Resting Functional Connectivity of the Periaqueductal Gray Is Associated With Normal Inhibition and Pathological Facilitation in Conditioned Pain Modulation.
Resting Functional Connectivity of the Periaqueductal Gray Is Associated With Normal Inhibition and Pathological Facilitation in Conditioned Pain Modulation.
复制标题
DOI：
10.1016/j.jpain.2018.01.001
复制
发表时间：
2018-06
期刊：
影响因子：
--
通讯作者：
Harte SE
中科院分区：
文献类型：
--
作者：
Harper DE;Ichesco E;Schrepf A;Hampson JP;Clauw DJ;Schmidt-Wilcke T;Harris RE;Harte SE
条件性疼痛调节（CPM），一种心理物理学范式，通常用于推断内源性疼痛改变系统的完整性，通过观察一种有害刺激对另一种有害刺激的影响，以前已经确定了纤维肌痛（FM）和其他慢性疼痛条件的内源性镇痛不足。这种缺陷的机制，无论是抑制不足和/或主动促进，在很大程度上是未知的。本横断面研究使用了行为CPM测试，基于体素的形态测量（VBM）和静息状态功能连接的组合，以确定健康对照组（HC; n=14）和FM患者（n=15）中CPM的神经相关性，并探讨可以解释在我们的患者样本中观察到的疼痛促进CPM的差异。VBM确定了一个集群，包括周围导水管灰质（PAG），其中包含显着较少的灰质体积FM患者。在这两组中，该集群和皮质疼痛处理区域之间的静息连接性更高，与更有效的抑制CPM相关，而PAG与背侧脑桥的连接性仅在HC中与更大的CPM抑制相关。更大的PAG连接到脑桥尾侧/延髓头端，这是疼痛抑制HC，与FM疼痛易化。这些发现表明PAG静息功能连接强度的变化可以解释CPM的一些正常变异。此外，在FM患者中观察到的疼痛易化CPM可能涉及中枢神经系统中疼痛抑制过程的衰减和疼痛易化过程的放大。
Conditioned pain modulation (CPM), a psychophysical paradigm that is commonly used to infer the integrity of endogenous pain-altering systems by observation of the effect of one noxious stimulus on another, has previously identified deficient endogenous analgesia in fibromyalgia (FM) and other chronic pain conditions. The mechanisms underlying this deficiency, be they insufficient inhibition and/or active facilitation, are largely unknown. The present cross sectional study used a combination of behavioral CPM testing, voxel based morphometry (VBM), and resting state functional connectivity to identify neural correlates of CPM in healthy controls (HC; n=14) and FM patients (n=15), and to probe for differences that could explain the pain-facilitative CPM that was observed in our patient sample. VBM identified a cluster encompassing the periaqueductal gray (PAG) that contained significantly less gray matter volume in FM patients. Higher resting connectivity between this cluster and cortical pain processing regions was associated with more efficient inhibitory CPM in both groups, whereas PAG connectivity with the dorsal pons was associated with greater CPM inhibition only in HC. Greater PAG connectivity to the caudal pons/rostral medulla, which was pain-inhibitory in HC, was associated with pain facilitation in FM. These findings indicate that variation in the strength of the PAG's resting functional connectivity can explain some of the normal variability in CPM. In addition, pain-facilitative CPM observed in FM patients likely involves both attenuation of pain inhibitory and amplification of pain facilitative processes in the central nervous system.