September 2021
Volume 21, Issue 9
Open Access
Vision Sciences Society Annual Meeting Abstract  |   September 2021
More and faster secondary saccades after a lesion to the posterior parietal cortex
Author Affiliations
  • Sanne Böing
    Utrecht University
  • Jasper H. Fabius
    University of Glasgow
  • Tanja C.W. Nijboer
    Utrecht University
    Center of Excellence for Rehabilitation Medicine, University Medical Center Utrecht and De Hoogstraat Rehabilitation
  • Stefan Van der Stigchel
    Utrecht University
Journal of Vision September 2021, Vol.21, 1985. doi:
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      Sanne Böing, Jasper H. Fabius, Tanja C.W. Nijboer, Stefan Van der Stigchel; More and faster secondary saccades after a lesion to the posterior parietal cortex. Journal of Vision 2021;21(9):1985.

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      © ARVO (1962-2015); The Authors (2016-present)

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Background: The posterior parietal cortex (PPC) was thought to be indispensable for processing extraretinal signals to generate accurate secondary saccades (S2). However, recent studies show that patients with chronic PPC lesions use some form of extraretinal signals to perform S2s or to perform the intrasaccadic displacement task. Hence, a PPC lesion might result in less reliable processing of extraretinal signals, instead of completely abolishing it. In this study, we investigated whether this lesser extraretinal reliability manifests itself as a decreased or delayed S2 initiation. Method: Patients and healthy controls performed a saccadic localization task (prosaccades) in two conditions. In one condition the target remained visible after the execution of the primary saccade (S1), in the other condition, the target was removed from the screen for 1 second. In the second condition, but not the first, accurate corrections (i.e. S2 generation) of S1 error relied more on extraretinal signals. S2 generation was analysed using linear mixed-effects modelling. Additive hazards analyses were performed to assess the time course of S2 generation within groups. Results: Although patients demonstrated slower S1 execution and lower S1 amplitudes than controls, they were able to generate S2s in order to overcome S1 inaccuracy, both when the target remained visible and when it was removed after S1. Furthermore, patients showed more and seemingly earlier S2 generation. Conclusion: These findings support the hypothesis that a PPC lesion does not abolish the use of extraretinal signals. Although patients’ behaviour differed from that of healthy controls and could therefore be regarded as deviant, we suggest that the observed change in oculomotor behaviour after a PPC lesion reflects an adjustment to increased sensorimotor noise. This implies that more and faster S2s could be optimal given the PPC lesion.


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