Temporal lobe involvement in Japanese encephalitis: problems in differential diagnosis

Abstract

Background and purpose: On MR imaging and CT, Japanese encephalitis (JE) shows lesions in the thalami, substantia nigra, basal ganglia, cerebral cortex, cerebellum, brain stem, and white matter, whereas temporal lobe involvement is characteristically seen in Herpes simplex encephalitis (HSE). Temporal lobe involvement in JE may cause problems in differentiating it from HSE. We undertook this study to show the temporal lobe involvement pattern in JE and highlight differentiating features from temporal lobe involvement in HSE.

Methods: Sixty-two patients with JE underwent CT or MR imaging or both. MR imaging was done in 53 and CT in 53. The diagnosis of JE was confirmed by cerebrospinal fluid (CSF) IgM enzyme-linked immunosorbent assay.

Results: Eleven (17.7%) patients showed temporal lobe involvement with abnormal MR imaging in all. All the patients showed hippocampal involvement. Two patients showed extension of lesions into the amygdala and uncus with insular involvement in 1. The rest of the temporal lobe was spared. All patients had thalamic and substantia nigra involvement with basal ganglia involvement in 7. Six of 9 CT scans were abnormal and the temporal lesions were seen in 2.

Conclusions: The temporal lobe involvement pattern is fairly characteristic and mostly involves the hippocampus, usually sparing the rest of the temporal lobe. This and the concurrent involvement of the thalami, substantia nigra (SN), and basal ganglia allow differentiation from HSE. However, if the temporal lobe involvement is more severe, laboratory tests may be the only way to differentiate it from HSE, and it may be prudent to start antiviral therapy in the interim period.

Fig 1.

Patient 3. Fourteen-year-old boy. A, T2-weighted axial image: bilateral thalamic lesions (black arrows). Note left hippocampal tail involvement (white arrow). B, T2-weighted coronal image shows bilateral thalamic (black arrows), substantia nigra (white arrows), and left hippocampal body involvement (large white arrow). C, Image more posterior than B shows hippocampal tail involvement on the left side (arrow). D, Axial T2-weighted image shows bilateral substantia nigra lesions (arrows).

Fig 2.

Patient 4. Eighteen-year-old man. A, Axial T2-weighted image. Lesions are seen in both caudate heads and thalami (arrows). B, Coronal T2-weighted image shows bilateral hippocampal body involvement (arrows). C, Axial T2-weighted image shows the lesions involving the hippocampal tails (arrows). Note lesions in the caudate heads (white arrowheads). D, Axial T2-weighted image done 3 months after C shows resolution of the hippocampal tail lesions (arrows). The caudate head lesions have resolved (white arrowheads). E, CT scan done in the acute stage shows brain swelling and bilateral subtle thalamic lesions (arrows). The hippocampal and basal ganglia involvement was not apparent on this CT scan (not shown in the figure). F, Follow-up CT scan, done 3 months after E, shows reduction in the edema and resolution of thalamic lesions.

Fig 3.

Patient 7. Fifty-year-old woman. A, Axial T2-weighted image shows left hippocampal head and body involvement (arrow). There is extension into the amygdala. Note bilateral substantia nigra lesions (large white arrow). B, Axial T2-weighted image shows bilateral thalamic and basal ganglia lesions (black arrows). Note left-sided insular involvement (white arrow).

Fig 4.

Patient 5. Twenty-nine-year-old man. A, Coronal T2-weighted image shows bilateral hippocampal body involvement (black arrows). Note bilateral thalamic and substantia nigra involvement (white arrows). B, Axial T2-weighted image shows bilateral hippocampal tail involvement (arrows). C, Axial CT scan done at the same time as A and B shows hypoattenuated left mesial temporal lobe lesion. Note resemblance to Herpes simplex virus encephalitis. The right-sided involvement is not seen. The thalamic and substantia nigra lesions are not visible (not shown in the figure). D and E, Follow-up axial and coronal T2-weighted MR done 2.5 months after A and B shows clearing up of the lesions in thalamus, substantia nigra, and hippocampus.