Several studies recently have looked at the relationship between irritable bowel syndrome and increased pain sensitivity.
The authors of “Increased Pain Sensitivity among Adults Reporting Irritable Bowel Syndrome Symptoms in a Large Population-Based Study,” published in Pain, examined the association between increased somatic pain sensitivity and irritable bowel syndrome (IBS) in a large population-based sample. They also tested whether this association was independent of sex, age, comorbid chronic pain, and psychological distress.
Participants’ pain sensitivity was tested by assessing heat-pain threshold (N=4054), pressure-pain threshold (N=4689), and cold-pressor pain intensity and tolerance (N=10,487).
Compared with control subjects, participants with IBS had reduced cold-pressor tolerance, increased cold-pressor pain intensity ratings, and lower heat-pain thresholds, after adjusting for sex and age, results that were “only slightly attenuated and remained significant when controlling for comorbid chronic pain and psychological distress.”
The authors wrote that “Heat- and cold-pressor pain sensitivity was greatest for the IBS reporting severe chronic abdominal pain, indicating that hyperalgesia in IBS is related to degree of clinical pain rather than to the diagnosis per se. Because all pain tests were all carried out on the upper extremities, our findings indicate the presence of widespread hyperalgesia in IBS, which may be a contributing factor to the high rate of comorbid pain seen in this patient group.”
Other studies have also found that IBS is associated with increased pain sensitivity. The authors of “Central and Peripheral Hypersensitivity in the Irritable Bowel Syndrome,” published in 2010 in Pain, evaluated “pain threshold and tolerance and sensory and affective ratings of contact thermal, mechanical pressure, ischemic stimuli, and cold pressor stimuli” in a cohort of 78 diarrhea-predominant IBS (D-IBS) and 57 healthy controls. They reported that “a subset of IBS patients demonstrated the presence of somatic hypersensitivity to thermal, ischemic, and cold pressor nociceptive stimuli.”
The author of this study noted that “Many hypotheses have been proposed to explain IBS including alterations in intestinal motility and visceral hypersensitivity, alterations in brain-gut regulatory pathways, postinfectious or postinflammatory changes in digestive neuroimmune function, and alterations in intestinal microflora as possible mechanisms. Among them, mounting evidence suggests that visceral hypersensitivity plays an important role in the pathogenesis of IBS.”