Leanne Tamm , Jonathan A. Dudley , Sarah L. Karalunas , John O. Simon , Thomas C. Maloney , Gowtham Atluri , Jeffery N. Epstein
{"title":"Exploring the neural basis of reaction time variability in ADHD: The importance of examining data at the trial level","authors":"Leanne Tamm , Jonathan A. Dudley , Sarah L. Karalunas , John O. Simon , Thomas C. Maloney , Gowtham Atluri , Jeffery N. Epstein","doi":"10.1016/j.ynirp.2025.100263","DOIUrl":null,"url":null,"abstract":"<div><div>Patients with ADHD evidence elevated reaction time variability (RTV) due to periodic long reaction times (RTs). Even though reaction time variability (RTV) reflects intraindividual differences in RT across time, prior research exploring the neural basis of RTV in ADHD has primarily examined associations between neural activation and summary RTV outcomes (e.g., standard deviation of reaction time, tau). Here, we explore group differences in the neural basis of RTV by examining association between trial-level RTs and fMRI BOLD activation obtained during a Stop Signal Task in a large (<em>n</em> = 5719) sample of 9- to 10-year-old children participating in the Adolescent Brain Cognitive Development (ABCD) study. Children with ADHD demonstrated greater RTV than those without ADHD. ADHD-related group differences were not observed between fMRI BOLD activation and summary RTV outcomes. At the trial level, longer RTs were associated with increased BOLD activation in salience/ventral attention and executive control networks and decreased BOLD activation in the default mode network, consistent with time-on-task effects (i.e., stimulus processing time) in which long RTs require maintaining task-positive activation and DMN suppression for more time than short RTs. Moreover, children with ADHD showed weaker associations between long RTs and BOLD activation in these regions than children without ADHD supporting models that point to dysregulated competition between the DMN and executive network as mechanism of cognitive impairment in ADHD.</div></div>","PeriodicalId":74277,"journal":{"name":"Neuroimage. Reports","volume":"5 2","pages":"Article 100263"},"PeriodicalIF":0.0000,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroimage. Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666956025000315","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Neuroscience","Score":null,"Total":0}
引用次数: 0
Abstract
Patients with ADHD evidence elevated reaction time variability (RTV) due to periodic long reaction times (RTs). Even though reaction time variability (RTV) reflects intraindividual differences in RT across time, prior research exploring the neural basis of RTV in ADHD has primarily examined associations between neural activation and summary RTV outcomes (e.g., standard deviation of reaction time, tau). Here, we explore group differences in the neural basis of RTV by examining association between trial-level RTs and fMRI BOLD activation obtained during a Stop Signal Task in a large (n = 5719) sample of 9- to 10-year-old children participating in the Adolescent Brain Cognitive Development (ABCD) study. Children with ADHD demonstrated greater RTV than those without ADHD. ADHD-related group differences were not observed between fMRI BOLD activation and summary RTV outcomes. At the trial level, longer RTs were associated with increased BOLD activation in salience/ventral attention and executive control networks and decreased BOLD activation in the default mode network, consistent with time-on-task effects (i.e., stimulus processing time) in which long RTs require maintaining task-positive activation and DMN suppression for more time than short RTs. Moreover, children with ADHD showed weaker associations between long RTs and BOLD activation in these regions than children without ADHD supporting models that point to dysregulated competition between the DMN and executive network as mechanism of cognitive impairment in ADHD.