There is generally no treatment to cure color deficiencies. ″The American Optometric Association reports a contact lens on one eye can increase the ability to differentiate between colors, though nothing can make you truly see the deficient color.″

Optometrists can supply colored spectacle lenses or a single red-tint contact lens to wear on the non-dominant eye, but although this may improve discrimination of some colors, it can make other colors more difficult to distinguish. A 1981 review of various studies to evaluate the effect of the X-chrom contact lens concluded that, while the lens may allow the wearer to achieve a better score on certain color vision tests, it did not correct color vision in the natural environment. A case history using the X-Chrom lens for a rod monochromat is reported and an X-Chrom manual is online.

Lenses that filter certain wavelengths of light can allow people with a cone anomaly, but not dichromacy, to see better separation of colors, especially those with classic "red/green" color blindness. They work by notching out wavelengths that strongly stimulate both red and green cones in a deuter- or protanomalous person, improving the distinction between the two cones' signals. As of 2013, sunglasses that notch out color wavelengths are available commercially.

There is generally no treatment to cure achromatopsia. However, dark red or plum colored filters are very helpful in controlling light sensitivity.

Since 2003, there is a cybernetic device called eyeborg that allows people to perceive color through sound waves. Achromatopsic artist Neil Harbisson was the first to use such a device in early 2004, the eyeborg allowed him to start painting in color by memorizing the sound of each color.

Moreover, there is some research on gene therapy for animals with achromatopsia, with positive results on mice and young dogs, but less effectiveness on older dogs. However, no experiments have been made on humans. There are many challenges to conducting gene therapy on humans. See Gene therapy for color blindness for more details about it.

Since there is no cure for albinism, it is managed through lifestyle adjustments. People with albinism need to take care not to sunburn and should have regular healthy skin checks by a dermatologist.

For the most part, treatment of the eye conditions consists of visual rehabilitation. Surgery is possible on the extra-ocular muscles to decrease strabismus. Nystagmus-damping surgery can also be performed, to reduce the "shaking" of the eyes back and forth. The effectiveness of all these procedures varies greatly and depends on individual circumstances.

Glasses, low vision aids, large-print materials, and bright angled reading lights can help individuals with albinism. Some people with albinism do well using bifocals (with a strong reading lens), prescription reading glasses, hand-held devices such as magnifiers or monoculars or wearable devices like eSight

and Brainport.

Albinism is often associated with the absence of an iris in the eye. Contact lenses may be colored to block light transmission through the aniridic eye. Some use bioptics, glasses which have small telescopes mounted on, in, or behind their regular lenses, so that they can look through either the regular lens or the telescope. Newer designs of bioptics use smaller light-weight lenses. Some US states allow the use of bioptic telescopes for driving motor vehicles. (See also NOAH bulletin "Low Vision Aids".)

To support those with albinism, and their families, the National Organization for Albinism and Hypopigmentation was set up to provide a network of resources and information.

There is no cure for retinitis pigmentosa, but the efficacy and safety of various prospective treatments are currently being evaluated. The efficiency of various supplements, such as Vitamin A, DHA, and Lutein, in delaying disease progression remains an unresolved, yet prospective treatment option. Clinical trials investigating optic prosthetic devices, gene therapy mechanisms, and retinal sheet transplantations are active areas of study in the partial restoration of vision in retinitis pigmentosa patients.

Studies have demonstrated the delay of rod photoreceptor degeneration by the daily intake of 15000 IU (equivalent to 4.5 mg) of vitamin A palmitate; thus, stalling disease progression in some patients. Recent investigations have shown that proper vitamin A supplementation can postpone blindness by up to 10 years (by reducing the 10% loss pa to 8.3% pa) in some patients in certain stages of the disease.

The Argus retinal prosthesis became the first approved treatment for the disease in February 2011, and is currently available in Germany, France, Italy, and the UK. Interim results on 30 patients long term trials were published in 2012. The Argus II retinal implant has also received market approval in the US. The device may help adults with RP who have lost the ability to perceive shapes and movement to be more mobile and to perform day-to-day activities. In June 2013, twelve hospitals in the US announced they would soon accept consultation for patients with RP in preparation for the launch of Argus II later that year. The Alpha-IMS is a subretinal implant involving the surgical implantation of a small image-recording chip beneath the optic fovea. Measures of visual improvements from Alpha-IMS studies require the demonstration of the device's safety before proceeding with clinical trials and granting market approval.

The goal of gene therapy studies is to virally supplement retinal cells expressing mutant genes associated with the retinitis pigmentosa phenotype with healthy forms of the gene; thus, allowing the repair and proper functioning of retinal photoreceptor cells in response to the instructions associated with the inserted healthy gene. Clinical trials investigating the insertion of the healthy RPE65 gene in retinas expressing the LCA2 retinitis pigmentosa phenotype measured modest improvements in vision; however, the degradation of retinal photoreceptors continued at the disease-related rate. Likely, gene therapy may preserve remaining healthy retinal cells while failing to repair the earlier accumulation of damage in already diseased photoreceptor cells. Response to gene therapy would theoretically benefit young patients exhibiting the shortest progression of photoreceptor decline; thus, correlating to a higher possibility of cell rescue via the healthy inserted gene.

The progressive nature of and lack of a definitive cure for retinitis pigmentosa contribute to the inevitably discouraging outlook for patients with this disease. While complete blindness is rare, the patient's visual acuity and visual field will continue to decline as initial rod photoreceptor and later cone photoreceptor degradation proceeds. Possible treatments remain in the research and clinical trial stages; however, treatment studies concerning visual restoration in retinitis pigmentosa prove promising for the future.

Studies indicate that children carrying the disease genotype benefit from presymptomatic counseling in order to prepare for the physical and social implications associated with progressive vision loss. While the psychological prognosis can be slightly alleviated with active counseling the physical implications and progression of the disease depend largely on the age of initial symptom manifestation and the rate of photoreceptor degradation, rather than access to prospective treatments. Corrective visual aids and personalized vision therapy provided by Low Vision Specialists may help patients correct slight disturbances in visual acuity and optimize their remaining visual field. Support groups, vision insurance, and lifestyle therapy are additional useful tools for those managing progressive visual decline.

Though there is no treatment for Cone dystrophy, certain supplements may help in delaying the progression of the disease.

The beta-carotenoids, lutein and zeaxanthin, have been evidenced to reduce the risk of developing age related macular degeneration (AMD), and may therefore provide similar benefits to Cone dystrophy sufferers.

Consuming omega-3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid) has been correlated with a reduced progression of early AMD, and in conjunction with low glycemic index foods, with reduced progression of advanced AMD, and may therefore delay the progression of cone dystrophy.

Currently, there is no treatment for the disease. However, ophthalmologists recommend wearing sunglasses and hats outdoors and blue-light blocking glasses when exposed to artificial light sources, such as screens and lights. Tobacco smoke and second-hand smoke should be avoided. Animal studies also show that high doses of vitamin A can be detrimental by building up more lipofuscin toxin. Dietary non-supplemental vitamin A intake may not further the disease progression.

Clinical trials are being conducted with promising early results. The trials may one day lead to treatments that might halt, and possibly even reverse, the effects of Stargardt disease using stem cell therapy, gene therapy, or pharmacotherapy.

The Argus retinal prosthesis, an electronic retinal implant, was successfully fitted to a 67-year-old woman in Italy at the Careggi Hospital in 2016. The patient had a very advanced stage of Stargardt’s disease, and a total absence of peripheral and central visual fields.

Genetic testing can confirm albinism and what variety it is, but offers no medical benefits except in the cases of non-OCA disorders that cause albinism "along with" other medical problems which may be treatable. There is no 'cure' for Albinism. The "symptoms" of albinism can be assisted by various methods.

Dichromacy ("di" meaning "two" and "chroma" meaning "color") is the state of having two types of functioning color receptors, called cone cells, in the eyes. Organisms with dichromacy are called dichromats. Dichromats can match any color they see with a mixture of no more than two pure spectral lights. By comparison, trichromats require three pure spectral lights to match all colors that they can perceive, and tetrachromats require four.

Dichromacy in humans is a color vision defect in which one of the three basic color mechanisms is absent or not functioning. It is hereditary and sex-linked, predominantly affecting males. Dichromacy occurs when one of the cone pigments is missing and color is reduced to two dimensions.

The following may provide relief:

- Cold compresses

- Pad and bandage with antibiotics drops for 24 hours, heals most of the cases

- anaesthetic drops should not be used

- Oral analgesics if pain is intolerable

- Single dose of tranquilizers

In the early stages, there are a few treatment options. Laser surgery or cryotherapy (freezing) can be used to destroy the abnormal blood vessels, thus halting progression of the disease. However, if the leaking blood vessels are clustered around the optic nerve, this treatment is not recommended as accidental damage to the nerve itself can result in permanent blindness. Although Coats' disease tends to progress to visual loss, it may stop progressing on its own, either temporarily or permanently. Cases have been documented in which the condition even reverses itself. However, once total retinal detachment occurs, sight loss is permanent in most cases. Removal of the eye (enucleation) is an option if pain or further complications arise.

There are various kinds of color blindness:

- Protanopia is a severe form of red-green color blindness, in which there is impairment in perception of very long wavelengths, such as reds. To these individuals, reds are perceived as beige or grey and greens tend to look beige or grey like reds. It is also the most common type of dichromacy today. This problem occurs because patients do not have the red cone cells in the retina. Protanomaly is a less severe version.

- Deuteranopia consists of an impairment in perceiving medium wavelengths, such as greens. Deuteranomaly is a less severe form of deuteranopia. Those with deuteranomaly cannot see reds and greens like those without this condition; however, they can still distinguish them in most cases. It is very similar to protanopia. In this form, patients do not have green cone cells in the retina, which makes it hard to see the green color.

- A rarer form of color blindness is tritanopia, where there exists an inability to perceive short wavelengths, such as blues. Sufferers have trouble distinguishing between yellow and blue. They tend to confuse greens and blues, and yellow can appear pink. This is the rarest of all dichromacy, and occurs in around 1 in 100,000 people. Patients do not have the blue cone cells in the retina.

Acquired heterochromia is usually due to injury, inflammation, the use of certain eyedrops that damages the iris, or tumors.

An odd-eyed cat is a cat with one blue eye and one eye either green, yellow, or brown. This is a feline form of complete heterochromia, a condition that occurs in some other animals. The condition most commonly affects white-colored cats, but may be found in a cat of any color, provided that it possesses the white spotting gene.

There are good results from multiple doses of intravitreal injections of anti-VEGF drugs such as bevacizumab. A 2017 systematic review update found moderate evidence that aflibercept may have advantages in improving visual outcomes over bevacizumab and ranibizumab, after one year. Present recommended treatment for diabetic macular edema is Modified Grid laser photocoagulation combined with multiple injections of anti-VEGF drugs.

Treatment of toxic and nutritional optic neuropathy is dictated by the cause of the disorder.

- Toxic optic neuropathy is treated by identification and removal of the offending agent. Depending upon the individual affected, the nature of the agent, total exposure prior to removal, and degree of vision loss at the time of diagnosis, the prognosis is variable.

- Nutritional optic neuropathy is treated with improved nutrition. A well-balanced diet with plenty of protein and green leafy vegetables, vitamin supplementation (thiamine, vitamin B, folic acid, multivitamins), and reduction of smoking and/or drinking are the mainstay of treatment. Again, prognosis is variable and dependent upon the affected individual, treatment compliance, and degree of vision loss at diagnosis.

In both toxic and nutritional neuropathy, vision generally recovers to normal over several days to weeks, though it may take months for full restoration and there is always the risk of permanent vision loss. Visual acuity usually recovers before color vision.

The odd-eyed coloring is caused when either the epistatic (dominant) white gene (which masks any other color genes and turns a cat completely white) or the white spotting gene (which is the gene responsible for bicolor and tuxedo cats) prevents melanin (pigment) granules from reaching one eye during development, resulting in a cat with one blue eye and one green, yellow, or brown eye. The condition only rarely occurs in cats that lack both the dominant white and the white spotting gene.

Triamcinolone is a long acting steroid preparation. When injected in the vitreous cavity, it decreases the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, and results in an increase in visual acuity. The effect of triamcinolone is transient, lasting up to three months, which necessitates repeated injections for maintaining the beneficial effect. Best results of intravitreal Triamcinolone have been found in eyes that have already undergone cataract surgery. Complications of intravitreal injection of triamcinolone include cataract, steroid-induced glaucoma and endophthalmitis. A systematic review found evidence that eyes treated with the intravitreal injection of triamcinolone had better visual acuity outcomes compared to eyes treated with macular laser grid photocoagulation, or sham injections.

Achromatopsia (ACHM), also known as total color blindness, is a medical syndrome that exhibits symptoms relating to at least five conditions. The term may refer to acquired conditions such as cerebral achromatopsia, also known as color agnosia, but it typically refers to an autosomal recessive congenital color vision condition, the inability to perceive color and to achieve satisfactory visual acuity at high light levels (typically exterior daylight). The syndrome is also present in an incomplete form which is more properly defined as dyschromatopsia. It is estimated to affect 1 in 40,000 live births worldwide.

There is some discussion as to whether achromats can see color or not. As illustrated in "The Island of the Colorblind" by Oliver Sacks, some achromats cannot see color, only black, white, and shades of grey. With five different genes currently known to cause similar symptoms, it may be that some do see marginal levels of color differentiation due to different gene characteristics. With such small sample sizes and low response rates, it is difficult to accurately diagnose the 'typical achromatic conditions'. If the light level during testing is optimized for them, they may achieve corrected visual acuity of 20/100 to 20/150 at lower light levels, regardless of the absence of color. One common trait is hemeralopia or blindness in full sun. In patients with achromatopsia, the cone system and fibres carrying color information remain intact. This indicates that the mechanism used to construct colors is defective.

Nyctalopia (from Greek νύκτ-, "nykt-" "night"; ἀλαός, "alaos" "blind, not seeing", and ὄψ, "ops" "eye"), also called night-blindness, is a condition making it difficult or impossible to see in relatively low light. It is a symptom of several eye diseases. Night blindness may exist from birth, or be caused by injury or malnutrition (for example, vitamin A deficiency). It can be described as insufficient adaptation to darkness.

The most common cause of nyctalopia is retinitis pigmentosa, a disorder in which the rod cells in the retina gradually lose their ability to respond to the light. Patients suffering from this genetic condition have progressive nyctalopia and eventually their daytime vision may also be affected. In X-linked congenital stationary night blindness, from birth the rods either do not work at all, or work very little, but the condition doesn't get worse.

Another cause of night blindness is a deficiency of retinol, or vitamin A, found in fish oils, liver and dairy products.

The opposite problem, the inability to see in bright light, is known as "hemeralopia" and is much rarer.

Since the outer area of the retina is made up of more rods than cones, loss of peripheral vision often results in night blindness. Individuals suffering from night blindness not only see poorly at night, but also require extra time for their eyes to adjust from brightly lit areas to dim ones. Contrast vision may also be greatly reduced.

Rods contain a receptor-protein called rhodopsin. When light falls on rhodopsin, it undergoes a series of conformational changes ultimately generating electrical signals which are carried to the brain via the optic nerve. In the absence of light, rhodopsin is regenerated. The body synthesizes rhodopsin from vitamin A, which is why a deficiency in vitamin A causes poor night vision.

Refractive "vision correction" surgery (especially PRK with the complication of "haze") may rarely cause a reduction in best night-time acuity due to the impairment of contrast sensitivity function (CSF) which is induced by intraocular light-scatter resulting from surgical intervention in the natural structural integrity of the cornea.

Heterochromia has also been observed in those with Duane syndrome.

Aulus Cornelius Celsus, writing ca. 30 AD, described night blindness and recommended an effective dietary supplement: "There is besides a weakness of the eyes, owing to which people see well enough indeed in the daytime but not at all at night; in women whose menstruation is regular this does not happen. But success sufferers should anoint their eyeballs with the stuff dripping from a liver whilst roasting, preferably of a he-goat, or failing that of a she-goat; and as well they should eat some of the liver itself."

Historically, nyctalopia, also known as moonblink, was a temporary night blindness believed to be caused by sleeping in moonlight in the tropics.

In the French language, and have inverse meanings, the first naming the ability to see in the dark as well as in plain light, and the second the inability to do so. It is thought that this inversion from Latin happened during the 2nd century AD, even though the ancient greek νυκτάλωψ ("nuktálōps") has been used in both senses.

Treatment modalities currently under clinical investigation include cell therapy, gene therapy and oral therapies.

Regarding cell therapy, Advanced Cell Technology, now called Ocata Therapeutics, has completed Phase I/II multicenter clinical trial using retinal cells derived from human embryonic stem cells (hESCs) to treat patients with Stargardt. After treating and collecting data on 18 patients, Advanced Cell was given approval to test its stem cell therapy on patients with 20/100 vision. In October 2014, the results of the Phase I/II clinical trial were published in "the Lancet".

Research at the preclinical (animal) stage include a new compound that can remove lipofuscin from retinal pigment epithelial cells.

Distortion of vision refers to straight lines not appearing straight, but instead bent, crooked, or wavy. Usually this is caused by distortion of the retina itself. This distortion can herald a loss of vision in macular degeneration, so anyone with distorted vision should seek medical attention by an ophthalmologist promptly. Other conditions leading to swelling of the retina can cause this distortion, such as macular edema and central serous chorioretinopathy.

An Amsler grid can be supplied by an ophthalmologist so that the vision can be monitored for distortion in people who may be predisposed to this problem.

Tunnel vision implies that the peripheral vision, or side vision, is lost, while the central vision remains. Thus, the vision is like looking through a tunnel, or through a paper towel roll. Some disorders that can cause this include:

Glaucoma - severe glaucoma can result in loss of nearly all of the peripheral vision, with a small island of central vision remaining. Sometimes even this island of vision can be lost as well.

Retinitis pigmentosa - This is usually a hereditary disorder which can be part of numerous syndromes. It is more common in males. The peripheral retina develops pigmentary deposits, and the peripheral vision gradually becomes worse and worse. The central vision can be affected eventually as well. People with this problem may have trouble getting around in the dark. Cataract can be a complication as well. There is no known treatment for this disorder, and supplements of Vitamin A have not been proven to help.

Punctate Inner Choroidopathy - This condition is where vessels gro (( material is missing ))

Stroke - a stroke involving both sides of the visual part of the brain may wipe out nearly all of the peripheral vision. Fortunately, this is a very rare occurrence