Obsessive-compulsive disorder (OCD) has been related to a hyperactive frontal-striatal-thalamic circuit and associated with altered mechanisms of action and error monitoring. In the present study, we examined whether these results only hold for errors in choice reaction time experiments and Stroop tasks or extend to errors of commission in a Go/NoGo task, as well. We investigated the electrophysiological correlates of error monitoring in 11 patients with OCD and 11 age-, sex-, and education-matched healthy controls using event-related potentials (ERPs). Participants performed a Go/NoGo task while a 64-channel EEG was recorded. Our study focused on three ERP components: the error-related negativity (ERN)/error negativity (Ne), the “early” error positivity (“early” Pe) reflecting automatic error processing, and the “late” error positivity (“late” Pe), which is thought to mirror the awareness of erroneous responses. Artifact-free EEG-segments were used to compute ERPs on correct Go trials and incorrect NoGo trials (i.e., errors of commission), separately. Patients with OCD showed enhanced (more negative) ERN/Ne amplitudes compared to control subjects. Groups did not differ with regard to the early Pe component and the late Pe component. Our results support the view that compulsivity in OCD patients is related to hyper-functioning error monitoring processes.

Borderline personality disorder (BPD) has been related to a dysfunction of anterior cingulate cortex, amygdala, and prefrontal cortex and has been associated clinically with impulsivity, affective instability, and significant interpersonal distress. We examined 17 patients with BPD and 17 age-, sex-, and education matched control participants with no history of Axis I or II psychopathology using event-related potentials (ERPs). Participants performed a hybrid flanker-Go/Nogo task while multichannel EEG was recorded. Our study focused on two ERP components: the Nogo-N2 and the Nogo-P3, which have been discussed in the context of response inhibition and response conflict. ERPs were computed on correct Go trials (button press) and correct Nogo trials (no button press), separately. Groups did not differ with regard to the Nogo-N2. However, BPD patients showed reduced Nogo-P3 amplitudes. For the entire group (n = 34) we found a negative correlation with the Barratt Impulsiveness Scale (BIS-10) and Becks's depression inventory (BDI). The present study is the first to examine Nogo-N2 and Nogo-P3 in BPD and provides further evidence for impaired response inhibition in BPD patients.

Impulsiveness has been linked to fast guesses and premature responses in reaction time tasks like the Eriksen flanker task or the Go/Nogo task. In the present study, healthy subjects without history of DSM-IV Axis I or II psychopathology were examined. Impulsiveness was determined by calculating individual reaction times (as a function of general response speed) in order to split the entire group (n = 26) in a subgroup with a more controlled response style (low impulsiveness [LI] group; n = 13) and a subgroup with a more impulsive response style (high impulsiveness [HI] group; n = 13). Subjects performed a Go/Nogo task while a multi-channel EEG was recorded. Two event-related potentials (ERP) were of special interest: the Nogo-N2 and -P3 component. HI subjects had significantly reduced (less positive) Nogo-P3 amplitudes compared to LI subjects whereas groups did not differ with regard to the Nogo-N2. These results corroborate previous findings of reduced Nogo-P3 amplitudes in samples with enhanced levels of impulsiveness. Moreover, present data suggest that there is a broader range of impulsiveness even in healthy subjects which might mask or pronounce between-group differences in clinical studies. Therefore, different levels of impulsiveness in control groups should be carefully taken into account in further ERP studies.

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