Perceiving Collision Impacts in Alzheimer's Disease: The Effect of Retinal Eccentricity on Optic Flow Deficits.

Nam-Gyoon Kim

doi:10.3389/fnagi.2015.00218

Abstract

The present study explored whether the optic flow deficit in Alzheimer’s disease (AD) reported in the literature transfers to different types of optic flow, in particular, one that specifies collision impacts with upcoming surfaces, with a special focus on the effect of retinal eccentricity. Displays simulated observer movement over a ground plane toward obstacles lying in the observer’s path. Optical expansion was modulated by varying . The visual field was masked either centrally (peripheral vision) or peripherally (central vision) using masks ranging from 10° to 30° in diameter in steps of 10°. Participants were asked to indicate whether their approach would result in “collision” or “no collision” with the obstacles. Results showed that AD patients’ sensitivity to was severely compromised, not only for central vision but also for peripheral vision, compared to age- and education-matched elderly controls. The results demonstrated that AD patients’ optic flow deficit is not limited to radial optic flow but includes also the optical pattern engendered by . Further deterioration in the capacity to extract to determine potential collisions in conjunction with the inability to extract heading information from radial optic flow would exacerbate AD patients’ difficulties in navigation and visuospatial orientation.

Highlights

Cognitive impairment characterized by progressive memory loss is the most profound feature of Alzheimer’s disease (AD), vision is impaired
The present study explored whether the optic flow deficit Duffy and colleagues described in AD patients transfers to different types of optic flow, in particular, one that specifies collision impacts with upcoming surfaces, with a special focus on the effect of retinal eccentricity
Is the optic flow deficit in AD reported by Duffy and colleagues confined to radial optic flow or is it a more general symptom reflecting the inability of AD patients to perceive the consequences of their own movement, irrespective of movement type? Second, do abnormalities in the parasol ganglion cells, those in the retinal periphery, and the neural structures in the subsequent relay stations of the subcortical and cortical pathways, including those in MT and MST, contribute to the optic flow deficit in AD?

Summary

Introduction

Cognitive impairment characterized by progressive memory loss is the most profound feature of Alzheimer’s disease (AD), vision is impaired (for reviews, see Cronin-Golomb and Gilmore, 2003; Kirby et al, 2010; Valenti, 2010). One of the less well known forms of visual impairment in AD is optic flow deficit (Page and Duffy, 1999, 2003; Tetewsky and Duffy, 1999; O’Brien et al, 2001; Kavcic and Duffy, 2003; Mapstone et al, 2003, 2008; Monacelli et al, 2003; Duffy et al, 2004; Kavcic et al, 2006; Mapstone and Duffy, 2010). Optic flow refers to the changing optical structure at a moving point of observation (Gibson, 1966, 1986). Because optic flow is generated by an observer moving in the environment, its structure is specific to the very movement that engendered it.

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Results

Discussion

Conclusion