Suzan Erica, Treister Roi, Pud Dorit, Haddad May, Eisenberg Elon
Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel; Institute of Pain Medicine, Rambam Health Care Campus, Haifa, Israel.
Pain Med. 2015 Jan;16(1):168-75. doi: 10.1111/pme.12565. Epub 2014 Sep 12.
Conditioned pain modulation (CPM) and offset analgesia (OA) are considered to represent paradigms of descending inhibitory pain modulation in humans. This study tested the effects of hydromorphone therapy on descending inhibitory pain modulation, as measured by changes from baseline in the magnitudes of CPM and OA.
Prospective evaluation.
Institute of Pain Medicine, Rambam Health Care Campus.
Patients with chronic radicular pain.
Thirty patients received 4 weeks of oral hydromorphone treatment at an individually titrated dose (mean ± standard deviation dose of 11.6 ± 4.8 mg/day). CPM and OA were assessed before and after hydromorphone treatment. CPM was assessed by subtracting the response to a painful phasic heat stimulus administered simultaneously with a conditioning cold pain stimulus, from the response to the same heat stimulus administered alone. The OA paradigm consisted of a three-temperature stimuli train (T1 = 49°C [5 seconds], T2 = 50°C [5 seconds], and T3 = 49°C [20 seconds]). The magnitude of OA was quantified by subtracting minimal pain scores obtained during T3 from the maximal pain scores obtained during T2.
CPM scores changed from a baseline of 17.7 ± 20.6 to 21 ± 20.4 following treatment, and OA scores changed from 7.8 ± 20.5 to 9.7 ± 14.6. Wilcoxon signed rank test indicated that these changes were not significant (CPM: P = 0.22; OA: P = 0.44). McNemar test revealed that the percentage of patients who exhibited a change in the direction of CPM or OA in response to hydromorphone treatment was not significant (CPM: P = 0.37; OA: P = 0.48).
These results suggest that the descending inhibitory pain modulation, as manifested in humans by CPM and OA, is unlikely to be mediated by hydromorphone therapy.
条件性疼痛调制(CPM)和抵消性镇痛(OA)被认为是人类下行性抑制性疼痛调制的范例。本研究测试了氢吗啡酮治疗对下行性抑制性疼痛调制的影响,通过CPM和OA幅度相对于基线的变化来衡量。
前瞻性评估。
兰巴姆医疗保健校园疼痛医学研究所。
慢性根性疼痛患者。
30名患者接受了为期4周的口服氢吗啡酮治疗,剂量为个体化滴定剂量(平均±标准差剂量为11.6±4.8毫克/天)。在氢吗啡酮治疗前后评估CPM和OA。CPM通过将与条件性冷痛刺激同时施加的疼痛相位热刺激的反应,减去单独施加相同热刺激的反应来评估。OA范例包括一个三温度刺激序列(T1 = 49°C [5秒],T2 = 50°C [5秒],T3 = 49°C [20秒])。OA的幅度通过从T2期间获得的最大疼痛评分中减去T3期间获得的最小疼痛评分来量化。
治疗后CPM评分从基线的17.7±20.6变为21±20.4,OA评分从7.8±20.5变为9.7±14.6。Wilcoxon符号秩检验表明这些变化不显著(CPM:P = 0.22;OA:P = 0.44)。McNemar检验显示,因氢吗啡酮治疗而在CPM或OA方向上出现变化的患者百分比不显著(CPM:P = 0.37;OA:P = 0.48)。
这些结果表明,在人类中由CPM和OA表现出的下行性抑制性疼痛调制不太可能由氢吗啡酮治疗介导。