April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
Effect of Injected Neurochemicals on Ocular Growth in a Homeomorphic Biomechanical Model of the Eye
Author Affiliations & Notes
  • G. K. Hung
    Biomedical Engineering, Rutgers University, Piscataway, New Jersey
  • K. J. Ciuffreda
    Vision Sciences, SUNY College of Optometry, New York, New York
  • Footnotes
    Commercial Relationships  G.K. Hung, None; K.J. Ciuffreda, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3687. doi:
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      G. K. Hung, K. J. Ciuffreda; Effect of Injected Neurochemicals on Ocular Growth in a Homeomorphic Biomechanical Model of the Eye. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3687.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : To investigate in a homeomorphic biomechanical model the effects of the interaction between retinal defocus change and local injection of neurochemicals, with known myopigenic or anti-myopigenic properties, on ocular shape and rate of growth.

Methods: : Simulations of a model of the eye based on the Incremental Retinal-Defocus Theory (IRDT) was presented previously at ARVO (2009, #3946). The homeomorphic biomechanical model consisted of a distributed assembly of masses and springs that represent the outer shell of the eyeball. It has 30 connected nodes forming a circle, where each node consists of a mass that is attached by two springs. For a given simulated optical defocus condition, a decrease in blur circle size at a node decreases the spring constant of the adjacent springs. A Matlab simulation program was used to demonstrate the emmetropization process via changes in retinal defocus as specified by IRDT. To further investigate the model properties, simulated doses of neurochemicals were injected at local retinal regions. The effect of a neurochemical in the model was to modify the spring constants of the nearby springs. The neurochemicals included dopamine, 7-methylxanthine, atropine, apomorphine, pirenzepine, glucagons, timolol, TGF-β, retinoic acid, and insulin. Based on research references, these neurochemicals range from being strongly anti-myopigenic to strongly myopigenic.

Results: : Various combination of changes in retinal defocus and local injections of neurochemicals were tested. The results showed ocular growth changes that were consistent with IRDT and the known myopigenic or anti-myopigenic effects of the neurochemicals. For example, simulation of the simultaneous presentation of a decrease in retinal defocus (which is myopigenic) and the local injection of anti-myopigenic neurochemical, such as 7-methylxanthine, showed retardation of excessive ocular growth at the local region. On the other hand, presentation of an increase in retinal defocus (which is anti-myopigenic) and the local injection of a myopigenic neurochemical such as retinoic acid showed overall slower axial growth rate but a bulging at the local region.

Conclusions: : Our homeomorphic biomechanical model can serve as a framework for understanding the mechanisms underlying neurochemical cascades in myopegenesis and the potential for drug therapy to retard ocular growth so as to prevent the onset and/or progression of myopia.

Keywords: myopia • drug toxicity/drug effects • emmetropization 

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