Vestibular Evoked Myogenic Potentials
Brandon Isaacson, M.D.
March 3, 2005

This is a 47-year-old gentleman who presented with symptoms of constant lightheadedness; pulsatile tinnitus, which increased in the recumbent position; autophony, which disappeared in the recumbent position; and severe episodic dizziness. He described his dizziness as shifting of the visual surround in the presence of loud noises.

On physical exam, pneumatic otoscopy and tragal pressure caused no symptoms. His Weber lateralized to the right ear with the 256 tuning fork and bone conduction was greater than air conduction in that ear on further testing.

This is his audiogram and temporal bone CT scan. He had a low frequency conductive hearing loss; and on further evaluation, given his symptoms, it was suspected that he had superior canal dehiscence and the CT scan in the coronal plane confirmed that. On the right superior canal, you can see there is no bone overlying it.

Given that he had these fairly prominent symptoms and we could not elicit his symptoms with tragal pressure or pneumatic otoscopy, we were still concerned about the diagnosis and whether his symptoms were actually caused by the superior canal dehiscence, so we ordered VEMP testing, which is vestibular evoked myogenic potentials, and this is basically a threshold gram of the vestibular evoked myogenic potentials. Normally, these potentials disappear at approximately 85 dB; and, as you can see in the left ear, although it is not as nice of a curve, but there is, in fact, a VEMP present at 95 dB. It is still there at 85, but not quite, and then it is pretty obvious in the right ear at 95 dB, and all the way down to almost 65 or 55 dB. So, when the normal thresholds are typically around 85 dB or above, this was fairly supportive of the diagnosis, and the patient is currently scheduled to undergo a middle fossa craniotomy with a plugging of the superior canal on the right side.

So, what is the role of the vestibular system? It is to stabilize vision, control posture and register orientation. This picture on the right demonstrates the utricle, which is only in the horizontal plane and the saccule, which is oriented to the vertical plane. The otoliths are sensitive organs within the vestibule, and they are able to detect linear acceleration and the perception of gravity, as well as centrifugal force.

The anatomy of the otoliths. The actual otoliths themselves are calcium carbonate pistols. They have, compared to the surrounding indolin fluid that has a specific gravity of 1, the specific gravity of about 2.2, so they are sensitive to gravity motion and, therefore, allow the otoliths to work in the fashion that they do. The basic structure of the otolith function is depicted on the right on the picture, and that shows that the otoliths are the most superficial layer followed by a gel layer. The stereociliary and kinocilium of the vestibular hair cells are embedded in that gel layer. Therefore, when you get movement of the otoliths relative to gravity or linear acceleration, it causes deflection of the stereocilium either towards or away from the kinocilium, activating the hair cells or causing decreased action potential firing.

This is a histology slide of the otolith origins, and it shows the exact same structure as I have showed you before—the otoliths on top, the hair cells on the bottom layer, and then in between is that gel layer where the steriociliary and kinociliary are embedded.

So, the actual anatomy of the individual otoliths—there is the utricle and the saccule, and the utricle is oriented on a horizontal plane, or on an axial plane, while the saccule is actually oriented in a sagittal or parasagittal plane. The utricle is almost a circular structure, while the saccule is more oblong. The hair cell orientation is different as opposed to the cuppula in the semicircular canals. In the cuppula, all the kinocilium are facing the same way, either towards the utricle or away from the utricle. In the horizontal canal, they are towards the utricle, and in the vertical canals are away from the utricle. The otolith organs are actually kind of bisected by a line called the striola. In the utricle they are directed towards the striola and in the saccule, they have the opposite direction. That menas that only need essentially one set of otoliths in order to function, because they basically sense direct movement in all directions or acceleration in the forward and aft direction, side-to-side, as well as in an up and down fashion like in an elevator. If you were to not have a sacule, you would probably have a hard time telling you were moving in an elevator, aside from your proprioceptive input from the rest of your body.

This slide, basically depicts how these things work. In particular, this is focusing mainly on the utricle, just for ease of description. When you tilt your head backwards, the otoconia are deflected backwards, and therefore cause activation of some of the hair cells that are facing towards that way and decreased activation of some of the other cells that are facing away from the striola, and then the same works for the forward motion or acceleration and deceleration.

So, what are the symptoms of actual otolith dysfunction? They are a little bit different from the classic vertigo that we always hear of or rotatory vertigo where the patient comes in describing room-spinning vertigo. With otolith dysfunction, the patient basically has a sensation of linear motion or the feeling of actual falling or of lateral pulsion, which is kind of being pushed to one side or the other or forward or backward. They also have difficulties with aligning objects in the horizontal or vertical plane and that actually is taken advantage of in something called the subjective visual vertical, which is another otolith test where a digital line is basically presented on the wall and they have to line it up to whether it’s either directly perpendicular to the horizon or parallel and then you measure the angles between the actual horizontal or the vertical. It should be either 90 degrees or 180 degrees. If it’s not, they basically have signs of otolith dysfunction.

So, what is the history of vestibular evoked myogenic potentials? Iit goes back to Tullio, who actually described the sound sensitivity of the vestibular system. Later, Bickford, Jacobson, and Cody discovered that a loud acoustic stimulus produced a myogenic inion response, and the inion is actually the back of the skull where a lot of the cervical muscles insert. They theorized that this inion response was from the vestibular system. Later it was actually discovered that the sacule had the lowest sensitivity to sound within the vestibule.

So people were initially excited about the potential of using vestibular evoked myogenic potentials, but then it went by the wayside and wasn’t really reintroduced until 1994, by Kovach, who basically was able to stimulate the sacule and record actual potentials from the cervical musculature. He discovered that these potentials were actually retained in patients who had profound sensorineural hearing loss. That confirmed that these were actually from the vestibule and not the cochlea. In patients who actually underwent vestibular nerve section, these potentials actually disappeared. So, it was pretty much isolated to the vestibular nerve and vestibular system and not the cochlea. There are two actual potentials that are measured. One is the P13-N23, which is a positive and negative deflection that occurs at 13 and 23 milliseconds respectively, and that is of vestibular origin. Tthen there is a later potential, which has not been used as much in clinical practice or in research, which is the N34 and P34, and those again correspond to the 34 and 44 millisecond latency and N means negative, and P means positive.

In 2002, when people were still debating on whether these actually arise from sacule, an investigator studied seven patients with significant malformations of the cochlea and vestibular system. Some of these patients actually had no semicircular canals but still had some vestibule and either present or absent cochlea. Almost all these patients had moderate to profound hearing loss. Despite this, all these patients, including the ones with absent semicircular canals had vestibular evoked myogenic potentials. So, if they don’t have semicircular canals, they don’t have much of a cochlea, and they have profound hearing loss, it pretty much isolates this to the utricle or sacule.

So, what is vestibular evoked myogenic potential? It is basically an inhibitor response that is recorded in a tonically-contracting sternocleidomastoid muscle. It can also be recorded in other muscles, including the trapezius muscle. There is actually an excitatory loop that is recorded in other muscles, but this is the one that has been clinically used and also used in research. This response is actually generated by either clicks, which are broadband stimulus; low-frequency tone pitch, anywhere from 250 to 1000 Hz. Skull taps are actually used in certain scenarios.

Again, as I already talked about, in which otolith is the VEMP originating? As I mentioned earlier, this is present in deaf patients. It is absent in vestibular nerve section patients. From prior research, it was discovered that the sacular nerve fibres had the lowest threshold to acoustic stimulation. So, in a guinea pig model, they looked at the actual individual nerve fibers arising from each individual semicircular canal as well as the utricle and sacule, and found that the sacular nerves were the ones to have the lowest threshold to response to acoustic stimuli.

What is the reflex arc? How does this work? It starts with sound presentation to the ear. It is transduced through the middle ear and then stimulates the actual sacular hair cells. The sacular fibers of the inferior vestibular nerve are activated, and it gets transmitted to lateral vestibular nucleus, the medial vestibular spinal tract, and then goes to an inhibitory motor neuron or directly. It either goes through two reflex arcs. There is a disynaptic and a trisynapticpathway. These are depicted on the picture on the right. If you look all the way to the left, there is a stimulatory neuron that basically enervates two inhibitory neurons, which are represented by black circles that directly inhibit the nuclei, the motor neurons, going to the sternocleidomastoid muscles and the neck flexor muscles. And then there is a disynaptic pathway where the inferior vestibular stimulates an inhibitory neuron which directly inhibits the motor nucleus of the motor neuron for the neck flexor muscles. This y was worked out in a cat model.

So what are the responses that can be recorded from a vestibular evoked myogenic potential? There are three basic measures. There is the threshold, the latency, and the amplitude. Of the these three, probably threshold has been, so far, the most clinically useful. And that is basically the point at which the vestibular evoked myogenic potential can be recorded. It is basically depicted by this picture on the right where the Y-axis shows the decibel sound presentation and the X-axis is the latency. The P13 and N23 latencies are seen on the x-axis and that refers to latency; and you have an obvious response at 103 dB. As you go further down in decibels, the response gets less in amplitude until it disappears at approximately 65 dB. This is in another patient that has apparent canal dehiscence.

Threshold is thought to be a measure of actual cochlear vestibular impedence. In other words, if you have another opening or third window in the inner ear, the threshold is actually going to be decreased because your impedence is decreased within the system.

The next measure is latency, and that reflects the time in which these potentials occur. This is not as useful, and it is a fairly constant perimeter. The only thing it has actually shown to be somewhat useful for is in patients with multiple sclerosis. Those patients often either had no vestibular evoked myogenic potentials or they had significantly prolonged latencies. That is indicative of a nerve impulse conduction block. Essentially, a lot of these patients have isolated lesions in the brain stem and along the vestibular spinal tract. Therefore, if you will, there is a conduction block of the response and so you have a prolonged latency.

The amplitude is actually just measured from the P13 to N23, and that actually has been used in clinical practice. However, it is a fairly variable response, and it can be variable even between ears of the same patienty. So far, that hasn’t been quite as useful as the other two measures, in particular, threshold.

So what are the clinical applications? Well, like all vestibular tests, it is a helpful test for site of lesion testing. This really doesn’t replace a good history on a patient who presents with vestibular problems. Particularly, it is very helpful, as I mentioned before, for fistula or dehiscence of the otocapsule. Also, it can be potentially useful for follow-up with clinical distortion in the ear, such as Ménière’s disease.

What is the testing protocol? In order to have this test work, the actual amplitude of the response is proportional to the amount of time of contraction you have in the sternocleidomastoid muscle; so, the more contracted the muscle is, the higher your amplitude is and the more consistent your response is going to be. There are three different positions people describe in measuring vestibular evoked myogenic potentials. The patient can be placed in the supine position with the neck flexed; they can be placed supine with the head rotated away from the test ear and then with the neck flexed; and then sitting with the head rotated away from the test ear. All these serve to basically activate the sternocleidomastoid muscle. The more that muscle is contracted, the greater the increase in the amplitude of the response.

There are three different stimuli that have been used—broadband clicks; tone versed, particularly low frequency tone verse - the tuning curve of the sacule is anywhere from 250 to 750 Hz; and skull taps. Again, skull taps haven’t been used as much, and they basically try to elicit response with a reflex hammer. I don’t know of any patients who want to be whacked in the head with a reflex hammer, but it is actually useful in conductive hearing loss. Patients that have a conductive hearing loss, can’t transfer the sound from the external ear, through the middle ear, and into the inner ear; therefore, if they have a conductive hearing loss of greater than 20 dB, they are not going to have vestibular evoked myogenic potentials. So a skull tap actually directly stimulates the vestibule and therefore can give you a response.

Some clinical conditions this may be useful in are: 1) vestibular neuritis, which basically presents with acute onset dizziness, vertigo, and disequilibrium. The patient can have nausea and usually has no evidence of hearing loss. If there is hearing loss, it is typical to classify this as labyrinthitis. The actual acute phase of the condition lasts for about 24 to 48 hours and then there is gradual improvement. A few things in the diagnosis are excluding other neurologic deficits. Obviously, if they have other cranial nerves that are affected, you have to worry about a vascular etiology for the diagnosis. The pathophysiology of vestibular neuritis is mainly thought to be related to a viral infection, particularly reactivation of a herpes virus. It is thought to usually arise in the superior vestibular nerve. The other theory is that it arises from loss of blood supply to the vestibule or the inner ear. This is a less popular of a theory. Again, it is felt to most commonly arise from inflammation or reactivation of a viral infection in the superior vestibular nerve. So what are the sequelae of vestibular neuritis? Well, most of these patients recover. Sometimes they can have some prolonged disequilibrium or later develop hydrops. Actually, about a third of them can develop benign paroxysmal positional vertigo. This is actually where VEMPs have been used in testing. Some of the other diagnostic procedures you can do in vestibular neuritis are an MRI, an audiogram, and calorics. While MRIs are not frequently performed, the main reason to do so would be if you suspect something else is going on or the clinical history doesn’t fit with the diagnosis. Often you do not really want to subject the patient to a caloric test in the middle of an episode of vestibular neuritis. What is would show is usually absent or significantly reduced caloric responses on the affected side, as the calorics are a reflection of lateral semicircular canal function. This is enervated by the superior vestibular nerve.

Murofushi in 1996 looked at 47 patients with the diagnosis of vestibular neuritis. Sixteen of these patients, or a third of them, had absent vestibular evoked myogenic potentials. None of these patients developed benign paroxysmal positional vertigo. So what does this mean? Well, basically, if you think about it, the VEMP response is generated by the inferior vestibular nerve and it rises from the sacule. The benign paroxysmal positional vertigo actually arises in the posterior semicircular canal in most cases—90 to 95 percent of cases. So, if the inferior vestibular nerve is affected by the vestibular neuritis, even if they do have otoconia within the posterior canal, if the nerve is not working, then they are not going to get these symptoms. In the 10 patients who actually did develop benign paroxysmal positional vertigo, all of them had an intact VEMP, which is sort of the opposing portion, where they had their inferior vestibular nerve, which worked, but if they had a VEMP, they were more likely to get benign paroxysmal positional vertigo because the inferior vestibular nerve was intact. Again, the last statement basically summarizes this, that patients who have vestibular neuritis who have active VEMPs are unlikely to go on and develop benign paroxysmal positional vertigo.

So what about Ménière’s disease? Again, the symptoms for Ménière’s disease are typically, 3 of these 4 symptoms. Classically, you have to have two episodes of vertigo, aural fullness, fluctuating hearing, and tinnitus. The diagnostic modalities include imaging to rule out other causes; audiometry (usually patients can have a low frequency hearing loss); balance function testing can often help; glycerol testing with an audiogram has also been described as a distortion product due to acoustic emissions; and, as I have mentioned also, used in VEMP testing; and electrocochleography.

One of the first studies was actually by de Waele, and she wanted to assess whether the sacule actually was dysfunctional in patients with Ménière’s. She used 59 patients and 71 controls, and 54 percent of the patients with Ménière’s had no vestibular evoked myogenic potential. Actually, in the patients who did have VEMPs, there was really no difference in latency or amplitude compared to controls. In this case, it didn’t seem as useful; however, if you test most patients or controls, almost all of them will have a vestibular evoked myogenic potential. This basically shows that the sacule is dysfunctional or not working in a significant portion of Ménière’s patients. The patients that actually have low frequency hearing loss, the worse their hearing was in the low frequency range, the more likely they were to have an absent VEMP. So perhaps it can be used to follow patients with Ménière’s to see how much inner ear function they have left. Also of note is if they had no VEMP response, they did very poor on condition 5 in posturography, and that is indicative of vestibular dysfunction.

Another study used 29 patients who just had symptoms of mild dizziness or vertigo and did not really have any other symptoms of Ménière’s. They had a control set of patients, although they didn’t really report the data on them. They looked at pure tone audiometry, otoacoustic emissions and VEMPs, and they looked at pre and post administration of glycerol. With glycerol administration, typically, the audiogram, if the patient has Ménière’s, will improve. The researchers wanted to look at this affect with otoacoustic emissions and VEMPs. They found that in 58 ears, 14 of the patients, or 24 percent of the ears, actually had a positive glycerol test on the audiogram. And then, with otoacoustic emissions, 31 percent had a positive test and with VEMPs, 27.5 percent of the ears had a positive test.

Comparing the three tests and looking at them, there wasn’t necessarily a really good correlation between the three tests. In other words, if you had a positive audiogram glycerol test, you may not necessarily have a distortion product otoacoustic emission that was positive or a VEMP that was positive. What they theorized was that maybe the little acoustic emissions and VEMPs could be used to test individual problems.

Rauch used VEMPs to assign the diseased ear in patients with Ménière’s. He used 20 patients with unilateral Ménière’s disease and compared caloric asymmetry with vestibular evoked myogenic potentials using a 250 Hz tone burst. Most people described caloric asymmetry as a 25 percent difference. In his study, he used it as an absolute and just basically said if there was a 5 percent difference in the calorics between ears, then that was considered positive. And then, for VEMPs, obviously, if they had a decreased threshold or absent VEMPs, then that was considered a positive.

Tthey bascially showed that if the VEMP was corrected in assigning the diseased ear 80 percent of the time, while caloric asymmetry at 5 percent was 85 percent correct. If you looked at them both together, they were always able to kind of identify the ear. Hhowever, there were some contradictory points where a VEMP may show one ear and the caloric may show another. So, it was not necessarily that useful and most people would still use the audiogram to assign which ear was affected.

Another excellent study by Rauch was more interesting. This study discussed 34 patients with unilateral Ménière’s and 14 controls. Most normal patients with vestibular evoked myogenic potentials had their best or lowest threshold and best response at approximately 500 Hz tone-verse thresholds. In patients with Ménière’s, this actual tuning curve shifted towards 1000 Hz. So basically, as the frequency of the tone pip increased, the amplitude of the VEMP increased and the threshold decreased in patients with Ménière’s disease. And that was actually shown in the diseased ear as well as the unaffected ear. So, that was fairly interesting and that may reflect that some of these patients may go on to develop bilateral Ménière’s.

So what about acoustic neuroma? Again, symptoms for this are: hearing loss, tinnitus, and disequilibrium. Vertigo is unusual. If they are very large tumors, there may be ataxia and dysmetria. The diagnostic methods are: audiometry, if there is an asymmetric hearing loss; absent reflexes; ABR (delayed or absent wave 5, or a total absence of the ABR). ENG testing can sometimes be considered helpful, and MRI, obviously, is currently the gold standard, and I don’t think that’s going to change.

But what about VEMPs with acoustic neuroma patients? It may be helpful in actually predicting nerve origin of the tumor, and this would be particularly relevant in patients who have intact hearing who may be good candidates for hearing preservation. Most studies have shown basically that tumors that arrive off the superior vestibular nerve have a better prognosis of hearing preservation surgery with small tumors as opposed to tumors on the inferior vestibular nerve where you actually have to kind of move the facial nerve out of the way, and you are certainly a lot closer to the blood supply to the cochlea. So, if they have an absent VEMP and a small tumor, you could theorize that the tumor arises off the inferior vestibular nerve, and they may not have as good of a prognosis for hearing preservation; whereas if they have normal VEMPs and have some calorics, that indicates more of a superior vestibular nerve tumor and again probably a better prognosis for preserving hearing.

These two studies I have listed here that looked at the presence or absence or decreased amplitude of a VEMP response in patients with acoustic neuromas. Basically, it showed that close to 80 percent of patients either had no VEMP response in their tumor ear or they had a significantly decreased amplitude.

In the first study of patients with acoustic neuromas, they also looked at latency as a measure of diagnosing acoustic neuromas and only 10.5 percent of the patients had a prolonged latency. Actually, those were in patients with very large tumors, so one could theorize that if there is significant brain stem compression, then obviously this is going to affect your conduction velocity, such as in multiple sclerosis patients.

So what about superior canal dehiscence? Thus far, this has actually been probably the most interesting thing evaluated by vestibular evoked myogenic potentials. The classic symptoms and signs are sound-induced vertigo, which is the Tullio phenomenon; pressure-induced ocular deviation, which is Hennebert’s sign, and that can be either with pneumatic otoscopy or tragral compression. Sometimes, these patients can present with an isolated conductive hearing loss with no vestibular symptoms and usually it is at the low frequencies. Sometimes patients can have negative bone conduction thresholds, and there have been several reports of patients being operated on for this conductive hearing loss, undergoing middle ear exploration and a stapedotomy with no change in their hearing after the operation. They then went on to get further testing, and they were actually discovered to have superior canal dehiscence as the cause of their conductive hearing loss.

So how do you diagnose superior canal dehiscence? Well, certainly history and physical exam are very important and paramount. The other things that you can use to confirm your diagnosis are high-resolution CT scan, which is the current regimen, and also VEMPs. I think these two are actually complementary in this case, such as the index case, where we had a positive CT scan, but we elicited the symptoms on physical exam and so we used the vestibular evoked myogenic potentials to further confirm our diagnosis.

Again, this basically shows a threshold gram, basically, of a left ear and a right ear on a patient with left superior canal dehiscence. On the right ear, there is an obvious response at 103 dB, and then there still may be a response at 100 dB, and then nothing at 95 dB; while in the affected ear, the actual response goes all the way down to 70 dB, which is, you know, pretty impressive considering patients usually lose the response in anywhere from 95 to 85 dB. So this helps support the diagnosis of left superior canal dehiscence.

On the CT scan, this is a coronal scan on the right and then a reconstructed image on the left showing the imaging in the plane of superior canal, showing a fairly obvious dehiscence. This is actually one of those patients who had a low frequency conductive hearing loss, underwent a stapedectomy with no improvement, and you can see the prosthesis there, and then they were later found to have a superior canal dehiscence.

So what are the problems with vestibular evoked myogenic potentials? Well, currently, there are a lot. Iif you look at all the literature, there are variable methods of performing this test, particularly with positions, what type of stimulus they use, and how they record it. So there is really no uniform testing protocol as there is, for example, in something like ABR. There is not a lot of data on normal subjects, so we don’t really have a reference bank. That will probably go by individual balance labs getting their own normal subjects and establishing their own normal data. You can’t really use these in a setting of conductive hearing loss. If you have a 20 dB air-bone gap in a middle ear effusion or ossicular discontinuity, then using tone-pitch or clicks are really not going to elicit this. There may a role for using skull taps in that situation.

Probably the main problem is that you are not really measuring the actual physiologic function of the sacule. The sacule, you know, vestibularly, or back in development, it was an auditory receptor. It still is actually in fish, but in humans, it is mainly an organ of sensing gravity and linear acceleration, not its usual physiologic function, and it certainly would be preferable to measure physiologic function as opposed to vestibular function.

So what are some future developments with VEMPs? Well, one would be to develop, again, uniform testing primers so centers can compare their data, both for normative-end patients who are affected by vestibular conditions.There are a few physiologic tests that are more involved. One is off-axis rotation and rotary chair and the subjective horizontal visual or vertical. Those are more tests of utricular function, but it would be nice to compare some type of physiologic function of the VEMP to see how they correlate. It certainly has a role in actually monitoring ototoxicity, particularly in patients with chronic chemotherapy or antimicrobial therapy, patients who have cystic fibrosis and are on long-term aminoglycoside therapy—they are certainly at risk for vestibular toxicity—as well as patients on chemotherapy. Right now, the only test we have are audiometry, particularly high frequency audiometry, and rotary chair. Those are all tests of cochlear toxicity and not vestibular toxicity. Certainly, hearing impairment is a very disabling condition, but bilateral vestibular paralysis is also very impairing, it is not practical for patients to have rotary chair testing on a daily basis or even on a weekly basis to monitor for ototoxicity. VEMP is something that can be done at the bedside and may be able to be used to monitor this. It can also be used to monitor changes during chemical labyrinthectomy for Ménière’s patients. Again, this hasn’t been described. And then, in general, just the multifactorial balance disorder patients, patients who have fallen or elderly patients who have declined vestibular function - it may be helpful in localizing the problem and maybe designing rehabilitation strategies.

Case Presentation:

RJ is a 47 year-old male who presented with a three year history of constant light-headedness, and episodes of severe dizziness. His dizziness was further described as shifting of vision with exposure to loud noise. He also described right pulsatile tinnitus which increased in the recumbent position. Autophony and awareness of respiration which disappeared in the recumbent position was also noted.

On physical exam, tragal pressure and pneumatic otoscopy did not elicit the previously described visual symptoms. Weber testing lateralized to the right ear with 256Hz tuning fork and bone conduction was greater than air conduction. Findings of the 512Hz tuning fork were normal. Audiometric testing demonstrated a bilateral low frequency conductive loss. MRI, MRA and ENG were normal. Temporal bone computed tomography demonstrated a dehiscence of the right superior semicircular canal. Vestibular evoked myogenic potentials demonstrated a decreased threshold in the right ear of 50dB compared to 85dB in the left ear.

The patient has been scheduled for a middle fossa craniotomy with plugging of the right superior canal.

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