Department of Integrative Biology and Physiology, University of California, Los Angeles, CA 90095 USA; Neuroscience Department, International School for Advanced Studies (SISSA), Bonomea 265, Trieste, Italy.
Department of Integrative Biology and Physiology, University of California, Los Angeles, CA 90095 USA.
Prog Neurobiol. 2018 Jan;160:64-81. doi: 10.1016/j.pneurobio.2017.10.004. Epub 2017 Nov 2.
Preclinical and clinical neurophysiological and neurorehabilitation research has generated rather surprising levels of recovery of volitional sensory-motor function in persons with chronic motor paralysis following a spinal cord injury. The key factor in this recovery is largely activity-dependent plasticity of spinal and supraspinal networks. This key factor can be triggered by neuromodulation of these networks with electrical and pharmacological interventions. This review addresses some of the systems-level physiological mechanisms that might explain the effects of electrical modulation and how repetitive training facilitates the recovery of volitional motor control. In particular, we substantiate the hypotheses that: (1) in the majority of spinal lesions, a critical number and type of neurons in the region of the injury survive, but cannot conduct action potentials, and thus are electrically non-responsive; (2) these neuronal networks within the lesioned area can be neuromodulated to a transformed state of electrical competency; (3) these two factors enable the potential for extensive activity-dependent reorganization of neuronal networks in the spinal cord and brain, and (4) propriospinal networks play a critical role in driving this activity-dependent reorganization after injury. Real-time proprioceptive input to spinal networks provides the template for reorganization of spinal networks that play a leading role in the level of coordination of motor pools required to perform a given functional task. Repetitive exposure of multi-segmental sensory-motor networks to the dynamics of task-specific sensory input as occurs with repetitive training can functionally reshape spinal and supraspinal connectivity thus re-enabling one to perform complex motor tasks, even years post injury.
临床前和临床神经生理学和神经康复研究表明,脊髓损伤后慢性运动麻痹患者的随意感觉运动功能有相当惊人的恢复水平。这种恢复的关键因素主要是脊髓和脊髓上网络的活动依赖性可塑性。这一关键因素可以通过电刺激和药物干预对这些网络进行神经调节来触发。这篇综述探讨了一些可能解释电调节效果的系统水平生理机制,以及重复训练如何促进随意运动控制的恢复。特别是,我们证实了以下假设:(1)在大多数脊髓损伤中,损伤区域有一定数量和类型的神经元存活,但不能传导动作电位,因此没有电反应;(2)可以将损伤区域内的这些神经元网络神经调节为电活性的转化状态;(3)这两个因素使得脊髓和大脑中的神经元网络有广泛的活动依赖性重组的潜力;(4)固有脊髓网络在损伤后驱动这种活动依赖性重组中发挥关键作用。实时本体感觉输入到脊髓网络为脊髓网络的重组提供了模板,这些网络在执行特定功能任务所需的运动池协调水平中起着主导作用。多节段感觉运动网络重复暴露于特定任务的感觉输入动态中,就像重复训练一样,可以对脊髓和脊髓上的连接进行功能重塑,从而使患者能够在受伤多年后完成复杂的运动任务。