Distinguishing Adolescents With ADHD From Their Unaffected Siblings and Healthy Comparison Subjects by Neural Activation Patterns During Response Inhibition
Dysfunctional response inhibition is a key executive function impairment in attention deficit hyperactivity disorder (ADHD). Still, behavioral response inhibition measures do not consistently differentiate affected from unaffected individuals. The authors therefore investigated neural correlates of...
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| Veröffentlicht in: | The American journal of psychiatry Jg. 172; H. 7; S. 674 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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01.07.2015
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| ISSN: | 1535-7228, 1535-7228 |
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| Abstract | Dysfunctional response inhibition is a key executive function impairment in attention deficit hyperactivity disorder (ADHD). Still, behavioral response inhibition measures do not consistently differentiate affected from unaffected individuals. The authors therefore investigated neural correlates of response inhibition and the familial nature of these neural correlates.
Functional MRI measurements of neural activation during the stop-signal task and behavioral measures of response inhibition were obtained in adolescents and young adults with ADHD (N=185), their unaffected siblings (N=111), and healthy comparison subjects (N=124).
Stop-signal task reaction times were longer and error rates were higher in participants with ADHD, but not in their unaffected siblings, while reaction time variability was higher in both groups than in comparison subjects. Relative to comparison subjects, participants with ADHD and unaffected siblings had neural hypoactivation in frontal-striatal and frontal-parietal networks, whereby activation in inferior frontal and temporal/parietal nodes in unaffected siblings was intermediate between levels of participants with ADHD and comparison subjects. Furthermore, neural activation in inferior frontal nodes correlated with stop-signal reaction times, and activation in both inferior frontal and temporal/parietal nodes correlated with ADHD severity.
Neural activation alterations in ADHD are more robust than behavioral response inhibition deficits and explain variance in response inhibition and ADHD severity. Although only affected participants with ADHD have deficient response inhibition, hypoactivation in inferior frontal and temporal-parietal nodes in unaffected siblings supports the familial nature of the underlying neural process. Activation deficits in these nodes may be useful as endophenotypes that extend beyond the affected individuals in the family. |
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| AbstractList | Dysfunctional response inhibition is a key executive function impairment in attention deficit hyperactivity disorder (ADHD). Still, behavioral response inhibition measures do not consistently differentiate affected from unaffected individuals. The authors therefore investigated neural correlates of response inhibition and the familial nature of these neural correlates.OBJECTIVEDysfunctional response inhibition is a key executive function impairment in attention deficit hyperactivity disorder (ADHD). Still, behavioral response inhibition measures do not consistently differentiate affected from unaffected individuals. The authors therefore investigated neural correlates of response inhibition and the familial nature of these neural correlates.Functional MRI measurements of neural activation during the stop-signal task and behavioral measures of response inhibition were obtained in adolescents and young adults with ADHD (N=185), their unaffected siblings (N=111), and healthy comparison subjects (N=124).METHODSFunctional MRI measurements of neural activation during the stop-signal task and behavioral measures of response inhibition were obtained in adolescents and young adults with ADHD (N=185), their unaffected siblings (N=111), and healthy comparison subjects (N=124).Stop-signal task reaction times were longer and error rates were higher in participants with ADHD, but not in their unaffected siblings, while reaction time variability was higher in both groups than in comparison subjects. Relative to comparison subjects, participants with ADHD and unaffected siblings had neural hypoactivation in frontal-striatal and frontal-parietal networks, whereby activation in inferior frontal and temporal/parietal nodes in unaffected siblings was intermediate between levels of participants with ADHD and comparison subjects. Furthermore, neural activation in inferior frontal nodes correlated with stop-signal reaction times, and activation in both inferior frontal and temporal/parietal nodes correlated with ADHD severity.RESULTSStop-signal task reaction times were longer and error rates were higher in participants with ADHD, but not in their unaffected siblings, while reaction time variability was higher in both groups than in comparison subjects. Relative to comparison subjects, participants with ADHD and unaffected siblings had neural hypoactivation in frontal-striatal and frontal-parietal networks, whereby activation in inferior frontal and temporal/parietal nodes in unaffected siblings was intermediate between levels of participants with ADHD and comparison subjects. Furthermore, neural activation in inferior frontal nodes correlated with stop-signal reaction times, and activation in both inferior frontal and temporal/parietal nodes correlated with ADHD severity.Neural activation alterations in ADHD are more robust than behavioral response inhibition deficits and explain variance in response inhibition and ADHD severity. Although only affected participants with ADHD have deficient response inhibition, hypoactivation in inferior frontal and temporal-parietal nodes in unaffected siblings supports the familial nature of the underlying neural process. Activation deficits in these nodes may be useful as endophenotypes that extend beyond the affected individuals in the family.CONCLUSIONSNeural activation alterations in ADHD are more robust than behavioral response inhibition deficits and explain variance in response inhibition and ADHD severity. Although only affected participants with ADHD have deficient response inhibition, hypoactivation in inferior frontal and temporal-parietal nodes in unaffected siblings supports the familial nature of the underlying neural process. Activation deficits in these nodes may be useful as endophenotypes that extend beyond the affected individuals in the family. Dysfunctional response inhibition is a key executive function impairment in attention deficit hyperactivity disorder (ADHD). Still, behavioral response inhibition measures do not consistently differentiate affected from unaffected individuals. The authors therefore investigated neural correlates of response inhibition and the familial nature of these neural correlates. Functional MRI measurements of neural activation during the stop-signal task and behavioral measures of response inhibition were obtained in adolescents and young adults with ADHD (N=185), their unaffected siblings (N=111), and healthy comparison subjects (N=124). Stop-signal task reaction times were longer and error rates were higher in participants with ADHD, but not in their unaffected siblings, while reaction time variability was higher in both groups than in comparison subjects. Relative to comparison subjects, participants with ADHD and unaffected siblings had neural hypoactivation in frontal-striatal and frontal-parietal networks, whereby activation in inferior frontal and temporal/parietal nodes in unaffected siblings was intermediate between levels of participants with ADHD and comparison subjects. Furthermore, neural activation in inferior frontal nodes correlated with stop-signal reaction times, and activation in both inferior frontal and temporal/parietal nodes correlated with ADHD severity. Neural activation alterations in ADHD are more robust than behavioral response inhibition deficits and explain variance in response inhibition and ADHD severity. Although only affected participants with ADHD have deficient response inhibition, hypoactivation in inferior frontal and temporal-parietal nodes in unaffected siblings supports the familial nature of the underlying neural process. Activation deficits in these nodes may be useful as endophenotypes that extend beyond the affected individuals in the family. |
| Author | Buitelaar, Jan K Hoekstra, Pieter J Mennes, Maarten Heslenfeld, Dirk van Rooij, Daan Faraone, Stephen V Oosterlaan, Jaap Hartman, Catharina A Franke, Barbara von Rhein, Daniel Thissen, Andrieke J A M Zwiers, Marcel P Rommelse, Nanda |
| Author_xml | – sequence: 1 givenname: Daan surname: van Rooij fullname: van Rooij, Daan organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 2 givenname: Pieter J surname: Hoekstra fullname: Hoekstra, Pieter J organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 3 givenname: Maarten surname: Mennes fullname: Mennes, Maarten organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 4 givenname: Daniel surname: von Rhein fullname: von Rhein, Daniel organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 5 givenname: Andrieke J A M surname: Thissen fullname: Thissen, Andrieke J A M organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 6 givenname: Dirk surname: Heslenfeld fullname: Heslenfeld, Dirk organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 7 givenname: Marcel P surname: Zwiers fullname: Zwiers, Marcel P organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 8 givenname: Stephen V surname: Faraone fullname: Faraone, Stephen V organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 9 givenname: Jaap surname: Oosterlaan fullname: Oosterlaan, Jaap organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 10 givenname: Barbara surname: Franke fullname: Franke, Barbara organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 11 givenname: Nanda surname: Rommelse fullname: Rommelse, Nanda organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 12 givenname: Jan K surname: Buitelaar fullname: Buitelaar, Jan K organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y – sequence: 13 givenname: Catharina A surname: Hartman fullname: Hartman, Catharina A organization: From the Department of Psychiatry, University Medical Center, University of Groningen, Groningen, the Netherlands; the Department of Cognitive Neuroscience, the Department of Psychiatry, and the Department of Human Genetics, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Center, Nijmegen, the Netherlands; Karakter Child and Adolescent Psychiatry University Center Nijmegen, Nijmegen, the Netherlands; the Department of Psychology, VU University Amsterdam, Amsterdam, the Netherlands; and the Department of Psychiatry and the Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, N.Y |
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| Snippet | Dysfunctional response inhibition is a key executive function impairment in attention deficit hyperactivity disorder (ADHD). Still, behavioral response... |
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| SubjectTerms | Adolescent Attention - physiology Attention Deficit Disorder with Hyperactivity - diagnosis Attention Deficit Disorder with Hyperactivity - genetics Attention Deficit Disorder with Hyperactivity - physiopathology Brain Mapping Cerebral Cortex - physiopathology Executive Function Female Follow-Up Studies Humans Impulsive Behavior - physiology Inhibition (Psychology) Magnetic Resonance Imaging Male Neuropsychological Tests Psychomotor Performance - physiology Reaction Time - physiology Reference Values |
| Title | Distinguishing Adolescents With ADHD From Their Unaffected Siblings and Healthy Comparison Subjects by Neural Activation Patterns During Response Inhibition |
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