الفهرس يوجد فقط 14 صفحة متاحة للعرض العام
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المستخلص
Stroke is a leading cause of death and the most common cause of neurological disability in adults (Rothwell et al, 2005). About 15–20% of patients with Stroke have a preceding Transient ischemic attack (Rothwell and Warlow, 2005).
Transient ischemic attack provides a golden opportunity for Stroke prevention. Therefore, it should be treated as a medical emergency with prompt investigations to determine the mechanism of ischemia and subsequent preventive therapy. The risk of Stroke after TIA is estimated to be 10%-20% in the first 90 days. This risk is time-dependent with 50% of the risk occurring in the first 48hours (Johnston and Hill, 2004).
The classic definition of TIA is a sudden focal neurologic deficit that lasts for less than 24 hours, presumed to be of vascular origin, and confined to an area of the brain or eye perfused by a specific artery (Wilterdink and Easton, 1992).
The vast majority of TIAs are brief with symptoms lasting less than an hour and recent studies of TIAs using highly sensitive neuroimaging techniques have shown that patients with complete resolution of symptoms may still have evidence of continuing tissue damage. Moreover, MRI of patients with TIA have shown that new areas of restricted diffusion are present in nearly half of the patients, particularly if their symptoms lasted more than one hour, which demonstrates that permanent ischemia may result in Transient symptoms, thus challenging the older, arbitrary definition of 24 hours of symptom duration ( Kidwell et al, 1999).