Widespread attenuating changes in brain connectivity associated with the general factor of psychopathology in 9- and 10-year olds.

Convergent research identifies a general factor ("P factor") that confers transdiagnostic risk for psychopathology. Large-scale networks are key organizational units of the human brain. However, studies of altered network connectivity patterns associated with the P factor are limited, especially in early adolescence when most mental disorders are first emerging. We studied 11,875 9- and 10-year olds from the Adolescent Brain and Cognitive Development (ABCD) study, of whom 6593 had high-quality resting-state scans. Network contingency analysis was used to identify altered interconnections associated with the P factor among 16 large-scale networks. These connectivity changes were then further characterized with quadrant analysis that quantified the directionality of P factor effects in relation to neurotypical patterns of positive versus negative connectivity across connections. The results showed that the P factor was associated with altered connectivity across 28 network cells (i.e., sets of connections linking pairs of networks); pPERMUTATION values < 0.05 FDR-corrected for multiple comparisons. Higher P factor scores were associated with hypoconnectivity within default network and hyperconnectivity between default network and multiple control networks. Among connections within these 28 significant cells, the P factor was predominantly associated with "attenuating" effects (67%; pPERMUTATION < 0.0002), i.e., reduced connectivity at neurotypically positive connections and increased connectivity at neurotypically negative connections. These results demonstrate that the general factor of psychopathology produces attenuating changes across multiple networks including default network, involved in spontaneous responses, and control networks involved in cognitive control. Moreover, they clarify mechanisms of transdiagnostic risk for psychopathology and invite further research into developmental causes of distributed attenuated connectivity.

Using the Diffusion Model to Explain Cognitive Deficits in Attention Deficit Hyperactivity Disorder.

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.

Is Poor Working Memory a Transdiagnostic Risk Factor for Psychopathology?

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.