Central Sensitization (CS) refers to an amplification of neural signaling within the central nervous system, resulting in pain hypersensitivity (Woolf, 2011). Symptoms of CS include allodynia, hyperalgesia, expansion of the receptive field beyond the area of peripheral nerve supply, and prolonged pain after a stimulus has been removed (Latremoliere & Woolf, 2009). A number of CSrelated biological mechanisms have been identified, including dysregulation of ascending and descending tracks in the central nervous system (Ren & Dubner, 2002; Yunus, 2007; Heinricher et al., 2009; van Wijk & Veldhuijzen, 2010; Kindler, Bennett, & Jones, 2011); overactivation of glial cells, resulting in the release of proinflammatory cytokines (Ji, Berta, & Nedergaard, 2013; Loggia et al., 2015; Nijs et al., 2017); dysfunction of the stress system, including the hypothalamic–pituitary–adrenal axis (Van Houdenhove & Luyten, 2009); decreased production of paininhibiting neurotransmitters, and increased production of painaugmenting neurotransmitters, including excess production of brainderived neurotropic factor (BDNF) (Caumo et al., 2016; Deitos et al., 2015; Nijs, Meeus et al., 2015; Phillips & Clauw, 2011; Trang, Beggs, & Salter, 2011). Central Sensitization has been most often identified with fibromyalgia, and associated chronic widespread pain and sensitivity, with no observable pathology or nociceptive etiology. However, CS has also been identified in subsets of patients with clear evidence of tissue trauma, pathology, and/or nociceptive components, including multiple sclerosis (FernándezdelasPeñas et al., 2015), osteoarthritis (Akinci et al., 2016; Lluch, Torres, Nijs, & DOI: 10.1111/jabr.12123

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中央敏化清单：用户手册

中枢敏化 (CS) 是指中枢神经系统内神经信号的放大，导致疼痛超敏反应 (Woolf, 2011)。CS 的症状包括异常性疼痛、痛觉过敏、感受野扩张超出周围神经供应区域，以及刺激消除后的长时间疼痛（Latremoliere & Woolf，2009）。已经确定了许多与 CS 相关的生物机制，包括中枢神经系统中上行和下行轨道的失调（Ren & Dubner，2002；Yunus，2007；Heinricher 等，2009；van Wijk & Veldhuijzen，2010；Kindler, Bennett , & 琼斯, 2011); 神经胶质细胞过度活化，导致促炎细胞因子的释放（Ji、Berta 和 Nedergaard，2013 年；Loggia 等人，2015 年；Nijs 等人，2017 年）；压力系统功能障碍，包括下丘脑-垂体-肾上腺轴（Van Houdenhove & Luyten，2009）；减少疼痛抑制神经递质的产生，增加镇痛神经递质的产生，包括脑源性神经营养因子 (BDNF) 的过量产生（Caumo 等人，2016 年；Deitos 等人，2015 年；Nijs、Meeus 等人，2015 年；Phillips & Clauw） ，2011 年；Trang、Beggs 和 Salter，2011 年）。中枢敏化最常与纤维肌痛以及相关的慢性广泛疼痛和敏感性相关，没有可观察到的病理学或伤害性病因。然而，在具有明确组织创伤、病理和/或伤害性成分证据的患者亚组中也发现了 CS，包括多发性硬化症（FernándezdelasPeñas 等，2015）、骨关节炎（Akinci 等，2016；Lluch，Torres , 奈斯, &