The predominant cause of nutritional optic neuropathy is thought to be deficiency of B-complex vitamins, particularly thiamine (vitamin B), cyanocobalamin (vitamin B) and recently copper Deficiency of pyridoxine (vitamin B), niacin (vitamin B), riboflavin (vitamin B), and/or folic acid also seems to play a role. Those individuals who abuse alcohol and tobacco are at greater risk because they tend to be malnourished. Those with pernicious anemia are also at risk due to an impaired ability to absorb vitamin B from the intestinal tract.

There are several causes of toxic optic neuropathy. Among these are: ingestion of methanol (wood alcohol), ethylene glycol (automotive antifreeze), disulfiram (used to treat chronic alcoholism), halogenated hydroquinolones (amebicidal medications), ethambutol and isoniazid (tuberculosis treatment), and antibiotics such as linezolid and chloramphenicol. Tobacco is also a major cause of toxic optic neuropathy.

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

The cause of this condition is not presently known. It appears to be inherited in an autosomal dominant fashion.

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.

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

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.

It has been suggested that the disease follows a x-linked pattern of inheritance though studies done on this particular disease are few.

Acorea, microphthalmia and cataract syndrome is a rare genetically inherited condition.

Intraoperative floppy iris syndrome (IFIS) is a complication that may occur during cataract extraction in certain patients. This syndrome is characterized by a flaccid iris which billows in response to ordinary intraocular fluid currents, a propensity for this floppy iris to prolapse towards the area of cataract extraction during surgery, and progressive intraoperative pupil constriction despite standard procedures to prevent this.

IFIS has been associated with tamsulosin (e.g., Flomax), a medication widely prescribed for urinary symptoms associated with benign prostatic hyperplasia (BPH). Tamsulosin is a selective alpha blocker that works by relaxing the bladder and prostatic smooth muscle. As such, it also relaxes the iris dilator muscle by binding to its postsynaptic nerve endings. Even if a patient has only taken tamsulosin once in their life, that dose is enough to cause IFIS during cataract extraction indefinitely. Various alpha-blockers are associated with IFIS, but tamsulosin has a stronger association than the others.

A joint statement of two ophthalmologic societies states that "the other major class of drugs to treat BPH — 5-alpha reductase inhibitors — do not appear to cause IFIS to any significant degree." 5-ARIs include finasteride, a medication typically used as first line therapy for BPH and androgenic alopecia. The medication is also associated with cataract formation.

IFIS may also be associated with other causes of small pupil like synechiae, pseudoexfoliation and other medications (used for conditions such as glaucoma, diabetes and high blood pressure). IFIS does not usually cause significant changes in postoperative outcomes. Patients may experience more pain, a longer recovery period, and less improvement in visual acuity than a patient with an uncomplicated cataract removal.

The severity of the condition is not linked to the duration of tamsulosin intake.

Zonular cataract and nystagmus, also referred as Nystagmus with congenital zonular cataract is a rare congenital disease associated with Nystagmus and zonular cataract of the eye.

The cataract-microcornea syndrome is the association of congenital cataract and microcornea.

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).

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.

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).

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.

Aniridia may be broadly divided into hereditary and sporadic forms. Hereditary aniridia is usually transmitted in an autosomal dominant manner (each offspring has a 50% chance of being affected), although rare autosomal recessive forms (such as Gillespie syndrome) have also been reported. Sporadic aniridia mutations may affect the WT1 region adjacent to the AN2 aniridia region, causing a kidney cancer called nephroblastoma (Wilms tumor). These patients often also have genitourinary abnormalities and intellectual disability (WAGR syndrome).

Several different mutations may affect the PAX6 gene. Some mutations appear to inhibit gene function more than others, with subsequent variability in the severity of the disease. Thus, some aniridic individuals are only missing a relatively small amount of iris, do not have foveal hypoplasia, and retain relatively normal vision. Presumably, the genetic defect in these individuals causes less "heterozygous insufficiency," meaning they retain enough gene function to yield a milder phenotype.

- AN

- Aniridia and absent patella

- Aniridia, microcornea, and spontaneously reabsorbed cataract

- Aniridia, cerebellar ataxia, and mental deficiency (Gillespie syndrome)

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.

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.

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.

A galactosemic cataract is cataract which is associated with the consequences of galactosemia.

The presence of presenile cataract, noticeable in galactosemic infants as young as a few days old, is highly associated with two distinct types of galactosemia: GALT deficiency and to a greater extent, GALK deficiency.

An impairment or deficiency in the enzyme, galactose-1-phosphate uridyltransferase (GALT), results in classic galactosemia, or Type I galactosemia. Classic galactosemia is a rare (1 in 47,000 live births), autosomal recessive disease that presents with symptoms soon after birth when a baby begins lactose ingestion. Symptoms include life-threatening illnesses such as jaundice, hepatosplenomegaly (enlarged spleen and liver), hypoglycemia, renal tubular dysfunction, muscle hypotonia (decreased tone and muscle strength), sepsis (presence of harmful bacteria and their toxins in tissues), and cataract among others. The prevalence of cataract among classic galactosemics is markedly less than among galactokinase-deficient patients due to the extremely high levels of galactitol found in the latter. Classic galactosemia patients typically exhibit urinary galactitol levels of only 98 to 800 mmol/mol creatine compared to normal levels of 2 to 78 mmol/mol creatine.

Galactokinase (GALK) deficiency, or Type II galactosemia, is also a rare (1 in 100,000 live births), autosomal recessive disease that leads to variable galactokinase activity levels: ranging from high GALK efficiency to undetectably-low GALK efficiency. The early onset of cataract is the main clinical manifestation of Type II galactosemics, most likely due to the high concentration of galactitol found in this population. GALK deficient patients exposed to high-galactose diets show extreme levels of galactitol in blood and urine. Studies on galactokinase-deficient patients have shown that nearly two-thirds of ingested galactose can be accounted for by galactose and galactitol levels in the urine. Urinary levels of galactitol in these subjects approach 2500 mmol/mol creatine as compared to 2 to 78 mmol/mol creatine in control patients.

A decrease in activity in the third major enzymes of galactose metabolism, UDP galactose-4'-epimerase (GALE), is the cause of Type III galactosemia. GALE deficiency is an extremely rare, autosomal recessive disease that appears to be most common among the Japanese population (1 in 23,000 live births among Japanese population). While the link between GALE deficiency and cataract prevalence seems to be ambiguous, experiments on this topic have been conducted. A recent 2000 study in Munich, Germany analyzed the activity levels of the GALE enzyme in various tissues and cells in patients with cataract. The experiment concluded that while patients with cataract seldom exhibited an acute decrease in GALE activity in blood cells, "the GALE activity in the lens of cataract patients was, on the other hand, significantly decreased". The study's results are depicted below. The extreme decrease in GALE activity in the lens of cataract patients seems to suggest an irrefutable connection between Type III galactosemia and cataract development.

Vitreous touch syndrome, also known as vitreous wick syndrome is a late complication of intra capsular cataract extraction wherein the vitreous bulges through the pupillary aperture, and touches and attaches to the corneal endothelium.

Patients usually do not require treatment due to benign nature of the disease. In case cataract develops patients generally do well with cataract surgery.