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Recently we showed that when a patient comes to the vestibular
clinic with acute vertigo and nausea, the clinician, by using the
results of new objective measures of peripheral vestibular function
can be confi dent it is an acute attack of vestibular neuritis rather than
an acute attack of M é ni è re ’ s disease or an acute attack of labyrinthitis
(Manzari et al, 2011, 2013). But how can the recovery of the patient
after vestibular neuritis be measured? That is the crucial question
for vestibular compensation. Here we show that measures at regular
intervals by the new simple objective measurement of horizontal
semicircular canal function, the video head impulse test (vHIT;
MacDougall et al, 2009), provide the answer. The results from two
extreme patients raise important questions about the mechanism of
recovery after unilateral vestibular loss.
The new tests are (1) the vHIT test of semicircular canal func-
tion, (2) the ocular vestibular-evoked myogenic potential (oVEMP),
and (3) the cervical vestibular evoked myogenic potential (cVEMP).
The video head impulse test (vHIT) is a clinically realistic way of
measuring semicircular canal function quickly and accurately in a
way which is well tolerated by patients, even during intense nau-
sea. Simultaneous measures in the same person by both vHIT and
scleral search coils have shown that the accuracy of vHIT matches
the search coil technique in testing dynamic semicircular canal func-
tion (MacDougall et al, 2009; 2013). The ocular vestibular evoked
myogenic potential (oVEMP) tests predominantly utricular function,
and the cervical vestibular evoked myogenic potential (cVEMP) tests
predominantly saccular function (Curthoys, 2010, 2012).
Vestibular evoked myogenic potentials (VEMPs) are small poten-
tials in response to sound and vibration stimulation recorded by sur-
face electrodes on the skin above activated muscles. Physiological
evidence shows that air-conducted sound and bone-conducted vibra-
tion activates otolithic receptors and afferent neurons and results in:
A short latency inhibitory potential (the cVEMP p13-n23) 1.
recorded over the ipsilateral tensed sternocleidomastoid muscles
predominantly due to saccular input, and
A short latency excitatory potential (the oVEMP n10) recorded 2.
over inferior oblique eye muscles beneath the contralateral eye
as the patient looks upward, predominantly due to utricular input.
The oVEMP is a crossed , ascending, excitatory, utriculo-ocular
response. The cVEMP p13-n23 is an uncrossed , descending,
inhibitory, sacculo-collic response.
There is now a wealth of physiological and clinical evidence support-
ing the use of these VEMPs as indicators of the state of peripheral
utricular and saccular function (see Curthoys, 2012 for a review).
Design and Methods
To test saccular function, the cVEMP p13-n23 was measured to
repeated short-tone bursts of 500-Hz bone conducted vibration
(BCV) each lasting 7 milliseconds, at a rate of 4/s, for 50 pre-
sentations. To test utricular function the oVEMP n10 to the same
stimuli was measured. The stimuli were delivered by a Bruel and
Clinical note
Vestibular function after vestibular neuritis
L. Manzari * , A.M. Burgess † , H.G. MacDougall † & I.S. Curthoys †
* MSA ENT Academy Center, Cassino (FR), Italy, and † Vestibular Research Laboratory, School of Psychology, The University of Sydney, NSW, Australia
Abstract Objective: To measure horizontal semicircular canal function over days, weeks, and months after an acute attack of vestibular neuritis. Design: The video head impulse test (vHIT)
was used to measure the eye movement response to small unpredictable passive head turns at intervals after the attack. Study sample: Two patients diagnosed with acute right unilateral
vestibular neuritis. Results: There was full restoration of horizontal canal function in one patient (A) as shown by the return of the slow phase eye velocity response to unpredict-
able head turns, while in the other patient (B) there was little or no recovery of horizontal canal function. Instead this second patient generated covert saccades during head turns.
Conclusion: Despite the objective evidence of their very different recovery patterns, both patients reported, at the fi nal test, being happy and feeling well recovered, even though in one
of the patients there was clear absence of horizontal canal function. The results indicate covert saccades seem a successful way of compensating for loss of horizontal canal function
after unilateral vestibular neuritis. Factors other than recovery of the slow phase eye velocity are signifi cant for patient recovery.
Key Words: Vestibular; labyrinth; vestibular neuritis; head impulse test; vestibular compensation; saccades
Correspondence: Ian S. Curthoys, Vestibular Research Laboratory, School of Psychology, University of Sydney, Sydney. NSW 2006, Australia. E-mail: ianc@psych.usyd.
edu.au
(Received 19 January 2013; accepted 22 May 2013)
ISSN 1499-2027 print/ISSN 1708-8186 online © 2013 British Society of Audiology, International Society of Audiology, and Nordic Audiological Society
DOI: 10.3109/14992027.2013.809485
International Journal of Audiology 2013; Early Online: 1–6
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Kjaer minishaker 4810 to the midline of the forehead at the hairline
(a location called Fz). In both cases the stimuli were generated and
the responses averaged using a Chartr EP 200 averager (Otometrics,
Denmark).
The vHIT system consists of a pair of lightweight, tightly-fi tting
goggles on which is mounted a very small, light, fast, fi re-wire cam-
era and a half silvered mirror which refl ects the image of the patient ’ s
eye into the camera. A small sensor on the goggles measures head
movement. The whole goggle system is lightweight (about 60 g) and
must be secured tightly to the head to minimize slippage, because
any slippage of the goggles relative to the eye will be registered as
a movement of the eye and so generate artifactual data. The eye
movement is recorded at 250 Hz. The stimuli are brief, passive,
unpredictable, horizontal head turns to the left or right through an
angle of about 10 – 20 ° in 0.5 s, delivered by the clinician while the
patient is asked to keep fi xating a target spot on the wall. Head turns
towards the affected ear cause a reduced slow phase compensatory
eye velocity response with the consequence that the eyes are taken,
with the head, off target and a saccade is necessary to regain fi xa-
tion on the target spot as per instructions. These saccades may occur
after the end of the head turn when head velocity has returned to
zero (overt saccades), or actually during the head turn itself when
the head velocity is greater than zero (and such saccades are called
covert saccades because they are almost impossible for the clinician
to detect by visual inspection) (Weber et al, 2008, 2009).
vHIT provides two indicators of semicircular canal functional
state: (1) the VOR gain which is the ratio of slow phase compensa-
tory eye velocity to head velocity, and (2) the saccade pattern —
whether saccades occur during the head movement (covert saccades)
or after it (overt saccades). By using vHIT at intervals after the acute
attack, the clinician can follow the dynamic function of the horizon-
tal semicircular canal during vestibular neuritis or labyrinthitis, and
determine whether the dynamic function of the canal does or does
not recover.
Vestibular neuritis patients Two patients, one man (identifi ed as A) and one woman (B), both aged
36, were referred for the fi rst time to our tertiary referral neurotological
center (MSA ENT Center, Cassino, Italy) respectively on the 23rd Jan-
uary 2012 and 10th June 2011. On the basis of the results of a battery of
objective tests of otolithic and semicircular canal function (see below)
both patients were diagnosed as having right-sided vestibular neuritis.
They both came to the clinic with acute vestibular syndrome (long
lasting rotatory vertigo, nausea, pallor, and vomiting). The patients did
not remember closed cranial trauma, and the anamnesis showed no
notable systemic disease such as diabetes or cardiovascular problems.
There were no cochlear symptoms, such as tinnitus or fullness or acute
hearing loss either before, during, or after the onset of the acute vertigo,
so it was presumed that they were not patients with M é ni è re ’ s disease
or involvement of the cochlea or labyrinthitis.
At the time of the fi rst visit all symptoms reported by the patients
were evaluated with a standardized set of tests including bed-side
examination (Table 1). Otoscopy fi ndings were normal. Both patients
were submitted to instrumental audio vestibular tests: audiometry,
tympanometry with stapedial refl exes, and auditory brainstem response
which were all normal for the patient ’ s age. Vestibular sense organ
testing showed marked losses. Firstly, Fitzgerald – Hallpike caloric
testing showed hyporesponsiveness of the right horizontal canal of
the affected ear. The pattern of horizontal, torsional, and vertical eye
movement components were measured with three-dimensional infrared
video-oculography (50-Hz sampling; Torsio VNG Ulmer; Synapsys,
Marseille, France) during spontaneous nystagmus; during head shaking
nystagmus; during the Dix-Hallpike manoeuvre, and during the head
roll manoeuvre for positional and positioning nystagmus. At the time
of the acute attack, both patients showed spontaneous nystagmus with
horizontal and torsional components; the horizontal quick phase being
directed toward the left (healthy) side. There was no evidence of BPPV
or positional nystagmus.
Both patients were referred to a tertiary radiology center for a
magnetic resonance imaging scan (MRI) of the posterior cranial
fossa using paramagnetic contrast enhancement. In both patients
radiologic evaluation revealed normal and symmetrical eighth
cranial nerves and normal signal from midbrain and posterior
cranial fossa.
The patients received oral steroids in the fi rst period of the disease,
seven days at least. It was recommended to resume daily activities as
soon as possible. A specifi c vestibular rehabilitation training was not
recommended. Over the next months the same patients were tested
on repeated occasions even when the acute subjective symptoms had
completely disappeared.
Abbreviations
BCV Bone-conducted vibration
cVEMP Cervical vestibular evoked myogenic potential
oVEMP Ocular vestibular evoked myogenic potential
SCM Sternocleidomastoid muscle
vHIT Video head impulse test
VOR Vestibulo-ocular refl ex
Table 1. Summary of clinical data of patients.
Neurotological evaluation
Audiometry
PTA scores
Patient Affected ear Gender Age, years
Spontaneous nystagmus
Head-shaking nystagmus
Canal paresis
Vibration-induced nystagmus MRI Right ear Left ear
A R M 36 Ny L/H Ny L/H 56% Ny L/H Normal 10.00 dB 10.00 dB
B R F 37 Ny L/H Ny L/H 67% Ny L/H Normal 10.00 dB 10.00 dB
L: left; R: right; F: female; M: male; dB: decibel; Ny: nystagmus; L/H: nystagmus with the horizontal quick-phase component to the left. Spontaneous
nystagmus: nystagmus that appears while the patient is in darkness without a fi xation light. Head-shaking nystagmus: nystagmus that appears after vigorous
horizontal headshaking for about 15 seconds at a frequency of about 2 Hz. Vibration-induced Nystagmus: nystagmus that appears after bone-conducted
vibration is applied to the mastoid bone while the patient is in darkness. MRI: magnetic resonance imaging scan. PTA scores (pure-tone audiometry average
scores): 500, 1000, 2000, 3000 Hz (considered frequencies).
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Vestibular function after vestibular neuritis 3
p13n23n10
R eye
L eye
R eye
L eye8 May 2012
R eye
L eye23 Jan 2012
R eye
L eye15 June 2012
10 ms
R SCM
L SCM
R SCM
L SCM8 May 2012
R SCM
L SCM
23 Jan 2012
R SCM
L SCM
15 June 2012
10 ms
–+
10 μV
10 June 2011 10 June 2011
–+
100 μV
oVEMPs cVEMPs
Patient A
Patient B
Figure 1. Records of oVEMP (left column) and cVEMP (right
column) responses for patients A (upper panel) and B (lower panel),
tested by 500-Hz BCV at Fz at the acute phase (top row) and after
recovery (bottom row). The approximate epoch of the oVEMP n10
potentials are marked by a yellow bar, and similarly the epoch of
the cVEMP p13 and n23 are marked by a blue bar. The p13 and
n23 responses are indicated by short vertical tick marks. In the fi rst
session of 23 Jan 2012, patient A shows reduced otolith function in
the right ear (both reduced utricular function shown by oVEMP n10
beneath the left eye, and reduced saccular function shown by cVEMP
p13-n23 over the right SCM). By the second session of 15 June
2012, the saccular function in the right ear had recovered, as shown
by a detectable p13-n23 response in the right SCM, approximately
symmetrical with the p13-n23 response in the left SCM. In the same
ear, utricular function as shown by n10 in the left eye was still small.
In the fi rst session of 10 June 2011, patient B shows absent saccular
and utricular function in the right ear, similar to the fi rst session for
patient A. By the second session of 8 May 2012 neither utricular nor
saccular function in the right ear had recovered in this patient, as
shown by absent n10 responses in the left eye and absent p13-n23
responses in the right SCM.
Results
In both patients 500-Hz BCV at Fz caused asymmetrical cVEMP
responses with reduced or absent p13-n23 potential over the ipsilat-
eral (right) contracted sternocleidomastoid (SCM) muscle, but with
potentials in the normal range for the Cassino clinic (130 � 65 μ V
(SD) n � 54; (Manzari et al, 2012) over the contralateral SCM, and
so it was concluded that the saccular afferents in the right inferior
vestibular nerve were affected in both patients (Figure 1).
The objective test of utricular function — the n10 component of
the ocular vestibular evoked myogenic potential (the oVEMP n10)
to the same 500-Hz Fz BCV stimulus — showed absent n10 potentials
beneath the left eye (the contralesional eye), in both patients with
n10s beneath the right eye being in the normal range for the Cassino
clinic (5.7 � 2.6 μ V (SD), n � 54; Manzari et al, 2012) — resulting
in an oVEMP n10 asymmetry ratio (AR) of 100% for both patients
(Figure 1), indicating that the utricular afferents in the right superior
vestibular nerve were affected in both patients.
This result indicates that the utricular afferents in the right superior
vestibular nerve were affected since the oVEMP is a crossed response
(Iwasaki et al, 2007). Testing horizontal canal function (described
below) showed reduced horizontal canal function for rightwards head
rotations. The combination of the reduced right horizontal canal func-
tion, the reduced right utricular function, and the reduced right saccular
function, in the absence of any cochlear symptoms, led to the diagnosis
of right vestibular neuritis for both patients.
At the time of the fi rst visit dynamic horizontal canal function was
tested by vHIT and the results of that test are shown in the uppermost
panels of Figures 2 and 3. For both patients vHIT showed a clearly
impaired right horizontal VOR gain when their head was abruptly,
unpredictably, passively turned to the right, whereas similar head turns
to the left (the healthy side) had normal VOR gain. At testing on this
fi rst occasion during the ipsilesional rightward passive head turns,
patients also showed a series of overt saccades and some covert sacca-
des and these saccades also confi rm inadequate right horizontal canal
VOR dynamic function (Weber et al, 2008). After the fi rst evaluation
both patients were regularly retested at the Cassino clinic (at the dates
shown on the panels in the fi gures) to evaluate the time course of the
recovery of the dynamic VOR from the acute neuritis. Both patients
were evaluated until they themselves declared they were ‘ cured ’ and
that subjectively their balance felt normal. For Patient A the time
to reach this stage was short — only about fi ve months, whereas for
Patient B the time was much longer (about 11 months) before the
patient declared herself fully recovered. In contrast to these subjective
reports of good recovery, the objective measures of semicircular canal
function by vHIT showed two totally different pictures of recovery of
dynamic semicircular canal function. In the fi rst case (A) there was
complete recovery – full restoration of horizontal canal function with
normal slow phase eye velocity and VOR gain close to 1.0 — whereas
in the second case (B) there was a complete absence of any recovery
of horizontal canal function.
Discussion
What factor(s) could explain this very similar subjective evaluation,
in light of the very different objective evidence? The results suggest
that saccades may play a major role in the recovery. In response
to the passive, unpredictable head rotation with high acceleration,
patient B showed a pattern of saccades evolving from a combina-
tion of overt and covert saccades at the acute stage (10 June 2011)
to covert saccades only at testing 11 months later (8 May 2012;
Figure 3). This patient, like many others, generated very small covert
saccades during the passive high acceleration head movements; and
these may hold the key to understanding compensation of vestibulo-
ocular symptoms in some patients.
Two distinct neural circuits underlie the generation of horizontal
eye movements: one for slow phase eye movements and the other for
generating quick phases and saccades (for a review, see Curthoys,
2002). There are interconnections between these circuits but each
can be considered separately. Slow phase eye velocity in response to
head turns is generated by the direct three neuron pathway: receptor/
vestibular nucleus/abducens motoneurons/eye muscles.
Quick phases and saccades are generated by a separate neural
circuit involving a network of burst neurons and pause neurons in
the brainstem close to abducens nucleus. The quick phase circuit can
be triggered by vestibular input (and so generate the quick phase of
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3
0
1
2
Peak Head Velocity (deg/s)
GAIN
Left Lateral Right Lateral
Left Lateral Right Lateral
Left Lateral Right Lateral
Left Lateral Right Lateral
250
–100
–50
–100
–50
–100
–50
–100
–50
0
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0
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–100
–50
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–100
–50
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–100
–50
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0
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Right: mean 0.58 SD 0.05 n 22
Left: mean 0.96 SD 0.07 n 22
LeftRight
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Peak Head Velocity (deg/s)0 100 200
0 100 200
0 100 200
0 100 200
GAIN LeftRight
3
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Peak Head Velocity (deg/s)
GAIN LeftRight
3
0
1
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Peak Head Velocity (deg/s)
GAIN LeftRight
deg/ s deg/ s
Right: mean 0.94 SD 0.04 n 20
Left: mean 1.08 SD 0.03 n 20
SD 0.05Right : mean 0.77
SD 0.04Left: mean 1.01
n 18
n 19
Right: mean 1.03 SD 0.06 n 16
Left: mean 1.19 SD 0.03 n 18
2012/01/23
2012/02/27
2012/03/28
Time (ms) Time (ms)
Time (ms) Time (ms)
Time (ms) Time (ms)
Time (ms) Time (ms)
deg/ s deg/ s
deg/ s deg/ s
deg/ s deg/ s
6000 100 200 300 400 500 6000 100 200 300 400 500
6000 100 200 300 400 500 6000 100 200 300 400 500
6000 100 200 300 400 500 6000 100 200 300 400 500
6000 100 200 300 400 500 6000 100 200 300 400 500
EyeHead
Figure 2. Objective measures of horizontal semicircular canal function at four testing occasions for patient A with acute unilateral (right)
vestibular neuritis: occasion 1 (23 Jan 2012) and at succeeding times thereafter. Each panel shows superimposed time series of head velocity
(blue) and the corresponding eye velocity (orange) for the tests of horizontal canal dynamic function using vHIT. The signs of head velocity
for leftward impulses and of eye velocity for rightward impulses have been inverted to allow for easier comparison. Each panel also shows
the horizontal VOR gains versus peak head velocity for the head-impulse data shown in that panel. Closed circles: leftward impulses; open
circles: rightward impulses. The mean and 95% confi dence intervals for gains in leftward and rightward impulses are shown at the right of
each Gain plot. Normal horizontal VOR gains are about 0.7 – 1.0 (MacDougall et al, 2009). For rotations to the affected side, eye velocity
is substantially less than the corresponding head velocity during the head turn so the VOR is signifi cantly less than for head turns to the
healthy side. There is a shower of saccades at the end of the head turn (black arrow). On each succeeding testing occasion, for head turns
to the affected side the slow phase eye velocity improves and the corrective saccades reduce in frequency and size until at the fi nal test,
VOR gain is 1.03 (in the normal range) and there are virtually no corrective saccades and it is concluded that horizontal semicircular canal
function has been fully restored after the neuritis.
vestibular nystagmus during prolonged canal activation) but can also
be triggered by other inputs, e.g. descending axons from the superior
colliculus causing voluntary saccades. There is evidence that input
from neck afferents can also trigger this quick phase neural circuit
(Barmack et al, 1989). In healthy subjects these two neural circuits
interact so that prolonged semicircular canal input from a maintained
acceleration results in slow phase compensatory eye movements, inter-
rupted by the quick return phases of vestibular nystagmus. In both of
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3
0
1
2
Peak Head Velocity (deg/s)0 100 200
GAIN
SDRight: mean
SDLeft: mean
LeftRight
n
n
2011/06/10
3
0
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Peak Head Velocity (deg/s)0 100 200
GAIN
SDRight: mean
SDLeft: mean
LeftRight
n
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2011/08/22
3
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Peak Head Velocity (deg/s)0 100 200
GAIN
SDRight: mean
SDLeft: mean
LeftRight
n
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2011/12/21
3
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Peak Head Velocity (deg/s)
0 100 200
GAIN
SDRight: mean
SDLeft: mean
LeftRight
n
n
2012/05/08
Left Lateral Right Lateral250
-10 0
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Head
0
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-5 0
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Time (ms)6000 100 200 300 400 500
de g/ s de g/ s
Time (ms)6000 100 200 300 400 500
Left Lateral250
-10 0
-5 0
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200
250
-10 0
-5 0
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Time (ms)6000 100 200 300 400 500
deg/s deg/s
Time (ms)6000 100 200 300 400 500
Left Lateral
Right Lateral
Right Lateral250
-10 0
-5 0
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-10 0
-5 0
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Time (ms)6000 100 200 300 400 500
0.130.56
0. 071.03
16
16
0.050.49
0. 060.97
25
21
0.070.50
0. 051.02
28
24
0.050.46
0. 031.01
19
18
Figure 3. The corresponding records for patient B who was also diagnosed with an acute (right) vestibular neuritis on occasion 1 (10
June 2011) and then tested at succeeding times thereafter. In this patient also the eye velocity is substantially less than head velocity on
occasion 1, but in contrast to patient A, the eye velocity response during the head impulse does not change over the succeeding tests and
at the fi nal test on 8 May 2012 the VOR gain remained at 0.46, about the same (slightly smaller) than the original VOR gain of 0.56. In
the later tests there is a shift of the saccadic pattern so that the saccades tend to be much more clustered and to be initiated during the head
turn (i.e. before the head velocity has returned to zero) and so are classifi ed as covert saccades. This is strong evidence that the slow phase
eye velocity to high acceleration head impulses does not change over time, and so we conclude that the neuritis has caused long term and
probably permanent damage. There is evidence of changes in the pattern of saccades. At the last test this patient reported good balance
function and considered that they had recovered.
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the patients here the horizontal slow phase mechanism was disabled at
the acute stage (as shown by the very low gain VOR) most probably
because of the acute damage to the superior vestibular nerve. However
the quick phase mechanism was unaffected as shown by the saccades
at each head turn. Over time in Patient A the slow phase mechanism
returned (the VOR gain increased) and as it did so the quick phases
become progressively smaller. In Patient B there is no recovery of the
slow phase at all, so even after many months it is just the saccades
which are present in response to the head turn. However the temporal
location of these saccades has moved so they occur during the head
movement and so are termed covert saccades.
Why are covert saccades so potentially valuable? Firstly because
they achieve the goal of keeping fi xation on the target and they do
so by effectively bypassing the neural circuits generating the slow
phase eye velocity (which are non-functional because of the reduced
or absent vestibular input) and instead use the independent neural
circuits for saccade generation. Secondly because visual perception
is attenuated — effectively blanked — by a process called saccadic
suppression during and after the saccade (Matin, 1974).
The major question remains ‘ what triggers covert saccades? ’ Why
do we suggest that these covert saccades may be produced by neck
afferent input (Macdougall & Curthoys, 2012)? Because one patient
with known surgical bilateral complete vestibular loss produced
covert saccades with exactly correct direction for 300 successive head
rotations (Weber et al, 2009). This is simply too high a success rate
to attribute it to anticipation or prediction. We have suggested the
covert saccades could be produced by neck afferents being triggered
at the very start of the head turn (Macdougall & Curthoys, 2012).
We stress that this is NOT the cervico-ocular refl ex which acts to
generate slow compensatory eye movements in response to neck input
(Yakushin et al, 2011) but a saccade which is triggered by activation
of neck receptors at the start of the head turn. Given their total loss
of vestibular input and the improbability of generating 300 successive
saccades in the correct direction by means of anticipation or prediction
we consider neck afferent input as a likely cause of covert saccades.
It is of particular interest that in both patients the measures of
otolithic function show unilateral loss of utricular function at the
acute stage and no recovery. Neither of these patients was troubled
by the unilaterally absent utricular input. Just as many patients with
total loss of all vestibular function from one ear may recover com-
pletely and resume normal life styles and be perfectly happy, so these
tests are showing that patients with isolated loss of individual ves-
tibular sense organs can also recover and resume normal lifestyles.
It may be thought that caloric tests delivered to these two patients
at comparable intervals would have given a similar result. In our
experience patients must be persuaded to have one caloric test and
are very reluctant to commit to successive calorics. Furthermore the
caloric test measures horizontal canal function and only the slow
phase eye velocity, and could not have shown the shift in response
towards covert saccades which we think to be of special signifi cance
for the successful compensation of patient B in the face of absent
horizontal canal function.
Conclusions
Tracking vestibular function from patients presented with acute
vestibular neuritis, over days, weeks, and months after the acute
attack, using the vHIT test and other new tests of vestibular
function, provides very useful information about their vestibular
compensation, and highlights the apparent value of covert saccades
in vestibular compensation.
Acknowledgements
We are grateful for the support of NH & MRC of Australia (1046826)
and of the Garnett Passe and Rodney Williams Memorial Foundation.
Ian Curthoys is funded by project grants from the National Health
and Medical Research Council of Australia and the Garnett Passe and
Rodney Williams Memorial Foundation. Ann Burgess and Hamish G.
MacDougall are funded by a project grant from the National Health
and Medical Research Council of Australia and the Garnett Passe and
Rodney Williams Memorial Foundation, respectively.
Declaration of interest : Hamish G. MacDougall and Ian Curthoys
are unpaid consultants to GN Otometrics, Taastrup, Denmark. The
authors have no other funding, fi nancial relationships, or confl icts
of interest to disclose.
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