The thalamocortical contribution to epilepsy.
The experimental literature has dealt intensively with the cortical contribution to epilepsy. Possibly because of the direction of technological advance, much less attention has been paid to the role of other structures. A model which emphasizes the role of some of those non-cortical structures, specifically that of thalamocortical modulation of cortical excitability, is developed. Some aspects of the petit mal seizure, a seizure type considered by some investigators to involve thalamocortical mechanisms, are predicted by the model. Although the thalamocortical mechanisms under study are not the only mechanisms underlying seizures, a full understanding of the phenomenology of epilepsy needs to take into account the role of subcortical modification of cortical activities in addition to other mechanisms. Gloor has described two types of epileptogenesis: type I characteristic of non-convulsive seizures and type II characteristics of convulsions. There is disagreement as to whether or not the two mechanisms represent qualitatively different phenomena. Utilizing the thalamocortical model, it can be shown that the two types of epileptogenesis are qualitatively different. Furthermore, the thalamocortical model leads to a possible explanation of clinically different profiles of antiepileptic efficacy of medications.
Department of Neurology, University of Arkansas for Medical Sciences, Little Rock 72205.
W J
WJ
Nowack
G C
GC
Theodoridis
D000818:Animals; D000927:Anticonvulsants / Q000627:therapeutic use; D002540:Cerebral Cortex / Q000503:physiopathology; D004827:Epilepsy / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D008954:Models, Biological; D008962:Models, Theoretical; D013788:Thalamus / Q000503:physiopathology
D000927:Anticonvulsants