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C.-S. Kee, L. Deng; Longitudinal Changes in the Magnitudes of Astigmatism and Ocular Axial Components in Normal and Lens-Induced Myopic Chicks. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1036. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Astigmatism is associated with spherical ametropia in both clinical and experimental eye studies. However, although it is known that myopia or hyperopia is largely due to the alterations in ocular axial components, it is unclear whether astigmatism is related to altered axial eye growth. This study aimed to examine the longitudinal changes in the magnitudes of astigmatism and ocular axial components in normal and experimentally-induced myopic chicks.
Longitudinal data were collected from control (no treatment, n=9) and treated birds (-10 D lens, n=9) during both the treatment (days 5 to 12) and recovery period (days 12 to 19). Refractive errors and ocular components’ axial dimensions were measured by using a Hartinger's refractometer and high-frequency A-scan ultrasonography (30MHz), respectively. For each period, the relationship between the magnitude of refractive astigmatism and those of individual ocular axial components was tested by a linear mixed effect model. Both variables being tested were adjusted by subtracting the mean values of control birds from respective data points. Because each of the six ocular components was separately tested, a more conservative standard was employed by using p<0.01 to identify any significant relationship.
In contrast to a natural decrease in the magnitude of astigmatism, chicks treated with -10D lenses developed significant amounts of astigmatism during the treatment period (day 12: mean ± SD = 3.2 ± 1.3 vs. 0.5 ± 0.5 D, p<0.001) concomitant with myopic eye growth. This experimentally-induced astigmatism decreased rapidly following the removal of the treatment lenses (day 19: 0.2 ± 0.4 vs. 0.2 ± 0.4 D, p=0.76). Regression analysis showed that the changes in astigmatic magnitudes were significantly related to the changes in vitreous chamber depth during both the treatment (slope = 4.48, p<0.001) and recovery period (slope = 5.40, p<0.0001). In addition, choroidal thickness was significantly related to the changes in astigmatic magnitudes during the recovery (slope = -5.21, p<0.001), but not the treatment period (slope = -1.83, p=0.80). Neither the changes in lens thickness nor those in anterior chamber depth were significantly related to the changes in astigmatic magnitude.
Our results indicate that the genesis of astigmatism is closely related to the alterations in the posterior ocular axial components. Further studies are needed to determine how and to what extent abnormal posterior axial eye growth promote the development of astigmatic errors.
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