Abstract
Although the identification of neural pathways for histamine-induced itch was a breakthrough in itch research, other pathways also seem to be involved in itch. In regard to itch of atopic dermatitis, neural sensitization complicates its mechanisms. Inflammatory mediators such as bradykinin that, normally, do not induce itch can function as pruritogens under neural sensitization, which also affects the treatment to a considerable extent. Complete inhibition of skin inflammation is, for now, the most effective way to suppress itching in atopic dermatitis, since there might be countless potential mediators inducing itch. Centrally acting anti-pruritic drugs as well as drugs against neural sensitization are prospective treatments for itch of atopic dermatitis.
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