Figure 1 Initial brain imaging (A–C) patient 1; (D–F) patient 2; (G–I) patient 3; (J–L) patient 4; and (M) patient 2. Initial brain imaging (A–C) patient.

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Figure 1 Initial brain imaging (A–C) patient 1; (D–F) patient 2; (G–I) patient 3; (J–L) patient 4; and (M) patient 2. Initial brain imaging (A–C) patient 1; (D–F) patient 2; (G–I) patient 3; (J–L) patient 4; and (M) patient 2. Brain fluid-attenuated inversion recovery (FLAIR) MRI performed on admission (A–C) revealed abnormally high intensity at the dorsal pons, bilateral insular cortex, and subcortical region in patient 1. According to FLAIR MRI, patient 2 and patient 4 had similar brain lesions, including abnormalities around the inferior horn of the lateral ventricle (D, J) and diffuse high intensity in the deep white matter of the frontotemporoparietal regions (E, K). These lesions are mainly confined to the white matter, as revealed by the relative sparing of the cortex, and are enhanced by gadolinium administration in T1-weighted MRI (F, L). In contrast, FLAIR MRI of patient 3 revealed patchy lesions in the subcortical area of the left temporal lobe (G) and in the basal ganglion (H). Contrast-enhanced FLAIR MRI revealed hyperintense lesions along the left central sulcus (I). Sagittal T2-weighted images depict an inhomogeneously hyperintense spinal cord, stretching from the cervico-occipital junction to the thoracic cord region (M). Yusuke Sakiyama et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e143 © 2015 American Academy of Neurology