Many applications for iPhone and iPad have been developed to help colorblind people to view the colors in a better way. Many applications launch a sort of simulation of colorblind vision to make normal-view people understand how the color-blinds see the world. Others allow a correction of the image grabbed from the camera with a special "daltonizer" algorithm.

The GNOME desktop environment provides colorblind accessibility using the gnome-mag and the libcolorblind software. Using a gnome applet, the user may switch a color filter on and off, choosing from a set of possible color transformations that will displace the colors in order to disambiguate them. The software enables, for instance, a colorblind person to see the numbers in the Ishihara test.

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.

Blindness can occur in combination with such conditions as intellectual disability, autism spectrum disorders, cerebral palsy, hearing impairments, and epilepsy. Blindness in combination with hearing loss is known as deafblindness.

It has been estimated that over half of completely blind people have non-24-hour sleep–wake disorder, a condition in which a person's circadian rhythm, normally slightly longer than 24 hours, is not entrained (synchronized) to the light/dark cycle.

The World Health Organization estimates that 80% of visual loss is either preventable or curable with treatment. This includes cataracts, onchocerciasis, trachoma, glaucoma, diabetic retinopathy, uncorrected refractive errors, and some cases of childhood blindness. The Center for Disease Control and Prevention estimates that half of blindness in the United States is preventable.

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.

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.

Vitamin A supplementation plays an important role, specifically vitamin A deficiency is a top causes of preventable childhood blindness. Though in measles cases, the administration of the vitamin to offset visual impairment has not been proven effective, as of yet.

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.

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.

As with some newborn mammals, all cats are blue-eyed as kittens, and may change as the newborn ages. The differences in an odd-eyed kitten's eye color might not be noticeable, save upon close inspection. Odd-eyed kittens have a different shade of blue in each eye. The color of the odd eye changes over a period of months–for example, from blue to green to yellow or from green to blue to yellow–until it reaches its final, adult color.

Risk factors such as UVB exposure and smoking can be addressed. Although no means of preventing cataracts has been scientifically proven, wearing sunglasses that counteract ultraviolet light may slow their development. While adequate intake of antioxidants (such as vitamins A, C, and E) has been thought to protect against the risk of cataracts, clinical trials have shown no benefit from supplements; though evidence is mixed, but weakly positive, for a potential protective effect of the nutrients lutein and zeaxanthin. Statin use is somewhat associated with a lower risk of nuclear sclerotic cataracts.

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

Heterochromia has also been observed in those with Duane syndrome.

People with hemeralopia may benefit from sunglasses. Wherever possible, environmental illumination should be adjusted to comfortable level. Light-filtering lenses appear to help in people reporting photophobia.

Otherwise, treatment relies on identifying and treating any underlying disorder.

is a program launched by the International Agency for the Prevention of Blindness (IAPB) and is supported by the WHO in 1999 that has made controlling blindness in children a high priority.

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.

Low vitamin C intake and serum levels have been associated with greater cataract rates. However, use of supplements of vitamin C has not demonstrated benefit.

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.

Hemeralopia (from Greek "ημέρα", hemera "day"; and "αλαός", alaos "blindness") is the inability to see clearly in bright light and is the exact opposite of nyctalopia (night blindness). Hemera was the Greek goddess of day and Nyx was the goddess of night. However, it has been used in an opposite sense by many non-English-speaking doctors. It can be described as insufficient adaptation to bright light. It is also called heliophobia and day blindness.

In hemeralopia, daytime vision gets worse, characterised by photoaversion (dislike/avoidance of light) rather than photophobia (eye discomfort/pain in light) which is typical of inflammations of eye. Nighttime vision largely remains unchanged due to the use of rods as opposed to cones (during the day), which are affected by hemeralopia and in turn degrade the daytime optical response. Hence many patients feel they see better at dusk than in daytime.

Controversies exist around eliminating this disorder from breeding Collies. Some veterinarians advocate only breeding dogs with no evidence of disease, but this would eliminate a large portion of potential breeding stock. Because of this, others recommend only breeding mildly affected dogs, but this would never completely eradicate the condition. Also, mild cases of choroidal hypoplasia may become pigmented and therefore undiagnosable by the age of three to seven months. If puppies are not checked for CEA before this happens, they may be mistaken for normal and bred as such. Checking for CEA by seven weeks of age can eliminate this possibility. Diagnosis is also difficult in dogs with coats of dilute color because lack of pigment in the choroid of these animals can be confused with choroidal hypoplasia. Also, because of the lack of choroidal pigment, mild choroidal hypoplasia is difficult to see, and therefore cases of CEA may be missed.

Until recently, the only way to know if a dog was a carrier was for it to produce an affected puppy. However, a genetic test for CEA became available at the beginning of 2005, developed by the Baker Institute for Animal Health, Cornell University, and administered through OptiGen. The test can determine whether a dog is affected, a carrier, or clear, and is therefore a useful tool in determining a particular dog's suitability for breeding.

Prophylaxis consists of periodic administration of Vitamin A supplements. WHO recommended schedule, which is universally recommended is as follows:

- Infants 6–12 months old and any older children weighing less than 8 kg - 100,000 IU orally every 3–6 months

- Children over 1 year and under 6 years of age - 200,000 IU orally every 6 months

- Infants less than 6 months old, who are not being breastfed - 50,000 IU orally should be given before they attain the age of 6 months

Future treatments may involve retinal transplants, artificial retinal implants, gene therapy, stem cells, nutritional supplements, and/or drug therapies.

2006: UK researchers transplanted mouse stem cells which were at an advanced stage of development, and already programmed to develop into photoreceptor cells, into mice that had been genetically induced to mimic the human conditions of retinitis pigmentosa and age-related macular degeneration. These photoreceptors developed and made the necessary neural connections to the animal's retinal nerve cells, a key step in the restoration of sight. Previously it was believed that the mature retina has no regenerative ability. This research may in the future lead to using transplants in humans to relieve blindness.

2008: Scientists at the Osaka Bioscience Institute have identified a protein, named Pikachurin, which they believe could lead to a treatment for retinitis pigmentosa.

2008: Retinitis pigmentosa was attempted to be linked to gene expression of FAM46A.

2010: A possible gene therapy seems to work in mice.

2012: Scientists at the Columbia University Medical Center showed on an animal model that gene therapy and induced pluripotent stem cell therapy may be viable options for treating retinitis pigmentosa in the future.

2012: Scientists at the University of Miami Bascom Palmer Eye Institute presented data showing protection of photoreceptors in an animal model when eyes were injected with mesencephalic astrocyte-derived neurotrophic factor (MANF).

Researchers at the University of California, Berkeley were able to restore vision to blind mice by exploiting a "photoswitch" that activates retinal ganglion cells in animals with damaged rod and cone cells.

2015: A study by Bakondi et al. at Cedars-Sinai Medical Center showed that CRISPR/Cas9 can be used to treat rats with the autosomal dominant form of retinitis pigmentosa.

2016: RetroSense Therapeutics aimed to inject viruses with DNA from light-sensitive algae into the eyes of several blind people (who have retinitis pigmentosa). If successful, they will be able to see in black and white.

Treatment can occur in two ways: treating symptoms and treating the deficiency. Treatment of symptoms usually includes the use of artificial tears in the form of eye drops, increasing the humidity of the environment with humidifiers, and wearing wraparound glasses when outdoors. Treatment of the deficiency can be accomplished with a Vitamin A or multivitamin supplement or by eating foods rich in Vitamin A. Treatment with supplements and/or diet can be successful until the disease progresses as far as corneal ulceration, at which point only an extreme surgery can offer a chance of returning sight.

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.