Abstracts

Rationale: There is a long-standing hypothesis that prolonged febrile seizures (PFS), the most common form of childhood CSE, cause mesial temporal sclerosis (MTS). CSE may result in acute hippocampal changes but whether this leads to long-term damage or MTS is uncertain. Radiological features of MTS may not be evident until several years post-CSE, but hippocampal volume reduction and/or asymmetry could be identified earlier. From an ongoing follow-up study investigating outcomes of a unique prospectively ascertained paediatric population-based cohort, we report quantitative hippocampal volumetry results a mean of 8.5 years post-CSE. Methods: Brain MRI was performed on a Siemens 1.5T scanner and T1-weighted images acquired using a three-dimensional fast low angle shot (3D FLASH) sequence providing 1mm³ isometric voxels. Hippocampal volumetry was performed using FSL software v4.1.9. Images were reformatted in a tilted coronal plane perpendicular to the long axis of the hippocampus and each hippocampal slice was manually measured independently by 2 investigators blind to clinical details. The hippocampal volume (HV) was measured on each side and right-left asymmetry calculated using asymmetry index (AI= (HV Right- HV Left) / 0.5x (HV Right+ HV Left). Coefficient of variation (CoV) was calculated to determine inter- and intra-rater agreement for HV measurements. Intracranial volume (ICV) was calculated using Brain Extraction Tool (BET) in FSL. HV and AIs were compared across aetiological groups using univariate ANOVA and post-hoc tests with Bonferroni correction in SPSS v21. Results: Hippocampal volumetry was performed on 144 children (70 healthy controls, 30 PFS, 12 acute symptomatic, 20 remote symptomatic and 12 idiopathic/unclassified CSE). The mean interval between CSE and MRI was 8.5 (range 6.3-10) years. Demographic and volumetry data are presented in table 1. CoV was 5.79 for inter- and 5.13 for intra-rater agreement. HV was significantly correlated with ICV (p=0.008) and age (p=0.015). There was no significant difference in mean corrected HV across the aetiological groups except the remote symptomatic group. Mean HV for remote symptomatic group was 553mm³ (95%CI 259-848, p=0.021) lower than controls. The AI for the remote symptomatic group was significantly higher compared with all the other groups (p<0.05 for all). There was no significant difference in the corrected mean HV or AI between PFS, acute symptomatic, idiopathic/unclassified CSE and controls. Three children with PFS who subsequently developed epilepsy had HV and AI in the normal range. One child with a history of CSE with meningitis had AI of 0.46, and neuroimaging features of unilateral MTS, but no epilepsy. Conclusions: On group analysis, hippocampal growth in children who had PFS, acute symptomatic and idiopathic/unclassified CSE is not impaired at a mean follow-up of 8.5 years post-CSE. Children with remote symptomatic CSE have a significant reduction in hippocampal volume and increased asymmetry compared to all the other groups.