Many people of East Asian descent are prone to developing angle closure glaucoma due to shallower anterior chamber depths, with the majority of cases of glaucoma in this population consisting of some form of angle closure. Higher rates of glaucoma have also been reported for Inuit populations, compared to white populations, in Canada and Greenland.

No clear evidence indicates vitamin deficiencies cause glaucoma in humans. It follows, then, that oral vitamin supplementation is not a recommended treatment for glaucoma. Caffeine increases intraocular pressure in those with glaucoma, but does not appear to affect normal individuals.

In the United States, the incidence of primary congenital glaucoma is about one in 10,000 live births. Worldwide, the incidence ranges from a low of 1:22,000 in Northern Ireland to a high of 1:2,500 in Saudi Arabia and 1:1,250 in Romania. In about two-thirds of cases, it is bilateral. The distribution between males and females varies with geography. In North America and Europe it is more common in boys, whereas in Japan it is more common in girls.

- Congenital glaucoma

- Incidence: one in every 10000-15000 live births.

- Bilateral in up to 80% of cases.

- Most cases are sporadic (90%). However, in the remaining 10% there appears to be a strong familial component.

The number of cases is around 0.5 to 0.7 per 10,000 births, making it a relatively rare condition.

Colobomas can be associated with a mutation in the "PAX2" gene.

Eye abnormalities have been shown to occur in over 90% of children with fetal alcohol syndrome.

Scientists are studying different populations and relationships to try to learn more about the disease. They have found associations with different groups but it is not yet clear what the underlying factors are and how they affect different peoples around the world.

- Glaucoma patients. While PEX and glaucoma are believed to be related, there are cases of persons with PEX without glaucoma, and persons with glaucoma without PEX. Generally, a person with PEX is considered as having a risk of developing glaucoma, and vice versa. One study suggested that the PEX was present in 12% of glaucoma patients. Another found that PEX was present in 6% of an "open-angle glaucoma" group. Pseudoexfoliation syndrome is considered to be the most common of identifiable causes of glaucoma. If PEX is diagnosed without glaucoma, there is a high risk of a patient subsequently developing glaucoma.

- Country and region. Prevalence of PEX varies by geography. In Europe, differing levels of PEX were found; 5% in England, 6% in Norway, 4% in Germany, 1% in Greece, and 6% in France. One contrary report suggested that levels of PEX were higher among Greek people. One study of a county in Minnesota found that the prevalence of PEX was 25.9 cases per 100,000 people. It is reportedly high in northern European countries such as Norway, Sweden and Finland, as well as among the Sami people of northern Europe, and high among Arabic populations, but relatively rare among African Americans and Eskimos. In southern Africa, prevalence was found to be 19% of patients in a glaucoma clinic attending to persons of the Bantu tribes.

- Race. It varies considerably according to race.

- Gender. It affects women more than men. One report was that women were three times more likely than men to develop PEX.

- Age. Older persons are more likely to develop PEX. And persons younger than 50 are highly unlikely to have PEX. A study in Norway found that the prevalence of PEX of persons aged 50–59 was 0.4% while it was 7.9% for persons aged 80–89 years. If a person is going to develop PEX, the average age in which this will happen is between 69 and 75 years, according to the Norwegian study. A second corroborating report suggested that it happens primarily to people 70 and older. While older people are more likely to develop PEX, it is not seen as a "normal" part of aging.

- Other diseases. Sometimes PEX is associated with the development of medical problems other than merely glaucoma. There are conflicting reports about whether PEX is associated with problems of the heart or brain; one study suggested no correlations while other studies found statistical links with Alzheimer's disease, senile dementia, cerebral atrophy, chronic cerebral ischemia, stroke, transient ischemic attacks, heart disease, and hearing loss.

Terrier breeds are predisposed to lens luxation, and it is probably inherited in the Sealyham Terrier, Jack Russell Terrier, Wirehaired Fox Terrier, Rat Terrier, Teddy Roosevelt Terrier, Tibetan Terrier, Miniature Bull Terrier, Shar Pei, and Border Collie. The mode of inheritance in the Tibetan Terrier and Shar Pei is likely autosomal recessive. Labrador Retrievers and Australian Cattle Dogs are also predisposed.

Congenital heterochromia is usually inherited as an autosomal dominant trait.

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.

Some pedigrees suggest inherited primary congenital is autosomal dominant but three major autosomal recessive loci have been identified:

- GLC3A – on chromosome 2 (2p21)

- GLC3B – on chromosome 1 (1p36)

- GLC3C – on chromosome 14 (14q24.3)

Anisocoria is a common condition, defined by a difference of 0.4 mm or more between the sizes of the pupils of the eyes.

Anisocoria has various causes:

- Physiological anisocoria: About 20% of normal people have a slight difference in pupil size which is known as physiological anisocoria. In this condition, the difference between pupils is usually less than 1 mm.

- Horner's syndrome

- Mechanical anisocoria: Occasionally previous trauma, eye surgery, or inflammation (uveitis, angle closure glaucoma) can lead to adhesions between the iris and the lens.

- Adie tonic pupil: Tonic pupil is usually an isolated benign entity, presenting in young women. It may be associated with loss of deep tendon reflex (Adie's syndrome). Tonic pupil is characterized by delayed dilation of iris especially after near stimulus, segmental iris constriction, and sensitivity of pupil to a weak solution of pilocarpine.

- Oculomotor nerve palsy: Ischemia, intracranial aneurysm, demyelinating diseases (e.g., multiple sclerosis), head trauma, and brain tumors are the most common causes of oculomotor nerve palsy in adults. In ischemic lesions of the oculomotor nerve, pupillary function is usually spared whereas in compressive lesions the pupil is involved.

- Pharmacological agents with anticholinergic or sympathomimetic properties will cause anisocoria, particularly if instilled in one eye. Some examples of pharmacological agents which may affect the pupils include pilocarpine, cocaine, tropicamide, MDMA, dextromethorphan, and ergolines. Alkaloids present in plants of the genera "Brugmansia" and "Datura", such as scopolamine, may also induce anisocoria.

- Migraines

With posterior lens luxation, the lens falls back into the vitreous humour and lies on the floor of the eye. This type causes fewer problems than anterior lens luxation, although glaucoma or ocular inflammation may occur. Surgery is used to treat dogs with significant symptoms. Removal of the lens before it moves to the anterior chamber may prevent secondary glaucoma.

According to recent research not a single theory is able to explain the cause fully. However current plausible theories include infection with "Toxoplasma gondii", Herpes simplex virus, Rubella, neurogenic causes, and autoimmune pathology.

Untreated glaucoma leads to total blindness. Surgical treatment is required. Presently-utilized surgical procedures include goniotomy, trabeculotomy, or trabeculectomy.

Anisocoria is a condition characterized by an unequal size of the eyes' pupils. Affecting 20% of the population, it can be an entirely harmless condition or a symptom of more serious medical problems.

Causes of photophobia relating directly to the eye itself include:

- Achromatopsia

- Aniridia

- Anticholinergic drugs may cause photophobia by paralyzing the iris sphincter muscle.

- Aphakia (absence of the lens of the eye)

- Blepharitis

- Buphthalmos (abnormally narrow angle between the cornea and iris)

- Cataracts

- Coloboma

- Cone dystrophy

- Congenital abnormalities of the eye

- Viral conjunctivitis ("pink eye")

- Corneal abrasion

- Corneal dystrophy

- Corneal ulcer

- Disruption of the corneal epithelium, such as that caused by a corneal foreign body or keratitis

- Ectopia lentis

- Endophthalmitis

- Eye trauma caused by disease, injury, or infection such as chalazion, episcleritis, glaucoma, keratoconus, or optic nerve hypoplasia

- Hydrophthalmos, or congenital glaucoma

- Iritis

- The drug isotretinoin (Accutane/Roaccutane) has been associated with photophobia

- Optic neuritis

- Pigment dispersion syndrome

- Pupillary dilation (naturally or chemically induced)

- Retinal detachment

- Scarring of the cornea or sclera

- Uveitis

The cause of pseudoexfoliation glaucoma is generally unknown.

PEX is generally believed to be a systemic disorder, possibly of the basement membrane of the eye. Researchers have noticed deposits of PEX material in various parts of the body, including in the skin, heart, lungs, liver, kidneys, and elsewhere. Nevertheless, what is puzzling is that PEX tends to happen in only one eye first, which scientists call "unilaterality", and in some cases, gradually afflicts the other eye, which is termed "bilaterality". According to this reasoning, if PEX were a systemic disorder, then both eyes should be affected at the same time, but they are not. There are contrasting reports about the extent and speed with which PEX moves from one eye to both eyes. According to one report, PEX develops in the second eye in 40% of cases. A contrasting report was that PEX can be found in both eyes in almost all situations if an electron microscope is used to examine the second eye, or if a biopsy of the conjunctiva was done, but that the extent of PEX is the second eye was much less than the first one. A different report suggested that two thirds of PEX patients had flakes in only one eye. In one long term study, patients with PEX in only one eye were studied, and it was found that over time, 13% progressed to having both eyes afflicted by PEX. Scientists believe that elevated levels of plasma homocysteine are a risk factor for cardiovascular disease, and two studies have found higher levels of plasma homocysteine in PEX patients, or elevated homocysteine concentrations in tear fluids produced by the eye.

There is speculation that PEX may be caused by oxidative damage and the presence of "free radicals", although the exact nature of how this might happen is still under study. Studies of PEX patients have found a decrease in the concentrations of ascorbic acid, increase in concentrations of malondialdehyde, and an increase in concentrations of 8-iso-prostaglandinF2a.

There is speculation that genetics may play a role in PEX. A predisposition to develop PEX later in life may be an inherited characteristic, according to one account. One report suggested the genetic component was "strong". One study performed in Iceland and Sweden has associated PEX with polymorphisms in gene LOXL1. A report suggested that a specific gene named LOXL1 which was a member of the family of enzymes which play a role in the linking of collagen and elastin inside cells. LOXL1 was responsible for "all the heritability" of PEX, according to one source. Two distinct mutations in which a single nucleotide was changed, or called a "single nucleotide polymorphism" or SNP, was discovered in Scandinavian populations and confirmed in other populations, and may be involved with the onset of PEX.

Researchers are investigating whether factors such as exposure to ultraviolet light, living in northern latitudes, or altitude influence the onset of PEX. One report suggested that climate was not a factor related to PEX. Another report suggested a possible link to sunlight as well as a possible autoimmune response, or possibly a virus.

Pigment dispersion syndrome (PDS) is an affliction of the eye that can lead to a form of glaucoma known as pigmentary glaucoma. It takes place when pigment cells slough off from the back of the iris and float around in the aqueous humor. Over time, these pigment cells can accumulate in the anterior chamber in such a way that it can begin to clog the trabecular meshwork (the major site of aqueous humour drainage), which can in turn prevent the aqueous humour from draining and therefore increases the pressure inside the eye. With PDS, the intraocular pressure tends to spike at times and then can return to normal. Exercise has been shown to contribute to spikes in pressure as well. When the pressure is great enough to cause damage to the optic nerve, this is called pigmentary glaucoma. As with all types of glaucoma, when damage happens to the optic nerve fibers, the vision loss that occurs is irreversible and painless.

This condition is rare, but occurs most often in Caucasians, particularly men, and the age of onset is relatively low: mid 20s to 40s. As the crystalline lens hardens with age, the lens zonules pull away from the iris and the syndrome lessens and stops. Most sufferers are nearsighted.

There is no cure yet, but pigmentary glaucoma can be managed with eye drops or treated with simple surgeries. One of the surgeries is the YAG laser procedure in which a laser is used to break up the pigment clogs, and reduce pressure. If caught early and treated, chances of glaucoma are greatly reduced. Sufferers are often advised not to engage in high-impact sports such as long-distance running or martial arts, as strong impacts can cause more pigment cells to slough off.

A 2016 Cochrane Review sought to determine the effectiveness of YAG laser iridotomy versus no laser iridotomy for pigment dispersion syndrome and pigmentary glaucoma, in 195 participants, across five studies. No clear benefits in preventing loss of visual field were found for eyes treated with peripheral laser iridotomy. There was weak evidence suggesting that laser iridotomy could be more effective in lowering intraocular pressure in eyes versus no treatment.

Buphthalmos (plural: buphthalmoses) is enlargement of the eyeball and is most commonly seen in infants and young children. It is sometimes referred to as buphthalmia (plural buphthalmias). It usually appears in the newborn period or the first 3 months of life. and in most cases indicates the presence of congenital (infantile) glaucoma, which is a disorder in which elevated pressures within the eye lead to structural eye damage and vision loss.

Aniridia is the absence of the iris, usually involving both eyes. It can be congenital or caused by a penetrant injury. Isolated aniridia is a congenital disorder which is not limited to a defect in iris development, but is a panocular condition with macular and optic nerve hypoplasia, cataract, and corneal changes. Vision may be severely compromised and the disorder is frequently associated with a number of ocular complications: nystagmus, amblyopia, buphthalmos, and cataract. Aniridia in some individuals occurs as part of a syndrome, such as WAGR syndrome (kidney nephroblastoma (Wilms tumour), genitourinary anomalies and intellectual disability), or Gillespie syndrome (cerebellar ataxia).

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.

Over many years, glaucoma has been defined by an intraocular pressure of more than 20 or 20 mm Hg. Incompatible with this (now obsolete) definition of glaucoma was the ever larger number of cases that have been reported in medical literature in the 1980s and 1990s who had the typical signs of glaucomatous damage, like optic nerve head excavation and thinning of the retinal nerve fiber layer, while these patients had an IOP that would generally have been regarded as "normal". It is now widely estimated that a larger percentage of patients with primary open-angle glaucoma (POAG) are suffering from normal tension glaucoma: probably half of all POAG patients in Europe and the majority of POAG patients in East Asia. Among Americans of Japanese descent, for instance, the prevalence of NTG is about four times as high as the prevalence of the "classical glaucoma" with an IOP of 22 mm Hg and higher. The pillar of the current understanding of normal tension glaucoma is a reduced IOP tolerance of the retinal ganglion cells and the cells in the optic nerve head - an IOP of, for example, 17 or 19 mm Hg that would not affect a healthy eye leads to damage in the eye of an NTG patient.

As the name implies, it is the bulge of weak sclera lined by ciliary body, which occurs about 2–3 mm away from the limbus. Its common causes are thinning of sclera following perforating injury, scleritis & absolute glaucoma.

it is part of anterior staphyloma

It is the name given to the localised bulge in limbal area, lined by the root of the iris. It results due to ectasia of weak scar tissue formed at the limbus, following healing of a perforating injury or a peripheral corneal ulcer. There may be associated secondary angle closure glaucoma, may cause progression of the bulge if not treated. Defective vision occurs due to marked corneal astigmatism. Treatment consists of localised staphylectomy under heavy doses of oral steroids.

The pressure within the eye is maintained by the balance between the fluid that enters the eye through the ciliary body and the fluid that exits the eye through the trabecular meshwork.