Painful stimuli evoke itch in patients with chronic pruritus

Ikoma, Akihiko; Fartasch, Manigé; Heyer, G.; Miyachi, Yoshiki; Handwerker, Hermann O.; Schmelz, Martin

doi:10.1212/wnl.62.2.212

Cited by 184 publications

(190 citation statements)

References 35 publications

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“…62) This finding is consistent with the clinical feature of chronic pruritus such as atopic dermatitis that patients are often urged to keep scratching once they start it, suggesting that scratching does not only inhibit but also generate itch. on the other hand, pain sensitization causes a contrastive phenomenon.…”

Section: Itch Sensitizationsupporting

confidence: 79%

Updated Neurophysiology of Itch

Ikoma¹

2013

Biological & Pharmaceutical Bulletin

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The unique physiological features of histamine-sensitive C-fibers and spinothalamic tract neurons support the hypothesis of itch specific pathway, whereas subsequent studies on cowhage-induced itch have provided evidence against it, suggesting the presence of multiple neural pathways for itch. Not only peripheral pruritogens but also spinal neural receptors are involved in the control of itch, and will be the target of treatment. Itch sensitization in chronic pruritus is another crucial factor that needs to be considered in the treatment. Neuropathic itch is the type of itch that occurs when nerve fibers are damaged or injured and spontaneous firing of nerves takes place, and plays a major role in itch accompanying some pathological conditions such as herpes zoster. The complexity of itch is due to the broad range of mediators involved and the large variety of neural mechanisms behind.

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Section: Itch Sensitizationsupporting

confidence: 79%

Updated Neurophysiology of Itch

Ikoma¹

2013

Biological & Pharmaceutical Bulletin

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“…It has been shown that itch can be evoked in patients with atopic dermatitis by mechanical, electrical, thermal, and low-pH stimuli that are normally painful (19). This finding is consistent with one of the well-known clinical features of patients with atopic dermatitis that they cannot stop scratching once they start it.…”

Section: Itch Sensitization In Atopic Dermatitissupporting

confidence: 79%

Analysis of the Mechanism for the Development of Allergic Skin Inflammation and the Application for Its Treatment: Mechanisms and Management of Itch in Atopic Dermatitis

Ikoma

2009

J Pharmacol Sci

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Abstract. Although the identification of neural pathways for histamine-induced itch was a breakthrough in itch research, other pathways also seem to be involved in itch. In regard to itch of atopic dermatitis, neural sensitization complicates its mechanisms. Inflammatory mediators such as bradykinin that, normally, do not induce itch can function as pruritogens under neural sensitization, which also affects the treatment to a considerable extent. Complete inhibition of skin inflammation is, for now, the most effective way to suppress itching in atopic dermatitis, since there might be countless potential mediators inducing itch. Centrally acting anti-pruritic drugs as well as drugs against neural sensitization are prospective treatments for itch of atopic dermatitis.

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“…In certain pathological conditions, it may also modulate the modality of the sensation. It has been observed that in lesioned areas of atopic dermatitis patients, nociceptive stimuli such as bradykinin treatment or electrical stimuli are perceived as itching and not as pain [56,57] .…”

Section: Sensitization and Regulatory Mechanisms Of Itch And Painmentioning

confidence: 99%

Molecular Mechanisms of Itch and Pain: An Overview

Lee

2015

Itch Pain

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Itch and pain are two distinct sensory modalities elicited by noxious and pruritic stimuli, respectively. The cellular and electrophysiological characteristics of itch and pain are very similar; thus discerning the mechanical difference between these two sensory modalities has long been elusive. Recent advances in this field have revealed various neuronal receptors responsible for itch and pain signal transduction and transmission. These studies have identified a distinct sub-population of sensory neurons responsible for itch signal transduction. In addition, itch and pain information conveyed to the spinal cord are processed and regulated by distinct spinal cord neurons. Although both itch and pain senses are required for our daily lives, chronic and hyper-sensation of itch and pain results in a debilitating disease state. Studies have now begun to elucidate mechanisms for the sensitization of pain and itch and also to unravel counter-regulatory mechanisms between itch and pain at the spinal cord level. Interestingly, toll-like receptors (TLRs), an innate immune receptor, has been implicated in the central sensitization of both pain and itch. In this review, we will briefly provide an overview of the molecular mechanisms of itch and pain. Additionally, we will discuss the recently uncovered role of TLRs in itch and pain sensation.

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Painful stimuli evoke itch in patients with chronic pruritus

Cited by 184 publications

References 35 publications

Updated Neurophysiology of Itch

Updated Neurophysiology of Itch

Analysis of the Mechanism for the Development of Allergic Skin Inflammation and the Application for Its Treatment: Mechanisms and Management of Itch in Atopic Dermatitis

Molecular Mechanisms of Itch and Pain: An Overview

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