Developmental patterns of inhibition and fronto-basal-ganglia white matter organisation in healthy children and children with attention-deficit/hyperactivity disorder.

Abstract

There is robust evidence implicating inhibitory deficits as a fundamental behavioural phenotype in children with attention-deficit/hyperactivity disorder (ADHD). However, prior studies have not directly investigated the role in which white matter properties within the fronto-basal-ganglia circuit may play in the development of inhibitory control deficits in this group. Combining recent advancements in brain-behavioural modelling, we mapped the development of stop-signal task (SST) performance and fronto-basal-ganglia maturation in a longitudinal sample of children aged 9-14 with and without ADHD. In a large sample of 135 ADHD and 138 non-ADHD children, we found that the ADHD group had poorer inhibitory control (i.e., longer stop-signal reaction times) across age compared to non-ADHD controls. When applying the novel parametric race model, this group effect was driven by higher within-subject variability (sigma) and higher number of extreme responses (tau) on stop trials. The ADHD group also displayed higher within-subject variability on correct responses to go stimuli. Moreover, we observed the ADHD group committing more task-based failures such as responding on stop trials (trigger failures) and omissions on go trials (go failures) compared to non-ADHD controls, suggesting the contribution of attentional lapses to poorer response inhibition performance. In contrast, longitudinal modelling of fixel-based analysis measures revealed no significant group differences in the maturation of fronto-basal-ganglia fibre cross-section in a subsample (74 ADHD and 73 non-ADHD children). Finally, brain-behavioural models revealed that age-related changes in fronto-basal-ganglia morphology (fibre cross-section) were significantly associated with reductions in the variability of the correct go-trial responses (sigma.true) and skew of the stop-trial distribution (tauS). However, this effect did not differ between ADHD and typically developing children. Overall, our findings support the growing consensus suggesting that attentional deficits subserve ADHD-related inhibitory dysfunction. Furthermore, we show novel evidence suggesting that while children with ADHD are consistently performing worse on the SST than their non-affected peers, they appear to have comparable rates of neurocognitive maturation across this period.