No controlled trials have established the effectiveness of treatments for the prevention of attacks. Many clinicians agree that long term immunosuppression is required to reduce the frequency and severity of attacks, while others argue the exact opposite. Commonly used immunosuppressant treatments include azathioprine (Imuran) plus prednisone, mycophenolate mofetil plus prednisone, mitoxantrone, intravenous immunoglobulin (IVIG), and cyclophosphamide.

Though the disease is known to be auto-antibodies mediated, B-cell depletion has been tried with the monoclonal antibody rituximab, showing good results.

Several other disease modifying therapies are being tried. In 2007, Devic's disease was reported to be responsive to glatiramer acetate and to low-dose corticosteroids. Use of Mycophenolate mofetil is also currently under research.

Currently, there is no cure for Devic's disease, but symptoms can be treated. Some patients recover, but many are left with impairment of vision and limbs, which can be severe.

The list of these diseases depends of the author, but usually are included:

- multiple sclerosis, normally defined by the dissemination in time and space of demyelinating lesions, with two (or sometimes three) clinical presentations:

- Relapsing-Onset multiple sclerosis, the most known and extended variant, normally consisting of two distinct clinical phases (Remitent-Recidivant, RRMS, and Secondary Progressive, SPMS)

- Progressive-Onset MS, most known as Primary progressive MS including a special genetic variant named rapidly progressive multiple sclerosis.

- Optic-spinal MS, or opticospinal, clinical and pathological variant of multiple sclerosis which often include visual symptoms and have a more severe course than typical MS. Though multiple scars (scleroses) are present in CNS, and they comply with the dissemination criteria, and sometimes is classified as clinically definite multiple sclerosis, currently is considered outside the scope of Multiple Sclerosis and inside the scope of Devic's disease, though it is uncertain if this applies to all cases. Also a variant affecting mainly the spinal cord and the cortex has been proposed

- Neuromyelitis optica (NMO), and its associated "spectrum of disorders" (NMOSD), currently considered a common syndrome for at least three separated diseases:, mainly produced by AQP4 autoimmune channelopathy, though other variants exists, some with anti-MOG and some others idiopathic. Some researchers think that there could exist an overlapping between Anti-NMDA receptor encephalitis cases and neuromyelitis optica or acute disseminated encephalomyelitis.

- Anti-MOG associated spectrum, often clinically presented as an anti-MOG autoimmune encephalomyelitis, but can also appear as negative NMO or atypical multiple sclerosis

- CRION (Chronic relapsing inflammatory optic neuritis): A distinct clinical entity from other inflammatory demyelinating diseases including multiple sclerosis (MS), neuromyelitis optica-immunoglobulin G (NMO-IgG) spectrum disease, and idiopathic relapsing optic neuritis.

- Acute disseminated encephalomyelitis or ADEM, a closely related disorder in which a known virus or vaccine triggers autoimmunity against myelin.

- Acute hemorrhagic leukoencephalitis, possibly a variant of Acute disseminated encephalomyelitis

- Balo concentric sclerosis, an unusual presentation of plaques forming concentrenic circles, which can sometimes get better spontaneously.

- Schilder disease or diffuse myelinoclastic sclerosis: is a rare disease that presents clinically as a pseudotumoural demyelinating lesion; and is more common in children.

- Marburg multiple sclerosis, an aggressive form, also known as malignant, fulminant or acute MS.

- Tumefactive multiple sclerosis: lesions whose size is more than 2 cm, with mass effect, oedema and/or ring enhancement

- Solitary sclerosis: This variant has been recently proposed (2012) by Mayo Clinic researches. though it was also reported by other groups more or less at the same time. It is defined as isolated demyelinating lesions which produce a progressive myelopathy similar to primary progressive MS, and is currently considered a synonym for tumefactive multiple sclerosis.

Some inflammatory conditions are associated with the presence of scleroses in the CNS. Optic neuritis (monophasic and recurrent) and Transverse myelitis (monophasic and recurrent)

As MS is an active field for research, the list is not closed or definitive. For example, some diseases like Susac's syndrome (MS has an important vascular component), leukoaraiosis, myalgic encephalomyelitis (aka chronic fatigue syndrome) or autoimmune variants of peripheral neuropathies like Guillain–Barré syndrome or progressive inflammatory neuropathy could be included assuming the autoimmune model. Also Leukodystrophy (which see) and its sub-conditions: Adrenoleukodystrophy and Adrenomyeloneuropathy could be in the list. Venous induced demyelination has also been proposed as a hypothetical MS variant produced by CCSVI.

Recent research has identified some possible new variants, like the possibility to separate primary progressive MS, PPMS, after recent findings seem to point that it is pathologically a very different disease.

Also an OPA1 variant and aKIR4.1 multiple sclerosis variant was reported in 2012 and later reported again, which could be considered a different disease (as Devic disease did before), and can represent up to a 47% of the MS cases. Finally, there exist some reports of an aquaporine-related multiple sclerosis, related to vegetal aquaporine proteins.

Though for the most of the cases these diseases are still idiopathic, recent researchs have found the causes for some of them, making them not idiopathic anymore. There are currently two identified auto-antibodies and a genetic variant. The autoantibodies are anti-AQP4 and anti-MOG so far and the genetic variant is a mutation in the gene NR1H3.

Current treatment is aimed at easing the symptoms, reducing inflammation, and controlling the immune system. The quality of the evidence for treating the oral ulcers associated with Behçet's disease, however, is poor.

High-dose corticosteroid therapy is often used for severe disease manifestations. Anti-TNF therapy such as infliximab has shown promise in treating the uveitis associated with the disease. Another Anti-TNF agent, etanercept, may be useful in people with mainly skin and mucosal symptoms.

Interferon alpha-2a may also be an effective alternative treatment, particularly for the genital and oral ulcers as well as ocular lesions. Azathioprine, when used in combination with interferon alpha-2b also shows promise, and colchicine can be useful for treating some genital ulcers, erythema nodosum, and arthritis.

Thalidomide has also been used due to its immune-modifying effect. Dapsone and rebamipide have been shown, in small studies, to have beneficial results for mucocutaneous lesions.

Given its rarity, the optimal treatment for acute optic neuropathy in Behçet's disease has not been established. Early identification and treatment is essential. Response to ciclosporin, periocular triamcinolone, and IV methylprednisone followed by oral prednisone has been reported although relapses leading to irreversible visual loss may occur even with treatment. Immunosuppressants such as interferon alpha and tumour necrosis factor antagonists may improve though not completely reverse symptoms of ocular Behçet's disease, which may progress over time despite treatment. When symptoms are limited to the anterior chamber of the eye prognosis is improved. Posterior involvement, particularly optic nerve involvement, is a poor prognostic indicator. Secondary optic nerve atrophy is frequently irreversible. Lumbar puncture or surgical treatment may be required to prevent optic atrophy in cases of intracranial hypertension refractory to treatment with immunomodulators and steroids.

IVIG could be a treatment for severe or complicated cases.

Adult-onset Still's disease is treated with anti-inflammatory drugs. Steroids such as prednisone are used to treat severe symptoms of Still's. Other commonly used medications include hydroxychloroquine, penicillamine, azathioprine, methotrexate, etanercept, anakinra, cyclophosphamide, adalimumab, rituximab, and infliximab.

Newer drugs target interleukin-1 (IL-1), particularly IL-1β. A randomized, multicenter trial reported better outcomes in a group of 12 patients treated with anakinra than in a group of 10 patients taking other disease-modifying antirheumatic drugs. Other anti-IL1β drugs are being developed, including canakinumab and rilonacept.

The condition "juvenile-onset Still's disease" is now usually grouped under juvenile rheumatoid arthritis. However, there is some evidence that the two conditions are closely related.

Surgical treatment of arterial manifestations of BD bears many pitfalls, since the obliterative endarteritis of vasa vasorum causes thickening of the medial layer and splitting of elastin fibers. Therefore, anastomotic pseudoaneurysms are likely to form, as well as pseudoaneurysms at the site of puncture in case of angiography or endovascular treatment; furthermore, early graft occlusion may occur.

For these reasons, invasive treatment should not be performed in the acute and active phases of the disease when inflammation is at its peak. The evaluation of disease’s activity is usually based on relapsing symptoms, ESR (erythrocyte sedimentation rate), and serum levels of CRP (C‐reactive protein).

Endovascular treatment can be an effective and safe alternative to open surgery, with less postoperative complications, faster recovery time, and reduced need for intensive care, while offering patency rates and procedural success rates comparable with those of surgery. This notwithstanding, long‐term results of endovascular treatment in BD are still to be determined.

Researchers are investigating whether levels of a protein named calprotectin could be used to improve diagnosis and monitoring.

Recent research into treatments for Dercum's disease has identified liposuction as a possible treatment. The researchers wanted to assess the use of liposuction on the affected adipose tissue to see if pain was reduced in the affected patient. The results of this study suggested that pain was reduced in patients for a short period of time. As time had passed the patients pain level had once again increased. The study found that pain was reduced only for a period of time and that all symptoms had come back within 5 years. Other recent treatments include Transcutaneous Electrical Stimulation has in one case proven to safely and effectively reduce the symptoms of the disease. This type of therapy is typically used in the treatment of painful inflammatory conditions. Treatments included 10 consecutive sessions over a 6-month period. After 4 months of treatment pain was reduced and after 6 months of treatment pain was even further reduced.

CVAC sessions

Cyclic Variations in Adaptive Conditioning (CVAC) is a method of touch free cyclic hypobaric pneumatic compression for treatment of tissue edema and, therefore, edema-associated pain. As a pilot study, 10 participants with AD completed pain and quality of life questionnaires before and after 20–40 minutes of CVAC process daily for 5 days. After treatment, there was a significant decrease in pain as measured by the Pain Catastrophizing Scale and the Visual Analogue Scale, but there was no change in pain quality by the McGill Pain Questionnaire. However, there were no changes in the Pain Disability Index or Pittsburgh Sleep Quality Index. This study suggests a potential treatment role for CVAC, and the authors recommended randomized controlled clinical trials.

The term "chronic Lyme disease" is often applied to several different sets of people. One usage refers to people suffering from the symptoms of untreated and disseminated late-stage Lyme disease: arthritis, peripheral neuropathy and/or encephalomyelitis. The term is also applied to people who have had the disease in the past and some symptoms remain after antibiotic treatment, which is also called post-Lyme disease syndrome. A third and controversial use of the term applies to patients with nonspecific symptoms, such as fatigue, who show no objective evidence they have been infected with Lyme disease in the past, since the standard diagnostic tests for infection are negative.

The Centers for Disease Control and Prevention state that some people after a "course of antibiotics will have lingering symptoms of fatigue, pain, or joint and muscle aches. In some cases, these can last for more than 6 months. Although often called 'chronic Lyme disease', this condition is properly known as 'post-treatment Lyme disease syndrome' (PTLDS)". This is estimated to occur in less than 5% of people who had Lyme disease and were treated.

While it is undisputed people can have severe symptoms, the cause and appropriate treatment are controversial. The symptoms may represent "for all intents and purposes" fibromyalgia or chronic fatigue syndrome. A few doctors attribute these symptoms to persistent infection with "Borrelia", or co-infections with other tick-borne pathogens, such as "Ehrlichia" and "Babesia". Other doctors believe that the initial infection may cause an autoimmune reaction that continues to cause serious symptoms even after the bacteria have been eliminated by antibiotics. A review looked at several animal studies that found persistence of live but disabled spirochetes following treatment of "B. burgdorferi" infection with antibiotics. The authors noted that none of the lingering spirochetes were associated with inflamed tissues and criticized the studies for not considering adequately the different pharmacodynamics and pharmacokinetics of the antibiotics used to treat the animals in the trials versus what would be expected to be used to treat humans. The authors concluded, "There is no scientific evidence to support the hypothesis that such spirochetes, should they exist in humans, are the cause of post-Lyme disease syndrome."

Major US medical authorities, including the Infectious Diseases Society of America, the American Academy of Neurology, and the National Institutes of Health, have stated there is no convincing evidence that "Borrelia" is involved in the various symptoms classed as chronic Lyme disease, and advise against long-term antibiotic treatment as ineffective and possibly harmful. Prolonged antibiotic therapy presents significant risks and can have dangerous side effects. Randomized placebo-controlled studies have shown that antibiotics offer no sustained benefit in people with "chronic Lyme"; with evidence of both placebo effects and significant adverse effects from such treatment. An advocacy group called the International Lyme And Associated Diseases Society (ILADS) argues the persistence of "B. burgdorferi" may be responsible for manifestations of late Lyme disease symptoms. It has questioned the generalizability and reliability of some of the above trials and the reliability of the current diagnostic tests.

Vaccination is the only known method to prevent the development of tumors when chickens are infected with the virus. However, administration of vaccines does not prevent transmission of the virus, i.e., the vaccine is not sterilizing. However, it does reduce the amount of virus shed in the dander, hence reduces horizontal spread of the disease. Marek's disease does not spread vertically. The vaccine was introduced in 1970 and the scientist credited with its development is Dr. Ben Roy Burmester and Dr. Frank J Siccardi. Before that, Marek's disease caused substantial revenue loss in the poultry industries of the United States and the United Kingdom. The vaccine can be administered to one-day-old chicks through subcutaneous inoculation or by "in ovo" vaccination when the eggs are transferred from the incubator to the hatcher. "In ovo" vaccination is the preferred method, as it does not require handling of the chicks and can be done rapidly by automated methods. Immunity develops within two weeks.

The vaccine originally contained the antigenically similar turkey herpesvirus, which is serotype 3 of MDV. However, because vaccination does not prevent infection with the virus, the Marek's disease virus has evolved increased virulence and resistance to this vaccine. As a result, current vaccines use a combination of vaccines consisting of HVT and gallid herpesvirus type 3 or an attenuated MDV strain, CVI988-Rispens (ATCvet code: ).

The twins require the use of wheelchairs for mobility and are unable to speak without the assistance of electronic speaking aids. They experience persistent and painful muscle spasms which are worsened by emotional distress. They are currently living with their parents, with the assistance of hospice workers. Doctors continue to administer tests to the twins in search of a treatment.

Treatment of mixed cryoglobulinemic disease is, similar to type I disease, directed toward treating any underlying disorder. This includes malignant (particularly Waldenström's macroglobulinemia in type II disease), infectious, or autoimmune diseases in type II and III disease. Recently, evidence of hepatitis C infection has been reported in the majority of mixed disease cases with rates being 70-90% in areas with high incidences of hepatitis C. The most effective therapy for hepatitis C-associated cryoglobulinemic disease consists of a combination of anti-viral drugs, pegylated INFα and ribavirin; depletion of B cells using rituximab in combination with antiviral therapy or used alone in patients refractory to antiviral therapy has also proven successful in treating the hepatitis C-associated disease. Data on the treatment of infectious causes other than hepatitis C for the mixed disease are limited. A current recommendation treats the underlying disease with appropriate antiviral, anti-bacterial, or anti-fungal agents, if available; in cases refractory to an appropriate drug, the addition of immunosuppressive drugs to the therapeutic regimen may improve results. Mixed cryoglobulinemic disease associated with autoimmune disorders is treated with immunosuppressive drugs: combination of a corticosteroid with either cyclophosphamide, azathioprine, or mycophenolate or combination of a corticosteroid with rituximab have been used successfully to treated mixed disease associated with autoimmune disorders.

All patients with symptomatic cryoglobulinemia are advised to avoid, or protect their extremities, from exposure to cold temperatures. Refrigerators, freezers, and air-conditioning represent dangers of such exposure.

Chronic Lyme disease is a generally unrecognised diagnosis that encompasses "a broad array of illnesses or symptom complexes for which there is no reproducible or convincing scientific evidence of any relationship to "B. burgdorferi" infection." There is no clinical evidence that "chronic" Lyme disease is caused by a persistent infection. It is distinct from post-treatment Lyme disease syndrome, a set of lingering symptoms which may persist after successful treatment of infection with Lyme spirochetes. The symptoms of "chronic Lyme" are generic and non-specific "symptoms of life".

A number of alternative treatments are promoted for "chronic Lyme disease", of which possibly the most controversial and harmful is long-term antibiotic therapy, particularly intravenous antibiotics. Most medical authorities advise against long-term antibiotic treatment for Lyme disease, though they agree that some patients do experience lingering symptoms. Following disciplinary proceedings by State medical licensing boards in the United States, a subculture of "Lyme literate" physicians has successfully lobbied for specific legal protections, exempting them from the standard of care and Infectious Diseases Society of America treatment guidelines. This "troubling" political interference in medical care has been criticised as an example of "legislative alchemy", the process whereby pseudomedicine is legislated into practice.

The disease appears to be progressive in nature. The Fields twins started having problems when they were four years old. By the time they had reached the age of nine, they were having difficulty walking and needed frames to assist them with walking. Their muscles have been gradually deteriorating over time. The disease affects the twins' nerves, causing them to make involuntary muscle movements such as trembling in the hands.

The extent of the disease is still unknown as the two women are only 21. However, the disease has had no apparent effect on their brains or personalities. Doctors do not know if the disease is fatal and, if so, what the life expectancy of one with this disease is. If the cause of the disease is genetic, there is a chance that the twins could pass it on to their future children.

Binswanger's disease has no cure and has been shown to be the most severe impairment of all of the vascular dementias. The best way to manage the vascular risk factors that contribute to poor perfusion in the brain is to treat the cause, such as chronic hypertension or diabetes. It has been shown that current Alzheimer’s medication, donepezil (trade name Aricept), may help Binswanger’s Disease patients as well . Donepezil increases the acetylcholine in the brain through a choline esterase inhibitor which deactivates the enzyme that breaks down acetylcholine. Alzheimer as well as Binswanger patients have low levels of acetylcholine and this helps to restore the normal levels of neurotransmitters in the brain. This drug may improve memory, awareness, and the ability to function. If no medical interception of the disease is performed then the disease will continue to worsen as the patient ages due to the continuing atrophy of the white matter from whatever was its original cause.

Marek's disease is a highly contagious viral neoplastic disease in chickens. It is named after József Marek, a Hungarian veterinarian. Marek's disease is caused by an alphaherpesvirus known as 'Marek's disease virus' (MDV) or "Gallid alphaherpesvirus 2" (GaHV-2). The disease is characterized by the presence of T cell lymphoma as well as infiltration of nerves and organs by lymphocytes. Viruses "related" to MDV appear to be benign and can be used as vaccine strains to prevent Marek's disease. For example, the related Herpesvirus of Turkeys (HVT), causes no apparent disease in turkeys and continues to be used as a vaccine strain for prevention of Marek's disease (see below). Birds infected with GaHV-2 can be carriers and shedders of the virus for life. Newborn chicks are protected by maternal antibodies for a few weeks. After infection, microscopic lesions are present after one to two weeks, and gross lesions are present after three to four weeks. The virus is spread in dander from feather follicles and transmitted by inhalation.

Pogosta disease is a viral disease, established to be identical with other diseases, Karelian fever and Ockelbo disease. The names are derived from the words Pogosta, Karelia and Ockelbo, respectively.

The symptoms of the disease include usually rash, as well as mild fever and other flu-like symptoms; in most cases the symptoms last less than 5 days. However, in some cases, the patients develop a painful arthritis. There are no known chemical agents available to treat the disease.

It has long been suspected that the disease is caused by a Sindbis-like virus, a positive-stranded RNA virus belonging to the Alphavirus genus and family Togaviridae. In 2002 a strain of Sindbis was isolated from patients during an outbreak of the Pogosta disease in Finland, confirming the hypothesis.

This disease is mainly found in the Eastern parts of Finland; a typical Pogosta disease patient is a middle-aged person who has been infected through a mosquito bite while picking berries in the autumn. The prevalence of the disease is about 100 diagnosed cases every year, with larger outbreaks occurring in 7-year intervals.

Treatment is with penicillin, ampicillin, tetracycline, or co-trimoxazole for one to two years. Any treatment lasting less than a year has an approximate relapse rate of 40%. Recent expert opinion is that Whipple's disease should be treated with doxycycline with hydroxychloroquine for 12 to 18 months. Sulfonamides (sulfadiazine or sulfamethoxazole) may be added for treatment of neurological symptoms.

Whipple's disease is a rare, systemic infectious disease caused by the bacterium "Tropheryma whipplei". First described by George Hoyt Whipple in 1907 and commonly considered a gastrointestinal disorder, Whipple's disease primarily causes malabsorption but may affect any part of the body including the heart, brain, joints, skin, lungs and the eyes. Weight loss, diarrhea, joint pain, and arthritis are common presenting symptoms, but the presentation can be highly variable and approximately 15% of patients do not have these classic signs and symptoms.

Whipple's disease is significantly more common in men, with 87% of the patients being male. When recognized and treated, Whipple's disease can usually be cured with long-term antibiotic therapy; if the disease is left untreated, it is ultimately fatal.

Infections are treated with antibiotics, particularly doxycycline, and the acute symptoms appear to respond to these drugs.

No serious long-term effects are known for this disease, but preliminary evidence suggests, if such symptoms do occur, they are less severe than those associated with Lyme disease.

Some patients have no symptoms, spontaneous remission, or a relapsing/remitting course, making it difficult to decide whether therapy is needed. In 2002, authors from Sapienza University of Rome stated on the basis of a comprehensive literature review that "clinical observation without treatment is advisable when possible."

Therapeutic options include surgery, radiation therapy, and chemotherapy. Surgery is used to remove single lymph nodes, central nervous system lesions, or localized cutaneous disease. In 2014, Dalia and colleagues wrote that for patients with extensive or systemic Rosai–Dorfman disease, "a standard of care has not been established" concerning radiotherapy and chemotherapy.