Neuropediatrics 2006; 37 - PS4_1_2
DOI: 10.1055/s-2006-945787

HIPPOCAMPAL VOLUMES AND DIFFUSION WEIGHTED IMAGE FINDINGS IN CHILDREN WITH PROLONGED FEBRILE SEIZURES: COMPARISON WITH SEIZURE DURATION AND EEG FINDINGS

J Natsume 1, N Bernasconi 1, M Miyauchi 1, M Naiki 1, T Yokotsuka 1, S Itomi 1, A Sofue 1, A Bernasconi 1
  • 1Department of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan

Objectives: There is continued debate on whether status epilepticus can cause acute hippocampal damage, which could lead to mesial temporal lobe epilepsy. Our purpose was to assess hippocampal volumes (HV) and signal changes on diffusion weighted imaging (DWI) in patients with prolonged febrile seizures (PFS) and compare them with the seizure duration or EEG findings.

Methods: We studied 12 children within five days of a first episode of PFS. The hippocampus was segmented manually on a high-resolution MRI and signal intensity abnormalities were evaluated visually on DWI. Seizure duration ranged from 40 to 95 minutes. In 7/12 patients, seizures lasted 60 minutes or longer despite intravenous infusion of diazepam. HV in patients were compared with those of 13 controls. HV abnormalities were correlated to seizure duration. DWI abnormalities were compared with HV, seizure duration and EEG abnormalities.

Results: The HV of patients were not significantly different from those of controls. However, when considering only patients with PFS for 60 minutes or longer, HV were significantly larger than in controls. In patients, there was a positive correlation between HV and seizure duration. DWI showed unilateral hippocampal hyperintensity in three patients with intractable seizures, and ipsilateral thalamic hyperintensity in two of them. EEG within 48 hours showed unilateral abnormalities ipsilateral to the side of DWI abnormalities.

Conclusion: Large HV and hippocampal hyperintensity on DWI were seen in patients with intractable PFS. Our results suggest that medically intractable PFS may cause structural changes in limbic structures that could promote epileptogenesis.