Abstract

In a previous study, we postulated a divergence in reflexive versus voluntary saccade behavior in Parkinson’s disease (PD) patients and hypothesized a fronto-striatal dysfunction. The voluntary saccade tasks included antisaccades (AS) and remembered saccades (RemS). However, multiple cognitive processes are involved in AS and RemS and the procedures lack a visual target. The present study had two main objectives. Firstly, we wanted to extend our previous findings of disturbed AS and RemS to other intentional (endogenous, “voluntary”) saccades but now with a visible target. Therefore, an intentional prosaccade (IpS) task was used. Secondly, we investigated whether there is a different saccade behavior in PD patients and controls in conditions where the central fixation stimulus is extinguished shortly before the onset of the peripheral target (the so called gap condition) to assess the role of disengagement of visual fixation. With respect to the first objective, the present study found a clear dissociation between the performances of PD patients on reflexive saccade (RS) versus IpS tasks. Patients did not differ from controls in latency or error rate of RS. However, in the IpS task, latency was longer and error rate was higher in PD patients. Thus, the present study provides evidence that PD patients are deficient in intentional saccade tasks independent from the fact whether a target is visible or not. As to the second objective, saccades of PD patients did show a shorter latency in the gap than in the no gap condition. This suggests that the gap effect is not dominantly dependent on nigro-collicular neuronal circuits that are affected in PD. In the patients, the gap effect was reliable in the RS task, but not in the IpS condition. These discordant gap findings might suggest modulation of selected neuronal circuits involved in early sensorimotor processing. The present findings do not to support the hypothesis that impaired saccade behavior in PD patients is merely dependent on the presence or the absence of visual fixation and suggests a higher order psychomotor dysfunction, presumably of intentional nature. The dorsolateral prefrontal cortex might correspond to the premotor cognitive dysfunction site. However, an additional involvement of the frontal eye field can not be excluded from the present study.

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