Networks: Interactions between Cortico-Thalamo-Cortical and Limbic Seizures

Abstract

It has been hypothesized that the mechanisms underlying limbic (focal) seizures are distinctively different from those responsible for typical absence (generalized) seizures. Absence seizures, which are typically associated with paroxysmal alterations in consciousness and 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. To study the dissimilarities between focal limbic and generalized typical absence seizures, we developed a new paradigm in which we combined a kindling model of limbic seizures with genetic absence epilepsy model in rats. © 2009 Elsevier Ltd All rights reserved.