Wildsoet C, Wallman J
School of Optometry, Queensland University of Technology and Vision, University of Queensland, Brisbane, Australia.
Vision Res. 1995 May;35(9):1175-94. doi: 10.1016/0042-6989(94)00233-c.
It is known that when hyperopic or myopic defocus is imposed on chick eyes by spectacle lenses, they rapidly compensate, becoming myopic or hyperopic respectively, by altering the depth of their vitreous chamber. Changes in two components--ocular length and choroidal thickness--underlie this rapid compensation. With monocular lens treatment, hyperopic defocus imposed by negative lenses resulted in substantially increased ocular elongation and a slight thinning of the choroid, both changes resulting in myopia; myopic defocus imposed by positive lenses resulted a dramatic increase in choroidal thickness, which pushed the retina forward toward the image plane, and a slight decrease in ocular elongation, both changes resulting in hyperopia. The refractive error after 5 days of lens wear correlated well with vitreous chamber depth, which reflected the changes in both choroidal thickness and ocular length. The degree of compensation for lenses was not affected by whether the fellow eye was covered or open. Both form-deprivation myopia and lens-induced myopia declined with age in parallel, but wearing a -15 D lens produced more myopia than did form deprivation. The spectacle lenses affected the refractive error not only of the lens-wearing eye, but also, to a much lesser degree, of the untreated fellow eye. At lens removal refractive errors were opposite in sign to the lense worn, and the subsequent changes in choroidal thickness and ocular length were also opposite to those that occurred when the lenses were in place. In this situation as well, effects of the spectacle lenses on the fellow eyes were observed. Eyes with no functional afferent connection to the brain because of either prior optic nerve section or intraocular tetrodotoxin injections showed compensatory changes to imposed defocus, but these were limited to compensation for imposed myopic defocus, at least for the eyes with optic nerve section. In addition, optic nerve section, but not tetrodotoxin treatment, moved the set-point of the visual compensatory mechanism toward hyperopia. Optic nerve section prevents myopia in response to negative lenses but not to diffusers, suggesting that compensation for hyperopia requires the central nervous system.
已知当通过眼镜片对鸡眼施加远视或近视性离焦时,它们会通过改变玻璃体腔的深度迅速进行代偿,分别变为近视或远视。这种快速代偿的基础是两个组成部分的变化——眼轴长度和脉络膜厚度。单眼镜片治疗时,负镜片施加的远视性离焦导致眼轴明显伸长和脉络膜轻度变薄,这两种变化均导致近视;正镜片施加的近视性离焦导致脉络膜厚度显著增加,使视网膜向像平面推进,以及眼轴轻度缩短,这两种变化均导致远视。戴镜5天后的屈光不正与玻璃体腔深度密切相关,而玻璃体腔深度反映了脉络膜厚度和眼轴长度的变化。镜片的代偿程度不受对侧眼是遮盖还是开放的影响。形觉剥夺性近视和镜片诱导性近视均随年龄增长而平行下降,但佩戴-15D镜片比形觉剥夺产生的近视更多。眼镜片不仅影响戴镜眼的屈光不正,而且对未治疗的对侧眼也有较小程度的影响。摘除镜片时,屈光不正的符号与戴镜时相反,随后脉络膜厚度和眼轴长度的变化也与镜片在位时相反。在这种情况下,也观察到了眼镜片对对侧眼的影响。由于先前的视神经切断或眼内注射河豚毒素而与大脑没有功能性传入连接的眼睛,对施加的离焦有代偿性变化,但这些变化仅限于对施加的近视性离焦的代偿,至少对于视神经切断的眼睛是这样。此外,视神经切断而非河豚毒素治疗使视觉代偿机制的设定点向远视移动。视神经切断可防止因负镜片而非漫射器引起的近视,这表明远视的代偿需要中枢神经系统。