In the ischemic focus, the processes of decay of the brain tissue begin, leading to acidification of a significant amount of space outside the affected area (E. Escuret, 1995). There is changing the relationship between the capillary system, glial cells and neurons. Capillary permeability increases. In the outbreak increases neuronophagy. Destruction develops in those brain formations whose neurons are involved in the process of retro- and anterograde degeneration. Against this background, almost immediately after a stroke, the reparative processes begin, which are primarily due to normalization of the cerebral circulation, although directly in the ischemic focus such a recovery is never complete.
In strokes, the characteristics of SCP may change under the influence of destructive processes in the pathological focus, accompanied by the death of capillaries, nerve and glial cells, as well as as a result of changes in the thyroid chorus of the brain as a whole.
Most of the studies of SCP in disorders of cerebral blood circulation were performed under experimental conditions with the removal of constant potentials directly from the cerebral cortex, when membrane membrane potentials of neurons and glia are the main source of SCP. In acute disorders of cerebral circulation in a dog, caused by applying a ligature to the middle cerebral artery (SMA), a significant negative shift in SCP occurs in the affected area, which occurs when the ligature is weakened. In animals with large changes in SCP, there is also a more pronounced neurological deficit. If the AMP did not change during ligation of the MCA, then the animals had no neurological symptoms (LU Anthony et al., 1963). In cats with occlusion of MCA in the affected area, the SCP was displaced in a negative direction by an average of 9.1 + 1.0 mV (T. Schima et al., 1983). SCP changes,recorded from the surface of the brain during ischemia, mainly due to a drop in the membrane potentials of nerve and glial cells.
In patients with focal brain damage during the registration of SCP from the head surface, it is established that ischemic damage to the cortex manifests itself in the form of a SCP negative shift of 10–20 mV, whereas a subcortical lesion causes a positive potential shift (K. Sano et al., 1977; H .V. Ponomareva, 1986). The latter is understandable, since if the blood circulation in the cortex is not impaired, then, due to secondary acidification of the brain, SCP rises.
We examined 26 patients aged from 34 to 72 years with acute cerebral circulation impairment or its consequences in the MCA basin (mainly superficial branches). The cortical branches of the MCA supply blood to a large part of the temporal region, as well as to the frontal, central and parietal regions. The duration of acute cerebrovascular accident in patients was from 2 weeks to 4 years. The diagnosis was made on the basis of clinical and paraclinical data. In the anamnesis, the patients had an acute violation of cerebral circulation with the development of hemiparesis and hemihypesthesia in the contralateral foci of the extremities, and a violation of higher mental functions was also observed . Gradually, during treatment, partial regression of neurological symptoms was noted.
In a clinical picture syndromes of frustration of the higher brain functions, movements and sensitivity came to light. The syndrome of disorders of higher brain functions was manifested in left hemispheric infarctions in the form of sensory-motor aphasia, which in some cases was combined with alexia, acalculia, apraxia, and in the case of right-brain infarction, in the form of underestimating its defect. The majority of patients had a central cranial nerve lesion, more often it was manifested by insufficiency of the facial nerve, others – hypoglossal. The syndrome of motor disorders in the form of hemiparesis in the extremities opposite to the infarction site was in all patients. In 13 patients with left-hemispheric lesion and in a patient with right-hemispheric stroke, the motor defect was pronounced, and in 6 patients the hemiparesis was mainly of a reflex nature:the strength of the limbs was reduced slightly, the tone was not changed, anisoreflexia was detected, but there were no pathological signs. The syndrome of sensory disturbances, observed in 8 patients with left hemispheric heart attack, was manifested by right hemihepesthesia. The diagnosis was supplemented with the necessary paraclinical examination methods: EEG, Echo EG, REG, X-ray of the skull, and in some cases cerebral angiography.