Ординатура / Офтальмология / Английские материалы / Ocular Periphery and Disorders_Dartt, Bex, Amore_2011

made in the steepest corneal meridian to reduce postoperative astigmatism. Penetrating keratoplasty is sometimes needed in severe cases of irregular corneal astigmatism. In this case, the resulting corneal shape can be altered by increasing or decreasing the tensile forces created by sutures. It is even possible to remove corneal material in one meridian, a wedge resection, to stretch the cornea, and change its shape. For healthy eyes, laser refractive surgery and conductive keratoplasty are the two techniques commonly used to treat ocular astigmatism. Toric intraocular lens implants also exist that can be used to correct ocular astigmatism and these may be used following cataract surgery or clear lens extraction.

Not Correcting Ocular Astigmatism

It is not always desirable or necessary to correct ocular astigmatism in adults. The most useful property of astigmatism is that, if one is accepting limited amounts of blur, it creates depth of focus in the eye. As mentioned earlier, for near tasks blur along a vertical meridian can usually be tolerated more readily than horizontal blur. An individual with against-the-rule simple myopic astigmatism will have vertical blur conjugate with a near distance equivalent to the amount of astigmatism and horizontal blur conjugate with distance vision. As long as this patient can tolerate the distance blur, they will have functional vision at both distance and near without accommodative effort. Such a situation would be useful for later presbyopes and pseudophakes and free the individual from needing any form of optical correction.

In addition, in some instances where individuals have very different ocular astigmatism in each eye the fusion difficulties that occur with spectacle correction make binocular vision impossible. If contact lenses cannot be tolerated and surgery is not an option, then there may be no alternative than to significantly undercorrect the astigmatism in the nondominant eye and allow visual suppression of the resulting blurred image to occur.

Finally, it is sometimes the case that an individual with high levels of ocular astigmatism has a measureable change in that astigmatism but is not complaining of any significant visual difficulties. One would be very cautious about changing any refractive correction in this individual

as the perceptual adaptation to the meridional magnification differences would be affected by doing so and the person may end up feeling that he/she see worse rather than better. The same is true when large changes to the ocular astigmatism are found that do cause symptoms. Adapting to large changes in the correction can be intolerable for some people.

Summary

Although ocular astigmatism is very common, affecting two out of every three adults, visually disabling ocular astigmatism is much less common, affecting only one in five. Correcting this astigmatism is straightforward in the great majority of cases, although the measurement and correction of both irregular astigmatism and high degrees of regular astigmatism remain challenging. Astigmatism induced when looking obliquely through spectacles is well controlled by using the appropriate lens design and contact lens and surgical correction of astigmatism is successful in many instances, even though the uptake of these latter forms of refractive correction is still low. Measuring and correcting irregular astigmatism has improved with the use of more accurate assessment of the corneal surface and with wave front aberrometry to sample the local refractive powers across a fine array of pupil locations. Optimally correcting irregular astigmatism with custom contact lenses and surgical refractive correction is proving to be challenging but successful trials have been performed.

See also: Hyperopia; Myopia; Refractive Surgery.

Further Reading

Freeman, M. H. and Hull, C. C. (2003). Optics, 11th edn. London: Butterworth-Heinemann.

Harris, W. F., Raasch, T. W., and Thibos, L. N. (1997). Optometry and Vision Science: Feature Issue on Visual Optics 6: 339–463.

Rabbetts, R. B. (2007). Bennett and Rabbetts’ Clinical Visual Optics, 4th edn. London: Butterworth-Heinemann.

Read, S. A., Collins, M. J., and Carney, L. G. (2007). A review of astigmatism and its possible genesis. Clinical and Experimental Optometry 90: 5–19.

Glossary

Accommodation – The changes in optical power by the eye in order to maintain a clear image (focus) as objects are moved closer. This occurs through a process of ciliary muscle contraction and zonular relaxation that causes the elastic-like lens to round up and increase its optical power. Natural loss of accommodation with increasing age is called presbyopia.

Astigmatism – An optical defect in which refractive power is not uniform in all directions (meridians). Light rays entering the eye are bent unequally by different meridians that prevent formation of a sharp image focus on the retina.

Choroidal neovascularization – The creation of new, weak and leaky, blood vessels in the choroid layer of the eye. It is a common symptom of wet age-related macular degeneration and of pathological myopia. Glaucoma – The neuropathy that affects the optic nerve of the eye and involves loss of retinal ganglion cells in a characteristic pattern causing peripheral visual-field defects.

Retinal detachment – A disorder of the eye in which some layers of the retina peel away from its underlying layers of support tissue. It is a medical emergency and if untreated it may cause partial or total vision loss.

Definition of Myopia: Health and

Economic Implications

Myopia, also called nearor shortsightedness, refers to the refractive state of the eye whereby the images of distant objects are focused in front of the retina when the accommodation system is relaxed. It can also be described as the refractive error in which the point conjugate with the retina, the far point of the eye, is located at some finite point in front of the eye. Therefore, light entering the eye has to originate from near objects, within the eye’s focal point, or diverged by concave lenses (minus power) in order to be focused on the retina of the myopic eye (Figure 1). Distant objects are otherwise perceived as blurred, hence the term nearsightedness. Squinting of the eyes is another symptom of myopia which can, rarely, produce headaches.

Myopia, in particular high myopia, is directly or indirectly associated with a number of ocular health complications that are potentially blinding. Moderate and high levels of myopia – greater than 5.00D – are a predisposing risk factor of reghmatogenous retinal detachment (lifetime risk is greater than 9%). High myopia is also a predisposing factor for open-angle glaucoma, myopic retinopathy, and myopic maculopathy. The increased elongation of the globe may be associated with degenerative changes in the sclera, choroid, Bruch’s membrane, retinal pigment epithelium (RPE), and neurosensory retina. There is increased incidence of fundus (posterior part of the eye) lesions (Figure 2) such as posterior staphyloma, atrophy of RPE and choroid, lacquer cracks in Bruch’s membrane, subretinal hemorrhages, lattice degeneration, pavingstone degeneration, pigmentary degeneration, white with or without pressure, retinal holes or tears, posterior vitreous detachment, macular holes, and choroidal neovascularization (CNV). Of these, CNV is the most common vision-threatening complication. Keratoconus, lens opacities, and increased complications following cataract surgery and pigmentary glaucoma are other associated complications. Although various methods of optical correction of myopia are possible, none changes the abnormally large size and shape of the myopic eye, with consequent thinning of the various layers, and therefore the risk of complications remains. Therefore, frequent complete eye health examinations, with pupillary dilation for comprehensive examination of the fundus, are necessary.

Myopia is a significant public health problem and its rapid increase in prevalence in recent decades is associated with a significant financial burden. In the United States, the annual direct cost of refractive correction with eye glasses alone is estimated to be at least $3.8 billion. Further adding to the cost of myopia are eye examinations, time off work, other optical corrections (e.g., contact lenses), refractive surgery, and other treatments. In the United States, correction of refractive errors, including the cost of glasses, contact lenses and refractive surgery, consumed over 12 billion dollars in 1990.

Although blurred vision resulting from myopia can often be corrected with visual aids, such as glasses, contact lenses, or refractive surgery, uncorrected refractive error is the major cause of visual impairment worldwide, accounting for at least 33% of visual impairments. In the United States, it is estimated that 5.3% of the visual impairments are due to uncorrected refractive errors. In addition, myopia – even if corrected – can be an impediment in certain professions; for example, military pilots and police officers.

Figure 1 (From top to bottom) Schematic drawing (color) of an emmetropic eye (top) with parallel rays of light focusing at the retina; a longer myopic eye (middle) with parallel rays of light focusing in front of the retina; and a longer myopic eye corrected with a concave lens, the light rays are diverged and now focus at the retina (bottom).

Natural History of Myopia

Emmetropization is the process whereby the refractive components and the axial length of the eye come into balance during postnatal development in order to induce emmetropia (no refractive error). Most infants are hyperopic, and in those born myopic, the myopia typically decreases to reach emmetropia by toddler age. However, in a small population, for instance, premature infants with retinopathy of prematurity, myopia is present at birth and does not regress. By 12 months of age, the frequency distribution of the spherical equivalent becomes leptokurtic (as it is in adults) with the peak at low hyperopia. Results of a large longitudinal study by Gwiazda and colleagues, in 2000, showed that infantile astigmatism is associated with increased astigmatism and myopia during the school years.

Myopia typically develops during the school years, progressing until adulthood, but it may also develop in adults. Progression typically ceases in the teenage years, although it may continue into the 30s. Generally, the annual progression is close to 0.50D in juvenile (8–12- year-old) Caucasians and double that for juvenile Asians. There is a correlation with the age of onset and the final refractive status in adulthood, that is, children who become myopic at an earlier age (6 vs. 11 years) have a higher risk for myopia progression and higher degree of myopia later on.

Refractive error in the adult population follows a leptokurtic distribution with the peak around emmetropia. Later in life, a myopic refractive shift may result due to crystalline lens changes.

Structural Correlates, Molecular and

Anatomical Changes in Myopia

In the Aristotelian writings (c 330 BC), the condition of shortsightedness was already documented. The optics of myopia, however, were first elucidated by Johannes

Kepler in his initial Clarification of Ophthalmic Dioptrics

(1604) when he correctly assumed that the incident light was brought to a focus in front of the retina. The reason for the displacement of the focus in myopic eyes elicited much attention. Some authors believed it was due to abnormal convexity of the lens; others attributed the defect either to an increased convexity of the cornea or to undue length of the globe, while some others described anatomically the unusual distance between the lens and the retina.

Biometric investigations of myopic eyes have confirmed that increased axial length of the eye, particularly vitreous chamber elongation, is the main structural correlate in human myopia. Steeper corneal radius, deeper anterior chambers, and thinner crystalline lenses have also been found; however, these are less consistent findings. The relationship between the eye’s axial length and corneal radii (normally 3/1) is generally increased in myopic eyes. Retinal thickness is increased in the fovea, but decreases toward the periphery and it is significantly thinner in myopic eyes beyond the macula. In the 1990s, some studies showed that intraocular pressure (IOP) was related to myopia in children and therefore associated to the pathogenesis of myopia. However, a number of recent studies have refuted this theory with findings of no association between IOP and refractive error prior to or after the onset of myopia in children. Differences in the results may have resulted from ethnic differences.

The protein composition in aqueous humor is different in myopic eyes, suggesting that those proteins could indicate a potential biomarker for myopia development. However, most myopic changes are found in the posterior segment of the eye. The sclera of myopic eyes, even with low or moderate amounts of myopia, exhibits a number of structural changes due to the stretching of the eye, including increased extensibility, narrowing and dissociation of collagen fiber bundles, increased prevalence of stellate fibrils, severe thinning, and reduced collagen content, among others. These differences in scleral structure, and therefore its functionality, translate into a relatively thinned and weakened sclera. As myopic eyes expand during myopia development, the sclera must increase its surface area. Either new tissue must be added or existing tissue remodeled. Results of biochemical and histological studies are generally consistent with the hypothesis of active remodeling of the sclera during myopic growth. Regulatory changes in scleral metabolism could be rapidly evoked by a change in visual conditions which can also regulate the direction of change in eye size (toward hyperopia or myopia). The sclera’s role on regulating eye growth and emmetropization and its potential role for preventing myopia warrant further investigation.

Signaling cascades link retinal image processing to scleral growth in myopia. Chemical messengers are released from the retina toward the RPE where secondary

messengers are released through Bruch’s membrane and transmitted through the choroid to the sclera. The role of substances and transmitters in the retina and choroid, such as glucagons, insulin, early growth response factor-1 (EGR1 or ZENK), dopamine, nitric oxide synthase (NOS) inhibitors, gamma aminobutyric acid (GABA), muscarinic receptor subtypes (M1 and M4), and acetylcholine, is being investigated. Jody Rada and Lisa Palmer have suggested that increased choroidal permeability may represent a mechanism for controlling the rate of delivery of bioactive factors to the sclera to regulate the rate of glycosaminoglycan synthesis in the posterior sclera. Changes in collagen subtype expression and turnover of the normal scleral matrix (matrix metalloproteinase-2) are ultimately responsible for the anatomical changes in collagen fibril morphology and tissue thinning found in myopia. A role of growth factors, such as transforming growth factor beta and specific matrix–cell receptors (integrins), and altered scleral cell phenotype (myofibroblasts), in the scleral regulation of myopia development has been suggested. In addition, several research centers are beginning to map the myopia-associated locus and to identify the gene(s) responsible for myopia (see the section titled ‘Etiology of myopia’).

Anthropometric measures such as body stature and weight have been associated to myopia. The Genes in Myopia (GEM) Twin Study group from Australia has recently (2008) reported that individuals in the heaviest quartile of weight of their study population had an increased incidence of myopia compared to those in the lightest weight quartile, but the relationship was significant only for females. Previous investigations have also associated myopia with taller and heavier individuals, but not all studies agree.

Classifications of Myopia

The pattern of myopia development is complex and variable; therefore, it makes more sense to refer to ‘‘myopias’’ rather than a single condition of myopia. This complex pattern makes a classification of myopia difficult and has resulted in numerous different classifications being postulated, including:

. Classification according to the degree of myopia. (1) Low,

(2) moderate, and (3) high. The limits are still arbitrary, a consensus among experts is necessary if studies of prevalence are to be compared. Typically, low myopia refers to amounts between 0.50D and less than 3.00D; moderate refers to amounts between 3.00D and 6.00D; and high would be greater than 6.00D.

. Ophthalmologic classification based on the fundus changes.

(1) Simple or physiological (no fundus changes) and (2) degenerative or pathological myopia (fundus anomalies).

. Classification according to progression of myopia. In 1984, Donders subdivided myopia progression into (1) stationary, (2) temporarily progressive, and (3) chronically progressive (also called malignant or deleterious) myopia. Nowadays, researchers classify myopia based on the progression of the refractive power: (1) stable myopia refers to the refractive error that has not increased more than -0.25D in a period greater than 2years, and

(2) progressing myopia refers to greater increases over that period.

. Classification according to the age of onset. Typically classified as (1) congenital, (2) infantile, (3) juvenile, and (4) adult myopia. It may also be classified as (1) congenital versus (2) acquired. Research studies classify myopia based on the age of onset: (1) late-onset (15 years or older), and (2) early-onset myopia (14 years or younger).

. Classification according to the combination of components of the eye. (1) Refractive, correlation or combination myopia, and (2) component myopia (e.g., due to corneal curvature myopia, lens myopia, and axial myopia).

. Classification according to presumed etiology. (1) Environmental versus (2) genetic. Also: (1) physiological myopia,

(2) school myopia (due to close work), and (3) excessive myopia (i.e., caused by diseases).

. Genetic classification. Dominant type, recessive type, a sex-linked recessive type, etc.

. Biological classification of myopia. (1) Physiological or simple myopia as a biological variation of the normal distribution of the eye components, and (2) pathological (progressive or magna) myopia as falling outside the normal distribution.

Clinical forms of myopia include: nocturnal myopia, due to drift in the accommodation state that increases the power of the eye under scotopic conditions, and pseudomyopia, false myopia due to physiological or pathological increased accommodation state.

Epidemiology of Myopia

In the early 1980s, more than 25% of the adult population in the United States and up to 75% in other developed countries, such as Taiwan, was myopic. Twenty years later, approximately 50% of general population in USA and up to 84% of the 16to 18-year-old group in Taiwan was myopic. Based on a serial cross-sectional study from the Singapore Armed Forces, myopia prevalence has increased in military conscripts from 26% in the late 1970s, to 43% in the 1980s, 66% in the mid-1990s, and to 83% in the late 1990s.

The prevalence of myopia varies with age; it is low in young children, increases in school-age children and young adult cohorts, and decreases in older age groups. Within populations, myopia tends to be initially observed

at the ages of 6–8 years with the average annual progression quoted as ranging from 0.10D to 0.60D. Chinese children are predominantly myopic; in 1990, the prevalence was 37% and 50% in the 6–12-year-old group and 13–18-year-old group, respectively. Recent studies in China and Sweden show that the prevalence of myopia is now higher for teenagers. Prevalence is even higher among Taiwanese children: 56% of 12-year-old children and 76% of 15-year-old children are myopes. In the later 1990s in Japan, 43.5% of 12-year-old children and 66% of 17-year-olds were myopes. It can be appreciated that there are racial differences within groups of same-age populations, for example, Chinese and Taiwanese populations show higher prevalence rates than other populations. Myopia prevalence declines to some extent in the population over 45 years of age, which is likely due to an increased prevalence rate in younger populations than an age difference.

The prevalence of myopia varies considerably between races, although it is difficult to ascertain the influence of environmental factors on these differences. In an attempt to account for environmental differences, a number of studies have investigated differences in racial groups living in the same location. In 1999, Lam and Edwards reviewed previous studies on myopia prevalence and concluded that the greatest prevalence of myopia occurs among Japanese, Chinese, and some Native American tribes. These studies take into account that the prevalence of myopia is lower in rural populations and it is affected by educational attainment and socioeconomic status.

Some studies have found a slightly higher prevalence of myopia in females than in males; however, not all agree on this. It seems that the differences in gender are found if the prevalence is measured in younger adults when males and females are not at the same growth level.

Etiology of Myopia

It is currently accepted that the etiology of myopia is complex with genetic and environmental factors playing a role. Understanding the relative contributions of genetic and environmental components is necessary to establish the mechanisms of myopia development and further attempt to arrest its progression. Separating these components is not trivial; for example, educational attainment is strongly influenced by genes, and therefore this risk factor should not solely be considered as an environmental risk factor; twins typically have the same environmental factors and hence should not be considered merely a genetic component.

A century ago, in 1913, Steiger showed that myopia is influenced by genetic factors and is an expression of a range within the normal distribution. A number of early

and recent studies with twins have shown that the concordance of refractive error is greater in monozygotic twins, indicating the existence of a genetic factor in myopia. Further, twin studies have provided evidence of correlation and heritability of a number of traits implicated in myopia. However, there are limitations associated to these studies.

The use of twin studies is also important in the identification of myopia’s gene loci. A number of genetic loci have been identified as being linked with myopia. These include loci for high myopia occurring at Xq28 (MYP1), 18p11.31 (MYP 2), 12q23-24 (MYP3), 7q36 (MYP4), 17q21-22 (MYP 5), 4q22-27 (MYP11), and 2q37.1 (MYP12). Other candidate loci have been linked with low and moderate (common) myopia: 22q12 (MYP6), 11p13 (MYP7), 3q26 (MYP8), and 4q12 (MYP9). These linkages provide evidence that myopia is a polygenic disease with multiple and different alleles likely to contribute to different disease subtypes. Multiple familial studies also support a genetic component in myopia, suggesting a definite genetic basis for high myopia, and likely for low myopia. However, to date no candidate genes have been shown to account for even a modest fraction of the familial risk of myopia, and data are conflicting about whether a true association exists. It is likely that there is substantial genetic heterogeneity. In addition, further studies need to assess the relative roles of environmental factors and genetic influences, such as interactions of early-age nearwork and genotype, and the identification of phenotypes for etiologically different subgroups of myopia, for example, age of onset, presence of retinal degenerative changes, or response to treatments. See Schaeffel et al., Young, and the Genes of Myopia (GEM) Twin Group studies in the further reading section for reviews on the molecular basis of myopia.

Environmental factors, particularly nearwork, have been associated to myopia for centuries. Even though associated, nearwork has not yet been proven to be a causative factor. A number of aspects related to nearwork have been associated to myopia development and progression, including reading, cognitive effort during nearwork (with associated educational level and intelligence), lighting, and working distance. Accommodation and inaccuracies of the accommodation response are associated with myopia. Children who are to become myopic show greater inaccuracies of accommodation (greater lags) during near tasks. Accommodation effort, inaccuracies of the accommodation system during distance viewing, and accommodation flexibility have also been associated to myopia (nearwork-induced transient myopia (NITM) – a shift in refractive error due to inability to relax the accommodation).

Evidence for active and visually guided emmetropization (and its failures, such as myopia) is beyond refute. A number of animal models of myopia show that emmetropization can be manipulated and myopia can be induced. Manipulation of the environment can be achieved by imposing a close-work environment, or most commonly by lens-induced myopia (using high-power negative – concave – lenses) or form-deprivation myopia (using diffuser lenses, sutured lids, etc.; Figure 3). The most common animal models for myopia are chicks, mice, pigs, and tree shrews. Defocus blur is thought to be the primary cue for emmetropization and myopia. Emmetropization uses blur as visual feedback to regulate eye growth; the system requires detection of blur probably at the level of outer retina (perhaps amacrine and bipolar cells) – via diffusion of signals across RPE and choroid – to then alter scleral matrix (likely through a modulation of proteoglycan synthesis). The amount of defocus blur may increase in those

individuals who adapt more to blur, and hence blur adaptation may be a risk factor for myopia. The balance between central and peripheral defocus has been related to myopia, and animal models show that peripheral defocus alone can influence the rate of axial eye growth. Optical aberrations have been suggested to play a role in myopization, as some studies have found higher levels of aberrations in myopic eyes, but their association with myopia is not clear.

Among environmental factors, increasing educational demand seems to be a risk factor for development of myopia. When comparing university student populations with general populations, a much higher rate of myopia progression is found in the university populations. For example, significant differences have been found in the prevalence of myopia among Norwegian university students when compared to the general population of Norway and other Nordic countries. The prevalence of myopia has also been found to be greater in Greek university students and Scandinavian medical students than in the general population of the respective countries. In an interesting study in 1993, Zylbermann and coworkers showed that myopia was more prevalent in Orthodox Jewish boys in Jerusalem compared to Jewish girls, since boys spend up to 16 h day reading religious text, whereas girls receive a similar education to that in Western countries. Educational demands have also been cited as a risk factor in the prevalence of myopia in Young’s 1969 work with Eskimo families in Alaska; while only two of the 130 Eskimo parents (all illiterate) were myopic, 60% of the children (required to attend school) became myopic.

Studies show that other environmental factors, such as light levels (related to latitude and the absence of ultraviolet (UV) radiation), contamination, diet, and parental smoking, have been associated to the development of myopia but there is no proven causation.

Children who spend more daytime outdoors are less likely to become myopic. This was a key discussion during the 12th International Myopia Conference in Australia. Following Jones and colleagues’ first report in 2002 on the beneficial effects of outdoor exposure, others have found that it is the amount of time spent outdoors, rather than any particular physical activity as it was previously suggested, which may help retard myopia. There is consensus among myopia research groups (Orinda Longitudinal Study of Myopia, Sydney Myopia Study, and Singapore Sharable Content Object Reference Model (SCORM) study) that outdoor time is protective against myopia. The mechanism for this protective effect is unknown.

Mutti and coworkers (in 2002), the Correction of Myopia Evaluation Trial (COMET) group (in 2005), and others have found that parental myopia is a high-risk factor for myopia. Parental myopia may affect myopia with both genetic and environmental components. A theory of genetic predisposition to myopia with environmental

triggers, such as nearwork, urban life, and reduced outdoor exposure, is commonly accepted at present. For an update on molecular, structural, and functional studies in humans and animals, including twin studies; prevalence, progression, and risk factors in myopia; the influence of nearwork and outdoor activity in myopia; and therapies for myopia see the 2009 work by McBrien and coworkers.

Correction and Prevention: Clinical

Management of Myopia

Myopia may be corrected using visual optical aids such as spectacles, contact lenses, or, increasingly, refractive surgery. Correction of myopia is achieved by placing minor power (concave) lenses in front of the eye (Figure 1). The power of the lenses is measured in diopters (D) and corresponds to the inverse of the focal power of the lens. The eye care provider measures the refractive correction using objective (i.e., retinoscopy and autorefractometer) and subjective techniques to determine the lowest-power diverging lens that achieves best visual acuity. A binocular and eye health examination is required to establish the appropriate prescription.

As per the American Optometric Association guidelines, the goals for management of the patient with myopia are clear, comfortable, efficient binocular vision and good ocular health. Low levels of myopia (less than 3.00D) are not corrected in infants and toddlers as it may disappear within 2 years of age and their visual world is close anyway, that is, they can see as far as they need to. Older children or young children with higher amounts of myopia need to be corrected to allow the visual system appropriate development with clear visual input. For adolescents and adults, in general, any degree of myopia should be corrected any time the patient is adversely affected by the lack of clear distance vision; therefore, patients’ needs are taken into account when prescribing a myopic correction. Astigmatism may occur in conjunction with myopia. When the degree of myopia is different ( 2.00D) between the two eyes, the condition is called anisometropic myopia (anisomyopia). The material of choice for the eye glasses will also depend on the patient’s characteristics (e.g., polycarbonate lenses are given to children) and the degree of the myopia (e.g., high-index, thinner lenses are recommended for higher prescriptions). Contact lenses (soft or gas permeable) are typically well accepted by myopic patients as the size of the retinal image is larger than with glasses, and they avoid visual-field restrictions. Whether spectacles or contact lenses are preferable in a given case depends upon numerous factors, including patient age, motivation, compliance, corneal physiology, and financial considerations. Orthokeratology is a technique of contact lens fitting which flattens the corneal surface over time to transiently reduce myopia.

A number of options to correct myopia with refractive surgery are available. Since the approval of the use of the excimer laser in the 1990s to reshape the cornea, there has been significant development in the correction of myopia. Laser refractive surgery has surpassed other conventional surgical techniques in safety and efficacy. The suitability of refractive surgery needs to be determined on a case- to-case basis and after a thoughtful discussion between the surgeon and the patient. Current refractive surgery options include:

1.Excimer laser photorefractive keratectomy (PRK). A procedure in which the corneal power is decreased by laser ablation of the central cornea, the corneal epithelium is scraped away to allow the reshaping of the corneal stroma.

2.Laser-assisted in situ keratomileusis (LASIK). This was introduced in the mid-1990s and largely replaced PRK. Unlike PRK, a flap is made in the epithelium to permit access to the stroma. LASIK avoids most of the problems of corneal haze, postoperative pain, and slow rehabilitation seen in PRK, but complications are sometimes associated with the flap. Some studies show that LASIK surgery has predictable and stable results in refractive and visual outcomes in correcting moderate to high myopia on long-term follow-up. Refractive

stability is maintained over 7 years, with no evidence of progressive late-onset complications. Recently, an alternative mechanical, epi-LASIK technique has shown comparable effective results to LASEK.

3.Laser epithelial keratomileusis (LASEK). In this procedure, the epithelium is treated with alcohol and then peeled back to permit reshaping of the underlying layer. It avoids all flap-related complications associated with LASIK and has less postoperative pain and faster recovery than PRK.

4.Wavefront-guided (WFG), or custom LASIK. This technique is used to avoid the induced positive spherical aberration typically found after conventional LASIK procedures. It is more advantageous with large pupils (most studies of conventional LASIK have shown a relationship between the diameter of the low-light pupil and complains of visual symptoms after surgery). However, WFG LASIK has all the same risks of conventional surgery.

5.A new procedure of PRK with intraoperative use of topical mitomicym C seems to be more effective than LASIK surgery for moderate myopia.

6.A number of surgical techniques use phakic intraocular lenses implanted in the posterior chamber. These are used for the correction of high myopia.

Despite significant advances, certain limitations and complications exist in these refractive surgery procedures and patient education is essential before a decision is taken. In this rapidly changing field, co-management of patients and consultation of most recent literature are necessary.

None of these correction techniques prevents or treats the condition. A number of approaches and techniques, which are discussed below, have been advocated over the years to prevent, inhibit, and attempt to reverse myopia development.

Positive Additions for Nearwork

The underlying principle of using positive additions is to reduce the accommodative demand at near, as increased accommodative effort is thought to play a role in the development of myopia. Positive additions may be achieved with the undercorrection of spectacles which also leads to a distance undercorrection and therefore defocused images; hence, the use of bifocals and progressive lenses has been suggested. The technique is supported by animal research that has shown that wearing positive lenses induces hyperopia. However, good results on the use of positive additions may not be only dependent on reducing the magnitude of accommodation, but on other oculomotor factors as well. Results of different studies are contradictory, although some reduction in the rate of myopia progression has been found to occur. In particular, the COMET group has found that the progression of myopia slows down in myopic children who have esophoria at near and are treated with positive additions in the form of progressive addition lenses (PALs). Ongoing longitudinal studies are being undertaken in this area.

Contact Lenses

Although some studies have shown that contact lenses (especially hard contact lenses) reduce myopia progression, the mechanism of action is not well understood. However, the success of these techniques is thought to result from corneal curvature changes produced by the contact lenses, which suggests that the changes may be transient.

Vision Therapy and Biofeedback Training

Various forms of accommodative vision therapy have been advocated in the treatment of myopia. The aim of a training program is to reinforce and establish control over the accommodative response. Although there are reports that these techniques can induce a reduction in myopia, there are no masked studies with objective data supporting the usefulness of vision therapy for correcting or preventing the progression of myopia. In most published reports the quantified test was solely unaided visual acuity which improvement may be explained by an improved ability to interpret a blurred retinal image. Myopes of low degree commonly report that their vision seems poorer upon removal of their spectacles compared to that after a period without spectacle wear. This phenomenon is called blur adaptation and accounts for very small to no additive improvement in visual performance.

Rigorous research studies are needed if accommodation biofeedback is to qualify as a method of clinical treatment of myopia.

Pharmacological Treatment

The first drugs to treat the progression of myopia were chosen based on the belief that myopia could be controlled either by the relaxation of accommodation or the reduction of IOP. Hence, cycloplegic agents such as tropicamide and atropine, and adrenergic antagonistic agents have been used in the past with no success. The difficulties resulting from the regular instillation of drugs, such as inconvenience, reading problems, discomfort, pupillary mydriasis, and the possibility of other adverse reactions to the drug, in addition to the lack of clear evidence of the effectiveness of these agents, provoked abandonment of these techniques. Although none of these pharmacological agents used has demonstrated an ability to control myopic progression successfully, for the past few years new approaches to myopia control are considering the importance of muscarinic receptors in myopia development. M1 antagonist pirenzepine and atropine are the newest drugs used in the attempt to slow down the progression of myopia. Atropine is the only pharmacological agent currently studied in clinical trials. Although the site of action of these drugs is unknown, studies in chicks suggest that these drugs act on the cartilaginous sclera to transiently inhibit glycosaminoglycan synthesis and slow down myopia development. Growth factors, such as insulin-like growth factor 1 (IGF-1), basic fibroblast growth factor (bFGF), and retinoic acid have been shown to be effective at controlling ocular growth in animal models and are promising therapeutic agents for high human myopia. Future therapies to slow down the progression of myopia in humans will be directed at altering the retinal–scleral signaling cascade involved in emmetropization.

Correction and Prevention: Clinical

Management of Myopia?

In conclusion, the limited success achieved by the various methods of myopia control should not necessarily be interpreted as providing the absence of any relationship between myopia and nearwork. It is possible that once axial elongation has begun, continued visual feedback would produce additional axial elongation irrespective of any external intervention.

Further Reading

American Optometric Association (1997). Care of the Patient with Myopia, Optometric Clinical Practice Guideline. Association of Optometrists. http://www.aoa.org/myopia.xml (accessed Jun. 2009).

Charman, W. N. (2005). Aberrations and myopia. Ophthalmic and Physiological Optics 25: 285–301.

Chen, C. Y.-C. (2007). Heritability and shared environment estimates for myopia and associated ocular biometric traits: The genes in myopia (GEM) family study. Human Genetics 121: 511–520.

Curtin, B. J. (1985). The Myopias: Basic Science and Clinical Management. Philadelphia, PA: Harper and Row.

Dirani, M., Shekar, S. N., and Baird, P. N. (2008). Adult-onset myopia: The genes in myopia (GEM) twin study. Investigative Ophthalmology and Vision Science 49: 3324–3327.

Gilmartin, B. (2004). Myopia: Precedents for research in the twenty-first century. Clinical and Experimental Ophthalmology 32(3): 305–324.

Grosvenor, T. P. (1998). Clinical Management of Myopia. Boston, MA: Butterworth-Heinemann.

Gwiazda, J., Hyman, L., Dong, L. M., et al. (2007). Factors associated with high myopia after 7 years of follow-up in the Correction of Myopia Evaluation Trial (COMET) cohort. Ophthalmic Epidemiology 14(4): 230–237.

Jones, L., Sinnott, L. T., Mutti, D. O., et al. (2007). Parental history of myopia, sports and outdoor activities, and future myopia.

Investigative Ophthalmology and Vision Science 48: 3524–3532. Kurzt, D., Hyman, L., Gwiazda, J. E., et al. (2007). Role of parental

myopia in the progression of myopia and its interaction with treatment in COMET children. Investigative Ophthalmology and Vision Science 48(2): 562–570.

McBrien, N. A., Young, T. L., Pang, C. P., et al. (2009). Myopia: Recent advances in molecular studies; prevalence, progression and risk factors; emmetropization; therapies; optical links; peripheral refraction; sclera and ocular growth; signalling cascades; and animal models. Optometry and Vision Science 86(1): 45–66.

Rada, J. A. and Palmer, L. (2007). Choroidal regulation of scleral glycosaminoglycan synthesis during recovery from induced myopia.

Investigative Ophthalmology and Vision Science 48: 2957–2966. Rosenfield, M. and Gilmartin, B. (1998). Myopia and Nearwork. Oxford:

Butterworth-Heinemann.

Saw, S.-M., Gazzard, G., Au Eong, K. G., and Tan, D. T. (2002). Myopia: Attempts to arrest progression. British Journal of Ophthalmology 86: 1306–1311.

Saw, S.-M., Tong, L., Chua, W. H., et al. (2005). Incidence and progression of myopia in singaporean school children. Investigative Ophthalmology and Vision Science 46: 51–57.

Schaeffel, F., Simon, P., Feldkaemper, M., Ohngemach, S., and Williams, R. W. (2003). Molecular biology of myopia. An invited review. Clinical and Experimental Optometry 86(5): 295–307.

Wade, N. J. (1999). A Natural History Of Vision. Cambridge, MA: MIT Press.

Wallman, J. and Winawer, J. (2004). Homeostasis of eye growth and the question of myopia. Neuron 43: 447–468.

Young, T. L. (2009). Molecular genetics of human myopia: An update.

Optometry and Vision Science 86(1): E8–E22.

Relevant Website

Glossary

Anisometropia – A condition in which the two eyes have unequal refractive power so that the two eyes are in different states of myopia.

Astigmatism – An optical defect causing blurred images due to failure to focus a point object into a sharp image on the retina.

Sensitive period – An early developmental period that is particularly sensitive to development of amblyopia.

Snellen acuity – Clarity of vision as measured by eye care professionals using a chart called the Snellen chart.

Strabismus – Misregistration or misalignment of the images from the two eyes preventing the development of binocular vision.

What Is Amblyopia?

Amblyopia (from the Greek, amblyos – blunt; opia – vision) is a developmental abnormality that results from physiological alterations in the visual cortex and impairs form vision. Amblyopia is clinically important because, aside from refractive error, it is the most frequent cause of vision loss in infants and young children, occurring naturally in about 2–4% of the population; and it is of basic interest because it reflects the neural impairment which can occur when normal visual development is disrupted. The damage produced by amblyopia is generally expressed in the clinical setting as a loss of visual acuity in an apparently healthy eye, despite appropriate optical correction; however, there is a great deal of evidence showing that amblyopia results in a broad range of neural, perceptual, and clinical abnormalities. Currently, there is no positive diagnostic test for amblyopia. Instead, amblyopia is diagnosed by exclusion: in patients with conditions such as strabismus and anisometropia, a diagnosis of amblyopia is made through the exclusion of uncorrected refractive error and underlying ocular pathology. Amblyopic patients (especially those with strabismic amblyopia) often exhibit crowding problems, meaning they have better visual acuity when letters are presented in isolation than when they are presented in a line or a full chart.

Clinically, crowding may be a useful sign to aid in the diagnosis of amblyopia.

Amblyopia Is a Significant Public Health

Problem

Amblyopia can easily be reversed or eliminated when diagnosed and treated early in life. Thus, there is a premium on early detection of amblyopia and its risk factors. It has been estimated that perhaps as many as three-quarters of a million preschoolers are at risk for amblyopia in the United States, and roughly half of those may not be detected before school age. Moreover, detection is likely to be more delayed in low socioeconomic areas. Improved vision screening and access to treatment could, in principle, eliminate amblyopia as a public health issue.

Types of Amblyopia

Amblyopia comes in different sizes (degree of loss) and flavors (types). The presence of amblyopia is almost always associated with an early history of abnormal visual experience: binocular misregistration (i.e., strabismus – a turned eye), image degradation (high refractive error and astigmatism, anisometropia), or, less commonly, form deprivation (congenital cataract, ptosis). The severity of the amblyopia appears to be associated with the degree of imbalance between the two eyes (e.g., dense unilateral cataract results in severe loss), and to the age at which the amblyogenic factor occurred. Precisely how these factors interact is as yet unknown, but it is evident that different early visual experiences result in different functional losses in amblyopia, and a significant factor that distinguishes performance among amblyopes is the presence or absence of binocular function. Binocular function is much more likely to be damaged when amblyopia results from binocular misregistration (strabismus) than from image blur (anisometropia).

The Site(s) of Amblyopia

A longstanding question is the site of damage in amblyopia. Current opinion places the earliest functional physiological abnormalities in cortical area V1. Exhaustive anatomical and physiological experiments failed to find retinal alterations in monkeys reared with experimentally induced amblyopia. These same animals had marked