The physiology of vomiting

Abstract

In contrast to the perception of nausea, the physiology of the vomiting reflex (emesis) is generally established. This “complex” reflex serves a defensive function to expel noxious chemicals from the upper gastrointestinal tract (GI). Oddly, not all mammals possess this reflex, lacking in rodents and lagomorphs that makeup approximately 40 % of extant mammalian species. Four sensory pathways trigger the emetic reflex: (1) GI vagal afferents; (2) area postrema for detection of circulating toxins; (3) vestibular complex for motion sickness; and (4) forebrain descending pathways for cognitive and learned responses. These sensory inputs converge on a common caudal hindbrain network, a central pattern generator, which produces the motor event sequence of emesis. Although vomiting is useful to avoid food poisoning, it is maladaptive in numerous clinical conditions, including treatments with cytotoxic cancer chemotherapy agents, inhalational anesthesia for surgery, and opioids for pain control; vomiting is also prominent in chronic diseases, such as diabetic gastroparesis and cyclic vomiting syndrome. Clinically significant vomiting is only partly controlled with available antiemetic drugs; thus, research on the physiology of vomiting remains an important field for developing new therapies.