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首页> 中文期刊> 《中华核医学与分子影像杂志》 >失眠障碍患者脑多巴胺D2受体改变及其意义初探

失眠障碍患者脑多巴胺D2受体改变及其意义初探

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Objective To explore the changes of dopamine D2 receptor in dopamine pathway in in-somnia patients and discuss its clinical significance. Methods From January 2016 to December 2016, 15 patients with insomnia (1 male, 14 females, age:(44.3±8.6) years) and 15 gender-/age-matched-healthy volunteers (control group;3 males, 12 females, age:(40.5±9.0) years) were included to undergo resting brain 11C-Raclopride PET/CT imaging. The D2 receptor binding potential (BPND) of the dopamine pathway was calculated by molecular imaging and kinetic analysis toolbox ( MIAKAT) software. The BP ND , Hamilton depression scale ( HAMD) , transient and graphics memory scale results were compared with two-sample t test and Mann-Whitney u test between the two groups. Pearson correlation analysis was used to evaluate the correlation between BPND(nucleus accumbens, caudate nucleus, putamen) and Pittsburgh sleep quality in-dex ( PSQI) , HAMD, course of disease, transient memory and graphical memory scale scores in the patient group. Results The BP ND in bilateral putamen, nucleus accumbens and left caudate nucleus of patients was lower than that of controls( left putamen:z=-2.717, right putamen:z=-2.883, both P<0.01;left nu-cleus accumbens:t=-2.269, right nucleus accumbens:t=-2.410, both P<0.05;left caudate nucleus:t=-2.632,P<0. 05), but the BPND level of right caudate nucleus was not significantly different(z=-0.850, P>0.05) . The scores of HAMD in the patient group were higher than those in control group ( t=10. 273, P<0. 01), while the scores of instantaneous memory (t=-4.888, P<0.01) and graphical memory scale (t=-2.624, P<0.05) were lower. There were significant negative correlations between the BP ND of bilateral nucleus ac-cumbens, caudate nucleus and putamen and the course of insomnia in the patient group ( r range:-0.761 to-0.682, all P<0.01) . Conclusion Patients with insomnia have abnormal neurotransmitter system of dopa-mine D2 and it may play a role in the pathogenesis of insomnia.%目的 探讨失眠障碍患者脑多巴胺通路多巴胺D2受体变化及其意义.方法 纳入2016年1月至12月确诊的失眠障碍患者15例[男1例,女14例,年龄(44.3±8.6)岁]与健康志愿者(对照)15名[男3名,女12名,年龄(40.5±9.0)岁],2组性别、年龄匹配.研究对象接受静息脑11C-雷氯必利(Raclopride)PET/CT显像,应用分子影像动态分析工具箱(MIAKAT)软件计算多巴胺通路多巴胺D2受体结合力.采用两样本t检验或Mann-Whitney u检验比较患者组与对照组D2受体结合力及汉密尔顿抑郁量表(HAMD)、瞬时记忆、图形记忆量表评分差异.应用Pearson相关分析评价患者组伏隔核、尾状核、壳核D2受体结合力与匹兹堡睡眠质量指数(PSQI)、HAMD评分、病程、瞬时记忆及图形记忆量表评分的相关性.结果 患者组较对照组双侧壳核(左侧:z=-2.717,右侧:z=-2.883,均P<0.01)、双侧伏隔核(左侧:t=-2.269,右侧:t=-2.410,均P<0.05)、左侧尾状核(t=-2.632,P<0.05)多巴胺D2受体结合力减低,右侧尾状核多巴胺D2受体结合力差异无统计学意义(z=-0.850,P>0.05).患者组HAMD评分较对照组高(t=10.273,P<0.01),瞬时记忆(t=-4.888,P<0.01)及图形记忆(t=-2.624,P<0.05)量表评分较对照组低.患者组双侧伏隔核、尾状核、壳核D2受体结合力与失眠病程均呈负相关(r值:-0.761～-0.682,均P<0.01).结论 失眠障碍患者存在脑内多巴胺D2神经递质系统异常,该异常可能在失眠障碍的发病中起一定作用.

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