POST-INFECTIOUS EPILEPSY

Recently, substantial evidence has been obtained regarding the possible involvement of inflammatory processes in epileptogenesis. Thus, several studies have established increased synthesis of specific inflammatory mediators in the brain of patients and corresponding activation of some pro-inflammatory pathways in seizure foci, as well as involvement of oxidative stress. Information has also emerged that some chronic infections, such as neurocysticercosis, HIV and herpes, without causing acute cerebral pathology, are capable of provoking epileptic seizures and even subsequent formation of refractory epilepsy. This review summarizes experimental and clinical research data on the connection between epilepsy and chronically occurring infectious diseases and neuroinflammation.