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The purpose of the present paper was to determine error-monitoring ability and its relationship with executive function in patients with schizophrenia. In order to evaluate error-monitoring ability, the error negativity (Ne) and error positivity (Pe) were measured using the Stroop task. The correct-related negativity (CRN) and positivity (Pc) were also measured. In addition, neuropsychological tests were administered in order to evaluate executive function. The patients with schizophrenia had significantly reduced Ne and augmented CRN amplitudes, but the Pe and Pc amplitudes of the patients were comparable to those of the controls. In addition, the Ne amplitude, measured at Fcz was positively correlated with the Trail Making Test (TMT), part B response time, and the categories achieved on the Wisconsin Card Sorting Test (WCST) in patients with schizophrenia. No significant correlations were found between Ne amplitude and performance on the neuropsychological tests in the controls. And no associations were detected between CRN, Pe, Pc amplitudes and neuropsychological performance, in either the patients with schizophrenia or the controls. Reduced Ne amplitudes and augmented CRN amplitudes in patients with schizophrenia suggest the dysfunctional behavior-monitoring system in these patients. The functional significances of Ne and Pe are discussed.

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Although regional brain abnormalities underlying spatial working memory (SWM) deficits in schizophrenia have been identified, little is known about which brain circuits are functionally disrupted in the SWM network in schizophrenia. We investigated SWM-related interregional functional connectivity in schizophrenia using functional magnetic resonance imaging (fMRI) data collected during a memory task that required analysis of spatial information in object structure. Twelve schizophrenia patients and eleven normal control subjects participated. Patients had SWM performance deficits and deficient neural activation in various brain areas, especially in the high SWM load condition. Examination of the covariation of regional brain activations elicited by the SWM task revealed evidence of functional disconnection between prefrontal and posterior visual association areas in schizophrenia. Under low SMW load, we found reduced functional associations between dorsolateral prefrontal cortex (DLPFC) and inferior temporal cortex (ITC) in the right hemisphere in patients. Under high SWM load, we found evidence for further functional disconnection in patients, including additional reduced functional associations between left DLPFC and right visual areas, including the posterior parietal cortex (PPC), fusiform gyrus, and V1, as well as between right inferior frontal cortex and right PPC. Greater prefrontal-posterior cortical functional connectivity was associated with better SWM performance in controls, but not in patients. These results suggest that prefrontal-posterior functional connectivity associated with the maintenance and control of visual information is central to SWM, and that disruption of this functional network underlies SWM deficits in schizophrenia.

Deficits in response inhibition have been observed in schizophrenia and bipolar disorder; however, the neural origins of the abnormalities and their relevance to genetic liability for psychosis are unknown. We used a stop‐signal task to examine motor inhibition and associated neural processes in schizophrenia patients (n = 57), bipolar disorder patients (n = 21), first‐degree biological relatives of patients with schizophrenia (n = 34), and healthy controls (n = 56). Schizophrenia patients demonstrated motor control deficits reflected in longer stop‐signal reaction times and elongated reaction times. With the possibility of needing to inhibit a button press, both schizophrenia and bipolar disorder patients showed diminished reductions of the P300 brain response and only the healthy controls demonstrated adjustments in response execution time, as measured by response‐locked lateralized readiness potentials. Schizotypal traits in the biological relatives were associated with less P300 modulation consistent with the motor‐related anomalies being associated with subtle schizophrenia‐spectrum symptomatology in family members. The two patient groups had elongated response selection processes as manifest in the delayed onset of the stimulus‐locked lateralized readiness potential. The bipolar disorder group was unique in showing significantly diminished neural responses to the stop‐signal to inhibit a response. Antipsychotic medication dosage was related to worse motor inhibition, thus motor inhibition deficits in schizophrenia may be partially explained by the effect of pharmacological agents. Failed modulation of brain processes in relation to response inhibition probability and the lengthening of motor response selection appear to be transdiagnostic abnormalities spanning schizophrenia and bipolar disorder.

Time-frequency-spatial analysis identified process- and frequency-specific neural synchrony abnormalities underlying WM deficits in schizophrenia.

Although errant saccadic eye movements may mark genetic factors in schizophrenia, little is known about abnormal brain activity that precedes saccades in individuals with genetic liability for schizophrenia. We investigated electrophysiological activity preceding prosaccades and antisaccades in schizophrenia patients, first-degree biological relatives of schizophrenia patients, and control subjects. Prior to antisaccades patients had reduced potentials over lateral prefrontal cortex. Smaller potentials were associated with worse antisaccade performance. Relatives also exhibited reduced pre-saccadic potentials over lateral frontal cortex but additionally had reduced potentials over parietal cortex. Both patients and relatives tended toward increased activity over orbital frontal cortex prior to saccades. Results are consistent with lateral prefrontal dysfunction marking genetic liability for schizophrenia and underlying deficient saccadic control.

Background: Measures of the coherence of electroencephalography (EEG) time-series recorded at spatially distant points on the scalp are often used by researchers to characterize the dynamic interactions of brain regions. In dense-array EEG recordings, one or more electrode signals often contain prominent artifact necessitating replacement of the recorded data with an estimated signal using interpolation from data in valid recordings from the surrounding electrodes. Typically the signal estimation is carried out using spherical spline interpolation (SSI; Perrin et al., 1989); however, it is shown that this can introduce an erroneous increase in coherence between signals because the estimated signal is derived from elements in common recordings from other electrode sites. Although SSI performance depends on three SSI parameters, including interpolation order m, the Legendre polynomial order n, and regularization parameter λ, clear guidelines on how to optimally choose parameters have yet to be established for ensuring the temporal features of interpolated signals are accurate.