Basic mechanisms of generalized absence seizures

AbstractGeneralized absence seizures are neurophysiologically, pharmacologically, and developmentally unique and comprise the primary seizure type in a number of different absence epilepsy syndromes. Over the last 10 years, the availability of a number of animal models of generalized absence seizures and of sophisticated in vitro electrophysiological techniques that allow investigation of cortical and thalamic networks has begun to shed light on the pathogenesis of this disorder. The basic underlying mechanism appears to involve thalamocortical circuitry and the generation of abnormal oscillatory rhythms from that particular neuronal network. Biochemical mechanisms operative within thalamocortical circuitry during this neuronal oscillation seem to entail phase‐locked ‐aminobutyric acid (GABA)B‐mediated inhibition alternating with glutamate‐mediated excitation. The basic cellular mechanism operative within this tension between excitation and inhibition appears to involve the T‐type calcium current. Local circuitry within the thalamus may influence these oscillatory rhythms by GABAA‐mediated inhibition. Pharmacological factors at play external to thalamocortical circuitry include cho