New concepts concerning the neural mechanisms of infantile strabismus and amblyopia

Abstract

AbstractInfantile strabismus results in a loss of binocularity in the primary visual cortex. Beyond the primary visual cortex, the contralateral eye dominates while the temporal retinal signal appears to lose influence. This may either be caused by inadequate retinotopic matching between the nasal and temporal retinal signals (e.g. albinism or agenesis of the corpus callosum), or the result of a lack of normal sensory input. Dominance of the crossing retinal signal might also explain the motor characteristics of infantile esotropia (asymmetric OKN, latent nystagmus, DVD). Only 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). Amblyopia seems to be the result of active suppression by the crossing ganglion cells of the non‐amblyopic eye. Early‐onset monocular deprivation is thought to produce competitive imbalance for synaptic sites, which in turn results in a reduced proportion of functionally binocular neurons.Amblyopia treatment may aim at an optimal binocular balance and pharmacological treatment after the critical period.