PREDOCTORAL FELLOWSHIP PROGRAM (DISABILITY)

博士前奖学金计划（残疾）

• 批准号: 2519094
• 负责人: Joseph M. Hidler
• 金额: $ 1.35万
• 依托单位: REHABILITATION INSTITUTE OF CHICAGO D/B/A SHIRLEY RYAN ABILITYLAB
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-08-23 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/2519094
• 关键词: ankle; biological models; clinical research; human subject; motor neurons; muscle contraction; neuromuscular function; oscillography; spasm; spinal cord injury; stretch reflex

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.

阵挛被描述为一种不自主的有节奏的肌肉收缩， 伴随着脚踝肌肉的痉挛，发生在有 累及下行运动通路的病变。目前，有一个大型的 关于阵挛的原因的辩论，围绕两种不同的假设。 第一个提出了脊髓神经振荡器的存在，以及 第二，这种振荡是由于过度活动伸展的不稳定性造成的。 反射形成高增益负反馈调节器。因此。这个 总体目标是调查导致 阵挛。我们认为，在运动通路受损后， 运动神经元池的兴奋性因减少而增加 脊椎上或区域抑制性输入，增强了 边际稳定的系统。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总参数模型。 人类的脚踝将被开发出来。然后，将完成系统识别 在脚踝肌肉上确定模型组件的属性。 第三，阵挛行为，如振荡频率和肌肉长度 变化将在病理受试者中进行测量，受到不同 摄动，以及不同的惯性载荷。最后，进行了仿真 运动神经元阈值和当前频率关系将在#年调整 研究运动神经元池兴奋性的模型 影响脚踝反射的行为。基于A/S的控制系统 分析，我们将评估这些变化是否促进了振荡 人类脚踝反射中的行为(阵挛)。