Nijs Jo, Loggia Marco L, Polli Andrea, Moens Maarten, Huysmans Eva, Goudman Lisa, Meeus Mira, Vanderweeën Luc, Ickmans Kelly, Clauw Daniel
a Department of physiotherapy, human physiology and anatomy , Pain in Motion International Research Group, Vrije Universiteit Brussel , Brussels , Belgium.
b Department of Physiotherapy, Human Physiology and Anatomy, Faculty of Physical Education & Physiotherapy , Vrije Universiteit Brussel , Brussels , Belgium.
Expert Opin Ther Targets. 2017 Aug;21(8):817-826. doi: 10.1080/14728222.2017.1353603. Epub 2017 Jul 12.
The mechanism of sensitization of the central nervous system partly explains the chronic pain experience in many patients, but the etiological mechanisms of this central nervous system dysfunction are poorly understood. Recently, an increasing number of studies suggest that aberrant glial activation takes part in the establishment and/or maintenance of central sensitization. Areas covered: This review focused on preclinical work and mostly on the neurobiochemistry studied in animals, with limited human studies available. Glial overactivation results in a low-grade neuroinflammatory state, characterized by high levels of BDNF, IL-1β, TNF-α, which in turn increases the excitability of the central nervous system neurons through mechanisms like long-term potentiation and increased synaptic efficiency. Aberrant glial activity in chronic pain might have been triggered by severe stress exposure, and/or sleeping disturbances, each of which are established initiating factors for chronic pain development. Expert opinion: Potential treatment avenues include several pharmacological options for diminishing glial activity, as well as conservative interventions like sleep management, stress management and exercise therapy. Pharmacological options include propentofylline, minocycline, β -adrenergic receptor antagonists, and cannabidiol. Before translating these findings from basic science to clinical settings, more human studies exploring the outlined mechanisms in chronic pain patients are needed.
中枢神经系统致敏机制部分解释了许多患者的慢性疼痛体验，但这种中枢神经系统功能障碍的病因机制尚不清楚。最近，越来越多的研究表明，异常的胶质细胞激活参与了中枢致敏的建立和/或维持。涵盖领域：本综述聚焦于临床前研究工作，主要是动物神经生物化学研究，可供参考的人体研究有限。胶质细胞过度激活会导致低度神经炎症状态，其特征是脑源性神经营养因子（BDNF）、白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）水平升高，进而通过长时程增强和突触效率增加等机制提高中枢神经系统神经元的兴奋性。慢性疼痛中异常的胶质细胞活动可能由严重应激暴露和/或睡眠障碍引发，而这两者都是慢性疼痛发展的既定起始因素。专家观点：潜在的治疗途径包括几种降低胶质细胞活性的药理学选择，以及睡眠管理、压力管理和运动疗法等保守干预措施。药理学选择包括丙戊茶碱、米诺环素、β-肾上腺素能受体拮抗剂和大麻二酚。在将这些基础科学研究结果转化为临床应用之前，需要更多针对慢性疼痛患者探索上述机制的人体研究。
