This condition is usually unilateral, and its symptoms vary from none to mild blurring and discomfort. Signs include diffuse iris atrophy and small white keratic precipitates (deposits on the inner surface of the cornea), cells presenting in the anterior chamber as well as the anterior vitreous. Glaucoma and cataract occur frequently.

Eye floaters and loss of accommodation are among the earliest symptoms. The disease may progress to severe uveitis with pain and photophobia. Commonly the eye remains relatively painless while the inflammatory disease spreads through the uvea, where characteristic focal infiltrates in the choroid named Dalén-Fuchs nodules can be seen. The retina, however, usually remains uninvolved, although perivascular cuffing of the retinal vessels with inflammatory cells may occur. Papilledema, secondary glaucoma, vitiligo, and poliosis of the eyelashes may accompany SO.

Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Neovascularisation (growth of new abnormal vessels) is possible and any eye surgery, such as cataract surgery, can cause bleeding from the fragile vessels in the atrophic iris causing accumulation of blood in anterior chamber of the eye, also known as hyphema.

Sympathetic ophthalmia (SO) or Sympathetic uveitis is a bilateral diffuse granulomatous uveitis (a kind of inflammation) of both eyes following trauma to one eye. It can leave the patient completely blind. Symptoms may develop from days to several years after a penetrating eye injury.

Intermediate uveitis is a form of uveitis localized to the vitreous and peripheral retina. Primary sites of inflammation include the vitreous of which other such entities as pars planitis, posterior cyclitis, and hyalitis are encompassed. Intermediate uveitis may either be an isolated eye disease or associated with the development of a systemic disease such as multiple sclerosis or sarcoidosis. As such, intermediate uveitis may be the first expression of a systemic condition. Infectious causes of intermediate uveitis include Epstein-Barr virus infection, Lyme disease, HTLV-1 virus infection, cat scratch disease, and hepatitis C.

Permanent loss of vision is most commonly seen in patients with chronic cystoid macular edema (CME). Every effort must be made to eradicate CME when present. Other less common causes of visual loss include retinal detachment, glaucoma, band keratopathy, cataract, vitreous hemorrhage, epiretinal membrane and choroidal neovascularization.

First signs of a Fuchs spot are distorted sight of straight lines near the fovea, which some days later turn to the typical well-circumscribed patches after absorption of haemorrhage, and a pigmented scar remains. As in macular degeneration, central sight is affected. Atrophy leads to the loss of two or more lines of the Snellen chart.

The following are not classified as diseases of the eye and adnexa (H00-H59) by the World Health Organization:

- (B36.1) Keratomycosis — fungal infection of the cornea

- (E50.6-E50.7) Xerophthalmia — dry eyes, caused by vitamin A deficiency

- (Q13.1) Aniridia — a rare congenital eye condition leading to underdevelopment or even absence of the iris of the eye

Fuchs' dystrophy, also referred to as Fuchs' corneal endothelial dystrophy (FCED) and Fuchs' endothelial dystrophy (FED), is a slowly progressing corneal dystrophy that usually affects both eyes and is slightly more common in women than in men. Although early signs of Fuchs' dystrophy are sometimes seen in people in their 30s and 40s, the disease rarely affects vision until people reach their 50s and 60s.

The condition was first described by Austrian ophthalmologist Ernst Fuchs (1851–1930), after whom it is named. In 1910, Fuchs first reported 13 cases of central corneal clouding, loss of corneal sensation and the formation of epithelial bullae, or blisters, which he labeled 'dystrophia epithelialis corneae'. It was characterized by late onset, slow progression, decreased visual acuity in the morning, lack of inflammation, diffuse corneal opacity, intense centrally, and roughened epithelium with vesicle-like features.

A shift to the understanding of FCED as primarily a disease of the corneal endothelium resulted after a number of observations in the 1920s. Crystal-like features of the endothelium were noted by Kraupa in 1920, who suggested that the epithelial changes were dependent on the endothelium. Using a slit lamp, Vogt described the excrescences associated with FCD as drop-like in appearance in 1921. In 1924, Graves then provided an extremely detailed explanation of the endothelial elevations visible with slit-lamp biomicroscopy. A patient with unilateral epithelial dystrophy and bilateral endothelial changes was described by the Friedenwalds in 1925; subsequent involvement of the second eye led them to emphasize that endothelial changes preceded epithelial changes. As only a subset of patients with endothelial changes proceeded to epithelial involvement, Graves stated on 19 October 1925 to the New York Academy of Medicine that "Fuchs' epithelial dystrophy may be a very late sequel to severer cases of the deeper affection".

FED may be discovered as an incidental finding at a routine visit to an optometrist. or by an ophthalmologist during assessment for cataract surgery. As a result of irregularities on the inner surface of the cornea, affected individuals may simply notice a reduction in the quality of vision or glare or haloes particularly when driving at night. Individuals with symptomatic Fuchs' dystrophy typically awaken with blurred vision which improves during the day. This occurs because the cornea is normally more swollen in the morning due to nocturnal fluid retention in the absence of normal evaporation due to the lids being closed. During waking hours this fluid evaporates once the eyes are open. As the disease worsens vision remains blurred despite evaporation due to endothelial pump failure and fluid retention. As Fuchs' dystrophy typically occurs in older individuals there may also be cataract of the lens, which also reduces vision.

Researchers are finding that Fuchs' is a genetically heterogeneous disease, and many different genes and loci have been associated as contributing to a small percentage of overall Fuchs' cases. Certain genetic lesions have been correlated with more severe disease and earlier onset. Therefore, some individuals may experience symptoms of the disease at a much earlier age, while others may not experience symptoms until late in life.

This is a partial list of human eye diseases and disorders.

The World Health Organization publishes a classification of known diseases and injuries, the International Statistical Classification of Diseases and Related Health Problems, or ICD-10. This list uses that classification.

Although intermediate uveitis can develop at any age, it primarily afflicts children and young adults. There is a bimodal distribution with one peak in the second decade and another peak in the third or fourth decade.

In the United States the proportion of patients with intermediate uveitis is estimated to be 4-8% of uveitis cases in referral centers. The National Institutes of Health reports a higher percentage (15%), which may indicate improved awareness or the nature of the uveitis referral clinic. In the pediatric population, intermediate uveitis can account for up to 25% of uveitis cases.

The Fuchs spot or sometimes Forster-Fuchs' retinal spot is a degeneration of the macula in case of high myopia. It is named after the two persons who first described it: Ernst Fuchs, who described a pigmented lesion in 1901, and Forster, who described subretinal neovascularisation in 1862. The size of the spots are proportionate to the severity of the pathological myopia.

Disease begins with vesicles that coalesce. There is severe progressing edema and rupture may occur in 24 hours or less.

A corneal dystrophy can be caused by an accumulation of extraneous material in the cornea, including lipids and cholesterol crystals.

Corneal dystrophy may not significantly affect vision in the early stages. However, it does require proper evaluation and treatment for restoration of optimal vision. Corneal dystrophies usually manifest themselves during the first or second decade but sometimes later. It appears as grayish white lines, circles, or clouding of the cornea. Corneal dystrophy can also have a crystalline appearance.

There are over 20 corneal dystrophies that affect all parts of the cornea. These diseases share many traits:

- They are usually inherited.

- They affect the right and left eyes equally.

- They are not caused by outside factors, such as injury or diet.

- Most progress gradually.

- Most usually begin in one of the five corneal layers and may later spread to nearby layers.

- Most do not affect other parts of the body, nor are they related to diseases affecting other parts of the eye or body.

- Most can occur in otherwise totally healthy people, male or female.

Corneal dystrophies affect vision in widely differing ways. Some cause severe visual impairment, while a few cause no vision problems and are diagnosed during a specialized eye examination by an ophthalmologist. Other dystrophies may cause repeated episodes of pain without leading to permanent loss of vision.

Bullous keratopathy is a pathological condition in which small vesicles, or "bullae", are formed in the cornea due to endothelial dysfunction.

In a healthy cornea, endothelial cells keeps the tissue from excess fluid absorption, pumping it back into the aqueous humor. When affected by some reason, such as Fuchs' dystrophy or a trauma during cataract removal, endothelial cells suffer mortality or damage. The corneal endothelial cells normally do not undergo mitotic cell division, and cell loss results in permanent loss of function. When endothelial cell counts drop too low, the pump starts failing to function and fluid moves anterior into the stroma and epithelium. The excess fluid precipitates swelling of the cornea. As fluid accumulates between the basal epithelium cells, blister like formations form (bullae) and they undergo painful ruptures releasing their fluid content to the surface. These characteristic malformations disrupt vision and create pain sensations.

Treatment can include hyperosmotic eye drops to reduce swelling (5% sodium chloride), bandage contact lenses to reduce discomfort, glaucoma medications to reduce the flow of fluid into the cornea, and surgical procedures to replace the damaged tissue. The most common types of surgical treatment are Descemet's stripping automated endothelial keratoplasty (DSAEK) and Descemet's membrane endothelial keratoplasty (DMEK).

Symptoms of pterygium include persistent redness, inflammation, foreign body sensation, tearing, dry and itchy eyes. In advanced cases the pterygium can affect vision as it invades the cornea with the potential of obscuring the optical center of the cornea and inducing astigmatism and corneal scarring. Many patients do complain of the cosmetic appearance of the eye either with some of the symptoms above or as their major complaint.

Retinal vasculitis presents as painless, decrease of visual acuity (blurry vision), visual floaters, scotomas (dark spot in vision), decreased ability to distinguish colors, and metamorphopsia (distortion of images such as linear images).

Ophthalmic examination may reveal neovascularization (creation of new vessels in the retina), retinal vessel narrowing, retinal vessel cuffing, retinal hemorrhage, or possible vitritis (inflammation of the vitreous body) or choroiditis (inflammation of the choroid).

A pterygium is a pinkish, triangular tissue growth on the cornea of the eye. It typically starts on the cornea near the nose. It may slowly grow but rarely grows so large that the pupil is covered. Often both eyes are involved.

The cause is unclear. It appears to be partly related to long term exposure to UV light and dust. Genetic factors also appear to be involved. It is a benign growth. Other conditions that can look similar include a pinguecula, tumor, or Terrien's marginal corneal degeneration.

Prevention may include wearing sunglasses and a hat if in an area with strong sunlight. Among those with the condition, an eye lubricant can help with symptoms. Surgical removal is typically only recommended if the ability to see is affected. Following surgery a pterygium may recur in around half of cases.

The frequency of the condition varies from 1% to 33% in various regions of the world. It occurs more commonly among males than females and in people who live closer to the equator. The condition becomes more common with age. The condition has been described since at least 1000 BC.

In the beginning, medical officials defined ABCD syndrome by the four key characteristics of the syndrome. In the first case study of the Kurdish girl, researches described her as having "albinism and a black lock at the right temporo-occipital region along Blaschko lines, her eyelashes and brows were white, the irises in her eyes appeared to be blue, she had spots of retinal depigmentation, and she did not react to noise." The albinism is interesting in this diagnosis because the skin of an affected individual is albino pale besides the brown patches of mispigmented skin. The "black locks" described and seen in clinical pictures of the infants are thick patches of black hair above the ears that form a half circle reaching to the other ear to make a crest shape.

As identified in this first case study and stated in a dictionary of dermatologic syndromes, ABCD syndrome has many notable features, including "snow white hair in patches, distinct black locks of hair, skin white except brown macules, deafness, irises gray to blue, nystagmus, photophobia, poor visual activity, normal melanocytes in pigmented hair and skin, and absent melanocytes in areas of leukoderma." Individuals have the blue/gray irises typical of people affected by blindness. The C of ABCD syndrome is what distinguishes this genetic disorder from BADS and it involves cell migration disorder of the neurocytes of the gut. This characteristic occurs when nerve cells do not function correctly in the gut, which results in aganglionosis: The intestines’ failure to move food along the digestive tract. Deafness or being unresponsive to noise due to very low quality of hearing was reported in every case of ABCD syndrome. The characteristics of ABCD syndrome are clearly evident in an inflicted individual.

No longer considered a separate syndrome, ABCD syndrome is today considered to be a variation of Shah-Waardenburg type IV. Waardenburg syndrome (WS) is described as "the combination of sensorineural hearing loss, hypopigmentation of skin and hair, and pigmentary disturbances of the irides." Hearing loss and deafness, skin mispigmentation and albinism, and pigmentary changes in irises are the similarities between WS and ABCD. According to a dictionary of dermatologic syndromes, Waardenburg syndrome has many notable features, including "depigmentation of hair and skin – white forelock and premature graying of hair, confluent thick eyebrows, heterochromic irides or hypopigmentation of iris, laterally displaced inner canthi, congenital sensorineural deafness, broad nasal root, autosomal dominant disorder, and other associated findings, including black forelocks."

ABCD syndrome is the acronym for albinism, black lock, cell migration disorder of the neurocytes of the gut, and sensorineural deafness. It has been found to be caused by mutation in the endothelin B receptor gene (EDNRB).

Convulsive symptoms include painful seizures and spasms, diarrhea, paresthesias, itching, mental effects including mania or psychosis, headaches, nausea and vomiting. Usually the gastrointestinal effects precede central nervous system effects.

The dry gangrene is a result of vasoconstriction induced by the ergotamine-ergocristine alkaloids of the fungus. It affects the more poorly vascularized distal structures, such as the fingers and toes. Symptoms include desquamation or peeling, weak peripheral pulses, loss of peripheral sensation, edema and ultimately the death and loss of affected tissues. Vasoconstriction is treated with vasodilators.

Dyscalculia involves frequent difficulties with everyday arithmetic tasks such as the following:

- Difficulty reading analog clocks

- Difficulty stating which of two numbers is larger.

- Inability to comprehend financial planning or budgeting, sometimes even at a basic level; for example, estimating the cost of the items in a shopping basket or balancing a checkbook.

- Inconsistent results in addition, subtraction, multiplication and division.

- Visualizing numbers as meaningless or nonsensical symbols, rather than perceiving them as characters indicating a numerical value. (Hence the misnomer, "math dyslexia")

- Difficulty with multiplication, subtraction, addition, and division tables, mental arithmetic, etc.

- Problems with differentiating between left and right.

- A "warped" sense of spatial awareness, or an understanding of shapes, distance, or volume that seems more like guesswork than actual comprehension.

- Difficulty with time, directions, recalling schedules, sequences of events. Difficulty keeping track of time. Frequently late or early.

- Poor memory (retention & retrieval) of math concepts; may be able to perform math operations one day, but draw a blank the next. May be able to do book work but then fails tests.

- Difficulty reading musical notation.

- Difficulty with choreographed dance steps.

- Difficulty working backwards in time (e.g. What time to leave if needing to be somewhere at 'X' time).

- Having particular difficulty mentally estimating the measurement of an object or distance (e.g., whether something is 3 or 6 meters (10 or 20 feet) away).

- When writing, reading and recalling numbers, mistakes may occur in the areas such as: number additions, substitutions, transpositions, omissions, and reversals.

- Inability to grasp and remember mathematical concepts, rules, formulae, and sequences.

- Inability to concentrate on mentally intensive tasks.

- Mistaken recollection of names. Poor name/face retrieval. May substitute names beginning with same letter.