中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (1): 58-60.doi: 10.4103/1673-5374.169634

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

脊髓震荡:重复伤害的潜在风险

  

  • 收稿日期:2015-10-12 出版日期:2016-01-15 发布日期:2016-01-15
  • 基金资助:

    这项工作是由美国国立卫生研究院PO1 NS055976以及克雷格·H·尼尔森基金会支持。

Spinal cord concussion: studying the potential risks of repetitive injury

Itzhak Fischer, Christopher Haas, Ramesh Raghupathi, Ying Jin   

  1. Drexel University College of Medicine, Department of Neurobiology & Anatomy, Philadelphia, PA, USA
  • Received:2015-10-12 Online:2016-01-15 Published:2016-01-15
  • Contact: Itzhak Fischer, Ph.D., ifischer@drexelmed.edu.
  • Supported by:

    This work was supported by NIH PO1 NS055976, Craig H. Neilsen Foundation. We are grateful for the technical and graphical
    help provided by Julien Bouyer.

摘要:

脊髓震荡是指脊髓遭受强烈震荡后立即发生迟缓性瘫痪,损伤的平面以下感觉运动反射和植物神经功能全部丧失。因为在组织形态学上并没有病理变化发生,只是暂时性功能抑制,可以在数分钟或数小时内可以完全恢复。脊髓震荡的定义由Obersteiner于1879年最早提出,系指脊髓损伤后发生的一种可逆性功能紊乱。其特点为损伤平面以下脊髓功能的迅速、完全恢复。一般认为其恢复时间不超过24-48h。Obersteiner曾提出“神经元分子紊乱”学说,也有人认为脊髓震荡可能为间接暴力所导致的一种脊髓损伤。目前对其认识还相当肤浅,其原因主要在于脊髓震荡在临床上非常少见,而恢复时间又非常短暂,所以在对其进行深入研究时遇到许多难题。与慢性创伤性脑损伤相比,我们对脊髓震荡的直接后果和长期影响知之甚少。这是一种难以理解的现象,因为相关报道一直很少,并且未得到充分研究,而一些反复损伤的稀少数据也仅限于临床病例,没有足够的实验动物模型报道。为了解决这个问题,美国德雷塞尔大学医学院Itzhak Fischer教授的研究团队从2014年开始致力于研究开发强调重复性损伤的脊髓震荡动物模型。理想情况是,脊髓震荡模型应该使用密闭伤害更精确地模拟见于临床帘线震荡的拉伸或轴向载荷,如损伤通常发生在脊髓较小宫颈管或狭窄加剧而造成的过伸或过度屈曲。该定量损伤模型需要具有再现性,然而这使得旨在暴露脊髓的必要大多数脊髓损伤的动物模型中无法进行直接应用。因此Itzhak Fischer教授表示他们脊髓震荡模型的设计目的是突出易感性和反复损伤的功能性后果。这项研究只是脊髓震荡临床前工作的第一步,其将为理解损伤的病因提供一个机制框架,以便更好地指导与运动损伤相关的临床决策。Itzhak Fischer教授预计,他们实验室和其他人的未来工作应该集中在阐明脊髓震荡后脊髓易感性的关键参数,即相对时间,位置和损伤的严重程度。为了最大限度地提高本工作与动物模型基础研究的有效性,应协调脊髓和脑挫伤损伤的临床观察和基础研究。

Abstract:

Spinal cord concussion is a variant of mild spinal cord injury, clinically designated as transient paraplegia or neurapraxia, and characterized by variable degrees of sensory impairment and motor weakness that typically resolves within 24–72 hours without permanent deficits. Ideally, a model of spinal concussion should use a closed injury to more accurately model the stretching or axial loading seen in clinical cord concussion, as injuries typically occur as a result of hyperextension or hyperflexion of the spinal cord exacerbated by smaller cervical canals or stenosis. The need for reproducible, quantitative injury models, however, makes the direct application of forces on the exposed spinal cord a necessary trade off for most of animal models of SCI. Our model is designed to represent spinal cord concussion, and to highlight the susceptibility and functional consequences of repeated injury. This study, however, is only a first step in preclinical work on the risks associated with spinal concussion, which will provide a mechanistic framework for understanding the etiology of the injury as well as better guide clinical decision-making for RTP following contact sports injuries. We anticipate that future work from our laboratory and others will elucidate the key parameters of spinal vulnerability following spinal concussion with respect to the time, location, and severity of the injury. To maximize the effectiveness of this work the basic research with animal models should be coordinated with clinical observations and studies of both spinal and brain contusion injuries.