Book contents
- Frontmatter
- Contents
- List of contributors
- General introduction
- Section 1 Chronic models in intact animals – concepts and questions
- Introduction
- 1 The kindling model of epilepsy
- 2 Focal trigger zones and pathways of propagation in seizure generation
- 3 Genetic models of the epilepsies
- 4 Noradrenergic modulation of excitability: transplantation approaches to epilepsy research
- 5 Sensitivity of the immature central nervous system to epileptogenic stimuli
- Section 2 Features of the epileptogenic brain
- Section 3 ‘Normal’ brain mechanisms that support epileptiform activities
- Recent advances
- Index
2 - Focal trigger zones and pathways of propagation in seizure generation
from Section 1 - Chronic models in intact animals – concepts and questions
Published online by Cambridge University Press: 03 May 2010
- Frontmatter
- Contents
- List of contributors
- General introduction
- Section 1 Chronic models in intact animals – concepts and questions
- Introduction
- 1 The kindling model of epilepsy
- 2 Focal trigger zones and pathways of propagation in seizure generation
- 3 Genetic models of the epilepsies
- 4 Noradrenergic modulation of excitability: transplantation approaches to epilepsy research
- 5 Sensitivity of the immature central nervous system to epileptogenic stimuli
- Section 2 Features of the epileptogenic brain
- Section 3 ‘Normal’ brain mechanisms that support epileptiform activities
- Recent advances
- Index
Summary
Introduction
It is becoming increasingly evident that epileptogenic processes derive in part from an imbalance between excitatory and inhibitory controls in selected brain regions. Determining the nature of such imbalances, where and how they relate to convulsive seizure generation, and how they may be corrected, requires an understanding of neural mechanisms of propagated seizure development in the brain. Presently, there is a large gap between our knowledge of synaptic mechanisms involved in local epileptiform discharge in vitro and our observations in vivo of the convulsant and anticonvulsant actions of systemically administered drugs. Within this gap are the myriad of neural pathways connecting brain regions and forming complex circuits that can both propagate seizures and act to prevent them.
The neural circuitry involved in the initiation and propagation of seizures is extensive, intricate and variable with seizure type. It is clear that there are no neural circuits unique to seizures, but that seizure activity represents abnormal neuronal discharge conducted along circuits that are normally utilized for physiological processes. Moreover, several constellations of brain circuits exist that are potential substrates for propagated seizures. Thus, much in the same way that there is no single ‘memory’ circuit in the brain, seizures may be generated and propagated within any of several functionally distinct circuits.
- Type
- Chapter
- Information
- EpilepsyModels, Mechanisms and Concepts, pp. 48 - 93Publisher: Cambridge University PressPrint publication year: 1993
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