Neuronal mechanisms underlying focal convulsions and secondary generalised convulsions have been extensively investigated at many different levels, from the biochemical, through the cellular to the intact brain. Numerous pathogenic processes relevant to epilepsy are now known. Experimental models suggest that alterations to the shape, connectivity and receptor-chemistry of individual neurons increase their excitability and the resultant increases in activity lead to changes of the local ionic environment that further causes enhanced excitability. As a consequence of the latter, neuronal firing rates increase and there is a shift from single-firing- to burst-firing-behaviours in populations of neurons and, possibly, also several changes in the way populations of neurons communicate, namely, from 'synaptic' to 'electric' and from orthodromic to antidromic. As a consequence, massive neuronal synchronisation occurs, the correlate of the focal or secondarily generalised attack. Because of experimental difficulties in studying the widespread and evolving neuronal activities in freely behaving animals, a precise correlation between states of neuronal activation and convulsive behaviour is still unclear. (C) 2000 Harcourt Publishers Ltd.
- Animal model
- Partial epilepsy