Durazzo Timothy C, Gazdzinski Stefan, Banys Peter, Meyerhoff Dieter J
San Francisco Veterans Administration Medical Center, MRS Unit (114M), 4150 Clement St., San Francisco, CA 94121, USA.
Alcohol Clin Exp Res. 2004 Dec;28(12):1849-60. doi: 10.1097/01.alc.0000148112.92525.ac.
Cigarette smoking is common among alcohol-dependent individuals. Nevertheless, previous research has typically not accounted for the potential independent or compounding effects of cigarette smoking on alcohol-induced brain injury and neurocognition.
Twenty-four 1-week-abstinent recovering alcoholics (RAs; 14 smokers and 10 nonsmokers) in treatment and 26 light-drinking controls (7 smokers and 19 nonsmokers) were compared on measures of common brain metabolites in gray matter and white matter of the major lobes, basal ganglia, midbrain, and cerebellar vermis, obtained via multislice short-echo time proton magnetic resonance spectroscopic imaging. Smoking and nonsmoking RAs were also contrasted on measures of neurocognitive functioning, as well as laboratory markers of drinking severity and nutritional status.
Chronic alcohol dependence, independent of smoking, was associated with lower concentrations of frontal N-acetylaspartate (NAA) and frontal choline-containing compounds, as well as lower parietal and thalamic choline. Smoking RAs had lower NAA concentrations in frontal white matter and midbrain and lower midbrain choline than nonsmoking RAs. A four-group analysis of covariance also demonstrated that chronic cigarette smoking was associated with lower midbrain NAA and choline and with lower vermian choline. In smoking RAs, heavier drinking was associated with heavier smoking, which correlated with numerous subcortical metabolite abnormalities. The 1-week-abstinent smoking and nonsmoking RAs did not differ significantly on a brief neurocognitive battery. In smoking RAs, lower cerebellar vermis NAA was associated with poorer visuomotor scanning speed and incidental learning, and in nonsmoking RAs lower vermis NAA was related to poorer visuospatial learning and memory.
These human in vivo proton magnetic resonance spectroscopic imaging findings indicate that chronic cigarette smoking exacerbates chronic alcohol-induced neuronal injury and cell membrane damage in the frontal lobes of RAs and has independent adverse effects on neuronal viability and cell membranes in the midbrain and on cell membranes of the cerebellar vermis. Higher smoking levels are associated with metabolite concentrations in select subcortical structures. Greater consideration of the potential effects of comorbid cigarette smoking on alcohol-induced brain damage and other diseases affecting the central nervous system is warranted.
吸烟在酒精依赖个体中很常见。然而,以往的研究通常没有考虑吸烟对酒精所致脑损伤和神经认知的潜在独立或复合影响。
对24名戒酒1周的康复期酗酒者(RAs;14名吸烟者和10名非吸烟者)和26名轻度饮酒对照者(7名吸烟者和日19名非吸烟者)进行比较,通过多层短回波时间质子磁共振波谱成像测量主要脑叶、基底神经节、中脑和小脑蚓部灰质和白质中的常见脑代谢物。吸烟和不吸烟的RAs在神经认知功能测量以及饮酒严重程度和营养状况的实验室指标方面也进行了对比。
慢性酒精依赖与吸烟无关,与额叶N-乙酰天门冬氨酸(NAA)和额叶含胆碱化合物浓度降低以及顶叶和丘脑胆碱含量降低有关。吸烟的RAs额叶白质和中脑的NAA浓度低于不吸烟的RAs,中脑胆碱含量也较低。四组协方差分析还表明,长期吸烟与中脑NAA和胆碱含量降低以及蚓部胆碱含量降低有关。在吸烟的RAs中,饮酒量越大与吸烟量越大相关,这与许多皮质下代谢物异常有关。在简短的神经认知测试中,戒酒1周的吸烟和不吸烟RAs没有显著差异。在吸烟的RAs中,小脑蚓部NAA含量较低与视觉运动扫描速度较差和附带学习能力较差有关,而在不吸烟的RAs中,蚓部NAA含量较低与视觉空间学习和记忆较差有关。
这些人体活体质子磁共振波谱成像结果表明,长期吸烟会加剧慢性酒精引起的RAs额叶神经元损伤和细胞膜损伤,并对中脑神经元活力和细胞膜以及小脑蚓部细胞膜产生独立的不利影响。吸烟水平越高与特定皮质下结构中的代谢物浓度相关。有必要更多地考虑合并吸烟对酒精所致脑损伤和其他影响中枢神经系统疾病的潜在影响。