Altered experimental pain perception after cerebellar infarction

Altered experimental pain perception after cerebellar infarction
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DOI:
10.1016/j.pain.2014.04.006
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发表时间:
2014-07-01
期刊:
影响因子:
7.4
通讯作者:
Straube, Andreas
Straube, Andreas
中科院分区:
医学1区
文献类型:
--
作者:
Ruscheweyh, Ruth;Kuehnel, Maria;Straube, Andreas

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动物研究表明,小脑除了运动功能外,还在疼痛处理和调节中发挥作用,这可能是因为它与前额叶皮层和脑干区域的广泛联系,这些区域参与了下行疼痛控制。与此同时,人类成像研究表明,小脑激活疼痛刺激的反应。然而,目前尚不清楚小脑病变是否影响人类的疼痛感知。在本研究中,我们使用实验性疼痛测试比较急性疼痛感知和内源性疼痛抑制30例患者1至11年后小脑梗死和30名性别和年龄匹配的健康对照组。与对照组相比,患者对急性热刺激的疼痛感知显著增加(44 ℃-48 ℃,患者的平均疼痛强度等级为3.4 +/-2.8,对照组为1.5 +/-1.7 [在0-10的数字等级量表上],P <0.01)和重复256 mN针刺刺激(1.3 +/- 1.9 vs 0.6 +/- 1.0 [0-10],P <0.05)。患者的热痛觉过敏在梗死同侧的身体侧更明显。此外,与对照组相比,患者表现出减少的抵消镇痛(疼痛强度评分变化:0.0% +/- 15.8% vs-16.9%+/-36.3%,P <0.05)和减少的安慰剂镇痛(疼痛强度评分变化:-1.0 +/- 1.1 vs-1.8 +/- 1.3 [0-10],P <0.05)。相比之下,两组之间的热痛阈值和压力痛阈值没有显著差异。这些结果表明,小脑梗死后,患者认为热和重复的机械刺激比健康对照受试者更痛苦,内源性疼痛抑制机制(抵消和安慰剂镇痛)的激活不足。这表明小脑在人类疼痛感知和调节中的作用以前被低估了。(C)2014年国际疼痛研究协会。Elsevier B. V.出版,保留所有权利。
Animal studies have suggested that the cerebellum, in addition to its motor functions, also has a role in pain processing and modulation, possibly because of its extensive connections with the prefrontal cortex and with brainstem regions involved in descending pain control. Consistently, human imaging studies have shown cerebellar activation in response to painful stimulation. However, it is presently not clear whether cerebellar lesions affect pain perception in humans. In the present study, we used experimental pain testing to compare acute pain perception and endogenous pain inhibition in 30 patients 1 to 11 years after cerebellar infarction and in 30 sex- and age-matched healthy control subjects. Compared to controls, patients exhibited a significantly increased pain perception in response to acute heat stimuli (44 degrees C-48 degrees C, average pain intensity rating for patients 3.4 +/- 2.8 and for controls 1.5 +/- 1.7 [on a numeric rating scale of 0-10], P < .01) and to repeated 256 mN pinprick stimuli (1.3 +/- 1.9 vs 0.6 +/- 1.0 [0-10], P < .05). Heat hyperalgesia in patients was more pronounced on the body side ipsilateral to the infarction. In addition, patients showed reduced offset analgesia (change in pain intensity rating: 0.0% +/- 15.8% vs -16.9% +/- 36.3%, P < .05) and reduced placebo analgesia (change in pain intensity rating: -1.0 +/- 1.1 vs -1.8 +/- 1.3 [0-10], P < .05) compared to controls. In contrast, heat and pressure pain thresholds were not significantly different between groups. These results show that, after cerebellar infarction, patients perceive heat and repeated mechanical stimuli as more painful than do healthy control subjects and have deficient activation of endogenous pain inhibitory mechanisms (offset and placebo analgesia). This suggests that the cerebellum has a previously underestimated role in human pain perception and modulation. (C) 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.