Torebjörk Erik, Wahren LisKarin, Wallin Gunnar, Hallin Rolf, Koltzenburg Martin
Department of Clinical Neurophysiology, University Hospital in Uppsala, Sweden Department of Clinical Neurophysiology, University Hospital in Gothenburg, Sweden Department of Clinical Neurophysiology, University Hospital in Huddinge, Sweden Department of Neurology, University of Würzburg, Germany.
Pain. 1995 Oct;63(1):11-20. doi: 10.1016/0304-3959(95)00140-N.
We have tested the effects of cutaneous application of noradrenaline in 35 patients presenting with neuropathic pain. Depending on the outcome of sympatholytic interventions the patients were considered to have sympathetically maintained pain (SMP; n = 25) or sympathetically independent pain (SIP; n = 10). Iontophoretic application or cutaneous injection of noradrenaline into symptomatic skin aggravated pain and mechanical or thermal hyperalgesia in 7/25 SMP patients. Results from differential nerve blocks suggested that noradrenaline-induced ongoing pain and heat hyperalgesia were signalled by unmyelinated afferents, while touch-evoked pain and cold hyperalgesia were signalled by myelinated afferents. In none of the remaining 18/25 SMP patients, 10 SIP patients or 18 normal subjects did application of noradrenaline result in any appreciable increase of pain. A follow-up of 12 patients (initially 9 SMP, 3 SIP) after 12-16 years showed that one individual (previously SMP) was healthy, while 3 patients still suffered from SMP and 8 from SIP. Of the 5 SMP patients who had noradrenaline-induced pain at the initial examination, only 1 SMP patient still responded to noradrenaline with pain and hyperalgesia. Three other patients had changed to SIP and 1 individual was healthy. None of these 4 and none of the 7 initially noradrenaline-unresponsive patients experienced pain to the noradrenaline challenge at follow-up. Thus, cutaneous noradrenaline application can aggravate the pain in some, but not all SMP patients. THe abnormal noradrenaline reaction can change over time as can the pain relieving effects of sympatholytic therapy.
我们对35例神经性疼痛患者进行了皮肤应用去甲肾上腺素的效果测试。根据交感神经阻滞干预的结果，这些患者被认为患有交感神经维持性疼痛（SMP；n = 25）或交感神经独立性疼痛（SIP；n = 10）。对有症状的皮肤进行离子电渗法应用或注射去甲肾上腺素会使7/25例SMP患者的疼痛及机械性或热痛觉过敏加重。差异神经阻滞的结果表明，去甲肾上腺素诱发的持续性疼痛和热痛觉过敏由无髓传入神经传导信号，而触觉诱发的疼痛和冷痛觉过敏由有髓传入神经传导信号。在其余的18/25例SMP患者、10例SIP患者或18例正常受试者中，应用去甲肾上腺素均未导致疼痛有任何明显增加。对12例患者（最初9例SMP，3例SIP）进行12 - 16年的随访发现，1例个体（之前为SMP）健康，3例患者仍患有SMP，8例患有SIP。在初始检查时有去甲肾上腺素诱发疼痛的5例SMP患者中，只有1例SMP患者对去甲肾上腺素仍有疼痛和痛觉过敏反应。另外3例患者已转变为SIP，1例个体健康。这4例患者以及最初对去甲肾上腺素无反应的7例患者在随访时对去甲肾上腺素激发试验均未出现疼痛。因此，皮肤应用去甲肾上腺素可使部分而非全部SMP患者的疼痛加重。异常的去甲肾上腺素反应会随时间变化，交感神经阻滞治疗的止痛效果也会如此。
