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Category: Analysis

Description: Depression is a common neuropsychiatric consequence of traumatic brain injury (TBI) in adults. An emerging literature suggests depression may also occur at increased rates in adolescents following a TBI. Separately, spontaneous depression—i.e., not acquired via brain injury—has been linked to aberrant responses to the anticipation or receipt of rewards in motivational neural circuitry, which can be normalized following the use of pharmacologic or neurostimulation-based treatments for depression. Recent trials have begun to examine the efficacy of these same treatments for depression in patients with TBI, but it remains unknown whether there are common or distinct neural bases of spontaneous versus acquired depression. Determining whether motivational neural circuit responses to rewards are affected in acquired depression is therefore a vital step to i) providing empirical support for the translation of existing evidence-based treatments for depression to adolescents with acquired depression following TBI, and ii) providing further support for this prospective biomarker for identifying and monitoring treatment-induced change in depression. In this Registered Report, we will use the Adolescent Brain Cognitive Development (ABCD) consortium dataset to test the overarching research question that a disruption in functional neural responses to rewards is present in patients with acquired depression after TBI. Notably, ABCD provides an unparalleled opportunity to examine the trajectory of neuropsychiatric symptoms and behavior problems longitudinally within adolescent subjects—i.e., we can isolate TBI-specific variance independent from premorbid functioning. Specifically, here we focus on a comparison between N=42 adolescents that experienced an mTBI between ABCD MRI imaging acquisition visits, and N=42 well-matched control participants. We will first test the hypothesis that there will be significant increases in pre-post-injury depressive symptoms in mTBI patients relative to controls. Second, we hypothesize that mTBI will be associated with blunted recruitment of motivational neural circuitry during the anticipation or receipt of incentives on the ABCD study’s Monetary Incentive Delay (MID) fMRI paradigm, specifically focusing on pre-post-injury changes in recruitment of striatum, anterior cingulate cortex (ACC), and anterior insula (aINS). Third, we will test the hypothesis that aberrant recruitment of these neural circuits during the MID paradigm mediates the impact of mTBI on depression in adolescence. The proposed Registered Report will provide critical evidence for the shared vs. distinct functional neural mechanisms driving neurodevelopmental vs acquired depression. Regardless of our findings these data will provide critical evidence regarding the current standard of care for depression following mTBI in adolescence.