Sachs H, Russell J A, Christman D R, Cook B
Department of Neurology, State University of New York at Stony Brook.
Arch Neurol. 1987 Dec;44(12):1242-51. doi: 10.1001/archneur.1987.00520240024007.
That chronic alcoholism yields devastating effects to the central nervous systems of its victims is well known, but the actual physiologic mechanisms underlying that deterioration have yet to be completely identified. What is also known is that many chronic alcoholics seem to recover brain function after a protracted period of abstinence, but the actual mechanisms of that restoration are also not well understood. Using positron emission tomography with the tracer 11C-2-deoxy-D-glucose as a probe to measure regional cerebral metabolic rate of glucose (RCMRGlu), we compared the magnitudes of glucose consumption in 44 brain regions between a group of newly abstinent chronic alcoholics without Korsakoff's psychosis and a control group of normal nonalcoholic subjects whose range of age was that of the alcoholic group. We found that RCMRGlu measurements in the brains of alcoholics were significantly lower than in the brains of the control group, and that there were many fewer significant interregional correlations in the brains of the alcoholics than in the brains of the control group. We also found no significant correlation between age and global metabolic rate of glucose in either group. However, even though the number of alcoholic subjects was too few to allow a reliable statistical comparison, the measurements suggest that chronic alcoholics over the age of 50 years suffer a greater decrease of RCMRGlu values than do their counterparts under the age of 50 years. While resting in a bland environment, neither alcoholic nor control subjects were found to have significant differences in RCMRGlu values between their brain hemispheres. In contrast to this similarity, normal dextrous subjects responded to a nonverbal auditory stimulus by increasing the metabolic rate of glucose in their right hemispheres while eight of nine chronic alcoholics did not. The results of this pilot study point to arguments that the alcoholic brain metabolizes glucose at a lower rate than do normal brains, that there are fewer region-to-region functional relationships in the alcoholic brain than in the normal brain, and that alcoholics may be impaired in right hemispheric processing. In subsequent investigations, we will measure the metabolic changes that follow abstinence, if any, by tracking subjects throughout an interval of rehabilitation. Also, we intend to test the findings of this study by measuring greater numbers of alcoholic subjects to separate the consequences of measurement variability, age, and chance from the underlying biologic processes that seem to be affected by chronic alcoholism.
长期酗酒对受害者的中枢神经系统会产生毁灭性影响，这是众所周知的，但导致这种退化的实际生理机制尚未完全明确。同样已知的是，许多慢性酗酒者在长期戒酒之后似乎能恢复脑功能，但其恢复的实际机制也未得到充分理解。我们以正电子发射断层扫描技术，用示踪剂11C - 2 - 脱氧 - D - 葡萄糖作为探针来测量局部脑葡萄糖代谢率（RCMRGlu），比较了一组无柯萨科夫精神病的新戒酒慢性酗酒者与年龄范围与酗酒组相同的正常非酗酒对照组44个脑区的葡萄糖消耗量。我们发现，酗酒者大脑中的RCMRGlu测量值显著低于对照组大脑，且酗酒者大脑中区域间的显著相关性比对照组大脑少得多。我们还发现两组中年龄与整体葡萄糖代谢率之间均无显著相关性。然而，尽管酗酒者的数量太少，无法进行可靠的统计比较，但测量结果表明，50岁以上的慢性酗酒者的RCMRGlu值下降幅度比50岁以下的酗酒者更大。在平淡环境中静息时，未发现酗酒者和对照组受试者大脑半球之间的RCMRGlu值有显著差异。与这种相似性形成对比的是，正常灵巧的受试者在对非语言听觉刺激做出反应时，其右半球的葡萄糖代谢率会增加，而9名慢性酗酒者中有8名没有这种反应。这项初步研究的结果表明，酗酒者大脑代谢葡萄糖的速率低于正常大脑，酗酒者大脑中区域间的功能关系比正常大脑少，而且酗酒者右半球的处理功能可能受损。在后续研究中，我们将通过在整个康复期间跟踪受试者来测量戒酒（如果有）后随之而来的代谢变化。此外，我们打算通过测量更多的酗酒者来验证本研究的结果，以区分测量变异性、年龄和偶然性的影响与似乎受慢性酗酒影响的潜在生物学过程。
