Endogenous opioidergic dysregulation of pain in fibromyalgia: a PET and fMRI study.
Endogenous opioidergic dysregulation of pain in fibromyalgia: a PET and fMRI study.
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DOI：
10.1097/j.pain.0000000000000633
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发表时间：
2016-10
期刊：
影响因子：
7.4
通讯作者：
Harris RE
中科院分区：
文献类型：
--
作者：
Schrepf A;Harper DE;Harte SE;Wang H;Ichesco E;Hampson JP;Zubieta JK;Clauw DJ;Harris RE
内源性阿片系统功能障碍可能导致纤维肌痛（FM）的慢性疼痛，但尚不清楚这种功能障碍是否与已建立的痛觉过敏的神经生物学标志物有关。我们以前曾报道，与健康对照组相比，FM患者的m-阿片受体（莫尔）的可用性在几个疼痛处理脑区降低。在本研究中，我们比较了疼痛诱发的功能磁共振成像与内源性莫尔结合和临床疼痛评级的女性阿片类药物初治患者FM（n 5 - 18）使用全脑分析和我们以前的研究感兴趣的地区。在抗伤害性脑区，包括背外侧前额叶皮层（r 5 0.81，P，0.001）和前扣带皮层的多个区域（所有r。0.67;所有P均为0.02），降低的莫尔可用性与疼痛诱发的神经活动减少相关。此外，降低的莫尔可用性与丘脑底核中较低的脑激活相关（r 5 0.47，P 5 0.050）。在许多这些地区，疼痛诱发的活动和莫尔结合电位也与较低的临床情感疼痛评级。这些发现首次将内源性阿片系统张力与临床疼痛人群中局部疼痛诱发的脑活动联系起来。我们的数据表明，FM中内源性阿片系统的失调可能会导致传入伤害性刺激对抗伤害性脑区的兴奋减少，从而导致该人群中常见的痛觉过敏和异常性疼痛。我们提出了一个概念模型的情感性疼痛失调FM。
Endogenous opioid system dysfunction potentially contributes to chronic pain in fibromyalgia (FM), but it is unknown if this dysfunction is related to established neurobiological markers of hyperalgesia. We previously reported that m-opioid receptor (MOR) availability was reduced in patients with FM as compared with healthy controls in several pain-processing brain regions. In the present study, we compared pain-evoked functional magnetic resonance imaging with endogenous MOR binding and clinical pain ratings in female opioid-naive patients with FM (n 5 18) using whole-brain analyses and regions of interest from our previous research. Within antinociceptive brain regions, including the dorsolateral prefrontal cortex (r 5 0.81, P, 0.001) and multiple regions of the anterior cingulate cortex (all r. 0.67; all P, 0.02), reduced MOR availability was associated with decreased pain-evoked neural activity. Additionally, reduced MOR availability was associated with lower brain activation in the nucleus accumbens (r 5 0.47, P 5 0.050). In many of these regions, pain-evoked activity and MOR binding potential were also associated with lower clinical affective pain ratings. These findings are the first to link endogenous opioid system tone to regional pain-evoked brain activity in a clinical pain population. Our data suggest that dysregulation of the endogenous opioid system in FM could lead to less excitation in antinociceptive brain regions by incoming noxious stimulation, resulting in the hyperalgesia and allodynia commonly observed in this population. We propose a conceptual model of affective pain dysregulation in FM.
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