A closer look at the evolution of the eye and the brain provides a possible explanation for both the origin of infantile
esotropia and its motor characteristics. In the course of evolution, the eyes have moved from a lateral to a frontal position. Consequently, the monocular visual fields started to overlap resulting in a
binocular visual field. In lateral-eyed animals, the retinae project to the contralateral visual cortices only. These projections are also found in
binocular mammals and birds with
binocular visual fields but in addition there are uncrossed projections from the temporal retinae to the visual cortex. The partial chiasmal decussation and the corpus callosum provide the necessary structure that allows binocular vision to develop. Disruption of normal
binocular development causes a loss of binocularity in the primary visual cortex and beyond. Beyond the primary visual cortex, the contralateral eye dominates while the temporal
retinal signal appears to lose influence. Loss or absence of binocular vision in infantile
esotropia may be caused by inadequate retinotopic matching between the nasal and temporal
retinal signals like in
albinism with an abnormal or asymmetric chiasmal decussation or agenesis of the corpus callosum. Dominance of the crossing
retinal signal might also explain the motor characteristics of infantile
esotropia (asymmetric OKN, latent nystagmus, DVD). A normal
binocular cortical signal will predominate over the evolutionary older, originally non-
binocular,
retinal projections to the superior colliculi (CS) and the accessory optic system (AOS). A suppressed temporal
retinal signal paves the way for the re-emergence of eye movements driven by one eye, as in lateral-eyed non-
binocular animals.