Peter Bex

Peter Bex is the latest addition to the Schepens faculty. He received his PhD in Vision Science from Cardiff University, UK, in 1994. His thesis project was an applied study of perceptual failures experienced by pilots reading dynamic information on computer-generated cockpit displays. This was followed by post-doctoral research positions at McGill University in Montreal and at the University of Rochester, NY. Peter studied optics, used laser systems to present images directly on the retina, and began to examine visual function in the natural environment. Under natural conditions, existing computational models of visual processing are frustrated because of the complex and dynamic content of real scenes compared with laboratory or clinical stimuli. Peter then returned to the UK to take up a faculty position at the Institute of Ophthalmology in London in 2000, where he concentrated on translational research between basic and clinical vision science. Our understanding of visual processing is largely based on studies of the central vision of healthy, young subjects; Peter began to update our understanding of visual processing to deal with the effects of ageing and eye disease. This year, Peter joined the Schepens, where he is continuing this work and applying it to clinical populations, including those suffering from glaucoma, age-related macular degeneration, and amblyopia.

 
Figure 1. Your blind spot. Close your right eye and look at the airplane on the right or close your left eye and look at the airplane on the left. When you move closer to the page (around 6 inches or so), the other plane will fall within your blind spot and disappear. Just as we are unaware of this blind area of our vision, people are often unaware of blind areas caused by eye disease until the loss has become catastrophic. 

A fundamental challenge confronting clinical vision scientists concerns the remarkable plasticity and redundancy of the human visual system. For example, we are usually unaware that objects falling within the blind spot (where the optic nerve leaves the eye) are not visible, as shown in Figure 1. Likewise, blind spots caused by neurodegenerative disease or retinal insult may go undetected until significant vision loss has occurred, by which time it may be too late for the most effective treatments to be offered. A key objective of current behavioral vision research concerns the early detection, diagnosis, and monitoring of visual impairment.This endeavor is also a cornerstone for the development and assessment of new treatments and neuro-protective approaches, where sensitive measurement of visual function and dysfunction forms an essential part of evaluating treatment outcomes. 

Detection of Glaucoma

Glaucoma causes steady loss of peripheral vision and is the second leading cause of blindness in the developed world. Increases in life expectancy mean that around 80 million people worldwide are expected to have glaucoma by 2020. Early treatment for glaucoma can significantly reduce the progression of the disease but any lost vision is currently irreversible. It is thus essential to diagnose the disease as early as possible; however, most screening techniques for glaucoma work only once significant vision loss has already occurred.
Researchers are, therefore, working on new behavioral techniques that ask people to detect or discriminate carefully specified images. An understanding of the functional roles of different classes of retinal cells is an essential part of this process. For example, some retinal cells are involved in color vision, while others are insensitive to color but contribute to the perception of motion. Likewise, some cells have rapid response times, while others respond more slowly. We now know that some classes of retinal cell are more vulnerable to the early stages of glaucoma than others and we can combine this knowledge with an understanding of their stimulus selectivity and response properties to refine stimuli and tasks that isolate only the most vulnerable cells. These cells should show a sensitivity loss before other classes of cell and we can use this sensitivity loss for early diagnosis and to evaluate new and emerging neuro-protective interventions.

Visual Function in Age-Related Macular Degeneration

Age-related macular degeneration (AMD) causes blindness in the high-resolution area of central vision. Approximately 12 million people suffer from AMD and this figure is set to rise as our population ages. Treatment of macular disease with conventional ophthalmic techniques is of limited benefit in the majority of cases, forcing people to depend on their poor-resolution peripheral vision and severely impairing essential tasks such as mobility, face recognition and reading.

Figure 2. Crowding. If you fixate on the cross, the letter E is the same size (magnification), contrast and distance on the left and right. However, the adjacent letters on the right make it much harder to identify the middle letter. This effect is called crowding and it is crowding rather than acuity that limits vision across the majority of the visual field. 

The structure of the peripheral retina of people with AMD can be relatively intact, yet it supports greatly impoverished vision. This is true even in normally sighted people. To experience this for yourself, try reading words a couple of lines below where you are currently looking or recognizing the expressions of people if you look at the top of their heads. This phenomenon, illustrated in Figure 2, is known as crowding and it is a key factor limiting visual function in people with AMD. Vision scientists are trying to understand how visual processing and eye-movement behavior differ between central and peripheral visual fields. We are trying to learn the functional organization of the visual system that is responsible for these differences, so that we can develop new assistive devices that circumvent these problems. We are also beginning to understand some of the mechanisms of perceptual learning and neural plasticity that underlie the improvements in visual sensitivity seen in training programs. Techniques that minimize the effects of crowding, along with training that helps people learn to use their residual vision more effectively, will drive visual rehabilitation programs. Furthermore, our understanding of perceptual learning processes will be a critical stage for training people to use any new prosthetic and regenerated retinal implants that may be developed in the future.  

Amblyopia

Abnormal binocular vision in childhood can lead to the development of amblyopia in the absence of any observable ocular pathology. Amblyopia is commonly known as ‘lazy eye’ and is the leading cause of visual impairment in childhood, affecting approximately 3% of the population. The visual experience of amblyopia varies, but is often described as distorted rather than blurred, as illustrated in Figure 3b.

With no evident ocular pathology, treatments for amblyopia depend on perceptual learning techniques. The main treatments for amblyopia temporarily impair vision in the better eye with eye patches or drops. These treatments force the child to use her amblyopic eye, which would otherwise be suppressed by the better eye. Treatment is effective in around 75% of juvenile cases, but in fewer than half of adult cases. Relatively little is known about how treatment works and why is sometimes doesn’t, whether full stereo vision is restored, and levels of recidivism. Vision scientists are currently trying to understand the normal and abnormal development of binocular vision and to develop more-structured training programs to combine with patching or eye drops. Recent data from animal studies suggest that correcting the de-correlation between the images in each eye (for example, when an image resembles 3a with one eye, but 3b or 3c with the other) is critical for reversing amblyopia. It is likely that new, more-widely effective treatments for amblyopia will involve a correction for binocular de-correlation.