June 2016
Volume 57, Issue 7
Open Access
Letters to the Editor  |   June 2016
Motion Responses in Human Strabismus: What Optokinesis in the Deviating Eye Is Telling Us
Author Affiliations & Notes
  • Michael C. Brodsky
    Department of Ophthalmology and Neurology Mayo Clinic, Rochester, Minnesota, United States.
Investigative Ophthalmology & Visual Science June 2016, Vol.57, 2990. doi:10.1167/iovs.16-19569
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      Michael C. Brodsky; Motion Responses in Human Strabismus: What Optokinesis in the Deviating Eye Is Telling Us. Invest. Ophthalmol. Vis. Sci. 2016;57(7):2990. doi: 10.1167/iovs.16-19569.

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      © ARVO (1962-2015); The Authors (2016-present)

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In their recent study, Agaoglu et al.1 used dichoptic stimulation in two monkeys with early-onset strabismus to demonstrate that the peripheral retina of the deviating eye can generate optokinetic responses. This optokinetic response in the nonfixating eye has been identified and characterized in a recent study that was overlooked by the authors.2 We examined horizontal optokinetic responses in 10 patients with infantile esotropia who displayed the characteristic monocular nasotemporal optokinetic asymmetry that accompanies this condition. 
As expected, we observed that when one eye was covered and the fixing eye was viewing a temporally moving optokinetic target on a drum, poor optokinetic responses were present. However, when the nonfixing eye was uncovered to allow binocular viewing while the drum rotation continued, brisk binocular optokinetic responses immediately developed due to the intact nasalward optokinetic input that was being presented to the peripheral retina of the esodeviated nonfixating eye.2 These optokinetic responses were followed within a few seconds by a fixation shift to the previously nonfixating eye (except in patients with preexisting amblyopia in the nonfixating eye). 
This optokinetic uncover test demonstrated that the nonfixating eye can drive the optokinetic responses in humans with infantile esotropia. However, our observation that peripheral optokinetic responses generated by the nasal retina of the nonfixating eye dominated the temporalward optokinetic input to the fixating eye suggested that these peripheral retinal responses must be driven by the subcortical optokinetic system (i.e., the accessory optic system and nucleus of the optic tract). 
In their discussion, Agaoglu et al.1 concluded that these peripheral optokinetic responses were probably cortical in origin. Our findings suggest that a defining feature of infantile strabismus lies in the preservation of a functioning subcortical optokinetic system (an extrafoveal response to full-field optic flow). Although these subcortical optokinetic pathways are normally extinguished after 2 months of life in normal binocular humans,3 infantile strabismus may impede cortical development to potentiate their function. Since foveal pursuit is a cortical function, it seems unlikely that peripheral optokinetic responses would override foveal pursuit if both were cortical in origin. This subcortical mechanism would still be compatible with cortical suppression of the deviating eye.4 Preserved subcortical optokinetic responses would also explain the prominent torsional eye movements in infantile strabismus, as these may be subserved in part by optokinetic nuclei within the accessory optic system.4,5 In a larger sense, infantile strabismus may create a natural “dichoptic” state preserving access to dual optokinetic systems. 
References
Agaoglu S, Agaoglu MN, Das VE. Motion information via the nonfixating eye can drive optokinetic nystagmus in strabismus. Invest Ophthalmol Vis Sci. 2015; 56: 6423–6432.
Brodsky MC, Klaehn L. The optokinetic uncover test: a new insight into infantile esotopia. JAMA Ophthalmol. 2013; 131: 759–765.
Braddick O, Atkinson J. Development of human visual function. Vision Res. 2011; 51: 1588–1609.
Schor CM. Subcortical binocular suppression affects development of latent and optokinetic nystagmus. Am J Optom Physiol Opt. 1983; 60: 481–502.
Brodsky MC. The accessory optic system: the fugitive visual control syndrome in infantile strabismus. Arch Ophthalmol. 2012; 130; 1055–1058.
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