Current epilepsy treatment is mostly symptomatic and seems not to influence the underlying pathology or progression of the disease [1,2]. One-third of the patients are still resistant to current therapies [2–4]. The presence of inflammation, without known autoimmune or infectious etiology has been reported in epilepsy in the past two decades and has been considered an important mechanism for epileptogenesis [for review see [4–7]]. A ‘neuromodulatory’ role of various inflammatory molecules like cytokines, chemokines and prostaglandins in epilepsy models has been described by both a direct action on neurons, and by an autocrine receptor stimulation in glia cells which influence glianeuronal communication [3,8,9].
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