Myopia (Ancient Greek: μυωπία, muōpia, from myein "to shut" – ops (gen. opos) "eye"), commonly known as being nearsighted (American English) and shortsighted (British English), is a condition of the eye where the light that comes in does not directly focus on the retina but in front of it, causing the image that one sees when looking at a distant object to be out of focus, but in focus when looking at a close object.
Eye care professionals most commonly correct myopia through the use of corrective lenses, such as glasses or contact lenses. It may also be corrected by refractive surgery, though there are cases of associated side effects. The corrective lenses have a negative optical power (i.e. have a net concave effect) which compensates for the excessive positive diopters of the myopic eye. Negative diopters are generally used to describe the severity of the myopia, as this is the value of the lens to correct the eye. High-degree myopia, or severe myopia, is defined as -6 diopters or worse.
Axial myopia is attributed to an increase in the eye's axial length.
Refractive myopia is attributed to the condition of the refractive elements of the eye. Borish further subclassified refractive myopia:
Curvature myopia is attributed to excessive, or increased, curvature of one or more of the refractive surfaces of the eye, especially the cornea. In those with Cohen syndrome, myopia appears to result from high corneal and lenticular power.
Elevation of blood-glucose levels can also cause edema (swelling) of the crystalline lens as a result of sorbitol (sugar alcohol) accumulating in the lens. This edema often causes temporary myopia (nearsightedness).
Various forms of myopia have been described by their clinical appearance:
Simple myopia, more common than other types of myopia, is characterized by an eye that is too long for its optical power (which is determined by the cornea and crystalline lens) or optically too powerful for its axial length. Both genetic and environmental factors, particularly significant amounts of near work, are thought to contribute to the development of simple myopia.
Degenerative myopia, also known as malignant, pathological, or progressive myopia, is characterized by marked fundus changes, such as posterior staphyloma, and associated with a high refractive error and subnormal visual acuity after correction. This form of myopia gets progressively worse over time. Degenerative myopia has been reported as one of the main causes of visual impairment.
Nocturnal myopia, also known as night or twilight myopia, is a condition in which the eye has a greater difficulty seeing in low-illumination areas, even though its daytime vision is normal. Essentially, the eye's far point of an individual's focus varies with the level of light. Night myopia is believed to be caused by pupils dilating to let more light in, which adds aberrations, resulting in becoming more nearsighted. A stronger prescription for myopic night drivers is often needed. Younger people are more likely to be affected by night myopia than the elderly.
Index myopia is attributed to variation in the index of refraction of one or more of the ocular media. Cataracts may lead to index myopia.
Form deprivation myopia occurs when the eyesight is deprived by limited illumination and vision range, or the eye is modified with artificial lenses or deprived of clear form vision. In lower vertebrates, this kind of myopia seems to be reversible within short periods of time. Myopia is often induced this way in various animal models to study the pathogenesis and mechanism of myopia development.
Nearwork-induced transient myopia (NITM) is defined as short-term myopic far point shift immediately following a sustained near visual task. Some authors argue for a link between NITM and the development of permanent myopia.
Myopia is sometimes classified by the age at onset:
Congenital myopia, also known as infantile myopia, is present at birth and persists through infancy.
Youth onset myopia occurs in the early childhood or teenage, and the ocular power can keep varying until the age of 21, before which any form of corrective surgery is usually not recommended by ophthalmic specialists around the world.
School myopia appears during childhood, particularly the school-age years. This form of myopia is attributed to the use of the eyes for close work during the school years.
Adult onset myopia
Early adult onset myopia occurs between ages 20 and 40.
Myopia presents with blurry distance vision, but generally gives good near vision. In high myopia, even near vision is affected as objects must be extremely close to the eyes to see clearly, and patients cannot read without their glasses prescribed for distance. On fundoscopic examination of the eye, the optic nerve appears to be tilted and an area of white sclera could be seen on next to the disc with a line of hyperpigmentation separating this area from normal retina. The macula will have some retinal pigmentary changes and sometimes will have subretinal hemorrhages. The retina in myopic patients is thin and thorough evaluation of the periphery might show retinal holes and lattice degeneration. In addition, myopic patients might develop choroidal neovascularization in the macula.
Education and IQ
A number of studies have shown the incidence of myopia increases with level of education, and many studies have shown a correlation between myopia and a higher intelligence quotient (IQ).
A 2008 literature review reported studies in several nations have found a relationship between myopia and higher IQ and between myopia and school achievement. A common explanation for myopia is near-work. Regarding the relationship to IQ, several explanations have been proposed. One is that the myopic child is better adapted at reading, and reads and studies more, which increases intelligence. The reverse explanation is that the intelligent and studious child reads more, which causes myopia. Still another explanation is that pleiotropic gene(s) affect the size of both brain and eyes simultaneously. According to the two most recent studies, higher IQ may be associated with myopia in schoolchildren, independent of books read per week.
Other personal characteristics, such as value systems, school achievements, time spent in reading for pleasure, language abilities and time spent in sport activities correlated to the occurrence of myopia in studies.
Other risk factors
Heredity appears as an important factor associated with juvenile myopia, with smaller contributions from more near work, higher school achievement and less time in sports activity.
The National Institutes of Health says there is no known way of preventing myopia, and the use of glasses or contact lenses does not affect its progression. There is no universally accepted method of preventing myopia; proposed procedures have not been studied for effectiveness.
Commonly attempted preventive methods include wearing reading glasses, eye drops and participating in more outdoor activities. Some[which?] clinicians and researchers recommend plus power (convex) lenses in the form of reading glasses when engaged in close work or reading instead of using single focal concave lens glasses commonly prescribed. The reasoning behind a convex lens's possible effectiveness in preventing myopia is as follows: a convex lens's refractive property of converging light is used in reading glasses to help reduce the accommodation needed when reading and doing close work. Although accommodation is irrelevant in Medina's quantitative model of myopia, it reaches the same conclusion.
For people with presbyopia, whose eyes' lenses can not accommodate enough for very near focus, reading glasses help converge the light before it enters the eye to complement the refractive power of the eye lens, so near objects focus clearly on the retina. By reducing the focusing effort needed (accommodation), reading glasses or convex lenses essentially relax the focusing ciliary muscles and may consequently reduce chances of developing myopia. Inexpensive nonprescription reading glasses are commonly sold in drug stores and dollar stores. Alternatively, reading glasses fitted by optometrists have a wider range of styles and lens choices.
A Malaysian study reported in New Scientist suggested undercorrection of myopia caused more rapid progression of myopia. However, the reliability of these data has been called into question. Many myopia treatment studies suffer from any of a number of design drawbacks: small numbers, lack of adequate control group, failure to mask examiners from knowledge of treatments used, etc.
Pirenzepine eyedrops had a limited effect on retarding myopic progression in a recent, placebo-controlled, double-blind, prospective-controlled study.
Researchers at the University of Cambridge have found that a lack of outdoor play could be linked to myopia.
Glasses are commonly used to address near-sightedness.
Compensating for myopia using a corrective lens.
Eyeglasses, contact lenses, and refractive surgery are the primary options to treat the visual symptoms of those with myopia. Lens implants are now available offering an alternative to glasses or contact lenses for myopics for whom laser surgery is not an option. Orthokeratology is the practice of using special rigid contact lenses to flatten the cornea to reduce myopia. Occasionally, pinhole glasses are used by patients with low-level myopia. These work by reducing the blur circle formed on the retina, but their adverse effects on peripheral vision, contrast and brightness make them unsuitable in most situations.
Glasses may have the potential to make the eyes worse, as they increase the accommodation needed by the eyes to focus. Evidence of this can be seen when people with higher prescriptions have a harder time with activities like reading because their eyes grow tired faster. Stronger prescriptions require a higher accommodation by the eyes to focus through them, which can, over time, worsen eyesight, requiring yet another prescription, in a continuous but quickening cycle.Contact lenses of equivalent prescription may not result in the same effect as eyeglasses, as they are closer to the eyes and may require less accommodation.
Glasses work by using optical lenses bringing the image a viewer closer so that it can be focused by their myopic eyes. Large amounts of near work while wearing glasses can be very detrimental to the eyes and can be a cause of worsening nearsightedness. However, the eyestrain caused by not wearing glasses when they are needed can also be a risk factor. The best way to avoid needing new lenses is by reducing the amount of near work, which forces the eyes into a continuous near-focusing position that eventually causes or increases myopia, by taking frequent breaks from near work, and by only wearing glasses when they are needed.Reading glasses can also be worn during near work to decrease the strain on the eye, especially when already wearing corrective lenses, as they work in the opposite fashion to normal lenses. Using this practice may have the potential to prevent nearsightedness or slow its progression.
Prismatic color distortion shown with a camera set for nearsighted focus, and using −9.5 diopter eyeglasses to correct the camera's myopia. (left) Close-up of color shifting through corner of eyeglasses. The light and dark borders visible between color swatches do not exist. (right)
For people with a high degree of myopia, very strong eyeglass prescriptions are needed to correct the focus error. However, strong eyeglass prescriptions have a negative side effect in that off-axis viewing of objects away from the center of the lens results in prismatic movement and separation of colors, known as chromatic aberration. This prismatic distortion is visible to the wearer as color fringes around strongly contrasting colors. The fringes move around as the wearer's gaze through the lenses changes, and the prismatic shifting reverses on either side, above, and below the exact center of the lenses. Color fringing can make accurate drawing and painting difficult for users of strong eyeglass prescriptions.
Strongly nearsighted wearers of contact lenses do not experience chromatic aberration because the lens moves with the cornea and always stays centered in the middle of the wearer's gaze.
Various methods have been employed in an attempt to decrease the progression of myopia. Dr Chua Weihan and his team at National Eye Centre Singapore have conducted large scale studies on the effect of atropine of varying strength in stabilizing, and in some case, reducing myopia. The use of reading glasses when doing close work may provide success by reducing or eliminating the need to accommodate. Altering the use of eyeglasses between full-time, part-time, and not at all does not appear to alter myopia progression. The American Optometric Association's Clinical Practice Guidelines for Myopia refers to numerous studies which indicated the effectiveness of bifocal lenses and recommends it as the method for "Myopia Control". In some studies, bifocal and progressive lenses have not shown significant differences in altering the progression of myopia. More recently, robust studies on children have shown orthokeratology and centre distance bifocal contact lenses may arrest myopic development.
Scleral reinforcement surgery is aimed to cover the thinning posterior pole with a supportive material to withstand intraocular pressure and prevent further progression of the posterior staphyloma. The strain is reduced, although damage from the pathological process cannot be reversed. By stopping the progression of the disease, vision may be maintained or improved.
A systematic review of interventions performed to slow the progression of myopia in children under the age of 18 showed that anti-muscarinic topical medications were effective in slowing myopia in participants, when compared to placebo. These treatments include pirenzepine gel, cyclopentolate eye drops, and atropine eye drops. While these treatments were shown to be effective in slowing the progression of myopia, side effects included light sensitivity and near blur.
A number of alternative therapies exist including eye exercises and relaxation techniques, such as the Bates method. However, the efficacy of these practices is disputed by scientists and eye care practitioners.[unreliable source?] A 2005 review of scientific papers on the subject concluded that there was "no clear scientific evidence" that eye exercises were effective in treating myopia.
In the 1980s and 1990s, biofeedback created a flurry of interest as a possible treatment for myopia. A 1997 review of this biofeedback research concluded "controlled studies to validate such methods ... have been rare and contradictory." One study found that myopes could improve their visual acuity with biofeedback training, but that this improvement was "instrument-specific" and did not generalize to other measures or situations. In another study, an "improvement" in visual acuity was found, but the authors concluded this could be a result of subjects learning the task. Finally, in an evaluation of a training system designed to improve acuity, "no significant difference was found between the control and experimental subjects".
The global refractive errors has been estimated to affect 800 million to 2.3 billion. The incidence of myopia within sampled population often varies with age, country, sex, race, ethnicity, occupation, environment, and other factors. Variability in testing and data collection methods makes comparisons of prevalence and progression difficult.
The prevalence of myopia has been reported as high as 70–90% in some Asian countries, 30–40% in Europe and the United States, and 10–20% in Africa. Myopia is less common in African people and associated diaspora. In Americans between the ages of 12 and 54, myopia has been found to affect African Americans less than Caucasians.
In some parts of Asia, myopia is very common. Singapore is believed to have the highest prevalence of myopia in the world; up to 80% of people there have myopia, but the accurate figure is unknown.China's myopia rate is 31%: 400 million of its 1.3 billion people are myopic. The prevalence of myopia in high school in China is 77.3%, and in college is more than 80%. In some areas, such as China and Malaysia, up to 41% of the adult population is myopic to 1.00 dpt, and up to 80% to 0.5 dpt. A study of Jordanian adults aged 17 to 40 found over half (53.7%) were myopic. However, some research suggests the prevalence of myopia in India in the general population is only 6.9%.
In first-year undergraduate students in the United Kingdom found 50% of British whites and 53.4% of British Asians were myopic. In Greece, the prevalence of myopia among 15- to 18-year-old students was found to be 36.8%. A recent review found 26.6% of Western Europeans aged 40 or over have at least −1.00 diopters of myopia and 4.6% have at least −5.00 diopters.
Myopia is common in the United States, with research suggesting this condition has increased dramatically in recent decades. In 1971–1972, the National Health and Nutrition Examination Survey provided the earliest nationally representative estimates for myopia prevalence in the U.S., and found the prevalence in persons aged 12–54 was 25.0%. Using the same method, in 1999–2004, myopia prevalence was estimated to have climbed to 41.6%.
A study of 2,523 children in grades 1 to 8 (age, 5–17 years) found nearly one in 10 (9.2%) have at least − 0.75 diopters of myopia . In this study, 12.8% had at least +1.25 D hyperopia (farsightedness), and 28.4% had at least 1.00-D difference between the two principal meridians (cycloplegic autorefraction) astigmatism. For myopia, Asians had the highest prevalence (18.5%), followed by Hispanics (13.2%). Caucasian children had the lowest prevalence of myopia (4.4%), which was not significantly different from African Americans (6.6%).
A recent review found 25.4% of Americans aged 40 or over have at least −1.00 diopters of myopia and 4.5% have at least −5.00 diopters.
In Australia, the overall prevalence of myopia (worse than −0.50 diopters) has been estimated to be 17%. In one recent study, less than one in 10 (8.4%) Australian children between the ages of four and 12 were found to have myopia greater than −0.50 diopters. A recent review found 16.4% of Australians aged 40 or over have at least −1.00 diopters of myopia and 2.5% have at least −5.00 diopters.
In Brazil, a 2005 study estimated 6.4% of Brazilians between the ages of 12 and 59 had −1.00 diopter of myopia or more, compared with 2.7% of the indigenous people in northwestern Brazil. Another found nearly 1 in 8 (13.3%) of the students in the city of Natal were myopic.
Society and culture
The terms "myopia" and "myopic" (or the common terms "shortsightedness" or "shortsighted", respectively) have been used metaphorically to refer to cognitive thinking and decision making that is narrow in scope or lacking in foresight or in concern for wider interests or for longer-term consequences. It is often used to describe a decision that may be beneficial in the present, but detrimental in the future, or a viewpoint that fails to consider anything outside a very narrow and limited range. Hyperopia, the biological opposite of myopia, may also be used metaphorically for a value system or motivation that exhibits "farsighted" or possibly visionary thinking and behavior; that is, emphasizing long-term interests at the apparent expense of near-term benefit.
Normally eye development is largely genetically controlled, but it has been shown that the visual environment is an important factor in determining ocular development . Some research suggests that myopia may be inherited from one's parents.
Genetic basis for myopia
Genetically, linkage studies have identified 18 possible loci on 15 different chromosomes that are associated with myopia, but none of these loci are part of the candidate genes that cause myopia. Instead of a simple one-gene locus controlling the onset of myopia, a complex interaction of many mutated proteins acting in concert may be the cause. Instead of myopia being caused by a defect in a structural protein, defects in the control of these structural proteins might be the actual cause of myopia. A collaboration of all myopia studies worldwide, identified 16 new loci for refractive error in individuals of European ancestry, of which 8 were shared with Asians. The new loci include candidate genes with functions in neurotransmission, ion transport, retinoic acid metabolism, extracellular matrix remodeling and eye development. The carriers of the high-risk genes have a tenfold increased risk of myopia.
To induce myopia in lower as well as higher vertebrates, translucent goggles can be sutured over the eye, either before or after natural eye opening. Form-deprived myopia (FDM) induced with a diffuser, like the goggles mentioned, shows significant myopic shifts. Anatomically, the changes in axial length of the eye seem to be the major factor contributing to this type of myopia. Diurnal growth rhythms of the eye have also been shown to play a large part in FDM. Chemically, daytime retinal dopamine levels drop about 30%.
Normal eyes grow during the day and shrink during the night, but occluded eyes are shown to grow both during the day and the night. Because of this, FDM is a result of the lack of growth inhibition at night rather than the expected excessive growth during the day, when the actual light deprivation occurred. Elevated levels of retinal dopamine transporter (which is directly involved in controlling retinal dopamine levels) in the RPE have been shown to be associated with FDM.
Dopamine is a major neurotransmitter in the retina involved in signal transmission in the visual system. In the retinal inner nuclear layer, a dopaminergic neuronal network has been visualized in amacrine cells. Also, retinal dopamine is involved in the regulation of electrical coupling between horizontal cells and the retinomotor movement of photoreceptor cells. Although FDM-related elongations in axial length and drops in dopamine levels are significant, after the diffuser is removed, a complete refraction recovery is seen within four days in some laboratory mice. Although significant, what is even more intriguing is that within just two days of diffuser removal, an early rise and eventual normalization of retinal dopamine levels in the eye are seen. This suggests dopamine participates in visually guided eye growth regulation, and these fluctuations are not just a response to the FDM.
L-Dopa has been shown to re-establish circadian rhythms in animals whose circadian rhythms have been abolished. Dopamine, a major metabolite of levodopa, releases in response to light, and helps establish circadian clocks that drive daily rhythms of protein phosphorylation in photoreceptor cells. Because retinal dopamine levels are controlled on a circadian pattern, intravitreal injection of L-dopa in animals that have lost dopamine and circadian rhythms has been shown to correct these patterns, especially in heart rate, temperature, and locomotor activity. The occluders block light completely for the animals, which does not allow them to establish correct circadian rhythms, which leads to dopamine depletion. This depletion can be rectified with injections of L-dopa and hopefully contribute to the recovery from FDM.
L-Dopa metabolism is important to consider due to its extensive presystemic metabolism, rapid absorption in the proximal small intestine and short plasma half-life. The major metabolites of L-dopa are dopamine, dihydroxyphenylacetic acid, homovanillic acid, and 3-O-methyldopa and 3-methoxytyramine. Levodopa can be converted into dopamine in the presence of aromatic L-amino acid decarboxylase (L-AAAD). L-AAAD activity in rat retinas is modulated by environmental light, and this modulation is associated with dopamine D1 receptors and alpha 2 adrenoceptors. Also, the synthesis and release of dopamine are light dependent, and light accelerates the formation of dopamine from exogenous L-Dopa.
Past treatments with dopamine has been used as the gold-standard drug in the treatment of Parkinson's disease and low-dose administration of the drug has been the most effective treatment of Parkinson’s. Possible treatments involving dopamine in preventing a decrease in visual acuity have been shown to be successful in the past. L-Dopa treatment in children with amblyopia showed an improvement in visual acuity. In rabbits, injections of dopamine prevented the myopic shift and vitreous chamber and axial elongation typically associated with FDM. In guinea pigs, systemic L-dopa has been shown to inhibit the myopic shift associated with FDM, and has compensated for the drop in retinal dopamine levels. These experiments show promise in treating myopia in humans.
Side effects of L-dopa have been experimentally determined. L-Dopa and some of its metabolites have been shown to have pro-oxidant properties, and oxidative stress has been shown to increase the pathogenesis of Parkinson's disease. This promotion of free-radical formation by L-dopa does seem to directly affect its possible future treatment of myopia because free-radicals could cause further damage to those proteins responsible for controlling structural proteins in the eye. Levodopa and some of its metabolites such as dopa/dopamine quinone have also been shown to be toxic for nigral neurons. This toxic effect must be analyzed before treatment with levodopa for myopia to prevent damaging effects to these neurons.
L-Dopa inhibits myopic shifts
In guinea pigs, intraperitoneal injections of L-dopa have shown to inhibit the myopic shift associated with FDM and have compensated to the drop in retinal dopamine levels. In this study specifically, 60 animals were used and the L-dopa treatments inhibited the myopic shift (from −3.62 ± 0.98 D to −1.50 ± 0.38 D; p < 0.001) due to goggles occluding and compensated retinal dopamine (from 0.65 ± 0.10 ng to 1.33 ± 0.23 ng; p < 0.001). Daily L-dopa (10 mg/kg) was shown to increase the dopamine content in striatum. The axial length and retinal dopamine changes were positively correlated in the normal control eyes, deprived eyes, and L-dopa-treated deprived eyes. The increase in retinal dopamine and subsequent retardation of myopia may be associated with the fact that exogenous L-dopa was converted into dopamine. This suggests retinal dopaminergic function in the development of form-deprivation myopia in guinea pigs. The inhibitory effect of L-dopa on FDM may be associated with the fact that retinal L-AAAD can convert it into dopamine to balance the deficiency in the retina of the deprived eyes.
Areas of future research include intraperitoneal injection of L-dopa; its use at 10 mg/kg could not completely suppress the development of form-deprivation myopia. Perhaps the dose may be too low to completely suppress myopia. Another possibility of the incomplete suppression of myopia may be because it is a complex process, and retinal dopamine content is only one factor. It is also unclear whether systemic application of L-dopa is able to suppress the development of form-deprivation myopia.
There are two main theories for the ultimate evolutionary cause for myopia with implications in evolutionary medicine. They both stem back to mismatch theory, which is the idea that the environment to which the human body was adapted over millions of years does not match our current environment. The transition from the hunter-gatherer lifestyle to the modern Western lifestyle has facilitated the development of chronic, noninfectious diseases such as myopia. Studies of modern hunter-gatherer populations in Africa and Inuit populations in the Arctic point to environmental factors as the leading cause of myopia  In ancestral populations, myopic genes would have been strongly selected against because of the survival disadvantage they caused.
“Near work” or “Close work” hypothesis
This hypothesis, also referred to as the “use-abuse theory”  states that many aspects of our modern environment involve near work, which strains our eyes. Examples include reading and looking at pixelated screens of computers and phones for long periods of time. A majority of people in the developed world spend most, if not all, of their days doing tasks defined as “close work”, steadily building up a pressure in the eye, as the ciliary fibers that focus the eye are constantly contracting in an effort to follow words on a page. This is especially exacerbated in children whose eyes are still developing; their eyes may grow permanently elongated and myopic. This hypothesis helps elucidate why some associations between myopia, intelligence, and education were made in some studies in the 20th century. People who have more access to education likely read much more and likely score higher on intelligence tests, therefore creating a spurious association between intelligence and myopia. This spurious association further explains the social and geographical patterns and trends in rates of myopia worldwide. Some trends include Africans and people of African descent having lower rates of myopia while Asians and people of Jewish descent have higher rates of myopia, perhaps due to differential education opportunities. See: http://myopiacausedbynearwork.blogspot.com/2014/05/accommodative-hysteresis-possible-cause.html for a more recent interpretation of the effects of near work;
"Visual stimuli" hypothesis
Although not mutually exclusive with the other hypotheses presented, the visual stimuli hypothesis adds another layer of mismatch to explain the modern prevalence of myopia. There is evidence that lack of normal visual stimuli causes improper development of the eyeball. In this case, “normal” refers to the environmental stimuli that the eyeball evolved for over hundreds of millions of years. These stimuli would include diverse natural environments—the ocean, the jungle, the forest, and the savannah plains, among other dynamic visually exciting environments. Modern humans who spend most of their time indoors, in dimly or fluorescently lit buildings are not giving their eyes the appropriate stimuli to which they had evolved and may contribute to the development of myopia. Experiments where animals such as kittens and monkeys had their eyes sewn shut for long periods of time also show eyeball elongation, demonstrating that complete lack of stimuli also causes improper growth trajectories of the eyeball. Further research shows that people, and children especially, who spend more time doing physical activity and outdoor activity have lower rates of myopia, relating the increased magnitude and complexity of the visual stimuli encountered during these types of activities.
^Chen JC, Schmid KL, Brown B (2003). "The autonomic control of accommodation and implications for human myopia development: A review". Ophthalmic & physiological optics : the journal of the British College of Ophthalmic Opticians (Optometrists)23 (5): 401–422. doi:10.1046/j.1475-1313.2003.00135.x. PMID12950887.
^Cassin, B. and Solomon, S. (2001) Dictionary of Eye Terminology. Gainesville, Florida: Triad Publishing Company, ISBN 0937404632.
^Vukojević N, Sikić J, Curković T, Juratovac Z, Katusić D, Sarić B, Jukić T (2005). "Axial eye length after retinal detachment surgery". Collegium antropologicum29 (Suppl 1): 25–27. PMID16193671.
^Metge P, Donnadieu M (1993). "Myopia and cataract". La Revue du praticien (in French) 43 (14): 1784–1786. PMID8310218.
^Zhu X, Park TW, Winawer J, Wallman J (2005). "In a Matter of Minutes, the Eye Can Know Which Way to Grow". Investigative Ophthalmology and Visual Science46 (7): 2238–2241. doi:10.1167/iovs.04-0956. PMID15980206.
^Cordain L, Eaton SB, Miller JB, Lindeberg S, Jensen C (2002). "An evolutionary analysis of the aetiology and pathogenesis of juvenile-onset myopia". Acta Ophthalmologica Scandinavica80: 125–135. doi:10.1034/j.1600-0420.2002.800203.x. PMID11952477.
^Siatkowski RM, Cotter S, Miller JM, Scher CA, Crockett RS, Novack GD (2004). "Safety and efficacy of 2% pirenzepine ophthalmic gel in children with myopia: a 1-year, multicenter, double-masked, placebo-controlled parallel study". Arch Ophthalmol122 (11): 1667–74. doi:10.1001/archopht.122.11.1667. PMID15534128.
^Cho P, Cheung SW, Edwards M (2005). "The longitudinal orthokeratology research in children (LORIC) in Hong Kong: A pilot study on refractive changes and myopic control". Current eye research30 (1): 71–80. doi:10.1080/02713680590907256. PMID15875367.
^Rawstron JA, Burley CD, Elder MJ (2005). "A systematic review of the applicability and efficacy of eye exercises". J Pediatr Ophthalmol Strabismus42 (2): 82–8. PMID15825744.
^Rupolo G, Angi M, Sabbadin E, Caucci S, Pilotto E, Racano E, de Bertolini C (1997). "Treating myopia with acoustic biofeedback: A prospective study on the evolution of visual acuity and psychological distress". Psychosomatic medicine59 (3): 313–317. PMID9178342.
^ abcKempen JH, Mitchell P, Lee KE, Tielsch JM, Broman AT, Taylor HR, Ikram MK, Congdon NG, O'Colmain BJ (2004). "The prevalence of refractive errors among adults in the United States, Western Europe, and Australia". Arch. Ophthalmol.122 (4): 495–505. doi:10.1001/archopht.122.4.495. PMID15078666.
^Garcia CA, Oréfice F, Nobre GF, Souza Dde B, Rocha ML, Vianna RN (2005). "[Prevalence of refractive errors in students in Northeastern Brazil.]". Arq Bras Oftalmol (in Portuguese) 68 (3): 321–5. doi:10.1590/S0004-27492005000300009. PMID16059562.
^Jacobi FK, Pusch CM (2010). "A decade in search of myopia genes". Frontiers in bioscience : a journal and virtual library15: 359–372. doi:10.2741/3625. PMID20036825.
^Verhoeven VJ, Hysi PG, Wojciechowski R, Fan Q, Guggenheim JA, Höhn R, MacGregor S, Hewitt AW, Nag A, Cheng CY, Yonova-Doing E, Zhou X, Ikram MK, Buitendijk GH, McMahon G, Kemp JP, Pourcain BS, Simpson CL, Mäkelä KM, Lehtimäki T, Kähönen M, Paterson AD, Hosseini SM, Wong HS, Xu L, Jonas JB, Pärssinen O, Wedenoja J, Yip SP, Ho DW, Pang CP, Chen LJ, Burdon KP, Craig JE, Klein BE, Klein R, Haller T, Metspalu A, Khor CC, Tai ES, Aung T, Vithana E, Tay WT, Barathi VA, Chen P, Li R, Liao J, Zheng Y, Ong RT, Döring A, Evans DM, Timpson NJ, Verkerk AJ, Meitinger T, Raitakari O, Hawthorne F, Spector TD, Karssen LC, Pirastu M, Murgia F, Ang W, Mishra A, Montgomery GW, Pennell CE, Cumberland PM, Cotlarciuc I, Mitchell P, Wang JJ, Schache M, Janmahasatian S, Janmahasathian S, Igo RP, Lass JH, Chew E, Iyengar SK, Gorgels TG, Rudan I, Hayward C, Wright AF, Polasek O, Vatavuk Z, Wilson JF, Fleck B, Zeller T, Mirshahi A, Müller C, Uitterlinden AG, Rivadeneira F, Vingerling JR, Hofman A, Oostra BA, Amin N, Bergen AA, Teo YY, Rahi JS, Vitart V, Williams C, Baird PN, Wong TY, Oexle K, Pfeiffer N, Mackey DA, Young TL, van Duijn CM, Saw SM, Bailey-Wilson JE, Stambolian D, Klaver CC, Hammond CJ (2013). "Genome-wide meta-analyses of multiancestry cohorts identify multiple new susceptibility loci for refractive error and myopia". Nature Genetics45 (3): 314–318. doi:10.1038/ng.2554. PMC3740568. PMID23396134.
^Ji FT, Li Q, Zhu YL, Jiang LQ, Zhou XT, Pan MZ, Qu J (2009). "Form deprivation myopia in C57BL/6 mice". Chinese journal of ophthalmology45 (11): 1020–1026. PMID20137422.
^Tejedor J, de la Villa P (2003). "Refractive changes induced by form deprivation in the mouse eye". Investigative ophthalmology & visual science44 (1): 32–36. doi:10.1167/iovs.01-1171. PMID12506052.
^ abBoulamery A, Simon N, Vidal J, Bruguerolle B (2010). "Effects of L-Dopa on Circadian Rhythms of 6-Ohda Striatal Lesioned Rats: A Radiotelemetric Study". Chronobiology International27 (2): 251–264. doi:10.3109/07420521003664213. PMID20370468.
^Weiss S, Schaeffel F (1993). "Diurnal growth rhythms in the chicken eye: Relation to myopia development and retinal dopamine levels". Journal of comparative physiology. A, Sensory, neural, and behavioral physiology172 (3): 263–270. doi:10.1007/BF00216608. PMID8510054.
^Xi X, Chu R, Zhou X, Lu Y, Liu X (2002). "Retinal dopamine transporter in experimental myopia". Chinese medical journal115 (7): 1027–1030. PMID12150736.
^McMahon DG, Brown DR (1994). "Modulation of gap-junction channel gating at zebrafish retinal electrical synapses". Journal of neurophysiology72 (5): 2257–2268. PMID7533830.
^Pendrak K, Nguyen T, Lin T, Capehart C, Zhu X, Stone RA (1997). "Retinal dopamine in the recovery from experimental myopia". Current eye research16 (2): 152–157. doi:10.1076/ceyr.220.127.116.1190. PMID9068946.
^Fernandez N, Garcia JJ, Diez MJ, Sahagun AM, Díez R, Sierra M (2010). "Effects of dietary factors on levodopa pharmacokinetics". Expert Opinion on Drug Metabolism & Toxicology6 (5): 633–642. doi:10.1517/17425251003674364. PMID20384552.
^O'Malley KL, Harmon S, Moffat M, Uhland-Smith A, Wong S (1995). "The human aromatic L-amino acid decarboxylase gene can be alternatively spliced to generate unique protein isoforms". Journal of neurochemistry65 (6): 2409–2416. doi:10.1046/j.1471-4159.1995.65062409.x. PMID7595534.
^Hadjiconstantinou M, Rossetti Z, Silvia C, Krajnc D, Neff NH (1988). "Aromatic L-amino acid decarboxylase activity of the rat retina is modulated in vivo by environmental light". Journal of neurochemistry51 (5): 1560–1564. doi:10.1111/j.1471-4159.1988.tb01125.x. PMID3139836.
^Rossetti ZL, Silvia CP, Krajnc D, Neff NH, Hadjiconstantinou M (1990). "Aromatic L-amino acid decarboxylase is modulated by D1 dopamine receptors in rat retina". Journal of neurochemistry54 (3): 787–791. doi:10.1111/j.1471-4159.1990.tb02320.x. PMID2137529.
^Leguire LE, Komaromy KL, Nairus TM, Rogers GL (2002). "Long-term follow-up of L-dopa treatment in children with amblyopia". Journal of pediatric ophthalmology and strabismus39 (6): 326–330; quiz 330–6. PMID12458842.
^Gao Q, Liu Q, Ma P, Zhong X, Wu J, Ge J (2006). "Effects of direct intravitreal dopamine injections on the development of lid-suture induced myopia in rabbits". Graefe's Archive for Clinical and Experimental Ophthalmology244 (10): 1329–1335. doi:10.1007/s00417-006-0254-1. PMID16550409.
^Martignoni E, Blandini F, Godi L, Desideri S, Pacchetti C, Mancini F, Nappi G (1999). "Peripheral markers of oxidative stress in Parkinson's disease. The role of L-DOPA". Free radical biology & medicine27 (3–4): 428–437. doi:10.1016/S0891-5849(99)00075-1. PMID10468218.
^Hattoria N, Wanga M, Taka H, Fujimura T, Yoritaka A, Kubo S, Mochizuki H (2009). "Toxic effects of dopamine metabolism in Parkinson's disease". Parkinsonism & Related Disorders15: S35–S38. doi:10.1016/S1353-8020(09)70010-0. PMID19131041.
^Holm, S. (1937) The ocular refraction state of the Palaeo-Negroids in Gabon, French Equatorial Africa. Acta Ophthalmology 13(suppl.): 1-299.
^Young, F.A., et al. (1969). The transmission of refractive errors within Eskimo families. American Journal of Optometry and Archives of the American Academy of Optometry 46: 676-85.
^ abAngle, John, and David A. Wissman (1980). Epidemiology of Myopia. American Journal of Epidemiology 111: 220-228.
^ abcdLieberman, Daniel E. The Story of the Human Body: Evolution, Health, and Disease. New York: Pantheon Books, 2013. Print
^Shaw, Seang-Mei (2001). Nearwork in early-onset myopia. Investigative Ophthalmology and Visual Science. 43: 332-339.
^Nadell, M.C., and M.J. Hirsch (1958). The relationship between intelligence and the refractive state in a selected high school sample. American Journal of Optometry and Archives of AMerican Academy of Optometry 35: 321-326.
^Ebenholtz, SM,Citek, K (1995). Absence of adaptive plasticity after voluntary vergence and accommodation. Vision Research. 35: 2773-2783.
^Ebenholtz, SM (1991). Accommodative Hysteresis: Fundamental Asymmetry in Decay Rate After Near and Far Focusing. Investigative Ophthalmology & Visual Science.32: 148-153.
^Smith III, E.L., G.W. Maguire, and J.T. Watson (1980). Axial lengths and refractive errors in kittens reared with an optically induced anisometropia. Investigate Ophthalmology and Vision Science 19: 1250-55.
^Hubel D., T.N. Weisel (1985). Myopia and eye enlargement after neonatal lid fusion in monkeys. Nature 266: 485-88.
^Dirani, M., et al. (2009). Outdoor activity and myopia in Singapore teenage children. British Journal of Ophthalmology 93: 997-1000.
^Rose, K.A., et al. (2008). Outdoor activity reduces the prevalence of myopia in children. Ophthalmology 115: 1279-85.