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[压力反射敏感性与慢性疼痛:发病机制意义及临床应用]

[Baroreflex sensitivity and chronic pain : Pathogenetic significance and clinical implications].

作者信息

Meller T, Stiehm F, Malinowski R, Thieme K

机构信息

Institut für Medizinische Psychologie, Fachbereich Medizin, Philipps-Universität Marburg, Karl-von-Frisch-Str. 4, 35032, Marburg, Deutschland.

Vitanas Klinik für Geriatrie, Geesthacht, Deutschland.

出版信息

Schmerz. 2016 Oct;30(5):470-476. doi: 10.1007/s00482-016-0150-5.

Abstract

The interaction of cardiovascular dynamics and pain perception is an important component of intrinsic pain regulation. In healthy subjects acute pain stimuli cause increased sympathetic arousal and increased mean arterial pressure. Arterial baroreceptors sense phasic blood pressure changes and relay the information to the lower brainstem via the dorsomedial nucleus tractus solitarius (dmNTS). Projections in the brainstem and also higher cortical areas result in elevation of blood pressure as part of the autonomic nervous system as well as modulation of sleep, anxiety and pain. In healthy subjects there is an inverse relationship between blood pressure and pain sensitivity but this relationship is impaired in chronic pain patients. Persistent stress, pain behavior and classical and operant conditioning mechanisms reduce baroreflex sensitivity (BRS) and dmNTS activity in a subgroup of patients. This leads to a decrease of autonomic regulatory function as well as reduced pain inhibition. Importantly, baroreflex function can be modulated by cognitive and affective processes. This article reviews the role of the baroreflex arc as a possible crucial factor in the development and maintenance of chronic pain. The importance of learning mechanisms is described. Mechanism-based individualized treatment approaches for patients with hypertensive stress reactivity are also critically discussed.

摘要

心血管动力学与疼痛感知之间的相互作用是内在疼痛调节的重要组成部分。在健康受试者中,急性疼痛刺激会导致交感神经兴奋增加和平均动脉压升高。动脉压力感受器感知相位血压变化,并通过孤束核背内侧核(dmNTS)将信息传递至脑桥下部。脑干以及更高皮层区域的投射会导致血压升高,这是自主神经系统的一部分,同时也会调节睡眠、焦虑和疼痛。在健康受试者中,血压与疼痛敏感性呈负相关,但在慢性疼痛患者中这种关系受损。持续的压力、疼痛行为以及经典和操作性条件反射机制会降低一部分患者的压力反射敏感性(BRS)和dmNTS活性。这会导致自主调节功能下降以及疼痛抑制减弱。重要的是,压力反射功能可通过认知和情感过程进行调节。本文综述了压力反射弧在慢性疼痛发生和维持过程中作为一个可能的关键因素所起的作用。描述了学习机制的重要性。还对基于机制的高血压应激反应性患者个体化治疗方法进行了批判性讨论。

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