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Astigmatism Shift in Low-Astigmatism Myopic Children Wearing Highly Aspherical Lenslets: A Self- Controlled Cohort Study

This self-controlled cohort study reveals that highly aspherical lenslets (HAL) accelerate astigmatism progression exclusively in myopic children with low baseline astigmatism by disrupting the compensatory balance between corneal and internal astigmatism, without compromising the treatment's core efficacy in controlling axial elongation.

Original authors: Kaihuai Yu, Yuejia Peng, Jin Zhang, Haoqi Lan, Qiaolan Zheng, Jie Chen, Wuhe Chen

Published 2026-07-05

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CC BY 4.0

Original authors: Kaihuai Yu, Yuejia Peng, Jin Zhang, Haoqi Lan, Qiaolan Zheng, Jie Chen, Wuhe Chen

Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). ✨ This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer

The Big Picture: A New Glasses Lens vs. The Old One

Imagine you have a pair of glasses designed to stop your eyes from getting longer (which causes nearsightedness). This new type of lens, called HAL (Highly Aspherical Lenslets), is like a "smart shield" that works very well to stop your eyes from growing too long.

However, doctors noticed something strange: while these lenses were great at stopping eye growth, they seemed to be making some children's eyes slightly more "tilted" or uneven (a condition called astigmatism).

This study wanted to answer three questions:

Does this new lens actually make astigmatism worse?
If it does, why does it happen?
Does this "tilt" ruin the lens's ability to stop nearsightedness?

The Experiment: The "Time-Travel" Comparison

Instead of comparing two different groups of kids (which is like comparing apples to oranges because every kid is different), the researchers used a clever trick. They looked at the same 359 children over time.

Phase 1: The kids wore regular, standard glasses (SVL) for 6 months to a year.
Phase 2: The same kids switched to the new "smart shield" lenses (HAL) for another 6 months to a year.

This is like testing a car's fuel efficiency by driving the exact same car on the same route with two different types of gas. It removes the guesswork about whether the driver or the car was the problem.

The Findings: Who Gets the "Tilt"?

The study found that the new lenses only caused a problem for a specific group of kids: those who started with very little or no astigmatism (less than 1.00 Diopter).

The "Flat" Eyes: For kids whose eyes were already very round and flat (low astigmatism), the new lenses acted like a gentle wind pushing against a sail, causing their eyes to become slightly more tilted over time.
The "Already Tilted" Eyes: For kids who already had a significant amount of astigmatism, the new lenses did not make it worse. Their eyes stayed just as they were.

The Analogy: Think of astigmatism like a wobbly table leg.

If the table is already wobbly (high astigmatism), putting a new heavy object on it (the HAL lens) doesn't make it wobble more; it was already unstable.
If the table is perfectly flat and stable (low astigmatism), that same heavy object pushes it just enough to create a new wobble.

The "Why": The Tug-of-War Inside the Eye

The researchers dug deeper to find out why this happened. They looked at two parts of the eye:

The Cornea: The clear front window of the eye.
The Internal Lens: The lens sitting inside the eye.

Normally, these two parts act like a tug-of-war team. If the front window (cornea) gets a little more tilted, the inner lens naturally tilts the opposite way to cancel it out. This is called compensation. It's like two people holding a rope; if one pulls left, the other pulls right to keep the rope straight.

What the study found:
When kids with "flat" eyes wore the new HAL lenses, the front window (cornea) started tilting more. However, the inner lens failed to pull back to cancel it out. The "tug-of-war" balance was broken. The result? The eye ended up slightly more tilted than before.

The Good News: The "Shield" Still Works

The most important finding is that this new tilt does not ruin the lens's main job.

Even though the eyes of the "flat" kids got a little more tilted, the new lenses were still extremely effective at stopping the eyes from growing longer.

The Analogy: Imagine you are wearing a raincoat (the lens) to stay dry. The study found that while the raincoat might make your hat tilt slightly to the side (astigmatism), it still keeps you completely dry (stops myopia). The tilt doesn't make the raincoat fail.

Summary for Parents and Patients

Does the new lens stop nearsightedness? Yes, very effectively.
Does it cause astigmatism? Only for kids who started with almost no astigmatism.
Is it dangerous? No. The slight increase in astigmatism is small and does not stop the lens from protecting the eye from getting worse.
What should we do? Doctors should keep an eye on kids with very low astigmatism who wear these lenses, just to make sure the "tilt" doesn't get too big, but they shouldn't worry that the main treatment is failing.

In short: The new lens is a powerful tool that stops eyes from growing too long. It might slightly nudge the "balance" of some children's eyes, but it doesn't break the tool's ability to do its most important job.

Technical Summary: Astigmatism Shift in Low-Astigmatism Myopic Children Wearing Highly Aspherical Lenslets

Problem Statement
Highly Aspherical Lenslets (HAL), a type of peripheral defocus spectacle lens (PDSL), are widely prescribed for myopia control due to their efficacy in slowing axial elongation. However, emerging evidence suggests that PDSL designs, particularly HAL, may inadvertently induce astigmatic shifts. Previous literature presents conflicting findings: some studies report accelerated astigmatism progression with HAL, while others find no significant difference compared to controls. Furthermore, the anatomical origin of these shifts—whether they arise from corneal changes, internal ocular components, or a disruption in the compensatory balance between them—remains unclear due to a lack of comprehensive biometric data in prior studies. This study aims to evaluate the impact of HAL on astigmatism progression, elucidate its anatomical origin, and determine if such astigmatic alterations compromise the lens's core myopia control efficacy.

Methodology
This research employed a retrospective, self-controlled cohort design involving 359 myopic children (aged 3–16 years) from Wenzhou Medical University. The study design minimized inter-individual variability by having each participant sequentially wear single-vision lenses (SVL) followed by HAL, with each phase lasting either 6 months or 1 year.

Data Collection: Comprehensive ophthalmic examinations were conducted, including cycloplegic refraction, corneal topography (IOLMaster), and axial length (AL) measurements.
Vector Analysis: Astigmatism data were converted into orthogonal power vectors ( $J_0$ and $J_{45}$ ) to analyze Total Astigmatism (TA), Corneal Astigmatism (CA), and Internal Astigmatism (IA). IA was calculated as the vectorial difference between TA and CA.
Compensation Factor (CF): A compensation factor was calculated to quantify the relationship between CA and IA, categorizing eyes as having full compensation, under-compensation, or over-compensation.
Statistical Approach: Linear regression assessed baseline TA as a predictor of astigmatic differences between lens phases. Subgroup analyses stratified participants by baseline astigmatism (<1.00 D vs. ≥1.00 D). Mediation analysis was used to test whether TA changes mediated the effect of HAL on axial elongation.

Key Contributions

Differentiation by Baseline Astigmatism: The study identifies that the astigmatic effect of HAL is not uniform but is strictly confined to children with no or low baseline astigmatism (<1.00 D). In this subgroup, HAL significantly accelerated astigmatism progression compared to SVL. Conversely, children with moderate to high baseline astigmatism showed no significant difference in progression between the two lens types.
Mechanistic Insight into Compensation: Through vector decomposition, the study reveals that the astigmatic shift is driven by a disruption in the compensatory balance between corneal and internal astigmatism. Under HAL wear, CA ( $J_0$ ) increased significantly, while IA ( $J_0$ ) decreased correspondingly. In low-astigmatism eyes, this internal compensation failed to match the corneal increase, resulting in a net rise in total astigmatism. In contrast, high-astigmatism eyes maintained stability through a matched reduction in IA.
Functional Dissociation: The research demonstrates a functional dissociation between astigmatic side effects and myopia control efficacy. Mediation analysis confirmed that the observed astigmatic shifts did not mediate the effect of HAL on axial elongation control.

Results

Astigmatism Progression: In the low-baseline astigmatism group, TA progression was significantly higher with HAL than with SVL at both 6 months (HAL: 0.11 ± 0.23 D vs. SVL: 0.02 ± 0.23 D, $P=0.006$ ) and 1 year (HAL: 0.21 ± 0.31 D vs. SVL: 0.03 ± 0.24 D, $P<0.001$ ).
Vector Components: The increase in astigmatism was primarily driven by the $J_0$ component (with-the-rule/against-the-rule). CA $J_0$ increased while IA $J_0$ decreased, showing a strong negative correlation ( $r \approx -0.97$ ). $J_{45}$ (oblique) components remained stable.
Compensation Shift: Transition rates showed a significant loss of "full compensation" and a gain of "under-compensation" in the low-astigmatism group during the HAL phase compared to SVL.
Myopia Control Efficacy: HAL remained highly effective in suppressing axial elongation compared to SVL (e.g., 0.11 mm vs. 0.42 mm at 1 year, $P<0.001$ ). The astigmatic shift did not diminish this efficacy.

Significance and Claims
The paper claims that while HAL induces a statistically significant astigmatic shift, this effect is exclusive to children with low baseline astigmatism and involves a specific disruption of the corneal-internal compensatory mechanism. Crucially, the authors assert that this astigmatic alteration does not compromise the core myopia control efficacy of the lens.

The study concludes that the astigmatic shift is likely a lens-specific effect independent of natural myopia progression, potentially caused by asymmetric mechanical forces from the aspherical lenslets or accommodative microfluctuations. While the mean increase in astigmatism (0.18 D absolute difference at 1 year) may be of limited clinical relevance for the average patient, the authors note that approximately 30% of low-astigmatism children experienced a clinically noticeable increase ( $\ge$ 0.50 D). The findings support the overall safety profile of HAL regarding myopia control but suggest that clinicians should monitor astigmatic changes closely in children with low baseline astigmatism. The study does not propose immediate changes to lens design but suggests that understanding this compensatory disruption could inform future optimizations of peripheral defocus lenses.