Dizziness is the third most common ma -jor medical symptom reported in gen-eral medical clinics1 and accounts for
about 3%–5% of visits across care settings.2 In
the United States, this translates to 10 million
ambulatory visits per year because of dizziness,3
with roughly 25% of these visits to emergency
departments.2 Many patients have transient or
episodic symptoms that last seconds, minutes or
hours, but some have prolonged dizziness that
persists continuously for days to weeks.4
In this article, we use the term “dizziness” to
encompass vertigo, presyncope, unsteadi ness,
and other nonspecific forms of dizziness. When
dizziness de velops acutely, is accompanied by
nausea or vomiting, unsteady gait, nystagmus
and intolerance to head motion, and persists for a
day or more, the clinical condition is known as
acute vestibular syndrome.5,6 We define isolated
acute vestibular syndrome (with or without hear-
ing loss) as occurring in the absence of focal
neurologic signs such as hemiparesis, hemi -
sensory loss or gaze palsy. Transient dizziness
has a differential diagnosis distinct from that of
acute vestibular syndrome, and the approach to
diagnosis should differ accordingly.7 In this
review, we focus on acute vestibular syndrome,
whether isolated or not.
Most patients with acute vestibular syndrome
have an acute, benign, self-limited condition pre-
sumed to be viral or postviral. The condition is
usually called vestibular neuritis but is some-
times referred to as vestibular neuronitis, laby -
rinthitis, neurolabyrinthitis or acute peripheral
vestibulopathy.5,6 Some authors distinguish be -
tween labyrinthitis and vestibular neuritis based
on the presence of auditory symptoms at presen-
tation;8 however, this distinction is inconsistently
applied, and the terms are often used inter-
changeably. In this article, we include labyrinth -
itis and vestibular neuritis together as peripheral
causes of acute vestibular syndrome — that is,
pathology localized to the inner ear (labyrinth) or
eighth cranial (vestibular) nerve — as distin-
guished from central causes affecting vestibular
connections in the central nervous system. Al -
though peripheral causes are more common,
dangerous central causes, particularly ischemic
stroke in the brainstem or cerebellum, can mimic
benign peripheral causes closely.6,9–13
The evidence base for diagnosing the cause of
dizziness is limited.14 There is growing evidence
that the cause of acute vestibular syndrome is mis-
diagnosed in many patients15–19 and that frontline
physicians are eager for diagnostic guidelines.20,21
Regional variation in diagnostic practice is proba-
bly common,3 but little is known about factors
influencing diagnostic accuracy (e.g., access to
technology, availability of consultants, nature of
training, cultural or linguistic differences).
Narrative reviews have highlighted the im -
portance of accurately assessing the risk of dan-
gerous disorders, particularly ischemic stroke in
the posterior fossa, and have emphasized the util-
ity of a focused history and physical examination
in these patients.5,22–24 However, we are un aware
of any systematic re views, practice parameters or
fully validated clinical decision rules applicable
to unselected patients with acute, prolonged
dizziness that offer evidence-based guidance for
the diagnosis and management of acute vestibular
syndrome. We therefore performed a systematic
review and synthesis of the medical literature,
focusing on bedside diagnostic predictors.
Does my dizzy patient have a stroke? A systematic review
of bedside diagnosis in acute vestibular syndrome
Alexander A. Tarnutzer MD, Aaron L. Berkowitz MD PhD, Karen A. Robinson PhD, Yu-Hsiang Hsieh PhD,
David E. Newman-Toker MD PhD
Competing interests: None
declared.
This article has been peer
reviewed.
Correspondence to:
Dr. David E. Newman-Toker,
toker@jhu.edu
CMAJ 2011. DOI:10.1503
/cmaj.100174
ReviewCMAJ
• The most common causes of acute vestibular syndrome are vestibular
neuritis (often called labyrinthitis) and ischemic stroke in the brainstem
or cerebellum.
• Vertebrobasilar ischemic stroke may closely mimic peripheral vestibular
disorders, with obvious focal neurologic signs absent in more than half
of people presenting with acute vestibular syndrome due to stroke.
• Computed tomography has poor sensitivity in acute stroke, and
diffusion-weighted magnetic resonance imaging (MRI) misses up to
one in five strokes in the posterior fossa in the first 24–48 hours.
• Expert opinion suggests a combination of focused history and physical
examination as the initial approach to evaluating whether acute
vestibular syndrome is due to stroke.
• A three-component bedside oculomotor examination — HINTS (horizontal
head impulse test, nystagmus and test of skew) — identifies stroke with
high sensitivity and specificity in patients with acute vestibular syndrome
and rules out stroke more effectively than early diffusion-weighted MRI.
Key points
© 2011 Canadian Medical Association or its licensors CMAJ, June 14, 2011, 183(9) E571
Literature review and analysis
Details of the search strategy appear in Appendix
1. In brief, we searched MEDLINE to identify
English- language observational studies on the clin-
ical features, diagnostic evaluation and differential
diagnosis of acute vestibular syndrome published
through Dec. 4, 2009. We also performed a man-
ual search of the bibliographies of eligible articles.
Titles and abstracts of identified articles were
screened independently by two reviewers
(A.A.T. and A.L.B.). Articles were excluded if
they lacked original patient data, offered no
symptom data about dizziness, provided no
information about diagnostic accuracy for acute
central or peripheral vestibulopathies, did not
evaluate patients in the acute stage of disease,
involved patients under age 18 years or re ported
on fewer than five patients. Full-text versions of
eligible articles were re viewed independently by
the same two reviewers. A third reviewer (D.N.-
T.) verified the eligibility of selected articles and
settled any discrepancies.
One unmasked rater (A.A.T.) assessed the
strength of the reference standards used in the
included studies to distinguish between a peripheral
and a central cause of acute vestibular syndrome. A
second unmasked rater (D.N.-T.) verified the
strength of the reference standard. (Definitions of
the criteria used to assess the strength of the refer-
ence standards appear in Appendix 1.)
Information abstracted from each article
included study type, number of patients with dizzi-
ness, inclusion criteria and study site. Also ex -
tracted were data on the diagnostic tests used and
the proportion of patients with positive or negative
test results. Where appropriate, we attempted to
contact authors regarding study details.
For each test that was used in two or more stud-
ies, we calculated the pooled sensitivity, speci-
ficity, and positive and negative likelihood ratios
(and 95% confidence intervals [CIs]) for the test.25
No formal tests of heterogeneity were applied, but
we conducted a prospectively de fined subgroup
analysis that compared findings in stroke patients
who had an infarction in the territory of the ante-
rior inferior cerebellar artery with findings in those
who had cerebellar infarctions in other vascular
territories (posterior in ferior cerebellar artery or
superior cerebellar artery). All p values were two-
sided, with significance set at p < 0.05.
In instances where evidence derived from our
systematic review was incomplete, we included
expert opinion and critically reviewed related
evidence to support or refute such opinion. Evi-
dence failing to meet strict inclusion criteria was
considered part of the critical review.
Details of the results of our literature search
appear in Appendix 1 and Figure 1. Our system-
atic search identified 779 unique citations. We
re viewed 139 full-text articles and their bibli-
ographies and found 27 articles reporting data
from 21 studies that met the inclusion criteria.
Review
E572 CMAJ, June 14, 2011, 183(9)
Excluded n = 12
• No medium- or high-quality
reference standard used to rule
in or rule out stroke†
Excluded n = 640
• Not in English n = 2
• Lacked original patient data n = 151
• No symptom data about dizziness
n = 113
• No information about diagnostic
accuracy for acute central or
peripheral vestibulopathies n = 67
• Patients not evaluated in acute stage
of disease n = 172
• Included fewer than five patients
n = 135
Citations identified through
search of MEDLINE database
n = 779
Excluded n = 117
• No information about diagnostic
accuracy for acute central or
peripheral vestibulopathies n = 59
• Patients not evaluated in acute stage
of disease n = 36
• No symptom data about dizziness
n = 11
• Patients aged < 18 years n = 6
• Article could not be retrieved n = 3
• Included fewer than five patients n = 2
Articles identified
for full-text review
n = 139
Articles included in the
systematic review
n = 15 (10 studies)
Articles identified
through review of
bibliographies of
selected articles n = 5
Satisfied inclusion
criteria
n = 22
Articles considered for
systematic review
n = 27 (21 studies*)
Figure 1: Flow diagram indicating selection of articles. *In two articles26,27 (n =
108), published by a single research group, it is unclear whether each article
reports on an entirely distinct or partially overlapping group of patients (see
Table 1 for details). There could be as many as 28 patients counted more than
once. †The criteria used to assess the strength of the reference standards used
to rule in or rule out stroke appear in Appendix 1.
We excluded 12 articles reporting data from 11
studies because of inadequate diagnostic refer-
ence standards, which left 10 studies describing
a total of 392 patients. Details of these studies
appear in Table 1.
How common is acute vestibular
syndrome?
We found no direct studies of the incidence of
acute vestibular syndrome as a clinical presenta-
tion. Vestibular neuritis, probably the most com-
mon cause of acute vestibular syndrome, has an
estimated annual incidence of 3.5 per 100 000
population based on a single retrospective survey
of neuro-otology clinics in Japan.36 Data from a
nationally representative sample of emergency
departments in the United States indicate that, of
2.6 million visits annually because of dizziness,
acute vestibular syndrome from a peripheral
cause (i.e., vestibular neuritis or labyrinthitis) is
diagnosed in 6% of patients, which corresponds
to about 150 000 visits each year.2,18 Another 4%
of patients receive a cerebrovascular diagnosis,
and 22% leave the emergency department with-
out a causal diagnosis (i.e., they receive a diag-
nosis of “dizziness or vertigo”),2,18 many of
whom probably presented with acute vestibular
syndrome. From a survey of the general popula-
tion in Germany, 11% of those who reported
dizziness indicated that the symptom had lasted
for more than a day.4 In a US-based study in -
volving consecutive patients who visited an
emergency department because of dizziness,37
27% (47/175) of those who had any dizziness in
the 24 hours before their visit still had dizziness
in the emergency department that had not remit-
ted since it began (unpublished data). Thus, we
estimate that about 10% to 20% of patients who
present with acute dizziness to the emergency
department have acute vestibular syndrome,
which corresponds to about 250 000 to 500 000
visits to an emergency department each year in
the United States alone.
What are the most common
causes?
In our systematic review, we found no studies of
all presentations of acute vestibular syndrome.
Only three studies enrolled relatively unselected,
consecutive populations.6,9,11 Vestibular neuritis
was the most common peripheral cause of acute
ves tibular syndrome, and there were no patients
with labrynthitis (i.e., peripheral cause of acute
vestibular syndrome with auditory symptoms)
reported in these studies. However, two studies
expressly excluded patients with auditory symp-
toms,9,11 and the third excluded patients with a
history of recurrent auditory symptoms.6
The most common central causes of acute
vestibular syndrome reported in these three
studies are listed in Table 2. Central causes mim-
icking vestibular neuritis (sometimes called
“pseudoneuritis”11) were predominantly cere-
brovascular (83%) and demyelinating conditions
(11%). Two studies prospectively en rolled pa -
tients at high risk for stroke using age or vascular
risk factors as entry criteria,6,9 which probably
led to overrepresentation of cerebro vascular pa -
tients; the third study used a case–control design
and did not report the method for sampling pa -
tients in the control group.11 The remaining seven
studies included in the systematic review fo -
cused only on patients with acute dizziness who
had a diagnosis of stroke.10,26−28,31−33
None of the included studies was large
enough to identify rare but important causes
such as Wernicke syndrome,38 bacterial laby -
rinthitis39 or brainstem encephalitis.40 Box 1
shows a suggested differential diagnosis for
acute vestibular syndrome adapted from narra-
tive reviews written by specialists in the field of
vestibular disorders.8,24
Findings from our systematic review do not
allow a definitive statement about the relative
prevalence of vestibular neuritis versus stroke
among unselected patients presenting with acute
vestibular syndrome. We can, however, roughly
estimate the proportion of patients presenting
with acute vestibular syndrome who have stroke,
using data on the annual incidence of stroke and
prevalence of dizziness among stroke patients.
Of 795 000 strokes per year in the United
States,45 about 18% are located in the posterior
fossa,46 and about 50%–70% are associated with
dizziness as a prominent or presenting symp-
tom.22,47 Thus, we estimate that there are about
70 000 to 100 000 strokes per year in the United
States with dizziness as a prominent or present-
ing symptom. Considering the approximate inci-
dence of acute vestibular syndrome calculated
earlier (about 250 000 to 500 000 per year in the
United States), we estimate the true proportion
of acute vestibular syndrome due to stroke to be
about 25% ± 15%.
What elements of clinical history
are useful for diagnosis?
Certain clinical findings from history-taking help
to distinguish between stroke and vestibular neu-
ritis in patients presenting with acute vestibular
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CMAJ, June 14, 2011, 183(9) E573
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E574 CMAJ, June 14, 2011, 183(9)
Table 1: Characteristics of studies included in the systematic review of bedside diagnostic predictors of stroke in patients with acute
vestibular syndrome (AVS)
Study
No. of patients
screened
(no. included
in study)
Study population
(study focus)
Study
site
Diagnostic
reference
standards
Strength of
reference
standard to
rule in/rule out
stroke* Study design Comments
Rubenstein
et al.28
7 (7) AVS and diagnosis of
cerebellar stroke or
hemorrhage (clinical
findings)
NR • CT (all
patients)
Medium/NA Retrospective
case series
Clinical evaluation delayed
relative to onset of symptoms
up to 7 d.
Norrving et al.9
(preliminary
report in
Magnusson
et al.29,30)
24 (24) AVS for > 48 h and
age 50–75 yr (clinical
findings and electro-
oculography)
ED/HA • MRI without
DWI (n = 22)
• CT (n = 2)
Medium/
Medium
Prospective
cross-sectional
study
(consecutive
cases)
Only 4 patients had CT in acute
phase; MRI was performed 14–
44 d after onset of symptoms.
Patients with brainstem/
cerebellar dysfunction other
than nystagmus were excluded.
Kim et al.31 30 (30) Acute isolated vertigo
and diagnosis of stroke
(clinical findings)
ED/HA • MRI without
DWI (n = 17)
• CT (n = 13)
Medium/NA Prospective case
series (possibly
consecutive)
CT obtained in all patients. MRI
obtained in those with initially
negative CT.
Chen et al.32 295 (7) Acute vertigo and
diagnosis of brainstem
stroke (clinical findings,
caloric testing and
vestibular-evoked
myogenic potentials)
ED/HA • MRI without
DWI (all
patients)
Medium/NA Retrospective
case series
(possibly
consecutive)
Unclear whether patients with
cerebellar infarctions were
considered or included.
Lee et al.26† 28 (28) Acute audiovestibular
loss and diagnosis of
vertebrobasilar
infarction (clinical
findings and audiometric
assessment)
ED/HA • MRI with
DWI (all
patients)
High/NA Prospective case
series
(consecutive)
Retrospective analysis of data
from a prospective stroke
registry.
Lee et al.10 25 (25) AVS and diagnosis of
cerebellar infarction
(clinical findings and
audiovestibular testing,
vascular territory)
ED/HA • MRI with
DWI, and MRA
(all patients)
High/NA Prospective case
series
(consecutive)
Patients with brainstem/
cerebellar dysfunction other than
nystagmus were excluded.
Retrospective analysis of data
from a prospective stroke
registry.
Cnyrim et al.11 NR (83) AVS and diagnosis of
vestibular neuritis or
pseudoneuritis
(diagnosis, clinical
features)
ED • MRI with
DWI (all
patients)
High/Medium Case–control
study (possibly
prospective,
possibly
consecutive)
Initial MRI obtained within 5 d
of symptom onset; no further
breakdown provided. No follow-
up MRI or clinical follow-up in
patients with initially negative
MRI. Patients with hearing loss or
brainstem/cerebellar dysfunction
other than nystagmus were
excluded. Retrospective data
analysis. Selection of controls not
described.
Moon et al.33 7 (7) Acute vertigo and
diagnosis of isolated
infarction of the cerebellar
nodulus (clinical features,
audiovestibular findings)
ED/HA • MRI with
DWI, and MRA
(all patients)
High/NA Retrospective
case series
One of 8 patients reported had a
transient positional vertigo
syndrome rather than AVS.
Kattah et al.6
(preliminary
report in
Newman-Toker
et al.12)
121 (101) AVS and ≥ 1 risk factor
for stroke (diagnosis,
clinical features,
imaging)
ED/HA • MRI with
DWI (all
patients)
High/High Prospective
cross-sectional
study
(consecutive
cases)
Patients with initially negative
MRI underwent repeat MRI
owing to unexplained signs
suggesting central location.
Lee et al.27†
(preliminary
report in Lee
et al.34 and Lee
and Cho35)
80 (80) AVS and AICA stroke
(audio-vestibular
findings, topography of
lesion)
ED/HA • MRI with
DWI, and MRA
(all patients)
High/NA Prospective case
series
(consecutive)
Retrospective analysis of data
from prospective stroke registry.
Most MRIs obtained within 30 d
after symptom onset.
Note: AICA = anterior inferior cerebellar artery, AVS = acute vestibular syndrome, CT = computed tomography, DWI = diffusion-weighted imaging, ED = emergency
department, HA = hospital admission, MRA = magnetic resonance angiography, MRI = magnetic resonance imaging, NA = not applicable, NR = not reported.
*The strength of the reference standard used to rule stroke in or out was rated as high, medium or low (criteria are defined in Appendix 1).
†In these two studies,26,27 published by a single research group and focused on AVS with hearing loss and AICA stroke, it is unclear whether they report on entirely
distinct or partially overlapping groups of patients. In the 2009 study,27 the authors state that 23 patients were reported on previously; they cite several prior
studies (including the 2002 manuscript34) but do not include their 2005 manuscript26 in the list of related publications. Accordingly, we have included this 2005
article as representing a separate study, rather than as a preliminary report of the later manuscript. However, the 28 patients reported in the 2005 study were
from the same university-based stroke registry reported by the au