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.

The incidence and prevalence of PMD are unknown, and no studies have yet investigated its prevalence or incidence. However, it is generally agreed that PMD is a very rare condition. Some uncertainty regarding the incidence of PMD may be attributed to its confusion with keratoconus. PMD is not linked to race or age, although most cases present early in life, between 20 and 40 years of age. While PMD is usually considered to affect men and women equally, some studies suggest that it may affect men more frequently.

Several diseases have been observed in patients with PMD. However, no causal relationships have been established between any of the associated diseases and the pathogenesis of PMD. Such diseases include: chronic open-angle glaucoma, retinitis pigmentosa, retinal lattice degeneration, scleroderma, kerato-conjunctivitis, eczema, and hyperthyroidism.

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.

It is a much rarer condition than keratoconus, which is the most common of the cornea. Similar to keratoconus it is typically diagnosed in the patient's adolescent years and attains its most severe state in the twenties and thirties.

Cigarette smoking has been shown to double the rate of nuclear sclerotic cataracts and triple the rate of posterior subcapsular cataracts. Evidence is conflicting over the effect of alcohol. Some surveys have shown a link, but others which followed people over longer terms have not.

Keratoglobus continues to be a somewhat mysterious disease, but it can be successfully managed with a variety of clinical and surgical techniques. The patient is at risk for globe perforation because the thinned out cornea is extremely weak.

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.

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.

In studies of the genetic predisposition of refractive error, there is a correlation between environmental factors and the risk of developing myopia. Myopia has been observed in individuals with visually intensive occupations. Reading has also been found to be a predictor of myopia in children. It has been reported that children with myopia spent significantly more time reading than non-myopic children who spent more time playing outdoors. Socioeconomic status and higher levels of education have also been reported to be a risk factor for myopia.

Before LASIK surgery, people must be examined for possible risk factors such as keratoconus.

Abnormal corneal topography compromises of keratoconus, pellucid marginal degeneration, or forme fruste keratoconus with an I-S value of 1.4 or more is the most significant risk factor. Low age, low residual stromal bed (RSB) thickness, low preoperative corneal thickness, and high myopia are other important risk factors.

Visual function declines as a result of the irregular corneal shape, resulting in astigmatism, and causing a distortion in vision. Deterioration can become severe over time.

The number of children who suffer from blindness worldwide is approximately 1.4 million. 75% of the world’s blind children live in Africa and Asia. A 2014 review indicated that an estimated of 238,500 children with bilateral blindness (rate 1.2/1,000) in the Eastern Mediterranean region.

In general, approximately one-third of congenital cataracts are a component of a more extensive syndrome or disease (e.g., cataract resulting from congenital rubella syndrome), one-third occur as an isolated inherited trait, and one-third result from undetermined causes. Metabolic diseases tend to be more commonly associated with bilateral cataracts.

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.

Given that episodes tend to occur on awakening and managed by use of good 'wetting agents', approaches to be taken to help prevent episodes include:

- Environmental:

- ensuring that the air is humidified rather than dry, not overheated and without excessive airflow over the face. Also avoiding irritants such as cigarette smoke.

- use of protective glasses especially when gardening or playing with children.

- General personal measures:

- maintaining general hydration levels with adequate fluid intake.

- not sleeping-in late as the cornea tends to dry out the longer the eyelids are closed.

- Pre-bed routine:

- routine use of long-lasting eye ointments applied before going to bed.

- occasional use of the anti-inflammatory eyedrop FML (prescribed by an ophthalmologist or optometrist) before going to bed if the affected eye feels inflamed, dry or gritty

- use of a hyperosmotic (hypertonic) ointment before bed reduces the amount of water in the epithelium, strengthening its structure

- use the pressure patch as mentioned above.

- use surgical tape to keep the eye closed (if Nocturnal Lagophthalmos is a factor)

- Waking options:

- learn to wake with eyes closed and still and keeping artificial tear drops within reach so that they may be squirted under the inner corner of the eyelids if the eyes feel uncomfortable upon waking.

- It has also been suggested that the eyelids should be rubbed gently, or pulled slowly open with your fingers, before trying to open them, or keeping the affected eye closed while "looking" left and right to help spread lubricating tears. If the patient's eyelids feel stuck to the cornea on waking and no intense pain is present, use a fingertip to press firmly on the eyelid to push the eye's natural lubricants onto the affected area. This procedure frees the eyelid from the cornea and prevents tearing of the cornea.

Six genes have been found to be associated with the condition. These genes include BANP-ZNF469, COL4A4, FOXO1, FNDC3B, IMMP2L and RXRA-COL5A1. Others likely also exist.

A 2012 review could not find strong evidence for any cause, although many theories have been discredited. Because twins and relatives are more likely to get myopia under similar circumstances, there must be a hereditary factor. Myopic shifts seen during growth spurts of childhood and adolescence, as well as in acromegaly, indicates a relationship between the timing of myopic development and the release of human growth hormone. However, the lack of correlation between height and myopia seems to suggest the relationship between human growth hormone and myopia is complex.

Myopia has been increasing rapidly throughout the developed world, suggesting environmental factors must be important. Quite similarly, the mechanisms of emmetropization are still unclear. Emmetropization is the process by which a child's eye grows and changes to become less hyperopic. It is thought that the same triggers and signals that cause this growth may also play a role in the eye growing beyond the point of emmetropia and into myopia.

In one study, heredity was an important factor associated with juvenile myopia, with smaller contributions from more near work, higher school achievement, and less time in sports activity.

Long hours of exposure to daylight appears to be a protective factor. Lack of outdoor play could be linked to myopia.

Other personal characteristics, such as value systems, school achievements, time spent in reading for pleasure, language abilities, and time spent in sport activities all correlated to the occurrence of myopia in studies.

Patients with keratoconus typically present initially with mild astigmatism and myopia, commonly at the onset of puberty, and are diagnosed by the late teenage years or early 20s. The disease can, however, present or progress at any age; in rare cases, keratoconus can present in children or not until later adulthood. A diagnosis of the disease at an early age may indicate a greater risk of severity in later life. Patients' vision will seem to fluctuate over a period of months, driving them to change lens prescriptions frequently, but as the condition worsens, contact lenses are required in the majority of cases. The course of the disorder can be quite variable, with some patients remaining stable for years or indefinitely, while others progress rapidly or experience occasional exacerbations over a long and otherwise steady course. Most commonly, keratoconus progresses for a period of 10 to 20 years before the course of the disease generally ceases in the third and fourth decades of life.

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.

According to an American study nearly three in 10 children (28.4%) between the ages of five and 17 have astigmatism. A recent Brazilian study found that 34% of the students in one city were astigmatic. Regarding the prevalence in adults, a recent study in Bangladesh found that nearly 1 in 3 (32.4%) of those over the age of 30 had astigmatism.

A Polish study published in 2005 revealed "with-the-rule astigmatism" may lead to the onset of myopia.

A number of studies have found the prevalence of astigmatism increases with age.

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.

Approximately 50% of all congenital cataract cases may have a genetic cause which is quite heterogeneous. It is known that different mutations in the same gene can cause similar cataract patterns, while the highly variable morphologies of cataracts within some families suggest that the same mutation in a single gene can lead to different phenotypes. More than 25 loci and genes on different chromosomes have been associated with congenital cataract. Mutations in distinct genes, which encode the main cytoplasmic proteins of human lens, have been associated with cataracts of various morphologies, including genes encoding crystallins (CRYA, CRYB, and CRYG), lens specific connexins (Cx43, Cx46, and Cx50), major intrinsic protein (MIP) or Aquaporin, cytoskeletal structural proteins, paired-like homeodomain transcription factor 3 (PITX3), avian musculoaponeurotic fibrosarcoma (MAF), and heat shock transcription factor 4 (HSF4).

Lens subluxation is also seen in dogs and is characterized by a partial displacement of the lens. It can be recognized by trembling of the iris (iridodonesis) or lens (phacodonesis) and the presence of an aphakic crescent (an area of the pupil where the lens is absent). Other signs of lens subluxation include mild conjunctival redness, vitreous humour degeneration, prolapse of the vitreous into the anterior chamber, and an increase or decrease of anterior chamber depth. Removal of the lens before it completely luxates into the anterior chamber may prevent secondary glaucoma. A nonsurgical alternative involves the use of a miotic to constrict the pupil and prevent the lens from luxating into the anterior chamber.

The yearly cost of correcting refractive errors is estimated at 3.9 to 7.2 billion dollars in the United States.