@entity2516 in a primate model of strabismus and XXXX .

@entity5770 @entity2516 @entity3467 @entity735 @entity9529 @entity346 @entity4457
PURPOSE: To evaluate the development of @entity2516 in a primate model of sensory strabismus and @entity346 . 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 @entity5770 and @entity346 . The first @entity735 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 @entity735 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 @entity735 . The rate of emmetropization was slightly faster for the first @entity735 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 @entity3467 was produced by a brief period of reverse neonatal eyelid closure in a model of @entity9529 . It is suggested that infantile lid closure, @entity346 , or @entity4457 after neonatal visual disruption may be associated with a failure of normal emmetropization.
