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. 2022 Dec 15;22:486. doi: 10.1186/s12883-022-03025-1

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — A-D F/64, widespread leukoencephalopathy with frontal lobe predominance and corticomedullary junction DWI high intensity, involving corpus callosum and external capsule. E–F F/55, patchy frontal lobe leukoencephalopathy with corticomedullary junction DWI high intensity. G-H F/59, frontal lobe and external capsule DWI high intensity with splenium of corpus callosum lesions. I-J M/61, symmetrical lesions on brachium pontis and DWI high intensity. K-L F/54, asymmetrical distribution of frontal lobe leukoencephalopathy. M–N F/45, widespread leukoencephalopathy with grey matter involvement, left predominance. O-P F/54, progression of leukoencephalopathy after 4 years follow-up. Q-R F/51, extensive increase of corticomedullary junction DWI high signal after 2 months follow up, while no change in FLAIR sequence. (FLAIR: A, B, E, G, K, O, P; T2-weighted: I, M; DWI: C, D, F, H, J, L, N, Q, R)