School of Psychology, Murdoch University, Perth, WA 6150, Australia.
Pain Med. 2011 Dec;12(12):1784-807. doi: 10.1111/j.1526-4637.2011.01273.x. Epub 2011 Nov 14.
To review the implications of a local overproduction of tumor necrosis factor-α for the pathogenesis and treatment of complex regional pain syndrome.
Elevated local production of tumor necrosis factor-α contributes to prolonged inflammation in the early stages of complex regional pain syndrome. Consequences could include hypoxia and necrosis of local tissues.
We conducted a review of articles published since 2000 on tumor necrosis factor-α in complex regional pain syndrome.
We propose that exaggerated local inflammation, subsequent inhibition of N-type calcium channel currents in sympathetic vasoconstrictor neurons and reduced sympathetic neurotransmitter release from perivascular terminals disrupt sympathetic cutaneous vasoconstrictor activity in complex regional pain syndrome. The resultant microvascular disturbance could exacerbate inflammation in the affected limb. In addition, an underactive cholinergic anti-inflammatory pathway might lead to overproduction of tumor necrosis factor-α. The results of large, randomized controlled treatment studies that test the efficacy of selective anti-tumor necrosis factor-α drugs in complex regional pain syndrome are not yet available. However, numerous small-scale studies and case reports indicate that anti-inflammatory drug treatments that directly or indirectly target tumor necrosis factor-α ameliorate pain and other symptoms in some cases.
An exaggerated inflammatory cytokine cascade may contribute to sensory and autonomic disturbances in complex regional pain syndrome. Further investigation of anti-tumor necrosis factor-α therapy as a cost-effective treatment option for this devastating disease is required. Whether increased activity in the cholinergic anti-inflammatory pathway provides therapeutic benefits for complex regional pain syndrome also warrants further investigation.
探讨肿瘤坏死因子-α局部过度产生对复杂性区域疼痛综合征发病机制和治疗的影响。
肿瘤坏死因子-α局部水平升高可导致复杂性区域疼痛综合征早期炎症持续存在，其后果可能包括局部组织缺氧和坏死。
我们对 2000 年以来发表的有关复杂性区域疼痛综合征中肿瘤坏死因子-α的文章进行了综述。
我们提出，过度的局部炎症、随后交感神经血管收缩神经元 N 型钙通道电流抑制以及血管周围终端交感神经递质释放减少，破坏了复杂性区域疼痛综合征中交感皮肤血管收缩活性。由此产生的微血管紊乱可能使受累肢体的炎症恶化。此外，胆碱能抗炎途径功能不足可能导致肿瘤坏死因子-α过度产生。目前尚无大型随机对照治疗研究来检验选择性抗肿瘤坏死因子-α药物治疗复杂性区域疼痛综合征的疗效，但许多小规模研究和病例报告表明，一些情况下直接或间接靶向肿瘤坏死因子-α的抗炎药物治疗可改善疼痛和其他症状。
过度的炎症细胞因子级联反应可能导致复杂性区域疼痛综合征的感觉和自主神经紊乱。需要进一步研究抗肿瘤坏死因子-α治疗作为这种破坏性疾病的一种具有成本效益的治疗选择。胆碱能抗炎途径活性增加是否为复杂性区域疼痛综合征提供治疗益处也值得进一步研究。
