Absence of congruency sequence effects reveals neurocognitive inflexibility in Parkinson's disease

• How is instantaneous and sequence-dependent cognition affected by Parkinson's disease?
• Instantaneous action selection under conflict is normal in Parkinson's disease.
• Modulation of action selection through time is disturbed in Parkinson's disease.
• N2 findings support different effects on instantaneous and sequence-dependent cognition.
• LRP findings support different effects on instantaneous and sequence-dependent cognition.

The effects of Parkinson's disease (PD) on action selection in conflictual situations were examined in an experiment using the flanker task in combination with event-related brain potentials (ERPs). More specifically, we investigated the effects of PD on behavioral and neuronal indicators of both instantaneous (within-trial flanker congruency effects) and sequence-dependent (between-trial congruency sequence effects) distractor interference. Consistent with the existing literature, congruency-sensitive ERP components (i.e., fronto-central N2 and positive ‘dips’ of the lateralized readiness potential, LRP) were observed over medial-frontal and lateral–central regions, respectively. For situations requiring instantaneous action control, patients with PD and healthy controls showed similar congruency effects on reaction time, as well as on N2 and LRP ‘dip’ amplitudes. As expected, controls showed reliable congruency sequence effects on reaction time, as well as on N2 and LRP ‘dip’ amplitudes. However, patients with PD were completely unaffected by the congruence sequence across consecutive trials, as revealed by reaction time, as well as by N2 and LRP ‘dip’ amplitudes. The data imply that the effects of PD on action selection are largely restricted to a lack of adaptive modulation in time which we refer to as neurocognitive inflexibility, in the context of relatively spared abilities to instantaneously exert control over action selection. The findings are discussed in terms of basal ganglia dysfunction induced by PD which results primarily either in executive function deficits or in aberrant habit formation.