A study looks at the long-term impact that preeclampsia can have on mothers' brains. Plus: A study examines the impact of maternal obesity on a child's risk of childhood epilepsy.
A small case-control study by European researchers sheds new light on the long-term cerebral impact that preeclampsia has on mothers. Published in Neurology, the data-from magnetic resonance imaging (MRI) of the brain-suggest that changes to cerebral white and gray matter do not end with delivery.
Eighty-three women who had a preeclamptic or normotensive pregnancies (controls) in the past 5 to 15 years were included in the analysis. The women with preeclampsia histories were aged 42.8±5.1 years versus 40.6±5.5 for those with normotensive pregnancies.
All of the participants underwent MRI, and microstructural integrity of their brains was measured by assessing white matter structure using voxel-based segmentation of fluid-attenuation inversion recovery sequences. Voxel-based analysis was also performed of gray matter volumes to adjust for skull size.
Cortical gray matter volume was lower in the women with preeclampsia than in the controls (523.2 ±30.1 vs 544.4 ±44.7 mL, P<0.05) and both groups had white matter lesions. The changes, however, were more extensive in the women with preeclampsia, who had increased temporal lobe white matter disease (lesion volume: 23.2±24.9 vs 10.9±15.0 µL, P<0.05) and altered microstructural integrity (radial diffusivity: 538±19 vs 526±18 x 10-6 mm2/s, P<0.01), which also extended to the occipital and parietal lobes.
In bivariate regression analysis, temporal white matter changes were significantly associated with blood pressure and serum concentration of high-density lipoprotein. However, the researchers found that in women with a history of preeclampsia, the degree of temporal white matter change was independent of their current cardiovascular risk profile (P<0.05) and increased with time from the index pregnancy (P<0.05), consistent with a persistent susceptibility after delivery.
In women with preeclampsia, the authors said, “Clinical management at the time of pregnancy and ongoing risk factor modification after delivery are both likely to be important in reducing cerebrovascular disease later in life.” They suggested more aggressive cardiovascular prevention strategies after preeclampsia to reduce cumulative and ongoing damage and more careful attention to neurologic symptoms because the differences in cortical volumes and white matter changes may be harbingers of increased risk of cognitive complaints including disturbances of memory and concentration.
Does obesity increase risk of childhood epilepsy?
A new Swedish study in JAMA Neurology looks at the impact of overweight or obesity in early pregnancy on the risk of childhood epilepsy.
The researchers looked at 1,441,623 live single births that occurred at 22 or more completed gestational weeks from January 1997 to December 2011. The Sweden Medical Birth Register and National Patient Register provided the information on epilepsy diagnoses and obesity-related pregnancy and neonatal complications. Following adjustment for maternal age, country of origin, education level, cohabitation with partner, height, smoking, maternal epilepsy, and year of delivery, multivariate Cox proportional hazard regression models were used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs).
Of the 1,421,551 children with covariate information, 7592 (0.5%) were diagnosed with epilepsy. Overall incidence of epilepsy in children aged 28 days to 16 years was 6.79 per 10,000 child-years. When compared to offspring of normal-weight mothers (body mass index [BMI] 18.5 to < 25.0), adjusted HRs of epilepsy by maternal BMI categories were overweight (BMI 25.0 to <30.0), 1.11 (95% CI, 1.04-1.17); obesity grade I (BMI 30.0 to <35.0), 1.20 (95% CI, 1.10-1.31); obesity grade II (BMI 35.0 to <40.0), 1.30 (95% CI, 1.12-1.50); and obesity grade III (BMI ≥ 40.0), 1.82 (95% CI, 1.46-2.26).
Rates of epilepsy were significantly increased in children with malformation of the nervous system (adjusted HR, 46.4; 95% CI, 42.2-51.0), neonatal convulsions (adjusted HR, 33.5; 95% CI, 30.1-37.4), and with hypoxic ischemic encephalopathy (adjusted HR, 23.6; 95% CI, 20.6-27.1). Neonatal jaundice was associated with a more than 50% increased risk of epilepsy (adjusted HR, 1.47; 95% CI, 1.33-1.63). Among children with respiratory distress syndrome (adjusted HR, 2.43; 2.21-2.66) and neonatal hypoglycemia (adjusted HR, 2.10; 95% CI, 1.90-2.33), the rates of epilepsy were doubled. Obesity-related pregnancy or neonatal complications could not explain the elevated risk of epilepsy in the children of overweight or obese mothers.
The investigators concluded that childhood epilepsy increases when mothers are overweight or obese, in a dose-response manner. They argued that preventing or reducing obesity could be an important way to reduce the incidence of childhood epilepsy.