December 1995
Volume 36, Issue 13
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Articles  |   December 1995
Refractive error and axial length in a primate model of strabismus and congenital nystagmus.
Author Affiliations
  • M X Repka
    Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
  • R J Tusa
    Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Investigative Ophthalmology & Visual Science December 1995, Vol.36, 2672-2677. doi:
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      M X Repka, R J Tusa; Refractive error and axial length in a primate model of strabismus and congenital nystagmus.. Invest. Ophthalmol. Vis. Sci. 1995;36(13):2672-2677.

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Abstract

PURPOSE: To evaluate the development of refractive error and axial length in a primate model of sensory strabismus and nystagmus. METHODS: Four macaque monkeys had alternating tarsorraphy beginning within 24 hours of birth. One eye was closed for 25 days, and when it opened, the second eye immediately was closed for the next 25 days. Cycloplegic refractions and axial lengths were determined prospectively for three animals for 1 year or more. These data were compared to those of three unsutured control macaques raised under otherwise similar conditions. RESULTS: Each experimental animal developed exotropia and nystagmus. The first occluded eyes were significantly more hypermetropic than the control eyes at 1 month of age (+7.25 D +/- 1.95 D versus +1.92 D +/- 1.27 D; P < 0.02) and remained significantly more hypermetropic throughout the study. The second occluded eyes were more hypermetropic than the control eyes at 1 month (+2.42 D +/- 2.13 D versus +1.92 D +/- 1.27 D; P = 0.20), but less hypermetropic than the first occluded eyes. The rate of emmetropization was slightly faster for the first occluded eyes than for the control eyes (-0.12 D/month compared to -0.03 D/month). The mean axial length measurements of the experimental and control eyes were the same at 1 month, and their rates of change over time were identical. CONCLUSIONS: Persistent hypermetropia was produced by a brief period of reverse neonatal eyelid closure in a model of congenital-like nystagmus. It is suggested that infantile lid closure, nystagmus, or amblyopia after neonatal visual disruption may be associated with a failure of normal emmetropization.

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