Typological features of the brain in normal conditions and in cerebral hypoperfusion
Journal: RUDN Journal of Medicine (Vol.24, No. 4)Publication Date: 2020-11-24
Authors : V. Chrishtop; T. Rumyantseva; V. Nikonorova;
Page : 346-353
Keywords : cerebral hypoperfusion; stress resistance; cognitive abilities; brain;
Abstract
Relevance. Stress resistance and cognitive abilities of the patient, forming the personal component of the rehabilitation potential, have a significant impact on the course and recovery period after cerebral hypoxia of various origins. The adaptation of rehabilitation measures to the individual characteristics of the patient will significantly increase the effectiveness of rehabilitation measures for stroke and neurodegenerative diseases. The aim of this work is to generalize experimental and clinical studies characterizing the influence of individual characteristics of higher nervous activity on the course of cerebral hypoperfusion. Materials and methods . The study of literary sources of scientometric scientific bases for the last 15 years has been carried out. Results . The level of stress resistance is based on alternative biochemical strategies of neuronal metabolism of macroergs and neurotransmitters. At the organismic level, this is realized in a greater base voltage of the stress-activating system and a smaller reserve capacity of the sympathoadrenal system. In general, this leads to more severe cerebral hypoperfusion in stress-resistant individuals and slower recovery and is correlated with a high baseline sympathetic nervous system tone, insulin and testosterone concentrations. At the same time, a low level of stress resistance determines a greater sensitivity to exogenous corrective influences in cerebral hypoperfusion. The level of cognitive ability is associated with astrocytic responses and the organization of synaptic ensembles. The participation of astrocytes in the regulation of glutamate levels probably has a combined effect on both the state of cognitive mechanisms and damage to the components of neuroglial assemblies during hypoxia. This is also due to the release of S100β +, which, in turn, enhances the coordinated oscillations of neurons in the medial prefrontal cortex and hippocampus and may be the cause of greater damage to the cells of the cerebral hemispheres of the brain in animals with a high level of cognitive abilities in the cerebral hypoperfusion model.
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Last modified: 2020-11-24 17:42:45