Transient Ischaemic Attacks

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Transient Ischaemic Attack written for patients

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. The duration is no more than 24 hours and a deficit that lasts longer than 24 hours is defined as a stroke.[1] The majority of TIAs last for less than 30 minutes.

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  • TIAs affect 35 people per 100,000 of the population each year.[1] 
  • TIA is more common with increasing age. It is rare under the age of 60.
  • It affects men more than women and black races are at greater risk.
  • About 15% of first stroke victims have had a preceding TIA.

Risk factors

It has the same risk factors as for stroke. See also the separate article on Stroke Prevention.

It is usually embolic, may be thrombotic, and occasionally haemorrhagic (unlikely to produce a reversible lesion).

  • It affects the carotid area in about 80% and the vertebrobasilar area in about 20%. The efficacy of collateral flow through Willis' circle is often much less than may be expected from the basic anatomy, especially with advancing years.
  • 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 but this is difficult to ascertain.

Any person who presents with a short-lived acute-onset neurological syndrome, that might be due to cerebrovascular disturbance (fully resolved or resolving rapidly when first seen) should be assessed to establish the diagnosis and to determine whether the cause is vascular (about 50% are not). Secondary cardiovascular prevention measures which can reduce the risk of recurrence should then be identified.[1] 

History

  • A TIA may last anything from a few minutes to 24 hours. The usual duration is about 10 to 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.

Carotid territory (80%)

  • 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. This is a great simplification and the matter is discussed more fully in the separate article on Dysarthria and Dysphasia.
  • 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 (20%)

  • 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 age 60, 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 may 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 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.

The patient will need to be referred to a specialist centre within seven days but some of the investigations should be carried out before referral.

Primary care

  • Check urine for glucose.
  • FBC, ESR.
  • U&E, fasting lipids and glucose.
  • LFTs and TSH.
  • ECG may show atrial fibrillation, myocardial infarction or evidence of myocardial ischaemia
  • Note: coagulation studies (especially in younger patients and more so in venous thromboembolism rather than arterial thrombosis) and antiphospholipid antibodies may be appropriate but are best discussed with specialists initially.

Secondary care

The Royal College of Physicians (RCP) guidelines recommend:[1] 

  • People who have had a suspected TIA should be assessed by a specialist (within one week of symptom onset) before a decision on brain imaging is made.
  • People who have had a suspected TIA who need brain imaging (ie the vascular territory or pathology is uncertain) should undergo diffusion-weighted MRI except where contra-indicated, in which case CT should be used.
  • People who have a suspected TIA at high risk of stroke (eg, an ABCD2 score of 4 or above - see below) in whom vascular territory or pathology is uncertain should undergo urgent brain imaging (preferably diffusion-weighted MRI).
  • People with a suspected TIA at low risk of stroke (eg, an ABCD2 score of less than 4) in whom vascular territory or pathology is uncertain should undergo brain imaging within one week of onset of symptoms (preferably diffusion-weighted MRI).

The following are likely to be requested from the specialist service:

  • If there is suggestion of problems with the heart, including atrial fibrillation, echocardiogram may show atrial thrombus, aneurysm of the anterior wall of the left ventricle with mural thrombus, atrial myxoma or left side valve disease.
  • Cardiac monitoring may show paroxysmal atrial fibrillation.
  • Doppler studies of the carotid and vertebral arteries may show narrowing. This investigation may be followed by carotid angiography and carotid endarterectomy if stenosis is a least 70%
  • CT or MRI scan of the brain may show an area of reduced blood flow or an unsuspected infarct. MRI scanning tends to be more sensitive and to give better images of carotid and vertebral arteries. It may also demonstrate the rare cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
  • It may be argued that full investigation for coronary heart disease should be initiated, as the most common cause of death after TIA is a myocardial infarction.
  • 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; 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).[2] The risk of subsequent stroke is not as high as for TIA.[3] 

Secondary prevention (see below) includes the use of antiplatelet therapy, antihypertensive, and lipid-modifying treatments, the management of atrial fibrillation if present and the management of any other underlying or risk factors, including diabetes.

Driving[4] 

Group 1 (car or motorcycle)

  • Must not drive for one month.
  • No need to notify DVLA after a single TIA.
  • Multiple TIAs over a short period: require three months free from further attacks before resuming driving and DVLA should be notified.

Group 2 (lorry or bus)

  • Licence refused or revoked for one year following a stroke or TIA.

Assessment of the risk of stroke

An ABCD2 score of more than 4 suggests high risk of an early stroke.[5][6]

Scoring System for Risk of Stroke after TIA (ABCD2 Score)
AgeAge >601
Blood pressureBP>140 systolic and/or >90 diastolic1
Clinical featuresUnilateral weakness2
 Speech disturbance without weakness1
 Other0
Duration of symptoms>60 minutes2
 10-59 minutes1
 <10 minutes0
DiabetesPresence of diabetes1

RCP recommendations[1] 

  • All patients with a TIA should be seen by a specialist in neurovascular disease (eg, in a specialist neurovascular clinic or an acute stroke unit).
  • People with a suspected TIA should be assessed as soon as possible for their risk of subsequent stroke by using a validated scoring system such as ABCD2 (as above).
  • Patients with suspected TIA who are at high risk of stroke (eg, an ABCD2 score of 4 or above) should receive:
    • Aspirin or clopidogrel (each as a 300 mg loading dose and then 75 mg daily) and a statin started immediately.
    • NB: clopidogrel is not licensed for the management of TIA and therefore the National Institute for Health and Care Excellence (NICE) and the British National Formulary (BNF) recommend aspirin plus modified-release dipyridamole.[7] 
    • Specialist assessment and investigation within 24 hours of onset of symptoms.
    • Measures for secondary cardiovascular prevention introduced as soon as the diagnosis is confirmed, including discussion of individual risk factors.
  • People with crescendo TIA (two or more TIAs in a week), atrial fibrillation or those on anticoagulants should be treated as being at high risk of stroke even if they may have an ABCD2 score of 3 or below.
  • Patients with suspected TIA who are at low risk of stroke (eg, an ABCD2 score of 3 or below) should receive:
    • Aspirin or clopidogrel (each as a 300 mg loading dose and then 75 mg daily) and a statin.
    • NB: clopidogrel is not licensed for the management of TIA and therefore NICE and the BNF recommend aspirin plus modified-release dipyridamole.[7] 
    • Specialist assessment and investigations as soon as possible, but definitely within one week of onset of symptoms.
    • Measures for secondary prevention introduced as soon as the diagnosis is confirmed, including discussion of individual risk factors.
  • People who have had a TIA but present late (more than one week after their last symptom has resolved) should be treated as though they are at a lower risk of stroke.
  • Patients with TIA in atrial fibrillation should be anticoagulated in the TIA clinic once intracranial bleeding has been excluded and if there are no other contra-indications.

If the patient is in atrial fibrillation, management of that condition is required. In persistent atrial fibrillation there is benefit from anticoagulation but there is no evidence of any such benefit in the absence of atrial fibrillation.[8] 

Carotid stenosis

See the separate article on Carotid Artery Stenosis.

All people with TIA, who after specialist assessment are considered candidates for carotid endarterectomy, should have carotid imaging conducted urgently to facilitate carotid surgery, which should be undertaken within seven days of the onset of symptoms.[1] 

The risk of stroke within two days of a TIA is 3%; within seven days the risk is 5%.The risk of stroke after a TIA increases with higher ABCD2 score:[9] 

  • 2-day stroke risk on ABCD2 Score: 0-3 = 1.0%, 4-5 = 4.1%, 6-7 = 8.1%
  • 7-day stroke risk on ABCD2 Score: 0-3 = 1.2%, 4-5 = 5.9%, 6-7 = 11.7%

Other factors associated with an increased risk of stroke soon after a TIA include:[10] 

  • 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.

See also the separate article on Prevention of Cardiovascular Disease.

  • Lifestyle advice should always include smoking cessation, weight loss if overweight or obese, and a healthy diet. Exercise should also be encouraged.[11] 
  • If there is atrial fibrillation or another source for systemic emboli, this must be addressed. The relative merits of the various approaches to the management of atrial fibrillation are discussed elsewhere. Anticoagulation is usually required if the rhythm cannot be converted but anticoagulants are of no value in the absence of atrial fibrillation.[8] 
  • Hypertension must be controlled.
  • Everyone should be on antiplatelet medication of some sort.
  • Diabetes, if it exists, must be well controlled.
  • Hyperlipidaemia must be addressed. There is evidence that statin therapy in patients with a history of ischaemic stroke or TIA significantly reduces the risk of subsequent major coronary events but only marginally reduces the risk of stroke recurrence.[12] 

Further reading & references

  1. National clinical guidelines for stroke (fourth edition); Royal College of Physicians (2012)
  2. 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.
  3. 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.
  4. Assessing fitness to drive: guide for medical professionals; Driver and Vehicle Licensing Agency
  5. Worster A; ACP Journal Club. Review: 3 prediction rules, particularly ABCD, identify ED patients who can be discharged with low risk for stroke after TIA. Ann Intern Med. 2009 Sep 15;151(6):JC3-15.
  6. Sheehan OC, Merwick A, Kelly LA, et al; Diagnostic Usefulness of the ABCD2 Score to Distinguish Transient Ischemic Attack and Minor Ischemic Stroke From Noncerebrovascular Events. The North Dublin TIA Study. Stroke. 2009 Sep 10.
  7. British National Formulary
  8. De Schryver EL, Algra A, Kappelle LJ, et al; Vitamin K antagonists versus antiplatelet therapy after transient ischaemic attack or minor ischaemic stroke of presumed arterial origin. Cochrane Database Syst Rev. 2012 Sep 12;9:CD001342. doi: 10.1002/14651858.CD001342.pub3.
  9. Bhatt A, Jani V; The ABCD and ABCD2 Scores and the Risk of Stroke following a TIA: A Narrative Review. ISRN Neurol. 2011;2011:518621. doi: 10.5402/2011/518621. Epub 2011 Jul 21.
  10. Stroke and TIA; NICE CKS, February 2009
  11. Diep L, Kwagyan J, Kurantsin-Mills J, et al; Association of physical activity level and stroke outcomes in men and women: a meta-analysis. J Womens Health (Larchmt). 2010 Oct;19(10):1815-22. doi: 10.1089/jwh.2009.1708.
  12. Manktelow BN, Potter JF; Interventions in the management of serum lipids for preventing stroke recurrence. Cochrane Database Syst Rev. 2009 Jul 8;(3):CD002091. doi: 10.1002/14651858.CD002091.pub2.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Gurvinder Rull
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
2882 (v28)
Last Checked:
14/03/2014
Next Review:
13/03/2019

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