White matter lesions

Mohamad Habes, Aristeidis Sotiras, Guray Erus, Jon B. Toledo, Deborah Janowitz, David A. Wolk, Haochang Shou, Nick R. Bryan, Jimit Doshi, Henry Völzke, Ulf Schminke, Wolfgang Hoffmann (+3 others)
2018 Neurology  
Objectives To investigate spatial heterogeneity of white matter lesions or hyperintensities (WMH). Methods MRI scans of 1,836 participants (median age 52.2 ± 13.16 years) encompassing a wide age range (22-84 years) from the cross-sectional Study of Health in Pomerania (Germany) were included as discovery set identifying spatially distinct components of WMH using a structural covariance approach. Scans of 307 participants (median age 73.8 ± 10.2 years, with 747 observations) from the Baltimore
more » ... ngitudinal Study of Aging (United States) were included to examine differences in longitudinal progression of these components. The associations of these components with vascular risk factors, cortical atrophy, Alzheimer disease (AD) genetics, and cognition were then investigated using linear regression. Results WMH were found to occur nonuniformly, with higher frequency within spatially heterogeneous patterns encoded by 4 components, which were consistent with common categorizations of deep and periventricular WMH, while further dividing the latter into posterior, frontal, and dorsal components. Temporal trends of the components differed both cross-sectionally and longitudinally. Frontal periventricular WMH were most distinctive as they appeared in the fifth decade of life, whereas the other components appeared later in life during the sixth decade. Furthermore, frontal WMH were associated with systolic blood pressure and with pronounced atrophy including AD-related regions. AD polygenic risk score was associated with the dorsal periventricular component in the elderly. Cognitive decline was associated with the dorsal component. Conclusions These results support the hypothesis that the appearance of WMH follows age and diseasedependent regional distribution patterns, potentially influenced by differential underlying pathophysiologic mechanisms, and possibly with a differential link to vascular and neurodegenerative changes. ‡These authors contributed equally to this work. Glossary AD = Alzheimer disease; BLSA = Baltimore Longitudinal Study of Aging; deep = deep white matter; dors. = dorsal periventricular; fron. = frontal periventricular; post. = posterior periventricular; SHIP = Study of Health in Pomerania; WMH = white matter hyperintensities; WMHC = white matter hyperintensities component. Academy of Neurology. Unauthorized reproduction of this article is prohibited. , education, and SHIP subcohorts. d Models were adjusted for age, sex, education, and SHIP subcohorts.
doi:10.1212/wnl.0000000000006116 pmid:30076276 pmcid:PMC6139818 fatcat:26j4otbdo5catgglup6oj3cj4a