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Alteration of Regional Cerebral Glucose Metabolic Rate in Non-Korsakoff Chronic Alcoholism
Howard Sachs, MD, PhD;
Jerome A. G. Russell, PhD;
David R. Christman, DSc;
Bryan Cook, MD
Arch Neurol. 1987;44(12):1242-1251.
Abstract
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• 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 tracer11C-2-deoxy-D-glucose as a probe to measure regional cerebral metabolic rate of glucose (RCMRGIu), 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 RCMRGIu 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 RCMRGIu values than do their counter-parts under the age of 50 years. While resting in a bland environment, neither alcoholic nor control subjects were found to have significant differences in RCMRGIu 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.
Author Affiliations
From the Department of Neurology, State University of New York at Stony Brook (Dr Sachs); Northport (NY) Veterans Administration Medical Center (Drs Sachs and Cook); and the Department of Chemistry, Brookhaven National Laboratory, Upton, NY (Drs Sachs, Russell, and Christman).
Footnotes
Accepted for publication July 29, 1987.
Presented in part at the American Academy of Neurology, New York, April 9, 1987.
Reprint requests to Brookhaven National Laboratory, Department of Chemistry, Bldg 555, Upton, NY 11973 (Dr Christman).
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