{"title":"屈光发育 II:正常和近视眼发育模型。","authors":"Jos J Rozema, Arezoo Farzanfar","doi":"10.1111/opo.13412","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>During refractive development, eye growth is controlled by a combination of genetically pre-programmed processes and retinal feedback to minimise the refractive error. This work presents a basic differential model of how this process may take place.</p><p><strong>Methods: </strong>The description starts from two bi-exponential descriptions of the axial power P<sub>ax</sub> (or dioptric distance) and total refractive power P<sub>eye</sub>, the difference between which corresponds with the spherical refractive error S. This description is rewritten as an ordinary differential equation and supplemented by a retinal feedback function that combines retinal blur (closed loop) with a term describing excessive axial growth (open loop). This model is controlled by a total of 18 parameters that allow for a wide variety of developmental behaviours.</p><p><strong>Results: </strong>The proposed model reproduces refractive development growth curves found in the literature for both healthy and myopic eyes. An early onset of myopisation, a large growth term and a high minimum for the crystalline lens power all lead to higher degrees of myopia. Assigning more importance to the feedback than to the pre-programmed growth makes the model more sensitive to myopogenic influences. Applying refractive corrections to the model, undercorrection is found to produce more myopia. The model compensates for a low-powered imposed lens and can return to (near) emmetropia if that imposed lens is removed quickly thereafter. Finally, simulating the effect of a diffuser leads to high myopia.</p><p><strong>Conclusion: </strong>Using a series of basic assumptions, the proposed model recreates many well-known experimental and clinical results about refractive development from the literature while placing them in a standardised context. This contributes to a broader understanding of the origins of refractive errors, and future versions may help in the development of solutions for myopia control.</p>","PeriodicalId":19522,"journal":{"name":"Ophthalmic and Physiological Optics","volume":null,"pages":null},"PeriodicalIF":2.8000,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Refractive development II: Modelling normal and myopic eye growth.\",\"authors\":\"Jos J Rozema, Arezoo Farzanfar\",\"doi\":\"10.1111/opo.13412\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>During refractive development, eye growth is controlled by a combination of genetically pre-programmed processes and retinal feedback to minimise the refractive error. This work presents a basic differential model of how this process may take place.</p><p><strong>Methods: </strong>The description starts from two bi-exponential descriptions of the axial power P<sub>ax</sub> (or dioptric distance) and total refractive power P<sub>eye</sub>, the difference between which corresponds with the spherical refractive error S. This description is rewritten as an ordinary differential equation and supplemented by a retinal feedback function that combines retinal blur (closed loop) with a term describing excessive axial growth (open loop). This model is controlled by a total of 18 parameters that allow for a wide variety of developmental behaviours.</p><p><strong>Results: </strong>The proposed model reproduces refractive development growth curves found in the literature for both healthy and myopic eyes. An early onset of myopisation, a large growth term and a high minimum for the crystalline lens power all lead to higher degrees of myopia. Assigning more importance to the feedback than to the pre-programmed growth makes the model more sensitive to myopogenic influences. Applying refractive corrections to the model, undercorrection is found to produce more myopia. The model compensates for a low-powered imposed lens and can return to (near) emmetropia if that imposed lens is removed quickly thereafter. Finally, simulating the effect of a diffuser leads to high myopia.</p><p><strong>Conclusion: </strong>Using a series of basic assumptions, the proposed model recreates many well-known experimental and clinical results about refractive development from the literature while placing them in a standardised context. 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引用次数: 0
摘要
目的:在屈光发育过程中,眼睛的生长受到基因预编程过程和视网膜反馈的共同控制,以最大限度地减少屈光不正。本研究提出了这一过程的基本微分模型:该模型从轴向功率 Pax(或屈光距离)和总屈光功率 Peye 的两个双指数描述开始,两者之差与球面屈光不正 S 相对应。该描述被改写为常微分方程,并辅以视网膜反馈函数,将视网膜模糊(闭环)与描述过度轴向增长(开环)的项结合起来。该模型由总共 18 个参数控制,可实现多种发育行为:结果:所提出的模型再现了文献中健康眼睛和近视眼的屈光发育增长曲线。近视发生早、增长项大、晶状体功率最小值高都会导致近视度数增加。与预设的增长相比,反馈更为重要,这使得模型对近视发生的影响更为敏感。在对模型进行屈光矫正时,发现矫正不足会产生更多近视。该模型可对低倍外加镜片进行补偿,如果随后迅速移除外加镜片,则可恢复到(近)散光状态。最后,模拟散光器的效果会导致高度近视:利用一系列基本假设,所提出的模型再现了文献中有关屈光发展的许多著名实验和临床结果,同时将这些结果置于标准化的环境中。这有助于人们更广泛地了解屈光不正的起源,未来的版本可能有助于近视控制解决方案的开发。
Refractive development II: Modelling normal and myopic eye growth.
Purpose: During refractive development, eye growth is controlled by a combination of genetically pre-programmed processes and retinal feedback to minimise the refractive error. This work presents a basic differential model of how this process may take place.
Methods: The description starts from two bi-exponential descriptions of the axial power Pax (or dioptric distance) and total refractive power Peye, the difference between which corresponds with the spherical refractive error S. This description is rewritten as an ordinary differential equation and supplemented by a retinal feedback function that combines retinal blur (closed loop) with a term describing excessive axial growth (open loop). This model is controlled by a total of 18 parameters that allow for a wide variety of developmental behaviours.
Results: The proposed model reproduces refractive development growth curves found in the literature for both healthy and myopic eyes. An early onset of myopisation, a large growth term and a high minimum for the crystalline lens power all lead to higher degrees of myopia. Assigning more importance to the feedback than to the pre-programmed growth makes the model more sensitive to myopogenic influences. Applying refractive corrections to the model, undercorrection is found to produce more myopia. The model compensates for a low-powered imposed lens and can return to (near) emmetropia if that imposed lens is removed quickly thereafter. Finally, simulating the effect of a diffuser leads to high myopia.
Conclusion: Using a series of basic assumptions, the proposed model recreates many well-known experimental and clinical results about refractive development from the literature while placing them in a standardised context. This contributes to a broader understanding of the origins of refractive errors, and future versions may help in the development of solutions for myopia control.
期刊介绍:
Ophthalmic & Physiological Optics, first published in 1925, is a leading international interdisciplinary journal that addresses basic and applied questions pertinent to contemporary research in vision science and optometry.
OPO publishes original research papers, technical notes, reviews and letters and will interest researchers, educators and clinicians concerned with the development, use and restoration of vision.