A 12-year-old male presented with severe headache, high grade fever with chills and rigors, and convulsions, for the last 7 days. His CSF picture was suggestive of viral meningitis.
Imaging findings on T2W and FLAIR images include heterogeneous hyperintensity involving both thalami (Fig 1, 3) and the pons (Fig 2, 3). On T1W images both thalami and the pons appear heterogeneously hypointense (Fig. 4, 5). These areas show restricted diffusion on DWI and corresponding ADC. (Fig. 6, 7). Both thalami and the pons are enlarged.
Japanese encephalitis (JE) is a primary viral encephalitis caused by the Japanese encephalitis virus. The Japanese encephalitis virus is an RNA Flavi virus. It is transmitted by its vector culex mosquito. Its virus reservoirs are domestic pigs and wild birds. Japanese encephalitis is mainly prevalent in Southeast Asia, including Japan, Korea, Thailand, and India. In most temperate areas of Asia, Japanese encephalitis virus is transmitted mainly during the warm season. In tropics and subtropics, transmission occurs during the rainy season and in rice-cultivating regions [1-3].
Symptoms include high grade fever, malaise, headache, altered mental status and convulsion. It usually occurs in a monophasic pattern in which the patient gradually recovers with or without persistent signs of neurological injury. A biphasic pattern of Japanese encephalitis has been encountered in which there is a relapse of symptoms within a few days or weeks after recovery from the early phase [1, 2, 4, 5].
Laboratory diagnosis of Japanese encephalitis is done by testing serum or cerebrospinal fluid (CSF) to detect virus-specific Ig M antibodies. Radiological diagnosis is made by its characteristic findings on MRI of the brain. Involvements of bilateral thalami is the most frequent and characteristic finding. On T1 weighted images it shows low signal, on T2 weighted and on FLAIR images it shows high signal, and on Diffusion Weighted images it shows restricted diffusion. On GRE it may show patchy areas of blooming if haemorrhage is present, which occurs 4 to 5 days after infection. Other areas of the brain may be involved, such as the basal ganglia, brain stem, cerebellum, cerebral cortex, spinal cord and substantia nigra. While clinical presentation and CSF findings are non specific and suggestive of meningitis, the MRI findings would be consistent with Japanese encephalitis in the setting of a patient who presents in an endemic area. In areas where it is uncommon, for example in Europe, the fact that MRI findings are very suggestive of Japanese encephalitis may not be apparent to someone who has not encountered it before [1-5].
Prognosis is poor with a high grade of mortality. The mortality among those with encephalitis is as high as 30%.
Safe and effective Japanese encephalitis vaccines are available to prevent disease. In endemic areas, vaccinations are given providing life long immunity. There is no specific antiviral treatment or cure available for Japanese Encephalitis. Treatment is symptomatic, like for fever and convulsion. Other treatment consists of supportive therapy to stabilize the patient.
Differential Diagnosis List
Viral infection- Rabies
Bilateral Thalamic infarcts
Inborn error of metabolism - wilson's disease
Metabolic disease-Reye's syndrome.
Mitochondrial disease-Leigh syndrome.
Leukodystrophies- Krabbe's disease.