The Miami Project to Cure Paralysis, University of Miami, and Bruce W. Carter Department of Veterans Affairs Medical Center, Miami, Florida 33136, and.
Shirley Ryan Ability Lab, Northwestern University, and Hines Veterans Affairs Medical Center, Chicago, Illinois 60611.
J Neurosci. 2019 Oct 2;39(40):7872-7881. doi: 10.1523/JNEUROSCI.1106-19.2019. Epub 2019 Aug 14.
Damage to the corticospinal and reticulospinal tract has been associated with spasticity in humans with upper motor neuron lesions. We hypothesized that these descending motor pathways distinctly contribute to the control of a spastic muscle in humans with incomplete spinal cord injury (SCI). To test this hypothesis, we examined motor-evoked potentials (MEPs) elicited by transcranial magnetic stimulation over the leg representation of the primary motor cortex, maximal voluntary contractions (MVCs), and the StartReact response (shortening in reaction time evoked by a startling stimulus) in the quadriceps femoris muscle in male and females with and without incomplete SCI. A total of 66.7% of the SCI participants showed symptoms of spasticity, whereas the other 33.3% showed no or low levels of spasticity. We found that participants with spasticity had smaller MEPs and MVCs and larger StartReact compared with participants with no or low spasticity and control subjects. These results were consistently present in spastic subjects but not in the other populations. Clinical scores of spasticity were negatively correlated with MEP-max and MVC values and positively correlated with shortening in reaction time. These findings provide evidence for lesser corticospinal and larger reticulospinal influences to spastic muscles in humans with SCI and suggest that these imbalanced contributions are important for motor recovery. Although spasticity is one of the most common symptoms manifested in humans with spinal cord injury (SCI) to date, its mechanisms of action remain poorly understood. We provide evidence, for the first time, of imbalanced contributions of the corticospinal and reticulospinal tract to control a spastic muscle in humans with chronic incomplete SCI. We found that participants with SCI with spasticity showed small corticospinal responses and maximal voluntary contractions and larger reticulospinal gain compared with participants with no or low spasticity and control subjects. These results were consistently present in spastic subjects but not in the other populations. We showed that imbalanced corticospinal and reticulospinal tract contributions are more pronounced in participants with chronic incomplete SCI with lesser recovery.
皮质脊髓束和网状脊髓束的损伤与上运动神经元损伤患者的痉挛有关。我们假设这些下行运动通路对不完全性脊髓损伤（SCI）患者痉挛肌肉的控制有明显的贡献。为了验证这一假设，我们检查了经颅磁刺激刺激初级运动皮层腿部代表区引起的运动诱发电位（MEPs）、最大自主收缩（MVCs）和股四头肌的 StartReact 反应（惊跳刺激诱发的反应时缩短）在有无不完全性 SCI 的男性和女性中。共有 66.7%的 SCI 参与者表现出痉挛症状，而其余 33.3%的参与者表现出无痉挛或低水平痉挛。我们发现，痉挛参与者的 MEPs 和 MVCs 较小，而 StartReact 较大，与无痉挛或低痉挛参与者和对照组相比。这些结果在痉挛组中一直存在，但在其他人群中则不存在。痉挛的临床评分与 MEP-max 和 MVC 值呈负相关，与反应时缩短呈正相关。这些发现为 SCI 患者痉挛肌肉中皮质脊髓和网状脊髓影响较小提供了证据，并表明这些不平衡的贡献对运动恢复很重要。尽管痉挛是迄今为止脊髓损伤（SCI）患者最常见的症状之一，但其作用机制仍知之甚少。我们首次提供了证据，证明慢性不完全性 SCI 患者的皮质脊髓和网状脊髓通路对控制痉挛肌肉的不平衡贡献。我们发现，痉挛的 SCI 参与者的皮质脊髓反应和最大自主收缩较小，网状脊髓增益较大，与无痉挛或低痉挛参与者和对照组相比。这些结果在痉挛组中一直存在，但在其他人群中则不存在。我们表明，不平衡的皮质脊髓和网状脊髓通路贡献在恢复较差的慢性不完全性 SCI 参与者中更为明显。
