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作 者:Julie Ouerfelli-Ethier Aarlenne Z.Khan Laure Pisella
机构地区:[1]School of Optometry,University of Montreal,Montreal,QC,Canada [2]ImpAct,INSERM UM1028,CNRS UMR 5292,University Claude Bernard Lyon 1,Bron,France
出 处:《Annals of Eye Science》2019年第1期189-189,共1页眼科学年鉴(英文)
摘 要:Background:Performing an anti-saccade relies on two mechanisms:(I)inhibiting an automatic saccade to a target,and(II)generating,instead,a voluntary saccade to a location other than this visual target.It remains unclear where and how these two processes are implemented to ensure the production of correct anti-saccades.Previous research in optic ataxia has implicated the posterior parietal cortex(PPC)in anti-pointing,implying a possible role of the PPC in anti-saccade production.Methods:Here,we tested how three patients with unilateral or bilateral damage to the PPC,as well as six neurologically intact controls,perform different types of anti-saccade:classic anti-saccades(180°rotation)or mirror saccades(90°rotation)across and within hemi-fields.Results:We showed that PPC damaged patients were impaired in anti-saccade production for their contralesional visual fields.This was reflected in a longer period of erroneous pro-saccades,longer latencies associated with correct anti-saccades to the contralesional visual field and more imprecise anti-saccades.Conclusions:Our results thus suggest that PPC damage results in delayed and prolonged competing saccade planning processes between two locations(i.e.,visual target and saccade goal location).Taken together,our results provide evidence for a crucial role of the PPC in parallel mechanisms underlying anti-saccade performance.
关 键 词:Saccade planning anti-saccade inhibition posterior parietal cortex(PPC)
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