• O Tomkins, I Shelef, I Kaizerman, A Eliushin, Z Afawi, A Misk, M Gidon, A Cohen, D Zumsteg, and A Friedman.
• Department of Physiology, Zlotowski Center for Neuroscience, Ben-Gurion University, 84105 Beer-Sheva, Israel.
• J. Neurol. Neurosurg. Psychiatr. 2008 Jul 1; 79 (7): 774-7.

BackgroundTraumatic brain injury (TBI) is an important cause of focal epilepsy. Animal experiments indicate that disruption of the blood-brain barrier (BBB) plays a critical role in the pathogenesis of post-traumatic epilepsy (PTE).ObjectiveTo investigate the frequency, extent and functional correlates of increased BBB permeability in patient with PTE.Methods32 head trauma patients were included in the study, with 17 suffering from PTE. Patients underwent brain MRI (bMRI) and were evaluated for BBB disruption, using a novel semi-quantitative technique. Cortical dysfunction was measured using electroencephalography (EEG), and localised using standardised low-resolution brain electromagnetic tomography (sLORETA).ResultsSpectral EEG analyses revealed significant slowing in patients with TBI, with no significant differences between patients with epilepsy and those without. Although bMRI revealed that patients with PTE were more likely to present with intracortical lesions (p = 0.02), no differences in the size of the lesion were found between the groups (p = 0.19). Increased BBB permeability was found in 76.9% of patients with PTE compared with 33.3% of patients without epilepsy (p = 0.047), and could be observed years following the trauma. Cerebral cortex volume with BBB disruption was larger in patients with PTE (p = 0.001). In 70% of patients, slow (delta band) activity was co-localised, by sLORETA, with regions showing BBB disruption.ConclusionsLasting BBB pathology is common in patients with mild TBI, with increased frequency and extent being observed in patients with PTE. A correlation between disrupted BBB and abnormal neuronal activity is suggested.

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