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and MRI demonstrates a higher diagnostic value than in poor clinical outcomes. [13,18] A significantly higher
CT, especially when assessing site, range, quantity, proportion of abnormal CT scans and abnormal MRI
and extent of infection. Thalamic changes, especially has been reported when evaluating NCC/JE-coinfected
bilateral involvement, could be used to help diagnosis lesions. [18] JE in association with cerebral venous sinus
JE in endemic areas. thrombosis has also been reported with the help of MRI
and MR venography. [19]
Lesions can also be observed in the substantia
nigra, brain stem, cerebellum, cerebral cortex, and In this study, 65 patients took MRI examination in
white matter. [8-10] One study reported changes in the 92 patients. Thirty patients (46.15%) presented with
thalamus (94%), basal ganglia (35.5%), midbrain (58%), inflammatory lesions between 2 and 32 days after
cerebellum (25.8%), pons (19%), and cerebral onset, 3 patients (10.00%) presented in the initial
cortex (19%) on MRI. MRI lesions are generally phase, 19 patients (63.63%) in the acute phase, and
[8]
hypointense on T1 and hyperintense on T2 and FLAIR 8 patients (26.67%) in convalescence. Handique [15] has
images. FLAIR is the most useful sequence for detecting reported 90.00% MRI sensitivity during the 1st week of
lesions and defining the extent of supratentorial JE infection. However, in this study, 13 of 30 (43.33%)
lesions. On FLAIR images, cerebral lesions can be patients presented with lesions on MRI during the
better observed, but T2-weighted imaging is better for 1st week of JE infection. Our patients were first treated
evaluating the midbrain and brain stem. [11] Thalamic at other hospitals, and some patients were too ill for
lesions may demonstrate mixed intensity on T1 and T2 early examination, so their MRI examinations were
imaging in the subacute phase, which may be suggestive not timely, which may explain the low sensitivity in
of hemorrhagic changes. The involvement of temporal this study.
[12]
lobe has also been observed in some studies, [8,13,14] but
all reported patients also demonstrated involvement However, this study does show changes in the thalamus
of the thalamus and substantia nigra. [14] Temporal lobe (93.33%), basal ganglia (36.67%), hippocampus (33.33%),
involvement is fairly characteristic and mostly involves mid-brain (33.33%), pons (3.33%), and cerebral cortex
the hippocampus, usually sparing the rest of the (16.67%) on MRI [Figure 1]. Except for one patient, all
temporal lobe. Because JEV takes a hematogenous route patients demonstrated hippocampal involvement on
during the invasion and infects the blood supply in parts MRI that was accompanied by thalami involvement. The
of the thalamus, cerebral peduncles, hippocampus, and gray matter areas of the brain, including the thalamus
uncus, [14] this may explain concurrent involvement in and hippocampus, were primarily affected by JEV on
the medial temporal lobe along with the thalami and autopsy. [20] These areas are associated with increases in
substantia nigra. The hippocampal involvement was activated and phagocytic microglia. Srivastava et al.
[21]
[22]
most commonly in the tail and body, occasionally in have reported that JEV RNA load in different brain
the head and amygdala. [14,15] The presence of typical regions of rat with higher affinity of JEV to thalamus
JE lesions in the thalami, substantia nigra, and basal and mid brain compared to other regions. These may
ganglia, along with temporal lobe involvement, explain the commonly affected areas observed on
may help differentiate JE from herpes simplex virus imaging. Three patients were examined using both
encephalitis (HSE). Sawlani [11] has reported that MRI CT and MRI, but only MRI revealed lesions. One MRI
techniques such as FLAIR and diffusion weighted reexamination reported lesion reduction following
imaging (DWI) can be used to evaluate HSE and JE. DWI treatment, while another reported enlarged lesions. That
and apparent diffusion coefficients mapping (ADC) can may be the first study that used early MRI examination
differentiate cytotoxic edema from vasogenic edema. [16] and did not observe the peak of brain injury. Three
Significantly restricted diffusion and low average ADC patients showed inflammatory lesions in combination
values have been observed in the acute phase lesions with ischemic infarction on MRI. All of these patients
in HSE patients, whereas JE lesions do not show demonstrated risk factors that are also shared with
restricted diffusion or significantly low ADC values severe encephalitis, such as hypertension and age.
in the acute phase (whereas chronic phase lesions Basumatary et al. have reported that changes on MRI
[4]
show restricted diffusion and high ADC values). [11] or CT in combination with thalamic involvement are
However, Prakash et al. [17] have reported restricted significantly related with dystonia. However, other
diffusion and low ADC values in the acute phase JE. clinical symptoms, such as behavioral abnormalities,
Coinfection of neurocysticercosis (NCC) and JE has seizure, coma level, and death, do not demonstrate a
also been observed by MRI and CT, which may result significant correlation with radiological abnormalities.

Neuroimmunol Neuroinflammation | Volume 1 | Issue 1 | June 2014 31