Publication Abstract Display
Type: Published Abstract
Title: [H] Spectroscopy reveals selective vulnerability of frontal white matter in abstinent alcoholics.
Authors: Schweinsburg BC, Alhassoon OM, Taylor MJ, Videen JS, Brown GG, Patterson TL, Grant I
Year: 2001
Publication: Journal of the International Neuropsychological Society
Volume: 7 Issue: 2 Pages: 191
Abstract:Neuropsychological and magnetic resonance imaging investigations have suggested that the human frontal lobes seem particularly sensitive to the neurotoxic effects of alcohol. Quantitative volumetry has revealed that white matter changes may account for the brain shrinkage associated with alcohol consumption, however, the nature of this change is not well understood. Single-voxel [1H] magnetic resonance spectroscopy (MRS) was used to characterize the metabolic change associated with chronic alcoholism in frontal (FWM) and posterior (PWM) brain white matter regions, and to determine the relationship between brain metabolism and neuropsychological functioning.We hypothesized that the FWM would be differentially impacted by alcohol consumption compared to a PWM region, and these alterations would be associated with neuropsychological dysfunction. Twenty-seven recently detoxified alcoholics [RDA: M age: 39.8 (7.2); M education 13.4 (1.7); M length of abstinence 33.2 (7.1)] and 14 controls [CON: M age: 37.6 (8.2); M education 14.0 (1.6)] were examined using MRS (PRESS, TE 5 35 ms, TR 5 3000 ms). Concentrations of N-acetylaspartate (NAA), choline, creatine, and myo-Inositol were calculated. Repeated measures ANOVA revealed a Group 3 Region interaction for concentration of NAA [F (1,39)= 5.90, p= .02] Follow-upanalyses showed RDA had significantly lower NAA in the FWM, [t(39)=4.07, p=.0002], while RDA and CON had similar concentrations of NAA in the PWM. No between-group changes were found for the other metabolites, and no relationship between brain metabolism and neuropsychological functioning was found. The results indicated that the frontal lobes are particularly susceptible to axonal injury after long-term alcohol consumption. This is consistent with rodent models of alcoholism and may be due to altered blood flow and0or glutamate0NMDA mediated injury.

return to publications listing