Pathophysiology of Cerebral Ischemia

Abstract

Cerebrovascular accident (CVA) is the sudden interruption or decrease of blood supply (oxygen and glucose) to the brain resulting in cerebral infarction, permanent neurological damage, severe functional limitations and death. Stroke is the second most common cause of death worldwide and the leading cause in Brazil. The risk factors for CVA include systemic arterial hypertension and other vascular diseases, diabetes mellitus, sedentarism, dyslipidemia, and smoking. These risk factors are at high prevalence, globaly, increasing the prospects for new incidents of the disease. Currently, the treatment options for CVA are limited, partially because many promising medicines presented intolerable side effects or limited therapeutic effects in the clinical trials. In the acute and subacute phases of the CVA the therapeutic goals are to protect the neurons at risk, increase the endogenous capacity of the central nervous system (CNS) to regenerate itself, and diminish functional sequelae. This review discusses the role of molecular mechanisms underlying CVA is the key for new therapeutic discoveries aiming at neuroprotection, neuroregeneration and neurogenesis.