Abstract
Essential infantile esotropia is generated by prenuclear visual pathways that increase esotonus and gradually drive the eyes into a convergent position. Contrary to the prevailing notion that infantile esotropia reflects a primary disturbance within the visual cortex, accumulating evidence suggests that infantile esotropia is generated by lower subcortical centers that subserve nasalward optokinesis. These phylogenetically older visuo-vestibular pathways include the nucleus of the optic tract, accessory optic system, inferior olive, cerebellar flocculus, and vestibular nucleus. In humans, the subcortical visual system is normally turned off after the first few months of infancy but retains its function in children who develop infantile esotropia. Mutations or other perturbations that prolong subcortical neuroplasticity may therefore lead to a persistent simultaneous nasalward optokinetic imbalance in both eyes to generate infantile esotropia. Deficits in cortical motion processing and monocular nasotemporal asymmetry to foveated optokinetic targets are likely the effect, rather than the cause, of infantile esotropia.
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