Catching the Rebound From Myopia Treatment

The importance of monitoring myopia progression is at its highest at the ‘end’  of treatment, as rebound can negate years of valuable treatment if not considered and monitored.

Firstly, treatment must be continued for much longer than the two years most publications of study results indicate. To ensure the best long-term results, treatment is now considered necessary for a longer period based on the axial growth expected at different ages¹ and the evidence that discontinuation of some interventions leads to rebound growth.^2,3 The evidence on the rate of rebound for each modality is still under investigation, and it will be difficult to obtain given the various confounders, such as age, ethnicity, lifestyle, and treatment dose, which can interact with progression rate.⁴

Rebound in Myopia

Rebound is defined as an increase in axial growth that occurs when certain myopia interventions are discontinued. But true rebound is not just faster progression once stopping compared to the rate while on treatment. Publications have varied in how this has been calculated, further confusing matters. The true rebound is defined as faster progression than a control (untreated) group, age- and ethnicity-matched, after cessation.² Specifically, a faster rate compared to matched children who never received treatment (Figure 1).

Figure 1: Mean annualised rebound of axial elongation (in mm) following the cessation of myopia control treatment for six categories of myopia control treatment. Note that the right-hand scale for myopia progression is inverted. Error bars are ±1 standard deviation.¹

Although this is the benchmark of true rebound, it is also important to assess whether stopping treatment early means that the patient who might still progress fast will ‘lose the benefit’ of continued treatment.

Peripheral defocus spectacle lenses. Not all myopia interventions result in rebound at treatment cessation. Peripheral defocus spectacle lenses and dual-focus contact lenses have been well documented to not result in rebound after cessation.

The long-term use of defocus incorporated multiple segments (DIMS) design lenses has been examined by comparing axial progression between a group using DIMS for six years and another group using DIMS for 3.5 years, followed by single-vision lenses for the following 2.5 years. No rebound was reported after switching to single-vision lenses, with a cohort age-average of 16 years.⁵

A crossover study with Vietnamese children found no rebound with the use of highly aspherical lenslet (HAL) spectacle lenses over six months.⁶ This study was further analysed to ensure the true rebound was calculated by comparing the groups when untreated, and it was found to be an even lower value of suspected rebound.² Longer-term studies would help to review this, especially in a younger age group. Given the difficulties of achieving this, we will need to rely on real-world studies going forward.

Dual focus contact lenses. Long-term studies, using dual-focus contact lenses with peripheral add power, have reported minimal rebound after one year of treatment cessation.⁷ In another study comparing single-vision contact lenses with extended depth of focus and dual focus contact lenses, no significant rebound was noted over six months.⁸ Although there is a limitation of the number of studies and specifics like different age groups, the consensus is that rebound is not a significant concern with this modality of myopia intervention.²

Orthokeratology. Rebound in orthokeratology (OK) can only be assessed by axial change, as the refraction changes are induced on the cornea by wearing the rigid contact lens. The reports have been varied, with rebound documented, however, in varying amounts. One study, with a one-month follow-up, reported minimal rebound.⁹ However, most other studies demonstrate rebound varying when calculated for annualised true rebound: +0.03,10 +0.11,11 and +0.14 mm.¹² All these studies had small cohort sizes and followed, on average, for six months or less, with most of the cohort aged around 14 years.² Managing this rebound is difficult, as weaning from OK is limited by the effects on vision with intermittent wear.¹³ Treatment options include longer treatment to prevent progression when the eye is known to be at high risk. Alternatively, either combining with another modality (often atropine is also used) or transitioning to a different modality can be considered. None of these options has been studied.

Low-dose atropine drops. Rebound has been most extensively studied with the use of atropine myopia intervention. The concentration of atropine used has been reported to be dose-related to the measured rebound. The ATOM: atropine 1% study reported +0.20 mm rebound after one year of cessation.¹⁴ Interestingly, this study used atropine 1% in only one eye (the other was the control), and the long-term follow-up study published in 2024 (ATLAS study) demonstrated that the anisometropia dissipated over time and the treatment effect was lost.¹⁵ ATOM 2, at concentrations of 0.5%, 0.25%, and 0.01%, also had a year washout, and a rebound was noted that appeared to be dose-related.¹⁶ The recent ATLAS study following these subjects has highlighted the need for monitoring and longer treatment, with no significant difference between treatment and control groups. The study also highlighted that the use of atropine to control myopia may result in rebound, which seemed to remove any treatment benefit over time.¹⁵

The LAMP study examined atropine concentrations of 0.05, 0.025, and 0.01%, and in the third year, the groups were re-randomised to continue or discontinue treatment¹⁷ (Table 1).

Table 1. The rebound from atropine calculated over one year, was less when calculated for true rebound.¹³

If the progression is analysed for true rebound compared to a matched no-treatment group, the rebound is dose-related but lower than once thought. Bullimore and Brenan recalculated the rebound to be negligible with atropine 0.025% and 0.01%, and mild (+0.03 mm over one year) with atropine 0.05%.² In another study using the same calculation method, atropine 0.01% was found to have a significant rebound after six months of use (+0.10 mm; annualised), which was less than that with atropine 0.1% (+0.13 mm) compared to control.^2,18

The difficulty with the data is the varying treatment and cessation periods, and the inclusion age of the participants. The summary is that there is a dose-related rebound effect with atropine drops, which may be smaller than once thought, but given the results of the ATLAS study, it should not be underestimated. Recent choroidal thickness studies suggest that higher-dose atropine (1%) may act on distinct choroidal layers to mediate the rebound response, which was not observed with atropine 0.01% in this study.¹⁹

Repeated low-level red-light therapy. Repeated low-level red-light (RLRL) therapy is the latest myopia tool to enter the Australian market. It has been shown to be highly effective in controlling myopia progression.²⁰ Two studies have reported rebound, which is the greatest among all myopia intervention modalities.³ Chen et al. have documented an annualised rebound of +0.33 mm, extrapolated from a three-month cessation.^2,21 Xiong et al. reported +0.28 mm at one year cessation.²² Consistently, RLRL demonstrates the highest efficacy and the greatest rebound, so extra care is recommended. Further studies examining longer-term exposure and cessation will help clarify the rebound risk associated with RLRL.

Treatment Plans and Options

When developing the management plan for your patient, the initial assessment and ongoing follow-up will help identify risk factors for rebound. Much like the risks of myopia progression in general, a rebound needs assessment to ensure the treatment effect is not eliminated over time. Predictors for rebound are categorised in Figure 2.

Figure 2. Predictors to assess when managing the risk of rebound.

Age of the patient. It is clear from the literature that a child under 10 is destined to continue to elongate and hence progress with their myopia. Although some patients will slow down earlier, generally, stopping treatment early will reduce the final success rate.

Treatment. As described above, treatment with OK, atropine, and RLRL has a significant risk of rebound compared to peripheral defocus glasses and dual-focus contact lenses. Different atropine concentrations also need to be considered, with higher concentrations more likely to lead to greater rebound.

Family history. High myopia runs in families, so be aware of family history. A history of high myopia will increase the risk of the patient progressing faster and for longer.

Axial change. Monitoring progression will give you a growth trend for that child. Waiting for the natural slowing of growth in adolescence can help plan for the timing to minimise the rebound effect.

Environmental confounders. If your patient is inclined to spend time indoors and do a lot of near work, longer treatment is recommended, as these activities promote faster eye growth. Often, environmental factors confound the genetics, with parental myopia often occurring together with poor lifestyle routines. This is not a rule, but it is often the case and important to discuss with the patient and family.

So What is Best Practice?

The options include: weaning treatment, stopping treatment, transitioning treatment, and combining treatments.

A recent publication has advocated a weaning regimen with atropine and RLRL based on progression assessment of axial measurement change.¹³ In this publication, it was recommended that a child under 10 years of age continue treatment. In a child aged 10–14 years with progression of less than 0.2 mm over one year, or a child aged 14–16 years with progression of less than 0.1 mm over one year, weaning could be considered.¹³ The recommendations to wean included weaning the dose and then the frequency. If on atropine, first reduce the concentration (e.g., from 0.05% to 0.025%) every three months. Then reduce the frequency from nightly to every second night.¹³

This regime would take a long time, and the uncertainty around variable changes during this period would only add to the confusion, for example, seasonal variation in growth. Another approach is to monitor the eye’s elongation, recognising that during adolescence, the growth rate should decrease. Watching the axial change slow to less than 0.05 mm per six months over two visits provides some reassurance that natural growth is slowing. My approach is to stop atropine at the current dose if this trend is apparent. Furthermore, I often encourage the use of peripheral defocus glasses as a transition, or in combination if they are already using them, and discuss the need for lifestyle changes to aid the retardation of progression. This combination allows a control modality to remain present while atropine drops are reduced. I monitor for the next six months and restart atropine if a significant rebound is observed.

Given the high efficacy observed in studies using RLRL, weaning does seem a logical plan. Since the full treatment schedule is three minutes, twice a day, four hours apart, for five days a week, weaning involves reducing the treatment to once a day for three months, then reducing the frequency and number of days a week of RLRL treatment.¹³ For example twice daily would be reduced to daily over five days then to three times a week, then once a week. This weaning regimen has not been tested in any study and is suggested as a potential treatment paradigm.

Summary

Rebound needs to be considered and planned for as part of your patient’s myopia management to achieve optimal clinical outcomes. Also, although peripheral defocus glasses and dual-focus contact lenses do not appear to exhibit significant rebound, how they can mitigate the rebound documented with other modalities remains to be studied. Monitoring elongation provides the best guide to treatment effects, your patient’s individualised growth trend, and any post-treatment acceleration. Future studies in this area will be complex and difficult to assess among known confounders. Real-world data will need to guide us to achieve best practice and best results.

References 

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19. Xu H, Ye L, Peng Y, et al. Potential choroidal mechanisms underlying atropine’s antimyopic and rebound effects: A mediation analysis in a randomized clinical trial. Invest Ophthalmol Vis Sci 2023;64(4):13. doi: 10.1167/iovs.64.4.13.
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