Giesecke Thorsten, Gracely Richard H, Grant Masilo A B, Nachemson Alf, Petzke Frank, Williams David A, Clauw Daniel J
University of Michigan, Ann Arbor, MI 48106, USA.
Arthritis Rheum. 2004 Feb;50(2):613-23. doi: 10.1002/art.20063.
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).
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.
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 fibromyalgia 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.
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.
对于许多慢性下腰痛（CLBP）患者而言，病因不明。在其他特发性慢性疼痛病症中，感觉测试和功能磁共振成像（fMRI）已确定存在全身性疼痛敏感性增加、痛觉过敏以及大脑处理过程改变的情况，这表明在此类病症中疼痛处理存在中枢性增强。我们比较了将这两种方法应用于特发性CLBP患者（n = 11）、广泛性疼痛患者（纤维肌痛；n = 16）和健康对照受试者（n = 11）的结果。
CLBP患者的下腰痛持续至少12个月，且MRI/影像学检查未发现病因。在一个中性部位（拇指指甲）进行实验性疼痛测试，以评估所有受试者的压痛阈值。对于fMRI研究，在同一部位施加等压力（2千克）和等主观疼痛强度（轻度疼痛）的刺激。
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存在痛觉过敏；产生轻度疼痛所需的压力在对照组（5.6千克）明显高于CLBP患者（3.9千克）（P = 0.03）或纤维肌痛患者（3.5千克）（P = 0.006）。当对三组施加等量压力时，fMRI在CLBP组和纤维肌痛组的疼痛相关皮质区域检测到5个共同的神经元激活区域（对侧初级和次级[S2]体感皮层、顶下小叶、小脑以及同侧S2）。相同的刺激在对照组仅导致一次激活（在对侧S2体感皮层）。当三组受试者接受诱发主观上相等疼痛的刺激时，fMRI显示三组均存在共同的神经元激活。
在相同压力水平下，CLBP或纤维肌痛患者经历的疼痛明显更多，并且在疼痛相关皮质区域表现出更广泛、共同的神经元激活模式。当施加诱发同等疼痛反应的刺激时（与对照组相比，两组患者所需压力明显更低），三组之间的神经元激活相似。这些发现与特发性CLBP患者存在中枢性疼痛处理增强的情况一致。
