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. 2024 Oct 11;19:376. doi: 10.1186/s13023-024-03365-w

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© The Author(s) 2024

Open Access This 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 — Brain MRI for our patients. Patient 1 (1 A): MRI showed bilateral underdeveloped insula, frontal, temporal and occipital lobes, microgyria, decreased white-matter volume, dilated bilateral lateral ventricles, bilateral symmetrical T2-weighted imaging (T2WI) multiple hyperintense lesions in the basal ganglia, thalamus and lenticular nucleus (a) and a thin corpus callosum (b); Patient 2 (1B): MRI showed frontal subdural fluid, bilateral hemispheric brain atrophy, multiple hyperintense lesions in the basal ganglia, globus pallidus, thalamus, midbrain and cerebral peduncles (a), and a thin corpus callosum (b); Patient 4 (1 C): Brain MRI revealed hyperintensity of the bilateral basal ganglia on symmetrical T2-weighted imaging (T2WI) (a) and a thin corpus callosum (b)