Postnatal growth and emmetropization

Refractive error is a mismatch between the optical refractive determinants of the eye (corneal curvature, lens power and location, and axial length). At birth, the eye is rarely emmetropic, and is significantly smaller than the adult eye (Table 5.1); the refractive error of the newborn eye ranges between +2.0 and +4.0 diopters (D) with an almost normal (Gaussian) distribution (Fig. 5.1A).⁵ Within 2 years, this variability of refractive error decreases and the mean value shifts so that the eye becomes closer to emmetropia. The population distribution becomes more leptokurtotic, which means it is more clustered around the mean value (Fig. 5.1B). This process is called emmetropization and, within populations, it is possible to predict shifts in refractive error so that most of the infants born hyperopic become emmetropic by 6 to 8 years of age. Eye growth is rapid, and reaches 90% of adult proportions by the age of 4. As the cornea flattens, it loses refractive power, which is balanced by increasing axial length. Whether this balance is guided by genetically encoded mechanisms or is affected by environmental influences has been debated for centuries. Most likely both nature and nurture affect the way the eye develops. By adulthood, the distribution of refractive error is similarly leptokurtotic, and there is a left skew in the distribution of the myopic subjects (Fig. 5.1C).⁶

Table 5.1 Newborn vs. adult ocular parameters

	Newborn	Adult
Axial length	16.8 mm	23.0 mm
Mean keratometry	55 D	43 D
Optic nerve length	24 mm	30 mm
Corneal diameter	10 mm	10.6 mm (vertical) × 11.7 mm (horiz.)
Corneal thickness	581 µm	545 µm
Pars plana length	0.5–1.05 mm	3.5–4 mm
Orbital volume	7 cc	30 cc

Fig. 5.1 Distribution of refractive error at different ages. (A) At 3 months of age; (B) at 20 months of age (from Mutti et al. Invest Ophthalmol Vis Sci 2005; 46: 3074–80); (C) an adult population distribution (in 1958 British Birth Cohort age 45 years)

(from Simpson et al. Invest Ophthalmol Vis Sci 2007; 48: 4421–5).

Support for the assertion that eye growth is genetically regulated comes from studies of heritability and epidemiology. Almost all studies of refractive error, and in particular myopia, have shown that the strongest risk factors are having one or two parents who are myopic,⁷ and pediatric ophthalmologists recognize the hyperopic/esotropic family attending their practices. While this might be ascribed to families sharing the same environmental risk factors, twin studies control for this shared environment by comparing concordance between monozygotic (identical) and dizygotic (fraternal) twin pairs. Twin studies, across ages and cultures, show a high heritability of refractive error, of the order of 80–90%.^8,⁹ This is not to say that the environment is not important. Strong temporal trends in myopia prevalence must be due to environmental factors. However, genetic factors appear important in determining where a person lies within the population distribution of a society at a particular time. Recently, genome-wide association studies have reported the association of several genes with refractive error,^10,¹¹ and further genes will be identified. Like many complex traits, myopia susceptibility is conferred by many genes of small effect.

While Kepler suggested a local eye-mediated control of refractive error in the 17th century, myopia studies have been difficult to design, given the need for longitudinal data, and difficulties measuring the amount of close activity in children, and trying to control for factors including lighting, nutritional and other measures. There has been relatively little research into hyperopia, but risk factors for myopia are generally protective for hyperopia and vice versa.

There is a significant association of myopia with near work, educational level of attainment, and IQ.¹² The classic study by Zylbermann et al.¹³

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