagnosis and the case for urgent secondary prevention both depend on it.

• Diffusion-weighted MRI - the imaging of choice, since it can detect a small acute infarct that would reclassify the event as a stroke rather than a TIA, and helps localise the likely vascular territory
• CT head - if MRI is not readily available, mainly to exclude an alternative diagnosis such as haemorrhage or a mass lesion
• Carotid Doppler ultrasound - urgently, for any anterior circulation event, to identify stenosis amenable to endarterectomy
• ECG - looking for atrial fibrillation
• Prolonged ECG monitoring - if cardioembolism is suspected but the initial ECG is normal
• Bloods: FBC (polycythaemia, thrombocythaemia), glucose and HbA1c, lipid profile, U&Es, clotting
• Echocardiography - if a cardiac source is suspected, particularly in younger patients

Management

Immediate

Aspirin 300 mg should be given immediately to anyone with a suspected TIA, unless there is a contraindication (bleeding disorder, already on an anticoagulant - seek specialist advice) or the diagnosis is clearly not vascular.²

Secondary prevention

Prevention is started immediately, at the point of diagnosis, rather than deferred to a later clinic - the risk of stroke is front-loaded into the days after a TIA.

• Antiplatelet therapy: clopidogrel 75 mg once daily is first-line long-term; aspirin plus dipyridamole is an alternative if clopidogrel is not tolerated
• Anticoagulation: a DOAC replaces antiplatelet therapy if atrial fibrillation or another cardioembolic source is found, once haemorrhage has been excluded
• High-intensity statin: atorvastatin 20-80 mg regardless of baseline cholesterol
• Blood pressure control to standard targets, once the diagnosis is confirmed
• Carotid endarterectomy: for symptomatic carotid stenosis of 50-99% (NASCET criteria), performed within 2 weeks of the event wherever possible - benefit falls sharply the longer surgery is delayed
• Smoking cessation, diabetic control, and lifestyle modification

Complications

The overriding concern is progression to a completed, disabling stroke - risk is highest in the first 48 hours and remains substantially elevated for weeks. Anxiety and fear of a further event are common and should be addressed explicitly, as should the practical impact of a temporary driving ban on employment and independence.

Red flags

The purpose of the TIA pathway is to intervene during the narrow window in which recurrence risk is highest. The features below indicate a patient at the upper end of that risk, in whom same-day rather than next-day assessment is appropriate.

Prognosis

Without treatment, the risk of stroke after a TIA is high - historically quoted as around 1 in 12 (8%) within the first week and up to 1 in 5 within 3 months, concentrated heavily in the first 48 hours. With prompt assessment, imaging and secondary prevention, this risk falls by roughly 80%, which is why the 24-hour pathway exists and why a TIA should never be treated as a minor or reassuring event.⁴

The reason urgent assessment is so effective is that the recurrence risk is heavily front-loaded. The mechanism that produced the TIA - an unstable carotid plaque, or an atrial thrombus - is usually still present and still active in the hours and days afterwards. Intervening at that point, with antiplatelet therapy, a statin, blood pressure control and, where indicated, carotid surgery, removes or stabilises the source before it embolises again.

This explains why the same interventions delivered weeks later achieve far less. The EXPRESS study demonstrated that moving assessment and treatment from a median of several days to the same day reduced 90-day stroke risk by around 80%, which is a larger effect than almost any drug in stroke medicine and is achieved purely by changing the speed of the pathway.

A final point concerns diagnostic humility. TIA is diagnosed retrospectively from a history of symptoms that have resolved, and a meaningful proportion of referrals turn out to be mimics - migraine, syncope, seizure or functional symptoms. Overdiagnosis carries real costs: lifelong antiplatelet therapy, a driving ban, insurance consequences and considerable anxiety. Where the history is genuinely not suggestive of a focal ischaemic event, saying so clearly and looking for the true cause is better medicine than defensively labelling every transient symptom a TIA.