Characterisation of capsaicin-induced mechanical hyperalgesia as a marker for altered nociceptive processing in patients with rheumatoid arthritis
Characterisation of capsaicin-induced mechanical hyperalgesia as a marker for altered nociceptive processing in patients with rheumatoid arthritis
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DOI：
10.1016/s0304-3959(97)03361-7
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发表时间：
1997-06-01
期刊：
影响因子：
7.4
通讯作者：
Kidd, BL
中科院分区：
文献类型：
--
作者：
Morris, VH;Cruwys, SC;Kidd, BL
类风湿性关节炎（RA）的特点是疼痛和压痛，不仅发生在发炎或受损的关节上，而且还发生在明显正常的组织上。实验模型表明这些特征是由周围和中枢神经元内的敏感性变化引起的，但缺乏来自人类疾病的直接证据。目前，大多数临床研究评估的是整体疼痛体验，而不是伤害感受通路各组成部分的活动。因此，本研究的目的是评估使用基于辣椒素的技术来量化 RA 患者神经元敏感性的变化。首先将20μl的辣椒素溶液(0.03mg/ml)局部施用到对照受试者和RA患者前臂上明显正常的皮肤上30分钟。然后使用 74.4 mN von Frey 毛发在不同时间点测量随后对针刺刺激的机械痛觉过敏的发展。确定了痛觉过敏的面积与许多临床测量之间的关系。在正常受试者中，辣椒素引起的机械性痛觉过敏随着年龄的增长而下降（r = 0.47，P < 0.01）。正常受试者和 RA 患者痛觉过敏的发生时间相似。然而，35 名 RA 患者中痛觉过敏的最大面积要大得多； 254.3 +/- 20.7 cm(2)，与 35 名正常对照相比； 109 +/- 7.5 厘米(2) (P < 0.001)。痛觉过敏面积与关节压痛综合评分之间存在明显关联（r = 0.47，P < 0.01），但与总体疼痛评分或全身炎症标志物无关。这些结果为 RA 中感觉纤维群的敏感性增强提供了证据。类风湿患者前臂的外周感觉活动先前已被证明是正常的，结果表明这种疾病中存在增强的中枢机制。辣椒素引起的痛觉过敏与 RA 患者关节压痛之间的相关性表明，关节症状部分是由中枢因素而非完全是外周因素引起的。该研究支持使用基于辣椒素的技术来探索以慢性疼痛为特征的临床疾病的伤害感受机制。 (C) 1997 年国际疼痛研究协会。
Rheumatoid arthritis (RA) is characterised by pain and tenderness not only over inflamed or damaged joints, but also over apparently normal tissues. Experimental models suggest that these features result from changes of sensitivity within both peripheral and central neurones, but direct evidence from human disease is lacking. At present, most clinical studies have evaluated overall pain experience rather than activity within components of the nociceptive pathway. Therefore, the aim of this study was to assess the use of a capsaicin-based technique to quantify changes of neuronal sensitivity in patients with RA. First 20 mu l of capsaicin in solution (0.03 mg/ml) was applied topically for 30 min to apparently normal skin on the forearm of control subjects and patients with RA. The subsequent development of mechanical hyperalgesia to pinprick stimuli was then measured at various time points using a 74.4-mN von Frey hair. The relationship between the area of hyperalgesia and a number of clinical measures was determined. Capsaicin-induced mechanical hyperalgesia was found to decline with age in normal subjects (r = 0.47, P < 0.01). The development of hyperalgesia had a similar time course in normal subjects and patients with RA. The maximum area of hyperalgesia, however, was substantially larger in 35 RA patients; 254.3 +/- 20.7 cm(2), compared with 35 normal controls; 109 +/- 7.5 cm(2) (P < 0.001). An association was apparent between hyperalgesic area and a composite score of joint tenderness (r = 0.47, P < 0.01), but not with overall pain score ora systemic marker of inflammation. These results provide evidence for enhanced sensitisation of a population of sensory fibres in RA. Peripheral sensory activity over the forearms of rheumatoid patients has previously been shown to be normal and the results suggest the presence of enhanced central mechanisms in this disorder. The correlation between capsaicin-induced hyperalgesia and joint tenderness in the RA patients implies that joint symptoms arise partially as a result of central, and not exclusively peripheral, factors. The study supports the use of capsaicin-based techniques to explore nociceptive mechanisms in clinical disorders characterised by chronic pain. (C) 1997 International Association for the Study of Pain.