Transient ischemic attack

Last reviewed:October 2019

Last updated:October 2019

Summary

Cerebral ischemia 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 neurologic deficit, aggressive treatment for stroke should not be delayed in the hope that the symptoms will spontaneously resolve.

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

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

In addition to a complete neurologic exam 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 subclinical cerebral infarction.

Definition

A transient ischemic attack (TIA) is a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, 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 neurologic deficit.

History and exam

Key diagnostic factors

patient/caregiver report of focal neurologic 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 neurologic deficit on exam
absence of positive symptoms (shaking, scotoma, spasm)
absence of headache
history of migraine
absence of seizure prior to neurologic deficit
no history of epilepsy
family or personal history of premature stroke, miscarriage, or venous thromboembolism
carotid bruit

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