Table of Contents
Epilepsy Research and Treatment
Volume 2011, Article ID 143908, 10 pages
http://dx.doi.org/10.1155/2011/143908
Review Article

Blood-Brain Barrier Dysfunction in Epileptogenesis of the Temporal Lobe

1Departments of Physiology and Neurobiology, Ben-Gurion University of the Negev, Beersheva 84105, Israel
2Neurocure Research Center, Institute of Neurophysiology, Charité Universitätsmedizin, Berlin 10117, Germany
3Biomedical Engineering, Ben-Gurion University of the Negev, Beersheva 84105, Israel

Received 11 October 2010; Accepted 14 March 2011

Academic Editor: Heidrun Potschka

Copyright © 2011 Itai Weissberg et al. This is an open access article distributed under the , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Epilepsy of the temporal lobe (TLE) is the most common form of focal epilepsy, and in adults, it most frequently develops after injury. However, the mechanisms by which a normal functioning brain turns into an epileptic one still remain obscure. Recent studies point to vascular involvement and particularly blood-brain barrier (BBB) dysfunction in the development of epilepsy. The BBB is a specialized structure which functions to control the neuronal extracellular milieu. BBB dysfunction is found in many diseases of the central nervous system, including stroke, traumatic injuries, tumors and infections. Interestingly, all these insults may initiate an epileptogenic process which eventually leads to spontaneous, recurrent seizures. This epileptogenic time frame usually lasts weeks, months, or even years in man, and days to weeks in rodents and may serve as a “window of opportunity” for the prevention of epilepsy. However, no prevention strategy exists, stressing the importance of research into the mechanisms of epileptogenesis. Here, we will underscore recent experiments suggesting that BBB dysfunction directly induces epileptogenesis. We will provide new evidence to support the hypothesis that BBB breakdown and specifically exposure of temporal lobe structures to the most common serum protein, albumin, is sufficient to induce epileptogenesis.