Heterogeneity in development of aspects of working memory predicts longitudinal attention deficit hyperactivity disorder symptom change.

Abstract

The role of cognitive mechanisms in the clinical course of neurodevelopmental disorders is poorly understood. Attention Deficit Hyperactivity Disorder (ADHD) is emblematic in that numerous alterations in cognitive development are apparent, yet how they relate to changes in symptom expression with age is unclear. To resolve the role of cognitive mechanisms in ADHD, a developmental perspective that takes into account expected within-group heterogeneity is needed. Method The current study uses an accelerated longitudinal design and latent trajectory growth mixture models in a sample of children ages 7–13 years carefully characterized as with (n=437) and without (n=297) ADHD to: 1) identify heterogeneous developmental trajectories for response inhibition, visual spatial working memory maintenance, and delayed reward discounting and 2) to assess the relationships between these cognitive trajectories and ADHD symptom change. Results Best-fitting models indicated multiple trajectory classes in both the ADHD and typically-developing samples, as well as distinct relationships between each cognitive process and ADHD symptom change. Developmental change in response inhibition and delayed reward discounting were unrelated to ADHD symptom change, while individual differences in the rate of visual spatial working memory maintenance improvement predicted symptom remission in ADHD. Conclusion Characterizing heterogeneity in cognitive development will be crucial for clarifying mechanisms of symptom persistence and recovery. Results here suggest working memory maintenance may be uniquely related to ADHD symptom improvement.

Is there any incremental benefit to conducting neuroimaging and neurocognitive assessments in the diagnosis of ADHD in young children? A machine learning investigation

“…Subparts of the cingulate cortex, including the anterior and middle-posterior cingulate cortex have been previously implicated in ADHD research (Rubia, 2018). This region has been previously associated with cognitive and impulse control, and a decreased connectivity between the anterior cingulate and the posterior parietal cortex in ADHD has been observed in prior research [see Vogt (2019) The intraparietal sulcus is a very significant contributor to working memory (Chein et al, 2003;Cowan, 2016;Cowan et al, 2011;Oztekin et al, 2009;Smith & Jonides, 1998;Xu & Chun, 2006), and working memory deficits have been commonly observed in previous ADHD research (Hammer et al, 2015;Karalunas et al, 2017;Palladino & Ferrari, 2013;Raiker et al, 2019;Raiker et al, 2012). Notably, this region has been previously implicated for its importance in supporting focus of attention during WM operations in healthy adults (Cowan et al, 2011;Oztekin et al, 2009).…”

Is an irritable ADHD profile traceable using personality dimensions? Replicability, stability, and predictive value over time of data-driven profiles

“…(3) our sample was characterised by a restricted age range (6)(7)(8)(9)(10)(11) as opposed to the larger age range (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18) in [23]; (4) recruitment strategies differed (community sample vs. clinically based). The possible effect of these factors on the identified communities should be examined in future studies.…”

How do stimulant treatments for ADHD work? Evidence for mediation by improved cognition

“…From these theories, it follows that amelioration of ADHD‐related deficits in cognition should result in clinical improvement. Indeed, there is evidence that maturation of cognitive function predicts ADHD remission (e.g., Halperin, Trampush, Miller, Marks, & Newcorn, ; Karalunas et al., ; c.f., Coghill, Hayward, Rhodes, Grimmer, & Matthews, ). In ADHD intervention work, cognitive functions have been hypothesized as treatment mechanisms for stimulant and nonstimulant medications (e.g., Arnsten, ; Gamo, Wang, & Arnsten, ; Robbins & Arnsten, ) and are common targets for the development of nonpharmacologic interventions (see, for example, Cortese et al., ; Halperin & Healey, ; Halperin et al., ).…”