Table of Contents
Cardiovascular Psychiatry and Neurology
Volume 2011, Article ID 765923, 11 pages
http://dx.doi.org/10.1155/2011/765923
Research Article

Blood-Brain Barrier Breakdown Following Traumatic Brain Injury: A Possible Role in Posttraumatic Epilepsy

1Departments of Physiology and Neurobiology, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, 84105 Beer-Sheva, Israel
2Department of Ophthalmology, Bnai Zion Medical Center, Haifa, Israel
3Department of Neuroradiology, Soroka University Medical Center and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel
4Department of Neurosurgery, Soroka University Medical Center and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel
5Department of Biomedical Engineering, Ben-Gurion University of the Negev, Beer-Sheva, Israel

Received 30 October 2010; Accepted 2 January 2011

Academic Editor: Daniela Kaufer

Copyright © 2011 Oren Tomkins et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Recent animal experiments indicate a critical role for opening of the blood-brain barrier (BBB) in the pathogenesis of post-traumatic epilepsy (PTE). This study aimed to investigate the frequency, extent, and functional correlates of BBB disruption in epileptic patients following mild traumatic brain injury (TBI). Thirty-seven TBI patients were included in this study, 19 of whom suffered from PTE. All underwent electroencephalographic (EEG) recordings and brain magnetic resonance imaging (bMRI). bMRIs were evaluated for BBB disruption using novel quantitative techniques. Cortical dysfunction was localized using standardized low-resolution brain electromagnetic tomography (sLORETA). TBI patients displayed significant EEG slowing compared to controls with no significant differences between PTE and nonepileptic patients. BBB disruption was found in 82.4% of PTE compared to 25% of non-epileptic patients (𝑃=.001) and could be observed even years following the trauma. The volume of cerebral cortex with BBB disruption was significantly larger in PTE patients (𝑃=.001). Slow wave EEG activity was localized to the same region of BBB disruption in 70% of patients and correlated to the volume of BBB disrupted cortex. We finally present a patient suffering from early cortical dysfunction and BBB breakdown with a gradual and parallel resolution of both pathologies. Our findings demonstrate that BBB pathology is frequently found following mild TBI. Lasting BBB breakdown is found with increased frequency and extent in PTE patients. Based on recent animal studies and the colocalization found between the region of disrupted BBB and abnormal EEG activity, we suggest a role for a vascular lesion in the pathogenesis of PTE.