Purpose: Human infants at greatest risk for esotropia are those who suffer cerebral insults that could decorrelate signals from the 2 eyes during an early critical period of binocular, visuomotor development. The author reared normal infant monkeys, under conditions of binocular decorrelation, to determine if this alone was sufficient to cause esotropia and associated behavioral as well as neuroanatomic deficits.

Methods: Binocular decorrelation was imposed using prism-goggles for durations of 3 to 24 weeks (in 6 experimental, 2 control monkeys). Behavioral recordings were obtained, followed by neuroanatomic analysis of ocular dominance columns and binocular, horizontal connections in the striate visual cortex (area V1).

Results: Concomitant, constant esotropia developed in each monkey exposed to decorrelation for a duration of 12 to 24 weeks. The severity of ocular motor signs (esotropia-angle; dissociated vertical deviation; latent nystagmus; pursuit/optokinetic tracking asymmetry; fusional vergence deficits), and the loss of V1 binocular connections, increased as a function of decorrelation duration. Stereopsis was deficient and motion visual evoked potentials were asymmetric. Monkeys exposed to decorrelation for 3 weeks showed transient esotropia but regained normal visuomotor behaviors and binocular V1 connections.

Conclusions: Binocular decorrelation is a sufficient cause of infantile esotropia when imposed during a critical period of visuomotor development. The systematic relationship between severity of visuomotor sign, and severity of V1 connectivity deficit, provides a neuroanatomic mechanism for several of these signs. Restoration of binocular fusion and V1 connections, after short durations of decorrelation, helps explain the benefits of early repair in human strabismus.