A lecture presented by Dr. Krystel Huxlin, Professor of Ophthalmology, Associate Chair for Research, Flaum Eye Institute, University of Rochester
Biography
Dr. Krystel Huxlin is the James V. Aquavella Professor of Ophthalmology and Associate Chair for Research in the Department of Ophthalmology and Flaum Eye Institute at the University of Rochester, Rochester, NY, USA. She also serves as the Associate Director of the Center for Visual Science and co-Director of its Training program. She holds secondary appointments in the Institute of Optics, the Departments of Neuroscience and Brain & Cognitive Sciences at the University of Rochester. Dr. Huxlin earned her bachelor’s (1991) and doctorate (1994) degrees in Neuroscience at the University of Sydney, Australia, before joining the Ophthalmology faculty at the University of Rochester (1999). Her work seeks to understand how visual functions can be restored after damage to the adult visual system. An author on more than 90 peer-reviewed publications and book chapters, she holds 10 patents and divides her attention between studying perceptual plasticity in damaged visual systems and manipulating molecular substrates of corneal wound healing to prevent and treat scarring, and to restore optical quality following insults to the ocular surface. She is also part of the team that developed LIRIC, a novel, non-surgical paradigm for laser refractive error correction. She was the inaugural President of the Rochester Society For Neuroscience Chapter, is a reviewing editor for eLife and the Journal of Vision and is a member of the Board of Directors of the Vision Sciences Society, for whom she currently serves as President-elect.
Abstract
In humans, damage to the primary visual cortex (V1) causes a loss of vision over large regions of the visual field, referred to as cortically-induced blindness (CB). This afflicts between ¼ and ½ of stroke victims, with rates rising worldwide. A major barrier these patients encounter is that in contrast with early-onset physical therapies prescribed to rehabilitate motor cortex damage, there are no accepted vision restoration therapies for CB. Over the last 2 decades, the assumption that damaged, adult visual systems cannot recover functionally has been challenged by research in both humans and animal models. Human studies, which have been largely restricted to chronic CB patients whose deficits are deemed stable and permanent, point to one method consistently able to recover vision after V1 damage: visual training to detect or discriminate stimuli in the blind field. Our group was responsible for key developments in this approach, leading to mechanistic insights, but also uncovering key barriers to implementation. Among them is the fact that recovery in chronic CB requires months of daily training and the vision restored is lowcontrast, coarse and restricted to the blind field perimeter, limiting its usefulness in everyday life. Evidence suggests that some of these limitations may arise because some chronic patients lose neurons that contribute to vision fundamentals not only in V1, but also – through trans-synaptic, retrograde degeneration - in the thalamus and retina. In contrast, there is little evidence of such degeneration in subacute CB patients (<3 months post-stroke). Moreover, when trained, subacute patients recover the same discrimination abilities as chronic patients but do so faster and over larger areas of their blind field. These data form a strong premise for refocusing investigative efforts on substantial differences in plastic potential between subacute and chronic stroke-affected visual systems, and on defining how they can best be exploited to maximize visual restoration in CB