Timothy C. Hain, MD • Page last modified: August 1, 2022
The vibration test is a recent development in clinical vestibular assessment. It has been made possible by the wide availability of video Frenzel goggles, which are devices which allow one to observe a subjects eyes in complete darkness. First described by Lucke (1973), vibration over the head or neck may elicit a vigorous nystagmus, and furthermore, the nystagmus is frequently direction specific and allows you to identify the "bad ear" (it beats away). We will sometimes use the abbreviation "VIN" for vibration induced nystagmus.
|Device used for vibration test (cost -- about $25). This is a Sunbeam/Oster shower massager. We presently use "Wahl" 2-speed massagers that offer both a 60 and 120 Hz stimulus.|
A source of vibration, such as a hand-held shower massager is firmly applied to the mastoid, vertex, anterior or posterior neck of a subject. Others have used a "TheraSpa Turbo Brookstone" (White et al, 2007), or a variety of much more expensive devices sold by medical supply companies.
You can use other vibrators/massagers -- it is not very critical except we advise against battery powered devices (which vary according to their charge status). In Europe, perhaps because they use a 50 Hz electrical system, the common device used is a 100 Hz vibrator (Dumas et al, 2016). As noted above, the "Wahl" 2-speed massager that we presently use in the clinic has a 60 and 120 Hz setting.
The other device that you need is a video-frenzel goggle system. Optical Frenzel goggles just don't work for this test -- you need complete darkness.
|Method of vibration test. A Wahl shower massager is applied firmly to the lower edge of the sternocleidomastoid. The lower frequency setting is used (60 hz).|
There are two general methods to do the bedside vibration test -- vibration of the neck, and vibration of the skull.
Generally we use the neck -- we apply vibration to the lower edge of the sternocleidomastoid (SCM) as we want to avoid the carotid artery area, but the exact location is not at all critical as long as the sternocleidomastoid is located and the pressure is firm. Interestingly, one can sometimes even get VIN by vibrating the deltoid muscle, but the most convenient place is generally the SCM. The eyes are observed with a device such as a video-Frenzel goggle system. No light can be allowed. The subject is sitting upright, without instruction other than to look straight ahead. Most European studies of neck vibration state that they used the "dorsal neck muscles" (e.g. Michel et al, 2001). It is possible that these are "apple/orange" situations as we generally stimulate the very SCM muscle which is lateral to anterior.
The other method, which is favored by Dumas (2016), is to apply the vibration to the mastoid area and vertex of the skull. This methodology increases the relative amount of stimulation to the inner ear as opposed to the neck. One would not think that this method would stimulate the neck to any great extent.
|Vibration induced nystagmus. This patient has a 60% left weakness. There is a 3 deg/sec right-beating spontaneous nystagmus, which increases to about 10 deg/sec when vibration is applied to either sternocleidomastoid with a device that produces a 60 cycle vibration (a shower massager).|
A positive response is a horizontal nystagmus that beats in the same direction, for vibration on both sides of the neck. Above is shown a strong nystagmus, typical of vestibular neuritis or post-ITG. It is actually more common to have no spontaneous nystagmus at all, but a powerful nystagmus produced by vibration. This would be typical of the compensated unilateral loss.
Another example of the typical positive vibration test is shown here (movie, 7 meg). This individual has a complete unilateral vestibular loss secondary to removal of an acoustic neuroma on the right side 30 years prior. There is a strong nystagmus beating to the left, for vibration on either side. The subject cannot see because of the goggles which occlude vision. The vibration source is a conventional shower massager as shown above. This example illustrates that vibration induced nystagmus generally persists as long as the unilateral loss persists. In acoustic neuroma patients -- this means forever.
Any type of unilateral vestibular loss is generally very productive of VIN. This includes, for example, acoustic neuromas. (Negrevergne et al, 2003).
According to Michel et al (2001), VIN is present in about 6% of normal persons.
Ipsiversive VIN (DCVN)
It is common for vibration to produce a nystagmus that beats to the left for vibration of the left neck, and to the right on vibration of the right neck. This is an "ipsi" versive DCVN. This response seems to be more frequent in older people, and has no association with any known disease. Perhaps it relates greater reliance on the neck in older people, as their ears degrade.
Occasionally (perhaps 1% of the iDCVN), there is a contraversive nystagmus that beats opposite to the side being vibrated. cDVCN. Again, there is no clinical correlation as yet.
This link is to a video of a weak cDCVN (courtesy of Dr. Dario Yacovino).
Occasionally there are large differences in the intensity of nystagmus between one side and the other. The clinical significance of this is unclear. We speculate that some of the asymmetry is due to technical issues (i.e. inconsistent application of the vibration), and that some of it is related to differences in neck proprioception. We think this is much more common in persons who have had neck surgery. We do not have an opinion about this situation with skull vibration, but we would think it would be less prominent as skull vibration is transmitted through the entire skull, although obviously falling off as a function of distance.
Nuti and Mandela (2005) reported on asymmetry of the mastoid vibration test. They stated "In the few patients in whom mastoid vibration nystagmus was elicited only from one side, or when there was a clear difference in intensity of the nystagmus induced on the two sides, the stimulated side was more often the affected side. " This suggests that the nystagmus, at least in these cases, was not from the remaining inner ear.
The term "perverted" is generally used to describe a non-horizontal nystagmus elicited by some stimulus, where a horizontal nystagmus is expected. Fpor example, a vertical nystagmus or a torsional nystagmus.
|2 examples of upbeating nystagmus induced by vibration on either side. This is of unknown significance, but it is quite rare, unless very strong vibration is used. It may relate to where the source of vibration is placed on the head.|
Nystagmus that is vectored other than horizontally, is of unknown significance. Following the convention in ENG testing, this response can be called "perverted", because it goes in unconventional directions. In some cases it may be due to release from fixation suppression. This is generally upbeating, but downbeating and even torsional nystagmus is rarely encountered. In SCD, vertical nystagmus is occasionally reported (see below).
In theory, unexpected VIN might be due to release of fixation -- perhaps neck input was suppressing a nystagmus. Also, entirely in theory, perhaps vertical VIN is due to a relative lack of upward or downward sensors in the inner ear, assuming that vibration stimulates everything. We don't really know.
The vibration test nystagmus (as far as we know) persists forever. Well, at least as long as the vestibular weakness persists. Below is an example of a patient post-acoustic removal 1 year prior to testing (image courtesy of Dr. Dario Yacovino). Vibration nystagmus is stronger than head-shaking nystagmus. HSN usually becomes smaller in the territory between 50-100% loss, while vibration nystagmus scales more linearly with the extent of loss. (unpublished observations of the author). Of course, there is no caloric nystagmus (bottom right):
Here again is a link to vibration nystagmus in a patient whose acoustic was removed 30 years prior. (movie, 7 meg). This individual has a complete unilateral vestibular loss secondary to removal of an acoustic neuroma on the right side 30 years prior. There is a strong nystagmus beating to the left, for vibration on either side. The subject cannot see because of the goggles which occlude vision. The vibration source is a conventional shower massager as shown above.
There is a suprisingly large literature documenting the utility of neck vibration in diagnosis of dizziness. There is also a large basic science literature documenting the deleterious effects of vibration on posture.
Vibration of the neck is a moderately reliable method of localizing the side of a unilateral vestibular lesion. In complete darkness, vibration induces a nystagmus that resembles that seen acutely, prior to compensation. Vibration induced nystagmus persists over decades, unlike spontaneous nystagmus. Vibration testing was abnormal in generic vestibular neuritis in 91% of patients, and 94% of those patients with Ramsey-Hunt type of vestibular neuritis (Kim et al, 2015).
Koo et al (2011) compared VIN to caloric and the time constant of the rotatory chair test. VIN was a better test than HSN or spontaneous nystagmus, althought hey were all rather similar. There was a weak (0.451) correlation with caloric paresis, and also a weak correlation with the time constant. One would not think that it would correlate that well with TC, as the TC does not reflect relative vestibular paresis, but can be affected by bilateral as well. On the other hand, one would expect a better correlation with canal paresis.
We ourselves have found that vibration induced nystagmus is an excellent method of determining whether or not transtympanic gentamicin treatment for Meniere's disease will stop vertigo attacks. (unpublished data of the author). Presumably this is due to unilateral vestibular damage. We also use it when patients with Meniere's, who have had TTG, get worse. If there is no VIN -- perhaps more gentamicin is needed. This does not always work.
Clinical uses of the vibration test that we find dubious
Vibration to diagnose SCD -- we are dubious.
This is basically the subject of bedside diagnosis of SCD, which is discussed in more detail here.
Vibration of the posterior neck is reported by a few investigators to be useful in diagnosis of SCD, but we are dubious ourselves. According to White et al (2007), it induces a downbeating nystagmus (White et al, 2007). We have not found this to be true in our SCD population. Dumas et al (2014) suggested that vibration of the vertex and mastoids of the skull in 17 subjects with SCD largely produces an upbeating nystagmus. However there were other directions too -- he stated "In SCD, VIN was observed in 82% of patients with a primarily torsional, horizontal, and vertical (up-beating) component in 40%, 30%, and 30%, " So quite a mixture.
In a later study, Dumas et al (2019) examined 40 patients with similar skull vibration technique, and reported that "VIN torsional and horizontal components observed on vertex location in 88% beat toward the lesion side in 95%, and can be obtained up to 800Hz (around 500Hz being optimal). SVIN slow-phase-velocity was significantly higher on vertex stimulation at 100 and 300Hz (P=0.04) than on mastoids." Both upbeating and downbeating nystagmus was observed. Torsion and horizontal was seen beating towards the lesion side (e.g. suggesting an exitatory vestibular mechanism). It is difficult to see how one could get both upbeating and downbeating nystagmus from a purely vestibular stimulus.
In our own clinical practice, we don't think that vibration of the neck (SCM) induces consistent nystagmus in SCD (note how Dumas said there was a mixture), and in those who have upbeating nystagmus, most have BPPV and not SCD. Still, if we saw a torsional nystagmus, we would pay attention and look hard for SCD with an oVEMP. The valsalva test and bone-conducted sound (throught the wrist) is probably more effective than VIN in suggesting the existence of SCD at the bedside. The oVEMP test is currently the best lab test to establish SCD, without doing a CT scan, although occasionally it does have false negatives.
Vibration of the mastoid in Meniere's disease - dubious as well.
One would not expect that any bedside protocol would be able to diagnose Meniere's disease for several reasons. First it fluctuates. Second, the brunt of the damage in Meniere's is to the hearing organ. It takes a very long time for vestibular damage to be sustained in Meniere's. So, the general idea that a vestibular bedside test can somehow identify Meniere's, at least in reliable fashion, seems rather unlikely. It does seem possible that one might be able to pick out unusual combinations -- perhaps nystagmus going in the wrong direction as hearing deficits however.
Hong et al (2007) suggested that vibration over the mastoid was somewhat localizing, generally producing contralesional nystagmus, especially in persons with more vestibular damage. There are many problems with this study - -mastoid location (see comments above), and also a protocol where the side eliciting bigger VIN was used. We prefer a protocol where only VIN is accepted that goes the same direction for each sides, and also a protocol where the neck rather than the mastoid is stimulated. Still, we do agree that occasionally a wrong-way VIN is seen.
Marques and Perez-Fernandez (2012), reported VIN in 73 of 97 patients with Meniere's disease. It is difficult to know what this means.
There are several possibilities -- the inner ear (including semicircular canals and otolith organs), the neck proprioceptors, or perhaps a combination of both. Another possibilty is that vibration "releases" a spontaneous nystagmus in some way, held in abeyance by some central circuit. Certainly there are examples of how nystagmus can be reversed simply by mental effort (e.g. latent nystagmus).
It is also well established that neck muscle vibration shifts the idea of straight ahead. Jamal et al (2019), wrote "Under unilateral NMV, the visual environment moves towards the side opposite the vibration (LoE II) and the subject's experience of "straight ahead" is shifted towards the side of the vibration (LoE II). " (NMV means neck muscle vibration). Additionally, according to Calvin-Figuiere et al (1999), "In humans, vibration applied to muscle tendons evokes illusory sensations of movement that are usually associated with an excitatory tonic response in muscles antagonistic to those vibrated (antagonist vibratory response or AVR). " Furthermore, "That the AVR is observed only when a kinesthetic illusion is evoked, together with the similarities between voluntary contractions and AVRs, suggests that this vibration-induced motor response may result from a perceptual-to-motor transformation of proprioceptive information, rather than from spinal reflex mechanisms."
There is also a substantial literature about "stepping around nystagmus" or "podokinetic" nystagmus, first described by Bles (1983), as well as a neurophysiological underpinning of changes in neck responsive units post vestibular loss (mainly due to Cullen). These lines of investigation provide an underlying physiology suggesting that neck stimulation could cause nystagmus.
Inner ear mechanism:
It is rather obvious that vibration of the head excites the inner ear, including the cochlea, the canals, and the otoliths, as after all, responding to sound and vibration is the core reason that these sense organs exist. Vulovic and Curthoys (2011) examined nystagmus in Guinea Pigs (without any vestibular lesion), and reported that there was nystagmus produced by vibration, that was lessened by ablation of the vestibular system with gentamicin. This is not an exact match to the usual situation of VIN, as these Guinea Pigs lacked a vestibular imbalance. It is also interesting that the nystagmus was lessened, but not abolished by vestibular damage. This suggests the possibilty of a dual mechanism.
Karlberg, Aw, Black, Todd, MacDougall and Halmagyi (2003) stated "While altered proprioceptive inputs from neck muscles might be important in the mechanism of vibration-induced ocular torsion and nystagmus after unilateral vestibular deafferentation, vibratory stimulation of vestibular receptors in the intact labyrinth also appears to have an important role. " Thus Karlberg and co-authors explicitly suggested a dual source.
Trying to put it together: Probably it is a mixture.
Considering the general qualities of VIN -- immediate onset and offset, one would not think that this would be a vestibular nystagmus because of the lack of nystagmus after the vibration is removed. All peripheral vestibular nystagmus (to the writers knowledge anyway), have a secondary phase that goes in the opposite direction of the primary nystagmus, and that builds up over time. So in other words, one would expect after a minutes of vibration, to have an opposite directed nystagmus in the dark. This suggests that one of the other theories than inner ear is more likely.
Another observation made by Nuti and Mandela, that when VIN is very asymmetrical (from the mastoid), the stronger response is generally from the "bad ear" side. This observation argues against the idea that the source of the nystagmus is the remaining ear.
Well, more room for research.
Vibration induced nystagmus is (in our opinion) about as useful as the "HIT" or head impulse test, but oddly enough, far less research has been done on vibration. Some basic questions that we think would be of interest: