Amblyopia

Benjamin Jastrzembski MD

Neuro-Ophthalmology & Neuro-Otology

Updated 08.21.2022
Released 01.30.2003
Expires For CME 08.21.2025

Amblyopia

Author: Benjamin Jastrzembski MD

See Contributor Disclosures

Editor: Heather E Moss MD PhD

Amblyopia

In This Article

Quick Link

Introduction

Overview

Amblyopia is poor vision caused by abnormal visual experience during childhood brain development (02). This common disorder occurs in an estimated prevalence of 1.4% (36; 13; 32; 31; 15). Unless treated during childhood, the loss of vision is almost always permanent. Amblyopia treatment often requires penalization of the better-seeing eye to stimulate central visual processing in the worse-seeing, amblyopic eye. New treatment options for amblyopia are becoming available that use virtual reality headsets.

Key points

	• Amblyopia is a reduction in visual acuity secondary to abnormal central visual processing in one or both eyes due to refractive error, strabismus, or visual deprivation.
	• Treatment of amblyopia involves addressing the underlying cause of vision loss with or without penalization of the better-seeing eye.
	• Amblyopia treatment is most effective at younger ages.
	• Vision loss from amblyopia can be permanent if it is not treated in a timely fashion.

Historical note and terminology

The term “amblyopia” is derived from the Greek amblys, meaning “blunt,” and ops, meaning “eye,” indicating a “dullness” or incomplete loss of vision rather than complete blindness (10). The early clinical understanding of this disorder is traced to George Louis Leclerc, Comte de Buffon, who in 1743 proposed the use of occlusion of the sound eye to “force” the amblyopic eye to see better (10). The understandings of amblyopia was advanced by the work of Hubel and Wiesel, who won the Nobel Prize in 1981 for their experiments blocking light from a single eye in kittens and young monkeys. Hubel and Wiesel demonstrated anatomic changes in the visual cortex as well as impairment of vision in the young animals that had been temporarily deprived of vision. In contrast, blocking visual input in adult animals made no difference on the anatomy of the visual cortex or the vision. Hubel and Wiesel concluded that there exists a critical period of neuroplasticity in early life during which visual stimulation is required for normal visual cortex development (53; 54). As a result of their work and subsequent studies by other investigators, the concept of amblyopia as a developmental visual disorder was established (48; 29; 43).

Clinical manifestations

Presentation and course

A period of abnormal visual input to the brain from one or both eyes during development causes amblyopia. The impaired visual experience during the critical period of visual cortex plasticity results in abnormal central processing of visual input. The degree of vision loss may vary from a minimal decrease of acuity to light-perception only vision. Total loss of vision (no light perception) does not occur in amblyopia without the presence of other ocular disease. Unless treated during childhood, the visual deficit will nearly always persist into adulthood and throughout life (44; 24).

Amblyopia is categorized as (A) refractive, (B) strabismic, and (C) deprivational. More than one category of amblyopia is frequently found in a single individual. In refractive amblyopia, optical defocus degrades the image that is sent to the brain causing impaired visual cortex development. Refractive amblyopia is distinct and more challenging to treat than refractive error. In refractive error, appropriate optical correction of blur by glasses or contact lenses will result in immediate normal “best-corrected” visual acuity. In refractive amblyopia, the acuity will remain suboptimal even after eliminating image blur with appropriate glasses or contact lenses, demonstrating abnormalities in central visual processing. Anisometropia, in which the refractive error differs between the two eyes, is much more likely to cause amblyopia than isometropia, in which the refractive error is equal in the two eyes (13; 31). Full-time correction of the refractive error alone may improve vision and resolve refractive amblyopia with time, but in some cases, penalization therapy such as patching may be needed to improve the vision of the amblyopic eye (06).

The second category of amblyopia is strabismic. In strabismus, the two eyes point in different directions. If the images from the two eyes are so disparate that they cannot be fused by the brain, diplopia or suppression of one image occurs. Older children and adults frequently experience diplopia in this scenario. The young child does not experience diplopia; instead, the visual cortex suppresses the image from the nondominant eye. Over time, the suppression impairs the ability to interpret the image from the nondominant eye causing unilateral amblyopia and reduced binocularity. The severity of the suppression is directly correlated to the degree of impairment in visual acuity and binocularity (26). Isolated strabismic amblyopia is unilateral, but not all patients with strabismus develop amblyopia. Strabismic amblyopia is more commonly associated with esotropia (convergent eye deviation or crossed eyes) than with exotropia (divergent eye deviation or “walleyed”) (49).

The last category of amblyopia is deprivation or occlusion amblyopia. This is the least common form of amblyopia and the most difficult to treat. It may be unilateral or bilateral. As indicated by its name, it is caused by a structural abnormality that obstructs the visual axis of the eye(s). Examples of these occlusions include congenital or acquired cataracts, corneal opacities from trauma or infection, ptosis occluding the pupil, or vitreous or retinal hemorrhage as is observed in nonaccidental infantile trauma, for example. An infant is exquisitely sensitive to deprivation amblyopia, so concern for congenital cataracts or other ophthalmic disorders in an infant should be referred to pediatric ophthalmology for evaluation on an urgent basis. Even with optimal surgical care as well as aggressive treatment of amblyopia, removal of a cataract in an infant is unlikely to return visual acuity to normal.

In general, amblyopia may occur at any time during visual immaturity, even if there are new circumstances that did not exist at birth. For example, if a child develops a visually significant cataract at 5 years of age, irreversible vision loss from amblyopia may develop if the cataract is not addressed during the critical period of visual development. The critical period of visual development in humans is from birth to approximately 9 years of age. The risk of developing amblyopia, as well as the speed of its onset, is inversely proportional to the age of the patient. Earlier initiation of amblyopia management results in better visual outcomes, although there is some improvement in teenagers who have not been previously treated (42). Therefore, the American Academy of Ophthalmology Preferred Practice Patterns recommends offering treatment to children of any age, even those in their adolescent years (52).

The diagnosis of unilateral amblyopia is more common than bilateral amblyopia. Unilateral amblyopia presents as a difference in best-corrected vision between the eyes. Although this differential may in fact be very small, it is clinically accepted that a verbal child must have a 2-line or greater difference in optotype identification, which is usually tested with letters or pictures, to be classified as amblyopic. This minimum differential is meant to decrease the significant potential for false positives that may occur when testing the vision of young verbal children. Observation of comparative monocular fixation attention or behavior is used to assess infants and preverbal children.

Prognosis and complications

The age at risk for the development of amblyopia is from birth to approximately 9 years of age. Unless treated before 9 years of age, amblyopia will almost always persist unchanged for life into adulthood (44; 24).

Clinical vignette

A 10-month-old healthy male was referred for examination and treatment of an esotropia. The ocular misalignment was first noted at 3 months of age. He had received no previous treatment for the problem. Medical and family histories were noncontributory.

Examination. In order to evaluate the vision in this preverbal infant, he was placed on the parent’s lap, and his attention was drawn to a small toy that was held approximately 2 feet from his face. With the left eye covered, the right eye was central and steady, and it maintained fixation. When the occluder was then switched to the right (normal vision) eye, the child objected and moved the examiner’s hand away to see around the occlusion. When the right eye was covered, the left eye was central and steady, but it did not maintain fixation when the right eye was uncovered. This objection to occlusion of the right eye indicated that the vision of the left eye was significantly less than that of the right eye and that amblyopia was present.

The esotropia measured 50 prism diopters using the Krimsky method. This involves shining a penlight at the infant’s eyes and placing prisms of increasing strength in front of the left eye in a step-wise approach until the light reflexes are aligned. Careful observation of the extraocular movements showed features consistent with infantile esotropia. Extraocular movements with both eyes open initially suggested a possible limitation of abduction in the left eye (version movement). However, a closer look using the Doll’s head maneuver while simultaneously covering the right eye demonstrated full abduction of the left eye (duction movement). There was also subtle elevation of each eye in adduction, consistent with inferior oblique overaction, another feature common in infantile esotropia. Otherwise, the comprehensive examination was normal. Observation of the ocular adnexa, the pupils, and anterior segment were performed and were within normal limits. The patient had a dilated fundus examination, which showed normal optic nerves and retinae as well as a cycloplegic refraction that showed low, age-appropriate hyperopia.

For this infant, the severity of his esotropia and his young age puts him at high risk for profound strabismic amblyopia and loss of binocular vision. Given this, it was discussed with the family to consider this as a lifelong condition that can be managed, but not necessarily cured. The amblyopia was treated with patching of the normal-vision right eye two hours daily. The family was concerned that the patching itself could produce a deprivation amblyopia in the better-seeing right eye. There is indeed a risk of overpenalization causing a reverse/occlusion amblyopia, and this risk is inversely proportional to the patient’s age or and level of visual immaturity. Therefore, close serial monitoring of the patient during amblyopia treatment was performed. If an occlusion/reverse amblyopia is induced by patching, it is almost always correctable. In addition to the amblyopia therapy, strabismus surgery was also promptly performed before age 1 year to correct the esotropia. Prior to the surgery, the family was cautioned that patching would still be required after the strabismus surgery, that the development of binocular vision does not always occur despite an excellent post-op ocular alignment, and that individuals with infantile esotropia frequently require more than one strabismus surgery over their lifetime.

The patient was followed throughout childhood with decreasing frequency as he became less sensitive to amblyopia with age. By his teenage years, he achieved an excellent result with a best-corrected visual acuity of 20/40 in his weaker left eye, and 20/15 in his right eye. He had a small angle residual esotropia that was observed in the eye clinic, but he reported that the eye misalignment was not observed by his peers or even his family. He denied any psychosocial stress from the residual strabismus.

This clinical vignette is a composite and does not describe a specific individual.

Prevention

Early detection and treatment of the major risk factors for amblyopia, namely strabismus, refractive error, and visual deprivation, prevents or mitigates amblyopia.

Preventive monitoring is especially important for postsurgical patients, as these families sometimes mistakenly consider surgery as curative treatment for not only strabismus but also amblyopia. After strabismus surgery, children must be followed at least until age 9 to monitor for amblyopia. Similarly, postsurgical ptosis, cataract, or eye trauma patients require monitoring to identify early amblyopia and prevent its progression. As a child ages, the risk of developing amblyopia diminishes.

There is growing awareness of the prevalence and treatment options for childhood myopia (47; 18; 38; 03). However, refractive error is distinct from refractive amblyopia, and if the vision is correctable to a normal level with glasses, only refractive error is present, not refractive amblyopia. The presence of anisometropia (difference in refractive error between the two eyes) greatly increases the likelihood that refractive amblyopia will develop (13; 31). In all cases of refractive error, and especially in cases of anisometropia, the early use of appropriate glasses in young children is sometimes sufficient to prevent refractive amblyopia.

Although low outdoor light exposure and near work among children are established risk factors for myopia progression, there has also been growing concern in the general public concerning screen time as a risk factor for refractive error/refractive amblyopia. There is presently no scientific evidence that the use of near screen time is a risk factor for refractive amblyopia, although the American Academy of Pediatrics recommends limiting screen time to promote overall child development (07). As far as the effect of near screen time on myopic progression, in a study of Dutch teenagers who spent an average of about 4 hours on their smartphones a day, smartphone use was only minimally associated with myopia (11). Distance from the eyes to the phone screen was not correlated with myopic progression. The effect of screen time may be more pronounced on preteen children, however.

Differential diagnosis

Confusing conditions

Amblyopia must be distinguished from other causes of visual impairment, particularly cerebral visual impairment. Cerebral visual impairment (CVI) is defined as decreased vision from postgeniculate visual pathway brain damage and is most commonly seen in children with a history of perinatal hypoxic-ischemic damage. It is more common in children born prematurely, and as many as 93% of cerebral visual impairment patients have seizures (04). The key distinguishing factor is that amblyopia is secondary to abnormal visual input to the brain, whereas cerebral visual impairment is caused by abnormalities in the brain itself.

Associated or underlying disorders

Amblyopia is often confused with its associated risk factors namely strabismus, refractive error, or causes of visual deprivation such as cataracts or trauma. Although closely related, amblyopia and its associated ophthalmic diseases are distinct. Amblyopia refers only to abnormal central processing of visual input secondary to impaired visual experience during the critical period of early childhood. In turn, this impaired brain development is caused by abnormal visual experience from an ophthalmic disease such as cataracts or strabismus. The distinction is important because if the ophthalmic disease is acquired after the critical period of early childhood, it will not cause amblyopia. For example, a traumatic cataract acquired in a teenager will not cause deprivational amblyopia. If the cataract is removed surgically, even years later, normal visual acuity may be achieved, as the brain visual processing developed normally prior to the injury. In contrast, a traumatic cataract before age 9 has a high risk of causing deprivational amblyopia as central visual processing is still developing.

Management

Refractive error. Treatment of refractive error alone improves vision in refractive amblyopia and to a lesser degree strabismic amblyopia (06; 05; 55). Glasses are the most common modality and are often well tolerated by children if they are properly fitted by an optician familiar with children. It is important to choose a pair of spectacles that the child can wear for all waking hours and that does not allow them to look over the frames. Although ordering glasses on the internet without evaluation by an in-person optician is more affordable in the U.S., this is not recommended due to the difficulty of fitting glasses in children. Contact lenses are indicated in specific clinical scenarios (eg, in postsurgical cataract patients or for myopia control). The risks of contact lens use and proper care must be explained. Elective use of contact lenses for refractive error alone in young children may be considered on a case-by-case basis depending on the parents’ and physician’s evaluation of the child’s ability to comply with hygiene requirements.

Occlusion. The most widely accepted and time-proven treatment of an amblyopic eye is occlusion of the better-seeing fellow eye. Patching is performed on a part-time basis, with studies demonstrating equivalent results between 2 and 6 hours of daily patching for moderate amblyopia (39). For severe amblyopia, 6 hours of patching a day is recommended (19). Patching earlier in life results in better visual outcomes with children under age 7 years having superior improvement compared to older children undergoing similar patching times (14). Teenagers who have not previously been treated for amblyopia may still benefit from occlusion therapy (42).

Covering the better-seeing eye prevents the child from seeing well during occlusion therapy. As a result, compliance is often be a serious problem limiting the effectiveness of patching (45). If well explained by the physician to understanding parents, occlusion therapy is effective (09; 28).

During occlusion therapy for amblyopia, some practitioners have suggested near visual activities for their patients (19; 39). The presumption is that these activities performed at near viewing stimulate the visual system of the brain and help alleviate the amblyopia. However, a controlled, randomized study comparing 2 hours of patching combined with either 2 hours of near activities (eg, reading, writing, playing computer games) or 2 hours of distance activities (eg, outdoor play, television viewing at a distance of at least 6 feet) demonstrated no difference in visual acuity improvement between the 2 groups (36).

Pharmacologic treatment. Chronic cycloplegia of the unaffected eye with 1 drop daily of atropine sulfate 1% solution is comparable in effect to occlusion therapy in children with moderate amblyopia ages 3 to 7 years who are not nearsighted or myopic (22; 35). Atropine is also effective if given for 2 consecutive days a week, or “weekend atropine,” instead of daily (40). Atropine blurs or penalizes the better-seeing eye and thereby improves the vision of the amblyopic eye without a patch. A slightly higher degree of acceptability has been reported for atropine compared with patching treatment (41).

Dichoptic treatment. Dichoptic treatment, where the amblyopic eye receives a higher contrast stimulus and the better-seeing eye contrast is reduced during visual tasks, has also shown for amblyopia treatment. Initial trials showed mixed results, but effectiveness may have been limited by games that were relatively unappealing to children (17; 46; 20; 21; 16; 30). A dichoptic device that provides a menu of age-appropriate video media using a virtual reality (VR) headset (Luminopia One) showed an improvement of one-line of vision compared to a control group at 12 weeks in children ages 4 to 7 compared to full-time glasses use. The device is FDA-approved for the treatment of strabismic or refractive amblyopia in children ages 4 to 7.

Surgery. For deprivation amblyopia, it is essential that the structural issue underlying the amblyopia (eg, cataract, ptosis) be treated, usually with surgical intervention. In the case of strabismus, surgical correction will not improve an associated strabismic amblyopic. Treatment for strabismic amblyopia is often begun prior to surgical correction of the strabismus.

For children with refractive amblyopia from large refractive error who do not tolerate glasses or contact lenses, refractive surgery such as photorefractive keratectomy (PRK) laser-assisted in situ keratomileusis (LASIK) may be used (34).

Other treatments. Perceptual learning techniques that present images hypothesized to correspond to the receptive field of the visual cortex may be effective in treating amblyopia, although further research is needed (56; 57; 24). RevitalVision, a computerized perceptual learning amblyopia treatment system, is presently FDA-approved for the treatment of amblyopia in individuals 9 years of age and older.

Levodopa has been studied as a potential pharmacologic therapy to augment occlusion therapy, but results have not been definitively positive (25; 33; 37; 12). A randomized, double-masked placebo-controlled study of the use of levodopa/carbidopa for the treatment of refractory amblyopia in older children did not demonstrate any benefit over 2 hours of daily patching (37).

There is insufficient evidence to support the use of vision therapy eye exercise for the treatment of amblyopia (52).

References

01: Baker FH. Effects of visual deprivation and strabismus on the response of neurons in the visual cortex of the monkey, including studies on the striate and prestriate cortex in the normal animal. Brain Res 1974;66:185-208.
02: Birch EE. Amblyopia and binocular vision. Prog Retin Eye Res 2013;33:67–84.** PMID 23201436
03: Chamberlain P, Peixoto-de-Matos SC, Logan NS, Ngo C, Jones D, Young G. A 3-year randomized clinical trial of MiSight Lenses for myopia control. Optom Vis Sci 2019;96(8):556-67. PMID 31343513
04: Chang MY, Borchert MS. Advances in the evaluation and management of cortical/cerebral visual impairment in children. Surv Ophthalmol 2020;65(6):708-24. PMID 32199940
05: Chen P, Chen J, Tai M, et al. Anisometropic amblyopia treated with spectacle correction alone: possible factors predicting success and time to start patching. Am J Ophthalmol 2007;143:54-60. PMID 17113556
06: Cotter SA, Pediatric Eye Disease Investigator Group, Edwards AR, Wallace DK, et al. Treatment of anisometropic amblyopia in children with refractive correction. Ophthalmology 2006;113(6):895-903. PMID 16751032
07: Council on Communications and Media. Media and young minds. Pediatrics 2016;138(5):e20162591. PMID 27940793
08: Crawford ML, Blake R, Cool SJ, von Noorden GK. Physiological consequences of unilateral and bilateral eye closure in macaque monkeys: some further observations. Brain Res 1975;84:150-4. PMID 1111823
09: Dorey SE, Adams GG, Lee JP, Sloper JJ. Intensive occlusion therapy for amblyopia. Br J Ophthalmol 2001;85:310-3. PMID 11222336
10: Duke-Elder S. Anomalies of ocular motility. In: Ocular motility and strabismus. St. Louis: Mosby, 1973:292-4.
11: Enthoven CA, Polling JR, Verzijden T, et al. Smartphone use associated with refractive error in teenagers. Ophthalmology 2021;128(12):1681-8. PMID 34245754
12: Farvardin M, Khalili MR, Behnia M. Levodopa plus occlusion therapy versus occlusion therapy alone for children with anisometropic amblyopia. J Ophthalmic Vis Res 2019;14(4):457-64. PMID 31875101
13: Friedman DS, Repka MX, Katz J, et al. Prevalence of amblyopia and strabismus in white and African American children aged 6 through 71 months the Baltimore Pediatric Eye Disease Study. Ophthalmology 2009;116(11):2128-34. PMID 19762084
14: Fronius M, Cirina L, Ackermann H, Kohnen T, Diehl CM. Efficiency of electronically monitored amblyopia treatment between 5 and 16 years of age: New insight into declining susceptibility of the visual system. Vision Res 2014;103:11-9. PMID 25130409
15: Fu Z, Hong H, Su Z, Lou B, Pan CW, Liu H. Global prevalence of amblyopia and disease burden projections through 2040: a systematic review and meta-analysis. Br J Ophthalmol 2020;104(8):1164-70.** PMID 31704700
16: Gao TY, Guo CX, Babu RJ, et al.; BRAVO Study Team. Effectiveness of a binocular video game vs placebo video game for improving visual functions in older children, teenagers, and adults aith amblyopia: a randomized clinical trial. JAMA Ophthalmol 2018;136(2):172-81. PMID 29302694
17: Hess RF, Thompson B. Amblyopia and the binocular approach to its therapy. Vision Res 2015;114:4-16. PMID 25906685
18: Holden BA, Fricke TR, Wilson DA, et al. Global prevalence of myopia and high myopia and temporal trends from 2000 through 2050. Ophthalmology 2016;123(5):1036-42. PMID 26875007
19: Holmes JM, Kraker RT, Beck RW, et al. A randomized trial of prescribed patching regimens for treatment of severe amblyopia in children. Ophthalmology 2003;110(11):2075-87. PMID 14597512
20: Holmes JM, Manh VM, Lazar EL, et al. Effect of a binocular iPad game vs part-time patching in children aged 5 to 12 years with amblyopia: a randomized clinical trial. JAMA Ophthalmol 2016;134(12):1391-1400. PMID 27812703
21: Kelly KR, Jost RM, Dao L, Beauchamp CL, Leffler JN, Birch EE. Binocular iPad game vs patching for treatment of amblyopia in children: a randomized clinical trial. JAMA Ophthalmol 2016;134(12):1402-8. PMID 27832248
22: Kushner BJ. Atropine vs. patching for the treatment of moderate amblyopia in children. Arch Ophthalmol 2002;120:387-8. PMID 11879145
23: Lee KM, Lee SH, Kim NY, et al. Binocularity and spatial frequency dependence of calcarine activation in two types of amblyopia. Neurosci Res 2001;40:147-53. PMID 11377753
24: Lee YH, Maniglia M, Velez F, Demer JL, Seitz AR, Pineles S. Short-term perceptual learning game does not improve patching-resistant amblyopia in older children. J Pediatr Ophthalmol Strabismus 2020;57(3):176-84. PMID 32453851
25: Leguire LE, Komaromy KL, Nairus TM, Rogers GL. Long-term follow-up of L-dopa treatment in children with amblyopia. J Pediatr Ophthalmol Strabismus 2002;39:326-30. PMID 12458842
26: Li J, Thompson B, Lam CSY, et al. The role of suppression in amblyopia. Invest Ophthalmol Vis Sci 2011;52(7):4169. PMID 21447685
27: Loh AR, Chiang MF. Pediatric vision screening. Pediatr Rev 2018;39(5):225-34. PMID 29716965
28: Loudon S, Polling JR, Simonsz HJ. A preliminary report about the relation between visual acuity increase and compliance in patching therapy for amblyopia. Strabismus 2002;10:79-82. PMID 12221485
29: Lowel S, Engelmann R. Neuroanatomical and neurophysiological consequences of strabismus: changes in the structure and functional organization of the primary visual cortex in cats with alternating fixation and strabismic amblyopia. Strabismus 2002;10:95-105. PMID 12221487
30: Manh VM, Holmes JM, Lazar EL, et al; Pediatric Eye Disease Investigator Group. A randomized trial of a binocular ipad game versus part-time patching in children aged 13 to 16 years with amblyopia. Am J Ophthalmol 2018;186:104-15. PMID 29196184
31: McKean-Cowdin R, Cotter SA, Tarczy-Hornoch K, et al. Prevalence of amblyopia or strabismus in asian and non-Hispanic white preschool children: multi-ethnic pediatric eye disease study. Ophthalmology 2013;120(10):2117-24. PMID 23697956
32: Pai AS, Rose KA, Leone JF, et al. Amblyopia prevalence and risk factors in Australian preschool children. Ophthalmology 2012;119(1):138-44. PMID 2196326
33: Pandey PK, Chaudhuri Z, Kumar M, Satyabala K, Sharma P. Effect of levodopa and carbidopa in human amblyopia. J Pediatr Ophthalmol Strabismus 2002;39:81-9. PMID 11911549
34: Paysse EA, Tychsen L, Stahl E. Pediatric refractive surgery: Corneal and intraocular techniques and beyond. J AAPOS 2012;16(3):291-7. PMID 22681949
35: Pediatric Eye Disease Investigator Group. A randomized trial of atropine vs. patching for treatment of moderate amblyopia in children. Arch Ophthalmol 2002;120(3):268-78. PMID 11879129
36: Pediatric Eye Disease Investigator Group. A randomized trial of near versus distance activities while patching for amblyopia in children aged 3 to less than 7 years. Ophthalmology 2008;115(11):2071-8. PMID 18789533
37: Pediatric Eye Disease Investigator Group, Repka MX, Kraker RT, et al. A randomized trial of levodopa as treatment for residual amblyopia in older children. Ophthalmology 2015;122(5):874-81. PMID 25676904
38: Pineles SL, Kraker RT, VanderVeen DK, et al. Atropine for the prevention of myopia progression in children. Ophthalmology 2017;124(12):1857-66.** PMID 28669492
39: Repka MX, Beck RW, Holmes JM, et al. A randomized trial of patching regimens for treatment of moderate amblyopia in children. Arch Ophthalmol 2003;121(5):603-11. PMID 12742836
40: Repka MX, Cotter SA, Beck RW, et al. A randomized trial of atropine regimens for treatment of moderate amblyopia in children. Ophthalmology 2004;111(11):2076-85. PMID 15522375
41: Repka MX, Wallace DK, Beck RW, et al; PEDIG. Two-year follow-up of a 6-month randomized trial of atropine vs patching for treatment of moderate amblyopia in children. Arch Ophthalmol 2005;123(2):149-57. PMID 15710809
42: Scheiman MM, Hertle RW, Beck RW, et al. Randomized trial of treatment of amblyopia in children aged 7 to 17 years. Arch Ophthalmol 2005;123(4):437-47. PMID 15824215
43: Schroder JH, Fries P, Roelfsema PR, Singer W, Engel AK. Ocular dominance in extrastriate cortex of strabismic amblyopic cats. Vision Res 2002;42:29-39. PMID 11804629
44: Scott WE, Dickey CF. Stability of visual acuity in amblyopic patients after visual maturity. Graefes Arch Clin Exp Ophthalmol 1998;266(2):154-7. PMID 3360344
45: Simonsz HJ, Polling JR, Voorn R, et al. Electronic monitoring of treatment compliance in patching for amblyopia. Strabismus 1999;7:113-23. PMID 10420216
46: Vedamurthy I, Nahum M, Huang SJ, et al. A dichoptic custom-made action video game as a treatment for adult amblyopia. Vision Res 2015;114:173-87. PMID 25917239
47: Vitale S, Sperduto RD, Ferris FL 3rd. Increased prevalence of myopia in the United States between 1971-1972 and 1999-2004. Arch Ophthalmol 2009;127(12):1632. PMID 20008719
48: von Noorden GK. Amblyopia: a multidisciplinary approach. Invest Ophthalmol Vis Sci 1985;26:1704-16. PMID 3934105
49: von Noorden GK. Examination of the patient – IV. In: Binocular vision and ocular motility: theory and management of strabismus. 6th edition. St. Louis: CV Mosby, 2001:249.
50: von Noorden GK, Crawford ML. The lateral geniculate nucleus in human strabismic amblyopia. Invest Ophthlamol Vis Sci 1992;33(9):2729-32. PMID 1639619
51: von Noorden GK, Middleditch PR. Histology of the monkey lateral geniculate nucleus after unilateral lid closure and experimental strabismus: further observations. Invest Ophthalmol 1975;14:674-83. PMID 808514
52: Wallace DK, Repka MX, Lee KA, Melia M, Christiansen SP, Morse CL, et al. Amblyopia Preferred Practice Pattern®. Ophthalmology 2018;125(1):P105-42.** PMID 29108744
53: Wiesel TN, Hubel DH. Single-cell responses in striate cortex of kittens deprived of vision in one eye. J Neurophysiol 1963;26:1003-17. PMID 14084161
54: Wiesel TN, Hubel DH. Comparison of the effects of unilateral and bilateral eye closure on cortical unit responses in kittens. J Neurophysiol 1965;28(6):1029-40. PMID 5883730
55: Writing Committee for the Pediatric Eye Disease Investigator Group, Cotter SA, Foster NC, et al. Optical treatment of strabismic and combined strabismic-anisometropic amblyopia. Ophthalmology 2012;119(1):150-8. PMID 21959371
56: Yalcin E, Balci O. Efficacy of perceptual vision therapy in enhancing visual acuity and contrast sensitivity function in adult hypermetropic anisometropic amblyopia. Clin Ophthalmol 2014;8:49-53. PMID 24376340
57: Zhang JY, Cong LJ, Klein SA, Levi DM, Yu C. Perceptual learning improves adult amblyopic vision through rule-based cognitive compensation. Invest Ophthalmol Vis Sci 2014;55(4):2020-30. PMID 24550359

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Benjamin Jastrzembski MD

Dr. Jastrzembski of University of California, Davis has no relevant financial relationships to disclose.
See Profile

Editor

Heather E Moss MD PhD

Dr. Moss of Stanford University has no relevant financial relationships to disclose.
See Profile

Former Authors

Iris S Kassem MD PhD
Jeffrey N Bloom MD and Stacy L Pineles MD

Patient Profile

Age range of presentation: 0 month to 12 years
Sex preponderance: male=female
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-9: Amblyopia, unspecified: 368.00

Amblyopia, strabismic: 368.01

Amblyopia, deprivation: 368.02

Amblyopia, refractive: 368.03
ICD-10: Amblyopia ex anopsia: H53.0

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Amblyopia

Associated Disorders

Anisometropia
Congenital cataract
Congenital corneal opacity
Congenital ptosis
Strabismus

Differential Diagnosis

any unilateral vision loss
any bilateral vision loss
other visual abnormalities
optic nerve atrophy
nonamblyopic vision abnormalities

Amblyopia

Amblyopia

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Brain death/death by neurologic criteria

Hepatic encephalopathy

Bowel dysfunction in neurologic disorders

Coma due to primary brainstem and diencephalic lesions

Giant cell arteritis

Ischemic optic neuropathy

Transient visual loss

Vestibular schwannoma

Amblyopia

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Brain death/death by neurologic criteria

Hepatic encephalopathy

Bowel dysfunction in neurologic disorders

Coma due to primary brainstem and diencephalic lesions

Giant cell arteritis

Ischemic optic neuropathy

Transient visual loss

Vestibular schwannoma

This is an article preview.
Start a Free Account
to access the full version.