Abstracts

Rationale: Inflammatory processes contribute to blood-brain-barrier (BBB) breakdown and proconvulsive penetration of leukocytes in the central nervous system (CNS) in active epilepsy. This process is regulated via multiple adhesion molecules like intercellular adhesion molecule 1 (ICAM-1): Blocking ICAM-1 prevented occurrence of SE in animal models (Fabene et al. 2009). Therefore, we performed a prospective study in patients with active epilepsy on possible systemic changes of ICAM-1.Methods: 20 patients with well characterized focal epilepsy were included (7 male (35%), age 40.7 11.7 years). Blood drawing was performed at a seizure free interval for baseline (minimum of 3 days) and immediately, 1 and 24 hours after a complex partial (CPS) or secondary generalized tonic-clonic seizure (sGTCS). Distribution of ICAM-1 on CD3+ leukocyte subsets, CD56+ NK cells and CD14+ monocytes was analyzed using flow cytometry.Results: ICAM-1 on NK cells increased significantly immediately postictally compared to baseline (25.7% 13.1% vs. 15.1% 5.7%, p=0.014) and decreased again one hour after the seizure (16,45% 8,9%). This finding remained the same comparing complex partial and secondary generalized seizures separately (CPS: 14.9% 4.4% vs. 21.6% 9.6%, p=0.046; sGTCS: 16.5% 7.4% vs. 35.3% 13%, p=0.011). Comparison of CD3+ marked cells did not show any significant changes (p=0.37), neither did monocytes (p=0.55).Conclusions: The results show that ICAM-1 on NK cells is altered also in human focal epilepsy in the acute postictal state. The increase was detectable in both complex partial and secondary generalized seizures. The exact contribution of this finding to human icto- or epileptogenesis is subject to further studies.