Timothy C. Hain, MD Return to Index. Please read our disclaimer Page last modified: July 4, 2015
See also: Anatomy of vestibular compensation
The vestibular system is the inner ear and associated circuits in the nervous system that sense motion of the body (mainly the head), and use this to control movement and posture.
We have two ears, and there are several illnesses where one ear may get shut down, either temporarily or permanently. When this happens, the inner ears become imbalanced, and also do not react fully for a given head movement. There is inappropriate vestibular tone, and incorrect vestibular gain. This causes spontaneous nystagmus and oscillopsia.
Vestibular compensation is the central nervous system process that adapts to these two problems -- getting rid of imbalance in tone, and readjusting gain. These are separate processes that occur with different time courses.
Recovery from vestibular lesions has been observed clinically for over 100 years (Von Bechterew, 1883). Many of the earliest investigations reported on the effects of various lesions on Bechterew (1883) nystagmus, which arises on destruction of the second labyrinth in hemilabyrinthectomized animals. Ewald noted that compensation is upset by blinding (1892). Magnus (1924) demonstrated a transient Bechterew nystagmus in decerebrate animals. Siegel and Demetriades (1925) reported compensation even after cerebellectomy. Schaefer and Meyer (1974) found that plaster casts applied to the hindlimbs of animals impaired compensation. Similarly compensation is impaired by unilateral cerebral decortication (di Giorgio, 1939), destruction of the inferior olives (Llinas and Walton, 1977), and postbrachial section of the cord (Azzena, 1969; Azzena et al, 1976). Key work related to adaptive plasticity of the VOR was published in 1976 (Gonshor and Jones, 1976) where it was found that normal animals can even reverse their VOR, given an appropriate demand.
Experimental models used in humans are generally "experiments of nature", including individuals who have had vestibular nerve section, removal of acoustic neuromas, and canal plugging for treatment of BPPV or Superior Canal Dehiscence (SCD).
Static and dynamic vestibular deficits
After an acute unilateral loss of peripheral vestibular function, there are numerous well known postural and oculomotor deficits that appear. These can be subdivided into static and dynamic deficits -- static signs are present without head movement and dynamic signs are present only during head movement. Static signs include mainly postural asymmetries and spontaneous nystagmus. Dynamic signs include depressed and asymmetrical VOR, and diminished vestibulocular reflexes. Associated with these signs are behavioral changes usually aimed at minimizing the risk of fall by adopting a more cautious stance, and also a reduced propensity to move the head, to avoid dynamic problems.
Recovery can occur through four processes outlined below
Methods of compensation
Recovery from peripheral vestibular lesions is a complex, multimodal process with the potential for important interactions between components. These processes are ordinarily all initiated simultaneously, are partially redundant, and with the exception of restoration of peripheral function, they are all competitive. By this I mean that the success of one process may eliminate the need for another process and thereby reduce its efficacy or development. This naturally then leads to the conclusion that recovery patterns may be idiosyncratic. An individual who uses vision and prediction very well might never develop good brainstem compensation for diminished dynamic vestibular responses. One then might wonder about optimality : is there one “best” pattern of vestibular compensation that we as clinicians should be striving to foster, or is the body “wise” enough to choose the optimal compensatory strategy in each individual ? We will next consider each of these processes in more detail.
Process 1: Restoration of peripheral function:
Many processes that impair vestibular function are time-limited, and recovery occurs because the lesion has disappeared rather than because of any neurological mechanism invoked by the patient. The most common causes of vestibular vertigo are listed below.
Table 1: Proportion of patients that recover spontaneously from vestibular disorders
Proportion of Otologic Vertigo
Fraction that recover spontaneously
Aggregate proportion that recovers
BPPV (Benign Paroxysmal Positional Vertigo)
80% recover by 6 months
2 hours-2 days
50% recover by 2 months
Bilateral Vestibular Loss
25% recover by 6 months
Note that almost half of patients with vertigo related to vestibular neuritis recover caloric responses spontaneously. We will develop subsequently the idea that unnecessary vestibular compensation may be harmful. This leads us to our first, counter-intuitive conclusion:
Vestibular compensation is unnecessary (and probably counterproductive) in almost half of all patients with clinical vestibular disorders.
Process 2: Brainstem mechanisms that implement vestibular compensation:
After a unilateral vestibular ablation there are two types of deficits for which a correction is required; a static imbalance related to differences in the levels of tonic discharge within the vestibular nuclei, and a dynamic disturbance, related to the loss of one half of afferent input.
Table 3: Deficits following unilateral vestibular loss
Head, body and ocular tilt
sensory input not needed
Movement induced visual disturbance
Needs sensory input
Grossly, one may say that that the static compensation system works very well, and that the dynamic compensation system has significant problems when considering recovery from vestibular lesions. We will now consider these processes individually.
Restoration of static balance: Immediately after unilateral labyrinthectomy there is complete loss of neural activity on the ipsilateral vestibular nucleus accompanied by increased activity in the contralateral vestibular nucleus (Precht et al, 1966: Mccabe and Ryu, 1969; McCabe et al, 1972). The sudden loss of resting activity relates to loss of peripheral input combined with continued commissural inhibition from the intact side. The increased activity on the contralateral side is presumed due to the removal of commissural inhibition from the lesioned side. In cat and guinea pig, several weeks after the onset of the injury the mean resting activity of the vestibular nucleus neurons on both sides are almost equal (Markham et al, 1977, 1984; Ris et al, 1995).
Resolution of spontaneous nystagmus is fast. In rat, guinea pigs and cat, spontaneous nystagmus is gone by 48 hours (Jensen, 1979; Llinas and Walton 1977; Sirkin et al, 1984; Vibert el al, 1993). In guinea pigs, spontaneous nystagmus abates by 50% by 15 hours post lesion even though the deafferented vestibular nucleus neurons have no spontaneous activity (Vidal et al, 1998). In monkeys the process appears to take a little longer -- Fetter and Zee(1988) found that a 9 deg/sec nystagmus was still present after three months. Furthermore, it was independent of exposure to light. Fisch reported that in humans with vestibular neurectomies, nystagmus was maximal in the first post-operative week but decreased rapidly thereafter, being only 3 deg/sec for the next three years (Fisch, 1973). Thus the compensation process for tone imbalance resulting in nystagmus appears to happen quickly and without the need of sensory input.
A mechanism called the “cerebellar clamp” has been postulated to explain the rapid resolution of spontaneous nystagmus (McCabe et al, 1972). They wrote that “in response to a massive asymmetry of discharges into the cerebellum occasioned by the sudden deafferentation of the vestibular nuclei of one side (by unilateral labyrinthectomy), cerebellar inhibition imposes a shutdown of the intact side, to rebalance the asymmetry at the lowest level”. Fisch also felt that in patients post-neurectomy, there was strong central inhibition for the first four weeks followed by a more gradual process when central inhibition is gradually reduced. During the period of the cerebellar clamp, the dynamic VOR is necessarily poor. This may be the reason why Maoli, Precht and Reid found improvements in VOR in lesioned cats occurred much more slowly than adaptive plasticity in normal animals (1983). Recent research in animals (Balaban) has shown that there is increased metabolic activity in the inferior olive and vestibulocerebellum (posterior vermis) 6 hours after unilateral nerve section. This may be the equivalent of the “cerebellar clamp”. This increase in metabolic activity persists chronically and presumably reflects an internal re-balancing of the vestibular brainstem related to internal feedback loops. The vestibular commissures do not appear to be necessary for static compensation to occur or its maintenance.
Static compensation is robust. Resolution of spontaneous nystagmus occurs independently of visual input in monkeys (Fetter and Zee, 1988) and is also little affected by somatosensory input in baboons and guinea pigs (Lacour et al, 1976;Schaefer and Meyer, 1975). Potential substrates for static adaptation include the denervation hypersensitivity to vestibular input in the vestibular nucleus (Curthoys and Halmagyi, 1996), greater reliance on commissures (Dieringer and Straka, 1998), and the activity deriving from the deep cerebellar nuclei and the inferior olive (Zee, 1994). Because cats with labyrinthectomy recover more quickly than those with unilateral loss induced by neurectomy, restoration of resting activity may also derive from surviving primary vestibular neurons (Cass and Goshgarian, 1991). However, human studies have not supported the idea that labyrinthectomy patients do any better than nerve sections (Takemori et al, 1984).
Postural deviation appears to be mainly derived from asymmetrical otolith activity. In frogs, postural symptoms are attributed primarily to the asymmetry in utricular input (Dieringer and Strata, 1998). Head posture normalizes with a time constant of about 21 days, unrelated to whether the lesion is pre or post-ganglionic. There are substantial differences among species. Rabbits do not recover a normal head posture after hemilabyrinthectomy, while rodents regain a normal head posture within 3 days and humans barely exhibit a postural deficit of the head at all (Dieringer N, 1995). In the guinea pig head deviation is also related to asymmetries in otolith input.
Section of the vestibular commissures does not impair postural vestibular compensation in guinea pig (Smith et al, 1986) suggesting that commissural activity does not play a strong role in static compensation in this animal. Postural normalization is closely correlated with recovery of resting discharge in 2nd order vestibular neurons, which occurs in roughly 2 days (Ris et al, 1995). However in frogs, postural vestibular compensation (see following paragraph) does appear to be related to increased synaptic efficacy of commissural fibers to the sectioned side (Dieringer and Straka, 1998).The compensation process for tone imbalance resulting in postural deviation may also depend on contributions from somatosensory inputs in animals (Jensen, 1979; Schaefer and Meyer, 1975).
Recovery of Dynamic VOR to hemi-labyrinthine lesion
Barsma and Collewign, 1974
Maoli et al, 1983
Maoli and Precht, 1985
Deficient maculo and canal-ocular reflexes at 1 year
Hamann et al, 1998
2/3 normal by 1 month
Vibert et al, 1993
Symmetric at 3 mo for 30 deg/sec, asym. at 240
Symmetric at 1 mo. for 120 deg/sec, asymmetric at 240
Fetter and Zee, 1988
Takahashi et al, 1977
Wolfe and Kos, 1977
Baloh et al, 1984
Takahashi et al, 1984
Allum et al, 1988
Maas et al, 1989
Fetter and Dichgans, 1990
Restoration of dynamic VOR. Recovery has been studied in the rabbit, cat, guinea pig, monkey, and human. Fetter and Zee studied restoration of VOR gain after unilateral labyrinthectomy in monkeys (1988). There was no increase in gain until exposure to light. Furthermore, improvements are lost after bilateral occipital lobectomy. It has previously been shown that dynamic adaptive changes are also lost after removal of the vestibulocerebellum (Robinson, 1976; Haddad et al, 1977). These results suggest that adaptation of VOR gain is a dynamic process that requires visual experience for its acquisition and is dependent on CNS structures for maintenance (Zee, 1994). Potential substrates for mediation of dynamic adaptation include the flocculus, inferior olive, and vestibular commissures (Galiana et al, 1984). Precht showed that cutting of the vestibular commissure in cat eliminates rotational sensitivity of ipsilateral type-I cells showing that recovery of in cat dynamic VOR probably requires commissar participation.
In humans, dynamic compensation appears to take on the order of months, as opposed to the quicker process of static compensation.
On a neural basis, it is clear that recovery of the dynamic VOR requires recovery of vestibular neuron sensitivity to velocity and acceleration. There are several mechanisms. A component of recovery clearly relates to restoration of tonic firing on the ipsilateral side (for labyrinthectomy and nerve section), or in other words, should be correlated with loss of the tonic offset. This mechanism works in essence because more neurons are active, being out of inhibitory cutoff, and also implies a direction dependent gain nonlinearity, as is observed in behavioral data. This could, in theory, compensate only up to a 50% VOR level, as after labyrinthectomy, half of the input is gone. This mechanism is supported experimentally by many studies (e.g. Smith and Curthoys, 1988).
A second component relates to increased sensitivity of central neurons, as clearly with only half of the input remaining, for recovery to occur, central sensitivity must double. For sensitivity to increase on the side ipsilateral to the lesion, information must necessarily be transferred from the intact side to the lesioned side, presumably via the vestibular commissures. Such increases in sensitivity have been observed (Hamann and Lannou, 1988; Newlands and Perachio, 1989)
Table 5: Cell types in the vestibular nucleus, according to firing characteristics
Vestibular only (VO)
Fuchs and Kimm, 1975
Vestibular and pause during saccades
Fuchs and Kimm, 1975
Keller and Kamath, 1975
Tomlinson and Robinson, 1984
Eye position, vestibular input, pause
Tomlinson and Robinson, 1984
Scudder and Fuchs, 1992
Eye-head velocity cells
eye velocity minus head velocity (gaze velocity)
Scudder and Fuchs, 1992
Floccular target neurons (FTN)
PVP like cells that diminish responsiveness during vestibular suppression
Lisberger et al, 1994
There are many subpopulations of neurons in the vestibular nucleus (see table above). It is presently unclear the degree to which each population is altered during the process of vestibular compensation, but Lisberger and colleagues (1984) have argued that the FTN are the critical modifiable element in VOR plasticity. If true, the FTN may also be the modifiable element in vestibular dynamic compensation. If the plasticity pathways are also used for compensation (which would be reasonable), one would expect that after vestibular compensation, plasticity may be “used up”. This concept was tested by Maoli and Precht (1985), who reported that additional plastic change induced by visual stimuli was possible even after labyrinthectomy, although cats with labyrinthectomy compensated much more slowly than normal animals (Maoli, Precht and Reid, 1983).
Dynamic compensation, at least driven by the labyrinth, may never be perfect following hemilabyrinthectomy. Typically recovery is best for low velocities or accelerations, but fails for higher velocities/accelerations, suggesting saturation phenomena (Halmagyi et al, 1990; Paige, 1983).
Table 6: What Amount of Compensation do we need ?
Condition Lesion Need from CNS
BPPV (Benign Paroxysmal Positional Vertigo)
1 canal hyperactive
Suppress 1 canal
Episodic imbalance Transient suppression of one inner ear
0-50% loss 1-2x Gain
Bilateral Vestibular Loss
50-100% loss 2x-infinite gain
50% loss 2x gain
Table 7: How much plasticity do we have available ?
Need Lesion Response Species Authors
Spectacle 1.7-1.9x Monkey Miles and Eighmy 2x lat. Canal plug 1.6x Monkey Paige, 1983 2x lat. Canal plug 0 Cat Baker et al, 1982 2x labyrinthectomy 1.5x (estimate) Cat Cass and Goshgarian, 1991
Adaptive Plasticity in the VOR was illustrated in a dramatic fashion in an experiment of Gonshor and Melvill Jones (1976). They forced the VOR to reverse itself by rotating human subjects with mirror-reversed vision ("Dove" prisms). Thus when a subject was experiencing right-going vestibular stimulation, instead of the usual left-going eye movements of the normal VOR, the eyes would have to move to the right in the head for image stabilization. For this paradigm there was a progressive maintained attenuation of VOR gain which was carried over to the next day. After several weeks using reversing dove prisms, it was shown that a VOR reappeared in approximately the reverse direction (Gonshor and Melvill Jones, 1976)
Miles and colleagues, using monkeys, continued to study this issue. Using magnifying or minifying spectacles, aimed at asking for augmentation or attenuation, they were able to document adaptive changes of the VOR gain up to 1.8X, for 2.0 glasses. The relevance to studies in normal animals to animals with lesions was questioned by Maoli, Precht and Reid (1983) who reported that cats with unilateral lesions compensated much more slowly than normal animals.
Central mechanisms: It is clear that adaptive plasticity is obtained through a combination of the action of the cerebellum and the brainstem. A direct brainstem pathway exists between the vestibular nuclei and the oculomotor nuclei. Adaptive VOR changes could be mediated via either changes in the properties of this direct pathway, or through indirect side-pathways that augment or overwhelm the direct pathway.
Table 8: Evidence for critical period
Lacour et al, 1989
Lacour et al, 1976
Yes (Guinea pigs)
VOR – low velocity
Fetter and Zee, 1988
VOR – high velocity
Fetter and Zee, 1988
Lacour et al, 1976
No (Guinea pigs)
Critical period ? Some investigators have reported that unless visual experience is allowed early after a labyrinthine lesion, recovery is suboptimal (Lacour et al, 1989). Fetter and Zee (1988) did not generally find this as monkeys kept in the dark for 4 days after lesion and then allowed normal visual experience, generally showed recovery of dynamic VOR at about the same rate as monkeys who were kept in the dark for the first days. There was one important exception – for high-velocity rotations toward the lesioned side, recovery was delayed in monkeys initially deprived of vision. There appears to be more evidence for a critical period in postural control than in the VOR (Zee, 1994). According to Herdman and associates (1995), it is still unclear whether there is a critical period in humans for recovery from acute vestibular imbalance, but exercises early after acoustic neuroma resection facilitate the rate of recovery of postural stability.
Context Specificity: VOR gain adaptation is context specific. Baker and associates have showed that cats can be trained to change the gain of their VOR differently with one ear down than when the other ear is down. This demonstrates that VOR adaptation can be changed by static otolithic signals.
There are a variety of possible sensory inputs that can be used to substitute for lost vestibular input (Courjon et al, 1982; Putkonen et al, 1977). Visual tracking is well known to be used as a substitute for vestibular input, although smooth pursuit fails at frequencies above 0.5 Hz.
There is considerable evidence that the brain can use other canals to substitute for unilateral canal plugs (Bohmer et al, 1982), such as are used to treat SCD and occasional refractory BPPV. The brain can also apparently use otolith inputs. Bohmer et al (1982, 1985), studied canal-plugged monkeys and found recovery of VOR at high frequency sinusoids, with a gain near normal at 4 hz. They attributed this recovery to preserved otolithic information.
Cervical inputs are also a well known source for an incomplete compensatory response resembling the VOR. Baker et al (1982) studied canal plugged cats and reported increase of the COR gain to about 0.1, two weeks post-lesion. Dichgans and associates showed that in monkeys with bilateral labyrinthectomy, the COR grows to a gain of about 0.3 at 7 weeks post-lesion (1973). The same authors also concluded that these animals could modulate the gain of their COR during active head movements. The situation appears to be more complicated in humans although it has been studied occasionally (Bronstein and Hood, 1986; Jurgens and Mergner, 1989; Kasai and Zee, 1978), and COR measurements appear very dependent on instruction suggesting either voluntary modulation or prediction. Recently clinicians have noticed that vibration of neck muscles reliably creates a nystagmus in persons with unilateral loss. This likely represents another compensatory pathway, which has so far been little studied.
Prediction or anticipation seems particularly likely to be a mechanism of recovery for individuals who are vestibularly impaired. It is well known that the VOR gain can be modulated, or in other words, enhanced or suppressed, by voluntary effort (Barr et al, 1976). There are also suggestions that the COR gain can be modulated (Kasai and Zee, 1978). In animals, use of prediction has been postulated in bilateral canal plugged cats (Baker et al, 1982) and monkeys with bilateral labyrinthectomy (Dichgans et al, 1973). In the latter study, the combination of the COR with prediction enabled the animals to obtain a total gain of 90% at seven weeks, but only with active head movements.
Saccadic substitution or supplementation involves production of saccades in the direction of the VOR (or in other words, oppositely directed to fast-phases which oppose the VOR), in an attempt to maintain fixation on a visual target (Segal and Katsarkas, 1988). As vision is suppressed during saccades, the point of this putative mechanism must be to put the eye on the object of regard after the saccade is over. It has been well documented in subsequent studies where it was termed "VCUS" (Tian et al, 2000). Recent investigators have renamed this phenomenon "covert" vs. "overt" saccades.
Physical therapy, which frequently involves use of voluntary head or body movement, presumably promotes use of substitution, modulation and prediction. One would expect that this recovery mechanism would be best facilitated by natural activities, such as occur while walking or climbing, and might be less well promoted by special sensory arrangements.
Process 4: Behavioral changes which minimize the impact of vestibular disturbance
Like substitution, little attention has also been paid to adaptive strategies which decrease the need for vestibular input. If head movement can be limited in frequency, visual tracking mechanisms may be adequate to substitute for an absent or reduced VOR. If challenges to balance can be minimized, risk of falling or at least mis-stepping can be reduced. Berthoz (1985) observed reduction of rapid head movements to the side of vestibular injury. These mechanisms seem likely to be those most facilitated by physical therapy.
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.