Ramamirtham Ramkumar, Kee Chea-Su, Hung Li-Fang, Qiao-Grider Ying, Huang Juan, Roorda Austin, Smith Earl L
College of Optometry, University of Houston, 505 J Davis Armistead Building, Houston, TX 77204-2020, USA.
Vision Res. 2007 Sep;47(21):2751-66. doi: 10.1016/j.visres.2007.07.014. Epub 2007 Sep 6.
The purpose of this study was to investigate the relationship between refractive errors and high-order aberrations in infant rhesus monkeys. Specifically, we compared the monochromatic wave aberrations measured with a Shack-Hartman wavefront sensor between normal monkeys and monkeys with vision-induced refractive errors. Shortly after birth, both normal monkeys and treated monkeys reared with optically induced defocus or form deprivation showed a decrease in the magnitude of high-order aberrations with age. However, the decrease in aberrations was typically smaller in the treated animals. Thus, at the end of the lens-rearing period, higher than normal amounts of aberrations were observed in treated eyes, both hyperopic and myopic eyes and treated eyes that developed astigmatism, but not spherical ametropias. The total RMS wavefront error increased with the degree of spherical refractive error, but was not correlated with the degree of astigmatism. Both myopic and hyperopic treated eyes showed elevated amounts of coma and trefoil and the degree of trefoil increased with the degree of spherical ametropia. Myopic eyes also exhibited a much higher prevalence of positive spherical aberration than normal or treated hyperopic eyes. Following the onset of unrestricted vision, the amount of high-order aberrations decreased in the treated monkeys that also recovered from the experimentally induced refractive errors. Our results demonstrate that high-order aberrations are influenced by visual experience in young primates and that the increase in high-order aberrations in our treated monkeys appears to be an optical byproduct of the vision-induced alterations in ocular growth that underlie changes in refractive error. The results from our study suggest that the higher amounts of wave aberrations observed in ametropic humans are likely to be a consequence, rather than a cause, of abnormal refractive development.
本研究的目的是调查幼年恒河猴屈光不正与高阶像差之间的关系。具体而言,我们比较了正常猴子和患有视觉诱导性屈光不正的猴子使用沙克-哈特曼波前传感器测量的单色波像差。出生后不久,正常猴子以及通过光学诱导散焦或形觉剥夺饲养的实验猴子,其高阶像差的幅度均随年龄增长而降低。然而,实验猴子高阶像差的降低幅度通常较小。因此,在晶状体饲养期结束时,在远视、近视以及出现散光的实验眼(但非单纯性屈光不正眼)中观察到像差量高于正常水平。总均方根波前误差随球镜屈光不正度数增加而增大,但与散光度数无关。近视和远视实验眼均显示彗差和三叶草像差增加,且三叶草像差程度随球镜屈光不正度数增加而增大。与正常或远视实验眼相比,近视眼中正球差的发生率也更高。在恢复无限制视觉后,实验诱导性屈光不正已恢复的实验猴子的高阶像差量减少。我们的结果表明,高阶像差受幼年灵长类动物视觉经验的影响,且我们实验猴子中高阶像差的增加似乎是视觉诱导的眼生长改变的光学副产品,而这种改变是屈光不正变化的基础。我们研究的结果表明,在屈光不正人群中观察到的较高波像差量可能是异常屈光发育的结果而非原因。