In terms of the treatment of cytomegalovirus retinitis, oral valganciclovir, intravenous ganciclovir, IV foscarnet, and IV cidofovir are all efficient in the treatment of this condition. Also intravitreal injections, an injection of medicine into the vitreous near the retina, of foscarnet in concomitance with oral valganciclovir can be used for treatment as well.

Often individuals with CMV retinitis will need surgery for either retinal detachment or intravitreal instillation of ganciclovir. Retinal detachment occurs in up to 29% of affected eyes, repair being most effective with endolaser and silicone oil endotamponade.Intravitreal ganciclovir implant has the benefit of less systemic toxicity. An adverse effect of this is retinal detachment (and vitreous hemorrhage), also there is no systemic beneficial effect for cytomegalovirus organ disease.

It is extremely important to see an ophthalmologist regularly. Research indicates that supplements slow the disease and lessen the symptoms. Supplements such as Vitamin A, lutein, omega-3 fatty acid DHA have shown to help this disease. While supplements may help lessen the symptoms, retinitis itself is not curable. Additionally, devices such as low-vision magnifiers can be used to aid vision in patients suffering from despaired vision due to retinitis. Rehabilitation services may also aid the patient so that patients may use their vision in a more effective manner. Lastly, it is advisable to wear sunglasses even on gloomy days to protect your eyes from any ultraviolet light.

There are two types of retinitis: Retinitis pigmentosa (RP) and cytomegalovirus (CMV) retinitis. Both conditions result in the swelling and damage to the retinitis. However, the key difference in both these conditions is that Retinitis pigmentosa is a genetic eye disease that you inherit from one or both of your parents. On the other hand, CMV retinitis develops from a viral infection in the retina. Although there is no cure for this disease, there are steps you can take to protect your eyes from worsening. Supplements can slow the progression of the disease and alleviate symptoms temporarily. Research also shows that vitamin A, lutein, and omega-3 fatty acids also help alleviate symptoms.

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.

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.

If the nematode can be seen by an ophthalmologist, which occurs in less than half of cases, it should be treated with photocoagulation for extramacular location and surgical removal in case the larva is lying in the macula. After the worm is killed, visual acuity loss usually does not progress. Alternatively, Antihelminthic treatment such as high dose oral Albendazole and prednisolone may be used.

Macular edema sometimes occurs for a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops. Prophylactic use of Nonsteroidal anti-inflammatory drugs has been reported to reduce the risk of macular edema to some extent.

In 2010 the US FDA approved the use of Lucentis intravitreal injections for macular edema.

Iluvien, a sustained release intravitreal implant developed by Alimera Sciences, has been approved in Austria, Portugal and the U.K. for the treatment of vision impairment associated with chronic diabetic macular edema (DME) considered insufficiently responsive to available therapies. Additional EU country approvals are anticipated.

In 2013 Lucentis by intravitreal injection was approved by the National Institute for Health and Care Excellence in the UK for the treatment of macular edema caused by diabetes and/or retinal vein occlusion.

On July 29, 2014, Eylea (aflibercept), an intravitreal injection produced by Regeneron Pharmaceuticals Inc., was approved to treat DME in the United States.

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

Gene therapy is currently not a treatment option, however human clinical trials for both choroideremia and Leber's congenital amaurosis (LCA) have produced somewhat promising results.

Clinical trials of gene therapy for patients with LCA began in 2008 at three different sites. In general, these studies found the therapy to be safe, somewhat effective, and promising as a future treatment for similar retinal diseases.

In 2011, the first gene therapy treatment for choroideremia was administered. The surgery was performed by Robert MacLaren, Professor of Ophthalmology at the University of Oxford and leader of the Clinical Ophthalmology Research Group at the Nuffield Laboratory of Ophthalmology (NLO).

In the study, 2 doses of the AAV.REP1 vector were injected subretinally in 12 patients with choroideremia.

There study had 2 objectives:

- to assess the safety and tolerability of the AAV.REP1 vector

- to observe the therapeutic benefit, or slowing of the retinal degeneration, of the gene therapy during the study and at a 24-month post-treatment time point

Despite retinal detachment caused by the injection, the study observed initial improved rod and cone function, warranting further study.

In 2016, researchers were optimistic that the positive results of 32 choroideremia patients treated over four and a half years with gene therapy in four countries could be long-lasting.

While nothing currently can be done to stop or reverse the retinal degeneration, there are steps that can be taken to slow the rate of vision loss. UV-blocking sunglasses for outdoors, appropriate dietary intake of fresh fruit and leafy green vegetables, antioxidant vitamin supplements, and regular intake of dietary omega-3 very-long-chain fatty acids are all recommended.

One study found that a dietary supplement of lutein increases macular pigment levels in patients with choroideremia. Over a long period of time, these elevated levels of pigmentation could slow retinal degeneration. Additional interventions that may be needed include surgical correction of retinal detachment and cataracts, low vision services, and counseling to help cope with depression, loss of independence, and anxiety over job loss.

Currently treatment of ARN consists of antiviral therapy administered orally. Typical antiviral agents used include famciclovir, valganciclovir, and valacyclovir. While on these medications, a patient's kidney function should be watched. Some physician's also may administer the antiviral agents via intravitreal delivery. Though controversial, some physicians administer steroids (prednisone) and antithrombotic therapy (aspirin).

Some commonly admistered antiviral agents are as follows:

- Acyclovir

- Famciclovir

- Valacyclovir

- Gancicilovir

- Valganciclovir

In a study done published by the British Journal of Ophthalmology, the cases of ARN/BARN reported in 2001-2002 in the UK, Varicella Zoster Virus was the most common culprit for the disease and presented mostly in men than in women.

Researchers have also looked at two cases of ARN in patients who have been diagnosed with an immunodeficiency virus. The disease presented itself more so in the outer retina until it progressed far enough to then affect the inner retina. The patients were not so responsive to the antiviral agents given to them through an IV, acyclovir specifically. The cases progressed to retinal detachment. The patients tested positive for the herpes virus. Researchers are now wondering if this type of ARN is specific to those who have the immunodeficiency virus.

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.

Cytomegalovirus (a type of herpes virus) is what causes cytomegalovirus retinitis. Other types of herpes viruses include herpes simplex viruses and Epstein-Barr virus. Once an individual is infected with these viruses they stay in the body for life. What triggers the virus to reactivate are the following (though CMV can also be congenital).

- Leukemia

- AIDS

- Immunosuppressive chemotherapy

Retinal dysplasia is an eye disease affecting the retina of animals and, less commonly, humans. It is usually a nonprogressive disease and can be caused by viral infections, drugs, vitamin A deficiency, or genetic defects. Retinal dysplasia is characterized by folds or rosettes (round clumps) of the retinal tissue.

Photic retinopathy generally goes away on its own over time, but there is no specific treatment known to be reliable for speeding recovery. One path sometimes attempted, which has unclear results, is to treat the initial macular edema with corticosteroids.

This is a partial list of human eye diseases and disorders.

The World Health Organization publishes a classification of known diseases and injuries, the International Statistical Classification of Diseases and Related Health Problems, or ICD-10. This list uses that classification.

Most cases of retinal dysplasia in dogs are hereditary. It can involve one or both retinas. Retinal dysplasia can be focal, multifocal, geographic, or accompanied by retinal detachment. Focal and multifocal retinal dysplasia appears as streaks and dots in the central retina. Geographic retinal dysplasia appears as an irregular or horseshoe-shaped area of mixed hyper or hyporeflectivity in the central retina. Retinal detachment occurs with complete retinal dysplasia, and is accompanied by blindness in that eye. Cataracts or glaucoma can also occur secondary to retinal dysplasia. Other causes of retinal dysplasia in dogs include infection with canine adenovirus or canine herpesvirus, or radiation of the eye in newborns.

Optic disc drusen are found clinically in about 1% of the population but this increases to 3.4% in individuals with a family history of ODD. About two thirds to three quarters of clinical cases are bilateral. A necropsy study of 737 cases showed a 2.4% incidence with 2 out of 15 (13%) bilateral, perhaps indicating the insidious nature of many cases. An autosomal dominant inheritance pattern with incomplete penetrance and associated inherited dysplasia of the optic disc and its blood supply is suspected. Males and females are affected at equal rates. Caucasians are the most susceptible ethnic group. Certain conditions have been associated with disc drusen such as retinitis pigmentosa, angioid streaks, Usher syndrome, Noonan syndrome and Alagille syndrome. Optic disc drusen are not related to Bruch membrane drusen of the retina which have been associated with age-related macular degeneration.

Generally speaking, people diagnosed with photic retinopathy recover visual acuity completely within two months, though more severe cases may take longer, or not see complete recovery at all.

DUSN may be caused by a helminthic infection with Toxocara canis, Baylisascaris procyonis, or Ancylostoma caninum. The characteristic lesions are believed to result from a single nematode migrating within the subretinal space. Although previously thought to be endemic in some areas, that belief was likely due to under awareness. DUSN has been diagnosed in patients in many countries and climates including America, Brazil, China and India.

It was described by Chuta Oguchi (1875-1945), a Japanese ophthalmologist, in 1907. The characteristic fundal appearances were described by Mizuo in 1913.

Treatment of the disease is limited. In the People's Republic of China, high doses of Vitamin K and zinc are infused but thus treatment has been declared as quackery in the Republic of China (Taiwan) and by the Timor Leste Academy of Ophthalmology. In the U.S., afflicted persons have taken high doses of zinc (240 mg every two hours).

Oguchi disease, also called congenital stationary night blindness, Oguchi type 1 or Oguchi disease 1, is an autosomal recessive form of congenital stationary night blindness associated with fundus discoloration and abnormally slow dark adaptation.

Acute posterior multifocal placoid pigment epitheliopathy (APMPPE) primarily occurs in adults (with a mean age of 27). Symptoms include blurred vision in both eyes, but the onset may occur at a different time in each eye. There are yellow-white placoid lesions in the posterior pole at the level of the RPE. Some suggest a genetic predisposition to the disease, while others postulate an abnormal immune response to a virus.

The severity and prognosis vary with the type of mutation involved.