Shared impairments in inhibitory control, rather than representing a transdiagnostic endophenotype in ADHD and OCD, were associated with disorder-differential functional and structural abnormalities. Patients with ADHD showed smaller and underfunctioning ventrolateral prefrontal/insular-striatal regions whereas patients with OCD showed larger and hyperfunctioning insular-striatal regions that may be poorly controlled by smaller and underfunctioning rostro/dorsal medial prefrontal regions.

Objective: Autism spectrum disorder (ASD) and obsessive-compulsive disorder (OCD) share inhibitory control deficits possibly underlying poor control over stereotyped/repetitive and compulsive behaviours, respectively. However, it is unclear whether these symptom profiles are mediated by common or distinct neural profiles. This comparative multimodal meta-analysis assessed shared and disorder-specific neuroanatomy and neurofunction of inhibitory functions. Methods:A comparative meta-analysis of 62 voxel-based morphometry (VBM) and 26 functional magnetic resonance imaging (fMRI) studies of inhibitory control was conducted comparing grey matter volume (GMV) and activation abnormalities between ASD (sMRI:911;fMRI:188) and OCD (sMRI:928;fMRI:247) patients versus controls. Multimodal meta-analysis compared groups across VBM and fMRI.Results: Both disorders shared reduced function and structure in rostral/dorsomedial prefrontal cortex including anterior cingulate. OCD had disorder-specific increase in structure and function of left basal ganglia (BG)/insula relative to controls and ASD, who had reduced right BG/insula volumes versus OCD. In fMRI, ASD patients showed disorder-specific reduced left dorsolateral-prefrontal activation and reduced posterior cingulate deactivation, while OCD patients showed temporoparietal underactivation. Conclusions:The multimodal comparative meta-analysis shows shared and disorder-specific abnormalities. While rostro-dorsomedial prefrontal cortex was smaller in structure and function in both disorders, this was concomitant with increased structure and function in BG/insula in OCD, but a reduction in ASD, presumably reflecting a disorder-specific fronto-striato-insular dysregulation in OCD in the form of poor frontal control over overactive BG, and a fronto-striato-insular maldevelopment in ASD with reduced structure and function in this network. Disorder-differential mechanisms appear to drive overlapping phenotypes of inhibitory control abnormalities in ASD and OCD. Carlisi et al.3

BackgroundPeople with attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) have abnormalities in frontal, temporal, parietal and striato-thalamic networks. It is unclear to what extent these abnormalities are distinctive or shared. This comparative meta-analysis aimed to identify the most consistent disorder-differentiating and shared structural and functional abnormalities.MethodsSystematic literature search was conducted for whole-brain voxel-based morphometry (VBM) and functional magnetic resonance imaging (fMRI) studies of cognitive control comparing people with ASD or ADHD with typically developing controls. Regional gray matter volume (GMV) and fMRI abnormalities during cognitive control were compared in the overall sample and in age-, sex- and IQ-matched subgroups with seed-based d mapping meta-analytic methods.ResultsEighty-six independent VBM (1533 ADHD and 1295 controls; 1445 ASD and 1477 controls) and 60 fMRI datasets (1001 ADHD and 1004 controls; 335 ASD and 353 controls) were identified. The VBM meta-analyses revealed ADHD-differentiating decreased ventromedial orbitofrontal (z = 2.22, p < 0.0001) but ASD-differentiating increased bilateral temporal and right dorsolateral prefrontal GMV (zs ⩾ 1.64, ps ⩽ 0.002). The fMRI meta-analyses of cognitive control revealed ASD-differentiating medial prefrontal underactivation but overactivation in bilateral ventrolateral prefrontal cortices and precuneus (zs ⩾ 1.04, ps ⩽ 0.003). During motor response inhibition specifically, ADHD relative to ASD showed right inferior fronto-striatal underactivation (zs ⩾ 1.14, ps ⩽ 0.003) but shared right anterior insula underactivation.ConclusionsPeople with ADHD and ASD have mostly distinct structural abnormalities, with enlarged fronto-temporal GMV in ASD and reduced orbitofrontal GMV in ADHD; and mostly distinct functional abnormalities, which were more pronounced in ASD.

Objective: For the first time, we use a longitudinal population-based autism cohort to chart the trajectories of cognition and autism symptoms from childhood to early adulthood and identify features that predict the level of function and change with development. Method: Latent growth curve models were fitted to data from the Special Needs and Autism Project cohort at three time points: 12, 16, and 23 years. Outcome measures were IQ and parent-reported Social Responsiveness Scale autism symptoms. Of the 158 participants with an autism spectrum disorder at 12 years, 126 (80%) were reassessed at 23 years. Child, family, and contextual characteristics obtained at 12 years predicted intercept and slope of the trajectories. Results: Both trajectories showed considerable variability. IQ increased significantly by a mean of 7.48 points from 12 to 23 years, whereas autism symptoms remained unchanged. In multivariate analysis, full-scale IQ was predicted by initial language level and school type (mainstream/specialist). Participants with a history of early language regression showed significantly greater IQ gains. Autism symptoms were predicted by Social Communication Questionnaire scores (lifetime version) and emotional and behavioral problems. Participants attending mainstream schools showed significantly fewer autism disorder symptoms at 23 years than those in specialist settings; this finding was robust to propensity score analysis for confounding. Conclusion: Our findings suggest continued cognitive increments for many people with autism across the adolescent period, Q6 but a lack of improvement in autism symptoms. Our finding of school influences on autism symptoms requires replication in other cohorts and settings before drawing any implications for mechanisms or policy.