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Major depressive disorder (MDD) is highly prevalent in individuals with anorexia nervosa (AN) and is a predictor of greater clinical severity. However, there is a limited amount of evidence supporting the use of psychotropic medications for its management. A systematic scoping review was conducted to assess the current literature on brain stimulation treatments for AN with comorbid MDD, with a specific focus on MDD treatment response and weight restoration. This review was conducted according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, and the PubMed, PsycInfo, and MEDLINE databases were searched until July 2022 using specific key words related to AN and brain stimulation treatments. A total of 373 citations were identified, and 49 treatment studies that met the inclusion criteria were included in the review. The initial evidence suggests that electroconvulsive therapy, repetitive transcranial magnetic stimulation, and deep-brain stimulation may be effective in managing comorbid MDD in AN. Emerging evidence suggests that transcranial direct current stimulation may have a positive effect on body mass index in individuals with severe to extreme AN. However, there is a need for the development of better measurement techniques for assessing the severity of depression in the context of AN. Controlled trials that are adequately designed to account for these limitations are highly warranted for deep-brain stimulation, electroconvulsive therapy, and repetitive transcranial magnetic stimulation and hold promise for providing clinically meaningful results.

ObjectiveTo examine the association between gestational age at birth and risk of clinically diagnosed intellectual disability (ID) week by week to provide a detailed description of ID risk across the entire range of gestational ages and by severity of ID.MethodsAll individuals born alive in Sweden 1974–2017 were prospectively followed up from birth until 2017 using national registers. The HRs for ID according to weekly gestational age and gestational age categories were determined using Cox models. Sibling analyses were conducted to adjust for familial confounding.ResultsThe study included 3 572 845 live births. During the follow-up, 26 596 ID cases were registered. The adjusted weekly estimates showed a gradual increase in risk of ID from week 40 to week 24 (adjusted HR37weeks=1.80 (1.74 to 1.87), aHR32weeks=3.93 (3.73 to 4.13), aHR28weeks=7.53 (6.95 to 8.16), aHR24weeks=21.58 (18.62 to 25.00)) and from week 41 onwards (aHR42weeks=1.26 (1.19 to 1.32)), with statistically significantly higher risks across the range of gestational age compared with infants born at week 40. The associations were consistent in mild, moderate and severe/profound ID but most prominent for severe/profound ID.ConclusionThe risk of ID increased weekly as the date of delivery moved away from 40 weeks, both preterm and post-term. The results remained robust after detailed adjustment for confounding, including familial confounding.

IMPORTANCE: There is growing concern about the long-term neurologic effects of prenatal exposure to maternal overweight and obesity. The causes of epilepsy are poorly understood and, in more than 60% of the patients, no definitive cause can be determined. OBJECTIVES: To investigate the association between early pregnancy body mass index (BMI) and the risk of childhood epilepsy and examine associations between obesity-related pregnancy and neonatal complications and risks of childhood epilepsy. DESIGN, SETTING, AND PARTICIPANTS: A population-based cohort study of 1 441 623 live single births at 22 or more completed gestational weeks in Sweden from January 1, 1997, to December 31, 2011, was conducted. The diagnosis of epilepsy as well as obesity-related pregnancy and neonatal complications were based on information from the Sweden Medical Birth Register and National Patient Register. Multivariate Cox proportional hazards regression models were used to estimate adjusted hazard ratios (HRs) and 95% CIs after adjusting for maternal age, country of origin, educational level, cohabitation with partner, height, smoking, maternal epilepsy, and year of delivery. Data analysis was conducted from June 1 to December 15, 2016. MAIN OUTCOMES AND MEASURES: Risk of childhood epilepsy. RESULTS: Of the 1 421 551 children born between January 1, 1997, and December 31, 2011, with covariate information available, 7592 (0.5%) were diagnosed with epilepsy through December 31, 2012. Of these 3530 (46.5%) were female. The overall incidence of epilepsy in children aged 28 days to 16 years was 6.79 per 10 000 child-years. Compared with offspring of normal-weight mothers (BMI 18.5 to <25.0), adjusted HRs of epilepsy by maternal BMI categories were as follows: 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). The rates of epilepsy were considerably increased for children with malformations of the nervous system (adjusted HR, 46.4; 95% CI, 42.2-51.0), hypoxic ischemic encephalopathy (adjusted HR, 23.6; 95% CI, 20.6-27.1), and neonatal convulsions (adjusted HR, 33.5; 95% CI, 30.1-37.4). The rates of epilepsy were doubled among children with neonatal hypoglycemia (adjusted HR, 2.10; 95% CI, 1.90-2.33) and respiratory distress syndrome (adjusted HR, 2.43; 2.21-2.66), and neonatal jaundice was associated with more than a 50% increased risk of epilepsy (adjusted HR, 1.47; 95% CI, 1.33-1.63). The elevated risk of epilepsy in children of overweight or obese mothers was not explained by obesity-related pregnancy or neonatal complications. CONCLUSIONS AND RELEVANCE: The rates of childhood epilepsy increased with maternal overweight or obesity in a dose-response manner. Given that overweight and obesity are modifiable, prevention of obesity may be an important public health strategy to reduce the incidence of childhood epilepsy.

(Abstracted from BMJ2018;360:k207)Population-based studies have found an increased risk of epilepsy and cerebral palsy (CP) associated with infants found to have a low Apgar score. Research has found a temporal association, as a low Apgar score at 5 minutes has been found to confer a higher risk than a correspondingly low Apgar score at 1 minute.

Idiopathic toe-walking (ITW) is a condition in which otherwise healthy children walk on their toes. The diagnosis is a diagnosis of exclusion. The aim of this study was to elucidate the occurrence of neuropsychiatric symptoms among 5- to 13-year-old children with ITW.

(Abstracted from JAMA2017;317(9):925–936)Prevalence of cerebral palsy (CP) rose between 1998 and 2006, and few preventable risk factors are known for this most common pediatric motor disability. Maternal obesity, a risk factor for neonatal complications such as preterm delivery and asphyxia-related neonatal morbidities, has been suggested to be associated with CP.

ObjectiveTo investigate associations between Apgar score at five and 10 minutes across the entire range of score values (from 0 to 10) and risks of childhood cerebral palsy or epilepsy, and to analyse the effect of changes in Apgar scores from five to 10 minutes after birth in infants born ≥37 completed weeks.Design, setting, and participantsPopulation based cohort study in Sweden, including 1 213 470 non-malformed live singleton infants, born at term between 1999 and 2012. Data on maternal and pregnancy characteristics and diagnoses of cerebral palsy and epilepsy were obtained by individual record linkages of nationwide Swedish registries.ExposuresApgar scores at five and 10 minutes.Main outcome measureCerebral palsy and epilepsy diagnosed up to 16 years of age. Adjusted hazard ratios were calculated, along with 95% confidence intervals.Results1221 (0.1%) children were diagnosed as having cerebral palsy and 3975 (0.3%) as having epilepsy. Compared with children with an Apgar score of 10 at five minutes, the adjusted hazard ratio for cerebral palsy increased steadily with decreasing Apgar score: from 1.9 (95% confidence interval 1.6 to 2.2) for an Apgar score of 9 to 277.7 (154.4 to 499.5) for an Apgar score of 0. Similar and even stronger associations were obtained between Apgar scores at 10 minutes and cerebral palsy. Associations between Apgar scores and epilepsy were less pronounced, but increased hazard ratios were noted in infants with a five minute Apgar score of 7 or less and a 10 minute Apgar score of 8 or less. Compared with infants with an Apgar of 9-10 at both five and 10 minutes, hazard ratios of cerebral palsy and epilepsy were higher among infants with a five minute Apgar score of 7-8 and a 10 minute Apgar score of 9-10.ConclusionRisks of cerebral palsy and epilepsy are inversely associated with five minute and 10 minute Apgar scores across the entire range of Apgar scores.