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

Stress-related changes in visceral perception resulting in enhanced sensitivity to physiological and/or experimental visceral stimuli along with hypervigilance are considered to play a critical role in the pathophysiology of irritable bowel syndrome (IBS) (Elsenbruch et al., 2010; Mayer et al., 2008; Mulak & Bonaz, 2004; Posserud et al., 2004). Visceral hypersensitivity present in about two-thirds of IBS patients has been considered a biological marker in IBS (Bouin et al., 2002; Mertz et al., 1995). 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). Evidence of spinal nociceptive facilitation in IBS has been also provided (Coffin et al., 2004). Over the past 15 years, various animal models have been developed to gain a deeper insight into the central and peripheral mechanisms of visceral hypersensitivity (Holschneider et al., 2011; Mayer et al., 2008). However, only recently has the role of alterations in descending pain modulatory pathways in the pathophysiology of IBS and experimental models of IBS been recognized (Berman et al., 2008; Larauche et al., 2011a; Larauche et al., 2011b; WilderSmith et al., 2004). In this chapter, we will review the recent developments on stress-related modulation of visceral sensitivity to colorectal distension (CRD), with a special focus on alterations in stress-induced visceral analgesia and pain inhibitory mechanisms.