Commentary on Peripheral and Central Contributions to Hyperalgesia in Irritable Bowel Syndrome

Abstract

The article by Price et al 14 Price D.D. Zhou Q. Moshiree B. Robinson M.E. Verne G.N. Peripheral and central contributions to hyperalgesia in the irritable bowel syndrome. J Pain. 2006; 7 (Epub online April 5, 2006): 529-535 Abstract Full Text Full Text PDF PubMed Scopus (114) Google Scholar presents a disease model for a common functional gastrointestinal syndrome, irritable bowel syndrome (IBS), developed by an accomplished and respected interdisciplinary group of pain researchers and gastroenterologists. The model is based on a series of well-designed studies on the mechanisms mediating altered perceptual responses to aversive visceral and somatic stimuli. Based largely on their own observations made in healthy control subjects and different IBS patient populations, the authors propose a disease model in which tonic afferent input from the rectum maintains a state of central sensitization (lumbosacral spinal hyperexcitability) which can be modulated by central influences, including those occurring during the placebo response. The proposed model, which is analogous to disease models of neurogenic pain, is based on several key observations by the authors that suggest that IBS patients demonstrate the following: 1) enhanced perceptual responses to aversive rectal stimuli; 2) thermal somatic hyperalgesia in both lower and upper extremities; 3) enhanced activation in brain regions, which are part of the central pain matrix during both visceral and somatic pain stimuli (these neuroimaging findings were associated with visceral and somatic hyperalgesia); 4) enhanced spinal cord processing of visceral stimuli (a finding also present in a neonatal injury rodent model of chronic visceral and somatic hyperalgesia); 5) both rectal and somatic hyperalgesia, as well as that IBS symptoms are reduced by intrarectal lidocaine administration; and 6) that intrarectal placebo is also associated with IBS pain relief.