As providers we often struggle to understand how our patients experience illness in relationship to their disease, such as the data that is discernible from x-ray, endoscopy or histopathology. With structural disorders such as IBD or peptic ulcer disease we often assume that the patient’s symptoms correlate highly with the evident disease activity. However, a patient’s illness, or their perception of ill health, may vary considerably from their disease, or the externally verifiable evidence of a pathological state.

One important example of this possible incongruity can be noted in inflammatory bowel disease (IBD), ulcerative colitis or Crohn’s disease. Some patients with active and ulcerating IBD may have few symptoms and may not even present for treatment until a complication such as bleeding, obstruction, or abscess arises. That is because mucosal inflammation alone is not sufficient in many cases to cause pain or other GI symptoms. The pain of IBD relates to penetrating ulcers that reach neural plexi, fistulas, obstruction or severe inflammation. In contrast, it is not uncommon for us to see patients with IBD who report marked pain and diarrhea, but with endoscopic or radiological mild or microscopic disease, a similar phenotype to that of post-infectious irritable bowel syndrome (PI-IBS). We now call this entity IBD-IBS. Both IBD-IBS and PI-IBS share similar pathophysiological origins with evidence for mucosal inflammation (more so in IBD) often in response to infection which then leads to loss of mucosal membrane integrity, cytokine activation and upregulation of myenteric nerves causing pain. The dissociation between illness and disease in IBD is most evident since the use of potent biological anti-TNF agents that can literally wipe out observable disease, yet visceral sensitization may occur from prior inflammation leading to abdominal pain and diarrhea in up to 20% of patients treated with these potent agents.

The chronic pain of illnesses like IBD-IBS is biopsychosocial: a multidimensional process with sensory, emotional, and cognitive contributions to the experience that relates to:

  1. Ascending visceral pain transmission,
  2. Peripheral amplification of visceral signals
  3. Reduced inhibition by the CNS of ascending pain signals at the level of the dorsal horn and 4) central amplification via psychological distress.

As a result, chronic pain involves dysregulation of neurophysiological processes at spinal and supraspinal levels. Additionally, with chronic pain increased afferent visceral stimuli do not contribute as much as CNS upregulation of incoming visceral afferent signals, which can bring even regulatory (normally subliminal) signals to a point of conscious awareness and distress.

Our understanding of IBD-IBS pain in terms of both peripheral (gut) and central (brain and spinal cord) acting factors leads to important therapeutic implications for the treating physician. The management of centrally driven chronic pain may evoke more centrally targeted treatments in addition to or instead of anti-inflammatory agents, for example. Antidepressants, including SNRIs and TCAs, and psychological treatments, including CBT and hypnosis, are examples of centrally targeted therapies for chronic pain as might occur in IBD-IBS. Narcotic use should be avoided as continued use can escalate gastrointestinal symptoms, leading to opioid induced constipation (OIC) or the infrequently recognized narcotic bowel syndrome (NBS) in which opioids paradoxically increase pain.

For further information on the concept of IBD-IBS and also central modulation in chronic pain please refer to:

Grover,M.; Herfarth,H.; Drossman,D.A. The functional-organic dichotomy: Post-infectious irritable bowel syndrome and inflammatory bowel disease-irritable bowel syndrome. Clinical Gastroenterology and Heptatology 2009; 7:48-53

Grover,M.; Drossman,D.A.Pain management in inflammatory bowel disease; IBD Monitor 2009;10:1-10

 Douglas A. Drossman, MD