Early stages may be asymptomatic and may not require any intervention. Initial treatment may include hypertonic eyedrops and ointment to reduce the corneal edema and may offer symptomatic improvement prior to surgical intervention.

Suboptimal vision caused by corneal dystrophy usually requires surgical intervention in the form of corneal transplantation. Penetrating keratoplasty, a common type of corneal transplantation, is commonly performed for extensive corneal dystrophy.

With penetrating keratoplasty (corneal transplant), the long-term results are good to excellent. Recent surgical improvements have been made which have increased the success rate for this procedure. However, recurrence of the disease in the donor graft may happen. Superficial corneal dystrophies do not need a penetrating keratoplasty as the deeper corneal tissue is unaffected, therefore a lamellar keratoplasty may be used instead.

Phototherapeutic keratectomy (PTK) can be used to excise or ablate the abnormal corneal tissue. Patients with superficial corneal opacities are suitable candidates for a this procedure.

Treatment is aimed at managing the symptoms of the disease. A form of laser eye surgery named keratectomy may help with the superficial corneal scarring. In more severe cases, a partial or complete corneal transplantation may be considered. However, it is common for the dystrophy to recur within the grafted tissue.

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

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

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

Corneal transplant is not needed except in very severe and late cases.

Light sensitivity may be overcome by wearing tinted glassess.

Currently this sub-type of muscular dystrophy has no cure and no "definitive" treatment exists. Treatment offers preventative tactics to delay muscle breakdown and increase life expectancy. Stretching and physical therapy can increase mobility. Treatment also includes correcting skeletal abnormalities through orthopedic surgery and other orthopedic techniques. Antiepileptic medication is administered to help prevent seizures. ACE inhibitors and beta blockers help treat heart conditions, and respiratory assistance is more than likely needed at some point for the affected individual

In case of corneal erosion, a doctor may prescribe eye drops and ointments to reduce the friction on the eroded cornea. In some cases, an eye patch may be used to immobilize the eyelids. With effective care, these erosions usually heal within three to seven days, although occasional sensations of pain may occur for the next six-to-eight weeks. As patients with LCD suffer with dry eyes as a result of erosion, a new technique involving the insertion of punctal plugs (both upper and lower) can reduce the amount of drops used a day, aiding ocular stability.

By about age 40, some people with lattice dystrophy will have scarring under the epithelium, resulting in a haze on the cornea that can greatly obscure vision. In this case, a corneal transplantation may be needed. There have been many cases in which teenage patients have had the procedure, which accounts for the change in severity of the condition from person to person.

Although people with lattice dystrophy have an excellent chance for a successful corneal transplantation, the disease may also arise in the donor cornea in as little as three years. In one study, about half of the transplant patients with lattice dystrophy had a recurrence of the disease between two and 26 years after the operation. Of these, 15 percent required a second corneal transplant. Early lattice and recurrent lattice arising in the donor cornea responds well to treatment with the excimer laser.

Phototherapeutic keratectomy (PTK) using [Excimer laser] can restore and preserve useful visual function for a significant period of time in patients with anterior corneal dystrophies.

Currently no cure or specific treatment exists to eliminate the symptoms or stop the disease progression. A consistent diet planned with the help of a dietitian along with exercises taught by a speech therapist can assist with mild symptoms of dysphagia. Surgical intervention can also help temporarily manage symptoms related to the ptosis and dysphagia. Cutting one of the throat muscles internally, an operation called cricopharyngeal myotomy, can be one way to ease symptoms in more severe cases.

Physical therapy and specifically designed exercises may assist with proximal limb weakness, though there is still no current definitive data showing it will stop the progress of the disease. Many of those affected with the proximal limb weakness will eventually require assistive devices such as a wheelchair. As with all surgical procedures, they come with many risk factors. As the dysphagia becomes more severe, patients become malnourished, lose significant weight, become dehydrated and suffer from repeated incidents of aspiration pneumonia. These last two are often the cause of death.

Treatment for Ullrich congenital muscular dystrophy can consist of physical therapy and regular stretching. Respiratory support may be needed at some point by the affected individual.

Though cardiac complications are not a concern in this type of CMD, in regards to respiratory issues ventilation via a tracheostomy is a possibility in some cases.

There is currently no cure for or treatment specific to myotonic dystrophy. Therefore, the focus is on managing the complications of the disease, particularly those relating to the cardiopulmonary system as these account for 70% of deaths due to DM1. Pacemaker insertion may be required for individuals with cardiac conduction abnormalities. Improving the quality of life which can be measured using specific questionnaires is also a main objective of the medical care. Central sleep apnea or obstructive sleep apnea may cause excessive daytime sleepiness, and these individuals should undergo a sleep study. Non-invasive ventilation may be offered if there is an abnormality. Otherwise, there is evidence for the use of modafinil as a central nervous system stimulant, although a Cochrane review has described the evidence thus far as inconclusive.

Some small studies have suggested that imipramine, clomipramine and taurine may be useful in the treatment of myotonia. However, due to the weak evidence and potential side effects such as cardiac arrhythmias, these treatments are rarely used. A recent study in December 2015 showed that a common FDA approved antibiotic, Erythromycin reduced myotonia in mice. Human studies are planned for erythromycin. Erythromycin has been used successfully in patients with gastric issues.

Altered splicing of the muscle-specific chloride channel 1 (ClC-1) has been shown to cause the myotonic phenotype of DM1 and is reversible in mouse models using Morpholino antisense to modify splicing of ClC-1 mRNA.

Currently, there is no cure for muscular dystrophy. In terms of management, physical therapy, occupational therapy, orthotic intervention (e.g., ankle-foot orthosis), speech therapy, and respiratory therapy may be helpful. Low intensity corticosteroids such as prednisone, and deflazacort may help to maintain muscle tone. Orthoses (orthopedic appliances used for support) and corrective orthopedic surgery may be needed to improve the quality of life in some cases. The cardiac problems that occur with EDMD and myotonic muscular dystrophy may require a pacemaker. The myotonia (delayed relaxation of a muscle after a strong contraction) occurring in myotonic muscular dystrophy may be treated with medications such as quinine.

Occupational therapy assists the individual with MD to engage in activities of daily living (such as self-feeding and self-care activities) and leisure activities at the most independent level possible. This may be achieved with use of adaptive equipment or the use of energy-conservation techniques. Occupational therapy may implement changes to a person's environment, both at home or work, to increase the individual's function and accessibility; furthermore, it addresses psychosocial changes and cognitive decline which may accompany MD, and provides support and education about the disease to the family and individual.

Combined strengthening and aerobic training at moderate intensity was deemed safe for individuals with neuromuscular diseases. The combination was found to increase muscle strength. Specifically, aerobic exercise via stationary bicycle with an ergometer was found to be safe and effective in improving fitness in people with DM1. The strength training or aerobic exercise may promote muscle and cardiorespiratory function, while preventing further disuse atrophy. Cardiovascular impairments and myotonic sensitivities to exercise and temperature necessitate close monitoring of people and educating people in self-monitoring during exercise via the Borg scale, heart rate monitors, and other physical exertion measurements.

There is no known cure for Becker muscular dystrophy yet. Treatment is aimed at control of symptoms to maximize the quality of life which can be measured by specific questionnaires. Activity is encouraged. Inactivity (such as bed rest) or sitting down for too long can worsen the muscle disease. Physical therapy may be helpful to maintain muscle strength. Orthopedic appliances such as braces and wheelchairs may improve mobility and self-care.

Immunosuppressant steroids have been known to help slow the progression of Becker muscular dystrophy. The drug prednisone contributes to an increased production of the protein utrophin which closely resembles dystrophin, the protein that is defective in BMD.

The cardiac problems that occur with EDMD and myotonic muscular dystrophy may require a pacemaker.

The investigational drug Debio-025 is a known inhibitor of the protein cyclophilin D, which regulates the swelling of mitochondria in response to cellular injury. Researchers decided to test the drug in mice engineered to carry MD after earlier laboratory tests showed deleting a gene that encodes cycolphilin D reduced swelling and reversed or prevented the disease’s muscle-damaging characteristics. According to a review by Bushby, et al. if a primary protein is not functioning properly then maybe another protein could take its place by augmenting it. Upregulation of compensatory proteins has been done in models of transgenic mice.

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.

The prognosis of this sub-type of MD indicates that the affected individual may eventually have feeding difficulties. Surgery, at some point, might be an option for scoliosis.

Scoliosis which is a sideways curve of the persons vertebrate, is determined by a variety of factors, including the degree (mild or severe), in which case if possible a brace might be used by the individual

Treatment for limb-girdle muscular dystrophy can take the form of exercise and physical therapy which are advised to maintain as much muscle strength and joint flexibility as possible, there are few studies corroborating the effectiveness of exercise. Physical therapy and exercise "may" prevent the rapid progression of the disease rather than halt or reverse it. Calipers, as an example, may be used to maintain mobility and quality of life. Careful attention to lung and heart health is required, corticosteroids in LGMD 2C-F individuals, shows some improvement

Additionally individuals can follow "management" that follows:

- Occupational therapy

- Respiratory therapy

- Speech therapy

- Neutralizing antibody to myostatin should not be pursued

In terms of the prognosis of limb-girdle muscular dystrophy in its mildest form, affected individuals have near-normal muscle strength and function. LGMD isn't typically a fatal disease, though it may eventually weaken the heart and respiratory muscles, leading to illness or death due to secondary disorders. The frequency of limb-girdle muscular dystrophy ranges from 1 in 14,500 (in some instances 1 in 123,000)

Prognosis depends on the individual form of MD. In some cases, a person with a muscle disease will get progressively weaker to the extent that it shortens lifespan due to heart and breathing complications. However, some of the muscle diseases do not affect life expectancy at all, and ongoing research is attempting to find cures and treatments to slow muscle weakness.

Phototherapeutic keratectomy (PTK) done by an ophthalmologist can restore and preserve useful visual function for a significant period of time in patients with anterior corneal dystrophies including EBMD.

Reis-Bücklers corneal dystrophy is not associated with any systemic conditions.

In terms of the management of congenital muscular dystrophy the American Academy of Neurology recommends that the individuals

need to have monitoring of cardiac function, respiratory, and gastrointestinal. Additionally it is believed that therapy in speech, orthopedic and physical areas, would improve the persons quality of life.

While there is currently no cure available, it is important to preserve muscle activity and any available correction of skeletal abnormalities (as scoliosis).Orthopedic procedures, like spinal fusion, maintains/increases the individuals prospect for more physical movement.

The treatment (management) of Emery–Dreifuss muscular dystrophy can be done via several methods, however secondary complications should be consider in terms of the progression of EDMD, therefore cardiac defibrillators may be needed at some point by the affected individual. Other possible forms of management and treatment are the following:

- Orthopaedics

- Surgery

- Monitor/treat any cardiac issues

- Respiratory aid

- Physical therapy

Recurrence within a few years occurs in all patients following corneal transplantation. Soft contact lenses are effective in decreasing recurrences.

There is a variety of research under way targeted at various forms of limb-girdle muscular dystrophy. Among the methods thought to hold promise for treatment include gene transfer therapy, which works by inserting in cells of defective genes with a healthy gene.

According to a review by Bengtsson et al. some success with AAV-mediated gene therapies (for different disorders) have increased interest in researchers, with CRISPR/Cas9 and exon-skipping helping these therapeutic goals along. Limb-girdle muscular dystrophies has many different types which are due to different gene mutations. LGMD2D is caused by a mutation in the α-sarcoglycan gene.Future treatment could be had by gene therapy through recombinant adeno-associated vectors.

Conversely, according to a review by Straub, et al. there are several research issues that need to be targeted, the rareness of the disease, our poor understanding of the mechanism of LGMD2, and absence of patient cohorts, consequently biomarkers for individuals with LGMD2 are lacking. The review goes on to state that animal models for LGMD2 have been used to analyse therapeutic medications. Also adding that while prednisone has been used and has had positive effects on affected LGMD2 individuals there is still no evidence of its effectiveness in trials that are placebo-controlled

Fukuyama congenital muscular dystrophy has a poor prognosis. Most children with FCMD reach a maximum mobility at sitting upright and sliding. Due to the compounded effects of continually worsening heart problems, impaired mental development, problems swallowing and additional complications, children with FCMD rarely live through adolescence, the disorder proves fatal by age 20.

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.