Abstract
BACKGROUNDS AND OBJECTIVES: Visceral pain shows many pathophysiological properties that make this form of pain unique, not only because of the clinical properties of the sensation but also because the neurobiological mechanisms that mediate the sensory process. This study aimed at reviewing the pathophysiology of visceral pain. CONTENTS: The activation and sensitization of visceral nociceptors are heavily influenced by the secretory and motor properties of the microenvironment where the sensory receptors are located. In some cases, epithelial cells can play a direct role in the activation of primary sensory neurons. Subclinical alterations of the visceral epithelium can contribute to enhanced visceral sensitivity. Central hypersensitivity induced by visceral activation can be caused by mobilization of AMPA receptors from the cytosol to the membrane of nociceptive neurons. In addition, functional pain syndromes, such as the Irritable Bowel Syndrome, could be triggered or maintained by hormonal alterations, particularly those involving sex hormones such as estrogen. CONCLUSION: The neurobiological mechanisms that mediate visceral pain are sufficiently unique to preclude interpreting visceral pain conditions purely as a direct extrapolation of what we know about somatic pain. The functional properties of visceral nociceptors are different from those of their somatic counterparts and the microenvironment where visceral nociceptors are located, and especially the motor and secretory functions of organs like the gut, play a key role in the activation and sensitization of visceral sensory receptors.
Highlights
The neurobiological mechanisms that mediate visceral pain are sufficiently unique to preclude interpreting visceral pain conditions purely as a direct extrapolation of what we know about somatic pain
In some cases visceral hyperalgesia appears in the absence of an identifiable peripheral cause, perhaps as a consequence of the sensitization and hyperexcitability of visceral afferents evoked by subclinical changes in their microenvironment
Hyperalgesia is the most prominent feature of the visceral pain process and is the expression of hypersensitivity of the pain pathway induced by the sensitization of the peripheral receptors that signal visceral sensory events or of the neurons that transmit and process this sensory information to the central nervous system (CNS)
Summary
The basic model of visceral hyperalgesia shown in figure 1A includes the peripheral origin of primary hyperalgesia due to nociceptor sensitization and the alteration in the central processing of afferent impulses from low threshold mechanoreceptors that results in referred secondary hyperalgesia. This alteration is initially triggered and later maintained by the enhanced afferent discharges from the primary hyperalgesic area. In the case of referred visceral hyperalgesia the primary focus is located in an internal organ, where nociceptors are sensitized by the originating stimulus and send enhanced discharges to the central nervous system (CNS) There, these impulses trigger and maintain a secondary hyperalgesic area that, in this case, is referred to the surface of the body[1]. This study aimed at reviewing the pathophysiology of visceral pain
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