Neuroscience and Cell Biology, 301 University Boulevard, Route 1043, University of Texas Medical Branch, Galveston, Texas 77555-1043, USA.
Exp Neurol. 2008 Nov;214(1):6-9. doi: 10.1016/j.expneurol.2008.07.016. Epub 2008 Jul 29.
Research focused on improving recovery of function, including the reduction of central neuropathic pain (CNP) after spinal cord injury (SCI) is essential. After SCI, regional neuropathic pain syndromes above, at and below the level or spinal injury develop and are thought to have different mechanisms, but may share common dysfunctional glial mechanisms. Detloff et al., [Detloff, M.R., Fisher, L.C., McGaughy, V., Longbrake, E.E., Popovich, P.G., Basso, D.M., Remote activation of microglia and pro-inflammatory cytokines predict the onset and severity of below-level neuropathic pain after spinal cord injury in rats. Exp. Neurol. (2008), doi: 10.1016/j.expneurol.2008.04.009.] describe events in the lumbar region of the spinal cord after a midthoracic SCI injury, the so called "below-level" pain and compares the findings to peripheral nerve lesion findings. This commentary briefly reviews glial contributions and intracellular signaling mechanisms, both neuronal and glial, that provide the substrate for CNP after SCI, including the persistent glial production of factors that can maintain sensitization of dorsal horn neurons in segments remote from the spinal injury; ie. dorsal horn hyperexcitability to formerly non noxious stimuli that become noxious after SCI resulting in allodynia. The term "gliopathy" is proposed to describe the dysfunctional and maladaptive response of glial cells, specifically astrocytes and microglia, to neural injury that is initiated by the sudden injury induced increase in extracellular concentrations of glutamate and concomitant production of several proinflammatory molecules. It is important to understand the roles that different glia play in "gliopathy", a condition that appears to persist after SCI. Furthermore, targeted treatment of gliopathy will attenuate mechanical allodynia in both central and peripheral neuropathic pain syndromes.
研究重点在于改善功能恢复，包括减少脊髓损伤（SCI）后的中枢神经性疼痛（CNP）。SCI 后，在损伤水平以上、以下和损伤水平处会出现区域性神经性疼痛综合征，这些疼痛综合征被认为具有不同的机制，但可能具有共同的功能障碍性神经胶质机制。Detloff 等人，[Detloff, M.R., Fisher, L.C., McGaughy, V., Longbrake, E.E., Popovich, P.G., Basso, D.M., Remote activation of microglia and pro-inflammatory cytokines predict the onset and severity of below-level neuropathic pain after spinal cord injury in rats. Exp. Neurol. (2008), doi: 10.1016/j.expneurol.2008.04.009.]描述了中胸段 SCI 损伤后脊髓腰区的事件，即所谓的“损伤以下”疼痛，并将这些发现与周围神经损伤的发现进行了比较。本评论简要回顾了胶质细胞的贡献和细胞内信号转导机制，包括神经元和神经胶质细胞，这些机制为 SCI 后 CNP 提供了基础，包括胶质细胞持续产生的因子可以维持脊髓损伤远隔部位背角神经元的敏化；即背角神经元对以前非伤害性刺激的超敏反应，在 SCI 后这些刺激变得具有伤害性，从而导致痛觉过敏。提出“神经胶质病”这一术语是为了描述胶质细胞（特别是星形胶质细胞和小胶质细胞）对神经损伤的功能障碍和适应性不良反应，这种反应是由细胞外谷氨酸浓度的突然升高和几种促炎分子的共同产生引起的。了解不同胶质细胞在“神经胶质病”中的作用非常重要，这种情况似乎在 SCI 后仍然存在。此外，靶向治疗神经胶质病可以减轻中枢和周围神经性疼痛综合征中的机械性痛觉过敏。
