Historically, itch was defined relative to pain as a function of “soothing” an itch with a scratch reflex. Under this method of itch inhibition, this twentieth-century hypothesis initially proposed that the close relationship between these two distinct sensations operate within identical neural circuitry by way of intensity (Von Frey, 1922). Percepts were coded by level of assignment writing service stimuli intensity; itchy modalities were the result of low level neuronal activation and pain responses generated at higher levels. ( McMahon and Koltzenburg, 1992 ). Evidence against intensity theory has since developed as subsiding painful stimuli was not shown to evoke itch at lower frequencies ( Handwerker et al., 1991 ; Ochoa and Torebjork, 1989 ) and alternatively, increasing itch stimuli did not induce pain responses ( Tucket, 1982). With the identification of distinct “itch specific” sensory afferent fibers ( Han et al., 2013), intensity theory ultimately led into Specificity Theory which suggests that there exists distinguishable afferent fibers for detection of itch and pain stimuli.