Editor’s note: This is the first of several planned articles to appear in 2019 on myopia management.
Very few things in science are definitive and, therefore, not subject to continual debate and revision, as new evidence emerges. Myopia is not one of these few things.
Here, I will wade through what we know and what we do not know about the refractive disorder.
DEFINITION AND PROGRESSION
What we know about myopia that it is a refractive condition in which the eye is generally too long to provide clear optics, resulting in blurred distance vision. What we don’t know about myopia is how it really should be defined, for example what variables indicate onset and what the consequences of that definition might be.
What we know about progression is that various ocular changes, such as peripheral hyperopic defocus, increased lag of accommodation or changes in binocular vision, may be observed prior to myopia onset and progression. But they have also been reported after onset.1 What we don’t know is whether there is a difference between a pre-myope experiencing a rapid reduction of hyperopia accompanied by an accelerated axial elongation and a child experiencing exactly the same growth pattern, but who has earned the status of a true myope, having passed the barrier of -0.75 D. Depending on how the onset of myopia is defined, ocular changes, such as increased accommodative lag, experienced after the onset of myopia — and thus consequences of myopia — might more properly be considered as contributors to the onset of accelerated axial growth, which occurred during hyperopia but could be considered the beginning of the myopic process.2-6
PREVALENCE
What we think we know is that the prevalence has been increasing all around the world, particularly in urban East Asian countries, where one recent study shows a 23% increase over the last decade.7 What we don’t know is why, when that East Asian population relocates to Australia or Mongolia, they experience dramatically lower levels of myopia.7,8
PREVENTION
What we know is that evidence from multiple studies show time spent outdoors is linked with a protective effect, in terms of delaying the onset of myopia, and is less suggestive of controlling progression once myopia has begun.9-11 What we don’t know is what it is about outdoor exposure or activities that might be responsible. Could it be light intensity, differences in light spectrum outdoors or that most time spent outdoors involves viewing distance objects? This is yet to be determined.12,13
What most practicing optometrists know through patient encounters is near work activities increase the risks for developing myopia and influence the rate of progression, as well as the duration of progression. What we don’t know is whether these anecdotal findings are well-supported in the literature, as there are many studies that find near work to be a factor,11,14-18 and many that fail to show a relationship.11,14-18 What we don’t know is how to separately assess whether there is a protective effect from being outdoors or a stimulative effect from being indoors.19
SIGNS
What we know is a number of studies suggest a link between myopia onset and progression and various accommodative and binocular vision measures.6,20-22 What we also know is the best control in such studies show a limited impact of optical devices on these measures.1,23-26 What we know is while esophoria has been linked to the onset and progression of myopia, and has been used as a basis for the treatment of myopia progression, the findings are quite mixed, with most revealing no effects.1,23-24,27 What we don’t know is why optometrists base their treatment decisions on the behavior of the eyes when viewing a near object while one eye is covered. What we do know is the most effective optical treatment reported to date involves the measurement of the alignment of the eyes under binocular viewing conditions, using a measurement of eso fixation disparity as the determinant of the treatment group and for prescribing the particular bifocal add power, rather than using a monocular measurement of phoria.28 What we don’t know is why no other researchers have utilized this method of assessing eye alignment and, when they do take binocular vision into account, why they still use a monocular measure of binocular vision to determine the treatment protocol.
CONTROL/TREATMENT
With regard to myopia progression control, what we do know is that prescribing single vision spectacle lenses or contact lenses has been the standard of care during the time over which myopia rates have skyrocketed. What we don’t know is why optometrists and ophthalmologists continue to choose these options in treating their patients. We also think we know that undercorrection of myopia either is ineffective in slowing progression or may actually accelerate progression.29,30 A recent study, though, found that significant undercorrection of myopia from not correcting the myopia, resulted in less myopia progression than full correction.31 What we don’t know is why when doctors insist that undercorrection causes myopia and that all myopes must have full corrections, they don’t insist that those children be reappointed every month to look for progression and to keep increasing the minus power to somehow combat the increase in myopia.
What we do know is that atropine, in various dosages, quite convincingly, controls myopia progression and axial elongation.32-39 What we also know is abrupt discontinuation of many pharmaceuticals that suppress receptors, including atropine, maximizes the rebound phenomenon, and in the case of atropine specifically, there is a greater loss of treatment effect in the higher doses, as compared to the lower doses.37,40-42 What we don’t know is why none of the existing, ongoing or planned atropine trials have sought to answer the question: “What is the most effective way to prescribe or discontinue atropine, so as to avoid or limit a rebound phenomenon, which can dramatically reverse the myopia control effect desired?”
What we do know is since the atropine studies have been interpreted to mean that the myopia-controlling effects of atropine are (unlike any drug ever studied) largely dose independent and side effects are (like virtually every drug ever studied) dose dependent, the lowest possible dose will have the best possible results.37,42 One has to wonder why atropine should behave so dramatically different than every other drug? We do know that if studies are designed to test dose-dependent treatment effects and then are designed to maximize the reversing effects of the rebound after abrupt discontinuation, dose-dependent treatment effects will be obscured.
We do know from various studies that atropine’s myopia-controlling effects are not caused by cycloplegia, as the effects persist in animals after severing ciliary nerves.43 What we have learned is atropine appears to act in the inner retina to magnify the retinal response to myopic defocus, and that it appears to inhibit choroidal thinning in response to hyperopic defocus while not suppressing the choroidal thickening found with myopic defocus.44,45
What we think we know is that orthokeratology has greater myopia control effects in children who have large pupils, and we think we know atropine added to orthokeratology may increase the myopia control effects.46-48 What we don’t know is whether this apparent additive effect is due to the larger pupils created by the atropine and/or the inherent mechanisms involved with atropine treatments.
We do know the average myopia control found in multiple orthokeratology studies is around 50%.49,50 We also know that in most of those studies, there are greater treatment effects found in either higher refractive errors or with greater corneal shape changes induced.51-53 What we don’t know is whether alternative designs intended to maximize the corneal shape changes, regardless of the initial prescription, will result in outcomes of lower levels of myopia.
What we do know is the risks of microbial keratitis with overnight orthokeratology is similar to the risks reported for overnight soft contact lenses.54 What we don’t know is whether those studies confirmed those risks or if more studies need to be done.
What we do know is the average myopia progression control found in many studies of multifocal or bifocal contact lenses is around 40%.28,49,55-58 What we don’t know about these lenses is whether they need to be distance center multifocals, as those are the only designs with published results, whether there is any effect of add power, whether there are any ways to optimize their designs to maximize treatment effects and whether there might be additive positive effects when combined with atropine.
HOW DO WE ACT?
Continuing research in the definition, prevalence, progression, prevention, signs and control is needed to fill in the gaps of what we don’t know about myopia. Additional information resources include: Essilor’s new Myopia Taskforce, Treehouse Eyes, which conducts The Myopia Meeting, Brien Holden Vision Institute, Global Specialty Lens Symposium and the Vision by Design meeting.* OM
*This list will be updated at OptometricManagement.com .
References
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