Daisuke Koshiyama1, Makoto Miyakoshi2, Kumiko Tanaka-Koshiyama1, Yash B Joshi3, Joyce Sprock3, David L Braff3, Gregory A Light3. 1. Department of Psychiatry, University of California San Diego, La Jolla, CA, USA. 2. Swartz Center for Neural Computation, University of California San Diego, La Jolla, CA, USA. Electronic address: mmiyakoshi@ucsd.edu. 3. Department of Psychiatry, University of California San Diego, La Jolla, CA, USA; VISN-22 Mental Illness, Research, Education and Clinical Center (MIRECC), VA San Diego Healthcare System, San Diego, CA, USA.
Abstract
BACKGROUND: Schizophrenia patients have abnormal electroencephalographic (EEG) power over multiple frequency bands, even at rest, though the primary neural generators and spatiotemporal dynamics of these abnormalities are largely unknown. Disturbances in the precise synchronization of oscillations within and across cortical sources may underlie abnormal resting-state EEG activity in schizophrenia patients. METHODS: A novel assessment method was applied to identify the independent contributing sources of resting-state EEG and assess the phase discontinuity in schizophrenia patients (N = 148) and healthy subjects (N = 143). RESULTS: A network of 11 primary contributing sources of scalp EEG was identified in both groups. Schizophrenia patients showed abnormal elevations of EEG power in the temporal region in the theta, beta, and gamma-bands, as well as the posterior cingulate gyrus in the delta, theta, alpha, and beta-bands. The higher theta-band power in the middle temporal gyrus was significantly correlated with verbal memory impairment in patients. The peak frequency of alpha was lower in patients in the cingulate and temporal regions. Furthermore, patients showed a higher rate of alpha phase discontinuity in the temporal region as well as a lower rate of theta phase discontinuity in the temporal and posterior cingulate regions. CONCLUSIONS: Abnormal rates of phase discontinuity of alpha- and theta-band, abnormal elevations of EEG power in multiple bands, and a lower peak frequency of alpha were identified in schizophrenia patients at rest. Clarification of the mechanistic substrates of abnormal phase discontinuity may clarify core pathophysiologic abnormalities of schizophrenia and contribute to the development of novel biomarkers for therapeutic interventions.
BACKGROUND: Schizophrenia patients have abnormal electroencephalographic (EEG) power over multiple frequency bands, even at rest, though the primary neural generators and spatiotemporal dynamics of these abnormalities are largely unknown. Disturbances in the precise synchronization of oscillations within and across cortical sources may underlie abnormal resting-state EEG activity in schizophrenia patients. METHODS: A novel assessment method was applied to identify the independent contributing sources of resting-state EEG and assess the phase discontinuity in schizophrenia patients (N = 148) and healthy subjects (N = 143). RESULTS: A network of 11 primary contributing sources of scalp EEG was identified in both groups. Schizophrenia patients showed abnormal elevations of EEG power in the temporal region in the theta, beta, and gamma-bands, as well as the posterior cingulate gyrus in the delta, theta, alpha, and beta-bands. The higher theta-band power in the middle temporal gyrus was significantly correlated with verbal memory impairment in patients. The peak frequency of alpha was lower in patients in the cingulate and temporal regions. Furthermore, patients showed a higher rate of alpha phase discontinuity in the temporal region as well as a lower rate of theta phase discontinuity in the temporal and posterior cingulate regions. CONCLUSIONS: Abnormal rates of phase discontinuity of alpha- and theta-band, abnormal elevations of EEG power in multiple bands, and a lower peak frequency of alpha were identified in schizophrenia patients at rest. Clarification of the mechanistic substrates of abnormal phase discontinuity may clarify core pathophysiologic abnormalities of schizophrenia and contribute to the development of novel biomarkers for therapeutic interventions.
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