INTERNEURONAL CIRCUITS IN HUMAN SPINAL CORD INJURY

神经元间通路在脑出血的发生中起重要作用。 脊髓损伤的痉挛(SCI)。在SCI之后，键的中断 脊椎下行通路导致不受控制的反射运动 腿。这些反射运动由协调的屈曲或伸展组成 髋关节、膝盖和脚踝对特定的外部感觉或本体感觉的反应 暗示。我们推测脊髓损伤释放功能性神经元间回路，使 它们对于传入输入是可访问的。这些回路包括神经元间 负责众所周知的屈曲撤退反射的通路，这是 在脊髓损伤中被夸大，以及一种新的反射反应的出现，伸肌 痉挛。对传入通路和负责的神经元间系统的知识 屈肌痉挛是基于屈肌退缩反射的类比。 然而，关于伸肌痉挛的起源几乎没有任何信息。 在SCI中。 我们的第一个目标是测试屈肌痉挛是否由 屈肌的负荷敏感型肌肉传入。我们假定 与负荷敏感相关的神经元间通路的超兴奋性 传入可以产生自我兴奋，有效地建立一种积极的 反馈环路。这一机制将为长期的、 与屈肌痉挛相关的重复性肌肉激活。我们将对此进行测试 脊髓损伤受试者在屈肌反射过程中改变肌肉负荷的假说 使用肌肉刺激和强加的运动。影响将使用以下方法来衡量 关节扭矩和肌电测量。 对于伸肌痉挛，我们假设观察到的运动行为导致 脊髓损伤后脊髓运动通路的释放。我们将对此进行测试 通过研究传入是否调制伸肌痉挛提出假说 来自髋屈肌和脚踝伸肌的信息。因为本体感髋关节 屈肌传入和Lb组踝伸肌传入在 运动的调节，以此类推，我们期望显示伸肌痉挛 是这些运动反射的表现。伸肌痉挛将是 使用一种测量关节扭矩响应的新型仪器进行量化 强制移动会触发。 这项研究中制定的原则将成为新疗法的基础 脊髓损伤的痉挛方式。

Interneuronal pathways play a significant role in the origin of spasticity in spinal cord injury (SCI.). Following SCI, the interruption of key descending spinal pathways results in uncontrolled reflex movements of the legs. These reflex movements consist of coordinated flexion or extension of the hip, knee and ankle in response to specific exteroceptive or proprioceptive cues. We postulate that SCI releases functional interneuronal circuits, making them accessible to afferent inputs. These circuits include interneuronal pathways responsible for the well-know flexion withdrawal reflex, which Is exaggerated in SCI, and the emergence of a novel reflex response, the extensor spasm. Knowledge of the afferent pathways and interneuronal systems responsible for flexor spasms is based on this analogy to the flexion withdrawal reflex. However, there is virtually no information about the origins of extensor spasms in SCI. Our first aim is to test whether flexor spasms are peripherally mediated by load-sensitive muscle afferents of the flexors. We postulate that hvperexcitability of the interneuronal pathways associated with load sensitive afferents could produce self excitation, effectively establishing a positive feedback loop. This mechanism would provide an explanation for the prolonged, repetitive muscle activation associated with flexor spasms. We will test this hypothesis in SCI subjects by altering the muscle load during the flexor reflex using muscle stimulation and imposed movements. Effects will be measured using joint torque and electromyographic measurements. For extensor spasms, we hypothesize that the observed motor behavior results from the release of spinal locomotor pathways following SCI. We will test this hypothesis by investigating whether extensor spasms are modulated by afferent information from hip flexors and ankle extensors. Since the proprioceptive hip flexor afferents and group lb ankle extensor afferents play a prominent role in the modulation of locomotion, by analogy we expect to show that extensor spasms are the manifestation of these locomotor reflexes. Extensor spasms will be quantified using a novel apparatus that measures the joint torque response to imposed movement triggers. The principles developed in this study will form the basis for new treatment modalities for spasticity in spinal cord injury.