Cerebral mechanisms of experimental hyperalgesia in fibromyalgia

被引:41
作者
Burgmer, M. [1 ]
Pfleiderer, B. [2 ]
Maihoefner, C. [3 ]
Gaubitz, M.
Wessolleck, E. [4 ]
Heuft, G. [1 ]
Pogatzki-Zahn, E. [5 ]
机构
[1] Univ Hosp Munster, Dept Psychosomat & Psychotherapy, Munster, Germany
[2] Univ Hosp Munster, Dept Clin Radiol, Munster, Germany
[3] Univ Hosp Erlangen, Dept Neurol, Erlangen, Germany
[4] Hannover Med Sch, Clin Laryngol Rhinol & Otol, D-3000 Hannover, Germany
[5] Univ Hosp Munster, Dept Anesthesiol & Intens Care, Munster, Germany
关键词
PRESSURE-PAIN THRESHOLDS; INDUCED SECONDARY HYPERALGESIA; 2ND PAIN; TEMPORAL SUMMATION; HUMAN BRAIN; MODULATION; ACTIVATION; HEAT; SENSITIZATION; STIMULATION;
D O I
10.1002/j.1532-2149.2011.00058.x
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
The present study examined the hyperresponsiveness of the central nervous system in patients with fibromyalgia syndrome (FMS) related to mechanical hyperalgesia. The goals were to differentiate between increased pain ratings and hyperalgesia related either to peripheral or to central sensitization and to correlate with cerebral activation pattern. Seventeen patients and 17 healthy controls were examined, placing an experimental incision in the right volar forearm and causing tonic pain. Experimental pain, primary and secondary hyperalgesia were assessed during the time course of the experimental pain, and the changes in hyperalgesia were correlated to brain activation (functional magnetic resonance imaging). Patients with FMS experienced the experimental pain during the time course as more painful than healthy controls (Fscore = 3.93, pscore = 0.008). While they did not present a different course of primary hyperalgesia (Fscore = 1.01, pscore = 0.40), they did show greater secondary hyperalgesia (Fscore = 5.45, pscore = 0.004). In patients with FMS, the cerebral pattern corresponding to secondary hyperalgesia was altered. The activity in the dorsolateral prefrontal cortex was inversely correlated with secondary hyperalgesia in healthy controls (R = -0.34 p = 0.005); in patients, this correlation was disrupted (R = 0.19 p = 0.12). These findings point to an alteration of pain transmission at the central level in FMS (e. g., loss of inhibition) and might be related to changes in cerebral-midbrain-spinal mechanisms of pain inhibition.
引用
收藏
页码:636 / 647
页数:12
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