Limbic encephalitis is a rare condition with no randomised-controlled trials to guide treatment. Treatments that have been tried include intravenous immunoglobulin, plasmapheresis, corticosteroids, cyclophosphamide and rituximab.

If an associated tumour is found, then recovery is not possible until the tumour is removed. Unfortunately, this is not always possible, especially if the tumour is malignant and advanced.

If people are found to have a tumor, the long-term prognosis is generally better and the chance of relapse is much lower. This is because the tumour can be removed surgically, thus eradicating the source of autoantibodies. In general, early diagnosis and aggressive treatment is believed to improve patient outcomes, but this remains impossible to know without data from randomized controlled trials. Given that the majority of patients are initially seen by psychiatrists, it is critical that all physicians (especially psychiatrists) consider anti-NMDA receptor encephalitis as a possible cause of acute psychosis in young patients with no past neuropsychiatric history.

- If a tumor is detected, its removal should occur in conjunction with first-line immunotherapy. This involves steroids to suppress the immune system, intravenous immunoglobulin, and plasmapheresis to physically remove autoantibodies. A study of 577 patients showed that over four weeks, about half the patients improved after receiving first-line immunotherapy.

- Second-line immunotherapy includes rituximab, a monoclonal antibody that targets the CD20 receptor on the surface of B cells, thus destroying the self-reactive B cells. Cyclophosphamide, an alkylating agent that cross-links DNA and is used to treat both cancer and autoimmune diseases, has sometimes proven useful when other therapies have failed.

- Other medications, such as alemtuzumab, remain experimental.

The disease is incurable once manifested, so there is no specific drug therapy for TBE. Symptomatic brain damage requires hospitalization and supportive care based on syndrome severity. Anti-inflammatory drugs, such as corticosteroids, may be considered under specific circumstances for symptomatic relief. Tracheal intubation and respiratory support may be necessary.

Prevention includes non-specific (tick-bite prevention, tick checks) and specific prophylaxis in the form of a vaccine. TBE immunoglobulin is no longer used. Tick-borne encephalitis vaccine is very effective and available in many disease endemic areas and in travel clinics.

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.

The recovery process from anti-NMDA encephalitis can take many months. The symptoms reappear in reverse order: The patient may begin to experience psychosis again, leading many people to falsely believe the patient is not recovering. As the recovery process continues on, the psychosis fades. Lastly, the person's social behavior and executive functions begin to improve.

Modern treatment approaches to encephalitis lethargica include immunomodulating therapies, and treatments to remediate specific symptoms.

Treatment for encephalitis lethargica in the early stages is patient stabilization, which may be very difficult. There is little evidence so far of a consistent effective treatment for the initial stages, though some patients given steroids have seen improvement.The disease becomes progressive, with evidence of brain damage similar to Parkinson's disease.

Treatment is then symptomatic. Levodopa (-DOPA) and other anti-parkinson drugs often produce dramatic responses; however, most patients given -DOPA experience s of the disease that are short lived.

No specific therapy is available at present for La Crosse encephalitis, and management is limited to alleviating the symptoms and balancing fluids and electrolyte levels. Intravenous ribavirin is effective against La Crosse encephalitis virus in the laboratory, and several studies in patients with severe, brain biopsy confirmed, La Crosse encephalitis are ongoing.

In a trial with 15 children being infected with La Crosse viral encephalitis were treated at certain phases with ribavirin (RBV). RBV appeared to be safe at moderate doses. At escalated doses of RBV, adverse events occurred and then the trial was discontinued. Nonetheless, this was the largest study of antiviral treatment for La Crosse encephalitis.

In one case, cloxacillin, ceftriaxone, and amphotericin B were tried.

Two patients survived after being successfully treated with a therapy consisting of flucytosine, pentamidine, fluconazole, sulfadiazine and azithromycin. Thioridazine was also given. Successful treatment in these cases was credited to "awareness of "Balamuthia" as the causative agent of encephalitis and early initiation of antimicrobial therapy."

Antiviral therapy: as early as possible

10~15mg/kg every 8 hours for 14~21d

5~10mg/kg every 12hours for 14~21d

immune therapy: interferon

symptomatic therapy

High fever: physical regulation of body temperature

Seizure: antiepileptic drugs

high intracranial pressure-20%mannitol

Infections: antibiotic drugs

Treatments of proven efficacy are currently limited mostly to herpes viruses and human immunodeficiency virus. The herpes virus is of two types: herpes type 1 (HSV-1, or oral herpes) and herpes type 2 (HSV-2, or genital herpes). Although there is no particular cure; there are treatments that can relieve the symptoms. Drugs like Famvir, Zovirax, and Valtrex are among the drugs used, but these medications can only decrease pain and shorten the healing time. They can also decrease the total number of outbreaks in the surrounding. Warm baths also may relive the pain of genital herpes.

Human Immunodeficiency Virus Infection (HIV) is treated by using a combination of medications to fight against the HIV infection in the body. This is called antiretroviral therapy (ART). ART is not a cure, but it can control the virus so that a person can live a longer, healthier life and reduce the risk of transmitting HIV to others around him. ART involves taking a combination of HIV medicines (called an HIV regimen) every day, exactly as prescribed by the doctor. These HIV medicines prevent HIV Virus from multiplying (making copies of itself in the body), which reduces the amount of HIV in the body. Having less HIV in the body gives the immune system a chance to recover and fight off infections and cancers. Even though there is still some HIV in the body, the immune system is strong enough to fight off infections and cancers. By reducing the amount of HIV in the body, HIV medicines also reduce the risk of transmitting the virus to others. ART is recommended for all people with HIV, regardless of how long they’ve had the virus or how healthy they are. If left untreated, HIV will attack the immune system and eventually progress to AIDS.

Even with treatment, the condition is often fatal, and there are very few recorded survivors, almost all of whom suffered permanent neurocognitive deficits. Antifungal drugs including ketoconazole, miconazole, 5-flucytosine and pentamidine have been shown to be effective against GAE-causing organisms in laboratory tests.

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.

Most patients reported in the literature have been given treatments suitable for autoimmune neurological diseases, such as corticosteroids, plasmapheresis and/or intravenous immunoglobulin, and most have made a good recovery. The condition is too rare for controlled trials to have been undertaken.

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.

There is no specific treatment for Japanese encephalitis and treatment is supportive, with assistance given for feeding, breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol. There is no transmission from person to person and therefore patients do not need to be isolated.

A breakthrough in the field of Japanese encephalitis therapeutics is the identification of macrophage receptor involvement in the disease severity. A recent report of an Indian group demonstrates the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in Japanese Encephalitis infection of the brain. This transcriptomic study provides a hypothesis of neuroinflammation and a new lead in development of appropriate therapeutic against Japanese encephalitis.

Where an underlying neoplasm is the cause, treatment of this condition is indicated in order to reduce progression of symptoms. For cases without a known cause, treatment involves suppression of the immune system with corticosteroid treatment, intravenous immunoglobulin, immunosuppressive agents like Rituximab, Cellcept, or Imuran or plasmapheresis.

Immunosuppressive therapies, encompassing corticosteroids, azathioprine, methotrexate and more recently, rituximab, are the mainstay of therapy. Other treatments include PE, IVIG, and thymectomy. Patients reportedly exhibited a heterogenous response to immunomodulation.

Antiepileptics can be used for symptomatic relief of peripheral nerve hyperexcitability. Indeed, some patients have exhibited a spontaneous remission of symptoms.

Most people recover from West Nile virus without treatment. No specific treatment is available for WNV infection. In mild cases over the counter pain relievers can help ease mild headaches and muscle aches in adults. In severe cases treatment consists of supportive care that often involves hospitalization, intravenous fluids, pain medication, respiratory support, and prevention of secondary infections.

During the acute stage, treatment is aimed at reducing the inflammation. As in other inflammatory diseases, steroids may be used first of all, either as a short course of high-dose treatment, or in a lower dose for long-term treatment. Intravenous immunoglobulin is also effective both in the short term and in the long term, particularly in adults where it has been proposed as first-line treatment. Other similar treatments include plasmapheresis and tacrolimus, though there is less evidence for these. None of these treatments can prevent permanent disability from developing.

During the residual stage of the illness when there is no longer active inflammation, treatment is aimed at improving the remaining symptoms. Standard anti-epileptic drugs are usually ineffective in controlling seizures, and it may be necessary to surgically remove or disconnect the affected cerebral hemisphere, in an operation called hemispherectomy. This usually results in further weakness, hemianopsia and cognitive problems, but the other side of the brain may be able to take over some of the function, particularly in young children. The operation may not be advisable if the left hemisphere is affected, since this hemisphere contains most of the parts of the brain that control language. However, hemispherectomy is often very effective in reducing seizures.

Herpesviral Encephalitis can be treated with high-dose intravenous acyclovir. Without treatment, HSE results in rapid death in approximately 70% of cases; survivors suffer severe neurological damage. When treated, HSE is still fatal in one-third of cases, and causes serious long-term neurological damage in over half of survivors. Twenty percent of treated patients recover with minor damage. Only a small population of survivors (2.5%) regain completely normal brain function. Indeed, many amnesic cases in the scientific literature have etiologies involving HSE. Earlier treatment (within 48 hours of symptom onset) improves the chances of a good recovery. Rarely, treated individuals can have relapse of infection weeks to months later. There is evidence that aberrant inflammation triggered by herpes simplex can result in granulomatous inflammation in the brain, which responds to steroids. While the herpes virus can be spread, encephalitis itself is not infectious. Other viruses can cause similar symptoms of encephalitis, though usually milder (Herpesvirus 6, varicella zoster virus, Epstein-Barr, cytomegalovirus, coxsackievirus, etc.).

People reduce the chance of getting infected with LACV by preventing mosquito bites. There is no vaccine or preventive drug.

Prevention measures against LACV include reducing exposure to mosquito bites. Use repellent such as DEET and picaridin, while spending time outside, especially at during the daytime - from dawn until dusk. "Aedes triseriatus" mosquitoes that transmit (LACV) are most active during the day. Wear long sleeves, pants and socks while outdoors. Ensure all screens are in good condition to prevent mosquitoes from entering your home. "Aedes triseriatus" prefer treeholes to lay eggs in. Also, remove stagnant water such as old tires, birdbaths, flower pots, and barrels.

Infection with Japanese encephalitis confers lifelong immunity. There are currently three vaccines available: SA14-14-2, IC51 (marketed in Australia and New Zealand as JESPECT and elsewhere as IXIARO) and ChimeriVax-JE (marketed as IMOJEV). All current vaccines are based on the genotype III virus.

A formalin-inactivated mouse-brain derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan, Korea, Taiwan, and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program.

The most common adverse effects are redness and pain at the injection site. Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. However where the vaccine is not produced in mouse brains but in vitro using cell culture there is little adverse effects compared to placebo, the main side effects are headache and myalgia.

The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer. The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk. Furthermore, there is also no data available regarding the interchangeability of other JE vaccines and IXIARO.

In September 2012 the Indian firm Biological E. Limited has launched an inactivated cell culture derived vaccine based on SA 14-14-2 strain which was developed in a technology transfer agreement with Intercell and is a thiomersal-free vaccine.

There is no cure for EEE. Treatment consists of corticosteroids, anticonvulsants, and supportive measures (treating symptoms) such as intravenous fluids, tracheal intubation, and antipyretics. About four percent of humans known to be infected develop symptoms, with a total of about six cases per year in the US. A third of these cases die, and many survivors suffer permanent brain damage.

Corticosteroids are administered through IV or orally. They cause lymphocytopenia, a condition where white blood cell levels are abnormally low. Corticosteroids cause white blood cell death, lowering their numbers throughout the body. They also cause white blood cells to recirculate away from the area of damage (the retina). This minimizes damage caused by the antibodies produced by the white blood cells. Often, this is treatment is combined with plasmapheresis. Instead of treating the plasma and blood cells, they are replaced with a healthy donor mixture. Patients who respond positively show improved visual fields and an almost complete disappearance of anti-retinal antibodies.

Plasmapheresis involves separating blood into two parts - blood cells and plasma. The blood plasma components, such as the antibodies, are treated outside of the body. After removal of the disease-associated antibodies, the blood cells and plasma are transfused back into the body. Response to this treatment depends on how much retinal damage has been done. Patients who respond positively show significant visual gains.