Some models of saccade generation make a distinction between the ‘when’

and the ‘where’ systems of saccade control, in which saccade latencies and gain are determined by different neural processes (Findlay & Walker, 1999). The ‘when’ system, which determines saccade latency, reflects directly the build-up of activity in saccade neurons in the intermediate layer of the SC. The ‘where’ system, which determines saccade gain, reflects patterns of neural activity across multiple brainstem structures during saccade execution. It is therefore not surprising that the discrimination task abnormally affected only saccade this website latency in the PD group. The release of attention promoted by the demands of the discrimination task may directly change only the excitability of saccade-triggering neurons in the SC. The association of smaller mean saccade gain with worse performance Sunitinib of the discrimination task in the PD group is consistent with the suggestion that the amount of pre-saccadic visual processing at the saccade target location determines the spatial accuracy of saccades

(Findlay, 1982; Findlay & Walker, 1999). Thus, in PD saccadic hypometria may be associated with a deficit in pre-saccadic visual processing. PD patients often have difficulty ignoring distracting visual stimuli in tasks where endogenous attentional selection competes with visual inputs (Deijen et al., 2006; Machado et al., 2009). Although our paradigm induced two types of abnormal saccadic facilitation in our PD group – one endogenous and another exogenous – the number of directional errors generated in the PD group did not differ from the control group. The performance of the discrimination task induced both groups to make more directional errors, but only in trials with symbol-changes at non-target locations. We propose that a

premature release of attention from fixation, induced by the intention to perform the discrimination task, allowed the peripheral symbol-changes to trigger a number of inappropriate saccades in both groups. The frequency of these directional errors depended on the timing of Phospholipase D1 the symbol-change (the SOA): fewer errors were made in trials with longer SOAs. This suggests that the triggering of a directional error was less likely if the symbol-change occurred at a time when the saccade target selection process was further advanced. The similarity of the slopes of this effect in the PD and the control group suggests that the time course of the target selection process is normal in PD at least in this paradigm. Others have recently proposed neurophysiological explanations for the apparently contradictory changes in the saccade system observed in PD (hyper-reflexivity, together with impaired saccade initiation). Chambers & Prescott (2010) proposed that in PD fixation-related inhibition in the SC might decay abnormally quickly and Terao et al.