University of California, San Francisco (UCSF)

Neural Mechanisms of Strabismus

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In the Laboratory for Visual Neuroscience as UCSF Medical Center, we are seeking to discover how visual perception occurs in the human brain. To pursue this objective we are studying a disease that affects children called strabismus. In this condition the eyes become crossed, leading to loss of stereoscopic depth perception, and often to amblyopia (lazy eye). In most cases, it is not clear why the eyes cease to fuse normally on visual targets. It appears that once the eyes begin to cross, children learn rapidly to avoid double vision by suppressing the image from the deviated eye. Thus, the corrective signal for realignment of the eyes is lost.

We are investigating the neural mechanisms responsible for visual suppression in the hope of developing new strategies for strabismus prevention. Our research has shown that each eye is represented in the human visual cortex within parallel, dovetailed slabs of tissue called ocular dominance columns. In strabismus, metabolic activity is reduced within the ocular dominance columns serving the suppressed eye. Our hypothesis is that these columns provide a switch-like mechanism for inhibitory brain pathways to turn off perception of signals emanating from the deviated eye.

To investigate this possibility, we are studying neural function in macaque monkeys raised with strabismus. The animals alternate fixation between the two eyes, just like children with strabismus. We have determined which eye they prefer to use for fixation and have mapped the pattern of visual suppression that occurs under natural viewing. Currently, we are recording cellular activity in the visual cortex to compare responses in ocular dominance columns corresponding to the fixating, perceiving eye versus the deviated, suppressed eye. Through these studies we hope to identify the cellular mechanisms responsible for suppression in strabismus, and those vital for perception in normal individuals.