The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
复制标题
肌痛性脑脊髓炎/慢性疲劳综合征（ME/CFS）的神经炎症病理学研究
DOI：
10.3389/fphys.2017.00088
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发表时间：
2017-02-17
影响因子：
4
通讯作者：
Glassford, Julian A. G.
中科院分区：
文献类型：
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作者：
Glassford, Julian A. G.
肌痛性脑脊髓炎/慢性疲劳综合征（ME/CFS）是一种病因不明的使人衰弱的多系统慢性疾病，被世界卫生组织（WHO）归类为神经系统疾病。该疾病的症状似乎源于多种慢性神经障碍和相关扭曲以及有害感觉信号和神经免疫激活的慢性性。本文结合了一个简要的审查和讨论生物医学研究认为相关的这一基本概念的角度来看。其目的是为利益攸关方提供一个简明、综合的疾病模式大纲，以帮助揭开这一重大公共卫生问题的神秘面纱。主要的病因是：（A）在脊椎区域骨和神经肌肉组织的压缩、收缩、应变或损伤的背景下，影响不利神经兴奋的姿势/生物力学疼痛信号传导;（B）在长期的亲免疫性神经营养感染的背景下，特别是涉及亲淋巴细胞/亲胶质细胞/胶质细胞毒性的变化的免疫介导的炎症后遗症;（C）因子A和B的组合。在这样的条件下持续的神经胶质活化与氧化和亚硝化应激、神经炎症和神经敏感性相关。这些过程共同增强了涉及内分泌通路畸变、免疫和线粒体功能障碍以及神经变性的多系统紊乱的可能性，并且倾向于更难治的协同神经胶质功能障碍（胶质病）、自身免疫和中枢神经元致敏。
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating multi-systemic chronic illness of unknown etiology, classified as a neurological disorder by the World Health Organization (WHO). The symptomatology of the condition appears to emanate from a variety of sources of chronic neurological disturbance and associated distortions, and chronicity, in noxious sensory signaling and neuroimmune activation. This article incorporates a summary review and discussion of biomedical research considered relevant to this essential conception perspective. It is intended to provide stakeholders with a concise, integrated outline disease model in order to help demystify this major public health problem. The primary etiopathological factors presented are: (A) Postural/biomechanical pain signaling, affecting adverse neuroexcitation, in the context of compression, constriction, strain, or damage of vertebral-regional bone and neuromuscular tissues; (B) Immune mediated inflammatory sequelae, in the context of prolonged immunotropic neurotrophic infection-with lymphotropic/gliotropic/glio-toxic varieties implicated in particular; (C) A combination of factors A and B. Sustained glial activation under such conditions is associated with oxidative and nitrosative stress, neuroinflammation, and neural sensitivity. These processes collectively enhance the potential for multi-systemic disarray involving endocrine pathway aberration, immune and mitochondrial dysfunction, and neurodegeneration, and tend toward still more intractable synergistic neuro-glial dysfunction (gliopathy), autoimmunity, and central neuronal sensitization.