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Updated: Jun 19, 2026

In vitro Functional Characterization of Mouse Colorectal Afferent Endings
Published on: January 21, 2015
Widespread hypersensitivity is related to altered pain inhibition processes in irritable bowel syndrome
Mathieu Piché1, Marianne Arsenault, Pierre Poitras
1Department of Physiology, Université de Montréal, Montreal, Que., Canada H3T 1J4 Department of Stomatology, Université de Montréal, Montreal, Que., Canada H3T 1J4 Groupe de recherche sur le système nerveux central (GRSNC), Université de Montréal, Montreal, Que., Canada H3T 1J4 Centre de recherche en neuropsychologie et cognition (CERNEC), Université de Montréal, Montreal, Que., Canada H3T 1J4 Centre de recherche de l'Institut universitaire de gériatrie de Montréal (CRIUGM), Université de Montréal, Montreal, Que., Canada H3T 1J4 Service de Gastroentérologie de l'Hôpital Saint-Luc du CHUM, Université de Montréal, Montreal, Que., Canada H3T 1J4 Département de chiropratique, Université du Québec à Trois-Rvières, Que., Canada G9A 5H7.
Abstract:
The mechanisms of chronic pain in irritable bowel syndrome (IBS) have been widely investigated but remain unclear. The present study investigated the relation between visceral hypersensitivity, cutaneous thermal sensitivity, and central pain mechanisms. Rectal sensitivity was assessed with a barostat, and forearm and calf sensitivity with a contact thermode. Central mechanisms were assessed by counterirritation using sustained cold-pain to the hand and painful electric shocks to the ankle. Psychological symptoms were also assessed, using questionnaires. Female volunteers with diarrhea-predominant IBS (n=27) and healthy controls (n=25) participated in the study. IBS patients had lower rectal and calf pain thresholds compared to controls (p's<0.05). IBS patients also reported more pain than controls for rectal distensions, and heat pain on the calf and forearm (all p's<0.001). Cold-pain inhibited shock-pain in controls but not IBS patients (controls: -13.5+/-5.3 vs IBS: +1.9+/-10.5; p<0.01). In addition, visceral hypersensitivity was significantly correlated to cutaneous thermal hypersensitivity and pain inhibition deficits, although effects were only weak and moderate, respectively. Furthermore, covariance analyses indicated that psychological factors accounted for group differences in visceral hypersensitivity and pain inhibition deficits. In conclusion, this study confirms the relation between altered pain inhibition processes and widespread hypersensitivity in IBS. The present results also suggests that psychological symptoms and altered pain processing in IBS patients may reflect at least in part, common underlying mechanisms.
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