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Basal ganglia structures comprise a portion of the neural circuitry that is hypothesized to coordinate the selection and suppression of competing responses. Parkinson's disease (PD) may produce a dysfunction in these structures that alters this capacity, making it difficult for patients with PD to suppress interference arising from the automatic activation of salient or overlearned responses. Empirical observations thus far have confirmed this assumption in some studies, but not in others, due presumably to considerable inter-individual variability among PD patients. In an attempt to help resolve this controversy, we measured the performance of 50 PD patients and 25 healthy controls on an arrow version of the Eriksen flanker task in which participants were required to select a response based on the direction of a target arrow that was flanked by arrows pointing in the same (congruent) or opposite (incongruent) direction. Consistent with previous findings, reaction time (RT) increased with incongruent flankers compared to congruent or neutral flankers, and this cost of incongruence was greater among PD patients. Two novel findings are reported. First, distributional analyses, guided by dual-process models of conflict effects and the activation–suppression hypothesis, revealed that PD patients are less efficient at suppressing the activation of conflicting responses, even when matched to healthy controls on RT in a neutral condition. Second, this reduced efficiency was apparent in half of the PD patients, whereas the remaining patients were as efficient as healthy controls. These findings suggest that although poor suppression of conflicting responses is an important feature of PD, it is not evident in all medicated patients.

Responding optimally in a visual environment often requires attentional navigation of relevant and irrelevant stimuli as well as the capacity to control responses that might be signaled by these stimuli. In some instances, a response to a visual stimulus is overlearned and activation related to this response may be triggered automatically by the presence of the stimulus, even if the stimulus is irrelevant to the task at hand. Depending on the circumstances, this automatic stimulus–response activation can be advantageous or disadvantageous to performance. For instance, when automatic response activation anticipates a preferred course of action, the speed and accuracy of selecting the preferred response is facilitated (Burle, van den Wildenberg, & Ridderinkhof, 2005). In contrast, conflict between an automatically activated response and a preferred response interferes with the speed and accuracy of selecting the preferred response (Botvinick, Braver, Barch, Carter, & Cohen, 2001). In the case of conflict, cognitive control is necessary to suppress the automatic response activation in order to minimize interference with the selection of the preferred action (Ridderinkhof, van den Wildenberg, Segalowitz, & Carter, 2004a; Ridderinkhof, van den Wildenberg, Wijnen, & Burle, 2004b). Anyone who has attempted to type a sentence quickly using a keyboard with an unfamiliar key arrangement can appreciate the amount of cognitive control required to suppress the automatic, overlearned keystrokes (e.g., typing with a Dvorak key arrangement after learning a Qwerty layout).

The action selection and inhibition model of basal ganglia function offers an influential and intriguing framework for understanding some of the cognitive deficits produced by PD. Here we demonstrate that PD can produce poor interference control during action selection relative to healthy controls, and the basis of this problem stems from less effective suppression of what appears to be a more strongly activated incorrect response. Not all patients show a strong pattern of poor inhibitory control; however, when controlling for baseline RT, there is a hypothesized pattern of stronger activation of an incorrect response followed by poorer suppression of this response among PD patients. Future work is needed to determine what neuropathological processes are responsible for cognitive control deficits among PD patients, what factors contribute to the variability of cognitive control deficits among PD patients, and whether all PD patients eventually show similar deficits.