The Ishihara color test, which consists of a series of pictures of colored spots, is the test most often used to diagnose red–green color deficiencies. A figure (usually one or more Arabic digits) is embedded in the picture as a number of spots in a slightly different color, and can be seen with normal color vision, but not with a particular color defect. The full set of tests has a variety of figure/background color combinations, and enable diagnosis of which particular visual defect is present. The anomaloscope, described above, is also used in diagnosing anomalous trichromacy.

Because the Ishihara color test contains only numerals, it may not be useful in diagnosing young children, who have not yet learned to use numerals. In the interest of identifying these problems early on in life, alternative color vision tests were developed using only symbols (square, circle, car).

Besides the Ishihara color test, the US Navy and US Army also allow testing with the Farnsworth Lantern Test. This test allows 30% of color deficient individuals, whose deficiency is not too severe, to pass.

Another test used by clinicians to measure chromatic discrimination is the Farnsworth-Munsell 100 hue test. The patient is asked to arrange a set of colored caps or chips to form a gradual transition of color between two anchor caps.

The HRR color test (developed by Hardy, Rand, and Rittler) is a red–green color test that, unlike the Ishihara, also has plates for the detection of the tritan defects.

Most clinical tests are designed to be fast, simple, and effective at identifying broad categories of color blindness. In academic studies of color blindness, on the other hand, there is more interest in developing flexible tests to collect thorough datasets, identify copunctal points, and measure just noticeable differences.

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.

It is important that people be examined by someone specializing in low vision care prior to other rehabilitation training to rule out potential medical or surgical correction for the problem and to establish a careful baseline refraction and prescription of both normal and low vision glasses and optical aids. Only a doctor is qualified to evaluate visual functioning of a compromised visual system effectively. The American Medical Association provides an approach to evaluating visual loss as it affects an individual's ability to perform activities of daily living.

Screening adults who have no symptoms is of uncertain benefit.

Visual impairment has the ability to create consequences for health and well being. Visual impairment is increasing especially among older people. It is recognized that those individuals with visual impairment are likely to have limited access to information and healthcare facilities, and may not receive the best care possible because not all health care professionals are aware of specific needs related to vision.

- A prerequisite of effective health care could very well be having staff that are aware that people may have problems with vision.

- Communication and different ways of being able to communicate with visually impaired clients must be tailored to individual needs and available at all times.

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.

The diagnosis of childhood blindness is done via methods to ascertain the degree of visual impairment in the affected child doing so via "dilating eye drops" and the proceeding eye exam.

According to colour vision researchers at the Medical College of Wisconsin (including Jay Neitz), each of the three standard colour-detecting cones in the retina of trichromats – blue, green and red – can pick up about 100 different gradations of colour. If each detector is independent of the others, simple exponentiation gives a total number of colours discernible by an average human as their product, or about 1 million; nevertheless, other researchers have put the number at upwards of 2.3 million. Exponentiation suggests that a dichromat (such as a human with red-green color blindness) would be able to distinguish about 10,000 different colours, but no such calculation has been verified by psychophysical testing.

Furthermore, dichromats have a significantly higher threshold than trichromats for coloured stimuli flickering at low (1 Hz) frequencies. At higher (10 or 16 Hz) frequencies, dichromats perform as well as or better than trichromats.. This means such animals would still observe the flicker instead of a temporally fused visual percept as is the case in human movie watching at a high enough frame rate.

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.

In segmental heterochromia, sometimes referred to as sectoral heterochromia, areas of the same iris contains two completely different colors.

Segmental heterochromia is rare in humans; it is estimated that only about 1% of the population have it.

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.

Heterochromia is classified primarily by onset: as either genetic or acquired.

Although a distinction is frequently made between heterochromia that affects an eye completely or only partially (segmental heterochromia), it is often classified as either genetic (due to mosaicism or congenital) or acquired, with mention as to whether the affected iris or portion of the iris is darker or lighter. Most cases of heterochromia are hereditary, caused by certain diseases and syndromes. Sometimes one eye may change color following disease or injury.

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.

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.

Serious complications of cataract surgery include retinal detachment and endophthalmitis. In both cases, patients notice a sudden decrease in vision. In endophthalmitis, patients often describe pain. Retinal detachment frequently presents with unilateral visual field defects, blurring of vision, flashes of light, or floating spots.

The risk of retinal detachment was estimated as about 0.4% within 5.5 years, corresponding to a 2.3-fold risk increase compared to naturally expected incidence, with older studies reporting a substantially higher risk. The incidence is increasing over time in a somewhat linear manner, and the risk increase lasts for at least 20 years after the procedure. Particular risk factors are younger age, male sex, longer axial length, and complications during surgery. In the highest risk group of patients, the incidence of pseudophakic retinal detachment may be as high as 20%.

The risk of endophthalmitis occurring after surgery is less than one in 1000.

Corneal edema and cystoid macular edema are less serious but more common, and occur because of persistent swelling at the front of the eye in corneal edema or back of the eye in cystoid macular edema. They are normally the result of excessive inflammation following surgery, and in both cases, patients may notice blurred, foggy vision. They normally improve with time and with application of anti-inflammatory drops. The risk of either occurring is around one in 100. It is unclear whether NSAIDs or corticosteroids are superior at reducing postoperative inflammation.

Posterior capsular opacification, also known as after-cataract, is a condition in which months or years after successful cataract surgery, vision deteriorates or problems with glare and light scattering recur, usually due to thickening of the back or posterior capsule surrounding the implanted lens, so-called 'posterior lens capsule opacification'. Growth of natural lens cells remaining after the natural lens was removed may be the cause, and the younger the patient, the greater the chance of this occurring. Management involves cutting a small, circular area in the posterior capsule with targeted beams of energy from a laser, called capsulotomy, after the type of laser used. The laser can be aimed very accurately, and the small part of the capsule which is cut falls harmlessly to the bottom of the inside of the eye. This procedure leaves sufficient capsule to hold the lens in place, but removes enough to allow light to pass directly through to the retina. Serious side effects are rare. Posterior capsular opacification is common and occurs following up to one in four operations, but these rates are decreasing following the introduction of modern intraocular lenses together with a better understanding of the causes.

Vitreous touch syndrome is a possible complication of intracapsular cataract extraction.

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.

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.

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.

Although there has been extensive research in the past decades on this disease, there is still no evidence based therapies for this condition. This condition is often diagnosed at an early age; usually as a teenager or young adult.

To make a specific diagnosis, intraocular fluid samples may be taken and sent for analysis. In some cases, blood or cerebrospinal fluid (CSF) are also tested. Imaging may be done to help make the diagnosis.

An accurate diagnosis of retinitis pigmentosa relies on the documentation of the progressive loss photoreceptor cell function, confirmed by a combination of visual field and visual acuity tests, fundus and optical coherence imagery, and electroretinography (ERG),

Visual field and acuity tests measure and compare the size of the patient's field of vision and the clarity of their visual perception with the standard visual measurements associated with healthy 20/20 vision. Clinical diagnostic features indicative of retinitis pigmentosa include a substantially small and progressively decreasing visual area in the visual field test, and compromised levels of clarity measured during the visual acuity test. Additionally, optical tomography such as fundus and retinal (optical coherence) imagery provide further diagnostic tools when determining an RP diagnosis. Photographing the back of the dilated eye allows the confirmation of bone spicule accumulation in the fundus, which presents during the later stages of RP retinal degeneration. Combined with cross-sectional imagery of optical coherence tomography, which provides clues into photoreceptor thickness, retinal layer morphology, and retinal pigment epithelium physiology, fundus imagery can help determine the state of RP progression.

While visual field and acuity test results combined with retinal imagery support the diagnosis of retinitis pigmentosa, additional testing is necessary to confirm other pathological features of this disease. Electroretinography (ERG) confirms the RP diagnosis by evaluating functional aspects associated with photoreceptor degeneration, and can detect physiological abnormalities before the initial manifestation of symptoms. An electrode lens is applied to the eye as photoreceptor response to varying degrees of quick light pulses is measured. Patients exhibiting the retinitis pigmentosa phenotype would show decreased or delayed electrical response in the rod photoreceptors, as well as possibly compromised cone photoreceptor cell response.

The patient's family history is also considered when determining a diagnosis due to the genetic mode of inheritance of retinitis pigmentosa. At least 35 different genes or loci are known to cause "nonsyndromic RP" (RP that is not the result of another disease or part of a wider syndrome). Indications of the RP mutation type can be determine through DNA testing, which is available on a clinical basis for:

- (autosomal recessive, Bothnia type RP)

- (autosomal dominant, RP1)

- (autosomal dominant, RP4)

- (autosomal dominant, RP7)

- (autosomal dominant, RP13)

- (autosomal dominant, RP18)

- CRB1 (autosomal recessive, RP12)

- (autosomal recessive, RP19)

- (autosomal recessive, RP20)

For all other genes (e.g. DHDDS), molecular genetic testing is available on a research basis only.

RP can be inherited in an autosomal dominant, autosomal recessive, or X-linked manner. X-linked RP can be either recessive, affecting primarily only males, or dominant, affecting both males and females, although males are usually more mildly affected. Some digenic (controlled by two genes) and mitochondrial forms have also been described.

Genetic counseling depends on an accurate diagnosis, determination of the mode of inheritance in each family, and results of molecular genetic testing.

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.

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.

There are two types of retinitis: Retinitis pigmentosa (RP) and cytomegalovirus (CMV) retinitis. Both conditions result in the swelling and damage to the retinitis. However, the key difference in both these conditions is that Retinitis pigmentosa is a genetic eye disease that you inherit from one or both of your parents. On the other hand, CMV retinitis develops from a viral infection in the retina. Although there is no cure for this disease, there are steps you can take to protect your eyes from worsening. Supplements can slow the progression of the disease and alleviate symptoms temporarily. Research also shows that vitamin A, lutein, and omega-3 fatty acids also help alleviate symptoms.

The long-term prognosis for patients with Stargardt disease is widely variable although the majority of people will progress to legal blindness.

Stargardt disease has no impact on general health and life expectancy is normal. Some patients, usually those with the late onset form, can maintain excellent visual acuities for extended periods, and are therefore able to perform tasks such as reading or driving.