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Jun. 17, 2026
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Amblyopia
- Updated 04.07.2026
- Released 01.30.2003
- Expires For CME 04.07.2029
Amblyopia
Introduction
Overview
Amblyopia is defined as reduced visual acuity caused by the lack of receiving a focused image on the fovea during early childhood (02). The deficit is nearly always limited to one eye. It occurs in three settings: anisometropia, ocular misalignment (strabismus), and a lesion of the lid or ocular media that prevents formation of an image on the fovea (deprivation). Amblyopia occurs with an estimated prevalence of 1.4% (33; 10; 29; 28; 12). Unless treated during childhood, the impaired visual acuity is generally permanent. Amblyopia treatment often requires favoring vision in the amblyopic eye by discouraging vision in the non-amblyopic eye (“penalization”). New treatment options for amblyopia that use virtual reality headsets are becoming available.
Key points
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• Amblyopia is a reduction in visual acuity secondary to abnormal visual processing in one or both eyes due to uncorrected refractive error, ocular misalignment (strabismus), or visual deprivation. | |
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• Treatment of amblyopia involves addressing its underlying cause, as well as temporarily weakening visual processing by the better-seeing eye (“penalization”). | |
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• Treatment is most effective when undertaken soon after diagnosis. | |
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• If not treated early, visual impairment from amblyopia will usually be permanent. |
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 (08). 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 normally sighted eye to “force” the amblyopic eye to see better (08). The understanding 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 (48; 49). 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. By contrast, blocking visual input in adult animals made no difference in the anatomy of the visual cortex or in vision. These investigators concluded that there is a critical period of neuroplasticity in early life during which visual stimulation is required for normal visual cortex development. As a result of their work and subsequent studies by other investigators, amblyopia was recognized as a developmental visual disorder (43; 26; 39).
Clinical manifestations
Presentation and course
In early childhood, the lack of a focused image presented to the fovea results in impaired visual input to the brain. The impaired visual input during the critical period of visual cortical plasticity results in subnormal visual acuity in the affected eye and incomplete visual cortex development in those regions receiving input from the affected eye. The degree of vision loss may vary from a minimal decrease in acuity to bare light perception. Total loss of vision (no light perception) does not occur in amblyopia without the presence of other disease. Unless treated during childhood, the visual deficit will nearly always persist (40; 21).
Amblyopia is categorized as refractive, strabismic, or 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 cannot usually be eliminated by correcting the refractive error alone. Because of the abnormalities in central visual processing that exist in refractive amblyopia, visual acuity will remain subnormal even after eliminating image blur with appropriate spectacles or contact lenses. The associated amblyopia must also be addressed.
The most common cause of refractive amblyopia is anisometropia, in which the refractive error differs between the two eyes (10; 28). The eye with the higher refractive error typically becomes amblyopic. Correction of the refractive error is the first step in therapy, but it is usually also necessary to disfavor the vision in the non-amblyopic eye by means of occlusion or by blocking accommodation (“penalization”) (05).
In strabismic amblyopia, the eyes are misaligned. One eye fixates the viewed target with the fovea; the other eye fixates the viewed target with a non-foveal element of the retina. In order to avoid diplopia, the youthful brain automatically suppresses the image perceived by the deviating eye. Over time, suppression causes amblyopia in the non-fixating eye and reduced binocularity. The severity of the suppression is directly correlated to the degree of impairment in visual acuity and binocularity (23). Strabismic amblyopia is more commonly associated with esotropia (convergent eye deviation or crossed eyes) than with exotropia (divergent eye deviation or “wall eyes”) (44).
The third category of amblyopia, and the least common, is deprivation. It may affect one eye or both. The cause is a structural abnormality that obstructs the visual axis. Examples include congenital cataracts, corneal opacities from trauma or infection, ptosis occluding the pupil, and vitreous or retinal hemorrhage as is often observed in nonaccidental infantile trauma. An infant is exquisitely sensitive to deprivation amblyopia, so concern for congenital cataracts or other ophthalmic disorders in an infant should be referred for urgent evaluation. However, even prompt cataract extraction is unlikely to restore normal visual acuity.
The critical period of visual development in humans lasts until approximately 9 years of age. Amblyopia may occur at any time during that period. 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 promptly addressed. 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 even some improvement in children treated initially in the second decade of life (38). The American Academy of Ophthalmology Preferred Practice Patterns recommends offering treatment to children of any age, even those in their adolescent years (47).
Amblyopia is most often limited to one eye, presenting as a difference in best-corrected vision between the two eyes. A difference in visual acuity of at least two optotype lines is accepted as a necessary minimum for a diagnosis of amblyopia. Such a minimum differential is meant to decrease the potential for false positive diagnoses. In preverbal children, where optotype visual acuity cannot be readily assessed, other methods must be used to diagnose amblyopia.
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 (40; 21).
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. Medical and family histories were noncontributory. In order to evaluate the vision in this preverbal infant, 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 maintained steady fixation. When the occluder was then moved to the right eye, the child moved the examiner’s hand away to see around the occluder. This objection to occlusion of the right eye indicated that the vision of the left eye was poorer than that of the right eye and that amblyopia might be the cause.
The child had an esotropia that measured 50 prism diopters using the Krimsky method, which involves shining a penlight at the infant’s eyes and placing prisms of increasing strength in front of the left eye in a stepwise approach until the light reflexes are aligned. Ocular excursions were normal except for subtle supraduction of each eye in adduction, consistent with inferior oblique overaction, a feature common in infantile esotropia. Otherwise, the ophthalmologic examination was normal.
The diagnosis was infantile esotropia. He was at high risk for profound strabismic amblyopia and loss of binocular vision. The amblyopia was treated with patching of the right eye for 2 hours daily. The timing of occlusion is designed to avoid occlusion amblyopia, a risk that is inversely proportional to the patient’s age. 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-operative ocular alignment, and that patients with infantile esotropia frequently require more than one strabismus surgery.
By his teenage years, the patient had achieved a visual acuity of 20/40 in the amblyopic left eye and had maintained a visual acuity 20/15 in the right eye. There was a small residual esotropia that was not noticeable to peers or family.
Biological basis
Etiology and pathogenesis
The pathogenesis of amblyopia is unsettled. Refractive amblyopia appears to be due to a decrease of the spatial resolution of neurons (20). Strabismus prevents stimulation of corresponding retinal points in each eye so that binocularity is disrupted. Visual deprivation produces physiological and anatomic changes of the visual pathways in animal models (48; 49). It results in a loss of binocularly driven cortical neurons and a loss of neurons responding to the amblyopic eye (01; 06). In addition to these abnormalities in the visual cortex, histologic changes have also been detected in the lateral geniculate bodies in deprivational and strabismic amblyopia (46; 45).
Epidemiology
The estimated global prevalence of amblyopia is approximately 1.4% (33; 10; 29; 28; 12). However, the accuracy of these estimates is poor due to the lack of data from certain regions and differences in study methodologies (12).
Prevention
Early detection of the major risk factors, namely refractive error, strabismus, and visual deprivation, improves the prevention of amblyopia.
After surgery for strabismus, monitoring for amblyopia must be maintained as patient families sometimes mistakenly consider surgery to be curative treatment for amblyopia. Children must be followed postoperatively until at least 9 years of age. Children with ptosis, cataract, or eye trauma require monitoring to identify early amblyopia and prevent its progression. As a child ages, the risk of developing amblyopia diminishes.
The presence of anisometropia (difference in refractive error between the two eyes) greatly increases the likelihood that refractive amblyopia will develop (10; 28). Early correction of anisometropia in young children is important, but may not eliminate amblyopia, which must be managed separately.
Differential diagnosis
Confusing conditions
The diagnosis of amblyopia is made by exclusion of other causes of visual impairment, including simple uncorrected refractive error, ocular media imperfections, retinal disorders, and optic nerve and other visual pathway disorders.
Amblyopia should not be diagnosed when visual impairment affects both eyes. The only exception to this rule is very high hyperopic refractive error, which should be evident during refraction.
When refractive, ocular media, retinal, and visual pathway disorders have been excluded, there remains the rare binocular impairment caused by visual cortex dysfunction (“cerebral visual impairment”). This diagnosis is most commonly made in children with a history of perinatal hypoxic-ischemic damage, often associated with premature birth and neonatal seizures (03).
Diagnostic workup
The basic diagnostic test for amblyopia is an age-appropriate determination of the visual acuity of each eye with identification of the source causing the amblyopia. Guidelines have been published for pediatric vision screening and referral criteria (24). In preverbal children, assessment of visual acuity is based on fixation and following of visual stimuli and relatively more resistance to occlusion of an eye. Verbal children should be asked to identify a series of letters or pictures on each acuity line.
Amblyopia is defined as visual acuity below that which is expected for age or a difference of two lines or more on the visual acuity chart. If such a deficit is identified, examination must be directed at excluding non-amblyopic causes of reduced visual acuity. It is well to remember that amblyopia may be identified at any age. But because there are no markers for amblyopia, it is a presumptive diagnosis based on the presence of at least one of its three settings (anisometropia, strabismus, visual deprivation) and once non-amblyopic causes have been excluded.
Management
Refractive error. Treatment of refractive error alone sometimes improves vision in refractive amblyopia and in strabismic amblyopia (05; 04; 50). However, penalization of the non-amblyopic eye is often necessary. Ordering spectacles on the Internet is not recommended due to the difficulty of fitting glasses in children. Contact lenses are indicated in specific clinical scenarios, such as after cataract extraction or in myopia control.
Occlusion. The most widely accepted and time-proven treatment of amblyopia is occlusion of the non-amblyopic 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 (35). For severe amblyopia, 6 hours of patching a day is recommended (15). Patching earlier in life results in better visual outcomes in children younger than 7 years old (11). Teenagers who have not previously been treated for amblyopia may also benefit from occlusion therapy (38).
Because occlusion of the non-amblyopic eye initially reduces visual acuity, compliance is often a serious problem limiting the effectiveness of patching (41), especially if it is not thoroughly explained to parents (07; 25).
Although there had been recommendations to have children devote activities to near visual tasks during occlusion therapy (15; 35), a randomized study comparing patching with and without emphasis on near activities demonstrated no difference in amblyopia relief (33).
Pharmacologic treatment. By blocking accommodation, pharmacologic cycloplegia of the non-amblyopic eye blurs its vision for near visual tasks. Treatment with one drop daily of atropine sulfate 1% solution was found to be comparable in relieving amblyopia to occlusion therapy in non-myopic children under 7 years old with moderate amblyopia (19; 32). Atropine given for two consecutive days a week (“weekend atropine”) is equally effective (36). Pharmacologic penalization has received higher acceptance than patching by families with amblyopic children (37).
Dichoptic treatment. Dichoptic treatment involves increasing the contrast of stimuli viewed by the amblyopic eye and reducing contrast received by the non-amblyopic eye. Effectiveness in relieving amblyopia was limited by games that were relatively unappealing to children (14; 42; 16; 18; 13; 27). A dichoptic device that provides a menu of age-appropriate video media using a virtual reality (VR) headset (Luminopia One) showed a one-line visual acuity improvement compared to the prescription of spectacles alone. This treatment is FDA-approved for refractive and strabismic amblyopia in children ages 4 to 7. Several similar treatments using VR headsets have also had promising results compared to patching (17; 51).
Surgery. For deprivation amblyopia, treatment is directed at the occluding structure, commonly cataract or ptosis. But for strabismic amblyopia, surgical correction of the ocular misalignment alone will not improve an associated amblyopia. In fact, penalization is often begun prior to surgical intervention.
For children with refractive amblyopia from large refractive error who do not tolerate spectacles or contact lenses, refractive surgery such as photorefractive keratectomy (PRK) or laser-assisted in situ keratomileusis (LASIK) may be used (31).
Other treatments. Further research is necessary to prove that perceptual learning techniques that present images hypothesized to correspond to the receptive field of the visual cortex are effective in treating amblyopia (52; 53; 21). However, RevitalVision, a computerized perceptual learning amblyopia treatment system, is FDA-approved for treatment in patients aged 9 years or older.
Levodopa has been studied as a potential pharmacologic therapy to augment occlusion therapy, but results have not been clearly positive (22; 30; 34; 09). 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 relative to 2 hours of daily patching (34).
There is insufficient evidence to support the use of vision therapy eye exercises for the treatment of amblyopia (47).
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Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Author
-
Jonathan D Trobe MD
Dr. Trobe of the University of Michigan has no relevant financial relationships to disclose.
See Profile
Former Authors
- Jeffrey N Bloom MD
- Stacy L Pineles MD
- Iris S Kassem MD PhD
- Benjamin Jastrzembski MD
- Heather E Moss MD PhD
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-10
-
- Amblyopia ex anopsia: H53.0
- ICD-11
-
- Impairment of binocular functions: 9D46
- Other specified disorder of the optic nerve: 9C40.Y
- Other specified symptoms or signs involving the visual system: MC1Y
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