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Samuel Eckmann, Lukas Klimmasch, Bertram Shi, Jochen Triesch; A model of the development of anisometropic amblyopia through recruitment of interocular suppression. Journal of Vision 2018;18(10):942. doi: 10.1167/18.10.942.
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In anisometropia the two eyes have different refractive power, preventing simultaneous focusing with both eyes. When not treated early enough this can lead to amblyopia and a permanent loss of stereopsis. In this case, instead of fusing the information from both eyes, the brain suppresses signals from the central region of one eye. The mechanisms underlying this development are not well understood. To shed light on this question, we propose the first computational model for how this suppression may develop. This model extends an earlier model of the simultaneous development of accommodation and vergence control. That earlier model is formulated in the active efficient coding framework, a recent generalization of classic efficient coding theories to active perception. It describes the simultaneous development of receptive field properties and eye movement control to maximize the system's overall coding efficiency. We extend that earlier model to include interocular suppression by introducing a mechanism where strong responses from monocular neurons suppress the signals from the other eye. In the healthy case without anisometropia, the model learns to accommodate correctly and to perform precise vergence eye movements. In anisometropic cases where the ranges over which the two eyes can focus differ, an amyblopia-like state develops, where one eye is reliably suppressed by the other. This causes receptive fields to become increasingly monocular and to favor the dominant eye. However, by recruiting neurons that retain binocular receptive fields, the system is able to maintain the capacity for vergence control. Interestingly, for one myopic and one hyperopic eye, the model develops monovision, i.e., it learns to focus on objects at close distances with the myopic eye and on objects at far distances with the hyperopic eye. In conclusion, we present the first computational model of how anisometropia may lead to amblyopia by recruiting interocular suppression mechanisms.
Meeting abstract presented at VSS 2018
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