Altered structural brain asymmetry in autism spectrum disorder (ASD) has been reported. However, findings have been inconsistent, likely due to limited sample sizes. Here we investigated 1,774 individuals with ASD and 1,809 controls, from 54 independent data sets of the ENIGMA consortium. ASD was significantly associated with alterations of cortical thickness asymmetry in mostly medial frontal, orbitofrontal, cingulate and inferior temporal areas, and also with asymmetry of orbitofrontal surface area. These differences generally involved reduced asymmetry in individuals with ASD compared to controls. Furthermore, putamen volume asymmetry was significantly increased in ASD. The largest case-control effect size was Cohen’sd = −0.13, for asymmetry of superior frontal cortical thickness. Most effects did not depend on age, sex, IQ, severity or medication use. Altered lateralized neurodevelopment may therefore be a feature of ASD, affecting widespread brain regions with diverse functions. Large-scale analysis was necessary to quantify subtle alterations of brain structural asymmetry in ASD.

Error monitoring by the posterior medial frontal cortex (pMFC) has been linked to post-error behavioral adaptation effects and cognitive control dynamics in lateral prefrontal cortex (LPFC). It remains unknown, however, whether control adjustments following errors produce post-error behavioral adjustments (PEBAs) by inhibiting inappropriate responses or facilitating goal-directed ones. Here we used functional magnetic resonance imaging to investigate the hemodynamic correlates of PEBAs in a stimulus–response compatibility task. Our task was designed to test whether PEBAs are implemented by suppressing motor responses primed by irrelevant stimulus features (face location), redirecting attention to relevant features (face gender), or both or neither of these possibilities. Independent of PEBAs, error-related pMFC activation was followed by post-error recruitment of prefrontal and parietal control regions and, crucially, both (1) suppressed response-related activity in sensorimotor cortex and (2) enhanced target processing in face-sensitive sensory cortex (“fusiform face area”). More importantly, by investigating the covariation between post-error hemodynamic activity and individual differences in PEBAs, we showed that modulation of task-related motor and sensory processing was dependent on whether participants produced generally slower responses (“post-error slowing”; PES) or selectively reduced interference effects (“post-error reduction of interference”; PERI), respectively. Each of these behaviorally dependent effects was mediated by distinct LPFC control mechanisms (PES: inferior frontal junction; PERI: superior frontal sulcus). While establishing relationships between PEBAs and cognitive control, our findings suggest that the neural architecture underlying sequential behavioral adaptation may be determined primarily by how control is executed by the individual when adjustments are needed.

Background: Individuals with anorexia nervosa are thought to exert excessive self-control to inhibit primary drives. Methods: This study used functional MRI (fMRI) to interrogate interactions between the neural correlates of cognitive control and motivational processes in the brain reward system during the anticipation of monetary reward and reward-related feedback. In order to avoid confounding effects of undernutrition, we studied female participants recovered from anorexia nervosa and closely matched healthy female controls. The fMRI analysis (including node-to-node functional connectivity) followed a region of interest approach based on models of the brain reward system and cognitive control regions implicated in anorexia nervosa: the ventral striatum, medial orbitofrontal cortex (mOFC) and dorsolateral prefrontal cortex (DLPFC). Results: We included 30 recovered patients and 30 controls in our study. There were no behavioural differences and no differences in hemodynamic responses of the ventral striatum and the mOFC in the 2 phases of the task. However, relative to controls, recovered patients showed elevated DLPFC activity during the anticipation phase, failed to deactivate this region during the feedback phase and displayed greater functional coupling between the DLPFC and mOFC. Recovered patients also had stronger associations than controls between anticipation-related DLPFC responses and instrumental responding. Limitations: The results we obtained using monetary stimuli might not generalize to other forms of reward. Conclusion: Unaltered neural responses in ventral limbic reward networks but increased recruitment of and connectivity with lateral–frontal brain circuitry in recovered patients suggests an elevated degree of self-regulatory processes in response to rewarding stimuli. An imbalance between brain systems subserving bottom–up and top–down processes may be a trait marker of the disorder.