PDF(Pubmed)
Abstract：
UNASSIGNED: Mechanisms underlying myofascial temporomandibular disorder (mTMD) are poorly understood. One theory is dysfunction in the central mediation of pain, specifically in enhanced facilitatory pain modulation. Because mechanisms leading to central sensitization may differ for joint and muscle pain, this study of mTMD addressed phenotypic heterogeneity by temporomandibular (TM) joint pain in the examination of quantitative sensory testing (QST).
UNASSIGNED: The stimulus dependent increase in second pain (temporal summation (TS)) and associated aftersensations (AS) were examined across groups of women with mTMD with TM joint pain and without, and a demographically matched control group.
UNASSIGNED: TS was slightly more evident in mTMD without joint pain vs with (p = 0.035), but AS were most robustly persistent in the group with joint pain vs without (p < 0.002).
UNASSIGNED: While both subgroups demonstrated evidence of central sensitization relative to controls on one of two measures, differences in QST results, if replicated, may point to possible differences in the mechanisms that yield central sensitization. Alternatively, it may represent methodological artifacts that need to be addressed. Therefore, greater consideration should be given to symptom-based phenotypes in studies examining TS and AS.
UNASSIGNED: The stimulus dependent increase in second pain (temporal summation (TS)) and associated aftersensations (AS) were examined across groups of women with mTMD with TM joint pain and without, and a demographically matched control group.
UNASSIGNED: TS was slightly more evident in mTMD without joint pain vs with (p = 0.035), but AS were most robustly persistent in the group with joint pain vs without (p < 0.002).
UNASSIGNED: While both subgroups demonstrated evidence of central sensitization relative to controls on one of two measures, differences in QST results, if replicated, may point to possible differences in the mechanisms that yield central sensitization. Alternatively, it may represent methodological artifacts that need to be addressed. Therefore, greater consideration should be given to symptom-based phenotypes in studies examining TS and AS.
摘要：
未经证实：肌筋膜颞下颌关节紊乱病（mTMD）的潜在机制知之甚少。一种理论是疼痛的中枢调解功能障碍，特别是在增强的促进疼痛调节中。因为关节和肌肉疼痛导致中枢致敏的机制可能不同，这项mTMD研究在定量感觉测试（QST）检查中通过颞下颌（TM）关节痛解决了表型异质性。
UNASSIGNED：在患有TM关节痛和无TM关节痛的mTMD女性组中检查了刺激依赖性第二疼痛（时间总和（TS））和相关的后感（AS）的增加，和人口统计学匹配的对照组。
UNASSIGNED：TS在无关节疼痛的mTMD中比（p=0.035）更明显，但与无关节痛组相比，AS最强烈地持续存在（p<0.002）。
UNASSIGNED：虽然两个亚组都显示了相对于对照的中枢致敏证据，QST结果的差异，如果复制，可能指出产生中枢致敏的机制可能存在差异。或者，它可能代表需要解决的方法论工件。因此,在检查TS和AS的研究中，应更多地考虑基于症状的表型。
UNASSIGNED：在患有TM关节痛和无TM关节痛的mTMD女性组中检查了刺激依赖性第二疼痛（时间总和（TS））和相关的后感（AS）的增加，和人口统计学匹配的对照组。
UNASSIGNED：TS在无关节疼痛的mTMD中比（p=0.035）更明显，但与无关节痛组相比，AS最强烈地持续存在（p<0.002）。
UNASSIGNED：虽然两个亚组都显示了相对于对照的中枢致敏证据，QST结果的差异，如果复制，可能指出产生中枢致敏的机制可能存在差异。或者，它可能代表需要解决的方法论工件。因此,在检查TS和AS的研究中，应更多地考虑基于症状的表型。
