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What do we really mean by emmetropisation
Author(s) -
Morgan I.
Publication year - 2017
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2017.02742
Subject(s) - emmetropia , refraction , elongation , optics , lens (geology) , refractive error , vitreous chamber , optometry , ophthalmology , human eye , physics , medicine , materials science , visual acuity , metallurgy , ultimate tensile strength
Summary One of the distinctive features of refractive development is the establishment of a tight distribution of refraction by the age of 2. This can be explained by work on animal models showing that hyperopic defocus promotes, while myopic defocus slows, axial elongation, with precise compensation for the imposed refractive error. It has therefore been assumed that the end‐point of human refractive development is tightly defined emmetropia, with an active mechanism for maintaining emmetropia. But in fact, human refractions generally stabilize in the mildly hyperopic range – a state which can be maintained until adult life. With educational pressures, many children become transiently emmetropic, but then progress to myopia, consistent with evidence that early emmetropia is a major risk factor for myopia. Recent work has demonstrated another control over axial elongation, based on increased release of dopamine by bright light which slows axial elongation. Refractive development in humans can be better explained if myopic defocus signals weaken after the age of 2, and once loss of lens power has slowed, the only process able to counter axial elongation associated with education is provided by the light‐dopamine pathway.