Functional pain syndromes, including such common disorders as irritable bowel syndrome (within the field of gastroenterology); chronic pelvic pain (in gynecology); interstitial cystitis/painful bladder syndrome (in urology); fibromyalgia (in rheumatology) and others cross multiple disciplines affecting more than 20% of the population worldwide and are more common in women. Inflammation is not a common pathophysiological pathway for a number of chronic (including functional) diseases. One of the possible explanations for this phenomenon is the neuronal reorganization associated with pain transmission (nociception), but the mechanisms of the crosstalk are unclear. Moreover, clinical presentations of functional syndromes often lack a specific pathology in the affected organ but may respond to a visceral cross-sensitization in which increased nociceptive input from an inflamed organ (i.e., uterus) sensitizes neurons that receive convergent input from an unaffected organ (i.e., colon or bladder). This mini-review focuses on the novel mechanisms for possible therapeutic interventions associated with the visceral pain primarily focusing on visceral nociceptors located within primary afferent neurons of dorsal root ganglia. Since there are observed gender differences in prevalence of functional diseases, it is proposed that estrogen may modulate nociceptor sensitization. Understanding these gender differences and neuronal reorganization associated with visceral pain will be the basis of translational efforts to modulate viscerally mediated mechanisms or functional disorders with ultimate goal to develop new therapies to treat functional disorders.
Buy this Article