Tiihonen J, Vilkman H, Räsänen P, Ryynänen O P, Hakko H, Bergman J, Hämäläinen T, Laakso A, Haaparanta-Solin M, Solin O, Kuoppamäki M, Syvälahti E, Hietala J
Department of Forensic Psychiatry, University of Kuopio, Finland.
Mol Psychiatry. 1998 Mar;3(2):156-61. doi: 10.1038/sj.mp.4000365.
Recent in vivo studies have shown low dopamine D2 receptor and dopamine transporter densities among late onset (type 1) alcoholics. We have now studied 6-[18F]-FDOPA (FDOPA) uptake in 10 type 1 alcoholics and eight matched controls to test the hypothesis that striatal presynaptic dopamine function is lower among alcoholics. Markedly low FDOPA uptake (Ki) was observed in the left caudate of two alcoholic patients, but the mean striatal uptake values of the patient group were higher than those of the control group. The greatest difference was observed in the mean FDOPA intake in the left putamen, which was 28% higher in the patient group (t = 3.00, P = 0.008, d.f. = 16, independent samples t-test), and in the right caudate (difference 36%, t = 2.87, P = 0.01). The elevated FDOPA uptake in putamen and caudate correlated with poor Wisconsin Card Sorting Test (WCST) performance (error %) among alcoholics (correlation coefficients from 0.49 to 0.56), which suggests that the magnitude of presynaptic dopamine function alteration correlates with the degree of disability to modify one's behavior. The results do not give support to the hypothesis of generally decreased striatal dopamine turnover in type 1 alcoholism, but on the contrary indicate an increased presynaptic dopamine function. This may represent a compensatory mechanism to low postsynaptic DA function. The low presynaptic DA function observed in the left caudate of two patients suggests that type 1 alcoholism may be a heterogeneous disorder.
近期的体内研究表明，晚发性（1型）酒精中毒患者的多巴胺D2受体和多巴胺转运体密度较低。我们现在对10名1型酒精中毒患者和8名匹配的对照组进行了6-[18F]-氟多巴（FDOPA）摄取研究，以检验酒精中毒患者纹状体突触前多巴胺功能较低这一假设。在两名酒精中毒患者的左侧尾状核中观察到明显较低的FDOPA摄取（Ki），但患者组的平均纹状体摄取值高于对照组。在左侧壳核的平均FDOPA摄取中观察到最大差异，患者组高出28%（t = 3.00，P = 0.008，自由度 = 16，独立样本t检验），右侧尾状核也有差异（差异36%，t = 2.87，P = 0.01）。壳核和尾状核中FDOPA摄取的升高与酒精中毒患者威斯康星卡片分类测验（WCST）表现不佳（错误率%）相关（相关系数为0.49至0.56），这表明突触前多巴胺功能改变的程度与改变行为的残疾程度相关。结果不支持1型酒精中毒患者纹状体多巴胺周转率普遍降低的假设，相反表明突触前多巴胺功能增强。这可能代表了对突触后多巴胺功能低下的一种补偿机制。在两名患者左侧尾状核中观察到的突触前多巴胺功能低下表明，1型酒精中毒可能是一种异质性疾病。
