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Neurocognitive markers of late‐onset ADHD: a 6‐year longitudinal study
Author(s) -
Ilbegi Shahrzad,
Buitelaar Jan K.,
Hoekstra Pieter J.,
Hartman Catharina A.,
Franke Barbara,
Faraone Stephen V.,
Oosterlaan Jaap,
Luman Marjolein,
Lieshout Marloes,
Rommelse Nanda N.J.
Publication year - 2021
Publication title -
journal of child psychology and psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.652
H-Index - 211
eISSN - 1469-7610
pISSN - 0021-9630
DOI - 10.1111/jcpp.13272
Subject(s) - neurocognitive , psychology , attention deficit hyperactivity disorder , longitudinal study , el niño , sibling , cognition , developmental psychology , clinical psychology , psychiatry , audiology , pediatrics , medicine , pathology
Background There is an increased interest in ‘late‐onset’ attention‐deficit/hyperactivity disorder (ADHD), referring to the onset of clinically significant ADHD symptoms after the age of 12 years. This study aimed to examine whether unaffected siblings with late‐onset ADHD could be differentiated from stable unaffected siblings by their neurocognitive functioning in childhood. Methods We report findings from a 6‐year prospective, longitudinal study of the Dutch part of the International Multicenter ADHD Genetics (IMAGE) study, including individuals with childhood‐onset (persistent) ADHD ( n = 193), their siblings with late‐onset ADHD ( n = 34), their stable unaffected siblings ( n = 111) and healthy controls ( n = 186). At study entry (mean age: 11.3) and follow‐up (mean age: 17.01), participants were assessed for ADHD by structured psychiatric interviews and multi‐informant questionnaires. Several neurocognitive functions were assessed at baseline and after 6 years, including time reproduction, timing variability (reaction time variability and time production variability), reaction time speed, motor control and working memory; intelligence was taken as a measure of overall neurocognitive functioning. Results Siblings with late‐onset ADHD were similar to individuals with childhood‐onset ADHD in showing longer reaction times and/or higher error rates on all neurocognitive measures at baseline and follow‐up, when compared to healthy controls. They differed from stable unaffected siblings (who were similar to healthy controls) by greater reaction time variability and timing production variability at baseline. No significant group by time interaction was found for any of the tasks. Conclusions For unaffected siblings of individuals with ADHD, reaction time variability and timing production variability may serve as neurocognitive marker for late‐onset ADHD.