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Most of what is written and believed about pain and nociceptors originates from studies of the “somatic” (non-visceral) sensory system. As a result, the unique features of visceral pain are often overlooked
In the clinic, the management of visceral pain is typically poor, and drugs that are used with some efficacy to treat somatic pain often present unwanted effects on the viscera
This review provides evidence of functional, morphological, and biochemical differences between visceral and non-visceral afferents, with a focus on potential nociceptive roles, and also considers some of the potential mechanisms of visceral mechanosensation.
We have reviewed evidence here that visceral nociceptors—or, more accurately, visceral afferents with the potential to transmit nociceptive information—differ from non-visceral (somatic) afferents in a number of ways, including their morphology and the channels and receptors they contain.
In humans, visceral pain has a number of characteristics that distinguish it from pain originating from non-visceral structures, and these differences are most likely responsible for the symptoms experienced by patients with a visceral disease such as IBS
Somatic pain relief strategies typically work poorly for the management of visceral pain, and a better understanding of the visceral nociceptor (along with central mechanisms not discussed here) is vital to the development of new therapies for visceral pain management.
Although CGRP- and TRPV1-containing DRG somata are more common in visceral sensory neurons, these and other potential surrogates do not reliably distinguish visceral from non-visceral nociceptors. Until such a marker (or constellation of markers) is found, identification of nociceptors requires functional assessment.