Background The postpartum state is associated with a substantially increased risk of thrombosis. It is uncertain to what extent this heightened risk persists beyond the conventionally defined 6-week postpartum period. Methods Using claims data on all discharges from nonfederal emergency departments and acute care hospitals in California, we identified women who were hospitalized for labor and delivery between January 1, 2005, and June 30, 2010. We used validated diagnosis codes to identify a composite primary outcome of ischemic stroke, acute myocardial infarction, or venous thromboembolism. We then used conditional logistic regression to assess each patient's likelihood of a first thrombotic event during sequential 6-week periods after delivery, as compared with the corresponding 6-week period 1 year later. Results Among the 1,687,930 women with a first recorded delivery, 1015 had a thrombotic event (248 cases of stroke, 47 cases of myocardial infarction, and 720 cases of venous thromboembolism) in the period of 1 year plus up to 24 weeks after delivery. The risk of primary thrombotic events was markedly higher within 6 weeks after delivery than in the same period 1 year later, with 411 events versus 38 events, for an absolute risk difference of 22.1 events (95% confidence interval [CI], 19.6 to 24.6) per 100,000 deliveries and an odds ratio of 10.8 (95% CI, 7.8 to 15.1). There was also a modest but significant increase in risk during the period of 7 to 12 weeks after delivery as compared with the same period 1 year later, with 95 versus 44 events, for an absolute risk difference of 3.0 events (95% CI, 1.6 to 4.5) per 100,000 deliveries and an odds ratio of 2.2 (95% CI, 1.5 to 3.1). Risks of thrombotic events were not significantly increased beyond the first 12 weeks after delivery. Conclusions Among patients in our study, an elevated risk of thrombosis persisted until at least 12 weeks after delivery. However, the absolute increase in risk beyond 6 weeks after delivery was low. (Funded by the National Institute of Neurological Disorders and Stroke.)

Background and Purpose The risk of stroke and other postpartum cerebrovascular disease (CVD) occurring after hospital discharge for labor and delivery is uncertain. Methods We performed a retrospective cohort study using administrative databases to identify all pregnant women who were hospitalized for labor and delivery at nonfederal, acute care hospitals in California from 2005 through 2011 and who were discharged without an International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis of CVD. The primary outcome was an acute CVD composite defined as any ischemic stroke, intracranial hemorrhage, cerebral venous sinus thrombosis, pituitary apoplexy, carotid/vertebral artery dissection, hypertensive encephalopathy, or other acute CVD occurring after hospital discharge and prior to 6 weeks after labor and delivery. Descriptive statistics were used to estimate the incidence of postdischarge CVD. Multivariate logistic regression was used to evaluate the association between selected baseline factors and postdischarge CVD. Results The rate of any postdischarge acute CVD was 14.8 per 100,000 patients (95% CI 13.2-16.5). Risk factors for any acute CVD were eclampsia (OR 10.1, 95% CI 3.09-32.8), chronic kidney disease (OR 5.4, 95% CI 2.5-11.8), black race (OR 2.5, 95% CI 1.9-3.3), preeclampsia (OR 2.1, 95% CI 1.6-2.8), pregnancy-related hematologic disorders (OR 1.8, 95% CI 1.3-2.5), and age (OR 1.5 per decade, 95% CI 1.3-1.8). Conclusion The incidence of postpartum acute CVD after hospital discharge for labor and delivery is similar to rates reported for all postpartum events in prior publications, suggesting that a substantial proportion of postpartum CVD occurs after discharge.

IntroductionEpilepsy mortality rates are rising. It is unknown whether rates are rising due to an increase in epilepsy prevalence, changes in epilepsy causes of death, increase in the lethality or epilepsy or failures of treatment. To address these questions, we compare epilepsy mortality rates in the USA with all-cause and all-neurological mortality for the years 1999 to 2017.ObjectivesTo determine changes in US epilepsy mortality rates versus all-cause mortality, and to evaluate changes in the leading causes of death in people with epilepsy.DesignRetrospective population-based multiple cause-of-death study.Primary outcomeChange in age-adjusted epilepsy mortality rates compared with mortality rates for all-cause and all-neurological mortality.Secondary outcomeChanges in the leading causes of death in epilepsy.ResultsFrom 1999 to 2017, epilepsy mortality rates in the USA increased 98.8%, from 5.83 per million in 1999 to 11.59 per million (95% CI 88.2%–110.0%), while all-cause mortality declined 16.4% from 8756.34 per million to 7319.17 per million (95% CI 16.3% to 16.6%). For the same period, all-neurological mortality increased 80.8% from 309.21 to 558.97 per million (95% CI 79.4%–82.1%). The proportion of people with epilepsy who died due to neoplasms, vascular dementia and Alzheimer’s increased by 52.3%, 210.1% and 216.8%, respectively. During the same period, the proportion who died due to epilepsy declined 27.1%, while ischaemic heart disease as a cause of death fell 42.6% (p<0.001).ConclusionsEpilepsy mortality rates in the USA increased significantly from 1999 to 2017. Likely causes include increases in all-neurological mortality, increased epilepsy prevalence and changes in the underlying causes of death in epilepsy, led by increases in vascular dementia and Alzheimer’s. An important finding is that ischaemic heart disease and epilepsy itself are declining as underlying causes of death in people with epilepsy.

Serial MRS imaging showed significant improvement in lactate peaks and NAA/Cho ratios that corresponded with clinical improvement after L-arginine therapy. Given this correlation between radiologic and clinical improvement, MRS may be a useful biomarker assessing response to treatment in MELAS.