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Melody Ying Y. Huang, Chien-Cheng Chen, Christopher J. Bockisch, Dominik Straumann; Doomed to Move the Eyes: Infantile Nystagmus-Like Eye Movements in Healthy Human Subjects. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3016.
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The optokinetic response (OKR) is characterized by involuntary eye movements that help stabilize whole-field motion on the retina in order to preserve visual acuity. The neuronal circuit underlying the OKR is a negative feedback (closed-loop) system that relies on retinal slip velocity information from the retinal ganglion cells. In this study, we tested how manipulation of the retinal slip velocity alters the behavior of this sensory-motor system.
Healthy human subjects, wearing eye tracking goggles, were placed in front of a diffusive screen on which sinusoidal black and white gratings were projected. The stationary gratings were displaced according to eye movements so as to create the illusion of a magnified or even reversed retinal slip (illusory retinal slip = true retinal slip multiplied by a desired factor). The experimental paradigm consisted of eighteen conditions with different retinal slip multiplication factors. Eye movements were recorded by EyeSeeCam® tracking system at a frame rate of 220 frames per second and analyzed by a custom-made software.
While positive multiplication factors lead to little eye movements, negative multiplication factors, i.e., reversed illusory retinal slips, evoked vigorous eye movements with eye position waveforms typically found in infantile nystagmus syndrome (INS). Whole-field motion turned out to be necessary for this phenomenon since replacing the whole-field grating with a single dot failed to elicit nystagmoid eye movements.
In healthy subjects, the OKR works as a negative feedback loop sensory-motor system that attempts to reduce the retinal slip velocity (i.e., error signal). The experimental setup presented here enabled us to simulate a positive feedback in healthy subjects via the illusion of a reversed error signal. The resulting eye movements that resemble INS suggest that a wrong visual input to the OKR system may play a role in the pathomechanism of INS. This may particularly be the case in patients with abnormal optic nerve projections such as seen in albinism.
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