Neural reward processing among children with conduct disorder and mild traumatic brain injury in the ABCD study

Conduct disorder and childhood head injuries frequently co-occur and are linked to a higher risk of later delinquency. While both are known to disrupt reward-related neural circuits, this study investigated whether their combined presence leads to a unique disruption in these pathways, potentially accounting for the increased risk of delinquency.

Using neuroimaging data from the baseline (age 9-10) assessment from the Adolescent Brain and Cognitive Development (ABCD) study, four groups were compared: children with conduct disorder (CD, n = 588), a mild traumatic brain injury (mTBI, n = 1,216), both (mTBI+CD, n = 252), and typically developing controls (TD, n = 705). Neural activation in eight regions of interest (amygdala, hippocampus, nucleus accumbens, caudal anterior cingulate cortex, rostral anterior cingulate cortex, medial orbitofrontal cortex, thalamus, and insula) during reward anticipation and receipt were assessed during the monetary incentive delay task.

After controlling for several covariates, including sex, ADHD, and internalizing problems, the mTBI+CD group displayed greater left amygdala and hippocampal activation during reward receipt compared to all other groups. While they displayed increased activation in the right hippocampus and thalamus compared to TD controls and the right hippocampus compared to the mTBI group, they did not differ from the CD group. No group differences emerged during reward anticipation.

Increased left amygdala and hippocampus activation in children with conduct disorder and a history of mild traumatic brain injury may reflect robust encoding of emotionally charged reward experiences, potentially reinforcing memory-guided, reward-seeking behaviors.