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.
Date:
13 November 2019, 16:00 (Wednesday, 5th week, Michaelmas 2019)
Venue:
Sherrington Library, off Parks Road OX1 3PT
Speaker:
Professor Filiz Onat (Department of Pharmacology and Clinical Pharmacology, Marmara University School of Medicine, Istanbul, Turkey)
Organising department:
Department of Physiology, Anatomy and Genetics (DPAG)
Organiser:
Professor Zoltan Molnar (DPAG, University of Oxford)
Organiser contact email address:
zoltan.molnar@dpag.ox.ac.uk
Host:
Professor Zoltan Molnar (DPAG, University of Oxford)
Part of:
Neuroscience Theme Guest Speakers (DPAG)
Booking required?:
Not required
Audience:
Members of the University only
Editor:
Talitha Smith
