Division of Allergy and Clinical Immunology, Johns Hopkins School of Medicine, Baltimore, MD, USA.
Clin Exp Allergy. 2012 Jan;42(1):8-19. doi: 10.1111/j.1365-2222.2011.03791.x. Epub 2011 Jun 6.
Chronic itch represents a burdensome clinical problem that can originate from a variety of aetiologies. Pruriceptive itch originates following the activation of peripheral sensory nerve endings following damage or exposure to inflammatory mediators and ascends to the brain through the spinal thalamic tract. Much insight has been gained into the understanding of the mechanisms underlying pruriceptive itch through studies using humans and experimental animals. More than one sensory nerve subtype is thought to subserve pruriceptive itch which includes both unmyelinated C-fibres and thinly myelinated Aδ nerve fibres. There are a myriad of mediators capable of stimulating these afferent nerves leading to itch, including biogenic amines, proteases, cytokines, and peptides. Some of these mediators can also evoke sensations of pain and the sensory processing underlying both sensations overlaps in complex ways. Studies have demonstrated that both peripheral and central sensitization to pruritogenic stimuli occur during chronic itch.
慢性瘙痒是一种令人痛苦的临床问题，可能由多种病因引起。伤害感受性瘙痒源于外周感觉神经末梢在损伤或暴露于炎症介质后被激活，并通过脊髓丘脑束上升到大脑。通过对人类和实验动物的研究，人们对瘙痒产生的机制有了更深入的了解。人们认为，不止一种感觉神经亚型参与了瘙痒，包括无髓鞘 C 纤维和薄髓鞘 Aδ 神经纤维。有无数种介质能够刺激这些传入神经，导致瘙痒，包括生物胺、蛋白酶、细胞因子和肽。其中一些介质还可以引起疼痛感觉，而这两种感觉的感觉处理在复杂的方式中重叠。研究表明，慢性瘙痒时，对致痒刺激的外周和中枢敏化都会发生。
