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神经病理性疼痛病理生理学中的炎症。

Inflammation in the pathophysiology of neuropathic pain.

机构信息

Department of Neurology, University of Würzburg, Würzburg, Germany.

Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO, USA.

出版信息

Pain. 2018 Mar;159(3):595-602. doi: 10.1097/j.pain.0000000000001122.

DOI:10.1097/j.pain.0000000000001122
PMID:29447138
Abstract

Peripheral nerve injuries and diseases often lead to pain persisting beyond the resolution of damage, indicating an active disease-promoting process, which may result in chronic pain. This is regarded as a maladaptive mechanism resulting from neuroinflammation that originally serves to promote regeneration and healing. Knowledge on these physiological and pathophysiological processes has accumulated over the last few decades and has started to yield potential therapeutic targets. Key players are macrophages, T-lymphocytes, cytokines, and chemokines. In the spinal cord and brain, microglia and astrocytes are involved. Recently, data have been emerging on the regulation of these players. MicroRNAs and other noncoding RNAs have been discussed as potential master switches that may link nerve injury, pain, and inflammation. Clinical disorders most intensely studied in the context of neuroinflammation and pain are the complex regional pain syndrome, polyneuropathies, postherpetic neuralgia, and the fibromyalgia syndrome, in which recently a neuropathic component has been described. Research from several groups has shown an important role of both proinflammatory and anti-inflammatory cytokines in neuropathic and other chronic pain states in humans. There is ample evidence of an analgesic action of anti-inflammatory cytokines in animal models. The interplay of anti-inflammatory cytokines and the nociceptive system provides possibilities and challenges concerning treatment strategies based on this concept.

摘要

周围神经损伤和疾病常导致损伤愈合后仍持续存在疼痛,表明存在促进疾病进展的活跃过程,这可能导致慢性疼痛。这被认为是一种神经炎症原有的适应性机制,最初是为了促进再生和愈合。过去几十年中,人们对这些生理和病理生理过程的认识不断积累,并开始产生潜在的治疗靶点。关键的参与者是巨噬细胞、T 淋巴细胞、细胞因子和趋化因子。在脊髓和大脑中,小胶质细胞和星形胶质细胞也参与其中。最近,关于这些参与者的调控数据不断涌现。microRNAs 和其他非编码 RNA 被认为是潜在的主开关,可能将神经损伤、疼痛和炎症联系起来。在神经炎症和疼痛的背景下,研究最深入的临床疾病是复杂性区域疼痛综合征、多发性神经病、带状疱疹后神经痛和纤维肌痛综合征,最近已经描述了其神经病理性成分。几个研究小组的研究表明,促炎和抗炎细胞因子在人类神经病理性和其他慢性疼痛状态中均起着重要作用。有大量证据表明抗炎细胞因子在动物模型中具有镇痛作用。抗炎细胞因子与伤害感受系统的相互作用为基于这一概念的治疗策略提供了可能性和挑战。

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