“Wylie, Ridderinkhof, Bashore, & van den Wildenberg (2010). The effect of Parkinson’s disease on the dynamics of on-line and proactive cognitive control during action selection.” – Article summary

Processing irrelevant visual information sometimes activates incorrect response impulses. The engagement of cognitive control to suppress these impulses and make proactive adjustments to reduce the future impact of incorrect impulses may rely on the integrity of frontal-basal ganglia circuitry. In Parkinson’s disease, motor symptom severity is associated with within-trial (i.e. on-line) control of response impulses. This implies that basal ganglia dysfunction produced by Parkinson’s disease has selective effects on cognitive control mechanisms engaged to resolve response conflict. The primary deficits are in the on-line suppression of incorrect responses occurring in the context of a relatively spared ability to adjust control proactively and minimize future conflict.

Inhibition of stimulus-driven response impulses can be beneficial to the speed and accuracy of emitted responses. However, activation of an unwanted response may also interfere with selection of a desired response or lead to response error. On-line control refers to mechanisms to suppress incorrect response activation. Proactive control refers to adjusting control mechanisms to better adapt to future response conflict.

Response interference tasks induce conflict between a response impulse that is driven automatically by an irrelevant feature of a stimulus display and a response that is selected deliberately by the processing of relevant stimulus features.

In the Simon task, people have to make a hand movement towards a spatial location as indicated by a coloured circle. The Simon effect refers to the detrimental influence on performance of non-corresponding trials relative to the facilitative influence of corresponding trials. Non-corresponding means that the spatial location of the trial (i.e. hemisphere wise) is incongruent with the preferred movement.

This is typically explained through dual-route processing models. These models state that the spatial location or the irrelevant dimension automatically and rapidly activates the corresponding response via a direct processing route. The relevant feature engages a deliberately processing route which utilizes a slower controlled processing mechanism to translate the feature in the correct response. On corresponding trials, the direct and the deliberate route converge. On non-corresponding trials, the direct and the deliberate route conflict, slowing reaction time and increasing error rate. The size of the Simon effect reflects the extra demands and time required to suppress the interference caused by the incorrect response activation in non-corresponding trials.

It is possible that interference control mechanisms can be adjusted proactively between trials. Control processes may be tightened by trials that follow conflict trials and vice versa. This means that the Simon effect reduces following trials with response conflict.

The basal ganglia is believed to contribute to the neural mechanisms involved in the focused selection and inhibition of action. To release motor pathways from inhibition, the output structures of the basal ganglia that correspond to a particular movement must be selectively inhibited by upstream basal ganglia projections.

The direct pathway of the basal ganglia provides inhibitory control over the output structures. The indirect pathway of the basal ganglia excites basal ganglia output structures, increasing inhibition. Thus, the direct pathway decreases inhibition whereas the indirect pathway increases inhibition of an action. The basal ganglia can suppress and facilitate response commands that are competing for access to the motor system.

The ability to suppress conflicting responses may be vulnerable in the case of basal ganglia dysfunction (e.g. Parkinson’s disease). Patients with Parkinson’s disease were less effective at resolving response interference by suppressing incorrect response tendencies than healthy controls. When faced with conflict on an immediately preceding trial, participants were able to adapt to this conflict and minimize it when it occurred on the subsequent trial. Patients with Parkinson’s disease were not different than healthy controls in the ability to proactively adapt to conflict between trials.

There appeared to be a clear increase in incorrect trials when non-corresponding trials were preceded by corresponding trials. Following non-corresponding trials, a conflict adaptation process is engaged that reduces the impact of incorrect response capture on the subsequent trial. After facing and resolving the conflict induced by a non-corresponding trial, participants proactively activated control processes to minimize automatic response capture on the next trial. Healthy controls achieved better control over initial response capture following conflict.

Simon effects are sensitive to sequential effects. The Simon effects are larger for trials preceded by corresponding than for non-corresponding trials. Patients with Parkinson’s disease showed less efficient inhibition than healthy controls.

After making an error, participants slowed their reaction time on a subsequent trial and engaged control processes between trials to reduce interfering effects of conflict on the subsequent trial. Patients with Parkinson’s disease were similar to healthy controls in their ability to adapt proactively after making a response error.

More severe motor symptoms in Parkinson’s disease is associated with larger Simon effects on reaction time, accuracy and a higher proportion of fast errors on non-corresponding trials. With increases in motor symptom severity, there is an increase in response capture and less proficient suppression of the incorrect response. Increases in motor symptom severity was unrelated to measures when it comes to trials preceded by correct responses on non-corresponding trials. It was also not associated with the Simon effect on trials following an error and unrelated to a slowing of reaction time on corresponding and non-corresponding trials that were preceded by an error.

Patients with Parkinson’s disease with the most severe motor symptoms made more fast errors than patients with the least severe motor symptoms.

It is likely that patients with Parkinson’s disease did not experience enhanced conflict or show impairment in their proficiency at resolving response conflict induced by automatic processing of irrelevant spatial information. The strength of the initial response capture was most likely similar between patients with Parkinson’s disease and healthy controls.

Patients with Parkinson’s disease were less proficient at suppressing the interference arising from incorrect response capture. The ability to suppress initiated but not yet executed responses is disrupted by Parkinson’s disease and influenced by its treatment. This means that one important feature of Parkinson’s disease is a dysfunction in inhibitory control processes that operate during action selection. This especially occurs in situations where there is response conflict.

With increasing motor severity, there is a pattern of stronger response capture and less proficient suppression of response impulses. After experiencing response conflict, healthy adults are able to adjust cognitive control proactively to minimize the interfering effects of conflict that might occur on a subsequent trial. Patients with Parkinson’s disease were very similar in this. However, among patients with Parkinson’s disease, proactive control was less effective at reducing the strength of response capture by the direct route.

Selective suppression was less efficient among patients with Parkinson’s disease for both preceding trial types (i.e. corresponding or not corresponding). After facing conflict, proactive control of initial response capture allows one to respond more quickly to non-correspondence than to correspondence. This is also shown in patients with Parkinson’s disease, although the magnitude of this is reduced.

The feature integration model states that features of a stimulus and the response to it for each trial are coded into a memory event that can be activated by overlapping features in the subsequent trial. If one of the features are present in the next trial, the memory event is activated and this produces facilitation effects or interference effects, depending on whether the feature and responses mismatch.

Basal ganglia structures play an important role in the focused selection and inhibition of responses, providing a potential neural circuitry for implementing interference control. In Parkinson’s disease, there is a reduction in the capacity to suppress automatic capture by conflicting responses increases interference during response selection.