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Blood-Brain Barrier Disruption in Post-Traumatic Epilepsy
  1. O Tomkins (tomkins{at}
  1. Ben-Gurion University of the Negev, Israel
    1. I Shelef (shelef{at}
    1. Soroka Medical Center, Israel
      1. I Kaizerman (idnak{at}
      1. Ben-Gurion University of the Negev, Israel
        1. A Misk (dr_misk53{at}
        1. Al-Quds University, Palestinian Territory, Occupied
          1. Z Afawi (afawi{at}
          1. Tel-Aviv Sourasky Medical Center, Israel
            1. A Eliushin
            1. Soroka Medical Center, Israel
              1. M Gidon (micky{at}
              1. Soroka Medical Center, Israel
                1. A Cohen (avicohen{at}
                1. Soroka Medical Center, Israel
                  1. D Zumsteg
                  1. University Hospital Zurich, Swaziland
                    1. A Friedman (alonf{at}
                    1. Ben-Gurion University of the Negev, Israel


                      Background: Traumatic 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).

                      Objective: To investigate the frequency, extent and functional correlates of increased BBB permeability following in PTE patients.

                      Methods: 32 head trauma patients were included in the study, with 17 suffering from PTE. Patients underwent brain magnetic resonance imaging (bMRI) and were evaluated for BBB disruption, using a novel semi-quantitative technique. Cortical dysfunction was measured using electroencephalography (EEG), and localized using standardized low resolution brain electromagnetic tomography (sLORETA).

                      Results: Spectral EEG analyses revealed significant slowing in TBI patients with no significant differences between epileptic and non-epileptic patients. While bMRI revealed that PTE patients 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 PTE compared to 33.3% of non-epileptic patients (p=0.047), and could be observed years following the trauma. Cerebral cortex volume with BBB disruption was larger in PTE patients (p=0.001). In 70% of patients, slow (delta band) activity was co-localized, by sLORETA, with regions showing BBB disruption.

                      Conclusions: Lasting BBB pathology is common in mild TBI patients, with increased frequency and extent in PTE patients. A correlation between disrupted BBB and abnormal neuronal activity is suggested.

                      • Blood-Brain Barrier
                      • Electroencephalography
                      • Magnetic Resonance Imaging
                      • Post-Traumatic Epilepsy

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