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慢性疼痛评估基础指南:从神经生理学到床边。

Basic guide to chronic pain assessment: from neurophysiology to bedside.

机构信息

Department of Medical Science and Public Health, University of Cagliari, Cagliari, Italy -

Department of Anesthesia, Resuscitation and Pain Therapy, Sacred Heart Catholic University, Rome, Italy.

出版信息

Minerva Anestesiol. 2020 Dec;86(12):1321-1330. doi: 10.23736/S0375-9393.20.14573-5.

Abstract

Chronic musculoskeletal pain is a highly prevalent condition that is commonly encountered in both general and specialist practice. Nonetheless, it still represents a significant challenge to the practitioners because of the lack of substantial evidence-based guidance. This review aimed to summarize the main pathophysiological mechanisms of chronic pain offering a mechanism-oriented approach to diagnosis and management. We believe that a basic knowledge of the physical signs and symptoms of these mechanisms could empower the clinician to choose appropriate medication and identify high-risk pain patients. Central sensitization and neuropathic features may arise in previously nociceptive and inflammatory pain syndromes. Central sensitization is a functional remodeling of the spinal cord, where light touch afferents are recruited by nociceptive second-order neurons. Neuropathic features include both negative signs, such as reduced perception of vibration and touch, and positive symptoms, such as paroxysmal electric shock pain, due to ectopic discharge. These phenomena are the neurobiological basis of the commonly defined refractory chronic pain. Early detection and specific treatment of these mechanisms are required in order to restrain the reinforcement of pronociceptive remodeling of the nervous system.

摘要

慢性肌肉骨骼疼痛是一种普遍存在的病症,在普通和专科实践中都很常见。尽管如此,由于缺乏实质性的循证指导,它仍然对从业者构成重大挑战。本综述旨在总结慢性疼痛的主要病理生理机制,为诊断和治疗提供一种基于机制的方法。我们相信,对这些机制的物理体征和症状有基本的了解,可以使临床医生能够选择合适的药物,并识别出高风险的疼痛患者。在以前的伤害感受性和炎症性疼痛综合征中,可能会出现中枢敏化和神经病理性特征。中枢敏化是脊髓的功能重塑,其中轻触传入纤维被伤害性二级神经元募集。神经病理性特征包括负性征象,如振动和触觉感知降低,以及阳性症状,如由于异位放电引起的阵发性电击样疼痛。这些现象是通常定义的难治性慢性疼痛的神经生物学基础。需要早期发现和特定治疗这些机制,以抑制伤害感受性重塑的神经系统的增强。

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