In severe cases of PM and DM with systemic signs, an initial three to five days on intravenous corticosteroid (methylprednisolone) may be used; but normally treatment begins with a single daily (after breakfast) high dose of oral corticosteroid (prednisone). After a month or so the strength of every second day's dose is very gradually reduced over three to four months, to minimize the negative effects of the prednisone. When a high dose of prednisone cannot be reduced without losing muscle strength, or when prednisone is effective but it is producing significant complications, "steroid sparing" oral immunosuppressants such as azathioprine, mycophenolate mofetil, methotrexate and cyclosporine, may be used in combination with reduced prednisone. Some of these steroid sparing drugs can take several months to demonstrate an effect.

To minimize side effects, patients on corticosteroids should follow a strict high-protein, low-carbohydrate, low-salt diet; and with long-term corticosteroid use a daily calcium supplement and weekly vitamin D supplement (and a weekly dose of Fosamax for postmenopausal women) should be considered.

For patients not responding to this approach there is weak evidence supporting the use of intravenous immunoglobulin, ciclosporin, tacrolimus, mycophenolate mofetil and other agents; and trials of rituximab have indicated a potential therapeutic effect.

There is no standard course of treatment to slow or stop the progression of the disease. sIBM patients do not reliably respond to the anti-inflammatory, immunosuppressant, or immunomodulatory medications. Management is symptomatic. Prevention of falls is an important consideration. Specialized exercise therapy may supplement treatment to enhance quality of life. Physical therapy is recommended to teach the patient a home exercise program, to teach how to compensate during mobility-gait training with an assistive device, transfers and bed mobility.

There have been few randomized treatment trials, due to the relative rarity of inflammatory myopathies. The goal of treatment is improvement in activities of daily living and muscle strength. Suppression of immune system activity (immunosuppression) is the treatment strategy. Patients with PM or DM almost always improve to some degree in response to treatment, at least initially, and many recover fully with maintenance therapy. (If there is no initial improvement from treatment of PM or DM, the diagnosis should be carefully re-examined.) There is no proven effective therapy for IBM, and most IBM patients will need assistive devices such as a cane, a walking frame or a wheelchair. The later in life IBM arises, the more aggressive it appears to be.

When sIBM was originally described, the major feature noted was muscle inflammation. Two other disorders were also known to display muscle inflammation, and sIBM was classified along with them. They are dermatomyositis (DM) and polymyositis (PM) and all three illnesses were called idiopathic (of unknown origin) myositis or inflammatory myopathies.

It appears that sIBM and polymyositis share some features, especially the initial sequence of immune system activation, however, polmyositis comes on over weeks or months, does not display the subsequent muscle degeneration and protein abnormalities as seen in IBM, and as well, polymyositis tends to respond well to treatments, IBM does not. IBM is often confused with (misdiagnosed as) polymyositis. Polymyositis that does not respond to treatment is likely IBM.

Dermatomyositis shares a number of similar physical symptoms and histopathological traits as polymyositis, but exhibits a skin rash not seen in polymyositis or sIBM. It may have different root causes unrelated to either polymyositis or sIBM.

The first line treatment for polymyositis is corticosteroids. Specialized exercise therapy may supplement treatment to enhance quality of life.

Polymyositis, like dermatomyositis, strikes females with greater frequency than males.

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.

There is no cure for dermatomyositis, but the symptoms can be treated. Options include medication, physical therapy, exercise, heat therapy (including microwave and ultrasound), orthotics and assistive devices, and rest. The standard treatment for dermatomyositis is a corticosteroid drug, given either in pill form or intravenously. Immunosuppressant drugs, such as azathioprine and methotrexate, may reduce inflammation in people who do not respond well to prednisone. Periodic treatment using intravenous immunoglobulin can also improve recovery. Other immunosuppressive agents used to treat the inflammation associated with dermatomyositis include cyclosporine A, cyclophosphamide, and tacrolimus. Physical therapy is usually recommended to prevent muscle atrophy and to regain muscle strength and range of motion. Many individuals with dermatomyositis may need a topical ointment, such as topical corticosteroids, for their skin disorder. They should wear a high-protection sunscreen and protective clothing. Surgery may be required to remove calcium deposits that cause nerve pain and recurrent infections.

Antimalarial medications, especially hydroxychloroquine and chloroquine, are used to treat the rashes, as they are in similar conditions.

Rituximab is used when people don't respond to other treatments.

As of 2016, treatments for amyopathic dermatomyositis in adults did not have a strong evidence base; published treatments included antimalarial medications, steroids, taken or orally or applied to the skin, calcineurin inhibitors applied to the skin, dapsone, Intravenous immunoglobulin (IVIG), methotrexate, azathioprine, and mycophenolate mofetil. None appear to be very effective but among them, IVIG has had the best outcomes.

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.

Polymyositis and dermatomyositis are first treated with high doses of a corticosteroids

A 2009 review noted that muscle weakness usually begins after age 20 and after 20–30 years, the person usually requires a wheel chair for mobility. There was no mention of increased mortality.

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.

Before the advent of modern treatments such as prednisone, intravenous immunoglobulin, plasmapheresis, chemotherapies, and other drugs, the prognosis was poor.

The cutaneous manifestations of dermatomyositis may or may not improve with therapy in parallel with the improvement of the myositis. In some people, the weakness and rash resolve together. In others, the two are not linked, with one or the other being more challenging to control. Often, cutaneous disease persists after adequate control of the muscle disease.

The risk of death from the condition is much higher if the heart or lungs are affected.

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.

Clinical studies have revealed that camptocormia may be hereditary; however, the inheritance mechanism remains unclear. Current areas of research include molecular and genetic studies aimed at elucidating a possible inheritance model along with molecular pathological mechanisms and proteins responsible for BSS. This research will help will facilitate improvement in the classification, diagnosis, and treatment of the condition. In addition, new technologies and animal models of postural abnormalities are being developed to understand camptocormia and design more effective treatment methods.

Myositis is inflammation or swelling of the muscles. Injury, medicines, infection, or an immune disorder can lead to myositis. It is a documented side effect of the lipid-lowering drugs statins and fibrates.

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

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

This condition can lead to excess pressure on the spine, causing pain and discomfort. If the spine is bent too far, a patient may have difficulties breathing because of the pressure of the spine pressed against the lungs. Camptocormia may also lead to muscle weakness in the upper back and to arthritis and other bone-degeneration diseases. Because of loss of bone strength, injury to the spine and slipped discs become increasingly significant. Camptocormia can lead to infection, tumors, and diseases of the endocrine system and connective tissues. The success of the treatment method is largely dependent on the patient, but response to therapeutic methods is generally low.

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.

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.

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.

In the treatment of polyneuropathies one must ascertain and manage the cause, among management activities are: weight decrease, use of a walking aid, and occupational therapist assistance. Additionally BP control in those with diabetes is helpful, while intravenous immunoglobulin is used for multifocal motor neuropathy.

According to Lopate, et al., methylprednisolone is a viable treatment for chronic inflammatory demyelinative polyneuropathy (which can also be treated with intravenous immunoglobulin) The author(s) also indicate that prednisone has greater adverse effects in such treatment, as opposed to intermittent (high-doses) of the aforementioned medication.

According to Wu, et al., in critical illness polyneuropathy supportive and preventive therapy are important for the affected individual, as well as, avoiding (or limiting) corticosteroids.

While the exact incidence is unknown, estimates range from 33 - 57 percent of patients staying in the ICU for longer than 7 days. More exact data is difficult to obtain, since variation exists in defining the condition.

The three main risk factors for CIP and CIM are sepsis and systemic inflammatory response syndrome (SIRS), and multi-organ failure. Reported rates of CIP/CIM in people with sepsis and SIRS range from 68 to 100 percent. Additional risk factors for developing CIP/CIM include: female gender, high blood sugar (hyperglycemia), low serum albumin, and immobility. A greater severity of illness increases the risk of CIP/CIM. Such risk factors include: multi-organ dysfunction, renal failure, renal replacement therapy, duration of organ dysfunction, duration of ICU stay, low albumin, and central neurologic failure.

Certain medications are associated with CIP/CIM, such as corticosteroids, neuromuscular blocking agents, vasopressors, catecholamines, and intravenous nutrition (parenteral nutrition). Research has produced inconsistent results for the impact of hypoxia, hypotension, hyperpyrexia, and increased age on the risk of CIP/CIM. The use of aminoglycosides is "not" an independent risk for the development of CIP/CIM.

The importance of correctly recognizing progressive muscular atrophy as opposed to ALS is important for several reasons.

- 1) the prognosis is a little better. A recent study found the 5-year survival rate in PMA to be 33% (vs 20% in ALS) and the 10-year survival rate to be 12% (vs 6% in ALS).

- 2) Patients with PMA do not suffer from the cognitive change identified in certain groups of patients with MND.

- 3) Because PMA patients do not have UMN signs, they usually do not meet the "World Federation of Neurology El Escorial Research Criteria" for “Definite” or “Probable” ALS and so are ineligible to participate in the majority of clinical research trials such as drugs trials or brain scans.

- 4) Because of its rarity (even compared to ALS) and confusion about the condition, some insurance policies or local healthcare policies may not recognize PMA as being the life-changing illness that it is. In cases where being classified as being PMA rather than ALS is likely to restrict access to services, it may be preferable to be diagnosed as "slowly progressive ALS" or "lower motor neuron predominant" ALS.

An initial diagnosis of PMA could turn out to be slowly progressive ALS many years later, sometimes even decades after the initial diagnosis. The occurrence of upper motor neurone symptoms such as brisk reflexes, spasticity, or a Babinski sign would indicate a progression to ALS; the correct diagnosis is also occasionally made on autopsy.