BLIND EYES FREE

There is abundant evidence that the performance of these eye movements, including the vestibulo-ocular reflex, is optimized by visual feedback –. In species with a fovea (a specialized area of the retina providing high visual acuity), saccades redirect the line of sight (the angle of gaze) toward features of interest. However, even while stationary, during attempted fixation of an earth-fixed target, small eye movements (microsaccades, drift, and tremor) are generated to prevent sensory adaptation, which would cause fading of the visual percept. During locomotion, vestibular and visual tracking mechanisms act to stabilize the retinal image. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist.Įye movements evolved to serve vision.

The work is made available under the Creative Commons CC0 public domain dedication.įunding: This study was supported by the National Institutes of Health (NIH R01 EY06717), the Department of Veterans Affairs, and the Evenor Armington Fund of Case Medical Center.

This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. Received: DecemAccepted: JanuPublished: February 18, 2013 PLoS ONE 8(2):īarrow Neurological Institute, United States of America Inputs that bypass this neural network, such as projections to motoneurons for upward saccades, remain conjugate.Ĭitation: Schneider RM, Thurtell MJ, Eisele S, Lincoff N, Bala E, Leigh RJ (2013) Neurological Basis for Eye Movements of the Blind. Whereas monocular visual loss causes disjunctive gaze instability, binocular blindness causes both disjunctive and conjugate gaze instability (drifts and nystagmus). We conclude that the neural gaze-stabilizing network, which contains neurons with both binocular and monocular discharge preferences, is under adaptive visual control. Accurate saccades could be made to somatosensory cues by an individual with acquired blindness, but voluntary saccades were absent in an individual with congenital blindness. Bilateral visual loss caused eye drifts that were larger than following monocular visual loss or in control subjects. In individuals with late monocular visual loss, gaze stability was more similar to control subjects.

These vertical eye drifts were much more disjunctive than upward saccades. During binocular viewing, patients with early-onset monocular loss of vision showed greater instability of vertical gaze in the eye with visual loss and, to a lesser extent, in the normal eye, compared with control subjects.

We tested the hypothesis that gaze instability following visual impairment is caused by loss of inputs that normally optimize the performance of the neural network (integrator), which ensures both monocular and conjugate gaze stability. We also measured saccades to visual or somatosensory cues. We measured binocular gaze using the magnetic search coil technique during attempted fixation (monocular or binocular viewing) of 4 individuals with childhood-onset of monocular visual loss, 2 individuals with late-onset monocular visual loss due to age-related macular degeneration, 2 individuals with bilateral visual loss, and 20 healthy control subjects. Visual loss is known to cause greater instability of gaze, but reported comparisons with normal subjects using reliable measurement techniques are few. When normal subjects fix their eyes upon a stationary target, their gaze is not perfectly still, due to small movements that prevent visual fading.

BLIND EYES FREE

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