Ben H Jansen1, Anant Hegde, Nashaat N Boutros. 1. Department of Electrical and Computer Engineering, University of Houston, Houston, TX 77204-4005, USA. bjansen@uh.edu
Abstract
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 (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. RESULTS: 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). 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.
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 schizophreniapatients suffer from phase synchronization deficits as compared to normal subjects. METHODS: The auditory EPs from 20 normal subjects and 19 schizophreniapatients 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. RESULTS: The S1 stimulus produced significantly less (P < 0.05) phase synchronization in schizophreniapatients 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). CONCLUSIONS:Schizophreniapatients 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.
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