The CDC MMWR report advised, "To prevent infections in general, persons should stay home if they are ill, wash their hands often with soap and water, avoid close contact (such as touching and shaking hands) with those who are ill, and clean and disinfect frequently touched surfaces."

Unlike polio, acute flaccid myelitis can not currently be prevented with a vaccine.

Efforts to develop a vaccine for the virus depend on whether multiple strains of enteroviruses actually cause acute flaccid myelitis, and if so, whether a vaccine can be designed to protect against them all.

No controlled clinical trials have been conducted on ADEM treatment, but aggressive treatment aimed at rapidly reducing inflammation of the CNS is standard. The widely accepted first-line treatment is high doses of intravenous corticosteroids, such as methylprednisolone or dexamethasone, followed by 3–6 weeks of gradually lower oral doses of prednisolone. Patients treated with methylprednisolone have shown better outcomes than those treated with dexamethasone. Oral tapers of less than three weeks duration show a higher chance of relapsing, and tend to show poorer outcomes. Other anti-inflammatory and immunosuppressive therapies have been reported to show beneficial effect, such as plasmapheresis, high doses of intravenous immunoglobulin (IVIg), mitoxantrone and cyclophosphamide. These are considered alternative therapies, used when corticosteroids cannot be used or fail to show an effect.

There is some evidence to suggest that patients may respond to a combination of methylprednisolone and immunoglobulins if they fail to respond to either separately

In a study of 16 children with ADEM, 10 recovered completely after high-dose methylprednisolone, one severe case that failed to respond to steroids recovered completely after IV Ig; the five most severe cases -with ADAM and severe peripheral neuropathy- were treated with combined high-dose methylprednisolone and immunoglobulin, two remained paraplegic, one had motor and cognitive handicaps, and two recovered. A recent review of IVIg treatment of ADEM (of which the previous study formed the bulk of the cases) found that 70% of children showed complete recovery after treatment with IVIg, or IVIg plus corticosteroids. A study of IVIg treatment in adults with ADEM showed that IVIg seems more effective in treating sensory and motor disturbances, while steroids seem more effective in treating impairments of cognition, consciousness and rigor. This same study found one subject, a 71-year-old man who had not responded to steroids, that responded to an IVIg treatment 58 days after disease onset.

According to a ProMED article, disease in sheep has been controlled in the UK by a vaccine (ATCvet code: QI04AA01), originally developed by Scotland's Moredun Research Institute by Prof John Russell Greig. In 2009, however, a shortage of vaccine combined with an increase in the number of ticks found in sheep pasture areas cause an increased risk of this disease.

Treatment (which is based on supportive care) is as follows:

Pyrimethamine-based maintenance therapy is often used to treat Toxoplasmic Encephalitis (TE), which is caused by Toxoplasma gondii and can be life-threatening for people with weak immune systems. The use of highly active antiretroviral therapy (HAART), in conjunction with the established pyrimethamine-based maintenance therapy, decreases the chance of relapse in patients with HIV and TE from approximately 18% to 11%. This is a significant difference as relapse may impact the severity and prognosis of disease and result in an increase in healthcare expenditure.

Prophylactic vaccination is available against poliomyelitis, measles, Japanese encephalitis, and rabies. Hyper immune immunoglobulin has been used for prophylaxis of measles, herpes zoster virus, HSV-2, vaccine, rabies, and some other infections in high-risk groups.

Given that some conditions as MS show cortical damage together with the WM damage, there has been interest if this can appear as a secondary damage of the WM. It seems that some researchers claim so.

Vaccination is available against tick-borne and Japanese encephalitis and should be considered for at-risk individuals. Post-infectious encephalomyelitis complicating smallpox vaccination is avoidable, for all intents and purposes, as smallpox is nearly eradicated. Contraindication to Pertussis immunization should be observed in patients with encephalitis.

Experimental allergic encephalomyelitis (EAE) is an animal model of CNS inflammation and demyelination frequently used to investigate potential MS treatments. An acute monophasic illness, EAE is far more similar to ADEM than MS.

There is some evidence that there may be a relationship between BoDV-1 infection and psychiatric disease.

In 1990, Janice E. Clements and colleagues reported in the journal "Science" that antibodies to a protein encoded by the BoDV-1 genome are found in the blood of patients with behavioral disorders. In the early 1990s, researchers in Germany, America, and Japan conducted an investigation of 5000 patients with psychiatric disorders and 1000 controls, in which a significantly higher percentage of patients than controls were positive for BoDV-1 antibodies. Subsequent studies have also presented evidence for an association between BoDV-1 and human psychiatric disorders. However, not all researchers consider the link between BoDV-1 and human psychiatric disease to be conclusively proven. A recent study found no BoDV-1 antibodies in 62 patients with the deficit form of schizophrenia.

Additional evidence for a role of BoDV-1 in psychiatric disorders comes from reports that the drug amantadine, which is used to treat influenza infections, has had some success in treating depression and clearing BoDV-1 infection. Counter-claims state that Borna virus infections are not cleared by amantadine. The issue is further complicated by the fact that amantadine is also used in the treatment of Parkinson's disease and may have direct effects on the nervous system.

Should the viral progression be diagnosed during stage 1 (even during late stage 1 when stage 2 symptoms start to manifest themselves) then treatment to combat the infection can be administered successfully—there is no cure for SSPE but if it is caught early enough then the sufferer can respond to the treatment and prevent symptom recurrence by taking the medication for the rest of their life. The treatment for the SSPE infection is the immunomodulator interferon and specific antiviral medication—ribavirin and inosine pranobex are specifically used to greater effect than antivirals such as amantadine.

For those who have progressed to stage 2 or beyond, the disease is incurable. For patients in the terminal phase of the disease there is a palliative care and treatment scheme—this involves anticonvulsant therapy (to help with the body's progressive loss of control of the nervous system causing gradually more intensive spasms/convulsions) alongside supportive measures to help maintain vital functioning. It is fairly standard as the infection spreads and symptoms intensify that feeding tubes need to be inserted to keep a nutritional balance. As the disease progresses to its most advanced phase, the patient will need constant nursing as normal bodily function declines to the complete collapse of the nervous system.

Combinations of treatment for SSPE include:

- Oral inosine pranobex (oral isoprinosine) combined with intrathecal (injection through a lumbar puncture into the spinal fluid) or intraventricular interferon alpha.

- Oral inosine pranobex (oral isoprinosine) combined with interferon beta.

- Intrathecal interferon alpha combined with intravenous ribavirin.

SSPE is a rare condition, although there is still relatively high incidence in Asia and the Middle East. However, the number of reported cases is declining since the introduction of the measles vaccine—eradication of the measles virus prevents the SSPE mutation and therefore the progression of the disease or even the initial infection itself.

Louping ill is caused by RNA virus called Louping ill virus. Louping ill virus belongs to genus Flavivirus, family Flaviviridae.

There are four subtypes: British, Irish, Spanish and Turkish.

Development of new therapies has been hindered by the lack of appropriate animal model systems for some important viruses and also because of the difficulty in conducting human clinical trials for diseases that are rare. Nonetheless, numerous innovative approaches to antiviral therapy are available including candidate thiazolide and purazinecarboxamide derivatives with potential broad-spectrum antiviral efficacy. New herpes virus drugs include viral helicase-primase and terminase inhibitors. A promising new area of research involves therapies based on enhanced understanding of host antiviral immune responses.

Demyelination is produced by injection of brain extracts, CNS proteins (such as myelin basic protein), or peptides from such protein emulsified in an adjuvant such as complete Freund's adjuvant. The presence of the adjuvant allows the generation of inflammatory responses to the protein/peptides. In many protocols, mice are coinjected with pertussis toxin to break down the blood-brain barrier and allow immune cells access to the CNS tissue. This immunisation leads to multiple small disseminated lesions of demyelination (as well as micro-necroses) in the brain and spinal cord and the onset of clinical symptoms.

Although sharing some features, mostly demyelination, this model, first introduced in 1930s, differs from human MS in several ways. EAE either kills animals or leaves them with permanent disabilities; animals with EAE also suffer severe nerve inflammation, and the time course of EAE is entirely different from MS, being the main antigen (MBP) in charge.

Since each case is different, the following are possible treatments that patients might receive in the management of myelitis.

- Intravenous steroids

High-dose intravenous methyl-prednisolone for 3–5 days is considered as a standard of care for patients suspected to have acute myelitis, unless there are compelling reasons otherwise. The decision to offer continued steroids or add a new treatment is often based on the clinical course and MRI appearance at the end of 5 days of steroids.

- Plasma exchange (PLEX)

Patients with moderate to aggressive forms of disease who don’t show much improvement after being treated with intravenous and oral steroids will be treated with PLEX. Retrospective studies of patients with TM treated with IV steroids followed by PLEX showed a positive outcome. It also has been shown to be effective with other autoimmune or inflammatory central nervous system disorders. Particular benefit has been shown with patients who are in the acute or subacute stage of the myelitis showing active inflammation on MRI. However, because of the risks implied by the lumbar puncture procedure, this intervention is determined by the treating physician on a case-by-case basis.

- Immunosuppressants/Immunomodulatory agents

Myelitis with no definite cause seldom recurs, but for others, myelitis may be a manifestation of other diseases that are mentioned above. In these cases, ongoing treatment with medications that modulate or suppress the immune system may be necessary. Sometimes there is no specific treatment. Either way, aggressive rehabilitation and long-term symptom management are an integral part of the healthcare plan.

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

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.

Currently the mechanism of spread and infection is unknown despite the tedious epidemiological, clinical, and neurological studies that have been conducted. Recent Studies show Horizontal Disease Transmission, or the transmission of a disease from one individual to another of the same generation. It appears that VE is an infectious disease; however, the incubation period would have to be very extensive (in excess of 5 years). Many infected individuals attribute the initial symptoms as a result of a plunge in frigid waters. So far, no causative agent has been found in blood, spinal fluid, or brain tissue.

The theory of autoimmune attack claims that a person with neuroimmunologic disorders have genetic predisposition to auto-immune disorder, and the environmental factors would trigger the disease. The specific genetics in myelitis is not completely understood. It is believed that the immune system response could be to viral, bacterial, fungal, or parasitic infection; however, it is not known why the immune system attacks itself. Especially, for immune system to cause inflammatory response anywhere in the central nervous system, the cells from immune system must pass through the blood brain barrier. In the case of myelitis, not only is the immune system dysfunctional, but the dysfunction also crosses this protective blood brain barrier to affect the spinal cord.

The mortality rate of the virus largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate, where complications such as pneumonia and encephalitis are more common. In older dogs that develop distemper encephalomyelitis, vestibular disease may present. Around 15% of canine inflammatory central nervous system diseases are a result of CDV.

The first antibodies to BoDV-1 in humans were discovered in the mid-1980s. Since then, there have been conflicting results from various studies in regards to whether an association exists between the agent and clinical disease. Antibodies to BoDV-1, which indicate prior infection, and BoDV-1 antigen have also been detected in blood donors.

Encephalomyelitis is inflammation of the brain and spinal cord. Various types of encephalomyelitis include:

- "Acute disseminated encephalomyelitis" or "postinfectious encephalomyelitis", a demyelinating disease of the brain and spinal cord, possibly triggered by viral infection.

- "Encephalomyelitis disseminata", a synonym for multiple sclerosis.

- "AntiMOG associated encephalomyelitis", one of the underlying conditions for the phenotype neuromyelitis optica and in general all the spectrum of MOG autoantibody-associated demyelinating diseases.

- "Equine encephalomyelitis", also called "equine encephalitis", a potentially fatal mosquito-borne viral disease that infects horses and humans.

- "Myalgic encephalomyelitis", a disease involving presumed inflammation of the central nervous system with symptoms of muscle pain and fatigue; the term has sometimes been used interchangeably with "chronic fatigue syndrome", though there is still controversy over the distinction.

- "Experimental autoimmune encephalomyelitis" (EAE), an animal model of brain inflammation.

- Progressive encephalomyelitis with rigidity and myoclonus (PERM) – A kind of stiff person syndrome.

- AIDS related encephalomyelitis, caused by opportunistic Human T-lymphotropic virus type III (HTLV-III) infection.

Unfortunately a vaccine for malignant catarrhal fever (MCF) has not yet been developed. Developing a vaccine has been difficult because the virus will not grow in cell culture and until recently it was not known why. Researchers at the Agricultural Research Service (ARS) found that the virus undergoes changes within the animal's body, a process known as "cell tropism switching". In cell tropism switching, the virus targets different cells at different points in its life cycle. This phenomenon explains why it has been impossible to grow the virus on any one particular cell culture.

Because the virus is transmitted from sheep to bison and cattle, researchers are first focusing on the viral life cycle in sheep. The viral life cycle is outlined in three stages: entry, maintenance, and shedding. Entry occurs through the sheep's nasal cavity and enters into the lungs where it replicates. The virus undergoes a tropic change and infects lymphocytes, also known as white blood cells, which play a role in the sheep's immune system. In the maintenance stage the virus remains on the sheep's lymphocytes and circulates the body. Finally, during the shedding stage, the virus undergoes another change and shifts its target cells from lymphocytes to nasal cavity cells, where it is then shed through nasal secretions. This discovery undoubtedly puts scientists on the right track for developing a vaccine – starting with the correct cell culture for each stage of the virus lifecycle – but ARS researchers are also looking into alternative methods to develop a vaccine. Researchers are experimenting with the MCF virus that infects topi (an African antelope) because it will grow in cell culture and does not infect cattle. Researchers hope that inserting genes from the sheep MCF virus into the topi MCF virus will ultimately be an effective MCF vaccine for cattle and bison. While there is much ground left to cover, scientists are getting closer and closer to developing a vaccine.