ABSTRACT
Irritable bowel syndrome (IBS), a chronic episodic medical condition associated with abdominal pain or discomfort and altered bowel habits, is the most common reason for referral to gastroenterologists and is responsible for combined direct and indirect costs of up to $30 billion per year in the United States (1,2). Despite the fact that pain is the defining element of this syndrome, much of the earlier literature dealt predominantly with the disturbances in bowel function. It is only recently that pain itself has come in focus, and several plausible theories have been put forward based on experimental and phenomenological studies. As will be apparent from this chapter, we are still not close to forming any definitive conclusions. In part, this is due to the nature of the subject itself-pain is perhaps the most subjective of the various symptom components in IBS and has been incompletely and/or inaccurately characterized in this syndrome (3). Thus, it is conceivable that there are several different types (qualitatively as well as quantitatively) of pain in patients with IBS, each with its own causative phenomena. This is in all probability a reflection of the heterogeneous nature of the syndrome itself. It is hoped that with increasing mechanistic insight, we will be able to cull out distinct disorders from the ‘‘mixed bag’’ that we call IBS today. This in turn will allow us to discriminate between those instances when pain (or discomfort) is a secondary (and perhaps relatively minor) accompaniment to diarrhea, constipation, or bloating that results from a primary bowel problem (such as one caused by persistent ‘‘microinflammation’’ or small bowel bacterial overgrowth) or when changes in central circuitry (such as those induced in a vulnerable nervous system by stress) result in pain being as prominent a symptom, if not more, than disturbed bowel function. Another way of framing this question is by analogy to the classification of somatic pain, based on putative neurophysiologic mechanisms. According to this, pain can be either nociceptive or neuropathic, the former due to persistent stimulation of peripheral nociceptors by local injury and/or inflammation, while the latter is independent of nociceptor stimulation, implying changes in the pain pathways (either peripheral or central) that result in persistent, aberrant signaling.
