Refractive development II: Modelling normal and myopic eye growth.
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| Title: | Refractive development II: Modelling normal and myopic eye growth. |
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| Authors: | Rozema, Jos J. (AUTHOR), Farzanfar, Arezoo (AUTHOR) |
| Source: | Ophthalmic & Physiological Optics. Jan2025, Vol. 45 Issue 1, p120-134. 15p. |
| Subjects: | Refractive errors, Crystalline lens, Ordinary differential equations, Visual accommodation, Myopia |
| Abstract: | 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. [ABSTRACT FROM AUTHOR] |
| Copyright of Ophthalmic & Physiological Optics is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | 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. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 02755408 |
| DOI: | 10.1111/opo.13412 |
