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Published on: July 9, 2016
Decorrelation of cerebral visual inputs as the sufficient cause of infantile esotropia
Lawrence Tychsen1, Michael Richards, Agnes M F Wong
1From the Departments of Ophthalmology and Visual Sciences.
Insights
Binocular decorrelation alone can cause infantile esotropia in infant monkeys during a critical developmental period. The severity of esotropia and visual cortex deficits correlated with decorrelation duration, suggesting a mechanism for strabismus.
Area of Science:
- Neuroscience
- Developmental Biology
- Ophthalmology
Background:
- Infants at risk for esotropia often experience cerebral insults affecting binocular vision during critical developmental periods.
- Understanding the sole impact of binocular signal decorrelation is crucial for infantile esotropia etiology.
Purpose of the Study:
- To determine if binocular decorrelation alone is sufficient to induce esotropia in infant monkeys.
- To investigate associated behavioral and neuroanatomic deficits resulting from binocular decorrelation.
Main Methods:
- Infant monkeys were reared with prism-goggles inducing binocular decorrelation for 3-24 weeks.
- Behavioral assessments and neuroanatomic analysis of the striate visual cortex (V1) were performed.
Main Results:
- Monkeys exposed to decorrelation for 6-24 weeks developed constant esotropia.
- Increased decorrelation duration led to more severe ocular motor signs and V1 binocular connection loss.
- Short-term decorrelation (3 weeks) resulted in transient esotropia with subsequent recovery.
Conclusions:
- Binocular decorrelation is a sufficient cause of infantile esotropia during a critical developmental window.
- The correlation between visuomotor signs and V1 connectivity deficits offers a neuroanatomic explanation.
- Recovery after short-term decorrelation supports the benefits of early strabismus intervention in humans.
Background And Purpose:
Human infants at greatest risk for esotropia are those who suffer cerebral insults that could decorrelate signals from the two eyes during an early critical period of binocular, visuomotor development. The authors 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 3-24 weeks (control monkeys wore plano goggles), emulating unrepaired strabismus of durations 3 months to 2 years in human infants. 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 6-24 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 visually evoked potentials were asymmetric. Monkeys exposed to decorrelation for 3 weeks showed transient esotropia, but regained normal alignment, 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 signs and severity of V1 connectivity deficits provides a neuroanatomic mechanism for these signs. Restoration of binocular fusion and V1 connections after short durations of decorrelation helps explain the benefits of early strabismus repair in humans.
