Disrupted effective connectivity of the sensorimotor network in amyotrophic lateral sclerosis
Disrupted effective connectivity of the sensorimotor network in amyotrophic lateral sclerosis
复制标题
DOI：
10.1007/s00415-015-8013-z
复制
发表时间：
2016-03-01
影响因子：
6
通讯作者：
Jiang, Tianzi
中科院分区：
文献类型：
--
作者：
Fang, Xiaojing;Zhang, Yuanchao;Jiang, Tianzi
虽然功能失调的感觉运动网络（SMN）经常参与肌萎缩侧索硬化症（ALS）的发病机制，但该网络内的因果关系尚未得到探讨。在这项研究中，频谱动态因果模型应用于静息态功能磁共振成像数据，以估计20名ALS患者和21名健康对照者队列中SMN的因果关系。首先使用独立成分分析提取SMN成分，然后在两组之间进行比较，以确定SMN的异常。在ALS患者中，我们发现左侧初级运动皮层（M1），左侧初级体感皮层（S1）和右侧辅助运动皮层（SMA）的显著区域活动改变。在这些区域中，频谱DCM显示左侧M1和右侧SMA之间缺少闭环电路，并且在ALS中失去了从右侧SMA到左侧S1的投影。这些发现可能反映了ALS运动神经元缺失对运动功能的影响，并为ALS感觉运动神经回路的崩溃提供了令人信服的证据。总之，这项研究阐明了一个神经生物学模型，可以解释ALS中SMN的功能障碍，并提供了更深入的了解这种疾病的病理生理学。
Although dysfunctional sensorimotor network (SMN) has been frequently involved in the pathogenesis of amyotrophic lateral sclerosis (ALS), the causal relationship within this network remains unexplored. In this study, spectral dynamic causal modeling was applied to resting-state functional magnetic resonance imaging data to estimate the causal relationship of SMN in a cohort of 20 ALS patients and 21 healthy controls. The SMN components were first extracted using an independent component analysis, and then compared between the two groups to identify the abnormalities in SMN. In ALS patients, we found significant regional activity alterations in the left primary motor cortex (M1), the left primary somatosensory cortex (S1), and the right supplementary motor cortex (SMA). Among these regions, spectral DCM revealed missing closed-loop circuit between the left M1 and the right SMA, and lost projection from the right SMA to the left S1 in ALS. These findings may reflect the influences of the loss of motor neurons on motor function in ALS, and provide compelling evidence for a breakdown of the sensorimotor neural circuits in ALS. In conclusion, this study elucidates a neurobiological model that may explain the functional impairments of the SMN in ALS, and provides much deeper insights into the pathophysiology of this disease.