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White and Gray Matter Abnormalities in Manifest Huntington's Disease: Cross‐Sectional and Longitudinal Analysis
Author(s) -
Sweidan Wafaa,
Bao Fen,
Bozorgzad NavidSeraji,
George Edwin
Publication year - 2020
Publication title -
journal of neuroimaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.822
H-Index - 64
eISSN - 1552-6569
pISSN - 1051-2284
DOI - 10.1111/jon.12699
Subject(s) - white matter , medicine , putamen , atrophy , globus pallidus , corpus callosum , fractional anisotropy , magnetic resonance imaging , thalamus , pathology , diffusion mri , cardiology , basal ganglia , neuroscience , psychology , central nervous system , radiology
BACKGROUND AND PURPOSE Early white matter (WM) changes and cortical atrophy in Huntington's disease (HD) are often evident before disease onset and extend through the brain during manifest stages. The trajectory of these brain abnormalities in symptomatic stages remains relatively unexplored. The aim of this study is to investigate how the pattern of WM and gray matter (GM) alterations progress over time. METHODS We investigated alterations in brain WM, cortical thickness, and subcortical structures using diffusion and structural magnetic resonance imaging, in manifest HD patients ( n = 13) compared to age‐matched healthy controls ( n = 11). Imaging and clinical data for the HD group were collected at follow‐up (7 months) to explore possible longitudinal changes. RESULTS Cross‐sectional analyses identified significant posterior cortical thinning ( P < .05) and symmetric fractional anisotropy (FA) reduction ( P < .01) in brain WM of HD group compared to HC. These changes were strongly correlated with impairment in motor symptoms and processing speed. Subcortical atrophy was significant in caudate, putamen, globus pallidus, and thalamus ( P < .001). Regions of interest analysis revealed a significant reduction in FA of the corpus callosum (CC) (–2.19%, P < .05) upon follow‐up, whereas no significant cortical thinning and subcortical atrophy was found. CONCLUSIONS This study showed broad GM and WM abnormalities in manifest HD patients. Reductions in FA and cortical thinning correlated significantly with the disturbances of motor and cognitive processing that describe HD. Follow‐up assessment showed that the CC is compromised in the absence of detectable GM changes or motor decline, suggesting it plays an important role in disease progression.