In this paper, we consider the domain of executive functions (EFs) and their possible role in developmental psychopathologies. We first consider general theoretical and measurement issues involved in studying EFs and then review studies of EFs in four developmental psychopathologies: attention deficit hyperactivity disorder (ADHD), conduct disorder (CD), autism, and Tourette syndrome (TS). Our review reveals that EF deficits are consistently found in both ADHD and autism but not in CD (without ADHD) or in TS. Moreover, both the severity and profile of EF deficits appears to differ across ADHD and autism. Molar EF deficits are more severe in the latter than the former. In the few studies of more specific EF tasks, there are impairments in motor inhibition in ADHD but not in autism, whereas there are impairments in verbal working memory in autism but not ADHD. We close with a discussion of implications for future research.

Context Autism is considered the most heritable of neurodevelopmental disorders, mainly because of the large difference in concordance rates between monozygotic and dizygotic twins. Objective To provide rigorous quantitative estimates of genetic heritability of autism and the effects of shared environment. Design, Setting, and Participants Twin pairs with at least 1 twin with an autism spectrum disorder (ASD) born between 1987 and 2004were identified through the California Department of Developmental Services. Main Outcome Measures Structured diagnostic assessments (Autism Diagnostic Interview–Revised and Autism Diagnostic Observation Schedule) were completed on 192 twin pairs. Concordance rates were calculated and parametric models were fitted for 2 definitions, 1 narrow (strict autism) and 1 broad (ASD). Results For strict autism, probandwise concordance for male twins was 0.58 for 40 monozygotic pairs (95% confidence interval [CI], 0.42–0.74) and 0.21 for 31 dizygotic pairs (95% CI, 0.09–0.43); for female twins, the concordance was 0.60 for 7 monozygotic pairs (95% CI, 0.28–0.90) and 0.27 for 10 dizygotic pairs (95% CI, 0.09–0.69). For ASD, the probandwise concordance for male twins was 0.77 for 45 monozygotic pairs (95% CI, 0.65–0.86) and 0.31 for 45 dizygotic pairs (95% CI, 0.16–0.46); for female twins, the concordance was 0.50 for 9 monozygotic pairs (95% CI, 0.16–0.84) and 0.36 for 13 dizygotic pairs (95% CI, 0.11–0.60). A large proportion of the variance in liability can be explained by shared environmental factors (55%; 95% CI, 9%–81% for autism and 58%; 95% CI, 30%–80% for ASD) in addition to moderate genetic heritability (37%; 95% CI, 8%–84% for autism and 38%; 95% CI, 14%–67% for ASD). Conclusion Susceptibility to ASD has moderate genetic heritability and a substantial shared twin environmental component.

A group of high-functioning autistic individuals was compared to a clinical control group matched on VIQ, age, sex and SES. Significant group differences were found on executive function, theory of mind, emotion perception and verbal memory tests, but not on spatial or other control measures. Second-order theory of mind and executive function deficits were widespread among the autistic group, while first-order theory of mind deficits were found in only a subset of the sample. The relationship of executive function and theory of mind deficits to each other, and their primacy to autism, are discussed.

WHAT'S KNOWN ON THIS SUBJECT:The sibling recurrence risk of autism has been estimated to be between 3% and 10%. Previous research was affected by small samples and selection, stoppage, and reporting limitations. Updated estimates of recurrence risk are needed. WHAT THIS STUDY ADDS:Studying a large sample and using a prospective longitudinal design, this study demonstrated that the sibling recurrence risk of autism spectrum disorder is substantially higher than previous estimates. This elevated risk has important implications for infant screening and genetic counseling. abstract OBJECTIVE: The recurrence risk of autism spectrum disorders (ASD) is estimated to be between 3% and 10%, but previous research was limited by small sample sizes and biases related to ascertainment, reporting, and stoppage factors. This study used prospective methods to obtain an updated estimate of sibling recurrence risk for ASD. METHODS:A prospective longitudinal study of infants at risk for ASD was conducted by a multisite international network, the Baby Siblings Research Consortium. Infants (n ϭ 664) with an older biological sibling with ASD were followed from early in life to 36 months, when they were classified as having or not having ASD. An ASD classification required surpassing the cutoff of the Autism Diagnostic Observation Schedule and receiving a clinical diagnosis from an expert clinician. RESULTS:A total of 18.7% of the infants developed ASD. Infant gender and the presence of Ͼ1 older affected sibling were significant predictors of ASD outcome, and there was an almost threefold increase in risk for male subjects and an additional twofold increase in risk if there was Ͼ1 older affected sibling. The age of the infant at study enrollment, the gender and functioning level of the infant's older sibling, and other demographic factors did not predict ASD outcome. CONCLUSIONS:The sibling recurrence rate of ASD is higher than suggested by previous estimates. The size of the current sample and prospective nature of data collection minimized many limitations of previous studies of sibling recurrence. Clinical implications, including genetic counseling, are discussed. Pediatrics 2011;128:e488-e495 AUTHORS:

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