For decades, interactions between the enteric neuromuscular apparatus and the central nervous system have served as the primary focus of pathophysiological research in the functional gastrointestinal disorders. The accumulation of patient reports, as well as clinical observations, has belatedly led to an interest in the role of various luminal factors and their interactions with each other and the host in functional gastrointestinal disorders. Most prominent among these factors has been the role of food. As a consequence, while not always evidence-based, dietary interventions are enjoying a renaissance in irritable bowel syndrome management. Not surprisingly, given its exploration in many disease states, the gut microbiota has also been studied in functional gastrointestinal disorders; data remain inconclusive. Likewise, there is also a considerable body of experimental and some clinical data to link functional gastrointestinal disorders pathogenesis to disturbances in epithelial barrier integrity, abnormal entero-endocrine signaling and immune activation. These data provide growing evidence supporting the existence of micro-organic changes, particularly in subgroups of patients with functional dyspepsia and IBS. However, their exact role in the complex pathophysiology and symptom generation of functional gastrointestinal disorders needs to be further studied and elucidated particularly with longitudinal and interventional studies.

These findings suggest that the Rome criteria combined with a lack of red flags have a very high predictive value for diagnosing irritable bowel syndrome. Application of these diagnostic criteria has the potential to alter utilization of health care resources.

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It has long been established that neural reflexes are involved in the regulation of gastrointestinal vascular function, in particular the mucosal hyperemia that follows food ingestion. However, more precise identification of reflex pathways involved in the control of mucosal blood flow had not previously been forthcoming because of a lack of adequate methods to examine resistance arterioles within the intestinal wall. Recent advances have employed novel in vitro preparations and videomicroscopic techniques to investigate the neural control of the gastrointestinal microvasculature and involvement of intrinsic and extrinsic vasodilatory neurons in mucosal reflexes. Vasoconstrictor innervation to submucosal arterioles is mediated solely by extrinsic sympathetic nerves that release ATP onto arteriolar P2n-purinoceptors. Neurogenic vasodilation of submucosal arterioles occurs by release of acetylcholine and/or neuropeptides from intrinsic submucosal neurons as well as by release of substance P and calcitonin gene-related peptide from extrinsic sensory nerves. Both vasodilator pathways can be activated independently by mucosal stimulation, and both have afferent and efferent components confined to the mucosa and submucosal neuronal plexus. We speculate that the intrinsic enteric cholinergic reflex pathways are involved in local physiological control of mucosal blood flow, whereas extrinsic sensory reflex pathways are preferentially activated during inflammatory states.