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Lesions to right posterior parietal cortex impair visual depth perception from disparity but not motion cues.

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Peer-reviewed

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Article

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Authors

Murphy, Aidan P 
Leopold, David A 
Humphreys, Glyn W 
Welchman, Andrew E 

Abstract

The posterior parietal cortex (PPC) is understood to be active when observers perceive three-dimensional (3D) structure. However, it is not clear how central this activity is in the construction of 3D spatial representations. Here, we examine whether PPC is essential for two aspects of visual depth perception by testing patients with lesions affecting this region. First, we measured subjects' ability to discriminate depth structure in various 3D surfaces and objects using binocular disparity. Patients with lesions to right PPC (N = 3) exhibited marked perceptual deficits on these tasks, whereas those with left hemisphere lesions (N = 2) were able to reliably discriminate depth as accurately as control subjects. Second, we presented an ambiguous 3D stimulus defined by structure from motion to determine whether PPC lesions influence the rate of bistable perceptual alternations. Patients' percept durations for the 3D stimulus were generally within a normal range, although the two patients with bilateral PPC lesions showed the fastest perceptual alternation rates in our sample. Intermittent stimulus presentation reduced the reversal rate similarly across subjects. Together, the results suggest that PPC plays a causal role in both inferring and maintaining the perception of 3D structure with stereopsis supported primarily by the right hemisphere, but do not lend support to the view that PPC is a critical contributor to bistable perceptual alternations.This article is part of the themed issue 'Vision in our three-dimensional world'.

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Keywords

binocular vision, bistable, depth perception, parietal cortex, structure from motion, Aged, Aged, 80 and over, Brain Diseases, Cues, Depth Perception, Female, Humans, Male, Middle Aged, Motion, Parietal Lobe, Perceptual Disorders, Visual Perception

Journal Title

Philos Trans R Soc Lond B Biol Sci

Conference Name

Journal ISSN

0962-8436
1471-2970

Volume Title

371

Publisher

Royal Society Publishing
Sponsorship
Wellcome Trust (095183/Z/10/Z)
This research was supported by a Wellcome Trust-NIH PhD studentship (WT091467MA) to A.P.M., a Wellcome Trust Fellowship (095183/Z/10/Z) to A.E.W., and grants from the MRC and the Stroke Association to G.W.H. D.A.L. and A.P.M. are supported by the Intramural program of the National Institutes of Health