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The benzodiazepines are a family of sedating medications used both for treatment of anxiety and vertigo. The purpose of this page is to review current evidence regarding the effects of benzodiazepines on vestibular function. The bottom line is that there is little experimental data, and that current dogma (not well substantiated) is that benzodiazepines suppress vestibular responses and also suppress compensation.
Commonly prescribed benzodiazepines include diazepam (Valium), lorazepam (Ativan), Klonazepam, alprazolam (Xanax) and many others. These drugs are largely used to treat anxiety, but also are used to induce sleep, and a variety of other purposes. They generally are not toxic, in the sense that they generally do not damage organ systems, but also generally are associated with addiction and tolerance.
Benzodiazepines are GABA modulators, acting centrally to suppress vestibular responses. They increase the affinity of chloride channel opening (Soto et al, 2013). There are differential effects across benzodiazepines on Gaba-A receptor subtypes. In small doses, these drugs are extremely useful. Addiction, impaired memory, increased risk of falling, and possibly impaired vestibular compensation are their main shortcomings.
Lorazepam and Klonazepam are a particularly useful agents when treating dizziness because of its effectiveness and simple kinetics. Addiction, the biggest problem, can usually be avoided by keeping the dose to 0.5 mg twice/day or less. Other problems include higher incidence of car accidents (risk x1.5), and hip fractures (risk x 1.8) (Ray, Griffin et al. 1987; Ray, Fought et al. 1992). Fall risk is increased in the elderly by roughly the same proportions.
Nevertheless, low doses of diazepam (Valium) (2 mg) can be quite effective for dizziness. 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. Long acting benzodiazepines are not helpful for relief of vertigo.
It is our opinion (with partial confirmation in the literature) that benzodiazepines decrease vestibular gain and also decrease phase. This results in a total response (gain * time constant) that can be normal, but with a relatively long time constant and lower gain. Although this is our general opinion, reinforced by considerable clinical experience, experimental evidence for the effect on the time constant is almost non-existent.
Morrow and Young (2007) observed that large doses of benzodiazepines can reduce the gain of the VOR, almost eliminating it in large doses. This is also the author's opinion.
Barmack and Pettorossi stated that diazepam suppressed the activity of "secondary vestibular neurons", lasting 15-60 minutes (1980). We think that this statement is equivalent to saying that diazepam reduces VOR gain, which is certainly true. They also reported that a dose of 1/2mg/kg (in rabbits) reduced the HVOR gain by 50% (Barmack and Pettorossi, 1980b). The equivalent dose in humans would be 35 mg -- this is far more than nearly any human can tolerate without going to sleep. Of course, rabbits are not people, but again we would agree that diazepam, even in relatively small doses, reduces the gain of the VOR. Our impression, based on experience with patients, is that diazepam also increases the time-constant (i.e. reduces phase lead). Pettorossi et al (1982) suggested that diazepam enhances cerebellar inhibition of vestibular neurons, based on animal experiments. Perhaps this is the mechanism for the effects on gain and phase, suggested above.
Blau et al (2005) reported that there were no effects of 10 mg/day of diazepam administered for 14 days on the rotatory chair test. They reported "CONCLUSIONS: Clinically, the DZ subjects' scores remained within the normal ranges for vestibulo-ocular phase and gain, suggesting that patients in whom drug cessation is problematic may not have to discontinue DZ before testing with the SHA rotational system. ". We disagree entirely with this report from many experiences with patients on benzodiazepines. It may be that the "normal ranges" were too wide for these investigators.
Overall, there is remarkably little data on the effect of benzodiazepines on VOR gain and phase. It seems certain that it suppresses gain, and we also think it is highly likely that it increases the time constant and increases phase lag (e.g. reduces phase lead). Someone should do a study.
Dogma states that benzodiazepines impair vestibular compensation. There are several variants of compensation -- static and dynamic. Static compensation has to do with restoration of tone. This happens, generally speaking, irrespective of the drug environment.
Martin et al (1996) reported that "These results suggest that even high doses of diazepam before and following UL do not result in an impairment of compensation of SN in guinea pig." It is our impression that SN (spontaneous nystagmus) compensates irregardless of medication, and we think this is a reasonable supposition.
Peppard (1986) suggested that amphetamines improved compensation, but that "other drugs" had either little effect on recovery or hindered it.
Ishikawa and Igarashi found no major effect on balance or nystagmus in monkeys given diazepam (1984). We find this peculiar.
Diazepam did not delay vestibular compensation in the cat (Bernstein et al, 1972).
Overall, no substantial data appears to be present to substantiate the dogma that there is an adverse effect of benzodiazepines on compensation of vestibular responses.
Benzodiazepines are commonly used in emergency departments and medical offices to treat vertigo. We think this is reasonable, abeit in small doses. By small, we mean 5mg of diazepam (or less), or 1 mg of lorazepam (or less).
Marill et al (2000) reported that "CONCLUSION: Our results suggest that dimenhydrinate was more effective in relieving vertigo and less sedating than lorazepam at the intravenous doses administered in this study." They used lorazepam 2 mg, and comapred dimenhydrinate 50 mg. We think that these authors simply used too much lorazepam (see above).
Lader et al (1999) suggested that "The benzodiazepines are now recognised as major drugs of abuse and addiction. Other drug and non-drug therapies are available and have a superior risk benefit ratio in long-term use. It is concluded that benzodiazepines should be reserved for short-term use--up to 4 weeks--and in conservative dosage. " We are in agreement.
Overall, benzodiazepines are commonly used to treat dizziness. In our opinion, they are best used in small doses, and ideally for a limited time (e.g. a month). Some patients require small amounts on a daily basis to suppress dizziness. Here it is important to avoid addiction.