The Purpose of Functional Mapping in Focal Cerebral Ischemia

Abstract

Experimental results obtained during the last decade [3, 5, 6] have demonstrated that cerebral cell damage following focal ischemia is not caused by a single event, but develops as the result of a cascade of pathogenetic steps. The primary event is the regional fall in cerebral blood flow (CBF) below a critical threshold, which differs for the maintenance of function and morphological integrity of the nerve cells [1]. Insufficient blood and oxygen supply causes alterations in metabolism, especially glycolysis, and depletion of primary (ATP, PCr) and secondary (glucose) energy reserves; leads to changes in the electrophysiological properties of the nerve cells; and finally causes the depolarization of membranes by excessive changes in ion homeostasis. The fate of a cell is determined not only by the severity of the ischemic event but also by its duration, which even at the initial stage allows a limited period of time during which complete recovery is possible if reperfusion above a critical value can be achieved.