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Transient cervical nerve root compression in the rat induces bilateral forepaw allodynia and spinal glial activation: mechanical factors in painful neck injuries.

机译:大鼠短暂性颈神经根受压可引起双侧前爪异常性疼痛和脊髓神经胶质激活:颈痛的机械因素。

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STUDY DESIGN: An in vivo rat model of transient cervical nerve root compression. OBJECTIVES: To investigate the potential for cervical nerve root compression to produce behavioral hypersensitivity and examine its dependence on compression. SUMMARY OF BACKGROUND DATA: Clinically, nerve root injury has been hypothesized as a potential source of neck pain, particularly because cervical nerve roots are at mechanical risk for injury during neck loading. Lumbar radiculopathy models of nerve root ligation show that mechanical allodynia and spinal glial changes depend on nerve root deformation magnitude. However, no investigation has been performed to examine cervical nerve root compression as a cause of pain. METHODS: Two compressive forces (10 and 60 grams force [gf]) were transiently applied to the C7 nerve roots unilaterally using microvascular clips in separate groups (n = 12 each). Sham procedures were also performed in a separate group of rats (n = 12). Bilateral forepaw mechanical allodynia was monitored after surgery for 7 days. On day 7, spinal glial activation was assessed using immunohistochemistry to investigate its dependence on nerve root compressive force, in the context of behavioral hypersensitivity. RESULTS: Bilateral allodynia was observed following injury, which was significantly (P < 0.042) increased over sham and baseline responses. No difference in allodynia was found between the 10 and 60 gf injuries. Astrocytic and microglial activation were observed in the ipsilateral dorsal horn following compression, with only astrocytic activation paralleling allodynia patterns. CONCLUSIONS: Results imply a force threshold exists less than 10 gf for persistent pain symptoms following transient cervical nerve root compression. Findings also suggest that spinal glial activation may be related to behavioral sensitivity and may modulate cervical nerve root mediated pain.
机译:研究设计:短暂性颈神经根受压的体内大鼠模型。目的:研究颈神经根受压产生行为超敏反应的可能性,并研究其对受压的依赖性。背景数据摘要:临床上,神经根损伤被认为是可能引起的颈部疼痛,特别是因为颈神经根在颈部负荷期间处于机械性损伤风险中。腰神经根结扎的神经根模型表明,机械性异常性疼痛和脊髓神经胶质的改变取决于神经根的变形幅度。但是,尚未进行检查以检查颈神经根受压是疼痛的原因。方法:在不同的组中,分别使用微血管夹(n = 12),分别向C7神经根单侧施加两个压缩力(10和60克力[gf])。在另一组大鼠(n = 12)中也进行了假手术。术后7天监测双侧前爪机械性异常性疼痛。在第7天,在行为超敏性的情况下,使用免疫组织化学评估了脊髓神经胶质细胞的活化,以研究其对神经根压缩力的依赖性。结果:受伤后观察到双侧异常性疼痛,与假手术和基线反应相比明显增加(P <0.042)。在10 gf和60 gf的损伤之间,痛觉异常没有差异。压缩后,在同侧背角观察到星形胶质细胞和小胶质细胞活化,只有星形胶质细胞活化与异常性疼痛平行。结论:结果表明暂时性颈神经根受压后持续疼痛症状的力阈值小于10 gf。研究结果还表明,脊髓神经胶质激活可能与行为敏感性有关,并且可以调节颈神经根介导的疼痛。

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