Abstract
Experimental and clinical evidence have demonstrated the increased synthesis of specific inflammatory mediators, and the upregulation of their cognate receptors in the chronic epileptic brain, indicating that some proinflammatory pathways are activated in seizure foci. Inhibition of experimental seizures by pharmacological interference with specific proinflammatory signaling, together with evidence of changes in intrinsic susceptibility to seizures in transgenic mice with perturbed inflammatory pathways, was instrumental to establish the concept that brain inflammation has a role in the etiopathogenesis of seizures. Increasing evidence also highlights the possible involvement of inflammatory processes arising in the injured brain in the development of epilepsy (i.e., in epileptogenesis). Since brain inflammation in epilepsy is not a mere epiphenomenon of the pathology but is likely involved in the mechanisms underlying neuronal hyperexcitability, the onset of seizures and their recurrence, it might be considered as a biomarker of disease development and severity, and, as such, could be used for diagnostic, prognostic or therapeutic purposes, provided that adequate noninvasive methodologies are developed to detect and quantify brain inflammation in humans.