Risk factors such as UVB exposure and smoking can be addressed. Although no means of preventing cataracts has been scientifically proven, wearing sunglasses that counteract ultraviolet light may slow their development. While adequate intake of antioxidants (such as vitamins A, C, and E) has been thought to protect against the risk of cataracts, clinical trials have shown no benefit from supplements; though evidence is mixed, but weakly positive, for a potential protective effect of the nutrients lutein and zeaxanthin. Statin use is somewhat associated with a lower risk of nuclear sclerotic cataracts.

N-Acetylcarnosine drops have been investigated as a medical treatment for cataracts. The drops are believed to work by reducing oxidation and glycation damage in the lens, particularly reducing crystallin crosslinking. Some benefit has been shown in small manufacturer sponsored randomized controlled trials but further independent corroboration is still required.

Femtosecond laser mode-locking, used during cataract surgery, was originally used to cut accurate and predictable flaps in LASIK surgery, and has been introduced to cataract surgery. The incision at the junction of the sclera and cornea and the hole in capsule during capsulorhexis, traditionally made with a handheld blade, needle, and forceps, are dependent on skill and experience of the surgeon. Sophisticated three-dimensional images of the eyes can be used to guide lasers to make these incisions. can also then break up the cataract as in phacoemulsification.

Stem cells have been used in a clinical trial for lens regeneration in twelve children under the age of two with cataracts present at birth. The children were followed for six months, so it is unknown what the long-term results will be, and it is unknown if this procedure would work in adults.

A 2009 study, widely reported in the popular press, has suggested that repetitive transcranial magnetic stimulation may temporarily improve contrast sensitivity and spatial resolution in the affected eye of adults with amblyopia. This approach is still under development, and the results await verification by other researchers. It has also been suggested that comparable results can be achieved using different types of brain stimulation such as anodal transcranial direct current stimulation and theta burst rTMS.

A 2013 study concluded that converging evidence indicates decorrelated binocular experience plays a pivotal role in the genesis of amblyopia and the associated residual deficits. Another study of 2013 suggests that playing a version of the popular game Tetris that is modified such that each eye sees separate components of the game may also help to treat this condition in adults. Furthermore, it has been proposed that the effects of this kind of therapy may be further enhanced by noninvasive brain stimulation as shown by a recent study using anodal tDCS.

A 2014 Cochrane review sought to determine the effectiveness of occlusion treatment on patients with sensory deprivation amblyopia, but no trials were found eligible to be included in the review. However, good outcomes from occlusion treatment for sensory deprivation amblyopia likely rely on compliance with the treatment.

In general, the younger the child, the greater the urgency in removing the cataract, because of the risk of amblyopia. For optimal visual development in newborns and young infants, a visually significant unilateral congenital cataract should be detected and removed before age 6 weeks, and visually significant bilateral congenital cataracts should be removed before age 10 weeks.

Some congenital cataracts are too small to affect vision, therefore no surgery or treatment will be done. If they are superficial and small, an ophthalmologist will continue to monitor them throughout a patient's life. Commonly, a patient with small congenital cataracts that do not affect vision will eventually be affected later in life; generally this will take decades to occur.

Although the best outcome is achieved if treatment is started before age 8, children older than age 12 and some adults can show improvement in the affected eye. Children from 9 to 11 who wore an eye patch and performed near-point activities (vision therapy) were four times as likely to show a two-line improvement on a standard 11-line eye chart than children with amblyopia who did not receive treatment. Adolescents aged 13 to 17 showed improvement, as well, albeit to a lesser degree than younger children. Whether such improvements are only temporary, however, is uncertain, particularly if treatment is discontinued.

Tentative evidence shows that perceptual training may be beneficial in adults.

Virtual-reality computer games where each eye receives different signals of the virtual world that the player's brain must combine to successfully play the game have shown some promise in improving both monocularity in the affected eye, as well as binocularity.

In general, strabismus can be approached and treated with a variety of procedures. Depending on the individual case, treatment options include:

- Correction of refractive errors by glasses

- Prism therapy (if tolerated, to manage diplopia)

- Patching (mainly to manage amblyopia in children and diplopia in adults)

- Botulinum toxin injection

- Surgical correction

Surgical correction of the hypertropia is desired to achieve binocularity, manage diplopia and/or correct the cosmetic defect. Steps to achieve the same depend on mechanism of the hypertropia and identification of the offending muscles causing the misalignment. Various surgical procedures have been described and should be offered after careful examination of eyes, including a detailed orthoptic examination focussing on the disturbances in ocular motility and visual status. Specialty fellowship trained pediatric ophthalmologists and strabismus surgeons are best equipped to deal with these complex procedures.

Cell based therapies using bone marrow stem cells as well as retinal pigment epithelial transplantation are being studied. A number of trials have occurred in humans with encouraging results.

Cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.

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.

A practical application of AMD-associated genetic markers is in the prediction of progression of AMD from early stages of the disease to neovascularization.

Though there is no treatment for Cone dystrophy, certain supplements may help in delaying the progression of the disease.

The beta-carotenoids, lutein and zeaxanthin, have been evidenced to reduce the risk of developing age related macular degeneration (AMD), and may therefore provide similar benefits to Cone dystrophy sufferers.

Consuming omega-3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid) has been correlated with a reduced progression of early AMD, and in conjunction with low glycemic index foods, with reduced progression of advanced AMD, and may therefore delay the progression of cone dystrophy.

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.

Congenital nystagmus has traditionally been viewed as non-treatable, but medications have been discovered in recent years that show promise in some patients. In 1980, researchers discovered that a drug called baclofen could effectively stop periodic alternating nystagmus. Subsequently, gabapentin, an anticonvulsant, was found to cause improvement in about half the patients who received it to relieve symptoms of nystagmus. Other drugs found to be effective against nystagmus in some patients include memantine, levetiracetam, 3,4-diaminopyridine (available in the US to eligible patients with downbeat nystagmus at no cost under an expanded access program), 4-aminopyridine, and acetazolamide. Several therapeutic approaches, such as contact lenses, drugs, surgery, and low vision rehabilitation have also been proposed. For example, it has been proposed that mini-telescopic eyeglasses suppress nystagmus.

Surgical treatment of Congenital Nystagmus is aimed at improving the abnormal head posture, simulating artificial divergence or weakening the horizontal recti muscles. Clinical trials of a surgery to treat nystagmus (known as tenotomy) concluded in 2001. Tenotomy is now being performed regularly at numerous centres around the world. The surgery developed by Louis F. Dell'Osso Ph.D. aims to reduce the eye shaking (oscillations), which in turn tends to improve visual acuity.

Acupuncture has conflicting evidence as to having beneficial effects on the symptoms of nystagmus. Benefits have been seen in treatments where acupuncture points of the neck were used, specifically points on the sternocleidomastoid muscle. Benefits of acupuncture for treatment of nystagmus include a reduction in frequency and decreased slow phase velocities which led to an increase in foveation duration periods both during and after treatment. By the standards of evidence-based medicine, the quality of these studies can be considered poor (for example, Ishikawa has a study sample size of just six, is unblinded and without proper control), and given high quality studies showing that acupuncture has no effect beyond placebo, the results of these studies have to be considered clinically irrelevant until higher quality studies are produced.

Physical therapy or Occupational therapy is also used to treat nystagmus. Treatment consist of learning compensatory strategies to take over for the impaired system.

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

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

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.

Galactosemic infants present clinical symptoms just days after the onset of a galactose diet. They include difficulty feeding, diarrhea, lethargy, hypotonia, jaundice, cataract, and hepatomegaly (enlarged liver). If not treated immediately, and many times even with treatment, severe mental retardation, verbal dyspraxia (difficulty), motor abnormalities, and reproductive complications may ensue. The most effective treatment for many of the initial symptoms is complete removal of galactose from the diet. Breast milk and cow's milk should be replaced with soy alternatives. Infant formula based on casein hydrolysates and dextrin maltose as a carbohydrate source can also be used for initial management, but are still high in galactose. The reason for long-term complications despite a discontinuation of the galactose diet is vaguely understood. However, it has been suggested that endogenous (internal) production of galactose may be the cause.

The treatment for galactosemic cataract is no different from general galactosemia treatment. In fact, galactosemic cataract is one of the few symptoms that is actually reversible. Infants should be immediately removed from a galactose diet when symptoms present, and the cataract should disappear and visibility should return to normal. Aldose reductase inhibitors, such as sorbinil, have also proven promising in preventing and reversing galactosemic cataracts. AR inhibitors hinder aldose reductase from synthesizing galactitol in the lens, and thus restricts the osmotic swelling of the lens fibers. Other AR inhibitors include the acetic acid compounds zopolrestat, tolrestat, alrestatin, and epalrestat. Many of these compounds have not been successful in clinical trials due to adverse pharmokinetic properties, inadequate efficacy and efficiency, and toxic side effects. Testing on such drug-treatments continues in order to determine potential long-term complications, and for a more detailed mechanism of how AR inhibitors prevent and reverse the galactosemic cataract.

Distorted vision is a symptom with several different possible causes.

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

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.

Nystagmus is a relatively common clinical condition, affecting one in several thousand people. A survey conducted in Oxfordshire, United Kingdom found that by the age of two, one in every 670 children had manifested nystagmus. Authors of another study in the United Kingdom estimated an incidence of 24 in 10,000 (~0.240 %), noting an apparently higher rate amongst white Europeans than in individuals of Asian origin.

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.

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

This type of PRA has an early onset of severe vision loss. It is caused by a defect in the gene for cGMP-phosphodiesterase, which leads to retinal levels of cyclic guanosine monophosphate ten times normal.

Although advancement has been slow to come during the decades of research dedicated to the galactosemic cataract, some notable additions have been made. In 2006, Michael L. Mulhern and colleagues further investigated the effects of the osmotic swelling on galactosemic cataract development. Experiments were based on systematic observation of rats fed a 50% galactose diet. According to Mulhern, 7 to 9 days after the onset of the galactose diet, lenses appeared hydrated and highly vacuolated. Lens fibers became liquefied after nine days of the diet, and nuclear cataract formation appeared after 15 days of the diet.

The experiment concluded that

Apoptosis in lens epithelial cells (LEC) is linked to cataract formation. Essentially, the study suggested that the mechanism outlined by Friedenwald and Kinoshita, which centers on osmotic swelling of the lens fibers, is just the beginning in a cascade of events that causes and progresses the galactosemic cataract. Mulhern determined that osmotic swelling is actually a cataractogenic stressor that leads to LEC apoptosis. This is because osmotic swelling of lens fibers considerably strains LEC endoplasmic reticula. As the endoplasmic reticulum is the principal site of protein synthesis, stressors on the ER can cause proteins to become misfolded. The subsequent accumulation of misfolded proteins in the ER activates the unfolded protein response (UPR) in LECs. In agreement, it was later observed on galactosemic yeast models, the activation of UPR upon galactose treatment. UPR initiates apoptosis, or cell death, by various mechanisms, one of which is the release of reactive oxygen species (ROS). Thus, according to recent findings, osmotic swelling, UPR, oxidative damage, and the resultant LEC apoptosis all play key roles in the onset and progression of the galactosemic cataract. Other studies claim that the oxidative damage in LECs is less a result of the release of ROS and more because of the competition between aldose reductase and glutathione reductase for nicotinamide adenine dinucleotide phosphate (NADPH). Aldose reductase requires NADPH for the reduction of galactose to galactitol, while glutathione reductase utilizes NADPH to reduce glutathione disulfide (GSSG) to its sulfhydryl form, GSH. GSH is an important cellular antioxidant. Therefore, what exactly the key roles are for these cataractogenic factors is not yet fully understood or agreed upon by researchers.