Amblyopia (`lazy eye'), the loss of visual acuity in one eye that cannot be corrected by glasses, is the most common cause of monocular vision loss worldwide and affects 3-5% of population. In addition to the acuity loss, a high proportion of amblyopic patients lack binocular function and depth perception. The combined loss of acuity and depth perception has a significant impact on the quality of life in amblyopes. The standard clinical treatment is to patch the non-amblyopic fellow eye to promote the use of the amblyopic eye in children. Adults are usually not treated, because amblyopia has long been considered untreatable in adults. With occlusion therapy, the success rate ranges from 60% to 80% with 20-25% recurrence following treatment, leaving about one third of affected children with amblyopia that persists into adulthood. This project seeks to understand the failure of current treatment approaches and proposes alternative therapies for those amblyopic patients who do not respond well to the conventional regimen. We believe that visual suppression, the fundamental factor in amblyopic visual loss, is a great barrier to treatment. We propose that visual suppression in amblyopia may be a form of long-term attentional neglect and that learning to attend to the amblyopic eye may overcome this neglect and improve visual function in the amblyopic eye. To test this hypothesis, Aim 1 will examine cortical suppression in amblyopic individuals with and without residual binocular function, because these two groups of patients have different treatment outcomes. Non-binocular amblyopes are more difficult to treat and often regress following treatment.
Aim 2 will measure both the strength and the latency of selective visual attention in individuals with amblyopia, and will correlate these results with the suppression measurements in Aim 1.
Aim 3 will investigate whether manipulating attention in the amblyopic eye can modulate cortical suppression.
Aim 4 will test the hypothesis that suppression can be alleviated and visual function will be improved by training the amblyopic eye with high attention-demand tasks. We will use both conventional perceptual learning tasks (low attention-demand tasks) and high attention-demand tasks to train individuals with amblyopia. We will track and evaluate visual function (acuity and stereopsis), depth of suppression, and attentional modulation during training by using visual psychophysics coupled to frequency-tagged source-localized EEG measurements. The knowledge gained from this study will contribute significantly to a broader understanding of the neural basis of visual suppression and the development of amblyopia. Our results will shed light on why amblyopic therapy often fails, and will indicate more efficient treatment strategies, especially for those who do not response well to conventional treatment.
Amblyopia (`lazy eye') is the most common cause of monocular vision loss worldwide and affects 3-5% of population. With current patching treatment, the success rate is about 60-80% with 20-25% recurrence following treatment, leaving about one third of affected children with amblyopia that persists into adulthood. This project seeks reasons for the failure of current treatment approaches. The knowledge gained from this study will contribute significantly to a broader understanding of the neural basis of visual suppression and the development of amblyopia. Our results will shed light on why amblyopic therapy often fails, and will indicate more efficient treatment strategies, especially fo those who do not response well to conventional treatment.
Hou, Chuan; Good, William V; Norcia, Anthony M (2018) Detection of Amblyopia Using Sweep VEP Vernier and Grating Acuity. Invest Ophthalmol Vis Sci 59:1435-1442 |
Hou, Chuan; Kim, Yee-Joon; Verghese, Preeti (2017) Cortical sources of Vernier acuity in the human visual system: An EEG-source imaging study. J Vis 17:2 |
Hou, Chuan; Kim, Yee-Joon; Lai, Xin Jie et al. (2016) Degraded attentional modulation of cortical neural populations in strabismic amblyopia. J Vis 16:16 |