Abstract

The development of hyperthermia (≥38.3 °C) in severe traumatic brain injury (TBI) is associated with increased levels of disability and mortality, since it critically affects the development of secondary brain damage. At the cellular level, hyperthermia causes structural and functional changes in neurons through disruption of depolarization, transmembrane ion transport, cell signaling mechanisms, and damage to mitochondrial function. Hyperthermia can lead to necrosis or apoptosis of neurons. Among the systemic effects of hyperthermia is an increase in the permeability of the blood - brain barrier, causing the development of intracranial hypertension. This publication presents the pathophysiological mechanisms of the development of hyperthermia and its participation as a factor of brain damage in severe TBI, diagnostic criteria for hyperthermia of central origin and modern methods of controlled normothermia.

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