Evidence of executive dysfunction in autism spectrum disorders (ASD) across development remains mixed and establishing its role is critical for guiding diagnosis and intervention. The primary objectives of this meta-analysis is to analyse executive function (EF) performance in ASD, the fractionation across EF subdomains, the clinical utility of EF measures and the influence of multiple moderators (for example, age, gender, diagnosis, measure characteristics). The Embase, Medline and PsychINFO databases were searched to identify peer-reviewed studies published since the inclusion of Autism in DSM-III (1980) up to end of June 2016 that compared EF in ASD with neurotypical controls. A random-effects model was used and moderators were tested using subgroup analysis. The primary outcome measure was Hedges’ g effect size for EF and moderator factors. Clinical sensitivity was determined by the overlap percentage statistic (OL%). Results were reported according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. A total of 235 studies comprising 14 081 participants were included (N, ASD=6816, Control=7265). A moderate overall effect size for reduced EF (Hedges’ g=0.48, 95% confidence interval (CI) 0.43–0.53) was found with similar effect sizes across each domain. The majority of moderator comparisons were not significant although the overall effect of executive dysfunction has gradually reduced since the introduction of ASD. Only a small number of EF measures achieved clinical sensitivity. This study confirms a broad executive dysfunction in ASD that is relatively stable across development. The fractionation of executive dysfunction into individual subdomains was not supported, nor was diagnostic sensitivity. Development of feasible EF measures focussing on clinical sensitivity for diagnosis and treatment studies should be a priority.

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Previous systematic reviews and meta-analyses have identified cognitive deficits in adults with obstructive sleep apnoea (OSA). However, quantitative analysis of the association between OSA and neuropsychological performance has not been conducted specifically in older adults, for whom there is a greater risk of cognitive decline. We searched Medline, Embase and PsycINFO through August 2016 for studies describing associations between OSA and neuropsychological outcomes in people aged>50 years. Meta-analyses were performed on these studies for overall cognition and within cognitive domains. Subgroup analyses were performed taking into account risk of bias and moderating differences in study design. 13 studies met eligibility criteria for analysis. A small negative association was found between OSA and all neuropsychological outcomes combined, g=0.18(95% CI 0.04-0.32), and in memory and processing speed domains. Small case-control studies from sleep clinic populations observed the greatest associations, while larger cohort studies from community samples illustrated no association. Analysis accounting for publication bias resulted in a null overall association, g=0.02 (95%CI -0.12 to 0.16). Associations between OSA and cognition in later life are highly variable and the findings differ based on the type and setting of study. It appears some older adults may be at risk of cognitive impairments attributable to OSA; however, the risk of bias renders the evidence inconclusive. High quality research is warranted in clinically diagnosed OSA patients as well as those already experiencing neuropsychological impairment and who may be regarded at higher risk of further cognitive decline.