Henriksson Karl G
Department of Rehabilitation Medicine, Faculty of Health Sciences, Linkoping University, Pain Clinic, University Hospital, Linkoping, SE-581 85, Sweden.
Curr Pain Headache Rep. 2003 Dec;7(6):426-32. doi: 10.1007/s11916-003-0058-5.
The aim of this review is to present research that has a bearing on the pathogenesis of hypersensitivity in muscle pain syndromes. Allodynia and hyperalgesia in these syndromes can be segmental or generalized and temporary or permanent. Hypersensitivity in muscle pain conditions in the clinic is best diagnosed by determining the pressure pain threshold. In a disorder such as fibromyalgia, decreased pain thresholds also are found at sites where there is no tenderness. Pathogenetic mechanisms for allodynia and hyperalgesia can be identified at several levels of the nociceptive system, from the nociceptors in the muscle to the cortex. Central sensitization of nociceptive neurons in the dorsal horn and a disturbed balance between inhibitory and facilitatory impulses in the descending tracts from the brain stem to the dorsal horn are the main mechanisms for pain hypersensitivity. Changes in function, biochemical make-up, and synaptic connections in the nociceptive neurons in the dorsal horn are considered to be caused by neuronal plasticity.
本综述的目的是介绍与肌肉疼痛综合征中超敏反应发病机制相关的研究。这些综合征中的痛觉过敏和痛觉超敏可为节段性或全身性的,也可为暂时性或永久性的。临床上,肌肉疼痛状况下的超敏反应最好通过测定压力痛阈来诊断。在诸如纤维肌痛之类的病症中,在无压痛的部位也发现疼痛阈值降低。从肌肉中的伤害感受器到皮层,在伤害感受系统的几个层面都可确定痛觉过敏和痛觉超敏的发病机制。背角伤害性神经元的中枢敏化以及从脑干到背角的下行传导束中抑制性和易化性冲动之间的平衡失调是疼痛超敏的主要机制。背角伤害性神经元的功能、生化组成和突触连接的变化被认为是由神经元可塑性引起的。