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Japanese encephalitis (JE) is one of many viral encephalitides and results from infection with the Japanese encephalitis virus.
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At the onset of the disease patients present with severe rigors, fevers and headache. As it progresses to the acute encephalitic stage, meningo-encephalitic symptoms such as neck rigidity, cachexia, hemiparesis and convulsions become prevalent.
JE is caused by the JE virus, a single-stranded RNA flavivirus. Domestic pigs and wild birds are reservoirs for the virus, which is spread by mosquitoes. It is prevalent in India, Southeast Asia and East Asia 5.
Bilateral thalamic involvement is classical regardless of CT or MR imaging. Other areas may be involved are midbrain, pons, cerebellum, basal ganglia, cerebral cortex and spinal cord. However, imaging within 3-4 days of the onset of disease may not reveal hemorrhagic lesions.
- symmetric or asymmetric bilateral thalamic hypodensities
- may not detect subacute or chronic hemorrhage
- parenchymal edema in affected regions:
- DWI: variable restricted diffusion
- T1: low signal
- T2/FLAIR: high signal
- if hemorrhage is present:
- GRE: patchy blooming
Treatment and prognosis
Only supportive treatment is available. Higher mortality rate in children. Vaccination may be preventive in endemic areas, although infection with JE confers lifelong immunity.
Other infectious causes that can cause a similar imaging pattern include:
- other flavivirus encephalitides (e.g. Murray Valley encephalitis, West Nile fever, dengue encephalitis)
- eastern equine encephalitis
herpes simplex encephalitis
- it is important to differentiate JE from herpes simplex encephalitis, as the latter can be treated with antivirals
- although typically temporal lobe involvement
Causes of T2 hyperintense basal ganglia lesions can also be considered.
Hemorrhagic thalamic lesions can also be a result of:
- deep cerebral vein thrombosis
- basilar artery thrombosis: rarely tentorial herniation following head injury may cause thalamic infarcts
Radiologists may face a diagnostic challenge when CT/MRI findings of both JE and neurocysticercosis (NCC) are seen in the same patient.1
Theoretically, both JE and NCC share some common epidemiological factors; and in both conditions, pig acts as the intermediate carrier. Studies show that the occurrence of JE and NCC in the same patient is not just a coincidence, albeit, NCC predisposes a person to JE infection. Keeping in mind this fact may help radiologists and clinicians in proper and early management of the patient who present with mixed clinical scenario.
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- 3. Kumar S, Misra UK, Kalita J et-al. MRI in Japanese encephalitis. Neuroradiology. 1997;39 (3): 180-4. Pubmed citation
- 4. Prakash M, Kumar S, Gupta RK. Diffusion-weighted MR imaging in Japanese encephalitis. J Comput Assist Tomogr. 2004;28 (6): 756-61. Pubmed citation
- 5. Mehra, Shibani, and U. C. Garga. "Role of imaging in herpes and Japanese encephalitis–Two cases and review of literature." Journal, Indian Academy of Clinical Medicine 13.4 (2012): 339.
- Handique SK, Barkataky N. MR imaging in biphasic Japanese encephalitis. AJNR Am J Neuroradiol. 2008;29 (3): E3. doi:10.3174/ajnr.A0862 - Pubmed citation