New Research Leads the Way for Developing Better Treatments for CVI

In the U.S., Cerebral/cortical visual impairment (CVI) — damage to the central visual pathways that results in a spectrum of visual deficits — is the most frequent diagnosis of children with visual impairment younger than three years of age (24%). CVI is also a leading cause of visual impairment in children of developing nations.

Despite this prevalence, the treatment of CVI is an unmet clinical need. CVI is associated with a variety of perinatal complications — including congenital central nervous system malformations, traumatic brain injury, cerebral vascular accidents and metabolic disorders. Yet CVI is most commonly connected to perinatal hypoxia, a temporary reduction in oxygenation of blood or restriction of blood circulation before, during or immediately after birth. 

A prominent barrier to effective treatment is the lack of a pre-clinical model for investigating how and where perturbations to brain circuitry arise and how aberrant brain circuitry causes different types and severity of visual impairment. Recently, a team of researchers led by Aaron McGee, PhD, professor of Translational Neurosciences with the University of Arizona College of Medicine – Phoenix, may have established such a model.

In a study recently published as the cover story in Experimental Neurology, Dr. McGee and his co-researchers performed a series of tests to assess motor and visual function for a pre-clinical model of CVI based on perinatal hypoxia. 

“The goal for this project was to develop an experimental framework for identifying where and how CVI perturbs the circuits of the brain that mediate vision so that we can develop compensatory therapeutic interventions,” said Dr. McGee.

They discovered that transient hypoxia causes enduring impairments in visual acuity and binocular depth perception. These deficits in vision were associated with problems in the development of the visual thalamus and differences in the responses of neurons in visual cortex. Poor acuity and depth perception are often symptoms of CVI.

“This study is a prime example of how basic science can be applied to pursue therapeutic strategies for this challenging visual disorder that lacks effective treatment options — a key initiative of the current strategic plan of the National Eye Institute,” said William Guido, PhD, co-corresponding author on the study and former chair of the Department of Anatomical Sciences and Neurobiology at the University of Louisville.

At present, there is no treatment to restore the visual pathways damaged in CVI. Community resources, such as the Perkins School for the Blind, focus on improving diagnosis of CVI, as well as developing environmental modifications and individualized educational programming for affected children. The hope is that this research will lead to treatments that target the visual circuitry in the brain that could be used in conjunction with these accommodations to improve vision for children and adults with CVI.

“This works is a prime example of how basic science can translate to develop treatment strategies for a pressing and unmet clinical need,” said Dr. McGee.

Driving Discovery with Aaron McGee, PhD