Error processing in normal aging and in basal ganglia disorders.

Recently it has been shown that effects of aging and pathologically induced changes of basal ganglia structures may have quite similar effects on cognitive functions mediated by the medial prefrontal cortex. The question appears, if this pattern may be assignable to other cognitive functions that are mediated via the basal ganglia and medial prefrontal brain areas. Error processing is a component of executive functions that also depends on these areas and especially on the anterior cingulate cortex (ACC). Hence we ask, if error processing functions are differentially modulated by normal aging and basal ganglia diseases. Error processing mechanisms in these groups were investigated using a cognitive event-related potential (ERP), the error negativity. Enrolling an extended sample of young and elderly controls, as well as patients with Parkinson's and Huntington's disease, we show that modulations of error processing differ between aging, different basal ganglia diseases. Despite that the examined basal ganglia disorder groups (Parkinson's and Huntington's disease) differ in their age they show similar modulations in error processing, suggesting that aging effects are overridden by pathogenic effects. The study shows that it may be valuable to compare aging not only to different forms of basal ganglia disorders in order to gain knowledge about age- and disease-related mechanisms and the effects of these on cognitive functions. Diseases of the basal ganglia may impact error processing above and beyond the effects of normal aging. Although many aging, Parkinson's disease and Huntington's disease studies on error processing functions have already been published, this study ties together several related observations across all of these groups in one experiment.

Error processing in patients with Parkinson's disease: the influence of medication state.

One of the hallmarks of Parkinson's disease (PD) is a depletion of dopamine. Error processing, as reflected in a component of the event-related potential, the so-called error (related) negativity (Ne or ERN) is likely dependent on the midbrain dopaminergic system. In case of an unfavourable event such as an error, this system is assumed to send an error signal to the mediofrontal cortex, which elicits the Ne. Hence, the Ne should be altered in patients with PD. In fact, we earlier found a reduction of the Ne in medicated patients with PD in different tasks while another group found no such reduction in "off-medication" patients in a flanker task. In the present study, we reinvestigated this issue by measuring the Ne in a large group of treated PD patients in the "on"- and "off"-parkinsonian medication state and in matched control subjects in a flanker task. The Ne was found to be the same in the "on-medication" and "off-medication" state, while the motor score in the Unified Parkinson's Disease Rating Scale was different. In both medication states the Ne was smaller in the patients than in the controls. The results show that the Ne reduction found earlier is unaffected by short-term differences in parkinsonian medication. The question remains open whether the long-term medication could have contributed to the Ne reduction.

Effects of stimulus-response compatibility in Parkinson's disease: a psychophysiological analysis.

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.