Source localization (LORETA) of the error-related-negativity (ERN/Ne) and positivity (Pe).

We investigated error processing of 39 subjects engaging the Eriksen flanker task. In all 39 subjects a pronounced negative deflection (ERN/Ne) and a later positive component (Pe) were observed after incorrect as compared to correct responses. The neural sources of both components were analyzed using LORETA source localization. For the negative component (ERN/Ne) we found significantly higher brain electrical activity in medial prefrontal areas for incorrect responses, whereas the positive component (Pe) was localized nearby but more rostral within the anterior cingulate cortex (ACC). Thus, different neural generators were found for the ERN/Ne and the Pe, which further supports the notion that both error-related components represent different aspects of error processing.

Allelic variation of serotonin transporter function modulates the brain electrical response for error processing.

A functional length variation in the transcriptional control region of the serotonin transporter gene (5-HTTLPR) influences brain function, personality traits, and susceptibility to psychiatric disorders. Here we measured prefrontal brain function by means of event-related potentials during an error processing paradigm. Physiologically, occurrence of an error elicits two specific electrical responses in the prefrontal cortex, the early error related negativity (Ne/ERN) and the later occurring error positivity (Pe), reflecting different components of error processing. Healthy subjects with one or two copies of the low-activity 5-HTTLPR short variant showed significantly higher amplitudes of the Ne/ERN and a trend to higher amplitudes of the Pe as compared to age- and gender-matched individuals homozygous for the long allele. Performance measures and latencies of these ERP-components did not differ between groups. These results indicate that the 5-HTTLPR short variant is associated with enhanced responsiveness of the brain and further supports the notion that prefrontal brain function is influenced by allelic variation in serotonin transporter function.

Sensory gating deficit in a subtype of chronic schizophrenic patients.

The dual click P50 paradigm has been established as a neurophysiological method to detect gating mechanisms. Studies of schizophrenic patients have shown that an insufficient reduction of the P50 amplitude after the second relative to the first stimulus indicates a deficient sensory gating mechanism. The aim of this study was to compare the P50 responses in the dual click paradigm of healthy volunteers to those of patients with different psychotic disorders, especially with regard to psychopathology and nosology according to ICD-10 and DSM-IV and to the classification system of Leonhard. A total of 34 patients and 12 healthy volunteers were investigated electrophysiologically while they performed the P50 dual click experiment. Patients with prominent negative symptoms and without perceptual abnormalities and patients with a hebephrenic subtype of schizophrenia showed less suppression in the dual click P50 paradigm than did healthy controls. Patients with brief/acute and transient psychotic disorders or cycloid psychoses did not differ from healthy volunteers with regard to suppression in the dual click P50 paradigm. No striking influence of gender, age, duration of disease and present medication was found. The findings confirm the lack of sensory gating measured by the dual click P50 paradigms in some but not all patients with schizophrenia. Both subtype of schizophrenia and current form of psychopathology appear to be related to the presence or absence of abnormal sensory gating.

Face-specific event-related potential in humans is independent from facial expression.

A face-specific brain EEG potential at approximately 160 ms after stimulus presentation has recently been described by various research groups. Most of these studies analysed this face-specific brain potential using smiling faces as stimuli. In electrophysiological studies, however, differences in amplitude due to the emotional valence of the stimuli were described as early as 100 ms after stimulus presentation. In order to investigate the effect of facial expressions with different emotional content on face-specific brain EEG potentials, event-related potentials (ERPs) to faces with sad, happy and neutral expressions were compared to ERPs elicited with buildings in 16 healthy subjects. A face-specific potential at vertex approximately 160 ms after stimulus presentation has been verified in the present study. No significant differences in latency or amplitude of this component were found for different facial expressions.