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Offset analgesia: The role of peripheral and central mechanisms

机译:偏移镇痛:外围和中央机制的作用

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Abstract Background Offset Analgesia ( OA ) can be evoked by a three‐heat‐stimulus train (T1‐T2‐T3), with T1 (5?s) and T3 (20?s) having the same temperature (e.g. 48?°C) and T2 (5?s) being slightly higher (1–3?°C). OA is defined as a disproportional pain reduction caused by the slight temperature decrease from T2 to T3. As the pain modulatory mechanisms behind OA are still poorly understood, the current study aimed to investigate the role of peripheral and central mechanisms by applying heat stimuli to the same location and to different unilateral and bilateral locations. Method Young healthy volunteers participated in the study. A ‘standard‐ OA ’ paradigm (48–49–48?°C) was applied to the non‐dominant volar forearm (T1–T2–T3 applied on the same location). ‘Unilateral‐ OA ’ trials were applied on three different locations of the non‐dominant volar forearm (the same dermatome). ‘Bilateral‐ OA ’ trials were applied by shifting T1–T2–T3 between dominant and non‐dominant volar forearms. A constant stimulus of 48?°C was applied as control for the evoked pain. The pain intensities were continuously recorded using an electronic visual analogue scale. Results The largest pain intensity reduction was reported for the ‘standard‐ OA ’ paradigm ( p ??0.001) compared with the control stimulus. Both ‘Unilateral‐ OA ’ and ‘Bilateral‐ OA ’ trials caused a significant pain reduction ( p ??0.05) compared with the control; however, the pain reduction was less than that evoked by ‘standard‐ OA ’ ( p ??0.05). Conclusion This study showed that OA could be elicited when the stimuli were applied both to the same and to different locations (ipsi‐ and contralateral) indicating that peripheral as well as central mechanisms are involved in mediating OA . Significance This study investigated offset analgesia by applying thermal painful stimuli to the ipsi‐ and bilateral forearms in healthy subjects and found that both peripheral and central mechanisms seem to mediate offset analgesia.
机译:摘要背景偏移镇痛(OA)可以通过三热刺激列车(T1-T2-T3)引起,具有具有相同温度的T1(5·S)和T3(20μl)(例如48Ω·℃ )和T2(5?s)略高(1-3°C)。 OA被定义为由T2至T3的略微温度降低引起的分类疼痛减少。随着OA后面的疼痛调制机制仍然不知所措,目前的研究旨在通过将热刺激应用于同一位置和不同单侧和双边地点来研究外围和中枢机制的作用。方法年轻健康志愿者参加了这项研究。将“标准OA”范式(48-49-48°C)施加到非显性Volar前臂(在同一位置施加的T1-T2-T3)。 “单侧OA”试验应用于非显性vlar前臂(同样皮肤物)的三个不同地点。通过在显性和非显性vlar前臂之间移位T1-T2-T3来应用'双侧OA'试验。将48℃的恒定刺激施用为诱发疼痛的控制。使用电子视觉模拟量表连续记录疼痛强度。结果,与对照刺激相比,“标准织物”范式(Pα.<0.001)报道了最大疼痛强度降低。与对照相比,“双侧织物”和“双侧织物”试验均导致显着的疼痛减少(P?&Δ0.05);然而,疼痛减少少于“标准织物”(P≥β0)引起的疼痛。结论本研究表明,当刺激施用刺激和不同的位置(IPSI和对侧)时,可以引发OA,表明外周以及中枢机制参与介导的OA。意义本研究通过对健康受试者的IPSI和双侧前臂施加热疼痛刺激来研究偏移镇痛,发现外周和中枢机制似乎介导抵消镇痛。

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  • 来源
    《European journal of pain :》 |2018年第1期|共8页
  • 作者单位

    Center for Sensory‐Motor Interaction (SMI)Aalborg UniversityDenmark;

    Center for Sensory‐Motor Interaction (SMI)Aalborg UniversityDenmark;

    Center for Sensory‐Motor Interaction (SMI)Aalborg UniversityDenmark;

    Center for Sensory‐Motor Interaction (SMI)Aalborg UniversityDenmark;

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  • 正文语种 eng
  • 中图分类 诊断学;
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