Philadelphia, August 13, 2018 - According to a study in Biological Psychiatry, physical brain injury in children contributes to the development of attention-deficit/hyperactivity disorder (ADHD), distinct from genetic risk for the disorder.
In the study, youth who reported ADHD symptoms and had a history of mild traumatic brain injury (TBI), such as a concussion, did not have an increased genetic risk for the disorder. This is in contrast to developmental ADHD, which is caused in part by the small cumulative effects of multiple ADHD-related genes.
"This article suggests that there are at least two forms of ADHD. One that is an expression of a risk inherited within families and the other which develops after traumatic brain injury," said John Krystal, MD, Editor of Biological Psychiatry. "The latter is of particular interest in light of the growing evidence that contact sports and combat are associated with higher rates of traumatic brain injury than we previously recognized," he added.
"Mild traumatic brain injury (which includes concussion) is very common in adolescents; epidemiological data show that approximately 1 in 5 report a previous mild traumatic brain injury," said senior author Anne Wheeler, PhD, of SickKids Research Institute and University of Toronto, Canada. This rate is alarming considering that as many as 50 percent of children develop ADHD symptoms soon after the injury. Although symptoms resolve over time in most children, others convert to a diagnosis of ADHD.
In the study, first author Sonja Stojanovski, a doctoral student in Dr. Wheeler's laboratory, and colleagues compared the origins of ADHD symptoms in 418 youth with a history of TBI and 3,193 with no TBI, all of whom were between 8 and 22 years old. Genetic risk score was associated with increased ADHD symptom severity, but only in youth without TBI. There was no association in those with TBI, meaning that genetic predisposition does not appear to make children more vulnerable to developing ADHD after brain injury.
The researchers also looked for hallmark abnormalities in brain structure associated with the disorder. The association between volumes of ADHD-related brain structures and ADHD symptom severity was similar between the two groups. However, an analysis of the connections bridging the two brain hemispheres revealed opposite relationships with ADHD symptoms between the groups. The structural findings indicate the presence of both similar and distinct neural mechanisms that cause ADHD after TBI.
"When thinking about treating youth with ADHD it is important to understand what the underlying causes are and how they may differ from person to person to move towards a personalized medicine approach," said Dr. Wheeler. According to the findings of this study, this personalized approach may be based on whether a patient has experienced TBI.
###
Notes for editors
The article is "Polygenic Risk and Neural Substrates of Attention-Deficit/Hyperactivity Disorder Symptoms in Youth with a History of Mild Traumatic Brain Injury," by Sonja Stojanovski, Daniel Felsky, Joseph Viviano, Saba Shahab, Rutwik Bangali, Christie Burton, Gabriel A. Devenyi, Lauren J. O'Donnell, Peter Szatmari, M. Mallar Chakravarty, Stephanie Ameis, Russell Schachar, Aristotle N. Voineskos, and Anne L. Wheeler (https://doi.org/10.1016/j.biopsych.2018.06.024). It appears in Biological Psychiatry , published by Elsevier.
Copies of this paper are available to credentialed journalists upon request; please contact Rhiannon Bugno at Biol.Psych@UTSouthwestern.edu or +1 214 648 0880. Journalists wishing to interview the authors may contact Anne Wheeler at anne.wheeler@sickkids.ca or +1 416 813 7654 ext 309585.
The authors' affiliations and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, MD, is Chairman of the Department of Psychiatry at the Yale University School of Medicine, Chief of Psychiatry at Yale-New Haven Hospital, and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
About Biological Psychiatry
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 6th out of 142 Psychiatry titles and 9th out of 261 Neurosciences titles in the Journal Citations Reports® published by Thomson Reuters. The 2017 Impact Factor score for Biological Psychiatry is 11.982. http://www.biologicalpsychiatryjournal.com
About Elsevier
Elsevier is a global information analytics business that helps institutions and professionals advance healthcare, open science and improve performance for the benefit of humanity. Elsevier provides digital solutions and tools in the areas of strategic research management, R&D performance, clinical decision support and professional education, including ScienceDirect, Scopus, SciVal, ClinicalKey and Sherpath. Elsevier publishes over 2,500 digitized journals, including The Lancet and Cell, more than 38,000 e-book titles and many iconic reference works, including Gray's Anatomy. Elsevier is part of RELX Group, a global provider of information and analytics for professionals and business customers across industries. http://www.elsevier.com
Media contact
Rhiannon Bugno, Editorial Office
Biological Psychiatry
+1 214 648 0880
Biol.Psych@UTSouthwestern.edu
Journal
Biological Psychiatry