INVITED REVIEW
Clinical Evaluation of the Vestibular Nerve Using Vestibular Evoked
Myogenic Potentials
Jamie M. Bogle
Department of Otolaryngology, Mayo Clinic Arizona, Scottsdale, Arizona, U.S.A.
Summary: Vestibular evoked myogenic potentials are currently
the most clinically accessible method to evaluate the otolith
reflex pathways. These responses provide unique information
regarding the status of the utriculo-ocular and sacculo-collic
reflex pathways, information that has previously been
unavailable. Vestibular evoked myogenic potentials are recorded
from tonically contracted target muscles known to be innervated
by these respective otolith organs. Diagnosticians can use
vestibular evoked myogenic potentials to better evaluate the
overall integrity of the inner ear and neural pathways; however,
E valuation of the vestibular system has historically been limited
to tests of the lateral semicircular canal, superior branch of the
vestibular nerve (CN VIII), and resultant angular vestibulo-ocular
reflex pathway. In recent years, additional methods of vestibular
nerve testing in the clinic have enhanced understanding of inner
ear disorders and function, leading to improved diagnosis and
patient management.
The vestibular system lies within the bony labyrinth of the
temporal bone. This system includes three semicircular canals
(lateral, anterior, and posterior) responsible for detection and
coding of angular acceleration. The remaining two end organs,
the saccule and the utricle, are collectively described as the
otolith organs and are responsible for detecting linear accelera-
tion, including the effects of gravity. Importantly, the saccule and
utricle are innervated by the inferior and superior branches of the
vestibular nerve, respectively, facilitating evaluation of both
neural pathways.1
EVOLUTION OF VESTIBULAR NERVE TESTING
Vestibular nerve testing began in its current form in 1964
when Bickford, Jacobson, and Cody reported a sound-induced
evoked potential recorded at the inion.2 These responses were
hypothesized to originate from the cerebellum; however, further
investigation found that the response amplitude varied with the
level of underlying tonic electromyography (EMG) of the neck.
These interesting potentials were unfortunately abandoned after
finding no significant clinical application at that time. Thirty
years later, Colebatch and Halmagyi revisited these responses as
they reported a case evaluating a short-latency myogenic
potential recorded from the tonically contracted
The author has no funding or conflicts of interest to disclose.
Address correspondence and reprint requests to Jamie M. Bogle, AuD, PhD,
Department of Otolaryngology, Mayo Clinic Arizona, 13400 E Shea
Boulevard, Scottsdale, AZ 85259, U.S.A.; e-mail: bogle.jamie@mayo.edu.
Copyright Ó 2018 by the American Clinical Neurophysiology Society
ISSN: 0736-0258/18/3501-0039
DOI 10.1097/WNP.0000000000000422
clinicalneurophys.com Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018
there are specific considerations for each otolith reflex protocol.
In addition, specific patient populations may require protocol
variations to better evaluate atypical function of the inner ear
organs, vestibular nerve transmission, or subsequent reflex
pathways. This is a review of the clinical application and
interpretation of cervical and ocular vestibular evoked myogenic
potentials.
Key Words: Vestibular, Evoked potentials, Otolith.
(J Clin Neurophysiol 2018;35: 39–47)
sternocleidomastoid (SCM) muscle before and after vestibular
nerve section. The clear absence of the evoked potential noted
after vestibular nerve section highlighted the importance of the
vestibular system in generating this potential.3,4
VESTIBULAR EVOKED MYOGENIC POTENTIALS
Vestibular evoked myogenic potentials (VEMPs) are cur-
rently the most clinically accessible method to evaluate the
otolith reflex pathways. These reflexes provide unique informa-
tion to the vestibular diagnostician as to the status of both the
superior and inferior branches of the vestibular nerved
information that was previously unavailable. Vestibular evoked
myogenic potentials are evoked potentials recorded from specific
muscle sites known to be innervated by the utricle and saccule,
respectively. Each of the otolith reflex pathways will be further
described below; however, there are some recording parameters
that are similar for both.
Appropriate stimuli are needed to reliably evoke VEMPs. In
general, all stimuli must provide sufficient translation of the
otolith organs to trigger the reflex.4–7 The vestibular system has
frequency tuning for acoustic stimuli, as evidenced by increased
response rate and amplitude of VEMP responses to low-
frequency stimuli. Each otolith organ is somewhat different in
the underlying rationale for its optimal frequency response. The
saccule has frequency tuning that may relate to its significant
evolutionary role in auditory function. Auditory function in the
saccule has been demonstrated for mammals with a reported
resonant frequency range between 200 and 1,000 Hz.8 This has
been replicated in human clinical VEMP studies that demonstrate
a typical resonant frequency for air- and bone-conducted stimuli
between 200 and 500 Hz.9–12 The utricle demonstrates similar
acoustic tuning as the saccule, although this may be due to the
physical characteristics of the utricle and not due to an
evolutionary role in audition. The utricle is less firmly attached
to the temporal bone than the saccule, and research suggests that
this may contribute to its low-frequency tuning as it is able to
39
 J. M. Bogle Clinical Evaluation of the Vestibular Nerve

vibrate more freely.13 Utricular frequency tuning has also been

demonstrated in human VEMP trials, with lower frequency
stimuli (e.g., 500 Hz) providing improved response presence and
amplitude in comparison to higher and lower frequencies.14,15
The acoustic intensity needed to demonstrate increased
vestibular nerve firing is high for animal models (saccule:
approximately 90 dB SPL; utricle: approximately 120 dB
SPL).8,16 Most clinical protocols use air-conducted stimuli
between 120 and 130 dB SPL.10,14,16–19 Care should be taken
to use the lowest stimulus intensity for the shortest exposure time
possible to minimize the risk of acoustic trauma.20 The sound
pressure resulting from high-intensity, low-frequency stimuli
shifts the endolymph within the vestibule, shearing the otolith
end organ hair cells and triggering the reflex. The acoustic
stimulus creates a force throughout the inner ear, but auditory
perception is not necessary and individuals with significant
hearing impairment may demonstrate appropriate VEMPs.21 FIG. 1. Typical cervical vestibular evoked myogenic potential
Importantly, acoustic stimuli must be able to travel unimpeded (cVEMP) using 500 Hz toneburst stimuli (122 dB pSPL, 4 ms
through the outer and middle ear space to provide enough duration, 5 Hz rate). Response demonstrates appropriate latencies
translational force to the otolith organs. Atypical function along (P1 ¼ 14.65 ms, N1 ¼ 21.88 ms) and uncorrected amplitude value
the transmission pathway, such as fluid in the middle ear space, (P1-N1 amplitude ¼ 117.99 mV).
will reduce the force conducted through the vestibule, reducing
or obliterating the response.22 That said, acoustic stimuli are the sacculo-collic reflex by recording the inhibition of the SCM
most commonly used in the clinic due to accessibility.18 Another in response to otolith translation.36
option for VEMP recording is mechanical stimulation. Mechan-
ical stimuli are transmitted to the otolith organs more efficiently Method
than air-conducted stimuli23,24; there are several methods for Numerous protocols are available for cVEMP recording.
providing a mechanical, or bone-conducted, stimulus. Clinically, Tables 1 and 2 provide commonly used stimulus and recording
bone-conduction may be completed using standard bone oscil- parameters for cVEMP. The remaining method discussion will
lation devices,23 although often the force output is not sufficient focus on parameters that may lead to considerable variability in
to stimulate the otolith organs. Researchers have incorporated cVEMP data.
other methods for producing adequate bone-conducted stimuli,
including including Br€uel & Kjæl’s Type 4810 Mini-Shaker
(Nærum, Denmark)25 or a reflex hammer attached to an electronic Electrode Placement
trigger.26,27 These devices allow for efficient stimulation of the Cervical VEMPs are typically completed using a 1-channel
vestibular system. While these options are not available in the montage. Noninverting electrodes are commonly placed on the
typical clinical vestibular laboratory, they do provide possibilities upper third of the tonically contracted SCM muscle ipsilateral to
for future development and improved protocols. the stimulus (Fig. 2). The inverting electrode may be placed on

Cervical Vestibular Evoked Myogenic Potentials TABLE 1. Example Cervical and Ocular Vestibular Evoked
Cervical VEMPs (cVEMPs) are responses obtained from the Myogenic Potential (VEMP) Stimulus Parameters
tonically contracted ipsilateral SCM muscle, describing an Cervical VEMP Ocular VEMP
inhibition of the vestibulo- or sacculo-collic reflex.28,29 The
Air-conducted stimuli
resulting reduction in EMG level is interpreted as a loss of
Frequency 400–700 Hz, 400–700 Hz,
postural muscle tone.30 Cervical VEMPs are biphasic with typically 500 Hz typically 500 Hz
a positive deflection (P1) occurring at approximately 13 ms Intensity 120–130 dB SPL max 120–130 dB SPL max
and subsequent negative deflection (N1) at approximately 23 ms. Gating Blackman Blackman
Note, cVEMP tracings are often inverted in the literature (Fig. 1). Duration #7 ms #7 ms
Evidence from animal and human models hypothesize Rate #5 Hz #5 Hz
that the saccule is the primary end organ responsible for Presentation Monaural Monaural/binaural
cVEMP generation.31,32 From the peripheral end organ, the Bone-conducted stimuli
cVEMP pathway travels through the inferior branch of the Frequency 100–500 Hz 100–500 Hz
vestibular nerve (CN VIII) to Scarpa’s ganglion,8,33 terminat- Intensity 31.6 N peak 31.6 N peak
Gating Blackman Blackman
ing within the vestibular nuclei. The descending reflex
Duration #7 ms #7 ms
pathway continues through the medial vestibulo-spinal Rate #5 Hz #5 Hz
tract through the motonucleus of CN XI and finally to the Presentation Binaural Binaural
SCM.4,34,35 This disynaptic pathway describes the

40 Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018 clinicalneurophys.com

 Clinical Evaluation of the Vestibular Nerve J. M. Bogle

TABLE 2. Example Cervical and Ocular Vestibular Evoked

Myogenic Potential (VEMP) Recording Parameters
Cervical VEMP Ocular VEMP
Electrode placement
Noninverting Upper third of Inferior oblique
sternocleidomastoid muscle
Inverting Forehead or Chin or nose
sternoclavicular junction
Ground Forehead or dorsum Forehead or dorsum
Electrode impedances ,10 kU ,10 kU
Channels 1-/2-channel 1-/2-channel
Amplification 5,000 100,000
Artifact rejection Disabled Disabled
Bandpass filter 10–250 Hz 10–1,500 Hz
Epoch 100 ms 100 ms
Samples per average 50–100 100–150

the sternum21 or forehead37 with the ground electrode on the

forehead or dorsum as needed.

Participation
Cervical VEMP testing requires active patient participation
to provide appropriate contraction of the SCM muscle and
subsequent increase in underlying EMG level. In some cases, the
patient is seated and turns the head,38 while in others, the patient
is in a reclined or supine position while completing the head turn
(Fig. 2).39 Importantly, the cVEMP requires active contraction of
the ipsilateral SCM because of the reflex’s inhibitory nature36;
therefore, understanding the effects of underlying EMG level is
important for response interpretation. The amplitude of the
cVEMP response will vary based on the level of SCM muscle
contractiondincreased muscle contraction leads to increased
cVEMP amplitude.40
Active participation is commonly used in cVEMP testing.
Establishing a standard level of muscle contraction has been
reported as a method of reducing EMG variability and therefore
standardizing the cVEMP response. There are generally two
options available. First, as the underlying EMG level signifi-
cantly impacts cVEMP amplitude, monitoring, and stabilizing
this variable should provide more consistent responses. Research
has described the linear effect of EMG level on cVEMP
amplitude when instructing the patient to achieve various target
EMG levels.40 Generally, these active participation methods
require the participant to maintain a specific EMG level for the
duration of testing. This may be done by providing a visual target
to the patient to maintain an appropriate amount of muscle
contraction.
Another option for obtaining reliable cVEMP responses is
using a maximum contraction method. In this method, the patient
is reclined to 308 recumbent (Fig. 2). From this position, the
patient is instructed to lift the head from the chair with the
assumption that the weight of the head remains the same for both
sidesdtherefore, the amount of SCM muscle contraction
between sides should be similar. This method has demonstrated
reliable responses with no significant amplitude differences noted
in control participants39,41 and has demonstrated significantly
FIG. 2. Common electrode placement for cervical vestibular
evoked myogenic potential (cVEMP) recording. In this montage, the
inverting electrode is on the forehead, noninverting on the upper
third of the sternocleidomastoid, and the ground on the dorsum.
There are several other options available that provide reliable
cVEMP responses.
higher response rates than other methods.42 As the underlying
EMG level obtained with the maximum contraction method is
expected to be greater than that obtained with setting a prede-
termined target EMG level (Fig. 3), the clinical values obtained
among these methods will vary. Establishing a standard protocol
within the clinical laboratory is important to understand when
otolith reflex pathway pathology may be present.
Interpretation
Cervical VEMP interpretation includes analysis of response
latency and amplitude. Two major latency components are
evaluated for cVEMP responses. The P1 component typically
occurs around 13 ms, whereas the following N1 component
occurs around 23 ms. These values are consistent between the
patient participation methods described above.10,39,43 Latency
does not shift with stimulus intensity changes or EMG level;
however, N1 latency may demonstrate a fatigue effect describing
reduced muscle drive associated with prolonged testing.40,44
P1-N1 amplitude is most commonly reported in relation to
otolith reflex pathway function. Cervical VEMP amplitude is

clinicalneurophys.com Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018 41

 J. M. Bogle Clinical Evaluation of the Vestibular Nerve

FIG. 3. Example of the effects of change of

prestimulus electromyography (EMG) level
on raw cervical vestibular evoked myogenic
potential (cVEMP) amplitude using
a maximum contraction participation
method. A, Prestimulus EMG values
between 40 and 70 mV, providing a P1-N1
amplitude of 90 mV. B, EMG values between
100 and 130 mV, providing an increased
N1-P1 amplitude value of 264.91 mV. No
significant changes in latency values were
noted.

a summation of saccule/inferior vestibular nerve function, Ocular Vestibular Evoked Myogenic Potentials
intensity of the stimulus, and muscle drive. Care must be taken Ocular vestibular evoked myogenic potentials (oVEMPs)
when recording cVEMPs as any of these factors may lead to are a more recently described response. Ocular VEMPs are
reduced response amplitude. There is a wide variability in obtained from the contralateral inferior oblique muscle, describ-
reported P1-N1 amplitudes, especially when various participation ing an excitation of the translational vestibulo-ocular reflex.50
methods are compared. For those methods with a specified EMG Ocular VEMPs are often multiphasic; however, the primary
target level, response amplitudes tend to be smaller than those biphasic response is typically reported (Fig. 4).
obtained with the maximum contraction method.37,40,45 Because Evidence from human and animal models hypothesizes that
of this, various methods of amplitude normalization have been the utricle is the primary end organ responsible for oVEMP
reported. Some laboratories have the capability to normalize the generation. From the peripheral end organ, the oVEMP pathway
response amplitude by the prestimulus EMG level. In these cases, travels through the superior branch of CN VIII to Scarpa’s
the averaged prestimulus EMG level is used to adjust the ganglion, terminating within the vestibular nuclei. The ascending
resulting response amplitude, theoretically providing a method pathway crosses through the medial longitudinal fasciculus to the
for controlling fatigue and other interpatient differences. Some motonucleus of CN III and finally to the contralateral inferior
methods provide real-time rectification of the prestimulus interval oblique muscle. This pathway describes the utriculo-ocular reflex
and apply this value to each individual epoch,4 whereas others pathway. As this pathway is stimulated, the resulting recording is
provide a post hoc normalization based on the averaged prestimulus an excitation of the inferior oblique muscle.31,51,52
EMG level. These measures have demonstrated effectiveness for
some studies in adjusting for the underlying EMG level.46,47
Specifically, these methods may work well when evaluating Method
responses with lower prestimulus EMG levels, e.g., those obtained Numerous protocols are available for oVEMP recording.
using pre-set EMG targets. There is evidence, however, that this Tables 1 and 2 provide commonly used stimulus and recording
response may not demonstrate a linear growth function. As the parameters for oVEMPs. The remaining method discussion
underlying EMG level increases, the resulting amplitude saturates.
This has been described especially when using strong muscle
contractions.23,37,45,48
Inner ear asymmetry is often considered in the vestibular
diagnostic laboratory as an indicator of pathology. Amplitude
asymmetry ratio is a metric used to evaluate the difference in
cVEMP response between sides (amplitude asymmetry ¼ [right
amplitude 2 left amplitude]/[right amplitude 1 left amplitude]).
This is a useful metric due to the high variability of amplitudes
noted in this response, but it is influenced by SCM muscle
fatigue. Clinical laboratory normative data often report appro-
priate amplitude asymmetry ratios as less than approximately
47%.39,44,46
Threshold describes the lowest stimulus intensity needed to
record a reliable response. Threshold is a function of several
factors, including the health of the saccule/inferior vestibular
nerve and underlying EMG level. Determining the specific
threshold in general is not useful in evaluating this response FIG. 4. Typical ocular vestibular evoked myogenic potential
with some exception, as in the presence of third window (oVEMP) response using 500 Hz toneburst stimuli (122 dB SPL, 4 ms
disorders which are described later. Control participants demon- duration, Blackman gating, 5 Hz rate). Response demonstrates
strate typical thresholds of 100 to 120 dB SPL with differences of appropriate latencies (N1 ¼ 11.13 ms, P1 ¼ 16.21 ms) and
10 dB or less between sides.49 amplitude value (N1-P1 amplitude ¼ 8.37 mV).

42 Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018 clinicalneurophys.com

 Clinical Evaluation of the Vestibular Nerve
will focus on parameters that may lead to variability in
oVEMP data.
Electrode Placement
Ocular VEMPs can be recorded using a one- or two-channel
montage. Noninverting electrodes are placed under each eye
somewhat laterally to better position the electrode over the
inferior oblique motor point (Fig. 5).53 The inverting electrode
may be placed on the nose,54 chin,1 or inner canthus.53 Response
contamination should be considered when determining appropri-
ate inverting electrode placement. Nearby reference electrode
positions, such as directly under the noninverting electrode, may
lead to phase cancellation, significantly reducing the amplitude
by as much as 30%.36,55 The ground electrode may be placed on
the forehead, sternum, dorsum, or elsewhere as needed
Presentation
Unilateral or bilateral oVEMP recordings are feasible for
air-conducted stimuli. Because the translational vestibulo-ocular
reflex is mostly a crossed reflex and because of the consistent
FIG. 5. Common electrode placement for ocular vestibular evoked
myogenic potential (oVEMP) recording. In this montage, the
noninverting electrode is placed laterally on the belly of each
inferior oblique muscle, inverting on the chin, and the ground on
the forehead. There are several other options available that provide
reliable oVEMP responses.
clinicalneurophys.com Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018
J. M. Bogle
binocular eye position, it is possible to record simultaneous
oVEMPs; however, there may be some interaction when using
a binaural acoustic stimulus due to interference from ipsilateral
utricular projections.56 Research has found that binaural stimu-
lation can produce increased amplitudes and response prevalence
at low repetition rates and reduce asymmetry ratios.56,57 How-
ever, binaural stimulation has been associated with reduced
response prevalence at higher stimulus repetition rates when
compared with monaural stimulation. It is important to maintain
a lower stimulation rate (#5 Hz) for consistent binaural
responses and consider the underlying effects of possible
ipsilateral utricular involvement in the response.57
Gaze Effect
Patient participation is much reduced for oVEMP testing,
but not eliminated. Ocular VEMP protocols require some level of
gaze elevation to reliably record these responses. In general,
oVEMP response amplitude increases with increasing gaze up to
358, but with no significant difference between 358 and at
a “maximum” gaze angle.58
Interpretation
Ocular VEMP interpretation includes analysis of response
latency and amplitude. While oVEMPs may be multiphasic, two
major latency components are evaluated for oVEMP responses.
These latencies will vary with stimulus typedair-conduction
stimuli demonstrate later responses than bone-conduction
because of the reduced efficiency of this stimulus. For air-
conducted stimuli, the N1 component occurs around 12 ms with
the following P1 component occurring around 17 ms. Interpeak
latencies should remain below 7 ms.55 Bone-conduction stimuli
typically produce shorter-latency responses, generally noted to
begin around 8 ms.59
N1-P1 amplitude is commonly reported in relation to otolith
reflex pathway function. Ocular VEMP amplitude is described as
a summation of utricule/superior vestibular nerve function,
intensity of the stimulus, and muscle drive. Again, care must
be taken when recording these responses because any of these
factors may lead to reduced amplitude or absent responses.
Importantly, the patient must maintain appropriate eye gaze
position for reliable responses. Typical response amplitude varies
with stimulus type (air-vs. bone-conduction), electrode montage,
and gaze elevation. Establishing clinical normative data is
important to appropriately evaluate this response. For typical
air-conducted stimuli (500 Hz), average amplitudes of approx-
imately 4 mV are reported,55 while bone-conducted stimuli
provide average amplitudes of approximately 15 mV.54
Ocular VEMP amplitude asymmetry is often considered to
be an indicator of pathology. Amplitude asymmetry ratio is
a metric used to evaluate the difference in response between sides
(amplitude asymmetry ¼ [right amplitude 2 left amplitude]/
[right amplitude 1 left amplitude]). Asymmetry because of
muscle contraction is less concerning for oVEMP testing, and
fatigue is generally not considered a significant issue. Clinical
laboratory normative data often report appropriate amplitude
asymmetry ratios of less than approximately 34%.55
43
 J. M. Bogle
Threshold is a function of several factors, including health
of the utricle/superior vestibular nerve and underlying EMG level
(i.e., gaze position). Determining this specific value in general is
not useful in evaluating this response, with some exception as in
the presence of third window disorders to be described later.
Typical oVEMP thresholds range between 100 to 120 dB SPL.55
Clinical Applications
Vestibular evoked myogenic potentials are commonly used
clinical measures of otolith reflex pathway function. The following
will briefly describe common findings for patients with conditions
affecting the peripheral and central vestibular systems, as well as the
effect of aging.
Peripheral Vestibular Considerations
Peripheral vestibulopathy has been historically limited to
lateral semicircular canal function, evaluating the superior
vestibular nerve and angular vestibulo-ocular reflex pathway.
Additional information obtained from otolith reflex testing has
expanded our understanding of peripheral disorders.
Third Window Disorders
Vestibular evoked myogenic potentials are commonly used
to evaluate patients suspected of having third window disorders,
such as superior semicircular canal dehiscence, with abnormal
VEMPs considered a defining characteristic of these disorders.
An unanticipated opening into the vestibular labyrinth creates an
amplified response to acoustic or mechanical VEMP stimuli,
leading to significantly more robust VEMP responses.60 In these
cases, it may be expected for VEMP thresholds to be approx-
imately 20 dB below typical responses. Interpeak amplitude is
also an important marker for possible third window pathology,
especially for oVEMP responses. Patients with known third
window disorders have demonstrated oVEMP interpeak ampli-
tudes of 12 times those of control patients. Further exploration of
these responses has found that as stimulus energy is uncommonly
shunted through the labyrinth, a typically inappropriate stimulus
frequency (e.g., 4,000 Hz) may provide a simple method to
evaluate a patient for suspected third window disorders. Manzari
et al61 noted that 100% of patients with diagnosed third window
disorder demonstrated present responses to 4,000 Hz air-
conducted oVEMP stimuli; no control patients had responses
to this frequency.
Méniere Disease
Méniere disease is an acquired inner ear disorder associated
with both hearing and vestibular dysfunction due to an abnormal
accumulation of endolymph. Vestibular evoked myogenic poten-
tial responses in patients with Méniere disease are varied, likely
because of the progressive nature of the disorder. Reduced
amplitudes for both cVEMP and oVEMP have been noted, as
well as prolonged cVEMP latencies and significant oVEMP
threshold elevations in some patients, but not for all. There is
notable overlap in VEMP responses for patients with Méniere
disease and controls, which does limit the diagnostic utility of
using VEMP testing alone as a diagnostic metric for dysfunc-
tion.62 Further exploration of improving the sensitivity of VEMP
44 Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018
Clinical Evaluation of the Vestibular Nerve
testing for those with Méniere disease has evaluated a possible
change in frequency tuning. As the frequency tuning of the
otolith organs is related to size, location, and inner ear fluid
pressure,1,9,13 alterations in these may lead to variability in the
VEMP tuning curve. Although most VEMP literature uses low-
frequency stimuli, dilation of the inner ear due to excessive
endolymph accumulation and increased inner ear pressure may
alter the frequency tuning of the inner ear. Maxwell et al63
reported using VEMP amplitude ratios for 500 and 1,000 Hz
stimuli, noting reasonable accuracy in identifying patients with
clinically certain Méniere disease. These findings suggest that
evaluation at higher frequencies (e.g., 1,000 Hz) may provide
insight into evaluating patients with questionable Méniere
disease.
Neural Transduction Considerations
The otolith reflex pathways are not solely used to evaluate
the peripheral vestibular end organs. Vestibular evoked myo-
genic potentials are reflexes and as such can be used to describe
abnormalities along the complete reflex arc. Additional work has
been completed to evaluate the usefulness of VEMP responses in
cases of abnormal neural transmission.
Vestibular Neuritis
Vestibular neuritis is a unilateral vestibulopathy that
presents with a sudden episode of vertigo and imbalance.
Vestibular evoked myogenic potentials have been important in
evaluating this condition, as specific information regarding the
status of both the superior and inferior branches of the vestibular
nerve can be evaluated. Vestibular neuritis generally affects the
superior branch of the vestibular nerve and can be evaluated
using oVEMPs as well as other measures of vestibulo-ocular
reflex function (e.g., caloric testing, head impulse testing). A
smaller portion of patients with acute vertiginous symptoms may
present with vestibular neuritis, specifically affecting the inferior
branch of the vestibular nerve. These unique cases present with
isolated abnormalities of the inferior nerve branch (i.e., cVEMP,
posterior semicircular canal head thrust test), and require
investigation of inferior nerve branch function to improve patient
management.64
Vestibular Schwannoma
Vestibular schwannoma is a histologically benign tumor that
arises from the Schwann cells of either branch of the vestibular
nerve as it courses through the internal auditory canal. Current
literature is not clear as to the typical clinical diagnostic
presentation of this disorder; however, dizziness, imbalance
and asymmetric hearing loss are common. Generally, oVEMPs
are reported as more sensitive to vestibular schwannoma than
cVEMPs but inclusion of both otolith reflex evaluations, along
with diagnostic hearing testing (i.e., cochlear nerve branch), can
provide information about the breadth of function of CN VIII.
Vestibular evoked myogenic potential involvement of either
branch of the vestibular nerve has been described for up to
approximately 80% of patients with known vestibular schwan-
noma; unfortunately, there are reported cases of known tumor
with normal VEMP responses.65
clinicalneurophys.com
 Clinical Evaluation of the Vestibular Nerve
Central Vestibulopathy Considerations
Numerous studies have evaluated central vestibulopathy
using VEMP methodology. Currently, there is conflicting
evidence for many conditions, including specific cerebellar and
brainstem infarcts and cerebellar ataxia; however, a lesion
anywhere along the utriculo-ocular or sacculo-collic reflex
pathways may affect the VEMP. Localization of the lesion is
key to VEMP interpretation, as VEMPs will only be impacted in
cases where the lesion influences the otolith reflex pathways. For
example, although cVEMPs may be quite helpful in documenting
abnormality in patients with lesions affecting the lower pons and/
or upper medulla, it is less useful in documenting abnormalities
of the midbrain.66 Conversely, oVEMPs are more likely to detect
midbrain lesions, as well as pontine and medullary involve-
ment.67 Further exploration will prove useful in determining the
sensitivity of VEMP to these specific lesions.
Multiple Sclerosis
Dizziness is commonly reported by patients with multiple
sclerosis, even when clear lesions are not noted on imaging.
Vestibular evoked myogenic potential responses demonstrate
a variety of abnormalities, with prolonged latencies and absent
responses as the most commonly reported likely because of
expected damage to the myelin sheaths or axons. Up to 50% of
cVEMP responses in individuals with central demyelinating disease
are described as abnormal.68,69 Ocular VEMPs may provide
additional information regarding neural integrity, especially along
the medial longitudinal fasciculus and ocular pathways. Gabelic
et al68 reported that up to 70% of patients with multiple sclerosis
have demonstrated abnormal oVEMP response latency or absent
waveforms. This finding is in line with additional reports demon-
strating that 85% of patients with internuclear ophthalmoplegia,
common in multiple sclerosis, present with abnormal oVEMPs.70 It
is feasible that VEMPs may be used to supplement diagnostic
management and to monitor disease progression in patients with
multiple sclerosis.
Migraine
Dizziness is commonly reported in patients with a headache
history, and vestibular migraine is believed to be a common
cause of vertigo. The clinical presentation of patients with
suspected vestibular migraine is variable. General imbalance is
reported in over half of patients, whereas a sense of rotational
(50%) or “rocking” (35%) vertigo is common.71 Vestibular
evoked myogenic potentials have been used to evaluate patients
with migraine, especially for those presenting with dizziness.
Vestibular evoked myogenic potentials can demonstrate abnor-
malities in amplitude, asymmetry ratio, and response prevalence.
Zaleski et al71 reported the VEMP profiles of patients with
diagnosed vestibular migraine, finding that while 8% of patients
demonstrated abnormalities in cVEMP responses, 61% of
oVEMP responses were abnormal (30% bilaterally absent, 31%
significantly asymmetric). The underlying pathophysiology for
these abnormalities has not been described, but these results
suggest that the translational vestibulo-ocular reflex pathway may
be especially vulnerable to dysfunction associated with vestibular
migraine.
clinicalneurophys.com Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018
J. M. Bogle
Aging Considerations
With increasing age, VEMPs become less sensitive. Even
when controlling for underlying EMG level (i.e., possible decrease
in muscle tone), adults older than 60 years are less likely to
demonstrate reliable responses or may produce responses signifi-
cantly reduced from their younger counterparts.10,15 Interpretation of
data for those over 60 years of age, therefore, becomes more
complicated because an absent response noted on VEMP testing
may or may not be related to an underlying abnormality contributing
to symptoms of dizziness or imbalance.
Limitations
Vestibular evoked myogenic potentials are commonly used
measures of otolith reflex pathway function and provide information
not otherwise available in the clinical setting. There are important
considerations for VEMP interpretation. As many clinics have
access to air-conducted stimuli, understanding the health of the
auditory system is important for VEMP interpretation because
conductive hearing loss can lead to significant alteration of these
responses. Unfortunately, the high intensity needed for air-
conducted stimuli limits the use of VEMP for patients with
sensitivity to loud sounds. Care should be taken to minimize the
stimulus intensity for these patients or consider alternative stimulus
modalities. Importantly, VEMPs are measures of a reflex pathway,
and as such, are nonspecific. An abnormality anywhere along the
otolith reflex pathway can lead to alteration of this response.
Incorporating these considerations along with the patient’s medical
history and clinical presentation allow for more appropriate VEMP
interpretation.
CONCLUSIONS
Vestibular evoked myogenic potentials are clinical diagnos-
tic measures providing information regarding the otolith reflex
pathways. Vestibular evoked myogenic potentials are an impor-
tant addition to the vestibular laboratory as they allow for
documentation of the vestibulo-collic and translational vestibulo-
ocular reflex pathways. These responses provide further infor-
mation regarding the status of the peripheral and central
vestibular systems across a wide range of pathologies.
REFERENCES
1. Jacobson G, Shepard N. Balance Function Assessment and Management.
2nd ed. San Diego: Plural, 2016.
2. Bickford R, Jacobson J, Cody D. Nature of average evoked potentials to
sound and other stimuli in man. Ann N Y Acad Sci 1964;112:204–223.
3. Colebatch J, Halmagyi M. Vestibular evoked myogenic potentials in
human neck muscles before and after unilateral vestibular deafferenta-
tion. Neurology 1992;42:1635–1636.
4. Colebatch J, Halmagyi G, Skuse N. Myogenic potentials generated by
a click-evoked vestibulocollic reflex. J Neurol Neurosurg Psychiatry
1994;57:190–197.
5. Sheykholeslami K, Murofushi T, Kermany M, Kaga K. Bone-conducted
evoked myogenic potentials from the sternocleidomastoid muscle. Acta
Otolaryngol 2000;120:731–734.
6. Welgampola M, Colebatch J. Characteristics and clinical applications of
vestibular-evoked myogenic potentials. Neurology 2005;64:1682–1688.
45
 J. M. Bogle
7. Cheng PW, Chen CC, Wang SJ, Young YH. Acoustic, mechanical and
galvanic stimulation modes elicit ocular vestibular-evoked myogenic
potentials. Clin Neurophysiol 2009;120:1841–1844.
8. McCue M, Guinan J. Spontaneous activity and frequency selectivity of
acoustically responsive vestibular afferents in the cat. J Neurophysiol
1995;74:1563–1572.
9. Todd N, Cody F, Banks J. A saccular origin of frequency tuning in
myogenic evoked potentials: implications for human responses to loud
sounds. Hear Res 2000;141:180–188.
10. Janky K, Shepard N. Vestibular evoked myogenic potential (VEMP)
testing: normative threshold response curves and effects of age. J Am
Acad Audiol 2009;20:514–522.
11. de Oliveira Barreto A, Colafemina J, de Lemos Menezes P. Saccular
sensitivity function measured by vestibular evoked myogenic potential.
Acta Otolaryngol 2011;131:618–623.
12. Sheykholeslami K, Kermany M, Kaga K. Frequency sensitivity range of
the saccule to bone-conducted stimuli measured by vestibular evoked
myogenic potentials. Hear Res 2001;160:58–62.
13. Todd N, Rosengren S, Govender S, Colebatch J. Low-frequency tuning
in the human vestibular-ocular projection is determined by both
peripheral and central mechanisms. Neurosci Lett 2009;458:43–47.
14. Murnane O, Akin F, Kelly K, Byrd S. Effects of stimulus and recording
parameters on the air conduction ocular vestibular evoked myogenic
potential. J Am Acad Audiol 2011;22:469–480.
15. Piker E, Jacobson G, Burkard R, McCaslin D, Hood L. Effects of
age on the tuning of the cVEMP and oVEMP. Ear Hear 2013;34:
e65–e73.
16. Govender S, Fernando T, Dennis D, Welgampola M, Colebatch J.
Properties of 500 Hz air- and bone-conducted vestibular evoked
myogenic potentials (VEMPs) in superior canal dehiscence. Clin
Neurophysiol 2016;127:2522–2531.
17. Krause E, Mayerhofer A, Gurkov R, et al. Effects of acoustic stimuli
used for vestibular evoked myogenic potential studies on cochlear
function. Otol Neurotol 2013;34:1186–1192.
18. Papathanasiou E, Murofushi T, Akin F, Colebatch J. International
guidelines for the clinical application of cervical vestibular evoked
myogenic potentials: an expert consensus report. Clin Neurophysiol
2014;125:658–666.
19. Piker E, Baloh R, Witsell D, Garrison D, Lee W. Assessment of the
clinical utility of cervical and ocular vestibular evoked myogenic
potential testing in elderly patients. Otol Neurotol 2015;36:1238–1244.
20. Portnuff C, Kleindienst S, Bogle J. Safe use of acoustic vestibular-
evoked myogenic potential stimuli: protocol and patient-specific con-
siderations. J Am Acad Audiol 2017;28:708–717.
21. Ackley R, Tamaki C, Oliszewski C, Inverso D. Vestibular evoked
myogenic potential assessment of deaf and hard of hearing patients.
Insights in Practice: Clinical Topics in Otoneurology. GN Otometrics
2004.
22. Mahdi P, Amali A, Pourbakht A, Yazdi A, Bassam A. Vestibular evoked
myogenic potential produced by bone-conducted stimuli: a study on its
basics and clinical applications in patients with conductive and
sensorineural hearing loss and a group with vestibular schwannoma.
Iran J Otorhinolaryngol 2013;25:141–146.
23. McNerney K, Burkard R. The vestibular evoked myogenic potential
(VEMP): air- versus bone-conducted stimuli. Ear Hear 2011;32:e6–e15.
24. Welgampola M, Rosengren S, Halmagyi M, Colebatch J. Vestibular
activation by bone conducted sound. J Neurol Neurosurg Psychiatry
2003;74:771–778.
25. Nguyen K, Welgampola M, Carey J. Test-retest reliability and age-
related characteristics of the ocular and cervical vestibular evoked
myogenic potential tests. Otol Neurotol 2010;31:793–802.
26. Halmagyi M, Yarvor R, Colebatch J. Tapping the head activates the
vestibular system: a new use for the clinical reflex hammer. Neurology
1995;45:1927–1929.
27. Iwasaki S, McGarvie L, Halmagyi M, et al. Head taps evoke a crossed
vestibulo-ocular reflex. Neurology 2007;68:1227–1229.
28. Colebatch J, Rothwell J. Motor unit excitability changes mediating
vestibulocollic reflexes in the sternocleidomastoid muscle. Clin Neuro-
physiol 2004;115:2567–2573.
29. Wit H, Kingma C. A simple model for the generation of the
vestibular evoked myogenic potential (VEMP). Clin Neurophysiol
2006;117:1354–1358.
30. Carey J, Amin N. Evolutionary changes in the cochlea and labyrinth:
solving the problem of sound transmission to the balance organs of
46 Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018
Clinical Evaluation of the Vestibular Nerve
the inner ear. Anat Rec A Discov Mol Cell Evol Biol 2006;288:482–
489.
31. Curthoys I. A critical review of the neurophysiological evidence
underlying clinical vestibular testing using sound, vibration and galvanic
stimuli. Clin Neurophysiol 2010;121:132–144.
32. Kushiro K, Zakir M, Ogawa Y, Sato H, Ushino Y. Saccular and utricular
inputs to sternocleidomastoid motoneurons of decerebrate cats. Exp
Brain Res 1999;126:410–416.
33. Murofushi T, Curthoys I. Physiological and anatomical study of click-
sensitive primary vestibular afferents in the Guinea pig. Acta Otolar-
yngol 1997;117:66–72.
34. Fitzgerald M, Comerford P, Tuffery A. Sources of innervation of the
neuromuscular spindles in sternomastoid and trapezius. J Anat
1982;134:471–490.
35. Krause H, Bremerich A, Herrmann M. The innervation of the trapezius
muscle in connection with radical neck-dissection. J Craniomaxillofac
Surg 1991;19:87–89.
36. Rosengren S, Todd N, Colebatch J. Vestibular-evoked extraocular
potentials produced by stimulation with bone-conducted sound. Clin
Neurophysiol 2005;116:1938–1948.
37. Bogle J, Zapala D, Criter R, Burkard R. The effect of muscle contraction
level on the cervical vestibular evoked myogenic potential (cVEMP):
usefulness of amplitude normalization. J Am Acad Audiol
2013;24:77–88.
38. Vanspauwen R, Wuyts F, van de Heyning P. Improving vestibular
evoked myogenic potential reliability by using a blood pressure
manometer. Laryngoscope 2006;116:131–135.
39. Isaradisaikul S, Strong D, Moushey J, Gabbard S, Ackley R, Jenkins H.
Reliability of vestibular evoked myogenic potentials in healthy subjects.
Otol Neurotol 2008;29:542–544.
40. Akin F, Murnane O, Panus P, Caruthers S, Wilkinson A, Proffitt T. The
influence of voluntary tonic EMG level on the vestibular-evoked
myogenic potential. J Rehabil Res Dev 2004;41:473–480.
41. Bush M, Jones R, Shinn J. The clinical reliability of vestibular evoked
myogenic potentials. Ear Nose Throat J 2010;89:170–176.
42. Wang CT, Young YH. Comparison of the head elevation versus rotation
methods in eliciting vestibular evoked myogenic potentials. Ear Hear
2006;27:376–381.
43. Beyea J, Zeitouni A. Vestibular evoked myogenic potentials in healthy
control subjects using the head rotation method. J Otolaryngol Head
Neck Surg 2008;37:522–527.
44. Zapala D, Brey R. Clinical experience with the vestibular evoked
myogenic potential. J Am Acad Audiol 2004;15:198–215.
45. McCaslin D, Fowler A, Jacobson G. Amplitude normalization reduces
cervical vestibular evoked myogenic potential (cVEMP) amplitude
asymmetries in normal subjects: proof of concept. J Am Acad Audiol
2014;25:268–277.
46. Kim K, Jung J, Lee J, Suh M. Capacity of rectified vestibular evoked
myogenic potential in correcting asymmetric muscle contraction power.
Clin Exp Otorhinolaryngol 2013;6:209–213.
47. Lee K, Kim M, Son E, Lim H, Bang J, Kang J. The usefulness of
rectified VEMP. Clin Exp Otorhinolaryngol 2008;1:143–147.
48. Rosengren S. Effects of muscle contraction on cervical vestibular evoked
myogenic potentials in normal subjects. Clin Neurophysiol
2015;126:2198–2206.
49. Isaradisaikul S, Navacharoen N, Hanprasertpong C, Kangsanarak J.
Cervical vestibular evoked myogenic potentials: norms and protocols. Int
J Otolaryngol 2012;2012:913515.
50. Weber K, Rosengren S, Michels R, Sturm V, Straumann D, Landau K.
Single motor unit activity in human extraocular muscles during the
vestibulo-ocular reflex. J Physiol 2012;590:3091–3101.
51. Curthoys I, Manzari L. Evidence missed: ocular vestibular-evoked
myogenic potentials differentiate utricular from saccular function.
Otolaryngol Head Neck Surg 2011;144:751–752.
52. Iwasaki S, Chihara Y, Smulders Y, et al. The role of the superior
vestibular nerve in generating ocular vestibular-evoked myogenic
potentials to bone conducted vibration at FZ. Clin Neurophysiol
2009;120:588–593.
53. Sandhu J, George S, Rea P. The effect of electrode positioning on the
ocular vestibular evoked myogenic potential to air-conducted sound.
Clin Neurophysiol 2013;124:1232–1236.
54. Vanspauwen R, Wuyts F, Krijger S, Maes L. Comparison of different
electrode configurations for the oVEMP with bone-conducted vibration.
Ear Hear 2017;38:205–211.
clinicalneurophys.com
 Clinical Evaluation of the Vestibular Nerve
55. Piker E, Jacobson G, McCaslin D, Hood L. Normal characteristics of the
ocular vestibular evoked myogenic potential. J Am Acad Audiol
2011;22:222–230.
56. Iwasaki S, Egami N, Inoue A, et al. Ocular vestibular evoked myogenic
potential elicited from binaural air-conducted stimulations: clinical
feasibility in patients with peripheral vestibular dysfunction. Acta
Otolaryngol 2013;133:708–713.
57. Bogle J, Zapala D, Burkhardt B, et al. The effect of repetition rate on air-
conducted ocular vestibular evoked myogenic potentials (oVEMPs). Am
J Audiol 2015;24:411–418.
58. Kantner C, Gurkov R. The effects of commonly used upward gaze
angles on ocular vestibular evoked myogenic potentials. Otol Neurotol
2014;35:289–293.
59. Iwasaki S, Smulders Y, Burgess A, et al. Ocular vestibular evoked
myogenic potentials to bone conducted vibration of the midline forehead
at Fz in health subjects. Clin Neurophysiol 2008;119:2135–2147.
60. Zuniga M, Janky K, Nguyen K, Welgampola M, Carey J. Ocular versus
cervical VEMPs in the diagnosis of superior semicircular canal
dehiscence syndrome. Otol Neurotol 2013;34:121–126.
61. Manzari L, Burgess A, McGarvie L, Curthoys I. An indicator of probable
semicircular canal dehiscence: ocular vestibular evoked myogenic
potentials to high frequencies. Otolaryngol Head Neck Surg
2013;149:142–145.
62. Johnson S, O’Beirne G, Lin E, Gourley J, Hornibrook J. oVEMPs and
cVEMPs in patients with “clinically certain” Meniere’s disease. Acta
Otolaryngol 2016;136:1029–1034.
clinicalneurophys.com Journal of Clinical Neurophysiology Volume 35, Number 1, January 2018
J. M. Bogle
63. Maxwell R, Jerin C, Gurkov R. Utilisation of multi-frequency VEMPs
improves diagnostic accuracy for Meniere’s disease. Eur Arch Otorhi-
nolaryngol 2017;274:85–93.
64. Kim J, Kim H. Inferior vestibular neuritis. J Neurol 2012;259:1553–
1560.
65. Chiarovano E, Darlington C, Vidal PP, Lamas G, de Waele C. The role of
cervical and ocular vestibular evoked myogenic potentials in the assessment
of patients with vestibular schwannomas. PLoS One 2014;9:e105026.
66. Itoh A, Kim Y, Yoshioka K, et al. Clinical study of vestibular-evoked
myogenic potentials and auditory brainstem responses in patients with
brainstem lesions. Acta Otolaryngol Suppl 2001;545:116–119.
67. Oh S, Kim J, Lee J, et al. Ocular vestibular evoked myogenic potentials
induced by air-conducted sound in patients with acute brainstem lesions.
Clin Neurophysiol 2013;124:770–778.
68. Gabelic T, Krbot M, Sefer A, Isgum V, Adamec I, Habek M. Ocular and
cervical vestibular evoked myogenic potentials in patients with multiple
sclerosis. J Clin Neurophysiol 2013;30:86–91.
69. Versino M, Colnaghi S, Callieco R, Bergamaschi R, Romani A, Cosi V.
Vestibular evoked myogenic potentials in multiple sclerosis patients.
Clin Neurophysiol 2002;113:1464–1469.
70. Rosengren S, Colebatch J. Ocular vestibular evoked myogenic potentials
are abnormal in internuclear ophthalmoplegia. Clin Neurophysiol
2011;122:1264–1267.
71. Zaleski A, Bogle J, Starling A, et al. Vestibular evoked myogenic
potentials in patients with vestibular migraine. Otol Neurotol
2015;36:295–302.
47