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Blood–brain barrier disruption in post-traumatic epilepsy
  1. O Tomkins3,
  2. I Shelef2,
  3. I Kaizerman3,
  4. A Eliushin2,
  5. Z Afawi4,
  6. A Misk5,
  7. M Gidon2,
  8. A Cohen2,
  9. D Zumsteg6,
  10. A Friedman1
  1. 1
    Departments of Physiology and Neurosurgery, Soroka Medical Center and Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel
  2. 2
    Department of Neuroradiology, Soroka Medical Center, Beer-Sheva, Israel
  3. 3
    Department of Physiology Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, Israel
  4. 4
    Department of Neurology, Tel-Aviv Sourasky Medical Center, Tel Aviv, Israel
  5. 5
    Department of Neurology, Shaare Zedek Medical Center, Jerusalem, Israel
  6. 6
    Department of Neurology, University Hospital Zurich, Zurich, Switzerland
  1. Alon Friedman, Departments of Physiology and Neurosurgery, Zlotowski Center for Neuroscience, Ben-Gurion University, 84105 Beer-Sheva, Israel; alonf{at}


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 in patient with PTE.

Methods: 32 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).

Results: Spectral 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.

Conclusions: Lasting 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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  • OT and IS contributed equally to this work

  • Competing interests: None declared.

  • Ethics approval: Ethics approval was obtained from the Soroka Medical Center Helsinki Committee.