Mechanisms of Weakness in Incomplete Spinal Cord Injury

脊髓损伤（SCI）患者的自发性肌无力和疲劳增加是功能独立性下降的两个主要损伤。然而，这些损伤的机制尚不完全清楚，目前也没有有效的治疗方法。本研究的主要目标是描述脊髓损伤患者在稳态收缩期间的人体运动单元（MUs）的招募和速率编码模式，并量化线性变化等长收缩期间的时变速率调制模式。拟议的实验包括使用细丝肌内电极记录胫骨前肌和三头肌表面肌在恒力或线性变化的等距收缩过程中的单毫米波。将对脊髓损伤患者的扭矩、表面肌电图和单MU数据进行分析和量化，并与对照组进行比较。本研究的主要假设是脊髓损伤后，节段性运动系统的下行神经调节输入被中断。这一假设将通过比较对照组和脊髓损伤患者的MU行为与神经调节后减少动物制剂记录的运动神经元行为来评估。我们的论点是，控制对象的非线性运动单元行为在性质上类似于神经调节后减少准备中的运动神经元行为。脊髓损伤患者非线性行为的缺失可能提示神经调节输入的缺失，这将为脊髓损伤后无力的药物治疗奠定基础。

Voluntary muscular weakness and increased fatigue in patients with spinal cord injuries (SCI) are two of the primary impairments underlying decreased functional independence. The mechanisms underlying these impairments are incompletely understood, however, and few effective treatments are currently available. The primary goals of this proposal are to characterize recruitment and rate coding patterns of human motor units (MUs) in patients with spinal cord injuries during steady-state contractions and to quantify the time-varying rate modulation patterns during linearly-varying isometric contractions. The proposed experiments involve use of fine wire intramuscular electrodes to record - from single MUs of tibialis anterior and triceps surae muscles during constant-force or linearly varying isometric contractions. Torque, surface electromyography, and single MU data will be analyzed and quantified in patients with SCI and compared to control subjects. The primary hypothesis of this proposed study is that descending neuromodulatory input to the segmental motor system is interrupted following SCI. This hypothesis will be assessed by comparing MU behavior from both control subjects and patients with spinal cord injury to motoneuron - behavior recorded from reduced animal preparations following neuromodulation. It is our contention that non-linear motor unit behavior in control subjects is qualitatively similar to motoneuron behavior in reduced preparations following neuromodulation. Absence of non-linear behavior in patients with SCI may suggested absence of neuromodulatory input, and would establish a foundation for pharmacological treatments for weakness following SCI..