Myopia: Attempts to arrest progression

Tan Tock Seng Hospital, Tumasik, 00, Singapore
British Journal of Ophthalmology (Impact Factor: 2.98). 12/2002; 86(11):1306-11. DOI: 10.1136/bjo.86.11.1306
Source: PubMed

ABSTRACT Previous studies have evaluated the efficacy of several interventions to decrease the progression of myopia. These include devices that alter the perception of the visual environment and pharmacological treatments. There is no conclusive evidence thus far that alteration of the pattern of spectacle wear, bifocals, ocular hypotensives, or contact lenses retards the progression of myopia. Several randomised clinical trials have demonstrated that the rate of progression of myopia is lower in children given atropine eye drops than those given placebo. However, atropine is associated with short term side effects such as photophobia and possible long term adverse events including light induced retinal damage and cataract formation. Other more selective antimuscarinic agents such as pirenzipine are presently being evaluated. Further well conducted randomised clinical trials with large sample sizes and adequate follow up designed to evaluate treatments to retard the progression of myopia should be conducted, since the identification of an effective intervention may have a greater public health impact on the burden and morbidity from myopia than the few treatments currently available.

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Available from: Kah-Guan Au Eong, Sep 26, 2015
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    • "Thus, myopia is suggested to be a multi-faceted phenomenon, and variety of attempts for its treatment were made throughout the world, including medical therapies [14], lens and eye exercises [15,16], and massage therapies [17]. Unfortunately, these attempts did not achieve cure or became the base for standard treatment. "
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    ABSTRACT: To evaluate the efficacy of two non-surgical interventions of vision improvement in children. A prospective, randomized, pilot study to compare fogging method and the use of head mounted 3D display. Subjects were children, between 5 to 15 years old, with normal best corrected visual acuity (BCVA) and up to -3D myopia. Subjects played a video game as near point work, and received one of the two methods of treatments. Measurements of uncorrected far visual acuity (UCVA), refraction with autorefractometer, and subjective accommodative amplitude were taken 3 times, at the baseline, after the near work, and after the treatment. Both methods applied after near work, improved UCVA. Head mounted 3D display group showed significant improvement in UCVA and resulted in better UCVA than baseline. Fogging group showed improvement in subjective accommodative amplitude. While 3D display group did not show change in the refraction, fogging group's myopic refraction showed significant increase indicating the eyes showed myopic change of eyes after near work and treatment. Despite our lack of clear knowledge in the mechanisms, both methods improved UCVA after the treatments. The improvement in UCVA was not correlated to measured refraction values. UCVA after near work can be improved by repeating near and distant accommodation by fogging and 3D image viewing, although at the different degrees. Further investigation on mechanisms of improvements and their clinical significance are warranted.
    The Open Ophthalmology Journal 10/2013; 7:69-48. DOI:10.2174/1874364101307010069
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    • "A recent study using the human scleral tissue showed that atropine increased FGF2 activation in a dose-dependent manner [33], while the authors also reported atropine reduced cell proliferation of scleral fibroblasts. Since atropine has been demonstrated to retard myopia progression in humans [34,35], their FGF2 expression pattern is unexpected and hard to explain (personal communication with the correspondent author of the study [33]). Similar to our finding, FGF2 was significantly upregulated in the choroid/RPE of minus lens-treated eyes (i.e., eyes of induced myopia) of primate marmoset monkeys as compared with plus lens-treated fellow eyes (i.e., eyes of induced hyperopia) [36]. "
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    ABSTRACT: Fibroblast growth factor-2 (FGF2) has been implied in the development of myopia according to previous studies investigating FGF2 in the sclera and retinal pigment epithelium. This study measured retinal FGF2 gene expression in an animal model and also tested for the association between single nucleotide polymorphisms (SNPs) in FGF2 and high myopia. The guinea pigs were assigned to 2 groups: form deprivation myopia (FDM) for two weeks and normal control (free of form deprivation). Biometric measurement was performed and FGF2 expression levels were compared among the FDM eyes, the fellow eyes of the FDM group and the normal eyes in retina. We also enrolled 1,064 cases (≤-6.0 D) and 1,001 controls (≥-1.5 D) from a Chinese population residing in Taiwan. Six tagging SNPs were genotyped to test for an association between genotypes and high myopia. The FDM eyes had the most prominent changes of refraction and axial length. Compared with the mRNA levels of FGF2 in the normal eyes, the FDM eyes had the highest levels of mRNA (p=0.0004) followed by the fellow eyes (p=0.002). The FDM and normal eyes became more myopic compared with the fellow eyes, but the fellow eyes became more hyperopic (p=0.004) in the end of the experiment which may be due to its relatively short axial length when compared with normal eyes (p=0.05). The SNP genotypes were all in Hardy-Weinberg equilibrium. However, none of the SNPs were significantly associated with high myopia (all p values >0.1). We identified a significant change of FGF2 expression in the FDM eyes but FGF2 genetic variants are unlikely to influence susceptibility to myopia. There may be a systemic effect to influence gene expression and refraction on the fellow eyes, which may perturb emmetropization in the fellow eyes. Our data also suggest using normal eyes rather than the fellow eyes as the control eyes when study the form deprivation myopia.
    Molecular vision 02/2012; 18:471-8. · 1.99 Impact Factor
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    • "It is reasonable to expect that the mechanism of action of muscarinic receptor antagonists in inhibiting myopia progression to be consistent across species. Although atropine [16,17] and pirenzepine (specific muscarinic receptor 1 (M1) antagonist) [18] have both been shown to reduce myopia progression via slowing of axial elongation, the exact mechanism is still unknown. It was found that the M1 receptor does not exist in the chick sclera [19] such evidence implies that muscarinic antagonists which prevents the progression of myopia in the chick either work through another muscarinic receptor subtype or through non-specific or non-receptor mediated mechanisms. "
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    ABSTRACT: To investigate the effect of atropine on the development of spectacle lens induced myopia in the mouse and to determine if the level of mRNAs for the muscarinic receptor subtypes (M(1) - M(5)) is affected by atropine treatment. Experimental myopia was developed in Balb/CJ (BJ) mice by placing -10 diopter spectacle lens on post-natal day 10 over the right eyes of 150 mice (n=10 in each group, 5 repetitions) for six weeks. After 2 weeks of lens wearing, the atropine group received a daily sub-conjunctival injection (10 µl) of 1% atropine sulfate and the saline group received daily 10 µl of 0.9% normal saline for 4 weeks. In addition, myopia was developed in C57BL/6 (B6) mice by placing -10 D spectacle lens on post-natal day 10 over the right eyes of 60 mice (n=10 in each group, 2 repetitions) for six weeks with and without atropine treatment. Refraction and axial length was measured at 2, 4, and 6 weeks after treatments. RT-PCR and northern blots were performed using specific primers for M(1)-M(5), and products sequenced. Real-time PCR was used to quantify message levels. Axial length of myopic eyes was 111% of their controls without atropine treatment and 103% of controls after atropine (p<0.01). Refraction shifted from myopic to emmetropic after atropine was administered in both pigmented and non-pigmented eyes. Corneal thickness, anterior chamber depth, corneal curvature and retinal thickness were not significantly different with and without atropine treatment (p=0.14). The lens thickness and vitreous chamber depth were significantly reduced after receiving atropine (p<0.05). Real-time PCR showed that message levels for M(1), M(3), and M(4) were upregulated in myopic sclera after atropine treatment, but M(2) and M(5) showed little change. The present study shows that 1% atropine reduces myopia progression in both pigmented and non-pigmented mice eyes. Axial length and vitreous chamber depth appear to be the main morphological parameters related to myopia. The results suggest that atropine may act on one or more muscarinic receptors to differentially regulate expression levels of specific receptors.
    Molecular vision 03/2011; 17:680-92. · 1.99 Impact Factor
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