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Excitation and Inhibition in Epilepsy

Published online by Cambridge University Press:  18 September 2015

Jerome Engel Jr.
Jerome Engel Jr.*
Affiliation:
Departments of Neurology and Neurobiology and the Brain Research Institute, UCLA School of Medicine, Los Angeles
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Abstract

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The term epileptic seizures is used to describe a variety of paroxysmal signs and symptoms resulting from a large number of underlying pathological processes. Generalized tonic-clonic convulsions, therefore, reflect entirely different basic neuronal mechanisms than those of typical absences. Animal research suggests that the former result from disturbances that involve disinhibilion, whereas the abnormality giving rise to the latter requires intact, if not enhanced, inhibition in order to sustain hypersynchronous neuronal discharges. Investigations in human mesial temporal lobe epilepsy and chronic experimental animal models indicate that partial seizures can also reflect multiple underlying mechanisms, with some disinhibitory in type, while others appear to be hypersynchronous and associated with enhanced inhibition. Just as more than one epileptogenic disturbance can result in transition to ictus, it is likely that more than one mechanism can be engaged to terminate epileptic seizures, that these diverse processes could result in different postictal manifestations, and that they could conceivably contribute differently to the development of interictal behavioral disturbances. An appreciation for the fact that epilepsy is not merely an increase in excitation and/or a decrease in inhibition, but a variety of complicated neuronal interactions in different patients, or even at different times in the same patient or same seizure, is essential to the development of effective treatments to control epileptic seizures and prevent their consequences.

Résumé

Résumé

Excitation et inhibition dans l’épilepsie. Le terme crise d’épilepsie est utilisé pour décrire une variété de signes et de symptômes paroxystiques résultant d’un grand nombre de processus pathologiques sous-jaeents. Les convulsions toniques-cloniques généralisées reflètent donc des mécanismes neuronaux de base qui sont entièrement différents de ceux des absences typiques. La recherche chez l’animal suggère que les premières résultent de perturbations qui impliquent une désinhibition, alors que les secondes résultent d’une anomalie qui requière une inhibition intacte ou même accrue pour maintenir des décharges neuronales hypersynchrones. L’investigation de l’épilepsie mésiale du lobe temporal chez l’humain et chez des modèles animaux d’épilepsie expérimentale chronique indiquent que les crises partielles peuvent également refléter des mécanismes sous-jacents multiples. dont quelques uns sont de type désinhibition alors que d’autres semblent être hypersynchrones et associés à une inhibition accrue. Comme plus d’une perturbation épileptogène peut prédisposer à l’ictus, il est également possible que plus d’un mécanisme peut être mobilisé pour mettre fin à une crise d’épilepsie, que ces divers processus pourraient donner lieu à des manifestations postcritiques différentes et qu’ils pourraient vraisemblablement contribuer différemment au développement de perturbations du comportement entre les crises. Il est essentiel de reconnaître que l’épilepsie n’est pas seulement une augmentation de l’excitation et/ou une diminution de l’inhibition, mais une variété d’interactions neuronales complexes chez différents patients ou même à différents moments chez le même patient ou pendant la même crise afin de développer des traitements efficaces pour contrôler les crises d’épilepsie et en prévenir les conséquences.

Type
Review Article
Information
Canadian Journal of Neurological Sciences , Volume 23 , Issue 3 , August 1996 , pp. 167 - 174
Copyright
Copyright © Canadian Neurological Sciences Federation 1996

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