Peripheral Mechanisms of Symptom Generation in Irritable Bowel Syndrome
There is considerable interest in the mechanisms that underlie symptom generation in irritable bowel syndrome (IBS) and particularly those mechanisms peripheral to higher centres in the nervous system. While the central nervous system is important in IBS, it is restricted largely to the role of beha...
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Format: | Article |
Language: | English |
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Wiley
2001-01-01
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Series: | Canadian Journal of Gastroenterology |
Online Access: | http://dx.doi.org/10.1155/2001/690794 |
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author | Stephen M Collins |
author_facet | Stephen M Collins |
author_sort | Stephen M Collins |
collection | DOAJ |
description | There is considerable interest in the mechanisms
that underlie symptom generation in irritable bowel syndrome
(IBS) and particularly those mechanisms peripheral to higher
centres in the nervous system. While the central nervous system
is important in IBS, it is restricted largely to the role of behaviour
in stress perception and symptom reporting. The gut and
the autonomic nervous system are principal areas of research in
identifying mechanisms underlying symptom generation and in
the identification of new targets for drug development. While
motility changes occur in IBS, they are neither specific nor predictable,
and this is one reason why drugs aimed at influencing
motility patterns have enjoyed limited success to date. This success
has prompted interest in sensory physiology to explain pain
and other discomforts expressed by patients with IBS. Patients
with IBS exhibit intolerance to rectal distension and other
manoeuvres of the gut, while exhibiting normal or raised thresholds
for somatic pain. The mechanisms underlying the development
of hyperalgesia or allodynia in the gut remain to be
determined. In other systems and experimental models, low
grade inflammation is a predicable inducer of these states, and
recent evidence suggests that a subpopulation of patients with
IBS develop chronic symptoms after acute gastroenteritis. This
and other inflammatory stimuli may induce a hyperalgesic state
and alter motor function in patients with IBS. Substances that
mediate these changes are not fully understood, but there is
growing recognition of the role of serotonin as a sensitizing
agent. |
format | Article |
id | doaj-art-7f35b56730ed442386f089e3181c5f6a |
institution | Kabale University |
issn | 0835-7900 |
language | English |
publishDate | 2001-01-01 |
publisher | Wiley |
record_format | Article |
series | Canadian Journal of Gastroenterology |
spelling | doaj-art-7f35b56730ed442386f089e3181c5f6a2025-02-03T01:29:17ZengWileyCanadian Journal of Gastroenterology0835-79002001-01-0115Suppl B14B16B10.1155/2001/690794Peripheral Mechanisms of Symptom Generation in Irritable Bowel SyndromeStephen M Collins0Division of Gastroenterology, McMaster University, Hamilton, Ontario, CanadaThere is considerable interest in the mechanisms that underlie symptom generation in irritable bowel syndrome (IBS) and particularly those mechanisms peripheral to higher centres in the nervous system. While the central nervous system is important in IBS, it is restricted largely to the role of behaviour in stress perception and symptom reporting. The gut and the autonomic nervous system are principal areas of research in identifying mechanisms underlying symptom generation and in the identification of new targets for drug development. While motility changes occur in IBS, they are neither specific nor predictable, and this is one reason why drugs aimed at influencing motility patterns have enjoyed limited success to date. This success has prompted interest in sensory physiology to explain pain and other discomforts expressed by patients with IBS. Patients with IBS exhibit intolerance to rectal distension and other manoeuvres of the gut, while exhibiting normal or raised thresholds for somatic pain. The mechanisms underlying the development of hyperalgesia or allodynia in the gut remain to be determined. In other systems and experimental models, low grade inflammation is a predicable inducer of these states, and recent evidence suggests that a subpopulation of patients with IBS develop chronic symptoms after acute gastroenteritis. This and other inflammatory stimuli may induce a hyperalgesic state and alter motor function in patients with IBS. Substances that mediate these changes are not fully understood, but there is growing recognition of the role of serotonin as a sensitizing agent.http://dx.doi.org/10.1155/2001/690794 |
spellingShingle | Stephen M Collins Peripheral Mechanisms of Symptom Generation in Irritable Bowel Syndrome Canadian Journal of Gastroenterology |
title | Peripheral Mechanisms of Symptom Generation in Irritable Bowel Syndrome |
title_full | Peripheral Mechanisms of Symptom Generation in Irritable Bowel Syndrome |
title_fullStr | Peripheral Mechanisms of Symptom Generation in Irritable Bowel Syndrome |
title_full_unstemmed | Peripheral Mechanisms of Symptom Generation in Irritable Bowel Syndrome |
title_short | Peripheral Mechanisms of Symptom Generation in Irritable Bowel Syndrome |
title_sort | peripheral mechanisms of symptom generation in irritable bowel syndrome |
url | http://dx.doi.org/10.1155/2001/690794 |
work_keys_str_mv | AT stephenmcollins peripheralmechanismsofsymptomgenerationinirritablebowelsyndrome |