This saves OPERATIONAL ...

This saves OPERATIONAL mechanisms of memory, perception, motor and language skills, but also violated programming activities: develops abnormal inactivity due to lack of switchable attention or, conversely, excessive impulsiveness due to instability of any attention, or various combinations thereof [1012] . Other pathogenic mechanisms of cognitive impairment Besides destruction of deep cerebral structures and the emergence of the phenomenon of separation from the secondary dysfunction of frontal brain regions in the pathogenesis of cognitive impairment undeniable role played by cerebral infarction of the cortical localization. Strategically important for the association of cognitive activity are areas of the frontal cortex and the junction area of ??the parieto-temporo-occipital cortex, as well as the structure gippokampovogo circle. In some cases you may experience post-stroke dementia associated with a history of cerebral infarction unit macrofocal strategic localization [4, 32, 40]. An equally important aspect of the pathogenesis of cognitive disorders in DE yavlyaetsyaprisoedinenie neurodegenerative process. According to pathomorphological data, the coexistence of vascular changes and markers of neurodegeneration of Alzheimer's character (senile amyloid plaques, neurofibrillary intracellular plexus, neuronal apoptosis medibazalnyh lobyh departments, the hippocampus and temporo-parietal lobes of the brain) is not rare. In these cases, one speaks of mixed vascular-degenerative dementia. The frequency of mixed dementia is much greater than expected for random coincidence of two diseases. This fact has a theoretical explanation: hypoxia is a factor in accelerating the neurodegenerative changes, moreover, are particularly sensitive to hypoxia, hippocampal neurons [27]. Therefore, cerebral vascular insufficiency is regarded now as a risk factor and one of the pathogenetic mechanisms of Alzheimer's disease. Thus, at least in some patients a significant contribution to the development of cognitive impairment makes concomitant degenerative process [34, 36]. Pathogenesis of emotional disorders in DE rather complex and heterogeneous pathogenesis of depressive symptoms appear at DOE and its relationship with cognitive disabilities. First, emotional disturbances, as well as cognitive, may be the result of secondary dysfunction of frontal brain regions. It is known that communication dorzolateralnoy frontal cortex and striatal complex are involved in the formation of positive emotional reinforcement for achieving the goal of activity. Violation of these bonds as a result of the phenomenon of separation will lead to failure of positive reinforcement and, as a consequence, chronic frustration, which is a prerequisite for depression [13, 38]. Depressive symptoms are regularly described in lesions of the frontal lobes of the brain with different etiologies [13]. However, it should be borne in mind that some of the manifestations of frontal dysfunction can mimic depression in the absence of a true reduction of background mood.