Grau James W, Baine Rachel E, Bean Paris A, Davis Jacob A, Fauss Gizelle N, Henwood Melissa K, Hudson Kelsey E, Johnston David T, Tarbet Megan M, Strain Misty M
Behavioral and Cellular Neuroscience, Department of Psychology, Texas A&M University, College Station, TX 77843, USA.
Behavioral and Cellular Neuroscience, Department of Psychology, Texas A&M University, College Station, TX 77843, USA.
Exp Neurol. 2020 Aug;330:113334. doi: 10.1016/j.expneurol.2020.113334. Epub 2020 Apr 28.
The present review explores the concept of learning within the context of neurorehabilitation after spinal cord injury (SCI). The aim of physical therapy and neurorehabilitation is to bring about a lasting change in function-to encourage learning. Traditionally, it was assumed that the adult spinal cord is hardwired-immutable and incapable of learning. Research has shown that neurons within the lower (lumbosacral) spinal cord can support learning after communication with the brain has been disrupted by means of a thoracic transection. Noxious stimulation can sensitize nociceptive circuits within the spinal cord, engaging signal pathways analogous to those implicated in brain-dependent learning and memory. After a spinal contusion injury, pain input can fuel hemorrhage, increase the area of tissue loss (secondary injury), and undermine long-term recovery. Neurons within the spinal cord are sensitive to environmental relations. This learning has a metaplastic effect that counters neural over-excitation and promotes adaptive learning through an up-regulation of brain-derived neurotrophic factor (BDNF). Exposure to rhythmic stimulation, treadmill training, and cycling also enhances the expression of BDNF and counters the development of nociceptive sensitization. SCI appears to enable plastic potential within the spinal cord by down-regulating the Cl co-transporter KCC2, which reduces GABAergic inhibition. This enables learning, but also fuels over-excitation and nociceptive sensitization. Pairing epidural stimulation with activation of motor pathways also promotes recovery after SCI. Stimulating motoneurons in response to activity within the motor cortex, or a targeted muscle, has a similar effect. It is suggested that a neurofunctionalist approach can foster the discovery of processes that impact spinal function and how they may be harnessed to foster recovery after SCI.
本综述探讨了脊髓损伤（SCI）后神经康复背景下的学习概念。物理治疗和神经康复的目的是实现功能的持久改变——促进学习。传统上，人们认为成人脊髓是固定不变的——不可改变且无法学习。研究表明，在胸段横断导致与大脑的通信中断后，脊髓下部（腰骶部）的神经元仍能支持学习。有害刺激可使脊髓内的伤害性回路敏感化，激活与脑依赖性学习和记忆相关的信号通路。脊髓挫伤损伤后，疼痛输入会加剧出血，增加组织损失面积（继发性损伤），并损害长期恢复。脊髓内的神经元对环境关系敏感。这种学习具有一种代谢性塑性效应，可对抗神经过度兴奋，并通过上调脑源性神经营养因子（BDNF）促进适应性学习。接受节律性刺激、跑步机训练和骑自行车也能增强BDNF的表达，并对抗伤害性敏感化的发展。SCI似乎通过下调氯离子共转运体KCC2来激活脊髓内的可塑性潜能，这会减少GABA能抑制作用。这既能促进学习，但也会加剧过度兴奋和伤害性敏感化。将硬膜外刺激与运动通路的激活相结合也能促进SCI后的恢复。响应运动皮层或目标肌肉内的活动刺激运动神经元也有类似效果。有人提出，一种神经功能主义方法可以促进对影响脊髓功能的过程以及如何利用这些过程促进SCI后恢复的发现。
