Model of human refractive error development.
Model of human refractive error development.
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人类屈光不正发展模型。
DOI：
10.1076/ceyr.19.1.41.5343
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发表时间：
1999
影响因子：
2
通讯作者：
Ciuffreda,KJ
中科院分区：
文献类型：
--
作者：
Hung,GK;Ciuffreda,KJ
目的构建一个屈光不正发展模型，以解释在前30年内远视眼（HYP）、正视眼（EMM）、早发性近视眼（EOM）和晚发性近视眼（LOM）屈光不正的不同相互作用机制和时间进程。在远视和近视两种模式下，对先前开发的近距离工作诱导的短暂近视（NITM）模型进行模拟，以获得四个屈光组的AE rms和屈光不正之间的临界关系。然后，在NITM模型中加入两个控制通路。基因控制的途径与角膜、透镜和眼球的长期生长有关。环境控制的途径与近距离工作过程中的视网膜散焦相关，其中高于阈值水平的重复误差（AE）的均方根（rms）导致眼球轴向长度增加。散焦引起的轴向长度变化的阈值根据经验确定为对应于四个折射组中的微分磁化率。两种途径的综合作用产生了总体屈光不正。将AE rms与屈光不正之间的关系与两种控制路径结合起来进行长期模拟（30岁：最初的15年使用远视范例，随后的15年使用近视范例）来量化四个屈光组中与日常近距离工作活动相关的屈光不正发展。确定远视屈光不正。HYP对视网膜散焦效应的敏感性最低或阈值最高，并保持在远视水平。在前2年，EMM表现出相对的近视转变，变为并保持正视。在近视组中，眼外肌表现出遗传控制的成分（从2岁开始）和散焦诱导的成分（从15岁开始），而在近视的发展中，眼外肌仅表现出散焦诱导的因素（从15岁开始）。此外，模拟表明正视化仅发生在小于0.5 D的“诱导”屈光不正，这与AE rms和屈光不正之间的非单调关系一致，其中最小AE rms发生在0.5 D。结论该模型表明，遗传和散焦-诱发性环境因素在不同屈光人群屈光不正的发生发展中起重要作用。该模型还提供了一个框架，进一步详细的定量分析过程中的屈光不正的发展和正视化。
PurposeTo construct a model of refractive error development that can account for the different interactive mechanisms and time courses of refractive error in the hyperope (HYP), emmetrope (EMM), early-onset myope (EOM), and late-onset myope (LOM) over the first 30 years of life.MethodsFirst, a baseline short-term (1 mo.) simulation of a previously developed nearwork-induced transient myopia (NITM) model was performed under both far- and near-viewing paradigms to obtain the critical relationships between AE rms and refractive error for the four refractive groups. Then, two control pathways were added to the NITM model. The genetically-controlled pathway was associated with the long-term growth of the cornea, lens, and the eyeball. The environmentally-controlled pathway was associated with retinal-defocus during nearwork, wherein the root mean square (rms) of the accommodative error (AE) above a threshold level resulted in an increase in axial length of the eyeball. The thresholds for defocus-induced axial length change were empirically determined to correspond to the differential susceptibility in the four refractive groups. The combination of effects from the two pathways produced the overall refractive error. The relationship between AE rms and refractive error was combined with the two control pathways for the long-term simulations (30 yrs: the initial 15 yrs using a far-viewing paradigm followed by an additional 15 yrs using a near-viewing paradigm) to quantify refractive error development as related to daily nearwork activity in the four refractive groups.ResultsAll refractive groups began early in life with a genetically-determined hyperopic refractive error. The HYP had the lowest susceptibility or highest threshold to retinal defocus effects, and remained at a hyperopic level. The EMM exhibited a relative myopic shift in the first 2 years to become and remain at emmetropia. In the myopic groups, the EOM exhibited both a genetically-controlled component (starting 2 years of age) and a defocus-induced component (starting at 15 years of age), whereas the LOM manifested only a defocus-induced factor (starting at 15 years of age) in the development of myopia. In addition, simulations indicated that emmetropization occurred only for "induced" refractive error that was less than 0.5 D, which was consistent with the non-monotonic relationship between AE rms and refractive error, wherein the minimum AE rms occurred at 0.5 D.ConclusionsThe model showed that both genetic and defocus-induced environmental factors play important roles in the development of refractive error in the different refractive groups. The model also provides a framework for further detailed quantitative analysis of the processes of refractive error development and emmetropization.