The Food and Drug Administration is recommending that physicians restrict prescribing high-dose Simvastatin (Zocor, Merck) to patients, given an increased risk of muscle damage. The FDA drug safety communication stated that physicians should limit using the 80-mg dose unless the patient has already been taking the drug for 12 months and there is no evidence of myopathy.

"Simvastatin 80 mg should not be started in new patients, including patients already taking lower doses of the drug," the agency states.

Because different types of myopathies are caused by many different pathways, there is no single treatment for myopathy. Treatments range from treatment of the symptoms to very specific cause-targeting treatments. Drug therapy, physical therapy, bracing for support, surgery, and massage are all current treatments for a variety of myopathies.

Currently, there are no treatments for any of the congenital myopathies. Depending on the severity, there are different therapies available to help alleviate any pain and aid patients in performing varying activities. For example, many congenital myopathy patients are involved in physical or occupational therapy in an attempt to strengthen their skeletal muscles. Orthopedic surgery is usually necessary to correct skeletal deformities secondary to muscle weakness, such as scoliosis. Survival is typically determined by the level of respiratory muscle insufficiency.

New research resources have become available for the NM community, such as the CMDIR (registry) and the CMD-TR (biorepository). These two resources connect families and individuals interested in participating in research with the scientists that aim to treat or cure NM. Some research on NM seeks to better understand the molecular effects the gene mutations have on muscle cells and the rest of the body and to observe any connections NM may have to other diseases and health complications.

Because lack of sialic acid appears to be part of the pathology of IBM caused by GNE mutations, clinical trials with sialic acid supplements, and with a precursor of sialic acid, N-Acetylmannosamine, have been conducted, and as of 2016 further trials were planned.

Currently there is no cure for myotubular or centronuclear myopathies. Treatment often focuses on trying to maximize functional abilities and minimize medical complications, and involvement by physicians specializing in Physical Medicine and Rehabilitation, and by physical therapists and occupational therapists.

Medical management generally involves efforts to prevent pulmonary complications, since lung infections can be fatal in patients lacking the muscle strength necessary to clear secretions via coughing. Medical devices to assist with coughing help patients maintain clear airways, avoiding mucous plugs and avoiding the need for tracheostomy tubes.

Monitoring for scoliosis is also important, since weakness of the trunk muscles can lead to deviations in spinal alignment, with resultant compromise of respiratory function. Many patients with congenital myopathies may eventually require surgical treatment of scoliosis.

Treatment is palliative, not curative (as of 2009).

Treatment options for lower limb weakness such as foot drop can be through the use of Ankle Foot Orthoses (AFOs) which can be designed or selected by an Orthotist based upon clinical need of the individual. Sometimes tuning of rigid AFOs can enhance knee stability.

Some cases of myotonia congenita do not require treatment, or it is determined that the risks of the medication outweigh the benefits. If necessary, however, symptoms of the disorder may be relieved with quinine, phenytoin, carbamazepine, mexiletine and other anticonvulsant drugs. Physical therapy and other rehabilitative measures may also be used to help muscle function. Genetic counseling is available.

Treatment for acquired noninflammatory myopathy is directed towards resolution of the underlying condition, pain management, and muscle rehabilitation.

Drug induced ANIMs can be reversed or improved by tapering off of the drugs and finding alternative care. Hyperthyroidism induced ANIM can be treated through anti-thyroid drugs, surgery and not eating foods high in Iodine such as kelp. Treatment of the hyperthyroidism results in complete recovery of the myopathy. ANIM caused by vitamin D deficiency can easily be resolved by taking vitamin supplements and increasing one's exposure to direct sunlight.

Pain can be managed through massaging affected areas and the use of nonsteroidal anti-inflammatory drugs (NSAIDs).

Exercise, physical therapy, and occupational therapy can be used to rehabilitate affected muscle areas and resist the atrophy process.

As with all myopathies, the use of walkers, canes, and braces can assist with the mobility of the afflicted individual.

Although there is no cure for NM, it is possible, and common for many people live healthy active lives even with moderate to severe cases. Research continues to seek ways to ameliorate debilitating symptoms and lengthen the life-span in quality ways for those affected. Some people have seen mild improvements in secretion handling, energy level, and physical functioning with supplemental L-tyrosine, an amino acid that is available through health centers. Some symptoms may worsen as the patient ages. Muscle loss increases with age naturally, but it is even more significant with nemaline myopathy.

For most horses, diet has a significant impact on the degree of clinical signs. PSSM horses fed diets high in nonstructural carbohydrates (NSC), which stimulate insulin secretion, have been shown to have increased severity of rhabdomyolysis with exercise. Current recommendations for horses with PSSM include a low-starch, high-fat diet. Low-starch diets produce low blood glucose and insulin levels after eating, which may reduce the amount of glucose taken up by the muscle cells. High fat diets increase free fatty acid concentrations in the blood, which may promote the use of fat for energy (via free fatty acid oxidation) over glucose metabolism. Horses with the most severe clinical signs often show the greatest improvement on the diet.

Dietary recommendations usually include a combination of calorie restriction, reduction of daily NSC content, and an increase in dietary fat. Diet recommendations need to be balanced with the animal's body condition score and exercise level, as it may be beneficial to wait on increasing dietary fat after an obese animal has lost weight. The diet should have <10% of digestible energy coming from NSC, and 15-20% of daily digestible energy coming from fat.

Although no cure currently exists, there is hope in treatment for this class of hereditary diseases with the use of an embryonic mitochondrial transplant.

Horses with PSSM show fewer clinical signs if their exercise is slowly increased over time (i.e. they are slowly conditioned). Additionally, they are much more likely to develop muscle stiffness and rhabdomyolysis if they are exercised after prolonged stall rest.

Horses generally have fewer clinical signs when asked to perform short bouts of work at maximal activity level (aerobic exercise), although they have difficulty achieving maximal speed and tire faster than unaffected horses. They have more muscle damage when asked to perform lower intensity activity over a longer period of time (aerobic activity), due to an energy deficit in the muscle.

The overall incidence of myotubular myopathy is 1 in 50,000 male live births. The incidence of other centronuclear myopathies is extremely rare, with there only being nineteen families identified with CNM throughout the world. The symptoms currently range from the majority who only need to walk with aids, from a stick to a walking frame, to total dependence on physical mobility aids such as wheelchairs and stand aids, but this latter variety is so rare that only two cases are known to the CNM "community".

Approximately 80% of males with a diagnosis of myotubular myopathy by muscle biopsy will have a mutation in MTM1 identifiable by genetic sequence analysis.

Many patients with myotubular myopathy die in infancy prior to receiving a formal diagnosis. When possible, muscle biopsy and genetic testing may still be helpful even after a neonatal death, since the diagnostic information can assist with family planning and genetic counseling as well as aiding in the accurate diagnosis of any relatives who might also have the same genetic abnormality.

It is not uncommon for drugs to damage muscle fibers. Particular families of drugs are known to induce myopathies on the molecular level, thus altering organelle function such as the mitochondria. Use of multiple drugs from these families in conjunction with one another can increase the risk of developing a myopathy. Many of the drugs associated with inducing myopathies in patients are found in rheumatology practice.

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.

In northern Scandinavia, the prevalence of myotonia congenita has been estimated at 1:10,000.

Myotonia congenita is estimated to affect 1 in 1,000,000 people worldwide.

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.

Prognosis strongly depends on which subtype of disease it is. Some are deadly in infancy but most are late onset and mostly manageable.

There is currently no cure for the disease but treatments to help the symptoms are available.

Myotubular myopathy, also known as centeronuclear myopathy, is recognized by pain during exercise and difficulty walking. People affected by this disease typically are wheel-chair-bound by middle adulthood, have weakness in the muscles involved in eye movement, nerve function disorders, and some form of intellectual disability. Myotubular myopathy is very rare, with less than 50 families currently affected.

Genetically, myotubular myopathy can have two causes: autosomal dominant and autosomal recessive. When caused by a mutation in the DNM2 gene, the disorder is autosomal dominant, meaning it can be passed on by one mutated gene. When the mutation takes place in the BIN1 gene, the disease is instead autosomal recessive, and both genes must be mutated for the disease to be inherited. Autosomal recessive onset is most common.

There is no specific treatment but triggering anesthetics are avoided and relatives are screened for "RYR1" mutations as these may make them susceptible to MH.

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.

While the disability can range from minor, occasional weakness to permanent muscle damage, inability to hold a normal job and use of a powerchair, most people function fairly well with drugs and lifestyle changes.

Mitochondrial myopathies are types of myopathies associated with mitochondrial disease. On biopsy, the muscle tissue of patients with these diseases usually demonstrate "ragged red" muscle fibers. These ragged-red fibers contain mild accumulations of glycogen and neutral lipids, and may show an increased reactivity for succinate dehydrogenase and a decreased reactivity for cytochrome c oxidase. Inheritance was believed to be maternal (non-Mendelian extranuclear). It is now known that certain nuclear DNA deletions can also cause mitochondrial myopathy such as the OPA1 gene deletion. There are several subcategories of mitochondrial myopathies.