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334 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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the head movement. In healthy people the eye movement is equal and opposite to the head movement, and
the image on the retina is stable and visual perception
is clear (see first half of Video 14–1). If there is a peripheral vestibular deficit, this basic reflex does not operate
properly, the eyes do not compensate adequately for
the head movement, so the image of the visual world is
smeared across the retina, causing the patient to experience blurred or bouncing vision during head movement. Because of these visual problems, many patients
with peripheral vestibular deficits are convinced that
there is something wrong with their eyes, but the real
problem is in their inner ear. Subjective visual problems are some of the first signs of peripheral vestibular disorders, and they are frequently associated with
reduced vestibular function. A major goal of clinical
vestibular testing is to quantify vestibular function of
each ear and to identify the level of function in each
vestibular labyrinth.
The functional state of the semicircular canals can
be assessed by measuring the corrective eye movement
during an unpredictable head movement. Obviously
this inference has to be made with due care because
many systems, apart from the semicircular canals, can
control eye movements. Voluntary smooth pursuit,
moving visual stimuli (optokinetic input), cervical
input, or the saccadic system can generate eye movements. Consequently, in order to test semicircular
canal function specifically, the contribution of these
additional sources of control must be excluded. How?
Measures of the eye movement response during the
first 100 ms of an unpredictable, passive, small, abrupt,
head turn with natural values of angular acceleration (1000–4000 deg/s/s) exclude these other sources
of oculomotor control because they are just too slow
to drive the compensatory eye movement response
during this early phase (Halmagyi & Curthoys, 1987,
1988). This test is called the head impulse test (HIT)
and each head turn is called a head impulse. Thanks
to the development of the video version of the head
impulse test (vHIT) (MacDougall, Weber, McGarvie,
Halmagyi, & Curthoys, 2009), that testing using natural values of head acceleration is now routine. Nevertheless the clinician also needs to be wary because
other central disorders along the neural pathway from
the inner ear to the eye muscles, or even disease or
dysfunction of the eye muscles themselves, can also
affect the eye movement response. To a large extent the
contribution of these factors can be checked by calibration and verifying smooth pursuit before the vHIT test
even begins.
There are six semicircular canals in the head (Figure 14–1), and they work in three matched pairs: left
horizontal-right horizontal (LH-RH), left anterior-right
Figure 14–1. A. Schematic view of the enlarged semi-
circular canals showing the orientations of the semicircular canals in the head, viewed looking straight down
on the head.
so they are very close to one another. Each semicircular
canal has a diameter of about 6 mm, and normally the
two labyrinths are about 70 mm apart in the head (Curthoys, Blanks, & Markham, 1977a, 1977b). The parallel
canals form three matched pairs.
left anterior;
posterior;
from the free educational iPhone or iPad app called
“aVOR,” developed by Hamish MacDougall and available on i
impulse: position, average velocity, average acceleration.
The two labyrinths have been translated
LH, left horizontal; LA,
LP, left posterior; RA, right anterior; RP, right
RH, right horizontal. These images are modified
Tunes. B. Approximate magnitudes of a head
posterior (LARP), and right anterior-left posterior
(RALP). Each pair works as a “push-pull” pair. That
means that while one canal is activated, the paired
canal is inhibited. The canals are not mutually perpendicular so it is not possible to stimulate any pair in total
isolation. Any head rotation causes a unique pattern
of activation of the six semicircular canals. Disease or
dysfunction can affect all canals in both ears (bilateral
vestibular loss [BVL]), or all the canals on one side (unilateral vestibular loss [UVL]), or just one individual
canal. The ideal test of peripheral vestibular function
is one that tests the function of each of the six semicircular canals specifically, using stimuli with natural
values of angular acceleration.
The Video Head Impulse Test: Overview
In clinical vHIT testing the patient’s head is passively
and unpredictably turned by the clinician, so the value
14. THE VIDEO HEAD IMPULSE TEST (vHIT) 335
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of the angular acceleration varies from one impulse to
the next. However, in vHIT, both the head movement
stimulus and the eye movement response are measured
exactly on every impulse, and the analysis relates each
eye movement response to the head movement stimulus which caused it. The patient is instructed to keep
staring at an “earth-fixed” fixation target on the wall in
front of him or her during the head turn and to return
his or her eyes to that target as quickly as possible if the
target is lost. It is most important that the patient does
not actively turn his or her own head — it must be a
passive, unpredictable head turn with an abrupt start and
stop — abrupt in order to generate the clinically acceptable values of angular acceleration. Each head turn is
called a head impulse or a trial.
Such a head impulse consists of a brief angular acceleration up to a peak head velocity, followed
immediately by an angular deceleration back to rest.
The semicircular canals of the inner ear are activated
by angular acceleration, and that activation drives the
eyes via short fast pathways from the semicircular
canal receptors to the eye muscles. In healthy subjects,
both eyes move conjugately to compensate for the passive head turn. (A brief outline of the physiological
evidence for this vestibulo-ocular response is given in
Figure 14–20B, later in this chapter.)
Consider the responses of a healthy individual.
After a very short latency (about 10 ms) from the onset
of the head turn there is a smooth compensatory eye
movement, with the velocity of the eye movement
almost exactly matching the velocity of the head movement. The result is that the subject’s gaze remains fixed
on the target irrespective of direction of the unpredictable, passive head turn (Halmagyi & Curthoys, 1988;
Figure 14−2). This is a very fast and remarkably accurate response. In healthy subjects it is said that VOR
gain is around 1.0, where VOR gain is defined as the
ratio of eye velocity to head velocity. (VOR gain and its
measurement are discussed in more detail below.)
For patients with UVL, as their head is turned to
their affected side (an “ipsilesional” head turn), the
semicircular canal function on the affected side is deficient, and so the neural drive from the affected semicircular canals to the eye muscles is inadequate. Thus
during such an ipsilesional head turn the patients’ eyes
do not compensate for the head turn, so they do not
stay on the earth-fixed target but are moved with the
head off the target. Consequently at the end of the head
turn the patients’ gaze is directed away from the fixation target and they must make a corrective saccade to
return gaze to the target as the instructions require (see
Figure 14–2). In many patients with semicircular canal
loss, that corrective saccade is often clear to the clinician viewing the patient’s eye movement; therefore, it
is called an “overt” saccade and its occurrence after a
head impulse is the telltale sign of deficient semicircular canal function on the side to which the head has
been turned. A left UVL means that leftward head turns
are not adequately compensated for — so the eye velocity is too low and there is a corrective saccade (to the
right) after a head turn to the left. The saccade is con-
firmation of the reduced eye velocity, and its presence
indicates a left horizontal canal loss. Similarly, a corrective saccade after a head turn to the right indicates
a right horizontal canal loss. Patients with BVL make
corrective saccades for head turns in both directions.
If a patient with a UVL is given a head turn to his
or her healthy side (a “contralesional” head turn), the
healthy canals drive the eyes, and so the eye movement
compensates for the head movement and the VOR
gain is about 1.0 or is only modestly reduced. But for
such UVL patients there is a clear asymmetry of VOR
between the healthy and the affected side. For patients
with BVL, VOR gains for both sides are significantly
less than normal values for healthy subjects in their age
band, so they make corrective saccades for both directions of head turn.
The vHIT test requires cooperation by patients: to
keep their eyes wide open, to keep fixating the target
on the wall, and to relax their neck muscles to allow
the clinician to turn their head passively. The patient
is instructed to try not to blink (“keep your eyes wide
open”), to relax their neck muscles (“become like a rag
doll”), and not to try to predict or to “help” with the
head turns. Video HIT requires passive, unpredictable head turns. Some people find it very difficult to
relax their neck muscles and so the clinician finds it
difficult to turn their head abruptly, even through a
very small angle. However, for this test to be a valid
indicator of vestibular function, the clinician must be
able to deliver a very small, abrupt movement which
is a “turn and stop.” The abrupt stop is every bit as
important as the abrupt start. There should be as little
overshooting or rebound of the head at the end of the
impulse as possible. It takes training and practice to be
able to do acceptable head impulses. With such “difficult” patients the clinician should aim to get just a few
quality head impulses, since each impulse is a test of
the canal function (see “How Many Impulses” below).
Some patients with vestibular loss can generate
a corrective saccade during the head turn itself, so the
clinician viewing the patient’s eye movements does not
see an overt saccade at the end of the head turn, and so
may wrongly conclude that the patient’s semicircular
canal function is normal (Weber et al., 2008a). A corrective saccade generated during the head impulse cannot
be detected by simple visual observation and so it is
called a covert saccade (covert = hidden), in contrast
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Healthy
Right
unilateral
loss
A - Before B - During head turn to rightC - At rest after head turn
figure 14–2. Full face view of the difference between the response of a healthy subject (top row ) and a patient
UVL on their right side (bottom row ) during a rightward clinical head impulse (large arrow in column B ). Before
with
the head turn (column A) the person is instructed to look at the examiner’s nose during the head turn, to try not to
blink, and to keep looking at the nose during the head turn. During the head turn, the eyes of the healthy subject
rotate to compensate for the head turn and so stay fixed on the examiner’s nose (column B
end of the rotation (column C
affected side (B
head rotation (i.e., to the right in this example). At the end of the head turn (column C
been dragged, with the head turn, off target, and so the patient must make a corrective saccade back (small
arrows beneath the eyes), to regain the fixation target on the examiner’s nose as instructed. A patient with right
UVL makes a corrective saccade after rightward head impulses, and a patient with a left UVL makes a corrective
saccade after leftward head impulses.
), the eyes do not compensate for the head turn, so the eyes move in the same direction as the
to the overt saccade made at the end of the head turn.
These covert saccades mean that it is necessary to
obtain objective measures of the eye movement during the head movement for the head impulse test to
be a valid indicator of vestibular function. Video HIT
provides that evidence by obtaining objective, accurate, high-speed measures of eye movements during
the brief abrupt head movements. By using a miniature, very fast video camera on lightweight, tightly fitting glasses securely attached to the head, it is possible
to measure the eye velocity during the head impulse
(MacDougall et al., 2009; Figure 14–3). A detailed explanation of the measurement procedure and the pitfalls
to avoid is given in the section “Doing the Test” below.
Video HIT quantifies the VOR simply, quickly, and
) — no corrective saccade is necessary. For the patient during the rotation to their
Still images from the aVOR app for iPhone.
accurately, and the recordings give objective evidence
of the presence of covert or overt corrective saccades. In
particular, covert saccades are readily detected by the
vHIT system. Video HIT quantifies the VOR not only
for horizontal but also for vertical semicircular canals
when the head is turned in the plane of the vertical
canals (see below), so it provides objective evidence
of the functional state of all six semicircular canals.
These tests with an earth-fixed target are now called
head impulse paradigm (HIMP) tests. We have also
developed a simple variant using the same camera
system and same head impulse but where the patient
is required to look at a moving spot on the wall during
the head turn — and this is called the suppression head
impulse (SHIMP) test (see below).
) and remain so at the
) the patient’s eyes have
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Figure 14–3. The Otometrics video head impulse goggles. The measured eye views the fixation target through a half-silvered mirror which
reflects an image of the eye onto the camera. A sensor within the
goggles detects head velocity.
VALIDATION OF THE VIDEO
HEAD IMPULSE TEST
Video HIT has been validated by comparing simultaneous measures of the same eye by both scleral search
coils and video in many healthy subjects and patients,
showing there was little systematic difference between
results from these two very different systems (MacDougall, McGarvie, Halmagyi, Curthoys, & Weber,
2013b; MacDougall et al., 2009). The vHIT system runs
on a laptop computer, is completely portable, and is
used in the research laboratory, the clinic, the hospital ward, the outpatient clinic, the ambulance. Importantly, testing is done in full light, in order to constrict
the pupil, so the test environment does not need any
special environmental conditions (like a dark room).
One very important application is the use of vHIT in
the emergency room, for testing the canal function of
patients presenting with severe vertigo and determining if the vertigo is due to peripheral vestibular loss
as opposed to a central stroke (Newman-Toker, Kattah,
Alvernia, & Wang, 2008).
EXAMPLES OF vHIT RESULTS
In carrying out vHIT it is essential to ensure the results
meet certain minimum standards: that the head velocity reaches or exceeds 150 deg/s, the eye velocity data
are not noisy, and the head impulse has minimal overshoot and rebound. The reasons for these minimal
standards will be explained below. Figure 14–4 shows
the results for a healthy subject (top row, A, B) and a
patient with UVL (bottom row, C, D). The figure shows
the superimposed records over time (called time series)
of the head velocity of every head turn and the eye
velocity of the corresponding eye movement response,
for leftward head turns (A, C) (testing the function of
the left horizontal canal) and rightward head turns (B,
D) testing the function of the right horizontal canal. In
this figure and later similar time series, the eye velocity records have been inverted and superimposed on
the head velocity records to show graphically how
closely eye velocity matches head velocity in healthy
subjects. ONLY after verifying that the time series are
acceptable should the clinician consider the VOR gain.
In this example each head impulse had similar peak
head velocities, and the repeatability of the stimulus
and response is evident at a glance. As is clear from
the closely matching eye and head velocity raw data,
the VOR gains are close to 1.0 for both leftward and
rightward head turns. Thus we can conclude that the
healthy subject’s horizontal semicircular canal function
is normal on both sides. This is a typical result for a
healthy subject.
Notice that although the eye velocity closely
matches head velocity, this healthy subject makes some
(very small) saccades for head turns in both directions (identified by small arrows in the figure). Many
healthy people have small overt and covert saccades
during head impulse testing. Even tiny saccades have
relatively high peak eye velocity and so they are easily detected by vHIT. Minor saccadic corrections to get
back exactly to the center of the fixation dot can have
high velocities and so are easily shown on the records.
These small saccades are not of clinical importance. The
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Figure 14–4. Superimposed time series of head velocity and (inverted) eye velocity during horizontal head impulses for a healthy subject (A , B ) and a patient with
a UVL (C, D ). For the healthy subject eye velocity matches head velocity for both
directions of rotation, so the eye velocity records superimpose the head velocity
records and the
which have no clinical significance. For the patient, for head turns to the affected
side, eye velocity is much lower than head velocity, so the VOR gain is around 0.5,
and there are many compensatory saccades
cades) or during the impulse (covert saccades).
to the patient’s healthy side is reduced (0.79), because the contribution from the
opposite (affected) side is reduced. Reproduced with permission from Curthoys and
Manzari (2017).
VOR gain is around 1.0. The person makes small saccades (arrows)
clinical indicator of semicircular canal function is the
eye velocity during the head impulse, and that is quantified by VOR gain.
It is important to realize that semicircular canal
stimulation generates slow phase corrective eye movements, not saccades. Saccades correct for inadequate
slow phase eye velocity. The clinician’s focus should
be primarily upon the slow phase eye velocity during the
head impulse and how closely it matches the head velocity, with the saccades acting as confirmation of reduced
eye velocity. In patients the saccades give information
that complements the evidence from the slow phase eye
velocity, but the more important indicator is the slow
phase eye velocity because that is what is being driven
by the semicircular canals. The confirmation from the
saccades is valuable but not primary. As we show
below, for any individual patient, simply changing the
— either after the impulse (overt sac-
The eye velocity for head turns
instructions (from HIMPs to SHIMPs) totally changes
the pattern of saccadic responses, without affecting
peripheral semicircular canal function and slow phase
eye velocity.
Examples of Patient Results:
Bilateral Vestibular Loss
Some patients have BVL possibly as a result of systemic
gentamicin for the treatment of a previous serious infection (Weber et al., 2009). Figures 14–5C and D shows
the time series of head impulses to the left and right for
a patient with BVL and, for comparison, representative
examples of responses from a healthy subject (Figures
14–5A and B) and a patient with UVL (Figures 14–5E
and F). In the patient with BVL, the VOR gain is very
figure 14–5. Time series results from testing a healthy subject (A, B), a patient with UVL (E, F), and a patient with
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BVL (C, D). A, B. For the healthy subject, the VOR gains (rightmost column) for both leftward (filled circles) and
rightward impulses (open circles) are close to 1.0, as expected given that the head and eye traces in panels (A)
and (B) are closely overlaid, and any corrective saccades are very small. C, D. A patient with a bilateral horizontal
canal loss. Eye velocities during the impulse do not match head velocity, and VOR gains are well below normal
values for impulses toward both sides. Large overt saccades are present for impulses to both left and right sides.
E,F. The patient with a left unilateral horizontal canal loss has reduced eye velocity for leftwards (“ipsilesional”)
head turns and so reduced VOR gain for impulses toward the affected left side. In confirmation there are overt
saccades after the impulse and some covert saccades. These are overt saccades because they occur after the
head has stopped moving, and so would probably be detectable by a trained eye. The objective records from vHIT
show these saccades very clearly.
339
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small for both directions of head turn, and those small
gains are corroborated by the overt saccades after the
head turns. The progressive loss of vestibular function
due to systemic gentamicin vestibulotoxicity cannot
simply be quantified by caloric testing because daily
calorics are unacceptable to most patients. But such
a progressive loss of semicircular canal function can
be measured objectively by vHIT objectively tracking
changes in semicircular canal function even at intervals
as short as a few minutes, if necessary.
For the patient with left UVL (Figures 14–5E and F),
the eye velocities for head turns toward the patient’s
healthy right ear (“contralesional” head turns) match
head velocity and so are very similar to that of the
healthy subject, and the VOR gains for these head
turns to the right ear are about 1.0 for every head
impulse. The measured VOR gains for the ipsilesional
(leftward) head turns are all around 0.3, which is substantially below the range of normal gains (0.72–1.20;
Table 14–1). For both directions of head turn, the VOR
gains vary from impulse to impulse — the VOR gain is
not always exactly 1.0 or always exactly 0.3. Notice in
particular that the eye velocity during the head turn to
the affected side is not 0.0 — there is a small and very
inadequate eye velocity response, and the physiological reason for such a weak response for head turns to
the affected ear is explained in Appendix 14–A. However, the overall pattern shown here is the common eye
velocity response pattern for a patient with a unilateral
loss of horizontal canal function; for example, a patient
with an acute left vestibular neuritis.
Notice also that in the examples, all the peak head
velocities are about 150 to 200 deg/s. Many patients
with UVL may show normal VOR gain for ipsilesional
head turns at low head velocities (e.g., 50 deg/s), so
that their vestibular loss only becomes apparent at
higher head velocities (above about 150 deg/s). For
this reason it is recommended that there should be trials where the head velocity is greater than 150 deg/s.
Clinicians should be cautious about accepting any test
result where this 150 deg/s velocity is not achieved. It
is more difficult to achieve these higher head velocities in patients with stiff necks, so some clinicians tend
not to achieve these higher values, but in that case the
results are not an adequate test of ipsilateral semicircular canal function and can be misleading, suggesting
that a patient has normal semicircular canal function
when the patient has a unilateral deficit, undetected
because the vestibular test is inadequate. The exception
to this recommendation is testing patients during acute
attacks of vertigo, where even low head velocities can
be very valuable in verifying the cause of the attack. In
our experience, achieving higher head velocities is a
matter of practice.
VOR GAIN
The head impulse seems such a simple test — a brief
abrupt head turn and a corresponding eye movement
response. Surely it is simple to quantify just how good
Table 14–1. Normative Data: Average VOR Gains and Average Horizontal VOR Gain Asymmetry for Healthy
Subjects from the Sydney Clinic.*
Horizontal
Left
Horizontal
N 28 28 29 29 29 29 28
Mean 0.92 1.00 0.96 0.92 0.95 0.98 5.9%
SD 0.06 0.07 0.12 0.17 0.12 0.15 3.7%
Lower
cutoff
Note. Full VOR gains across ages are given in McGarvie et al. (2015c).
* These numbers must be used with caution: they are only based on a relatively small sample of healthy subjects, and the mea-
sured VOR gain depends on the gain algorithm and the peak head velocity used. Figure 14–7 shows graphically the normative
VOR gain as average values at different velocities.
†
The VOR asymmetry values were calculated as [(VORlarger − VORsmaller) /(VORlarger + VORsmaller)] × 100. At high accelerations there is a systematic difference between the VOR gains in the two eyes dependent on the direction of the head turn
(Weber et al., 2008b), and since vHIT only tests one eye this is a source of asymmetry. For most clinical testing this interocular
source of asymmetry is small.
0.80 0.86 0.72 0.58 0.71 0.68 13.3%
Right
Horizontal
Left
Anterior
Left
Posterior
Right
Anterior
Right
Posterior
VOR Gain
Asymmetry
†
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the performance of the eye movement response is?
No. We have realized that the response is complex.
The initial approach by engineers to measuring performance by measuring VOR gain adopted such an
approach — just measure eye velocity and divide it by
head velocity. Unfortunately things are not that simple
— at what moment do you measure the eye velocity? It
is very different early in the response, when the head
acceleration is minimal, rather than later. And what
about the eye velocity during deceleration? Very few
people have tackled these questions. We developed
vHIT and so we are well aware of these (and other
related) matters, and we advocate for most clinical
tests to use a “global” measure of VOR gain — which is
a measure of the whole eye movement performance —
taking the whole (desaccaded) eye velocity response
and dividing it by the whole head velocity stimulus.
We advocate this in preference to measuring at a single
moment because such momentary measures can be
artifactual. Saccades are removed because the diagnostic indicator of semicircular canal function is slow
phase eye velocity, not saccades. Saccades correct for
the reduced VOR gain. This is an “area” gain, which
is essentially a measure of eye position with respect to
head position (Figure 14–6).
The VOR gain as we have defined it — area VOR
gain — has some advantages, but also has the drawback
that it obscures important response events during the
head impulse. For example, just exactly when and how
does the onset of the eye movement response occur?
New evidence suggests that the early response may be
an indicator of semicircular canal function in endolymphatic hydrops (Rey-Martinez, Burgess, & Curthoys,
2018). But these are matters on which future research
will elaborate — at present, the best clinical indicator is
area VOR gain. In the ICS Impulse system (Otometrics A/S, Taastrup, Denmark) the eye velocity record
is first desaccaded. The data point at the beginning of
the saccade is joined by a straight line to the data point
at the end of the saccade, and the saccade eye velocity
is removed. Then the area under the desaccaded eye
velocity curve from the start of the head velocity to the
end of the head velocity is calculated and compared
with the area under the head velocity curve from the
start of the head velocity until the moment when the
head velocity returns to zero. VOR gain is defined as
the ratio of these two areas. This is essentially a position gain, but our investigations have shown that this
mode of calculating gain is very resistant to artifact
due to glasses slip. It is a more functional measure of
gain, as the position error is the driver for the corrective
saccade, so VOR gain and the corrective saccade are
complementary.
Using such an area gain, the range of normality
is tight, in contrast to calorics. The average horizontal
VOR gain for vHIT for healthy subjects in our clinic
is 0.96 ± 0.12 (SD), so the mean gain ± 2 SDs (including 95% of the population) (Zar, 2010) is 1.20 to 0.72
(see Table 14–1; see also Figure 14–7). In other words
any VOR gain less than 0.72 or greater than 1.20 is considered to be abnormal. The average vHIT gain asymmetry ratio (comparable to the canal paresis score) for
high accelerations is 5.9% ± 3.7, so the normal range of
vHIT gain asymmetry in this group of healthy subjects
is from 0 to 13.3%, and a gain asymmetry greater than
13.3% is considered to be abnormal. This is smaller than
figure 14–6. In order to calculate VOR gain, the area under the eye velocity record (light gray ) is divided by the
area under the head velocity record (dark gray ). The figure shows how the ratio of those areas is around 1.0 in
healthy subjects (A) but UVL decreases that ratio (B). This area VOR gain is less affected by minor fluctuations
in eye velocity which can affect VOR gain calculated from instantaneous values of eye velocity records. Reproduced with permission from Curthoys and Manzari (2017).
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figure 14–7. Normative values for vHIT VOR gain at increasing peak head velocities across ages.
The average horizontal VOR gain for left and right horizontal canal stimulation across increasing
peak head velocities. Each panel shows the average VOR gain as a function of peak head velocity
together with a band (gray) of ± 2 standard deviations around the mean. The number of individuals tested in each age band is shown. Each band includes 95% of the population at that age. The
clear result is that VOR gain is around 1.0 for each decade age band with a small decline as the
peak head velocity increases. Reproduced with permission from McGarvie, MacDougall, Halmagyi,
Burgess, Weber, and Curthoys (2015c).
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the size of the normal range of canal paresis scores with
calorics, which is of the order of 0 to 25%. Thus, vHIT
can detect small asymmetries as well as whether VOR
gains for both directions of rotation are below normal, as occurs in BVL. For healthy subjects, VOR gain
changes very little with age, and an example is shown
in Figure 14–7 (from McGarvie et al., 2015c). Area VOR
gain for vHIT is much less susceptible to artifacts such
as glasses slip.
Why Is VOR Gain Not Exactly 1.0?
Textbooks give the impression that the VOR gain
should be exactly 1.0 in healthy subjects. In fact, this is
very rarely true. Perfectly healthy people who have no
symptoms of visual blur or oscillopsia can have gains
much smaller than 1.0 — for example, 0.85 or less — or
gains much higher than 1.0, up to 1.2. These people do
not complain of blur or oscillopsia during head movements. Why? There are probably a host of reasons.
VOR gain is not a fixed immutable quantity but can be
changed by a variety of procedures. Subjects who have
worn magnifying spectacles have increased VOR gain
even when the spectacles are removed. VOR gain also
increases above 1.0 for healthy subjects if the fixation
target is close. Cerebellar disorders can cause increased
or decreased VOR gain (Shaikh et al., 2013). Recent evidence indicates that hydrops may cause enhanced VOR
gain (Rey-Martinez et al., 2018).
VOR Gain Asymmetries
Clinicians carrying out vestibular tests are steeped in
the tradition of looking for asymmetries of semicircular canal function between the two sides, and the canal
paresis score is the measure of asymmetry of horizontal
semicircular canal function from caloric data. There are
different ways of quantifying VOR gain asymmetries for
vHIT data. One measure uses a version of the Jongkees
formula for calculating asymmetry (Weber et
VOR gain asymmetry (%) =
[(VORlarger − VORsmaller)/
(VORlarger + VORsmaller)] × 100
al., 2008a):
Video HIT and Vestibular Neuritis
and Vestibular Compensation
In many years of testing thousands of patients, we have
found no evidence of VOR adaptation or habituation
to repeated head impulses in the one testing occasion.
The pattern of saccades may change, even within a single testing session, but the VOR gain usually remains
fixed. Importantly there is no evidence of central compensation of the VOR to these high acceleration head
impulses (Halmagyi et al., 1990). In patients tested
immediately after and 1 year after vestibular neurectomy, there was no detectable change in ipsilesional
VOR gain. That same result is also found in some neuritis patients followed over a long time span (example
in Figure 14–8A). However the VOR of some patients
with vestibular neuritis does recover, as shown by
Figure 14–8B, and we attribute that to recovery from
the neuritis itself, allowing normal neural function
to return.
Saccades are a confirmation of the VOR gain, but it
is VOR gain which is the primary indicator of vestibular function. Many other factors apart from peripheral
semicircular canal function affect saccades, and so it
is VOR gain which is the clinically important primary
indicator of vestibular function. Saccades act to confirm
the VOR gain measure but they should not be used to
replace VOR gain. That confirmation is clearly shown
in Figure 14–8B, where, as the VOR progressively
increases after neuritis, the saccadic velocity decreases.
In particular, we caution against the new emphasis
on saccade velocity in vHIT testing, for the reason that
the velocity of the corrective saccade depends on overshoot and rebound of the head velocity. As the rebound
(or overshoot) velocity increases, there is progressively
reduced need for a corrective saccade, for a reason
which has nothing to do with peripheral vestibular
function. It has to do with the fact that the overshoot is
effectively changing the technical testing requirement
for a saccade. In the limit if the overshoot is as big as
the impulse, then no saccade is needed, since the head
has come back to the starting position and the patient
(even without vestibular function) is looking at the
earth-fixed target. It is very difficult to minimize overshoot and rebound, and it becomes even more difficult
at high peak velocities, such as those reported here.
One aspect of saccadic performance usually
changes in most patients with time after vestibular loss,
and that is the temporal spread (clustering) of saccades.
The corrective saccades of the typical early vestibular
neuritis patient are spread across a wide time band (see
Figure 14–8). But over time those saccades tend to cluster and move to being earlier and so become covert,
rather than overt. We suggest this is due to learning
processes during recovery (MacDougall & Curthoys,
2012; Rey-Martinez, Batuecas-Caletrio, Matino, &
Fernandez, 2015). The overt and covert saccades may
occur in tight clusters during or just after the head
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