Studies have identified the following abnormalities as risk factors for the development of BRVO:

- hypertension

- cardiovascular disease

- obesity

- glaucoma

Diabetes mellitus was not a major independent risk factor.

Familial transmission is now recognized in a small proportion of people with MacTel type 2; however, the nature of any related genetic defect or defects remains elusive. The MacTel genetic study team hopes that exome analysis in the affected population and relatives may be more successful in identifying related variants.

Age-related macular degeneration accounts for more than 54% of all vision loss in the white population in the USA. An estimated 8 million Americans are affected with early age-related macular degeneration, of whom over 1 million will develop advanced age-related macular degeneration within the next 5 years. In the UK, age-related macular degeneration is the cause of blindness in almost 42% of those who go blind aged 65–74 years, almost two-thirds of those aged 75–84 years, and almost three-quarters of those aged 85 years or older.

Macular degeneration is more likely to be found in Caucasians than in people of African descent.

The causes of macular edema are numerous and different causes may be inter-related.

- It is commonly associated with diabetes. Chronic or uncontrolled diabetes type 2 can affect peripheral blood vessels including those of the retina which may leak fluid, blood and occasionally fats into the retina causing it to swell.

- Age-related macular degeneration may cause macular edema. As individuals age there may be a natural deterioration in the macula which can lead to the depositing of drusen under the retina sometimes with the formation of abnormal blood vessels.

- Replacement of the lens as treatment for cataract can cause pseudophakic macular edema. (‘pseudophakia’ means ‘replacement lens’) also known as Irvine-Gass syndrome The surgery involved sometimes irritates the retina (and other parts of the eye) causing the capillaries in the retina to dilate and leak fluid into the retina. Less common today with modern lens replacement techniques.

- Chronic uveitis and intermediate uveitis can be a cause.

- Blockage of a vein in the retina can cause engorgement of the other retinal veins causing them to leak fluid under or into the retina. The blockage may be caused, among other things, by atherosclerosis, high blood pressure and glaucoma.

- A number of drugs can cause changes in the retina that can lead to macular edema. The effect of each drug is variable and some drugs have a lesser role in causation. The principal medication known to affect the retina are:- latanoprost, epinephrine, rosiglitazone, timolol and thiazolidinediones among others.

- A few congenital diseases are known to be associated with macular edema for example retinitis pigmentosa and retinoschisis.

Although a variety of complex classification schemes are described in the literature, there are essentially two forms of macular telangiectasia: type 1 and type 2. Type 1 is typically unilateral and occurs almost exclusively in males after the age of 40.

Type 2 is mostly bilateral, occurs equally in males and females.

This ocular pathology was first described by Iwanoff in 1865, and it has been shown to occur in about 7% of the population. It can occur more frequently in the older population with postmortem studies showing it in 2% of those aged 50 years and 20% in those aged 75 years.

All people with "diabetes mellitus" are at riskthose with Type I diabetes and those with Type II diabetes. The longer a person has diabetes, the higher their risk of developing some ocular problem. Between 40 and 45 percent of Americans diagnosed with diabetes have some stage of diabetic retinopathy. After 20 years of diabetes, nearly all patients with Type I diabetes and >60% of patients with Type II diabetes have some degree of retinopathy; however, these statistics were published in 2002 using data from four years earlier, limiting the usefulness of the research. The subjects would have been diagnosed with diabetes in the late 1970s, before modern fast acting insulin and home glucose testing.

Prior studies had also assumed a clear glycemic threshold between people at high and low risk of diabetic retinopathy.

However, it has been shown that the widely accepted WHO and American Diabetes Association diagnostic cutoff for diabetes of a fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) does not accurately identify diabetic retinopathy among patients. The cohort study included a multi-ethnic, cross-sectional adult population sample in the US, as well as two cross-sectional adult populations in Australia. For the US-based component of the study, the sensitivity was 34.7% and specificity was 86.6%. For patients at similar risk to those in this study (15.8% had diabetic retinopathy), this leads to a positive predictive value of 32.7% and negative predictive value of 87.6%.

Published rates vary between trials, the proposed explanation being differences in study methods and reporting of prevalence rather than incidence values.

During pregnancy, diabetic retinopathy may also be a problem for women with diabetes.

It is recommended that all pregnant women with diabetes have dilated eye examinations each trimester to protect their vision.

People with Down's syndrome, who have extra chromosome 21 material, almost never acquire diabetic retinopathy. This protection appears to be due to the elevated levels of endostatin, an anti-angiogenic protein, derived from collagen XVIII. The collagen XVIII gene is located on chromosome 21.

STGD1 is the most common form of inherited juvenile macular degeneration with a prevalence of approximately 1 in 10,000 births.

Cystoid macular edema (CME) involves fluid accumulation in the outer plexiform layer secondary to abnormal perifoveal retinal capillary permeability. The edema is termed "cystoid" as it appears cystic; however, lacking an epithelial coating, it is not truly cystic. The cause for CME can be remembered with the mnemonic "DEPRIVEN" (diabetes, epinepherine, pars planitis, retinitis pigmentosa, Irvine-Gass syndrome, venous occlusion, E2-prostaglandin analogues, nicotinic acid/niacin).

Diabetic macular edema (DME) is similarly caused by leaking macular capillaries. DME is the most common cause of visual loss in both proliferative, and non-proliferative diabetic retinopathy.

Studies indicate drusen associated with AMD are similar in molecular composition to Beta-Amyloid (βA) plaques and deposits in other age-related diseases such as Alzheimer's disease and atherosclerosis. This suggests that similar pathways may be involved in the etiologies of AMD and other age-related diseases.

Optic pits occur equally between men and women. They are seen in roughly 1 in 10,000 eyes, and approximately 85% of optic pits are found to be unilateral (i.e. in only one eye of any affected individual). About 70% are found on the temporal side (or lateral one-half) of the optic disc. Another 20% are found centrally, while the remaining pits are located either superiorly (in the upper one-half), inferiorly (in the lower one-half), or nasally (in the medial one-half towards the nose).

Optic disc drusen are found clinically in about 1% of the population but this increases to 3.4% in individuals with a family history of ODD. About two thirds to three quarters of clinical cases are bilateral. A necropsy study of 737 cases showed a 2.4% incidence with 2 out of 15 (13%) bilateral, perhaps indicating the insidious nature of many cases. An autosomal dominant inheritance pattern with incomplete penetrance and associated inherited dysplasia of the optic disc and its blood supply is suspected. Males and females are affected at equal rates. Caucasians are the most susceptible ethnic group. Certain conditions have been associated with disc drusen such as retinitis pigmentosa, angioid streaks, Usher syndrome, Noonan syndrome and Alagille syndrome. Optic disc drusen are not related to Bruch membrane drusen of the retina which have been associated with age-related macular degeneration.

In general, BRVO has a good prognosis: after 1 year 50–60% of eyes have been reported to have a final VA of 20/40 or better even without any treatment. With time the dramatic picture of an acute BRVO becomes more subtle, hemorrhages fade so that the retina can look almost normal. Collateral vessels develop to help drain the affected area.

No particular risk factors have been conclusively identified; however, there have been a few reports that demonstrate an autosomal dominant pattern of inheritance in some families. Therefore, a family history of optic pits may be a possible risk factor.

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.

There is no good evidence for any preventive actions, since it appears this is a natural response to aging changes in the vitreous. Posterior vitreous detachment (PVD) has been estimated to occur in over 75 per cent of the population over age 65, that PVD is essentially a harmless condition (although with some disturbing symptoms), and that it does not normally threaten sight. However, since epiretinal membrane appears to be a protective response to PVD, where inflammation, exudative fluid, and scar tissue is formed, it is possible that NSAIDs may reduce the inflammation response. Usually there are flashing light experiences and the emergence of floaters in the eye that herald changes in the vitreous before the epiretinal membrane forms g

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.

Macular degeneration is a condition affecting the tissues lying under the retina, while a macular hole involves damage from within the eye, at the junction between the vitreous and the retina itself. There is no relationship between the two diseases. Depending upon the degree of attachment or traction between the vitreous and the retina, there may be risk of developing a macular hole in the other eye. In those cases where the vitreous has already become separated from the retinal surface, there is very little chance of developing a macular hole in the other eye. On the other hand, when the vitreous remains adherent and pulling on the macular region in both eyes, then there may be a greater risk of developing a hole in the second eye. In very rare instances, trauma or other conditions lead to the development of a macular hole. In the vast majority of cases, however, macular holes develop spontaneously. As a result, there is no known way to prevent their development through any nutritional or chemical means, nor is there any way to know who is at risk for developing a hole prior to its appearance in one or both eyes.

Berlin's edema (commotio retinae) is a common condition caused by blunt injury to the eye. It is characterized by decreased vision in the injured eye a few hours after the injury. Under examination the retina appears opaque and white in colour in the periphery but the blood vessels are normally seen along with "cherry red spot" in the foveal reigion.This whitening is indicative of cell damage, which occurs in the retinal pigment epithelium and outer segment layer of photoreceptors. Damage to the outer segment often results in photoreceptor death through uncertain mechanisms. Usually there is no leakage of fluid and therefore it is not considered a true edema. The choroidal fluorescence in fluorescent angiography is absent. Visual acuity ranges from 20/20 to 20/400.

The prognosis is excellent except in case of complications of choroidal rupture, hemorrhage or pigment epithelial damage, but damage to the macula will result in poorer recovery. The outcome can be worsened in the case of retinal detachment, atrophy or hyperplasia. Visual field defects can occur. In late cases cystoid macular edema sometimes develops which can further lead to macular destruction.

Commotio retinae is usually self limiting and there is no treatment as such. It usually resolves in 3–4 weeks without any complications and sequelae.

Familial exudative vitreoretinopathy (FEVR) ( ) is a genetic disorder affecting the growth and development of blood vessels in the retina of the eye. This disease can lead to visual impairment and sometimes complete blindness in one or both eyes. FEVR is characterized by exudative leakage and hemorrhage of the blood vessels in the retina, along with incomplete vascularization of the peripheral retina. The disease process can lead to retinal folds, tears, and detachments.

Irvine–Gass syndrome, pseudophakic cystoid macular edema or postcataract CME is one of the most common causes of visual loss after cataract surgery. The syndrome is named in honor of S. Rodman Irvine and J. Donald M. Gass.

The incidence is more common in older types of cataract surgery, where postcataract CME could occur in 20–60% of patients, but with modern cataract surgery, incidence of Irvine–Gass syndrome have reduced significantly.

Replacement of the lens as treatment for cataract can cause pseudophakic macular edema. (‘pseudophakia’ means ‘replacement lens’) this could occur as the surgery involved sometimes irritates the retina (and other parts of the eye) causing the capillaries in the retina to dilate and leak fluid into the retina. This is less common today with modern lens replacement techniques

Few studies have examined the prevalence of FCED on a large scale. First assessed in a clinical setting, Fuchs himself estimated the occurrence of dystrophia epithelialis corneae to be one in every 2000 patients; a rate that is likely reflective of those who progress to advanced disease. Cross-sectional studies suggest a relatively higher prevalence of disease in European countries relative to other areas of the world. Fuchs' dystrophy rarely affects individuals under 50 years of age.

In the UK, screening for diabetic retinopathy is part of the standard of care for people with diabetes. After one normal screening in people with diabetes, further screening is recommended every two years. Teleophthalmology has been employed in these programs.

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.

Vitreomacular adhesion (VMA) is a human medical condition where the vitreous gel (or simply vitreous) of the human eye adheres to the retina in an abnormally strong manner. As the eye ages, it is common for the vitreous to separate from the retina. But if this separation is not complete, i.e. there is still an adhesion, this can create pulling forces on the retina that may result in subsequent loss or distortion of vision. The adhesion in of itself is not dangerous, but the resulting pathological vitreomacular traction (VMT) can cause severe ocular damage.

The current standard of care for treating these adhesions is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye. A biological agent for non-invasive treatment of adhesions called ocriplasmin has been approved by the FDA on Oct 17 2012.