Limbic encephalitis is associated with an autoimmune reaction. In non-paraneoplastic limbic enephalitis, this is typically due to infection (commonly herpes simplex virus) or as a systemic autoimmune disorder. Limbic encephalitis associated with cancer or tumors is called paraneoplastic limbic encephalitis.

It can be caused by a bacterial infection, such as bacterial meningitis, or may be a complication of a current infectious disease syphilis (secondary encephalitis).

Certain parasitic or protozoal infestations, such as toxoplasmosis, malaria, or primary amoebic meningoencephalitis, can also cause encephalitis in people with compromised immune systems. Lyme disease or "Bartonella henselae" may also cause encephalitis.

Other bacterial pathogens, like "Mycoplasma" and those causing rickettsial disease, cause inflammation of the meninges and consequently encephalitis. A non-infectious cause includes acute disseminated encephalitis which is demyelinated.

Limbic encephalitis is broadly grouped into two types: paraneoplastic limbic encephalitis and non-paraneoplastic limbic encephalitis.

- Paraneoplastic limbic encephalitis (PNLE) is caused by cancer or tumor, and may be treated by removal of the tumor.

- Non-paraneoplastic limbic encephalitis (NPLE) is not associated with cancer. More common than PNLE, it is caused by am infection, autoimmune disorder, or other condition that may never be identified.

Viral encephalitis can occur either as a direct effect of an acute infection, or as one of the sequelae of a latent infection. The majority of viral cases of encephalitis have an unknown cause, however the most common identifiable cause of viral encephalitis is from herpes simplex infection. Other causes of acute viral encephalitis are rabies virus, poliovirus, and measles virus.

Additional possible viral causes are arbovirus (St. Louis encephalitis, West Nile encephalitis virus), bunyavirus (La Crosse strain), arenavirus (lymphocytic choriomeningitis virus) and reovirus (Colorado tick virus). The Powassan virus is a rare cause of encephalitis.

The number of new cases a year is unknown. According to the California Encephalitis Project, the disease has a higher incidence than its individual viral counterparts in patients younger than 30. The largest case series to date characterized 577 patients with anti-NMDA receptor encephalitis. The epidemiological data were limited, but this study provides the best approximation of disease distribution. It found that women are disproportionally affected, with 81% of cases reported in female patients. Disease onset is skewed toward children, with a median age of diagnosis of 21 years. Over a third of cases were children, while only 5% of cases were patients over the age of 45. This same review found that 394 out of 501 patients (79%) had a good outcome by 24 months. 30 patients (6%) died, and the rest were left with mild to severe deficits. The study also confirmed that patients with the condition are more likely to be of Asian or African origin.

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 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.

While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60–90 days to recover. People with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple long term (>1+ years) somatic complaints such as tremor, and dysfunction in motor skills and executive functions. People with milder illness are just as likely as people with more severe illness to experience adverse outcomes. Recovery is marked by a long convalescence with fatigue. One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease.

Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).

Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation. For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension, and diabetes mellitus.

A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene "CCR5" gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of "CCR5" made up 4.0 to 4.5% of a sample of West Nile disease sufferers, while the incidence of the gene in the general population is only 1.0%.

Most common cause of autoimmune encephalitis after acute demyelinating encephalitis in England. More than 500 cases have been reported in literature till 2013. In California Encephalitis Project it was found >4 times as frequently as herpes simplex virus type 1 (HSV-1), varicella-zoster virus (VZV), and West Nile virus (WNV). Among patients with first-onset schizophrenia incidence varies between 6–10%.

- Age – frequently 5–76 years, Median age of patients was 23 years

- Sex – 80% Female

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.

The clinical features and course of the condition, the associated auto-antibodies against relevant antigens, and the response to treatment, all suggest that Bickerstaff brainstem encephalitis is an autoimmune disease. However, each of these criteria fails to fit a substantial proportion of patients, and there is no single test or feature which is diagnostic of Bickerstaff brainstem encephalitis. It is therefore possible that a proportion of cases are due to other causes, such as infection or lymphoma, but remain undiagnosed. It is also possible that there is more than one autoimmune disease that can cause an illness which would currently be diagnosed as Bickerstaff's. There is certainly overlap between Guillain–Barré syndrome, Miller Fisher syndrome and Bickerstaff brainstem encephalitis, as well as other conditions associated with anti-ganglioside antibodies such as chronic ophthalmoplegia with anti-GQ1b antibody.

and the pharyngo-cervico-brachial variant of GBS.

Borna disease is an infectious neurological syndrome of warm-blooded animals, caused by Borna disease viruses 1 and 2 (BoDV-1/2), both of which are members of the species "Mammalian 1 bornavirus". BoDV-1 an 2 cause abnormal behaviour and fatality. Borna disease viruses 1 and 2 are neurotropic viruses and members of the "Bornaviridae" family within the "Mononegavirales" order.

Although Borna disease viruses 1 and 2 are mainly seen as the causative agent of Borna disease in horses and other animals, they are also controversially discussed as human infectious agents and therefore as potential zoonotic agents. The role of BoDV-1 and -2 in human illness is controversial and it is yet to be established whether BoDV-1 or -2 cause any overt disease in humans. However, correlative evidence exists linking BoDV-1/2 infection with neuropsychiatric disorders such as bipolar disorder.

The mode of transmission of BoDV-1/2 is unclear but probably occurs through intranasal exposure to contaminated saliva or nasal secretions. Following infection, individuals may develop Borna disease, or may remain subclinical, possibly acting as a carrier of the virus.

The majority of MVEV infections are sub-clinical, i.e. do not produce disease symptoms, although some people may experience a mild form of the disease with symptoms such as fever, headaches, nausea and vomiting and only a very small number of these cases go on to develop MVE. In fact, serological surveys which measure the level of anti-MVEV antibodies within the population estimate that only 1 in 800-1000 of all infections result in clinical disease.

The incubation period following exposure to the virus is around 1 to 4 weeks. Following infection, a person will have lifelong immunity to the virus. When a patient appears to show MVE symptoms and has been in an MVE-endemic area during the wet season, when outbreaks usually occur, MVE infection must be confirmed by laboratory diagnosis, usually by detection of a significant rise of MVE-specific antibodies in the patient's serum.

Of those who contract MVE, one-quarter die from the disease.

Rocio viral encephalitis is an epidemic flaviviral disease of humans first observed in São Paulo State, Brazil, in 1975. Low-level enzootic transmission is likely continuing in the epidemic zone, and with increased deforestation and population expansion, additional epidemics caused by Rocio virus are highly probable. If migratory species of birds are, or become involved in, the virus transmission cycle, the competency of a wide variety of mosquito species for transmitting Rocio virus experimentally suggest that the virus may become more widely distributed. The encephalitis outbreak in the western hemisphere caused by West Nile virus, a related flavivirus, highlights the potential for arboviruses to cause severe problems far from their source enzootic foci.

The causative Rocio virus belongs to the genus "Flavivirus" (the same genus as the Zika virus) in family Flaviviridae and is closely related serologically to Ilhéus, St. Louis encephalitis, Japanese encephalitis and Murray Valley encephalitis viruses.

Guillain–Barré syndrome can lead to death as a result of a number of complications: severe infections, blood clots, and cardiac arrest likely due to autonomic neuropathy. Despite optimum care this occurs in about 5% of cases.

There is a variation in the rate and extent of recovery. The prognosis of Guillain–Barré syndrome is determined mainly by age (those over 40 may have a poorer outcome), and by the severity of symptoms after two weeks. Furthermore, those who experienced diarrhea before the onset of disease have a worse prognosis. On the nerve conduction study, the presence of conduction block predicts poorer outcome at 6 months. In those who have received intravenous immunoglobulins, a smaller increase in IgG in the blood two weeks after administration is associated with poorer mobility outcomes at six months than those whose IgG level increased substantially. If the disease continues to progress beyond four weeks, or there are multiple fluctuations in the severity (more than two in eight weeks), the diagnosis may be chronic inflammatory demyelinating polyneuropathy, which is treated differently.

In research studies, the outcome from an episode of Guillain–Barré syndrome is recorded on a scale from 0 to 6, where 0 denotes completely healthy, 1 very minor symptoms but able to run, 2 able to walk but not to run, 3 requiring a stick or other support, 4 confined to bed or chair, 5 requiring long-term respiratory support, 6 death.

The health-related quality of life (HRQL) after an attack of Guillain–Barré syndrome can be significantly impaired. About a fifth are unable to walk unaided after six months, and many experience chronic pain, fatigue and difficulty with work, education, hobbies and social activities. HRQL improves significantly in the first year.

Murray Valley encephalitis virus (MVEV) is a zoonotic flavivirus endemic to northern Australia and Papua New Guinea. It is the causal agent of Murray Valley encephalitis (previously known as Australian encephalitis or Australian X disease). In humans it can cause permanent neurological disease or death. MVEV is related to Kunjin virus which has a similar ecology but a lower morbidity rate. Although the arbovirus is endemic to Northern Australia, it has occasionally spread to the southern states during times of heavy rainfall during the summer monsoon season via seasonal flooding of the Murray-Darling river system. These outbreaks can be "...decades apart, with no or very few cases identified in between".

In Western countries, the number of new episodes per year has been estimated to be between 0.89 and 1.89 cases per 100,000 people. Children and young adults are less likely to be affected than the elderly: the risk increases by 20% for every decade of life. Men are more likely to develop Guillain–Barré syndrome than women; the relative risk for men is 1.78 compared to women.

The distribution of subtypes varies between countries. In Europe and the United States, 60–80% of people with Guillain–Barré syndrome have the demyelinating subtype (AIDP), and AMAN affects only a small number (6–7%). In Asia and Central and South America, that proportion is significantly higher (30–65%). This may be related to the exposure to different kinds of infection, but also the genetic characteristics of that population. Miller Fisher variant is thought to be more common in Southeast Asia.

During 1975 and 1976, Rocio virus was responsible for several epidemics of meningoencephalitis in coastal communities in southern São Paulo, Brazil. The outbreaks affected over 1,000 people and killed about 10% of those infected, but apparently responded well to treatment for viral encephalitides. The disease progresses rapidly after onset, with patients dying within 5 days of symptoms first appearing. The disease first presents with fever, headache, vomiting, and conjunctivitis, then progresses to neurological symptoms (confusion, disorientation, etc.) and muscle weakness; about one-third of cases enter a coma, and a third of those patients die, although supportive care such as intensive nursing and symptomatic treatment might reduce the case fatality rate to 4%. Survivors show neurological and psychological after-effects (sequelae) in about 20% of cases.

Bickerstaff brainstem encephalitis is a rare inflammatory disorder of the central nervous system, first described by Edwin Bickerstaff in 1951. It may also affect the peripheral nervous system, and has features in common with both Miller Fisher syndrome and Guillain–Barré syndrome.

In the United States each year approximately 1,000,000 individuals develop herpes zoster. Of those individuals approximately 10-18% develop postherpetic neuralgia.

Less than 10 percent of people younger than 60 develop postherpetic neuralgia after a bout of herpes zoster, while about 40 percent of people older than 60 do.

A person's sex also seems to have some role in the development of autoimmunity; that is, most autoimmune diseases are "sex-related". Nearly 75% of the more than 23.5 million Americans who suffer from autoimmune disease are women, although it is less-frequently acknowledged that millions of men also suffer from these diseases. According to the American Autoimmune Related Diseases Association (AARDA), autoimmune diseases that develop in men tend to be more severe. A few autoimmune diseases that men are just as or more likely to develop as women include: ankylosing spondylitis, type 1 diabetes mellitus, granulomatosis with polyangiitis, Crohn's disease, Primary sclerosing cholangitis and psoriasis.

The reasons for the sex role in autoimmunity vary. Women appear to generally mount larger inflammatory responses than men when their immune systems are triggered, increasing the risk of autoimmunity. Involvement of sex steroids is indicated by that many autoimmune diseases tend to fluctuate in accordance with hormonal changes, for example: during pregnancy, in the menstrual cycle, or when using oral contraception. A history of pregnancy also appears to leave a persistent increased risk for autoimmune disease. It has been suggested that the slight, direct exchange of cells between mothers and their children during pregnancy may induce autoimmunity. This would tip the gender balance in the direction of the female.

Another theory suggests the female high tendency to get autoimmunity is due to an imbalanced X chromosome inactivation. The X-inactivation skew theory, proposed by Princeton University's Jeff Stewart, has recently been confirmed experimentally in scleroderma and autoimmune thyroiditis. Other complex X-linked genetic susceptibility mechanisms are proposed and under investigation.

In 1995, the Food and Drug Administration (FDA) approved the Varicella vaccine to prevent chickenpox. Its effect on postherpetic neuralgia is still unknown. The vaccine—made from a weakened form of the varicella-zoster virus—may keep chickenpox from occurring in nonimmune children and adults, or at least lessen the risk of the chickenpox virus lying dormant in the body and reactivating later as shingles. If shingles could be prevented, postherpetic neuralgia could be completely avoided.

In May 2006 the Advisory Committee on Immunization Practices approved a new vaccine by Merck (Zostavax) against shingles. This vaccine is a more potent version of the chickenpox vaccine, and evidence shows that it reduces the incidence of postherpetic neuralgia. The CDC recommends use of this vaccine in all persons over 60 years old.