Postinflammatory visceral sensitivity and pain mechanisms

Neurogastroenterol Motil. 2008 May;20 Suppl 1:73-80. doi: 10.1111/j.1365-2982.2008.01110.x.

Abstract

The inflammatory reaction is normally tightly regulated, and as soon as the original insult has been cleared, a resolution phase starts that aims at leading the tissues back to a normal physiological state. However, after intestinal inflammation, a number of patients develop postinflammatory hypersensitivity symptoms, which can be defined as an excessive sensitivity to gut nociceptive stimulation. The pain experienced by those patients has been largely studied in the context of postinfectious intestinal diseases. The mechanisms of postinflammatory persistent visceral pain involve peripheral and central neuroplastic changes, low-grade chronic inflammation that sensitizes visceral afferent pathways and sensitization of non-neuronal resident cells of the gut. Several molecular determinants such as neurokinins, serotonin, proteases and voltage-gated ion channels seem to play a significant role in the control of postinflammatory visceral sensation. This review tries to give insights into the mechanisms of persistent visceral pain following the resolution of intestinal inflammation and tries to identify what needs to be done to further advance the field of postinflammatory hypersensitivity clinical management.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Hyperalgesia / etiology
  • Hyperalgesia / pathology
  • Hyperalgesia / physiopathology
  • Inflammation / complications
  • Inflammation / physiopathology
  • Nociceptors / physiology
  • Pain / etiology
  • Pain / pathology*
  • Pain / physiopathology*
  • Pain Measurement / methods
  • Pain Threshold / physiology
  • Visceral Afferents / pathology*
  • Visceral Afferents / physiology*