Clinical Review - Transient ischaemic attack

How to assess, diagnose and manage TIA in primary care. By Dr Sam Qureshi, Dr Angela Clarke and Professor Anthony Rudd.

TIAs are caused when a blood vessel becomes blocked (Photograph: Zephyr/SPL)
TIAs are caused when a blood vessel becomes blocked (Photograph: Zephyr/SPL)

Section 1: Epidemiology and aetiology

Every year in England approximately 20,000 people will have their first transient ischaemic attack (TIA)1 with an incidence rate of 0.5 in 1,000.

A large proportion of TIAs go unrecognised, with about half never coming to medical attention.2 Cerebrovascular disease is the third largest cause of death in England. It is the leading cause of disability in England, commonly affecting communication, motor function and sensation. Major strokes are often preceded by TIA, but are often not recognised by patients, so not reported.

The care of patients with TIA has improved dramatically in the past decade, with work focusing on early recognition and prevention of more disabling events. An understanding of the different mechanisms is crucial to treatment and prevention.

TIAs are caused when a blood vessel within the brain is blocked, either by thrombus or material from an atherosclerotic plaque. Cells die within the brain due to ischaemia, resulting in the clinical presentation.

TIA and stroke differ in terms of symptom duration, with TIA typically lasting for less than an hour. However, the aetiology and epidemiology are the same.

The classification for stroke is valuable in understanding the pathophysiology of TIA.

  • Large-artery events are caused by stenotic lesions in the internal carotid artery, anterior or middle cerebral arteries or in the posterior circulation in the vertebral or basilar territories. Any obstruction at these sites can cause TIA symptoms, especially if collateral circulation is inadequate.
  • Embolic events usually arise from a process starting from an extracranial large artery or from the heart, and occasionally from smaller vessels within the brain. Cardiac causes are most commonly secondary to AF or left ventricular disease.
  • Lacunar or small-vessel events are due to stenosis of one of the intracranial vessels, anterior from the middle cerebral artery or its branches and posteriorly from the vertebro-basilar system. The process involved here is usually atherosclerosis driven by risk factors such as hypertension and hypercholesterolaemia.

Section 2: Making the diagnosis

A diagnosis of TIA warrants urgent assessment by a specialist. All patients with ongoing symptoms suggestive of stroke rather than TIA should be urgently transferred to hospital.

TIA is a sudden onset of transient focal neurological deficit, often lasting for only a few minutes, although the definition is for all symptoms and signs to have completely resolved within 24 hours. Patients will often present late and, therefore, the diagnosis needs to be made on history rather than examination and investigation.

Differential diagnoses
In TIA, symptoms result from a sudden change in vascular dynamics, so they will be of sudden onset. Description of an insidious onset is not suggestive of TIA. The symptoms are also maximal at the time of onset followed by a gradual recovery. Symptoms that stutter or are intermittent are less suggestive of TIA and may represent other important diagnoses, such as migraine, tumours or demyelination. Symptoms that last for a few seconds and recurrent, frequent, stereotypical events are also unlikely to be due to TIA, and alternatives such as focal epilepsy should be considered.

Many have the perception that headache is part of a TIA syndrome. While the presentation of headache also warrants careful evaluation, isolated, severe headache is rare in TIA and more likely to be migraine.

Common conditions that mimic TIA include seizures, sepsis, delirium, hypoand hyperglycaemia, migraine, space-occupying lesions and functional disorders.

Symptoms of TIA
Anterior circulation symptoms involving the carotid artery circulation include unilateral weakness or numbness, speech disturbance, visual defects such as hemianopia or amaurosis fugax – a painless transient monocular blindness, classically described as a curtain descending across the visual field.

Posterior circulation symptoms involving the vertebro-basilar system include ataxia, articulation difficulty, diplopia, bilateral visual loss and again hemianopic visual defects. Isolated vertigo, syncope or amnesia are not usually caused by TIA.

The pattern of symptoms can help to reach a diagnosis. Symptoms relating to a specific neurological vascular territory are supportive of TIA. For example, unilateral weakness and aphasia, or visual field defects with other posterior circulation symptoms such as ataxia and dysarthria.

Patients with suspected TIA should receive aspirin immediately unless contraindicated, and have some initial basic investigations, most importantly a blood glucose, routine observations (pulse and BP) and ECG. The subsequent assessment, either in primary or secondary care, should include a stroke risk ABCD2 score (see table).3 This stratifies patients into high-risk (ABCD2 scores of four or more) and lower-risk patients. Many hospitals offer a daily TIA assessment service for patients requiring urgent or other hospital admission. Those at lower risk can be referred to a TIA clinic, where they should be seen, assessed and management instituted within seven days.3

Age >60 years = 1 point
BP >140/90mmHg = 1 point
Clinical features
  Unilateral weakness = 2 points
  Speech disturbance without weakness = 1 point
Duration of symptoms
  >60 minutes = 2 points
   10-59 minutes = 1 point
Diabetes = 1 point

Further investigations will be based on risk stratification and exclusion of differential diagnoses. This includes a full blood work-up and possible brain imaging. Diffusion-weighted MRI is the imaging modality of choice. It should be performed within seven days in low-risk patients and within 24 hours for those at high risk. When MRI is not possible, CT can be used. CT is especially useful in identifying haemorrhages and space-occupying lesions. It is reasonable not to perform brain imaging when the history is suggestive of migraine or metabolic derangement. The work-up will also include cardiac investigations to define the aetiology and facilitate appropriate treatment.

All patients with suspected TIA should have Doppler ultrasonography looking for carotid and vertebro-basilar disease. A Holter monitor and echocardiogram may be necessary.

Section 3: Managing the condition

The diagnostic work-up and management of TIA should be the same as with stroke but, in the case of TIA, risk stratification allows the decision of where and how quickly a specialist referral should be made.

It is essential that all patients undergo aggressive risk factor management (see box). Lifestyle advice should target as many of these risk factors as possible. Patients in whom TIA is suspected must be advised not to drive for one month or until further discussion in a TIA clinic.

Hypertension Current smoking
Hypercholesterolaemia High waist-to-hip ratio
High dietary risk score Lack of regular exercise
Diabetes mellitus Excess alcohol consumption
Psychological stress Cardiac causes (AF or previous MI)

Treatments with antiplatelet medication, antihypertensives and statins have been investigated, showing a potential reduction in stroke rate if introduced early.3 Some specific interventions are discussed below.

The use of aspirin in patients with previous TIA or stroke has been shown to reduce the risk of subsequent vascular events by 13%.4 Aspirin 300mg as a single dose should be started while investigations are pending.

Although occasionally TIA can be due to a small intracerebral haemorrhage, this is uncommon and it is reasonable to commence an antiplatelet drug without prior brain imaging.

The NICE recommendations for antiplatelet therapy after stroke are long-term combination of aspirin 75mg once a day (or clopidogrel if aspirin not tolerated) and dipyridamole modified release 200mg twice a day.

However, most stroke physicians cannot see a reason to adopt a different approach to antiplatelet therapy in TIA from that for stroke because they are clearly the same disease.

As a result, the forthcoming edition of the National Clinical Guidelines for Stroke support the use of clopidogrel first line after a TIA, only using the aspirin and dipyridamole combination if the patient is unable to tolerate clopidogrel.

Antihypertensive treatment is recommended for both the prevention of recurrent stroke and other vascular events post TIA. The absolute BP target should be individualised (more rigorous control in patients with diabetes). Observational studies and clinical trials support BP reduction for secondary prevention regardless of the initial BP.

Although the optimal drug regimen remains uncertain, available data from trials such as PROGRESS support the use of diuretics and the combination of diuretics and ACE inhibitors.5 Benefits have been linked to absolute BP reductions of approximately 10/5mmHg.6

Cholesterol-lowering drugs have been shown to be beneficial for both primary and secondary prevention.7

This should be tackled with dietary modification and the use of a statin if total cholesterol is over 3.5mmol/L.

Tight glucose control is important in patients with diabetes with TIA or ischaemic stroke, to reduce microvascular and macrovascular complications. The HbA1c should be optimised to below 7%.

Smoking increases the risk of stroke by about 50%. As a result, all TIA and ischaemic stroke patients should be encouraged to stop smoking and be signposted to smoking cessation services.

Carotid endarterectomy
Carotid endarterectomy is indicated in patients with TIA or stroke with a symptomatic carotid stenosis of 70-99%. Surgery needs to be performed as soon as possible after the TIA, with evidence suggesting that by 12 weeks, medical treatment is as effective at preventing recurrence as surgical.8

AF contributes to about 15% of ischaemic strokes and TIA. To date, anticoagulation with warfarin has been the mainstay of treatment, with risk-stratification tools such as CHAD2Vasc highly effective. Warfarin is more effective than aspirin.9

Newer anticoagulants, such as dabigatran (factor Xa inhibitor), which do not require monitoring, are emerging; however, they are more costly and have the disadvantage of being irreversible, should life-threatening bleeding occur.

Section 4: Prognosis

The prognosis of TIA and stroke is related to a timely diagnosis, referral to a specialist service and initiation of treatment, including secondary prevention.

The key factor in terms of the prognosis of TIAs is the risk of stroke and other vascular events such as MI and stroke following this first incident.10

Risk of stroke
More than 20% of strokes are preceded by a TIA, although this is often not noticed and reported by the patient.11

Statistics from interviews in Oxfordshire with patients who had a TIA between 2002 and 2007 found that 70% of patients did not correctly recognise their TIA. This causes a delay in seeking medical help.

Up to a third of recurrent strokes occur before the patient seeks any medical attention.

Reliable estimations of this risk are necessary for educating the population and planning effective service provision and appropriate follow-up by specialist services.12

It has been quoted that the early risk of stroke after TIA varies widely between 3% and 11% at seven days; a significant difference, with the lowest risk being when emergency treatment has been given by specialised stroke services.11

Preventing recurrence
It has been estimated that a high number of recurrent events might be prevented with the use of a specialist centralised approach encompassing adjustments such as dietary and lifestyle modification (current smoking, alcohol consumption, psychological stress) with concurrent medical interventions.

This will include appropriate urgent investigations and control of risk factors, such as hypertension and high cholesterol.

Lifestyle advice should target as many risk factors as possible.

Section 5: Case study

A 58-year-old man was brought to the emergency department by his family. During his routine morning walk he noticed a sudden onset of left facial numbness associated with a dull headache on the right posterior aspect of his head. He was staggering to the right side and feeling unsteady and nauseated, with no vomiting. He telephoned his wife, who noticed his speech was slow and slurred, but there was no word-finding difficulty. His family immediately took him to hospital.

There was a history of hypertension, hypercholesterolaemia, ischaemic heart disease (MI and PCI with bare metal stent in 2007) and probable TIA at the time of cardiac intervention. His medication included atenolol, ramipril, simvastatin, aspirin and clopidogrel.

When reviewed by emergency department staff (three hours after the onset of symptoms) the speech and balance had returned to normal. Examining his cardiovascular, respiratory and neurological systems revealed no abnormalities.

The history and examination was consistent with a TIA in the vertebro-basilar circulation. An ECG showed sinus bradycardia with no ischaemic changes. The chest X-ray and blood tests were all unremarkable and his random cholesterol result was 6mmol/L. His BP was slightly elevated at 160/80mmHg.

The patient's ABCD2 score was four. As this constitutes a moderate risk of stroke in the following 48 hours, he was admitted to the stroke unit. A diffusion-weighted brain MRI was performed (below), which showed an area of restricted diffusion in keeping with ischaemia in the inferior cerebellar artery (PICA) territory. There was also some suggestion that the right vertebral artery may be occluded and therefore an outpatient CT angiogram was organised, mainly to exclude vertebral artery dissection.

MRI showed an area of restricted diffusion in keeping with ischaemia in the inferior cerebellar artery (PICA) territtory (Photograph: Author image)

The diagnosis of a TIA was explained to the patient and he was discharged with appropriate secondary prevention to reduce the risk of stroke.

He was instructed not to drive for one month.

Section 6: Evidence base

Carotid endarterectomy may be indicated (Photograph: Sovereign, ISM/SPL)

Clinical trials
There is substantial evidence from clinical trials and observational studies to suggest that stroke can be prevented.

  • Early use of existing preventive strategies for stroke (EXPRESS) suggested that the 90-day risk of fatal or disabling stroke was reduced by 80% with urgent specialist clinic review.4
  • The perindopril protection against recurrent stroke study (PROGRESS) investigated the efficacy of BP lowering with perindopril in normotensive and hypertensive patients with a history of TIA or stroke.6 The trial involved 6,015 patients from 172 centres randomised to active treatment with perindopril (4mg daily) with or without indapamide, or placebo. Over the four-year observation period, active treatment reduced the risk of total major vascular events by 26%. Combination treatment with perindopril and indapamide reduced the risk of stroke by 43%. Treatment of patients with stroke with these two agents should be considered even when normotensive.
  • The Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial was the first to investigate the effect of cholesterol control with statins in patients with prior stroke or TIA and a normal cholesterol level.13 It examined 4,731 patients receiving either atorvastatin (80mg daily) or placebo. There was a significant reduction in cholesterol levels with treatment, and analysis of these data has reflected a reduction in stroke risk and favourable outcome.
  • The European Atrial Fibrillation Trial (EAFT) recruited 455 patients from 108 centres in a randomised trial.10 It suggested that warfarin was superior to placebo or aspirin in the prevention of stroke in patients with AF.



Click here to take a test on this article and claim a certificate on MIMS Learning


These further action points may allow you to earn more credits by increasing the time spent and the impact achieved.

  • Audit whether patients with TIAs have had an ABCD2 score.
  • Review how aggressive you are about stroke prevention in your patients with TIA.
  • Discuss with your patient partnership group how you can increase awareness of TIA among your patient group.


1. Lloyd-Jones D, Adams RJ, Brown TM et al. Heart disease and stroke statistics – 2010 update: a report from the American Heart Association. Circulation 2010; 121: e46-e215.

2. Coull A, Lovett J, Rothwell P, on behalf of the Oxford Vascular Study. Population-based study of early risk of stroke after transient ischaemic attack or minor stroke: implications for public education and organisation of services. BMJ 2004; 328: 326-8.

3. NICE. Stroke: diagnosis and initial management of acute stroke and transient ischaemic attack (TIA). London, NICE, 2008.

4. EXPRESS Transient Ischemic Attack study: Speed the process. Stroke 2008: 39: 2400-1.

5. Furie KL, Kasner SE, Adams RJ, et al. Guidelines for the prevention of stroke or transient ischaemic attack: a guideline for healthcare professionals from the American Heart Association. Stroke 2011; 42: 227-76.

6. PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Lancet 2001; 358: 1033-41.

7. Stephen M, Davis M, Geoffrey A et al. Secondary prevention after ischaemic stroke or transient ischaemic attack. N Engl J Med 2012; 366: 1914-22.

8. Amarenco P, Bogousslavsky J, Callahan A III et al. High-dose atorvastatin after stroke or TIA. N Eng J Med 2006; 355: 549-59.

9. Rothwell PM, Eliasziw M, Gutnikov SA et al. Endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and timing of surgery. Lancet 2004; 363: 915-24.

10. EAFT (European Atrial Fibrillation Trial) Study Group. Secondary prevention in non-rheumatic atrial fibrillation after TIA or minor stroke. Lancet 1993; 342: 1255-62.

11. Pendlebury ST, Rothwell PM. Risk of recurrent stroke, other vascular events and dementia after transient ischaemic attack and stroke. Cerebrovasc Dis 2009; 27 Suppl 3: 1-11.

12. Giles MF, Rothwell PM. Risk of stroke after transient ischaemic attack: a systematic review and meta-analysis. Lancet Neurol 2007; 6: 1063-72.

13. Callahan A, Amarenco P, Goldstein LB et al. Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) Trial. Arch Neurol 2011; 68(10): 1245-51.

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