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Original Articles

Pathological completion in the intact visual field of hemianopia patients

ORCID Icon, ORCID Icon, ORCID Icon & ORCID Icon
Pages 169-183 | Received 19 Dec 2016, Accepted 26 Jun 2017, Published online: 02 Aug 2017
 

ABSTRACT

We investigated figure segregation in the intact visual field (VF) of hemianopia patients. Three patients and matched controls performed a Yes–No figure detection task, where square or square fragments were embedded in a background of randomly oriented Gabor elements. We varied orientation and number of the fragment elements, stimulus eccentricity and background density (BD). Figure detection was impaired in all three patients in the entire intact VF, but potentially more pronounced in patients with cortical lesions. “Pathological completion” was most frequently observed for high BDs and for square fragments oriented towards the blind hemifield. Our findings confirm contour integration deficits in the intact VF of hemianopia patients. Further, our results indicate that (1) contour integration deficits are exacerbated by contextual interaction and (2) “pathological completion” appears to be more likely associated with lesions of cortical rather than geniculo-striate origin. The deficits point to increased lateral suppressive inputs from background elements.

Acknowledgements

The authors wish to thank U. Bunzenthal for excellent assistance in recruiting subjects. We are grateful to C. Altmann for making available his stimulus program, to B. Herwig for developing the software for stimulus generation, to U. Polat and L. Spillmann for insightful comments on the experiment design. We thank the subjects of this study for their time, understanding and collaborative spirit. Results were partly presented at the 38th European Conference on Visual Perception, 23–27 August 2015, Liverpool, UK. We are grateful to two anonymous reviewers whose detailed and constructive comments to an earlier version of the manuscript were helpful for improving the paper.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by the Swiss National Science Foundation (SNF) Grant #51NF40-158776, the National Centre of Competence in Research (NCCR) “SYNAPSY-The Synaptic Basis of Mental Diseases”, to OF and MHH from the École Polytechnique Fédérale de Lausanne, Switzerland.

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