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Myopia is a global public health issue with a worldwide prevalence of ∼30% and is estimated to rise to 50% by 2050. In addition to the burden associated with routine management of the condition, high myopia predisposes the eye to sight-threatening complications such as myopic maculopathy and glaucoma in adult life. Controlling onset and progression of myopia at a young age can reduce the risk of morbidity associated with high myopia. Progression of myopia can be slowed with various optical, environmental, and pharmaceutical strategies, of which atropine has proven to be the most effective. High-dose atropine (0.5%-1%) is the most effective, but it has significant trade-offs with respect to rebound of myopia on discontinuation and side effects such as photophobia and difficulty with near work (decreased accommodation). Low doses of atropine have been trialed and show a dose-dependent efficacy. However, its mode of action on the ocular tissues leading to slowing eye growth remains unclear and multiple mechanisms and sites in the eye have been postulated to play a role. This review summarizes the role of atropine in controlling myopia and the mechanisms studied to date.
Tran et al. (Tue,) studied this question.