SANTA BARBARA, CALIF. — The “itch-scratch” cycle is the dermatologic equivalent of chronic pain syndrome, and should be treated as such, Timothy G. Berger, M.D., said at the annual meeting of the California Society of Dermatology and Dermatologic Surgery.
Just as with chronic pain, there is a “reduced threshold” phenomenon that occurs with chronic itch, he explained.
Chronicity not only lowers the threshold for the sensation of itch, it also increases the intensity of itch. Also like pain, short bursts of spontaneous itch may occur, even when the skin is clear.
“This has to do with anatomic rewiring in the central nervous system,” said Dr. Berger, professor of clinical dermatology at the University of California, San Francisco.
“The premise for pain is to intervene early to stop that central rewiring. In itch, the same premise should be applied.”
Dr. Berger explained that exciting advances in neurobiology have begun to elucidate the mechanisms of itch, although certain important pieces of the puzzle have yet to be found.
Importantly, researchers have discovered that itch is not, as previously believed, a minor sensation of pain.
Rather, “there are specific itch nerves and there are specific pain nerves,” he said.
Itch-specific neurons are small, unmyelinated C fibers distributed into and near the epidermis, constituting about 10% of the sensory nerves. They have no response to pain, but do respond to histamine and certain plant species.
“These itch nerves have very extensive branches,” with a single itch-specific neuron feeding an 8.5-cm area. That's why, “when there's something that hurts, there's a little spot that hurts. When you itch, your whole arm itches,” he noted.
Specific receptors have been identified for pressure and for pain, but no specific itch receptor has been found, although Dr. Berger has confidence that one will be located. “It just can't be that there isn't one.”
Dr. Berger said there are connections between pain and itch, although the two act independently. “Itch” and “pain” channels interact, and the neural elements mediating them are identical, though separate.
Itch can be blocked by pain, which is why scratching relieves itching.
Conversely, blocking pain neurons can heighten the sensation of itch, as in the case of opiates inducing pruritus.
Another intriguing aspect to itch is the role played by inflammatory mediators—neuropeptides. Even when a patient's itch does not have a primary inflammatory etiology, inflammation can develop in response to itch through neuropeptides.
This explains why drugs with anti-inflammatory properties can sometimes be effective in treating itch.
Dr. Berger reviewed several novel drugs for treating itch:
▸ Thalidomide. Especially effective in prurigo nodularis, this drug can be used for itch at dosages of 50–200 mg daily. It may increase the risk of neuropathy, and should be used cautiously in dosages higher than 100 mg/day, at which there may be an increased risk of thrombosis.
▸ Mirtazapine (Remeron). At a dosage of 15–45 mg nightly, this unique antidepressant has potent antihistamine properties. “It will occasionally work in patients when other medications have not worked,” Dr. Berger said. It is sedating, but otherwise well tolerated.
▸ Ondansetron (Zofran). This serotonin 5-hydroxytryptamine-3 receptor blocker can be used in doses of 4 or 8 mg/day, especially for opiate-related itch.
▸ Paroxetine (Paxil). Another antidepressant, this is an SSRI unrelated to the others in its class. It is used for pruritus at a dosage of 20 mg/day. Its anti-itch properties are powerful enough that normal patients may develop pruritus upon stopping the drug.
Dr. Berger reported no conflicts of interest regarding any of these drugs.