Gazdzinski Stefan, Durazzo Timothy C, Weiner Michael W, Meyerhoff Dieter J
Center for Imaging of Neurodegenerative Diseases (CIND), Veterans Administration Medical Center, San Francisco, CA 94121, USA.
Alcohol. 2008 Mar;42(2):67-76. doi: 10.1016/j.alcohol.2008.01.002.
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 1 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.
几乎我们所了解的酒精使用障碍中神经生物学脑损伤的所有信息都来自于接受治疗的酗酒者的便利样本。最近的研究表明，与未接受过治疗的酗酒者相比，接受治疗的酗酒者存在更多的共病情况、更差的心理社会功能以及更高的依赖水平。因此，尚不清楚来自接受治疗的酗酒者便利样本的神经影像学结果是否能推广到整个酒精使用障碍人群。我们比较了35名戒酒1周的接受治疗的酗酒者（ALC）和32名未接受过治疗的重度饮酒者（HD）在1.5特斯拉体内磁共振成像获得的脑区体积和代谢物浓度，以评估潜在的组间差异。然后，我们评估了共病吸烟以及常见的人口统计学和临床变量是否介导了任何现有的神经生物学组间差异。与HD相比，ALC的脑叶灰质体积和丘脑较小，慢性吸烟会加剧这种情况。此外，与HD相比，ALC多个脑区中N-乙酰天门冬氨酸（一种公认的神经元活力标志物）、含胆碱代谢物（参与膜更新）和肌醇（一种假定的神经胶质细胞和渗透溶质标志物）的浓度较低。ALC与HD相比，白质中N-乙酰天门冬氨酸浓度较低可由研究前一年每月的平均饮酒量来解释。然而，其他组间差异不能通过共同的饮酒、人口统计学和临床变量（同时用作协变量）或排除患有共病情绪障碍的参与者来解释。综上所述，这表明酗酒者临床样本中的脑萎缩程度以及神经元和膜损伤程度不能推广到未寻求治疗的规模大得多的酒精使用障碍人群。
