Evidence of augmented central pain processing in idiopathic chronic low back pain
Evidence of augmented central pain processing in idiopathic chronic low back pain
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DOI：
10.1002/art.20063
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发表时间：
2004-02-01
影响因子：
--
通讯作者：
Clauw, DJ
中科院分区：
文献类型：
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作者：
Giesecke, T;Gracely, RH;Clauw, DJ
Objective.对于许多患有慢性腰痛（CLBP）的人来说，没有可识别的原因。在其他特发性慢性疼痛条件下，感觉测试和功能性磁共振成像（fMRI）已经确定了普遍增加的疼痛敏感性，痛觉过敏和改变大脑处理的发生，表明在这种情况下疼痛处理的中枢增强。我们比较了这两种方法应用于特发性CLBP患者（n = 11），广泛疼痛患者（纤维肌痛; n = 16）和健康对照组（n = 11）的结果。CLBP患者的腰痛持续至少12个月，MRI/影像学变化无法解释。在中性部位（缩略图）进行实验性疼痛测试，以评估所有受试者的压力-疼痛阈值。在fMRI研究中，将相同压力（2 kg）和相同主观疼痛强度（轻微剧烈疼痛）的刺激施加到同一部位。尽管CLBP组的压痛点数量较少，但实验性疼痛测试显示该组以及纤维肌痛组均出现痛觉过敏;对照组（5.6 kg）产生轻微剧烈疼痛所需的压力显著高于CLBP患者（3.9 kg）（P 0.03）或纤维肌痛患者（3.5 kg）（P 0.006）。当对3组施加等量的压力时，fMRI检测到CLBP和神经痛组中疼痛相关皮层区域的5个共同神经元激活区域（对侧初级和次级[S2]体感皮层，顶下小叶，小脑和同侧S2）。同样的刺激在对照组中只引起了一次激活（在对侧S2体感皮层）。当3组受试者接受主观上诱发相同疼痛的刺激时，fMRI显示3组受试者都有共同的神经元激活。在相同的压力水平下，CLBP或纤维肌痛患者的疼痛明显更多，并且在疼痛相关的皮层区域显示出更广泛，更常见的神经元激活模式。当施加引起同样疼痛反应的刺激时（与对照组相比，两个患者组需要显著较低的压力），3组之间的神经元激活相似。这些发现与特发性CLBP患者中枢疼痛处理增强的发生一致。
Objective. For many individuals with chronic low back pain (CLBP), there is no identifiable cause. In other idiopathic chronic pain conditions, sensory testing and functional magnetic resonance imaging (fMRI) have identified the occurrence of generalized increased pain sensitivity, hyperalgesia, and altered brain processing, suggesting central augmentation of pain processing in such conditions. We compared the results of both of these methods as applied to patients with idiopathic CLBP (n = 11), patients with widespread pain (fibromyalgia; n = 16), and healthy control subjects (n = 11).Methods. Patients with CLBP had low back pain persisting for at least 12 months that was unexplained by MRI/radiographic changes. Experimental pain testing was performed at a neutral site (thumbnail) to assess the pressure-pain threshold in all subjects. For fMRI studies, stimuli of equal pressure (2 kg) and of equal subjective pain intensity (slightly intense pain) were applied to this same site.Results. Despite low numbers of tender points in the CLBP group, experimental pain testing revealed hyperalgesia in this group as well as in the fibromyalgia group; the pressure required to produce slightly intense pain was significantly higher in the controls (5.6 kg) than in the patients with CLBP (3.9 kg) (P 0.03) or the patients with fibromyalgia (3.5 kg) (P 0.006). When equal amounts of pressure were applied to the 3 groups, fMRI detected 5 common regions of neuronal activation in pain-related cortical areas in the CLBP and fibrornyalgia groups (in the contralateral primary and secondary [S2] somatosensory cortices, inferior parietal lobule, cerebellum, and ipsilateral S2). This same stimulus resulted in only a single activation in controls (in the contralateral S2 somatosensory cortex). When subjects in the 3 groups received stimuli that evoked subjectively equal pain, fMRI revealed common neuronal activations in all 3 groups.Conclusion. At equal levels of pressure, patients with CLBP or fibromyalgia experienced significantly more pain and showed more extensive, common patterns of neuronal activation in pain-related cortical areas. When stimuli that elicited equally painful responses were applied (requiring significantly lower pressure in both patient groups as compared with the control group), neuronal activations were similar among the 3 groups. These findings are consistent with the occurrence of augmented central pain processing in patients with idiopathic CLBP.