Widespread hypersensitivity is related to altered pain inhibition processes in irritable bowel syndrome

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.

Modulation of Visceral Pain by Stress: Implications in Irritable Bowel Syndrome

“…The observed somatic hypersensitivity to cutaneous heat stimulation involved different regions of the body but was more pronounced in dermatomes in which afferents converge on spinal neurons receiving bowel afferents. These data suggest that the coexisting visceral and somatic hypersensitivity may depend on both viscerosomatic convergence and generalized spinal hyperexcitability (Piché et al, 2010). A deficit in endogenous pain modulation and somatic hypersensitivity have also been demonstrated in other recent studies in IBS patients (Heymen et al, 2010;Wilder-Smith et al 2004).…”

“…Based on recent clinical findings demonstrating that IBS patients have a compromised engagement of the inhibitory descending pain modulation systems (Berman et al, 2008;Coffin et al, 2004;Piché et al, 2010;Song et al, 2006;Wilder-Smith et al, 2004), gaining a deeper understanding of mechanisms involved in the expression of stress-induced visceral analgesia, or lack thereof, are promising avenues to be explored and may lead to new therapeutic targets for IBS. Therefore the use of non-invasive methods of monitoring VMR that allows the unraveling of the analgesic influence of stress on visceral pain represents a step forward to gain insight into the underlying mechanisms, in particular the neural substrates and neurochemistry of stress-related analgesia as established in the somatic pain field (Butler & Finn, 2009).…”

“…hot or cold water immersion tests (King et al, 2009;Wilder-Smith et al, 2004). Recent studies assessing the correlation between visceral and somatic hypersensitivity in diarrheapredominant IBS patients have shown that patients with rectal hypersensitivity display a clear concomitant deficit in somatic pain inhibition (Piché et al, 2010). The observed somatic hypersensitivity to cutaneous heat stimulation involved different regions of the body but was more pronounced in dermatomes in which afferents converge on spinal neurons receiving bowel afferents.…”

“…Numerous studies have also reported coexisting somatic hypersensitivity in IBS, although results are not unanimous (Chang et al, 2000;Iovino et al, 2006), most likely due to methodological issues, heterogeneity of IBS patient subgroups, or concomitant disorders (e.g., fibromyalgia) (Moshiree et al, 2007;Verne et al, 2001). The widespread character of hypersensitivity has been related to both peripheral and central mechanisms (Azpiroz et al, 2007;Piché et al, 2010). Alterations in the central nervous system (CNS) circuitries responsive to visceral input have been recently delineated in IBS patients compared with healthy subjects using functional brain imaging techniques (Song et al, 2006;Wilder-Smith et al, 2004).…”

(236) Impaired conditioned pain modulation in youth with functional abdominal pain

“…Diminished CPM (relative to control samples) has been observed in a variety of chronic pain conditions, including fibromyalgia [19,22], temporomandibular disorder [17], and chronic headache [32]. Impaired CPM has also been found in adults with IBS [14,17,31,51] and is linked to greater distress and discomfort in these individuals [15].Few evoked pain studies have been conducted in healthy youth [4,26,28,34] and only two have examined CPM [29,42]. Relatively little is known about experimental pain responses in youth with FAP.…”