June 1, 2020
By Thomas Aller, OD, FBCLA
As the prevalence of myopia grows throughout the world, the onset moves to younger ages, and higher levels are being seen in young adults, there is a developing consensus that treating myopia progression should have a goal of limiting the maximum level attained by an individual patient.1 That consensus, however, hasn’t yet led to broad adoption of myopia control in clinical practice.2 And while there is also no widespread agreement that myopia is a disease, there is general agreement that there are higher risks of certain ocular disorders and diseases with higher levels of myopia. These associations are well known for retinal tears and detachments, not well chronicled for the newly categorized myopia macular degeneration and not commonly appreciated for cataracts and glaucoma.3 For these conditions, we expect that the association with myopia is really an association with axial elongation, and that is why the goal of managing myopia progression should be to control axial elongation maximally.4 It may be many years (or perhaps never) before a study will conclude that 15 years of myopia suppression will reduce the consequences of pathologies linked with excess axial elongation. For this clinical dilemma, practitioners are limited to drawing logical conclusions from the existing literature and perhaps freed in the same instance to provide care to their patients that likely will benefit them years down the road, without waiting for multiple studies to prove it.
Five treatments are known or strongly expected to either delay the onset of myopia or slow the progression of myopia.5,6 Eye care practitioners may choose between atropine, multifocal contact lenses, orthokeratology, and in some markets, novel myopia control spectacle lenses. All of these treatments can be said to have studies that support the expectation of an average of 40 percent to 50 percent control as compared to various standard forms of myopia corrections.5 Crafting an effective treatment protocol requires evaluating the individual patient and working with them and with the parents to decide upon the best initial treatment strategy. For almost any treatment of any condition, there can be differences between the average treatment effect and the treatment effect for an individual. Every diopter matters7, and the condition we are trying to treat presumably causes irreversible damage to ocular structures. Therefore, specialty level myopia progression control obligates the eye care practitioner to not only tailor the initial treatment to the preferences, needs, and abilities of the individual patient but also to monitor the axial elongation that is occurring under treatment carefully and to modify the anti-myopia “dosage” or change the anti-myopia “medicine” to attempt to suppress axial elongation maximally.
Some will argue that in the absence of robust studies proving that changing a treatment strategy in an underperforming case, there is no justification for making a change. Several factors may make such studies unlikely and, if performed, unlikely to prove that changing treatment will help. There are seasonal differences in myopia progression so that if you start treatment in March or April and evaluate the progression in September or October and then change your treatment, you may not see a reduction in the progression rate over the next six months because myopia progression tends to be highest in the winter months. Myopia progression is not reliably linear, and there can be good years and bad years which may be related to behavior or environmental influences or not. Thus, an individual patient having a bad year under treatment “A” might have less progression next year under treatment “B” just because it is a different year and not necessarily because of your brilliant treatment decision. The third factor is with the generally observed slowing of myopia with age. An eyecare practitioner could expect that if the treatment were changed every year, the treatment effect would appear to improve every year.
Some studies hint at the value of additive treatments in that orthokeratology has been observed to be more effective with larger pupil sizes8 as well as perhaps more effective when combined with atropine. However, the studies are limited as well as in early phases.9 Even more compelling, it is clear that there is a dose-response relationship with higher percentages of atropine showing greater treatment effect.10 This gets a bit muddled in that all atropine studies abruptly discontinue the drug at the end of the treatment phase, triggering a rebound phenomenon that also seems to have a dose-response relationship, leading to more significant reductions in treatment effects for higher doses as compared to lower doses. This rebound phenomenon leads to the somewhat nonsensical conclusion that atropine might be the only drug in the universe that does not have a dose-response effect.
Deciding whether to increase the dose in a patient being treated with low dose atropine should be based on whether the patient is meeting the myopia control objectives and whether the current dosage is well tolerated. As with any treatment, the risks must be balanced by the benefits, so if an increased dosage creates unwelcome side effects, the dose should be reduced.
Deciding whether to add atropine to an existing optical strategy cannot be based on scientific studies because none attempt to answer that question. If you think that atropine and optical methods operate along the same pathway, you might anticipate minimal additional benefits. If you believe they operate along separate but parallel pathways, you might expect more robust effects. In terms of the risks associated with combined treatments, you could anticipate some visual disturbances with various forms of multifocal optics and larger pupil sizes, but always keep in mind that what likely would bother a presbyope or a night-driving adult, doesn’t tend to disturb a child.
While many cases could be cited from the author’s nearly 30 years of experience with active myopia management to show improved treatment effects with more aggressive treatments, many other cases might not have changed in the expected direction with such changes. What might be slightly more compelling is to analyze an ongoing case series of patients aged 6 to 14 at the onset of myopia control in which there were 157 times in which treatments were changed from less effective to more effective, or might have changed between two likely equally effective treatments, or might have changed from more effective to less effective. In this simplified analysis, which follows, we will just look at how the myopia progression rate changed after increased, decreased, and neutral treatment changes. Here, we are assuming that bifocal glasses or PALs are a weak treatment. Lower add MFCLs were expected to have a lower treatment effect than higher adds. If the distance zone size was decreased from previous treatment or the peripheral plus zone area was increased, this was viewed as more effective. Orthokeratology cases were not included in this analysis because axial lengths were not as routinely available as refractive data. Adding atropine or increasing the dose of atropine was presumed to be increasing myopia control. Table 1 shows the myopia progression rates before and after treatment changes, and there were little to no changes in myopia rates when treatments were judged as reduced or neutral. In contrast, increased myopia treatment effect resulted in a significant reduction in myopia progression rates. Keep in mind that in the clinical management of myopia, any reductions in treatment effect would be intended not to stimulate myopia but to improve the clinical acceptance of the treatment. Thus, we would not expect significant increases in myopia in this case series. Neutral treatment changes should be associated with reductions in myopia progression simply due to the anticipated decrease in progression with age. The observed substantial reductions in myopia progression match the intent of changing the treatments to more effective treatments.
Table 1. Changes in Treatment vs. Changes in Myopia Rates
|Change in Treatment Effect
|Number of Patients
|Changes in myopia rates D/Yr (SD)
|-0.01 (±0.74 D)*
|+0.05 (±0.71 D)*
|+0.41 (±0.66 D)*
* Statistically significant difference between all groups, Two-tailed T-test, p<0.01
Practitioners and scientists may draw different conclusions from these clinical observations, as well they should. As a clinician and a scientist, I try to make observations, ask questions about those observations, and track how treatments appear to affect results. It is often the case that great discoveries can come from simple clinical observations, but these observations must lead to further inquiry to develop into scientific discoveries. A lot of the parents of my patients are scientists, and they understand the value of good science, but they are also parents. I will often ask them when presenting various treatment choices, such as whether to make a particular change in treatment type or “dose,” if they want me to be their scientist or their doctor, and 97.5 percent of the time, they ask me to be their doctor. My advice to clinicians, based on 30 years of experience in active myopia progression control, is to listen to the scientists but don’t be afraid to observe and analyze the effects of your treatment choices with your patients. Remember that they usually will want you to be their doctor, not their scientist.
|Thomas Aller, OD, FBCLA, is a collaborator with the Brien Holden Vision Institute and a visiting scholar at the University of California, Berkeley School of Optometry.
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