J Neurochem. 2025 Aug;169(8):e70171. doi: 10.1111/jnc.70171.
ABSTRACT
Early-life seizure (ELS) represents a condition characterized by ictal events occurring during the early stages of childhood, with particularly high incidence in the neonatal period and infancy. ELS is triggered by a variety of causes, including simply a fever, perinatal asphyxia, brain damage, or genetic abnormalities. Emerging evidence indicates that ELS exerts profound and enduring effects on brain development, predisposing individuals to heightened risks of epilepsy persisting into adulthood. Several shared mechanisms underpin the increased adult epileptogenesis resulting from diverse ELS subtypes, including febrile seizures (FS), chemoconvulsants-induced seizures, and hypoxia-associated seizures. This review systematically examines the long-term consequences on adult epileptogenesis of ELS, focusing on maladaptive plasticity in neuronal networks, reactive gliosis, sustained neuroinflammatory responses, and progressive neuronal degeneration. Finally, we offer perspectives on intensive avenues for future research.
PMID:40734501 | DOI:10.1111/jnc.70171
