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.
Pathophysiology; Review; Visceral pain
