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首发和慢性精神分裂症急性期患者的感觉门控P50
引用本文:刘登堂,陈兴时,卓恺明,宋振华,吴彦,王继军,杨治良,徐一峰.首发和慢性精神分裂症急性期患者的感觉门控P50[J].上海精神医学,2010,22(6):339-342.
作者姓名:刘登堂  陈兴时  卓恺明  宋振华  吴彦  王继军  杨治良  徐一峰
作者单位:[1]上海交通大学医学院附属精神卫生中心,200030 [2]华东师范大学心理学系博士后流动站,200062
基金项目:中国博士后科学基金,上海市科学技术委员会自然基金资助项目,上海市卫生局科研课题项目,杨森科学委员会中国分会研究基金(JRCC)
摘    要:目的探讨病程对精神分裂症感觉门控抑制缺陷的影响。方法对58名健康志愿者、38例首发精神分裂症急性期患者和36例慢性精神分裂症急性期患者进行感觉门控研究。应用听觉P50抑制评估感觉门控,实验模式为条件刺激(S1)-测试刺激(S2)模式。结果首发患者、慢性患者及对照组的S1波幅分别为(3.7±2.5)μV、(4.5±2.0)μV和(5.8±3.8)μV(F=5.P〈053,.01),首发患者的S1波幅低于对照组(P〈0.01);S2波幅分别为(2.8±1.1)μV、(3.5±1.5)μV和(2.1±1.4)μV(F=11.47,P〈0.01),首发和慢性患者的S2波幅均高于对照组(P分别为0.02,小于0.01),并且慢性患者的S2波幅高于首发患者(P=0.02)。P50抑制指标在三组之间差异均有统计学意义(P均小于0.01),首发和慢性患者的S2/S1波幅比均大于对照组(P均小于0.01),而S1-S2波幅差值和100(1-S2/S1)均低于对照组(P均小于0.01),但首发患者和慢性患者之间P50抑制指标差异无统计学意义(P均大于0.05)。结论首发精神分裂症和慢性精神分裂症均存在明显的感觉门控P50抑制缺陷,病程对精神分裂症的感觉门控P50抑制缺陷无明显影响。

关 键 词:精神分裂症  感觉门控  听觉P50电位

Sensory gating P50 during the acute phase of schizophrenia in first-episode and in chronic patients
Liu Dengtang,Chen Xingshi,Zhuo Kaiming,Song Zhenghua,Wu Yan,Wang Jijun,Yang Zhiliang,Xu Yifeng.Sensory gating P50 during the acute phase of schizophrenia in first-episode and in chronic patients[J].Shanghai Archives of Psychiatry,2010,22(6):339-342.
Authors:Liu Dengtang  Chen Xingshi  Zhuo Kaiming  Song Zhenghua  Wu Yan  Wang Jijun  Yang Zhiliang  Xu Yifeng
Institution:1.1.Shanghai Mental Health Center,Shanghai Jiaotong University School of Medicine,Shanghai 200030;2.Department of Psychology, East China Normal University,Shanghai 200062
Abstract:Objective:Assess the relationship of disease course with the sensory gating P50 deficits in patients with schizophrenia. Methods: Fifty-eight healthy controls, 38 first-episode schizophrenic patients in the acute phase of illness and 36 chronic schizophrenic patients in acute relapses were enrolled in the study. Sensory gating was evaluated using the auditory P50 suppression test with the conditioning (S1)-testing (S2) paradigm. Results:Mean (±sd) S1 amplitudes in first-episode schizophrenia, chronic schizophrenia and healthy controls were (3.7±2.5)μV, (4.5±2.0)μV and (5.8±3.8)μV, respectively (F=5.53,P〈0.01); the S1 amplitude in first-episode schizophrenia was shorter than that in chronic schizophrenia(P〈0.01). S2 amplitudes in first-episode schizophrenia, chronic schizophrenia and healthy controls were (2.8±1.1)μV,(3.5±1.5)μV and (2.1±1.4)μV, respectively(F=11.47,P〈0.01); the S2 amplitudes in first-episode schizophrenia and chronic schizophrenia were both higher than that in healthy controls (P=0.02 and P〈0.01, respectively), and the S2 amplitude in chronic schizophrenia was higher than that in first-episode schizophrenia (P=0.02). Three P50 indicators of inhibition—S2/S1, S1-S2, and 100(1-S2/S1)—were all significantly different in the three groups of subjects(P’s0.01); follow-up pairwise comparisions found that the S2/S1 ratios in first-episode and chronic schizophrenia were both higher than that in healthy controls(P’s0.01)and the S1-S2 and 100(1-S2/S1) parameters in first-episode and chronic schizophrenia were both smaller than those in healthy controls(P’s0.01). However, no differences were found in these three P50 parameters between first-episode patients and chronic patents (all P’s0.05). Conclusion:Similary deficits in sensory gating during the acute phase of first-episode schizophrenia and acute episodes in patients with chronic schizophrenia suggest that sensory gating deficits in schizophrenia are not influenced by the course of the disease.
Keywords:Schizophrenia Sensory gating Auditory evoked potential P50
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