Chapter

Role of Blood-Brain Barrier Dysfunction in Epileptogenesis

Alon Friedman and Uwe Heinemann

in Jasper's Basic Mechanisms of the Epilepsies

Fourth edition

Published on behalf of ©Jeffrey L. Noebels, Massimo Avoli, Michael A. Rogawski, Richard W. Olsen, and Antonio V. Delgado-Escueta

Published in print July 2012 | ISBN: 9780199746545
Published online April 2013 | e-ISBN: 9780199322817 | DOI: http://dx.doi.org/10.1093/med/9780199746545.003.0027

Series: Contemporary Neurology Series

Role of Blood-Brain Barrier Dysfunction in Epileptogenesis

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Focal epilepsy typically arises from neuronal tissue either within or adjacent to a cortical lesion. About 30% of epilepsies are caused by acquired etiologies such as traumatic brain injury, stroke, infection, or prolonged febrile seizures.1 Injury-related acquired epilepsy is frequently resistant to medications and may be associated with other neurological impairments. In most animal models of acquired epilepsy (similar to the situation in humans), a period of days to weeks is required for the development of seizures.2,3 Typically, the initial insult is followed by a latent interval, referred to as epileptogenesis, in which cellular and structural reorganization occurs that ultimately leads to chronic recurrent epileptic seizures. While the molecular, anatomical, and electrophysiological activities in the epileptic focus have been described in great details (e.g., in refs. 4–8), the critical changes occurring following injury and before epileptic activity develops are mostly unknown. A better understanding of the molecular and physiological events during epileptogenesis is essential for the targeted development of preventive therapeutic approaches that are presently unavailable.1

Chapter.  5870 words.  Illustrated.

Subjects: Neurology

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