As of 2017, eleven disease-modifying medications have been approved by regulatory agencies for relapsing-remitting multiple sclerosis (RRMS). They are interferon beta-1a, interferon beta-1b, glatiramer acetate, mitoxantrone, natalizumab, fingolimod, teriflunomide, dimethyl fumarate, alemtuzumab, daclizumab, and ocrelizumab.

Their cost effectiveness as of 2012 is unclear. In May 2016 the FDA approved daclizumab for the treatment of relapsing multiple sclerosis in adults, with requirements for postmarketing studies and submission of a formal risk evaluation and mitigation strategy. In March 2017 the FDA approved ocrelizumab, a humanized anti-CD20 monoclonal antibody, as a treatment for RRMS, with requirements for several Phase IV clinical trials.

In RRMS they are modestly effective at decreasing the number of attacks. The interferons and glatiramer acetate are first-line treatments and are roughly equivalent, reducing relapses by approximately 30%. Early-initiated long-term therapy is safe and improves outcomes. Natalizumab reduces the relapse rate more than first-line agents; however, due to issues of adverse effects is a second-line agent reserved for those who do not respond to other treatments or with severe disease. Mitoxantrone, whose use is limited by severe adverse effects, is a third-line option for those who do not respond to other medications. Treatment of clinically isolated syndrome (CIS) with interferons decreases the chance of progressing to clinical MS. Efficacy of interferons and glatiramer acetate in children has been estimated to be roughly equivalent to that of adults. The role of some newer agents such as fingolimod, teriflunomide, and dimethyl fumarate, as of 2011, is not yet entirely clear.

As of 2017, rituximab was widely used off-label to treat RRMS.

During symptomatic attacks, administration of high doses of intravenous corticosteroids, such as methylprednisolone, is the usual therapy, with oral corticosteroids seeming to have a similar efficacy and safety profile. Although, in general, effective in the short term for relieving symptoms, corticosteroid treatments do not appear to have a significant impact on long-term recovery. The consequences of severe attacks that do not respond to corticosteroids might be treatable by plasmapheresis.

Management Corticosteroids may be effective in some patients. Additional treatment options are beta-interferon or immunosuppressive therapy. Otherwise management is supportive and includes physiotherapy, occupational therapy and nutritional support in the later stages as patients lose their ability to eat.

Fatigue is a common symptom and affects the daily life of individuals with MS. Changes in lifestyle are usually recommended to reduce fatigue. These include taking frequent naps and implementing exercise. MS patients who smoke are also advised to stop. Pharmacological treatment include anti-depressants and caffeine. Aspirin has also been experimented with and from clinical trial data, MS patients preferred using aspirin as compared to the placebo in the test. One hypothesis is that aspirin has an effect on the hypothalamus and can affect the perception of fatigue through altering the release of neurotransmitters and the autonomic responses.

There are no approved drugs for the treatment of cognitive dysfunction, however, some treatments have shown an association with improvements in cognitive function. One such treatment is "Ginkgo biloba", is a herb commonly used by patients with Alzheimer's disease.

Treatment typically involves improving the patient's quality of life. This is accomplished through the management of symptoms or slowing the rate of demyelination. Treatment can include medication, lifestyle changes (i.e. quit smoking, adjusting daily schedules to include rest periods and dietary changes), counselling, relaxation, physical exercise, patient education and, in some cases, deep brain thalamic stimulation (in the case of tremors). The progressive phase of MS appears driven by the innate immune system, which will directly contribute to the neurodegenerative changes that occur in progressive MS. Until now, there are no therapies that specifically target innate immune cells in MS. As the role of innate immunity in MS becomes better defined, it may be possible to better treat MS by targeting the innate immune system.

Treatments are patient-specific and depend on the symptoms that present with the disorder, as well as the progression of the condition.

There is currently no cure or standard procedure for treatment. A bone marrow transplant has been attempted on a child, but it made no improvement. Hydrocephalus may be seen in younger patients and can be relieved with surgery or by implanting a shunt to relieve pressure.

First-line treatment for CIDP is currently intravenous immunoglobulin (IVIG) and other treatments include corticosteroids (e.g. prednisone), and plasmapheresis (plasma exchange) which may be prescribed alone or in combination with an immunosuppressant drug. Recent controlled studies show subcutaneous immunoglobin (SCIG) appears to be as effective for CIDP treatment as IVIG in most patients, and with fewer systemic side effects.

IVIG and plasmapheresis have proven benefit in randomized, double-blind, placebo-controlled trials. Despite less definitive published evidence of efficacy, corticosteroids are considered standard therapies because of their long history of use and cost effectiveness. IVIG is probably the first-line CIDP treatment, but is extremely expensive. For example, in the U.S., a single 65 g dose of Gamunex brand in 2010 might be billed at the rate of $8,000 just for the immunoglobulin—not including other charges such as nurse administration. Gamunex brand IVIG is the only U.S. FDA approved treatment for CIDP, as in 2008 Talecris, the maker of Gamunex, received orphan drug status for this drug for the treatment of CIDP.

Immunosuppressive drugs are often of the cytotoxic (chemotherapy) class, including rituximab (Rituxan) which targets B cells, and cyclophosphamide, a drug which reduces the function of the immune system. Ciclosporin has also been used in CIDP but with less frequency as it is a newer approach. Ciclosporin is thought to bind to immunocompetent lymphocytes, especially T-lymphocytes.

Non-cytotoxic immunosuppressive treatments usually include the anti-rejection transplant drugs azathioprine (Imuran/Azoran) and mycophenolate mofetil (Cellcept). In the U.S., these drugs are used as "off-label" treatments for CIDP, meaning that their use here is accepted by the FDA, but that CIDP treatment is not explicitly indicated or approved in the drug literature. Before azathioprine is used, the patient should first have a blood test that ensures that azathioprine can safely be used.

Anti-thymocyte globulin (ATG), an immunosuppressive agent that selectively destroys T lymphocytes is being studied for use in CIDP. Anti-thymocyte globulin is the gamma globulin fraction of antiserum from animals that have been immunized against human thymocytes. It is a polyclonal antibody.

Although chemotherapeutic and immunosuppressive agents have shown to be effective in treating CIDP, significant evidence is lacking, mostly due to the heterogeneous nature of the disease in the patient population in addition to the lack of controlled trials.

A review of several treatments found that azathioprine, interferon alpha and methotrexate were not effective. Cyclophosphamide and rituximab seem to have some response. Mycophenolate mofetil may be of use in milder cases. Immunoglobulin and steroids are the first line choices for treatment. Rarely bone marrow transplantation has been performed.

Physical therapy and occupational therapy may improve muscle strength, activities of daily living, mobility, and minimize the shrinkage of muscles and tendons and distortions of the joints.

There are no effective drugs that inhibit or cure the virus infection without toxicity. Therefore, treatment aims at reversing the immune deficiency to slow or stop the disease progress. In patients on immunosuppression, this means stopping the drugs or using plasma exchange to accelerate the removal of the biologic agent that put the person at risk for PML.

In HIV-infected people, this may mean starting highly active antiretroviral therapy (HAART). AIDS patients starting HAART after being diagnosed with PML tend to have a slightly longer survival time than patients who were already on HAART and then develop PML. Some AIDS patients with PML have been able to survive for several years, with HAART. A rare complication of effective HAART is immune reconstitution inflammatory syndrome (IRIS), in which increased immune system activity actually increases the damage caused by the JCV infection; although IRIS can often be managed with medication, it is extremely dangerous in PML.

Cidofovir was studied as possible treatment for PML and has been used on a case by case basis, working in some, but not others.

Cytarabine (also known as ARA-C), a chemotherapy drug used to treat certain cancers, has been prescribed on an experimental basis for a small number of non-AIDS PML patients and stabilized the neurological condition of a minority of these patients. One patient regained some cognitive function lost as a result of PML.

In June 2010, the first case report appeared of a PML patient being successfully treated with the anti malaria drug mefloquine with activity against the JC virus. The patient cleared the virus and had no further neurological deterioration.

Two case reports of using interleukin-2 successfully have been published. Some success have been reported with mirtazapine, but this has not been demonstrated in clinical trials.

A number of drugs work against JC virus in cell culture, but there is no proven, effective therapy in humans.

For example, 1-O-hexadecyloxypropyl-cidofovir (CMX001), suppresses JCV but has been found to have toxicity at therapeutic dosage. The number of patients treated with other therapies is too low to demonstrate effectiveness.

There is a wide range of treatments for central nervous system diseases. These can range from surgery to neural rehabilitation or prescribed medications.

In the US, neuroborreliosis is typically treated with intravenous antibiotics which cross the blood–brain barrier, such as penicillins, ceftriaxone, or cefotaxime. One relatively small randomized controlled trial suggested ceftriaxone was more effective than penicillin in the treatment of neuroborreliosis. Small observational studies suggest ceftriaxone is also effective in children. The recommended duration of treatment is 14 to 28 days.

Several studies from Europe have suggested oral doxycycline is equally as effective as intravenous ceftriaxone in treating neuroborreliosis. Doxycycline has not been widely studied as a treatment in the US, but antibiotic sensitivities of prevailing European and US isolates of "Borrelia burgdorferi" tend to be identical. However, doxycycline is generally not prescribed to children due to the risk of bone and tooth damage.

Discreditied or doubtful treatments for neuroborreliosis include:

- Malariotherapy

- Hyperbaric oxygen therapy

- Colloidal silver

- Injections of hydrogen peroxide and bismacine

Exercise is a promising mechanism of prevention and treatment for various diseases characterized by neuroinflammation. Aerobic exercise is used widely to reduce inflammation in the periphery. Exercise has been shown to decreases proliferation of microglia in the brain, decrease hippocampal expression of immune-related genes, and reduce expression of inflammatory cytokines such as TNF-α.

Treatment of ALS2-related disorders includes physical therapy and occupational therapy to promote mobility and independence and use of computer technologies and devices to facilitate writing and voice communication.

There is no known cure to BVVL however a Dutch group have reported the first promising attempt at treatment of the disorder with high doses of riboflavin. This Riboflavin protocol seems to be beneficial in almost all cases. Specialist medical advice is of course essential to ensure the protocol is understood and followed correctly.

Patients will almost certainly require additional symptomatic treatment and supportive care. This must be specifically customized to the needs of the individual but could include mobility aids, hearing aids or cochlear implants, vision aids, gastrostomy feeding and assisted ventilation, while steroids may or may not help patients.

The first report of BVVL syndrome in Japanese literature was of a woman that had BVVL and showed improvement after such treatments. The patient was a sixty-year-old woman who had symptoms such as sensorineural deafness, weakness, and atrophy since she was 15 years old. Around the age of 49 the patient was officially diagnosed with BVVL, incubated, and then attached to a respirator to improve her CO2 narcosis. After the treatments, the patient still required respiratory assistance during sleep; however, the patient no longer needed assistance by a respirator during the daytime.

In terms of treatment for neuromuscular diseases (NMD), "exercise" might be a way of managing them, as NMD individuals would gain muscle strength. In a study aimed at results of exercise, in muscular dystrophy and Charcot-Marie-Tooth disease, the later benefited while the former did not show benefit; therefore, it depends on the disease Other management routes for NMD should be based on medicinal and surgical procedures, again depending on the underlying cause.

Experimentation has shown that manipulating the levels of thyroid hormone can be considered as a strategy to promote remyelination and prevent irreversible damage in Multiple sclerosis patients. N-cadherin agonists have been identified and observed to stimulate neurite growth and cell migration, key aspects of promoting axon growth and remyelination after injury or disease. It has been shown that intranasal administration of aTf (apotransferrin) can protect myelin and induce remyelination.

Much of the research referenced in this section has been conducted in 2012 and represents very new information about demyelinating diseases and potential therapies for them.

Topical treatment for the skin changes of scleroderma do not alter the disease course, but may improve pain and ulceration. A range of NSAIDs (nonsteroidal anti-inflammatory drugs) can be used to ease painful symptoms, such as naproxen. There is limited benefit from steroids such as prednisone. Episodes of Raynaud's phenomenon sometimes respond to nifedipine or other calcium channel blockers; severe digital ulceration may respond to prostacyclin analogue iloprost, and the dual endothelin-receptor antagonist bosentan may be beneficial for Raynaud's phenomenon. The skin tightness may be treated systemically with methotrexate and ciclosporin. and the skin thickness treated with penicillamine.

The prognosis of this disease is very variable and can take three different courses: a monophasic, not remitting;

remitting;

and finally, progressive, with increase in deficits.

Because neuroinflammation has been associated with a variety of neurodegenerative diseases, there is increasing interest to determine whether reducing inflammation will reverse neurodegeneration. Inhibiting inflammatory cytokines, such as IL-1β, decreases neuronal loss seen in neurodegenerative diseases. Current treatments for multiple sclerosis include interferon-B, Glatiramer actetate, and Mitoxantrone, which function by reducing or inhibiting T Cell activation, but have the side effect of systemic immunosuppression In Alzheimer's disease, the use of non-steroidal anti-inflammatory drugs decreases the risk of developing the disease. Current treatments for Alzheimer's disease include NSAIDs and glucocorticoids. NSAIDs function by blocking conversion of prostaglandin H2 into other prostaglandins (PGs) and thromboxane (TX). Prostoglandins and thromboxane act as inflammatory mediators and increase microvascular permeability.

Scleroderma renal crisis, the occurrence of acute renal failure and malignant hypertension (very high blood pressure with evidence of organ damage) in people with scleroderma, is effectively treated with drugs from the class of the ACE inhibitors. The benefit of ACE inhibitors extends even to those who have to commence dialysis to treat their kidney disease, and may give sufficient benefit to allow the discontinuation of renal replacement therapy.

Camurati–Engelmann disease is somewhat treatable. Glucocorticosteroids, which are anti-inflammatory and immunosuppressive agents, are used in some cases. This form of medication helps in bone strength, however can have multiple side effects. In several reports, successful treatment with glucocoricosteroids was described, as certain side effects can benefit a person with CED. This drug helps with pain and fatigue as well as some correction of radiographic abnormalities.

Alternative treatments such as massage, relaxation techniques (meditation, essential oils, spa baths, music therapy, etc.), gentle stretching, and especially heat therapy have been successfully used to an extent in conjunction with pain medications. A majority of CED patients require some form of analgesics, muscle relaxant, and/or sleep inducing medication to manage the pain, specifically if experiencing frequent or severe 'flare-ups' (e.g. during winter).

Natalizumab (Tysabri) was approved in 2004 by the FDA for multiple sclerosis (MS). It was subsequently withdrawn from the market by its manufacturer after it was linked with three cases of PML. All 3 initial cases were taking natalizumab in combination with interferon beta-1a. After a safety review the drug was returned to the market in 2006 as a monotherapy for MS under a special prescription program. As of May 2011, over 130 cases of PML had been reported in MS patients, all in patients who had taken natalizumab for more than a year. While none of them had taken the drug in combination with other disease-modifying treatments, previous use of MS treatments increases the risk of PML between 3 and 4-fold. The estimated prevalence of PML in MS is 1.5 cases per thousand natalizumab users. Around 20% of MS patients with PML die, and most of the rest are very disabled.

A person with MS developed PML and died during a 4-year course of dimethyl-fumarate.

Inflammatory demyelinating diseases (IDDs), sometimes called Idiopathic (IIDDs) because the unknown etiology of some of them, and sometimes known as borderline forms of multiple sclerosis, is a collection of multiple sclerosis variants, sometimes considered different diseases, but considered by others to form a spectrum differing only in terms of chronicity, severity, and clinical course.

Multiple Sclerosis for some people is a syndrome more than a single disease. It can be considered among the acquired demyelinating syndromes with a multiphasic instead of monophasic behaviour. Multiple sclerosis also has a prodromal stage in which an unknown underlying condition, able to damage the brain, is present, but no lesion has still developed.

It took its name from Otto Marburg. It can be diagnosed "in vivo" with an MRI scan.

If Marburg disease occurs in the form of a single large lesion, it can be radiologically indistinguishable from a brain tumor or abscess. It is usually lethal, but it has been found to be responsive to Mitoxantrone and Alemtuzumab, and it has also been responsive to autologous stem cell transplantation. Recent evidence shows that Marburg's presents a heterogeneous response to medication, as does standard MS.

Since pseudobulbar palsy is a syndrome associated with other diseases, treating the underlying disease may eventually reduce the symptoms of pseudobulbar palsy.

Possible pharmacological interventions for pseudobulbar affect include the tricyclic antidepressants, serotonin reuptake inhibitors, and a novel approach utilizing dextromethorphan and quinidine sulfate. Nuedexta is an FDA approved medication for pseudobulbar affect. Dextromethorphan, an N-methyl-D-aspartate receptor antagonist, inhibits glutamatergic transmission in the regions of the brainstem and cerebellum, which are hypothesized to be involved in pseudobulbar symptoms, and acts as a sigma ligand, binding to the sigma-1 receptors that mediate the emotional motor expression.