Hippocampal sclerosis after febrile status epilepticus: The FEBSTAT study

Male Clinical Sciences FEBSTAT Study Team Clinical sciences Neurodegenerative Hippocampus 03 medical and health sciences Status Epilepticus 0302 clinical medicine Risk Factors 2.1 Biological and endogenous factors Humans Prospective Studies Aetiology Preschool Child Epilepsy Neurology & Neurosurgery Sclerosis Biomedical and Clinical Sciences Neurosciences Infant Magnetic Resonance Imaging Brain Disorders Diffusion Magnetic Resonance Imaging Child, Preschool Biomedical Imaging Female Follow-Up Studies
DOI: 10.1002/ana.24081 Publication Date: 2013-12-07T11:51:21Z
ABSTRACT
ObjectiveWhether febrile status epilepticus (FSE) produces hippocampal sclerosis (HS) and temporal lobe epilepsy (TLE) has long been debated. Our objective is to determine whether FSE produces acute hippocampal injury that evolves to HS.MethodsFEBSTAT and 2 affiliated studies prospectively recruited 226 children aged 1 month to 6 years with FSE and controls with simple febrile seizures. All had acute magnetic resonance imaging (MRI), and follow‐up MRI was obtained approximately 1 year later in the majority. Visual interpretation by 2 neuroradiologists informed only of subject age was augmented by hippocampal volumetrics, analysis of the intrahippocampal distribution of T2 signal, and apparent diffusion coefficients.ResultsHippocampal T2 hyperintensity, maximum in Sommer's sector, occurred acutely after FSE in 22 of 226 children in association with increased volume. Follow‐up MRI obtained on 14 of the 22 with acute T2 hyperintensity showed HS in 10 and reduced hippocampal volume in 12. In contrast, follow‐up of 116 children without acute hyperintensity showed abnormal T2 signal in only 1 (following another episode of FSE). Furthermore, compared to controls with simple febrile seizures, FSE subjects with normal acute MRI had abnormally low right to left hippocampal volume ratios, smaller hippocampi initially, and reduced hippocampal growth.InterpretationHippocampal T2 hyperintensity after FSE represents acute injury often evolving to a radiological appearance of HS after 1 year. Furthermore, impaired growth of normal‐appearing hippocampi after FSE suggests subtle injury even in the absence of T2 hyperintensity. Longer follow‐up is needed to determine the relationship of these findings to TLE. ANN NEUROL 2014;75:178–185
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