Brietzke Aline Patrícia, Antunes Luciana Conceição, Carvalho Fabiana, Elkifury Jessica, Gasparin Assunta, Sanches Paulo Roberto Stefani, da Silva Junior Danton Pereira, Dussán-Sarria Jairo Alberto, Souza Andressa, da Silva Torres Iraci Lucena, Fregni Felipe, Md Wolnei Caumo
Post-Graduate Program in Medical Sciences, Medical Engineering Service.
Faculdade de Medicina da Universidade Federal do Rio Grande do Sul, Porto Alegre.
Medicine (Baltimore). 2019 Jan;98(3):e13477. doi: 10.1097/MD.0000000000013477.
Fibromyalgia (FM) is characterized by chronic widespread pain whose pathophysiological mechanism is related to central and peripheral nervous system dysfunction. Neuropathy of small nerve fibers has been implicated due to related pain descriptors, psychophysical pain, and neurophysiological testing, as well as skin biopsy studies. Nevertheless, this alteration alone has not been previously associated to the dysfunction in the descending pain modulatory system (DPMS) that is observed in FM. We hypothesize that they associated, thus, we conducted a cross-sectional exploratory study.To explore small fiber dysfunction using quantitative sensory testing (QST) is associated with the DPMS and other surrogates of nociceptive pathways alterations in FM.We run a cross-sectional study and recruited 41 women with FM, and 28 healthy female volunteers. We used the QST to measure the thermal heat threshold (HTT), heat pain threshold (HPT), heat pain tolerance (HPT), heat pain tolerance (HPTo), and conditional pain modulation task (CPM-task). Algometry was used to determine the pain pressure threshold (PPT). Scales to assess catastrophizing, anxiety, depression, and sleep disturbances were also applied. Serum brain-derived neurotrophic factor (BDNF) was measured as a marker of neuroplasticity. We run multivariate linear regression models by group to study their relationships.Samples differed in their psychophysical profile, where FM presented lower sensitivity and pain thresholds. In FM but not in the healthy subjects, regression models revealed that serum BDNF was related to HTT and CPM-Task (Hotelling Trace = 1.80, P < .001, power = 0.94, R = 0.64). HTT was directly related to CPM-Task (B = 0.98, P = .004, partial-η = 0.25), and to HPT (B = 1.61, P = .008, partial η = 0.21), but not to PPT. Meanwhile, BDNF relationship to CPM-Task was inverse (B = -0.04, P = .043, partial-η = 0.12), and to HPT was direct (B = -0.08, P = .03, partial-η = 0.14).These findings high spot that in FM the disinhibition of the DPMS is positively correlated with the dysfunction in peripheral sensory neurons assessed by QST and conversely with serum BDNF.
纤维肌痛(FM)的特征是慢性广泛性疼痛,其病理生理机制与中枢和外周神经系统功能障碍有关。由于相关的疼痛描述、心理物理性疼痛、神经生理学测试以及皮肤活检研究,小神经纤维的神经病变被牵连其中。然而,此前这种改变尚未与FM中观察到的下行疼痛调节系统(DPMS)功能障碍相关联。我们假设它们之间存在关联,因此,我们进行了一项横断面探索性研究。为了探究使用定量感觉测试(QST)检测到的小纤维功能障碍是否与FM中的DPMS以及伤害性感受通路改变的其他替代指标相关。我们开展了一项横断面研究,招募了41名患有FM的女性和28名健康女性志愿者。我们使用QST来测量热痛阈值(HTT)、热痛阈(HPT)、热痛耐受(HPT)、热痛耐受(HPTo)以及条件性疼痛调节任务(CPM任务)。使用压力测痛法来确定疼痛压力阈值(PPT)。还应用了评估灾难化、焦虑、抑郁和睡眠障碍的量表。测量血清脑源性神经营养因子(BDNF)作为神经可塑性的标志物。我们按组运行多元线性回归模型来研究它们之间的关系。样本在心理物理特征方面存在差异,FM患者表现出较低的敏感性和疼痛阈值。在FM患者而非健康受试者中,回归模型显示血清BDNF与HTT和CPM任务相关(霍特林迹值=1.80,P<0.001,功效=0.94,R=0.64)。HTT与CPM任务直接相关(B=0.98,P=0.004,偏η=0.25),与HPT也直接相关(B=1.61,P=0.008,偏η=0.21),但与PPT无关。同时,BDNF与CPM任务的关系呈负相关(B=-0.04,P=0.043,偏η=0.12),与HPT呈正相关(B=-0.08,P=0.03,偏η=0.14)。这些发现突出表明,在FM中,DPMS的去抑制与通过QST评估的外周感觉神经元功能障碍呈正相关,与血清BDNF呈负相关。