Contribution of different EEG frequencies to auditory evoked potential abnormalities in schizophrenia
Contribution of different EEG frequencies to auditory evoked potential abnormalities in schizophrenia
复制标题
DOI：
10.1016/j.clinph.2003.10.016
复制
发表时间：
2004-03-01
影响因子：
4.7
通讯作者：
Boutros, NN
中科院分区：
文献类型：
--
作者：
Jansen, BH;Hegde, A;Boutros, NN
目的：我们之前已经展示过 [Clin NeuroPhysol 2003； 114:79] 正在进行的脑电图 (EEG) 的相位重组在潜伏期在 50 到 200 毫秒之间的听觉诱发电位 (EP) 分量的生成中发挥着重要作用。在本研究中，我们调查了精神分裂症患者与正常人相比是否存在相位同步缺陷。方法：分析了 20 名正常人和 19 名精神分裂症患者的听觉 EP。 EP 是使用双刺激范例获得的，其中以 500 ms 的平均刺激间间隔和 8 s 的对间间隔传递两个相同的音调突发（Si 和 S）。分段普罗尼方法（PPM）用于将单次试验听觉诱发电位分解为不同的频带。比较每个频段的刺激前和刺激后相位直方图，以确定两个人群中听觉刺激产生的相位同步程度。结果：在 2-12 Hz 频率范围内，S-1 刺激在精神分裂症患者中产生的相位同步显着低于正常受试者 (P < 0.05)。对于 S-2 刺激，群体间相位同步差异要少得多且更小。两个群体的 S-1 比 S-2 表现出更多的相位同步。在正常人群中观察到 S-1 后 100 ms 的 N100 幅度和相位同步之间存在显着相关性（P < 0.01），但在精神分裂症组中却没有观察到。 S后200 ms P200振幅与相位同步之间的相关性在正常组（P < 0.01）和精神分裂症组（P < 0.03）中显着。结论：与正常对照组相比，精神分裂症患者在2-12 Hz频率范围内存在相位同步缺陷，尤其是对于第一次刺激。这种缺陷解释了 EP 振幅较低的原因，并且可能是导致精神分裂症受试者感觉门控减少的一个重要因素。意义：这里提出的研究有助于理解健康中感觉门控和精神分裂症中的门控缺陷的潜在机制。 (C) 2004 年国际临床神经生理学联合会。由爱思唯尔爱尔兰有限公司出版。保留所有权利。
Objective: We have shown previously [Clin Neurophysiol 2003; 114:79] that phase reorganization of the ongoing electroencephalogram (EEG) plays an important role in the generation of auditory evoked potential (EP) components with a latency between 50 and 200 ms. In the present study, we investigate whether schizophrenia patients suffer from phase synchronization deficits as compared to normal subjects.Methods: The auditory EPs from 20 normal subjects and 19 schizophrenia patients were analyzed. EPs were obtained using a double stimulus paradigm, in which two identical tone bursts (Si and S,) were delivered with an average inter-stimulus interval of 500 ms and an inter-pair interval of 8 s. The Piecewise Prony Method (PPM) was used to decompose single trial auditory evoked potentials into different frequency bands. Pre- and post-stimulus phase histograms were compared for each frequency band to determine the degree of phase synchronization produced by auditory stimulation in the two populations.Results: The S-1 stimulus produced significantly less (P < 0.05) phase synchronization in schizophrenia patients than in normal subjects in the 2-12 Hz frequency range. Far fewer and smaller inter-population phase synchronization differences were seen for the S-2 stimulus. Both populations showed more phase synchronization for S-1 than S-2. A significant correlation (P < 0.01) between N100 amplitude and phase synchronization 100 ms post S-1 was observed for the normal population but not for the schizophrenia group. The correlation between P200 amplitude and phase synchronization 200 ms post S, was significant for the normal group (P < 0.01) and the schizophrenia group (P < 0.03).Conclusions: Schizophrenia patients have a phase synchronization deficiency, as compared to a normal control group, especially for the first stimulus, in the 2-12 Hz frequency range. This deficiency explains the lower EP amplitudes and may be a significant factor contributing to reduced sensory gating reported in schizophrenic subjects. Significance: The research presented here contributes to the understanding of the mechanism underlying sensory gating in health and gating deficiencies in schizophrenia. (C) 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.