摘要: Decades of experimental work have established an imbalance excitation and inhibition as the leading mechanism transition from normal brain function to seizure. In epilepsy, these transitions are rare abrupt. Transition processes incorporating positive feedback, such activity-dependent disinhibition, could provide uncommon timing features. A rapidly expanding array genetic etiologies will help delineate molecular mechanism(s). This delineation entail quite a bit cell biology. The genes discovered so far more remarkable for their diversity than similarities.