Pain and inflammatory bowel disease

Abstract

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 iatrogenic as well as essential neuropsychiatric comorbidities 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.

Figures

FIGURE 1

Computerized tomography (A) and colonoscopic findings (B,C) in a patient with worsening abdominal pain, but no other symptoms of disease exacerbation. The CT scan shows wall thickening and enhancement in the neoterminal ileum, which was inflamed and strictured on colonoscopy.

FIGURE 2

Filiform stricture in a patient with isolated small bowel Crohn’s disease.

FIGURE 3

Colitis causes visceral hypersensitivity. Potentially noxious stimuli (eg, colorectal distension) trigger responses that encode stimulus intensity, as shown in panel A. Once a threshold is passed, pain is perceived as indicated by the box. In many disorders associated with pain the stimulus response relationship is shifted to the left (sensitization), as indicated by the dotted line. Previously innocuous stimuli cause pain (allodynia) and the perceived pain intensity of noxious stimuli is increase (hyperalgesia). (B) An example of sensitization due to experimental colitis in mice. Animals were tested at baseline and 3 days after induction of colitis. Responses to colorectal distension were assessed using electromyographic recordings of the abdominal wall muscles (VMR: visceromotor response). Filled circles indicate baseline conditions, open circles represent findings on day 3 after induction of colitis.

FIGURE 4

Acute experimental colitis causes hypersensitivity of the left foot tested with small filaments (mechanical hypersensitivity; A) or a radiant heat source (thermal hypersensitivity; B).

FIGURE 5

Conceptual model of pain in IBD patients. The inflammatory process sensitizes visceral afferent neurons, leading to increased central input and perception. The affective dimension of pain (valence) triggers emotional responses, which can result in enhanced worrying and hypervigilance, impairing descending inhibitory control mechanisms.