Slow, variable, and error-prone performance on speeded reaction time (RT) tasks has been well documented in childhood ADHD, but equally well documented is the context-dependent nature of those deficits, particularly with respect to event rate. As event rates increase (or, as the interstimulus intervals become shorter), RTs decrease, a pattern of performance that has long been interpreted as evidence that cognitive deficits in ADHD are a downstream consequence of a fundamental difficulty in the regulation of arousal to meet task demands. We test the extent to which this is a misinterpretation of the data that occurs when RT and accuracy are considered separately, as is common in neurocognitive research. In two samples of children aged 8–10 with (N = 97; 33 girls) and without (N = 39; 26 girls) ADHD, we used the diffusion model, an influential computational model of RT, to examine the effect of event rate on inhibitory control in a go-no-go task. Contrary to longstanding belief, we found that fast event rates slowed the rate at which children with ADHD accumulated evidence to make a decision to “no-go”, as indexed by drift rate. This in turn resulted in a higher proportion of failed inhibits, and occurred despite increased task engagement, as reflected by changes in the starting point of the decision process. Thus, although faster event rates increased task engagement among children with ADHD, the increased engagement was unable to counteract the concurrent slowing of processing speed to “no-go” decisions. Implications for theoretical models of ADHD and treatments are discussed.

In contrast to historical conceptualizations that framed psychological disorders as distinct, categorical conditions, it is now widely understood that co- and multi-morbidities between disorders are extensive. As a result, there has been a call to better understand the dimensional liabilities that are common to and influence the development of multiple psychopathologies, as supported and exemplified by the National Institutes of Mental Health (NIMH) Research Domain Criteria (RDoC) framework. We use a latent variable SEM approach to examine the degree to which working memory deficits represent a cognitive liability associated with the development of common and discrete dimensions of psychopathology. In a sample of 415 community recruited children aged 8-12 (n = 170 girls), we fit a bi-factor model to parent reports of behavior from the DISC-4 and BASC-2, and included a latent working memory factor as a predictor of the internalizing, externalizing, and general “p-factor.” We found that both the general “p-factor” and externalizing (but not internalizing) latent factor were significantly associated with working memory. When a bi-factor model of externalizing symptomology was fit to further explore this relationship, working memory was only correlated with the general externalizing dimension; correlation with specific inattention, hyperactive/impulsive, and oppositional factors did not survive once the general externalizing dimension was taken into consideration. These findings held regardless of the sex of the child. Our results suggest that working memory deficits represent both a common cognitive liability for mental health disorders, and a specific liability for externalizing disorders.

Objective: Deficits in the ability to perceive time have been proposed as an etiologic mechanism in the development of the cognitive and behavioral characteristics associated with ADHD. However, previous studies testing the presence of timing deficits have produced idiosyncratic results. This is in large part due to the underutilization of insights from basic timing research, and from the inherent difficulty that arises when a single index of performance (i.e., reaction time [RT] or accuracy) is used to index the health of what is essentially a multiple-component process. The current article utilizes a diffusion model approach to isolate the component processes involved in timing (i.e., internal clock speed, decision-making speed, speed/accuracy trade-off strategies, and nondecision time) using a well-validated timing task. Method: Fifty children with ADHD and 32 non-ADHD controls aged 8–12 completed a temporal bisection procedure. Results: Diffusion model parameters indicated that both the internal clock and decision-making speeds were slower among children with ADHD. However, the strength of evidence for slowed decision making far outweighed evidence for a slower internal clock. Conclusions: Slower evidence accumulation during decision making is domain-general deficit in ADHD. Such slowing is consistent with adaptive-gain theories, which posit that a suboptimal ratio of neural signal-to-noise is characteristic of children with ADHD.

It has previously been demonstrated that rats trained on the peak-interval procedure to associate two different cues with two different fixed interval schedules will generate a scalar peak function at an intermediate time when presented with the compound cue. This response pattern has been interpreted as resulting from the simultaneous retrieval of different temporal memories, and a consequential averaging process to resolve the ambiguity. In the present set of studies, we investigated the role that serotonin 1a receptors play in this process. In Experiment 1, rats were trained on a peak-interval procedure to associate the interoceptive states induced by saline and the 5-HT1a agonist, 8-OH-DPAT, with a 5 s or 20 s fixed-interval schedule signaled by the same tone cue (counter-balanced). While peak functions following administration of saline were centered at the appropriate time (5 s or 20 s), peak functions following administration of the agonist were centered around 7 s, irrespective of the reinforced time during training, suggesting agonist-induced disruption in selective temporal memory retrieval, resulting in increased ambiguity regarding the appropriate time at which to respond. In Experiment 2, rats were trained in a peak-interval procedure to associate a tone cue with a 10 s fixed interval and a light cue with a 20 s fixed interval. Administration of the 5-HT1a antagonist, WAY-100635, had no impact on timing when single cues were presented, but altered the intermediate, scalar, response to the stimulus compound, suggesting antagonist-induced disruption in the processes used to deal with temporal memory ambiguity. Together, these data suggest that manipulations of 5HT transmission at the 5-HT1a receptor cause changes in the temporal pattern of responding that are consistent with alterations in temporal memory processes and responses to temporal ambiguity.

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