Nausea and Vomiting

The physiologic purpose of nausea is to prevent food intake; that of vomiting is to expel food or other toxic substances present in the upper part of the GI tract.22,23 The vomiting center, located in the lateral reticular formation of the medulla is the origin of the final common pathway along which different impulses induce emesis. The second important medullary site is the chemoreceptor trigger zone located in the area postrema.

The chemoreceptor trigger zone, which is outside the blood-brain barrier is accessible to humoral stimuli (chemicals, toxins, viruses, ions) circulating either in the blood or in the cerebrospinal fluid. However, the chemoreceptor trigger zone can only initiate emesis through stimulation of the vomiting center. The vomiting center may also be activated directly by impulses that originate in the pharynx, the GI tract and the cerebral cortex.

Indeed, emotional trauma and unpleasant olfactory and visual stimuli may cause nausea and vomiting. Finally, stimulation of the vestibular apparatus (movements of the head, neck, and eye muscles) may cause nausea and vomiting by stimulating the vomiting center. Protracted vomiting may cause dehydration, electrolyte imbalance, malnutrition syndrome, and may result in mucosal laceration and upper GI hemorrhage.22,23

Nausea and vomiting have been found to be mediated by dopaminergic (D2), cholinergic, serotonergic (5‑HT3), and histaminergic (H1), receptors.22,23 Meclizine, a histamine H1‑receptor antagonist, is approved for the prevention of nausea, vomiting, motion sickness and vertigo.2,3,22,23 Nausea and vomiting, as a result of μ‑receptor activation in the medullary chemoreceptor trigger zone, are common ADRs associated with opioid analgesic therapy.