Brain Rehabilitation Research Ctr., Malcom Randall VA Medical Center, Gainesville, FL 32608-1135, USA.
J Neurophysiol. 2010 Feb;103(2):844-57. doi: 10.1152/jn.00825.2009. Epub 2009 Dec 9.
Evidence suggests that the nervous system controls motor tasks using a low-dimensional modular organization of muscle activation. However, it is not clear if such an organization applies to coordination of human walking, nor how nervous system injury may alter the organization of motor modules and their biomechanical outputs. We first tested the hypothesis that muscle activation patterns during walking are produced through the variable activation of a small set of motor modules. In 20 healthy control subjects, EMG signals from eight leg muscles were measured across a range of walking speeds. Four motor modules identified through nonnegative matrix factorization were sufficient to account for variability of muscle activation from step to step and across speeds. Next, consistent with the clinical notion of abnormal limb flexion-extension synergies post-stroke, we tested the hypothesis that subjects with post-stroke hemiparesis would have altered motor modules, leading to impaired walking performance. In post-stroke subjects (n = 55), a less complex coordination pattern was shown. Fewer modules were needed to account for muscle activation during walking at preferred speed compared with controls. Fewer modules resulted from merging of the modules observed in healthy controls, suggesting reduced independence of neural control signals. The number of modules was correlated to preferred walking speed, speed modulation, step length asymmetry, and propulsive asymmetry. Our results suggest a common modular organization of muscle coordination underlying walking in both healthy and post-stroke subjects. Identification of motor modules may lead to new insight into impaired locomotor coordination and the underlying neural systems.
有证据表明,神经系统通过肌肉激活的低维模块化组织来控制运动任务。然而,目前尚不清楚这种组织是否适用于人类行走的协调,也不清楚神经系统损伤如何改变运动模块的组织及其生物力学输出。我们首先测试了这样一个假设,即行走过程中的肌肉激活模式是通过一小部分运动模块的可变激活产生的。在 20 名健康对照者中,在一系列步行速度下测量了 8 条腿部肌肉的肌电图信号。通过非负矩阵分解识别出的四个运动模块足以解释肌肉激活在步与步之间以及在不同速度下的变化。接下来,与脑卒中后肢体弯曲-伸展协同作用异常的临床概念一致,我们测试了这样一个假设,即脑卒中后偏瘫患者的运动模块会发生改变,导致行走能力受损。在脑卒中患者(n=55)中,表现出更简单的协调模式。与对照组相比,在以自身偏好速度行走时,需要更少的模块来解释肌肉激活。在健康对照组中观察到的模块合并,导致需要更少的模块,这表明神经控制信号的独立性降低。模块的数量与偏好的行走速度、速度调节、步长不对称和推进力不对称相关。我们的研究结果表明,健康和脑卒中患者的行走运动协调具有共同的模块化组织。运动模块的识别可能为运动协调受损和潜在的神经系统提供新的见解。