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Relatively new are the 5HT3 agents (Zofran, Kytril).In theory, these agents might not be ideal for emesis related to vestibular imbalance.Clonazepam (Klonopin), is as effective a vestibular suppressant as lorazepam (Ganaca et al, 2002).The author prefers to avoid use of alprazolam (Xanax) for vestibular suppression, because of the potential for a difficult withdrawal syndrome.It is to be hoped that agents selective for vestibular subtypes of muscarinic receptors will eventually be developed or discovered among our presently available pharmacopoeia, as these agents may provide vestibular suppression with less side effects. This has been described for scopolamine (Luetje and Wooten 1996), and other anticholinergics may also have addiction syndromes. All the antihistamines in general use for control of vertigo also have anticholinergic activity.Withdrawal has been described from a similar agent to meclizine, diphenhydramine. With the possible exception of astemizole (Hismanal) in Meniere's disease (Turner and Jackson, 1989), antihistamines that do not cross the blood brain barrier, are not used to control vertigo.All anticholinergics used in the management of vertigo have prominent side effects of dry mouth, dilated pupils, and sedation.Scopolamine and atropine are nonspecific muscarinic receptor antagonists (Barton et al, 1994; Soto et al, 2013).
Injectables are used in the emergency room or inpatient settings. Some antihistamines commonly used as vestibular suppressants have significant antiemetic properties (e.g. When an oral agent is appropriate, this agent is generally the first to be used, because it rarely causes adverse effects any more severe than drowsiness.
We also highly recommend the neuropharmacology review article written by Soto et al (2013).
A discussion of drug treatment should start with a discussion of the neurotransmitters used to signal in the vestibular system. Vestibular suppressant and antiemetic drugs are the mainstay of treatment of vertigo.
Serafin and others (1993) reported that histamine increases firing in MVN cells, mediated through the H2 receptor.
H1 receptors are present in guinea pig vestibular nucleus, but they don't seem to be relevant to vertigo, and it does not appear that the therapeutic effects of H1 receptor blockers can be attributed to blockate of H1 (Timmerman, 1994).