Peripheral pain mechanisms in chronic widespread pain.
Peripheral pain mechanisms in chronic widespread pain.
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DOI：
10.1016/j.berh.2010.01.010
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发表时间：
2011-04
影响因子：
5.2
通讯作者：
Staud, Roland
中科院分区：
文献类型：
--
作者：
Staud, Roland
慢性广泛性疼痛(CWP)的临床症状包括纤维肌痛(FM)，包括疼痛、僵硬、主观无力和肌肉疲劳。煤工尘肺的肌肉疼痛通常被描述为波动的，通常与局部或全身性压痛(痛觉过敏和/或超敏)有关。这种与肌肉疼痛相关的压痛依赖于外周和/或中枢神经系统对外周刺激的反应增加，外周刺激可以是伤害性的(痛觉过敏)，也可以是非伤害性的(超感痛觉)。例如，肌肉痛觉过敏的患者会比正常对照组对疼痛的肌肉刺激的评分更高，而异位痛症患者可能会认为轻微的触摸是痛苦的，这是一个“正常”的人永远不会描述为痛苦的事情。CWP的外周和/或中枢神经系统改变的发病机制尚不清楚，但已涉及外周软组织改变。来自干预措施的间接证据表明，在像FM这样的CWP综合征患者中，减弱紧张性外周伤害性冲动的间接证据表明，总体FM疼痛依赖于外周输入。更重要的是，可以通过去除外周冲动输入来改善或消除超敏和痛觉过敏。煤工尘肺疼痛的另一个潜在机制是中枢去抑制。然而，这种疼痛机制也依赖于紧张性冲动的输入，即使只是不充分地抑制。因此，了解CWP的一个有希望的方法是确定深层组织中受体的异常活动是否对这种慢性疼痛障碍的发展和维持至关重要。大多数煤工尘肺患者存在局部组织异常，包括肌筋膜触发点、韧带触发点或关节和脊柱的骨性关节炎。虽然这些变化不能预测煤工尘肺的发展，但它们代表了重要的疼痛产生因素，可能会引发或延续慢性疼痛。局部化学介质，包括乳酸、三磷酸腺苷和细胞因子，似乎在煤工尘肺患者深层组织伤害性感受器的敏化中起着重要作用。因此，外周冲动输入和中枢性疼痛敏感性增加的组合可能是包括FM在内的广泛传播的慢性疼痛障碍的原因。
Clinical symptoms of chronic widespread pain (CWP) conditions including fibromyalgia (FM), include pain, stiffness, subjective weakness, and muscle fatigue. Muscle pain in CWP is usually described as fluctuating and often associated with local or generalized tenderness (hyperalgesia and/or allodynia). This tenderness related to muscle pain depends on increased peripheral and/or central nervous system responsiveness to peripheral stimuli which can be either noxious (hyperalgesia) or non-noxious (allodynia). For example, patients with muscle hyperalgesia will rate painful muscle stimuli higher than normal controls, whereas patients with allodynia may perceive light touch as painful, something that a “normal” individual will never describe as painful. The pathogenesis of such peripheral and/or central nervous system changes in CWP is unclear, but peripheral soft tissue changes have been implicated. Indirect evidence from interventions that attenuate tonic peripheral nociceptive impulses in patients with CWP syndromes like FM suggest that overall FM pain is dependent on peripheral input. More importantly, allodynia and hyperalgesia can be improved or abolished by removal of peripheral impulse input. Another potential mechanism for CWP pain is central disinhibition. However, this pain mechanism also depends on tonic impulse input, even if only inadequately inhibited. Thus a promising approach to understanding CWP is to determine whether abnormal activity of receptors in deep tissues is fundamental to the development and maintenance of this chronic pain disorder. Most CWP patients present with focal tissue abnormalities including myofascial trigger points, ligamentous trigger points, or osteoarthritis of the joints and spine. While not predictive for the development of CWP these changes nevertheless represent important pain generators that may initiate or perpetuate chronic pain. Local chemical mediators, including lactic acid, ATP, and cytokines seem to play an important role in sensitizing deep tissue nociceptors of CWP patients. Thus the combination of peripheral impulse input and increased central pain sensitivity may be responsible for wide-spread chronic pain disorders including FM.
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