Introduction

Progressive myopia is associated with multiple sight-threatening conditions such as cataract, retinal detachment, glaucoma, and lacquer cracks, as well as other conditions.^1-2 Uncorrected refractive error is the leading cause of visual disability among school-aged children. Table 1 shows risks factors that have been associated with myopia. The rates of myopia have been rising, and the associated visual morbidity and consequent decreased quality of life carry substantial cost, making myopia a significant public health concern. Although the cause of myopia has not been identified, effective measures to slow its progression during childhood have been the subject of many clinical trials and of animal research. The most popular treatment methods will be discussed. 

Progressive addition lenses

The use of progressive addition lenses (PALs) has been thought to decrease myopic progression. The Correction of Myopia Evaluation Trial (COMET) evaluated the effect of PALs compared with single vision lenses (SVLs) on the progression of juvenile-onset myopia.³ This study had three-year follow-up on 462 children aged 6 to 11 years old. It found that PALs did decrease myopic progression, with the treatment effect primarily shown in the first year. Although this study showed statistical significance in decreasing myopic progression, the magnitude of the change was not clinically significant.

In Hong Kong, a similar study was completed, comparing PALs to SVLs.⁴ The study used matched treatment and control groups. It found no evidence that progression of myopia was slowed by the wearing of PALs, either in terms of refractive error or of axial length.

Orthokeratology/peripheral optical blur

Orthokeratology (OOK) alters the structural integrity of the cornea.⁵ The theory behind its mechanism is that peripheral blur leads to decreased axial elongation. Over 100 cases are reported in the literature of infectious keratitis, including Acanthamoeba keratitis, as a consequence of OOK. Because of the potentially blinding complications, a report by the American Academy of Ophthalmology highlighted the need for further studies with a built-in wide safety margin.⁵ Recent research suggests that peripheral blur may in fact slow axial elongation, warranting further study of peripheral blur in slowing progressive myopia.⁶

Rigid gas-permeable contact lenses

Rigid gas-permeable (RGP) contact lenses have been used to decrease myopic progression. Katz and colleagues studied 298 children aged 6 to 12 years old over a 2-year period, comparing the study group wearing RGPs to a control group wearing spectacles.⁷ They found no difference in myopic progression between children who wore spectacles and those who consistently used RGPs. It is important to note that only 37.5% of patients in the RGP group completed the study.

Walline and colleagues studied soft contact lenses (SCLs) versus RGPs.⁸ Although they concluded that RGPs decreased myopic progression after 3 years when compared to SCLs, only 69% of patients who were initially prescribed RGPs continued to wear them for the full study time.

Atropine

Anti-muscarinic pharmaceutical agents have significant side effects, such as mydriasis and cycloplegia, that lead to near blur and photophobia. These make the long-term use of atropine difficult for the patient. Current practice involves using bifocals and transition lenses, along with atropine, to minimize these side effects. Atropine 1% has had a significant effect on decreasing myopic progression, as shown by the ATOM1 (Atropine in the Treatment of Myopia) study by Chia and colleagues.⁹ In the ATOM2 study, Chia and colleagues were the first to describe the effects of multiple low-dose strengths (0.5%, 0.1%, and 0.01%) of atropine.⁹ Their findings showed that lower concentrations of atropine were less effective between 0.01% and 0.5% (P < 0.05); however, axial lengths at 2 years were not significantly different between the three strengths of atropine. In addition, they found that atropine 0.01% had a negligible effect on accommodation and pupil size, and no effect on near visual acuity. They also found in subsequent studies that the 0.01% concentration of atropine decreased rebound myopic progression. Low-dose (0.01%) atropine is currently being used in clinical practice in Asia and the United States. A national study from the Pediatric Eye Disease Investigator Group (PEDIG) is pending.

Time outdoors

Laboratory experiments on animals showed that controlled bright non-ultraviolet (non-UV) light exposure prevents myopia.¹¹ This slowing of myopic progression can be blocked by administration of dopamine antagonists (spiperone).¹¹ These laboratory experiments provide evidence that bright light exposure stimulates dopamine release, which in turn decreases axial elongation. This also shows it is not UV light that prevents progressive myopia. These laboratory findings in Australia were supported by a study of Singapore teenage children showing that children who spent more time outdoors were less likely to be myopic.¹² Additional research by Neitz and Neitz at the University of Washington suggests that the wavelengths of outdoor light may be important in preventing myopic progression.¹³

Conclusion

High myopia carries significant morbidity and decreased quality of life. Several treatments to slow myopic progression exist, but much work must be done in isolating the causes and finding a universally accepted treatment method. Orthokeratology can cause sight-threatening complications, so widespread use of this practice has been discouraged in ophthalmology. Whether or not RGPs are efficacious has been subject to doubt scientifically. There is no substantiation to the efficacy of PALs, according to the COMET study. Low-dose atropine shows promise in slowing progression of myopia, but there are no randomized controlled trials to date on non-Asian children. Time outdoors seems to be an effective, simple, treatment and, with proper use of sunscreen, seems to be a reasonable first approach to discuss with parents. Multiple techniques may be necessary for some children.

References

1. Rada JA, Shelton S, Norton TT. The sclera and myopia. Exp Eye Res. 2006; 82:185-200.
2. Saw SM, Gazzard G, Shih‐Yen EC, Chua WH. Ophthalmic Physiol Opt. 2005; 25: 381–391.
3. Gwiazda J, Hyman L, Hussein M, et al. A randomized clinical trial of progressive addition lenses versus single vision lenses on the progression of myopia in children. Invest Ophthalmol Vis Sci. 2003; 44(4):1492-1500.
4. Edwards MH, Li RW, Lam CS, Lew JK, Yu BS. The Hong Kong progressive lens myopia control study: study design and main findings. Invest Ophthalmol Vis Sci. 2002; 43(9):2852-2858.
5. Van Meter WS, Musch DC, Jacobs DS, Kaufman SC, Reinhart WJ, Udell IJ, American Academy of Ophthalmology. Safety of overnight orthokeratology for myopia. Ophthalmology. 2008; 115(12):2301-2313.
6. Li SM, Kang MT, Wu SS, Liu LR, Li H, Chen Z, Wang N. Efficacy, safety and acceptability of orthokeratology on slowing axial elongation in myopic children by meta-analysis. Curr Eye Res. 2015; Aug 3:1-9. [Epub ahead of print]
7. Katz J, Schein OD, Levy B, et al. A randomized trial of rigid gas permeable contact lenses to reduce progression of children’s myopia. Am J Ophthalmol. 2003; 136:82-90.
8. Walline JJ, Jones LA, Mutti DO, Zadnik K. A randomized trial of the effects of rigid contact lenses on myopia progression. Arch Ophthalmol. 2004; 122:1760-1766.
9. Tong L, Huang XL, Koh AL, Zhang X, Tan DT, Chua WH. Atropine for the treatment of childhood myopia: effect on myopia progression after cessation of atropine. 2009; 116(3):572-579.
10. Chia A, Chua WH, Wen L, Fong A, Goon YY, Tan D. Atropine for the treatment of childhood myopia: changes after stopping atropine 0.01%, 0.1% and 0.5%. Am J Ophthalmol. 2014; 157(2):451-457.
11. French AN, Ashby RS, Morgan IG, Rose KA. Time outdoors and the prevention of myopia. Exp Eye Res. 2013;114:58-68. doi: 10.1016/j.exer.2013.04.018. Epub 2013 May 2.
12. Dirani M, Tong L, Gazzard G, et al. Outdoor activity and myopia in Singapore teenage children. Br J Ophthalmol. 2009; 93(8):997-1000.
13. Greenwald SH, Kuchenbecker JA, Roberson DK, Neitz M, Neitz J. S-opsin knockout mice with the endogenous M-opsin gene replaced by an L-opsin variant. Vis Neurosci. 2014 Jan;31(1):25-37.