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Low serum levels of 25-hydroxyvitamin D [25(OH)D] and low sunlight exposure are known risk factors for the development of multiple sclerosis. Add-on vitamin D supplementation trials in established multiple sclerosis have been inconclusive. The effects of vitamin D supplementation to prevent multiple sclerosis is unknown. We aimed to test the hypothesis that oral vitamin D3 supplementation in high-risk clinically isolated syndrome (abnormal MRI, at least three T2 brain and/or spinal cord lesions), delays time to conversion to definite multiple sclerosis, that the therapeutic effect is dose-dependent, and that all doses are safe and well tolerated. We conducted a double-blind trial in Australia and New Zealand. Eligible participants were randomized 1:1:1:1 to placebo, 1000, 5000 or 10 000 international units (IU) of oral vitamin D3 daily within each study centre (n = 23) and followed for up to 48 weeks. Between 2013 and 2021, we enrolled 204 participants. Brain MRI scans were performed at baseline, 24 and 48 weeks. The main study outcome was conversion to clinically definite multiple sclerosis based on the 2010 McDonald criteria defined as either a clinical relapse or new brain MRI T2 lesion development. We included 199 cases in the intention-to-treat analysis based on assigned dose. Of these, 116 converted to multiple sclerosis by 48 weeks (58%). Compared to placebo, the hazard ratios (95% confidence interval) for conversion were 1000 IU 0.87 (0.50, 1.50); 5000 IU 1.37 (0.82, 2.29); and 10 000 IU 1.28 (0.76, 2.14). In an adjusted model including age, sex, latitude, study centre and baseline symptom number, clinically isolated syndrome onset site, presence of infratentorial lesions and use of steroids, the hazard ratios (versus placebo) were 1000 IU 0.80 (0.45, 1.44); 5000 IU 1.36 (0.78, 2.38); and 10 000 IU 1.07 (0.62, 1.85). Vitamin D3 supplementation was safe and well tolerated. We did not demonstrate reduction in multiple sclerosis disease activity by vitamin D3 supplementation after a high-risk clinically isolated syndrome. [ABSTRACT FROM AUTHOR]

Objective: Stability and developmental effects of electroencephalography (EEG) and event related potential (ERP) correlates of ADHD are understudied. This pilot study examined stability and developmental changes in ERP and EEG metrics of interest. Methods: Thirty-seven 7 to 11-year-old children with ADHD and 15 typically developing (TD) children completed EEG twice, 11 to 36 months apart. A series of mixed effects linear models were run to examine stability and developmental effects of EEG and ERP metrics. Results: Stability and developmental effects of EEG and ERP correlates of ADHD varied considerably across metrics. P3 amplitude was stable over time and showed diverging developmental trajectories across groups. Developmental differences were apparent in error related ERPs and resting aperiodic exponent. Theta-beta ratio was stable over time among all children. Conclusions: Developmental trajectories of EEG and ERP correlates of ADHD are candidate diagnostic markers. Replication with larger samples is needed. [ABSTRACT FROM AUTHOR]

Pioneering longitudinal studies of boys with hyperactivity by Satterfield et al. 1 indicated that one of the most deleterious outcomes associated with attention-deficit/hyperactivity disorder (ADHD) is later antisocial behaviors. This risk grows when ADHD is accompanied by severe behavior problems.2 Though most children with ADHD will not go on to engage in criminal behavior, dimensional measures of externalizing behavior problems as well as categorical diagnoses of oppositional defiant disorder and conduct disorder have strong associations with ADHD. Moreover, cross-sectional studies of incarcerated adults indicate that 20% to 30% meet diagnostic criteria for ADHD.3 These associations between childhood ADHD, oppositional defiant disorder, and conduct disorder and later criminal behavior beg the question of whether treatment of ADHD can reduce the severity of, or in some cases prevent, criminal behavior. [ABSTRACT FROM AUTHOR]