Department of Spine Surgery, School of Medicine, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Department of Anesthesiology, Jinling Hospital, Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Cell Mol Neurobiol. 2024 Nov 28;44(1):81. doi: 10.1007/s10571-024-01517-x.
Regional neuropathic pain syndromes above, at, or below the site of spinal damage arise after spinal cord injury (SCI) and are believed to entail distinct pathways; nevertheless, they may share shared defective glial systems. Neuropathic pain after SCI is caused by glial cells, ectopic firing of neurons endings and their intra- and extracellular signaling mechanisms. One such mechanism occurs when stimuli that were previously non-noxious become so after the injury. This will exhibit a symptom of allodynia. Another mechanism is the release of substances by glia, which keeps the sensitivity of dorsal horn neurons even in regions distant from the site of injury. Here, we review, the models and identifications of SCI-induced neuropathic pain (SCI-NP), the mechanisms of SCI-NP related to glia, and the treatments of SCI-NP.
脊髓损伤(SCI)后出现的、位于损伤部位以上、以下或周围的区域性神经病理性疼痛综合征,被认为涉及不同的途径;然而,它们可能共享共同的缺陷神经胶质系统。SCI 后的神经病理性疼痛是由神经胶质细胞、神经元末梢的异位放电及其细胞内和细胞外信号转导机制引起的。一种这样的机制发生在以前无害的刺激物在受伤后变得有害时。这将表现出痛觉过敏的症状。另一种机制是神经胶质细胞释放物质,即使在远离损伤部位的区域,也能保持背角神经元的敏感性。在这里,我们综述了 SCI 诱导的神经病理性疼痛(SCI-NP)的模型和鉴定、与神经胶质有关的 SCI-NP 的机制,以及 SCI-NP 的治疗方法。
Cell Mol Neurobiol. 2024-11-28
Exp Neurol. 2008-7-29
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