Pattern of choroidal thickness in early-onset high myopia

Myopia is of diverse aetiology. A small proportion of myopia is clearly familial, generally early in onset and of high level, with defined chromosomal localisations and in some cases, causal genetic mutations. However, in economically developed societies, most myopia appears during childhood, particularly during the school years. The chromosomal localisations characterised so far for high familial myopia do not seem to be relevant to school myopia. Family correlations in refractive error and axial length are consistent with a genetic contribution to variations in school myopia, but potentially confound shared genes and shared environments. High heritability values are obtained from twin studies, but rest on contestable assumptions, and require further critical analysis, particularly in view of the low heritability values obtained from parent-offspring correlations where there has been rapid environmental change between generations. Since heritability is a population-specific parameter, the values obtained on twins cannot be extrapolated to define the genetic contribution to variation in the general population. In addition, high heritability sets no limit to the potential for environmentally induced change. There is in fact strong evidence for rapid, environmentally induced change in the prevalence of myopia, associated with increased education and urbanisation. These environmental impacts have been found in all major branches of the human family, defined in modern molecular terms, with the exception of the Pacific Islanders, where the evidence is too limited to draw conclusions. The idea that populations of East Asian origin have an intrinsically higher prevalence of myopia is not supported by the very low prevalence reported for them in rural areas, and by the high prevalence of myopia reported for Indians in Singapore. A propensity to develop myopia in "myopigenic" environments thus appears to be a common human characteristic. Overall, while there may be a small genetic contribution to school myopia, detectable under conditions of low environmental variation, environmental change appears to be the major factor increasing the prevalence of myopia around the world. There is, moreover, little evidence to support the idea that individuals or populations differ in their susceptibility to environmental risk factors.

To determine the incidence and progression rates of myopia in young Singaporean children. A prospective cohort study, the Singapore Cohort Study of the Risk Factors for Myopia (SCORM), was conducted in two schools in Singapore (1999-2002). Children aged 7 to 9 years (n=981) were followed up over a 3-year period. Cycloplegic autorefraction and biometry parameter measures were performed annually, according to the same protocol. The 3-year cumulative incidence rates were 47.7% (95% confidence interval [CI]: 42.2-53.3), 38.4% (95% CI: 31.4-45.4), and 32.4% (95% CI: 21.8-43.1) for 7-, 8-, and 9-year-old children, respectively. The 3-year cumulative incidence rates were higher in Chinese (49.5% vs. 27.2%) and in 7-year-old compared with 9-year-old children at baseline (47.7% vs. 32.4%), though the latter relationship was of borderline significance after adjustment for race, gender, amount of reading (books/week), and parental myopia (P=0.057). Premyopic children with greater axial lengths, vitreous chamber depths, and thinner lenses were more prone to the development of myopia, after controlling for age, gender, race, reading, and parental myopia. The 3-year mean cumulative myopia progression rates were -2.40 D (95% CI: -2.57 to -2.22) in 7-year-old myopic children, -1.97 (95% CI: -2.16 to -1.78) in 8-year-olds, and -1.71 (95% CI: -1.98 to -1.44) in 9-year-olds. Both the incidence and progression rates of myopia are high in Singaporean children.

Given the prominence of central vision in humans, it has been assumed that visual signals from the fovea dominate emmetropization. The purpose of this study was to examine the impact of peripheral vision on emmetropization. Bilateral, peripheral form deprivation was produced in 12 infant monkeys by rearing them with diffusers that had either 4- or 8-mm apertures centered on the pupils of each eye, to allow 24 degrees or 37 degrees of unrestricted central vision, respectively. At the end of the lens-rearing period, an argon laser was used to ablate the fovea in one eye of each of seven monkeys. Subsequently, all the animals were allowed unrestricted vision. Refractive error and axial dimensions were measured along the pupillary axis by retinoscopy and A-scan ultrasonography, respectively. Control data were obtained from 21 normal monkeys and 3 infants reared with binocular plano lenses. Nine of the 12 treated monkeys had refractive errors that fell outside the 10th- and 90th-percentile limits for the age-matched control subjects, and the average refractive error for the treated animals was more variable and significantly less hyperopic/more myopic (+0.03 +/- 2.39 D vs. +2.39 +/- 0.92 D). The refractive changes were symmetric in the two eyes of a given animal and axial in nature. After lens removal, all the treated monkeys recovered from the induced refractive errors. No interocular differences in the recovery process were observed in the animals with monocular foveal lesions. On the one hand, the peripheral retina can contribute to emmetropizing responses and to ametropias produced by an abnormal visual experience. On the other hand, unrestricted central vision is not sufficient to ensure normal refractive development, and the fovea is not essential for emmetropizing responses.