Elevated insular glutamate in fibromyalgia is associated with experimental pain.
Elevated insular glutamate in fibromyalgia is associated with experimental pain.
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DOI：
10.1002/art.24849
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发表时间：
2009-10
影响因子：
--
通讯作者：
Clauw, Daniel J.
中科院分区：
文献类型：
--
作者：
Harris, Richard E.;Sundgren, Pia C.;Craig, A. D.;Kirshenbaum, Eric;Sen, Ananda;Napadow, Vitaly;Clauw, Daniel J.
由增强的兴奋性和/或减少的抑制性神经传递引起的中枢性疼痛增强是功能性疼痛综合征（如纤维肌痛（FM））的病理生理学基础的一种提出的机制。多功能磁共振成像（fMRI）研究表明，在这种情况下，小脑延髓是神经元活动增强的区域。由于谷氨酸（Glu）是一种主要的皮质兴奋性神经递质，在疼痛神经传递的功能，我们假设，岛叶谷氨酸水平的增加将存在于FM患者，这种分子的浓度将与疼痛报告。19名FM患者和14名年龄和性别匹配的无疼痛对照者进行了加压疼痛测试和质子磁共振波谱（H-MRS）检查，其中在休息时检查了右前和右后腰椎。与对照组相比，FM患者的右后髓内Glu（平均值（SD）：FM 8.09（0.72）; HC 6.86（1.29）; p=0.009）以及谷氨酸和谷氨酰胺（例如Glx;平均值（SD）：FM 12.38（0.94）; HC 10.59（1.48）; p=0.001）水平显著更高。在该区域内未检测到任何其他主要代谢物的差异（所有p>0.05），并且在右前额叶内未检测到任何代谢物的组间差异（所有p>0.10）。在右后颅窝，两组中Glu和Glx水平较高与压痛阈值较低相关（Glu：r=-0.43; p=0.012; Glx：r=-0.50; p=0.003）。增强的谷氨酸能神经传递导致的高浓度的谷氨酸在后丘脑内可能发挥作用的病理生理FM和其他中枢疼痛增强综合征。
Central pain augmentation resulting from enhanced excitatory and/or decreased inhibitory neurotransmission is a proposed mechanism underlying the pathophysiology of functional pain syndromes such as fibromyalgia (FM). Multiple functional magnetic resonance imaging (fMRI) studies implicate the insula as a region of heightened neuronal activity in this condition. Since glutamate (Glu) is a major cortical excitatory neurotransmitter that functions in pain neurotransmission, we hypothesized that increased levels of insular Glu would be present in FM patients and that the concentration of this molecule would be correlated with pain report. 19 FM patients and 14 age- and sex-matched pain free controls underwent pressure pain testing and a proton magnetic resonance spectroscopy (H-MRS) session wherein the right anterior and right posterior insula were examined at rest. FM patients had significantly higher levels of Glu (mean(SD): FM 8.09(0.72); HC 6.86(1.29); p=0.009) and combined glutamate and glutamine (e.g. Glx; mean(SD): FM 12.38(0.94); HC 10.59(1.48); p=0.001) within the right posterior insula as compared to controls. No differences were detected in any of the other major metabolites within this region (all p>0.05) and no group differences were detected for any metabolite within the right anterior insula (all p>0.10). Within the right posterior insula, higher levels of Glu and Glx were associated with lower pressure pain thresholds across both groups (Glu: r=−0.43; p=0.012; Glx: r=−0.50; p=0.003). Enhanced glutamatergic neurotransmission resulting from higher concentrations of Glu within the posterior insula may play a role in the pathophysiology of FM and other central pain augmentation syndromes.
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