INTERNEURONAL CIRCUITS IN HUMAN SPINAL CORD INJURY

神经元间通路在神经元的起源中起着重要的作用。 脊髓损伤（SCI）痉挛。SCI之后，按键中断 下行的脊髓通路导致脊髓的不受控制的反射运动， 腿这些反射运动包括协调的屈曲或伸展的肌肉。 髋、膝和踝对特异性外感受或本体感受 线索我们假设SCI释放功能性神经元间回路， 它们可以被传入输入所访问。这些回路包括神经元间的 负责众所周知的屈曲撤回反射的途径， 在SCI中被夸大了，并且出现了一种新的反射反应，伸肌 痉挛传入通路和负责的神经元间系统的知识 用于屈肌痉挛的方法是基于这种与屈肌撤回反射的类比。 然而，几乎没有关于伸肌痉挛起源的信息 在SCI。 我们的第一个目的是测试屈肌痉挛是否是外周介导的 屈肌的负荷敏感性肌肉传入。我们推测 与负荷敏感性相关的神经元间通路的超兴奋性 传入神经可产生自我兴奋，有效地建立一个积极的 反馈回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。我们将测试这个 通过改变屈肌反射期间的肌肉负荷在SCI受试者中的假设 使用肌肉刺激和强制运动。将使用以下指标衡量效果： 关节扭矩和肌电图测量。 对于伸肌痉挛，我们假设观察到的运动行为导致 脊髓运动通路的释放。我们将测试这个 通过研究伸肌痉挛是否受到传入神经的调制， 来自髋屈肌和踝伸肌的信息。由于髋关节的本体感受 屈肌传入和lb组踝伸肌传入在 运动的调节，以此类推，我们希望能证明伸肌痉挛 是这些运动反射的表现伸肌痉挛 使用测量关节扭矩响应的新型装置进行量化， 强加的运动触发器。 这项研究中提出的原则将成为新疗法的基础 脊髓损伤痉挛的治疗方法。

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.