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The majority of patients with epilepsy maintain seizure control during pregnancy. The apparently higher risk of seizures among women treated with oxcarbazepine and the more frequent increases in drug load in the oxcarbazepine and lamotrigine cohorts prompts further studies on relationships with pharmacokinetic changes. Risks associated with status epilepticus appear to be lower than previously reported.

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Abstracts(4.2±1.4 vs 4.2±1.3). Third, the receptive language function was significantly improved after taking lamotrigine in PPVT (8y 4m±2y 4m vs 8y 10m±2y 4m, P <0.01). However, there were no significant changes in percentages of precise articulation and error pattern of consonants after taking lamotrigine (98.3% to 99.1%, P >0.05). Conclusions Our results suggest that lamotrigine can be used without significant negative effects on language function. Moreover, language functions, especially receptive language, were improved after lamotrigine initiation. Background Most pregnant women with chronic active epilepsy need to use antiepileptic drugs (AEDs) during pregnancy to prevent epileptic seizures that may threaten maternal and fetal well-being. Valproic acid (VPA) and carbamazepine (CBZ) have been associated with an increased risk of neural tube defects (NTDs) in the exposed fetus. Aim To investigate the spectrum of neural tube defects and associated central nervous system (CNS) and non-CNS malformations after prenatal exposure to CBZ and/or VPA. Methods NTDs in pregnancies in which CBZ and/or VPA were used during the first trimester were collected from 1970-2012 in the Netherlands. Type and location of the NTDs, associated CNS and non-CNS major malformations and relevant patient characteristics were analysed. Results 87 pregnancies were included. NTDs after exposure to CBZ or VPA were mostly caudally located, whereas a combination of CBZ and VPA was associated with a location shift of the NTD to the rostral side (Figure 1). There were no differences between CBZ and VPA in the percentage of associated CNS malformations and non-CNS malformations circa 75% and 45%. SPECTRUM OF NEURAL TUBE DEFECTS AFTER PRENATAL ANTIEPILEPTIC DRUG EXPOSURE: EXTENSIVE CASE SERIES