An increasing number of schizophrenia studies have been examining electroencephalography (EEG) data using time-frequency analysis, documenting illness-related abnormalities in neuronal oscillations and their synchronization, particularly in the gamma band. In this article, we review common methods of spectral decomposition of EEG, time-frequency analyses, types of measures that separately quantify magnitude and phase information from the EEG, and the influence of parameter choices on the analysis results. We then compare the degree of phase locking (ie, phase-locking factor) of the gamma band (36-50 Hz) response evoked about 50 milliseconds following the presentation of standard tones in 22 healthy controls and 21 medicated patients with schizophrenia. These tones were presented as part of an auditory oddball task performed by subjects while EEG was recorded from their scalps. The results showed prominent gamma band phase locking at frontal electrodes between 20 and 60 milliseconds following tone onset in healthy controls that was significantly reduced in patients with schizophrenia (P = .03). The finding suggests that the early-evoked gamma band response to auditory stimuli is deficiently synchronized in schizophrenia. We discuss the results in terms of pathophysiological mechanisms compromising event-related gamma phase synchrony in schizophrenia and further attempt to reconcile this finding with prior studies that failed to find this effect.

Introduction Only about one third of patients at high risk for psychosis based on current clinical criteria convert to a psychotic disorder within a 2.5-year follow-up period. Targeting clinical high-risk (CHR) individuals for preventive interventions could expose many to unnecessary treatments, underscoring the need to enhance predictive accuracy with non-clinical measures. Candidate measures include event-related potential (ERP) components with established sensitivity to schizophrenia. Here we examined the mismatch negativity (MMN) component of the ERP elicited automatically by auditory deviance in CHR and early illness schizophrenia (ESZ) patients. We also examined whether MMN predicted subsequent conversion to psychosis in CHR patients. Method MMN to auditory deviants (duration, frequency, and duration+frequency “double deviant”) were assessed in 44 healthy controls (HC), 19 ESZ, and 38 CHR patients. Within CHR patients, 15 converters to psychosis were compared to 16 non-converters with at least 12 months of clinical follow-up. Hierarchical Cox regression examined the ability of MMN to predict time to psychosis onset in CHR patients. Results Irrespective of deviant type, MMN was significantly reduced in ESZ and CHR patients relative to HC, and in CHR converters relative to non-converters. MMN did not significantly differentiate ESZ and CHR patients. The duration+frequency double deviant MMN, but not the single deviant MMNs, significantly predicted the time to psychosis onset in CHR patients. Conclusions Neurophysiological mechanisms underlying automatic processing of auditory deviance, as reflected by the duration+frequency double deviant MMN, are compromised prior to psychosis onset, and can enhance the prediction of psychosis risk among CHR patients.

During talking, a corollary discharge prepares cortex for self-generated sounds, minimizing responsiveness and providing a way to recognize sounds as self-generated. When we talk, we are the agent producing the sound and know what sound to expect. The auditory ERP N1 is normally suppressed during talking, but less so in schizophrenia, perhaps due to deficits in agency and expectancy inherent to talking. N1 was assessed in 27 patients (23 schizophrenia, 4 schizoaffective) and 26 controls. During talking, subjects said "ah" every 1-2 s. During agency, subjects pressed a button to deliver "ah" every 1-2 s. During expectancy, "ah" followed a visual warning. Talking yielded greatest N1 suppression in controls and greatest suppression failure in patients. Agency and expectancy had modest suppression effects on N1 and only in controls. Group differences in expectancy and agency could not account for failed corollary discharge during talking in patients.