利培酮对精神分裂症患者感觉门控P50缺陷的影响

目的探讨非典型抗精神病药物利培酮对精神分裂症患者感觉门控P50缺陷的影响。方法 26例急性期首发精神分裂症患者和25例急性期慢性精神分裂症患者入组,采用可变剂量（26 mg/d）的利培酮治疗,分别于治疗前及治疗46周后完成感觉门控P50测定。P50实验模式为听觉条件刺激（S1）-测试刺激（S2）模式。应用阳性与阴性症状量表（PANSS）评定精神症状,PANSS减分率评定疗效。结果治疗前P50测量指标在两组患者之间差异均无统计学意义（P〉0.05）,P50抑制指标与精神分裂症的病程、发作次数、精神症状（PANSS总分、阳性总分、阴性总分及一般精神病理分）之间均无相关性（P〉0.05）。治疗前后比较,除了S2波幅的组别主效应显著（P=0.02）外,其余P50测量指标的主效应及交互作用均不显著（P〉0.05）;利培酮对P50测量指标的影响与疗效无关。结论首发精神分裂症和慢性精神分裂症均存在感觉门控抑制缺陷。利培酮对首发和慢性精神分裂症的感觉门控P50抑制缺陷均无治疗改善作用。 更多还原

Effect of risperidone on sensory gating P50 deficit in patients with schizophrenia

Objective To investigate the effect of atypical antipsychotic medicine risperidone on sensory gating P50 deficit in patients with schizophrenia. Methods Twenty-six patients with first-episode schizophrenia and 25 patients with chronic schizophrenia were enrolled in the study. All patients were treated with risperidone of different doses (2 to 6 mg/d). All patients fulfilled the evaluation of sensory gating P50 with the conditioning (S1)-testing (S2) paradigm before treatment and 4 to 6 weeks after treatment. The psychotic symptoms were assessed with Positive and Negative Syndrome Scale (PANSS), and the therapeutic effects were evaluated with PANSS reduction rate. Results There was no significant difference in P50 parameters between the two groups before treatment (P>0.05), and there was no significant correlation between P50 inhibition parameters and disease course, psychotic episodes and psychiatric symptoms (PANSS total score, positive symptoms score, negative symptoms score and general psychopathology symptoms score) of schizophrenia (P>0.05). Except the group main effect for S2 amplitude (P=0.02), there was no significant change for main effect and interaction of the other P50 parameters after treatment (P>0.05). The effect of risperidone on P50 parameters was not related to the therapeutic effect. Conclusion Deficit in sensory gating inhibition exists in both first-episode schizophrenia and chronic schizophrenia, and risperidone in not effective in treating the deficit in sensory gating inhibition of schizophrenia.