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9
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Bedside Assessment of the
Vestibular System
Carrie W. Hoppes, Karen H. Lambert, and Devin L. McCaslin
INTRODUCTION AND HISTORY
“Bedside tests” of vestibular function are brief, informal assessments designed to help clinical neurophysiologists form hypotheses of what they will observe
during more formal quantitative testing. Alone, these
tests are capable of identifying relatively large asymmetries in unilateral vestibular impairments. They also
are valuable for quickly identifying patients with bilateral peripheral vestibular system impairments. As a
general statement, bedside tests can identify unilateral
vestibular impairments when caloric asymmetries are
approximately 40% to 50%. We describe in this chapter several of the most common and useful “bedside
tests” and present a brief description of their administration and interpretation. The majority of the chapter
describes what is currently known about the bedside
tests of the vestibular system but does not extend this
discussion to the evaluation of the oculomotor system,
as this topic is covered elsewhere in this text (see Chapters 3 and 10). Additionally, the sensitivity and specificity of each test is described along with the mechanism
of action of each test. Sensitivity is defined as the percentage of subjects known to be abnormal that produce an abnormal or positive test result. Specificity
is defined as the percentage of subjects known to be
normal who produce a normal or negative test result.
In 2013, members of the American Physical Therapy
Association’s Vestibular Evidence Database to Guide
Effectiveness (VEDGE) task force evaluated tests and
measures commonly used in the assessment of patients
with vestibular disorders. When available, the VEDGE
task force recommendation for each test is described.
EXAMINATION TO IDENTIFY SPONTANEOUS
VESTIBULAR
Introduction
The word nystagmus is derived from the Greek word
“nystazein” which translates to the word “nod.” This
refers to the situation when an individual is falling
asleep and the head drops down slowly and is followed
by the head being jerked quickly upward (i.e., mirroring the slow phase/fast phase of a beat of nystagmus).
Decades of research into this phenomenon has provided
investigators with a clear understanding of most types of
nystagmus. This chapter discusses vestibular nystagmus
only. This type of nystagmus is a cardinal sign indicating
that a static imbalance exists between the resting outputs
of the left and right peripheral vestibular systems.
Technique
Prior to beginning the search for spontaneous nystagmus (SN), a thorough history should be taken to determine whether the patient has any visual symptoms and
what, if any, other neurologic symptoms exist (Serra &
NYSTAGMUS
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Leigh, 2002). It is also advisable to compile and review
a list of the patient’s medications, as some can cause or
suppress nystagmus. Next, an evaluation of gross eye
movements is suggested. Specifically, check that the
patient has full range of movement for each eye and
record any evidence of strabismus (ocular misalignment). This can be performed by simply having the
patient follow the examiner’s finger in an “X” or “H”
pattern. Following this step, have the patient fixate on a
target that is at arm’s length away. Again, the examiner
can use a finger as the target. Similarly, the center gaze
subtest on an electronystagmography (ENG)/videonystagmography (VNG) test system light-bar provides a suitable target. If nystagmus is noted while the
patient is fixating on the target directly in front of him
or her, the amplitude and direction of nystagmus (vertical, horizontal, and torsional) should be recorded, as
should the presence of any differences in the nystagmus
between eyes. Once the search for SN has been completed with vision (in room light), VNG goggles should
be applied and the exam continued with vision denied.
When vision is denied, a patient no longer is capable
of using visual fixation mechanisms that activate subcortical inhibitory pathways connected to the vestibular nuclei (VN). This inhibitory action on the VN will
act significantly to suppress any vestibular-generated
SN. VNG goggles have been available for several years
and should be used whenever possible to help identify
nystagmus when vision is denied. Two primary advantages of infrared VNG goggles over traditional Frenzel
lenses are the following: (1) the patient cannot fixate
on anything inside the goggles as it is completely dark,
and (2) most systems allow the option to record so that
the eye movements can be further examined offline.
With vision denied and the patient sitting upright,
begin mental alerting tasks while examining the eyes
for any SN. If SN is noted with vision denied, again,
record the amplitude and direction of eye movements,
as well as any other characteristics (e.g., torsional components, whether right- or left-beating).
Results
Normal Result
No nystagmus is visible in room light or with vision
denied.
Abnormal Result
The direction of the fast phase and velocity (deg/s) of
the nystagmus should be documented as well as any
changes in these two parameters that occur with visual
fixation. Acute peripheral disorders of the labyrinth
and vestibular portion of the eighth nerve commonly
result in a direction-fixed horizontal-rotary nystagmus
the increases in amplitude when vision is denied.
For peripheral vestibular system impairments,
the nystagmus should increase in velocity when the
patient stares in the direction of the fast phase, become
smaller in velocity when the patient stares at midline,
and become smallest when the patient stares in the
direction of the slow phase. Those characteristics follow Alexander’s law (Alexander, 1912). It is important
that a comparison be made between nystagmus velocity with and without visual fixation, as central nervous
system disorders often produce nystagmus that is not
suppressed by fixation.
Mechanism
A primary function of the semicircular canals (SCCs)
is to transduce angular acceleration of the head into
a neural pattern that is routed through the vestibuloocular reflex (VOR). The VOR permits the maintenance
of clear vision during head movements. The SCCs are
organized in orthogonal planes allowing for a synergistic pairing between them. The vestibular nerves that
run from the SCCs to the vestibular nuclei maintain an
average baseline tonic firing rate of approximately 70
to 90 spikes per second (Goldberg & Fernandez, 1971).
When the head is accelerated in the plane of a particular
canal, the neurons connected to the canal of the leading
ear will assume a level of increased neural activity over
their resting rate. This is accompanied by a corresponding decrease in firing rate in the nerve associated with
the paired canal on the opposite side. This neural pattern is relayed rostrally through the central vestibular
system to the oculomotor nuclei, which provide tonus
to the oculomotor muscles. When an insult is incurred
by the peripheral vestibular system, specifically, to the
hair cells in the labyrinth or to the vestibular portion
of the eighth nerve, the tonic rate of firing is reduced on
the affected side. This unilateral loss of peripheral function creates an asymmetry in the tonic resting activity of the two peripheral vestibular systems similar to
that which normally occurs during movement of the
head. This asymmetry routed through the VOR results
in SN. This pathologic eye movement consists of a slow
conjugate deviation of the eyes away from the intact
side followed by a quick corrective movement toward
the side that has a level of increased neural firing. SN
is described by noting the direction of the fast phase,
even though it is the slow component that is generated
9. BEDSIDE ASSESSMENT OF THE VESTIBULAR SYSTEM 169
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by the vestibular system. SN due to an asymmetry in
the resting firing rate between the two end organs generates the illusion of rotary motion in the absence of
any head movement. Specifically, patients describe that
they feel as though they are rotating toward the intact
side. SN due to an acute loss of peripheral vestibular
function is primarily horizontal with a mild torsional
component.
Test Performance
The ability to identify SN following a unilateral vestibular system impairment is greatest within the first three
to seven days (Fetter & Dichgans, 1990). However, a
phenomenon known as vestibular compensation uses
a centrally mediated adaptive mechanism to restore
neural activity to the impaired side, which results in
a reduction in the amplitude of the SN and a cessation of the patient’s perception of vertigo. Depending
on the integrity of the neural structures responsible
for vestibular compensation, resolution of the SN may
take much longer (Cass, Kartush, & Graham, 1992; Furman, Balaban, & Pollack, 1997). Using SN to diagnose
an end-organ disorder is also complicated by the fact
that the damaged peripheral system can spontaneously
regain function and produce a paradoxical SN known
as recovery nystagmus that beats toward the affected
ear (Jacobson, Pearlstein, Henderson, Calder, & Rock,
1998; McClure & Lycett, 1978). Based on a study of
16 patients, recovery nystagmus should be considered
when the nystagmus is observed at a delayed time
point (17 days after onset), when there is a mismatch
between SN direction and canal paresis on caloric testing, and when there is high gain with contralesional
asymmetry on slow harmonic acceleration testing (Lee,
Son, Rah, Jung, & Suh, 2019). Vestibular compensation is dependent on factors such as the patient’s age
and activity level, the presence of one functioning end
organ, the patient’s use of vestibular suppressants, and
the presence of intact vestibular nuclei, posterior and
anterior vermis, flocculonodular lobe, and the inferior
olive (Igarashi & Ishikawa, 1985; Kaufman, Anderson, & Beitz, 1992). Due to the efficiency of vestibular
compensation, in most cases, unless a patient is seen
directly after the insult, there is a good chance there
will be no evidence of SN. Using the presence of SN
in room light as a bedside test to diagnose unilateral
vestibular dysfunction, therefore, is not recommended
without quantitative testing. The presence of SN demonstrating the characteristics described above is a good
sign that a peripheral asymmetry exists. However, due
to the intersubject variability and quality of central compensation mechanisms, it is impossible to determine the
degree and side of the impairment from the direction
of SN. There have been a few studies that have examined the sensitivity and specificity of SN for identifying
peripheral end-organ dysfunction (Table 9–1). Dayal,
Tarantino, Farkashidy, and Paradisgarten (1974) presented data from 302 patients with spontaneous, positional, or paroxysmal positional nystagmus. All of the
cases had a clinical diagnosis and there was no control
group. When only the peripheral disorders were examined, the presence of spontaneous activity was very low.
Table 9–1. Comparison of Studies Evaluating Spontaneous Nystagmus
Study n Controls Disorder Condition Sensitivity Specificity
Dayal, Tarantino,
Farkashidy, &
Paradisgarten (1974)
Guidetti, Monzani, &
Rovatti (2006)
Totals 963 48% 95%
302 0 Ménière’s 52% Could not
calculate
Labyrinthectomy 71% Could not
calculate
Acoustic neuroma 75% Could not
calculate
Vestibular neuritis 49% Could not
calculate
661 Peripheral Direct
observation
Vestibular Frenzel goggles 20% 96%
hypofunction VNG 48% 92%
19% 96%
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Specifically, the sensitivity of SN for Ménière’s disease
was 52%, for labyrinthectomy 71%, for acoustic neuroma 75%, and for vestibular neuritis 49%.
In a study by Guidetti, Monzani, and Rovatti
(2006), the sensitivity and specificity of SN to peripheral vestibular system hypofunction in 528 outpatients
and 133 control subjects was examined using three
methods. SN was identified using direct observation
in light, Frenzel lenses, and VNG. When patients with
peripheral vestibular impairments were examined for
SN using direct observation in light or wearing Frenzel
lenses, the sensitivity was low and there was no significant difference between the two methods. Specifically,
direct observation in light had a sensitivity of 19%,
whereas Frenzel lenses had a sensitivity of 20%. Both
techniques had a specificity of 96%. VNG, although
better, still only had a sensitivity of 48% and a specificity of 92%.
These findings suggest that using only the presence or absence of spontaneous nystagmus to diagnose
unilateral peripheral vestibular system hypofunction
(UVH) is unacceptable. Although the presence of SN
may lead an examiner to suspect UVH, the sensitivity
using the best techniques is less than 50%. As discussed
above, central compensation mechanisms among other
factors greatly influence whether SN will be observed.
Thus, when an organic vestibular disorder is suspected,
quantitative testing should be completed to confirm or
refute its existence.
THE HORIZONTAL HEAD-IMPULSE TEST
Introduction
a patient with bilateral peripheral vestibular loss will
exhibit abnormal catch-up saccades with head thrust
to either side. The HIT is now a routine component in
the bedside assessment of vestibular function that is
quickly and easily administered and interpreted. This
chapter addresses only the bedside version of the HIT
and not the video HIT (vHIT) that is described in depth
in Chapter 14.
Technique
To perform the test, the examiner gently grasps the
patient’s head and passively moves it through a low
amplitude, high velocity head turn (Figure 9–1). The
patient’s head should be tilted forward 30 degrees
in order to position the lateral SCCs coplanar to the
ground (Schubert, Tusa, Grine, & Herdman, 2004). The
head should be turned approximately 10 degrees off
center and then the patient is instructed to fixate on a
target (often the examiner’s nose) and maintain fixation
on it throughout the test. The examiner then gently
grasps the patient’s head on both sides and rapidly and
abruptly (>2000 deg/s2) rotates the patient’s head approximately 15 to 20 degrees to the midline, then repeats
the test on the other side. While the head is being rapidly turned the examiner observes the patient’s eyes to
confirm that they remain stationary on the target (a negative test). The examiner should be vigilant for a catchup saccade to refixate the target after the head movement is complete (a positive test). The direction of
testing should be randomized so that the patient cannot
predict the timing or direction of head turn, or a preplanned saccade might obscure a positive test result.
The head-impulse test (HIT) is a screening test that utilizes the oculocephalic response, or doll’s eye reflex,
to identify unilateral and bilateral peripheral vestibular system impairment. This reflex was originally
employed to identify vestibular function in comatose
or unresponsive patients (Fisher, 1969). In 1988, Halmagyi and Curthoys expanded the clinical utility of the
test with their description of its application in patients
with complete loss of labyrinth function. The ability,
or inability, of the patient to maintain fixation on a target during an extremely fast angular excursion of the
head can give the examiner some insight into the integrity of the lateral semicircular canal ipsilateral to the
direction of the head turn. As described in the initial
paper by Halmagyi and Curthoys (1988), a patient will
demonstrate an abnormal catch-up saccade when the
head is thrust toward the impaired side. It follows that
Results
Normal Result
A quick translation of a patient’s head to the patient’s
left should invoke a corresponding compensatory eye
movement to the right due to stimulation of the left
lateral SCC, and inhibition of the right lateral SCC.
This compensatory eye movement should be very
close to 180 degrees out of phase from the movement
of the head. Quick translation to the right will stimulate the right lateral SCC and inhibit the left lateral
SCC, resulting in a compensatory leftward eye movement to maintain the target on the fovea (Kelly, 1985).
When this occurs, fixation is maintained on the target
throughout the head acceleration (no catch-up saccade
is observed).
9. BEDSIDE ASSESSMENT OF THE VESTIBULAR SYSTEM 171
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Figure 9–1. A. The patient is instructed to fixate on a target directly in front of him or her. B. When the
patient’s head is rotated abruptly 15 to 20 degrees to one side the eyes should deviate 180 degrees
out of phase with the head thrust and remain fixed on the target. However, when the eyes cannot
maintain fixation on the target due to an impaired vestibular system, the eyes travel with the head
and come off the target. C.
to bring the eye back to the point of visual fixation.
In order to reacquire the target, a saccadic eye movement is generated
Abnormal Result
Damage to the left peripheral vestibular system will
result in a catch-up saccade to the right on left head
turn, and the maintenance of normal fixation through
a normal VOR with right head turn. The reverse is true
for damage to the right peripheral vestibular system.
Mechanism
While the horizontal VOR has been described in detail
in Chapter 1, this chapter describes the neural mechanism of the HIT using an adaptation of Halmagyi and
Curthoys’ (1988) description. It is important to remember that the two lateral SCCs are working in tandem
in a push-pull fashion and that the contribution and
integrity of both canals must be considered when
describing the mechanism of the HIT.
Gain is classically defined as output divided by
input. The purpose of the VOR is to keep an image centered on the retina when the head is moved. In order
to keep the eye stable and the retina on the target, output would have to be equal to input. If the input (head
impulse) matched output (VOR) perfectly, it would be
said to have gain of 1.
According to Halmagyi, Curthoys, and Cremer
(1990), when a high-frequency stimulus such as the
head impulse is applied to subjects with intact end
organs, the gain of the VOR in the yaw plane is very
close to 1 (0.94 ± 0.08 SD) at 122 deg/s head velocity.
Because the head movement is rapid (greater than
0.10 Hz) the VOR is evoked rather than the optokinetic
subsystem, resulting in a vestibular-driven compensatory eye movement that is close to 180 degrees out of
phase with the head movement. This has the effect of
keeping the retinas stable and on the target while the
head rotates around the eyes.
Halmagyi et al. (1990) have investigated the effect
of complete UVH on the HIT. When patients with a
complete loss of function of one end organ are subjected to the same head impulse as described above
(122 deg/s head velocity), the gain of the VOR has
been shown to drop to 0.20 (Halmagyi et al., 1990).
Thus, the electrical drive to the VOR is less than what
is necessary to maintain the 180 degree opposite phase
compensatory eye movement. Accordingly, a catchup saccade is required to bring the eye to the target. It
would be reasonable to expect that with complete unilateral loss of vestibular function on one side that VOR
gain would decrease to zero when the head is thrust
toward the impaired side. The reason the drop in gain
is not zero is that there are contributions to the VOR
from the contralateral end organ. Although the exact
neural mechanism is not completely understood, if the
head is turned toward the ipsilesional side, which in
this example is the right, utriculofugal endolymph flow
in the left lateral SCC will result in inhibition of the
172 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
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intact lateral SCC and become the primary (although
inefficient) source of drive toward the impaired side.
Halmagyi et al. (1990) suggest that as this utriculofugal
response from the intact side is so small, it is unlikely
to be an integral part of the bilaterally generated VOR.
Test Performance
An extensive body of literature exists concerning the
sensitivity and specificity of the HIT for identifying
lateral SCC paresis. The function of the lateral canal
can be assessed easily in the laboratory using caloric
testing and/or rotational testing. As such, most investigations have been designed using the bithermal caloric
test as the gold standard against which the HIT is compared. What must be kept in mind when reviewing the
relationship between caloric responses and the HIT is
that the two tests employ stimuli that are at opposite
ends of the frequency spectrum. The caloric response
is analogous to a rotational stimulus of 0.003 Hz (i.e.,
one cycle every 5.5 min), whereas the HIT represents
a high-frequency movement characteristic of those
occurring in everyday life. This is important to know,
as peripheral vestibular system disorders affect the
low-frequency spectrum earlier, and more severely,
than the high-frequency spectrum (Angelaki & Perachio, 1993). This phenomenon greatly favors the caloric
response being more sensitive than the HIT to peripheral vestibular impairment.
In the original description of the HIT by Halmagyi and Curthoys (1998), 12 experimental subjects who
had undergone unilateral vestibular neurectomy were
compared with a control group of 12 neurologically
intact subjects. Patients who have undergone a nerve
section surgical procedure usually have a complete loss
of vestibular function on the affected side. The initial
report described the HIT as having 100% sensitivity
and specificity. Subsequent studies examining the HIT
in patients with nerve sections also demonstrated high
degrees of sensitivity and specificity (Cremer et al.,
1998; Foster, Foster, Spindler, & Harris, 1994; Halmagyi,
Black, Thurtell, & Curthoys, 2003; Lehnen, Aw, Todd,
& Halmagyi, 1994). However, for any bedside test to
be considered useful to the clinician, it must have a
high sensitivity and specificity in a broader population. Although the previous studies demonstrated the
HIT to be highly sensitive and specific in subjects with
complete vestibular end-organ damage, the majority of patients who present to a dizziness clinic will
have UVH of varying magnitudes. Studies in Table 9–2
illustrate how the magnitude of UVH as represented
by unilateral caloric weakness is highly predictive of
whether an abnormal HIT will be observed. Whereas
the majority of the literature suggests that the sensitivity of the HIT increases as the degree of peripheral
vestibular system hypofunction increases, it can be
observed from the studies illustrated in Table 9–2 that
if a patient demonstrates a caloric asymmetry exceeding 40%, there is a high probability that the patient
will exhibit an abnormal HIT result regardless of the
technique used (Beynon, Jani, & Baguley, 1998; Harvey, Wood, & Feroah, 1997; Perez & Rama-Lopez, 2003;
Shepard, 1998). However, the fact remains that when
only the studies utilizing patients with partial vestibular hypofunction are considered, the mean sensitivity
of the HIT is approximately 46% and the specificity is
approximately 94%. The reader is directed to Chapter
14, where the vHIT is described.
The VEDGE task force determined that the HIT
was recommended for patients with acute (zero to six
weeks) and chronic (greater than six weeks) vestibular
disorders (Scherer et al., 2014). It was noted, however,
that the HIT does not provide a measure of central
compensation. The HIT test was Recommended for
patients with peripheral dysfunction and Reasonable
to Recommend at this time for patients with central
dysfunction for assessment of the VOR.
HEAD SHAKE
Introduction
When the head is shaken vigorously for 20 to 30 cycles
and then stopped, a transient vestibular nystagmus
may emerge in patients with peripheral and central
vestibular system disorders. Originally described by
Bárány (1907), this aberrant response has been termed
head-shaking nystagmus (HSN). The appearance of SN
following repetitive shaking of the head has led to the
development of a large body of literature referring to
what is today known as the head-shake test. The headshake test evolved from an early test described by Borries (1923) where the investigators described how head
shaking could change the nature of SN. Vogel (1929)
expanded this work and described how shaking the
head could elicit SN from patients who were in the
process of central compensation. The contemporary
head-shake test was described by Kamei and Kornhuber (1964). In this original report the patient was fitted
with Frenzel lenses and instructed to shake the head
back and forth 30 times in four different conditions,
after which the clinician observed the eyes for SN. The
four conditions varied in terms of plane and direc-
9. BEDSIDE ASSESSMENT OF THE VESTIBULAR SYSTEM 173
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table 9–2. Comparison of Studies Evaluating the Head Impulse Test
Study n Controls Disorder Condition Sensitivity Specificity
Halmagyi &
Curthoys (1988)
Cremer et al.
(1998)
Halmagyi, Black,
Thurtell, & Curthoys
(2003)
Foster, Foster,
Spindler, & Harris
(1994)
Lehnen, Aw, Todd,
& Halmagyi (1994)
Harvey & Wood
(1996)
Harvey, Wood, &
Feroah (1997)
Beynon, Jani, &
Baguley (1998)
12 12
10 9 Unilateral vestibular
4 0 Postvestibular
6 6 Complete surgical
16 Vestibular
112 Complaints of
105
150 Dizziness 34% Could not
Unilateral vestibular
neurectomy
100% 100% Could not
deafferentation (7),
Unilateral posterior
SCC occluded (3)
Active and
neurectomy
lesions or canal
paresis
neurectomy (9),
Vestibulocochlear
neurectomy (7)
dizziness
Dizziness 35% 95%
Passive head
movements
≤30%
>30%
UW
100% 100%
calculate
100% Could not
calculate
100% 97%
100% Could not
calculate
<39%
68%
97%
calculate
Perez & RamaLopez (2003)
Schubert, Tusa,
Grine, & Herdman
(2004)
Total 791 76% 94%
265
111 65
tion of head shake in an effort to elicit responses from
each of the semicircular canals. They included shaking
the head when it was tilted 30 degrees forward and
positioned normally, in the coronal plane, and in the
sagittal plane.
Vertigo 45% 91%
UVH (79)
B
VH (32)
Nonvestibular
dizziness (65)
71%
84%
to identify. Most VNG systems provide a digital video
recording option, which allows the examiner to review
the results without having the patient repeat the test.
In the absence of VNG equipment, a patient can also
be evaluated while wearing Frenzel lenses. Although
Frenzel lenses will help the examiner observe the eyes,
patients may still fixate on the inside of the goggles.
technique
When this occurs, HSN may be attenuated or elimi-
nated because of VOR cancellation mechanisms.
The optimal situation to evaluate the head-shake test
is with the patient wearing VNG goggles with vision
denied. This eliminates the possibility that the patient
will visually fixate on an object and reduce the intensity
and duration of HSN, thereby making it more difficult
To begin, the patient’s head is tilted forward 30
degrees to position the lateral semicircular canals parallel to the ground. If an active procedure is being performed, the patient is instructed to oscillate the head
from side to side approximately 30 to 45 degrees from
82%
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