Grimes Jeffrey S, Creech Suzannah K, Young Erin E, Vichaya Elisabeth G, Meagher Mary W
Department of Psychology, Texas A & M University, College Station, Texas 77843-4235, USA.
J Pain. 2009 Mar;10(3):282-92. doi: 10.1016/j.jpain.2008.09.005. Epub 2008 Dec 13.
Previous research indicates that exposure to shock decreases thermal pain sensitivity in humans. This hypoalgesia has been attributed to a centrally mediated fear state that activates descending inhibitory pathways. Animal research suggests that distraction alters the activation of these hypoalgesic systems. To determine whether the pain memory alters the activation of hypoalgesic systems in humans, the present study examined whether a post-shock distractor attenuates shock-induced hypoalgesia. If fear-inducing shocks are represented by a limited capacity working memory system, then a distractor should speed the decay of the hypoalgesia. Healthy men were randomly assigned to 1 of 4 groups: shock-distraction, shock-no distraction, no shock-distraction, and no shock-no distraction. Following baseline pain tests, participants in the shock groups were presented with 3 brief shocks. Immediately following shock, an unexpected vibration stimulus was presented to participants in the distraction groups. Both self-report and physiological (SCL, HR) measures indicated that shock exposure resulted in fear, arousal, and decreased pain sensitivity. Consistent with prior animal studies, presentation of a post-shock distractor sped the decay of shock-induced hypoalgesia. Specifically, the distraction group exhibited significantly less shock-induced hypoalgesia compared to the no-distraction group. These findings provide additional evidence for the involvement of memory processes in the activation of descending pain inhibitory pathways.
This study demonstrated that the presentation of a distracting stimulus immediately following 3 brief shocks attenuated shock-induced hypoalgesia in healthy human subjects. Understanding the impact of post-pain distraction on pain processing may have important clinical implications because it may influence patients' willingness to undergo future painful medical procedures.
先前的研究表明，遭受电击会降低人类对热痛的敏感性。这种痛觉减退归因于一种中枢介导的恐惧状态，该状态激活了下行抑制通路。动物研究表明，分心会改变这些痛觉减退系统的激活。为了确定疼痛记忆是否会改变人类痛觉减退系统的激活，本研究考察了电击后分心物是否会减弱电击诱发的痛觉减退。如果诱发恐惧的电击由容量有限的工作记忆系统表征，那么分心物应该会加速痛觉减退的消退。健康男性被随机分配到4组中的1组：电击-分心组、电击-无分心组、无电击-分心组和无电击-无分心组。在进行基线疼痛测试后，电击组的参与者接受3次短暂电击。电击后立即向分心组的参与者施加意外的振动刺激。自我报告和生理（皮肤电导率、心率）测量均表明，电击暴露导致恐惧、觉醒，并降低了疼痛敏感性。与先前的动物研究一致，电击后分心物的呈现加速了电击诱发的痛觉减退的消退。具体而言，与无分心组相比，分心组表现出明显更少的电击诱发的痛觉减退。这些发现为记忆过程参与下行疼痛抑制通路的激活提供了额外证据。
本研究表明，在3次短暂电击后立即呈现分心刺激可减弱健康人类受试者电击诱发的痛觉减退。了解疼痛后分心对疼痛处理的影响可能具有重要的临床意义，因为它可能影响患者接受未来痛苦医疗程序的意愿。
