Researchers at the University of Melbourne, Australia, measured the effect of temperature on brain sodium channel, Nav1.2, properties, using a computer model of the dentate gyrus granule cell. In animal models thermogenic seizures are hippocampal in origin (Dube C et al. 2000). The voltage dependance of activation became 7.6mV more negative when the temperature was increased from 37C to 41C. The direct effect of heat caused an increase in gating rates of sodium ion channels and a more negative activation with increased neuronal excitability. This dramatic increase in excitability due to increased temperature may be an important factor in the mechanism of a febrile seizure. [1]

COMMENT. The mechanism of febrile seizures is dependent on several factors, but especially height of body temperature and an individual’s febrile convulsive threshold. In addition to genetic susceptibility and cytokines, the neurotropic properties of certain viruses, age and level of immaturity, and water and electrolyte balance are contributing factors [2, 3]. The above study provides further explanations for the febrile seizure mecanism at a molecular level, and specifically the effect of body temperature on brain sodium channels.