Vertigo and motion sickness. Part II: pharmacologic treatment

Ear, Nose & Throat Journal, Jan, 2006 by Timothy P. Zajonc, Peter S. Roland

Miscellaneous agents. N-methyl-D-aspartate (NMDA) antagonists have been evaluated in animal models in an effort to find a drug that will serve as a broad-spectrum antiemetic. The selective competitive antagonist LY233053

has been shown to act in this capacity by blocking both motion- and chemical-induced emesis in cats. (72) The sites of action appear to be both the vestibular nuclei and later in the final common pathway for vomiting.

Animal studies have also shown that short adrenocorticotrophic hormone (ACTH) fragments relieve vertigo symptoms and accelerate their disappearance. (51,73,74) The site of action of one fragment, ORG 2766, appears to be in the vestibular nucleus complex itself.

Ineffective agents include ginger root and acetylleucine. Ginger root (Zingiber officinale) has been found to have no effect on motion sickness in rotary-chair tests and only a very mild effect on tachygastria in motion sickness. (75) Acetylleucine, which has been used in France since 1957, has no clinical trials to support its use; neither does the Ginkgo biloba extract EGb 761. (51)

Selecting a medication

It is possible to predict the clinical usefulness of some medications by referring to the neurophysiologic model for vertigo and motion sickness. For example, if a vestibular suppressant is successful for treating motion sickness, it will likely be useful for treating vertigo, as well. It is also important to consider a medication's onset of action. A drug with a rapid onset of action is required to treat acute vestibular vertigo or ongoing motion sickness, whereas a slow-acting medication is appropriate for chronic vertigo.

Editor's note

"Vertigo and motion sickness. Part I: Vestibular anatomy and physiology," appeared in the September 2005 issue of ENT Journal, pp. 58 1-4.

References

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