Abstract
Generalized hypersensitivity that extends into somatic areas is common in patients with irritable bowel syndrome (IBS). The sensitized state, particularly assessed by experimental methods, is known to persist even during remissions of clinical pain. It was hypothesized that disease-related nociceptive activity in the gut maintains a systemic-sensitized state. The present study evaluated responses to prolonged thermal stimuli maintained at constant temperature or constant pain intensity during stimulation. The effect of topically applied rectal lidocaine on heat sensitivity was also evaluated. The question is whether silencing potential intestinal neural activity (which may not always lead to a conscious pain experience) with lidocaine attenuates sensitization of somatic areas. Tests were also performed where lidocaine was applied orally to control for systemic or placebo effects of the drug. The IBS subjects exhibited a greater sensitivity to somatic heat stimuli compared to controls; however, lidocaine had no discernible effect on sensitization in this sample of IBS patients, where most of the individuals did not have clinical pain on the day of testing.
Highlights
Irritable bowel syndrome (IBS) is a common gastrointestinal disorder that consists of abdominal pain that can be associated with abnormal bowel movements [1]
Scores of Symptom Checklist were higher in IBS patients compared to healthy controls (Control: 96.8± 17.9; IBS: 102.7 ± 18.1; F (1, 21) = 5.129, P = 0.03)
The goal of this study was to verify the existence of somatic hypersensitivity on glabrous skin of the hands in IBS patients and determine the interaction between potential intestinal neural activity and somatic sensitization
Summary
Irritable bowel syndrome (IBS) is a common gastrointestinal disorder that consists of abdominal pain that can be associated with abnormal bowel movements [1]. Since natural variation of visceral pain occurs in IBS and other visceral pain disorders, one method to evaluate altered pain processing in IBS is to psychophysically assess responses to controlled experimentally induced stimuli [3, 4]. Like other chronic pain cohorts, IBS patients are often more sensitive to a range of experimentally applied stimuli. While the underlying pathophysiological mechanism(s) are still unclear, increased sensitivity to visceral pain in IBS patients appears to be influenced by altered processing of afferent information from the gut [7, 8]. Altered activity within primary visceral afferents secondarily induces changes in central processing mechanisms (e.g., NMDA-receptor-based signaling [14]), which manifests itself as allodynia and hyperalgesia to stimuli within the affected gastrointestinal tissue [3].
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