People should only be diagnosed with encephalitis if they have a decreased or altered level of consciousness, lethargy, or personality change for at least twenty-four hours without any other explainable cause. Diagnosing encephalitis is done via a variety of tests:

- Brain scan, done by MRI, can determine inflammation and differentiate from other possible causes.

- EEG, in monitoring brain activity, encephalitis will produce abnormal signal.

- Lumbar puncture (spinal tap), this helps determine via a test using the cerebral-spinal fluid, obtained from the lumbar region.

- Blood test

- Urine analysis

- Polymerase chain reaction (PCR) testing of the cerebrospinal fluid, to detect the presence of viral DNA which is a sign of viral encephalitis.

The diagnosis of limbic encephalitis is extremely difficult and it is usual for the diagnosis to be delayed for weeks. The key diagnostic test (detection of specific auto-antibodies in cerebrospinal fluid) is not routinely offered by most immunology laboratories. Some of the rarer auto-antibodies (e.g., NMDAR) have no commercially available assay and can only be measured by a very small number of research laboratories worldwide, further delaying diagnosis by weeks or months. Most patients with limbic encephalitis are initially diagnosed with herpes simplex encephalitis, because the two syndromes cannot be distinguished clinically. HHV-6 (human herpes virus 6) encephalitis is also clinically indistinguishable from limbic encephalitis.

There are two sets of diagnostic criteria used. The oldest are those proposed by Gultekin "et al." in 2000.

A revised set of criteria were proposed by Graus and Saiz in 2005.

The main distinction between the two sets of criteria is whether or not the detection of a paraneoplastic antibody is needed for diagnosis.

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.

The main antibodies within this group are those against Hu, Ma2, CV2, amphiphysin and Ri. The syndrome of anti-Ma2 encephalitis may be clinically mistaken for Whipple's disease.

Japanese encephalitis is diagnosed by commercially available tests detecting JE virus-specific IgM antibodies in serum and /or cerebrospinal fluid, for example by IgM capture ELISA.

JE virus IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. Therefore, positive IgM antibodies occasionally may reflect a past infection or vaccination. Serum collected within 10 days of illness onset may not have detectable IgM, and the test should be repeated on a convalescent sample. For patients with JE virus IgM antibodies, confirmatory neutralizing antibody testing should be performed.

Confirmatory testing in the US is only available at CDC and a few specialized reference laboratories. In fatal cases, nucleic acid amplification, and virus culture of autopsy tissues can be useful. Viral antigen can be shown in tissues by indirect fluorescent antibody staining.

Current or previous infection can be detected through a blood test. However, some authors note that such complement-fixation tests are insensitive and should not be used for diagnosis. Dr. Clare A. Dykewicz, "et al." state,

Clinical diagnosis of LCM can be made by the history of prodrome symptoms and by considering the period of time before the onset of meningitis symptoms, typically 15–21 days for LCM.

Pathological diagnosis of congenital infection is performed using either an immunofluorescent antibody (IFA) test or an enzyme immunoassay to detect specific antibody in blood or cerebrospinal fluid. A PCR assay has been recently developed which may be used in the future for prenatal diagnosis; however, the virus is not always present in the blood or CSF when the affected child is born." Diagnoses is subject to methodological shortcomings in regard to specificity and sensitivity of assays used. For this reason, LCMV may be more common than is realized.

Another detection assay is the reverse transcription polymerase chain reaction (RT-PCR) tests which may detect nucleic acids in the blood and cerebrospinal fluid.(CSF) Virus isolation is not used for diagnosis in most cases but it can be isolated from the blood or nasopharyngeal fluid early in the course of the disease, or from CSF in patients with meningitis. LCMV can be grown in a variety of cell lines including BHK21, L and Vero cells, and it may be identified with immuno-fluorescence. A diagnosis can also be made by the intracerebral inoculation of blood or CSF into mice.

There have been several proposed diagnostic criteria for Encephalitis Lethargica. One, which has been widely accepted, includes an acute or subacute encephalitic illness where all other known causes of encephalitis have been excluded. Another diagnostic criterion, suggested more recently,says that the diagnosis of Encephalitis Lethargica "may be considered if the patient’s condition cannot be attributed to any other known neurological condition and that they show the following signs: influenza-like signs; hypersomnolence (hypersomnia), wakeability, opthalmoplegia (paralysis of the muscles that control the movement of the eye), and psychiatric changes."

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.

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.

The TBE virus may be present in a seronegative strain or subtype. In such cases a marker for TBE infection is elevated IFN-g in CSF.

Viral antigen can usually be found in brain tissue. Serological testing can also be performed with an ELISA.

As in humans, the sensitivity of testing methods for rodents contributes to the accuracy of diagnosis. LCMV is typically identified through serology. However, in an endemically infected colony, more practical methods include MAP (mouse antibody production) and PCR testing. Another means of diagnosis is introducing a known naïve adult mouse to the suspect rodent colony. The introduced mouse will seroconvert, allowing use of immunofluorescence antibody (IFA), MFIA or ELISA to detect antibodies.

A number of various diseases may present with symptoms similar to those caused by a clinical West Nile virus infection. Those causing neuroinvasive disease symptoms include the enterovirus infection and bacterial meningitis. Accounting for differential diagnoses is a crucial step in the definitive diagnosis of WNV infection. Consideration of a differential diagnosis is required when a patient presents with unexplained febrile illness, extreme headache, encephalitis or meningitis. Diagnostic and serologic laboratory testing using polymerase chain reaction (PCR) testing and viral culture of CSF to identify the specific pathogen causing the symptoms, is the only currently available means of differentiating between causes of encephalitis and meningitis.

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.

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.).

Previous methods of diagnosis included HI, complement fixation, neutralization tests, and injecting the serum of infected individuals into mice. However, new research has introduced more efficient methods to diagnose KFDV. These methods include: nested RT-PCR, TaqMan-based real-time RT-PCR, and immunoglobin M antibodies detection by ELISA. The two methods involving PCR are able to function by attaching a primer to the NS-5 gene which is highly conserved among the genus to which KFDV belongs. The last method allows for the detections of anti-KFDV antibodies in patients.

Preliminary diagnosis is often based on the patient's clinical symptoms, places and dates of travel (if patient is from a nonendemic country or area), activities, and epidemiologic history of the location where infection occurred. A recent history of mosquito bites and an acute febrile illness associated with neurologic signs and symptoms should cause clinical suspicion of WNV.

Diagnosis of West Nile virus infections is generally accomplished by serologic testing of blood serum or cerebrospinal fluid (CSF), which is obtained via a lumbar puncture. Initial screening could be done using the ELISA technique detecting immunoglobulins in the sera of the tested individuals.

Typical findings of WNV infection include lymphocytic pleocytosis, elevated protein level, reference glucose and lactic acid levels, and no erythrocytes.

Definitive diagnosis of WNV is obtained through detection of virus-specific antibody IgM and neutralizing antibodies. Cases of West Nile virus meningitis and encephalitis that have been serologically confirmed produce similar degrees of CSF pleocytosis and are often associated with substantial CSF neutrophilia.

Specimens collected within eight days following onset of illness may not test positive for West Nile IgM, and testing should be repeated. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavavirus infection and is not by itself evidence of an acute West Nile virus infection.

If cases of suspected West Nile virus infection, sera should be collected on both the acute and

convalescent phases of the illness. Convalescent specimens should be collected 2–3 weeks after acute specimens.

It is common in serologic testing for cross-reactions to occur among flaviviruses such as dengue virus (DENV) and tick-borne encephalitis virus; this necessitates caution when evaluating serologic results of flaviviral infections.

Four FDA-cleared WNV IgM ELISA kits are commercially available from different manufacturers in the U.S., each of these kits is indicated for use on serum to aid in the presumptive laboratory diagnosis of WNV infection in patients with clinical symptoms of meningitis or encephalitis. Positive WNV test results obtained via use of these kits should be confirmed by additional testing at a state health department laboratory or CDC.

In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry, and virus culture of autopsy tissues can also be useful. Only a few state laboratories or other specialized laboratories, including those at CDC, are capable of doing this specialized testing.

Most individuals with HSE show a decrease in their level of consciousness and an altered mental state presenting as confusion, and changes in personality. Increased numbers of white blood cells can be found in patient's cerebrospinal fluid, without the presence of pathogenic bacteria and fungi. Patients typically have a fever and may have seizures. The electrical activity of the brain changes as the disease progresses, first showing abnormalities in one temporal lobe of the brain, which spread to the other temporal lobe 7–10 days later. Imaging by CT or MRI shows characteristic changes in the temporal lobes (see Figure). Definite diagnosis requires testing of the cerebrospinal fluid (CSF) by a lumbar puncture (spinal tap) for presence of the virus. The testing takes several days to perform, and patients with suspected Herpes encephalitis should be treated with acyclovir immediately while waiting for test results.

First and foremost is high level of clinical suspicion especially in young adults showing abnormal behavior as well as autonomic instability. The person may have alteration in level of sensorium and seizures as well during early stage of the illness. Clinical examination may further reveal delusions and hallucinations

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.

The diagnosis is considered when a child with congenital rubella develops progressive spasticity, ataxia, mental deterioration, and seizures. Testing involves at least CSF examination and serology. Elevated CSF total protein and globulin and elevated rubella antibody titers in CSF and serum occur. CT may show ventricular enlargement due to cerebellar atrophy and white matter disease. Brain biopsy may be necessary to exclude other causes of encephalitis or encephalopathy. Rubella virus cannot usually be recovered by viral culture or immunohistologic testing.

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.

Viral encephalitis is a type of encephalitis caused by a virus.

It is unclear if anticonvulsants used in people with viral encephalitis would prevent seizures.

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.

Arbovirus encephalitis refers to encephalitis that is caused by arbovirus infection.

There are many types of arboviral encephalitides found in the United States.

Examples include:

- California encephalitis

- Japanese encephalitis

- St. Louis encephalitis

- Tick-borne encephalitis

- West Nile fever

- Murray Valley encephalitis

The diagnosis of chickenpox is primarily based on the signs and symptoms, with typical early symptoms followed by a characteristic rash. Confirmation of the diagnosis is by examination of the fluid within the vesicles of the rash, or by testing blood for evidence of an acute immunologic response.

Vesicular fluid can be examined with a Tzanck smear, or by testing for direct fluorescent antibody. The fluid can also be "cultured", whereby attempts are made to grow the virus from a fluid sample. Blood tests can be used to identify a response to acute infection (IgM) or previous infection and subsequent immunity (IgG).

Prenatal diagnosis of fetal varicella infection can be performed using ultrasound, though a delay of 5 weeks following primary maternal infection is advised. A PCR (DNA) test of the mother's amniotic fluid can also be performed, though the risk of spontaneous abortion due to the amniocentesis procedure is higher than the risk of the baby's developing fetal varicella syndrome.