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Animal experiments, and particularly functional investigations on human chronically epileptic tissue as well as genetic studies in epilepsy patients and their families strongly suggest that some forms of epilepsy may share a pathogenetic mechanism: an alteration of voltage-gated sodium channels. This review summarizes recent data on changes of sodium channel expression, molecular structure and function associated with epilepsy, as well as on the interaction of new and established antiepileptic drugs with sodium currents. Although it remains to be determined precisely how and to what extent altered sodium-channel functions play a role in different epilepsy syndromes, future promising therapy approaches may include drugs modulating sodium currents, and particularly substances changing their inactivation characteristics.
Rüdiger Köhling (Fri,) studied this question.