November 2003

Neurophysiology of PruritusCutaneous Elicitation of Itch

Author Affiliations

From the Departments of Dermatology, University of Münster, Münster (Drs Ständer, Steinhoff, Metze, and Luger), Anesthesiology and Intensive Care Medicine, Faculty of Clinical Medicine, Mannheim (Dr Schmelz), and Social Medicine, Occupational and Environmental Dermatology, University of Heidelberg, Heidelberg (Dr Weisshaar), Germany. The authors have no relevant financial interest in this article.


Copyright 2003 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2003

Arch Dermatol. 2003;139(11):1463-1470. doi:10.1001/archderm.139.11.1463

Itching is defined as an unpleasant cutaneous sensation leading to the desire to scratch. It serves as a physiological self-protective mechanism as do other cutaneous sensations like pain, touch, vibration, cold, and heat to help defend the skin against harmful external agents. Pruritus can be evoked in the skin directly by mechanical and thermal stimuli or indirectly through chemical mediators. It may also be generated in the central nervous system independently of peripheral stimulation. Single-nerve-fiber recordings have shown that histamine-evoked itch is transmitted by selective slow-conducting subpopulations of unmyelinated C-polymodal neurons. Recent experimental studies using improved methods have demonstrated which of the suspected chemical itch mediators such as histamine, neuropeptides, prostaglandins, serotonin, acetylcholine, or bradykinin act pruritogenically on C-fibers. Moreover, investigations have revealed new receptor systems such as vanilloid, opioid, and cannabinoid receptors on cutaneous sensory nerve fibers that may modulate itch and thereby represent targets for antipruritic therapy. This review focuses on the peripheral generation of itch, including neurotransmitters, neuropeptides, and inflammatory mediators.