Journal
CLINICAL AND EXPERIMENTAL ALLERGY
Volume 42, Issue 1, Pages 8-19Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1365-2222.2011.03791.x
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Funding
- NHLBI NIH HHS [R01 HL062296, R01 HL038095-22, R01 HL038095] Funding Source: Medline
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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 Ad 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.
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