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Journal of Vestibular Research 27 (2017) 233–242
IOS Press
Clinical and video head impulse test
in the diagnosis of posterior circulation
stroke presenting as acute vestibular
syndrome in the emergency department
Ayse Gulera,1 , Funda Karbek Akarcab,1 , Cenk Eraslanc , Ceyda Tarhand , Cem Bilgend ,
Tayfun Kirazlid and Nese Celebisoya,∗
a Department
of Neurology, Ege University School of Medicine, Bornova, Izmir, Turkey
of Emergency, Ege University School of Medicine, Bornova, Izmir, Turkey
c Department of Radiology, Ege University School of Medicine, Bornova, Izmir, Turkey
d Department of Otorhinolaryngology, Ege University School of Medicine, Bornova, Izmir, Turkey
b Department
Received 23 November 2016
Accepted 28 June 2017
INTRODUCTION: Head impulse test (HIT) is the critical bedside examination which differentiates vestibular neuritis (VN)
from posterior circulation stroke (PCS) in acute vestibular syndrome (AVS). Video-oculography based HIT (vHIT) may have
aadditional strength in making the differentiation.
METHODS: Patients admitted to the emergency department of a tertiary-care medical center with AVS were studied. An
emergency specialist and a neurologist performed HIT. vHIT was conducted by an neuro-otology research fellow.
RESULTS: Forty patients 26 male, 14 female with a mean age of 49 years were included in the analyses. Final diagnoses
were VN in 24 and PCS in 16 patients.
In the VN group, clinical HIT was assessed as abnormal in 19(80%) cases by the emergency specialist and in 20(83%)
by the neurologist. In all PCS patients, HIT was recorded as normal both by the emergency specialist and the neurologist
(100%). On vHIT, patients with VN had significantly low gain values for both the ipsilesional and contralesional sides when
compared with the healthy controls, with significantly lower figures for the ipsilesional side (p < 0.001). All patients in this
group had normal DWI-MRI.
PCS patients had bilaterally low gain (p < 0.05) on vHIT. However, gain asymmetry was not significant. Subgroup analyses
according to presence of brainstem involvement revealed bilateral low gain (p < 0.05) in patients with brainstem infarction
(anterior inferior cerebellar artery-posterior inferior cerebellar artery stroke, AICA-PICA stroke) whereas patients with pure
cerebellar infarction (posterior inferior cerebellar artery-superior cerebellar artery stroke, PICA-SCA stroke) had gain values
similar to healthy controls.
With a gain cut-off ≤0.75 and gain asymmetry cut-off ≥17%, as determined by ROC analysis, 100% of PCS patients and
80% of VN patients were correctly diagnosed.
CONCLUSIONS: Clinical HIT, either performed by an emergency specialist or neurologist is equivalent to vHIT gain and
gain asymmetry analysis as conducted by neuro-otologist in the diagnosis of PCS, albeit mislabeling about 20% of VN
1 These
authors share the first authorship.
author: Nese Celebisoy, M.D., Prof., Department of Neurology, Ege University School of Medicine, Bornova,
35100, Izmir, Turkey. E-mail:
∗ Corresponding
ISSN 0957-4271/17/$35.00 © 2017 – IOS Press and the authors. All rights reserved
A. Guler et al. / Clinical and video head impulse test in the diagnosis of posterior circulation stroke
patients. vHIT does not appear to yield additional diagnostic information. These findings indicate the strength of clinical
HIT. Pure gain-based vHIT analysis seems limited and needs to be incorporated with saccade analysis.
Keywords: Acute vestibular syndrome, head impulse test, video-oculography based head impulse test, vestibular neuritis,
posterior circulation stroke
1. Introduction
Acute vestibular syndrome (AVS) is a clinical
syndrome of new onset continuous vertigo, nausea/vomiting, motion intolerance and gait instability
lasting days to weeks [9]. It has been reported to be
the diagnosis in approximately 10 to 20% of dizzy
patients admitted to emergency departments in US
[24]. The most common causes are vestibular neuritis
(VN) in ∼70% and posterior circulation stroke (PCS)
in ∼25% [24]. Though not considered as a stroke
symptom previously [5], recent evidence has revealed
that isolated vertigo is a common PCS presentation
[9, 24, 15, 12, 20]. Therefore, it is critical to differentiate stroke patients from patients with VN admitted
to the emergency department with features of AVS.
Current evidence indicates that bedside examinations
mainly involving eye movements can distinguish central lesions from peripheral ones [9, 24, 15, 16, 10].
HINTS battery involving head impulse test (HIT),
nystagmus, test of skew have approximately 99% sensitivity in diagnosing PCS [16, 23], whereas magnetic
resonance imaging (MRI) with diffusion-weighted
imaging (DWI) has a sensitivity of 80% to 85% in
the first 24 to 48 hours [16, 18].
The highest sensitivity component of the battery is
the horizontal HIT of vestibulo-ocular reflex (VOR)
[7]. Clinically a unilateral abnormal HIT has been
found in approximately 92% of cases with acute VN
[21]. It is present in less than 10% of stroke patients
generally those involving the labyrinth, vestibular
nerve or nucleus [11]. A sensitivity of ∼91% and
specificity of ∼100% has been reported for central
lesions in AVS [16].
Quantitative HIT, both video-oculography (VOG)
based HIT testing (vHIT) [14, 17] and the gold standard, search coil [3], have been previously studied
in AVS and can separate VN from posterior inferior
cerebellar artery (PICA) strokes. However, anterior
inferior cerebellar artery (AICA) strokes were at risk
of being misclassified based on VOR gain alone but
were correctly classified by corrective saccade analysis [3].
In this study our first aim was to assess the reliability of the clinical HIT results in the emergency
department to differentiate VN from PCS in AVS. The
second aim was to see if vHIT measurements yielded
additional information in making the differentiation.
2. Patients and methods
The method was similar to two previous studies
[3, 14]. Patients presenting to the emergency department of a tertiary-care medical center with AVS who
had acute vertigo, nystagmus, nausea or vomiting
and unsteady gait of less than 3 days in onset were
enrolled in a prospective cross-sectional study from
December 2013 to March 2016. Patients with a previous history of vestibular or ocular motor disorders
were excluded. All patients gave written informed
consent and the study was approved by the institutional ethics committee. The patients underwent
structured bedside examination including the HINTS
battery [9] plus bedside hearing by finger rub [16] first
by an emergency specialist (FK) and then by a neurologist (AG) who were blinded to each other’s findings.
Diagnosis of suspected central or peripheral lesion
were made without knowledge of patient history.
The noninvasive, quantitative video-oculography
device (ICS Impulse, GN Otometrics, Taastrup,
Denmark) was used to measure and record eye movements. The vHIT was conducted by a neuro-otology
research fellow (CK). The operator stood behind the
subject to hold the head and instructed the subject
to focus on a target approximately 1 meter away.
The lateral canals were stimulated with the head
inclined forward 30 degrees. At least 20 random
impulses with unpredictable timing with amplitudes
of 5–20 degrees and a head velocity of 50–250
degrees/second were performed. All vHIT trials were
assessed by an expert masked neuro-otologist (NÇ)
to classify as interpretable (no artifacts or fast eye
movements during the VOR) or uninterpretable. For
comparison vHIT recording was performed in 29 age
and sex matched healthy controls. Gain asymmetry was determined by using the formula used in a
previous study [25] which is as follows:
contralateral gain-ipsilateral gain/contralateral
gain+ipsilateral gainX100.
A. Guler et al. / Clinical and video head impulse test in the diagnosis of posterior circulation stroke
The diagnosis of VN was determined by the
presence of unidirectional spontaneous nystagmus
obeying Alexander’s law or unilateral gaze-evoked
nystagmus with the fast phase directed away from
the vestibular deficit, abnormal clinical HIT, no neurologic signs including absence of skew deviation and
normal DWI.
Any finding in the HINTS battery suspicious for
a central lesion i.e. presence of direction changing
nystagmus, a negative clinical head impulse test or
skew deviation indicated PCS.
All patients underwent MRI to confirm final diagnosis. Lesion was determined by a neuroradiologist
(CE); abnormal DWI was diagnosed as PCS.
3. Statistics
The IBM SPSS Statistics 23 software was used
for the statistical analyses. The Shapiro–Wilk test
was performed to check if the numerical data was
normally distributed in each group. Parametric tests
were used as normal distribution was conformed.
Comparison of the numerical data between groups
was performed by one-way ANOVA. Homogeneity
of variances was tested by Levene statistics. As the
variances were homogeneous, pairwise comparisons
following ANOVA was performed by Bonferroni test.
Paired t-test was used to test the significance of difference between the ipsilesional and contralesional VOR
gains. Receiver operating characteristic curve analysis was used to identify potential quantitative cut-off
points for differentiating VN from PCS. Categorical
variables were compared with Chi-square test. All the
tests were performed at a 0.05 level of significance
(p < 0.05).
3.1. Reliability assessment
The Kappa statistic was used to document interrater reliability and was reported as an overall mean
with standard deviation. Kappa statistic <0.00; poor,
0.00–0.20; slight, 0.21–0.40; fair, 0.41–0.60; moderate, 0.61–0.80: substantial and 0.81–1.00; excellent
were agreement between physician raters. p-value of
less than 0.05 was considered to be significant.
4. Results
Fifty-two AVS patients admitted to the Emergency
Department of Ege University Medical School were
Fig. 1. Flow diagram of patient screening, enrollment and final
present. Five were excluded because of a lack of
confirmatory neuroimaging. Three patients could not
cooperate with vHIT testing. In 4 patients vHIT
results were accepted as uninterpretable. Therefore
40 patients 26 (%65) male, 14 (%35) female with a
mean age of 49 years (19–82 years) were include in
the analyses. Final diagnoses were VN in 24 and PCS
in 16 patients (Fig. 1).
In 24 VN patients (12 male, 12 female) the mean
age was 46 years (range 19–82 years). Unidirectional spontaneous nystagmus was present in 9 and
unilateral gaze-evoked nystagmus was present in 6.
Clinical HIT was assessed as abnormal in 19(80%)
cases by the emergency specialist and in 20(83%)
by the neurologist. Four patients who were found to
have clinically normal HIT by the neurologist had
unilateral low gain and gain asymmetry on vHIT and
normal DWI indicating that the final diagnosis is VN.
In 16 patients (14 male, 2 female) with PCS the
mean age was 52 years (range 26–80 years). None
had additional cranial nerve or long tract sign. Skew
deviation was present in two (patient 11 and 13).
Two patients; one with a right lateral medullary+
cerebellar infarction and another with a right pontomedullary+ cerebellar infarction had left beating
nystagmus (patient 3 and 11). Direction changing
nystagmus was noted in seven (patients 2, 4, 6, 8–10,
and 12). In all clinical HIT was clinically assessed
A. Guler et al. / Clinical and video head impulse test in the diagnosis of posterior circulation stroke
Table 1
Clinical and radiological features of patients with posterior circulation stroke
HIT (Neu)
Cranial MRI
P, Patient; L, Left beating; DCN, Direction-changing nystagmus; ES, Emergency Specialist; Neu, Neurologist;
PICA, Posterior inferior cerebellar artery; AICA, Anterior inferior cerebellar artery; SCA, Superior cerebellar
as normal both by the emergency specialist and the
neurologist (100%). PCS was further classified radiologically into subgroups according topography and
vascular anatomy. In 9 with brainstem infarction,
either alone or associated with cerebellar infarction
(patient 3, 5, 7, 10, 11, 13–16), this was categorized as
AICA-PICA stroke. In 7 with pure cerebellar infarction without brainstem involvement (patient 1, 2, 4, 6,
8, 9 and 12) this was designated as PICA-SCA stroke
(Table 1).
The conformity of clinical HIT results reported
by the emergency specialist and the neurologist was
excellent and the κ coefficient was 0.86.
VOR gains in healthy controls and patients are
given in Table 2. When compared with the results
of healthy controls VOR gains of patients with VN
were low both for the ipsilesional and contralesional
sides reaching a statistical significance (p < 0.001
and p = 0.001 respectively). Gain asymmetry of
37.7% (± 20.2%) was also statistically significant
(p < 0.001).
Typical vHIT recordings of VN and all 16 PCS
are presented Fig. 2a and b respectively. Comparison
of the VOR gains of PCS with the healthy controls
showed that low gain values were present both for the
ipsilesional (p = 0.036) and contralesional (p = 0.021)
sides. However, gain in AICA-PICA stroke was
reduced both for the ipsilesional (p = 0.005) and
contralesional sides (p = 0.008) without significant
asymmetry (p = 0.71). In PICA-SCA stroke VOR
gains were not different from the healthy controls ipsilesionally (p = 1.00) or contralesionally
(p = 0.96) and there was no asymmetry (p = 0.065)
(Table 2).
Table 2
VOR gains in patient groups and healthy controls recorded by vHIT
Vestibular neuritis
Pure cerebellar infarction
Brainstem infarction
Healthy controls
VOR gain
Mean ± SD
95% CI
0,51 ± 0.19
0.83 ± 0.20
1,02 ± 0.13
0.97 ± 0.16
0,79 ± 0.25
0,80 ± 0.23
1.05 ± 0.21
1.01 ± 0.19
37.70 ± 20.20
6.62 ± 3.66
12.39 ± 5.75
10.81 ± 7.61
VOR: Vestibulo-ocular reflex. vHIT: Video head impulse test.
ratio (%)
A. Guler et al. / Clinical and video head impulse test in the diagnosis of posterior circulation stroke
Cut-off points for vHIT gain were determined by
receiver operating characteristic curve (ROC) analysis. The specificity was 93% at gain values ≤0.75
when the sensitivity was 96% for the VN group
(AUC = 0.977, SE: 0.017, 95%CI = 0.944–1.00,
p < 0.001). In 23 of the 24 VN gain values were
≤0.75. One of the 7 (14%) PICA-SCA stroke and
4 of the 9 (44%) AICA-PICA stroke had gain values ≤0.75. Gain asymmetry ≥17% was found to
have a sensitivity of 79% (19/24) and a specificity of 84% in diagnosis of VN (AUC = 0.896,
SE:0.04, 95%CI = 0.818–0.974, p < 0.001). None of
the 7 PICA-SCA strokes and just one (11%) AICAPICA stroke had an asymmetry ≥17%. With both
gain ≤0.75 and asymmetry ≥17% taken into consideration, 100% of PCS were correctly diagnosed but
only 80% of VN were correctly identified.
5. Discussion
In this study, clinical HIT was found to be abnormal
in about 80% of VN patients, regardless of speciality (emergency speciality: 80%; neurologist 83%).
In all of the 16 PCS (100%) HIT was found to be
normal both by the emergency specialist and the
neurologist. Clinical HIT allows identification of a
peripheral vestibular deficit with a sensitivity ranging
from 34% to 100%; complete vestibular loss is associated with the highest sensitivity [2, 6, 21]. Incomplete
vestibular loss, improper technique due to slow head
impulses and being conservative in rating HIT as deficient may explain normal HIT in our VN patients. We
confirm that frontline clinicians, irrespective of specialty, can confidently diagnose PCS based on normal
HIT. Abnormal clinical HIT has been reported in 9%
to 39% of patients with acute cerebellar or brainstem
strokes [1, 4, 15]. We found 100% sensitivity, perhaps
due to clinicians cognizant about the possibility of
HIT in PCS and therefore more likely to undercall
abnormal HIT.
Head impulses mainly drive the short latency,
oligosynaptic VOR pathways from the semicircular canals to the extraocular muscles. It is known
that high acceleration reveals VOR deficits better and
elicits larger overt catch-up saccades [25]. Catch-up
saccades that are imperceptible to clinical detection, termed covert saccades, are generated while the
head is still moving and reduces the sensitivity of
the test. Repeated testing has also been suggested
to avoid false-negative results [25]. Clinicians with
neuro-otological experience had lower HIT sensitivity (due to being more conservative in rating an
abnormal HIT) and higher specificity (better in identifying normal HIT) than clinicians without experience
[8]; the disagreement was mainly restricted to mild
deficit. The authors advised ordering quantitative
measurements, such as search coil or high speed
video methods when clinical HIT is not conclusive.
vHIT has been shown to measure VOR gains
accurately, equivalent to search coils, and can identify peripheral vestibular deficits in patients with
VN [13]. Both ipsi- and contralesional VOR gains
detected by vHIT in our VN patients were low when
compared to healthy controls and substantial asymmetry was present. Mildly reduced contralesional
gains has previously been reported [22], possibly
reflecting contribution to the VOR from ipsilateral canal excitation only when contralateral canal
inhibition is saturated by high acceleration head
impulse. The “on” and “off” direction gain asymmetry can be explained by push-pull cooperation
between the coplanar canals; the VOR, especially
at higher head acceleration, is driven better by
ipsilateral canal excitation than contralateral canal
inhibition [25].
Fig. 2a. Asymmetrically reduced VOR gain and overt saccades on the left side in a patient with vestibular neuritis.
A. Guler et al. / Clinical and video head impulse test in the diagnosis of posterior circulation stroke
Fig. 2b. (Continued)
VOR gains of our PCS patients were bilaterally low without a prominent asymmetry. This was
due to AICA-PICA strokes, as subgroup analysis
showed that gains recorded from PICA-SCA strokes
was not different from healthy controls (Table 2).
AICA strokes have been reported to show abnormal
VOR gains that can be confused with a peripheral lesion [3, 14]. Structures supplied by AICA,
such as vestibulo-oculomotor substrates and the
oligosynaptic pathways connecting them, are likely
affected [12]. Our AICA-PICA stroke had bilaterally reduced gains which was also reported in
previous studies [3, 14] and a case report with
isolated floccular infarction [19]. The explanation
seems to be the reciprocal interneuron connections between the vestibular nuclei as it is the
A. Guler et al. / Clinical and video head impulse test in the diagnosis of posterior circulation stroke
Fig. 2b. (Continued)
A. Guler et al. / Clinical and video head impulse test in the diagnosis of posterior circulation stroke
Fig. 2. (b) vHIT recordings and MRI findings of the patients with PCS within the order of Table 1. (vHIT: video head impulse test, PCS:
posterior circulation stroke).
A. Guler et al. / Clinical and video head impulse test in the diagnosis of posterior circulation stroke
case in VN, causing compensatory inhibition of the
contralateral vestibular nucleus, and the modulating role of flocculus on VOR in floccular lesions
[3, 19].
Our PICA-SCA stroke patients had normal and
symmetrical vHIT gains. Previous studies on PICA
strokes have shown normal clinical HIT in 99% of
patients [24, 16]. Normal vHIT results has been
reported and high-frequency VOR pathways was suggested to be unaffected in ischemia of the lateral
medulla and inferior cerebellum [14], both supplied
by the PICA. However, a search coil study reported
20% reduction in gains in PICA-SCA stroke [3], suggesting technical factors, such as goggle slippage,
were likely to account for normal range VOR gains
in our PICA-SCA stroke patients.
ROC analysis showed that using a gain cut-off
≤0.75, 96% of our VN patients could be diagnosed
with a specificity of 93%, but alarmingly 44% of
AICA-PICA and 14% of PICA-SCA strokes also had
gains ≤0.75. Using such gain cut-off would detect
most VN, but incorrectly diagnose nearly one in two
AICA-PICA stroke and one in seven of PICA-SCA
stroke as VN. A previous vHIT study has shown
about 90% specificity and sensitivity, using a gain
cut-off 0.75 [14]. In our study using a gain asymmetry
≥17% plus gain cut-off ≤0.75 improved diagnostic
accuracy, with 100% AICA-PICA strokes correctly
diagnosed and about 80% of VN detected. However
disappointingly this degree of diagnostic certainty
was not different from the percentage achieved by
clinical HIT. vHIT analysis did not add much in
making the diagnosis as both diagnostic methods led
to similar percentage of VN being misdiagnosed. A
search coil study has shown exceptional diagnostic
accuracy with both HIT gain and corrective saccade analysis [3]. Although search coil is unlikely
to be in widespread clinical use, its superiority over
vHIT is unquestionable and raises the possibility that
technical factors and artefact render vHIT gain less
diagnostically helpful.
Other than five patients with neuroimaging inadequacy, seven of the 52 AVS patients had to be
excluded as three could not cooperate with vHIT
testing and four had vHIT results uninterpretable
comprising approximately 14% of the overall group.
We did not repeat clinical and video HIT evaluation, and it is possible that diagnostic accuracy might
change over time, as the effect of ischemia can be
rapidly evolving. Our results cannot be generalized
to other causes of AVS, such as Meniere’s disease
and vestibular migraine.
In conclusion for now clinical HIT, performed by
emergency physicians or neuro-otoologists, seems
adequate in diagnostic evaluation AVS. If vHIT is
undertaken then both gain and gain asymmetry should
be taken in account. In the future the sensitivity
of vHIT analysis for PCS diagnosis needs to be
increased, possibility by incorporating saccade analysis, further refinement in video technology and
increased operator proficiency.
The authors would like to thank to Associate Prof
Timur Kose PhD for his contributions for the statistical analysis.
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