Linking binocular vision neuroscience with clinical practice

Binocularity in the human visual system poses two interesting and extremely challenging questions. The first, and perhaps most obvious stems from the singularity of perception even though the neural images we see originate as two separate monocular images. Mechanistically we can ask how and where do we convert two images into one? The second question is more of a “why” question. By converting lateral eyes with their inherent panoramic visual field into frontal eyes with overlapping binocular visual fields, primates have developed an extremely large blind region (the half of the world behind us). We generally accept that this sacrifice in visual field size was driven by the potential benefit of extracting information about the 3 dimension from overlapping right and left eye visual fields. For some people, both of these core processes of binocularity fail: a single fused binocular image is not achieved (when diplopia or suppression is present), and the ability to accurately represent the 3 dimension is lost (stereo-blindness). In addition to these failures in the core functions of the human binocular system, early imbalances in the quality of right and left eye neural images (e.g. due to anisometropia, monocular deprivation, and/or strabismus), can precipitate profound neurological changes at a cortical level which can lead to serious vision loss in one eye (amblyopia). Caring for patients with malfunctioning binocular visual systems is a core therapeutic responsibility of the eye care professions (optometry, ophthalmology and orthoptics) and significant advances in patient care and subsequent visual outcomes will be gained from a deeper understanding of how the human brain accomplishes full binocular integration. This feature issue on binocular vision brings together original articles and reviews from leading groups of neuroscientists, psychophysicists and clinical scientists from around the world who embrace the multidisciplinary nature of this topic. Our authors have taken on the big issues facing the research community tasked with understanding how binocular vision is meant to work, how it fails, and how to better treat those with compromised binocularity. These studies address deep issues about how the human brain functions with normal and abnormal binocular vision, as well as how it can be altered by therapy. Central to new clinical approaches to binocular vision therapy is the surprisingly novel and seemingly ironic notion that in order to recover binocularity one must experience binocularity. Hidden behind this deceptively simple idea is the deeper question of what binocularity is and how perceptual binocularity relates to neural binocularity, especially in those individuals with abnormal binocular visual systems? Using modern computational and psychophysical methods Georgeson and Wallis at Aston examine the three possible outcomes of binocular integration: fusion, diplopia and suppression. They examine the rules by which disparity affects the likelihood of single vision and the means by which it is achieved (fusion or suppression). Because stereopsis is only possible with correlated (fusible) right and left eye images, brain regions that respond selectively to correlated signals likely play a crucial in stereopsis. By varying the fusibility of random dot stimuli, Andrew Parker’s group at Oxford report increased responses to fusible stimuli in V3 that correlate with stereopsis, suggesting a critical role for V3 in human binocularity. This feature issue contains two related reviews from research groups in Canada: Mitchell and Duffy, provide an insightful analysis of the role of animal models in binocular vision research. They argue for, and cleverly demonstrate the value of binocular experience in the treatment of experimental deprivation amblyopia in kittens. Even short durations of binocular experience can off-set much longer periods of deprivation. Mitchell and Duffy set the stage for a more contemporary approach to vision therapy for amblyopia by reviewing some of the now classic work by Hubel and Wiesel and others. Studies of cat and monkey showed that even a seemingly complete loss of the deprived eye’s ability to drive neurons in visual cortex could be recovered by depriving the once seeing eye. Mitchell and Duffy show that this approach “works” in that it converts a once blind eye to a seeing eye, but by blinding the once seeing eye. However, recovery of vision in the originally deprived eye is fleeting and this eye eventually reverts to deep amblyopia, a regression that could only be prevented by including extensive periods of binocular exposure during the treatment period. Ironically, the preferred mix of patching and binocular exposure observed in these kitten studies may mirror the experience of children with less than perfect compliance to patching therapy. This review describes the intriguing finding that periods of darkness can recover plasticity within a developing visual system. Whereas Mitchell and Duffy’s review provides an contemporary summary of animal models of amblyopia treatment and highlights their clinical relevance to human amblyopia, Hess and colleagues summarize the key characteristics of human amblyopia and examine the clever strategies being developed to activate binocularity in human patients with amblyopia and strabismus. By degrading the visual input to the better eye, suppression of the amblyopic