Most patients can be treated non-surgically with eyeglasses, or contact lenses.

There is evidence suggesting corneal collagen cross-linking may be beneficial for patients with pellucid marginal degeneration. Research shows some promising results by combining collagen cross linking with photorefractive keratectomy, or with topography-guided transepithelial surface ablation.

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.

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.

Spectacles or RGP contact lenses can be used to manage the astigmatism. when the condition worsens, surgical correction may be required.

Barrage laser is at times done prophylactically around a hole or tear associated with lattice degeneration in an eye at risk of developing a retinal detachment. It is not known if surgical interventions such as laser photocoagulation or cryotherapy is effective in preventing retinal detachment in patients with lattice degeneration or "asymptomatic" retinal detachment. Laser photocoagulation has been shown to reduce risks of retinal detachment in "symptomatic" lattice degeneration. There are documented cases wherein retina detached from areas which were otherwise healthy despite being treated previously with laser.

Pterygium typically do not require surgery unless it grows to such an extent that it causes visual problems. Some of the symptoms such as irritation can be addressed with artificial tears. Surgery may also be considered for unmanageable symptoms.

A Cochrane review found conjunctival autograft surgery was less likely to have reoccurrence of the pterygium at 6 months compared to amniotic membrane transplant. More research is needed to determine which type of surgery resulted in better vision or quality of life. The additional use of mitomycin C is of unclear effect. Radiotherapy has also be used in an attempt to reduce the risk of recurrence.

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.

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.

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.

Treatments for corneal neovascularization are predominately off-lab with a multitude of complications as a result. The desired results from medical therapy may not always occur, ergo an invasive procedure may be needed to prevent further decrease in corneal avascularity.

For contact lenses related hypoxia, ceasing the use of contact lenses is the first step until corneal neovascularization is addressed by a physician. Modern rigid gas permeable and silicon hydrogel contact lenses have a much higher level of oxygen transmissibility, making them effective alternatives to help prevent corneal neovascularization.

Topical administration of steroids and non-steroid anti-inflammatory drugs are first-line treatment for individuals with CNV. The administration of steroids can increase the risk of infection, glaucoma, cataracts, herpes simplex recurrence. The anti-inflammatory drugs, however, increase the risk of corneal ulceration and melting.

Since VEGF plays an important role in vasculogenesis and pathologic neovascularization associated with eye diseases, a potential treatment for CNV is to inhibit VEGF activity by competing the binding of VEGF with specific neutralizing anti-VEGF antibody. VEGF inhibitors include pegatanib sodium, ranibizumab, and off-label bevacizumab are currently used for treatment of various retinal disease. Anti-VEGF antibodies such as the application of ranibizumab or bevacizumab have has been shown to reduce corneal neovascularization. Both ranibizumab and bevacizumab uses the same mechanism and inhibits all iso-forms of VEGF. The significant reduction in invasion of in-growth blood vessels in terms of neovascular area and vessel caliber suggests that treatment with ranibizumab induces thinning of the blood vessels, however, there's no significant change of the blood vessel's length. Using anti-VEGF antibodies to treat CNV has some limitations such as it is not a cure and may require repeated treatments to maintain positive effects over time. Topical and/or subconjunctival administration of bevaicizumab or ranibizumab have demonstrated short-term safety and efficacy, however long term effects have not been documented. Anti-VEGF therapy is currently an experimental treatment.

If the cornea is inflamed via corneal neovascularization, the suppression of enzymes can block CNV by compromising with corneal structural integrity. Corneal neovascularization can be suppressed with a combination of orally administration of doxycycline and with topical corticosteroid.

Surgical Options

Invasive solutions for corneal neovascularization are reserved when the medical therapies do not provide the desired results.

Invading blood tissues and ablating tissues in the cornea can be obstructed by the use of laser treatments such as Argon and s. Irradiation and/or damages to adjacent tissues caused by the procedure can result in corneal hemorrhage and corneal thinning. Obstruction of the blood vessels can be unsuccessful due to the depth, size, and, high blood flow rate of the vessels. In conjunction, thermal damage from the lasers can trigger inflammatory response which can exaggerate the neovascularization.

An effective treatment is photodynamic therapy, however, this treatment has limited clinical acceptance due to high costs and many potential complications involved that are also related to laser ablation. Complications can include irradiation from previously injected photosensitive dye inducing apoptosis and necrosis of the endothelium and basement membrane.

Diathermy and cautery is a treatment where an electrolysis needle is inserted into the feeder vessels in the limbus. The vessels are obstructed by a coagulating current through the use of unipolar diathermy unit or by thermal cautery.

Reduction of neovascularization has been achieved in rats by the topical instillation of commercially available triamcinolone and doxycycline.

Some evidence exists to suggest that the Angiotensin II receptor blocker drug telmisartan will prevent corneal neovascularization.

Recent treatment developments include topical application of bevacizumab, an anti-VEGF.

Treatment options include contact lenses, intrastromal corneal ring segments, corneal collagen cross-linking, or corneal transplant.

When cross-linking is performed only after the cornea becomes distorted, vision remains blurry even though the disease is stabilised. As a result, combining corneal collagen cross-linking with LASIK ('LASIK Xtra') aims to strengthen the cornea at the point of surgery and may be useful in cases where a very thin cornea is expected after the LASIK procedure. This would include cases of high spectacle power and people with thin corneas before surgery. Definitive evidence that the procedure can reduce the risk of corneal ectasia will only become available a number of years later as corneal ectasia, if it happens, usually occurs in the late post-operative period. Some study show that combining LASIK with cross-linking adds refractive stability to hyperopic treatments and may also do the same for very high myopic treatments.

In 2016, the FDA approved the KXL system and two photoenhancers for the treatment of corneal ectasia following refractive surgery.

No complications are encountered in most patients with lattice degeneration, although in young myopes, retinal detachment can occur. There are documented cases with macula-off retinal detachment in patients with asymptomatic lattice degeneration. Partial or complete vision loss almost always occurs in such cases. Currently there is no prevention or cure for lattice degeneration.

Treatment options include contact lenses and intrastromal corneal ring segments for correcting refractive errors caused by irregular corneal surface, corneal collagen cross-linking to strengthen a weak and ectatic cornea, or corneal transplant for advanced cases.

Usually being asymptomatic, drusen are typically found during routine eye exams where the pupils have been dilated.

Treatments for CCCA remain investigational. Altering hair care practices has not been proven to assist in hair rejuvenation. High-dose topical steroids, antibiotics, immunomodulators such as tacrolimus (Protopic) and pimecrolimus (Elidel), and anti-androgen/5alpha Reductase inhibitors have been used with unknown efficacy.

In terms of the management of spinal and bulbar muscular atrophy, no cure is known and treatment is supportive. Rehabilitation to slow muscle weakness can prove positive, though the prognosis indicates some individuals will require the use of a wheelchair in later stages of life.

Surgery may achieve correction of the spine, and early surgical intervention should be done in cases where prolonged survival is expected. Preferred nonsurgical treatment occurs due to the high rate of repeated dislocation of the hip.

Terrien marginal degeneration is a noninflammatory, unilateral or asymmetrically bilateral, slowly progressive thinning of the peripheral corneal stroma.

The cause of Terrien marginal degeneration is unknown, its prevalence is roughly equal between males and females, and it usually occurs in the second or third decade of life.

Electrical stimulation can promote nerve regeneration. The frequency of stimulation is an important factor in the success of both quality and quantity of axon regeneration as well as growth of the surrounding myelin and blood vessels that support the axon. Histological analysis and measurement of regeneration showed that low frequency stimulation had a more successful outcome than high frequency stimulation on regeneration of damaged sciatic nerves.

Surgery can be done in case a nerve has become cut or otherwise divided. Recovery of a nerve after surgical repair depends mainly on the age of the patient. Young children can recover close-to-normal nerve function. In contrast, a patient over 60 years old with a cut nerve in the hand would expect to recover only protective sensation, that is, the ability to distinguish hot/cold or sharp/dull. Many other factors also affect nerve recovery. The use of autologous nerve grafting procedures that involve redirection of regenerative donor nerve fibers into the graft conduit has been successful in restoring target muscle function. Localized delivery of soluble neurotrophic factors may help promote the rate of axon regeneration observed within these graft conduits.

An expanding area of nerve regeneration research deals with the development of scaffolding and bio-conduits. Scaffolding developed from biomaterial would be useful in nerve regeneration if they successfully exhibit essentially the same role as the endoneurial tubes and Schwann cell do in guiding regrowing axons.

Geographic Atrophy (GA), also known as atrophic age-related macular degeneration (AMD) or advanced dry AMD, is an advanced form of age-related macular degeneration that can result in the progressive and irreversible loss of retina (photoreceptors, retinal pigment epithelium, choriocappillaris) which can lead to a loss of visual function over time. It is estimated that GA affects >5 million people worldwide and approximately 1 million patients in the US, which is similar to the prevalence of neovascular (wet) AMD, the other advanced form of the disease.

The incidence of advanced AMD, both geographic atrophy and neovascular AMD, increases exponentially with age and while there are therapies for wet AMD, GA currently has no approved treatment options. The aim of most current clinical trials is to reduce the progression of GA lesion enlargement.

There is no cure for spinocerebellar ataxia, which is currently considered to be a progressive and irreversible disease, although not all types cause equally severe disability.

In general, treatments are directed towards alleviating symptoms, not the disease itself. Many patients with hereditary or idiopathic forms of ataxia have other symptoms in addition to ataxia. Medications or other therapies might be appropriate for some of these symptoms, which could include tremor, stiffness, depression, spasticity, and sleep disorders, among others. Both onset of initial symptoms and duration of disease are variable. If the disease is caused by a polyglutamine trinucleotide repeat CAG expansion, a longer expansion may lead to an earlier onset and a more radical progression of clinical symptoms. Typically, a person afflicted with this disease will eventually be unable to perform daily tasks (ADLs). However, rehabilitation therapists can help patients to maximize their ability of self-care and delay deterioration to certain extent. Researchers are exploring multiple avenues for a cure including RNAi and the use of Stem Cells and several other avenues.

On January 18, 2017 BioBlast Pharma announced completion of Phase 2a clinical trials of their medication, Trehalose, in the treatment of SCA3. BioBlast has received FDA Fast Track status and Orphan Drug status for their treatment. The information provided by BioBlast in their research indicates that they hope this treatment may prove efficacious in other SCA treatments that have similar pathology related to PolyA and PolyQ diseases.

In addition, Dr. Beverly Davidson has been working on a methodology using RNAi technology to find a potential cure for over 2 decades. Her research began in the mid-1990s and progressed to work with mouse models about a decade later and most recently has moved to a study with non-human primates. The results from her most recent research "are supportive of clinical application of this gene therapy". Dr. Davidson along with Dr. Pedro Gonzalez-Alegre are currently working to move this technique into a Phase 1 clinical trial.

Finally, another gene transfer technology discovered in 2011 has also been shown by Dr. Davidson to hold great promise and offers yet another avenue to a potential future cure.

Physical therapists can assist patients in maintaining their level of independence through therapeutic exercise programmes. One recent research report demonstrated a gain of 2 SARA points (Scale for the Assessment and Rating of Ataxia) from physical therapy. In general, physical therapy emphasises postural balance and gait training for ataxia patients. General conditioning such as range-of-motion exercises and muscle strengthening would also be included in therapeutic exercise programmes. Research showed that spinocerebellar ataxia 2 (SCA2) patients with a mild stage of the disease gained significant improvement in static balance and neurological indices after six months of a physical therapy exercise training program. Occupational therapists may assist patients with incoordination or ataxia issues through the use of adaptive devices. Such devices may include a cane, crutches, walker, or wheelchair for those with impaired gait. Other devices are available to assist with writing, feeding, and self care if hand and arm coordination are impaired. A randomised clinical trial revealed that an intensive rehabilitation program with physical and occupational therapies for patients with degenerative cerebellar diseases can significantly improve functional gains in ataxia, gait, and activities of daily living. Some level of improvement was shown to be maintained 24 weeks post-treatment. Speech language pathologists may use both behavioral intervention strategies as well as augmentative and alternative communication devices to help patients with impaired speech.