173

Acute Continuous Vertigo

Kevin A. Kerber, MD, MS1

1 Department of Neurology, University of Michigan Health System, Address for correspondence Kevin A. Kerber, MD, MS, Department of
Ann Arbor, Michigan Neurology, University of Michigan Health System, 1500 E. Medical
Center Dr., Ann Arbor, MI 48109 (e-mail: kakerber@umich.edu).
Semin Neurol 2013;33:173–178.

Abstract Acute continuous vertigo presentations are among the most feared presentations in
medicine. Although a self-limited disorder is the typical cause, a life-threatening stroke
can also occur. Differentiating a self-limited disorder from a life-threatening stroke can
be a challenge. Routinely collected information—such as stroke risk factors and findings
Keywords on the general neurologic examination—is not likely to enable the clinician to discrimi-
► dizziness nate between these causes. A focused oculomotor examination is a necessary compo-
► vertigo nent of the assessment, but is underused in routine care. The author describes the
► stroke challenges to diagnosing stroke in cases of acute continuous vertigo and provides an

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► vestibular neuritis approach to inform decision making at the bedside. Future research is necessary to
► clinical decision validate clinical decision support, assess generalizability, and demonstrate its impact on
making meaningful outcomes.

Acute continuous vertigo presentations are among the most-
feared presentations in medicine. Although the majority of these
presentations are caused by a self-limited disorder, such as
vestibular neuritis, many are caused by a potentially disabling
or life-threatening stroke.1–4 Dizziness-stroke presentations can
be challenging to identify because the lesion typically occurs in
the posterior circulation, generally the cerebellum. Cerebellar
lesions are not adequately represented by clinical stroke meas-
ures like the NIH (National Institutes of Health) Stroke Scale
because common neurologic deficits are often lacking in the
evaluation. Examination abnormalities in cerebellar stroke in-
clude eye-movement irregularities and imbalance, which can be
similar to or only subtly different from a common self-limited
disorder, vestibular neuritis. Even if there are only subtle deficits
on examination at the onset, a cerebellar stroke can lead to
herniation and death within a short time.5
No consensus guideline has been established for the evalu-
ation and management of patients with acute continuous
vertigo. Additionally, no consensus guideline exists for defining
what constitutes an acute continuous vertigo presentation. This
presentation is generally meant to group subjects with acute
and constant disorders of the vestibular system (either central
or peripheral). Yet, it is not likely that a criterion for these
presentations should be vertigo or its typical description (e.g.,
spinning, swaying). This is because patients are frequently not
reliable in their descriptions of dizziness symptoms.6 In fact,
more than half of dizziness patients who are asked to label the
type of symptom (i.e., “spinning or vertigo,” “about to faint,”
“unsteadiness,” “dizzy,” “lightheaded,” or “disoriented”) change
their responses when asked to label it again 5 to 10 minutes
later.6 In addition, 20% or more of patients with vestibular
disorders report only nonspecific dizziness or imbalance rather
than vertigo, while patients with nonvestibular disorders (e.g.,
myocardial infarction, panic disorder) frequently report verti-
go.6 For these reasons, the more precise way to define the
population of interest is by the presence of acute constant
dizziness symptoms (any dizziness, vertigo, or imbalance) and
through examination findings of nystagmus or imbalance.
In this article, the focus will be on distinguishing vestibular
neuritis from stroke presentations of acute continuous dizzi-
ness. Vestibular neuritis is the prototypical acute peripheral
vestibular system disorder and stroke is the most common
dangerous cause.3 However, clinicians should also be aware
that patients with other disorders can present with acute
continuous dizziness, nystagmus, and imbalance, including
demyelinating or inflammatory central nervous system le-
sions, vestibular migraine, and even benign paroxysmal
positional vertigo (particularly the horizontal canal variant).
Important Components of Diagnostic
Assessment and Decision Making
The main goal in the acute setting is to differentiate stroke
from vestibular neuritis. Because the principal goal of the

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174 Acute Continuous Vertigo Kerber

initial clinical assessment is to identify stroke patients, the
optimal evaluation and management of patients with acute
constant dizziness should be rooted in knowledge of the
prevalence of stroke in these presentations and the operating
characteristics (i.e., sensitivity and specificity) of any test used
in the diagnostic process (►Table 1).7 This information is
critical to making an accurate assessment of the probability of
stroke, which in turn informs decisions regarding further
testing or management. “Tests” in this context include bed-
side information (e.g., demographics, past medical history,
examination findings), laboratory tests, and imaging studies.
Unfortunately, the prevalence of stroke in presentations of
acute continuous dizziness has not been well defined. Data on
the prevalence of stroke are necessary to establish the pretest
probability of stroke, which is then used to estimate the
posttest likelihood of stroke after any testing.7 Published
studies report a prevalence of stroke in acute dizziness
populations that vary widely from as low as 3% to as high
as 72%.1–4,8 The low prevalence estimates are from popula-
tion-based or single-center observational studies, which
categories,1,4 there is still concern for misclassification be-
cause MRI or a detailed oculomotor examination (typically
not documented by emergency medicine doctors9) is re-
quired to diagnose stroke in many patients presenting with
isolated dizziness symptoms.8,10 The studies with the highest
prevalence of stroke are also not generalizable to a broad
acute-continuous-dizziness population because these were
referral populations selected to be at increased risk for stroke
etiology.3,8 It has been estimated that the true prevalence of
stroke in the dizziness population of interest is 10 to 40%.11
The results of diagnostic tests are used to adjust the
probability of the disorder so that the posttest probability
can be determined.7 For diagnostic tests to contribute mean-
ingful information, they must be reliable and accurate. They
must have been studied using rigorous methodology and
must have values of sensitivity and specificity that can result
in changes in clinical management within the population of
interest.12 An example of a test that does not contribute
meaningful information in this setting is the computed
tomography (CT) scan. CT scans are well known to be an

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include all patients with dizziness as a reason for the visit
or a dizziness diagnosis. Thus, these studies include patients
with recurrent positional attacks of dizziness, orthostatic
dizziness, chronic recurrent episodes of dizziness, and chron-
ic constant dizziness.1,2,4 Including all “dizziness” presenta-
tions dilutes the stroke-prevalence estimates because most of
these cases have a very low risk of stroke etiology; stroke is a
serious concern in acute continuous dizziness presentations.
The method used to determine the outcome in these studies
also introduces uncertainty about the findings because it was
based on routine care with the majority of patients not
undergoing specific bedside examination or magnetic reso-
nance imaging (MRI). Even though in some of these studies a
neurologist reviewed the medical records to validate outcome
inaccurate test for ischemic stroke (sensitivity, 16%; specific-
ity, 98%).13 By applying these test characteristics to a dizziness
patient with a 10% pretest probability of stroke and a negative
CT scan, the posttest probability only drops to 9%. This trivial
change is not sufficient to influence decisions about ischemic
stroke and renders the test of extremely low value in this
context.
Another important point regarding diagnostic testing and
decision making is that even when the key elements are
known (i.e., prevalence of the target disorder and the opera-
tional characteristics of tests), there will still need to be
important and often difficult decisions to make. It is not
realistic to think that the posttest probability will be defini-
tive (i.e., a 0% or 100% probability of the disorder). Instead,

Table 1 Important questions and issues to consider during the diagnostic evaluation

Question/Issue Why important

What is the prevalence Prevalence of the target disorder is the basis for diagnostic testing and decision
(pretest probability) of making. Without an accurate estimate of the pretest probability, the influence of any
stroke in this patient? diagnostic test cannot be determined.
What are the operating Sensitivity and specificity define the accuracy of a test, but have very little meaning
characteristics of the tests outside the context of the pretest probability of a disorder. These measures are used
being ordered/performed? to calculate the posttest probability. To be useful, studies that derive sensitivity and
How were these operating specificity must be performed in a relevant population of patients at a time of clinical
characteristics derived? uncertainty. The interpretation of the test must be blinded to the gold-standard
outcome determinant. Most studies reporting sensitivity and specificity are not
derived using methods to render the findings useful to clinical scenarios.
What is the posttest probability? The posttest probability is the final value (probability of the disorder of interest)
arrived at after considering the evaluation. This value is the basis for further testing
or management.
How will the test I am considering If the results of the test will not change clinical management, then why do it?
change my management?
How likely is it that the change in Favorably influencing the patient’s outcome is the ultimate goal. How likely is it that
management I anticipate making what you do will contribute to that goal?
(based on the test results) will
meaningfully impact the
patient’s outcome?

Seminars in Neurology Vol. 33 No. 3/2013


clinicians are left with an estimate of the probable outcome
upon which they will need to make management decisions.
What should be done if a patient has a 5% (1 in 20) probability
of stroke? How would that differ from a patient with a 1% (1 in
100), 0.2% (1 in 500), or 0.1% (1 in 1,000) probability of stroke?
Discriminating Vestibular Neuritis from
Stroke
Acute Continuous Dizziness due to Vestibular Neuritis
Vestibular neuritis is presumed to be caused by a viral or
postviral process involving the vestibular nerve. However, no
test exists to confirm the viral etiology. A subset of vestibular
neuritis cases likely has a vascular or demyelinating lesion
affecting the nerve (the eighth nerve has a large central glial
segment). The severity of vestibular neuritis is variable, with
some patients having relatively mild symptoms and others
being completely debilitated for days or weeks. Occasionally,
other cranial neuropathies can co-occur with vestibular
neuritis presentations, particularly those of the auditory
component of cranial nerve VIII or the facial nerve. If a facial
neuropathy is present, one should also search for cutaneous
vesicles around the auricle and external ear, which would
indicate the Ramsay Hunt syndrome, a disorder caused by the
varicella-zoster virus.
Patients with vestibular neuritis present with a highly
characteristic examination that includes unidirectional hori-
zontal nystagmus and a positive head-impulse test (HIT; also
referred to as the head-thrust test) (►Fig. 1).3 The fast phase
of the nystagmus is toward the healthy side. In the acute
phase, patients have nystagmus in their primary gaze that
increases in velocity with gaze in the direction the nystagmus
beats (e.g., right-beat nystagmus in primary gaze will increase
in velocity when looking to the right). As patients recover, the
nystagmus may only be apparent on gaze testing. If the
nystagmus changes direction with gaze (right beat on right
gaze, but then left beat on left gaze) or if vertical spontaneous
or gaze-evoked nystagmus is present, then a central lesion is
presumed. The HIT will be positive toward the affected side,
which is the side that is opposite the fast phase of nystagmus.
For example, if unidirectional right-beat nystagmus occurs,
the HIT will be expected to be positive after head movements
to the left. The HIT was first described in 198814; it can be
thought of as the afferent vestibular test because it is analo-
gous to the afferent pupillary defect. The HIT directly assesses
the vestibulo-ocular reflex (VOR), which links the vestibular
system to eye movements; a positive test localizes to the
vestibular nerve.
Acute Continuous Dizziness due to Stroke
When acute dizziness is the main or most prominent symp-
tom of stroke, other clues to the central lesion will be present
in most patients, though these clues may be subtle and
limited to central oculomotor abnormalities (►Table 2).3,15
If the exam uncovers new focal motor or sensory symptoms,
dysarthria, dysmetria, truncal ataxia, or Horner’s syndrome,
then a central lesion should be presumed. Although accom-
panying unilateral hearing loss has traditionally been consid-
Acute Continuous Vertigo Kerber 175
ered an indicator of a peripheral audiovestibular lesion,
hearing loss is also a characteristic of ischemia in the distri-
bution of the anterior inferior cerebellar artery.3,16 In cases of
isolated dizziness, no single factor adequately identifies
stroke. The oculomotor examination is probably the most
important component of the examination when trying to
assess the likelihood of stroke in patients with isolated
dizziness. Despite this, patients with stroke can present
with peripheral-appearing nystagmus (i.e., unidirectional
horizontal).3
Bedside Differentiation of Stroke from Vestibular Neuritis
To help clinicians discriminate ischemic neurologic presen-
tations from nonischemic presentations, several tests and
procedures have been developed. The ABCD2 Scale was
developed and validated as a tool to determine the risk of
subsequent stroke following a transient ischemic attack (TIA);
however, it likely differentiates cerebrovascular events from
noncerebrovascular events.17,18 The scale has been endorsed
by many medical societies for use in clinical decision making
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regarding acute neurologic symptoms.19 Components of the
ABCD2 score are age, blood pressure, clinical symptoms of
unilateral weakness or speech disturbance, duration, and
diabetes. The problem with the use of the ABCD2 score in
acute dizziness presentations is that it was not derived in this
specific population. As a result, some of the variables (i.e.,
duration and unilateral weakness) are less relevant, whereas
other important variables are not included. The value of the
ABCD2 scale in estimating the probability of stroke was
recently assessed specifically regarding acute dizziness pre-
sentations.20 Among 907 acute dizziness presentations in-
cluded in the study, 4.1% (37/907) had a cerebrovascular cause
(24 ischemic strokes, eight transient ischemic attacks, five
intracerebral hemorrhages). The proportion of patients hav-
ing a cerebrovascular cause was only 1% (5 of 512) in those
with an ABCD2 score  3, increased to 6.8% (25 of 369) in
those with ABCD2 score of 4–5, and 27% (7 of 26) in those with
ABCD2 score of 6–7. With a cutoff of  4 as the threshold for a
positive test, the sensitivity was 86% (32 of 37) and specificity
was 58% (507 of 870). However, this study is limited because
the stroke outcome was based on medical record review of
routine care, which is susceptible to misclassification partic-
ularly in the case of dizziness (only 11% underwent MRI). A
separate study used a prospective design to assess the accu-
racy of the ABCD2 score in acute dizziness patients.3 To be
included, patients also had to have examination findings of
nystagmus (spontaneous or gaze-evoked), nausea or vomit-
ing, head-motion intolerance, and new gait unsteadiness. In
this study, 98% of the participants had an MRI as part of their
routine care. As a result, this study is more focused on the
population of interest and has an outcome determinant with
less risk of misclassification. Applying the ABCD2 Scale in this
population ( 4 for a positive stroke determination), the
sensitivity was 61% (69 of 113) and the specificity was 62%
(48 of 77), respectively. Considering these sensitivity and
specificity values, a patient estimated to have a 25% pretest
probability of stroke who has an ABCD2 score of  3 would
still have a posttest probability of stroke equal to 7.4% (i.e., 1 of
Seminars in Neurology Vol. 33 No. 3/2013
176 Acute Continuous Vertigo Kerber

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Fig. 1 The head-impulse test. The head-impulse test is used to assess vestibular function and can be easily performed during the bedside
examination. This test specifically assesses the vestibulo-ocular reflex (VOR). The patient sits in front of the examiner and the examiner holds the
patient’s head steady in the midline. The patient is instructed to maintain gaze on the nose of the examiner. The examiner then quickly turns the
patient’s head 10 to 20 degrees to one side and observes the ability of the patient to keep the eyes locked on the examiner’s nose. If the patient’s
eyes stay locked on the examiner’s nose (i.e., no corrective saccade) (A), the peripheral vestibular system is assumed to be intact. If the patient’s
eyes move with the head (B) and the patient makes a voluntary eye movement back to the examiner’s nose (i.e., corrective saccade), a lesion of the
peripheral vestibular system, not a central nervous system (CNS) lesion is suggested. Thus, in a patient with acute continuous dizziness, the test
result shown in (A) would suggest a CNS lesion (because the VOR is intact), whereas the test result in (B) would suggest a peripheral vestibular
lesion on the right side (because the VOR is not intact). (Reprinted from Edlow JA, Newman-Toker DE, Savitz SI. Diagnosis and initial management
of cerebellar infarction. Lancet Neurol 2008;7(10):951–964).

every 13 patients in the group considered negative for stroke
by the ABCD2 Scale would be expected to have a stroke).
Recently, bedside oculomotor findings were grouped into
a three-step bedside examination clinical decision rule la-
beled the HINTS (head-impulse, nystagmus, and test-of-
skew) test.8 The findings from the HINTS examination that
suggest a central lesion can be remembered using the acro-
nym INFARCT (impulse normal, fast-phase alternating, refix-
ation on cover test). When interpreting the HINTS
examination, any of the three central signs results in the
test being considered positive for a central lesion. Among 190
patients presenting with acute dizziness and having nystag-
mus, head motion intolerance, and imbalance, HINTS (with
any of the three subtests being abnormal—recall that a
“negative” HIT is considered an abnormal finding) demon-
strated a sensitivity in identifying stroke of 96.5% (109 of 113
patients) and a specificity of 84.4% (65 of 77 patients), with
neuroimaging (MRI in 97%) considered as the gold standard of
stroke determinants.3 Applying this sensitivity and specificity
values to a patient presenting with a 25% probability of stroke,
a negative HINTS test would lower the probability to 1.4% (1
in 73 patients), whereas a positive test would increase the
probability to 73% (1 in < 2 patients). It should also be noted
that this study found that 15 of the ischemic stroke cases had
an initial MRI that was negative for acute stroke.3 In these
cases, a follow-up MRI (ordered because of clinical signs

Seminars in Neurology Vol. 33 No. 3/2013


Table 2 Features suggestive of a central nervous system lesion
in presentations of acute continuous dizziness
Oculomotor findings
Nystagmusa
Spontaneous pure vertical or torsionalb
Bidirectional gaze-evokedb
Gaze-evoked downbeatb
Skew deviationb
Ophthalmoparesis
(e.g., internuclear ophthalmoplegia)
Head impulse test without a corrective saccadeb
History of presentations
c
Other focal CNS symptoms
Significant cardiovascular risk factorsc
Other exam findings
Horner’s syndrome
CNS motor deficit
CNS sensory deficit
Dysarthria
Dysmetria
Truncal ataxia
Visual field defect
Altered level of alertness
Abbreviation: CNS, central nervous system.
a
Unidirectional horizontal nystagmus also occurs with lesions of the
central vestibular system.
b
Central patterns of nystagmus, normal head impulse test, and positive
skew, have been collectively developed in the HINTS (head-impulse,
nystagmus, and test-of-skew) assessment.
c 1 Kerber KA, Brown DL, Lisabeth LD, Smith MA, Morgenstern LB.
The value of other CNS symptoms and stroke risk factors has not been
well-defined in presentations of acute continuous dizziness. The ABCD2
(age, blood pressure, clinical features, duration of TIA, and presence of
diabetes) Scale is likely of only marginal value in this setting.
suggesting a central lesion) was positive. Most of the false-
negative MRIs were performed within 24 hours of symptom
onset. This finding, along with similar findings in other
studies,21 suggests that MRI may not have an optimal level
of sensitivity for detecting posterior fossa lesions when
performed in the acute period.
Studies of the results of HINTS examinations indicate that
the probability of stroke in acute continuous dizziness pre-
sentations can be accurately assessed, quickly and meaning-
fully, with bedside examination components.3 Powerful
bedside indicators of a peripheral vestibular lesion are unidi-
rectional horizontal nystagmus, a positive HIT, and no skew
deviation. However, these findings must be considered early-
phase diagnostic research results. The HINTS test has only
been recently developed and has not been prospectively
validated.3 Reliability of the examination findings has not
been measured. Highly specialized neurologists were the
examiners in these studies, so it is not known how well the
results would generalize to routine care settings.
Acute Continuous Vertigo Kerber 177
Portable devices have been developed that measure the
HIT.22 These devices consist of goggles that contain a high-
speed camera to capture eye movements and gyroscopes to
measure head movements. With this information, the VOR in
each direction can be measured. When assessed in 12 pa-
tients, the device-based measure of the HIT (including inter-
pretation of results by experts), nystagmus assessment, and
test-of-skew examination was 100% accurate in identifying
the six stroke cases and six peripheral vestibular cases
compared with the final radiographic gold-standard diagno-
ses.22 The use of this device could make the HINTS examina-
tion more reliable, accurate, and give generalizable results.
Future Steps
To optimize the efficiency and effectiveness of the evaluation
and management of patients presenting with acute continu-
ous dizziness, further research is required. The prevalence of
stroke in these presentations, using an optimal gold-standard
outcome determinant, needs to be defined in populations
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representative of routine care. Tools (e.g., laboratory/radio-
graphic tests, bedside clinical decision aids) to help adjust the
probability of stroke need to be developed and validated
using rigorous methods. Next, dissemination and implemen-
tation work and strategies, applying meaningful outcomes
such as patient health outcomes and health care efficiency
measures, need to be developed and tested. In the absence of
these future steps, it is likely that acute continuous dizziness
presentations will continue to be among the most-feared
presentations in medicine.
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