The association between BsmI polymorphism and risk factors for atherosclerosis in patients with epilepsy taking valproate

AbstractPurposeTo evaluate the association between the BsmI polymorphism and vascular risk factors or metabolic syndrome in patients with epilepsy treated with valproate.MethodsWe performed a cross-sectional study to determine glucose homeostasis, lipid profile, and evidence of metabolic syndrome, as well as the BsmI polymorphism in seizure free adults with epilepsy.ResultsWe recruited 75 patients with epilepsy to the current study. The frequency of the BsmI polymorphism was 22.7%. We found that patients with BsmI polymorphism had significantly higher total levels of triglycerides, total cholesterol, HDL-C and LDL-C. There were no differences in terms of fasting blood glucose level and fasting insulin levels between patients with the BsmI polymorphism and those with the wild type vitamin D receptor (VDR) gene. Insulin resistance was identified in 6 of 17 patients with the BsmI polymorphism, and 18 of 58 patients with the wild type VDR gene. We calculated the homeostasis model assessment (HOMA) index and found no difference in HOMA levels between the groups. Systolic blood pressure was higher in patients with the BsmI polymorphism. There was a higher prevalence of metabolic syndrome in patients with the BsmI polymorphism than in patients with the wild type gene. The prevalence of metabolic syndrome in BsmI polymorphism carriers was 64.7% compared with 41.4% in patients with the wild type VDR gene.ConclusionYoung patients with epilepsy taking valproate who carry the BsmI polymorphism are at an increased risk of having vascular risk factors

Does burst-suppression achieve seizure control in refractory status epilepticus?

Abstract Background The general principles in the administration of anesthetic drugs entail not only the suppression of seizure activity but also the achievement of electroencephalography burst suppression (BS). However, previous studies have reported conflicting results, possibly owing to the inclusion of various anesthetic agents, not all patients undergoing continuous electroencephalography (cEEG), and the inclusion of anoxic encephalopathy. This study aimed to analyze the effects of midazolam-induced BS on the occurrence outcomes in refractory status epilepticus patients. Methods Based on a prospective database of patients who had been diagnosed with status epilepticus via cEEG, multivariate Poisson regression modules were used to estimate the effect of midazolam-induced BS on breakthrough seizure, withdrawal seizure, intra-hospital complications, functional outcome at 3 months, and mortality. Modules were based on a pre-compiled directed acyclic graph (DAG). Results We included 51 non-anoxic encephalopathy, refractory status epilepticus patients. Burst suppression was achieved in 26 patients (51%); 25 patients (49%) had non-burst suppression on their cEEG. Breakthrough seizure was less often seen in the burst suppression group than in the non-burst suppression group. The incidence risk ratio [IRR] was 0.30 (95% confidence interval = 0.13–0.74). There was weak evidence of an association between BS and increased withdrawal seizure, but no association between BS and intra-hospital complications, mortality or functional outcomes was observed. Conclusion This study provides evidence that BS is safe and associated with less breakthrough seizures. Additionally, it was not associated with an increased rate of intra-hospital complications or long-term outcomes