Transient ischaemic attack

Last reviewed:October 2019

Last updated:October 2019

Summary

Cerebral ischaemia should be suspected when a patient presents with typical symptoms of rapidly resolving unilateral weakness or numbness, but also with less classic symptoms such as unilateral vision loss, diplopia, transient aphasia, or vertigo.

In a patient who presents with ongoing neurological deficit, aggressive treatment for stroke should not be delayed in the hope that the symptoms will spontaneously resolve.

Transient ischaemic attacks (TIAs) have considerable risk of early recurrent cerebral ischaemic events. Evaluation and initiation of secondary prevention should occur rapidly.

Evaluation focuses on work-up of underlying aetiology. Treatment hinges on secondary prevention with anticoagulants in cases of embolic aetiology or thrombophilia (acquired or inherited), or with antiplatelet therapy for non-embolic events. Modifiable risk factors such as carotid stenosis, hypertension, hyperlipidaemia, and unhealthy lifestyle are other targets of therapy.

In addition to a complete neurological examination and evaluation for diseases that mimic TIA, diagnostic imaging such as magnetic resonance imaging with diffusion-weighted images may be helpful to detect evidence of sub-clinical cerebral infarction.

Definition

A transient ischaemic attack (TIA) is a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.[1] The majority of TIAs resolve within the first hour, and diagnostic imaging allows recognition that some events with rapid clinical resolution are associated with permanent cerebral infarction.[2][3] The arbitrary definition of duration of symptoms for TIA should not deter aggressive therapy for a patient who presents with new neurological deficit.

History and exam

Key diagnostic factors

patient/carer report of focal neurological deficit
brief duration of symptoms

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Other diagnostic factors

history of extracranial atherosclerosis
history of cardiac disease
unilateral symptoms
increased BP on presentation
focal neurological deficit on examination
absence of positive symptoms (shaking, scotoma, spasm)
absence of headache
history of migraine
absence of seizure prior to neurological deficit
no history of epilepsy
family or personal history of premature stroke, miscarriage, or venous thromboembolism
carotid bruit

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