Amblyopia, otherwise known as lazy eye,[1] is a disorder of the visual system that is characterized by poor or indistinct vision in an eye that is otherwise physically normal, or out of proportion to associated structural abnormalities. It has been estimated to affect 1–5% of the population.[2]
The problem is caused by either no transmission or poor transmission of the visual stimulation through the optic nerve to the brain for a sustained period of dysfunction or during early childhood thus resulting in poor or dim vision. Amblyopia normally only affects one eye, but it is possible to be amblyopic in both eyes if both are similarly deprived of a good, clear visual image. Detecting the condition in early childhood increases the chance of successful treatment.
While the colloquialism "lazy eye" is frequently used to refer to amblyopia, the term is inaccurate because there is no "laziness" of either the eye or the amblyope involved in the condition. "Lazy brain" is a more accurate term to describe amblyopia. The term "lazy eye" is imprecise because it is also a layman's term for strabismus, particularly exotropia.[citation needed]
Physiology
Amblyopia is a developmental problem in the brain, not an organic problem in the eye (although organic problems can induce amblyopia which persist after the organic problem has resolved).[3] The part of the brain corresponding to the visual system from the affected eye is not stimulated properly, and develops abnormally. This has been confirmed via direct brain examination. David H. Hubel and Torsten Wiesel won the Nobel Prize in Physiology or Medicine in 1981 for their work demonstrating the irreversible damage to ocular dominance columns produced in kittens by sufficient visual deprivation during the so-called "critical period". The maximum critical period in humans is from birth to two years old.[4]
Symptoms
Many people with amblyopia, especially those who are only mildly so, are not even aware they have the condition until tested at older ages, since the vision in their stronger eye is normal. However, people who have severe amblyopia may experience associated visual disorders, most notably poor depth perception. Amblyopes may suffer from poor spatial acuity, low sensitivity to contrast and some "higher-level" deficits to vision such as reduced sensitivity to motion.[5] These deficits are usually specific to the amblyopic eye. Amblyopes also suffer from problems of binocular vision such as limited stereoscopic depth perception and usually have difficulty seeing the three-dimensional images in hidden stereoscopic displays such as autostereograms.[6] However perception of depth from monocular cues such as size, perspective, and motion parallax is normal.
Types
Amblyopia can be caused by deprivation of vision early in life by vision-obstructing disorders such as congenital cataracts, by strabismus (misaligned eyes), or by anisometropia (different degrees of myopia or hypermetropia in each eye).
Strabismic amblyopia
Strabismus, sometimes erroneously also called lazy eye, is a condition in which the eyes are misaligned. Strabismus usually results in normal vision in the preferred sighting (or "fellow") eye, but may cause abnormal vision in the deviating or strabismic eye due to the discrepancy between the images projecting to the brain from the two eyes.[7] Adult-onset strabismus usually causes double vision (diplopia), since the two eyes are not fixated on the same object. Children's brains, however, are more neuroplastic, and therefore can more easily adapt by suppressing images from one of the eyes, eliminating the double vision. This plastic response of the brain, however, interrupts the brain's normal development, resulting in the amblyopia. Strabismic amblyopia is treated by clarifying the visual image with glasses, and/or encouraging use of the amblyopic eye with an eyepatch over the dominant eye or pharmacologic penalization of it. Penalization usually consists of applying atropine drops to temporarily dilate the pupil, which leads to blurring of vision in the good eye. This helps to prevent the bullying and teasing associated with wearing a patch, although application of the eyedrops is more challenging. The ocular alignment itself may be treated with surgical or non-surgical methods, depending on the type and severity of the strabismus.[8]
Refractive or anisometropic amblyopia
Refractive amblyopia may result from anisometropia (unequal refractive error between the two eyes). Anisometropia exists when there is a difference in the refraction between the two eyes. The eye which provides the brain with a clearer image (closer to 20/20) typically becomes the dominant eye. The image in the other eye is blurred, which results in abnormal development of one half of the visual system. Refractive amblyopia is usually less severe than strabismic amblyopia and is commonly missed by primary care physicians because of its less dramatic appearance and lack of obvious physical manifestation, such as with strabismus.[9] Frequently, amblyopia is associated with a combination of anisometropia and strabismus.
Amblyopia in those that maintain binocular functions can be treated successfully up to a later age than those with strabismic amblyopia.
Pure refractive amblyopia is treated by correcting the refractive error early with prescription lenses and patching or penalizing the good eye.
Meridional amblyopia is a mild condition in which lines are seen less clearly at some orientations than others after full refractive correction. An individual who had an astigmatism at a young age that was not corrected by glasses will later have astigmatism that cannot be optically corrected.[citation needed]
Form-deprivation and occlusion amblyopia
Form-deprivation amblyopia (Amblyopia ex anopsia) results when the ocular media become opaque, such as is the case with cataracts or corneal scarring from forceps injuries during birth.[10] These opacities prevent adequate visual input from reaching the eye, and therefore disrupt development. If not treated in a timely fashion, amblyopia may persist even after the cause of the opacity is removed. Sometimes, drooping of the eyelid (ptosis) or some other problem causes the upper eyelid to physically occlude a child's vision, which may cause amblyopia quickly. Occlusion amblyopia may be a complication of a hemangioma that blocks some or all of the eye.
Treatment and prognosis
Treatments
Treatment of strabismic or anisometropic amblyopia consists of correcting the optical deficit and forcing use of the amblyopic eye, either by patching the good eye, or by instilling topical atropine in the eye with better vision. One should also be wary of over-patching or over-penalizing the good eye when treating for amblyopia, as this can create so-called "reverse amblyopia" in the other eye.[8][11]
Treatment of individuals age 9 through adult is possible through applied perceptual learning [12][13]
Form deprivation amblyopia is treated by removing the opacity as soon as possible followed by patching or penalizing the good eye to encourage use of the amblyopic eye.[8]
Clinical trials and experiments
Although the best outcome is achieved if treatment is started before age 5, research has shown that children older than age 10 and some adults can show improvement in the affected eye. Children from 7 to 12 who wore an eye patch and performed near point activities (vision therapy) were four times as likely to show a two line improvement on a standard 11 line eye chart than amblyopic children who did not receive treatment. Adolescents aged 13 to 17 showed improvement as well, albeit in smaller amounts than younger children. It is uncertain whether such improvements are only temporary, however, particularly if treatment is discontinued. [8][14]
Vision therapy programs are occasionally partially effective on motivated adults, at least in the short term.[15]
A recent study,[16] widely reported in the popular press,[17] has suggested that repetitive transcranial magnetic stimulation may temporarily improve contrast sensitivity and spatial resolution in the affected eye of amblyopic adults. These results await verification by other researchers.
Virtual reality computer games where each eye receives different signals of the virtual world that the player's brain must combine in order to successfully play the game have shown some promise in improving both monocularity in the affected eye as well as binocularity.[18] In at least one case, it has been reported that a video game (Nintendo's Mario Kart) has been successfully used to treat the disorder.[19]
References
1. ^ American Academy of Family Physicians (2007). "Information from your family doctor. Amblyopia ("lazy eye") in your child". American family physician 75 (3): 368. PMID 17304868.
2. ^ Weber, JL; Wood, Joanne (2005). "Amblyopia: Prevalence, Natural History, Functional Effects and Treatment" ([dead link] – Scholar search). Clinical and Experimental Optometry 88 (6): 365–375. doi:10.1111/j.1444-0938.2005.tb05102.x. PMID 16329744. http://www.optometrists.asn.au/gui/files/ceo886365.pdf.
3. ^ McKee, SP., Levi, DM., Movshon, JA. (2003). "The pattern of visual deficits in amblyopia" (PDF). J Vision 4 (5): 380–405. doi:10.1167/3.5.5. PMID 12875634. http://journalofvision.org/3/5/5/McKee-2003-jov-3-5-5.pdf.
4. ^ Jeffrey Cooper & Rachel Cooper. "All About Strabismus". Optometrists Network. http://www.strabismus.org/detection_diagnosis.html. Retrieved 2008-03-09.
5. ^ Hess, R.F., Mansouri, B., Dakin, S.C., & Allen, H.A. (2006). "Integration of local motion is normal in amblyopia". J Opt Soc Am a Opt Image Sci Vis 23 (5): 986–992. doi:10.1364/JOSAA.23.000986. PMID 16642175.
6. ^ Tyler, C.W. (2004). Binocular Vision In, Duane's Foundations of Clinical Ophthalmology. Vol. 2, Tasman W., Jaeger E.A. (Eds.), J.B. Lippincott Co.: Philadelphia.
7. ^ Levi, D.M. (2006). "Visual processing in amblyopia: human studies". Strabismus 14 (1): 11–19. doi:10.1080/09273970500536243. PMID 16513566.
8. ^ a b c d Holmes, Repka, Kraker & Clarke (2006). "The treatment of amblyopia". Strabismus 15 (1): 37–42. doi:10.1080/09273970500536227. PMID 16513568.
9. ^ "Commonly Missed Diagnoses in the Childhood Eye Examination". American Family Physician. August 15, 2001. http://www.aafp.org/afp/20010815/623.html.
10. ^ Angell et al.; Robb, RM; Berson, FG (1981). "Visual prognosis in patients with ruptures in Descemet's membrane due to forceps injuries". Arch Ophthalmol 99 (12): 2137. doi:10.1001/archopht.99.12.2137 (inactive 2010-01-05). PMID 7305711. http://archopht.ama-assn.org/cgi/content/abstract/99/12/2137.
11. ^ Amblyopia NEI Health Information
12. ^ Zhou, Y,et. al. (2005). ""Perceptual Learning Improves Contrast Sensitivity and Visual Acuity in Adults with Anisometropic Amblyopia"". Vision Research.
13. ^ Polat, U, et. al. (2004). ""Improving Vision in Adult Amblyopia by Perceptual Learning"". PNAS: 6692.
14. ^ Pediatric Eye Disease Investigator Group (2005). "Randomized trial of treatment of amblyopia in children aged 7 to 17 years". Archives of Ophthalmology 123 (April): 437–447. doi:10.1001/archopht.123.4.437. PMID 15824215.
15. ^ Treatment of Amblyopia (Lazy Eye)
16. ^ Benjamin Thompson, Behzad Mansouri, Lisa Koski, and Robert F. Hess (2008). "Brain Plasticity in the Adult: Modulation of Function in Amblyopia with rTMS". Current Biology 18 (14): 1067–1071. doi:10.1016/j.cub.2008.06.052. PMID 18635353. http://www.current-biology.com/content/article/abstract?uid=PIIS0960982208008087.
17. ^ National Public Radio. "Magnetic Pulses To Brain Help 'Lazy Eye'". http://www.npr.org/templates/story/story.php?storyId=92965339.
18. ^ BBC News: Video games tackle 'lazy eye'
19. ^ Destructoid: Mario Kart Saved Child's Eyesight
5. Polat U, Ma-Naim T, Belkin M, Sagi D. Improving vision in adult amblyopia by perceptual learning. PNAS. 2004 Apr 27;101(17):6692-7. Epub 2004 Apr 19.
2-Diplopia
Diplopia, commonly known as double vision, is the simultaneous perception of two images of a single object. These images may be displaced horizontally, vertically, or diagonally (i.e. both vertically and horizontally) in relation to each other.[1]
Causes
Diplopia has a diverse range of ophthalmologic, infectious, autoimmune, neurological, and neoplastic causes. A key pathological emphasis should be placed upon the Trochlear nerve (fourth cranial nerve) which causes weakness of the superior oblique muscle, resulting in a downward and inward gazing of the eyes.[citation needed]
• Trauma
• Multiple sclerosis
• Botulism
• Guillain-Barré syndrome
• Brain tumor
• Sinusitis
• Abscess
• Wernicke's syndrome
• Graves disease
• Orbital myositis
• Myasthenia gravis[1]
• Antimetropia
Binocular diplopia
Binocular diplopia is double vision arising as a result of the misalignment of the two eyes relative to each other, such as occurs in esotropia or exotropia. In such a case while the fovea of one eye is directed at the object of regard, the fovea of the other is directed elsewhere, and the image of the object of regard falls on an extra-foveal area of the retina.
The brain calculates the 'visual direction' of an object based upon the position of its image relative to the fovea. Images falling on the fovea are seen as being directly ahead, while those falling on retina outside the fovea may be seen as above, below, right or left of straight ahead depending upon the area of retina stimulated. Thus, when the eyes are misaligned, the brain will perceive two images of one target object, as the target object simultaneously stimulates different, non-corresponding, retinal areas in either eye, thus producing double vision.
This correlation of particular areas of the retina in one eye with the same areas in the other is known as retinal correspondence. This relationship also gives rise to an associated phenomenon of binocular diplopia, although one that is rarely noted by those experiencing diplopia: Because the fovea of one eye corresponds to the fovea of the other, images falling on the two foveas are 'projected' to the same point in space. Thus, when the eyes are misaligned, the brain will 'project' two different images in the same visual direction. This phenomenon is known as 'Confusion'.
The brain naturally guards against double vision. In an attempt to avoid double vision, the brain can sometimes ignore the image from one eye; a process known as suppression. The ability to suppress is to be found particularly in childhood when the brain is still developing. Thus, those with childhood strabismus almost never complain of diplopia while adults who develop strabismus almost always do. While this ability to suppress might seem a wholly positive adaptation to strabismus, in the developing child this can prevent the proper development of vision in the affected eye resulting in amblyopia. Some adults are also able to suppress their diplopia, but their suppression is rarely as deep or as effective and takes longer to establish. They are not at risk of permanently damaging their vision as a result though. It can appear sometimes, therefore, that diplopia disappears without medical intervention. However, in some cases the cause of the double vision may still be present.
Monocular diplopia
More rarely, diplopia can also occur when viewing with only one eye; this is called monocular diplopia, or, where the patient perceives more than two images, monocular polyopia. In this case, the differential diagnosis of multiple image perception includes the consideration of such conditions as corneal surface keratoconus, a structural defect within the eye, a lesion in the anterior visual cortex (rarely cause diplopia, more commonly polyopia or palinopsia) or non-organic conditions. Also, sub-luxation of the lens.
Temporary diplopia
Temporary diplopia can be caused by alcohol intoxication or head injuries, such as concussion. If temporary double vision does not resolve quickly, one should see an ophthalmologist immediately. It can also be a side effect of the anti-epileptic drugs Phenytoin and Zonisamide, and the anti-convulsant drug Lamotrigine, as well as the hypnotic drug Zolpidem and the dissociative drugs Ketamine and Dextromethorphan. Temporary diplopia can also be caused by tired and/or strained eye muscles, or by one crossing their own eyes at will. If diplopia appears with other symptoms such as fatigue and acute or chronic pain, the patient should see a doctor immediately.
Treatment for binocular diplopia
The appropriate treatment for binocular diplopia will depend upon the cause of the condition producing the symptoms. Efforts must first be made to identify and treat the underlying cause of the problem. Treatment options include prism lenses, vision therapy, surgery, and botulinum toxin. On occasions, in certain conditions such as the oculomotor nerve palsy for example, it may be necessary to occlude one eye either temporarily or permanently. Daily wear of prism lenses is a passive compensatory treatment. Vision therapy is an active treatment which retrains the visual and vestibular systems (brain, eye muscles, and body). Vision therapy may eliminate the need for daily wear of prism lenses but is only suitable for a minority of those with diplopic symptoms.
Voluntary diplopia
Some people are able to consciously uncouple their eyes, inducing double vision on purpose. These people do not consider their double vision dangerous or harmful, and may even consider it enjoyable. It makes viewing stereograms possible. It is a skill actively developed by pilots of Apache helicopters.[2]
References
1. ^ http://www.merck.com/mmpe/sec09/ch098/ch098e.html
• ^ Cassin, B. & Solomon, S. (1990) Dictionary of Eye Terminology. Gainesville, Florida: Triad Publishing Company
3-Myopia
Those with myopia see near objects clearly but far away objects appear blurred. With myopia, the eyeball is too long, or the cornea is too steep, so images are focused in the vitreous inside the eye rather than on the retina at the back of the eye. The opposite defect of myopia is hyperopia or "farsightedness" or "long-sightedness"—this is where the cornea is too flat or the eye is too small.
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, but this does have many risks and side effects. The corrective lenses have a negative optical power (i.e. are concave) which compensates for the excessive positive diopters of the myopic eye.
Alternative ideas and methods of treatment exist, most notably the claim that myopia is caused by excessive near sight work.[citation needed]
Classification
By cause
Borish and Duke-Elder classified myopia by cause:[3][4]
• Axial myopia is attributed to an increase in the eye's axial length.[5]
• Refractive myopia is attributed to the condition of the refractive elements of the eye.[5] Borish further subclassified refractive myopia:[3]
• Curvature myopia is attributed to excessive, or increased, curvature of one or more of the refractive surfaces of the eye, especially the cornea.[5] In those with Cohen syndrome, myopia appears to result from high corneal and lenticular power.[6]
• Index myopia is attributed to variation in the index of refraction of one or more of the ocular media.[5]
Elevation of blood-glucose levels can also cause edema (swelling) of the crystalline lens (hyperphacosorbitomyopicosis) as a result of sorbitol (sugar alcohol) accumulating in the lens. This edema often causes temporary myopia (nearsightedness). A common sign of hyperphacosorbitomyopicosis is blurring of distance vision while near vision remains adequate.[citation needed]
Clinical entity
Various forms of myopia have been described by their clinical appearance:[4][7]
• Simple myopia is more common than other types of myopia and 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.[8] Both genetic and environmental factors, particularly significant amounts of near work, are thought to contribute to the development of simple myopia.[8]
• 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.[5] This form of myopia gets progressively worse over time. Degenerative myopia has been reported as one of the main causes of visual impairment.[9]
• Nocturnal myopia, also known as night myopia 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.[10][11]
• Pseudomyopia is the blurring of distance vision brought about by spasm of the ciliary muscle.[12]
• Induced myopia, also known as acquired myopia, results from exposure to various pharmaceuticals, increases in glucose levels, nuclear sclerosis, oxygen toxicity (e.g., from diving or from oxygen and hyperbaric therapy) or other anomalous conditions.[8] The encircling bands used in the repair of retinal detachments may induce myopia by increasing the axial length of the eye.[13]
• Index myopia is attributed to variation in the index of refraction of one or more of the ocular media.[5] Cataracts may lead to index myopia.[14]
• Form deprivation myopia is a type of myopia that occurs when the eyesight is deprived by limited illumination and vision range,[15] or the eye is modified with artificial lenses[16] or deprived of clear form vision.[17][18] In lower vertebrates this kind of myopia seems to be reversible within short periods of time.[18] Myopia is often induced this way in various animal models to study the pathogenesis and mechanism of myopia development.[18]
• Nearwork Induced Transient Myopia (NITM), is defined as short-term myopic far point shift immediately following a sustained near visual task.[19] Some authors argue for a link between NITM and the development of permanent myopia.[20]
Degree
Myopia, which is measured in diopters by the strength or optical power of a corrective lens that focuses distant images on the retina, has also been classified by degree or severity:[2]
• Low myopia usually describes myopia of −3.00 diopters or less (i.e. closer to 0.00).[5]
• Medium myopia usually describes myopia between −3.00 and −6.00 diopters.[5] Those with moderate amounts of myopia are more likely to have pigment dispersion syndrome or pigmentary glaucoma.[21]
• High myopia usually describes myopia of −6.00 or more.[5] People with high myopia are more likely to have retinal detachments[22] and primary open angle glaucoma.[23] They are also more likely to experience floaters, shadow-like shapes which appear singly or in clusters in the field of vision.[24] Roughly 30% of myopes have high myopia.[25]
Age at onset
Myopia is sometimes classified by the age at onset:[2]
• Congenital myopia, also known as infantile myopia, is present at birth and persists through infancy.[8]
• Youth onset myopia occurs prior to age 20.[8]
• School myopia appears during childhood, particularly the school-age years.[26] This form of myopia is attributed to the use of the eyes for close work during the school years.[5]
• Adult onset myopia
• Early adult onset myopia occurs between ages 20 and 40.[8]
• Late adult onset myopia occurs after age 40.[8]
Signs and symptoms
Myopia presents with blurry distance vision but good near vision.
Cause
Because in the most common, "simple" myopia, the eye length is too long, any etiologic explanation must account for such axial elongation. To date, no single theory has been able to satisfactorily explain this elongation.
In the mid-1900s, mainstream ophthalmologists and optometrists believed myopia to be primarily hereditary; the influence of near work in its development seemed "incidental" and the increased prevalence of the condition with increasing age was viewed as a "statistical curiosity".[3][4][27]
Among mainstream researchers and eye care professionals, myopia is now thought to be a combination of genetic and environmental factors.[8][26][28]
There are currently two basic mechanisms believed to cause myopia: form deprivation (also known as pattern deprivation[29]) and optical defocus.[30] Form deprivation occurs when the image quality on the retina is reduced; optical defocus occurs when light focuses in front of or behind the retina. Numerous experiments with animals have shown that myopia can be artificially generated by inducing either of these conditions. In animal models wearing negative spectacle lenses, axial myopia has been shown to occur as the eye elongates to compensate for optical defocus.[30] The exact physiological mechanism of this image-controlled elongation of the eye is still unknown, but the mechanism has been described quantitatively with mathematical precision.[28][31][32] It has been suggested that accommodative lag leads to blur (i.e. optical defocus) which in turn stimulates axial elongation and myopia.[33]
Theories
• Combination of genetic and environmental factors—In China, myopia is more common in those with higher education background[34] and some studies suggest that near work may exacerbate a genetic predisposition to develop myopia.[35] Other studies have shown that near work (reading, computer games) may not be associated with myopic progression, however.[36][not in citation given] A "genetic susceptibility" to environmental factors has been postulated as one explanation for the varying degrees of myopia among individuals or populations,[37] but there exists some difference of opinion as to whether it exists.[26][38] High heritability simply means that most of the variation in a particular population at a particular time is due to genetic differences. If the environment changes—as, for example, it has by the introduction of televisions and computers—the incidence of myopia can change as a result, even though heritability remains high. From a slightly different point of view it could be concluded that—determined by heritage—some people are at a higher risk to develop myopia when exposed to modern environmental conditions with a lot of extensive near work like reading. In other words, it is often not the myopia itself which is inherited, but the reaction to specific environmental conditions—and this reaction can be the onset and the progression of myopia. Medina showed that myopia is a feedback process where genetic and environmental factors can coexist.[31]
• Genetic factors—The wide variability of the prevalence of myopia in different ethnic groups has been reported as additional evidence supporting the role of genetics in the development of myopia.[39] Measures of the heritability of myopia have yielded figures as high as 89%, and recent research has identified genes that may be responsible: defective versions of the PAX6 gene seem to be associated with myopia in twin studies.[40] Under this theory, the eye is slightly elongated front to back as a result of faults during development, causing images to be focused in front of the retina rather than directly on it. It is usually discovered during the pre-teen years between eight and twelve years of age. It most often worsens gradually as the eye grows during adolescence and then levels off as a person reaches adulthood. Genetic factors can work in various biochemical ways to cause myopia, a weak or degraded connective tissue is a very essential one. Genetic factors include an inherited, increased susceptibility for environmental influences like excessive near work, and the fact that some people do not develop myopia in spite of very adverse conditions is a clear indication that heredity is involved somehow in any case.
• Environmental factors—It has been suggested that a genetic susceptibility to myopia does not exist.[26] A high heritability of myopia (as for any other condition) does not mean that environmental factors and lifestyle have no effect on the development of the condition. Some recommend a variety of eye exercises to strengthen the ciliary muscle. Other theories suggest that the eyes become strained by the constant extra work involved in "nearwork" and get stuck in the near position, and eye exercises can help loosen the muscles up thereby freeing it for far vision. These primarily mechanical models appear to be in contrast to research results, which show that the myopic elongation of the eye can be caused by the image quality, with biochemical processes as the actuator. Common to both views is, however, that extensive near work and corresponding accommodation can be essential for the onset and the progression of myopia.
One Austrian study confirmed that the axial length of the eye does mildly increase while reading, but attributed this elongation due to contraction of the ciliary muscle during accommodation (the process by which the eye increases optical power to maintain a clear image focus), not "squeezing" of the extraocular muscles.[41]
Near work and nightlight exposure in childhood have been hypothesized as environmental risk factors for myopia.[42] Although one initial study indicated a strong association between myopia and nightlight exposure,[43] recent research has found none.[42][44][45][46]
• Near work. Near work has been implicated as a contributing factor to myopia in some studies, but refuted in others.[36] One recent study suggested that students exposed to extensive "near work" may be at a higher risk of developing myopia, whereas extended breaks from near work during summer or winter vacations may retard myopic progression.[47] Near work in certain cultures (e.g. Vanuatu) does not result in greater myopia[48][49][50] It has been hypothesized that this outcome may be a result of genetics or environmental factors such as diet or over-illumination, changes which seem to occur in Asian, Vanuatu and Inuit cultures acclimating to intensive early studies.[50]
• Time spent indoors – A number of studies have shown that children who spend more time outdoors have lower rates of myopia, possibly explaining the observed increase in myopia. It is theorized that the higher brightness or the larger distances outdoors play a role.[51]
• Diet and nutrition – One 2002 article suggested that myopia may be caused by over-consumption of bread in childhood, or in general by diets too rich in carbohydrates, which can lead to chronic hyperinsulinemia. Various other components of the diet, however, were made responsible for contributing to myopia as well, as summarized in a documentation.
• Stress has been postulated as a factor in the development of myopia.[52]
• The periods of eyelid closure during excess sleeping is another possible cause of myopia.[53]
Research
• A Turkish study found that accommodative convergence, rather than accommodation, may be a factor in the onset and progression of myopia in adults.[54]
• A recent Polish study revealed that "with-the-rule astigmatism" may lead to the creation of myopia.[55]
Benefits
Many people with myopia are able to read comfortably without eyeglasses even in advanced age. Myopes considering refractive surgery are advised that this may be a disadvantage after the age of 40 when the eyes become presbyopic and lose their ability to accommodate or change focus.
Diagnosis
A diagnosis of myopia is typically confirmed during an eye examination by an ophthalmologist, optometrist or orthoptist.[56] Frequently an autorefractor or retinoscope is used to give an initial objective assessment of the refractive status of each eye, then a phoropter is used to subjectively refine the patient's eyeglass prescription.
Prevention
There is no universally accepted method of preventing myopia.[8] Commonly attempted preventative methods include wearing reading glasses, eye drops and participating in more outdoor activities are described below. Some 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.[8][57] The reasoning behind a convex lens's possible effectiveness in preventing myopia is simple to understand: Convex lenses' refractive property of converging light are 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. The model teaches a very simple method to prevent myopia.[31] For people with Presbyopia, whose eye's lens 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.[58] 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.[59] Inexpensive non prescription 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.[60] A recent Malaysian study reported in New Scientist[61] suggested that undercorrection of myopia caused more rapid progression of myopia.[62] However, the reliability of these data has been called into question.[63] 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-control, double-blinded prospective controlled study.[64]
Daylight
Daylight may prevent myopia. Australian researchers had concluded that exposure to daylight appeared to play a critical role in restricting the growth of the eyeball, which is responsible for myopia or short-sightedness.[65] They compared children from other developed countries such as Singapore and Australian children spent about 2–3 hours a day outdoors which could increased dopamine in the eyes that restrict distorted shaping of the eyes.[66][67][68]
Management
Glasses are commonly used to address near-sightedness.
Eyeglasses, contact lenses, and refractive surgery are the primary options to treat the visual symptoms of those with myopia. 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.
Chromatic aberration of strong eyeglasses
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.
Eye-exercises and biofeedback
Practitioners and advocates of alternative therapies often recommend eye exercises and relaxation techniques such as the Bates method. However, the efficacy of these practices is disputed by scientists and eye care practitioners.[69] 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.[70]
In the 1980s and 1990s, there was a flurry of interest in biofeedback as a possible treatment for myopia. A 1997 review of this biofeedback research concluded that "controlled studies to validate such methods ... have been rare and contradictory."[71] It was found in one study that myopes could improve their visual acuity with biofeedback training, but that this improvement was "instrument-specific" and did not generalise to other measures or situations.[72] In another study an "improvement" in visual acuity was found but the authors concluded that this could be a result of subjects learning the task.[73] Finally, in an evaluation of a training system designed to improve acuity, "no significant difference was found between the control and experimental subjects".[74]
Myopia control
Epidemiology
The global prevalence of refractive errors has been estimated from 800 million to 2.3 billion.[79] The incidence of myopia within sampled population often varies with age, country, sex, race, ethnicity, occupation, environment, and other factors.[25][80] Variability in testing and data collection methods makes comparisons of prevalence and progression difficult.[81]
In some areas, such as China, India and Malaysia, up to 41% of the adult population is myopic to −1dpt,[82] up to 80% to −0.5dpt.[83]
A recent study involving first-year undergraduate students in the United Kingdom found that 50% of British whites and 53.4% of British Asians were myopic.[84]
In Australia, the overall prevalence of myopia (worse than −0.50 diopters) has been estimated to be 17%.[85] In one recent study, less than 1 in 10 (8.4%) Australian children between the ages of 4 and 12 were found to have myopia greater than −0.50 diopters.[86] A recent review found that 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.[87]
In Brazil, a 2005 study estimated that 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.[88] Another found nearly 1 in 8 (13.3%) of the students in the city of Natal were myopic.[89]
In Greece, the prevalence of myopia among 15 to 18 year old students was found to be 36.8%.[90]
In India, the prevalence of myopia in the general population has been reported to be only 6.9%.[90][91]
A recent review found that 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.[87]
In the United States, the prevalence of myopia has been estimated at 20%.[25] Nearly 1 in 10 (9.2%) American children between the ages of 5 and 17 have myopia.[92] Approximately 25% of Americans between the ages of 12 and 54 have the condition.[93] A recent review found that 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.[87]
A study of Jordanian adults aged 17 to 40 found that over half (53.7%) were myopic.[94]
Ethnicity and race
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.[80]
Myopia is less common in African people and associated diaspora.[25] In Americans between the ages of 12 and 54, myopia has been found to affect African Americans less than Caucasians.[93] Asians had the highest prevalence (18.5%), followed by Hispanics (13.2%). Caucasians had the lowest prevalence of myopia (4.4%), which was not significantly different from African Americans (6.6%). For hyperopia, Caucasians had the highest prevalence (19.3%), followed by Hispanics (12.7%). Asians had the lowest prevalence of hyperopia (6.3%) and were not significantly different from African Americans (6.4%). For astigmatism, Asians and Hispanics had the highest prevalences (33.6% and 36.9%, respectively) and did not differ from each other (P = .17). Blacks had the lowest prevalence of astigmatism (20.0%), followed by whites (26.4%).[95]
Education and myopia
A number of studies have shown that the incidence of myopia increases with level of education[90][93] and many studies[96] have shown a correlation between myopia and IQ, likely due to the confounding factor of formal education.
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.[97][98]
Society and culture
The terms myopia and myopic (or the common terms short sightedness or short sighted) have also been used metaphorically to refer to cognitive thinking and decision making that is narrow sighted or lacking in concern for wider interests or longer-term consequences.[99] 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 (see pragmatism, which tends to be myopic). Some antonyms of short sightedness are foreseeing, "forward thinking" and prophecy. Hyperopia, the biological opposite of myopia, is also used as a metaphor for those who exhibit "far-sighted" behavior; that is, over-prioritizing long-term interests at the expense of present enjoyment.[100]
Research
Normally eye development is largely genetically controlled, but it has been shown that the visual environment is an important factor in determining ocular development.
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.[101]
The Visual Environment and 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.[102] Form deprived myopia that is induced with a diffuser, like the goggles mentioned, shows significant myopic shifts.[103] Anatomically, the changes in axial length of the eye seem to be the major factor contributing to this type of myopia.[104] Diurnal growth rhythms of the eye have also been shown to play a large part in form-deprived myopia. Chemically, daytime retinal dopamine levels drop about 30%.[105] 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, form deprived myopia 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.[106] It has also been shown that an elevated level of retinal dopamine transporter (which is directly involved in controlling retinal dopamine levels) in the RPE is associated with FDM.[107]
The Role of Dopamine
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.[108] 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 4 days in some laboratory mice. Although this is significant, what is even more intriguing is that within just 2 days of diffuser removal, an early rise and eventual normalization of retinal dopamine levels in the eye are seen. This suggests that dopamine participates in visually guided eye growth regulation, and these fluctuations are not just a response to the FDM.[109] 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.[105] 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: The metabolism of L-Dopa 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 (DOPAC), homovanillic (HVA), and 3-O-methyldopa and 3-methoxytyramine.[110] Levodopa can be converted into dopamine in the presence of aromatic L-amino acid decarboxylase (L-AAAD).[111] L-AAAD activity in rat retinas is modulated by environmental light,[112] and this modulation is associated with dopamine D1 receptors [113] and alpha 2 adrenoceptor.[114] 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: L-Dopa 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 shown to be successful in the past. L-dopa treatment in children with amblyopia showed an improvement in visual acuity.[115] In rabbits, injections of dopamine prevented the myopic shift and vitreous chamber and axial elongation typically associated with FDM.[116] In guinea pigs, systemic L-dopa has shown to inhibit the myopic shift associated with FDM and has compensated to the drop in retinal dopamine levels.[117] These experiments show promise in treating myopia in humans.
• Possible Side Effects of Dopamine Treatment: Unfortunately, several 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.[118] This promotion of free-radical formation by L-Dopa does seem to directly effect its possible future treatment of myopia due to the fact that free-radicals could further cause damage to those proteins responsible for controlling structural proteins in the eye. It has also been shown that levodopa and some of its metabolites such as dopa/dopamine quinone are toxic for nigral neurons.[119] This toxic effect must be analyzed before treatment of levodopa for myopia to prevent damaging effects to these neurons.
L-DOPA Inhibits Myopic Shifts[117]
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 L-DOPA into dopamine to balance the deficiency in the retina of the deprived eyes.
• Areas of Future Research: Intraperitoneal injection of L-DOPA (10 mg/kg) could not completely suppress the development of form-deprivation myopia. Perhaps the dose of L-DOPA may be too low to completely suppress myopia. Another possibility of the incomplete suppression of myopia may lie in the fact that myopia is a complex process of which 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.
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72. ^ Randle RJ (1988). "Responses of myopes to volitional control training of accommodation.". Ophthalmic Physiol Opt 8 (3): 333–340. doi:10.1111/j.1475-1313.1988.tb01063.x. PMID 3269512.
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76. ^ Pärssinen O, Hemminki E, Klemetti A (July 1989). "Effect of spectacle use and accommodation on myopic progression: final results of a three-year randomised clinical trial among schoolchildren". Br J Ophthalmol 73 (7): 547–51. doi:10.1136/bjo.73.7.547. PMID 2667638. PMC 1041798. http://bjo.bmj.com/cgi/pmidlookup?view=long&pmid=2667638.
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78. ^ Bifocal soft contact lenses as a possible myopia control treatment: a case report involving identical twins. Aller TA, Wildsoet C. Clin Exp Optom. 2008 Jul;91(4):394-9. Erratum in: Clin Exp Optom. 2008 Sep;91(5):479. PMID: 18601670 [PubMed – indexed for MEDLINE]
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101. ^ Jacobi FK, Pusch CM. A decade in search of myopia genes. Front Biosci. 2010 Jan 1;15:359-72.
102. ^ Shen W, Vijayan M, Sivak JG. Inducing form-deprivation myopia in fish. Invest Ophthalmol Vis Sci. 2005 May;46(5):1797-803.
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4-Hyperopia
Hyperopia, and restoring of vision with convex lens.
People with hyperopia can experience blurred vision, asthenopia, accommodative dysfunction, binocular dysfunction, amblyopia, and strabismus.[1]
Hyperopia is often confused with presbyopia,[2][3] another condition that frequently causes blurry near vision.[4] Presbyopes who report good far vision typically experience blurry near vision because of a reduced accommodative amplitude brought about by natural aging changes with the crystalline lens.[4] It is also sometimes referred to as farsightedness, since in otherwise normally-sighted persons it makes it more difficult to focus on near objects than on far objects.[5]
The causes of hyperopia are typically genetic and involve an eye that is too short or a cornea that is too flat, so that images focus at a point behind the retina. People with hyperopia can usually see distant objects well, but have trouble focusing on nearby objects.
Classification of hyperopia
Hyperopia is typically classified according to clinical appearance, its severity, or how it relates to the eye's accommodative status.[1]
Classification by clinical appearance
• Simple hyperopia
• Pathological hyperopia
• Functional hyperopia
Diagnosis
Visual acuity is affected according to the amount of hyperopia, as well as the patient's age, visual demands, and accommodative ability.[1]
In severe cases of hyperopia from birth the brain has difficulty to merge the images that each individual eye see. This is because the images the brain receives from each eye is always blurred. A child with severe hyperopia has never seen objects in detail and might present with amblyopia or strabismus. If the brain never learns to see objects in detail, then there is a high chance that one eye will become dominant. The result is that the brain will block the impulses of the non-dominant eye with resulting amblyopia or strabismus. In contrast the child with myopia can see objects close to the eye in detail and does learn at an early age to see detail in objects.
The child with hyperopia will typically stand close, in front of a television. One would have expected that the child will stand far to see, but because the brain has never learned to see objects in detail and the child with hyperopia from birth presents with the picture of decreased visual perception.
The parents of a child with hyperopia do not always realize that the child has a problem at an early age. A hyperopic child might have problems with catching a ball because of blurred vision and because of a decreased ability to see three dimensional objects. The child will typically perform below average at school. As soon as a child starts identifying images a parent might find that the child cannot see small objects or pictures.
Treatment
Various eye care professionals, including ophthalmologists, optometrists, orthoptists, and opticians, are involved in the treatment and management of hyperopia. At the conclusion of an eye examination, an eye doctor may provide the patient with an eyeglass prescription for corrective lenses.
Minor amounts of hyperopia are sometimes left uncorrected. However, larger amounts may be corrected with convex lenses in eyeglasses or contact lenses. Convex lenses have a positive dioptric value, which causes the light to focus closer than its normal range.
Hyperopia is sometimes correctable with various refractive surgery procedures (LASIK). It can also be corrected with special convex lenses.
A child with severe hyperopia from birth will not see better with glasses when first fitted. This is because the brain must still learn to process the new detailed images received from the eyes and this learning process takes time.
References
1. ^ a b c American Optometric Association. Optometric Clinical Practice Guideline: Care of the patient with hyperopia. 1997.
2. ^ "Eye Health: Presbyopia and Your Eyes." WebMD.com. October, 2005. Accessed September 21, 2006.
3. ^ Chou B. "Refractive Error and Presbyopia." Refractive Source.com Accessed September 20, 2006.
4. ^ a b American Optometric Association. Optometric Clinical Practice Guideline: Care of the patient with presbyopia. 1998.
5. ^ Kazuo Tsubota, Brian S. Boxer Wacher, Dimitri T. Azar, and Douglas D. Koch, editors, , Hyperopia and Presbyopia, New York: Marcel Decker, 2003
5-Presbyopia
Similar to grey hair and wrinkles, presbyopia is a symptom caused by the natural course of aging. The first symptoms (described below) are usually first noticed between the ages of 40-50. The ability to focus on near objects declines throughout life, from an accommodation of about 20 dioptres (ability to focus at 50 mm away) in a child, to 10 dioptres at 25 (100 mm), and levels off at 0.5 to 1 dioptre at age 60 (ability to focus down to 1–2 meters only).
The word presbyopia comes from the Greek word presbys (πρέσβυς), meaning "old man" or "elder", and the Neolatin suffix -opia, meaning "sightedness".[1]
Symptoms
The first symptoms most people notice are difficulty reading fine print, particularly in low light conditions, eyestrain when reading for long periods, blur at near or momentarily blurred vision when transitioning between viewing distances. Many extreme presbyopes complain that their arms have become "too short" to hold reading material at a comfortable distance.[2]
Presbyopia, like other focus defects, becomes much less noticeable in bright sunlight. This is a result of the iris closing to a smaller diameter. As with any lens, increasing the focal ratio of the lens increases depth of field by reducing the level of blur of out-of-focus objects (compare the effect of aperture on depth of field in photography).
A delayed onset of seeking correction for presbyopia has been found among those with certain professions and those with miotic pupils.[3] In particular, farmers and homemakers seek correction later, whereas service workers and construction workers seek eyesight correction earlier.
Focusing mechanism of the eye
There is some confusion in articles and even textbooks over how the focusing mechanism of the eye actually works. In the classic book, 'Eye and Brain' by Gregory, for example, the lens is said to be suspended by a membrane, the 'zonula', which holds it under tension. The tension is released, by contraction of the ciliary muscle, to allow the lens to become more round, for close vision. This would seem to imply that the ciliary muscle, which is outside the zonula must be circumferential, contracting like a sphincter, to slacken the tension of the zonula pulling outwards on the lens. This is consistent with the fact that our eyes seem to be in the 'relaxed' state when focusing at infinity, and also explains why no amount of effort seems to enable a myopic person to see further away. Many texts, though, describe the 'ciliary muscles' (which seem more likely to be just elastic ligaments and not under any form of nervous control) as pulling the lens taut in order to focus at close range.[citation needed] This has the counter-intuitive effect of steepening the lens valve cytokinesis centrally (increasing its power) and flattening peripherally.
Interaction with myopia
Many people with myopia (near-sightedness) can read comfortably without eyeglasses or contact lenses even after age 40. However, their myopia does not disappear and the long-distance visual challenges remain. Myopes considering refractive surgery are advised that surgically correcting their nearsightedness may be a disadvantage after age 40, when the eyes become presbyopic and lose their ability to accommodate or change focus because they will then need to use glasses for reading. Myopes with astigmatism find near vision better, though not perfect, without glasses or contact lenses when presbyopia sets in, but the more astigmatism the poorer their uncorrected near vision.
A surgical technique offered is to create a "reading eye" and a "distance vision eye", a technique commonly used in contact lens practice, known as monovision. Monovision can be created with contact lenses or spectacles so that candidates for this procedure can determine if they are prepared to have their corneas reshaped by surgery to cause this effect permanently.
Treatment
Treatment for presbyopia has advanced significantly in recent years, thanks in no small part to the ready availability of inexpensive over-the-counter reading glasses with corrective lenses that cover a wide gamut of magnification levels. Contact lenses have also been used to correct the focusing loss that comes along with presbyopia. Some people choose to correct the focus problems with bifocals, giving them a wider range of vision without having to use a second set of glasses. As the focusing loss increases, prescription changes become more frequent.
In order to reduce the need for bifocals or reading glasses, some people choose contact lenses to correct one eye for near and one eye for far with a method called "monovision", which can interfere with depth perception due to loss of focusing ability in the other eye. There are also newer bifocal or multifocal contact lenses that attempt to correct both near and far vision with the same lens.[4]
Controversially, eye exercises have been touted as a way to delay the onset of presbyopia, but their effectiveness has not been demonstrated in medical research.[5] It has been observed that in some populations that do not consume animal protein, presbyopia is rare.[6]
Surgery
New surgical procedures may also provide solutions for those who do not want to wear glasses or contacts, including the implantation of accommodative intraocular lenses (IOLs). Scleral expansion bands, which increase the space between the ciliary body and lens, have not been found to provide predictable or consistent results in the treatment of presbyopia.[7] INTRACOR[8] has now been approved in Europe for treatment of both eyes (turning both corneas into multifocal lenses and so dispensing with the need for reading glasses).
PresbyLASIK, Conductive Keratoplasty, AcuFocus[9] are also worth consideration, but some use of reading glasses will still remain when light is poor, or when reading for extended periods of time.
Another treatment option for the correction of presbyopia in patients with emmetropia as well as in patients with myopia, hyperopia and astigmatism is Laser Blended Vision. In Laser Blended Vision, laser refractive surgery is used to correct the dominant eye mainly for distance vision and the non-dominant eye mainly for near vision, while the depth of field (i.e. the range of distances at which the image is in focus) of each eye is increased. As a result of the increased depth of field, the brain merges the two images, creating a blend zone, i.e. a zone which is in focus for both eyes. This allows the patient to see near, intermediate and far without glasses.[10][11][12]
References
1. ^ Direct translation courtesy of Merriam-Webster.com
2. ^ Robert Abel, The Eye Care Revolution: Prevent and Reverse Common Vision Problems, Kensington Books, 2004.
3. ^ García Serrano, JL; López Raya, R; Mylonopoulos Caripidis, T (Nov 2002). "Variables related to the first presbyopia correction" (Free full text). Archivos de la Sociedad Espanola de Oftalmologia 77 (11): 597–604. ISSN 0365-6691. PMID 12410405. http://www.oftalmo.com/seo/2002/11nov02/03.htm.
4. ^ Li, G; Mathine, DL; Valley, P; Ayräs, P; Haddock, JN; Giridhar, MS; Williby, G; Schwiegerling, J et al. (Apr 2006). "Switchable electro-optic diffractive lens with high efficiency for ophthalmic applications" (Free full text). Proceedings of the National Academy of Sciences of the United States of America 103 (16): 6100–4. doi:10.1073/pnas.0600850103. ISSN 0027-8424. PMID 16597675. PMC 1458838. http://www.pnas.org/cgi/pmidlookup?view=long&pmid=16597675.
5. ^ The lowdown on eye exercises, Harvard Medical School Family Health Guide http://www.health.harvard.edu/fhg/updates/update0903c.shtml
6. ^ The China Study, C. Campbell & T. Campbell, ISBN 9781932100662
7. ^ Malecaze, FJ; Gazagne, CS; Tarroux, MC; Gorrand, JM (Dec 2001). "Scleral expansion bands for presbyopia". Ophthalmology 108 (12): 2165–71. doi:10.1016/S0161-6420(01)00591-7. ISSN 0161-6420. PMID 11733253.
8. ^ www.technolaspv.com
9. ^ www.acufocus.com
10. ^ Reinstein DZ, Couch DG, Archer TJ. LASIK for Hyperopic Astigmatism and Presbyopia Using Micro-monovision With the Carl Zeiss Meditec MEL80. J Refract Surg. 2009;25:37-58
11. ^ Reinstein DZ, Archer TJ, Gobbe M. LASIK for the correction of myopic astigmatism and presbyopia using aspheric ablation profiles and a micro-monovision protocol with the Carl Zeiss Meditec MEL80. J Refract Surg. [In Press]
12. ^ Reinstein DZ, Archer TJ, Gobbe M. Outcomes of Presbyopic Micro-Monovision LASIK for Myopia, Hyperopia and Emmetropia. ESCRS. Berlin, 2008
6-Strabismus
Classification
Paralytic strabismus
Forms of paralytic strabismus include
• Third (oculomotor) nerve palsy
• Fourth (trochlear) nerve palsy
o Congenital fourth nerve palsy
• Sixth (abducent) nerve palsy
• Total (external) ophthalmoplegia
• Progressive external ophthalmoplegia
• Other
o Kearns-Sayre syndrome
Other strabismus
Other forms of strabismus include:
• Convergent concomitant/Divergent concomitant
o Esotropia
o Exotropia
• Vertical strabismus
o Hypertropia
o Hypotropia
• Other and unspecified heterotropia
o Microtropia
o Monofixation syndrome
• Heterophoria
o Esophoria
o Exophoria
• Mechanical strabismus
o Brown's sheath syndrome
• Other
o Duane syndrome
Signs and symptoms
One eye moves normally, while the other points in (esotropia or "crossed eyes"), out (exotropia), up (hypertropia) or down (hypotropia).
Strabismus is often referred to as "lazy eye". It is also referred to as "squint"[3], "crossed eye", "cock eye", "codeye" and "wall eye".[citation needed]
"Cross-eyed" means that when a person with strabismus looks at an object, one eye fixates the object and the other fixates with a convergence angle less than zero, that is the optic axes overconverge. "Wall-eyed" means that when a person with strabismus looks at an object, one eye fixates the object and the other fixates with a convergence angle greater than zero, that is the optic axes diverge from parallel.
Pathophysiology
More commonly however, squints are termed concominant (i.e. non paralytic). This means the squint is not caused by a lesion reducing innervation. The squint in this example is caused by a refractive error in one or both eyes. This refractive error causes poor vision in one eye and so stops the brain from being able to use both eyes together.
Diagnosis
During eye examinations, orthoptists, ophthalmologists and optometrists typically use a cover test to aid in the diagnosis of strabismus. If the eye being tested is the strabismic eye, then it will fixate on the object after the "straight" eye is covered, as long as the vision in this eye is good enough. If the "straight" eye is being tested, there will be no change in fixation, as it is already fixated. Depending on the direction that the strabismic eye deviates, the direction of deviation may be assessed. Exotropic is outwards (away from the midline) and esotropic is inwards (towards the nose); these are types of horizontal strabismus. "Hypertropia" is upward, and "Hypotropia" is downward; these are types of vertical strabismus, which are less common.
A simple screening test for strabismus is the Hirschberg test. A flashlight is shone in the patient's eye. When the patient is looking at the light, a reflection can be seen on the front surface of the pupil. If the eyes are properly aligned with one another, then the reflection will be in the same spot of each eye. Therefore, if the reflection is not in the same place in each eye, then the eyes aren't properly aligned.
Laterality
Strabismus may be classified as unilateral if the same eye consistently 'wanders', or alternating if either of the eyes can be seen to 'wander'. Alternation of the strabismus may occur spontaneously, with or without subjective awareness of the alternation. Alternation may also be seen following the cover test, with the previously 'wandering' eye remaining straight while the previously straight eye is now seen to be 'wandering' on removal of the cover. The cover-uncover test is used to diagnose the type of strabismus (also known as tropia) present.[2]
Onset
Strabismus may also be classified based on time of onset, either congenital, acquired or secondary to another pathological process, such as cataract.[2] Many infants are born with their eyes slightly misaligned. The best time for physicians to assess this is between ages 3 and 6 months. [4]
Differential diagnosis
Pseudostrabismus is the false appearance of strabismus. It generally occurs in infants and toddlers whose bridge of the nose is wide and flat, causing the appearance of strabismus. With age, the bridge of the child's nose narrows and the folds in the corner of the eyes go away. To detect the difference between pseudostrabismus and strabismus, a Hirschberg test may be used.
Management
Surgery to correct strabismus on an eight-month-old Nicaraguan infant.
As with other binocular vision disorders, the primary therapeutic goal for those with strabismus is comfortable, single, clear, normal binocular vision at all distances and directions of gaze.[5]
Whereas amblyopia, if minor and detected early, can often be corrected with use of an eyepatch on the dominant eye and/or vision therapy, the use of eyepatches is unlikely to change the angle of strabismus. Advanced strabismus is usually treated with a combination of eyeglasses or prisms, vision therapy, and surgery, depending on the underlying reason for the misalignment. Surgery does not change the vision; it attempts to align the eyes by shortening, lengthening, or changing the position of one or more of the extraocular eye muscles and is frequently the only way to achieve cosmetic improvement. Glasses affect the position by changing the person's reaction to focusing. Prisms change the way light, and therefore images, strike the eye, simulating a change in the eye position.
Early treatment of strabismus and/or amblyopia in infancy can reduce the chance of developing amblyopia and depth perception problems. Most children eventually recover from amblyopia by around age 10, if they have had the benefit of patches and corrective glasses. [4]
Eyes that remain misaligned can still develop visual problems. Although not a cure for strabismus, prism lenses can also be used to provide some comfort for sufferers and to prevent double vision from occurring.
Botulinum Toxin (Botox) may also be used in the treatment of strabismus, to improve cosmetic appearance. Most commonly used in adults, the toxin is injected in the stronger muscle, causing temporary paralysis. The treatment may need to be repeated 3-4 months later once the paralysis wears off. Common side effects are double vision, droopy eyelid, over correction and no effect. The side effects will resolve fairly quickly.
In adults with previously normal alignment, the onset of strabismus usually results in double vision (diplopia).
Prognosis
When strabismus is congenital or develops in infancy, it can cause amblyopia, in which the brain ignores input from the deviated eye. The appearance of strabismus may also be a cosmetic problem. One study reported that 85% of adult strabismus patients "reported that they had problems with work, school and sports because of their strabismus." The same study also reported that 70% said strabismus "had a negative effect on their self-image."[6]
References
1. ^ Online Etymology Dictionary
2. ^ a b c American Optometric Association. Optometric Clinical Practice Guideline: Care of the patient with strabismus: esotropia and exotropia. 1997.
3. ^ Squint (NHS health encyclopaedia)
4. ^ a b Nield, LS; Mangano, LM (April 2009). "Strabismus: What to Tell Parents and When to Consider Surgery". Consultant 49 (4). http://www.consultantlive.com/display/article/10162/1399809.
5. ^ Eskridge JB (October 1993). "Persistent diplopia associated with strabismus surgery". Optom Vis Sci 70 (10): 849–53. doi:10.1097/00006324-199310000-00013. PMID 8247489.
6. ^ Scribe/Alum Notes Winter 2001 – Template
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