In most MS-associated optic neuritis, visual function spontaneously improves over 2–3 months, and there is evidence that corticosteroid treatment does not affect the long term outcome. However, for optic neuritis that is not MS-associated (or atypical optic neuritis) the evidence is less clear and therefore the threshold for treatment with intravenous corticosteroids is lower. Intravenous corticosteroids also reduce the risk of developing MS in the following two years in patients with MRI lesions; but this effect disappears by the third year of follow up.

Paradoxically, oral administration of corticosteroids in this situation may lead to more recurrent attacks than in non-treated patients (though oral steroids are generally prescribed after the intravenous course, to wean the patient off the medication). This effect of corticosteroids seems to be limited to optic neuritis and has not been observed in other diseases treated with corticosteroids.

A Cochrane Systematic Review studied the effect of corticosteroids for treating people with acute optic neuritis. Specific corticosteroids studied included intravenous and oral methylprednisone, and oral prednisone. The authors conclude that current evidence does not show a benefit of either intravenous or oral corticosteroids for rate of recovery of vision (in terms of visual acuity, contrast sensitivity, or visual fields)..

AON is a rare disease and the natural history of the disease process is not well defined. Unlike typical optic neuritis, there is no association with multiple sclerosis, but the visual prognosis for AON is worse than typical optic neuritis. Thus AON patients have different treatment, and often receive chronic immunosuppression. No formal recommendation can be made regarding the best therapeutic approach. However, the available evidence to date supports treatment with corticosteroids and other immunosuppressive agents.

Early diagnosis and prompt treatment with systemic corticosteroids may restore some visual function but the patient may remain steroid dependent; vision often worsens when corticosteroids are tapered. As such, long-term steroid-sparing immunosuppressive agents may be required to limit the side-effects of steroids and minimize the risk of worsening vision.

Patients with optic disc drusen should be monitored periodically for ophthalmoscopy, Snellen acuity, contrast sensitivity, color vision, intraocular pressure and threshold visual fields. For those with visual field defects optical coherence tomography has been recommended for follow up of nerve fiber layer thickness. Associated conditions such as angioid streaks and retinitis pigmentosa should be screened for. Both the severity of optic disc drusen and the degree of intraocular pressure elevation have been associated with visual field loss. There is no widely accepted treatment for ODD, although some clinicians will prescribe eye drops designed to decrease the intra-ocular pressure and theoretically relieve mechanical stress on fibers of the optic disc. Rarely choroidal neovascular membranes may develop adjacent to the optic disc threatening bleeding and retinal scarring. Laser treatment or photodynamic therapy or other evolving therapies may prevent this complication.

Optic pits themselves do not need to be treated. However, patients should follow up with their eye care professional annually or even sooner if the patient notices any visual loss whatsoever. Treatment of PVD or serous retinal detachment will be necessary if either develops in a patient with an optic pit.

The acute uveitis phase of VKH is usually responsive to high-dose oral corticosteroids; parenteral administration is usually not required. However, ocular complications may require an subtenon or intravitreous injection of corticosteroids or bevacizumab. In refractory situations, other immunosuppressives such as cyclosporine, or tacrolimus, antimetabolites (azathioprine, mycophenolate mofetil or methotrexate), or biological agents such as intravenous immunoglobulins (IVIG) or infliximab may be needed.

Laser treatment of drusen has been studied. While it is possible to eliminate drusen with this treatment strategy, it has been shown that this fails to reduce the risk of developing the choroidal neovascularisation which causes the blindness associated with age-related macular degeneration.

There are good results from multiple doses of intravitreal injections of anti-VEGF drugs such as bevacizumab. A 2017 systematic review update found moderate evidence that aflibercept may have advantages in improving visual outcomes over bevacizumab and ranibizumab, after one year. Present recommended treatment for diabetic macular edema is Modified Grid laser photocoagulation combined with multiple injections of anti-VEGF drugs.

Triamcinolone is a long acting steroid preparation. When injected in the vitreous cavity, it decreases the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, and results in an increase in visual acuity. The effect of triamcinolone is transient, lasting up to three months, which necessitates repeated injections for maintaining the beneficial effect. Best results of intravitreal Triamcinolone have been found in eyes that have already undergone cataract surgery. Complications of intravitreal injection of triamcinolone include cataract, steroid-induced glaucoma and endophthalmitis. A systematic review found evidence that eyes treated with the intravitreal injection of triamcinolone had better visual acuity outcomes compared to eyes treated with macular laser grid photocoagulation, or sham injections.

Visual prognosis is generally good with prompt diagnosis and aggressive immunomodulatory treatment. Inner ear symptoms usually respond to corticosteroid therapy within weeks to months; hearing usually recovers completely. Chronic eye effects such as cataracts, glaucoma, and optic atrophy can occur. Skin changes usually persist despite therapy.

There is no cure for retinitis pigmentosa, but the efficacy and safety of various prospective treatments are currently being evaluated. The efficiency of various supplements, such as Vitamin A, DHA, and Lutein, in delaying disease progression remains an unresolved, yet prospective treatment option. Clinical trials investigating optic prosthetic devices, gene therapy mechanisms, and retinal sheet transplantations are active areas of study in the partial restoration of vision in retinitis pigmentosa patients.

Studies have demonstrated the delay of rod photoreceptor degeneration by the daily intake of 15000 IU (equivalent to 4.5 mg) of vitamin A palmitate; thus, stalling disease progression in some patients. Recent investigations have shown that proper vitamin A supplementation can postpone blindness by up to 10 years (by reducing the 10% loss pa to 8.3% pa) in some patients in certain stages of the disease.

The Argus retinal prosthesis became the first approved treatment for the disease in February 2011, and is currently available in Germany, France, Italy, and the UK. Interim results on 30 patients long term trials were published in 2012. The Argus II retinal implant has also received market approval in the US. The device may help adults with RP who have lost the ability to perceive shapes and movement to be more mobile and to perform day-to-day activities. In June 2013, twelve hospitals in the US announced they would soon accept consultation for patients with RP in preparation for the launch of Argus II later that year. The Alpha-IMS is a subretinal implant involving the surgical implantation of a small image-recording chip beneath the optic fovea. Measures of visual improvements from Alpha-IMS studies require the demonstration of the device's safety before proceeding with clinical trials and granting market approval.

The goal of gene therapy studies is to virally supplement retinal cells expressing mutant genes associated with the retinitis pigmentosa phenotype with healthy forms of the gene; thus, allowing the repair and proper functioning of retinal photoreceptor cells in response to the instructions associated with the inserted healthy gene. Clinical trials investigating the insertion of the healthy RPE65 gene in retinas expressing the LCA2 retinitis pigmentosa phenotype measured modest improvements in vision; however, the degradation of retinal photoreceptors continued at the disease-related rate. Likely, gene therapy may preserve remaining healthy retinal cells while failing to repair the earlier accumulation of damage in already diseased photoreceptor cells. Response to gene therapy would theoretically benefit young patients exhibiting the shortest progression of photoreceptor decline; thus, correlating to a higher possibility of cell rescue via the healthy inserted gene.

The progressive nature of and lack of a definitive cure for retinitis pigmentosa contribute to the inevitably discouraging outlook for patients with this disease. While complete blindness is rare, the patient's visual acuity and visual field will continue to decline as initial rod photoreceptor and later cone photoreceptor degradation proceeds. Possible treatments remain in the research and clinical trial stages; however, treatment studies concerning visual restoration in retinitis pigmentosa prove promising for the future.

Studies indicate that children carrying the disease genotype benefit from presymptomatic counseling in order to prepare for the physical and social implications associated with progressive vision loss. While the psychological prognosis can be slightly alleviated with active counseling the physical implications and progression of the disease depend largely on the age of initial symptom manifestation and the rate of photoreceptor degradation, rather than access to prospective treatments. Corrective visual aids and personalized vision therapy provided by Low Vision Specialists may help patients correct slight disturbances in visual acuity and optimize their remaining visual field. Support groups, vision insurance, and lifestyle therapy are additional useful tools for those managing progressive visual decline.

The most recognized cause of a toxic optic neuropathy is methanol intoxication. This can be a life-threatening event that normally accidentally occurs when the victim mistook, or substituted, methanol for ethyl alcohol. Blindness can occur with drinking as little as an ounce of methanol, but this can be counteracted by concurrent drinking of ethyl alcohol. The patient initially has nausea and vomiting, followed by respiratory distress, headache, and visual loss 18–48 hours after consumption. Without treatment, patients can go blind, and their pupils will dilate and stop reacting to light.

- Ethylene glycol, a component of automobile antifreeze, is a poison that is toxic to the whole body including the optic nerve. Consumption can be fatal, or recovery can occur with permanent neurologic and ophthalmologic deficits. While visual loss is not very common, increased intracranial pressure can cause bilateral optic disc swelling from cerebral edema. A clue to the cause of intoxication is the presence of oxalate crystals in the urine. Like methanol intoxication, treatment is ethanol consumption.

- Ethambutol, a drug commonly used to treat tuberculosis, is notorious for causing toxic optic neuropathy. Patients with vision loss from ethambutol toxicity lose vision in both eyes equally. This initially presents with problems with colors (dyschromatopsia) and can leave central visual deficits. If vision loss occurs while using ethambutol, it would be best to discontinue this medication under a doctor’s supervision. Vision can improve slowly after discontinuing ethambutol but rarely returns to baseline.

- Amiodarone is an antiarrhythmic medication commonly used for abnormal heart rhythms (atrial or ventricular tachyarrythmias). Most patients on this medication get corneal epithelial deposits, but this medication has also been controversially associated with NAION. Patients on amiodarone with new visual symptoms should be evaluated by an ophthalmologist.

- Tobacco exposure, most commonly through pipe and cigar smoking, can cause an optic neuropathy. Middle-aged or elderly men are often affected and present with painless, slowly progressive, color distortion and visual loss in both eyes. The mechanism is unclear, but this has been reported to be more common in individuals who are already suffering from malnutrition.

Currently, there is no treatment for the disease. However, ophthalmologists recommend wearing sunglasses and hats outdoors and blue-light blocking glasses when exposed to artificial light sources, such as screens and lights. Tobacco smoke and second-hand smoke should be avoided. Animal studies also show that high doses of vitamin A can be detrimental by building up more lipofuscin toxin. Dietary non-supplemental vitamin A intake may not further the disease progression.

Clinical trials are being conducted with promising early results. The trials may one day lead to treatments that might halt, and possibly even reverse, the effects of Stargardt disease using stem cell therapy, gene therapy, or pharmacotherapy.

The Argus retinal prosthesis, an electronic retinal implant, was successfully fitted to a 67-year-old woman in Italy at the Careggi Hospital in 2016. The patient had a very advanced stage of Stargardt’s disease, and a total absence of peripheral and central visual fields.

While radiation or chemotherapy may be helpful, treatment is often not necessary. Optical gliomas often cannot be surgically resected. If no visual symptoms wait 6 months and then in 6 months only treat if there are symptoms (visual loss, eye pain), otherwise do not treat.

A range of medications that act on the central nervous system has been found to be useful in managing neuropathic pain. Commonly used treatments include tricyclic antidepressants (such as nortriptyline or amitriptyline), the serotonin-norepinephrine reuptake inhibitor (SNRI) medication duloxetine, and antiepileptic therapies such as gabapentin, pregabalin, or sodium valproate. Few studies have examined whether nonsteroidal anti-inflammatory drugs are effective in treating peripheral neuropathy.

Symptomatic relief for the pain of peripheral neuropathy may be obtained by application of topical capsaicin. Capsaicin is the factor that causes heat in chili peppers. The evidence suggesting that capsaicin applied to the skin reduces pain for peripheral neuropathy is of moderate to low quality and should be interpreted carefully before using this treatment option. Local anesthesia often is used to counteract the initial discomfort of the capsaicin. Some current research in animal models has shown that depleting neurotrophin-3 may oppose the demyelination present in some peripheral neuropathies by increasing myelin formation.

High-quality evidence supports the use of cannabis for neuropathic pain.

Attacks are treated with short courses of high dosage intravenous corticosteroids such as methylprednisolone IV.

Plasmapheresis can be an effective treatment when attacks progress or do not respond to corticosteroid treatment. Clinical trials for these treatments contain very small numbers, and most are uncontrolled, though some report high success percentage.

CNV is conventionally treated with intravitreal injections of angiogenesis inhibitors (also known as "anti-VEGF" drugs) to control neovascularization and reduce the area of fluid below the retinal pigment epithelium. Angiogenesis inhibitors include pegaptanib, ranibizumab and bevacizumab (known by a variety of trade names, such as Macugen, Avastin or Lucentis). These inhibitors slow or stop the formation of new blood vessels (angiogenesis), typically by binding to or deactivating the transmission of vascular endothelial growth factor ('VEGF'), a signal protein produced by cells to stimulate formation of new blood vessels. The effectiveness of angiogenesis inhibitors has been shown to significantly improve visual prognosis with CNV, the recurrence rate for these neovascular areas remains high.

CNV may also be treated with photodynamic therapy coupled with a photosensitive drug such as verteporfin (Visudyne). The drug is given intravenously. It is then activated in the eye by a laser light. The drug destroys the new blood vessels, and prevents any new vessels forming by forming thrombi.

Several options exist for the treatment of BRVO. These treatments aim for the two of the most significant complications of BRVO, namely macular edema and neovascularization.

- Systemic treatment with oral Aspirin, subcutaneous Heparin, or intravenous thrombolysis have not been shown to be effective treatments for CRVO and for BRVO no reliable clinical trial has been published.

- Laser treatment of the macular area to reduce macular edema is indicated in patients who have 20/40 or worse vision and did not spontaneously improve for at least 3 months (to permit the maximum spontaneous resolution) after the development of the vein occlusion. It is typically administered with the argon laser and is focused on edematous retina within the arcades drained by the obstructed vein and avoiding the foveal avascular zone. Leaking microvascular abnormalities may be treated directly, but prominent collateral vessels should be avoided.

- The second indication of laser treatment is in case of neovascularization. Retinal photocoagulation is applied to the involved retina to cover the entire involved segment, extending from the arcade out to the periphery. Ischemia alone is not an indication for treatment provided that follow-up could be maintained.

- Preservative-free, nondispersive Triamcinolone acetonide in 1 or 4 mg dosage may be injected into the vitreous to treat macular edema but has complications including elevated intraocular pressure and development of cataract. Triamcinolone injection is shown to have similar effect on visual acuity when compared with standard care (Laser therapy), However, the rates of elevated intraocular pressure and cataract formation is much higher with the triamcinolone injection, especially the higher dosage. Intravitreal injection of Dexamethasone implant (Ozurdex; 700,350 μg) is being studied, its effect may last for 180 days. The injection may be repeated however with less pronounced effect. Although the implant was designed to cause less complications, pressure rise and cataract formation is noted with this treatment too.

- Anti-VEGF drugs such as Bevacizumab (Avastin; 1.25 -2.5 mg in 0.05ml) and Ranibizumab (lucentis) injections are being used and investigated. Intravitreal anti-VEGFs have a low incidence of adverse side effects compared with intravitreal corticosteroids, but are currently short acting requiring frequent injections. Anti-VEGF injection may be used for macular edema or neovascularization. The mechanism of action and duration of anti-VEGF effect on macular edema is currently unknown. The intraocular levels of VEGF are increased in eyes with macular edema secondary to BRVO and the elevated VEGF levels are correlated to the degree and severity of the areas of capillary nonperfusion and macular edema.

- Surgery is employed occasionally for longstanding vitreous hemorrhage and other serious complications such as epiretinal membrane and retinal detachment.

- Arteriovenous sheathotomy has been reported in small, uncontrolled series of patients with BRVO. BRVO typically occurs at arteriovenous crossings, where the artery and vein share a common adventitial sheath. In arteriovenous sheathotomy an incision is made in the adventitial sheath adjacent to the arteriovenous crossing and is extended along the membrane that holds the blood vessels in position to the point where they cross, the overlying artery is then separated from the vein.

Optic neuritis is a demyelinating inflammation of the optic nerve. It is also known as optic papillitis (when the head of the optic nerve is involved) and retrobulbar neuritis (when the posterior part of the nerve is involved). It is most often associated with multiple sclerosis, and it may lead to complete or partial loss of vision in one or both eyes.

Partial, transient vision loss (lasting less than one hour) can be an indication of early onset multiple sclerosis. Other possible diagnoses include: diabetes mellitus, low phosphorus levels, or hyperkalaemia.

No controlled trials have established the effectiveness of treatments for the prevention of attacks. Many clinicians agree that long term immunosuppression is required to reduce the frequency and severity of attacks, while others argue the exact opposite. Commonly used immunosuppressant treatments include azathioprine (Imuran) plus prednisone, mycophenolate mofetil plus prednisone, mitoxantrone, intravenous immunoglobulin (IVIG), and cyclophosphamide.

Though the disease is known to be auto-antibodies mediated, B-cell depletion has been tried with the monoclonal antibody rituximab, showing good results.

Several other disease modifying therapies are being tried. In 2007, Devic's disease was reported to be responsive to glatiramer acetate and to low-dose corticosteroids. Use of Mycophenolate mofetil is also currently under research.

The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.

Optic pits should be diagnosed by an eye care professional who can perform a thorough exam of the back of the eye using an ophthalmoscope.

More recently, the development of a special technology called optical coherence tomography (OCT) has allowed better visualization of the retinal layers. It has been used to demonstrate a marked reduction in the thickness of the retinal nerve fiber layer in the quadrant corresponding to the optic pit. This is not yet in standard use for diagnosis of an optic pit, but may be helpful in supporting a diagnosis.

The best treatment for light sensitivity is to address the underlying cause. Once the triggering factor is treated, photophobia disappears in many but not all cases.

People with photophobia will avert their eyes from direct light, such as sunlight and room lights. They may seek the shelter of a dark room. They may wear sunglasses designed to filter peripheral light and wide-brimmed sun hats.

Wearing sunglasses indoors can make symptoms worse over time as it will dark-adapt the retina which aggravates sensitivity to light. Indoor photophobia symptoms may be relieved with the use of precision tinted lenses which block the green-to-blue end of the light spectrum without blurring or impeding vision.

A paper by Stringham and Hammond, published in the "Journal of Food Science", reviews studies of effects of consuming Lutein and Zeaxanthin on visual performance, and notes a decrease in sensitivity to glare.

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.

Careful eye examination by an ophthalmologist or optometrist is critical for diagnosing symptomatic VMA. Imaging technologies such as optical coherence tomography (OCT) have significantly improved the accuracy of diagnosing symptomatic VMA.

A new FDA approved drug was released on the market late 2013. Jetrea (Brand name) or Ocriplasmin (Generic name) is the first drug of its kind used to treat vitreomacular adhension.

Mechanism of Action: Ocriplasmin is a truncated human plasmin with proteolytic activity against protein components of the vitreous body and vitreretinal interface. It dissolves the protein matrix responsible for the vitreomacular adhesion.

Adverse drug reactions: Decreased vision, potential for lens sublaxation, dyschromatopsia (yellow vision), eye pain, floaters, blurred vision.

New Drug comparison Rating gave Jetea a 5 indicating an important advance.

Previously, no recommended treatment was available for the patient with mild symptomatic VMA. In symptomatic VMA patients with more significant vision loss, the standard of care is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye, thereby surgically releasing the symptomatic VMA. In other words, vitrectomy induces PVD to release the traction/adhesion on the retina. An estimated 850,000 vitrectomy procedures are performed globally on an annual basis with 250,000 in the United States alone.

A standard PPV procedure can lead to serious complications including small-gauge PPV. Complications can include retinal detachment, retinal tears, endophthalmitis, and postoperative cataract formation. Additionally, PPV may result in incomplete separation, and it may potentially leave a nidus for vasoactive and vasoproliferative substances, or it may induce development of fibrovascular membranes. As with any invasive surgical procedure, PPV introduces trauma to the vitreous and surrounding tissue.

There are data showing that nonsurgical induction of PVD using ocriplasmin (a recombinant protease with activity against fibronectin and laminin) can offer the benefits of successful PVD while eliminating the risks associated with a surgical procedure, i.e. vitrectomy. Pharmacologic vitreolysis is an improvement over invasive surgery as it induces complete separation, creates a more physiologic state of the vitreomacular interface, prevents the development of fibrovascular membranes, is less traumatic to the vitreous, and is potentially prophylactic. As of 2012, ThromboGenics is still developing the ocriplasmin biological agent. Ocriplasmin is approved recently under the name Jetrea for use in the United States by the FDA.view.

An experimental test of injections of perfluoropropane (CF) on 15 symptomatic eyes of 14 patients showed that vitreomacular traction resolved in 6 eyes within 1 month and resolved in 3 more eyes within 6 months.