Japanese encephalitis

Japanese encephalitis (JE) is one of many viral encephalitides and results from infection with the Japanese encephalitis virus.

Clinical presentation

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. 

Pathology

Japanese encephalitis is caused by the Japanese encephalitis 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. 

Radiographic features

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.

CT

• symmetric or asymmetric bilateral thalamic hypodensities

• may not detect subacute or chronic hemorrhage

MRI

• 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 Japanese encephalitis confers lifelong immunity.

Differential diagnosis

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 Japanese encephalitis 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

Practical points

Radiologists may face a diagnostic challenge when CT/MRI findings of both Japanese encephalitis and neurocysticercosis (NCC) are seen in the same patient ¹.

Theoretically, both Japanese encephalitis and neurocysticercosis share some common epidemiological factors; and in both conditions, pig acts as the intermediate carrier. Studies show that the occurrence of Japanese encephalitis and neurocysticercosis in the same patient is not just a coincidence, albeit, neurocysticercosis predisposes a person to Japanese encephalitis 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.