Animal models have provided a wealth of information on mechanisms of epileptogenesis and comorbidogenesis, and have significantly advanced our ability to investigate the potential of new
therapies. Processes implicating
brain inflammation have been increasingly observed in
epilepsy research. Herein we discuss the progress on animal models of
epilepsy and comorbidities that inform us on the potential role of
inflammation in epileptogenesis and comorbidity pathogenesis in rodent models of
West syndrome and the Theiler's murine encephalomyelitis virus (TMEV) mouse model of
viral encephalitis-induced
epilepsy. Rat models of
infantile spasms were generated in rat pups after right intracerebral
injections of proinflammatory compounds (
lipopolysaccharides with or without
doxorubicin, or
cytokines) and were longitudinally monitored for epileptic
spasms and neurodevelopmental and cognitive deficits. Anti-inflammatory treatments were tested after the onset of
spasms. The TMEV mouse model was induced with intracerebral administration of TMEV and prospective monitoring for handling-induced
seizures or seizure susceptibility, as well as long-term evaluations of behavioral comorbidities of
epilepsy. Inflammatory processes are evident in both models and are implicated in the pathogenesis of the observed
seizures and comorbidities. A common feature of these models, based on the data so far available, is their pharmacoresistant profile. The presented data support the role of inflammatory pathways in epileptogenesis and comorbidities in two distinct
epilepsy models. Pharmacoresistance is a common feature of both
inflammation-based models. Utilization of these models may facilitate the identification of age-specific, syndrome- or etiology-specific
therapies for the
epilepsies and attendant comorbidities, including the
drug-resistant forms.