progressive myopia and intraocular pressure: what is the linkage?: a literature review

A CTA 0 P H T H A L M 0 L 0 GI CA (1988) Suoolement 185

Progressive myopia and intraocular pressure: what is the linkage?

A literature review

Ronald C. Pruett

Boston, MA, USA

Abstract. Progressive myopia may result from an inherited biomechanical weakness of the sclera that allows it to stretch (creep) in response to stress. In- creased intraocular pressure could be the mediator of stress produced by the inclined head position and the accommodation/convergence aspects of near work. This paper reviews data that relate to this hypothesis including work on sclera, intraocular pressure, animal models of myopia, and attempts at human treatment. Although the weight of evidence appears to support the proposed notion, no firm conclusion can be drawn due to imperfections in the design of prior studies. A future research agenda is proposed, including a controlled clinical trial of pharmacologically sustained ocular hypotension in young progressive myopes.

Key words: myopia progression - myopia prevention/ therapy - experimental myopia - scleral creep (dis- tensability) - intraocular pressure - near work - accommodation/convergence - glaucoma.

Polarized opinions of the past largely have been abandoned; few pure genetic or uselabuse theo- rists remain. Given the evidence, most now con- ceive of myopia as an anatomic/refractive state of the eye that may result from a number of in- fluences acting alone or in concert.

A predetermination by heredity is suggested by the prevalence or rarity of myopia among certain races or genetic isolates. Concordance between separately reared monozygotic twins and discor- dance between dizygotic twins raised in common give similar support, and there is an association between myopia and a number of heritable dis-

orders such as Marfan’s syndrome, Ehlers-Danlos syndrome, and the Wagner-Stickler syndrome. On the other hand, environmental factors can induce or influence the development of myopia. We know that near-space rearing of young primates fosters development of myopia, and epi- demiologists report myopic shifts in populations becoming more educated. Myopia has long been associated with near work, especially reading, and has been suspected of being the effect rather than the cause of intellectual development and socio- economic success. Occlusion or distortion of the image in the eye of the young can somehow induce myopia. In the laboratory investigations of this phenonenon, the genetic and uselabuse schools come together. An environmental manipulation (occlusion) can cause axial myopia, but the presence of a genetic substrate is evidenced by the fact that only certain species of young primates are so affected. Myopia must be multi- factorial.

Students of myopia would welcome a unifying theory that could gather these disparate observations into a rational pahtophysiologic schema. But this may be too much to hope for. It is likely that myopia is not one disease, but a collection of various developmental disorders that come from different directions to walk a final common path- way. If this is true, a number of means for prevention and treatment may by waiting to be invented, and the search will be long and tedious. Only if there were a shared mechanism could a ‘cure for myopia’ be anticipated.

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One factor that has been suspected as important is intraocular pressure (IOP). Although 1OP may not be the linchpin of physiologic myopia development, it may be a cofactor, and evaluation of its possible role in progressive myopia seems worth- while. This paper examines the linkage between progressive myopia and IOP. It articulates the long-standing hypothesis based on that notion, evaluates supporting data, draws conclusions, and suggests a future research agenda.

The Hypothesis

The anatomy and function of all biological sy- stems vary around a norm; this spectrum is an expression of DNA, RNA, and other cytoplasmic hereditary determinents and their response to environmental requirements. Ocular size and optics vary, the most common eccentricity being toward a larger, myopic eye. A number of possible explanations could be proposed. But considering that the anatomy and optics of the anterior segment are usually normal, shouldn’t we first con- sider that one or more of the three coats of the posterior segment is the target structure?

This hypothesis first supposes that the sclera of myopic eyes is abnormal. Due to genetically pre- scribed biochemical variations, some sclerae are biomechanically softer or harder, elastic or inelas- tic. This is simply Nature’s presentation to the environment to co-operate in the process of natural selection. But because humans are no longer hunter-gatherers, selection forces have changed in recent millennia. The primary premise, therefore, is that the sclera of the myopic individual is more prone than average to stretch (creep) in response to stress and that it also has poor me- mory (hysteresis) so that it gradually and pro- gressively becomes permanently deformed. As the scleral envelope enlarges, the choroid and retina are obligate followers.

A second premise is that the myopic eye is inclined to develop higher than average IOP. This too is genetically determined, perhaps through the organization of‘ the trabecular anatomy, itself a part of scleral anatomy. Some wonder whether ‘pressure produces myopia’; others, whether ‘myopia causes glaucoma’. It may be that neither causes the other but are both determined by

heredity and can be simultaneously expressed to more or less degree in different individuals. There is a possibility too that it is not so much sustained pressure as pulsed pressure that is destructive.

Given ‘weak’ sclera with low rigidity and the tendency toward elevated tension, one way the eye can accommodate is by stretching an enlarging. This might be accelerated and exaggerated if the IOP were spiked by positioning, accommodation, convergence, squeezing the lids, etc. In extreme cases the most plastic area of the adult sclera, the posterior pole, would develop a staphyloma. As the eye reaches its elastic limit in the high degrees of myopia, scleral ‘rigidity’ rises. Tissues can no longer stretch; they tear, lacquer cracks form, and choriocapillary hemorrhages and subretinal neo- vascular membranes complicate the problem. As the attenuation of the choroid and retina pro- gresses, secondary vitreous breakdown occurs, cataracts form, and the retina is more vulnerable to retinal detachment.

The Evidence

Intraocular pressure, mechanical stress, scleral creep, axial enlargment - what is the evidence? Why is the concept not universally endorsed? Why have treatments based on this notion generally not been accepted? Are there contradictory facts? Is there a way to find an answer? First, let’s examine what appears to be reasonably estab- lished concerning sclera and IOP in myopia. Second, do observations of experimental models and of human conditions tend to strengthen or weaken the hypothesis?

Sclera

True sclera, which is found only in vertebrates ( l) , is 68% water ( 2 ) . About 75% of its dry weight is collagen, the rest being non-collagenous proteins and mucopolysaccharides. Biochemical studies have shown chondroitin sulphate and at least two proteodermatan sulphate proteoglycans ( 3 ) . Some of these proteoglycans exist as intercellular fibers that form a matrix with the collagen bundles, but their possible role in disease is yet to be studied. Elastic tissue comprises less than 2% of the dry scleral weight (4). Is abnormal elastin present in myopic sclerae and is it related to scleral rigidity?

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(5). These questions are unanswerable at present, and their complexity is indicated by the fact that the Ehlers-Danlos syndrome alone can be divided on a clinical basis into at least eight subtypes (6). The biomechanical bases for this and other syn- dromes associated with myopia, such as Marfan’s, are unknown. Only in recent years has there been some scant evidence that collagen chemistry is abnormal; results are still preliminary (7-9).

We know more about the micro-architecture of the sclera than about its molecular structure, and there is strong evidence to suggest that collagen is anatomically different in myopia than in the emmetropic eye. In the normal eye the outer scleral layers contain mature, large-diameter collagen fibers (average 125 nm), whereas the inner layer shows immature, small-diameter fibers (average 62 nm) (10). It is believed that collagen is laid down by fibroblasts in the inner layer with gradual outward displacement. Observations of myopic abnormalities in fiber size and arrangement go back more than 30 years (1 1) and have been confirmed by current investigators (12- 14). The extreme of a staphyloma shows a predomi- nantly lamellar fiber bundle arrangement, smaller fibers and a greater range in their size, and peculiar fibrils star-shaped on cross section, all of which Curtin et al. (14) thought could be related to abnormal acidic glycosaminoglycan composition of the interfibrillary substance. The periodi- city of the cross striations in the collagen bundles is normal (about 65 nm). Other anatomical re- searchers, Rehak and Kubena (15, 16) looked for a common defect in the ultrastructure of the trabecular meshwork of human eyes with high myopia or glaucoma. None was found. In fact, the two conditions were markedly different, the inter- ti-abecular spaces being tight in glaucoma and loose in myopia.

The biomechanical behavior of sclera has been studied with a greater degree of sophistication recently (17). As a result we know that the relationship between stress (load) and strain (dimen- sional change) in the sclera is non-linear. That is, sclera is one of those materials that can change its elastic (Young’s) modulus as it is being stretched. The sclera becomes less compliant with increasing strain and also with increasing age. Recall that scleral rigidity is low in moderately high myopes and is greater in low and extremely high myopia (18). We know also that sclera is not so resistant to change in its radial dimension (thickness) but is

quite resistant to circumferential stretch, because its fibers run circumferentially. Despite that, sclera shows viscoelastic creep under stress with some tendency toward hysteresis. It is suspected that elasticity, creep, and hysteresis (19) are related to the progression of myopia as provoked by intraocular tension or other forces.

The meticulous measurements of Greene and his colleagues (20-24) support this proposition. They demonstrated that creep rate was related to IOP, time, and temperature in isolated rabbit eyes. Further, they showed that cyclic pulses of elevated IOP could cause irreversible deforma- tion as the plastic yield point was exceeded.

Curtin (25) measured the elasticity of adult human scleral strips and found that the material was more extensible posteriorly than anteriorly. He reminded us too that the posterior sclera is the last to develop ontogenetically and that it matures only after the completion of ocular growth of the eye at about 14 years. That is, scleral elasticity and plasticity are related to age.

The ability of the scleral shell to stretch is translated into axial elongation through pulsed or sustained, spiked or low-level, internal pressure. This would involve application of the Laplace equation for calculations of stress in the wall of a theoretical round eye of uniform composition.

Green (21) feels that scleral stress is exaggerated by the pull of extraocular muscles, especially posteriorly by the obliques, and that the stress is further concentrated by the presence of the scleral foramen. The latter is an extrapolation of a mechanical engineering principle that stress is greatly augmented around a circular hole in a plate under tension. Perkins (26) disagreed. After measuring the coefficient of ocular rigidity (k) in enucleated human eyes, he concluded that the lower value in myopic eyes was due largely to their greater volume rather than to any abnormal di- stensibility of the sclera. So strongly was Greene convinced by his data, however, that he recom- mended that the following therapeutic measures be considered for progressive myopia: atropine, plus lenses and/or base-in prisms, extraocular muscle surgery, scleral re-inforcement surgery, and drugs to lower the IOP. Additional methods for prevention and treatment have been suggested by others on the basis of this concept. These will be briefly reviewed later after we have examined more closely the relationship between IOP and myopia.

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lntraocular pressure

There are some dissenters, but most have claimed for many years that open angle glaucoma is more common among myopes and that myopia is present in a greater percentage of glaucoma patients than in the general population. In a case-control study among outpatients of a London clinic, Daubs & Crick (27) found no relationship between refractive error and ocular tension. Nor did Kragha (28) find a relationship in Nigerian subjects. However, David’s study (29) confirmed the association between myopia and IOP that was suggested as early as 1920 by Lange and Gilbert, cited by Knapp (33), and found by others (30-34). In fact, David re-iterated that myopia was a risk factor among those with ocular hypertension and added that ocular hypertension should be recognized as a risk factor among persons with myopia. After a review of the literature available to 1980, Ganley (35) also had concluded that myopia was a factor epidemologically associated with ocular hypertension.

Studies have varied in numbers of patients and methods of observation, but there is a consistent claim that IOP is correlated with the degree of myopia among the genetic mixes of numerous countries (25, 36-47). Curtin (25) reported that in myopia patients over 40 years of age who attended his clinic, 11.2% of those eyes with axial length greater than 26.5 mm and 23.1% of those greater than 30.5 mm were glaucomatous. Al- though other reported data are consistent with this observation, it has not gone unchallenged. Bonomi et al. (48) examined 137 anisometropic subjects to see if the IOP was higher in the more myopic eye. It was not, but they added that ‘. . .it is possible that bilateral myopes are genetically different from myopic anisometropes’. With re- gard to genetics, the majority of patients with pigmentary glaucoma/exfoliation syndrome are myopic (49-51), and Becker (52) claimed that they had a higher than normal incidence of HLA- B12, which is related to increased steroid re- sponsiveness. Studies in Shanghai (53) of HLA hereditary markers among subjects with ordinary high myopia and open angle glaucoma suggested that the two conditions were not linked in the genome. Mandelkorn et al. (54) studied the inheritance pattern among 23 members of four families with the pigmentary dispersion syndrome. Although the myopia and glaucoma were

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associated, the autosomal transmission of the traits appeared to be independent.

There is a good deal of evidence that the tension responses of highly myopic and glaucomatous or glaucoma-prone eyes are similar. In 1964, Becker & Hahn (55) advanced the idea that a rise in IOP following topical administration of cortisone was genetically determined and that it could identify heterozygote carriers of the glaucoma gene who, together with homozygous glaucoma patients, responded positively (56). This was confirmed by Armaly (57-59), but the recessive hereditary pattern of the response was disputed by Francois et al. (60). In 1966, Podos et al. (61) published their observations of steroid responses among high myopes. In 15 of 17 individuals there was a positive pressure rise. That stimulated additional investigation and speculation regarding this association. In a study in China (62), where 6.98% of the general population is highly myopic (63), there were significantly higher pressure responses in high myopes than in normal subjects. During our investigation conducted in Boston, we found that 19 of 20 (95%) eyes of 20 highly myopic patients with no detectable glaucoma were positive steroid responders and showed a reduced facility of outflow (C) during steroid provocation (64).

The finding that oral steroids produce pressure spikes in glaucoma patients led to speculation regarding endogenous cortisol production and its possible influence upon diurnal IOP variation (65). Glaucoma has occurred in myopia patients wearing contact lenses and using topical steroids (66), and monozygotic, myopic, glaucoma-suspect twins were found to be positive steroid responders (67). Brubaker & Halpin (68) were unsuccessful in inducing glaucoma in the eyes of rhesus monkeys with topical steroids, but they reported the case of an 18-year-old man who did have such a response. The tension rise was asymmetric, and the tension persisted in one eye that subsequently became axially myopic. Another 18-year-old with appar- ent unilateral steroid-induced glaucoma and secondary axial myopia was documented by Virgilio et al. (69). Interestingly the collagen of the sclera showed an abnormal ultrastructure that was inter- preted as an arrest in scleral collagen synthesis.

Steroids have been said to decrease the facility of outflow by the accumulation of glycosamino- glycans in the trabecular meshwork (70). Myopic eyes apparently are more vulnerable to this, and

perhaps also to the dispersal of pigment granules in the anterior chamber and to hyalyronic acid macromolecules that come forward from the vitreous following capsulotomy (7 1, 72). Even water loading and mydriasis produced a positive tension rise in 8.53% of cases (73).

IOP and reading

What about IOP and reading? Does head positioning and/or accommodation/convergence produce a tension rise and increase scleral stress? Here we are not considering prolonged, low-level stress but stress due to more acute short-lived events. The relationship between momentary fluctuations in IOP and the pathophysiology of damage is also of concern to glaucoma investigators (74). It has been shown, for example, that IOP variability is a better predictor of eyes that would develop visual field defects than is the highest or the mean IOP (75).

The position of the body and head are well known to affect IOP (76, 77), and posture was suspected of increasing myopia by Donders (78) more than 120 years ago. The extreme body position, inversion, raises arterial, venous, and intraocular pressure (79-8 1) and probably intra- cranial pressure (82). Simple changes in position, from sitting to supine, Krieglstein & Langham (83) found increased the tension 2.9 mmHg in normal and 3.9 mmHg in glaucomatous eyes under treatment. Low tension glaucomatous eyes responded to position also, and these investigations suggested that this was a pathogenic factor in the disease.

A number of authors think that the inclined position for reading (84), swaying the head back- ward and forward during reading (85), or simply ‘bad posture’ (86), while reading encourages myopic progression. Ferfilfein (87) studied this question in some detail and found that IOP increased in all inclined subjects and that the degree of increase was related to the angle of inclination and the duration in that position. He thought that the tension rise was due to venous outflow im- pairment and congestion. Interestingly the degree of rise was related to scleral thickness; that is, it was lower in myopic eyes with thin sclera.

Tokoro (88) confirmed these findings. High myopes had higher tensions than did low myopes, but the greater the degree of myopia, the less was the increase in tension with 45” forward head positioning and with the supine position. Tokoro

speculated that there was ‘slow reaction sensitivity’ and ‘changes in the blood circulation of the choroid’ in the highly myopic eye (89).

It seems clear that highly myopic eyes show a tension increase with inclination of the head that is inversely related to axial length and directly related to scleral thickness. Certainly the thickness of the choroidal vascular bed is decreased drama- tically in high degrees of myopia, and its percentage of the overall volume of the enlarged eye would be small, thus dampening the effect of vascular congestion. Perhaps the explanation is also related to scleral rigidity. Normal eyes, low- myopic eyes, and glaucomatous eyes with thicker and less elastic sclera would show a greater postural variation than the more elastic highly myopic eye. It would be interesting to know whether those extremely high myopes with increasing scleral rigidity would also show a greater postural response.

As we incline to read, we also converge and accommodate. Even simple horizontal eye movements elevate IOP 2-5 mmHg in normal subjects (90). Greene (2 1) believes that the eye movements associated with reading stress the sclera, and Coleman (91) made some direct TOP recordings in a human subject prior to enucleation. Squeez- ing of the lids could elevate the tension to 90 mmHg, horizontal and blinking movements can raise IOP by 10 mmHg. Accurate measurements of the pressure response to accommodation were not possible due to cycloplegia.

Coleman (92) has also described a unified model for accommodation and maintains that during accommodation there is a pressure gra- dient between the anterior chamber and the vitreous cavity. His direct recordings of aqueous and vitreous pressures during electrical stimul- ation of ciliary muscle activity confirmed the pressure difference in primate eyes (93). Young (94-96) demonstrated that if visual space were restricted to near viewing, it could produce myopia in the young primate eye, and this response could be blocked by atropine. Using an implantable transducer developed by Collins (97), Young later (98) showed increases in vitreous cavity pressure during accommodation in animals, supporting Coleman’s observations.

Myopia models

Attempts to simulate human myopia in laboratory animals began early in this century. There is now

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a large literature that was reviewed recently by Goss & Criswell (99) and Criswell 8c Goss (100). Accommodation, increased temperature, extraocular muscle tension on the sclera, IOP, and scleral stretch are recurrent themes.

The most fundamental conclusions that can be drawn from these experiments are that 1) myopia can be induced by a variety of manipulations in primates and subprimates, 2) both genetic and environmental factors are involved, and 3) there is in most species an early period that can be influenced and a later stage at which time the course appears to be set.

Young ( 10 1) believes that the plastic period ends at about 8 years of age in monkeys and 25-30 years of age in humans. More recently, since the pioneer work of Wiesel 8c Raviola (102), attention has been directed toward understanding the mechanisms of lid-occlusion/light-regulated myopia in primates, tree shrews (103), chickens ( 104), and other species.

Although IOP and scleral stress are still on the list of possible explanations for certain types of experimental myopia, the data to support this view are few or have not been gathered by the experimental protocols. Levinsohn ( 105), probably the earliest to suspect IOP, performed mano- metric measurements in macaque monkeys in which myopia was produced by prone positioning. The pressures were normal. He proposed that axial elongation was the eye’s response to relieve the stress produced by gravitational forces acting on the optic nerve at its point of exit from the sclera (106). Poos ( 107) failed to produce myopia by prone-positioning rabbits, by intermittently raising the vitreous pressure by injection while the body temperature was increased.

No significant changes in IOP were detected by various workers who conducted light-manipulation myopia experiments in developing chicks (log), adult chickens (1 lo), and monkeys (1 11). At this point the possible role of intraocular tension in various experimental models of myopia appears speculative, but it has not been totally explored.

Observations in humans

The number of publications describing the ratio- nale and presenting observations and statistics to support various therapies for progressive myopia is enormous. Goss ( 112) did a limited review of the literature in 1982, and Curtin (113) thoroughly

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surveyed the subject in his scholarly textbook of 1985. Some treatments are clearly based on the concept of scleral stress and creep, such as the various forms of re-inforcement scleroplasty, the use of vitamin A, calcium, etc, whose purpose it is to increase resistance. Others aim at decreasing stress.

Arciniegas ( 114- 116) has claimed that vitrectomy should be considered for reduction of pressure on the posterior pole. Some investigators have attempted control using medical means and most of these have tried cycloplegia and/or bifocal wear to prevent or relax accommodation (117, 118). This approach rests in part on the concept of hysteresis (1 19). It also implies that somehow accommodation/convergence generates a force that results in scleral expansion; it is founded on the belief that myopia is not totally determined by heredity, and that manipulation of environmental factors can make a difference (120, 12 1). Studies reported in recent years have included those of Bedrossian (197 1) (122), Gimbel (1973) (123), Kelly (1975) (124), Dyer (1979, 1980) (125, 126), Brodstein et al. (1984) (127), Brenner (1985) (128), and Goss (1986) (129). In general, the results have been favourable, suggesting that atropine/bifocals can reduce the rate of myopia progression. The work of Bedrossian (122) is unusual in that it used fellow eyes for a control, and it had a cross-over design. Critics are fast to point out the lack of controls in most studies, and one commented in 1985 that ‘there are methodo- logy flaws in all existing studies of the atropine treatment’ (130).

Another problem has been the high non-com- pliance and dropout rate due to the glare and inconvenience of mydriasis and cycloplegia. The potential for chronic mydriasis to allow photo- toxic effects also has been mentioned (13 1). These reasons, and the lingering doubt about its beneficial effect and permanence, have prevented cycloplegia from becoming a generally accepted method for preventing myopia progression.

It is noteworthy that a great deal of time, effort, and expense have been devoted to stuaying atropine as a treatment for myopia, without adequate controls and without a specific state- ment as to its theoretic mode of action. Investi- gations have been done in the belief that near work causes myopia, and the question simply has been: does atropine work? Many authors carefully avoid discussion of particulars, while others boldly

state that the mechanism of action is unknown. Some suggest or imply that atropine might prevent a permanent increase in the convexity of the lens surface (127), vitreous pressure (127), or increased intraocular tension ( 139) associated with reading.

Despite the fact that pressure seems the root suspicion of this medical approach, and also of those involving scleral re-inforcement or vitrectomy, there has been precious little activity to look for possible benefit from directly lowering the tension in myopic eyes. Wiener (132, 133) believed that myopes had adrenal insufficiency and that epinephrine might have . . .a beneficial influence on the softening or stretching ofthe sclera in progressive myopia’. He found topical epinephrine effective in reducing the rate of progression, as did Macdiarmid & Hamilton over 30 years later (134). One wonders whether the IOP was reduced by the epinephrine in these treated eyes.

An editor of a prestigious medical journal commented on the reasonableness of using tension-lowering drugs ‘ . . .when the eye is youthful and malleable, in the hope of lessening any stretching factor in the globe’, but noted sadly that he knew of unpublished data from Guy’s Hospital in London that adrenalin drops and acetazola- mide used over many years had produced only equivocal results (135). Curtin (136) has recom- mended the use of dipivephrine or timolol maleate, but only one inconclusive trial of timolol maleate is known to have been conducted thus far. Goldschmidt et al. (137) did a pilot study on 10 children with progressive myopia, aged 7- 12 years, who were treated for one year with 0.25% timolol drops twice daily. Although there was no significant change in the IOP in most of the children during treatment, there was a tendency for those who did respond with a lower tension to progress more slowly.

Conclusion

Our working hypothesis for myopia progression is old, and it somehow seems too simple, too obvious, unsophisticated. Despite that, it still has not been ruled out. In fact, there appears to be more evidence in support of it than against it. So why not accept it? The problem, I think, lies in the fact that there is no single study the results of

which will stand the rigors of scientific and statistical scrutiny so that all can believe its conclusions and commence treatment of patients. My only firm conclusion after studying the available information, therefore, is that the linkage between myopic progression and IOP is emminently worthy of serious controlled study.

Recommendations

Although there is a host of projects that a curious investigator might outline for support during the next five years, these would have my highest priority:

1) Apply the latest and developing techniques of molecular biology to the study of sclera in humans and in animal models of myopia.

2 ) Develop improved methods for the measuring of scleral rigidityielasticity that would be applicable in both laboratory and clinical settings.

3) Devise means to accurately monitor IOP as one of the parameters of experimentally induced myopia in animals.

4) Initiate a multicenter, double-blind, pro- spective clinical trial of pharmacologically sustained ocular hypotension in the treatment of progressive myopia in adolescent subjects. Timolol maleate, betaxolol, or dipivephrine might be considered for this purpose.

Comment

Some have dismissed myopia as not a ‘disease’ but a biologic variant for which there is no reason for worry or effort to prevent or reduce it; simply wear glasses (138)! But in 1979 the US Federal Trade Commission estimated that 1.3 billion dollars were spent yearly for corrective lenses for myopia (139). Presumably this figure did not include the cost of examinations by ophthalmolo- gists and optometrists, nor the cost of contact lens cleaning solutions and equipment, nor the cost of the more recently popularized refractive surgical procedures, in today’s dollars! The cost of myopia for the American society is great; when one con- siders that Asian populations have a prevalance of myopia over twice that of the US, the enormous weight of the world burden of myopia becomes more evident. This is without considering the

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disability and blindness that occur f rom the complications of high myopia: p remature cataract, glaucoma, macular degeneration, and retinal detachment .

Myopia is worth studying; it is worth preventing or reducing. The general public, the medical/ industrial complex, and the world community of visual scientists must join together to find a way.

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Author’s address:

R. C. Pruett, MD, P C, Myopia Research Unit of the Eye Research Institute of Retina Foundation and Retina Associates, 100 Charles River Plaza Cambridge Street 02114 Boston, MA, USA.

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progressive myopia and intraocular pressure: what is the linkage?: a literature review

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