Disruptive Behavior Problems, Callous-Unemotional Traits, and Regional Gray Matter Volume in the Adolescent Brain and Cognitive Development Study

Waller R, Hawes SW, Byrd AL, Dick AS, Sutherland MT, Riedel MC, Tobia MJ, Bottenhorn KL, Laird AR, Gonzalez R, Biol Psychiatry Cogn Neurosci Neuroimaging (2020).

Abstract

BACKGROUND: Neurobiological differences linked to socioemotional and cognitive processing are well documented in youths with disruptive behavior disorders (DBDs), especially youths with callous-unemotional (CU) traits. The current study expanded this literature by examining gray matter volume (GMV) differences among youths with DBD with CU traits (DBDCU+), youths with DBD without CU traits (DBD-only), and youths that were typically developing (TD). METHODS: Data were from the first full sample release of the Adolescent Brain and Cognitive Development Study (mean age = 9.49 years; 49% female). We tested whether the GMVs of 11 regions of interest selected a priori differentiated between our 3 groups: DBDCU+ (n = 288), DBD-only (n = 362), and TD (n = 915). Models accounted for demographic confounders, attention-deficit/hyperactivity disorder, and intracranial volume. We examined two potential moderators of the relationship between GMVs and group membership: sex and clinically significant anxiety (i.e., primary vs. secondary CU traits subtype). RESULTS: Youths in the DBDCU+ group had lower right amygdala GMV, and youths in the DBD-only group had lower bilateral amygdala GMV relative to TD youths. Youths in the DBDCU+ group had lower bilateral hippocampal GMV, and youths in the DBD-only group had lower left hippocampal GMV relative to TD youths. Youths in the DBDCU+ group evidenced lower left insula GMV relative to TD youths. Finally, youths in the DBD-only group had lower left superior frontal gyrus and lower right caudal anterior cingulate cortex GMVs relative to TD youths. There was no moderation of associations between GMV and group membership by sex. CONCLUSIONS: Our findings implicate structural aberrations in both the amygdala and hippocampus in the etiology of DBDs, with minimal evidence for differences based on the presence or absence of CU traits.