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***[[Constipation]]-prone [[Irritable bowel syndrome|IBS]] patients show fewer high-amplitude propagating [[Contraction|contractions]] (HAPCs) as compared to [[diarrhea]] prone [[Irritable bowel syndrome|IBS]] patients, delayed transit through the [[Colon (anatomy)|colon]] and decreased [[motility]].  
***[[Constipation]]-prone [[Irritable bowel syndrome|IBS]] patients show fewer high-amplitude propagating [[Contraction|contractions]] (HAPCs) as compared to [[diarrhea]] prone [[Irritable bowel syndrome|IBS]] patients, delayed transit through the [[Colon (anatomy)|colon]] and decreased [[motility]].  
***Changes in the [[Muscle|motor]] function of the [[Colon (anatomy)|colon]] are responsible for producing the [[Gastrointestinal tract|gastrointestinal]] symptoms of [[Irritable bowel syndrome|IBS]] such as altered [[Intestine|bowel]] habits and [[abdominal pain]].<ref name="pmid18456567" />
***Changes in the [[Muscle|motor]] function of the [[Colon (anatomy)|colon]] are responsible for producing the [[Gastrointestinal tract|gastrointestinal]] symptoms of [[Irritable bowel syndrome|IBS]] such as altered [[Intestine|bowel]] habits and [[abdominal pain]].<ref name="pmid18456567" />
**'''Visceral hypersensitivity:'''  
**'''Visceral hypersensitivity:'''
**IBS is associated with a decreased threshold for perception of [[Viscus|visceral]] stimuli (i.e. [[Viscus|visceral]] [[hypersensitivity]])<ref name="pmid18456567" /><ref name="pmid21537962">{{cite journal |vauthors=Barbara G, Cremon C, De Giorgio R, Dothel G, Zecchi L, Bellacosa L, Carini G, Stanghellini V, Corinaldesi R |title=Mechanisms underlying visceral hypersensitivity in irritable bowel syndrome |journal=Curr Gastroenterol Rep |volume=13 |issue=4 |pages=308–15 |year=2011 |pmid=21537962 |doi=10.1007/s11894-011-0195-7 |url=}}</ref><ref name="pmid2323511">{{cite journal |vauthors=Whitehead WE, Holtkotter B, Enck P, Hoelzl R, Holmes KD, Anthony J, Shabsin HS, Schuster MM |title=Tolerance for rectosigmoid distention in irritable bowel syndrome |journal=Gastroenterology |volume=98 |issue=5 Pt 1 |pages=1187–92 |year=1990 |pmid=2323511 |doi= |url=}}</ref>  
***IBS is associated with a decreased threshold for perception of [[Viscus|visceral]] stimuli (i.e. [[Viscus|visceral]] [[hypersensitivity]])<ref name="pmid18456567" /><ref name="pmid21537962">{{cite journal |vauthors=Barbara G, Cremon C, De Giorgio R, Dothel G, Zecchi L, Bellacosa L, Carini G, Stanghellini V, Corinaldesi R |title=Mechanisms underlying visceral hypersensitivity in irritable bowel syndrome |journal=Curr Gastroenterol Rep |volume=13 |issue=4 |pages=308–15 |year=2011 |pmid=21537962 |doi=10.1007/s11894-011-0195-7 |url=}}</ref><ref name="pmid2323511">{{cite journal |vauthors=Whitehead WE, Holtkotter B, Enck P, Hoelzl R, Holmes KD, Anthony J, Shabsin HS, Schuster MM |title=Tolerance for rectosigmoid distention in irritable bowel syndrome |journal=Gastroenterology |volume=98 |issue=5 Pt 1 |pages=1187–92 |year=1990 |pmid=2323511 |doi= |url=}}</ref>  
**[[Rectum|Rectal]] [[distension]] produces painful and non-painful sensations at lower volumes in [[Irritable bowel syndrome|IBS]] patients as compared to healthy controls, suggesting the presence of [[afferent]] pathway disturbances in [[Viscus|visceral]] [[Nerve|innervation]]<ref name="pmid7797041">{{cite journal |vauthors=Mertz H, Naliboff B, Munakata J, Niazi N, Mayer EA |title=Altered rectal perception is a biological marker of patients with irritable bowel syndrome |journal=Gastroenterology |volume=109 |issue=1 |pages=40–52 |year=1995 |pmid=7797041 |doi= |url=}}</ref><ref name="pmid2338274">{{cite journal |vauthors=Prior A, Maxton DG, Whorwell PJ |title=Anorectal manometry in irritable bowel syndrome: differences between diarrhoea and constipation predominant subjects |journal=Gut |volume=31 |issue=4 |pages=458–62 |year=1990 |pmid=2338274 |pmc=1378424 |doi= |url=}}</ref><ref name="pmid17919487">{{cite journal |vauthors=Posserud I, Syrous A, Lindström L, Tack J, Abrahamsson H, Simrén M |title=Altered rectal perception in irritable bowel syndrome is associated with symptom severity |journal=Gastroenterology |volume=133 |issue=4 |pages=1113–23 |year=2007 |pmid=17919487 |doi=10.1053/j.gastro.2007.07.024 |url=}}</ref><ref name="pmid12055583">{{cite journal |vauthors=Bouin M, Plourde V, Boivin M, Riberdy M, Lupien F, Laganière M, Verrier P, Poitras P |title=Rectal distention testing in patients with irritable bowel syndrome: sensitivity, specificity, and predictive values of pain sensory thresholds |journal=Gastroenterology |volume=122 |issue=7 |pages=1771–7 |year=2002 |pmid=12055583 |doi= |url=}}</ref>.  
***[[Rectum|Rectal]] [[distension]] produces painful and non-painful sensations at lower volumes in [[Irritable bowel syndrome|IBS]] patients as compared to healthy controls, suggesting the presence of [[afferent]] pathway disturbances in [[Viscus|visceral]] [[Nerve|innervation]]<ref name="pmid7797041">{{cite journal |vauthors=Mertz H, Naliboff B, Munakata J, Niazi N, Mayer EA |title=Altered rectal perception is a biological marker of patients with irritable bowel syndrome |journal=Gastroenterology |volume=109 |issue=1 |pages=40–52 |year=1995 |pmid=7797041 |doi= |url=}}</ref><ref name="pmid2338274">{{cite journal |vauthors=Prior A, Maxton DG, Whorwell PJ |title=Anorectal manometry in irritable bowel syndrome: differences between diarrhoea and constipation predominant subjects |journal=Gut |volume=31 |issue=4 |pages=458–62 |year=1990 |pmid=2338274 |pmc=1378424 |doi= |url=}}</ref><ref name="pmid17919487">{{cite journal |vauthors=Posserud I, Syrous A, Lindström L, Tack J, Abrahamsson H, Simrén M |title=Altered rectal perception in irritable bowel syndrome is associated with symptom severity |journal=Gastroenterology |volume=133 |issue=4 |pages=1113–23 |year=2007 |pmid=17919487 |doi=10.1053/j.gastro.2007.07.024 |url=}}</ref><ref name="pmid12055583">{{cite journal |vauthors=Bouin M, Plourde V, Boivin M, Riberdy M, Lupien F, Laganière M, Verrier P, Poitras P |title=Rectal distention testing in patients with irritable bowel syndrome: sensitivity, specificity, and predictive values of pain sensory thresholds |journal=Gastroenterology |volume=122 |issue=7 |pages=1771–7 |year=2002 |pmid=12055583 |doi= |url=}}</ref>.  
**[[Viscus|Visceral]] [[hypersensitivity]] contributes to [[Irritable bowel syndrome|IBS]] by involving the following:  
***[[Viscus|Visceral]] [[hypersensitivity]] contributes to [[Irritable bowel syndrome|IBS]] by involving the following:
**'''[[Spinal cord|Spinal]] hyperexcitability'''
****'''[[Spinal cord|Spinal]] hyperexcitability'''
***Secondary to activation of  [[Neurotransmitter|neurotransmitters]] such as:  
*****Secondary to activation of  [[Neurotransmitter|neurotransmitters]] such as:  
***[[NMDA receptor|N-methyl D aspartate (NMDA) receptor]]  
*****[[NMDA receptor|N-methyl D aspartate (NMDA) receptor]]  
***[[nitric oxide]]   
*****[[nitric oxide]]   
**'''Activation of specific [[Gastrointestinal tract|gastrointestinal]] mediators''' that lead to [[Afferent nerve|afferent]] [[nerve]] fiber sensitization:
****'''Activation of specific [[Gastrointestinal tract|gastrointestinal]] mediators''' that lead to [[Afferent nerve|afferent]] [[nerve]] fiber sensitization:
***[[kinins]]   
*****[[kinins]]   
***[[serotonin]]   
*****[[serotonin]]   
**'''Central ([[Brain stem|brainstem]] and [[Cerebral cortex|cortical]]) modulation''' with increased activation of anterior [[cingulate cortex]], [[thalamus]] and [[Insular cortex|insula]].
****'''Central ([[Brain stem|brainstem]] and [[Cerebral cortex|cortical]]) modulation''' with increased activation of anterior [[cingulate cortex]], [[thalamus]] and [[Insular cortex|insula]].
***These structures are involved in processing of pain.   
*****These structures are involved in processing of pain.   
***[[Cortical area|Cortical]] and [[brain stem]] modulation translate into long term hypersensitivity due to [[neuroplasticity]].  
*****[[Cortical area|Cortical]] and [[brain stem]] modulation translate into long term hypersensitivity due to [[neuroplasticity]].  
***Semi permanent changes(seen on functional [[magnetic resonance imaging]] and [[positron emission tomography]])  in the [[Nervous system|neural]] response to [[Viscus|visceral]] stimulation contribute to [[Viscus|visceral]] [[hypersensitivity]].''<ref name="pmid21537962" /><ref name="pmid10784583">{{cite journal |vauthors=Mertz H, Morgan V, Tanner G, Pickens D, Price R, Shyr Y, Kessler R |title=Regional cerebral activation in irritable bowel syndrome and control subjects with painful and nonpainful rectal distention |journal=Gastroenterology |volume=118 |issue=5 |pages=842–8 |year=2000 |pmid=10784583 |doi= |url=}}</ref>  ''  
*****Semi permanent changes(seen on functional [[magnetic resonance imaging]] and [[positron emission tomography]])  in the [[Nervous system|neural]] response to [[Viscus|visceral]] stimulation contribute to [[Viscus|visceral]] [[hypersensitivity]].''<ref name="pmid21537962" /><ref name="pmid10784583">{{cite journal |vauthors=Mertz H, Morgan V, Tanner G, Pickens D, Price R, Shyr Y, Kessler R |title=Regional cerebral activation in irritable bowel syndrome and control subjects with painful and nonpainful rectal distention |journal=Gastroenterology |volume=118 |issue=5 |pages=842–8 |year=2000 |pmid=10784583 |doi= |url=}}</ref>  ''  
**'''Recruitment of peripheral silent [[Nociceptor|nociceptors]]''' cause increased end [[Organ (anatomy)|organ]] sensitivity due to  
****'''Recruitment of peripheral silent [[Nociceptor|nociceptors]]''' cause increased end [[Organ (anatomy)|organ]] sensitivity due to  
***[[Hormone|hormonal]] activation ( increased [[serotonin]] affects [[Gastrointestinal tract|gastrointestinal]] [[motility]] and [[Viscus|visceral]] [[pain]] perception)  
*****[[Hormone|hormonal]] activation ( increased [[serotonin]] affects [[Gastrointestinal tract|gastrointestinal]] [[motility]] and [[Viscus|visceral]] [[pain]] perception)  
***[[Immunity (medical)|immune]] activation(recruitment of [[Inflammation|inflammatory]] mediators)<ref name="pmid21537962" />  
*****[[Immunity (medical)|immune]] activation(recruitment of [[Inflammation|inflammatory]] mediators)<ref name="pmid21537962" />  
{{familytree/start |summary=PE diagnosis Algorithm.}}
{{familytree/start |summary=PE diagnosis Algorithm.}}
{{familytree | | | | | | | | | |,|-| A01 |-| A02 | | | |A01=[[Spinal cord|Spinal]] hyperexcitability |A02= Activation of <br>• [[NMDA receptor|N-methyl D aspartate (NMDA) receptor]] <br>• [[nitric oxide]] }}
{{familytree | | | | | | | | | |,|-| A01 |-| A02 | | | |A01=[[Spinal cord|Spinal]] hyperexcitability |A02= Activation of <br>• [[NMDA receptor|N-methyl D aspartate (NMDA) receptor]] <br>• [[nitric oxide]] }}

Revision as of 02:07, 31 October 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

IBS is caused by the complex interaction of various factors such as intrinsic gastrointestinal factors, CNS dysregulation and psychosocial factors, genetic and environmental factors. Intrinsic gastrointestinal factors include motor abnormalities, visceral hypersensitivity, immune activation and mucosal inflammation, altered gut microbiota and abnormal serotonin pathways. Visceral hypersensitivity is a decreased threshold for the perception of visceral stimuli that affects spinal excitability brain stem and cortical modulation, activation of specific gastrointestinal mediators and recruitment of peripheral silent nociceptors. Immune activation and mucosal inflammation involves an interaction of lymphocytes, mast cells and proinflammatory cytokines. Environmental factors encompass dietary changes and infections. Psychosocial factors such as stress, anxiety and depression directly shape adult connectivity in the executive control network consisting of structures such as the insula, anterior cingulate cortex and the thalamus. Semipermanent/permanent changes in complex neural circuits lead to central pain amplification and contribute to abdominal pain in IBS patients. The dorsolateral prefrontal cortex activity (responsible for vigilance and alertness of the human brain) and the mid-cingulate cortex (engaged in attention pathways and responses) is reduced in IBS patients, which may lead to alterations in the subjective sensations of pain. Genetic factors also play a role in IBS. It has high twin concordance and familial aggregation. It is associated with Single nucleotide polymorphisms (SNPs) in genes involved in immune activation, neuropeptide hormone function, oxidative stress, nociception, permeability of the GI tract, host-microbiota interaction, inflammation, and TNF activity.

Pathophysiology

Pathogenesis

IBS is an interplay between four main factors:


 
 
 
 
 
CNS dysregulation and psychosocial factors
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Intrinsic gastrointestinal factors:
• Motor abnormalities
• Visceral hypersensitivity
• Immune activation and mucosal inflammation
• Altered gut microbiota
• Abnormal serotonin pathways
 
 
IRRITABLE BOWEL SYNDROME
 
 
 
Genetic factors:
• Twin concordance
• Familial aggregation
• Single Nucleotide Polymorphisms(SNPs)
• TNF polymorphism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Environmental factors
 
 
 

Environmental factors


 
 
 
 
 
 
 
 
 
 
 
 
Spinal hyperexcitability
 
Activation of
• N-methyl D aspartate (NMDA) receptor
• nitric oxide
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Central (brainstem and cortical) modulation
 
Increased activation of:
• Anterior cingulate cortex
• Thalamus
• insula
 
 
 
 
 
 
 
 
 
 
 
Visceral hypersensitivity
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Activation of specific gastrointestinal mediators
 
Kinins and serotonin activation lead to afferent nerve fiber sensitization
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Recruitment of peripheral silent nociceptors
 
Increased end organ sensitivity due to hormonal or immune activation
 
 
 
 
 
 




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