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
5 - Sensitivity of the immature central nervous system to epileptogenic stimuli
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
During the last ten years, there has been an increased interest in investigating the basic mechanisms of epilepsy in the immature brain. It was already known that the behavioral manifestations of seizures were age dependent but it was widely believed that in the immature central nervous system (CNS) inhibitory events predominated (Purpura & Housepian, 1961; Purpura, 1969, 1972). Therefore, it was assumed that the immature brain was not prone to seizures. However, the preponderance of recently acquired data indicates that the developing CNS is more susceptible to seizures than is the adult CNS. This concept is based on both epidemiological (Gibbs & Gibbs, 1963; Vernadakis & Woodbury, 1969; Hauser & Kurland, 1975; Woodbury, 1977) and experimental (Moshé et al., 1983; Albala et al., 1984; Schwartzkroin, 1984; Swann & Brady, 1984; Cavalheiro et al., 1987; Sperber & Moshé, 1988; Moshé, 1989) studies. Additional data have revealed that epileptogenesis during development may not be a linear event. There appear to be periods of increased seizure susceptibility, followed by relatively more resistant ‘developmental windows’ (Schwartzkroin, 1984; Moshé 1989; Moshé et al., 1992). Furthermore, since brain areas do not mature at the same time, epileptogenesis may differ from site to site.
- Type
- Chapter
- Information
- EpilepsyModels, Mechanisms and Concepts, pp. 171 - 198Publisher: Cambridge University PressPrint publication year: 1993
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