A possible mechanism underlying conditioned pain modulation.
A possible mechanism underlying conditioned pain modulation.
复制标题
条件性疼痛调节的可能机制。
DOI：
10.1016/j.pain.2014.02.011
复制
发表时间：
2014
期刊：
影响因子：
7.4
通讯作者：
King,ChristopherD
中科院分区：
文献类型：
--
作者：
King,ChristopherD
在过去的几年里，人们对抑制疼痛的能力，特别是与条件性疼痛调制(CPM)相关的能力的兴趣与日俱增。CPM通常被用来测量人类内源性疼痛抑制的效果，方法是在一定的时间模式下施加两个疼痛刺激，并评估第二个条件刺激对主要刺激的疼痛减轻程度。由此产生的抑制被认为是下行抑制机制激活的结果。CPM在临床研究中的应用为慢性疼痛中这些下行抑制机制的可能功能障碍提供了洞察力[14，26]。尽管已有研究表明纤维肌痛综合征(FMS)患者的CPM减少，但我们对内源性疼痛调制的潜在机制的了解存在缺陷，这凸显了进一步研究的必要性，特别是在慢性疼痛的背景下。Chalaye等人最近对一个潜在的机制进行了评估。该小组以前的一项研究[4]发现，在健康对照组中，心血管对条件性刺激(即冷水浴)的反应与CPM的大小呈正相关。在目前的研究[5]中，该范例在FMS患者中进行了评估。在CPM过程中进行了几个有趣的观察：(1)与对照组相比，在12℃下浸泡2分钟，FMS患者的心血管反应减弱(即收缩压[SBP]变化较小)；以及(2)SBP变化的幅度与CPM的幅度呈正相关(即，浸泡期间SBP上升更大=热敏感度下降更大)。在控制了浸泡时间后，其他心血管因素与CPM无关。Chalaye等人。可能提供了关于FMS疼痛调制缺陷的一块拼图，即对条件性刺激的心血管反应减弱。先前的研究表明，患有FMS的人调节心血管功能的能力受损[25]，包括对冷浸泡的交感反应性降低[20]。总体而言，FMS患者疼痛抑制功能障碍的部分原因可能是无法对条件性刺激产生“适当”的心血管反应。这项研究提出了几个与SBP和CPM效率之间的相互作用相关的问题，这些问题可能会指导未来这一领域的研究：
Over the past few years, interest in the ability to inhibit pain particularly related to conditioned pain modulation (CPM) has grown. CPM is commonly used to measure the efficacy of endogenous pain inhibition in humans by applying two painful stimuli in some temporal pattern and evaluating the degree of pain reduction of the primary stimulus by the second ‘‘conditioning’’stimulus. The resulting inhibition is thought to be a consequence of the activation of descending inhibitory mechanisms. The application of CPM in clinical studies has provided insights into the possible dysfunction of these descending inhibitory mechanisms in chronic pain [14, 26]. Although it has been shown that patients with fibromyalgia syndrome (FMS) exhibit reduced CPM, deficits in our understanding of the underlying mechanisms of endogenous pain modulation highlight the need for additional research particularly in the context of chronic pain.One potential mechanism was recently evaluated by Chalaye et al.[5]. A previous study by this group [4] found that cardiovascular responses to the conditioning stimulus (ie, cold water bath) were positively associated with the magnitude of CPM in healthy controls. In the current study [5], the paradigm was evaluated in patients with FMS. Several interesting observations were made during the CPM procedure:(1) individuals with FMS exhibited an attenuated cardiovascular response (ie, smaller changes in systolic blood pressure [SBP]) during a 2-minute immersion at 12 C compared to that in controls; and (2) the magnitude of the SBP change was positively associated with the magnitude of CPM (ie, greater increase in SBP during immersion= greater reduction in heat sensitivity). Additional cardiovascular factors were not associated with CPM after controlling for immersion time. Chalaye et al. may have offered 1 piece of the puzzle regarding deficits in pain modulation in FMS, namely, attenuated cardiovascular responsiveness to the conditioning stimulus. Previous studies have shown that individuals with FMS have an impaired ability to regulate cardiovascular functioning [25], including reduced sympathetic reactivity to cold immersion [20]. Overall, dysfunction of pain inhibition in FMS could be, in part, a result of an inability to mount a ‘‘proper’’cardiovascular response to the conditioning stimulus. The study raises several questions related to the interaction between SBP and CPM efficiency that may direct this area of research in the future: