Influences of Anxiety and Fear on Conditioned Pain Modulationin Healthy Individuals and Pain Patients

条件性疼痛调制(CPM)这一术语描述了“疼痛抑制疼痛”现象，这代表了一种脊髓上环路效应，其上中枢位于脑干。它是下行抑制控制系统的一部分，首次在纯生理学水平上被描述为弥漫性有害抑制控制(DNIC)。CPM测试已经变得非常流行，因为CPM的变化有望成为疼痛处理过程中性别和年龄差异的基础，更重要的是，似乎属于导致慢性疼痛发展的因素以及预测治疗效果的因素。因此，CPM已成为抑制性疼痛处理能力的标志。除了极少数例外，这一新出现的疼痛抑制标记物与高阶皮质下和皮质网络的功能关系以及心理对CPM效应的影响仍未被忽视，尽管高阶影响对下行疼痛抑制系统的影响已经被公认很长时间了。为了改变这种情况，并从疼痛处理的心理关键变量开始，将调查焦虑(威胁的预期)和恐惧(与威胁的对抗)以及内部(与有害刺激相关)和外部威胁(与有害刺激无关)的影响。这些因素的选择通常是基于对它们作用于疼痛处理的有效性的明确了解。这里的研究问题是，这些因素是否通过调节CPM而对疼痛产生影响。除了健康对照受试者，慢性肌肉骨骼疼痛患者将被调查，因为在这些患者中，情感对CPM的影响被认为更明显，并可能具有致病相关性。由于假设在病理生理学上相似(中枢敏感化)，但在疼痛严重程度(强度和扩散)和心理陪伴方面存在差异，纤维肌痛和慢性紧张型头痛(CTTH)患者将被作为临床模型进行研究。

The term Conditioned Pain Modulation (CPM) describes the 'pain inhibits pain' phenomenon, which represents a supra-spinal loop effect, with upper centres in the brain stem. It is part of the descending inhibitory control system, which has first been described at a pure physiological level as Diffuse Noxious Inhibitory Controls (DNIC). CPM testing has become very popular because changes in CPM have promised to underlie sex and age differences in pain processing and, even more importantly, seem to belong to the factors contributing to the development of chronic pain as well as to the factors predicting treatment efficacy. Thus, CPM has become a marker for the inhibitory pain processing capacity. With very few exceptions the functional relation of this emerging marker of pain inhibition with higher-order subcortical and cortical networks and psychological influences on CPM effects have yet been neglected although higher-order influences on descending pain inhibitory systems in general have been acknowledged for a long time. To change this situation and start with psychologically critical variables for pain processing, the influences of anxiety (anticipation of threat) and fear (confrontation with threat) as well as of internal (associated with noxious stimulation) and external threat (independent of noxious stimulation) will be investigated. The choice of these factors has been driven by definite knowledge of their efficiency in acting on pain processing in general. The research question here is whether these factors exert their influence on pain via modulation of CPM. Besides healthy control subjects, patients with chronic musculoskeletal pain will be investigated because in these patients the affective influences on CPM are assumed to be more pronounced and potentially of pathogenetic relevance. Due to presumed similarities in pathophysiology (central sensitization) but difference in pain severity (intensity and spread) and psychological accompaniments, patients with fibromyalgia and chronic tension-type headache (CTTH) will be studied as clinical models.