Benzodiazepines in dizziness -- what is the data ?

Timothy C. Hain, MD

Please read our disclaimerReturn to Index. • Page last modified: September 22, 2022

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.

Before beginning, lets acknowledge that benzodiazepines are addictive substances, and are a source of considerable passion on both sides of the issue regarding their utility for many purposes. Much of this page involves opinions of the author, Dr. Hain, who is a clinician who treats dizziness. It is important to realize that in situations like this, there will be many different opinions.

Background and quick overview:

Commonly prescribed benzodiazepines include diazepam (Valium), lorazepam (Ativan), Clonazepam, 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 largely involving suppression of the nervous system. 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 clonazepam are a particularly useful agents when treating dizziness because of their effectiveness and simple kinetics. Addiction, the biggest problem, can usually be avoided by keeping the dose to 0.5 mg/day or less (see discussion below). 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). Use of alprazolam (Xanax) for vestibular suppression is best avoided because of the potential for a difficult withdrawal syndrome. This is also sometimes seen with clonazepam. Very long acting benzodiazepines are not helpful for relief of vertigo. Shorter duration agents, such as lorazepam, are probably safer than the longer duration drugs (such as clonazepam) simply because there is less drug in the body considered over 24 hours.

Pharmacodynamics (i.e. how long does the effect of these drugs last ?).

There are many interesting things to consider concerning how these drugs are handled in the body. In particular, how strong are they (we will call this activity), how long do they last in the blood, how long does their effect last in the brain, and how does this all change as people develop tolerance.

In persons or animals that have never experienced these drugs, the following table illustrates roughly how powerful these are:

Table 1 -- Activity and Time constant of common benzodiazepines
Drug Lowest effective dose Time constant in the blood "Low dose" to manage chronic vertigo
Lorazepam 0.5 12-18 hours. 0.5 mg day
Clonazepam 0.5 30 hours 0.5 mg once/day
Diazepam 2 mg several, up to 24 hours. 2 mg twice/day
Alprazolam 0.25 mg 8 hours (6-12-15) Not recommended
Chlordiazepate 7.5 mg 10-30 hours Not recommended

These values all change in people who are tolerant both because the drug may be eliminated more rapidly as well as because the nervous system may develop resistance to the effects of these medications. The "activity" and timing also varies between sleepiness (i.e. sedation) and "dizziness". The "low dose" values above are the amounts that often control chronic dizziness, and also can generally be stopped abruptly without serious consequence (such as seizure) but nevertheless there will almost always be withdrawal effects such as anxiety/panic/sleep disturbance. . In people older than 65, we suggest an attempt to reduce benzodiazepine prescriptions, as older people are more sensitive to these medications as well as have other sources of impaired judgement and balance that make these drugs more dangerous.

Some individuals are "habituated" to benzodiazepines, and take far more than the doses above. Our thought is that these persons should be "tapered down" on benzodiazepines, aiming for the safer "low dose" values. The taper typically takes place over many months. We think that it is important to use prescription monitoring databases in this situation, and make it clear to patients that only a single medical provider will be controlling all benzodiazepine prescription. A contract is helpful. This is to prevent patients from "gaming" medical providers. There are often state prescription monitoring programs that can help.

Effects on VOR gain and phase.

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 not strong.

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.

Blair and Gavin (1979) investigated the effects of intravenous diazepam on the VOR of monkeys, and reported a decrease in gain and increase in time constant. The time constant is related to phase (see above). This fits with our clinical observations.

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.

Effects on compensation. (also see compensation page)

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.

Addiction to benzodiazepines

Addiction to benzodiazepines, as well as diversion of prescriptions for use as "street" drugs, is an immense problem. This subject seems to attract passionate appeals against their use, presumably being driven by emotionally trying experiences with addicts. Benzodiazepines, like ethanol containing beverages, are sometimes used to self-medicate anxiety, and for recreational purposes. Benzodiazepines are rarely sources of death from overdose, by themselves. Nevertheless, when mixed with other drugs, such as alcohol or opiates, benzodiazepines can be associated with death due to respiratory arrest. Thus prescription of benzodiazepines to persons prone to take "mind altering" substances, such as opiates, is particularly dangerous. It may be that use of benzodiazepines impairs the addicts "common sense" and makes it more likely that there will be a drug overdose of alcohol or opiates.

Practically, all benzodiazepines are addictive in the sense that they are associated with a withdrawall syndrome after prolonged use. This is of course also true for alcohol and opiates. Addiction is not necessarily a reason to avoid using a useful drug -- but it is part of the "cost benefit" equation. It has been our experience that intelligent, high functioning individuals (such as most attorneys or doctors), almost never take benzodiazepines. This is interesting.

The decision as to whether or not members of society should be allowed to ingest substances (such as beer, benzodiazepines, opiates or marijuana) that alter their judgement, is a legal one, and involves setting the "needle" selecting the amount to which society should be able to control their member's behavior. Of course, this varies from country to country.

From a medical perspective, benzodiazepines are very effective drugs to control vertigo. Medical practitioners are generally called upon to decide whether or not there is a reasonable medical purpose to use of benzodiazepines or opiates. In as much as these drugs are used to treat subjective sensations, these decisions generally have no basis in objective data, and depend on "judgement" calls. One wonders whether this decision is properly the province of all medical providers that can prescribe.

Lader et al (1999) suggested that "The benzodiazepines are now recognized 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. "

The author of this page, Dr. Hain, holds the opinion that medical use of benzodiazepines should be restricted to "low doses" -- i.e. presumably the same as "conservative dosage" mentioned by Lader above, as well as in the table above. There are rarely patients where doses greater than low doses seem justified - -these are generally people who have clear and objective signs of vertigo (i.e. strong nystagmus), that has not responded to other management. When patient's refuse reasonable medical management -- for example a surgical procedure to eliminate vertigo -- in favor of benzodiazepine usage, this creates an ethical problem that is best resolved by a sensible clinician. There is no iron clad rule.

Dr. Hain also feels that benzodiazepines should not be "first treatment" for dizziness, but rather should be part of a "stepped" protocol, beginning with alternatives (such as anticholinergic drugs -- usually meclizine). Individuals who are also taking other drugs that are often abused, such as opiates, are at higher risk, and prescriptions should be more limited. All of this being considered, there nevertheless are some patients who function well on low doses of benzodiazepines, and who are unable to function (e.g. work) without them. We think that "less harm" is done by continuing treatment than stopping.

Clinical effects of benzodiazepines on vertigo

Benzodiazepines are commonly used in emergency departments and medical offices to treat vertigo. We think this is reasonable, albeit in small doses. By small, we mean 5 mg of diazepam (usually less), or 1 mg of lorazepam (usually just 0.5 mg). We do not think that this amount of diazepam or lorazepam should be continued for long periods of time, for acute vertigo. However, if all else fails and given objective evidence for vertigo (e.g. nystagmus), we do think that chronic use is justifiable, based on a "less harm" reasoning.

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 compared dimenhydrinate 50 mg. We think that these authors simply used too much lorazepam (see above).

Hunter et al (2022) compared benzodiazepines to antihistamines for patients with acute vertigo. They wrote "Moderately strong evidence suggests that single-dose antihistamines provide greater vertigo relief at 2 hours than single-dose benzodiazepines." This study was a "metaanalysis" of other studies. They did not consider the diagnosis. It is generally felt that it is not the antihistamine effect but the anticholinergic that is the main mechanism of action, and we wonder how this review was structured. Antihistamines that don't get into the brain do nothing for dizziness. We don't agree with this paper's conclusion. As mentioned above, there is considerable passion pro and con about benzodiazepines -- similar to politics these days. It certainly doesn't match the common pattern of use of these medications in emergency settings.

We think a more nuanced approach would be helpful -- we think that benzodiazepines and anticholinergics are both not generally appropriate for the most common type of dizziness (BPPV). We think that both work for Meniere's disease quite well. We are dubious that either is appropriate for more than a few days for vestibular neuritis. So it depends.

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 by keeping the prescriptions low dose (see table above).