Transient ischaemic attacks
Peer reviewed by Dr Pippa Vincent, MRCGPLast updated by Dr Doug McKechnie, MRCGPLast updated 28 Jun 2024
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Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Transient ischaemic attack article more useful, or one of our other health articles.
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What are transient ischaemic attacks?
A transient ischaemic attack (TIA) is a temporary inadequacy of the circulation in part of the brain (a cerebral or retinal deficit) that gives a clinical picture similar to a stroke except that it is transient and reversible. Hence, TIA is a retrospective diagnosis.
Traditionally, a TIA is defined based on the duration of symptoms; neurological symptoms due to a presumed vascular event that resolve completely within 24 hours are considered to be a TIA, whereas symptoms lasting longer than 24 hours are defined as a stroke. In practice, 'true' TIAs (where there is no evidence of cerebral infarction) typically last only minutes, whereas longer events often show evidence of infarction on imaging and should really be considered 'strokes'.1
This concept, along with the increasing availability of MRIs, has led to an alternative tissue-based definition, whereby:2
A TIA is defined as an acute neurovascular syndrome attributable to a vascular territory that rapidly resolves, leaving no evidence of tissue infarction on a diffusion-weighted MRI.
If there is evidence of infarction on MRI, even if symptoms have resolved, this is instead considered an ischaemic stroke.
How common are transient ischaemic attacks? (epidemiology)
In the UK, the incidence of TIA is around 50 per 100,000 people per year.3
TIA is more common with increasing age. It is rare under the age of 60 years.
About 15% of first stroke victims have had a preceding TIA.4
Risk factors 5 6
TIAs have the same risk factors as for stroke. See also the separate Stroke prevention article.
Hypertension.
Smoking.
Diabetes mellitus.
Heart disease (valvular, ischaemic, atrial fibrillation).
Peripheral arterial disease.
Polycythaemia vera.
Carotid artery occlusion; carotid bruit.
Combined oral contraceptive pill.
Hyperlipidaemia.
Excess alcohol.
Clotting disorders.
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Causes of transient ischaemic attacks (aetiology)
It is usually embolic, may be thrombotic, and occasionally haemorrhagic (unlikely to produce a reversible lesion).
The most common source of emboli is the carotids, usually at the bifurcation.
They can originate in the heart with atrial fibrillation particularly, with mitral valve disease, or aortic valve disease, or from a mural thrombus forming on a myocardial infarct or a cardiac tumour - usually atrial myxoma.
The vertebrobasilar arteries may be a source.
Occasionally there is paradoxical embolism originating from the right side of the circulation.
Haemodynamic TIAs are rare. There is not necessarily total occlusion of the arteries, and circulation may merely be inadequate. Sometimes spasm may be involved.
Symptoms of transient ischaemic attacks (presentation) 67
Primary care responsibilities
A validated tool such as FAST (Face Arm Speech Test) should be used in primary care to screen people with sudden onset of neurological symptoms.
Exclude hypoglycaemia as a cause of these symptoms.
Any person presenting with acute neurological symptoms that resolve completely within 24 hours (ie suspected TIA) should be started on aspirin 300 mg, with the first dose given immediately (unless contra-indicated).
Any person presenting with a suspected TIA should be referred immediately and assessed urgently within 24 hours by a specialist physician in a neurovascular clinic or an acute stroke unit.8
Patients with a suspected TIA that occurred more than a week previously should be assessed by a stroke specialist clinician as soon as possible within 7 days.
Secondary prevention in addition to aspirin should be offered as soon as possible.
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History
A TIA may last anything from a few minutes to 24 hours. The usual duration is about 10-15 minutes. Onset is over a few minutes.
There may be changes in behaviour that are best described by a third party.
The clinical features will depend upon the part of the brain that becomes ischaemic. The majority of ischaemic events affect the carotid territory.
Carotid territory
Symptoms are usually unilateral and most often affect the motor area, causing unilateral weakness, affecting an arm, leg, or one side of the face. There may be dysarthria.
There may be sensory symptoms in the same areas.
If Broca's area is involved, there will also be difficulty with speech - called Broca's dysphasia. This produces inconsistent and unpredictable errors, usually substitution, with spontaneous speech containing fewer errors. See the separate Dysarthria and dysphasia article.
There may be amaurosis fugax (fleeting loss of vision), a unilateral loss indicative of retinal ischaemia, usually associated with emboli or stenosis of the ipsilateral carotid artery.
Vertebrobasilar territory
If the ophthalmic cortex is involved there will be a homonymous hemianopia that may present purely as ignoring one side of the visual field.
There may be bilateral visual impairment.
There may be hemiparesis, hemisensory symptoms, diplopia, vertigo, vomiting, dysarthria, dysphagia, or ataxia.
Ask both the patient and, if possible, those around, about weakness such as a drooping face, gait, confusion, dysarthria, loss of memory, or abnormal behaviour. Fleeting symptoms may be more obvious to those around than to the patient.
Ask about duration, intensity and fluctuation of symptoms.
Establish whether there were any simultaneous cardiac symptoms.
NB: global symptoms by themselves (unsteadiness, dizziness, syncope) are rarely due to TIA.
In addition to enquiring about the nature of the event, there are a number of other matters in the patient's history that require examination:
Has this happened before?
Has there been recent surgery, especially on the heart or carotids?
Has there been a previous stroke or any coronary heart disease?
Is hypertension being treated?
Is there known diabetes?
Are there any other significant illnesses? There may be a hypercoagulable state or vasculitis such as temporal arteritis.
If it presents in a person much younger than 60 years, has there been drug abuse, especially cocaine?
Examination
Neurological examination should be performed as for a stroke but, by the time the patient is seen, it should have reverted to normal.
Note overall attentiveness, ability to cooperate and verbal fluency.
Examination of the pulse may reveal abnormality of rate or rhythm. The artery may feel hard and rigid.
Check blood pressure (BP) in both arms.
Listen for a carotid bruit at the bifurcation and at the base of the neck for a vertebral bruit. However, a bruit can occur with minimal stenosis, and significant occlusion may be silent.
Check peripheral pulses.
Diagnosing transient ischaemic attacks (investigations)
TIAs require urgent referral to secondary care. Investigations are therefore usually undertaken by secondary care.
Secondary care investigations include:78
Brain imaging. MRI is the preferred modality to demonstrate the presence and distribution of ischaemia (if an infarct is present, this indicates a stroke rather than a TIA.
Patients should be assessed by a specialist physician before the decision to perform brain imaging is made, except when haemorrhage needs to be excluded (eg, patients taking an anticoagulant or with a bleeding disorder), when an unenhanced CT head should be performed urgently.
If a TIA is confirmed, further investigations include:
Urgent carotid imaging (duplex ultrasound, MR, or CT angiogram) to identify relevant severe carotid stenosis, in patients potentially suitable for carotid endarterectomy.
An ECG to look for arrhythmias (particularly atrial fibrillation) or other evidence of cardiac disease.
A 24-hour or longer cardiac monitor may be useful for detecting paroxysmal atrial fibrillation, particularly if there is no other apparent embolic source.
An echocardiogram to detect structural abnormalities such as valvular disease or an atrial thrombus.
Blood tests, such as:
A full blood count (to rule out polycythaemia).
A lipid profile.
Haemoglobin A1c.
Additional investigations may be requested in some cases, such as in younger people with no clear cause for a TIA. These might include:
A thrombophilia screen, eg, if antiphospholipid syndrome is suspected.
A bubble echocardiogram, to look for a patent foramen ovale.
Differential diagnosis
Before there is full recovery it is impossible to differentiate from a stroke.
Intracranial lesion (tumour or subdural haematoma). Beware of diagnosing TIA if there has been loss of consciousness, or convulsion.
Todd's paralysis:
Follows a seizure and is characterised by a temporary, usually unilateral, paralysis.
It may also affect speech or vision and usually resolves within 48 hours. The cause is unknown.
Todd's paresis (transient weakness of a hand, arm, or leg after partial seizure activity affecting that limb) is less severe and more common than Todd's paralysis.
Syncope due to cardiac arrhythmia.
Giant cell arteritis (temporal arteritis) has a very high ESR or CRP; there is often thickening and tenderness of the temporal artery, and monocular, temporary visual impairment is a frequent presentation.
Migraine, or migrainous aura.
Retinal or vitreous haemorrhage.
Focal epileptic seizure.
Labyrinthine disorders.
Transient global amnesia.
Psychological disorders (including hyperventilation).
Metabolic disturbance - eg, hypoglycaemia.
Features that do not fully fit for TIA are called transient neurological attacks (TNAs).9 The risk of subsequent stroke is not as high as for TIA.10
Management of transient ischaemic attacks
Initial management of suspected and confirmed TIA7
Offer aspirin (300 mg daily), unless contraindicated, to people who have had a suspected TIA, to be started immediately.
Refer immediately people who have had a suspected TIA for specialist assessment and investigation, to be seen within 24 hours of onset of symptoms.
Do not use scoring systems, such as ABCD2, to assess risk of subsequent stroke or to inform urgency of referral for people who have had a suspected or confirmed TIA.
Once the diagnosis of a TIA is confirmed:
Dual antiplatelets may be used in some patients, particularly patients seen within 24 hours of onset of a TIA or minor ischaemic stroke. Regimens include:
Aspirin and clopidogrel for 21 days, followed by clopidogrel monotherapy.
Aspirin and ticagrelor for 30 days, followed by either ticagrelor or clopidogrel monotherapy.
Anticoagulants should be initiated in secondary care for people with atrial fibrillation and a TIA or minor ischaemic strokes. These should be started as soon as possible, after imaging has excluded an intracranial haemorrhage.
High-intensity statin therapy (atorvastatin 20-80 mg) should start immediately.
Secondary prevention (in primary or secondary care) involves:8
Long-term use of antiplatelets (usually clopidogrel 75 mg), in people without AF.
Long-term anticoagulation, in people with AF.
Blood pressure control with antihypertensives as necessary.
The RCP guidelines recommend targeting a clinic systolic blood pressure of 130 mmHg or below, except in people with severe bilateral carotid artery stenosis, where they recommend a target of 140-150 mmHg.
Long-term lipid control by diet and the use of lipid-lowering medication.
The RCP guidelines recommend targeting a fasting LDL-c of below 1.8 mmol per litre, with escalation of the statin dose or addition of additional agents if this is not achieved.
Long-term diabetic glycaemic control.
Driving11
Group 1 (car or motorcycle)
Must not drive for one month.
Patients do not, however, need to inform the DVLA.
When more than one TIA is experienced, 1 month off driving is required following each episode of TIA.
Group 2 (lorry or bus)
Must not drive, and must notify the DVLA. A group 2 licence will be refused or revoked for one year following a stroke or TIA.
Carotid stenosis
See the separate Carotid artery stenosis article.
Prognosis
TIA is associated with a very high risk of stroke in the first month after the event and up to one year afterwards.8
Other factors associated with an increased risk of stroke include:6
Increased BP (ie sustained above 130/90 mm Hg).
Hyperlipidaemia.
Diabetes mellitus.
Atrial fibrillation and other cardiac arrhythmias.
Structural cardiac disease.
Carotid artery stenosis.
Lifestyle factors, including smoking, exercise, eating and dietary habits, and alcohol consumption.
A second TIA within one week.
Further reading and references
- McArthur KS, Quinn TJ, Dawson J, et al; Diagnosis and management of transient ischaemic attack and ischaemic stroke in the acute phase. BMJ. 2011 Mar 31;342:d1938. doi: 10.1136/bmj.d1938.
- Amin HP, Madsen TE, Bravata DM, et al; Diagnosis, Workup, Risk Reduction of Transient Ischemic Attack in the Emergency Department Setting: A Scientific Statement From the American Heart Association. Stroke. 2023 Mar;54(3):e109-e121. doi: 10.1161/STR.0000000000000418. Epub 2023 Jan 19.
- Zhang Y, Chapman AM, Plested M, et al; The Incidence, Prevalence, and Mortality of Stroke in France, Germany, Italy, Spain, the UK, and the US: A Literature Review. Stroke Res Treat. 2012;2012:436125. doi: 10.1155/2012/436125. Epub 2012 Mar 1.
- Hankey GJ. Impact of treatment of people with transient ischaemic attack on stroke incidence and public health. Cerebrovasc Dis 1996;6(suppl 1): 26-33.
- Khare S; Risk factors of transient ischemic attack: An overview. J Midlife Health. 2016 Jan-Mar;7(1):2-7. doi: 10.4103/0976-7800.179166.
- Stroke and TIA; NICE CKS, December 2023 (UK access only)
- Stroke and transient ischaemic attack in over 16s: diagnosis and initial management; NICE Guidance (May 2019 - last updated April 2022)
- National clinical guideline for stroke; Royal College of Physicians (2023)
- Fonseca AC, Canhao P; Diagnostic difficulties in the classification of transient neurological attacks. Eur J Neurol. 2011 Apr;18(4):644-8. doi: 10.1111/j.1468-1331.2010.03241.x. Epub 2010 Oct 18.
- Amort M, Fluri F, Schafer J, et al; Transient ischemic attack versus transient ischemic attack mimics: frequency, clinical characteristics and outcome. Cerebrovasc Dis. 2011;32(1):57-64. doi: 10.1159/000327034. Epub 2011 May 25.
- Assessing fitness to drive: guide for medical professionals; Driver and Vehicle Licensing Agency
Article history
The information on this page is written and peer reviewed by qualified clinicians.
Next review due: 27 Jun 2027
28 Jun 2024 | Latest version
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