denoting a disorder with no known or detectable organic basis to
explain the symptoms sometimes referred to as neurosis. Medical
history is replete with examples of diseases termed functional because
medical knowledge was incomplete and/or the technology to elucidate
the pathobiological mechanisms was not yet available.
Am J Physiol Gastrointest Liver Physiol. 2012 Mar 8. [Epub ahead of print]
Neural and neuro-immune mechanisms of visceral hypersensitivity in
irritable bowel syndrome.
Feng B, La JH, Schwartz ES, Gebhart GF.
Center for Pain Research, University of Pittsburgh.
Abstract
Irritable bowel syndrome (IBS) is characterized as 'functional'
because a pathobiological cause is not readily apparent.
Considerable evidence, however, documents that sensitizing
pro-inflammatory and lipotoxic lipids, mast cells and their products,
tryptases, enteroendocrine cells and mononuclear phagocytes and their
receptors are increased in tissues of IBS patients with colorectal
hypersensitivity.
It is also clear from recordings in animals of the colorectal afferent
innervation that afferents exhibit long-term changes in models of
persistent colorectal hypersensitivity. Such changes in afferent
excitability and responses to mechanical stimuli are consistent with
relief of discomfort and pain in IBS patients, including relief of
referred abdominal hypersensitivity, upon intra-rectal instillation of
local anesthetic.
In the aggregate, these experimental outcomes establish the importance
of afferent drive in IBS, consistent with a larger literature with
respect to other chronic conditions in which pain is a principal
complaint (e.g., neuropathic pain, painful bladder syndrome,
fibromyalgia).
Accordingly, colorectal afferents and the environment in which these
receptive endings reside constitute the focus of this review. That
environment includes under-studied and incompletely understood
contributions from immune-competent cells resident in and recruited
into the colorectum.
We close this review by highlighting deficiencies in existing
knowledge and identifying several areas for further investigation,
resolution of which we anticipate would significantly advance our
understanding of neural and neuro-immune contributions to IBS pain and
hypersensitivity.
http://ajpgi.physiology.org/content/early/2012/03/08/ajpgi.00542.2011.abstract
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