中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (4): 790-796.doi: 10.4103/1673-5374.353485

• 综述:周围神经损伤修复保护与再生 • 上一篇    下一篇

慢性压迫性脊髓损伤的血管事件及其病理生理学机制

  

  • 出版日期:2023-04-15 发布日期:2022-10-27
  • 基金资助:

    国家自然科学基金(81450020)

Pathophysiological mechanisms of chronic compressive spinal cord injury due to vascular events

Zhen-Xiao Ren1, Jing-Hui Xu1, Xing Cheng1, Gui-Xing Xu2, Hou-Qing Long1, *   

  1. 1Guangdong Provincial Key Laboratory of Orthopaedics and Traumatology/Department of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, China;  2Department of Neurosurgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, China
  • Online:2023-04-15 Published:2022-10-27
  • Contact: Hou-Qing Long, MD, houqinglong@163.com.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, No. 81450020 (to HQL).

摘要:

颈椎病是非外伤性脊髓损伤的主要原因。慢性静态和/或动态压迫性脊髓损伤是颈椎病的独特发病机制;在这种情况的发展过程中,微血管网络被压缩和破坏,导致同时出现缺血和缺氧。伴随着炎症,血液脊髓屏障的破坏和压缩部位的细胞凋亡是主要的病理变化。研究证实,血管再生和重塑通过促进血流和重建有效循环来满足神经修复所需的营养和氧气,有助于神经修复。手术减压是最有效的临床治疗。然而,一些患者在减压后仍有残留的神经功能障碍。因此,在压迫期间和减压后促进血管再通是对手术治疗的良好补充。这篇综述总结了慢性压迫性脊髓损伤的研究进展,包括压迫和减压后的生理和病理变化,以及血管损伤和修复的调节机制。

https://orcid.org/0000-0003-4306-2319 (Hou-Qing Long)

Abstract: Cervical spondylotic myelopathy is the main cause of non-traumatic spinal cord injury, with chronic static and/or dynamic compressive spinal cord injury as the unique pathogenesis. In the progression of this condition, the microvascular network is compressed and destroyed, resulting in ischemia and hypoxia. The main pathological changes are inflammation, damage to the blood spinal cord barriers, and cell apoptosis at the site of compression. Studies have confirmed that vascular regeneration and remodeling contribute to neural repair by promoting blood flow and the reconstruction of effective circulation to meet the nutrient and oxygen requirements for nerve repair. Surgical decompression is the most effective clinical treatment for this condition; however, in some patients, residual neurological dysfunction remains after decompression. Facilitating revascularization during compression and after decompression is therefore complementary to surgical treatment. In this review, we summarize the progress in research on chronic compressive spinal cord injury, covering both physiological and pathological changes after compression and decompression, and the regulatory mechanisms of vascular injury and repair.

Key words: angiogenesis, cervical spondylotic myelopathy, hypoxia, inflammation, ischemia, spinal cord injury, surgical decompression