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Febrile seizures (FS) are the most common type of seizures in infants and preschool children. Inflammatory mediators, which are known triggers of fever, have also been implicated as contributors to the onset of these seizures. Evidence that inflammation is present following FS and during established epilepsy suggests that it could also influence epileptogenesis. However, the potential involvement of inflammatory mediators to the epileptogenic process that may follow prolonged FS has yet to be fully determined. This article reviews the current state of our knowledge and major gaps that remain by focusing on four questions: Does inflammation contribute to the generation of FS? Does prolonged FS or febrile status epilepticus (SE) cause temporal lobe epilepsy in the absence of predisposing factors? Does inflammation contribute to the process by which febrile SE causes limbic epilepsy? And finally, can inflammation be a foundation for biomarkers and therapy for FS-induced epileptogenesis?

Chronic, limbic epilepsy was induced in male rats by a single systemic injection of lithium and pilocarpine. In two separate experiments, each 6 mo. in duration, the proportion of the population that displayed an overt motor seizure (head nodding, rearing, and forelimb clonus) within 10 min. each day after delivery of food pellets (despite food provided ad libitum) was recorded. Cumulative records for the numbers of rats in each population that displayed overt seizure for the first time during the observation period were plotted as a function of time. The occurrence of the saturated (approaching 100%) asymptote at about five months was interpreted to indicate that brief (10 min.) sampling over the 144 successive days that would compose a single 24-hr. period could serve as an estimate of the average probability of an overt seizure during an average 24-hr. period. If this assumption is correct, then these rats would have displayed about one overt seizure per day.

Two patients are reported, one with severe brain damage and epilepsy, and the other with limbic epilepsy, who were treated with unilateral microsurgical amygdalo-hippocampectomy for the control of rage and aggression. Both had significant improvement in their aggressiveness, and the second patient also improved in the frequency of his seizures and psychotic episodes. The significance of these observations for our understanding of the morphophysiological basis of rage and aggression is discussed.