Chapter 10 – Epidemiology of Refractive Errors

Chapter 10 – Epidemiology of Refractive Errors


• Presence of various refractive errors within demographic groups.

• Age and emmetropization.
• Genetic predisposition.
• Effects of visual environment.

• Current research.
• Interventions.

Studies that tabulate the distribution of refractive errors often employed data on young army recruits,[1] [2] which show the incidence of myopia to be about 10%. However, this group of healthy young men is not representative of the general population. A study in Sweden is only representative of Scandanavia—not of the United States! Stenstrom’s [3] study in Uppsala, Sweden, consisted of clinic patients, colleagues, nurses, and cadet officers, which is a group more reflective of the general population. His study showed that about 29% of the population have low myopia (=2D), 7% have moderate myopia (2–6D), and another 2.5% have high myopia (>6D). The great majority of his population (i.e., just under 70%) clustered between emmetropia and 2D of hyperopia, and the rest were high hyperopes and aphakes.
The spectacle-wearing population in a typical Western country provides a different focus on emmetropes. Bennett’s[4] study on the distribution of spectacles dispensed in England indicated that from the distribution of refractions carried out by the average eye clinician, about 20% are myopic and about 75% require prescriptions between -0.50D and +8.00D. Subtraction of Stenstrom’s estimate of the percentage of high hyperopes shows that about 65% of all refractive prescriptions are for presbyopes.
Pathological Myopia
Curtin[5] estimated that 2–3% of the population has pathological myopia (a condition in which there is an enlargement of the eyeball with a lengthening of the posterior segment). This group primarily falls into Stenstrom’s group of myopes of >6D. The term pathological is used because these patients show marked choroidal and retinal degenerative changes, a high incidence of retinal detachment, glaucoma, and increased occurrence of staphyloma development. At present, high myopia (>6D) is considered to be a sex-linked, recessive inherited disorder. [6] Fig. 10-1 illustrates the anatomy of the myopic crescent—note that as the eye enlarges, the sclera and choroid begin to show at the edge of the optic nerve (see Chapter 126 ).
Physiological or School Myopia
As noted by Stenstrom,[3] the vast majority of myopes are =2D; this type of myopia is called physiological or school myopia. The word physiological implies that this form of myopia is a normal, physiological response to a stress. In fact, substantial evidence exists that increased time spent reading from the early teen years to the mid-20s is related to the development of myopia.[7] [8] One of the authors also observed that over 60% of the average medical school class is myopic. That the long-term use of atropine eyedrops in conjunction with wearing bifocals stabilizes myopia also lends credence to this proposition.[9]
However, near work is not the sole cause of physiological myopia. Racial and ethnicity studies show that myopia is more prevalent among Asians and Jews and less prevalent among African-Americans.[6] (The results of a study in Taiwan showed the incidence of myopia to be about 12% in children 6 years of age or less, 55% in children 12 years of age or less, 76% in children 15 years of age or less, and 84% in those over 18 years of age.[10] ) Thus it appears that an inherited predisposition, linked with excessive close work during the student years, results in most of the cases of physiological myopia.
About 50% of full-term infants in their first years of life show astigmatism of over 1D.[11] [12] This may arise from the influence of the recti muscles that pull upon the delicate infant sclera because the astigmatism seems to change in different gaze directions. Howland et al.[13] suggested that the high astigmatism helps the infant to bracket the position of best focus while it learns to accommodate. By adulthood, this high incidence of astigmatism has disappeared. Studies show that about 15% of the adult population have astigmatism >1D and only 2% have astigmatism >3D. It is possible that much of the high astigmatism in the latter group is related to some form of intraocular surgery (e.g., corneal transplants, cataract surgery, or repair of corneal lacerations).
Although presbyopia is age related, its age of onset varies around the world. For example, presbyopia develops earlier in people who live closer to the equator.[14] [15] Specifically, the age of onset of presbyopia was noted to be 37 years in India, 39 years in Puerto Rico, 41 years in Israel, 42 years in Japan, 45 years in England, and 46 years in Norway (see Chapter 6 ). Further studies show the important variable to be ambient temperature rather than latitude. Thus, the higher the ambient temperature, the earlier the onset of presbyopia.
On the other hand, life expectancy is lower in developing countries, where the ambient temperatures are usually high. Thus, although presbyopia starts at a younger age in the developing world, fewer presbyopes are found in the general population. For example, in Haiti the prevalence rate of presbyopia is about 16% for the normal population, whereas in the United States it is 31%. The lower rate of presbyopia in Haiti is paradoxical.


Figure 10-1 Origin of the myopic crescent. As the eye enlarges, the choroid and retina gradually pull away from the temporal optic nerve head. Thus, in extreme cases, sclera is seen. In less extreme enlargement, choroid or a rim of pigment epithelium can be seen.
It is due to the fact that the average life span in Haiti is much shorter than in Western countries. Seen in perspective, presbyopia accounts for about 65% of all people who wear glasses in the developed Western countries. Thus, it is of little surprise that the first spectacles produced some time in the 14th century were created for presbyopes.
The overall refractive state of the eye is determined by four components:
• Corneal power (mean, 43D)
• Anterior chamber depth (mean, 3.4?mm)
• Crystalline lens power (mean, 21D)
• Axial length (mean, 24?mm)
Fig. 10-2 shows the distribution of total refraction and the four components just mentioned for 194 eyes.[16]
The most striking conclusion drawn from Fig. 10-2 is that, whereas each of the individual optical components may be considered to be randomly distributed, the overall refractive status does not show a normal distribution of refractive errors but shows a skew in the region of emmetropia. It seems that the various components cooperate to achieve a higher than expected incidence of refractive state between 0 diopter and +2 diopters.
This cooperation of components to produce a higher than expected incidence of emmetropia and lower hyperopia has been called emmetropization. [16] The process of emmetropization seems to be fully effective during the infantile growth of the eye. Specifically, the average sagittal diameter of the eye is approximately 18?mm at birth. By the age of 3 years, the axial length increases to about 23?mm. Such elongation of the eye theoretically yields a state of myopia of about 15D. Yet, during this period the data show that almost 75% of these young eyes are hyperopic.[17] Between 3 and 14 years of age, the elongation increases by, on average, an additional millimeter. Again, this should theoretically produce another 3D of myopia. Yet at 14 years of age, the average refractive state shows a strong clustering in the emmetropic neighborhood. Because the cornea and anterior chamber depth change very little during these periods of eye growth, it appears that the power of the crystalline lens changes to maintain emmetropia. It seems possible that the process is coordinated by the retina-brain complex, which might tune each component to ensure a sharp image. However, studies of infant monkeys that were raised in the dark or had the optic nerve sectioned suggest that emmetropization is largely programmed on a genetic basis.[18] The

Figure 10-2 Curves of distribution of refraction and its components in 194 eyes. (Adapted with permission from Sorsby A, Benjamin B, Davey JB, et al. Emmetropia and its aberrations. Med Res Counc Special Rep Serv. 1957; 293.)
experiments further showed that procedures that result in significant degradation of the retinal image, such as suture of the lids together or induction of a corneal opacity during the early growth period, influence the axial growth process. Surprisingly, these types of opacifications significantly increase the axial length and produce states of myopia of up to 12D. Such excessive image degradation seems to override the emmetropization process and result in high levels of axial myopia. The biological mechanism for this process seems to be a remodeling of posterior scleral tissue caused by a reduction in the synthesis of proteoglycans that is related to form deprivation. [19] [20]


1. Stromberg E. Uber refraktion und Achsenlange des menschlicken Auges. Acta Ophthalmol. 1936;14:281–93.

2. Sorsby A, Sheridan M, Leary GA. Vision, visual acuity and ocular refraction in young men. Br Med J. 1960;i:1394–8.

3. Stenstrom S. Untersuchungen uber die Variation and Kovariation des optischen Elemente des menschlichen Auges. Acta Ophthalmol. 1946;26(Suppl) (also English translation by Woolf D. Am J Optom. 1948;25:218–32).

4. Bennett AG. Lens usage in the supplementary ophthalmic service. Optician. 1965;149:131–7.

5. Curtin BJ. The myopias: basic science and clinical management. Philadelphia: Harper & Row; 1985.

6. Wold KC. Hereditary myopia. Arch Ophthalmol. 1949;42:225–35.

7. Angle J, Wissman DA. The epidemiology of myopia. Am J Epidemiol. 1980;111:220–31.

8. Hepsen IF, Evereklioglu C, Bayramlar H. The effect of reading and near-work on the development of emmetropic boys: a prospective, controlled, three-year follow-up study. Vision Res. 2001;41:2511–20.

9. Syniuta LA, Isenberg SJ. Atropine and bifocals can slow the progression of myopia in children. Binocul Vis Strabismus Q. 2001;16:201–2;227.

10. Luke LK, Yung–Feng S, Chong–Bin T, et al. Epidemiological study of ocular refraction amount school children in Taiwan. Invest Ophthalmol Vis Sci. 1996;6:1002.

11. Mohindra I, Held R, Gwiazda J, Brill S. Astigmatism in infants. Science. 1978; 202:329–31.


12. Bennett AG, Rabbits RB. Clinical visual optics, 2nd ed. London: Butterworths; 1989:50.

13. Howland HC, Atkinson J, Braddick O, French J. Astigmatism measured by photorefraction. Science. 1978;202:331–3.

14. Miranda MH. The environmental factor in the onset of presbyopia. In: Stark L, Obrecht G, eds. Presbyopia. New York: Professional Press; 1987.

15. Kleinstein RN. Epidemiology of presbyopia. In: Stark L, Obrecht G, eds. Presbyopia. New York: Professional Press; 1987.

16. Sorsby A, Benjamin B, Davey JB, et al. Emmetropia and its aberrations. Med Res Counc Special Rep Serv. 1957;293.

17. Cook RC, Glasscock RE. Refractive and ocular findings in the newborn. Am J Ophthalmol. 1951;34:1407–13.

18. Raviola E, Wiesel TN. An animal model of myopia. N Engl J Med. 1985;312: 1609–12.

19. Rada JA, Nickla D, Troilo D. Decreased proteoglycan synthesis associated with form deprivation in mature primate eyes. Invest Ophthalmol Vis Sci. 2000;41: 2050–8.

20. McBrien NA, Lawlor P, Gentle A. Scleral remodeling during the development and recovery from axial myopia in the tree shrew. Invest Ophthalmol Vis Sci. 2000;41:3713–19.


3 comments on “Chapter 10 – Epidemiology of Refractive Errors

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