Jansen Ben H, Hegde Anant, Boutros Nashaat N
Department of Electrical and Computer Engineering, University of Houston, Houston, TX 77204-4005, USA.
Clin Neurophysiol. 2004 Mar;115(3):523-33. doi: 10.1016/j.clinph.2003.10.016.
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.
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 (S1 and S2) 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.
The S1 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 S2 stimulus. Both populations showed more phase synchronization for S1 than S2. A significant correlation (P < 0.01) between N100 amplitude and phase synchronization 100 ms post S1 was observed for the normal population but not for the schizophrenia group. The correlation between P200 amplitude and phase synchronization 200 ms post S1 was significant for the normal group (P < 0.01) and the schizophrenia group (P < 0.03).
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.
The research presented here contributes to the understanding of the mechanism underlying sensory gating in health and gating deficiencies in schizophrenia.
我们之前已经表明[《临床神经生理学》2003年；114:79]，持续脑电图（EEG）的相位重组在潜伏期为50至200毫秒的听觉诱发电位（EP）成分的产生中起重要作用。在本研究中，我们调查与正常受试者相比，精神分裂症患者是否存在相位同步缺陷。
分析了20名正常受试者和19名精神分裂症患者的听觉EP。使用双刺激范式获得EP，其中两个相同的纯音脉冲（S1和S2）以平均500毫秒的刺激间隔和8秒的对间间隔呈现。采用分段 Prony 方法（PPM）将单次试验听觉诱发电位分解为不同频段。比较每个频段刺激前和刺激后的相位直方图，以确定两组人群中听觉刺激产生的相位同步程度。
在2至12赫兹频率范围内，精神分裂症患者中S1刺激产生的相位同步明显少于正常受试者（P < 0.05）。对于S2刺激，群体间相位同步差异少得多且小得多。两组人群中S1的相位同步都比S2更多。正常人群中观察到N100波幅与S1后100毫秒的相位同步之间存在显著相关性（P < 0.01），但精神分裂症组未观察到。正常组（P < 0.01）和精神分裂症组（P < 0.03）中P200波幅与S1后200毫秒的相位同步之间存在显著相关性。
与正常对照组相比，精神分裂症患者在2至12赫兹频率范围内存在相位同步缺陷，尤其是对于第一个刺激。这种缺陷解释了较低的EP波幅，并且可能是导致精神分裂症患者感觉门控降低的一个重要因素。
此处呈现的研究有助于理解健康状态下感觉门控的潜在机制以及精神分裂症中的门控缺陷。
