Typical findings for DE are ...

Typical findings for DE are focal and diffuse changes of white matter cysts and postischemic cerebral atrophy. According to some reports, the severity of white matter changes correlate with the severity of cognitive and affective disorders in ED [3,9,17,18]. Pharmacotherapy of mental disorders in the ED treatment of cognitive and emotional disorders in DE should be possible, or etiotropic patogenenticheskim. Because the basis of mental disorders as well as other symptoms of ED is vascular disease of the brain, the primary task of the doctor correction of risk factors of stroke and eliminate or reduce severity of chronic cerebral ischemia. Treatment of hypertension, the appointment of antiplatelet agents, surgical correction of atherosclerotic narrowing of major arteries, no doubt, helps to prevent the rise kognitivyh disorders and, according to some reports, reduced severity of existing cognitive defect. Also important is the control of hyperlipidemia, hyperglycemia, treatment of other systemic diseases [7]. Pathogenetically justified the use of drugs with vasoactive, neuroprotective and metabolic properties. Vasoactive drugs improve cerebral microcirculation by acting on arteriolar tone and blood rheology. Widely used in practice such drugs as tanakan, Vinpocetine, pentoxifylline, vazobral, calcium channel blockers (nimodipine, cinnarizine, flunarizin, etc.). These drugs have the potential to reduce the severity of cognitive impairment in the ED. In addition, as a rule, the greatest effect observed in the most mobile of cognitive areas, such as attention and memory strength [7]. The aim of neuroprotective drugs to improve survival of neurons in chronic ischemia and hypoxia, which promotes the growth of secondary prevention of cognitive and other neurological disorders. Given the important pathogenic role of lipid peroxidation in ischemic damage, neuroprotective effect may have drugs with antioxidant properties. We discuss how the probable antioxidant effect selegelina, tocopherol and Tanakan. The largest clinical experience with DOE is against Tanakan, which combines both vasoactive and neuroprotective properties. This drug in a number of studies have shown the ability to reduce the severity of cognitive, emotional and subjective symptoms of ED. However, the ability Tanakan modify the course of disease needs further study [8,19,28,31]. Neuroprotective potential have also drugs, reducing the content of intracellular calcium in neurons, such as nimodipine, because the accumulation of calcium enhances the energy processes and contributes to neuronal death. Symptomatic nootropic effect and the potential to modify the course of the disease is described as a blocker of NMDA-receptor akatinola memantine [7.36].