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Gray matter atrophy and freezing of gait in Parkinson's disease: Is the evidence black‐on‐white?
Author(s) -
Herman Talia,
RosenbergKatz Keren,
Jacob Yael,
Giladi Nir,
Hausdorff Jeffrey M.
Publication year - 2014
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.25697
Subject(s) - atrophy , white matter , parietal lobe , parkinson's disease , gait , psychology , voxel based morphometry , angular gyrus , voxel , balance (ability) , frontal lobe , medicine , neuroscience , physical medicine and rehabilitation , magnetic resonance imaging , cognition , disease , radiology
Objectives The pathophysiology underlying freezing of gait (FOG) in Parkinson's disease (PD) is poorly understood. We tested whether gray matter (GM) atrophy contributes to FOG in PD. Methods Voxel‐based morphometry quantified GM atrophy in 106 patients who were classified as freezers (n = 30) or nonfreezers (n = 76). Well‐matched smaller subgroups were also studied. Balance, gait, and cognitive function were assessed, and we evaluated the relationship between GM, FOG severity, and symptoms associated with FOG. Results GM was significantly reduced in the inferior parietal lobe and angular gyrus in the matched freezers (n = 22), compared to nonfreezers (n = 22; P < 0.015, cluster‐level corrected). In the entire cohort, FOG severity was related to bilateral caudate volumes. Conclusions GM atrophy in cortical (i.e., parietal lobe and angular gyrus) and subcortical areas (i.e., caudate) are related to FOG. Disparities among the existing findings suggest that inferences regarding specific brain regions should be made with caution. © 2013 International Parkinson and Movement Disorder Society