In ischemic stroke, an acute violation of cerebral circulation arising, as a rule, as a result of thrombosis, obliteration or embolism of cerebral vessels, the energy metabolism in the area of the pathological focus is sharply reduced ( EI Gusev et al., 1979) .
The pathophysiology of ischemic stroke depends on a decrease in cerebral blood flow. Ischemia results from sudden lack of oxygen and glucose. Oxidative phosphorylation fails, which is responsible for all other pathological reactions. As a result of the transition to anaerobic metabolism, the production of lactate and other acid products of metabolism increases. Ion pumps cell membranes are inactivated, which leads to disruption of ionic homeostasis. Ca and Na penetrate the cells, whereas out of neurons. The energy failure causes extracellular accumulation of the excitatory amino acid glutamate, resulting in hyperactivation of the NMDA receptor glutamate. Activation is also developing due to disturbances in the control system associated with blockade of magnesium ions by NMDA receptors. As a result, there is a massive influx of Ca, which is included in a series of enzymatic reactions involving phospholipases, proteases and endonucleases that break down cellular structures. Reperfusion causes brain damage by free radicals, the formation of which dramatically increases under the action of arachidonic acid, xanthine oxidase and nitric oxide. Reducing the energy supply of cells, as well as hyperactivation of enzymes and the production of free radicals, leads to cell death (E. Escuret, 1995; D. Lipscomb et al., 1998).
Energy metabolism in the neocortex may decrease not only when the focus is located in the cortex itself, but also in the subcortex, particularly in the thalamus, although here such a decrease is less pronounced (J. Baron et al., 1986; H. Chabriat et al ., 1992). Even in the absence of visible morphological damage, neurochemical changes are possible. It has been shown that in insult hemorrhage in the cortex, there is a significant deficit of benzodiazepine receptors, as well as directly in the area of stroke (J. Hatazawa, E. Shimosegawa, 1998).