Potential Mechanisms Underlying Centralized Pain and Emerging Therapeutic Interventions.
Potential Mechanisms Underlying Centralized Pain and Emerging Therapeutic Interventions.
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集中疼痛和新出现的治疗干预的潜在机制。
DOI：
10.3389/fncel.2018.00035
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发表时间：
2018
影响因子：
5.3
通讯作者：
Christianson JA
中科院分区：
文献类型：
--
作者：
Eller-Smith OC;Nicol AL;Christianson JA
集中性疼痛综合征与中枢神经系统内的变化有关，这些变化放大了外周输入和/或在没有有害刺激的情况下产生疼痛感知。特发性功能障碍通常被归类为集中疼痛综合征的例子包括纤维肌痛、慢性盆腔疼痛综合征、偏头痛和颞下颌紊乱。患者通常患有广泛性疼痛，与一种以上的特定综合征相关，并报告疲劳、情绪和睡眠障碍以及生活质量差。高度的症状合并症和缺乏明确的潜在病因使这些综合征难以治疗。这篇综述文章的主要目的是讨论中枢驱动的疼痛放大的潜在机制，以及它们如何导致诊断为集中疼痛综合征的患者的合并症增加、疼痛结果恶化和生活质量下降，并讨论新兴的非药物治疗方法，以改善与这些综合征相关的症状。下丘脑-垂体-肾上腺（HPA）轴的异常调节和输出通常与集中式疼痛疾病有关。下丘脑轴是主要的应激反应系统，它的激活导致下游皮质醇的产生和免疫反应的抑制。中枢性疼痛综合征的患者通常表现为皮质醇过高或过低，并有证据表明HPA轴下游信号的改变，包括肥大细胞（MC）浸润和激活增加，这可能导致附近伤害性传入事件的致敏。通过伤害感受器激活而增加的外周输入可导致“痛觉过敏启动”和/或“缠绕”，并最终通过中枢神经系统的长期增强而导致中枢敏化。其他中枢改变的证据已通过功能连通性和磁共振波谱的脑成像研究观察到，并被证明有助于纤维肌痛和慢性泌尿系统疼痛患者普遍疼痛和情绪不良。非药物疗法，包括运动和认知行为疗法（CBT），在治疗集中疼痛症状方面显示出很大的希望。
Centralized pain syndromes are associated with changes within the central nervous system that amplify peripheral input and/or generate the perception of pain in the absence of a noxious stimulus. Examples of idiopathic functional disorders that are often categorized as centralized pain syndromes include fibromyalgia, chronic pelvic pain syndromes, migraine, and temporomandibular disorder. Patients often suffer from widespread pain, associated with more than one specific syndrome, and report fatigue, mood and sleep disturbances, and poor quality of life. The high degree of symptom comorbidity and a lack of definitive underlying etiology make these syndromes notoriously difficult to treat. The main purpose of this review article is to discuss potential mechanisms of centrally-driven pain amplification and how they may contribute to increased comorbidity, poorer pain outcomes, and decreased quality of life in patients diagnosed with centralized pain syndromes, as well as discuss emerging non-pharmacological therapies that improve symptomology associated with these syndromes. Abnormal regulation and output of the hypothalamic-pituitary-adrenal (HPA) axis is commonly associated with centralized pain disorders. The HPA axis is the primary stress response system and its activation results in downstream production of cortisol and a dampening of the immune response. Patients with centralized pain syndromes often present with hyper- or hypocortisolism and evidence of altered downstream signaling from the HPA axis including increased Mast cell (MC) infiltration and activation, which can lead to sensitization of nearby nociceptive afferents. Increased peripheral input via nociceptor activation can lead to “hyperalgesic priming” and/or “wind-up” and eventually to central sensitization through long term potentiation in the central nervous system. Other evidence of central modifications has been observed through brain imaging studies of functional connectivity and magnetic resonance spectroscopy and are shown to contribute to the widespreadness of pain and poor mood in patients with fibromyalgia and chronic urological pain. Non-pharmacological therapeutics, including exercise and cognitive behavioral therapy (CBT), have shown great promise in treating symptoms of centralized pain.
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