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Briefly, a decision is made whether or not medical management has failed and whether or not more vigorous attempts at management are indicated. For intractable unilateral Menieres disease cases, we often presently advise a low dose gentamicin protocol. Persons who have intractable bilateral Meniere's disease are offered a trial of steroids with a safer immunosuppressant should this be effective, a modified gentamicin protocol, and very occasionally systemic aminoglycosides do deaden both ears. Trans (intra) tympanic injection of Gentamicin for control of intractable Meniere's disease. Nerve section for unilateral Meniere's that has not responded to low or high-dose gentamicin.
Intramuscular streptomycin for bilateral Meniere's disease that has not responded to low dose gentamicin. Use by otologic surgeons of this methodology is growing and papers supporting its use are proliferating very rapidly .
Studies using a brief period of administration, suggest that it is no better than placebo (Silverstein et al, 1998). On the other hand, if one has Meniere's disease in both ears (bilateral Meniere's disease), and one is not certain which one is causing dizzy attacks, it would seem reasonable to us to first try steroids. Intratympanic steroids combined with a viscous osmotic agent (hyaluronic acid) that reduces endolymph volume, has also been recently reported in an uncontrolled study to be effective (Selivanova et al, 2005) in persons who have failed intravenous steroids and vasodilators. Betahistine is a medication commonly used for Meniere's disease, with rather poor data establishing efficacy, but neverthless huge enthusiasm for its use world-wide in any case.
Multiple intratympanic steroid treatments for Meniere's disease is a promising treatment strategy. There is a trade off in cost, permanency of effect, and intrinsic risk between steroids and gentamicin.
In general, one needs to consider the input, central processing, and output for physiological responses. According to Naranjo, VEMP amplitudes are increased by threat and fear (Naranjo et al, 2016) showing that there are also other inputs to consider. According to Oh et al (2016), the cVEMPs are mediated by the vestibular nuclei and uncrossed medial vestibulospinal tract descending in the lower brainstem and spinal cord. The output for cVEMP responses is the sternocleidomastoid (SCM) muscle, which is innervated by the accessory (11th) cranial nerve. VEMPs are recorded using an evoked response computer, a sound generator, and surface electrodes to pick up neck muscle activation or other muscles if this is of interest. Higher than normal thresholds or low amplitudes may be found in persons with saccule disorders as well as conductive hearing loss. The general rule of thumb with hearing and cVEMP's is that conductive hearing loss obliterates air conducted VEMP's, and that sensorineural hearing loss does little or nothing to VEMP's. Figure: VEMP obtained in an individual with a modest left sided conductive hearing loss, using a Bio-Logic Navigator Pro.
Figure: cVEMP obtained in an individual with a profound right sensorineural hearing loss, using a Bio-Logic Navigator Pro. A potential pitfall in a person with a complete sensorineural hearing loss, is that one has no way of determining whether they also have also have a conductive component to their hearing loss.
The reflex scales to tonic EMG -- once again -- if you don't activate the neck muscle, you don't get a response. Another (but bad) method of obtaining activation is to have patients sit upright with their chin turned over the contralateral shoulder to tense the SCM muscle. Because the response is generally ipsilateral (carefully note the qualification), one theoretically can use bilateral stimuli and bilateral recording to reduce the number of trials (Huang et al, 2006; Young, 2006). Practically, one cannot do both -- 3 repetitions as well as thresholds, because of fatigue.
To rule out PAM potentials, you can run your cVEMP initially or perhaps in between other runs, without contracting the SCM. One can also broadly criticize all studies of VEMPs in that the core dogma driving the enthusiasm in doing VEMP tests is implausible.
Variability due to these technical problems might be reduced by adjusting for these factors.
We have experimented with this technique ourselves and decided that it was worse than using a very careful electrode placement and having patient's lift their head up straight (ensuring equal activation of both SCM). The number of studies using this test has grown remarkably, and we have devoted a separate page to oVEMPs.
We have studied acoustically generated VEMP's in the gastrocnemius and triceps (Ruddissil et al, 2008; Cherchi et al, 2009).
To summarize, although BC VEMP's are undoubtedly more reliable, their obvious problem lies in their inability to confine the stimulus to one ear. Basta et al reported similar results for 500 hz tone bursts (2007) but with lower overall amplitudes using a Viking system. At the present writing (2011), it appears to us that in normal persons, and using the Bio-logic Nav-Pro, average VEMP amplitude decline from approximately 150 at the age of 20 to approximately 75 at the age of 70.
The VEMP literature is rapidly increasing and it seems that there are considerable valuable diagnostic information to be obtained.
For some of the more popular disorders where VEMPs are used, we have separate pages, and have combined data from other VEMP protocols as well.
VEMP obtained in an individual with left sided Ramsay-Hunt syndrome, using a Bio-Logic Navigator Pro.
As most types of vestibular neuritis spare the inferior vestibular nerve, cVEMPs would be expected to generally be normal in vestibular neuritis.
Prolonged latency of cVEMPs has recently been suggested to be a sign of a retrocochlear (vestibular nerve) lesion, such as is found in vestibular neuritis. VEMP asymmetry in patient with small intracanalicular acoustic neuroma, without any hearing deficit.
In Vestibular neuritis, cVEMP's reportedly normalize more rapidly than canal related tests (Kim et al, 2008). Vestibular nerve sections fail to control intractable vertigo due to Meniere's disease in about 5% of patients. A potential pitfall in doing cVEMP's in persons with VNS are contralateral responses and extraneous responses (mainly posterior auricular muscle responses).
One might think that as VEMP's assess the saccule (an otolith organ), and because BPPV is thought to be due to another otolithic disease (loose otoconia from the utricle), that there might be abnormal VEMP's in persons with BPPV. We have not been impressed with sensitivity of cVEMPs to central disorders such as brainstem strokes.
Several groups (Wang and Young, 2007; Akin et al, 2012) reported that cVEMP's are reduced in persons with noise induced hearing loss. Instead our opinion is that there simply is reduction of air conducted VEMP's from hearing reduction. We do not think that this test should be done by people who are not familiar with hearing -- i.e. Regarding interpretation, it is simply not reasonable for general audiologists, who have no neurological background, to make inferences about brain function.
Akin FW, Murnane OD, Tampas JW, Clinard C, Byrd S, Kelly JK.The effect of noise exposure on the cervical vestibular evoked myogenic potential. Manzari L, Burgess AM, Curthoys IS.Ocular and cervical vestibular evoked myogenic potentials in response to bone-conducted vibration in patients with probable inferior vestibular neuritis. Manzari L, Burgess AM, McGarvie LA, Curthoys IS.Ocular and cervical vestibular evoked myogenic potentials to 500 Hz fz bone-conducted vibration in superior semicircular canal dehiscence. Meniere's Disease is thought to be triggered by immune reactions, metabolic disturbances within the inner ear, inner ear infections or trauma, possible allergic conditions, and other injures to the inner ear.
Hearing loss is generally most pronounced in the lower frequencies and is accompanied by a distinct sensation of pressure, fullness or a stopped-up feeling in the ear.
Sea shell-like roaring, ringing or bell-like noises in the ear (tinnitus) can be extremely distracting and bothersome. The clinical symptoms of Meniere's disease are thought to be caused by an increase in the fluid pressure within the delicate membranes of the inner ear. The classic theory is that during a Meniere's spell, the delicate membranes within the inner ear (cochlea) rupture.
Unfortunately, the sudden disruption of the normal inner ear tissues leads to injury of the tiny hair cells that are responsible for hearing and balance. In some patients, Meniere's disease is only intermittently bothersome and takes an overall mild course. Periods of increased symptoms, which are unpredictable and occur without warning, may be followed by long periods of improvement or even complete remission. Some blood tests are available to help rule out autoimmune inner ear disease that may simulate Meniere's Disease.
The history and quality of symptoms are very important in making the diagnosis of Meniere's disease.
On physical examination, the eardrums and neurological exam are usually normal, especially between the acute episodes of dizziness. A new test, vestibular evoked myopotentials, VEMP, are now being used to test patients who are suspected of having Meniere's Disease. High resolution CT scans may be performed to rule out superior semi-circular dehiscence syndrome (SSCDS).
Measurements of hemoglobin, blood sugar (glucose), cholesterol, immune system status, liver, kidney, thyroid function testing, and testing for infectious diseases such as syphilis, lyme disease, and infectious mononucleosis may be among the studies needed to rule out other conditions that may cause symptoms similar to those found in Meniere's disease.
Medical treatment is directed towards decreasing the frequency of attacks, stabilizing the hearing, and managing the episodes of vertigo when they occur. Medication(s) may be prescribed to reduce the severity of symptoms and possibly to decrease the frequency of Meniere's spells.
A recent treatment for patients with Meniere's Disease that is effecting both ears (Bilateral Meniere's Disease) is the administration of oral methotrexate in low, weekly doses. Vestibular (balance) rehabilitation programs may be useful in helping to adjust to the loss of balance function that is often seen in more advanced cases of Meniere's disease. Endolymphatic sac decompression is a surgical procedure performed to treat intractable Meniere's disease.
Other surgical procedures are available to treat Meniere's disease but must be tailored to the patient's individual needs and circumstances. For most patients with Meniere's Disease, a combination of lifestyle changes and medication leads to significant improvement. In the last few years, a minimally invasive procedure has been developed that can lead to a significant relief of vertigo with less surgical risk. Gentamicin is a common antibiotic that has been used for many years to treat serious bacterial infections intravenously. Both of these medications can be toxic when the large doses are given orally or intravenously.
Middle ear perfusion treatment of the inner ear with these medications has been performed at both academic and clinical medical centers in the United States. The success of Middle Ear Perfusion has been aided by advances in carbon dioxide lasers, fiberoptic endoscopic technology, and high definition video imaging. Dexamethasone seems to be most effective in patients with early Meniere's disease who have tinnitus, fluctuating hearing loss, and dizzy spells.
Middle Ear Perfusion is a promising treatment for Meniere's disease that does not respond to medical therapy. Atlas JT, Parnes LS: Intratympanic gentamicin titration therapy for intractable Meniere's Disease. Silverstein H, Arruda J, Rosenberg SI: Direct round window membrane application of gentamicin in the treatment of Meniere's disease. Kilpatrick JK, Sismanis A, Spencer RF, Wise CM: Low-dose oral methotrexate management of patients with bilateral Meniere's disease.
Marzo SJ, Leonetti JP: Intratympanic gentamicin therapy for persistent vertigo after endolymphatic sac surgery. Nakashima T, Naganawa S, Sugiura M, Teranishi M, Sone M, Hayashi H, Nakata S, Katayama N, Ishida IM.
The situation has changed greatly with gentamicin treatment in the last few years -- this document has recently been updated to reflect the very good results that have been obtained with a newer protocol - -low dose gentamicin. Disability is lessened in patients with Menieres after TTG treatment (Pfleiderer, 1998; Perez et al, 1999). A substantial advantage of TTG treatment is low cost, compared to alternative destructive treatments (i.e. The low dose method involves using 1-2 injections of gentamicin, waiting a month between injections. In our practice in Chicago, we have had excellent results with the low-dose variant, with excellent control of dizziness (100% so far) with no hearing damage at all.
A single dose treatment was reported by at the Mayo clinic, with 84% response rate of vertigo, and no change in hearing. The low dose of gentamicin over a prolonged time is likely to have a more uniform effect on the ear than brief, concentrated administrations (Pender, 2003), and also would seem likely to pose much lower risk to hearing.
Rarely, even after 6 injections, vertigo cannot be induced and vestibular function remains normal. Figure 2: The goal of high dose intratympanic gentamicin treatment is to reduce or eliminate vestibular function from one ear. Figure 2 above shows the expected result of high-dose gentamicin -- spontaneous nystagmus and vertigo.
The idea of the low-dose protocol is to do a small amount of permanent damage to the ear, just enough to permanently stop vertigo spells. TTG reduces the size of the summating potential of ECochG , which is a diagnostic test for Meniere's disease (Adamonis et al, 2000).
We think this conclusion is overly negative -- we think that the low dose gentamicin protocol is reasonably well established in the recent literature. When to stop treatment is also an issue, especially for the high-dose protocol with weekly injections. In our practice in Chicago, we have had good success in using vibration induced nystagmus to decide whether or not gentamicin has had an effect. There is literature that supports the idea that VEMP's are reduced or abolished following ITG.
It is very difficult to compete with the low-dose procedure in terms of results, because they are so good. Some groups have experimented with adding other agents to gentamicin, apparently in an attempt to make the solution more viscous and less likely to run down the eustachian tube as soon as the patient sits up. Ishiyama and associates (2007) reported pathology of the inner ear in a single patient with failed ITG (several attempts), followed by a successful labyrinthectomy.
We do not think that one needs to try the numerous treatments for Meniere's that are probably placebos, as these waste time and money, and low-dose gentamicin is very effective. Commercial gentamicin, rather than being a single chemical, actually consists of 3 related compounds.

Gentamicin is adminstered through the ear drum every month for a total of one or two administrations. This is because the gentamicin may only temporarily damage the hair cells, which can recover.
In persons with unilateral disease, one can combine a labyrinthectomy with a BAHA hearing device, and end up with more usable hearing after the labyrinthectomy. As steroids are neither curative nor long-lasting agents, brief intratympanic steroid treatments are obviously not able to cure Meniere's disease (Barrs, 2004; Dodson et al, 2004). Intratympanic dexamethasone versus high dosage of betahistine in the treatment of intractable unilateral Meniere disease. Longitudinal results with intratympanic dexamethasone in the treatment of Meniere's disease. Intratympanic Treatment of Intractable Unilateral Meniere Disease: Gentamicin or Dexamethasone? Simultaneous Labyrinthectomy With Cochlear Implantation in Patients With Bilateral Meniere's Disease. Therefore, lesions involving the vestibular nuclei can present abnormalities of cVEMPs and medullary lesions involving the descending MLF or the spinal accessory nucleus impair cVEMPs.
If either one of these structures were disturbed, one would expect alterations in the cVEMP as well.
A corollary, is that if you get a response without neck muscle activation, it isn't a VEMP (maybe a PAM ? In this case, some experts recommend simply tilting the entire body up by about 30 degrees, so that there is less torque needed by the patient to hold their head up (Colebatch, personal communication). We think this is a bad idea because you have no way of knowing how much tension the patient is producing, it is tiring, and patients can do something different on the right than on the left, without you knowing. We tried this method in our clinical practice, but discarded it for reasons explained below. Because there is a substantial response from the contralateral side on the left, one could assume wrongly that there was a present VEMP even in a person with a vestibular nerve section. There is some evidence that linked wrists might be a better choice for a reference though (Li et al, 1999).
It is faster but it reduces ones ability to localize the side of lesion because of crossover.
Headphones are less reliable than inserts, because small errors in headphone placement can result in substantial changes in sound intensity, and loss of a cVEMP. This is important if you are using equipment that doesn't produce optimally loud stimuli (see below).
After it went away when the sound generator was moved, we realized that the sound generator cannot be very close to the EMG leads.
This technique would seem quite reasonable for adjusting for differences in electrode placement as well as neck anatomy. They did not use our favored technique -- instead of lifting the head up straight, they had subjects lift and turn their heads. This is unsurprising as bone conduction stimulates both ears and one would think that averaging across two ears would be more reliable than one. Technically, averaging of electrical consequences of galvanic input is difficult because there is a large electrical artifact associated with the stimulus itself.
Galvanic stimulation excites distal vestibular nerve afferents, particularly those with irregular discharges, but any selectivity on this action on afferents arriving from the different vestibular end organs is uncertain. Galvanic VEMP's may be more reliable than acoustic VEMP's and thus be a better method of monitoring vestibulospinal connections through the spinal cord than acoustic VEMP's. These systems seem to produce lower amplitude results, perhaps due to differences in calibration. Ramsay-Hunt is a facial weakness, sometimes combined with 8th nerve neuritis, due to a recurrence of Herpes Zoster (the chicken-pox virus).
In fact, in our clinical practice in Chicago, we sometimes use the pattern of very abnormal VENG, accompanied by very normal cVEMP to strongly suggest Vestibular neuritis -- i.e. We are somewhat dubious about this and think that in this case the first wave of the cVEMP may simply be missing, but later waves related to cochlear function are preserved, causing the appearance of a prolonged latency. However, this conclusion is suspect as the VEMP technique used in this study (head-turning) is intrinsically flawed (see discussion above). The potentials shown are replicable but they lack the characteristic below-baseline displacement for P1 (see below).
The difficulty seems to be that the latencies in cVEMPs (at least with tone bursts), are so variable that there is inadequate sensitivity to disease. PSP is a rare degenerative disorder of the CNS that generally results in death within 5 years of diagnosis. The amplitude is low (30-50) but the latency is normal in this middle aged individual with genetically proven sca3 for 5 years, with gait ataxia, a small brainstem, and bilateral upgoing toes. A way around this may be to do bone-conduction cVEMPs when the air-conduction cVEMP is absent. Similarly, Zhou, Kenna, Stevens and Licameli (2008) reported cVEMP's are reduced in children with sensorineural hearing loss, and attributed this effect to saccule damage. Similarly, in our opinion, most physical therapists do not have appropriate audiology training to interpret cVEMP's. Galvanic and acoustic vestibular stimulation activate different populationso of vestibular afferents. Short latency responses in the averaged electro-oculogram elicited  by vibrational impulse stimuli applied upon the skull: could they reflect the vestibulo-ocular reflex function ? Head impulse test revealse residual semicircular canal function after vestibular neurectomy.
Click evoked EMG responses in sternocleidomastoid muscles: characteristics in normal subjects. An indicator of probable semicircular canal dehiscence: ocular vestibular evoked myogenic potentials to high frequencies.
Vestibular evoked myogenic potentials versus vestibular test battery in patients with Meniere's disease. Clinical Significance of Vestibular Evoked Myogenc Potentials in Benign Paroxysmal Positional Vertigo.
Vestibular-evoked myogenic potential thresholds normalize on plugging superior canal dehiscence. Acoustic clicks activate both the canal and otolith vestibulo-ocular reflex pathways in behaving monkeys. Augmentation of vestibular evoked myogenic potentials: An indication for distended saccular hydrops.
The mixing of inner ear fluids results in a sudden electrical discharge within the cochlea due to fluids with different electrolyte concentrations mixing together. It is possible that some, if not many, cases are due to a decrease in blood flow to the inner ear when the inner ear hydrostatic pressure prevents normal blood flow from reaching inner ear tissues.
This study enables visualization of the structures of the inner ear and brain in order to rule out tumors, strokes, multiple sclerosis, hydrocephalus, congenital anomalies, and other abnormalities which can cause dizziness and imbalance. In SSCDS, there is an erosion of the normal bone that covers the top of the superior semi-circular canal. Ultimately, the patient and a skilled ear specialist must evaluate the history, physical examinations, entire clinical picture, and test results together in order to arrive at a diagnosis.
Regular exercise, adequate rest, and control of other medical problems may be helpful as well. In this transmastoid surgical procedure, an incision is made behind the ear, and the mastoid bone is entered.
One procedure involves cutting the balance nerves (Vestibular Nerve Section) which is a neurosurgical procedure. However, some individuals will continue to have disabling symptoms in spite of comprehensive medical therapy.
This procedure involves the use of a carbon dioxide laser, small fiberoptic telescopes, and placement of steroids or ototoxic medication through a very small opening made in the eardrum. In an outpatient surgical center setting using intravenous sedation, a local anesthetic is used to numb the ear canal and the eardrum. Left Eardrum: Paparella Type I tube to aid in delivering additional doses of medication to the middle ear. Right Middle Ear: Mucosa removed from round window niche, exposing the round window membrane.
Right Eardrum: Paparella Type I tube to aid in delivering additional doses of medication to the middle ear. It is performed on an outpatient basis and appears to be safe, is much less invasive than older surgical techniques, and will hopefully benefit many patients who have either failed conservative medical management or who require a more active approach to their condition.
Dexamethasone perfusion of the labyrinth plus intravenous dexamethasone for Meniere's disease. Intratympanic injection of dexamethasone: time course of inner ear distribution and conversion to its active form. Intratympanic gentamicin treatment in Meniere's Disease: patients' experiences and outcomes. Intratympanic dexamethasone for sudden sensorineural hearing loss after failure of system treatment.
Dependence of hearing changes on the dose of intratympanically applied gentamicin: a meta-analysis using mathematical simulations of clinical drug delivery protocols. Combined intratympanic and systemic use of steroids for idiopathic sudden sensorineural hearing loss. Intratympanic versus intravenous delivery of dexamethasone and dexamethasone sodium phosphate to cochlear perilymph. Intratympanic steroid injections as a salvage treatment for sudden sensorineural hearing loss: a randomized, double-blind, placebo-controlled study.
Altered frequency dynamics of cervical and ocular vestibular evoked myogenic potentials in patients with Meniere's Disease. Intratympanic treatment of intractable unilateral Meniere's Disease: Gentamicin or Dexamethasone?
The effect of intratympanic methyl prednisolone and gentamicin injection on Meniere's Disease. Endolymphatic sac surgery versus intratympanic gentamicin for the treatment of intractable Meniere's Disease: a retrospective review with survey.
The main alternative to the mechanism being destruction of dark cells is the hypothesis that there is a partial damage to the vestibular hair cells.
2004) reported that low-dose methods have significantly poorer vertigo control (66.7% overall). If low-dose does indeed reduce pressure in the inner ear, it may be that hearing will deteriorate to a lesser extent.
We routinely recommend use of half-dose gentamicin in persons having this done who are over the age of 70. We don't think that this conjecture is correct, but it would be an interesting project for a researcher to investigate.
The treatment is stopped when vertigo ensues, indicating that the gentamicin is affecting the inner ear. At this point, treatment is stopped and another method of eliminating vestibular function is used (such as labyrinthectomy). This causes an imbalance between the two ears, and a spontaneous nystagmus or jumping of the eyes. This made sense as in a meta-analysis of variant methods was recently reported by Chia and others (Chia, Gamst et al. There would seem to be little advantage in experimenting with streptomycin as gentamicin works very well without appreciable risk to hearing when given at long intervals. A variant of titration method might be to continue injecting until the VEMP is greatly diminished. It is also difficult to understand the rationale of putting in a constant infusion of a drug, when it is well known from animals that gentamicin accumulates in the ear over many months.
It is hard to see how a drug that goes in and out of the ear in 3 days, costs quite a bit to the insurance system, and is associated with significant risks (of perforation) could make much positive difference to a lifelong illness. We see little reason why any other procedure should be advocated, unless low-dose gentamicin has already failed. We don't think that use of steroids here is a good idea, as it seems to bring on another complication. We presume that these individuals have a better ability to either adapt to vestibular lesions or recover from them. Oddly, we have found a few major medical centers, or even entire large metropolitan areas that seem to be unaware of the low dose gentamicin option. Examples of procedures that are probably placebos or at least only slightly effective, are the Menniett device, intratympanic steroids, and endolymphatic shunt surgery. The Effect of Intratympanic Methylprednisolone and Gentamicin Injection on Meniere's Disease.
Chemical labyrinthectomy for the worse ear of adult Nigerians with bilateral Meniere's disease: preliminary report of treatment outcomes.
We rarely recommend a shunt or sac procedure in our (non-surgical) practice -- we prefer low-dose gentamicin.
The risk to hearing and balance is minimal for this procedure (although there is substantial risk from older versions of this protocol).
We are unenthused about this idea for several reasons: First, surgical removal of the inner ear would make it impossible for hair cell regeneration to every be useful.
The present consensus is that one-time treatment has not yet been proven effective (Doyle et al, 2005) or to have a reasonable scientific basis. If they don't work, then either the choice of ear was wrong, both ears are active at the same time, or the diagnosis is wrong (migraine is the usual alternative confounding diagnosis in bilateral Menieres). If this methodology does indeed prove out, then the main issue would be to determine where this methodology belongs in the staged management of Menieres.
In our view, this is simply the combination of two short-lived treatments, but because hyaluronic acid is very viscous, the combination may keep the steroids in the ear for longer periods than simple injections of an aqueous solution, and might have better results due to this effect.
Supporting this train of thought, Albu et al (2014) recently reported that high-dose betahistine (i.e.
Sound stimulates the saccule, which activates the inferior vestibular nerve, lateral vestibular nucleus, 11th nerve nucleus, and then the sternocleidomastoid muscle (mostly ipsilaterally). In the author's laboratory, a Bio-Logic Navigator Pro does nearly all of the work, and sends the results to a desktop computer. It is a very big response, and as long as the person doing the test is attentive to details (getting the sound in both ears with proper placement of inserts or headphones, having the person lift their head through the entire trial, electrodes in the right place with proper impedance), it is very straightforward.
Although P1 is positive, it is shown negative on many cVEMPs, because of electrode placement (basically putting them on backwards).
Lower than normal thresholds as well as asymmetrical amplitudes are found in persons with Tullio's phenomenon, which is dizziness induced by sound.

Each side is about 250 microvolt in size (which is far above the lower limit of normal, about 70). This recording was obtained using binaural stimulation (see comments regarding this method). Thus, one could falsely conclude that there was no vestibular function on one side based on an absent VEMP.
We think this is an excellent idea, but at present there are no amplitude norms for this procedure.
Our recommendation, based on some unfortunate clinical experiences where binaural stimulation lead us astray, differs from others in the literature (e.g.
We do not agree -- we feel that amplitudes are more useful than thresholds, given a well standardized protocol.
See more discussion of the problems inherent in doing thresholds below under technical pitfalls.
Common things that go wrong here are asymmetrical placement of inserts, wax occluding one side, or a defective sound generator (the Bio-logic ones seem to go bad very often, when used for VEMPs -- it has happened to us 3 times in just 2 years !).
If you see stimulus artifact, or sinusoidal undulations to the trace, it is very likely that the electrodes are bad, someone put the sound generator box too close to the electrodes, the impedance was too high, or the evoked potential machine needs service.
The sound generator produces a magnetic field which induces a strong artifact, if one places it close to one of the electrical leads. Actually, there are three of these muscles -- posterior, superior and anterior auricular muscles - -all vestigial.
For reasons developed above, we think that a run or two of monaural stimulation is a very good idea.
While not emphasized much in the literature, VEMP tests likely involve input from many senses, and are not confined to saccule or utricle inputs as has been suggested.
It would seem to us to be not quite as reasonable for adjusting for differences in muscle activation, because this might easily change during the 2 minute cVEMP itself.
Because this method introduces the variability due to head turning, in our opinion, their experimental design was simply designed to fail.
It has been our general experience that the device that we use (Bio-Logic NavPro) produces larger potentials than most competing devices. VEMPs might, in theory, be useful for detecting residual function in the inferior vestibular nerve, as this branch of the vestibular nerve is sometimes intermingled with cochlear fibers (Lehnen et al, 2004). You should also check for the PAM (by doing a test with the head resting on the table) if there is something that appears to be a response on the sectioned side.
A possible confounding problem is that there may be middle ear disease after the injection due to the perforation required for transtympanic gentamicin.
As we are dubious that latency is a useful measure at all, we are also dubious about the use of cVEMP's in BPPV. This may be an artifact of our methodology (tone burst), which is temporally a longer stimulus than a click. While this substitutes for the bone conduction audiogram, it requires more testing and potentially may fatigue the patient.
While theoretically possible, we are dubious that a structure that requires 70db to elicit a minimal response would be very sensitive to noise.
We shudder to think of what might go on in a practice where testing is being done universally without any knowledge of whether the patient has a conductive hearing deficit, or sound-checks being done on the equipment. Meniere's Disease may be due to vessel inflammation (vasculitis), aging and narrowing of blood vessels, and additional unrecognized factors such as problems with calcium channel metabolism, etc. Classically, two muscles are used: (1) the sternocleidomastoid muscle (cervical VEMP or cVEMP) and (2) the inferior rectus muscle of the eye (ocular VEMP or oVEMP). The procedure is call "Laser Assisted Tympanotomy with Middle Ear Perfusion" or "LAT" for short. Treating the inner ear with very small, strategically-placed doses of gentamicin takes advantage of this effect by inactivating the sensory cells that cause episodes of vertigo.
Once the eardrum is numb, a carbon dioxide laser beam focused through a microscope is used to perform a Laser Assisted Tympanostomy (LAT) - an extremely small, bloodless opening in the eardrum approximately 2-3 mm. A randomized, double-blind, placebo-controlled clinical study to assess safety and clinical activity of OTO-104 given as a single intratympanic injection in patients with unilateral Meniere's disease. Several authors have reported that tinnitus or fullness may improve substantially after TTG (e.g. Most authors find that the control of vertigo is comparable to vestibular nerve section (about 90%). The low dose variant is relatively new, and there is not nearly as much data concerning outcome as the high-dose variant.
Recent studies in animals suggest that the type-I hair cells are the most sensitive, and the type-II hair cells are more resilient. In other words, the treatment is continued until there is evidence of damage to the inner ear. It should be noted, however, that small mammals like this have much thinner round window membranes than humans, and therefore may get a much larger amount of gentamicin over the same period of time.
We have also noted that all patients with successful low or high-dose gentamicin have strong vibration induced nystagmus. However, we have encountered one patient, who had migraine misdiagnosed as Meniere's, and who had 2 injections of gentamicin. 2004), the weekly titration method of delivery had the best results with both the best vertigo control and a trend towards less overall hearing loss. However, there are sometimes situations where one wants to get a lot of drug in fast, and accept more risk to hearing.
As has been mentioned already - - given the clear superiority of small-dose gentamicin over multiple dose protocols, there no longer seems to be any reason to give more than 1-2 injections, so titration is not really an issue. A problem with this idea is that the injection itself might cause a conductive hearing loss that interferes with the VEMP. They suggested that potential sources of recurrent vertigo in the patient include the contralateral ear (unlikely as labyrinthectomy worked), the saccule of the ipsilateral side (unlikely that saccule was spared by a drug that affected rest of the inner ear), and the severely damaged utricle (again unlikely).
This good experience is similar to the experience of others, even when they are less cautions than we are(Olusesi et al, 2014). It is best to go somewhere else if your otologist suggests that you will need 4 injections, or wants to repeat the injections in less than 1 month.
It would be interesting to know if use of the compound that is most vestibulotoxic might cause better results than the mixture of compounds. There is a large literature about the effect (or lack of effect) of this surgical treatment (see this page for more detail). This treatment is currently in clinical trials, and we expect that it will be eventually (i.e.
Thus it involves both making a hole in the ear drum (with the needle), as well as administering a drug to the inner ear (by diffusion across the round window membrane).
The core scientific difficulty is that steroids don't make any permanent alterations to the inner ear, and that they are gone from the ear in a short period of time (Harugnani et al, 2006). A comparison between steroids injected with and without hyaluronic acid would be a reasonable next step. The most reliable measure of the cVEMP response is the amplitude (Isaradisaikul et al, 2008). Prolonged latencies of P13 may be found in central disturbances (Murofushi et al, 2001), but practically these are very rarely encountered, and technical error is the source of most prolonged latencies. Artifacts can also go across the midline, which reduces much of the value of using a binaural stimulus. In our opinion, a minimum of two repetitions should be obtained on each side, to be sure that the VEMP is reproducible or absent, as the case may be.
At the present writing however, the clinical value of measuring latency (other than being sure you have a VEMP), remains somewhat elusive.
The literature suggests that amplitudes are more reliable than thresholds too (Isaradisaikul et al, 2008). A common quality control problem in the cVEMP is an overly nice technician who allows the patient to put their head down during the test.
This is an intrinsic problem with doing cVEMP's in very young children, and perhaps it should just not be attempted at all. Because cVEMP's are not far above the threshold provided by most evoked potential equipment, little things like not putting the insert in as far in one ear as the other can make a big difference. In our experience with the latter, the thing that routinely goes bad with the evoked potential machine are the connectors and the insert driver.
As nearly always one is trying to localize the side of lesion, we think that binaural cVEMP's are best avoided. Overall, it seems to us that their method may be better than the (poor) method of head-turning as it controls for intermittent effort which is a problem with the head-turning methodology. To us this suggests that a component of air-conducted VEMP response is either due to startle or multisensory convergence.
However, as cVEMPs require a very strong stimulus, it seems unlikely that they would be very sensitive.
We don't have any examples to show here, so we will just mention what is in the literature. This range overlapped substantially with age-matched controls, but may be another helpful method of identifying PSP. The saccule would more reasonably be damaged by excessive changes in linear acceleration as it is loaded by the otoconia. Foster has proposed that increase fluid pressure within the cochlea (endolymphatic hydrops) causes a decrease in blood flow to cochlear and vestibular tissues.
Genetic studies are being performed at The University of Iowa, Iowa City, IA as well as several other leading research centers. Distension of the saccule of the inner ear in Meniere's Disease is what is being indirectly measured and porvides diagnostic potential. However, it has been found to have limitations such as not completely resolving the vertigo and sometimes leading to additional hearing loss.
Three study groups were evaluated, each receiving a different number of doses of gentamicin. TTG treatment is also intrinsically of very low risk, especially compared to nerve section. However, right now, in our practice in Chicago as well as in other highly specialized settings, the low-dose protocol has become routine, as we think that it has even less risk and very good results. We also see no logical reason to combine dexamethasone (an intratympanic steroid) with streptomycin (an ototoxic antibiotic).
As vibration works so well, and we would not think that someone should be even doing gentamicin injections without the capability to do video-frenzel goggles, this idea doesn't seem to us to be worth pursuing.
It would also be interesting to know if different drug companies versions of gentamicin vary in their composition. The second is that if you do thresholds, you can't do a lot of repetition (because people get tired).
We presently continue to hold to the opinion that a careful, unrectified head-straight lifting VEMP is superior. We are not at all sure how pFL levels of 120 db relates to the ordinary problem with clinical bone vibrators that only produce 60 db. Head impulse tests for the posterior canal reveal residual function more more frequently than do cVEMPs (Lehnen et al, 2004). As VEMP circuitry is not thought to involve the cerebellum, it would be surprising to find abnormal VEMP's in any purely cerebellar condition. However, there is considerable emotional pain when the disease is difficult to control, and the spells are unpredictable.
Steroids, such as prednisone, can help reduce the severity of acute attacks but have significant side effects if taken for prolonged lengths of time.
The procedure usually requires an overnight stay in an outpatient surgery center and is of relatively low risk.
Overall study results showed control of vertigo in 75%, improvement in tinnitus in 48%, improvement in ear fullness in 62%, and hearing preservation in 90% of patients. Compared to labyrinthectomy, TTG treatment is also lower in risk because there is no need for general anesthesia. Because this procedure works so well, the experiments of the past that we detail below have all become somewhat irrelevant. It seems much more logical to us to use these one at a time rather than mixing them together.
As the problem in the past has mainly been hearing toxicity, procedures that are aimed to increase the dose delivered to the ear would seem irrational unless the ear is already deaf.
At a minimum, cVEMP's done in persons who are (perhaps) not cooperative should be done with equipment that can monitor the EMG. The third is that they don't always work -- low thresholds are NOT always accompanied by radiographic evidence of superior canal dehiscence.
In our own practice (see above), but we have only studied two patients and found abnormally reduced amplitude for age in one and an absent VEMP in the other. However, we do not know what causes the increase in fluid pressure within the cochlea (increased production of inner ear fluid, decreased reabsorption of the fluid, or a combination of both).
A fiberoptic examination of the middle ear and round window area is then performed using delicate 1.7 mm Middle Ear Endoscopes (lighted fiberoptic tubes) attached to a miniature television camera.
We are unenthused about the addition of steroids to gentamicin, or steroids to streptomycin (as discussed above).
A corollary is that if you really care that what you are measuring reflects the side you think you are measuring, don't use a bilateral cVEMP.
The literature about PAM is confused -- some authors may have mistaken the much larger cVEMP's for PAM responses, and vice versa.
These patients are unusual however and a longitudinal study would not be easy to carry out. As Machado-Joseph affects the brainstem, the mechanism for the reduced VEMP may lie in damage to other locations than the cerebellum. Again, the hearing loss may be due to patchy areas of ischemic tissue within the inner ear secondary to a lack of adequate blood flow. The round window is located and any scar tissue, adhesions, or obstructions that may be present are carefully removed. Our present position is that thresholds should not be done routinely, as they prevent one from doing a reliable amplitude. One could then still implant one ear, leaving both vestibular systems potential candidates for hair cell regeneration in the future.

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