Timothy C. Hain, MD Return to Index. Please read our disclaimer Page last modified: December 25, 2017
See also: Anatomy of vestibular compensation
DRUGS THAT AFFECT RATE OF VESTIBULAR COMPENSATION IN ANIMALS (Modified from Brandt, 1991, page 17)
If a patient has a permanent vestibular lesion, for instance an acoustic neuroma, it may be desirable to speed compensation. On the other hand, one might wish to retard compensation in persons with a transient vestibular lesion such as is often caused by Ménière's syndrome, or to prevent syndromes involving disturbed adaptation, such as the mal de debarquement syndrome.
According to this logic, benzodiazepines, steroids and dopamine blockers might harm persons with fixed vestibular lesions, through slowing down recovery. They might benefit persons with transient vestibular syndromes, by preventing unnecessary compensation. While steroids are potentially useful in common types of vertigo such as Meniere's disease and vestibular neuritis as antiemetics or to reduce unwanted immune mediated responses, they do not affect compensation or have direct effects on vestibular neurons (Alice et al, 1998).
The table above lists drugs known to affect the rate of compensation to vestibular lesions in animal models. Drugs that speed compensation are mainly stimulants, and drugs that retard compensation, sedatives. Most, if not all, vestibular suppressants retard compensation. Dopamine agonists speed compensation and antagonists slow compensation (Petrosini and Dell'Anna, 1993). Adrenergic agonists such as ephedrine and amphetamines are occasionally used in combination with vestibular suppressants. While they are most often used to counteract sedative effects of vestibular suppressants, they may also help by promoting vestibular compensation.
While no study has been made of this issue, it is likely that some antihypertensive agents and antipsychotic agents in clinical use slow vestibular compensation as in monkeys, depletion of catecholamines inhibits adaptive responses.
Drug effects on vestibular compensation by category
These drugs are GABA modulators, acting centrally to suppress vestibular responses. In small doses, benzodiazepines are extremely useful for management of vertigo. Addiction, impaired memory, increased risk of falling, and impaired vestibular compensation are their main shortcomings. Lorazepam is a particularly useful agent because of its effectiveness and simple kinetics. Lorazepam has no active metabolites. Addiction, the biggest problem, can be avoided by keeping the dose to 0.5 mg BID or less. Lorazepam can also be taken sublingually (1 mg) for an acute attack of vertigo. Similarly, low doses of diazepam (Valium™) (2 mg BID) can be quite effective. Relatively little information is available about addiction potential and efficacy of clonazepam (Klonopin™), but it appears as effective a vestibular suppressant as lorazepam. It is also usually prescribed in a dose of 0.5 mg twice/day. 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 usually not helpful for relief of vertigo.
Conventional wisdom states that benzodiazepines retard vestibular compensation.
Martin et al (1966) reported that diazepam does not impair compensation of spontaneous nystagmus in guinea pigs. This matters little, as spontaneous nystagmus is a process that is difficult to stop. Dynamic compensation is more important than static compensation.
Examples: Scopolamine, mixed antihistamine-anticholinergic (such as meclizine, and many otheres), some antidepressants (such as amitriptyline).
Anticholinergic medications are commonly used to treat vertigo because they are vestibular suppressants. Oddly enough, breaking the usual rule that sedatives block compensation, centrally acting anticholinergics produce a reversible overcompensation if administered after compensation has been attained to a vestibular imbalance (Zee 1988).
This may explain why occasional patients become dependent on Transderm-Scop™ and develop withdrawal symptoms (usually nausea and vertigo) when the patches are discontinued.
Dopamine agonists speed compensation and antagonists slow compensation (Petrosini et al. 1993).
Adrenergic agonists such as ephedrine and amphetamines are occasionally used in combination with vestibular suppressants. While they are most often used to counteract the sedative effects of vestibular suppressants, these stimulants may also help by promoting vestibular compensation. Amphetamines have been shown to speed recovery of motor function in stroke (Crisostomo et al. 1988). Calcium channel blockers such as verapamil also may enhance compensation (Smith et al. 1994). It seems likely that other antihypertensive agents, which act through adrenergic blocking or depleting, may slow vestibular compensation. It has also been suggested that betahistine may speed compensation (Colletti 2000). At this writing, there is very little clinical research data regarding the importance of these considerations (Smith et al. 1994).
While the precise role of histamine in central vestibular processing is uncertain, use of centrally acting antihistamines can prevent motion sickness and reduce the severity of its symptoms even if taken after the onset of symptoms (Takeda et al. 1989). All the antihistamines in general use for control of vertigo also have anticholinergic activity. Newer antihistamines that do not cross the blood brain barrier, are not used to treat vertigo.
Useful drugs where it is unknown whether they affect vestibular compensation.
The 5HT3 family of antinausea medications are immensely useful for nausea. Their effect on vestibular compensation is presently unclear.
Questionable and unconventional agents to modulate vestibular compensation.
Many substances, procedures and devices have been promoted as effective treatments of vertigo, many without clear proof of efficacy. The tendency to attribute curative properties to a bewildering number of medications and procedures has been particularly evident in the treatment of Meniere's disease (Torok 1977; Ruckenstein et al. 1991). It seems likely that most of these agents have minor or no pharmacologic efficacy, but they may function as placebos.
A recent study suggests that Ginkgo is similar in efficacy for vertigo as betahistine (Cesarani et al. 1998). Like Ginkgo Biloba, vertigoheel, a homeopathic remedy, has recently been compared to Serc, and found to be equivalent (Weiser et al. 1998). Baclofen and Amantadine, both centrally acting agents used generally in conditions unrelated to vertigo, are sometimes advocated for vertigo. Baclofen is most commonly used in patients in whom the diagnosis of microvascular compression of the eighth nerve is being considered. Amantadine is used in an attempt to promote compensation.
Bottom Line regarding drug effects on vestibular compensation.
Practically speaking, at this writing it seems prudent to avoid sedatives in situations where vestibular compensation is desirable, and perhaps also, to avoid as much as is practical dopamine blockers (such as antipsychotic agents) and adrenergic blockers. Anticholinergics such as scopolamine or as a component of a vestibular suppressant (e.g. Antivert), may be helpful. Most clinicians are not using adrenergic agonists such as ephedrine or amphetamine, and to the author's knowledge, no trials of ACTH or similar agents have been made.
A. Drug Treatment of Benign Paroxysmal Positional Vertigo (BPPV)
BPPV is the single most common type of vertigo, accounting for roughly 20% of all vertigo cases. BPPV is usually a transient condition, and no medications are appropriate. Occasional patients have prolonged positional symptoms. It seems unlikely that compensation can be attained for this situation, and vestibular suppressants seem reasonable.
B. Drug treatment of Ménière's Disease and other intermittent conditions such as SCD
Ménière's Disease is the second most common cause of vertigo of otologic origin. There are bouts of vertigo, typically lasting hours, as well as a slow decline in postural stability and hearing over years. Because Meniere's attacks are short lived, medications have little effect on compensation, and can be used without great concern.
Dogma holds that long term treatment of Meniere's with vestibular suppressants that slow down compensation, such as benzodiazepines, is unwise.
SCD (superior canal dehiscence) is also rarely treated with medications of any kind, as symptoms are triggered and brief. There is little concern about use of benzodiazepines, as compensation is generally not invoked.
C. Drug treatment of Vestibular Neuritis, considering vestibular compensation.
Vestibular neuritis is a monophasic self-limited condition that presents with vertigo, nausea, ataxia and nystagmus. These symptoms are brought about by an acute imbalance in vestibular tone combined with directionally asymmetrical response to head rotation. Vestibular neuritis is thought to be caused by a viral infection of the vestibular portion of the eighth cranial nerve. Mumps and various types of herpes viruses are possible infectious agents.
Evidence suggests that slightly more than half of patients with vestibular neuritis will recover completely (Bergenius et al. 1983) . Severe distress associated with constant vertigo, nausea and malaise usually lasts 2 or 3 days. Many patients are ready to return to their regular activities after a week and it is likely that in these instances there has been only a transient and incomplete vestibular lesion. However, a substantial proportion of patients may take as long as two months to improve substantially. On subsequent testing, this group often is demonstrated to have a continued unilateral paralysis of vestibular function.
Unfortunately, it is not possible to predict whether a patient will have a transient vestibular imbalance and recover quickly, or a permanent loss of function associated with a poorer prognosis. The implication for treatment is that if a permanent vestibular imbalance is made more tolerable by a vestibular suppressant medication, or central repair activity is partially blocked by a benzodiazepine or agent with dopamine blocking activity, the patient may not recover as rapidly as otherwise. Even bedrest may be poorly conceived since animal studies have shown that immobilization delays recovery from experimental vestibular lesions (Lacour et al. 1976) .
Thus, the treatment strategy for vestibular neuritis strongly considers vestibular compensation and involves use as few medications as possible and to encourage activity as practical. In the first few days of the illness, patients will usually severely restrict their activities as rapid head movements and activities such as sitting up or turning over in bed may cause increased vertigo. Vestibular suppressants and antiemetics are commonly used at this point, prescribed as suppositories if necessary. By the third day, it is usually possible to greatly reduce usage of vestibular suppressants and the patient should be encouraged to increase activity as tolerated.
Most patients recover completely within two months. Those that do not usually have a significant fixed vestibular paresis combined with central dysfunction that slows their compensation. For example, patients with alcoholic cerebellar degeneration or persons of advanced age may recover much more slowly. Patients with bigger deicits (e.g. 100% vestibular loss), will generally benefit more from vestibular rehabilitation than those with small deficits.
Most patients with vestibular neuritis can benefit from a program of physical therapy incorporating gait training and visual-vestibular exercises.
D. Drug Treatment of Bilateral Vestibular Paresis, considering vestibular compensation.
Bilateral vestibular paresis presents with oscillopsia, ataxia and mild vertigo. The typical patient is an individual who was recently treated for a serious infection, most often osteomyelitis or peritonitis. The infection is treated for several weeks with an ototoxic antibiotic (of which gentamicin is the most commonly encountered). The symptoms of bilateral vestibular paresis, ataxia and oscillopsia, manifest themselves when the patient recovers from their infection and tries to walk.
The long-term prognosis of these patients is good, although it may take many years before they achieve "normal" performance on functional evaluations. Unless there is a superimposed cerebellar lesion, substantial recovery is the rule. Most patients return to productive work within one year of exposure.
Vestibular compensation is the ONLY mechanism of recovery in bilateral vestibular paresis. Thus it takes first place in treatment strategies.
One should avoid medications that reduce vestibular compensation in bilateral vestibular paresis. This is not hard, as medications that reduce symptoms of other forms of otologic vertigo, such as the vestibular suppressants, generally make symptoms worse in bilateral vestibular paresis, and patients stop them. Vestibular suppressants must be eliminated in the management of this condition. It is also prudent to avoid medications with potential vestibular suppressant activity such as calcium channel blockers, and those that have central anticholinergic side effects (e.g. many of the tricyclic antidepressants).
Theoretically, in persons with some remaining vestibular function, medications that promote central plasticity might be helpful in treating bilateral vestibular paresis, and those that retard compensation would also slow or prevent recovery.
Dogma holds that benzodiazepines should be avoided in treatment of bilateral vestibular weakness, but evidence one way or the other is scanty. Of course, patients may wish to take a benzodiazepine to reduce anxiety, not caring that it could prolong their state of imbalance.
Bilateral vestibular paresis often responds well to physical therapy, which of course, is aimed at improving compensation.
E. Treatment of Central Vertigo , considering vestibular compensation
Vertigo caused by central nervous system dysfunction, or "central vertigo", is unusual. In the emergency room setting or otolaryngology clinic, a central cause of vertigo is identified in less than 5% of cases. Examples of central vertigo conditions are migraine associated vertigo and mal de debarquement syndrome.
There is a striking difference in the duration of symptoms between central vertigo associated with a fixed structural lesion of the nervous system and otologic vertigo in that in central vertigo, prolonged duration of symptoms are common. While patients with peripheral vestibular imbalance caused by a structural lesion of the vestibular nerve (e.g. vestibular neuritis) typically recover within months to a year, patients with central vertigo such as caused by the a stroke involving the cerebellum may continue to be distressed by ataxia, nausea, and the illusion of motion for years. Presumably the persistence of symptoms in patients with central vertigo reflects a defect in the central mechanisms that usually compensate for vestibular lesions.
One would also expect that attempts to promote vestibular compensation through brainstem or cerebellar mechanisms, would often fail, and that more attention here should be devoted to mechanisms that involve substitution or changes in behavior. In other words, "gaze stablization" exercises might be less useful emphasizis on effective use of appliances such as canes, walkers and footwear and avoidance of dangerous situations.
F. Drug treatment of disorders of compensation.
There are a few disorders in vestibular medicine that are attributed to inappropriate adaptation. Mal de Debarquement syndrome is attributed to an adaptive process for boat travel, that doesn't reverse after getting back on land. Visual vertigo, is attributed to reweighting of sensory systems so that vision is favored over vestibular. In both of these systems, the nervous system seems to be "stuck" in a maladaptive state. Medications that assist adaptation would seem more logical than one that retard adaptation.