Myopia has been recognised as a significant global health issue. Due to the urgency of the current situation, the European Society of Ophthalmology, in cooperation with the International Myopia Institute decided to publish this update (see article attached) of the current information and guidance on management of myopia. In summary, it discusses the following:
What is happening
In the last few decades, not only has the prevalence of myopia increased, but also the level of myopia, and with that, the risk of developing associated pathology like:
- Myopic maculopathy
- Optic Neuropathy
- Retinal Detachments
The World Health Organization (WHO) estimated that the number of people with myopia was:
- 2.6 Billion in 2020
and without intervention to slow down progression, will be:
- 3.3 Billion in 2030
- 4.9 Billion in 2050
This means that pathological myopia is predicted to become the most common cause of irreversible vision impairment and blindness.
What causes Myopia
50 years ago, the cause of myopia was believed to be mostly genetic.
It is now understood that myopia onset and progression, results from a complex interplay between visual/environmental conditions, and the genetic factors meant to modulate emmetropization (visually guided eye growth).
The emmetropization process:
- hyperopic retinal defocus (where there is a focus point behind the back of the eye)
- signals the retina to release biochemicals
- that travels through the retinal pigment epithelium (RPE) to the choroid
- where it changes the thickness of choroid thickness, moving the retina closer to the focal point of the eye (choroidal accommodation)
- biochemicals are also transmitted through the choroid to the sclera
- where it changes scleral extracellular matrix (ECM) synthesis
- which alters the biomechanical properties of the sclera
- which increases the length of the eye
- and makes the refractive state of the eye more myopic
Ocular and environmental factors that may affect retinal defocus, increasing axial length past the point of emmitropization (increasing myopia), include:
- Peripheral retinal defocus
- Lag of Accommodation
- Higher order aberrations
- Circadian rhythms
- Light intensity and spectral compositions
- Over stimulation of retinal OFF pathways
Myopia Risk Factors
- Myopia Onset. A high AC/A ratio was found to be a predictor of myopia onset, and began to increase approximately 4 years before the onset of myopia.
- Myopia Progression. After the onset of myopia, many children and young adults then showed reduced accommodative facility and greater accommodative convergence compared to age-matched emmetropic individuals. These deficits in accommodation in myopia may be a functional consequence of the equatorial enlargement of the eye. A higher accommodative lag was associated with faster progression of myopia.
- Time spent out-doors. To date, the most influential environmental factor associated with the onset of myopia, is less time spent outdoors. There are many different theories about whether the beneficial effect of time spent outdoors could be due to the brightness of light exposure, increased short-wavelength, ultraviolet light exposure and/or other mechanisms. Increasing time outdoors is effective in preventing the onset of myopia as well as in slowing the myopic shift in refractive error in non-myopic eyes.
- Near work. Spending more time at school or other near work activities is does mean spending less time outdoors. But evidence further suggest that with each 1 diopter per hour of near work, the odds of becoming more myopic increases by 2%.
- Black on white. A recent hypothesis suggests that the use of black text on a white background, overstimulates retinal OFF pathways, which decreases choroidal thickness (shown to be associated with myopia progression). White text on a black background leads to the opposite effect, with an overstimulation of the retinal ON pathways leading to choroid thinning. Therefore, reading white text from a black screen or tablet may inhibit myopia, while conventional black text on white background may stimulate myopia.
- Digital devices. Digital devices nowadays constitute a significant portion of our near work, and correlate with myopia. It has to be taken into account that digital devices may favour indoor lifestyles, and it has remained elusive whether it was a primary or secondary effect. Nonetheless, the increased availability and use of digital screens for both leisure and recreation by very young children may be further promoting myopia onset and progression.
- Parental myopia. Parental history of myopia correlates with the rate of axial elongation and increase in myopic refraction.
- Ethnicity. Evidence suggests differences between ethnic groups, but this may be due to environmental influences.
- Cognitive function and education. Evidence found a significant correlation between the genetic risk for refractive error and intelligence (defined by the number of years spent in formal education). But the mechanism linking education to myopia may be caused by defocus signals in the central and peripheral retina and persistent lag of accommodation.
Overall, it seems clear that myopia is caused and increased mostly by environmental and genetic factors interacting with each other.
Prevalence of myopia across age groups
Current studies suggest:
- The prevalence of Myopia is low in children younger than 6 years.
- The age of onset appears to be a strong predictor of high myopia.
- Parental myopia is associated with greater risk of early-onset myopia.
In the last half century, the incidence of myopia amongst the following age groups showed to have increased as follows:
- 7 – 10 years increased from 4.5% to 23.0%
- 11 – 14 years increased from 10.5% to 40.0%
- 15 – 18 years increased from 21.5% to 45.0%
The percentage of children with myopia who stabilise:
- By 15 years of age, are about 48%
- By 18 years of age, are about 77%
- By 21 years of age, are about 90%
- By 24 years of age, are most of the children, except the high myopes.
But the distribution of myopia in the population is expected to widen by 2050. A significant proportion of the population is expected to exhibiting myopia from 10 years, all the way to 79 years of age, with the bulk of late onset above 16 years of age. This reflects the significant lifestyle changes, mostly intensive near work over the past 10 to 25 years. This may well be exacerbated by changes in working patters following the Covid-19 pandemic, where we see increased time spend indoors and specifically on electronic devises.
To determine the first refraction in a child, cycloplegia must be used. Lack of cycloplegia in refractive error measurement increases the risk of misclassification for both myopia and hyperopia. The presence of <+0.75D of hyperopia at the age of 6 years indicates that myopia is likely to develop in the near future. One study found that white European children presenting with a refractive error of <+0.63D at 6–7 years and with at least one myopic parent, were shown to be likely to develop myopia by age 13 years. Those children with no myopic parents were likely to develop myopia by 16 years.
The visual complications of myopia are strongly related to axial length growth, thereby monitoring the axial length changes should be primary target for myopia management. Where axial biometry measures are available, these can also be informative in identifying children at risk for myopia who should be provided behavioural advice and monitored closely for the onset of myopia so that anti-myopia therapies can be applied. Axial lengths greater than 23.07 mm at 6–7 years are associated with a strong risk of future myopia.
Since the visual profile of the myopic child is characterised by higher accommodative lag, high AC/A ratio, esophoria at near and reduced accommodative flexibility, it would be important to include tests that evaluate the binocular vision and not only refraction. More attention needs to be paid to the management of binocular vision disorders.
It is suggested to screen children before the age of 6 years or in the first school year for family history of myopia, time spent outdoors, time performing close activities (like, cell phone or tablet use, playing with toys, handwork, reading, drawing, etc.), and binocular vision. Children with higher risk should be encouraged to spend more time outdoors as the key evidence-based strategy that appears effective in reducing the incidence of myopia.
Interventions for controlling myopia
- Optical Devices
- Surgical Interventions
Axial length is the most important metric to monitor in pre-myopic and myopic children.
Myopia generally progresses most rapidly during pre-teenage years (7 – 12 years), subsequently slowing through adolescence and adulthood. The mean age of myopia stabilisation is around 15.6 years od of age, with 95% of myopes stabilised by the age of 24 years.
Efficacy of some treatments may decrease after the first 6 months to 2 years of treatment.
The same treatments and protocols as applied in childhood may be applicable in later-onset myopia, although the available evidence is limited.
In case of atropine treatment parents and patients should be made aware that myopia progression may accelerate after stopping higher-dose atropine usage, but despite this rebound effect, the level of myopia post-treatment will be less than it would have been without treatment. The long-term use of atropine should only be undertaken with caution as long-term side effects have not been evaluated. It may be beneficial to tail off dosage or dose frequency at the end of treatment to minimise rebound effects. Results point to some loss of treatment efficacy with time with the higher concentrations of atropine, a study by which involved concentrations between 0.05% and 0.1%, suggested that treatment effects with low-dose atropine can be maintained for up to 4.5 years.
Discontinuation of ortho-K lens wear before age 14 has shown to lead to a more rapid increase in axial length over the next 7-month period, more so than single vision spectacle wearing controls. This slowed again with resumed lens wear for another 6 months. This suggests that ortho-K wear should not be discontinued before age 14.
Long-term use of soft myopia control contact lens and ortho-K is not contraindicated if ocular health is maintained through regular aftercares and strong compliance. No rebound effect was reported with soft contact lens for myopia control.
Progressive additional lenses showed only a small, long-term myopia control effect in comparison with contact lens corrections, except in specific cases.
Bifocal spectacle lenses might be a good solution for longevity treatment. A study of children wearing progressive addition lenses for 1year, then switched to single vision glasses for 1year showed no rebound.
Compliance and safety issues may require a change in treatment modality or a halting of treatment. Poor tolerance of visual side effects may also prompt cessation or change of myopia control therapy.
In conclusion, outdoor time is the most promising intervention method. There is consistent evidence of a benefit of slowing myopia development by the use of atropine eye drops, while the optimum concentration of atropine and the value of a combined use of atropine eye drops with optical devices are yet to be fully explored. There is also evidence of myopia control with soft multifocal contact lenses, orthokeratology, and new types of multifocal spectacle lenses. Information is constantly evolving, so it is important to stay abreast of studies published in the peer- reviewed literature.