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Origins of Increased Motoneuron Excitability in Hemispheric Stroke

半球中风运动神经元兴奋性增加的起源

基本信息

批准号：
9926904
负责人：
WILLIAM Zev RYMER
金额：
$ 31.75万
依托单位：
REHABILITATION INSTITUTE OF CHICAGO D/B/A SHIRLEY RYAN ABILITYLAB
依托单位国家：
美国
项目类别：
财政年份：
2016
资助国家：
美国
起止时间：
2016-06-08 至 2023-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9926904
关键词：
Address Affect Brain Stem Calcium Cell Nucleus Characteristics Clinical Complication Contracture Contralateral Coupled Cutaneous Data Deformity Diagnosis Disease Ear Electric Stimulation Electrophysiology (science)Excitatory Postsynaptic Potentials Exhibits Eye Fiber Flexor Forearm Functional disorder H-Reflex Human Hyperreflexia Isometric Exercise Joints Lead Left Length Limb structure Measures Membrane Methodology Motion Motor Motor Neurons Movement Muscle Muscle Hypertonia Muscle Spasticity Muscle Tonus Neck Neurons Norepinephrine Nuclear Phase Physiological Population Probability Property Records Recovery Reflex action Resistance Rest Sampling Serotonin Side Sodium Source Spinal Spinal Cord Stimulus Stretching Stroke Surface Survivors Synapses Synaptic Potentials System Techniques Technology Tendon structure Time Treatment outcome base biceps brachii muscle design falls hemiparetic stroke median nerve monoamine neurophysiology new technology novel novel therapeutic intervention personalized diagnostics public health relevance receptor recruit response reticulospinal tract sound spasticity spinal pathway stretch reflex stroke survivor tool vestibular pathway voltage

项目摘要

DESCRIPTION (provided by applicant): Spasticity is a common complication of hemispheric stroke, impacting 40% or more of stroke survivors. Its most visible clinical feature is muscular hypertonia, or increased resistance of a limb to externally imposed motion. If left untreated, this increase in tone can impede joint motion, limiting recovery of voluntary movement. In addition, spasticity may lead to persistent muscle shortening, giving rise to joint deformity, and to muscle contracture. The pathophysiology appears to depend on an enhancement of the stretch reflex response, but we do not know where this enhancement originates. Accordingly, this proposal seeks to explore the physiological origins of spastic hypertonia by examining several alternative hypotheses about the basic underlying mechanisms. First, there could be greater excitatory synaptic drive to the spinal motoneuron pool, arising from key descending spinal pathways such as the vestibulospinal and/or reticulospinal tracts. Second, there could be larger, and/or longer-duration Ia excitatory synaptic potentials (EPSP'S) in spinal motoneurons elicited by the muscle stretch. Third, there could be changes in the intrinsic membrane properties of motoneurons such as in voltage-gated conductances of motoneurons, giving rise to persistent inward currents, or "PIC's". We plan to explore these mechanisms in hemispheric stroke survivors, using advanced EMG recording technologies, coupled with the use of a novel tendon probe (the Linmot), which imposes controlled muscle length changes on the muscle (the biceps muscle) and records biceps muscle force. These approaches, when combined, should allow us to separate the relative contributions of the proposed mechanisms, and should help us to develop greater diagnostic precision about the physiological characteristics of spasticity, as well as to design novel therapeutic approaches.

描述（由申请人提供）：痉挛是半球卒中的常见并发症，影响40%或更多的卒中幸存者。其最明显的临床特征是肌肉张力亢进，或肢体对外部施加的运动的阻力增加。如果不治疗，紧张度的增加会阻碍关节运动，限制自主运动的恢复。此外，痉挛状态可能导致持续的肌肉缩短，引起关节畸形和肌肉挛缩。病理生理学似乎取决于牵张反射反应的增强，但我们不知道这种增强的起源。因此，本建议旨在探讨痉挛性肌张力亢进的生理起源，通过检查几个替代假说的基本机制。首先，可能有更大的兴奋性突触驱动脊髓运动神经元池，从关键的下行脊髓通路，如前庭和/或网状脊髓束。第二，可能有较大的，和/或较长的持续时间Ia兴奋性突触电位（EPSP'S）在脊髓运动神经元引起的肌肉拉伸。第三，运动神经元的内在膜特性可能发生变化，例如运动神经元的电压门控电导，从而产生持续的内向电流或“PIC”。我们计划在半球卒中幸存者中探索这些机制，使用先进的EMG记录技术，再加上使用一种新型肌腱探针（Linmot），该探针对肌肉（二头肌）施加受控的肌肉长度变化并记录二头肌肌力。这些方法，当结合起来，应该让我们分开的相对贡献的机制，并应帮助我们开发更高的诊断精度的痉挛的生理特征，以及设计新的治疗方法。