BACKGROUND: Nodding syndrome is an unexplained illness characterised by head-bobbing spells. The clinical and epidemiological features are incompletely described, and the explanation for the nodding and the underlying cause of nodding syndrome are unknown. We aimed to describe the clinical and neurological diagnostic features of this illness. METHODS: In December, 2009, we did a multifaceted investigation to assess epidemiological and clinical illness features in 13 parishes in Kitgum District, Uganda. We defined a case as a previously healthy child aged 5-15 years with reported nodding and at least one other neurological deficit. Children from a systematic sample of a case-control investigation were enrolled in a clinical case series which included history, physical assessment, and neurological examinations; a subset had electroencephalography (EEG), electromyography, brain MRI, CSF analysis, or a combination of these analyses. We reassessed the available children 8 months later. FINDINGS: We enrolled 23 children (median age 12 years, range 7-15 years) in the case-series investigation, all of whom reported at least daily head nodding. 14 children had reported seizures. Seven (30%) children had gross cognitive impairment, and children with nodding did worse on cognitive tasks than did age-matched controls, with significantly lower scores on tests of short-term recall and attention, semantic fluency and fund of knowledge, and motor praxis. We obtained CSF samples from 16 children, all of which had normal glucose and protein concentrations. EEG of 12 children with nodding syndrome showed disorganised, slow background (n=10), and interictal generalised 2.5-3.0 Hz spike and slow waves (n=10). Two children had nodding episodes during EEG, which showed generalised electrodecrement and paraspinal electromyography dropout consistent with atonic seizures. MRI in four of five children showed generalised cerebral and cerebellar atrophy. Reassessment of 12 children found that six worsened in their clinical condition between the first evaluation and the follow-up evaluation interval, as indicated by more frequent head nodding or seizure episodes, and none had cessation or decrease in frequency of these episodes. INTERPRETATION: Nodding syndrome is an epidemic epilepsy associated with encephalopathy, with head nodding caused by atonic seizures. The natural history, cause, and management of the disorder remain to be determined. FUNDING: Division of Global Disease Detection and Emergency Response, US Centers for Disease Control and Prevention.

The National Center on Birth Defects and Developmental Disabilities (NCBDDD) was established in April 2001 as a result of The Children’s Health Act of 2000.1 The supporters of the center’s creation wanted to raise the visibility of child health and disability at the CDC. From its inception, the NCBDDD included the established programs in birth defects, genetic disorders, developmental disabilities and disabilities and health, with a more than 30-year history in surveillance, research, and public health practice, including the training of public health professionals in these respective fields. | In 2003, the NCBDDD expanded with the addition of the blood disorders program, which initially had been established in response to the discovery that HIV, a bloodborne infection, highly affected people with hemophilia who required treatments using blood products. This led to the development of a comprehensive program to ensure optimal care for this and other populations affected by nonmalignant blood disorders.2 The current paper examines the health impact of the center’s work that was highlighted in a year-long reflection,“10 Years of Service”3;and provides a framework for how the NCBDDD will move forward with a renewed emphasis on enhancing public health and healthcare-system capacity to have greater health impact for the populations served.

The magnitude and causes of death among a cohort of children with epilepsy were determined. A follow-up study with a population-based cohort of 10-year-old children in the metropolitan Atlanta area with epilepsy was conducted. The National Death Index and linkage to State of Georgia death certificates were used to identify deaths. The authors estimated the expected numbers of deaths by applying mortality rates adjusted by age, race, and sex for the entire state of Georgia to the population for the follow-up period. Among the 688 children who were in the final epilepsy cohort, 64 deaths occurred; 20.6 deaths were expected (mortality ratio adjusted for age, race, and sex = 3.11). The mortality ratios for children with Lennox-Gastaut syndrome and infantile spasms were 13.92 and 11.91, respectively. Children and adolescents with epilepsy, especially those with Lennox-Gastaut syndrome or infantile spasms, have an increased risk of death.

Childhood obesity, defined as a body mass index (BMI; weight [kg]/height [m2]) ≥95th percentile for children or adolescents of the same age and sex, now affects 16% of 2- to 19-year-olds in the United States. An additional 15% are overweight, defined as a BMI between the 85th and 95th percentiles.1 Recent estimates suggest that 70% of obese children have at least one additional cardiovascular disease risk factor, like elevated blood pressure, hyperlipidemia, or hyperinsulinemia, and almost 40% have 2 or more.2 The obesity epidemic among children is now a national crisis to which we must all respond. | In this issue of Neurology®, researchers from Cincinnati Children’s Hospital raise the possibility that obesity is associated with new onset childhood epilepsy.3 In the selection of their control populations, the authors have tried to demonstrate that the increased prevalence of obesity among children with new onset seizures is unique to these patients and not a consequence of a sampling bias. Their observation that African Americans and Hispanics, among whom the prevalence of obesity is increased, were underrepresented in the new onset seizure group compared to a local control helps allay this concern about sampling.

OBJECTIVES: The reported increasing prevalence of autism spectrum disorder (ASD) and attendant health and family impact make monitoring of ASD prevalence a public health priority. METHODS: The prevalence of parent-reported diagnosis of ASD among US children aged 3 to 17 years was estimated from the 2007 National Survey of Children's Health (sample size: 78037). A child was considered to have ASD if a parent/guardian reported that a doctor or other health care provider had ever said that the child had ASD and that the child currently had the condition. The point-prevalence for ASD was calculated for those children meeting both criteria. We examined sociodemographic factors associated with current ASD and with a past (but not current) ASD diagnosis. The health care experiences for children in both ASD groups were explored. RESULTS: The weighted current ASD point-prevalence was 110 per 10,000. We estimate that 673,000 US children have ASD. Odds of having ASD were 4 times as large for boys than girls. Non-Hispanic (NH) black and multiracial children had lower odds of ASD than NH white children. Nearly 40% of those ever diagnosed with ASD did not currently have the condition; NH black children were more likely than NH white children to not have current ASD. Children in both ASD groups were less likely than children without ASD to receive care within a medical home. CONCLUSIONS: The observed point-prevalence is higher than previous US estimates. More inclusive survey questions, increased population awareness, and improved screening and identification by providers may partly explain this finding.