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The important new finding from Schwechter and colleagues is that hyperglycemia, itself, is proconvulsant. How can elevated glucose enhance seizure susceptibility? The answer to this crucial question regarding the mechanism of action awaits further research, as the mechanism per se is not addressed in this report. However, one clue to the answer might be gleaned from the authors's observation that hypoglycemia was associated with a higher seizure threshold. Other studies have indicated that restricting calories, thus inducing hypoglycemia, in the epilepsy-prone EL mouse also reduces seizure susceptibility (2). With any model that induces hypoglycemia, the role of ketosis must be excluded, as ketones themselves can affect seizure threshold (3). Moreover, multiple other mechanisms could explain hypoglycemia- and hyperglycemia-induced alterations of neuronal excitability. Furthermore, the effects of age on glucose balance and neuronal excitability must be delineated, as children with diabetes tend to develop seizures with hypoglycemia rather than with hyperglycemia. In addition to clarifying further the relation between hyperglycemia and seizures, Schwechter et al. highlight the link between metabolism and neuronal excitability and emphasize the need for further research on the long-term effects of hyperglycemia on various aspects of brain function.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=387262