Relapse to hazardous levels of alcohol consumption after treatment for alcohol use disorders is common. Investigation of the neurobiological correlates of resumption of hazardous drinking is necessary to clarify the mechanisms contributing to relapse
. Fifty-seven treatment-seeking alcohol-dependent participants (ALC) completed arterial spin labeling perfusion MRI of the frontal and parietal gray matter (GM) at 7
±3 days of abstinence (baseline). ALC participants were restudied after 35±11 days of abstinence (assessment point 2: AP2). Twenty-eight nonsmoking, light-drinking control participants (nsLD) from the community were studied with perfusion MRI. ALC participants were followed over 12 months after baseline study and were classified as abstainers (no alcohol consumption; n=19) and resumers (any alcohol consumption; n=38) at follow-up. Cross-sectional and longitudinal perfusion was compared in abstainers, resumers, and nsLD.At baseline, resumers demonstrated significantly lower frontal and parietal GM perfusion than nsLD and abstainers. Abstainers and nsLD were not different on frontal or parietal GM perfusion. No significant longitudinal perfusion changes were observed in abstainers and resumers. At AP2, resumers showed significantly lower frontal GM perfusion than nsLD and abstainers, whereas no group differences were observed for parietal GM. Abstainers and nsLD were not different on frontal GM perfusion.
The significantly decreased frontal GM perfusion in resumers compared with both abstainers and nsLD across the assessment interval suggests premorbid and/or acquired neurobiological abnormalities of the frontal GM in resumers.
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