Kobuch Sophie, Fazalbhoy Azharuddin, Brown Rachael, Henderson Luke A, Macefield Vaughan G
School of Medicine, Western Sydney University, Sydney, Australia.
Neuroscience Research Australia, Sydney, Australia.
Hum Brain Mapp. 2017 Feb;38(2):869-881. doi: 10.1002/hbm.23424. Epub 2016 Oct 3.
Experimentally induced tonic muscle pain evokes divergent muscle vasoconstrictor responses, with some individuals exhibiting a sustained increase in muscle sympathetic nerve activity (MSNA), and others a sustained decrease. These patterns cannot be predicted from an individual's baseline physiological or psychological measures. The aim of this study was to investigate whether the different muscle sympathetic responses to tonic muscle pain were associated with differential changes in regional brain activity. Functional magnetic resonance imaging (fMRI) of the brain was performed concurrently with microelectrode recording of MSNA from the peroneal nerve during a 40-min infusion of hypertonic saline into the ipsilateral tibialis anterior muscle. MSNA increased in 26 and decreased in 11 of 37 subjects during tonic muscle pain. Within the prefrontal and cingulate cortices, precuneus, nucleus accumbens, caudate nucleus, and dorsomedial hypothalamus, blood oxygen level dependent (BOLD) signal intensity increased in the increasing-MSNA group and remained at baseline or decreased in the decreasing-MSNA group. Similar responses occurred in the dorsolateral pons and in the region of the rostral ventrolateral medulla. By contrast, within the region of the dorsolateral periaqueductal gray (dlPAG) signal intensity initially increased in both groups but returned to baseline levels only in the increasing-MSNA group. These results suggest that the divergent sympathetic responses to muscle pain result from activation of a neural pathway that includes the dlPAG, an area thought to be responsible for the behavioral and cardiovascular responses to psychological rather than physical stressors. Hum Brain Mapp 38:869-881, 2017. © 2016 Wiley Periodicals, Inc.
实验性诱导的强直性肌肉疼痛会引发不同的肌肉血管收缩反应，一些个体表现出肌肉交感神经活动（MSNA）持续增加，而另一些个体则表现为持续减少。这些模式无法根据个体的基线生理或心理测量指标进行预测。本研究的目的是调查对强直性肌肉疼痛的不同肌肉交感反应是否与区域脑活动的差异变化相关。在向同侧胫前肌输注40分钟高渗盐水的过程中，对大脑进行功能磁共振成像（fMRI），同时用微电极记录腓神经的MSNA。在强直性肌肉疼痛期间，37名受试者中有26名的MSNA增加，11名减少。在前额叶和扣带回皮质、楔前叶、伏隔核、尾状核和背内侧下丘脑区域，MSNA增加组的血氧水平依赖（BOLD）信号强度增加，而MSNA减少组则保持在基线水平或下降。在脑桥背外侧和延髓头端腹外侧区域也出现了类似的反应。相比之下，在背外侧导水管周围灰质（dlPAG）区域，两组的信号强度最初均增加，但仅在MSNA增加组恢复到基线水平。这些结果表明，对肌肉疼痛的不同交感反应是由一条神经通路的激活引起的，该神经通路包括dlPAG，该区域被认为负责对心理而非身体应激源的行为和心血管反应。《人类大脑图谱》38:869 - 881，2017年。© 2016威利期刊公司。
