The human brain is remarkably efficient at processing noisy and at times discordant information from the natural world.  In addition to its high accuracy and low latency, the brain also has the capability to adapt and change itself.  For example, the brain can compensate for sensory loss due to injury, dysfunction, or disease by changing both its cortical structure and function. In particular, degenerative retinal diseases cause visual impairment that starts at different ages, progresses at a range of rates, and affects the visual pathway in unique ways.  Therefore, retinal disease provides an opportunity to understand the variety and versatility of plasticity in the eye and brain.

Our lab investigates the compensation and repurposing of visual brain regions in patients with low vision or blindness, and is specifically focused on multisensory perception.  By examining both the benefits and costs of plasticity in the adult brain, we aim to better understand neural adaptation, and thereby design devices, therapies, and multisensory training algorithms that engender cortical changes to improve patient visual function.

However, excessive adaptability in neural structure can also reduce the brain’s computational power, as well as hinder its long term sensory functionality.  For this reason, the brain places limitations on plasticity, including both confining extreme adaptability into critical periods and requiring long periods of sensory activation or deprivation to engender structural changes in adulthood.  Because of these restrictions on plasticity, functional brain changes that are easier to create are also easier to reverse.  In other words, the plasticity that reverses brain changes is often limited in the same ways as the plasticity generating those changes in the first place.

In the case of retinal blindness, the de-afferented or disconnected visual cortex adapts and often takes on new functional roles.  However, if vision is partially restored, the brain doesn’t necessarily revert to its original state.  The extent to which the adaptations due to visual deprivation linger, and how these persistent adaptations may generate a new sensory dynamic, are currently not well understood.  Ultimately, changes in cortical structure that took years or decades to engender due to visual impairment may take extended periods to reverse, or may not be reversible at all following partial visual restoration.  Limits on sensory organization reversal may restrict visual restoration patient long term functionality, as was shown in the case of cochlear implant patient outcomes.  As multiple methods of visual restoration are being developed (such as gene therapy, stem cell therapy, and prostheses), investigation of these neuroscience questions could enable a better understanding of sensory plasticity and improved patient outcomes.

One of our research projects in this domain is focused on studying the neuroplasticity that results from vision loss both before and after the partial restoration of vision with retinal prostheses.  In order to address this goal, we are using functional magnetic resonance imaging (fMRI) techniques to determine whether crossmodal changes during blindness hinder eventual visual rehabilitation.  This research could both aid in patient selection and also broaden current theories on the adaptability of the brain.

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