The production of inflammatory molecules in the brain has been described after seizure induction in experimental models as well as in epileptogenic tissue from clinical cases of epilepsy of different etiologies. Experimental studies in rodents show that inflammatory process in the brain can increase neuronal excitability via several mechanisms, including functional interaction with glutamate- and GABA-mediated neurotransmission. Specific anti-inflammatory treatments are anticonvulsant in experimental models and reduce pharmacoresistant seizures in selected epileptic syndromes. These observations suggest that brain inflammation could cause, or predispose, seizure occurrence. Further insights into this issue might open new perspectives for the pharmacological treatment of seizures and possibly for interfering with epileptogenesis.