TY - JOUR
T1 - Cortical thickness is associated with gait disturbances in cerebral small vessel disease
AU - de Laat, Karlijn F.
AU - Reid, Andrew T.
AU - Grim, David C.
AU - Evans, Alan C.
AU - Kötter, Rolf
AU - van Norden, Anouk G.W.
AU - de Leeuw, Frank Erik
N1 - Funding Information:
Dr De Leeuw received a personal fellowship of the Dutch Brain foundation (H04-12) and a clinical fellowship of the Netherlands Organization for Scientific Research (project number 40-00703-97-07197).
PY - 2012/1/16
Y1 - 2012/1/16
N2 - Although gait disturbances are present in a substantial portion of patients with cerebral small vessel disease (SVD), their pathogenesis has not been clarified as they are not entirely explained by the white matter lesions (WMLs) and lacunar infarcts. The role of cortical thickness in these patients remains largely unknown. We aimed to assess the regions of cortical thickness associated with distinct gait parameters in patients with SVD, and whether these associations were dependent on WMLs and lacunar infarcts. MRI data were obtained from 415 subjects with SVD, aged between 50 and 85. years. We assessed cortical thickness using surface-based cortical thickness analysis, and gait performance using the GAITRite system. Cortical thickness of predominantly the orbitofrontal and ventrolateral prefrontal cortex, the inferior parietal lobe, cingulate areas and visual association cortices was positively related to stride length. Thickness of the primary and supplementary motor cortices and the cingulate cortex was positively related to cadence, while thickness of the orbitofrontal and ventrolateral prefrontal cortex, anterior cingulate cortex and especially the inferior parietal lobe and superior temporal gyrus was negatively related to stride width. The associations with stride length and width were partially explained by the subcortical WMLs and lacunar infarcts. Cortical thickness may therefore be important in gait disturbances in individuals with SVD, with different cortical patterns for specific gait parameters. We suggest that cortical atrophy is part of the disease processes in patients with SVD.
AB - Although gait disturbances are present in a substantial portion of patients with cerebral small vessel disease (SVD), their pathogenesis has not been clarified as they are not entirely explained by the white matter lesions (WMLs) and lacunar infarcts. The role of cortical thickness in these patients remains largely unknown. We aimed to assess the regions of cortical thickness associated with distinct gait parameters in patients with SVD, and whether these associations were dependent on WMLs and lacunar infarcts. MRI data were obtained from 415 subjects with SVD, aged between 50 and 85. years. We assessed cortical thickness using surface-based cortical thickness analysis, and gait performance using the GAITRite system. Cortical thickness of predominantly the orbitofrontal and ventrolateral prefrontal cortex, the inferior parietal lobe, cingulate areas and visual association cortices was positively related to stride length. Thickness of the primary and supplementary motor cortices and the cingulate cortex was positively related to cadence, while thickness of the orbitofrontal and ventrolateral prefrontal cortex, anterior cingulate cortex and especially the inferior parietal lobe and superior temporal gyrus was negatively related to stride width. The associations with stride length and width were partially explained by the subcortical WMLs and lacunar infarcts. Cortical thickness may therefore be important in gait disturbances in individuals with SVD, with different cortical patterns for specific gait parameters. We suggest that cortical atrophy is part of the disease processes in patients with SVD.
KW - Cerebral small vessel disease
KW - Cortical thickness
KW - Gait
KW - Magnetic resonance imaging
UR - http://www.scopus.com/inward/record.url?scp=83055194503&partnerID=8YFLogxK
U2 - 10.1016/j.neuroimage.2011.08.005
DO - 10.1016/j.neuroimage.2011.08.005
M3 - Article
C2 - 21854857
AN - SCOPUS:83055194503
SN - 1053-8119
VL - 59
SP - 1478
EP - 1484
JO - Neuroimage
JF - Neuroimage
IS - 2
ER -