The long-term effects of febrile seizures on the hippocampal neuronal plasticity - clinical and experimental evidence.
Febrile seizures are the most common seizure disorder in childhood, but their long-term effects on the developing brains especially neuronal injury and neurocognitive function remain unresolved. Recent epidemiological studies reassure that most febrile seizures do not adversely affect global intelligence and hippocampal function, such as memory. However, there are concerns regarding those children who experience febrile seizures during the first postnatal year, having prior developmental delay and pre- or peri-natal events. Magnetic resonance imaging (MRI) studies confirmed that prolonged and focal FS can occasionally produce acute hippocampal injury that evolves into atrophy. Animal studies have revealed that the exposure of hippocampal neurons to experimental febrile seizures early in life, particularly prolonged or frequently repetitive FS, or together with brain malformation, may lead to sustained dysfunction of these cells, in spite of the absence of neuronal damage. Genetic studies suggest that the relationship between febrile seizures and subsequent epilepsy and neurocognitive dysfunction is sometimes genetic, but there are complex interactions with genetic or environmental modifiers. Therefore, there is a small group of children in whom febrile seizures-induced hippocampal injury might occur. Identification of the target population for subsequent mesial temporal sclerosis is important for prevention and early intervention.
Huang
Chao-Ching
CC
Institute of Clinical Medicine and Department of Pediatrics, National Cheng Kung University College of Medicine, Tainan, Taiwan.
Chang
Ying-Chao
YC
D000818:Animals; D001284:Atrophy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D003072:Cognition Disorders / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007223:Infant; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology*; D051381:Rats; D003294:Seizures, Febrile / Q000150:complications* / Q000503:physiopathology*; D013995:Time