心理社会应激和行为反馈对疼痛加工的影响及其与主观和神经内分泌参数的相关性。

IF 1.5 Q4 CLINICAL NEUROLOGY
Sarah Karen Schneider, Paul Pauli, Stefan Lautenbacher, Philipp Reicherts
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引用次数: 1

摘要

目的:以往关于应激性疼痛调节的研究表明,中度的心理应激通常会导致痛觉过敏,而较严重的心理应激则会导致痛觉减退。然而,现有的研究往往缺乏适当的控制条件来确定单纯的应力效应。同样,研究主要集中在对社会威胁的纯粹预期上,而没有考虑到社会评价的实际经验。因此,我们着手研究实际的社会上升和下降,并结合标准化的压力范式来评估疼痛感知的短期和长期变化及其与神经内分泌和主观压力参数的潜在关联。方法:我们将177名健康女性分配到四种实验条件中,一种是标准版的特里尔社会压力测试(TSST),随后有积极、消极或没有表现反馈,另一种是匹配良好但要求较低的安慰剂版的TSST。通过评分、唾液α -淀粉酶和唾液皮质醇来评估应激反应。为了捕获应激对疼痛的假定影响,测量了热痛阈值、相热痛刺激的评分和条件疼痛调节。结果:尽管压力诱导在很大程度上是成功的,但结果并不支持实验诱导的社会压力-无论是否随后的表现反馈-对女性疼痛的可靠影响。此外,我们发现疼痛调节与神经内分泌或主观应激反应的变化没有明确的关联。结论:我们的结果与先前的研究相反,这些研究反复证明了应激诱导的痛觉过敏或痛觉过敏。这可能是由于方法学上的原因,因为以前的研究通常具有关于施加压力源的高度异质性,样本量小,缺乏或不确定的控制条件。因此,我们的研究结果提出了一个问题,即在过去,实验性社会心理压力对女性疼痛调节的作用是否被高估了。未来的研究是必要的,应该采用参数应激诱导方法,包括良好匹配的控制任务,考虑参与者的性别/性别和相对于疼痛评估的应激反应的时间过程。该研究在“Deutsches Register Klinischer studen”(DRKS)上注册为DRKS00026946,也可以在世界卫生组织的搜索门户网站上找到。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of psychosocial stress and performance feedback on pain processing and its correlation with subjective and neuroendocrine parameters.

Objectives: Previous research on stress-induced pain modulation suggests that moderate psychological stress usually leads to hyperalgesia while more severe threat results in hypoalgesia. However, existing studies often lack suitable control conditions imperative to identify mere stress effects. Similarly, research mainly focused on pure anticipation of a social threat, not taking into consideration actual experiences of social evaluation. Therefore, we set out to investigate actual social up- and downgrading combined with a standardized stress paradigm to evaluate short-term and prolonged changes in pain perception and their potential association with neuroendocrine and subjective stress parameters.

Methods: We allocated 177 healthy women to four experimental conditions, either the standard version of the Trier Social Stress Test (TSST) followed by positive, negative or no performance feedback, or a well-matched but less demanding placebo version of the TSST. Stress responses were assessed with ratings, salivary alpha-amylase, and salivary cortisol. To capture putative effects of stress on pain, heat pain threshold, ratings of phasic heat pain stimuli, and conditioned pain modulation were measured.

Results: Despite a largely successful stress induction, results do not support a reliable influence of experimentally induced social stress-with or without subsequent performance feedback-on pain in women. Further, we found no clear association of pain modulation and changes in neuroendocrine or subjective stress responses.

Conclusions: Our results contrast previous studies, which repeatedly demonstrated stress-induced hypo- or hyperalgesia. This might be due to methodological reasons as former research was often characterized by high heterogeneity regarding the applied stressors, low sample sizes, and lacking or inconclusive control conditions. Thus, our results raise the question whether pain modulation in women by experimental psychosocial stress might have been overestimated in the past. Future research is necessary, which should employ parametric stress induction methods including well-matched control tasks, taking into consideration the participants' gender/sex and the time course of the stress response relative to pain assessment. The study is registered as DRKS00026946 at 'Deutsches Register Klinischer Studien' (DRKS) and can be also found at the World Health Organization's search portal.

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来源期刊
Scandinavian Journal of Pain
Scandinavian Journal of Pain CLINICAL NEUROLOGY-
CiteScore
3.30
自引率
6.20%
发文量
73
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