Forstenpointner Julia, Naleschinski Dennis, Wasner Gunnar, Hüllemann Philipp, Binder Andreas, Baron Ralf
Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.
Neurological Clinic, Kiel, Germany.
Pain Rep. 2019 Jan 18;4(1):e709. doi: 10.1097/PR9.0000000000000709. eCollection 2019 Jan-Feb.
Multiple mechanisms are involved in the development and persistence of neuropathic pain. Some patients with nerve damage will remain painless and develop a "loss of function" phenotype, whereas others develop painful neuropathies.
The aim of this study is to investigate the role of a peripheral nervous system sensitization by analyzing patients with and without pain.
The topical application of capsaicin was investigated in peripheral nociceptors. Two groups of patients (painful vs painless) with length-dependent neuropathies and small-fiber impairment were tested. Quantitative sensory testing was assessed before and after topical application of 0.6% capsaicin in the affected skin. In addition, blood perfusion measurements and an axon reflex flare assessment were performed.
Quantitative testing revealed that heat hyperalgesia was induced in all patients and volunteers ( < 0.01) without observing any significant differences between patient groups. By contrast, the extent of the axon reflex flare reaction ( < 0.01) as well as the blood perfusion ( < 0.05) was significantly greater in patients with pain than in neuropathy patients not experiencing pain.
Hyperexcitable vasoactive nociceptive C fibers might contribute to pain in peripheral neuropathies and therefore may serve as a key player in separating into a painless or painful condition.
神经性疼痛的发生和持续涉及多种机制。一些神经损伤患者将保持无痛状态并发展为“功能丧失”表型，而另一些患者则会发展为疼痛性神经病变。
本研究旨在通过分析有疼痛和无疼痛的患者来探讨外周神经系统致敏的作用。
研究了辣椒素在外周伤害感受器上的局部应用。对两组患有长度依赖性神经病变和小纤维损伤的患者（疼痛组与无痛组）进行了测试。在受影响的皮肤局部应用0.6%辣椒素之前和之后评估定量感觉测试。此外，还进行了血流灌注测量和轴突反射性潮红评估。
定量测试显示，所有患者和志愿者均诱发了热痛觉过敏（P<0.01），且未观察到患者组之间有任何显著差异。相比之下，有疼痛的患者轴突反射性潮红反应的程度（P<0.01）以及血流灌注（P<0.05）显著高于无疼痛的神经病变患者。
血管活性伤害性C纤维的过度兴奋可能导致外周神经病变中的疼痛，因此可能是区分无痛或疼痛状态的关键因素。
