4.2 Article

Are treated alcoholics representative of the entire population with alcohol use disorders? A magnetic resonance study of brain injury

期刊

ALCOHOL
卷 42, 期 2, 页码 67-76

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.alcohol.2008.01.002

关键词

alcohol use disorder; treatment; structural MRI; MR spectroscopy; brain

资金

  1. NATIONAL INSTITUTE ON AGING [P01AG019724] Funding Source: NIH RePORTER
  2. NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R01AA010788, P01AA011493] Funding Source: NIH RePORTER
  3. NIAAA NIH HHS [P01 AA011493-03S1, AA10788, R01 AA010788-09, P01 AA011493-04S1, R01 AA010788, R01 AA010788-07, R01 AA010788-10, R01 AA010788-12, R01 AA010788-11, P01 AA011493-04, R01 AA010788-08, AA11493, P01 AA011493-02S1, P01 AA011493, P01 AA011493-02, P01 AA011493-05, R01 AA010788-06, P01 AA011493-03] Funding Source: Medline
  4. NIA NIH HHS [P01 AG019724-050002, P01 AG019724] Funding Source: Medline

向作者/读者索取更多资源

Almost all we know about neurobiological brain injury in alcohol use disorders has been derived from convenience samples of treated alcoholics. Recent research has demonstrated more comorbid conditions, poorer psychosocial functioning, and higher dependence levels in treated alcoholics than in their treatment-naive counterparts. Thus, it is not clear whether neuroimaging results from convenience samples of treated alcoholics can be generalized to the entire population with alcohol use disorders. We compared 35 treated alcoholics at I week of abstinence (ALC) and 32 treatment-naive heavy drinkers (HD) on regional brain volumes and metabolite concentrations obtained by in vivo magnetic resonance at 1.5 Tesla to evaluate for potential group differences. Then, we evaluated whether comorbid cigarette smoking and common demographic and clinical variables mediated any existing neurobiological group differences. ALC demonstrated smaller lobar gray matter volumes and thalami than HD, exacerbated by chronic smoking. Furthermore, concentrations of N-acetyl-aspartate (an accepted marker of neuronal viability), choline-containing metabolites (involved in membrane turnover), and myo-inositol (a putative marker of glial cells and osmolyte) were lower in multiple brain regions of ALC compared to HD. The lower N-acetyl-aspartate concentrations in white matter of ALC versus HD were explained by average number of drinks per month over the year preceding study. However, the other group differences were not explained by common drinking, demographic, and clinical variables (used as covariates at the same time) or by excluding participants with comorbid mood disorders. Taken together, this suggests that the degree of brain atrophy, as well as neuronal and membrane injury in clinical samples of alcoholics cannot be generalized to the much larger population with alcohol use disorders that does not seek treatment. (C) 2008 Elsevier Inc. All rights reserved.

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