Itch pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
The central chemical involved in itching is histamine, a molecule released by mast cells in the skin. Histamine is the chemical that causes the itch and reddening. It binds to local nerve endings on specific receptors.
Itch can originate in the peripheral nervous system (dermal or neuropathic) or in the central nervous system (neuropathic, neurogenic, or psychogenic).[1]
Dermal/Pruritoceptive
Itch originating in the skin is considered pruritoceptive and can be induced by a variety of stimuli, including mechanical, chemical, thermal, and electrical stimulation. The primary afferent neurons responsible for histamine induced itch are unmyelinated C-fibers. In human C-fiber nociceptors, two major classes exist: mechano-responsive nociceptors and mechano-insensitive nociceptors. Mechano-responsive nociceptors have been in shown in studies to respond to mostly pain and mechano-insensitive receptors respond mostly to itch induced by histamine. However it does not explain mechanically induced itch or when itch is produced without a flare reaction which involves no histamine. Therefore it is possible that pruritoceptive nerve fibers have different classes of fibers, which is currently unclear in current research.[2]
Studies have been done to show that itch receptors are only found on the top two skin layers, the epidermis and the epidermal/dermal transition layers. Shelley and Arthur had verified the depth by injecting individual itch powder spicules (Mucuna pruriens) and found that maximal sensitivity was found at the basal cell layer or the innermost layer of the epidermis. Surgical removal of those skin layers removed the ability for a patient to perceive itch. Itch is never felt in muscle, joints, or inner organs, which show that deep tissue does not contain itch signaling apparatuses.[3]
Sensitivity to puritic stimuli is not even across the skin and has a random spot distribution with similar density to that of pain. The same substances that elicit itch upon intracutaneous injection (injection within the skin) elicit only pain when injected subcutaneously (beneath the skin). Itch is readily abolished in skin areas treated with nociceptor excitotoxin capsaicin but remains unchanged in skin areas which were rendered touch-insensitive by pretreatment with saponins, an anti-inflammatory agent. Although experimentally induced itch can still be perceived under a complete A-fiber conduction block, it is significantly diminished. Overall, itch sensation is mediated by A-delta and C nociceptors located in the uppermost layer of the skin.[4]
Neuropathic
Neuropathic itch can originate at any point along the afferent pathway as a result of damage of the nervous system. They could include diseases or disorders in the central nervous system or peripheral nervous system.[3] Examples of neuropathic itch in origin are nostalgia paresthetica, brachioradial pruritus, brain tumors, multiple sclerosis, peripheral neuropathy, and nerve irritation.[5]
Neurogenic
Neurogenic itch, which is itch induced centrally but with no neural damage, is often associated with increased accumulation of endogenous opioids and possibly synethetic opioids.[3]
Psychogenic
Itch is also associated with some psychiatric disorders such as delusions of parasitosis or related obsessive-compulsive disorders, for example neurotic scratching.[3]
References
- ↑ Yosipovitch, G., Greaves, M.W., Schmelz, M. (2003). Itch. The Lancet, 361(9358), 690-694.
- ↑ Ikoma, A., Steinhoff, M., Stander, S., Yosipovitch, G., Schmelz, M. (2006). The neurobiology of itch. Nature Reviews Neuroscience, 7(7), 535-547.
- ↑ 3.0 3.1 3.2 3.3
- ↑ Schmelz, M., Schmidt, R., Bickel, A., Handwerker, H.O., Torebjork, H.E. (1997). Specific C-Receptors for Itch in Human Skin. The Journal of Neuroscience, 17(20), 8003-8008.
- ↑ Bernhard, J.D. (2005). Itch and pruritus: what are they, and how should itches be classified? Dermatologic Therapy, 18, 288-291.