• B Bonaz.
• Department of Gastroenterology and Laboratory of Neurophysiology, Grenoble Faculty of Medicine and Hospital, Grenoble, France. Bruno.Bonaz@ujf-grenoble.fr
• J. Physiol. Pharmacol. 2003 Dec 1; 54 Suppl 4: 27-42.

AbstractChronic abdominal pain is the most distressing symptom in patients with functional digestive disorders (FDD). IBS is the most common gastrointestinal disorder seen in primary care and gastroenterology practice. IBS is a functional bowel disorder in which abdominal pain is associated with defaecation or a change in bowel habit, with features of disordered defecation and with distension. The underlying pathophysiology of IBS is unknown but a chronic visceral hyperalgesia, in the absence of detectable organic disease, is implicated. The exact location of abnormality of visceral pain processing is not known. Theories of its etiology have range widely from the original view that the disease represents a primary disturbance of gut mucosa to emerging conception of the syndrome as emanating from a complex disordered interaction between the digestive and nervous systems. Several lines of evidence suggest a strong modulatory or etiologic role of the central nervous system in the pathophysiology of IBS. A major advance in the understanding of the central mechanisms of pain processing has evolved from application of functional imaging techniques, as represented by positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). In humans, multiple components are involved in somato-visceral pain processings, including sensory-discriminative components, affective components, and cognitive components. Silverman et al, using PET, were the first to explore neural correlates of abdominal pain induced by rectal distension. If healthy subjects activated the ACC, the IBS patients did not while they presented an activation of the left PFC. These findings were consistent with an IBS model that includes both the exaggerated activation of a vigilance network (dorsolateral PFC) and a failure in pain inhibition network anterior cingulate cortex (ACC). In contrast, Mertz et al., using fMRI, observed that pain led to a greater activation of the ACC than did non-painful stimuli thus arguing for an up-regulation of afferent sensitivity to pain. Using fMRI, we also characterized cerebral loci activated by a rectal distension in healthy volunteers. The activation patterns presented a strong similarity with the central processing of somatic pain. In contrast, in a women predominant population of IBS patients, we did not observed any neuronal activation in locations activated in healthy volunteers (ACC, dorsolateral PFC) while a significant deactivation was observed in the IC and in the amygdala, a limbic structure with a role to assign emotional significance to a current experience related to anxiety and fear. Brain imaging techniques thus appear as useful tools to characterize normal and abnormal brain processing of visceral pain in patients with FDD. Reversal effects of chemical compounds targeting these abnormalities either at a peripheral or a central level should be of interest.

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