Elman Igor, Borsook David
Boonshoft School of Medicine, Wright State University, Dayton VA Medical Center, Dayton, OH, United States.
Harvard Medical School, Center for Pain and the Brain, Boston Children's Hospital, Massachusetts General Hospital, McLean Hospital, Boston, MA, United States.
Front Psychiatry. 2018 Feb 20;9:29. doi: 10.3389/fpsyt.2018.00029. eCollection 2018.
Pain is essential for avoidance of tissue damage and for promotion of healing. Notwithstanding the survival value, pain brings about emotional suffering reflected in fear and anxiety, which in turn augment pain thus giving rise to a self-sustaining feedforward loop. Given such reciprocal relationships, the present article uses neuroscientific conceptualizations of fear and anxiety as a theoretical framework for hitherto insufficiently understood pathophysiological mechanisms underlying chronic pain. To that end, searches of PubMed-indexed journals were performed using the following Medical Subject Headings' terms: pain and nociception plus amygdala, anxiety, cognitive, fear, sensory, and unconscious. Recursive sets of scientific and clinical evidence extracted from this literature review were summarized within the following key areas: (1) parallelism between acute pain and fear and between chronic pain and anxiety; (2) all are related to the evasion of sensory-perceived threats and are subserved by subcortical circuits mediating automatic threat-induced physiologic responses and defensive actions in conjunction with higher order corticolimbic networks (e.g., thalamocortical, thalamo-striato-cortical and amygdalo-cortical) generating conscious representations and valuation-based adaptive behaviors; (3) some instances of chronic pain and anxiety conditions are driven by the failure to diminish or block respective nociceptive information or unconscious treats from reaching conscious awareness; and (4) the neural correlates of pain-related conscious states and cognitions may become autonomous (i.e., dissociated) from the subcortical activity/function leading to the eventual chronicity. Identifying relative contributions of the diverse neuroanatomical sources, thus, offers prospects for the development of novel preventive, diagnostic, and therapeutic strategies in chronic pain patients.
疼痛对于避免组织损伤和促进愈合至关重要。尽管疼痛具有生存价值，但它会引发恐惧和焦虑等情绪痛苦，而这些情绪又会加剧疼痛，从而形成一个自我维持的前馈循环。鉴于这种相互关系，本文将恐惧和焦虑的神经科学概念作为理论框架，用于解释迄今为止尚未充分理解的慢性疼痛潜在病理生理机制。为此，我们使用以下医学主题词在PubMed索引期刊中进行了检索：疼痛与伤害感受，加上杏仁核、焦虑、认知、恐惧、感觉和无意识。从这篇文献综述中提取的一系列科学和临床证据总结在以下关键领域：（1）急性疼痛与恐惧、慢性疼痛与焦虑之间的平行关系；（2）所有这些都与逃避感官感知的威胁有关，并由皮层下回路介导，这些回路介导自动威胁诱发的生理反应和防御行为，同时与高阶皮质边缘网络（如丘脑皮质、丘脑-纹状体-皮质和杏仁核-皮质）协同作用，产生有意识的表征和基于评估的适应性行为；（3）某些慢性疼痛和焦虑状况是由于未能减少或阻止各自的伤害性信息或无意识威胁进入意识层面；（4）与疼痛相关的意识状态和认知的神经关联可能与皮层下活动/功能自主分离（即解离），从而导致最终的慢性化。因此，确定不同神经解剖学来源的相对贡献，为慢性疼痛患者开发新的预防、诊断和治疗策略提供了前景。
