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A Behavioral Screen for Heat-Induced Seizures in Mouse Models of Epilepsy
Published on: July 12, 2021
Inflammatory processes, febrile seizures, and subsequent epileptogenesis
ManKin Choy1, Céline M Dubé2, Markus Ehrengruber1
1Department of Pediatrics, University of California-Irvine, Irvine, CA.
Insights
Inflammation may contribute to febrile seizures (FS) and subsequent epilepsy. Further research is needed to determine if inflammatory mediators cause epilepsy after prolonged febrile seizures or febrile status epilepticus (SE).
Area of Science:
- Pediatric neurology
- Neuroinflammation
- Epileptogenesis
Background:
- Febrile seizures (FS) are common in young children and are linked to fever.
- Inflammatory mediators, triggers of fever, may also contribute to FS onset.
- Inflammation is observed post-FS and in epilepsy, suggesting a role in epileptogenesis.
Purpose of the Study:
- To review current knowledge on inflammation's role in FS and epileptogenesis.
- To identify gaps in understanding the link between prolonged FS/febrile status epilepticus (SE) and epilepsy.
- To explore inflammation's potential as a basis for biomarkers and therapies for FS-induced epileptogenesis.
Main Methods:
- Review of existing literature on febrile seizures, inflammation, and epilepsy.
- Focus on four key questions regarding inflammation's role.
- Analysis of the potential for inflammation to drive epileptogenesis following prolonged FS or SE.
Main Results:
- Evidence suggests inflammation contributes to FS generation.
- The role of prolonged FS or SE in causing temporal lobe epilepsy without predisposing factors requires further investigation.
- Inflammation's contribution to febrile SE-induced limbic epilepsy is not fully determined.
Conclusions:
- Inflammation is implicated in FS and may influence epileptogenesis.
- Further research is crucial to understand if prolonged FS or SE leads to epilepsy.
- Inflammation may offer potential for developing biomarkers and therapies for FS-induced epileptogenesis.
Abstract:
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?
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