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.

Risk factors for retinal detachment include severe myopia, retinal tears, trauma, family history, as well as complications from cataract surgery.

Retinal detachment can be mitigated in some cases when the warning signs are caught early. The most effective means of prevention and risk reduction is through education of the initial signs, and encouragement for people to seek ophthalmic medical attention if they have symptoms suggestive of a posterior vitreous detachment. Early examination allows detection of retinal tears which can be treated with laser or cryotherapy. This reduces the risk of retinal detachment in those who have tears from around 1:3 to 1:20. For this reason, the governing bodies in some sports require regular eye examination.

Trauma-related cases of retinal detachment can occur in high-impact sports or in high speed sports. Although some recommend avoiding activities that increase pressure in the eye, including diving and skydiving, there is little evidence to support this recommendation, especially in the general population. Nevertheless, ophthalmologists generally advise people with high degrees of myopia to try to avoid exposure to activities that have the potential for trauma, increase pressure on or within the eye itself, or include rapid acceleration and deceleration, such as bungee jumping or roller coaster rides.

Intraocular pressure spikes occur during any activity accompanied by the Valsalva maneuver, including weightlifting. An epidemiological study suggests that heavy manual lifting at work may be associated with increased risk of rhegmatogenous retinal detachment, but this relationship is not strong. In this study, obesity also appeared to increase the risk of retinal detachment. A high Body Mass Index (BMI) and elevated blood pressure have been identified as a risk factor in non-myopic individuals.

Genetic factors promoting local inflammation and photoreceptor degeneration may also be involved in the development of the disease.

Other risk factors include the following:

- Glaucoma

- AIDS

- Cataract surgery

- Diabetic retinopathy

- Eclampsia

- Family history of retinal detachment

- Homocysteinuria

- Malignant hypertension

- Metastatic cancer, which spreads to the eye (eye cancer)

- Retinoblastoma

- Severe myopia

- Smoking and passive smoking

- Stickler syndrome

- Von Hippel-Lindau disease

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.

The incidence of retinal detachment in otherwise normal eyes is around 5 new cases in 100,000 persons per year. Detachment is more frequent in middle-aged or elderly populations, with rates of around 20 in 100,000 per year. The lifetime risk in normal individuals is about 1 in 300. Asymptomatic retinal breaks are present in about 6% of eyes in both clinical and autopsy studies.

- Retinal detachment is more common in people with severe myopia (above 5–6 diopters), in whom the retina is more thinly stretched. In such patients, lifetime risk rises to 1 in 20. About two-thirds of cases of retinal detachment occur in myopics. Myopic retinal detachment patients tend to be younger than non-myopic ones.

- Retinal detachment is more frequent after surgery for cataracts. The estimated long-term prevalence of retinal detachment after cataract surgery is in the range of 5 to 16 per 1000 cataract operations, but is much higher in patients who are highly myopic, with a prevalence of up to 7% being reported in one study. One study found that the probability of experiencing retinal detachment within 10 years of cataract surgery may be about 5 times higher than in the absence of treatment.

- Tractional retinal detachments can also occur in patients with proliferative diabetic retinopathy or those with proliferative retinopathy of sickle cell disease. In proliferative retinopathy, abnormal blood vessels (neovascularization) grow within the retina and extend into the vitreous. In advanced disease, the vessels can pull the retina away from the back wall of the eye, leading to tractional retinal detachment.

Although retinal detachment usually occurs in just one eye, there is a 15% chance of it developing in the other eye, and this risk increases to 25–30% in patients who have had a retinal detachment and cataracts extracted from both eyes.

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.

Between 2 and 5% of the population in western countries have amblyopia. In the U.K., 90% of visual health appointments in the child are concerning amblyopia.

Depending on the chosen criterion for diagnosis, between 1 and 4% of the children have amblyopia.

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.

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

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.

Hypertropia may be either congenital or acquired, and misalignment is due to imbalance in extraocular muscle function. The superior rectus, inferior rectus, superior oblique, and inferior oblique muscles affect the vertical movement of the eyes. These muscles may be either paretic, restrictive (fibrosis) or overactive effect of the muscles. Congenital cases may have developmental abnormality due to abnormal muscle structure, usually muscle atrophy / hypertrophy or rarely, absence of the muscle and incorrect placement.

Specific & common causes include:

- Superior oblique Palsy / Congenital fourth nerve palsy

- Inferior oblique overaction

- Brown's syndrome

- Duane's retraction syndrome

- Double elevator palsy

- Fibrosis of rectus muscle in Graves Disease (most commonly inferior rectus is involved)

- Surgical trauma to the vertical muscles (e.g. during scleral buckling surgery or cataract surgery causing iatrogenic trauma to the vertical muscles).

Sudden onset hypertropia in a middle aged or elderly adult may be due to compression of the trochlear nerve and mass effect from a tumor, requiring urgent brain imaging using MRI to localise any space occupying lesion. It could also be due to infarction of blood vessels supplying the nerve, due to diabetes and atherosclerosis. In other instances it may be due to an abnormality of neuromuscular transmission, i.e., Myasthenia Gravis.

The National Eye Institute reports keratoconus is the most common corneal dystrophy in the United States, affecting about one in 2,000 Americans, but some reports place the figure as high as one in 500. The inconsistency may be due to variations in diagnostic criteria, with some cases of severe astigmatism interpreted as those of keratoconus, and" vice versa". A long-term study found a mean incidence rate of 2.0 new cases per 100,000 population per year. Some studies have suggested a higher prevalence amongst females, or that people of South Asian ethnicity are 4.4 times as likely to suffer from keratoconus as Caucasians, and are also more likely to be affected with the condition earlier.

Keratoconus is normally bilateral (affecting both eyes) although the distortion is usually asymmetric and is rarely completely identical in both corneas. Unilateral cases tend to be uncommon, and may in fact be very rare if a very mild condition in the better eye is simply below the limit of clinical detection. It is common for keratoconus to be diagnosed first in one eye and not until later in the other. As the condition then progresses in both eyes, the vision in the earlier-diagnosed eye will often remain poorer than that in its fellow.

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.

The vitreous (Latin for "glassy") humor is a gel which fills the eye behind the lens. Between it and the retina is the vitreous membrane. With age the vitreous humor changes, shrinking and developing pockets of liquefaction, similar to the way a gelatin dessert shrinks and detaches from the edge of a pan. At some stage the vitreous membrane may peel away from the retina. This is usually a sudden event, but it may also occur slowly over months.

Age and refractive error play a role in determining the onset of PVD in a healthy person. PVD is rare in emmetropic people under the age of 40 years, and increases with age to 86% in the 90s. Several studies have found a broad range of incidence of PVD, from 20% of autopsy cases to 57% in a more elderly population of patients (average age was 83.4 years).

People with myopia (nearsightedness) greater than 6 diopters are at higher risk of PVD at all ages.

Posterior vitreous detachment does not directly threaten vision. Even so, it is of increasing interest because the interaction between the vitreous body and the retina might play a decisive role in the development of major pathologic vitreoretinal conditions, such as epiretinal membrane.

PVD may also occur in cases of cataract surgery, within weeks or months of the surgery.

The vitreous membrane is more firmly attached to the retina anteriorly, at a structure called the vitreous base. The membrane does not normally detach from the vitreous base, although it can be detached with extreme trauma. However, the vitreous base may have an irregular posterior edge. When the edge is irregular, the forces of the vitreous membrane peeling off the retina can become concentrated at small posterior extensions of the vitreous base. Similarly, in some people with retinal lesions such as lattice retinal degeneration or chorio-retinal scars, the vitreous membrane may be abnormally adherent to the retina. If enough traction occurs the retina may tear at these points. If there are only small point tears, these can allow glial cells to enter the vitreous humor and proliferate to create a thin epiretinal membrane that distorts vision. In more severe cases, vitreous fluid may seep under the tear, separating the retina from the back of the eye, creating a retinal detachment. Trauma can be any form from a blunt force trauma to the face such as a boxer's punch or even in some cases has been known to be from extremely vigorous coughing or blowing of the nose.

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).

Refractive errors such as hyperopia and Anisometropia may be associated abnormalities found in patients with vertical strabismus.

The vertical miscoordination between the two eyes may lead to

- Strabismic amblyopia, (due to deprivation / suppression of the deviating eye)

- cosmetic defect (most noticed by parents of a young child and in photographs)

- Face turn, depending on presence of binocular vision in a particular gaze

- diplopia or double vision - more seen in adults (maturity / plasticity of neural pathways) and suppression mechanisms of the brain in sorting out the images from the two eyes.

- cyclotropia, a cyclotorsional deviation of the eyes (rotation around the visual axis), particularly when the root cause is an oblique muscle paresis causing the hypertropia.

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.

Distortion of vision refers to straight lines not appearing straight, but instead bent, crooked, or wavy. Usually this is caused by distortion of the retina itself. This distortion can herald a loss of vision in macular degeneration, so anyone with distorted vision should seek medical attention by an ophthalmologist promptly. Other conditions leading to swelling of the retina can cause this distortion, such as macular edema and central serous chorioretinopathy.

An Amsler grid can be supplied by an ophthalmologist so that the vision can be monitored for distortion in people who may be predisposed to this problem.

Tunnel vision implies that the peripheral vision, or side vision, is lost, while the central vision remains. Thus, the vision is like looking through a tunnel, or through a paper towel roll. Some disorders that can cause this include:

Glaucoma - severe glaucoma can result in loss of nearly all of the peripheral vision, with a small island of central vision remaining. Sometimes even this island of vision can be lost as well.

Retinitis pigmentosa - This is usually a hereditary disorder which can be part of numerous syndromes. It is more common in males. The peripheral retina develops pigmentary deposits, and the peripheral vision gradually becomes worse and worse. The central vision can be affected eventually as well. People with this problem may have trouble getting around in the dark. Cataract can be a complication as well. There is no known treatment for this disorder, and supplements of Vitamin A have not been proven to help.

Punctate Inner Choroidopathy - This condition is where vessels gro (( material is missing ))

Stroke - a stroke involving both sides of the visual part of the brain may wipe out nearly all of the peripheral vision. Fortunately, this is a very rare occurrence

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.

A posterior vitreous detachment (PVD) is a condition of the eye in which the vitreous membrane separates from the retina.

It refers to the separation of the posterior hyaloid membrane from the retina anywhere posterior to the vitreous base (a 3–4 mm wide attachment to the ora serrata).

The condition is common for older adults; over 75% of those over the age of 65 develop it. Although less common among people in their 40s or 50s, the condition is not rare for those individuals. Some research has found that the condition is more common among women.

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.

Deprivation amblyopia (amblyopia ex anopsia) results when the ocular media become opaque, such as is the case with congenital cataract or corneal haziness. These opacities prevent adequate visual input from reaching the eye, and disrupt development. If not treated in a timely fashion, amblyopia may persist even after the cause of the opacity is removed. Sometimes, drooping of the eyelid (ptosis) or some other problem causes the upper eyelid to physically occlude a child's vision, which may cause amblyopia quickly. Occlusion amblyopia may be a complication of a hemangioma that blocks some or all of the eye. Other possible causes of deprivation and occlusion amblyopia include obstruction in the vitreous and aphakia. Deprivation amblyopia accounts for less than 3% of all individuals affected by amblyopia.

The hyaloid artery, an artery running through the vitreous humour during the fetal stage of development, regresses in the third trimester of pregnancy. Its disintegration can sometimes leave cell matter.

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

Patients with retinal tears may experience floaters if red blood cells are released from leaky blood vessels, and those with uveitis or vitritis, as in toxoplasmosis, may experience multiple floaters and decreased vision due to the accumulation of white blood cells in the vitreous humour.

Other causes for floaters include cystoid macular edema and asteroid hyalosis. The latter is an anomaly of the vitreous humour, whereby calcium clumps attach themselves to the collagen network. The bodies that are formed in this way move slightly with eye movement, but then return to their fixed position.