Spinal Cord Injury Center, Balgrist University Hospital, Forchstrasse 340, 8008 Zürich, Switzerland.
Nat Rev Neurol. 2010 Mar;6(3):167-74. doi: 10.1038/nrneurol.2009.227. Epub 2010 Jan 26.
This Review discusses the spinal neuronal changes that occur after a complete spinal cord injury (SCI) in humans. Early after an SCI, neither locomotor nor spinal reflex activity can be evoked. Once spinal shock has resolved, locomotor activity and an early spinal reflex component reappear in response to appropriate peripheral afferent input. In the subsequent 4-8 months, clinical signs of spasticity appear, largely as a result of non-neuronal (for example, muscular) changes, whereas locomotor and spinal reflex activity undergo little change. At 9-12 months, the electromyographic amplitude in the leg muscles during assisted locomotion declines, accompanied by a decrease in the amplitude of the early spinal reflex component and an increase in the amplitude of a late spinal reflex component. This exhaustion of locomotor activity also occurs in nonambulatory patients with incomplete SCI. Neuronal dysfunction is fully established 1 year after the injury without further alterations in subsequent years. In chronic SCI, the absence of input from supraspinal sources has been suggested to lead to degradation of neuronal function below the level of the lesion or, alternatively, a predominance of inhibitory signaling to the locomotor pattern generator. Appropriate training and/or provision of afferent input to spinal neurons might help to prevent neuronal dysfunction in chronic SCI.
这篇综述讨论了人类完全性脊髓损伤（SCI）后脊髓神经元的变化。在 SCI 后早期，既不能诱发运动也不能诱发脊髓反射活动。一旦脊髓休克消退，运动活动和早期脊髓反射成分会再次出现，以响应适当的外周传入输入。在随后的 4-8 个月中，痉挛的临床症状出现，主要是由于非神经元（例如肌肉）的变化，而运动和脊髓反射活动几乎没有变化。在 9-12 个月时，辅助运动时腿部肌肉的肌电图幅度下降，同时早期脊髓反射成分的幅度减小，晚期脊髓反射成分的幅度增大。即使是不完全性 SCI 的非运动患者，其运动活动也会出现这种衰竭。在损伤后 1 年内，神经元功能障碍完全确立，随后几年没有进一步改变。在慢性 SCI 中，有人认为，由于缺乏来自皮质的输入，导致损伤以下水平的神经元功能退化，或者运动模式发生器中抑制信号占主导地位。适当的训练和/或向脊髓神经元提供传入输入可能有助于防止慢性 SCI 中的神经元功能障碍。
