Wegrzyn Jacek, Wciórka Jacek
Psychiatr Pol. 2004 May-Jun;38(3):395-408.
A pair of auditory stimuli presented in a 0.5 second interval cause a reduction of the P50 auditory evoked potential (P50 AEP) amplitude after the second stimuli in the pair. In some, but not all studies, a clear deficit of such P50 AEP gating was observed in schizophrenic patients. It was present constantly irrespective of the clinical state. This deficit was also found in first degree relatives of schizophrenic patients. However the results of the studies, as well as their interpretation remain controversial.
To differentiate between P50 AEP in groups of schizophrenic patients, their healthy first degree relatives, as well as those in the control group.
50 schizophrenic patients (ICD-10 criteria (DCR)) in early clinical improvement phase, 26 healthy first degree relatives, as well sa 46 healthy individuals with no psychiatric illness in the self-report and family history. All those studied were stimulated with 120 pairs of auditory stimuli (clicks), each of duration 2 mseconds and a sound intensity of 73 dB, with a 500 msecond interval between the stimuli in a pair (S1 and S2) every 8 seconds. A high-end filter of 70 Hz and low-end filter of 10 Hz were applied. Bio potentials were recorded from the head apex, relatively to the mastoid process (A1 + A2). Eyeball-movement artefacts were registered from the Fp1-A1 and Fp2-A2 potentials. The registered bio potentials were evened on-line.
Relative (i.e. evaluated in relation to the potential after S1) lowering of the P50 potential after S2 was the most significant in the healthy control group (75%), in the other groups usually there was an increase in the S2 potential--higher in the schizophrenic patient group (-45%) and lower in their first degree relatives (-11%).
(1) Healthy individuals suppressed the neurophysiologic response to the second pair of auditory stimuli much more than the schizophrenic patients and their healthy families. (2) No difference was seen in the suppression of the response between the schizophrenic patients and their first degree relatives. The results are coherent with the idea of the dysfunction of the P50 gating having endophenotypic traits as far as schizophrenia goes.
一对间隔0.5秒呈现的听觉刺激会导致该对刺激中第二个刺激后P50听觉诱发电位（P50 AEP）幅度降低。在一些但并非所有研究中，在精神分裂症患者中观察到这种P50 AEP门控存在明显缺陷。无论临床状态如何，该缺陷始终存在。在精神分裂症患者的一级亲属中也发现了这种缺陷。然而，这些研究的结果及其解释仍存在争议。
区分精神分裂症患者组、其健康一级亲属组以及对照组的P50 AEP。
50名处于临床早期改善阶段的精神分裂症患者（符合ICD - 10标准（DCR））、26名健康一级亲属以及46名自我报告和家族史中无精神疾病的健康个体。所有研究对象均接受120对听觉刺激（咔哒声），每对刺激持续时间为2毫秒，声强为73分贝，每对刺激（S1和S2）之间间隔500毫秒，每8秒重复一次。应用70赫兹的高端滤波器和10赫兹的低端滤波器。从头顶相对于乳突（A1 + A2）记录生物电位。从Fp1 - A1和Fp2 - A2电位记录眼球运动伪迹。记录的生物电位进行在线均衡。
相对于S1后的电位，S2后P50电位的相对降低（即相对于S1后的电位进行评估）在健康对照组中最为显著（75%），在其他组中，S2电位通常会升高——在精神分裂症患者组中升高幅度较大（-45%），在其一级亲属组中升高幅度较小（-11%）。
（1）健康个体对第二对听觉刺激的神经生理反应抑制程度远高于精神分裂症患者及其健康亲属。（2）精神分裂症患者与其一级亲属在反应抑制方面未发现差异。就精神分裂症而言，这些结果与P50门控功能障碍具有内表型特征的观点一致。
