The error negativity (Ne or ERN) is an event-related brain potential component, which is assumed to reflect error detection. Recently it has been hypothesized that the basal ganglia are assumed to play a crucial role in error detection. In the present study we ask whether the Ne is altered in patients with Parkinson's disease (PD), who have an impaired function of the basal ganglia. We recorded the Ne in patients and in matched controls, while they performed different tasks that require a relatively high cognitive control, which is supposed to pose particular problems on PD. The Ne was in fact smaller in the patients than in the controls in all tasks. Our results suggest an impairment of error detection in PD for different types of demanding tasks. This supports the hypothesis that the basal ganglia do play an important role for error detection in action monitoring.

The present study investigated the mechanisms underlying stimulus-response compatibility effects in Parkinson's disease patients and matched controls. Since basal ganglia are involved in the selection and inhibition of competing responses we examined whether basal ganglia dysfunction in Parkinson's disease leads to greater interference effects compared to the control subjects. Reaction times and lateralized movement-related cortical potentials (lateralized readiness potential: LRP) were recorded in two modified Eriksen flanker tasks. Both groups were influenced by compatibility conditions; interference was seen as enhanced reaction time and error rate, as well as incorrect early LRP and delayed late LRP in incongruent trials. Altogether, behavioral and electrophysiological measures showed the interference to be rather smaller for the patients than for the controls. In contrast, facilitation did not differ among groups. Hence the claim that Parkinson's disease patients are more influenced than controls by interfering directional stimuli appears not always valid.

Parkinson's disease (PD) is a neurodegenerative basal ganglia disorder accompanied by deficits in cognitive functions. One important executive function is the inhibition of responses. Due to basal ganglia damage, processes related to the selection of response are also dysfunctional. However, the relevance of deficits in response selection to processes related to response inhibition in PD is not clear. In this study we examined these processes by means of event-related potentials (ERPs) in two Go/Nogo tasks. In one task the stimulus-response mapping was compatible and in the other task it was incompatible with the meaning of the stimuli. The behavioural results show that PD patients were unaffected in the compatible response inhibition task but encountered problems in the incompatible one. In the ERPs the N2, generally reflecting response selection, was delayed for the PD compared to the control group. This suggests that response selection is delayed in PD. Moreover, the N2 was specifically enhanced in Nogo trials. This indicates that premotor inhibition, which is probably reflected by the Nogo-N2, is intensified in PD. The P3 was specifically attenuated and delayed after Nogo stimuli in the incompatible condition for PDs. Assuming that the Nogo-P3 reflects the evaluation of successful motor inhibition, our data show that this process is attenuated and delayed in PD but mainly in the incompatible task. The results suggest that inhibitory deficits in PD are only evident in complex (incompatible) stimulus-response mappings. These effects are probably due to an overstrain of striatal processes.