National Academies Press: OpenBook

Myopia: Prevalence and Progression (1989)

Chapter: Appendix A: The Biological Basis of Myopia

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Suggested Citation:"Appendix A: The Biological Basis of Myopia." National Research Council. 1989. Myopia: Prevalence and Progression. Washington, DC: The National Academies Press. doi: 10.17226/1420.
Page 43
Suggested Citation:"Appendix A: The Biological Basis of Myopia." National Research Council. 1989. Myopia: Prevalence and Progression. Washington, DC: The National Academies Press. doi: 10.17226/1420.
Page 44

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Appendix A The Biological Basis of Myopia While our natural tendency is to identify deviations from emmetropia, including myopia and hyperopia, as disorders or biological mistakes, this view has certain hazards. Since there is a substantial variation in the axial lengths of eyes, as well as in their optical power, it is not surprising that in all species there is some variation in how well these parameters are ~ . . matched optically, with the result that some eyes deviate from emmetropia in the myopic direction and others in the hyperopic direction. Relatively few eyes are precisely emmetropic by most precise dioptric measures. Another drawback of viewing ametropias as biological mistakes is that nearly all infants are born hyperopic, with large variability in refractive status. As eyes grow, three changes occur: (1) they become less hyperopic or become myopic; (2) they become less variable in refraction, and the shape of the distribution of refraction changes so that most eyes become nearly emmetropic and fewer eyes moderately ametropic than expected by a Gaussian distribution; and (3) the distribution curve becomes leptokur- totic (peaked). Thus the problem in assessing the prevalence of myopia lies in first deciding how far from emmetropia an eye must be to be considered myopic. Distant visual acuity is lost in direct proportion to the degree of myopia. A value as small as -0.25 D. will cause a slight lose; by contrast, young hyperopes without significant astigmatism retain acuity for distant vision even with refractive error. It is far from clear what developmental mechanisms are responsible for this "em- metropization" early in life. One possibility is that the eye or brain somehow can sense the direction and degree of ametropia and cause some component of the eye to grow in such a way that the eye becomes emmetropic. Alternatively, the eye may become more emmetropic simply because as it grows, its optical surfaces become less curved; consequently, optical power is reduced. As this reduction in total optical power occurs, any slight mismatch be- tween optical power and axial length will also have a progressively small effect on refractive error; consequently, the degree of myopia or hyperopia will decrease. Whatever the mechanism, it is clear that growth in the direction of myopia from an initially hyperopic state in the newborn is a normal biological phenomenon affecting most eyes. In cases of manifest myopia, what is abnormal is that the process does not stop at emmetropia and may even accelerate. It is now also clear that the amount of myopia is highly correlated with axial length of the eye and not at all correlated with the steepness of the corneal curvature. Most myopia found in any adult population is the result of changes that occurred after 43 1

44 the age of 7 and before the age of 16. This Is called adolescent or juvenile myopia. However it is beyond the scope of this report to evaluate in detail what factors in one's environment or experience might cause significant myopia to develop. While it seems plausible that the frequent onset of myopia during the early school years points to specific circumstances associated with school, such as reading, numerous other changes In growth and physiological function are occurring at this time. There is strong evidence that juvenile myopic shifts in males and females usually stabilize during the teens. Similarly, the more frequent occurrence of myopia in the children of myopes may point to similarities in the family environment or activities, as well as to a genetic component. These factors cannot easily be isolated. More puzzling yet is the development of myopia in young adulthood (adult-onset myopia), when the eye has stopped growing. Since this myopia development is often associated with intense study, it may be that the activities related to studying stimulate the eye's growth sufficiently to cause renewed growth, even in mature eyes. In some of these cases the myopia may arise, not from a change in the structure of the eye, but from its maintaining a continuous state of accommodation (spasm or tonic accommodation). This condition (pseudomyopia) might be expected to be limited by the amplitude of accommodation and, consequently, be absent when individuals lose all their accommodation in presbyopia. At present, it is unclear whether changes leading to young adult myopia involve axial elongation, as in juvenile myopia, or whether other mechan~me are responsible. So-called pathological myopia is not of direct interest to this report, since it occurs relatively infrequently and has no special predeliction to the young adult age group. Nev- ertheless, it is useful to understand that it is associated with pathological elongation of the anterior posterior axis. High levels of myopia frequently lead to blindness as a result of the rapidly increasing size of the posterior segment of the eye, causing degenerative changes in the retina (Curtin, 1985~. The pathophysiology of postnatal ocular expansion produces characteristic changes in the fundus appearance. The most common of these changes ~ crescent or conus formation. In this condition, a disparity exists between the areas of the overexpanded scleral shell and the retinal-choroid within. This disparity caused shifting of the choroid and retina temporally toward the ante of the globe that ~ expanded most. This "temporal shears results in a retraction of the laming vitrea (Rr~f~h'.~ m~mbrn.n-1 from t.h. t.-rnr`^ra1 ~;- . . .. . , ~.. . . . v ~,^_J _^ ~^ Van_ V_ ~- ^~- o^ 1 ~ · ~ ~ ~ · . OI one Op~lC nerve near, producing a crescentr~c area on the temporal aspect of the disk in which the lamina vitrea and its attached tissue, the choriocapilIaris and the retinal pigment epithelium, are absent. As a result, the inner aspect of the sclera becomes exposed and imparts a white color to the crescent area viewed ophthaImoscoPicallY. Sucertraction Is the ~.. . .. ~. ~.. .. converse ot the traction that produces crescent formation. With temporal shearing of the cooro~-ret~na upon the inner sclera, the optic nerve acts as a barrier to this process so that these inner ocular tissues become piled up and superimposed on the nasal margin of the optic nerve. An eye that presents with crescent formation, supertraction, or both has already expanded beyond its normal growth limit. Even moderate levels of myopia may show some of these fundus signs and may be associated with a higher incidence of retinal detachment and certain other degenerative processes affecting the eye. ., .

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This book considers the issues surrounding the occurrence, progression, and predictability of myopia (near-sightedness), with special emphasis on the 16- to 26-year-old population. Myopia reviews only the most pertinent published research in this area, analyzing the findings and drawing conclusions from these studies. The observations and recommendations will undoubtedly be of considerable interest to vision scientists and clinicians alike.


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