Abstracts

Rationale: The cause for most cases of childhood epilepsy remains unknown. Recent studies suggest the incidence of childhood epilepsy is decreasing, which may be attributable to improved diagnoses and or decreased environmental exposures. Increasing awareness of early life exposures and the subsequent risk for disease raises the possibility that factors during pregnancy influence the risk for childhood epilepsy. From an ongoing study we report preliminary findings on antenatal risk factors for childhood epilepsy. Methods: Our study population was obtained from the Norwegian Mother and Child Cohort Study (MoBa) a study of 107,408 children and their parents recruited from pregnancy. In MoBa, there are detailed prospectively collected individual-level socio-demographic, dietary and clinical data obtained from sequential pre-natal and post-natal questionnaires up to age 7 years. In order to increase chances of identifying epilepsy cases and minimise missing data on potential risk factors, we linked MoBa data to routine prospectively collected national data. Record matching was carried out with the Norwegian Patient Registry (NPR) that contains information on attendances to all hospitals and outpatient clinics in Norway, and the Medical Birth Registry of Norway (MBRN) which collects information on pregnancies and births for all children born in Norway. Epilepsy cases were defined as having a record of epilepsy diagnosis in the NPR (ICD-10 code G40.X)/parental report of epilepsy in MoBa questionnaires. Estimates of composition of maternal diets in pregnancy were obtained from MoBa food frequency questionnaires that provide reliable estimates of intake compared to biological markers. Logistic regression models were fitted to investigate risk factors for epilepsy. Results: To date, 563 children with epilepsy have been identified (Prevalence 0.6%, 95%CI 0.5-0.6%). After adjusting for socioeconomic status, in multivariable analyses the independent risk factors were maternal smoking during pregnancy (AOR 1.5, 95%CI 1.1-2.0), premature birth (32-36/40-OR 1.6, 95%CI 1.2-2.2; 23-31/40-AOR 3.0, 95%CI 1.9-4.8), APGAR <=3 (AOR 2.4, 95%CI 1.3-4.5), maternal history of epilepsy (AOR 3.5, 95%CI 2.1-5.8), and paternal history of epilepsy (AOR 3.8, 95%CI 2.1-6.5). There was a trend towards decreasing risk when parents have higher levels of education, although it was lessened when adjustment was made for maternal smoking (Paternal education > 16 years-AOR 0.6, 95%CI 0.4-0.8). We found no increased risk associated with parental age, lower intake of omega-3 (mean = 2.86, range 0-24 g/day) or omega-6 (mean= 77, range 0-330 mg/day) fatty acids, and no protective effect from breastfeeding.Conclusions: Smoking in pregnancy increases the risk for childhood epilepsy. A lack of association of childhood epilepsy and maternal fatty acid intake during pregnancy may be attributable to a high overall intake in MoBa. The role of other early life factors, including Vitamin D intake and maternal stress, are being investigated.