Summary Autism spectrum disorder (ASD), a neurodevelopmental disorder affecting nearly 1 in 88 children, is thought to result from aberrant brain connectivity. Remarkably, there have been no systematic attempts to characterize whole-brain connectivity in children with ASD. Here, we use neuroimaging to show there are more instances of greater functional connectivity in the brains of children with ASD compared with typically developing children. Hyper-connectivity in ASD was observed at the whole-brain and subsystems level, across long- and short-range connections, and was associated with higher levels of fluctuations in regional brain signals. Brain hyper-connectivity predicted symptom severity in ASD such that children with greater functional connectivity exhibited more severe social deficits. We replicated these findings in two additional independent cohorts, demonstrating again that at earlier ages, the brain in ASD is largely functionally hyper-connected in ways that contribute to social dysfunction. Our findings provide novel insights into brain mechanisms underlying childhood autism.

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In this paper, we review the most recent and often conflicting findings on conventional measures of executive control in autism spectrum disorders. We discuss the obstacles to accurate measurement of executive control, such as: its prolonged developmental trajectory; lack of consensus on its definition and if it is a unitary construct; the inherent complexity of executive control; and the difficulty measuring executive control functions in laboratory or clinical settings. We review the potential of an ecological validity framework to address some of these problems, and describe new tests claiming verisimilitude, or close resemblance to "real life" demands. We also review the concept of veridicality, which allows for the measurement of the ecological validity of any task, and discuss the few studies addressing ecological validity in individuals with autism. Our review suggests that a multi-source approach emphasizing veridicality may provide the most comprehensive assessment of executive control in autism. KeywordsExecutive Function; Autism; Ecological Validity; Asperger's; Cognitive Control; Neuropsychology Executive control is a widely studied construct in the field of autism spectrum disorders, henceforth referred to in this paper as autism. Though the research findings are inconsistent (see below), most clinicians, teachers, and family members agree that individuals with autism have difficulties with various aspects of executive control in their daily lives. This review will explore this discrepancy by addressing the following three questions:1. What do we know about conventional executive control tasks and autism? 2. Why is the executive control profile in autism so confusing?3. Where do we go from here?Our goal is to highlight novel areas of research in this field that could: advance the study of executive control in autism; improve its ability to capture the daily executive control obstacles that impair individuals with autism; and provide new targets for intervention.

The goal of the current study was to test whether deficits in processing speed (PS) may be a shared cognitive risk factor in reading disability (RD) and Attention Deficit/Hyperactivity Disorder (ADHD), which are known to be comorbid. Literature on ADHD and RD suggests that deficits on tasks with a speeded component are seen in both of these disorders individually. The current study examined a wide range of speeded tasks in RD, ADHD, comorbid RD+ADHD, and a control group to test whether RD and ADHD have similar profiles of PS deficits, and whether these deficits are shared by the two disorders. The results suggest that a general PS deficit exists in both clinical groups compared to controls, although children with RD demonstrate greater PS deficits than children with ADHD. Two tests (underadditivity and partial correlations) were conducted to test whether these PS deficits are shared. Since we found that PS deficits were underadditive in the comorbid group and that partialling PS reduced the correlation between RD and ADHD, it appears that PS is a shared cognitive risk factor that may help explain the comorbidity of these two disorders.

Objective While several studies have investigated developmental trajectories of executive functioning (EF) in autism spectrum disorders (ASD) using lab-based tasks, no study to date has directly measured how EF skills in everyday settings vary at different ages. The current study seeks to extend prior work by evaluating age-related differences in parent reported EF problems during childhood and adolescence in a large cross-sectional cohort of children with ASD. Methods 185 children with an ASD without intellectual disability participated in the study. Subjects were divided into four groups based on age (5–7; 8–10; 11–13; and 14–18 year olds). The four age groups did not differ in IQ, sex ratio, or autism symptoms. Results There were significant age effects (i.e., worsening scores with increasing age) in three BRIEF scale scores: Initiate (p=.007), Working Memory (p=.003), and Organization of Materials (p=.023). In addition, analysis of the BRIEF scale profile revealed that, although multiple scales were elevated, the Shift scale showed the greatest problems in both the youngest and oldest age cohorts. Conclusions Older children with ASD show greater EF problems compared to the normative sample than younger children with ASD. Specifically, there is a widening divergence from the normative sample in metacognitive executive abilities in children with ASD as they age. This, in combination with significant, albeit more stable, impairments in flexibility, has implications for the challenges faced by high functioning individuals with ASD as they attempt to enter mainstream work and social environments.

Individuals with ASD show atypical processing of social and nonsocial rewards. Findings support a broader interpretation of the social motivation hypothesis of ASD whereby general atypical reward processing encompasses social reward, nonsocial reward, and perhaps restricted interests. This meta-analysis also suggests that prior mixed results could be driven by sample age differences, warranting further study of the developmental trajectory for reward processing in ASD.

Recent estimates suggest that over 30% of children with autism spectrum disorders (ASD) meet diagnostic criteria for attention deficit/hyperactivity disorder (ADHD), and another 20% of children with ASD exhibit subthreshold clinical ADHD symptoms. Presence of ADHD symptoms in the context of ASD could have a variety of effects on cognition, autistic traits, and adaptive/ maladaptive behaviors including: exacerbating core ASD impairments; adding unique impairments specific to ADHD; producing new problems unreported in ASD or ADHD; having no clear impact; or producing some combination of these scenarios. Children with ASD and comorbid ADHD symptoms (ASD+ADHD; n=21), children with ASD without ADHD (ASD; n=28), and a typically developing control group (n=21) were included in the study; all groups were matched on age, gender-ratio, IQ, and socioeconomic status. Data were collected on verbal and spatial working memory, response inhibition, global executive control, autistic traits, adaptive functioning, and maladaptive behavior problems. In this sample, the presence of ADHD symptoms in ASD exacerbated impairments in executive control and adaptive behavior and resulted in higher autistic trait, and externalizing behavior ratings. ADHD symptoms were also associated with greater impairments on a lab measure of verbal working memory. These findings suggest that children with ASD+ADHD symptoms present with exacerbated impairments in some but not all domains of functioning relative to children with ASD, most notably in adaptive behavior and working memory. Therefore, ADHD may moderate the expression of components of the ASD cognitive and behavioral phenotype, but ASD+ADHD may not represent an etiologically distinct phenotype from ASD alone.Autism spectrum disorders (ASD) and attention deficit hyperactivity disorders (ADHD) are diagnosed based upon behavioral symptoms (APA, 2000). ASD is characterized by impairments in social functioning, communication, and restricted, repetitive behaviors/ interests, while ADHD is characterized by inattention and hyperactivity/impulsivity. Address Correspondence to: Benjamin E. Yerys, PhD, Children's Research Institute -Neuroscience, Children's National Medical Center, 111 Michigan Ave, NW, Washington, DC 20010, Phone: (202) Fax: (301) 765-5497. 2 When spatial working memory data is combined for the ASD and ASD+ADHD groups and then compared to the TYP group we find a significant difference in total between errors, t(56) =2.81, p<0.05, Cohen's d=0.61).There are no conflicts of interest, financial or otherwise, for the remaining authors involved directly or indirectly with this manuscript. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptAlthough the Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition Text Revision (DSM-IV-TR; APA, 2000) precludes a co-morbid diagnosis of ASD and ADHD, a recent study examining co-morbidity revealed that over 30% of children with highfunctioning ASD met diagnostic criteria for ADHD and a...

There is growing evidence of a camouflaging effect among females with autism spectrum disorder (ASD), particularly among those without intellectual disability, which may affect performance on gold-standard diagnostic measures. This study utilized an age- and IQ-matched sample of school-aged youth (n = 228) diagnosed with ASD to assess sex differences on the ADOS and ADI-R, parent-reported autistic traits, and adaptive skills. Although females and males were rated similarly on gold-standard diagnostic measures overall, females with higher IQs were less likely to meet criteria on the ADI-R. Females were also found to be significantly more impaired on parent reported autistic traits and adaptive skills. Overall, the findings suggest that some autistic females may be missed by current diagnostic procedures.