Forensic Neuropathology of Hyperthermia

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Heatstroke is defined as a core body temperature that rises above 40.6 ℃ and is accompanied by mental status abnormalities such as delirium, convulsions or coma resulting from exposure to environmental heat. There is fairly wide agreement that ethanol intake is a predisposing factor in heatstroke. This study was performed to identify the brain changes induced by heatstroke, using a mouse hyperthermia model with and without preceding ethanol administration. Exposure to heat of 40 ℃ until the core temperature reached to 42 ℃ followed by exposure to 37 ℃ for 15 min induced metabolic acidosis and respiratory alkalosis in mice. Immunohistochemistry of the brains of hyperthermia mice showed an increase in the number of c-fos immunoreactive neurons, as a marker of neuronal activation, in the central amygdaloid nucleus (CeA), which is involved in thermoregulation. Preceding ethanol administration maintained a high core temperature after heat exposure, induced hypotension, severe metabolic acidosis and respiratory failure, and accordingly, produced heatstroke, and further increased the number of c-fos immunoreactive neurons in the CeA in mice. These results indicate that hyperthermia is associated with neuronal activation in the CeA and is exacerbated by the presence of ethanol, implicating the pathophysiology and mechanisms of brain dysfunctions in the etiology of heatstroke.