Electrophysiology of Epileptic Tissue: What Pathologies are Epileptogenic?

Abstract

What defines the abnormality of epileptic tissue? What constitutes an epileptic focus? Experimental studies have been carried out for many years to try and answer these questins, and a large number of alterations have been proposed as basic to generation of epileptiform activity (Jasper et al., 1969; Lockard and Ward, 1980; Schwartzkroin and Wheal, 1984; DelgadoEscueta et al., 1986). Yet, our real information about the abnormalities intrinsic to the epileptic condition remains limited. In studying potential causes of abnormal cell electrical activity, we have become familiar with many of the normal properties of neocortical and hippocampal neurons, but have not been able to define the essential nature of the epileptic defect. Morphological, pharmacological, biochemical, and electrophysiological features have been suggested which could be involved in generation of epileptiform activity (Westrum et al., 1964; Heinemann et al., 1977; Woodbury and Kemp, 1977; French and Siggins, 1980; Schwartzkroin and Wyler, 1980; Lux and Heinemann, 1982; Ribak et al., 1982;. Dudek et al., 1983; Grisar et al., 1983; Scheibel et al., 1983; Schwartzkroin, 1983; DeLorenzo, 1984; Johnston and Brown, 1984; Somjen, 1984). For most of these, it remains unclear whether the abnormality is present before, and is responsible for, the development of epileptiform activity, or whether these abnormalities are produced as a result of abnormal electrical activity in the brain. It is this issue of defining causal, rather than correlative features of epileptogenesis that has been so difficult in epilepsy research. The drive for such causality has led to the establishment of a host of animal model systems.