Project summary
This proposal tests a novel `scotoma awareness' approach to aid those with Macular Degeneration (MD). MD
is the leading cause of central vision loss worldwide. MD patients spontaneously develop oculomotor strategies
to overcome loss of central vision, such as developing a new peripheral fixation spot to replace the fovea
(preferred retinal locus, or PRL). However, development of a PRL and the rate of success in developing one
vary greatly, meaning some patients live years without making effective use of their spared vision. Recent,
studies in Vision Science show that training healthy participants with gaze-contingent displays, obstructing
central vision (`simulated scotoma'), leads to development of PRLs at a faster time scale than found for MD
patients. Additionally, oculomotor metrics developed in our lab, are effective in characterizing individual eye
movement patterns in simulated scotoma participants. The ability to describe differences in compensatory
strategies in MD represents a crucial step towards individualized rehabilitative strategies, which could be
further improved by accelerating PRL development. However, it is unclear whether these results can be
reproduced in those with MD. It has been suggested that the visible, sharp-edged occluder in the gaze-
contingent displays increases scotoma awareness, thus accelerating PRL development. Many MD patients are
unaware of the location of their scotoma, with some persisting to use their damaged fovea as a fixation spot.
No study to date has translated the use of a simulated scotoma to promote rapid PRL development in MD
patients. As a first step towards addressing individual differences in patients and examine whether Vision
Science paradigms can be used as a rehabilitative tool in MD, we propose two Aims: In Aim 1 we will use a set
of oculomotor metrics to characterize individual profiles of compensation. In Aim 2 we will test the effectiveness
of the visible, simulated scotoma as a technique to promote the rapid development of a PRL. Patients will
undergo a `scotoma awareness' training, in which a simulated scotoma, individually tailored for each patient,
will be used to help them visualize their region of vision loss. Patients will be tested on the same metrics from
Aim 1 and a battery of visual and cognitive assessments before and after the `scotoma awareness' (or control)
sessions. This will enable quantification of the effect of scotoma awareness both in terms of visual abilities and
oculomotor strategies, and test the hypothesis that awareness of the location and extent of retinal damage
promotes fast PRL development. While challenging, the use of eye tracking techniques in patients could be
highly rewarding if this scotoma awareness procedure proves to be effective. A null result would be equally
informative, suggesting fundamental differences between physiological and simulated scotomas, thus
providing a limit in the use of simulations of retinal damage as a framework for the study of retinal pathologies
such as MD. This will provide a unique data set to help those developing interventions for central vision loss
understand how approaches to visual rehabilitation, and individual differences, give rise to training outcomes.