• Yannick Béjot, Corinne Aboa-Eboulé, Christine Marie, and Maurice Giroud.
• Université de Bourgogne, CHU de Dijon, Registre dijonnais des AVC, faculté de médecine de Dijon, IFR 100 Santé-STIC, EA 4184, service de neurologie, Réseau StrokAvenir, 21079 Dijon, France. ybejot@yahoo.fr
• Presse Med. 2011 Feb 1; 40 (2): 167-72.

AbstractTransient ischemic attack (TIA) is a well-recognized risk factor of ischemic stroke. Hence, 7 to 25% of ischemic stroke patients have a history of TIA, and the risk of ischemic stroke after TIA is about 15% at 3 months. However, epidemiological studies have demonstrated that among patients with ischemic stroke, those with a history of TIA have better functional and vital prognoses. This protective effect is particularly found in case of recent and short TIA, and in case of non-lacunar ischemic stroke. Hence, TIA can induce endogenous neuroprotection by the ischemic tolerance phenomenon that decreases the neurodegeneration usually caused by a severe cerebral ischemia in a non-preconditioned brain. The mechanisms of ischemic tolerance appear complex, multiple, and not fully understood. They involve changes in cellular gene expression, metabolic and signaling pathways, and enzymatic expression. The evidence of the neuroprotective effect of TIA offers interesting perspectives for the development of therapeutic strategies targeting the ischemic tolerance phenomenon.Copyright © 2010 Elsevier Masson SAS. All rights reserved.

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