G K Hung1, K J Ciuffreda. 1. Department of Biomedical Engineering, Rutgers University, Piscataway, NJ 08854-8014, USA. shoane@rci.rutgers.edu
Abstract
PURPOSE: To 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. METHODS: First, 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 AErms 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 AErms 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. RESULTS: All 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 AErms and refractive error, wherein the minimum AErms occurred at 0.5 D. CONCLUSIONS: The 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.
PURPOSE: To 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. METHODS: First, 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 AErms 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 AErms 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. RESULTS: All 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 AErms and refractive error, wherein the minimum AErms occurred at 0.5 D. CONCLUSIONS: The 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.