AAOpt 2022: Ten common misconceptions in myopia management

When interpreting study findings, take into consideration the similarity and the differences between the subjects recruited for the study versus the patient population each practitioner serves.

This article was reviewed by Maria Liu, OD, PhD, FAAO

Maria Liu, OD, PhD, FAAO, discussed 10 findings from myopia studies that are commonly mis-interpreted and have significant implications on the clinical management of progressive myopia during the American Academy of Optometry annual meeting in San Diego, California.

“Many study findings provided the evidence for association, however, being interpreted as the evidence for causation,” said Liu, who is an associate professor of clinical optometry at the University of California, Berkeley.

“It’s important to be mindful of the differences,” Liu said. “Ocular growth pattern and the efficacy of myopia control treatments are highly variable depending on the age, ethnicity, and the previous rate of progression. As a result, the interpretation of the study findings needs to take into consideration the similarity and the differences between the subjects recruited for the study versus the patient population each practitioner serves.”

Misconception 1: Heritability is pure evidence for genetic influence

Parents commonly state that “both of us are myopic, so there is nothing we can do to help our child’s myopia.”

However, evidence suggests causal interference of environmental factors. The incidence of myopia has rapidly increased globally, which cannot be explained by the rate of genetic changes and there is a lack of evidence for causal genes. Juvenile myopia is due to visual stress (causal effect) along with scleral resistibility (susceptibility factor).

Misconceptions 2 and 3: Axial length is closely associated with refractive error and is the most reliable predictor of myopia complications

Doctors may state that “your child’s myopia is mild, but the axial length is on the longer side so the risk of complications is higher,” or “your child’s myopia is moderate, but the axial length is shorter than other eyes of similar myopia, so the risk of complications is not as high.”

While research has shown a statistically significant association, this is not the same as predictive. The association between axial length and refractive error is not great enough for individual prediction and is highly confounded by age and myopia onset.

Misconceptions 4 and 5: Any axial length increase means myopia progression and relative axial length provides reliable quantification of anti-myopia efficacy

Doctors may state that “the anti-myopia efficacies among various clinical studies are very comparable, and the relative change of axial length is the perfect outcome measure.”

However, the comparison of anti-myopia efficacies across trials is not straightforward. The increase in axial length is a combined product of physiological growth and visually driven elongation. The younger the patient, the bigger part physiological axial growth plays when considering anti-myopia efficacy.

Misconception 6: The anti-myopia efficacy of OrthoK is primarily attributable to the induced para-central corneal steepening and its impact on peripheral defocus

The anti-myopia mechanisms of OrthoK are multifactorial. When looking at the different impact of pupil size on the peripheral defocus versus central higher-order aberrations, the marginal (peripheral) rays have a large impact from pupil size, projecting to the central retina. However,the paraxial and oblique rays have little impact.

The properties of competing defocus post-OrthoK include central flattening (size of the treatment area, asphericity, non-uniformity) and paracentral steepening (width and magnitude).

Misconception 7: OrthoK treatment has high specificity, and the back surface lens design determines anti-myopia dosage

Differences in OrthoK design, such as 6mm optical zone diameter (OZD) versus 5mm OZD, does not induce the same level of differences on the corneal surface. Significant individual variability is present with the same OrthoK design. The post-treatment corneal shape rather than the back surface lens design should be used as the “myopia-control dosage” in clinical studies.

Misconception 8: De-centered OrthoK treatment appears to provide better anti-myopia efficacy

The impact of lens decentration has multiple components including confounding from angle kappa; the direction of decentration, with superior and nasal being less visually detrimental, and a significant difference in imposed retinal blur; and magnitude of decentration. Therefore, the impact of lens decentration on myopia control efficacy should not be analyzed as a binary variable and instead needs to be categorized and quantified.

Misconception 9: The anti-myopia effect of low dose atropine is not mediated through its impact on accommodation. This implies that accommodation is not significantly involved in the development of myopia

The anti-myopia effect from low dose atropine is not mediated through cycloplegia. The effect is independent from its impact on accommodation and the exact target site is unclear. However, this should not be interpreted as the evidence that accommodation and/or near work do not play a role in the etiology of myopia.

Misconception 10: Impact of outdoor exposure or near work is linear and the measurements of both in clinical studies are highly reliable

Doctors may state that “it does not matter how your child takes the outdoor break as long as there is sufficient time for it.”

Not only the total amount but the pattern of outdoor breaks also matters. An outdoor break is more effective soon after sustained near work. Compensation to defocus depends on the duration and frequency of near work, while integration of competing defocus is non-linear on either the temporal or spatial scale.

Further, quantification of either the outdoor exposure or near work dosage using survey questions may not fully reflect the daily visual activities.