Intraocular pressure can be lowered with medication, usually eye drops. Several classes of medications are used to treat glaucoma, with several medications in each class.

Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate them or to communicate with the treating physician to improve the drug regimen. Initially, glaucoma drops may reasonably be started in either one or in both eyes. Wiping the eye with an absorbent pad after the administration of eye drops may result in fewer adverse effects, like the growth of eyelashes and hyperpigmentation in the eyelid.

Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an HMO found half failed to fill their prescriptions the first time, and one-fourth failed to refill their prescriptions a second time. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

The possible neuroprotective effects of various topical and systemic medications are also being investigated.

- Prostaglandin analogs, such as latanoprost, bimatoprost and travoprost, increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow.

- Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol, decrease aqueous humor production by the epithelium of the ciliary body.

- Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow.

- Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor).

- Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic glaucoma.

- Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.

Colobomas of the iris may be treated in a number of ways. A simple cosmetic solution is a specialized cosmetic contact lens with an artificial pupil aperture. Surgical repair of the iris defect is also possible. Surgeons can close the defect by stitching in some cases. More recently artificial iris prosthetic devices such as the Human Optics artificial iris have been used successfully by specialist surgeons. This device cannot be used if the natural lens is in place and is not suitable for children. Suture repair is a better option where the lens is still present.

Vision can be improved with glasses, contact lenses or even laser eye surgery but may be limited if the retina is affected or there is amblyopia.

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.

The modern goals of glaucoma management are to avoid glaucomatous damage and nerve damage, and preserve visual field and total quality of life for patients, with minimal side effects. This requires appropriate diagnostic techniques and follow-up examinations, and judicious selection of treatments for the individual patient. Although intraocular pressure is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment.

Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies, including nutritional compounds, some of which may be regarded by clinicians as safe for use now, while others are on trial.

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.

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.

Cataract removal can be performed at any stage and no longer requires ripening of the lens. Surgery is usually 'outpatient' and performed using local anesthesia. About 9 of 10 patients can achieve a corrected vision of 20/40 or better after surgery.

Several recent evaluations found that cataract surgery can meet expectations only when significant functional impairment due to cataracts exists before surgery. Visual function estimates such as VF-14 have been found to give more realistic estimates than visual acuity testing alone. In some developed countries, a trend to overuse cataract surgery has been noted, which may lead to disappointing results.

Phacoemulsification is the most widely used cataract surgery in the developed world. This procedure uses ultrasonic energy to emulsify the cataract lens. Phacoemulsification typically comprises six steps:

- Anaesthetic – The eye is numbed with either a subtenon injection around the eye (see: retrobulbar block) or topical anesthetic eye drops. The former also provides paralysis of the eye muscles.

- Corneal incision – Two cuts are made at the margin of the clear cornea to allow insertion of instruments into the eye.

- Capsulorhexis – A needle or small pair of forceps is used to create a circular hole in the capsule in which the lens sits.

- Phacoemulsification – A handheld ultrasonic probe is used to break up and emulsify the lens into liquid using the energy of ultrasound waves. The resulting 'emulsion' is sucked away.

- Irrigation and aspiration – The cortex, which is the soft outer layer of the cataract, is aspirated or sucked away. Fluid removed is continually replaced with a saline solution to prevent collapse of the structure of the anterior chamber (the front part of the eye).

- Lens insertion – A plastic, foldable lens is inserted into the capsular bag that formerly contained the natural lens. Some surgeons also inject an antibiotic into the eye to reduce the risk of infection. The final step is to inject salt water into the corneal wounds to cause the area to swell and seal the incision.

Extracapsular cataract extraction (ECCE) consists of removing the lens manually, but leaving the majority of the capsule intact. The lens is expressed through a 10- to 12-mm incision which is closed with sutures at the end of surgery. ECCE is less frequently performed than phacoemulsification, but can be useful when dealing with very hard cataracts or other situations where emulsification is problematic. Manual small incision cataract surgery (MSICS) has evolved from ECCE. In MSICS, the lens is removed through a self-sealing scleral tunnel wound in the sclera which, ideally, is watertight and does not require suturing. Although "small", the incision is still markedly larger than the portal in phacoemulsion. This surgery is increasingly popular in the developing world where access to phacoemulsification is still limited.

Intracapsular cataract extraction (ICCE) is rarely performed. The lens and surrounding capsule are removed in one piece through a large incision while pressure is applied to the vitreous membrane. The surgery has a high rate of complications.

Treatment of strabismic or anisometropic amblyopia consists of correcting the optical deficit (wearing the necessary spectacle prescription) and often forcing use of the amblyopic eye, by patching the good eye, or instilling topical atropine in the good eye, or both.

Concerning patching versus atropine, a drawback is seen in using atropine; the drops can have a side effect of creating nodules in the eye which a correctional ointment can counteract. One should also be wary of overpatching or overpenalizing the good eye when treating amblyopia, as this can create so-called "reverse amblyopia". Eye patching is usually done on a part-time schedule of about 4–6 hours a day. Treatment is continued as long as vision improves. It is not worthwhile continuing to patch for more than 6 months if no improvement continues. Treatment of individuals age 9 through to adulthood is possible through applied perceptual learning.

Deprivation amblyopia is treated by removing the opacity as soon as possible followed by patching or penalizing the good eye to encourage the use of the amblyopic eye. The earlier the treatment is initiated, the easier and faster the treatment is and the less psychologically damaging. Also, the chance of achieving 20/20 vision is greater if treatment is initiated early.

One of the German public health insurance providers, Barmer, has changed its policy to cover, as of 1 April 2014, the costs for an app for amblyopic children whose condition has so far not improved through patching. The app offers dedicated eye exercises which the patient performs while wearing an eyepatch.

Enzymatic vitreolysis has been trialled to treat vitreomacular traction (VMT) and anomalous posterior vitreous detachment. Whilst the mechanism of action may have an effect on clinically significant floaters, as of March 2015 there are no clinical trials being undertaken to determine whether this may be a therapeutic alternative to either i) conservative management, or ii) vitrectomy.

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.

While surgeries do exist to correct for severe cases of floaters, there are currently no medications (including eye drops) that can correct for this vitreous deterioration. Floaters are often caused by the normal aging process and will usually disappear as the brain learns to ignore them. Looking up/down and left/right will cause the floaters to leave the direct field of vision as the vitreous humour swirls around due to the sudden movement. If floaters significantly increase in numbers and/or severely affect vision, then one of the below surgeries may be necessary.

Currently, insufficient evidence is available to compare the safety and efficacy of surgical vitrectomy with laser vitreolysis for the treatment of floaters. A 2017 Cochrane Review did not find any relevant studies that compared the two treatments.

Aggressive marketing campaigns are currently promoting the use of laser vitreolysis for the treatment of floaters. No strong evidence currently exists for the treatment of floaters with laser vitreolysis. Currently, the strongest available evidence comparing these two treatment modalities are retrospective case series.

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.

Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (or tyres) to the sclera (the white outer coat of the eyeball). The bands push the wall of the eye inward against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of vitreous traction thereby allowing the retina to re-attach. Cryotherapy (freezing) is applied around retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling procedure. The buckle remains in situ. The most common side effect of a scleral operation is myopic shift. That is, the operated eye will be more short sighted after the operation. Radial scleral buckle is indicated for U-shaped tears or Fishmouth tears, and posterior breaks. Circumferential scleral buckle is indicated for multiple breaks, anterior breaks and wide breaks. Encircling buckles are indicated for breaks covering more than 2 quadrants of retinal area, lattice degeneration located on more than 2 quadrant of retinal area, undetectable breaks, and proliferative vitreous retinopathy.

The World Health Organization estimates that 80% of visual loss is either preventable or curable with treatment. This includes cataracts, onchocerciasis, trachoma, glaucoma, diabetic retinopathy, uncorrected refractive errors, and some cases of childhood blindness. The Center for Disease Control and Prevention estimates that half of blindness in the United States is preventable.

It can be treated with laser coagulation, and more commonly with medication that stops and sometimes reverses the growth of blood vessels.

A randomized control trial found that bevacizumab and ranibizumab had similar efficacy, and reported no significant increase in adverse events with bevacizumab. A 2014 Cochrane review found that the systemic safety of bevacizumab and ranibizumab are similar when used to treat neovascular AMD, except for gastrointestinal disorders. Bevacizumab however is not FDA approved for treatment of macular degeneration. A controversy in the UK involved the off-label use of cheaper bevacizumab over the approved, but expensive, ranibizumab. Ranibizumab is a smaller fragment, Fab fragment, of the parent bevacizumab molecule specifically designed for eye injections. Other approved antiangiogenic drugs for the treatment of neo-vascular AMD include pegaptanib and aflibercept.

The American Academy of Ophthalmology practice guidelines do not recommend laser coagulation therapy for macular degeneration, but state that it may be useful in people with new blood vessels in the choroid outside of the fovea who don't respond to drug treatment. There is strong evidence that laser coagulation will result in the disappearance of drusen but does not affect choroidal neovascularisation. A 2007 Cochrane review on found that laser photocoagulation of new blood vessels in the choroid outside of the fovea is effective and economical method, but that the benefits are limited for vessels next to or below the fovea.

Photodynamic therapy has also been used to treat wet AMD. The drug verteporfin is administered intravenously; light of a certain wavelength is then applied to the abnormal blood vessels. This activates the verteporfin destroying the vessels.

Cataract surgery could possibly improve visual outcomes for people with AMD, though there have been concerns of surgery increasing the progression of AMD. A randomized controlled trial found that people who underwent immediate cataract surgery (within 2 weeks) had improved visual acuity and better quality of life outcomes than those who underwent delayed cataract surgery (6 months).

No medical or surgical treatment is available for this condition.

Treatment is done by changing the optical magnification properties of the auxiliary optics (corrective lenses). The optical magnification properties of spectacle lenses can be adjusted by changing parameters like the base curve, vertex distance, and center thickness. Contact lenses may also provide a better optical magnification to reduce the difference in image size. The difference in magnification can also be eliminated by a combination of contact lenses and glasses (creating a weak telescope system). The optimum design solution will depend on different parameters like cost, cosmetic implications, and if the patient can tolerate wearing a contact lens.

Note however that before the optics can be designed, first the aniseikonia should be known=measured. When the image disparity is astigmatic (cylindrical) and not uniform, images can appear wider, taller, or diagonally different. When the disparity appears to vary across the visual field (field-dependent aniseikonia), as may be the case with an epiretinal membrane or retinal detachment, the aniseikonia cannot fully be corrected with traditional optical techniques like standard corrective lenses. However, partial correction often improves the patient's vision comfort significantly. Little is known yet about the possibilities of using surgical intervention to correct aniseikonia.

Aside from medical help, various sources provide information, rehabilitation, education, and work and social integration.

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.

A 2014 Cochrane Systematic Review studied the effectiveness of two anti-VEGF treatments, ranibizumab and pegaptanib, on patients suffering from macular edema caused by CRVO. Participants on both treatment groups showed a reduction in macular edema symptoms over six months.

Another Cochrane Review examined the effectiveness and safety of two intravitreal steroid treatments, triamcinolone acetonide and dexamethasone, for patients with from CRVO-ME. The results from one trial showed that patients treated with triamcinolone acetonide were significantly more likely to show improvements in visual acuity than those in the control group, though outcome data was missing for a large proportion of the control group. The second trial showed that patients treated with dexamethasone implants did not show improvements in visual acuity, compared to patients in the control group.

Evidence also suggests that intravitreal injections and implantation of steroids inside the eye can result in improved visual outcomes for patients with chronic or refractory diabetic macular edema.

In 2005, steroids were investigated for the treatment of macular edema due to retinal blood vessel blockage such as CRVO and BRVO.

When this magnification difference becomes excessive the effect can cause diplopia, suppression, disorientation, eyestrain, headache, and dizziness and balance disorders.

Non-surgical treatments of FCED may be used to treat symptoms of early disease. Medical management includes topical hypertonic saline, the use of a hairdryer to dehydrate the precorneal tear film, and therapeutic soft contact lenses. Hypertonic saline draws water out of the cornea through osmosis. When using a hairdryer, the patient is instructed to hold it at an arm's length or directed across the face on a cold setting, to dry out the epithelial blisters. This can be done two or three times a day. Definitive treatment, however, (especially with increased corneal edema) is surgical in the form of corneal transplantation. The most common types of surgery for FCED are Descemet's stripping automated endothelial keratoplasty (DSAEK) and Descemet's membrane endothelial keratoplasty (DMEK), which account for over half of corneal transplants in the United States.

More speculative future directions in the treatment of FED include in-vitro expansion of human corneal endothelial cells for transplantation, artificial corneas (keratoprosthesis) and genetic modification. Surgery where the central diseased endothelium is stripped off but not replaced with donor tissue, with subsequent Rho-Associated Kinase (ROCK) inhibition of endothelial cell division may offer a viable medical treatment.

A greater understanding of FED pathophysiology may assist in the future with the development of treatments to prevent progression of disease. Although much progress has been made in the research and treatment of FED, many questions remain to be answered. The exact causes of illness, the prediction of disease progression and delivery of an accurate prognosis, methods of prevention and effective nonsurgical treatment are all the subject of inquiries that necessitate an answer.

Increased attention must be given to research that can address the most basic questions of how the disease develops: what are the biomolecular pathways implicated in disease, and what genetic or environmental factors contribute to its progression? In addition to shaping our understanding of FED, identification of these factors would be essential for the prevention and management of this condition.

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.