Deficiency in endogenous modulation of prolonged heat pain in patients with Irritable Bowel Syndrome and Temporomandibular Disorder.
Deficiency in endogenous modulation of prolonged heat pain in patients with Irritable Bowel Syndrome and Temporomandibular Disorder.
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DOI：
10.1016/j.pain.2008.12.027
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发表时间：
2009-06
期刊：
影响因子：
7.4
通讯作者：
Riley JL 3rd
中科院分区：
文献类型：
--
作者：
King CD;Wong F;Currie T;Mauderli AP;Fillingim RB;Riley JL 3rd
患有肠易激综合征（IBS）和颞下颌关节紊乱病（TMD）的女性的特征是对实验性疼痛的敏感性增强。对这一观察结果的一个可能的解释是疼痛调制系统如弥漫性伤害抑制控制（DNIC）的缺陷。在一些使用短暂刺激的研究中，慢性疼痛患者表现出DNIC降低。本研究的目的是比较IBS和TMD患者对长时间热痛的敏感性和DNIC的疗效。施加于左手掌的热痛（实验刺激; 44.0 - 49.0 ° C）在三个30秒的试验期间在以下条件下跨越三个单独的测试阶段连续地评定：没有条件刺激;在右脚同时浸入23.0 ° C（对照）期间;以及在（DNIC; 8.0 - 16.0 ° C）水浴中的有害冷浸入期间。与对照组相比，IBS和TMD患者报告对热痛的敏感性增加，并且由于DNIC而未能表现出疼痛抑制。对照组在DNIC治疗期间疼痛明显减轻。这些发现支持了这样的观点，即慢性疼痛患者不仅对疼痛更敏感，而且表现出疼痛抑制的减少，这可能是因为内源性疼痛抑制系统功能障碍。
Females with Irritable Bowel Syndrome (IBS) and Temporomandibular Disorder (TMD) are characterized by enhanced sensitivity to experimental pain. One possible explanation for this observation is deficiencies in pain modulation systems like Diffuse Noxious Inhibitory Control (DNIC). In a few studies that used brief stimuli, chronic pain patients demonstrate reduced DNIC. The purpose of this study was to compare sensitivity to prolonged heat pain and the efficacy of DNIC in controls to IBS and TMD patients. Heat pain (experimental stimulus; 44.0-49.0°C), which was applied to left palm, was continuously rated during three 30-second trials across three separate testing sessions under the following conditions: without a conditioning stimulus; during concurrent immersion of the right foot in a 23.0°C (control); and during noxious cold immersion in a (DNIC; 8.0-16.0°C) water bath. Compared to controls, IBS and TMD patients reported increased sensitivity to heat pain and failed to demonstrate pain inhibition due to DNIC. Controls showed a significant reduction in pain during the DNIC session. These findings support the idea that chronic pain patients are not only more pain sensitive and demonstrate reduced pain inhibition by pain, possibly because of dysfunction of endogenous pain inhibition systems.
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