These findings suggest that a smaller prefrontal cortex is associated with early-onset drinking in individuals with comorbid mental disorders. Further studies are warranted to examine if a smaller prefrontal cortex represents a vulnerability to, or a consequence of, early-onset drinking.

While adolescent alcohol consumption has been asserted to adversely alter brain development, research in human adolescents has not yet provided us with sufficient evidence to support or refute this position. Brain constituents actively developing during adolescence include the prefrontal cortex, limbic system areas, and white matter myelin. These areas serving cognitive, behavioral, and emotional regulation may be particularly vulnerable to adverse alcohol effects. Alternatively, deficits or developmental delays in these structures and their functions may underlie liability to accelerated alcohol use trajectories in adolescence. This review will describe a conceptual framework for considering these relationships and summarize the available studies on the relationships among risk characteristics, alcohol involvement and brain development during this period. The cross-sectional designs and small samples characterizing available studies hamper definitive conclusions. This article will describe some of the opportunities contemporary neuroimaging techniques offer for advancing understanding of adolescent neurodevelopment and alcohol involvement.

Aims Adolescents with substance use disorders (SUD) have difficulties with cognitive, behavioral and affective regulation. White matter (WM) disorganization has been observed in adolescents with SUD and may be related to psychological dysregulation. This study compared adolescents with SUD and control adolescents to investigate relationships among psychological dysregulation, WM disorganization, and SUD symptoms. Design Cross-sectional observation. Setting Adolescents with SUD were recruited from SUD treatment programs. Controls were recruited from the community. Participants The 55 participants were ages 14–19; 35 with SUD, 20 controls without SUD. Measurements Psychological dysregulation was characterized by the Behavior Rating Inventory of Executive Function. WM disorganization was measured by diffusion tensor imaging, and fractional anisotropy, radial diffusivity and axial diffusivity were examined within cortical regions of interest. Findings Compared to controls, SUD adolescents showed significantly greater psychological dysregulation and prefrontal and parietal WM disorganization. WM disorganization was positively correlated with psychological dysregulation and cannabis-related symptoms. In multivariate mediation models, the results were consistent with both the Neurodevelopmental Immaturity model, in which WM disorganization leads to psychological dysregulation and cannabis-related symptoms, and with the Substance Effects Model, in which cannabis-related symptoms lead to WM disorganization and psychological dysregulation. Conclusions In adolescents, substance use disorder and psychological dysregulation appear to be associated with reduced frontoparietal network white matter maturation.

Child abuse predicted persistently elevated health-related symptoms primarily attributable to anxiety, and early signs of liver disease were attributable to AUD.

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