Emmetropisation and the aetiology of refractive errors

Abstract

The distribution of human refractive errors displays features that are not commonly seen in other biological variables. Compared with the more typical Gaussian distribution, adult refraction within a population typically has a negative skew and increased kurtosis (ie is leptokurtotic). This distribution arises from two apparently conflicting tendencies, first, the existence of a mechanism to control eye growth during infancy so as to bring refraction towards emmetropia/low hyperopia (ie emmetropisation) and second, the tendency of many human populations to develop myopia during later childhood and into adulthood. The distribution of refraction therefore changes significantly with age. Analysis of the processes involved in shaping refractive development allows for the creation of a life course model of refractive development. Monte Carlo simulations based on such a model can recreate the variation of refractive distributions seen from birth to adulthood and the impact of increasing myopia prevalence on refractive error distributions in Asia.

The progression of corrected myopia

“…This fall from emmetropia to a stabilization floor has been observed in a group of 469 corrected myopic children [20]. The model also explains the skewness towards myopia of the distribution of refractive errors [22]. Of course, leaving a myope uncorrected is not adequate for many people.…”

“…It is known that there is a distribution of refractive errors around zero diopters. The distribution is normal at birth and leptokurtic after emmetropization takes place [22]. The uncorrected end refraction is possibly determined genetically.…”

Problems in comparisons of data for the prevalence of myopia and the frequency distribution of ametropia

“…We argue first that the distribution of refractive errors is likely to be such that care must be exercised in inferring too much from simple measures of prevalence and mean refractive error, particularly when the threshold criterion used for defining myopia is set at a low value, and that, as recently emphasised by Flitcroft, the distribution of errors is of much greater significance for the understanding of the nature of any refractive changes that might be occurring. Further, when comparing effects in different age groups, allowance must be made for any gradual refractive changes, which may be an intrinsic part of the ageing process .…”

“…He gives details of a model of refractive development based on these mechanisms, which, with appropriate adjustment of parameters, leads to good simulations of the observed distributions at different ages. In a further paper, Flitcroft suggests that the failure of some eyes to emmetropise in early childhood, allied to the failure of some emmetropic eyes to maintain emmetropia in later childhood and the teenage years, leads at any age to two distinct populations of eyes. The “emmetropised” population is characterized by a relatively narrow Gaussian (normal) distribution, peaking near emmetropia.…”

Higher order aberrations, refractive error development and myopia control: a review

“…Axial length increases proportionately to a decrease in the dioptric power of the optical components of the eye, which suggests biological, passive regulation of eye growth, a process termed emmetropisation . Refractive errors are primarily determined by axial length changes that are disproportionate to the change in the ocular refractive power, where a slowed and increased rate of axial eye growth results in hyperopia and myopia, respectively, due to a failure in emmetropisation . Exposure of the eye to different visual experiences can disrupt emmetropisation, which suggests that the eye also uses visual input to actively influence eye growth in humans …”