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This study assessed the effects of modest sleep restriction and extension on children's neurobehavioral functioning (NBF). The sleep of 77 children (age: M = 10.6 years; range = 9.1-12.2 years) was monitored for 5 nights with activity monitors. These children (39 boys and 38 girls) were all attending regular 4th- and 6th-grade classes. Their NBF was assessed using computerized tests on the 2nd day of their normal sleep schedule. On the 3rd evening, the children were asked to extend or restrict their sleep by an hour on the following 3 nights. Their NBF was reassessed on the 6th day following the experimental sleep manipulation. Sleep restriction led to improved sleep quality and to reduced reported alertness. The sleep manipulation led to significant differential effects on NBF measures. These effects may have significant developmental and clinical implications.

The aim of this study was to examine the associations between sleep and neurobehavioral functioning (NBF) in school-age children. These variables were assessed for 135 unreferred, healthy school children (69 boys and 66 girls), from second-, fourth-, and sixth-grade classes. Objective assessment methods were used on the participants in their regular home settings. Sleep was monitored using actigraphy for 5 consecutive nights; and NBF was assessed using a computerized neurobehavioral evaluation system, administered twice, at different times of the day. Significant correlations between sleep-quality measures and NBF measures were found, particularly in the younger age group. Children with fragmented sleep were characterized by lower performance on NBF measures, particularly those associated with more complex tasks such as a continuous performance test and a symbol-digit substitution test. These children also had higher rates of behavior problems as reported by their parents on the Child Behavior Checklist. These results highlight the association between sleep quality, NBF, and behavior regulation in child development; and raise important questions about the origins of these associations and their developmental and clinical significance.

Autism symptoms, including impairments in language development, social interactions, and motor skills, have been difficult to model in rodents. Since children exposed in utero to sodium valproate (VPA) demonstrate behavioral and neuroanatomical abnormalities similar to those seen in autism, the neurodevelopmental effects of this antiepileptic agent were examined in mice following its pre-or postnatal administration. Exposed pups were evaluated in a battery of neurodevelopmental procedures designed to assess VPA-induced retardation (wherein a behavior fails to mature on schedule), regression (wherein a behavior does mature on time but then deteriorates), or intrusions (wherein normal behaviors are overshadowed by stereotypic or self-injurious behaviors). The resulting observations were interpreted in the context of this new strategy to model autism.

Childhood adversity is associated with altered reward processing, but little is known about whether this varies across distinct types of adversity. In a sample of 94 children (6–19 years), we investigated whether experiences of material deprivation, emotional deprivation, and trauma have differential associations with reward‐related behavior and white matter microstructure in tracts involved in reward processing. Material deprivation (food insecurity), but not emotional deprivation or trauma, was associated with poor reward performance. Adversity‐related influences on the integrity of white matter microstructure in frontostriatal tracts varied across childhood adversity types, and reductions in frontostriatal white matter integrity mediated the association of food insecurity with depressive symptoms. These findings document distinct behavioral and neurodevelopmental consequences of specific forms of adversity that have implications for psychopathology risk.

Purpose: We advanced a multifactorial, dynamic account of the complex, nonlinear interactions of motor, linguistic, and emotional factors contributing to the development of stuttering. Our purpose here is to update our account as the multifactorial dynamic pathways theory. Method: We review evidence related to how stuttering develops, including genetic/epigenetic factors; motor, linguistic, and emotional features; and advances in neuroimaging studies. We update evidence for our earlier claim: Although stuttering ultimately reflects impairment in speech sensorimotor processes, its course over the life span is strongly conditioned by linguistic and emotional factors. Results: Our current account places primary emphasis on the dynamic developmental context in which stuttering emerges and follows its course during the preschool years. Rapid changes in many neurobehavioral systems are ongoing, and critical interactions among these systems likely play a major role in determining persistence of or recovery from stuttering. Conclusion: Stuttering, or childhood onset fluency disorder (\"Diagnostic and Statistical Manual of Mental Disorders,\" 5th edition; American Psychiatric Association [APA], 2013), is a neurodevelopmental disorder that begins when neural networks supporting speech, language, and emotional functions are rapidly developing. The multifactorial dynamic pathways theory motivates experimental and clinical work to determine the specific factors that contribute to each child's pathway to the diagnosis of stuttering and those most likely to promote recovery.

Increased understanding of early neurobehavioural development is needed to prevent, identify, and treat childhood psychopathology most effectively at the earliest possible stage. Prospective birth cohorts can elucidate the association of genes, environment, and their interactions with neurobehavioural development. We conducted a systematic review of the birth cohort literature. On the basis of internet searches and 6,248 peer-reviewed references, 105 longitudinal epidemiological studies were identified. Twenty studies met inclusion criteria (prospectively recruited, population-based cohort studies, including at least one assessment before the end of the perinatal period and at least one assessment of behaviour, temperament/personality, neuropsychiatric or psychiatric status before 19 years of age), and their methodologies were reviewed in full. Whilst the birth cohort studies did examine some aspects of behaviour and neurodevelopment, observations in the early months and years were rare. Furthermore, aspects of sampling method, sample size, data collection, design, and breadth and depth of measurement in some studies made research questions about neurodevelopment difficult to answer. Existing birth cohort studies have yielded limited information on how pre- and perinatal factors and early neurodevelopment relate to child psychopathology. Further epidemiological research is required with a specific focus on early neurodevelopment. Studies are needed which include the measures of early childhood psychopathology and involve long-term follow-up.

This study investigated personality and neurobehavioral differences between 16 children with Asperger's Disorder, 15 children with High-Functioning Autism (HFA), and 31 controls, all ranging in age from 5-17 years, M age = 10.7 years, SD = 3.0. Parents rated their children's behaviors on a 44-item autistic symptoms survey and on the 200-item Coolidge Personality and Neuropsychological Inventory (Coolidge, Thede, Stewart, & Segal (2002a). The Coolidge Personality and Neuropsychological Inventory for Children (CPNI): Preliminary psychometric characteristics. \"Behavior Modification,\" 26, 550-566). The results indicated that the two clinical samples were significantly elevated on the Executive Function Deficits scale and Attention-Deficit/Hyperactivity Disorder (ADHD) scale compared to controls. There were more similarities than differences between the two clinical samples on the personality scales, although the Asperger's group scored significantly on the two scales with anxiety components.

Elucidating the mechanisms by which infant birth conditions shape development across lengthy periods is critical for understanding typical and pathological development and for targeted early interventions. This study examined how newborns' regulatory capacities impact 10-year outcomes via the bidirectional influences of child emotion regulation (ER) and reciprocal parenting across early development. Guided by dynamic systems theory, 125 infants were tested at seven time points: birth, 3, 6, 12, and 24 months and 5 and 10 years. Initial regulatory conditions were measured by respiratory sinus arrhythmia (RSA; vagal tone) and neurobehavioral regulation (Brazelton, 1973) at birth. At each assessment between 3 months and 5 years, infant ER was microcoded from age-appropriate paradigms and mother–child reciprocity observed during social interactions. Four regulation-related outcomes were measured at 10 years: child RSA, empathy measured by mother–child conflict discussion and a lab paradigm, accident proneness, and behavior problems. An autoregressive cross-lagged structural model indicated that infant birth conditions impacted 10-year outcomes via three mechanisms. First, child ER and reciprocal parenting were individually stable across development and were each predicted by regulatory birth conditions, describing gradual maturation of ER and reciprocity over time. Second, better ER skills at one time point were related to greater reciprocity at the next time point and vice versa, and these cross-time effects defined a field of individual-context mutual influences that mediated the links between neonatal RSA and 10-year outcomes. Third, direct associations emerged between neonatal regulation and outcome, suggesting that birth conditions may establish a neurobiological milieu that promotes a more mature and resilient system. These mechanisms describe distinct “attractor” states that constrain the system's future options, emphasize the importance of defining behavior-based phenotypes of heterotypic continuity, and suggest that infants may shape their development by initiating unique cascades of individual-context bidirectional effects.

Chronic sleep deprivation has been demonstrated to diminish cognitive performance, alter mood states, and concomitantly dysregulate inflammation and stress hormones. At present, however, there is little understanding of how an acute sleep deprivation may collectively affect these factors and alter functioning. The present study aimed to determine the extent to which 24-hours of sleep deprivation influences inflammatory cytokines, stress hormones, cognitive processing across domains, and emotion states. To that end, 23 participants (mean age = 20.78 years, SD = 2.87) filled out clinical health questionnaires measured by the Pittsburgh Sleep Quality Index, Morningness Eveningness Questionnaire, and Center for Epidemiological Studies Depression Scale. Actigraph was worn for 7 days across testing to record sleep duration. At each session participants underwent a series of measures, including saliva and blood samples for quantification of leptin, ghrelin, IL-1β, IL-6, CRP, and cortisol levels, they completed a cognitive battery using an iPad, and an emotion battery. We found that an acute sleep deprivation, limited to a 24 hr period, increases negative emotion states such as anxiety, fatigue, confusion, and depression. In conjunction, sleep deprivation results in increased inflammation and decreased cortisol levels in the morning, that are accompanied by deficits in vigilance and impulsivity. Combined, these results suggest that individuals who undergo 24hr sleep deprivation will induce systemic alterations to inflammation and endocrine functioning, while concomitantly increasing negative emotions.

Somatic disorders occur more often in adult psychiatric patients than in the general adult population. However, in child and adolescent psychiatry this association is unclear, mainly due to a lack of integration of existing data. To address this issue, we here present a systematic review on medical comorbidity in the two major developmental disorders autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) and formulate clinical recommendations. The literature was searched using the PubMed and PsycINFO databases (2000–1 May 2016) with the keywords “[((child and adolescent) AND (Autism OR Attention Deficit Hyperactivity Disorder* OR ADHD)) AND (“Cardiovascular Diseases” [Mesh] OR “Endocrine System Diseases” [Mesh] OR “Immune System Diseases” [Mesh] OR “Neurobehavioral Manifestations” [Mesh] OR “Gastrointestinal Disorders” [Mesh] OR Somatic OR Autoimmune disease OR Nervous system disease OR Infection OR Infectious disease)]. Two raters independently assessed the quality of the eligible studies. The initial search identified 5278 articles. Based on inclusion and exclusion criteria 104 papers were selected and subsequently subjected to a quality control. This quality was assessed according to a standardized and validated set of criteria and yielded 29 studies for inclusion. This thorough literature search provides an overview of relevant articles on medical comorbidity in ADHD and/or ASD, and shows that medical disorders in these children and adolescents appear to be widespread. Those who work with children with ASD and/or ADHD should be well aware of this and actively promote routine medical assessment. Additionally, case–control studies and population-based studies are needed to provide reliable prevalence estimates. Future studies should furthermore focus on a broader evaluation of medical disorders in children and adolescents with ADHD and/or ASD to improve treatment algorithm in this vulnerable group.