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Inhibition, reinforcement sensitivity and temporal information processing in ADHD and ADHD+ODD: evidence of a separate entity?

ABSTRACT: This study compared children with ADHD-only, ADHD+ODD and normal controls (age 8-12) on three key neurocognitive functions: response inhibition, reinforcement sensitivity, and temporal information processing. The goal was twofold: (a) to investigate neurocognitive impairments in children with ADHD-only and children with ADHD+ODD, and (b) to test whether ADHD+ODD is a more severe from of ADHD in terms of neurocognitive performance. In Experiment 1, inhibition abilities were measured using the Stop Task. In Experiment 2, reinforcement sensitivity and temporal information processing abilities were measured using a Timing Task with both a reward and penalty condition. Compared to controls, children with ADHD-only demonstrated impaired inhibitory control, showed more time underestimations, and showed performance deterioration in the face of reward and penalty. Children with ADHD+ODD performed in-between children with ADHD-only and controls in terms of inhibitory controls and the tendency to underestimate time, but were more impaired than controls and children with ADHD-only in terms of timing variability. In the face of reward and penalty children with ADHD+ODD improved their performance compared to a neutral condition, in contrast to children with ADHD-only. In the face of reward, the performance improvement in the ADHD+ODD group was disproportionally larger than that of controls. Taken together the findings suggest that, in terms of neurocognitive functioning, comorbid ADHD+ODD is a substantial different entity than ADHD-only.

SUBMITTER: Luman M

PROVIDER: S-EPMC2766046 | biostudies-other | 2009 Nov

REPOSITORIES: biostudies-other

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Project description:ObjectiveChildren with ADHD demonstrate impaired performance on a wide range of neuropsychological tests. It is unclear, however, whether ADHD is associated with many neurocognitive deficits or whether a small number of impairment(s) broadly influence test performance. The current study tests competing model predictions regarding two candidate causal mechanisms in ADHD: information processing speed and working memory.MethodA well-characterized sample of 86 children (Mage = 10.52, SDage = 1.54; 34 girls; 64% Caucasian/Non-Hispanic) with ADHD (n = 45) and without ADHD (n = 41) completed eight fully crossed experimental tasks that systematically manipulated working memory (BF?? = 1.80 × 10?³) and information processing speed (drift rate; BF?? = 7.61 × 10?).ResultsBayesian mixed-model ANOVAs indicated that increasing working memory demands produced significant reductions in information processing speed (drift rate; BF?? = 5.82 × 10??). In contrast, experimentally reducing children's information processing speed did not significantly change their working memory performance (BF?? = 1.31). ADHD status interacted with the working memory manipulation, such that the ADHD and non-ADHD groups showed equivalently high accuracy under the encoding-only conditions (BF?? = 3.45) but differed significantly under high working memory conditions (encoding + recall; BF?? = 19.58). Importantly, however, ADHD status failed to interact with (a) the working memory manipulation to differentially affect information processing speed and (b) the information processing speed manipulation to differentially affect working memory performance (all BF?? > 4.25).ConclusionsThese findings indicate that top-down executive control exerts significant effects on children's ability to quickly process information, but that working memory deficits and slowed information processing speed appear to be relatively independent impairments in ADHD. (PsycINFO Database Record (c) 2020 APA, all rights reserved).

Project description:ADHD is associated with altered dopamine regulated reinforcement learning on prediction errors. Despite evidence of categorically altered error processing in ADHD, neuroimaging advances have largely investigated models of normal reinforcement learning in greater detail. Further, although reinforcement leaning critically relies on ventral striatum exerting error magnitude related thresholding influences on substantia nigra (SN) and dorsal striatum, these thresholding influences have never been identified with neuroimaging. To identify such thresholding influences, we propose that error magnitude related activities must first be separated from opposite activities in overlapping neural regions during error detection. Here we separate error detection from magnitude related adjustment (post-error slowing) during inhibition errors in the stop signal task in typically developing (TD) and ADHD adolescents using fMRI. In TD, we predicted that: 1) deactivation of dorsal striatum on error detection interrupts ongoing processing, and should be proportional to right frontoparietal response phase activity that has been observed in the SST; 2) deactivation of ventral striatum on post-error slowing exerts thresholding influences on, and should be proportional to activity in dorsal striatum. In ADHD, we predicted that ventral striatum would instead correlate with heightened amygdala responses to errors. We found deactivation of dorsal striatum on error detection correlated with response-phase activity in both groups. In TD, post-error slowing deactivation of ventral striatum correlated with activation of dorsal striatum. In ADHD, ventral striatum correlated with heightened amygdala activity. Further, heightened activities in locus coeruleus (norepinephrine), raphe nucleus (serotonin) and medial septal nuclei (acetylcholine), which all compete for control of DA, and are altered in ADHD, exhibited altered correlations with SN. All correlations in TD were replicated in healthy adults. Results in TD are consistent with dopamine regulated reinforcement learning on post-error slowing. In ADHD, results are consistent with heightened activities in the amygdala and non-dopaminergic neurotransmitter nuclei preventing reinforcement learning.

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Inhibition, reinforcement sensitivity and temporal information processing in ADHD and ADHD+ODD: evidence of a separate entity?

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