Conditioned pain modulation and offset analgesia: Different avenues to inhibit pain.
Conditioned pain modulation and offset analgesia: Different avenues to inhibit pain.
复制标题
条件性疼痛调节和补偿镇痛：抑制疼痛的不同途径。
DOI：
10.1016/j.pain.2014.08.017
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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，身体调节感觉信息的能力一直是许多研究的焦点。在实验上，疼痛调制可以通过许多方法来评估，包括条件疼痛调制(CPM)和抵消止痛(OA)，如Nahman-Averuch等人目前的研究强调的那样。CPM通常通过第二个远程条件性刺激(即冷水浸泡[6，9，17，22，23])减少一个主要的疼痛刺激(即局部热刺激)而表现出来。相比之下，OA是通过使用延长的热脉冲来演示的，在该脉冲中，热模式温度(即1摄氏度)的轻微降低与疼痛强度的瞬时(10 S)降低相关[7，15，16，18，29，30]。虽然只有一小部分研究评估了相同队列中的CPM和OA[8，17，18，20]，但这些抑制模型的联合使用可能会让我们一窥个体抑制表型背后的不同特征，这可能对未来的实验和临床研究有意义。纳赫曼-阿维鲁奇等人的这项研究[15]旨在调查CPM和OA的心理物理和神经相关性之间的差异。使用相同的热刺激模式(即，对腿部施加49摄氏度的30s延长脉冲)，研究表明，在将对侧足部同时浸入中等疼痛的冷水浴(CPM诱导)和温度下降1摄氏度(OA诱导)的同时，热痛的主观分级都有所降低-观察结果与之前的研究一致[6，7，9，10，15，16，23，30]。然而，在两个模型中观察到的抑制程度并不相关，这表明潜在的抑制机制不同。证实了心理物理数据，每个范式的fMRI评估显示出皮质和皮质下活动的差异。总体而言，在CPM期间，在一些经典的疼痛相关区域观察到了广泛的失活，这与在OA范例中包括与导水管周围灰质(PAG)相关的脑干区域的激活形成了对比。根据目前的研究，疼痛调制的差异依赖于伤害性信息的空间(CPM)和时间(OA)呈现，这反过来又导致涉及疼痛感知和调制的区域的神经生物学活动的不同模式。更重要的是，这项研究增加了对不同抑制机制(CPM与OA)以及不同抑制范式(CPM的变体)的方法和含义的讨论。
The ability of the body to modulate sensory information has been a focus of a number of studies over the past several years. Experimentally, pain modulation can be assessed by a number of methods including conditioned pain modulation (CPM) and offset analgesia (OA) as highlighted in the current study by Nahman-Averbuch et al.[15]. CPM is frequently demonstrated through the reductions of a primary painful stimulus (ie, focal heat) by a second remote conditioning stimulus (ie, cold water immersion [6, 9, 17, 22, 23]). In contrast, OA is demonstrated by using a prolonged thermal pulse in which a slight reduction in the thermode temperature (ie, 1 C) is associated with a transient (10 s) reduction in pain intensity [7, 15, 16, 18, 29, 30]. Although only a small number of studies have evaluated CPM and OA in the same cohort [8, 17, 18, 20], the combined use of these inhibitory models may provide a glimpse into different characteristics underlying an individual’s inhibitory phenotype, which could have implications for future experimental and clinical research. The study by Nahman-Averbuch et al.[15] was designed to investigate differences between the psychophysical and neural correlates of CPM and OA. Using the same thermal stimulation paradigm (ie, 30s prolonged pulse at 49 C applied to the leg), the studies demonstrated reductions in the subjective ratings of heat pain during both concurrent immersion of the contralateral foot into moderately painful cold water bath (CPM induction) and following a 1 C temperature drop (OA induction)—observations that are in agreement with those of previous studies [6, 7, 9, 10, 15, 16, 23, 30]. However, the magnitude of inhibition observed in the 2 models did not correlate suggesting different mechanisms underlying inhibition. Confirming the psychophysical data, fMRI assessment of each paradigm demonstrated differences in cortical and subcortical activity. In general, widespread deactivations were observed in a number of classical pain-related areas during CPM, which was contrasted by activation in a number of areas including the brain stem region associated with the periaqueductal gray (PAG) during the OA paradigm. Based on the current study, differences in the modulation of pain are dependent on the spatial (CPM) and temporal (OA) presentation of nociceptive information, which in turn results in a differential pattern of neurobiological activity in areas involved in pain perception and modulation. More importantly, the study adds to the discussion about the methods and implications of different inhibitory mechanisms (CPM vs OA) and within different inhibitory paradigms (variations of CPM).