Department of Exercise Science, Physical Therapy Program, University of South Carolina, 921 Assembly Street, Columbia, South Carolina.
Department of Communication Sciences and Disorders, University of South Carolina, 915 Greene Street, Columbia, South Carolina.
Hum Brain Mapp. 2018 Jan;39(1):120-132. doi: 10.1002/hbm.23829. Epub 2017 Oct 5.
Advances in neuroimaging have enabled the mapping of white matter connections across the entire brain, allowing for a more thorough examination of the extent of white matter disconnection after stroke. To assess how cortical disconnection contributes to motor impairments, we examined the relationship between structural brain connectivity and upper and lower extremity motor function in individuals with chronic stroke. Forty-three participants [mean age: 59.7 (±11.2) years; time poststroke: 64.4 (±58.8) months] underwent clinical motor assessments and MRI scanning. Nonparametric correlation analyses were performed to examine the relationship between structural connectivity amid a subsection of the motor network and upper/lower extremity motor function. Standard multiple linear regression analyses were performed to examine the relationship between cortical necrosis and disconnection of three main cortical areas of motor control [primary motor cortex (M1), premotor cortex (PMC), and supplementary motor area (SMA)] and motor function. Anatomical connectivity between ipsilesional M1/SMA and the (1) cerebral peduncle, (2) thalamus, and (3) red nucleus were significantly correlated with upper and lower extremity motor performance (P ≤ 0.003). M1-M1 interhemispheric connectivity was also significantly correlated with gross manual dexterity of the affected upper extremity (P = 0.001). Regression models with M1 lesion load and M1 disconnection (adjusted for time poststroke) explained a significant amount of variance in upper extremity motor performance (R = 0.36-0.46) and gait speed (R = 0.46), with M1 disconnection an independent predictor of motor performance. Cortical disconnection, especially of ipsilesional M1, could significantly contribute to variability seen in locomotor and upper extremity motor function and recovery in chronic stroke. Hum Brain Mapp 39:120-132, 2018. © 2017 Wiley Periodicals, Inc.
神经影像学的进步使人们能够绘制整个大脑的白质连接图，从而更全面地检查中风后白质连接中断的程度。为了评估皮质连接中断如何导致运动障碍，我们检查了慢性中风患者大脑结构连接与上肢和下肢运动功能之间的关系。43 名参与者[平均年龄：59.7（±11.2）岁；中风后时间：64.4（±58.8）个月]接受了临床运动评估和 MRI 扫描。采用非参数相关分析来检查运动网络的一小部分结构连接与上肢/下肢运动功能之间的关系。进行标准多元线性回归分析，以检验皮质坏死与三个主要运动控制皮质区域[初级运动皮质（M1）、运动前皮质（PMC）和辅助运动区（SMA）]的皮质连接中断与运动功能之间的关系。患侧 M1/SMA 与（1）大脑脚、（2）丘脑和（3）红核之间的解剖学连接与上肢和下肢运动表现显著相关（P≤0.003）。M1-M1 半球间连接也与患侧上肢的总手工灵巧性显著相关（P=0.001）。调整中风后时间的 M1 病变负荷和 M1 连接缺失的回归模型可以解释上肢运动表现（R=0.36-0.46）和步态速度（R=0.46）的显著差异，M1 连接缺失是运动表现的独立预测因子。皮质连接中断，特别是患侧 M1 的连接中断，可能会显著影响慢性中风患者的运动和上肢运动功能以及恢复的变异性。人脑映射 39:120-132,2018。©2017 威利期刊公司
