Attenuation of experimental pruritus and mechanically evoked dysesthesiae in an area of cutaneous allodynia

Abstract

We investigated the effects of tactile allodynia on the itch and mechanically evoked dysesthesiae produced by an intradermal injection of histamine in human volunteers. After an intradermal injection of capsaicin into the volar surface of one forearm, there developed an area of tactile allodynia to stroking and hyperalgesia to pricking the skin. Histamine was then injected simultaneously into the area of allodynia (experimental arm) and into the opposite forearm (control arm). Magnitude estimates of itch were obtained every 15 s for 5 min, and the areas of cutaneous hyperalgesia (pricking-evoked pain), alloknesis (stroking-evoked itch), hyperknesis (pricking-evoked itch) and wheal and flare were measured. The areas of wheal and flare were not significantly different on the two arms. The magnitude of itch and the areas of hyperknesis and alloknesis developed normally on the control arm but were absent or greatly reduced on the experimental arm. Thus, both the itch and the alloknesis and hyperknesis normally induced by histamine were absent or greatly reduced when histamine was injected in an area of capsaicin-induced allodynia. These results are compatible with the hypothesis that activity in capsaicin-sensitive, nociceptive primary afferent neurons evokes a central neuronal inhibitory process that prevents or reduces the itch and mechanically evoked dysesthesiae normally produced by an intradermal injection of histamine.

Comparison of Responses of Primate Spinothalamic Tract Neurons to Pruritic and Algogenic Stimuli

“…Experimental itch and accompanying dysesthesiae were enhanced by a local anesthetic ) and attenuated in hyperalgesic skin surrounding a capsaicin injection ). These studies demonstrated functional interactions between pruritic and nociceptive neural systems and lend support to the hypothesis that the mechanisms subserving itch are inhibited centrally by mechanisms that underlie pain and hyperalgesia Brull et al 1999;Graham et al 1951;Nilsson et al 1997;Ward et al 1996).…”

“…Another property expected of a candidate pruriceptive neuron in the CNS is that its activity is inhibited by algesic stimuli applied to normal skin and by the development of algogenic dysesthetic states such as allodynia and hyperalgesia (Bickford 1938;Brull et al 1999;Graham et al 1951;Koppert et al 1993;Nilsson et al 1997;Ward et al 1996). Rather than being inhibited by capsaicin, most of the STT neurons in the present study were vigorously excited, after which they became sensitized to stroking and to punctate stimuli.…”

Effects of scratching and other counterstimuli on responses of trigeminothalamic tract neurons to itch-inducing stimuli in rats

“…Electrical stimulation at levels sufficient to induce pain also can reduce itch (Bickford 1938;Nilsson et al 1997;Ward et al 1996). Finally, application of the pain-inducing chemical capsaicin reduces histamine-induced itch in humans (Brull et al 1999). These findings suggest that many forms of noxious stimulation can reduce itch.…”

TRPV1 Mediates Histamine-Induced Itching via the Activation of Phospholipase A2and 12-Lipoxygenase

“…It is also noteworthy that noxious stimulation such as scratching, heat, cold, and capsaicin suppresses or relieves itch (Bickford, 1937;Ward et al, 1996;Weisshaar et al, 1998;Brull, 1999;Yosipovitch et al, 2005). Although the precise mechanisms are not known, it is generally accepted that nociceptive signals inhibit incoming itch signals by central mechanism (Bickford, 1937;Brull et al, 1999;Yosipovitch et al, 2005). Therefore, this central inhibitory effect of nociceptive signals on itch input in part explains why capsaicin evokes pain predominantly although it is highly likely to excite both nociceptors and pruritic sensory fibers.…”