Rebound Effects After Cessation of Myopia-Control Interventions: A Systematic Review

1. Introduction

The global rise in myopia [1,2], particularly in East and Southeast Asia [2], has become a major public health concern, with projections indicating that nearly half of the world’s population will be myopic by 2050 [2]. Since it often begins and progresses quickly in childhood, timely early interventions are essential. Myopia may result from disrupted emmetropization driven by the eye’s attempt to compensate for peripheral hyperopic blur [3,4], with Bruch’s membrane, comprising five structural layers, potentially exerting biomechanical influences on ocular shape and thereby contributing to both emmetropization and myopization [5]. In addition, myopia develops through complex interactions between genetic and environmental factors, with more than 450 associated genetic loci identified and key modifiable risks such as near work and reduced outdoor time playing significant roles [6].

Spectacle lenses have been used for myopia control in children and adolescents, with evidence from randomized controlled trials showing they can slow progression by affecting spherical refraction, axial length, and peripheral myopic defocus causing increase in choroidal thickness, making them a safe, non-invasive option to reduce high-myopia risk and guide lens selection [7,8,9,10]. In addition to spectacle lenses, other interventions such as gas-permeable contact lenses, orthokeratology lenses, and soft dual focus contact lenses have been extensively used for myopia control, offering alternative strategies to slow progression [11,12,13,14]. Atropine eye drops, particularly at low concentrations, have emerged as an effective, dose-dependent therapy for myopia control, with widespread use, especially in East Asia, helping to slow progression in high-risk children [15,16]. Randomized trials have demonstrated a clear dose-dependent efficacy of atropine for myopia control, with higher concentrations (0.5–1%) producing greater short-term reductions in spherical equivalent progression and axial elongation but at the cost of increased rebound after cessation [17] compared with low-dose atropine (0.01–0.05%) [18,19,20]. A novel molecule, 7-methylxanthine (7-MX), has emerged as a promising oral therapy for controlling myopia progression and excessive axial elongation [21]. Long-term clinical studies from Denmark demonstrate dose-dependent and sustained efficacy in children, with no significant safety concerns reported [21]. Repeated low-level red-light (RLRL) therapy, which enhances cellular energy supply and metabolism [22] to promote tissue repair [23], has recently attracted global attention as a novel scientific approach for myopia treatment [24,25,26].

Although there is convincing evidence for the efficacy of these different interventions for myopia control [9,16,27,28,29,30,31] uncertainties remain, particularly concerning the risk of myopic rebound following treatment cessation. The rebound effect, characterized by accelerated myopia progression in axial length or spherical equivalent following discontinuation of treatment, has been suggested as a major factor contributing to the relatively high discontinuation rates observed with various myopia control interventions [32]. Evidence suggests that optical interventions generally exhibit a lower magnitude of rebound compared with pharmacological or light-based therapies, although the latter typically demonstrate greater efficacy in slowing myopia progression during active treatment [33]. Understanding the potential for rebound is therefore essential for clinicians and patients when planning long-term management strategies, ensuring continuity of care, and selecting the most appropriate intervention for sustained myopia control.

Although several studies have evaluated that the rebound effect after stopping myopia control treatments varies widely and depends on the type and concentration of the intervention [16,34,35,36,37,38,39], to date, no systematic review has comprehensively analysed changes in axial length (AL) and spherical equivalent refraction (SER) after cessation of myopia control treatments across all study designs, including randomized and non-randomized studies. Also, the differences in study designs, treatment durations and washout periods have led to inconsistent findings, making the overall pattern of rebound unclear. Therefore, this systematic review aimed to summarize current evidence on the incidence, magnitude and possible predictors of rebound after cessation of myopia control treatments and to identify strategies that may help minimize rebound in practice.

2. Materials and Methods

2.1. Study Design, Data Source, and Search Strategy

In this systematic review, we aimed to evaluate the potential rebound effects that occur following the cessation of optical, pharmacological, and low-level light therapy interventions used for myopia control. This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines [40]. A systematic literature search was conducted, and 1027 articles published up to November 2025 were identified through the following databases: PubMed, Web of Science, Scopus, and ClinicalTrials.gov. The search combined three key concepts: myopia, treatment cessation or rebound, and relevant interventions, using the following Boolean strategy: (myopia OR nearsightedness) AND (discontinue OR cease OR cessation OR stop OR stopped OR rebound) AND (contact lens OR dual-focus contact lens OR MiSight contact lens OR extended depth of focus (EDOF) contact lens, OR orthokeratology OR spectacles OR Defocus incorporated multiple segments (DIMS) spectacles OR highly aspherical lenslets (HAL) OR atropine OR low-level light therapy OR LLLT). The reference lists of all retrieved articles were also reviewed to identify additional studies that met the inclusion criteria.

2.2. Study Selection

A total of 1027 studies were initially identified. After removing duplicates, the remaining articles underwent successive screening stages, including title, abstract, and full-text review. Three investigators independently performed the selection process according to these inclusion and exclusion criteria. Studies were included if they met the following criteria: (1) randomized controlled trials (RCTs) or other interventional studies, including post-hoc analyses reporting new findings on rebound effects; (2) studies reporting axial length (AL) and/or spherical equivalent (SE) measurements; and (3) studies enrolling children with myopia who underwent treatment for at least 6 months and subsequently discontinued the intervention for more than 2 weeks. There were no restrictions on country, follow-up duration, sample size, or study results.

Studies were excluded if they were unrelated to myopia control, did not report rebound effects after therapy cessation, were non-English publications, or appeared in unindexed journals. Titles and abstracts were first screened to remove clearly irrelevant studies. Full-text articles and eligible abstract-only publications were then assessed for eligibility based on reported post-cessation changes in axial length (AL) and/or spherical equivalent refraction (SER).

2.3. Data Extraction and Risk of Bias Assessment

Data from each included study were independently extracted and summarized in tables by three researchers. The following information was collected from each article: (1) author and year of publication, (2) study design, (3) follow-up duration (in months), (4) number of participants, (5) mean age of participants (in years), (6) participant sex distribution (male/female), (7) inclusion criteria, (8) intervention in the study group, (9) intervention in the control group, (10) baseline axial length (AL) and spherical equivalent refraction (SER), and (11) washout period of myopia control therapy in months.

The following data were extracted regarding outcomes of the studies: (12) continuation period rate of AL (mm)/SE (Ds), (13) cessation period rate of AL (mm)/SE (Ds), and (14) Rebound Effect. Rebound effects of myopia control therapies were defined as ‘(Progression during cessation period) − (Progression during continuation period)’. Rebound effect is classified into four levels based on changes in the AL or SE [41] as follows: “no rebound effect” (an AL ≤ 0 mm/year or SE ≥ 0 D/year); “weak rebound effect” (an AL from 0 to 0.09 mm/year or SE from 0 to −0.25 D/year); “moderate rebound effect” (an AL from 0.09 to 0.18 mm/year or SE from −0.25 to −0.50 D/year); and “strong rebound effect” (an AL ≥ 0.18 mm/year or SE ≤ −0.50 D/year).

Mean ± standard deviation (SD) values were calculated for each variable to summarize clinical outcomes and rebound effects. Specifically, the mean AL and SER rebound effect was determined based on the data reported in each study. The changes in AL and SER before and after cessation of treatment were manually extracted to calculate the differences in myopia progression during the treatment and discontinuation periods.

The studies that remained after abstract and full-text screenings were evaluated for methodological quality. To minimize the risk of bias, three authors independently assessed the included RCTs using the Cochrane Risk of Bias tool (without meta-analysis) [42], which considers the following domains: randomization process, adherence to intervention, missing outcome data, outcome measurement, selective reporting, and overall risk of bias. A synopsis of each study’s quality was generated based on these criteria to guide interpretation of the findings. For non-randomized studies, methodological quality was assessed using the Risk of Bias in Non-Randomized Studies of Interventions (ROBINS-I) tool [43], which evaluates potential bias across seven domains: confounding, participant selection, classification of interventions, deviations from intended interventions, missing data, outcome measurement, and selective reporting of results. A fourth author subsequently reviewed and compared these assessments to resolve discrepancies and ensure consistency.

The Robvis tool [44] was used to visually summarize the risk of bias across included studies. Robvis generates color-coded plots for each domain assessed by the Cochrane tool, providing a clear and thorough overview of study quality both individually and collectively included in this review.

3. Results

3.1. Literature Search

The study selection of this systemic review is outlined in Figure 1. Initially, 1027 studies were recorded. After eliminating the duplicates, and reviewing the abstract and full text articles, 21 studies, published between 2011 and 2025, were included in this systemic review. A total of 1927 participants including 907 females (47.07%) and 1020 males (52.93%) with average age of 10.8 ± 1.7 years were included in this review. After a structured and reproducible literature search, a total of 21 studies were identified which include HAL/DIMS spectacles [34,45], Soft multifocal contact lenses [36,46,48,51], Orthokeratology (Ortho-K) [35,37,47,49,50,52], atropine [53,54,55,56,57,58,59], and RLRL [38,39] studies. The mean washout period of the included studies was 10.6 ± 9.8 months. Table 1 presents the detailed characteristics of the studies included in this review.

3.2. Outcomes

The rebound effect outcomes are presented and summarized in Table 2 and Table 3 respectively. In most studies, axial length (AL) and spherical equivalent refraction (SER) values were higher in cessation groups than in groups that continued myopia control treatment. HAL/DIMS spectacles for myopia control interventions showed weak to moderate rebound effects after treatment cessation with a mean rebound of 0.09 ± 0.17 mm (0.06 to 0.11) in AL and −0.16 ± 0.43 D (-0.18 to -0.13) in SER. Multifocal contact lenses generally showed weak or no rebound after treatment cessation, whereas Ortho-K lenses were more frequently associated with moderate to strong rebound effects, suggesting a mean rebound of 0.05 ± 0.61 mm (-0.43 to 0.62) in AL and 0.05 ± 0.60 D (-0.22 to 0.41) in SER. Similarly, the mean rebound effect in atropine intervention was concentration-dependent and found to be 0.14 ± 0.19 mm (-0.02 to 0.35) in AL and -0.23 ± 0.47 D (-0.87 to 0.43) in SER. LLLT intervention showed moderate to strong rebound effects with the mean rebound effect of 0.23 ± 0.26 mm (0.15 to 0.30) in AL and -0.48 ± 0.37 D (-0.71 to -0.25) in SER.

In a comprehensive assessment of all myopia control interventions, the treatment continuation subgroup showed a mean axial length (AL) change of 0.15 ± 0.16 mm (range: −0.09 to 0.46) and a mean spherical equivalent refraction (SER) change of −0.25 ± 0.41 D (range: −0.67 to 0.38). In contrast, the treatment cessation subgroup demonstrated a mean AL change of 0.25 ± 0.26 mm (0.00 to 0.58) and a mean SER change of −0.55 ± 0.44 D (-1.15 to -0.01). These findings indicate a mean rebound effect of 0.11 ± 0.43 (-0.43 to 0.62) mm for AL and −0.20 ± 0.53 D for SER (-0.87 to 0.43), suggesting a intervention-dependent post-cessation increase in axial elongation and myopic progression.

3.3. Risk of Bias Assessment

Figure 2 presents the potential risk of bias in the included studies, assessed using the RoB 2 and ROBINS-I tools. Among the 16 RCTs, 13 studies [34,37,38,39,45,46,51,53,54,55,56,57,58] were assessed as having a low risk of bias, while 3 studies [36,47,48] had a moderate risk. Of the 5 non-RCTs, 2 studies [35,49] were rated as high risk and 3 studies [50,52,59] as moderate risk of bias. No RCTs were excluded, as more than 75% of them were at low risk of bias. For non-RCTs, although some studies had moderate or high risk of bias, studies with moderate risk comprised more than 50%, so all were retained in the review. The overall risk of bias summary of the domains used in each study is presented in Figure 3.

4. Discussion

Indeed, there are large volume of literature published over the past decade on myopia interventions [60], this systematic review aimed to assess changes in axial length (AL) and spherical equivalent (SE) after cessation of different myopia-control interventions, focusing on highly relevant original studies, including both randomized and non-randomized designs, identified through a targeted keyword-based search strategy. This review limited the summaries of rebound for optical (spectacles and contact lenses), atropine, and repeated low level laser therapies to randomized and non-randomized clinical trials for at least 1 year in duration, published before October 2025. Nonetheless, several included clinical trials lacked complete reporting of all checklist items (Table 1 and Table 2), which limited direct comparability across studies. While the trials were generally well conducted, detailed assessment of methodological quality and potential risk of bias identified deficiencies in reporting of certain required items.

Although myopia primarily develops in childhood, refractive changes can continue into adulthood [61], potentially predisposing individuals to rebound following intervention cessation. while the accelerated progression observed after treatment discontinuation. The effectiveness of current myopia-control strategies is demonstrated by their ability to significantly slow myopia progression during active treatment, and the rebound effects following treatment cessation [38,53] are clinically undesirable, however, these effects after treatment cessation serve as evidence of the effectiveness of myopia-control interventions, highlighting their role in suppressing ocular growth help prevent progression to high myopia. Because different interventions show varying rebound effects, it is important to study and compare these interventions to guide the selection of optimal strategies for future use.

4.1. Spectacles

Myopia-control spectacle lenses act by modifying peripheral retinal image signals, either by inducing peripheral myopic defocus [62] or by reducing retinal contrast [63]. These designs are based on the hypothesis that peripheral image quality influences ocular growth and myopia progression, and they typically combine a central distance-correction zone with surrounding treatment zones or contrast-modulating elements [62]. Therefore, the new-generation spectacle lens designs (HAL or DIMS) have been shown to effectively slow myopia progression in children [9,26,27].

However, a moderate rebound effect after cessation of HAL spectacles was found in a study by Sankaridurg et al. which [34]. In this study, children wearing highly aspherical lenslets (HAL) showed slower myopia progression than those with single-vision (SV) lenses. Switching from HAL to SV lenses led to increased progression, while switching from SV to HAL slowed progression. In contrast, Lam et al. [45] reported DIMS spectacle lenses provided a sustained effect of slowing myopia progression and axial elongation in myopic children who wore DIMS lenses for up to 6 years with weak rebound effect (approximately 0.22 D/year and 0.12 mm/year), after cessation of DIMS spectacles wear, with a longer duration of study and washout period of 72 and 30 months, respectively.

Although DIMS and HAL lenses were essentially equivalent in slowing myopia progression [64], the presence of a central distance-correction zone, extra peripheral myopic defocus, appears to play an important role in controlling myopia, particularly in influencing axial elongation [65]. The recently FDA-approved Essilor Stellest spectacle lens, based on the optical design of HAL lenses, has been clinically shown to slow myopia progression in children, with a 71% reduction in refractive progression and a 53% reduction in axial elongation over 24 months, and approximately 0.7 mm less axial elongation and 1.7 D less myopia progression over five years compared with conventional single-vision spectacles [66,67]. Its aspherical Lenslet design may potentially reduce rebound and provide enhanced long-term control, although post-cessation effects have yet to be assessed.

4.2. Contact Lens

Dual-focus contact lenses generate simultaneous clear and myopically defocused retinal images, with their myopia-control effect mediated primarily through altered central retinal activity [13]. Both inner and outer retinal responses increase predominantly within the central 10° under dual-focus conditions, with peak responses occurring at myopic defocus levels close to +2.00 D, indicating a centrally weighted retinal mechanism rather than peripheral signaling [13]. Optically, these lenses employ a central distance-correction zone surrounded by concentric peripheral zones alternating between distance correction and myopic defocus, enabling full refractive correction while maintaining consistent retinal exposure to myopic defocus across gaze directions, preserving visual acuity and normal accommodation [14]. Concerning post-treatment myopia progression, weak to moderate rebound effects were reported by Weng et al. [51], Ruiz-Pomeda et al. [36], and Anstice et al. [46] over follow-up periods ranging from 10 to 36 months, whereas no rebound effect was observed by Cheng et al. [48] after 42 months of follow-up.

Growing evidence [50] indicates that visual stimuli influence choroidal thickness changes involved in ocular growth regulation. Orthokeratology lenses have been shown to effectively control myopia in children, possibly through the induction of relative peripheral myopic defocus following lens wear; however, the precise underlying mechanism remains unclear. In orthokeratology treatment, refractive changes are difficult to assess because of corneal molding by the rigid gas-permeable lenses, so myopia progression is typically monitored using axial length measurements [68]. Rebound effects following cessation of orthokeratology lenses have been reported with varying magnitude across studies. Swarbrick et al. [47] reported a strong rebound after 12 months, while the other studies reported weak to moderate rebound, including Santodomingo-Rubido et al. [49] (24 months), Cho et al. [35] (24 months), Li et al. [50] (12 months), Wang et al. [52] (20 months), and Zhu et al. [37] (13 months). These findings suggest that the rebound effect after Ortho-K discontinuation is variable and may depend on follow-up duration, washout period, and study design.

Consistent with previous clinical evidence [69], both orthokeratology and dual-focus soft contact lenses demonstrate comparable efficacy in slowing myopia progression, allowing either modality to be selected in clinical practice based on patient preference, practitioner expertise, and individual suitability. Data on rebound effects following cessation of dual-focus contact lens wear remain limited, therefore, further longitudinal studies are required to compare the magnitude of rebound between dual-focus contact lenses and orthokeratology.

4.3. Atropine

Although the exact mechanism of atropine in myopia control is not fully understood, accumulating evidence suggests that atropine inhibits myopia progression through a multimodal mechanism involving retinal neuromodulation and downstream structural effects. Beyond muscarinic receptor blockade, atropine modulates retinal inhibitory and excitatory neurotransmitter pathways, enhancing dopaminergic signaling, a key inhibitor of axial elongation [70]. While muscarinic receptors contribute to ocular growth regulation, atropine’s antimyopic effect is not solely mediated by cholinergic pathways, indicating the involvement of additional, non-cholinergic mechanisms [71,72,73]. Downstream, atropine induces adaptive choroidal and scleral responses that collectively act to limit axial elongation [74,75].

Randomized trials and meta-analyses show that topical atropine slows childhood myopia in a concentration-dependent way, with higher concentrations (0.5–1%) giving the strongest short-term reductions but causing photophobia, accommodation loss, and rebound [76,77], while low doses (≤0.05%) provide a clinically meaningful effect with minimal side effects and excellent tolerability across Asian and Western populations [78,79]. Across atropine cessation studies, the magnitude of myopic rebound demonstrates a clear concentration-dependent pattern, occurring markedly after stopping ≥0.5% atropine but minimally with 0.01–0.05%, and while phased high-to-low-dose regimens reduce it but do not eliminate this effect [80,81]. In the ATOM2 follow-up, Chia et al.[53] reported substantially greater post-cessation myopia progression with higher atropine concentrations (0.5% and 0.1%) compared with minimal rebound after 0.01% treatment. This dose–response relationship was further supported by the LAMP washout analysis by Yam et al. [54], which showed progressively greater rebound in axial length with increasing prior atropine concentration, despite continued differences in on-treatment efficacy. Consistent with these findings, Medghalchi et al. [55] observed smaller rebound effects following cessation of 0.01% atropine compared with higher concentrations, while multiple recent studies evaluating 0.01% alone [56,57,58,59] reported weak or negligible rebound. Collectively, these results indicate that lower concentrations atropine particularly 0.01% provides the least rebound effect, however, further longitudinal studies are needed to compare these interventions.

Atropine efficacy for myopia control is both dose- and ethnicity-dependent, with higher concentrations producing greater reductions in spherical equivalent and axial elongation, and East Asian children demonstrating the largest treatment effect compared with South Asian and white European children [82]. In previous studies, although higher atropine concentrations have been associated with greater rebound, multiple evidence remains limited, particularly across ethnic groups since rebound effects may also vary by ethnicity, underscoring the need for further population-specific studies.

4.4. LLLT

Although the mechanism of low-level red-light therapy (LLLT) in myopia control is not fully understood, current evidence suggests that red-light exposure enhances retinal dopamine release, which regulates axial eye growth and choroidal thickness [83,84]. Through activation of retinal photoreceptors and downstream signaling pathways, LLLT increases choroidal blood perfusion, supports scleral remodeling, and ultimately slows axial elongation, thereby delaying myopia progression [37].

Since the use of low-level red-light therapy (LLLT) in myopia control is a relatively novel intervention [85], the available evidence remains limited. Nevertheless, findings from Xiong et al. [38] and Chen et al. [39] suggest a moderate to strong rebound effect following treatment cessation, warranting cautious interpretation and the need for further long-term, well-designed studies. Although no statistically significant differences were found among the three LRL powers, a trend suggests higher powers may be more effective [86]. Rebound effects may also vary with power, which requires further investigation with larger samples and longer follow-up.

Overall, in this systematic review, spectacle lenses and contact lens wear were associated with less rebound compared to atropine and LLLT interventions. Overall, Chia et al. [53] reported that 0.5% atropine caused the greatest rebound, followed by LLLT as reported by Xiong et al. [38]. Rebound effects after discontinuation of contact lenses appear variable, with some studies reporting weak or no rebound [46,48] and others observing stronger effects [47], likely influenced by follow-up duration, washout period, and study design. Emerging spectacle lens designs offer a safe and practical alternative for myopia control, avoiding the pharmacological side effects of atropine and the allergy, infection, and discomfort risks associated with contact lenses, while enabling greater autonomy for children [87]. However, dual-focus soft contact lenses [88], orthokeratology [89], and low-dose atropine [15,16] have all been shown to safely and effectively slow myopia progression in children, with DFCL reducing eye growth by 71% over three years, OK lenses supporting long-term control, and low-dose atropine demonstrating minimal rebound effects. Short-term studies have suggested the LLLT to be safe [25]; however, long-term studies are needed to fully assess its efficacy and potential rebound effects.

The dropout rate of due to spectacle non-tolerance is 2.1% ranging from 1.6% to 3.0%. The non-tolerance is reported majorly due to refraction error, (47.4%), followed by errors in communication (16.3%), dispensing (13.5%), non-adaptation (9.7%), data entry (8.7%), binocular vision (7.4%) and ocular pathology (6.4%) [90]. Reports indicate annual retention rate for soft contact lenses ranges from 17% to 26% [91,92], with the reasons of poor distance vision (26%), poor near vision (16%), discomfort (14%) and handling problems (15%), while that in orthokeratology lenses ranges from 3% to 9% [93,94] with the reasons of short sleep time, economic difficulties, poor effect after wearing the lenses , and corneal infiltrates.[95]. Repka MX et al.[96] reported a retention rate of 5% during low-dose atropine treatment of myopia. The dropout rate associated with red-light low-level (RLRL) therapy appears to be low [97]; however, it was not explicitly reported in the studies included in the present analysis and should therefore be systematically documented and evaluated in future evidence. High dropout rates can bias rebound estimates if participants with faster or slower post-cessation progression is selectively lost to follow-up, leading to under- or overestimation of true rebound effects making it difficult to reliably compare rebound effects across different myopia control interventions.

Experimental and clinical evidence suggests that ocular growth is regulated through a coordinated signaling cascade originating in the retina and transmitted via the retinal pigment epithelium and choroid to the sclera, the primary determinant of eye size and shape. During myopia development, scleral remodeling, characterized by altered collagen composition, extracellular matrix reorganization, and biomechanical weakening, facilitates axial elongation. Following cessation of myopia-control interventions, disruption of these growth-inhibitory signals may reactivate scleral remodeling processes, allow accelerated eye growth and contribute to rebound effects. This biological susceptibility may be particularly relevant in younger children and in eyes with established scleral thinning, where compensatory elongation may occur more rapidly [98,99]. Age may influence the magnitude of rebound following myopia control interventions, as younger children generally exhibit faster axial elongation. Supporting this, a comparative study of LLLT and orthokeratology found that younger children showed greater axial elongation under LLLT, whereas older children exhibited more pronounced choroidal thickening with OK lenses [85]. Although rebound was not assessed in this study, these age-dependent treatment responses suggest that the potential for rebound may vary across age groups. These areas warrant further investigation.

4.5. Strengths and Limitations

A key strength of this systematic review is that it includes both RCTs and non-RCTs, to the best of our knowledge, allowing for a comprehensive understanding of myopia control interventions with an overall low risk of bias.

The review is limited by heterogeneity among interventions, which may make direct comparisons difficult, and differences in follow-up durations and washout periods, potentially affecting the assessment of rebound and treatment effects. Inclusion of studies conducted several years apart may introduce bias due to changes in study design and methodology over time. Including both abstract-only and full-text articles could limit the depth and quality of extracted data, while studies from multiple countries may introduce variability in demographics and clinical characteristics, influencing the generalizability of results.

Future research should focus on long-term, well-designed studies to better evaluate the sustained efficacy and rebound effects of myopia control interventions, including LLLT, low-dose atropine, and optical therapies. Standardized study designs with uniform follow-up durations and washout periods are needed to reduce heterogeneity and allow for more reliable comparisons. Future studies should include large, multicenter cohorts with diverse ethnic population to better define dose-dependent rebound effects and optimize population-specific atropine treatment and discontinuation strategies, while mechanistic studies could further elucidate the pathways underlying treatment effects.

5. Conclusion

Each 1-diopter increase in myopia is associated with a 67% increase in myopic maculopathy prevalence, whereas slowing myopia progression by 1 diopter can reduce the risk by about 40%, irrespective of baseline myopia level [100]. In myopia control, progression at any level is important, because every diopter counts [100]. Beyond assessing rebound effects, this systematic review highlights the efficacy and significance of various interventions in reducing myopia progression and their potential long-term benefits for ocular health. In conclusion, this systematic review demonstrates that various myopia control interventions produce rebound effects of differing magnitude in different parameters including AL, SE, choroidal thickness and so on. Spectacle lenses and contact lenses showed the lowest rebound, whereas high-dose atropine and LLLT were associated with the greatest rebound, highlighting the dose-dependent nature of this phenomenon. Multiple studies suggest that the magnitude of rebound may also depend on follow-up duration, washout period, and study design, raising the possibility that greater myopia control during treatment could lead to a larger post-cessation rebound. Comprehensive future research is needed to clarify the precise mechanisms underlying these effects and to confirm these findings across diverse populations and study settings.