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354 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
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but perfectly normal vHIT response to natural values
of angular acceleration. A normal response on vHIT
shows that in response to the physiological, adequate
stimulus to the semicircular canal, semicircular canal
function is normal. A small or absent caloric response
may occur for a host of reasons unrelated to horizontal
semicircular canal function, such as an unusual external auditory meatus or unusual temporal bone density.
So, unsurprisingly, these two very different methods
of testing semicircular canals do not always produce
results which agree.
The correct way of identifying the true sensitivity and specificity of vHIT is to assess how well vHIT
can detect objectively identified UVL, and the only
group of patients in that category are those who have
undergone surgical removal of one vestibular nerve to
treat vestibular schwannoma. Our recent unpublished
measures of 20 such patients and 37 healthy subjects
showed that for detecting an objectively verified UVL,
the true sensitivity of vHIT was 1.0, the true specificity was 1.0, and the diagnostic accuracy was 100%. We
are not aware of comparable studies of the sensitivity
and specificity of the caloric test. With the caloric it is
not possible to obtain an absolute measure of horizontal semicircular canal function from the stimulation of
each ear. One reason is that there are such great variations between individuals in the pathways conveying
the thermal stimulus from the external ear canal to the
horizontal semicircular canal. So the magnitude of the
stimulus delivered to the canal receptors is not known.
The functional state of the other four vertical canals
cannot be evaluated by the caloric test. The vHIT test,
by contrast, provides an absolute measure of the function level of every semicircular canal separately. This
is possible because the stimulus, head rotation, is the
adequate, natural, physiological stimulus for the semicircular canals, and this stimulus is measured exactly
during the head turn. Similarly, the response to this
physiological stimulus
exactly. These simultaneous measures of the stimulus
and the response provide many significant advantages
compared with the caloric test. Most importantly vHIT
provides a measure of the gain of the vestibulo-ocular response for each canal individually. They allow
inspection of the form of the temporal profile of the eye
velocity response to every part of the stimulus during
different stimulus magnitudes — different peak head
velocities. This allows the clinician to identify absolute
loss of canal function, where there may be no asymmetry between the two sides but the canals on both sides
show a loss of function. Such BVL occurs with systemic
gentamicin ototoxicity (Weber et al., 2009). Caloric testing cannot provide this information with reliability.
— eye velocity — is measured
Video HIT tests can be given repeatedly — even only
minutes apart — and so the test is ideally suited to tracking changes in vestibular function (e.g., during disease
or during systemic gentamicin therapy or around the
time of an acute attack in Menière’s disease). Together
with vestibular-evoked myogenic potentials (VEMPs),
vHIT completes the ability to test the entire audiovestibular system (Curthoys, 2012).
gentamiCin ototoxiCity
The head impulse test can detect a small deterioration
in absolute bilateral semicircular canal function, e.g.,
due for example to the vestibulotoxic effects of gentamicin on the vestibular receptors in patients receiving
systemic antibiotic treatment. The progressive loss of
vestibular function due to systemic gentamicin cannot
be quantified by calorics because of the great variability
of the caloric responses and because daily calorics are
unacceptable to most patients. It is important to realize
that a single systemic injection of gentamicin can cause
almost total loss of vestibular function (Halmagyi &
Curthoys, 2018a). A progressive BVL can be detected
objectively even at the bedside by vHIT, since vHIT is
on a laptop and does not require specialized conditions.
Video HIT provides objective quantitative tracking of
changes in semicircular canal function at the bedside
during systemic gentamicin treatment even at intervals
as short as a few minutes if necessary. Similarly, vHIT
can quantify semicircular canal function in patients
receiving intratympanic gentamicin. It is now becoming common practice to use vHIT to “titrate” intratympanic gentamicin (ITG) dosages for treating Menière’s
disease. The patient is tested before and then one week
after ITG. The goal is to adjust the dosage to cause just
a small loss of peripheral canal function, rather than
total vestibular ablation (Marques, Manrique-Huarte,
& Perez-Fernandez, 2015). If there is no effect, a second intratympanic injection is given, etc. As the VOR
gains show a small loss, patients report reduced vertigo, but they retain a substantial part of their semicircular canal function.
méniÈre’s disease
Because it can be used at very short intervals, vHIT
is now starting to be used to monitor semicircular
canal function in patients with probable endolymphatic hydrops and patients with Ménière’s disease
14. THE VIDEO HEAD IMPULSE TEST (vHIT) 355
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even around the time of the attack. In many patients
with Menière’s disease there is a dissociation between
the results of vHIT testing and caloric testing — vHIT
shows normal canal function, whereas caloric testing
shows reduced or absent canal function (McGarvie,
Curthoys, MacDougall, & Halmagyi, 2015a, 2015b).
The reason for this dissociation is not known at present, but it may be due to the enlarged membranous
labyrinth in endolymphatic hydrops affecting the temperature transfer to the membranous semicircular duct
and thus the receptor activation.
THE SUPPRESSION HEAD
IMPULSE PARADIGM
In the usual head impulse test paradigm (which we
now term HIMP) the subject fixates an earth-fixed target (Figure 14–16A). The results from that test are now
complemented by a new variant we have introduced
which is called SHIMP (for suppression head impulse
paradigm) (MacDougall et al., 2015). The head turn
stimulus and the eye movement recording are identical. All that is changed are the instructions — from “look
at that fixed target on the wall” to “look at the moving
target.” In SHIMPs during the head turn the patient is
asked to stare at a laser spot on the wall projected from
a head mounted laser (Figure 14–16B). The head turn
stimulus is exactly the same in HIMPs and SHIMPs — brief,
unpredictable, high acceleration head turns — but in the
SHIMP protocol the subject is required to fixate a target
which moves with the head (second half of Video 14–1).
We call this new variant protocol SHIMP because we
expected suppression of the VOR to dominate. As
we have noted above, healthy subjects suppress their
VOR frequently in daily life, and they also do so in the
SHIMP paradigm, but it takes time (around 80 to 100
ms) for that VOR suppression to take place, and during that time the usual VOR is operating, just as in the
HIMP test. Independent evidence has shown that VOR
suppression in this passive, high acceleration paradigm
takes around 80 ms from the onset of the head turn
to become effective — so that it is just becoming effective at around the end of the head impulse stimulus.
During this 100-ms window, vHIT measures the slow
phase, just as it does during the HIMP paradigm. The
result is that both HIMPs and SHIMPs provide measures of the VOR! Subjects find this task very easy and
intuitive — they simply look at the spot as it appears
to jump from place to place as the clinician turns their
head. It is like watching a tennis match. Unbeknownst
to them, on each turn the clinician is getting excellent
data about how good the VOR is. Very quickly, subjects
Figure 14–16. The two test protocols: HIMPs and SHIMPs. A. In the usual proto-
col for head impulse testing (HIMP) the person is instructed to maintain fixation on an earth-fixed target during a small unpredictable passive head turn.
Because of the VOR healthy subjects do not make any large saccades. B. In the
SHIMP protocol the head turn is identical but the instructions are now to maintain fixation on a spot projected on the wall that moves with the head — it is
from a head-fixed laser in the glasses. Now healthy subjects make large saccades at the end of the impulse to regain the target spot (see text for explanation). Reproduced with permission from Halmagyi, Chen, MacDougall, Weber,
McGarvie and Curthoys (2017).
356 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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try to predict which way the spot will jump, and it is
imperative that the clinician try to minimize this prediction by always starting from a central point and
being as unpredictable as possible.
There is one very large difference between the
responses on HIMPs versus SHIMPs, and that is that
on SHIMPs, at the end of the head turn it is the healthy
subject who must make a saccade to regain the target,
whereas the patient without vestibular function does
not need to make a saccade. The reason is as follows.
Why do healthy subjects need to make a corrective saccade? Because during the head impulse the
VOR drives their eyes opposite to the direction of head
movement, and healthy subjects do not suppress their
VOR during that early stage (first ~80 ms) of the head
turn. Consequently their gaze is driven by their VOR
off the target. For example, as the head is turned to the
left, the fixation target moves to the left, the VOR drives
the eyes to the right, and so at the end of the impulse
the target is to the person’s left, but the subject’s gaze
is to the right, so the healthy subject must make a large
corrective saccade from right to left (anti-compensatory
for the head turn direction) to regain the target (Figure 14–17A). At the other extreme, for patients with
complete vestibular loss (Figure 14–17B), their VOR is
absent and so it does not drive their eyes off the headfixed target at all during the head impulse. At the end
of the impulse the patient’s eyes are still on target and
thus they do not make any corrective saccade. In sum:
in SHIMPs it is the healthy people who make corrective saccades and patients without vestibular function
who do not make corrective saccades. A simple rule is
that HIMP saccades are an indicator of vestibular loss,
whereas SHIMP saccades are an indicator of residual
figure 14–17. Superimposed time series of head and eye velocity records HIMPs and SHIMPs for a healthy subject
(A) and a patient with BVL (B). A. The results for the healthy subject show that for HIMPs eye velocity matches head
velocity during the impulses and there are minor corrective saccades at the end of the impulse. For SHIMPs eye
velocity matches head velocity during the impulses, but at the end of the impulse there are large corrective saccades to return gaze to the target. B. During HIMP trials, the patient with BVL elicits mostly overt positive catch-up
saccades after the head impulse. During SHIMP trials the same patient with BVL shows only very few saccades
after the end of the head impulse back to the head-fixed target, because their eyes have remained on the target
during the head impulse. In the SHIMP protocol it is the patient with vestibular loss who has no saccades, whereas
healthy subjects show large saccades — exactly the reverse of the saccadic pattern with the HIMP protocol. In a
healthy subject the slow phase eye velocity during the head impulses is the same for both HIMPs and SHIMPs, and
similarly for patients with vestibular loss. The SHIMP paradigm does not affect the slow phase eye velocity — only
the corrective saccades. Reproduced with permission of Wolters Kluwer Health, Inc. from MacDougall, McGarvie,
Halmagyi, Rogers, Manzari, Burgess, Curthoys and Weber (2016), A new saccadic indicator of peripheral vestibular
function based on the video head impulse test. Neurology, 87(4), 410–418. https://www.neurology.org/. Published
by the American Academy of Neurology.
14. THE VIDEO HEAD IMPULSE TEST (vHIT) 357
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vestibular function. Patients with UVL show large
SHIMP saccades for head turns to their healthy side
and small or absent SHIMP saccades for head turns to
their affected side (MacDougall et al., 2016; Shen et al.,
2016). The VOR gain during the head impulses is the
clinical indicator of vestibular function. The saccades
are again a confirmatory indicator of that vestibular
loss because, as stressed above, the size of the saccades (their peak saccade velocity) is affected by many
factors, especially the extent of rebound of the head
impulse. Overshoot and rebound reduce the size of the
saccadic velocity.
The SHIMP paradigm provides a complementary
measure of semicircular canal function to that from
HIMP, but VOR gain, measured from the slow phase
eye velocity, is similar for both HIMPs and SHIMPs
(MacDougall et al., 2016). Recent evidence is that in
SHIMPs VOR gain is (slightly) smaller than VOR gain
in HIMPs. Figure 14–18 shows HIMP and SHIMP
results for a patient with a UVL. The figure shows that
SHIMP has the advantage of usually effectively removing the covert saccades during the head impulses,
which cause problems in gain measurement in the standard HIMP protocol. SHIMP is a much more intuitive
figure 14–18. HIMP and SHIMP data for the horizontal canal tests for
a patient with UVL in the left ear. Top row: In the standard HIMP proto-
col, the gain of the VOR is greatly decreased for rotations towards the
affected left side (A), with large compensatory corrective saccades
(both overt and covert saccades). For rotations to the healthy side
(B), the gain is slightly lower than normal, with a few very small corrective saccades. In the SHIMP protocol, the VOR gains using the slow
phase eye velocity towards the affected (C) and healthy sides (D) are
similar to the corresponding gains for the HIMP protocol, but the saccade pattern is reversed. Towards the healthy side (D) there are very
large anti-compensatory SHIMP saccades at the end of the impulse.
Towards the affected side (C) there are a few late small saccades.
The gain of the VOR is not zero so the SHIMP saccades are very small
compared to the saccade amplitude for impulses to the healthy side
(D). Reproduced with permission from Curthoys and Manzari (2017).
358 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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test to carry out — the patient is just asked to look at the
spot. So language difficulties or cognitive deficits have
minimal impact. SHIMP is even easier to carry out at
the bedside than HIMP, and the corrective saccade is
much easier for the clinician to see.
NEW DEVELOPMENTS
1. The ability of vHIT testing to probe the function of
all canals has revealed unexpected outcomes. One
is that a rather surprising number of patients have
BVL of most (or all) semicircular canals. Prior to
vHIT the extent of vertical canal loss could not be
measured in a clinic. With vHIT it now can be. And
this pattern of reduced or absent function of all
canals (Ward, Agrawal, Hoffman, Carey, & Della
Santina, 2013) gives new understanding of patient
complaints.
2. Complementing that result is the equally unexpected result of the bilateral sparing of anterior canal
function, when other canals show loss (Tarnutzer,
Bockisch, Buffone, & Weber, 2017). Figure 14–19
shows data for a patient with bilateral loss of horizontal canal function, but bilateral sparing of both
anterior and posterior canals (Akdal et al., 2016).
3. As mentioned above, the use of vHIT to quantify
the progress of the loss of canal function during
intratympanic gentamicin is now widespread.
4. The dissociation of vHIT and caloric test results
may be an indicator of endolymphatic hydrops.
Figure 14–19. Results of testing all canals in a patient with BVL. Here there is
loss of function in both horizontal canals, but sparing of both anterior canals
and of both posterior canals. Video head impulse measures of patients with
BVL often reveal relative sparing of anterior semicircular canal function. This
clinical pattern may possibly indicate gentamicin vestibulotoxicity or Ménière’s
disease, or in Wernicke’s encephalopathy as in this patient, but also occurs in
BVL of unknown origin. Reprinted from Journal of the Neurological Sciences,
Vol. 365, Akdal, G., MacDougall, H. G., Chen, L., Tanrıverdizade, T., Yig˘itaslan,
O., and Halmagyi, G. M., Selective impairment of horizontal vestibulo-ocular
reflexes in acute Wernicke’s encephalopathy, pp. 167–168, © 2016, with permission from Elsevier.
14. THE VIDEO HEAD IMPULSE TEST (vHIT) 359
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ConClusion
Vestibular testing is being revolutionized by vHIT, and
when the results for vHIT are combined with the results
of the new ocular and cervical vestibular evoked myogenic potential (oVEMP and cVEMP) tests it is possible
to measure the function of all vestibular sense organs
(Curthoys, 2012).
Video HIT is very simple and does not require
specialized conditions — testing is done with the
patients sitting in an ordinary chair in a normally lit
room. Video HIT is undemanding and can be used on
patients as young as 3 years. Video HIT is a fast, simple
way of quickly, safely, and acceptably answering the
question: Which side is affected? Is the canal function
of each ear in the normal range? Video HIT allows
repeated testing even within a few minutes. It gives an
absolute level of canal function. It is very well tolerated
by patients and it allows measurement of the function
of all semicircular canals. The vHIT test is noninvasive,
safe, simple, and quick (less than 10 min to test both
sides), and very acceptable even to dizzy and nauseous
patients. The analysis software provides objective,
quantitative results in real time. In sharp contrast to
caloric stimuli, with vHIT the magnitude of the stimulus at each instant in time is known and can be related
directly to the response at that instant. Video HIT is
portable — it can be used in the clinic or at the bedside
or the emergency room, or even in the patient’s home.
Video HIT can be carried out even during acute attacks
of vertigo (e.g., in a patient during a Menière’s attack or
an attack of vestibular neuritis [Manzari et al., 2011]).
Videos assoCiated With this ChaPter
Video 14–1. How the horizontal head impulse
test is carried out at Royal Prince Alfred
Hospital Sydney for HIMPs and SHIMPs.
Video 14–2. How the standard LARP impulses
are carried out at Royal Prince Alfred Hospital
Sydney.
Video 14–3. How the standard RALP impulses
are carried out at Royal Prince Alfred Hospital
Sydney.
Acknowledgments. The vHIT test was developed with
the continued support of the Garnett Passe and Rodney Williams Memorial Foundation and the National
Health and Medical Research Council of Australia,
and we are grateful to those bodies. We published the
original paper for vHIT in 2009, and Otometrics DK
transformed our system into Impulse. We thank Jorge
Rey-Martínez, Julia Dlugaiczyk, and Matthieu Gomes
for their comments and suggestions on this chapter.
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Appendix 14–A
The Physiological Basis for the Head Impulse Test
Much of the following can be found interactively in the
free app for iPhone 4 (and later iPhones) called aVOR.
That app does not work on Android devices. The work
of Goldberg (2012) is a definitive source of physiological information about canal function.
How can the vestibular system achieve the speed
and precision of the VOR? The sensitivity and the precision of the VOR are the outcomes of neural interaction
between the signals from the two sets of semicircular
canals on each side of the head. One way of thinking
about this interaction is as follows: normally, with the
head still, the neural output from the vestibular receptors and afferents on the two sides causes balanced
(i.e., approximately equal) resting neural activity in
the cells in the two vestibular nuclei in the brainstem
(Figure 14–20). A head turn upsets that balance
neurons on the side toward the head turn are activated
and canal neurons on the other side are simultaneously
inhibited. That imbalanced neural activity triggers the
response — the corrective eye movement — as well as
sensations of turning and postural responses to ensure
that you do not fall.
— canal
Acceleration Versus Velocity
The mechanics of the semicircular canal convert the
angular acceleration of the head into an angular velocity signal. Physiological recordings from primary semicircular canal afferents have shown that the mechanics
of the semicircular canal-cupula system have effectively integrated the head acceleration stimulus to produce a neural signal corresponding to head velocity.
The passive head turn causes fluid flow in the
membranous duct of the semicircular canal, deflecting
the receptor hair cells on the crista in the ampulla in an
excitatory direction, so that the primary afferent neurons are activated (see Figure 14–20). Simultaneously
the same head turn causes fluid flow in the membranous duct of the semicircular canal on the opposite side
of the head. However, because of the orientation of the
receptor hair cells in that opposite canal, this head turn
causes these contralateral semicircular canal receptors
to be deflected in an inhibitory direction, so the afferent
neurons on this opposite side of the head are inhibited.
So the one head turn causes simultaneous complementary neural events in the two vestibular labyrinths
excitation on one side and inhibition on the other
(Figure 14–20B). It is a “push-pull” system. This reduction in the neural firing of these cells acts indirectly
to reduce the inhibition exerted on central vestibular
neurons. Reduced inhibition (called “disinhibition”) is
effectively excitatory. So in healthy subjects there are
two sources of vestibular drive to the eye muscles —
direct excitation and indirect excitation (disinhibition).
These sum and drive the eyes to compensate for the
head rotation with great speed and precision.
The contribution from the contralateral labyrinth
by indirect activation from disinhibition is effective
over only a small range of stimulus values, since the
neurons in the vestibular nuclei are relatively quickly
inhibited to silence during a high acceleration head
rotation. However, during a low acceleration head turn
to the affected side in a patient with a UVL, this source
of indirect excitation from the remaining healthy ear
can provide sufficient excitation to generate a compensatory eye movement response for ipsilesional head
turns that looks normal. That is why low accelerations
are to be avoided during clinical testing. This small
indirect excitation component is generated during the
low velocity part of the head impulse
ities this input probably does not contribute, and that is
why high-velocity head impulses are necessary to test
canal function. High acceleration head turns to the left
test the left horizontal semicircular canal. In patients
with UVL, the VOR gain for head turns to the healthy
side is frequently systematically smaller than 1.0
lacking the (small) functionally excitatory drive from
the affected side.
The detailed anatomical and physiological evidence underpinning this account is given by Curthoys
(2002) and Curthoys and Halmagyi (1995). The relative importance of the intercommunication between
the bilateral labyrinth inputs has been known since
the physiological work of Precht and Shimazu (1965),
Precht, Shimazu, and Markham (1966) and Markham,
Yagi, and Curthoys (1977).
— at higher veloc-
—
— it is
A.
https://t.me/medicina_free
figure 14–20. A. The semicircular canals are sym-
Direction of head turn
left horizontal
canal ampulla
Excited Inhibited
B.
Head movement
to left
Compensatory eye
movement to right
Eye muscles
Oculomotor nucleus
Abducens nucleus
head impulse to the left
+
-
-
II
-
Vestibular nucleus
Primary afferents
Horizontal
semicircular
canal
activated. Simultaneously, the receptors in the right horizontal canal are deflected in an inhibitory direction so the
primary afferent neurons from the right horizontal semicircular canal have reduced firing (dashed lines).
atory input from the left canal projects to the left vestibular nucleus and activates type I neurons that are excitatory
neurons which project to and excite neurons in the right abducens nucleus which project to the lateral rectus
eye muscle of the right eye and so act to generate the compensatory eye movement response to the right. This
response of the type I neurons in the vestibular nuclei is further increased because inhibition arising indirectly from
the right horizontal canal via the type II inhibitory neurons is reduced. This reduced inhibition is called disinhibition
and it is functionally excitatory. It is a secondary source of an excitatory drive arising from the opposite labyrinth.
So, in healthy subjects there are two sources of vestibular drive to the eye muscles — direct excitation and indirect
excitation (disinhibition). These sum and drive the eyes to compensate for the head rotation with great speed and
precision. After a UVL an ipsilesional head turn no longer causes the direct excitation, but still causes the indirect
excitation (the disinhibition) from the remaining healthy ear. For this reason, the VOR gain for ipsilesional head turns
in UVD patients is not zero. And the lack of this functionally excitatory drive from the affected side acts to decrease
the VOR gain for head rotations to the healthy side. Transmission through the vestibular nucleus can be inhibited
by cerebellar neurons, resulting in VOR suppression. It is stressed that this is a very basic figure showing just one of
the many neural circuits controlling vestibulo-ocular responses.
+
I
+
Left
Midline
right horizontal
canal ampulla
-
+
+
+
II
+
I
-
Right
metrical on the two sides of the head (see Figure
14–1) so a horizontal head turn causes opposite
effects in the paired semicircular canals on the two
sides of the head. The figure shows a schematic
view directly downward onto enlarged and translated human horizontal canals. Within the swelling
in the duct (the ampulla), there is a saddle-like
crista (here viewed edge-on) which is covered by
around 7,500 receptor hair cells, each projecting
into a jelly-like structure (the cupula) that seals the
membranous duct.
left in this example) causes fluid flow in an excitatory direction (arrow in the duct) in the left semicircular canal.
canal and so all 7,500 receptors on the crista in
the left canal are deflected in an excitatory direction resulting in an increase of neural activity of
all of the primary horizontal semicircular canal
afferents in the left vestibular nerve.
ously, that leftward head turn causes endolymph
flow in an inhibitory direction in the right semicircular canal (arrow in the duct
the receptors on the right crista to be deflected in
an inhibitory direction and so the neural activity
of all primary semicircular canal afferents on the
right is reduced.
LL-RL applies to accelerations in the planes of the
pairs of vertical canals
works.
Some of the neural mechanisms by which a
head turn generates a compensatory eye movement response. The neural connections in the
brainstem which have been extensively documented by physiological studies (references in
Curthoys, 2002). Excitatory neurons are shown as
filled hexagons; inhibitory neurons as open hexa-
-
Neurons that are activated (+) are shown as
gons.
thick darker traces, neurons with reduced firing (−)
are shown as light, dashed traces. The sequence is
as follows: during a leftward head turn the receptors in the left horizontal canal are deflected in
an excitatory direction and so the primary afferent neurons from the left semicircular canal are
The one head rotation (to the
This deflects the cupula in the left
), thus causing all
The same “push-pull” principle for
— LARP and RALP. B. How it
Simultane-
The excit-
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