Jianfeng Zhu, MD
BHVI

A network meta-analysis on myopia control found that use of atropine at different concentrations was significantly superior to other interventions (for example, progressive addition spectacle lenses, multifocal soft contact lenses, orthokeratology, more outdoor activities, etc.)¹

Other reviews and meta-analysis similarly concluded that there was less myopic progression with atropine and that both the efficacy and adverse effects were dose-dependent.^2,3

Later evidence suggested that the mechanism was via non-accommodative pathways,⁴ with some reports suggesting that atropine exerted its action via retinal amacrine cells and dopamine; when atropine binds to mAchR on the cells, they could release dopamine, which is considered to play a role in slowing myopia.

Atropine is a non-selective muscarinic acetylcholine receptor antagonist (mAchR), and the underlying mechanisms by which it controls myopia progression remain unclear. Initially, it was thought that the drug acted via accommodative mechanisms.

Later evidence suggested that the mechanism was via non-accommodative pathways,⁴ with some reports suggesting that atropine exerted its action via retinal amacrine cells and dopamine; when atropine binds to mAchR on the cells, they could release dopamine, which is considered to play a role in slowing myopia.^5-7 Other studies reported that atropine could be directly acting on sclera⁸ and might play a role in inhibiting glycosaminoglycan production and, thus, eye growth.^9,10