Abstracts

Rationale: Children with epilepsy are at increased risk of neurobehavioural impairments (NI) that have a significant impact on their quality of life. It is not known how much of this is caused by potentially modifiable factors, such as seizure frequency and medication or by pre-existing brain abnormalities that would cause problems even if seizures were well controlled. Reduced thalamic volume has been associated with NI in children with childhood absence epilepsy or complex partial seizures. There are no published studies investigating this issue in children with early onset epilepsy (EOE, onset <5 years) where the risk of NI is highest We hypothesise that there is a pre-existing subcortical abnormality in EOE compared to controls and that this is greater in children with epilepsy and NI. We present data from an ongoing study investigating the link between structural brain abnormalities and NI in EOE with a view to identifying potential predictive factors of NI Methods: Newly diagnosed EOE recruited as part of an ongoing prospective study on the incidence and risk factors of NI in EOE are being enrolled in this sub-study. Healthy controls, with no previous seizures or neurological abnormalities are also being enrolled. All participants are undergoing magnetic resonance imaging (MRI) including T1-weighted volumetric sequences (3D-FLASH/MPRAGE) and neurocognitive assessment. Assessment tools used include the Bayley Scales of Infant and Toddler Development (BSID-III), Wechsler Pre-School and Primary Scales of Intelligence (WPPSI-III), Social Responsiveness Scale-II (SRS-II) and Conners Early Childhood (C-EC). Patients are considered to have NI if they score > 1.5 standard deviations from population mean on one or more of the above tests. The FIRST segmentation tool (FSL 5.0, Oxford) was used to segment subcortical structures and the results visually assessed for errors. Volumes of the left and right thalami were recorded using this segmentation. Data was analysed in SPSS 19.0 (IBM) for Windows using univariate ANCOVA to compare groups with age as covariate. Results: 13 EOE (10 male, age 0-54 months, mean 25.9 months) and 25 controls (15 male, Age 2-65 months, mean 26.5 months) have been enrolled. Segmentation was successful in all except for one EOE. EOE had significantly smaller left (p=0.027) and right (p=0.048) thalamic volumes than controls after adjustment for age. EOE had a significantly higher rate of NI (7/13) than healthy controls (1/25, p < 0.001). EOE and NI had smaller left (5016mm³ vs 5650mm³) and right (4923mm³ vs 5516mm³) thalami compared to EOE without NI, but this was not statistically significant (p > 0.50 for both). Conclusions: To our knowledge, this is the first study showing that children with newly diagnosed early onset epilepsy show significant reductions in thalamic volume at diagnosis. They also have an increased incidence of NI. That both these are apparent at diagnosis is suggestive of pre-existing abnormality in a substantial proportion of EOE. Recruitment is ongoing to further examine the relationship between thalamic volume and NI in EOE.