May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Astigmatism Associated With Experimentally Induced Myopia or Hyperopia in Chickens
Author Affiliations & Notes
  • C.–S. Kee
    Department of BioScience, New England College of Optometry, Boston, MA
  • Footnotes
    Commercial Relationships  C. Kee, None.
  • Footnotes
    Support  NIH Grant EY11228
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3333. doi:
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      C.–S. Kee; Astigmatism Associated With Experimentally Induced Myopia or Hyperopia in Chickens . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3333.

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

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Purpose: : Astigmatism is a common refractive error in human populations but its etiology is poorly understood. Recent studies in monkeys have suggested that astigmatism may be a passive by–product of abnormal axial eye growth. This study aimed to examine the frequency and nature of the astigmatism that is associated with experimentally–induced axial ametropias in chickens.

Methods: : Exp.1 Four groups of chicks were raised under different visual manipulations known to induce axial ametropias: monocular form deprivation by translucent diffusers (n=14), monocular spherical defocus by –10D (n=6) or +10D lenses (n=6), and constant light (n=4). The visual manipulations started from 5 days of age and continued for a week. An age–matched group raised without any treatment served as a control group (n=13). Refractive development was followed closely by performing refractometry (Hartinger) without cycloplegia. Exp.2 To examine the contribution of corneal astigmatism, both refractometry and keratometry (Infrared photokeratometry) were performed on separate groups of birds reared with (form deprivation, n=5; +10D, n=8) or without visual manipulations (n=6). The treatment started at day 12 and continued for a week; measurements were performed at the end of the treatment period.

Results: : Exp.1 Significant amounts of astigmatism were associated with experimentally–induced refractive errors throughout the treatment period. In general, the magnitude of astigmatism increased systematically to a peak and subsequently decreased during the treatment period. At the end of the 7–day treatment period, twenty six of the 30 treated chicks exhibited astigmatism >1.4D (87%), whereas none of the control chicks had astigmatism >1.1D (mean ± SD = 5.9 ± 5.7D vs. 0.3 ± 0.4D; two sample t–test, p<0.0001). Interestingly, the untreated fellow eyes also exhibited higher than normal magnitudes of astigmatism (mean ± SD =1.9 ± 2.3D vs. 0.3 ± 0.4D; two sample t–test, p<0.005).The astigmatism (>1.4D) in the treated eyes was predominantly against–the–rule (69%, axis range=60°–120°). More importantly, the magnitude of astigmatism was significantly correlated with the magnitude of induced ametropia (Pearson’s r=0.5, p<0.01), and was directly proportional to the magnitude of corneal astigmatism (Exp.2, regression analysis, slope=1.2, p<0.01).

Conclusions: : Similar to macaque monkeys, visual conditions that alter the emmetropization process frequently promote the development of astigmatism in chickens. These results support the hypothesis that astigmatism is a passive by–product of abnormal axial eye growth.

Keywords: astigmatism • emmetropization • myopia 

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