| Autor: |
Singh, Mervyn, Skippen, Patrick, He, Jason, Thomson, Phoebe, Fuelscher, Ian, Caeyenberghs, Karen, Anderson, Vicki, Hyde, Christian, Silk, Timothy J. |
| Předmět: |
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| Zdroj: |
Human Brain Mapping; Oct2024, Vol. 45 Issue 15, p1-23, 23p |
| Abstrakt: |
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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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