These results suggest that fetal alcohol exposure should be considered a possible factor in the pathogenesis of childhood psychiatric disorders. These data provide clinically relevant information about the mental health problems that children with fetal alcohol exposure are likely to face.

BACKGROUND At least 60% of those treated for an alcohol use disorder will relapse. Empirical study of the integrity of the brain reward system (BRS) is critical to understanding the mechanisms of relapse as this collection of circuits is implicated in the development and maintenance of all forms of addictive disorders. This study compared thickness, surface area and volume in neocortical components of the BRS among non-smoking light drinking controls (Controls), individuals who remained abstinent and those who relapsed after treatment. METHODS Seventy-five treatment-seeking alcohol dependent individuals (abstinent for 7 ± 3 days) and 43 Controls completed 1.5T proton magnetic resonance imaging studies. Parcellated morphological data was obtained for following bilateral components of the BRS: rostral and caudal anterior cingulate cortex, insula, medial and lateral orbitofrontal cortex, rostral and caudal middle and superior frontal gyri, amygdala and hippocampus as well as for 26 other bilateral neocortical regions. Alcohol dependent participants were followed over 12-months after baseline study and were classified as Abstainers (no alcohol consumption; n=24) and Relapsers (any alcohol consumption; n=51) at follow-up. RESULTS Relapsers and Abstainers demonstrated lower cortical thickness in the vast majority of BRS regions as well as lower global thickness compared to Controls. Relapsers had lower total BRS surface area than both Controls and Abstainers, but Abstainers were not significantly different from Controls on any surface area measure. Relapsers demonstrated lower volumes than Controls in the majority of regions, while Abstainers showed lower volumes than Controls in the superior frontal gyrus, insula, amygdala and hippocampus, bilaterally. Relapsers exhibited smaller volumes than Abstainers in the right rostral middle and caudal middle frontal gyri and the lateral orbitofrontal cortex, bilaterally. In Relapsers, lower baseline volumes and surface areas in multiple regions were associated with a greater magnitude of post-treatment alcohol consumption. CONCLUSIONS Results suggest Relapsers demonstrated morphological abnormalities in regions involved in the “top down” regulation/modulation of internal drive states, emotions, reward processing and behavior, which may impart increased risk for the relapse/remit cycle that afflicts many with an AUD. Results also highlight the importance of examining both cortical thickness and surface area to better understand the nature of regional volume loss frequently observed in AUD. Results from this report are consistent with previous research implicating plastic neurobiological changes the brain reward system in the maintenance of addictive disorders.

These data provide an account of response inhibition-related brain functioning in youth with FASD. Furthermore, results suggest that the frontal-striatal circuitry thought to mediate inhibitory control is sensitive to alcohol teratogenesis.