中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (2): 329-330.doi: 10.4103/1673-5374.343901

• 观点:脊髓损伤修复保护与再生 • 上一篇    下一篇

开放性脊柱裂中炎性细胞因子的观点

  

  • 出版日期:2023-02-15 发布日期:2022-08-06

Perspective on inflammatory cytokines in open spinal dysraphism

Friederike Knerlich-Lukoschus*   

  1. Department of Neurosurgery, Section Pediatric Neurosurgery, University Medical Center Göttingen, Göttingen, Germany
  • Online:2023-02-15 Published:2022-08-06
  • Contact: Friederike Knerlich-Lukoschus, MD, PhD, friederike.knerlich-lukoschus@med.uni-goettingen.de.

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摘要： https://orcid.org/0000-0003-4907-015X (Friederike Knerlich-Lukoschus)

Abstract: Myelomeningocele (MMC) is a severe form of spinal dysraphism. Due to the failure of neural tube closure during early embryonic development, the affected part of the spinal cord is left open like a book at the back of the affected child. This malformed part of the spinal cord is not covered by its protective mesodermal and ectodermal derived layers. Consequently, the exposed neural tissue (i.e., the neural placode) is prone to injury during further intra-uterine development. Former investigations in sheep MMC models and ultrasound examinations in human fetuses demonstrated progressively decreased limb function during the later fetal course (Stiefel and Meuli, 2007). As a possible morphological correlate, Stiefel and Meuli (2007) demonstrated progressive tissue destruction of the initially intact appearing unfolded neural placode in curly tail/loop tail mouse fetuses. These observations were consistent with the hypothesis of secondary damage of the neural placode (so-called “second hit hypothesis”) (Heffez et al., 1990). According to this hypothesis, the “first hit” is considered the primary structural defect, which is due to faulty developmental processes. The size and location of the spinal cord abnormality within the spinal axis are important in determining the initial functional status. The assumed ongoing toxic and mechanical damaging impacts on the exposed neural placode are viewed as the “second hit”. The second hit presumably leads to additional deficits at and below the lesion level. These processes might also be responsible for further sequelae, like the development of secondary tethered cord syndrome (TCS), that typically occur during the later clinical course of the affected child. As in spinal cord injury (SCI), the second hit presumably induces further cellular and molecular lesion cascades in the placode, which are summarized under the term “third hit” (Figure 1A).