Mutual exclusive interactions between typical absence and limbic epilepsy

It has been hypothesized that the mechanisms underlying limbic (focal) epilepsy are distinctively different from those responsible for typical absence (generalized) epilepsy and its seizures. Absence seizures, which are typically associated with paroxysmal alterations in consciousness and 2.5-3 Hz spike-and-wave discharges in the EEG, are the major clinical manifestations of childhood and juvenile absence epilepsy. It has been suggested that the pathophysiology of absence seizures principally involves a predominance of inhibitory activity in cortico-thalamo-cortical circuits. In contrast, limbic seizures, clinically seen as representative of mesial temporal lobe epilepsy, have been shown to involve predominantly an excessive cellular hyperexcitability in the limbic system, with focal discharges in the EEG that can progress to secondary generalized convulsive seizures. In order to study the dissimilarities between limbic and generalized typical absence epilepsy, we developed a new paradigm in which we combined kindling as a limbic epilepsy model, with genetic absence epilepsy in rats.