Structural network communication differences in drug-naive depressed adolescents with non-suicidal self-injury and suicide attempts.

Background: Depression, non-suicidal self-injury (NSSI), and suicide attempts (SA) often co-occur during adolescence and are associated with long-term adverse health outcomes. Unfortunately, neural mechanisms underlying self-injury and SA are poorly understood in depressed adolescents but likely relate to the structural abnormalities in brain regions.

Aim: To investigate structural network communication within large-scale brain networks in adolescents with depression.

Methods: We constructed five distinct network communication models to evaluate structural network efficiency at the whole-brain level in adolescents with depression. Diffusion magnetic resonance imaging data were acquired from 32 healthy controls and 85 depressed adolescents, including 17 depressed adolescents without SA or NSSI (major depressive disorder group), 27 depressed adolescents with NSSI but no SA (NSSI group), and 41 depressed adolescents with SA and NSSI (NSSI + SA group).

Results: Significant differences in structural network communication were observed across the four groups, involving spatially widespread brain regions, particularly encompassing cortico-cortical connections (e.g., dorsal posterior cingulate gyrus and the right ventral posterior cingulate gyrus; connections based on precentral gyrus) and cortico-subcortical circuits (e.g., the nucleus accumbens-frontal circuit). In addition, we examined whether compromised communication efficiency was linked to clinical symptoms in the depressed adolescents. We observed significant correlations between network communication efficiencies and clinical scale scores derived from depressed adolescents with NSSI and SA.

Conclusion: This study provides evidence of structural network communication differences in depressed adolescents with NSSI and SA, highlighting impaired neuroanatomical communication efficiency as a potential contributor to their symptoms. These findings offer new insights into the pathophysiological mechanisms underlying the comorbidity of NSSI and SA in adolescent depression.