Pathophysiology of visceral pain

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.

Central and Peripheral Mechanism of Acupuncture Analgesia on Visceral Pain: A Systematic Review

“…Visceral pain, i.e., pain originating from the thoracic, abdominal, or pelvic regions, is a noticeable symptom associated with various clinical conditions [1, 2]. Visceral pain has different characteristics compared to somatic pain.…”

Acupuncture at Tàichōng (太冲 LR 3) for dysmenorrhea

“…True visceral pain arises as a diffuse and poorly defined sensation usually perceived in the midline of the body, at the lower sternum or upper abdomen [34] . Psychophysics of visceral pain differs from somatic pain, and it needs to be examined carefully while the neurological mechanism of somatic pain cannot extrapolate to visceral pain without qualification [35] . As said before, dysmenorrhea divided into primary and secondary.…”

Possible implications of animal models for the assessment of visceral pain

“…29 Functional pain states triggered by various factors (genetic, hormonal etc), resulting in central alteration of the sensory processing that mediates referred secondary hyperalgesia, can be activated even in the absence of a peripheral stimulation of the nociceptors. 31,32…”

“…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 CNS. Somatic and visceral hyperalgesia are similar in the sense that both include a peripheral component of enhanced activity from nociceptors and a central component of alteration in the central processing of low threshold inputs, but the peripheral component can generate a secondary hyperalgesia in case of visceral hyperalgesia 31 . Functional pain states triggered by various factors (genetic, hormonal etc), resulting in central alteration of the sensory processing that mediates referred secondary hyperalgesia, can be activated even in the absence of a peripheral stimulation of the nociceptors 31,32 …”

“…30 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 CNS. Somatic and visceral hyperalgesia are similar in the sense that both include a peripheral component of enhanced activity from nociceptors and a central component of alteration in the central processing of low threshold inputs, but the peripheral component can generate a secondary hyperalgesia in case of visceral hyperalgesia 31.…”