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      Enhanced Depth Navigation Through Augmented Reality Depth Mapping in Patients with Low Vision

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          Abstract

          Patients diagnosed with Retinitis Pigmentosa (RP) show, in the advanced stage of the disease, severely restricted peripheral vision causing poor mobility and decline in quality of life. This vision loss causes difficulty identifying obstacles and their relative distances. Thus, RP patients use mobility aids such as canes to navigate, especially in dark environments. A number of high-tech visual aids using virtual reality (VR) and sensory substitution have been developed to support or supplant traditional visual aids. These have not achieved widespread use because they are difficult to use or block off residual vision. This paper presents a unique depth to high-contrast pseudocolor mapping overlay developed and tested on a Microsoft Hololens 1 as a low vision aid for RP patients. A single-masked and randomized trial of the AR pseudocolor low vision aid to evaluate real world mobility and near obstacle avoidance was conducted consisting of 10 RP subjects. An FDA-validated functional obstacle course and a custom-made grasping setup were used. The use of the AR visual aid reduced collisions by 50% in mobility testing (p = 0.02), and by 70% in grasp testing (p = 0.03). This paper introduces a new technique, the pseudocolor wireframe, and reports the first significant statistics showing improvements for the population of RP patients with mobility and grasp.

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            Retinitis pigmentosa.

            Hereditary degenerations of the human retina are genetically heterogeneous, with well over 100 genes implicated so far. This Seminar focuses on the subset of diseases called retinitis pigmentosa, in which patients typically lose night vision in adolescence, side vision in young adulthood, and central vision in later life because of progressive loss of rod and cone photoreceptor cells. Measures of retinal function, such as the electroretinogram, show that photoreceptor function is diminished generally many years before symptomic night blindness, visual-field scotomas, or decreased visual acuity arise. More than 45 genes for retinitis pigmentosa have been identified. These genes account for only about 60% of all patients; the remainder have defects in as yet unidentified genes. Findings of controlled trials indicate that nutritional interventions, including vitamin A palmitate and omega-3-rich fish, slow progression of disease in many patients. Imminent treatments for retinitis pigmentosa are greatly anticipated, especially for genetically defined subsets of patients, because of newly identified genes, growing knowledge of affected biochemical pathways, and development of animal models.
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              Retinitis pigmentosa

              Retinitis pigmentosa (RP) is an inherited retinal dystrophy caused by the loss of photoreceptors and characterized by retinal pigment deposits visible on fundus examination. Prevalence of non syndromic RP is approximately 1/4,000. The most common form of RP is a rod-cone dystrophy, in which the first symptom is night blindness, followed by the progressive loss in the peripheral visual field in daylight, and eventually leading to blindness after several decades. Some extreme cases may have a rapid evolution over two decades or a slow progression that never leads to blindness. In some cases, the clinical presentation is a cone-rod dystrophy, in which the decrease in visual acuity predominates over the visual field loss. RP is usually non syndromic but there are also many syndromic forms, the most frequent being Usher syndrome. To date, 45 causative genes/loci have been identified in non syndromic RP (for the autosomal dominant, autosomal recessive, X-linked, and digenic forms). Clinical diagnosis is based on the presence of night blindness and peripheral visual field defects, lesions in the fundus, hypovolted electroretinogram traces, and progressive worsening of these signs. Molecular diagnosis can be made for some genes, but is not usually performed due to the tremendous genetic heterogeneity of the disease. Genetic counseling is always advised. Currently, there is no therapy that stops the evolution of the disease or restores the vision, so the visual prognosis is poor. The therapeutic approach is restricted to slowing down the degenerative process by sunlight protection and vitaminotherapy, treating the complications (cataract and macular edema), and helping patients to cope with the social and psychological impact of blindness. However, new therapeutic strategies are emerging from intensive research (gene therapy, neuroprotection, retinal prosthesis).
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                Author and article information

                Contributors
                nikolasa@stanford.edu
                humayun@med.usc.edu
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                2 August 2019
                2 August 2019
                2019
                : 9
                : 11230
                Affiliations
                [1 ]ISNI 0000 0001 2156 6853, GRID grid.42505.36, University of Southern California, USC Ginsburg Institute for Biomedical Therapeutics, ; Los Angeles, 90033 USA
                [2 ]ISNI 0000000419368956, GRID grid.168010.e, Stanford University, Department of Electrical Engineering, ; Stanford, 94301 USA
                [3 ]ISNI 0000 0001 2156 6853, GRID grid.42505.36, University of Southern California Keck School of Medicine, USC Roski Eye Institute, ; Los Angeles, 90033 USA
                Article
                47397
                10.1038/s41598-019-47397-w
                6677879
                31375713
                c3adabc2-2d1b-4324-acb1-16ea62f3ed5f
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 20 May 2019
                : 15 July 2019
                Categories
                Article
                Custom metadata
                © The Author(s) 2019

                Uncategorized
                translational research,software,biomedical engineering
                Uncategorized
                translational research, software, biomedical engineering

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