Study findings published in Biological Psychiatry showed that youth with history of traumatic brain injury reported greater ADHD symptom severity than those without injury.
Researchers also found that an increased genetic risk for ADHD was not associated with ADHD symptoms after a mild traumatic brain injury (TBI).
“While there are some established psychosocial premorbid risk factors for the development of ADHD post-TBI, to date it is not clear whether genetic risk for ADHD contributes to risk of developing ADHD following TBI and whether the neural substrates associated with ADHD symptoms are the same or different when a TBI has occurred,” Sonja Stojanovski, BS, from the neuroscience and mental health program at the Hospital for Sick Children, Toronto, and colleagues wrote.
The researchers examined whether ADHD symptoms were associated with genetic risk and brain structure among individuals aged 8 to 22 years with (n = 418) and without (n = 3,193) a history of TBI enrolled in a population-based study using medical history, ADHD symptoms, and genetic and neuroimaging data. To evaluate the connections between TBI history, genetic vulnerability, brain structure and ADHD symptoms, researchers examined:
- ADHD polygenic score in a discovery sample of those with ADHD (n = 19,099) and a control sample (n = 34,194);
- basal ganglia volumes; and
- fractional anisotropy in the corpus callosum and corona radiata.
The results indicated that when ADHD symptoms occur in conjunction with mild TBI, established genetic risk for ADHD might not be an important risk factor. Participants with mild TBI reported higher ADHD symptom severity than those without TBI (P = .002). Analysis showed that polygenic score was positively linked to ADHD symptoms in youths without TBI, but not in those with TBI.
The researchers also observed caudate volume was negatively associated with number of ADHD symptoms regardless of TBI history; however, the link between ADHD symptoms and structure of the genu of the corpus callosum was negative in the participants with TBI and positive in those without TBI. Furthermore, TBI history did not impact the link between basal ganglia volumes and ADHD symptoms.
The findings suggest that physical insult to the brain and resulting changes may contribute to the presentation of post-TBI ADHD symptoms in those with TBI, while genetic predisposition impacts developmentally acquired ADHD, Stojanozski and colleagues wrote.
“The identification of characteristic ADHD etiology in youths with a history of TBI is a first step toward understanding neurobiological and clinical heterogeneity, which will ideally pave the way for the development of tailored interventions that may differ among youths with ADHD, informed by presence or absence of TBI history,” the authors wrote. “Replication of these results in a comparable dataset will be an important next step.” – by Savannah Demko
Disclosure: Stojanovski reports no relevant financial disclosures.