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. 2023 Feb 4;9(2):e13470. doi: 10.1016/j.heliyon.2023.e13470

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© 2023 The Authors. Published by Elsevier Ltd.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 1 — MRI of the head and spinal cord. (A–D) On the 2nd day after admission. (A) the T2WI sequence showed hyperintensity in the left thalamus; (B) the FLAIR sequence showed hyperintensity in the left thalamus; (C and D) the FLAIR sequence showed that there was no obvious abnormal signal in the temporal lobe and semi-oval centers; (E–I). On the 6th day after admission. (E) the T2WI sequence showed a significant decrease in left thalamus hyperintensity compared with A; (F) the FLAIR sequence showed multiple asymmetric abnormally hyperintensity in bilateral temporal and occipital lobes at the temporal lobe level; (G) the FLAIR sequence showed multiple asymmetric abnormally hyperintensity in bilateral semi-oval centers; (H) the T2WI sequence showed abnormally hyperintensity of C3–C7 in the cervical spinal cord; (I) the T2WI sequence showed abnormally hyperintense signals in the conus spinal cord; (J–N) 2 months after illness. (J) the T2WI sequence showed dissipation of the left thalamic lesion; (K) the axial FLAIR sequence showed bilateral temporal lobe level lesion dissipation; (L) the FLAIR sequence showed significant dissipation of bilateral semi-oval centers lesion; (M) the T2WI sequence showed that the cervical medullary lesion was basically dispersed. (N) the T2WI sequence showed that the conus lesions were basically dispersed.