Stroke in children is rarely diagnosed in the time frame of 3 to 6 hours. Given the causes and outcome of stroke in children, this age group might benefit from thrombolysis and from neuroprotective therapy, yet the long delay in diagnosis in this age group excludes most cases from being considered for such treatments. This situation should encourage attempts to increase public and professional awareness of stroke in children and of the potential value of early diagnosis and treatment, preferably by broadening current educational efforts to all age groups.

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objective: To assess the association between obesity and primary headaches in children and adolescents. Methods and Procedures: In a prospective study, the short-questionnaire version based on existing International Headache Society diagnostic criteria was administered. Two hundred and seventy-three children and adolescents (61% females) aged 9-17 years were assessed. One hundred and sixteen (42.5%) subjects were of normal weight, 45 (16.5%) were at risk for overweight (BMI >85th and <95th percentile for age and gender) and 112 (41%) were overweight (BMI ≥95th percentile). The outcome measures were prevalence of headaches, type of headaches, association between headaches and elevated blood pressure in overweight subjects. Results: Headache was reported in 39 (14.3%) subjects, with a similar rate in females (14.5%) and males (14%). Among 39 subjects with headaches, 20 (17.9%) were overweight, 7 (15.6%) were at risk for overweight and 12 (10.3%) were normal-weight children. Among females, 7.7% of normal-weight group suffered from headaches, compared with 14.8% of the at risk for overweight group and 20.3% of the overweight group (P for trend 0.04). Among males, the occurrence of headaches was similar in all three weight groups (P = 0.96). The occurrence of headaches increased from 10.6% among children aged 9-11 years to 21.8% in the 15-18 years age group (P < 0.05). In multivariate analysis, a significant independent risk for headaches was present in overweight females (odds ratio (OR) = 3.93, 95% confidence interval (CI) 1.28-12.1) and in adolescents aged 15-18 years (OR = 2.62, 95% CI 1.07-6.45). Elevated blood pressure was not independently associated with headaches. Of the 15 children with migraine, 12 were either at risk for overweight or overweight. Discussion: Overweight females had an almost fourfold excess risk of headaches when compared with normal-weight girls.

This study assessed metabolic functioning of regional brain areas to address whether there is a neurometabolic profile reflecting the underlying neuropathology in individuals with autism spectrum disorders, and if varied profiles correlate with the clinical subtypes. Thirteen children (7-16 years) with autism spectrum disorders and 8 typically developing children were compared on (1)H-magnetic resonance spectroscopy data collected from hippocampus-amygdala and cerebellar regions. The autism spectrum disorder group had significantly lower N-acetyl-aspartate/creatine ratios bilaterally in the hippocampus-amygdala but not cerebellum, whereas myo-inositol/creatine was significantly increased in all measured regions. Choline/creatine was also significantly elevated in the left hippocampus-amygdala and cerebellar regions of children with autism spectrum disorder. Comparisons within the autism spectrum disorder group when clinically subdivided by history of speech delay revealed significant metabolic ratio differences. Magnetic resonance spectroscopy can provide important information regarding abnormal brain metabolism and clinical classification in autism spectrum disorders.

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This study examines major comorbidities in children with severe cerebral palsy and the feasibility of psychological tests for measuring abilities in a more impaired population. Eighty psychological evaluations of children with cerebral palsy aged 1.8 to 15.4 years (mean = 5.6) were analyzed. Major comorbid disorders were correlated with severity of motor disability. More than half of the cohort were diagnosed with severe cerebral palsy according to the Gross Motor Function Classification System. Multiple subtests were combined in order to assess the intellectual level. Normal intelligence was found in 22.5%, and 41.3% had moderate or severe intellectual impairment. Epilepsy occurred in 32.5% and attention-deficit hyperactivity disorder (ADHD) in 22.5%. Intellectual disability correlated with motor ability and with epilepsy. In a logistic regression model, epilepsy and motor ability score predicted 29.9% of IQ score variance. Intellectual impairment and epilepsy are common comorbidities. Subtests from different scales should be applied and interpreted with caution.

The substantial phenotypic heterogeneity in autism limits our understanding of its genetic etiology. To address this gap, here we investigated genetic differences between autistic individuals (nmax = 12,893) based on core and associated features of autism, co-occurring developmental disabilities and sex. We conducted a comprehensive factor analysis of core autism features in autistic individuals and identified six factors. Common genetic variants were associated with the core factors, but de novo variants were not. We found that higher autism polygenic scores (PGS) were associated with lower likelihood of co-occurring developmental disabilities in autistic individuals. Furthermore, in autistic individuals without co-occurring intellectual disability (ID), autism PGS are overinherited by autistic females compared to males. Finally, we observed higher SNP heritability for autistic males and for autistic individuals without ID. Deeper phenotypic characterization will be critical in determining how the complex underlying genetics shape cognition, behavior and co-occurring conditions in autism.

Numerous studies have attempted to identify early physiological abnormalities in infants and toddlers who later develop autism spectrum disorder (ASD). One potential measure of early neurophysiology is the auditory brainstem response (ABR), which has been reported to exhibit prolonged latencies in children with ASD. We examined whether prolonged ABR latencies appear in infancy, before the onset of ASD symptoms, and irrespective of hearing thresholds. To determine how early in development these differences appear, we retrospectively examined clinical ABR recordings of infants who were later diagnosed with ASD. Of the 118 children in the participant pool, 48 were excluded due to elevated ABR thresholds, genetic aberrations, or old testing age, leaving a sample of 70 children: 30 of which were tested at 0-3 months, and 40 were tested at toddlerhood (1.5-3.5 years). In the infant group, the ABR wave-V was significantly prolonged in those who later developed ASD as compared with case-matched controls (n 5 30). Classification of infants who later developed ASD and case-matched controls using this measure enabled accurate identification of ASD infants with 80% specificity and 70% sensitivity. In the group of toddlers with ASD, absolute and interpeak latencies were prolonged compared to clinical norms. Findings indicate that ABR latencies are significantly prolonged in infants who are later diagnosed with ASD irrespective of their hearing thresholds; suggesting that abnormal responses might be detected soon after birth. Further research is needed to determine if ABR might be a valid marker for ASD risk. Autism Res 2016, 9: 689-695.