Neurological disorders with general overheating of the body (scientific and literary review)

Abstract

Based on the understanding of the pathophysiology of heat stroke, it has been suggested that heat stroke can be considered as a form of hyperthermia that is associated with a systemic inflammatory response leading to a syndrome of multiple organ dysfunction in which encephalopathy predominates. Mechanisms of neuronal injury in heat stroke include: cellular effects (damage to membranes, mitochondria, and DNA, stimulation of excitotoxic mechanisms, protein denaturation), local effects (ischemia, inflammatory changes, edema, cytokine release, vascular damage), systemic effects (changes in cerebral blood flow, endotoxemia, translocation of bacteria through a dysfunctional gastrointestinal tract). Neurological manifestations of heat stroke develop in 3 stages according to the time of occurrence: acute, convalescent and late. In the acute stage, cerebral dysfunction prevails. Overheating of the body directly caused polyetiological cerebral dysfunction with deep suppression of consciousness in the acute stage; circulatory shock, hypoxia and cerebral ischemia, excessive accumulation of cytotoxic free radicals and oxidant brain damage developed. During the convalescence stage, cerebral dysfunction gradually decreases. This stage is characterized by transient cerebellar dysfunction. For the late stage, long-term neurological and cardiovascular complications with a constant risk of death are typical. When late stage with permanent neurologic deficits develop, cerebellar dysfunction is the most common symptom. The delayed onset of degeneration and deafferentation suggests that the syndrome is not caused by the primary lesion itself but may be a consequence of postsynaptic hypersensitivity or secondary reorganization of the involved pathways.