Sonja Stojanovski1, Daniel Felsky2, Joseph D Viviano3, Saba Shahab4, Rutwik Bangali3, Christie L Burton5, Gabriel A Devenyi6, Lauren J O'Donnell7, Peter Szatmari8, M Mallar Chakravarty9, Stephanie Ameis8, Russell Schachar10, Aristotle N Voineskos11, Anne L Wheeler12. 1. Neuroscience and Mental Health Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Physiology, University of Toronto, Toronto, Ontario, Canada. 2. Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Center for Translational and Computational Neuroimmunology, Department of Neurology, Columbia University Medical Center, New York; Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Cambridge, Massachusetts. 3. Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. 4. Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. 5. Neuroscience and Mental Health Program, Hospital for Sick Children, Toronto, Ontario, Canada. 6. Cerebral Imaging Centre, Douglas Institute, Montreal, Quebec, Canada; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. 7. Department of Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. 8. Neuroscience and Mental Health Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada; The Margaret and Wallace McCain Centre for Child, Youth and Family Mental Health, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. 9. Cerebral Imaging Centre, Douglas Institute, Montreal, Quebec, Canada; Department of Biomedical Engineering, McGill University, Montreal, Quebec, Canada; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. 10. Neuroscience and Mental Health Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada. 11. Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada; Campbell Family Mental Health Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada. 12. Neuroscience and Mental Health Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Physiology, University of Toronto, Toronto, Ontario, Canada. Electronic address: anne.wheeler@sickkids.ca.
Abstract
BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is a major sequela of traumatic brain injury (TBI) in youths. The objective of this study was to examine whether ADHD symptoms are differentially associated with genetic risk and brain structure in youths with and without a history of TBI. METHODS: Medical history, ADHD symptoms, genetic data, and neuroimaging data were obtained from a community sample of youths. ADHD symptom severity was compared between those with and without TBI (TBI n = 418, no TBI n = 3193). The relationship of TBI history, genetic vulnerability, brain structure, and ADHD symptoms was examined by assessing 1) ADHD polygenic score (discovery sample ADHD n = 19,099, control sample n = 34,194), 2) basal ganglia volumes, and 3) fractional anisotropy in the corpus callosum and corona radiata. RESULTS: Youths with TBI reported greater ADHD symptom severity compared with those without TBI. Polygenic score was positively associated with ADHD symptoms in youths without TBI but not in youths with TBI. The negative association between the caudate volume and ADHD symptoms was not moderated by a history of TBI. However, the relationship between ADHD symptoms and structure of the genu of the corpus callosum was negative in youths with TBI and positive in youths without TBI. CONCLUSIONS: The identification of distinct ADHD etiology in youths with TBI provides neurobiological insight into the clinical heterogeneity in the disorder. Results indicate that genetic predisposition to ADHD does not increase the risk for ADHD symptoms associated with TBI. ADHD symptoms associated with TBI may be a result of a mechanical insult rather than neurodevelopmental factors.
BACKGROUND:Attention-deficit/hyperactivity disorder (ADHD) is a major sequela of traumatic brain injury (TBI) in youths. The objective of this study was to examine whether ADHD symptoms are differentially associated with genetic risk and brain structure in youths with and without a history of TBI. METHODS: Medical history, ADHD symptoms, genetic data, and neuroimaging data were obtained from a community sample of youths. ADHD symptom severity was compared between those with and without TBI (TBI n = 418, no TBI n = 3193). The relationship of TBI history, genetic vulnerability, brain structure, and ADHD symptoms was examined by assessing 1) ADHD polygenic score (discovery sample ADHD n = 19,099, control sample n = 34,194), 2) basal ganglia volumes, and 3) fractional anisotropy in the corpus callosum and corona radiata. RESULTS: Youths with TBI reported greater ADHD symptom severity compared with those without TBI. Polygenic score was positively associated with ADHD symptoms in youths without TBI but not in youths with TBI. The negative association between the caudate volume and ADHD symptoms was not moderated by a history of TBI. However, the relationship between ADHD symptoms and structure of the genu of the corpus callosum was negative in youths with TBI and positive in youths without TBI. CONCLUSIONS: The identification of distinct ADHD etiology in youths with TBI provides neurobiological insight into the clinical heterogeneity in the disorder. Results indicate that genetic predisposition to ADHD does not increase the risk for ADHD symptoms associated with TBI. ADHD symptoms associated with TBI may be a result of a mechanical insult rather than neurodevelopmental factors.
Authors: Guido I Guberman; Sonja Stojanovski; Eman Nishat; Alain Ptito; Danilo Bzdok; Anne L Wheeler; Maxime Descoteaux Journal: Elife Date: 2022-05-17 Impact factor: 8.713
Authors: Michael A Mooney; Priya Bhatt; Robert J M Hermosillo; Peter Ryabinin; Molly Nikolas; Stephen V Faraone; Damien A Fair; Beth Wilmot; Joel T Nigg Journal: Psychol Med Date: 2020-01-24 Impact factor: 7.723
Authors: Stephen V Faraone; Tobias Banaschewski; David Coghill; Yi Zheng; Joseph Biederman; Mark A Bellgrove; Jeffrey H Newcorn; Martin Gignac; Nouf M Al Saud; Iris Manor; Luis Augusto Rohde; Li Yang; Samuele Cortese; Doron Almagor; Mark A Stein; Turki H Albatti; Haya F Aljoudi; Mohammed M J Alqahtani; Philip Asherson; Lukoye Atwoli; Sven Bölte; Jan K Buitelaar; Cleo L Crunelle; David Daley; Søren Dalsgaard; Manfred Döpfner; Stacey Espinet; Michael Fitzgerald; Barbara Franke; Manfred Gerlach; Jan Haavik; Catharina A Hartman; Cynthia M Hartung; Stephen P Hinshaw; Pieter J Hoekstra; Chris Hollis; Scott H Kollins; J J Sandra Kooij; Jonna Kuntsi; Henrik Larsson; Tingyu Li; Jing Liu; Eugene Merzon; Gregory Mattingly; Paulo Mattos; Suzanne McCarthy; Amori Yee Mikami; Brooke S G Molina; Joel T Nigg; Diane Purper-Ouakil; Olayinka O Omigbodun; Guilherme V Polanczyk; Yehuda Pollak; Alison S Poulton; Ravi Philip Rajkumar; Andrew Reding; Andreas Reif; Katya Rubia; Julia Rucklidge; Marcel Romanos; J Antoni Ramos-Quiroga; Arnt Schellekens; Anouk Scheres; Renata Schoeman; Julie B Schweitzer; Henal Shah; Mary V Solanto; Edmund Sonuga-Barke; César Soutullo; Hans-Christoph Steinhausen; James M Swanson; Anita Thapar; Gail Tripp; Geurt van de Glind; Wim van den Brink; Saskia Van der Oord; Andre Venter; Benedetto Vitiello; Susanne Walitza; Yufeng Wang Journal: Neurosci Biobehav Rev Date: 2021-02-04 Impact factor: 9.052