Abstract
Neuroimaging studies have shown that white matter damage accompanies excessive alcohol use, but the functional correlates of alcohol-related white matter disruption remain unknown. This study applied tract-based spatial statistics (TBSS) to diffusion tensor imaging (DTI) data from 332 heavy drinkers (mean age = 31.2 ± 9.4; 31% female) to obtain averaged fractional anisotropy (FA) values of 18 white matter tracts. Statistical analyses examined correlations of FA values with blood-oxygenation-level-dependent (BOLD) response to an alcohol taste cue, measured with functional magnetic resonance imaging (fMRI). FA values of nine white matter tracts (anterior corona radiata, body of corpus callosum, cingulate gyrus, external capsule, fornix, inferior frontooccipital fasciculus, posterior corona radiata, retrolenticular limb of internal capsule, and superior longitudinal fasciculus) were significantly, negatively correlated with BOLD activation in medial frontal gyrus, parahippocampal gyrus, fusiform gyrus, cingulum, thalamus, caudate, putamen, insula, and cerebellum. The inverse relation between white matter integrity and functional activation during the alcohol taste cue provides support for the hypothesis that lower white matter integrity in frontoparietal and corticolimbic networks is a factor in loss of control over alcohol consumption.
Highlights
Alcohol is the most readily available and commonly abused drug across all age groups in the United States (Substance Abuse and Mental Health Services Administration 2010), making alcohol-related brain damage a pressing public health concern
Brain and Behavior published by Wiley Periodicals, Inc
The objective of this study was to investigate the functional implications of individual differences in white matter integrity by testing whether fractional anisotropy (FA) values were related to blood-oxygenation-level-dependent (BOLD) response elicited by an alcohol taste cue in a sample of heavy drinkers
Summary
Alcohol is the most readily available and commonly abused drug across all age groups in the United States (Substance Abuse and Mental Health Services Administration 2010), making alcohol-related brain damage a pressing public health concern. White matter damage is a signature injury of alcohol use disorders (AUDs; Harper and Kril 1990; Kril and Halliday 1999). Evidence suggests that chronic alcohol abuse damages white matter on the cellular level by increasing oxidative stress (Crews and Nixon 2009; Fernandez-Lizarbe et al 2009; Pascual et al 2011) and downregulating genes critical to myelination (Lewohl et al 2000; Liu et al 2007). A recent meta-analysis of magnetic resonance imaging (MRI) studies comparing white matter volume in AUD and healthy control groups found a significant effect size of g = 0.304 for the white matter volume deficit associated with AUD diagnosis (Monnig et al 2012b).
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