Temporal Lobe Epilepsy: Morphological Abnormalities Associated with Genetic Epilepsies

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

Abstract

The relationships between structural brain abnormalities and epilepsy are poorly understood. Even in genetically-determined epilepsies, it is often unclear whether a neuropathological feature is causally related to seizure activity or is a secondary effect. We illustrate these two possibilities, using two genetic mouse 'knockout' models - p35-/-and Kv1.1-/-. In p35-/-mice, the gene deletion causes an abnormal pattern of brain development; this primary structural dysplasia in turn produces electrical and behavioral seizures. In Kv1.1-/-mice, the gene deletion is directly responsible for neuronal hyperexcitability and epilepsy, and neuropathological features appear secondarily as a result of intense recurrent seizure activity. Understanding the distinction between these two structure-function relationships is particularly important as we consider the development of novel therapies and points of intervention during epileptogenesis.

Original languageEnglish (US)
Title of host publicationEncyclopedia of Basic Epilepsy Research
PublisherElsevier Inc.
Pages1366-1373
Number of pages8
ISBN (Print)9780123739612
DOIs
StatePublished - Jan 1 2009

Keywords

  • Brain development
  • Cause-effect
  • Knockout models
  • Kv1.1
  • Neuropathology
  • P35
  • Potassium channel
  • Seizures

ASJC Scopus subject areas

  • Medicine(all)
  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Temporal Lobe Epilepsy: Morphological Abnormalities Associated with Genetic Epilepsies'. Together they form a unique fingerprint.

  • Cite this