Adler Lawrence E, Olincy Ann, Cawthra Ellen M, McRae Kara A, Harris Josette G, Nagamoto Herbert T, Waldo Merilyne C, Hall Mei-Hua, Bowles Amanda, Woodward Laurie, Ross Randal G, Freedman Robert
Box C268-26, Psychiatry, University of Colorado Health Science Ctr., 4200 East 9th Ave., Denver, CO 80262, USA.
Am J Psychiatry. 2004 Oct;161(10):1822-8. doi: 10.1176/ajp.161.10.1822.
Sensory gating deficits found in schizophrenia can be assessed by using a paired auditory stimulus paradigm to measure auditory evoked response. The ratio of the P50 response amplitude of the second or test stimulus to that of the first or conditioning stimulus is expressed as a percentage. Normal subjects generally suppress the second response and typically have ratios of less than 40%. Subjects with schizophrenia and half their first-degree relatives have deficits in sensory gating, with P50 ratios that are generally greater than 50%. Treatment with typical neuroleptics does not reverse this deficit. However, previous studies have shown that treatment with clozapine, an atypical neuroleptic, ameliorates this deficit in clinically responsive patients. This study sought to determine whether other atypical neuroleptics improve P50 ratios.
P50 evoked potential recordings were obtained from 132 patients with schizophrenia and 177 healthy comparison subjects. Eighty-eight patients were being treated with atypical neuroleptics (clozapine [N=26], olanzapine [N=31], risperidone [N=22], and quetiapine [N=9]). Thirty-four patients were taking typical neuroleptics, and 10 were unmedicated.
Healthy subjects exhibited P50 suppression that was significantly better than the schizophrenia patients receiving typical neuroleptics (mean=19.8% [SD=21.0%] versus 110.1% [SD=87.9%]). Patients receiving atypical neuroleptics had a mean P50 ratio that fell between these two means (mean=70.4%, SD=53.7%). When patients treated with different atypical neuroleptics were compared, only the clozapine group had mean P50 ratios that were in the normal range. All other groups exhibited auditory P50 response inhibition that was significantly poorer than that of the healthy subjects.
Improvement in P50 gating appears to be greatest in patients treated with clozapine.
精神分裂症患者存在的感觉门控缺陷可通过使用配对听觉刺激范式来测量听觉诱发电位进行评估。将第二个或测试刺激的P50反应振幅与第一个或条件刺激的P50反应振幅之比表示为百分比。正常受试者通常会抑制第二个反应，其比率通常低于40%。精神分裂症患者及其一级亲属中有一半存在感觉门控缺陷，其P50比率通常大于50%。使用典型抗精神病药物治疗并不能逆转这种缺陷。然而，先前的研究表明，使用非典型抗精神病药物氯氮平治疗可改善临床有反应患者的这种缺陷。本研究旨在确定其他非典型抗精神病药物是否能改善P50比率。
对132例精神分裂症患者和177名健康对照者进行P50诱发电位记录。88例患者正在接受非典型抗精神病药物治疗（氯氮平[N = 26]、奥氮平[N = 31]、利培酮[N = 22]和喹硫平[N = 9]）。34例患者正在服用典型抗精神病药物，10例未接受药物治疗。
健康受试者表现出的P50抑制明显优于接受典型抗精神病药物治疗的精神分裂症患者（平均值 = 19.8%[标准差 = 21.0%]对110.1%[标准差 = 87.9%]）。接受非典型抗精神病药物治疗的患者的平均P50比率介于这两个平均值之间（平均值 = 70.4%，标准差 = 53.7%）。当比较接受不同非典型抗精神病药物治疗的患者时，只有氯氮平组的平均P50比率处于正常范围内。所有其他组的听觉P50反应抑制明显比健康受试者差。
接受氯氮平治疗的患者P50门控改善似乎最大。
