纤维肌痛中的外周和中枢敏化:发病机制作用

Peripheral and central sensitization in fibromyalgia: pathogenetic role.

作者信息

Staud Roland, Smitherman Michael L

机构信息

Division of Rheumatology and Clinical Immunology, University of Florida, PO Box 100221, Gainesville, FL 32610-0221, USA.

出版信息

Curr Pain Headache Rep. 2002 Aug;6(4):259-66. doi: 10.1007/s11916-002-0046-1.

Abstract

Characteristic symptoms of fibromyalgia syndrome include widespread pain, fatigue, sleep abnormalities, and distress. Patients with fibromyalgia show psychophysical evidence of mechanical, thermal, and electrical hyperalgesia. Peripheral and central abnormalities of nociception have been described in fibromyalgia. Important nociceptor systems in the skin and muscles seem to undergo profound changes in patients with fibromyalgia through unknown mechanisms. They include sensitization of vanilloid receptor, acid-sensing ion channel receptors, and purino-receptors. Tissue mediators of inflammation and nerve growth factors can excite these receptors and cause extensive changes in pain sensitivity, but patients with fibromyalgia lack consistent evidence for inflammatory soft tissue abnormalities. Therefore, recent investigations have focused on central nervous system mechanisms of pain in fibromyalgia.

摘要

纤维肌痛综合征的典型症状包括广泛性疼痛、疲劳、睡眠异常和痛苦。纤维肌痛患者表现出机械性、热性和电性痛觉过敏的心理物理学证据。纤维肌痛中已描述了伤害感受的外周和中枢异常。皮肤和肌肉中的重要伤害感受器系统似乎在纤维肌痛患者中通过未知机制发生了深刻变化。这些变化包括香草酸受体、酸敏感离子通道受体和嘌呤受体的敏化。炎症组织介质和神经生长因子可激活这些受体并导致疼痛敏感性发生广泛变化,但纤维肌痛患者缺乏炎症性软组织异常的一致证据。因此,最近的研究集中在纤维肌痛疼痛的中枢神经系统机制上。

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