Abstract

The neurobiology of itch, which is formally known as pruritus, and its interaction with pain have been illustrated by the complexity of specific mediators, itch-related neuronal pathways and the central processing of itch. Scratch-induced pain can abolish itch, and analgesic opioids can generate itch, which indicates an antagonistic interaction. However, recent data suggest that there is a broad overlap between pain- and itch-related peripheral mediators and/or receptors, and there are astonishingly similar mechanisms of neuronal sensitization in the PNS and the CNS. The antagonistic interaction between pain and itch is already exploited in pruritus therapy, and current research concentrates on the identification of common targets for future analgesic and antipruritic therapy.

Author affiliations

1. Department of Dermatology, Kyoto University, Shogin-Kawahara-cho 54, Sakyo-ku, Kyoto 606-8507, Japan.
2. Department of Dermatology, IZKF Münster, and Boltzmann Institute for Immunobiology of the Skin,
3. Department of Dermatology, University Hospital, Von-Esmarch-Str. 58, 48149 Münster, Germany.
4. Departments of Dermatology, Neurobiology and Anatomy, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA.
5. Department of Anaesthesiology, Mannheim, University of Heidelberg, Theodor Kutzer Ufer 1–3, 68135 Manheim, Germany.

Correspondence to: Martin Schmelz⁵ Email: martin.schmelz@anaes.ma.uni-heidelberg.de

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