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Nausea and Vomiting (Professional) (cont.)


Progress has been made in understanding the neurophysiologic mechanisms that control nausea and vomiting (emesis) (N&V). Both are controlled or mediated by the central nervous system but by different mechanisms. Nausea is mediated through the autonomic nervous system. Vomiting results from the stimulation of a complex reflex that is coordinated by a putative true vomiting center, which may be located in the dorsolateral reticular formation near the medullary respiratory centers. The vomiting center presumably receives convergent afferent stimulation from several central neurologic pathways, including the following:[1,2]

  • A chemoreceptor trigger zone (CTZ).
  • The cerebral cortex and the limbic system in response to sensory stimulation (particularly smell and taste), psychologic distress, and pain.
  • The vestibular-labyrinthine apparatus of the inner ear in response to body motion.
  • Peripheral stimuli from visceral organs and vasculature (via vagal and spinal sympathetic nerves) as a result of exogenous chemicals and endogenous substances that accumulate during inflammation, ischemia, and irritation.

The CTZ is located in the area postrema, one of the circumventricular regions of the brain on the dorsal surface of the medulla oblongata at the caudal end of the fourth ventricle. Unlike vasculature within the blood-brain diffusion barrier, the area postrema is highly vascularized with fenestrated blood vessels, which lack tight junctions (zonae occludentes) between capillary endothelial cells. The CTZ is anatomically specialized to readily sample elements present in the circulating blood and cerebrospinal fluid (CSF).[3,4]

Currently, evidence indicates that acute emesis following chemotherapy is initiated by the release of neurotransmitters from cells that are susceptible to the presence of toxic substances in the blood or CSF. Area postrema cells in the CTZ and enterochromaffin cells within the intestinal mucosa are implicated in initiating and propagating afferent stimuli that ultimately converge on central structures corresponding to a vomiting center. The relative contribution from these multiple pathways culminating in N&V symptoms is complex and is postulated to account for the variable emetogenicity (intrinsic emetogenicity and mitigating factors [i.e., dosage, administration route, and exposure duration]) and emetogenic profile (i.e., time to onset, symptom severity, and duration) of agents.


  1. Pisters KM, Kris MG: Treatment-related nausea and vomiting. In: Berger A, Portenoy RK, Weissman DE, eds.: Principles and Practice of Supportive Oncology. Philadelphia, Pa: Lippincott-Raven Publishers, 1998, pp 165-199.
  2. Berger AM, Clark-Snow RA: Nausea and vomiting. In: DeVita VT Jr, Hellman S, Rosenberg SA, eds.: Cancer: Principles and Practice of Oncology. 5th ed. Philadelphia, Pa: Lippincott-Raven Publishers, 1997, 2705-2712.
  3. Andrews PL, Hawthorn J: The neurophysiology of vomiting. Baillieres Clin Gastroenterol 2 (1): 141-68, 1988.
  4. Miller AD, Leslie RA: The area postrema and vomiting. Front Neuroendocrinol 15 (4): 301-20, 1994.
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