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Deficits in Cognitive Control, Timing and Reward Sensitivity Appear to be Dissociable in ADHD

Recent neurobiological models of ADHD suggest that deficits in different neurobiological pathways may independently lead to symptoms of this disorder. At least three independent pathways may be involved: a dorsal frontostriatal pathway involved in cognitive control, a ventral frontostriatal pathway...

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Autores principales: de Zeeuw, Patrick, Weusten, Juliette, van Dijk, Sarai, van Belle, Janna, Durston, Sarah
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3517570/
https://www.ncbi.nlm.nih.gov/pubmed/23236497
http://dx.doi.org/10.1371/journal.pone.0051416
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author de Zeeuw, Patrick
Weusten, Juliette
van Dijk, Sarai
van Belle, Janna
Durston, Sarah
author_facet de Zeeuw, Patrick
Weusten, Juliette
van Dijk, Sarai
van Belle, Janna
Durston, Sarah
author_sort de Zeeuw, Patrick
collection PubMed
description Recent neurobiological models of ADHD suggest that deficits in different neurobiological pathways may independently lead to symptoms of this disorder. At least three independent pathways may be involved: a dorsal frontostriatal pathway involved in cognitive control, a ventral frontostriatal pathway involved in reward processing and a frontocerebellar pathway related to temporal processing. Importantly, we and others have suggested that disruptions in these three pathways should lead to separable deficits at the cognitive level. Furthermore, if these truly represent separate biological pathways to ADHD, these cognitive deficits should segregate between individuals with ADHD. The present study tests these hypotheses in a sample of children, adolescents and young adults with ADHD and controls. 149 Subjects participated in a short computerized battery assessing cognitive control, timing and reward sensitivity. We used Principal Component Analysis to find independent components underlying the variance in the data. The segregation of deficits between individuals was tested using Loglinear Analysis. We found four components, three of which were predicted by the model: Cognitive control, reward sensitivity and timing. Furthermore, 80% of subjects with ADHD that had a deficit were deficient on only one component. Loglinear Analysis statistically confirmed the independent segregation of deficits between individuals. We therefore conclude that cognitive control, timing and reward sensitivity were separable at a cognitive level and that deficits on these components segregated between individuals with ADHD. These results support a neurobiological framework of separate biological pathways to ADHD with separable cognitive deficits.
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spelling pubmed-35175702012-12-12 Deficits in Cognitive Control, Timing and Reward Sensitivity Appear to be Dissociable in ADHD de Zeeuw, Patrick Weusten, Juliette van Dijk, Sarai van Belle, Janna Durston, Sarah PLoS One Research Article Recent neurobiological models of ADHD suggest that deficits in different neurobiological pathways may independently lead to symptoms of this disorder. At least three independent pathways may be involved: a dorsal frontostriatal pathway involved in cognitive control, a ventral frontostriatal pathway involved in reward processing and a frontocerebellar pathway related to temporal processing. Importantly, we and others have suggested that disruptions in these three pathways should lead to separable deficits at the cognitive level. Furthermore, if these truly represent separate biological pathways to ADHD, these cognitive deficits should segregate between individuals with ADHD. The present study tests these hypotheses in a sample of children, adolescents and young adults with ADHD and controls. 149 Subjects participated in a short computerized battery assessing cognitive control, timing and reward sensitivity. We used Principal Component Analysis to find independent components underlying the variance in the data. The segregation of deficits between individuals was tested using Loglinear Analysis. We found four components, three of which were predicted by the model: Cognitive control, reward sensitivity and timing. Furthermore, 80% of subjects with ADHD that had a deficit were deficient on only one component. Loglinear Analysis statistically confirmed the independent segregation of deficits between individuals. We therefore conclude that cognitive control, timing and reward sensitivity were separable at a cognitive level and that deficits on these components segregated between individuals with ADHD. These results support a neurobiological framework of separate biological pathways to ADHD with separable cognitive deficits. Public Library of Science 2012-12-07 /pmc/articles/PMC3517570/ /pubmed/23236497 http://dx.doi.org/10.1371/journal.pone.0051416 Text en © 2012 de Zeeuw et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
de Zeeuw, Patrick
Weusten, Juliette
van Dijk, Sarai
van Belle, Janna
Durston, Sarah
Deficits in Cognitive Control, Timing and Reward Sensitivity Appear to be Dissociable in ADHD
title Deficits in Cognitive Control, Timing and Reward Sensitivity Appear to be Dissociable in ADHD
title_full Deficits in Cognitive Control, Timing and Reward Sensitivity Appear to be Dissociable in ADHD
title_fullStr Deficits in Cognitive Control, Timing and Reward Sensitivity Appear to be Dissociable in ADHD
title_full_unstemmed Deficits in Cognitive Control, Timing and Reward Sensitivity Appear to be Dissociable in ADHD
title_short Deficits in Cognitive Control, Timing and Reward Sensitivity Appear to be Dissociable in ADHD
title_sort deficits in cognitive control, timing and reward sensitivity appear to be dissociable in adhd
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3517570/
https://www.ncbi.nlm.nih.gov/pubmed/23236497
http://dx.doi.org/10.1371/journal.pone.0051416
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