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CSVD was evaluated using an age-related white matter change rating scale, Fazekas scale, enlarged perivascular spaces grading scale, lacunar infarction scale, Microbleed Anatomical Rating Scale, global cortical atrophy scale, and small-vessel disease score. Factors associated with MRI lesions, including sex, clinical subtype, disease severity, disease burden, genotype, and biomarkers, were also analyzed.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Of 71 patients, 16 (22.5%) experienced ischemic stroke. The incidences of lacunar infarctions, white matter hyperintensities, and cerebral microbleeds were 55%, 62%, and 33%, respectively. The abnormal MRI group had later disease onset, longer disease duration, and a higher Mainz Severity Score Index (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) than the normal MRI group. Patients with more severe clinical phenotypes also had higher CVSD-related scores. Sex and <jats:italic>GLA<\/jats:italic> mutational type were not closely associated with brain MRI lesions. Of the disease markers, the Mainz Severity Score Index and plasma globotriaosylsphingosine (Lyso-Gb<jats:sub>3<\/jats:sub>) were closely correlated with the majority of the MRI scores, whereas \u03b1-galactosidase A activity was not.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>Brain MRI revealed progressive lacunar infarctions, white matter hyperintensities, and decreased brain volume in patients with Fabry disease. Brain MRI lesions were closely related to onset-age; disease duration, severity, burden; and plasma\u00a0Lyso-Gb<jats:sub>3<\/jats:sub>. However, they were not associated with sex, \u03b1-galactosidase A activity, or <jats:italic>GLA<\/jats:italic> mutation type.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00415-023-11826-8","type":"journal-article","created":{"date-parts":[[2023,6,25]],"date-time":"2023-06-25T09:02:01Z","timestamp":1687683721000},"page":"4939-4948","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Brain MRI correlations with disease burden and biomarkers in Fabry disease"],"prefix":"10.1007","volume":"270","author":[{"given":"Yawen","family":"Zhao","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yunchuang","family":"Sun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuan","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6241-4207","authenticated-orcid":false,"given":"Wei","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhaoxia","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yun","family":"Yuan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yining","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2023,6,25]]},"reference":[{"issue":"Suppl 1","key":"11826_CR1","doi-asserted-by":"publisher","first-page":"s10","DOI":"10.1590\/1806-9282.66.S1.10","volume":"66","author":"TP Bernardes","year":"1992","unstructured":"Bernardes TP, Foresto RD, Kirsztajn GM (1992) Fabry disease: genetics, pathology, and treatment. 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