Siri D S Noordermeer1, Marjolein Luman2, Corina U Greven3, Kim Veroude4, Stephen V Faraone5, Catharina A Hartman6, Pieter J Hoekstra6, Barbara Franke7, Jan K Buitelaar8, Dirk J Heslenfeld2, Jaap Oosterlaan2. 1. Section of Clinical Neuropsychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. Electronic address: s.d.s.noordermeer@vu.nl. 2. Section of Clinical Neuropsychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. 3. Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands; Karakter Child and Adolescent Psychiatry University Center, Nijmegen, The Netherlands; Medical Research Council Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom. 4. Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands. 5. Departments of Psychiatry and Neuroscience and Physiology, State University of New York Upstate Medical University, Syracuse, New York; K.G. Jebsen Center, Bergen, Norway. 6. Department of Psychiatry, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. 7. Department of Human Genetics and Psychiatry, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands. 8. Department of Cognitive Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands; Karakter Child and Adolescent Psychiatry University Center, Nijmegen, The Netherlands.
Abstract
BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is associated with structural abnormalities in total gray matter, basal ganglia, and cerebellum. Findings of structural abnormalities in frontal and temporal lobes, amygdala, and insula are less consistent. Remarkably, the impact of comorbid oppositional defiant disorder (ODD) (comorbidity rates up to 60%) on these neuroanatomical differences is scarcely studied, while ODD (in combination with conduct disorder) has been associated with structural abnormalities of the frontal lobe, amygdala, and insula. The aim of this study was to investigate the effect of comorbid ODD on cerebral volume and cortical thickness in ADHD. METHODS: Three groups, 16 ± 3.5 years of age (mean ± SD; range 7-29 years), were studied on volumetric and cortical thickness characteristics using structural magnetic resonance imaging (surface-based morphometry): ADHD+ODD (n = 67), ADHD-only (n = 243), and control subjects (n = 233). Analyses included the moderators age, gender, IQ, and scan site. RESULTS: ADHD+ODD and ADHD-only showed volumetric reductions in total gray matter and (mainly) frontal brain areas. Stepwise volumetric reductions (ADHD+ODD < ADHD-only < control subjects) were found for mainly frontal regions, and ADHD+ODD was uniquely associated with reductions in several structures (e.g., the precuneus). In general, findings remained significant after accounting for ADHD symptom severity. There were no group differences in cortical thickness. Exploratory voxelwise analyses showed no group differences. CONCLUSIONS: ADHD+ODD and ADHD-only were associated with volumetric reductions in brain areas crucial for attention, (working) memory, and decision-making. Volumetric reductions of frontal lobes were largest in the ADHD+ODD group, possibly underlying observed larger impairments in neurocognitive functions. Previously reported striatal abnormalities in ADHD may be caused by comorbid conduct disorder rather than ODD.
BACKGROUND:Attention-deficit/hyperactivity disorder (ADHD) is associated with structural abnormalities in total gray matter, basal ganglia, and cerebellum. Findings of structural abnormalities in frontal and temporal lobes, amygdala, and insula are less consistent. Remarkably, the impact of comorbid oppositional defiant disorder (ODD) (comorbidity rates up to 60%) on these neuroanatomical differences is scarcely studied, while ODD (in combination with conduct disorder) has been associated with structural abnormalities of the frontal lobe, amygdala, and insula. The aim of this study was to investigate the effect of comorbid ODD on cerebral volume and cortical thickness in ADHD. METHODS: Three groups, 16 ± 3.5 years of age (mean ± SD; range 7-29 years), were studied on volumetric and cortical thickness characteristics using structural magnetic resonance imaging (surface-based morphometry): ADHD+ODD (n = 67), ADHD-only (n = 243), and control subjects (n = 233). Analyses included the moderators age, gender, IQ, and scan site. RESULTS:ADHD+ODD and ADHD-only showed volumetric reductions in total gray matter and (mainly) frontal brain areas. Stepwise volumetric reductions (ADHD+ODD < ADHD-only < control subjects) were found for mainly frontal regions, and ADHD+ODD was uniquely associated with reductions in several structures (e.g., the precuneus). In general, findings remained significant after accounting for ADHD symptom severity. There were no group differences in cortical thickness. Exploratory voxelwise analyses showed no group differences. CONCLUSIONS:ADHD+ODD and ADHD-only were associated with volumetric reductions in brain areas crucial for attention, (working) memory, and decision-making. Volumetric reductions of frontal lobes were largest in the ADHD+ODD group, possibly underlying observed larger impairments in neurocognitive functions. Previously reported striatal abnormalities in ADHD may be caused by comorbid conduct disorder rather than ODD.
Authors: Danielle S Kroll; Dana E Feldman; Szu-Yung Ariel Wang; Rui Zhang; Peter Manza; Corinde E Wiers; Nora D Volkow; Gene-Jack Wang Journal: J Neurol Sci Date: 2020-08-19 Impact factor: 3.181
Authors: Katyayani Singh; Mohan Jayaram; Maria Kaare; Este Leidmaa; Toomas Jagomäe; Indrek Heinla; Miriam A Hickey; Allen Kaasik; Michael K Schäfer; Jürgen Innos; Kersti Lilleväli; Mari-Anne Philips; Eero Vasar Journal: Sci Rep Date: 2019-04-01 Impact factor: 4.379