Kim Yeo Jin, Kwon Hun Ki, Lee Jong Min, Cho Hanna, Kim Hee Jin, Park Hee Kyung, Jung Na-Yeon, San Lee Jin, Lee Juyoun, Jang Young Kyoung, Kim Sung Tae, Lee Kyung Han, Choe Yearn Seong, Kim Yun Joong, Na Duk L, Seo Sang Won
From the Department of Neurology (Y.J.K., H.J.K., N.-Y.J., J.S.L., J.L., Y.K.J., D.L.N., S.W.S.), Neuroscience Center (Y.J.K., H.J.K., N.-Y.J., J.S.L., J.L., Y.K.J., D.L.N., S.W.S.), and Nuclear Medicine (K.H.L., Y.S.C.), Samsung Medical Center, Sungkyunkwan University School of Medicine; Department of Biomedical Engineering (H.K.K., J.M.L.), Hanyang University; Department of Neurology (H.C.), Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul; Department of Neurology (H.K.P.), Inje University Ilsan Paik Hospital, Goyang; and Radiology (S.T.K.) and Department of Neurology (Y.J.K.), Hallym University, Gangwon-do,Korea.
Neurology. 2016 Mar 29;86(13):1199-207. doi: 10.1212/WNL.0000000000002516. Epub 2016 Mar 2.
To investigate the topographic changes of white matter (WM) integrity and cortical thickness related to gait disturbances and determine whether these neural correlates mediate the association between cerebral small vessel disease (CSVD) and gait disturbances.
A total of 129 patients with subcortical vascular cognitive impairment were included. CSVD severity was quantified as global and regional WM hyperintensities (WMH) volume and lacune and microbleed numbers. Amyloid burdens were assessed using Pittsburgh compound B (PiB)-PET scanning. Gait score was measured using a standardized scale. WM integrity was assessed by applying tract-based spatial statistics. Cortical thickness was measured using surface-based methods. Path analysis for gait score was performed using regional CSVD markers as predictors and fractional anisotropy (FA) and cortical thickness as mediators.
Periventricular WMH (PWMH) volume was associated with gait score, regardless of other CSVD. PiB retention ratio was not associated with gait score. Gait score was correlated with FA in the frontal and parietal WM and bilateral corpus callosum and with cortical thinning in the bilateral frontal and lateral temporo-parieto-occipital regions. Path analysis for gait score showed that PWMH contributed to gait disturbances with the mediation of mean FA or cortical thickness.
Our findings suggest that WMH-related cortical thinning as well as disrupted integrity of periventricular WM is linked to gait disturbances.
研究与步态障碍相关的白质（WM）完整性和皮质厚度的地形变化，并确定这些神经关联是否介导脑小血管病（CSVD）与步态障碍之间的关联。
共纳入129例皮质下血管性认知障碍患者。CSVD严重程度通过全脑和局部WM高信号（WMH）体积以及腔隙和微出血数量进行量化。使用匹兹堡化合物B（PiB）-PET扫描评估淀粉样蛋白负荷。使用标准化量表测量步态评分。通过基于纤维束的空间统计学评估WM完整性。使用基于表面的方法测量皮质厚度。以区域CSVD标志物为预测因子，分数各向异性（FA）和皮质厚度为中介因子，对步态评分进行路径分析。
无论其他CSVD情况如何，脑室周围WMH（PWMH）体积均与步态评分相关。PiB滞留率与步态评分无关。步态评分与额叶和顶叶WM以及双侧胼胝体的FA以及双侧额叶和外侧颞顶枕区域的皮质变薄相关。步态评分的路径分析表明，PWMH通过平均FA或皮质厚度的中介作用导致步态障碍。
我们的研究结果表明，与WMH相关的皮质变薄以及脑室周围WM完整性破坏与步态障碍有关。
