Neurophysiology
Progress has been made in understanding the neurophysiologic mechanisms that
control nausea and vomiting. 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 nausea and
vomiting symptoms is complex and is postulated to account for the variable
emetogenicity (intrinsic emetogenicity and mitigating factors, i.e., dosage,
administration route, exposure duration) and emetogenic profile (i.e., time to
onset, symptom severity, and duration) of agents.
References
-
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.
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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.
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Andrews PL, Hawthorn J: The neurophysiology of vomiting. Baillieres Clin Gastroenterol 2 (1): 141-68, 1988.
[PUBMED Abstract]
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Miller AD, Leslie RA: The area postrema and vomiting. Front Neuroendocrinol 15 (4): 301-20, 1994.
[PUBMED Abstract]
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