Journal
EPILEPSIA
Volume 58, Issue -, Pages 39-47Publisher
WILEY
DOI: 10.1111/epi.13785
Keywords
Infantile spasms; Infection; Encephalitis; Therapies; Cytokines; Viral infection; Comorbidities; Epilepsy
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Funding
- National Institutes of Health (NIH) [R01 NS091170, U54NS100064]
- Department of Defense [W81XWH-13-1-0180]
- Infantile Spasms Initiative from CURE (Citizens United for Research in Epilepsy)
- Heffer Family Foundation
- Segal Family Foundation
- Abbe Goldstein/Joshua Lurie family
- National Institutes of Health (NINDS, NIH) [HHSN2712016 00048C]
- University of Washington School of Pharmacy
- Niedersachsen-Research Network on Neuroinfectiology (N-RENNT) of the Ministry of Science and Culture of Lower Saxony in Germany
- Laurie Marsh/Dan Levitz family
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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.
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