PREDOCTORAL FELLOWSHIP PROGRAM (DISABILITY)

阵挛被描述为一种不自主的节律性肌肉收缩， 伴随踝关节肌肉痉挛，发生在患有 涉及下行运动通路的病变。目前，有大量 关于阵挛原因的争论，围绕着两种不同的假设。 第一个提出了脊髓神经振荡器的存在， 第二，振荡是由于过度活跃的拉伸的不稳定性 反射形成高增益负反馈调节器。因此。的 总体目标是研究导致 阵挛我们认为，在运动通路损伤后， 运动神经元池的兴奋性增加，因为减少 脊髓上或区域性抑制性输入，增强了 稳定的系统。这一假设将分四个步骤进行检验。 首先，建立了牵张反射通路的集中参数模型。 将开发出人体踝关节。然后进行系统辨识 以确定模型组件的属性。 三是阵挛行为如振荡频率和肌肉长度 将在病理受试者中测量变化， 扰动和不同的惯性载荷。最后，模拟 运动神经元阈值与电流频率的关系将在 该模型旨在研究运动神经元池的兴奋性如何 影响踝反射的行为。基于控制系统 分析，我们将评估这些变化是否促进振荡 行为（阵挛）在人类脚踝反射。

CLONUS is described as an involuntary rhythmic muscle contraction which accompanies spasticity of ankle muscles, and occurs in people with lesions involving descending motor pathways. Currently, there is a large debate as to the causes of clonus, centering on two different hypotheses. The first proposes the existence of spinal neural oscillators, and the second that oscillation is due to instability of hyperactive stretch reflexes forming a high gain negative feedback regulator. Therefore. the overall objective is to investigate the underlying mechanisms causing clonus. We propose that following a lesion in motor pathways, the excitability of the motoneuron pool increases because of diminished supraspinal or regional inhibitory input, enhancing instability in a marginally stable system. This hypothesis will be tested in four steps. First, a lumped parameter model of the stretch reflex pathway in the human ankle will be developed. Then, systems identification will be done on ankle muscles to determine the properties of the models components. Third, clonus behavior such as oscillation frequency and muscle length change will be measured in pathological subjects, subjected to varying perturbations, and to differing inertial loads. Finally, simulated motoneuron threshold and current frequency relations will be adjusted in the model to examine how the excitability of the motoneuron pool influences the behavior of the ankle reflex. Based on a control systems analysis, we will assess whether these changes promote oscillatory behavior (clonus) in the human ankle reflex.