The neural pathways and receptors mediating the sensation of nausea need better characterization. For example, are the neural pathways the same for nausea as for vomiting? Since gastroparesis is much more common in women than in men, what gender differences are present in the relevant neural pathways that result in nausea? How similar or different are the pathways mediating nausea for different disorders, such as gastroparesis or cyclic vomiting syndrome. Is vomiting elicited differently in these disorders? Do agents that are efficacious for CINV also improve nausea and vomiting from gastrointestinal disorders? Should more of these agents be evaluated in GI diseases with prominent nausea and vomiting? In addition, are the pathways mediating nausea and vomiting in GI disorders, such gastroparesis or gastroparesis-like syndromes, similar to that for cyclic vomiting syndrome? To study the pathways in nausea and vomiting, animal models need to be developed. The shrew is an animal model in which vomiting can be studied. Currently, nausea is assessed only indirectly in animal models.

What is the proper clinical evaluation for these patients with nausea and vomiting? Currently, patients may seek care for their symptoms from their family medicine physician or internist and are then often referred to either a gastroenterologist, neurologist, or ENT physician. Each type of specialty might perform different tests and might treat patients differently. Better understanding of the evaluation of patients with chronic nausea and vomiting by different physicians may be helpful for all physicians. One area that is emerging is that for patients with gastroparesis, the symptoms do not correlate well with gastric emptying delays. Perhaps the symptoms that we attribute to delayed gastric emptying are from other gastric causes or non-gastric causes as reviewed in Chaps. 1, 3, and 4.