PMC8012135_01
(a, b) MRI brain of Case 1 showing bilateral T2 hyperintensities of the subcortical white matter of all the brain and splenium of the corpus callosum with associated diffusion restriction and signal change in thalami and pons. (c) Case 2: normal MRI brain on acute presentation. (d) Repeat MRI brain 50 days later showing bilateral T2 hyperintensity of the basal ganglia and parasagittal frontal lobes, anterior limb of the left internal capsule, insula, and subcortical white matter regions.
CRINM2021-6658000.001.jpg
PMC8012135_02_CRINM2021-6658000.001.jpg
fig1
MRI brain (Figure 1(d)) showed asymmetric bilateral high-signal lesions in the basal ganglia and the subcortical white matter in the frontal and temporal lobes, with involvement of the left internal capsule and left hippocampus. MRI orbits and spine, repeated CSF analysis, MOG antibodies (Table 1), and EEG were unremarkable.
PMC8012135_02
(a, b) MRI brain of Case 1 showing bilateral T2 hyperintensities of the subcortical white matter of all the brain and splenium of the corpus callosum with associated diffusion restriction and signal change in thalami and pons. (c) Case 2: normal MRI brain on acute presentation. (d) Repeat MRI brain 50 days later showing bilateral T2 hyperintensity of the basal ganglia and parasagittal frontal lobes, anterior limb of the left internal capsule, insula, and subcortical white matter regions.
CRINM2021-6658000.001.jpg
PMC8012135_02_CRINM2021-6658000.001.jpg
fig1
MRI brain (Figure 1(d)) showed asymmetric bilateral high-signal lesions in the basal ganglia and the subcortical white matter in the frontal and temporal lobes, with involvement of the left internal capsule and left hippocampus. MRI orbits and spine, repeated CSF analysis, MOG antibodies (Table 1), and EEG were unremarkable.