Viruses that tend to infect the central nervous system are usually neurotropic. The specific diagnosis of viral encephalitis requires PCR, serum biomarkers, or virus culture which may not available at acute setting, while clinical and routine laboratory findings are often non-specific. Imaging study is important in confirming the involvement of CNS by viral infection. MRI is much sensitive than CT in revealing acute brain and spinal cord lesions. The combination with gadolinium-based contrast medium and advanced sequences such as diffusion weighted imaging as well as MR spectroscopy could help early detection of lesion locations and thus prompt early antiviral treatment until proven otherwise. Imaging approaches to viral CNS infection depends on the knowledge of the patient conditions, such as ages, host immunity, clinical presentations (acute or subacute), geographic considerations and endemic incidence. The distribution of the lesions in the brain may sometimes suggest specific virus infection. This lecture will introduce the basic concepts and strategy of MR imaging approaches of common neurotropic viral encephalitis.

Neurotropic viruses have neuroinvasion property by the presence of virion surface glycoproteins. Common neurotropic viruses including the DNA or RNA types are herpes virus, varizella-zoster virus, cytomegalovirus, measles virus, influenza virus, rabies virus, JC virus, arbovirus, enterovirus, and retroviruses. Some emerging viruses such as Hendra and Nipah viruses, West Nile virus, enterovirus 71, also cause encephalopathy/encephalitis. Neurotropic viruses can cause acute or subacute neurological syndromes, depending on the virulence and cell levels being involved (figure 1)

Viral encephalitis may surge during outbreak of infection in different geographic distribution which may offer hints to the interpretation of neuroimaging. For example, West Nile encephalitis occurs in Middle East, Australia and Africa but fast spreading to North American in 1999. Hendra virus was found in Australia while Nipah virus caused endemic in Malaysia and Singapore also in 1999. Mosquito-borne arboviruses such as Japanese encephalitis virus and Dengue fever are prevalent in south Asia regions during the summer. Murray Valley encephalitis has similar clinical and imaging features to Japanese encephalitis while the former occurred in Australia (also called Australian encephalitis) and the latter in south Asia. In 1998, the epidemic enterovirus type 71 caused hundred more mortality due to irreversible rhombencephalitis in Taiwan. Other more well-known neurotropic viruses, such as herpes simplex viruses, varicella zoster virus, influenza viruses, and JC virus are worldwide.

In human immunodeficiency virus infection or in patients under immunomodulation therapy (Natalizumab for multiple sclerosis) and insufficient adaptive immune response, a secondary infection by John Cunningham virus (JCV) presenting with a catastrophic progressive multifocal leukoencephalopathy can be seen on T2-weighted MRI where mass effect is minimal and contrast enhancement is negligible. Patients with defective innate immune response subject to virus infection such as Human herpesvirus 1 and 6 encephalitis. The latter occur most often in organ transplant and lymphoproliferative disorders with immunosuppression. Tissue immune response to viral infection plays important role in term of acute and subacute presentation of clinical symptoms. For example, low grade inflammation is commonly seen in HIV infection while exaggerated inflammatory response can lead to a feature of the immune reconstitution inflammatory syndrome (IRIS).

The neuropathological features of viral encephalitis vary, depending on the specific cell involved. For examples, herpesvirus, rabies, and Japanese encephalitis virus more often involve neurons (gray matter) while JC virus, rubella, and measles virus affect astrocytes (white matters). Viruses that specifically infect oligodendroglia include measles virus that leads to subacute sclerosing panencephalitis, and JC virus that causes progressive multifocal leukoencephalopathy. HIV leads to microglia infestation.

There are some unique, though not specific, clinical/radiologic features in certain neurotropic viral encephalitis. For examples, mild encephalitis with a reversible splenial lesions (MERS) caused by influenza A and B viruses (figure 2), acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) and acute necrotizing encephalopathy (ANE) by influenza A and human herpes virus 6, rhombencephalitis by enterovirus type 71 (figure 3), and fulminant hemorrhagic and necrotizing meningoencephalitis in herpes simplex virus type 1 in immunocompetent patients, type 2 in neonates and children, In Japanese encephalitis virus (JEV), encephalitic involvement of dorsal thalami and substantia nigra along with clinical presentation of seizure and later appearance of movement disorder is typical.

Some non-viral encephalopathy such as paraneoplastic syndrome (limbic encephalitis with antibodies to intraneuronal antigens in small cell lung cancer and anti-NMDA receptor encephalopathy in patient with ovarian cancer) is indistinguishable clinically from herpes encephalitis or human herpes virus 6 encephalitis. Postinfectious or post-vaccine encephalomyelitis (ADEM) add more difficulty in acute assessment of viral encephalitis patients.