Peikert A, Hentrich M, Ochs G
Neurologische Klinik und Poliklinik, Technischen Universität, München, Federal Republic of Germany.
J Neurol. 1991 Dec;238(8):452-6. doi: 10.1007/BF00314653.
In order to evaluate the efficacy, time-course of action and predictors of response to topical capsaicin, 39 patients with chronic post-herpetic neuralgia (PHN), median duration 24 months, were treated with 0.025% capsaicin cream for 8 weeks. During therapy the patients rated their pain on a visual analogue scale (VAS) and a verbal outcome scale. A follow-up investigation was performed 10-12 months after study onset on the patients who had improved. Nineteen patients (48.7%) substantially improved after the 8-week trial; 5 (12.8%) discontinued therapy due to side-effects such as intolerable capsaicin-induced burning sensations (4) or mastitis (1); 15 (38.5%) reported no benefit. The decrease in VAS ratings was significant after 2 weeks of continuous application. Of the responders 72.2% were still improved at the follow-up; only one-third of them had continued application irregularly. Treatment effect was not dependent on patient's age, duration or localization of PHN (trigeminal involvement was excluded), sensory disturbance or pain character. Treatment response was not correlated with the incidence, time-course or severity of capsaicin-induced burning. If confirmed in controlled trials, the long-term results of this open, non-randomized study might indicate that the analgesic effect of capsaicin in PHN is mediated by both interference with neuropeptide metabolism and morphological changes (perhaps degeneration) of nociceptive afferents.
为了评估局部应用辣椒素的疗效、作用时程及反应预测因素,对39例慢性带状疱疹后神经痛(PHN)患者(中位病程24个月)用0.025%辣椒素乳膏治疗8周。治疗期间,患者根据视觉模拟量表(VAS)和语言结果量表对疼痛进行评分。对病情改善的患者在研究开始后10 - 12个月进行随访调查。8周试验后,19例患者(48.7%)病情显著改善;5例(12.8%)因难以忍受的辣椒素引起的烧灼感(4例)或乳腺炎(1例)等副作用而停止治疗;15例(38.5%)报告无疗效。连续应用2周后,VAS评分显著降低。在随访时,72.2%的有反应者病情仍有改善;其中只有三分之一的人不规则地继续用药。治疗效果不取决于患者的年龄、PHN的病程或部位(排除三叉神经受累)、感觉障碍或疼痛性质。治疗反应与辣椒素引起的烧灼感的发生率、时程或严重程度无关。如果在对照试验中得到证实,这项开放、非随机研究的长期结果可能表明,辣椒素在PHN中的镇痛作用是通过干扰神经肽代谢和伤害性传入神经的形态学变化(可能是退变)介导的。