Myopia has been known for more than 2000 years

and was first described by the ancient Greeks.1,2 However, despite the recorded use of convex lenses for presbyopia in the late 13th century in Florence, Italy, the correction of myopic refractive error had to await the development of concave lenses in the mid 16th century.  
 Myopia may be classified as “school myopia” or “adult onset myopia.”3 School myopia develops during the school age and stabilises around 15–17 years of age, while adult onset myopia develops in young adults. The aetiology, pathogenesis, and treatment of myopia have been hotly debated in the ophthalmic community for decades.4 There are several theories on the mechanism of development of myopia arising from disruption of the emmetropisation process. Emmetropisation is achieved when the optical power of the eye matches the axial length, resulting in a focused image of a distant object on the retina without accommodative effort.5 It has been proposed that overacting intraocular muscles may result in excessive accommodation and influence emmetropisation.6 The two basic mechanisms by which animal myopia may be induced are form deprivation and optical defocus. Form deprivation myopia can be induced by the application of translucent occluders over the animal’s eyes. Local retinal effects may occur and the resultant scleral growth modulated by chemicals such as dopamine, growth factors, and muscarinic antagonists.7–9 Negative spectacle lenses in chicks induce compensatory axial elongation and myopia.10