Neurological Basis for Eye Movements of the Blind

Abstract

When normal subjects fix their eyes upon a stationary target, their gaze is not perfectly still, due to small movements that prevent visual fading. Visual loss is known to cause greater instability of gaze, but reported comparisons with normal subjects using reliable measurement techniques are few. 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. We also measured saccades to visual or somatosensory cues. 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. 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. These vertical eye drifts were much more disjunctive than upward saccades. In individuals with late monocular visual loss, gaze stability was more similar to control subjects. Bilateral visual loss caused eye drifts that were larger than following monocular visual loss or in control subjects. 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. We conclude that the neural gaze-stabilizing network, which contains neurons with both binocular and monocular discharge preferences, is under adaptive visual control. Whereas monocular visual loss causes disjunctive gaze instability, binocular blindness causes both disjunctive and conjugate gaze instability (drifts and nystagmus). Inputs that bypass this neural network, such as projections to motoneurons for upward saccades, remain conjugate.

Importance of Eye Position on Spatial Localization in Blind Subjects Wearing an Argus II Retinal Prosthesis

“…However, quantify-ing VOR and correlating eye deviation with the degree of bias in spatial perception was not feasible in our study as a result of limitations in available eye-tracking systems. Infrared eye trackers require a calibration procedure that cannot be properly performed in blind individuals, 26 and the use of magnetic search coils is not acceptable in subjects wearing a retinal prosthesis, as the conjunctiva of affected individuals is vulnerable. 6 We therefore decided to video record eye and head movements.…”

Acquired pendular nystagmus

“…For example, study of patients with acquired monocular vision loss revealed small, low-frequency, irregular oscillations with a predominantly vertical component in the affected eye. [39] Study of nystagmus in these patients offers insight into the role that visual feedback plays in the maintenance of steady gaze in the absence of cerebellar or other central nervous system abnormalities.…”

“…[39] This predicts that loss of vision in one eye will affect the gaze stability of both eyes, with greater instability in the affected eye. Additionally, this predicts that movements that do not require the neural integrator, such as saccade, will be more conjugate than movements that require the neural integrator, such as the maintenance of steady gaze.…”

Gaze and pupil changes during navigation in age-related macular degeneration

“…In AMD, this may be due to eccentric fixation when central vision is lost 17. Additionally, loss of central vision may change gaze centres centrally 18. This may account for the increased fixation counts seen in this study with worsening central vision.…”