Journal
INFLAMMATORY BOWEL DISEASES
Volume 15, Issue 5, Pages 778-788Publisher
OXFORD UNIV PRESS INC
DOI: 10.1002/ibd.20848
Keywords
sensitization; hyperalgesia; inflammatory bowel disease
Categories
Funding
- NINDS NIH HHS [R01 NS050758] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS050758] Funding Source: NIH RePORTER
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Abdominal pain is a common symptom of inflammatory bowel disease (IBD); Crohn's disease, ulcerative colitis. Pain may arise from different mechanisms, which can include partial blockage and gut distention as well as severe intestinal inflammation. A majority of patients suffering from acute flares of IBD will experience pain, which will typically improve as disease activity decreases. However, a significant percentage of IBD patients continue experiencing symptoms of pain despite resolving inflammation and achieving what appears to be clinical remission. Current evidence suggests that sensory pathways sensitize during inflammation, leading to persistent changes in afferent neurons and central nervous system pain processing. Such persistent pain is not only a simple result of sensory input. Pain processing and even the activation of sensory pathways is modulated by arousal, emotion, and cognitive factors. Considering the high prevalence of latrogenic as well as essential neuropsychiatric commorbidities including anxiety and depression in IBD patients, these central modulating factors may significantly contribute to the clinical manifestation of chronic pain. The improved understanding of peripheral and central pain mechanisms is leading to new treatment strategies that view pain as a biopsychosocial problem. Thus, improving the underlying inflammation, decreasing the excitability of sensitized afferent pathways. and altering emotional and/or cognitive functions may be required to more effectively address the difficult and disabling disease manifestations.
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