The long-term neurodevelopmental outcomes of febrile seizures and underlying mechanisms

Febrile seizures (FSs) are convulsions caused by a sudden increase in body temperature during a fever. FSs are one of the commonest presentations in young children, occurring in up to 4% of children between the ages of about 6 months and 5 years old. FSs not only endanger children’s health, cause panic and anxiety to families, but also have many adverse consequences. Both clinical and animal studies show that FSs have detrimental effects on neurodevelopment, that cause attention deficit hyperactivity disorder (ADHD), increased susceptibility to epilepsy, hippocampal sclerosis and cognitive decline during adulthood. However, the mechanisms of FSs in developmental abnormalities and disease occurrence during adulthood have not been determined. This article provides an overview of the association of FSs with neurodevelopmental outcomes, outlining both the underlying mechanisms and the possible appropriate clinical biomarkers, from histological changes to cellular molecular mechanisms. The hippocampus is the brain region most significantly altered after FSs, but the motor cortex and subcortical white matter may also be involved in the development disorders induced by FSs. The occurrence of multiple diseases after FSs may share common mechanisms, and the long-term role of inflammation and γ-aminobutyric acid (GABA) system are currently well studied.