• DOI:10.1177/003591577506800829
• Corpus ID: 208793207

Itch

@article{Yosipovitch2003Itch,
  title={Itch},
  author={Gil Yosipovitch and Malcolm W. Greaves and Martin Schmelz},
  journal={The Lancet},
  year={2003},
  volume={361},
  pages={690-694}
}

• G. Yosipovitch, M. Greaves, M. Schmelz
• Published 1 August 1975
• The Lancet

Introduction to the Pharmacology and Physiology of Itch Studies with microelectrodes and with plant spicules containing potent itch-producing proteolytic enzymes demonstrated that itch receptors are a plexus of free nerve endings closely related to the dermo-epidermal zone. The receptors are stimulated by mediators, including histamine, released in inflamed itchy skin. Certain mediators, although not capable of causing itching alone, can potentiate the action of other itch-producing agents. This type of synergism has been demonstrated with prostaglandin E1, which potentiates the itching action of histamine in human skin. The observation that drugs which directly inhibit prostaglandin synthetase are not antipruritic may be explained by the low sensitivity of skin synthetase to this class of drug compared with synthetase of other tissues. Itch as well as pain is transmitted along small slowly-conducting sensory neurones to the cord. Whether the 'gate control' theory of pain also applies to itch is not known. Secondary neurones ascend to the second relay station in the thalamus. The evidence for tertiary neurones connecting thalamus and cortex is inferentialand derives partly from studies of the syndrome of congenital indifference to pain and itch. The phenomenon of central itching is of great interest. Anticholinesterases including diisopropyl fluorophosphate and physostigmine cause central itch, which raises the possibility that pruritus in some extensive itchy skin diseases might be due to acetylcholine released from damaged skin into the circulation. Measurement of itch presents serious difficulties. First, there is the obvious problem of subjectivity of sensation of itch. Secondly, there are no valid animal models for itch. Thirdly, there are no measurable direct electrophysiological changes in the cortex or in sensory neurones in response to itching. Newer objective indirect methods in man in which scratching in response to itching is measured are promising but perhaps the most potentially valuable future approach lies in measurement of biochemical responses to itching, for example changes of serum lipids or urinary catecholamine excretion.