Transient ischaemic attack

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, 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.

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

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

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

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] Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack. Stroke. 2009;40:2276-2293. http://stroke.ahajournals.org/content/40/6/2276.full http://www.ncbi.nlm.nih.gov/pubmed/19423857?tool=bestpractice.com This replaced the former definition of focal neurological impairment lasting less than 24 hours. 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] Kidwell CS, Alger JR, Di Salle F, et al. Diffusion MRI in patients with transient ischemic attacks. Stroke. 1999;30:1174-1180. http://stroke.ahajournals.org/content/30/6/1174.full http://www.ncbi.nlm.nih.gov/pubmed/10356095?tool=bestpractice.com [3] National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995;333:1581-1588. http://www.nejm.org/doi/full/10.1056/NEJM199512143332401#t=article http://www.ncbi.nlm.nih.gov/pubmed/7477192?tool=bestpractice.com The arbitrary definition of duration of symptoms for TIA should not deter aggressive therapy for a patient who presents with new neurological deficit.