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Related Experiment Videos

Basic pathophysiologic mechanisms in irritable bowel syndrome.

E A Mayer1, B D Naliboff, L Chang

  • 1UCLA/CURE Neuroenteric Disease Program, Department of Medicine, Physiology and Biobehavioral Sciences, UCLA School of Medicine, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. emayer@ucla.edu

Digestive Diseases (Basel, Switzerland)
|December 26, 2001
PubMed
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Irritable bowel syndrome (IBS) involves disrupted gut-brain communication, leading to altered motility and heightened visceral sensitivity. Central nervous system (CNS) stress circuits are hyperactive in IBS patients, impacting gut function and perception.

Area of Science:

  • Neurogastroenterology
  • Gastroenterology
  • Psychiatry

Background:

  • Irritable bowel syndrome (IBS) is characterized by gastrointestinal symptoms attributed to dysregulated gut motility, epithelial function, and visceral perception.
  • Patient heterogeneity suggests diverse underlying pathologies, potentially involving central nervous system (CNS) 'top-down' or peripheral 'bottom-up' models, or a combination.
  • Altered CNS regulation, particularly heightened responsiveness in stress/emotion circuits, is a key proposed mechanism for IBS symptom generation.

Purpose of the Study:

  • To explore the role of central nervous system (CNS) stress/emotion circuit responsiveness in the pathophysiology of Irritable Bowel Syndrome (IBS).
  • To elucidate the mechanisms by which CNS alterations influence brain-gut interactions and manifest as IBS symptoms.

Main Methods:

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  • Review of converging evidence on IBS pathophysiology.
  • Analysis of the role of the emotional motor system in mediating stress responses.
  • Examination of enhanced responsiveness in central stress circuits in IBS patients.

Main Results:

  • IBS symptom complex likely arises from altered gastrointestinal motility, epithelial function, and visceral perception.
  • Central nervous system (CNS) alterations, specifically enhanced responsiveness of stress/emotion circuits, provide a plausible mechanism for IBS.
  • IBS patients exhibit heightened responsiveness in these circuits, affecting gut motility, secretion, immune function, and sensory/emotional responses to visceral stimuli.

Conclusions:

  • The pathophysiology of IBS is heterogeneous, involving potential top-down (CNS) and/or bottom-up (peripheral) mechanisms.
  • Enhanced responsiveness of central stress/emotion circuits is a significant factor in IBS, mediating the impact of stressors on gut function and perception.
  • Understanding these brain-gut interactions is crucial for developing targeted IBS therapies.