ABSTRACT
Cerebral ischemia results from atherothrombosis, emboli, hypoperfusion or a variety of other causes that impair cerebral bloodflow (CBF) and lead to deprivation of both oxygen and glucose. When persistent and critical, such impairment in blood flow may eventually lead to neuronal death.1-4 Cells at the center of the ischemic focus, the ischemic core, may be especially vulnerable and may die within minutes of ischemic onset.3 Surrounding the ischemic core is an area of reduced perfusion in which cells are still viable, the ischemic penumbra.1,2,5-11 Cells in the ischemic penumbra are subjected to various pathological processes that may lead to their demise, and their survival is only possible for a limited amount of time.10,12-15 Spontaneous reperfusion usually occurs in the set-up of cerebral ischemia.16 While this process may reverse the ischemic damage when occurring early enough (e.g. transient ischemic attacks), it usually takes place at a much later time point when most penumbral cells have died. Essentially, the goal of neuronal protection therapies is to keep penumbral cells from dying until such time when spontaneous reperfusion occurs and surviving cells regain their functional capabilities.17
