Group differences in pain modulation: pain-free women compared to pain-free men and to women with TMD

Group differences in pain modulation: pain-free women compared to pain-free men and to women with TMD
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DOI:
10.1016/s0304-3959(01)00451-1
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发表时间:
2002-04-01
期刊:
影响因子:
7.4
通讯作者:
Maixner, W
Maixner, W
中科院分区:
医学1区
文献类型:
--
作者:
Bragdon, EE;Light, KC;Maixner, W

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以前报道的性别之间的实验性疼痛刺激的敏感性的差异,以及颞下颌关节紊乱病(TMD)患者和健康对照组之间,可能是由于部分组的差异,在两个疼痛调节机制:压力感受器反射弧和内源性阿片系统。22名无痛(PF)男性,20名PF女性和20名TMD女性进行了两次测试,在这两次测试中测量了热痛和缺血性手臂疼痛阈值和耐受性,但在一次测试中放松,在另一次测试中进行了实验室压力测试。血压(BP)和血浆β-内啡肽(β E)浓度在基线休息期间和在应力或放松期间进行测量。PF男性的热痛阈值和耐受性,但不是缺血性疼痛,超过了PF女性在这两个会议。PF妇女和TMD妇女对疼痛方式的敏感性没有差异;然而,PF妇女口服避孕药与缺血性疼痛阈值(IPTh)显著降低有关,而TMD患者与此无关。在单独的男性中,较高的基线收缩压(SBP)与这两天较高的热痛阈值和应激日的热痛耐受性相关。相反,在TMD女性中,较高的基线SBP与两天的较低的缺血性疼痛耐受性(IPTol)相关; PF女性的BP和疼痛敏感性无关。在男性中,但不是在PF或TMD女性,压力收缩压和舒张压呈正相关,热痛阈值和耐受性和较高的舒张期应激反应与较高的热痛和IPTh和耐受性。在压力日,较高的基线β E水平与PF妇女的IPTol较高密切相关,但与TMD妇女的IPTol较低轻微相关。因此,看来BP相关的镇痛机制(可能是压力感受器介导的)占主导地位的PF男性,而内源性阿片类药物的机制占主导地位的PF女性。应激增强了这些中枢机制的表达。女性TMDs似乎无法有效地参与正常的疼痛抑制系统;阿片受体脱敏和/或下调可能涉及,因为TMDs的β E产生似乎正常。(C)2002年国际疼痛研究协会。由Elsevier Science B. V.出版,版权所有。
Previously reported differences in sensitivity to experimental pain stimuli between the sexes, as well as between temporomandibular disorder (TMD) patients and healthy control subjects, may be attributable in part to group differences in two pain modulatory mechanisms: the baroreceptor reflex arc and the endogenous opioid system. Twenty-two pain-free (PF) men, 20 PF women and 20 women with TMD underwent two testing sessions in which heat pain and ischemic arm pain threshold and tolerance were measured during both sessions, but followed relaxation during one session and laboratory stress tasks during the other. Blood pressure (BP) and plasma beta-endorphin (betaE) concentration were measured during a baseline rest and during the stress or relaxation periods. PF men's threshold and tolerance for heat pain, but not for ischemic pain, exceeded that of PF women's during both sessions. PF women and TMD women did not differ in sensitivity to either pain modality; however, significantly lower ischemic pain threshold (IPTh) was linked to oral contraceptive use in PF women but not TMD patients. In the men alone, higher baseline systolic BP (SBP) was correlated with higher heat pain threshold on both days and heat pain tolerance on the stress day. Conversely, in TMD women, higher baseline SBP was correlated with lower ischemic pain tolerance (IPTol) on both days; BP and pain sensitivity were not related in PF women. In men, but not in PF or TMD women, stress systolic and diastolic BP were positively correlated with heat pain threshold and tolerance and higher diastolic reactivity to stress were correlated with higher heat pain and IPTh and tolerance. On the stress day, higher baseline betaE level was strongly associated with higher IPTol in PF women but marginally associated with lower IPTol in TMD women. Thus, it appears that a BP-related analgesic mechanism (probably baroreceptor-mediated) predominates in PF men, while an endogenous opioid mechanism predominates in PF women. Stress enhances the expression of these central mechanisms. Female TMDs appear unable to effectively engage normal pain-inhibitory systems; opioid receptor desensitization and/or downregulation are probably implicated, because TMDs' production of betaE appears normal. (C) 2002 International Association for the Study of Pain. Published by Elsevier Science B.V. All rights reserved.