Clinical and experimental data support the hypothesis that immune mechanisms may be a factor in a number of epilepsies such as Rasmussens encephalitis, Lennox-Gastaut syndrome, Landau-Kleffner syndrome, and temporal lobe epilepsy. Surgical epilepsy specimens have shown immunologic abnormalities, suggesting a broader role for immunopathology in the etiology of epilepsy. Inflammatory reactions occur in the brain in various central nervous system diseases, including autoimmune, neurodegenerative, and epileptic disorders. Proinflammatory and anti-inflammatory cytokines and related molecules have been described in the CNS and plasma, both in experimental models of seizure and in clinical cases of epilepsy. Inflammation involves both the innate and the adaptive immune systems and shares molecules and signaling pathways that are also activated by systemic infection. Experimental studies in rodents show that inflammatory reactions in the brain can enhance neuronal excitability, impair cell survival, and increase the permeability of the blood-brain barrier to blood-borne molecules and cells. The immune response is altered with the development of epilepsy, and seizures result. We provide an overview of the current knowledge implicating brain inflammation as a common predisposing factor for epilepsy, focusing particularly on clinical and basic evidence.
Keywords: Epilepsy, inflammation, blood-brain barrier, cytokines, human data, animal models
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