PHYSIOLOGY OF ITCHING

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Abstract
Itching represents a sensory quality which is identical with that of protopathic pain. Superficial tickling progresses to itching and itching to diffuse burning pain without critical change of the quality of sensation when the intensity of the stimulus is gradually increased. They have a longer latent period than other cutaneous sensations because they are mediated by the slowly conducting C fibers of Gasser and Erlanger. Whether tickling, itching or protopathic pain sensation is felt, depends on the frequency of impulses in these fibers. The sensations persist after the cessation of stimulation, the fibers being inclined to after-discharges and their impulses being capable of central summation. They often appear as after-sensations of other sensory perceptions. The clearest example of such combined impulses in different fiber sets is the double pain sensation following needle pricks. Itching is experienced in a rather pure form, and becomes accentuated or explosive if the epicritic sensitivity is depressed following injuries to the skin, to the peripheral nerve trunk, or to the central nervous system. Itching caused by pathologic processes is always based on such a condition. If the over-accentuation of protopathic sensitivity is pronounced, the slightest external stimuli, even if they are inadequate (e.g., touch and temp. stimuli) evoke itching. Polyphasic configurations in the electroneurogram of "second pain" impulses indicate the frequent branching of the corresponding axons. The ramifying axon system revealed by Lewis in experiments on hyperalgesia, although interpreted differently, also seems to be related to the perception of protopathic pain and itching. Radiation and poor localization of these sensations are explained by their originating from richly ramifying axons. According to this view there are 3 ramifying axon systems in the skin, the sympathetic, the antidromic vasodilator and the protopathic sensory system, all consisting of small unmyelinated fibers and all mediating diffuse effects by means of axon reflex impulses. Sympathetic and protopathic sensory systems often respond in coupled reactions to cutaneous stimuli but itching arises without any interference of the sympathetic fibers. Itching and antidromic vasodilatation are also frequently coupled with each other but there is no evidence that vasodilatation is a necessary factor in evoking itching. Supporting evidence has been presented for the theory that itching following skin injury and itching in skin lesion based on hypersensitivity reactions might be mediated by liberation of H-substance. However, liberation of histamine or of a similar substance cannot be responsible for itching which occurs without visible changes in the skin. The central inducement of itching, the scratch reflex and therapeutic considerations are briefly discussed.

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