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Vertigo and dizziness in the emergency room

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DOI: 10.1097/WCO.0000000000000769

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REVIEW

CURRENT
OPINION Vertigo and dizziness in the emergency room
Andreas Zwergal a,b and Marianne Dieterich a,b,c

Purpose of review
To provide an update on diagnostic algorithms for differential diagnosis of acute vertigo and dizziness and
swift identification of potentially harmful causes.
Recent findings
About 25% of patients with acute vertigo and dizziness have a potentially life-threatening diagnosis,
including stroke in 4–15%. Diagnostic work-up relies on the combination of symptom features (triggers,
duration, history of vertigo/dizziness, accompanying symptoms) and a comprehensive vestibular, ocular
motor, and balance exam. The latter includes head-impulse, head-shaking nystagmus, positional
nystagmus, gaze-holding, smooth pursuit, skew deviation, and Romberg’s test. Recent standardized
diagnostic algorithms (e.g., HINTS, TriAGeþ) suggest the combination of several elements to achieve a
good diagnostic accuracy in differentiation of central and peripheral vestibular causes. Neuroimaging with
MRI must be applied and interpreted with caution, as small strokes are frequently overlooked, especially in
the acute setting (false-negative rate of up to 50%).
Summary
Diagnostic differentiation of acute vertigo and dizziness remains a complex task, which can be tackled by
a structured clinical assessment focusing on symptom characteristics and constellations of ocular motor and
vestibular findings. Specific challenges arise in cases of transient or atypical vestibular syndromes.
Keywords
acute vestibular syndrome, central vestibular disorders, diffusion-weighted MRI, dizziness, ocular motor dysfunc-
tion, stroke, vertigo

INTRODUCTION Consequently, patients discharged from ED with a

Patients with acute vertigo and dizziness account for
about 4% of all visits and 20% of neurological con-
sultations in the emergency department (ED) [1]. The
majority of patients suffer from benign disorders,
with benign paroxysmal positional vertigo (BPPV),
orthostatic hypotension, acute unilateral vestibulop-
athy, vestibular migraine, and Menière’s disease
being the most frequent ones (Fig. 1). Up to 25% of
patients have a potentially life-threatening disease,
including cerebrovascular and cardiovascular events,
systemic metabolic, toxic, and inflammatory disor-
ders [2]. Stroke is the underlying cause in 4–15% of all
patients with acute vertigo and dizziness [1,2]. The
most frequent lesion localization is the cerebellum,
followed by the pontomedullary brainstem (Figs. 2
and 3). About 10% of strokes are missed at first
& ogy, SyNergy, Munich, Germany
contact in the ED [3 ]. Patients with mild or transient
dizziness, younger patients (<50 years), women, and
minorities are more frequently misdiagnosed [4,5]. In
a population-based registry study, 90% of transient
ischemic attacks (TIAs) in the posterior circulation
(with vestibular symptoms in half of patients), were
not recognized at first medical assessment [6].
suspected benign diagnosis of acute vertigo or dizzi-
ness had a 50-fold increased risk of being readmitted
to a hospital with a stroke diagnosis in the first week,
and a 9.3 times higher stroke risk after 30 days com-
pared with matched controls [6]. Likely reasons for
this deplorable situation are an overreliance on the
chief complaint (e.g., vertigo, dizziness) for differen-
tiation of peripheral and central causes, inadequate
knowledge or application of bedside ocular motor
examinations, and a high level of confidence in
imaging results, which may be often false-negative
a
Department of Neurology, University Hospital, Ludwig Maximilians Uni-
versity, bGerman Center for Vertigo and Balance Disorders, DSGZ,
Ludwig Maximilians University and cMunich Cluster of Systems Neurol-
Correspondence to Andreas Zwergal, MD, Department of Neurology and
German Center for Vertigo and Balance Disorders, DSGZ, Ludwig
Maximilians University, Munich, Marchioninistrasse 15, D-81377 Munich,
Germany. Tel: +49 89 4400 72571; fax: +49 89 4400 75584;
e-mail: andreas.zwergal@med.uni-muenchen.de
Curr Opin Neurol 2019, 32:000–000
DOI:10.1097/WCO.0000000000000769

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Neuro-otology

for stroke in the acute situation [7,8]. Therefore,

KEY POINTS
 25% of patients with acute vertigo or dizziness suffer
from a potentially life-threatening diagnosis, including
stroke in up to 15% of patients.
 The evaluation of triggers, symptom duration, history of
vertigo or dizziness, and accompanying features is of
greatest importance, whereas the symptom quality
(vertigo, dizziness, postural instability, disequilibrium)
does not help to differentiate peripheral from
central disorders.
 A comprehensive vestibular, ocular motor, and balance
exam has the highest diagnostic sensitivity to detect
stroke in the acute setting, as it allows central vestibular
pathologies to be differentiated from peripheral
vestibular disorders.
 Standardized diagnostic index tests (combining
symptom features with clinical signs) help to estimate
the risk for stroke.
 Early DWI-MRI has a poor diagnostic accuracy to
detect small strokes and therefore cannot replace
clinical examination and judgment.
physicians in the emergency services worldwide rank
vertigo and dizziness as one of the top priorities for
the development of better diagnostic algorithms [9].
DIAGNOSTIC APPROACHES
The currently favored diagnostic approaches rely on
an accurate assessment of the time course, triggers,
and duration of vestibular and accompanying non-
vestibular symptoms, a structured clinical ocular
motor exam, which may be supported by portable
video-oculography (VOG) devices, and a reasonable
selection and application of imaging methods. Vital
signs [blood pressure (BP), heart rate, oxygen satu-
ration, temperature] should be determined in all
acute presentations of vertigo and dizziness and
followed by more specific laboratory work-up, if
pathological, to account for general medical prob-
lems as the underlying cause (e.g., cardiovascular
disorders, infections). Overall, given the diversity of
presentations in acute vestibular disorders, the final
diagnosis in most cases results from a combination
of different features. Diagnostic index tests or

FIGURE 1. Frequency of diagnosis in acute vertigo/dizziness. In the entirety of acute vertigo or dizziness presentations,
benign paroxysmal positional vertigo (BPPV) is the most common cause (25%), followed by cardiovascular events (20%)
(orthostatic dysregulation/presyncope 12%, cardiac arrhythmia 5%, others 3%), and cerebrovascular events (14%) (8%
stroke, 5% transient ischemic attack, 1% intracranial hemorrhage). Acute unilateral vestibulopathy (12%) and attacks of
Menière’s disease (4%) are peripheral vestibular causes of vertigo/dizziness and must be differentiated from vestibular
migraine (5%). Systemic infections, intoxications, or metabolic dysregulations (e.g., hyponatriemia) have to be considered as
rarer causes. The estimation of frequency is based on previously published data [1,2] and personal data from the emergency
department of a tertiary referral center. The estimated mean value is depicted. The distribution of entities varies considerably
between studies and depends on the context of care (general physician, specialist, acute care).

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Vertigo and dizziness in the emergency ro om Zwergal and Dieterich

FIGURE 2. Prospective evaluation of lesion distribution in patients with isolated acute vertigo or dizziness (derived from the
EMVERT trial). The most frequent lesion site is found in the cerebellum (posterior inferior cerebellar artery territory), followed by
the pontomedullary brainstem. Level of sections depicted by z-MNI coordinates. Color bar (from red to yellow/white)
represents the percentage of lesions in an area (of all lesions).

FIGURE 3. Brainstem lesions and acute central vestibular syndrome. Overlap areas of brainstem infarct lesions in 23 patients
who presented with an acute vestibular syndrome due to a central rather than a peripheral lesion. MRI data from the literature
[10–14] are superimposed on four sections of the human brainstem (methods described in [15]). (a) Overlap area focusing on
the medial vestibular nucleus, VIIIm. (b) Overlap area focusing on the inferior cerebellar peduncle, ICP. (c) Overlap area
within the medial vestibular nucleus, VIIIm. (d) Overlap area within the superior vestibular nucleus, VIIIs, and the lateral
vestibular nucleus, VIII l. Reproduced with permission [16]. NPH, nucleus prepositus hypoglossi; sol, nucleus tractus solitarii; y,
y-group; VIIIsp, spinal part of vestibular nucleus.

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Neuro-otology
machine-learning algorithms may help in the future
to include different sources of information in diag-
nostic algorithms for acute vertigo or dizziness in
the ED [8].
SYMPTOM QUALITY AND
CHARACTERISTICS
The traditional method of symptom assessment in
acute vestibular disorders emphasized the type of
chief complaint, namely, vertigo, dizziness, postural
instability, or disequilibrium (for definition see
International Classification of Vestibular Disorders)
[17]. However, recent studies showed that this
approach has major limitations. The 2008 US
National Health Interview Survey indicated that
patients with suspected peripheral vestibular disor-
ders complained about pure vertigo in just one
quarter of cases, and different types of vertigo/dizzi-
ness in the remainder [18]. The prospective
EMVERT-trial found that stroke patients with iso-
lated vestibular or ocular motor symptoms com-
plained about dizziness in 45%, vertigo in 38%,
and double vision in 17% [19]. Lesions in the cere-
bellum presented with both vertigo and dizziness.
Lesions in the medulla tend to manifest with ver-
tigo, whereas lesions in the mesencephalon and
structures above tend to manifest with dizziness
or altered spatial perception [20]. Cortical lesions
rarely manifest with vertigo and are, in this case,
located in the parieto-insular region and less fre-
quently in the parietal cortex [15,21]. The mean
subjective intensity of vestibular symptoms in
stroke patients was lower than in patients with acute
unilateral vestibulopathy, but higher than in
patients with repetitive vestibular disorders. Given
the large overlap between groups, the symptom
intensity was not sufficient to distinguish peripheral
from central causes. The duration of symptoms in
vestibular stroke varied from less than 1 day (10%) to
1–4 days (40%) or more than 4 days (50% of cases)
and was therefore also not a sufficient indicator for
differentiation [19].
A more appropriate approach to assess the symp-
tom characteristics in acute vestibular disorders is
the TiTrATE algorithm, which stands for timing,
trigger, and targeted examination [22]. Timing refers
to the acuity of symptom onset and evolution of
symptoms, triggers to factors or actions that pro-
voked the onset of vestibular symptoms. A sponta-
neous, acute onset of vestibular symptoms increases
&
the risk of stroke 3.5-fold [23 ]. Vestibular TIAs may
present as spontaneous episodic vestibular symp-
toms, which last longer than 1 h in 50% of cases
[24,25]. In acute vestibular presentations, assess-
ment of accompanying symptoms is of great
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importance. Symptoms and signs, such as diplopia,
altered facial or body sensation, dysphagia, or limb
dysmetria, have a high sensitivity to indicate stroke
[21], but may be absent in patients with strategic
brainstem or cerebellar lesions [e.g., 16% of patients
with a posterior inferior cerebellar artery (PICA)
stroke] [26]. Headaches accompanying vestibular
symptoms must be considered as a red flag for
potential central lesions (e.g., due to artery dissec-
tion, cerebellar stroke with edema), but can also be
characteristically found in patients with vestibular
migraine [27]. In this case, the headache character-
istics may be helpful: phonophobia and photopho-
bia may indicate a potential migraine, while sudden
or sustained head and neck pain probably points to a
cerebrovascular event [28]. Hearing loss can be an
ambiguous accompanying symptom, as it can
appear in patients with Menière’s disease, but also
in about 50% of cases with an ischemia of the
anterior inferior cerebellar artery (AICA) which sup-
plies the labyrinthine artery [29].
VESTIBULAR, OCULAR MOTOR, AND
POSTURAL EXAM
In most cases, a comprehensive bedside vestibular,
ocular motor, and postural exam is the key to dif-
ferentiate peripheral or central causes of acute ver-
tigo and dizziness. It should include head impulse
testing (HIT) of the vestibulo–ocular reflex (VOR),
testing for head-shaking nystagmus or positional
nystagmus as well as signs of ocular tilt reaction
(OTR) [subjective visual vertical (SVV), skew devia-
tion, head tilt], assessment of smooth pursuit, gaze
holding, saccades, fixation suppression of VOR, and
&
postural control in Romberg’s test [6,30,31 ].
Pathological deviations of the SVV (>2.58) are
very sensitive to indicate acute unilateral lesions in
peripheral as well as central vestibular networks
&
[31 ]. About 95% of tegmental brainstem strokes
and 70% of cerebellar strokes show a pathological
&
deviation of SVV [31 ,32]. Due to the crossing of
vestibular graviceptive pathways at pontine level,
SVV deviations are ipsilesional in pontomedullary
brainstem lesions and contralesional in pontome-
sencephalic lesions. The amount of SVV deviation
&
decreases from lower to upper brainstem [31 ]
(Fig. 4). SVV deviations in acute cerebellar lesions
are mostly contralesional, especially if the dentate
nucleus is involved [32]. A specific application of
SVV measurements may be the differentiation of
acute central lesions from ‘benign’ vestibular
migraine, which can show central vestibular and
ocular motor signs during the attack [e.g., sponta-
neous nystagmus (SPN), central positional nystag-
mus] [33]. In contrast to vestibular stroke patients,
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Vertigo and dizziness in the emergency ro om Zwergal and Dieterich

FIGURE 4. Topography of deviations of subjective visual vertigo. Schematic graviceptive pathways together with the amount
(in deg) of subjective visual vertical deviation for ipsilateral and contralateral lesions depending on the level of acute unilateral
vestibular damage. The range of the mean values was calculated on the basis of previously published studies. The six major
messages are as follows: first, in peripheral and pontomedullary brainstem lesions, subjective visual vertical tilts are ipsilateral.
Second, in pontomesencephalic vestibular pathway lesions up to the interstitial nucleus of Cajal, subjective visual vertical tilts
are contralateral. Third, in cerebellar lesions, subjective visual vertical tilts are mostly contralesional, especially if the dentate
nucleus in involved. Fourth, in vestibular thalamic and cortical lesions, subjective visual vertical tilts may be either ipsilateral or
contralateral with an intraindividual consistency and an equal distribution interindividually. Fifth, the amount of subjective
visual vertical tilt is maximal in complete peripheral lesions, followed by tilt in brainstem. Sixth, acute vestibular symptoms
(vertigo, dizziness) are most frequently reported in brainstem and cerebellar lesions, while cortical lesions cause vertigo only
rarely. INC, interstitial nucleus of Cajal; MLF, medial longitudinal fascicle; PIVC, parieto-insular vestibular cortex; T, thalamus;
VN, vestibular nucleus. Adapted from [31 ]. &

patients with acute episodes of vestibular migraine
tend to have normal SVV values [34,35].
In patients with pontomedullary brainstem
and/or cerebellar lesions, presenting with SPN,
HINTS testing (head impulse test, gaze-evoked nys-
tagmus, test of skew) has a high sensitivity and
specificity to diagnose stroke [36]. A bilaterally nor-
mal head-impulse test in the presence of SPN is the
most sensitive indicator of a central origin by stroke,
followed by a gaze-evoked nystagmus in the oppo-
site direction to the SPN [36,37]. Skew deviation is a
very specific sign of a central lesion (95–100%), but
appears only in 40% of central lesions [38]. The
sensitivity of HINTS testing can be improved by
VOG-based quantification of the HIT (vHIT) [39–
41]. However, it is unclear how much the vHIT adds
to the differential diagnosis [42]. Potential limita-
tions of the HINTS approach are combined central–
peripheral pathologies (e.g., in AICA ischemia),
transient vestibular syndromes, and patients, whose
vestibular stroke presents without SPN (about 30–
40% of all patients with acute central vestibular
&
disorders) [8,29,43 ,44]. Therefore, its diagnostic
utility may not be generalized to all patients with
acute vestibular disorders.
In patients with acute vertigo or dizziness of
cerebellar origin, six main syndromes can be differ-
entiated based on clinical vestibular, ocular motor,
or postural signs (Fig. 5) [45]:
(1) Unilateral lesions of the nodulus and/or uvula show
an ipsilesional horizontal SPN, contraversive OTR,

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FIGURE 5. Vestibular, ocular motor, and postural findings in cerebellar stroke. The most frequent cerebellar lesion sites in
patients with acute vertigo or dizziness are shown alongside the most prevalent findings in the vestibular, ocular motor, and
postural exam. Different signs can be present in isolation or in combination. C, contralesional; I, ipsilesional; I > C, ipsilesional
more often than contralesional; OT, ocular torsion; OTR, ocular tilt reaction; SPN, spontaneous nystagmus; SVV, subjective
visual vertical; VOR, vestibulo–ocular reflex.

perverted head-shaking nystagmus (downbeat
nystagmus or direction-changing nystagmus after
horizontal head-shaking) [46], a central positional
nystagmus (apogeotropic nystagmus in ear-
down-position and downbeat nystagmus in
straight head hanging position) [47–50], a dimin-
ished tilt suppression of the postrotatory nystag-
mus [51], and contralesional lateropulsion in the
majority of cases [52].
(2) Isolated unilateral lesions of the flocculus are
considerably rare and can present with ipsile-
sional SPN, contralesional OTR, impaired ipsile-
sional smooth pursuit, and gaze holding [53].
The HIT may be bilaterally false-positive in these
lesions [54].
(3) Lesions of the cerebellar tonsil show an ipsile-
sional SPN in darkness, contralesional SVV devi-
ation, markedly impaired ipsilesional smooth
pursuit, and bilateral gaze-evoked nystagmus,
or isolated central positional nystagmus [55,56].
(4) Lesions of the inferior or middle cerebellar peduncle
present with ipsilesional SPN, contralesional
SVV and ocular torsion, impaired ipsilesional
smooth pursuit, and ipsilesional lateropulsion
[57,58].
(5) Ocular motor vermis lesions may cause central
positional nystagmus and saccadic hypermetria
to the lesion side [49,59]. Patients with more
extensive lesions to the anterior paravermis may
have pronounced gait and trunk ataxia [52].
(6) Lesions of the lateral posterior lobe including the
dentate nucleus regularly show a contralesional
OTR and ipsilesional lateropulsion [32,52].
DIAGNOSTIC INDEX TESTS FOR
CEREBROVASCULAR EVENTS
In recent years, several diagnostic index tests have
been described as helpful for differentiation of
peripheral and central causes of acute vertigo or
dizziness. In general, these index tests combine
different features from the patient history (e.g.,
symptom characteristics, cardiovascular risk pro-
file), clinical ocular motor exam (e.g., HIT,

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Vertigo and dizziness in the emergency ro om Zwergal and Dieterich

Table 1. Diagnostic index tests for acute vestibular disorders

Index test Features Application AUC Sen/Spec

HINTS [36] Head impulse test, gaze-evoked Acute vestibular syndrome 0.99 100/96%
nystagmus, test of skew with nystagmus
ABCD2 score [60,62] Age, blood pressure, clinical features, All acute vestibular 0.62–0.79 n.c.
duration of symptoms, diabetes disorders
PCI score [62] Blood pressure, diabetes, history of All acute vestibular 0.82 94/41%
stroke, rotation and rocking, speech disorders
difficulty, tinnitus, sensory deficit, gait
or limb ataxia
TriAGeþ score [23 ] Triggers, atrial fibrillation, male sex, All acute vestibular 0.82 77/72%
&

blood pressure >140/90 mmHg, disorders

brainstem or cerebellar dysfunction,
focal weakness, speech impairment,
dizziness, no history of dizziness/
vertigo
CATCH2 score [19] Central features, age, triggers, cover test All acute vestibular 0.88 85/77%
with skew deviation, head impulse disorders
test, history of dizziness/vertigo
NRL > 2.8 [64] Neutrophil to lymphocyte ratio All acute vestibular 0.82 86/78%
disorders
VAECCS [65] Abnormal ultrasound All acute vestibular n.c. 54/95%
disorders
Truncal ataxia score [66] Postural control during broad stance Acute vestibular syndrome n.c. 93/61%
STANDING [63 ] Spontaneous and positional nystagmus, Vestibular syndrome with n.c. 95/87%
&

nystagmus direction, head impulse nystagmus

test, test of equilibrium

The included features, modes of application, AUC values in ROC analysis, Sen, and Spec are reported for the respective test. AUC, area under the curve; ROC,
receiver operator characteristics; Sen, sensitivity; Spec, specificity.

nystagmus) and in some cases also biomarkers [8]
(for overview see Table 1). The ABCD2 score contrib-
utes to the diagnosis of vestibular stroke [61], but
seems to be inferior to HINTS and PCI score [61,62].
An ABCD2 score more than 5 is associated with
a stroke risk of 27%. The TriAGeþ score – a combi-
nation of symptom characteristics (e.g., triggers),
central clinical signs (e.g., dysarthria), and cardio-
vascular risk factors (e.g., BP) – can predict vestibu-
lar stroke with an overall accuracy of 82%
(sensitivity 96%, negative likelihood ratio 0.15), if
&
the cutoff is set to 5 [23 ]. The STANDING algorithm
(including assessment of spontaneous and posi-
tional nystagmus, nystagmus direction, and HIT)
detects a central cause of vestibular symptoms with
an overall accuracy of 88%, but is restricted to
&
patients with nystagmus [63 ]. A new diagnostic
index test called CATCH2 (central features, age,
triggers, cover test with skew deviation, HIT, history
of dizziness/vertigo) was composed from the pro-
spective EMVERT trial in 335 patients with isolated
vestibular or ocular motor symptoms (vertigo/dizzi-
ness, postural instability, double vision) and had an
overall accuracy of 88% to diagnose stroke [12]. This
test is applicable for the entirety of patients with
acute vestibular disorders, irrespective of the
presence of nystagmus. Other index tests have sug-
gested that neutrophil-to-lymphozyte ratio or ultra-
sound markers are helpful in diagnosis of vestibular
stroke [64,65].
BRAIN IMAGING
Neuroimaging in acute vertigo and dizziness is used
to an increasing extent in EDs and makes a relevant
contribution to the total expenses [67]. In US EDs,
about 40% of patients presenting with acute vestib-
ular disorders undergo cranial computed tomogra-
phy (CT) imaging and fewer than 3% MRI [67].
However, CT has a very low sensitivity (max.
16%) to identify posterior circulation stroke [68].
A CT scan is mostly indicated to exclude an acute
hemorrhage before intravenous thrombolysis or
antiplatelet therapy. CT angiography and perfusion
can show stenosis or occlusion of larger arteries (e.g.,
vertebral artery, PICA) and a mismatch of blood flow
and volume in larger cerebellar stroke, which may be
important for the decision to apply thrombolysis.
However, it is unable to detect smaller structural
lesions within the brainstem. MRI within the first
24 h after symptom onset may also miss about 20%
of larger strokes and up to 50% of brainstem and

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cerebellar strokes with a diameter less than 1 cm [69].
It seems that the false-negative rate cannot be solely
attributed to the slice thickness and imaging proto-
col, but to the delayed time course of diffusion-
weighted imaging (DWI) signal intensity in the pos-
terior circulation [70]. Consequently, an MRI for
detection of vestibular stroke should be performed
optimally more than 48 h after symptom onset [7].
Overall, MRI in the acute situation has a poorer
sensitivity compared with a comprehensive ocular
motor exam for several reasons [69]. Magnetic reso-
nance perfusion may be a promising method to
identify patients with acute transient vestibular syn-
& &
drome [43 ] and small stroke [71 ], but this will not be
easily available in EDs worldwide. A general use of
routine MRI is not cost-efficient and may lead to an
inappropriate reliance on imaging.
TREATMENT
The treatment of acute vestibular disorders follows
common guidelines (e.g., positioning maneuvers for
BPPV) and should be initiated in the ED. In acute
vestibular stroke, intravenous thrombolysis is indi-
cated, if the diagnosis is based on convincing evi-
dence from clinical ocular motor assessment, the
deficit is relevant (e.g., inability to stand freely),
and contraindications have been ruled out. A com-
mon dilemma is a prolonged door-to-needle time in
patients with posterior circulation stroke, which is
due to a misjudgment of symptoms and a lack of
standards for clinical assessment [72]. In scales which
are used for thrombolysis decisions like NIHSS, func-
tional consequences of vestibular lesions are under-
represented [73]. Although there are no larger trials
on functional outcomes of vestibular stroke, previous
case collections have suggested a high risk of perma-
nent morbidity and mortality (30–40%) in patients
with missed or untreated cerebellar strokes [74]. In
the future, better decision algorithms for thromboly-
sis therapy in acute vestibular disorders are needed
based on clinical signs and symptoms and structured
investigations of functional outcomes.
CONCLUSION
Patients with acute vertigo and dizziness should be
processed in a standardized way in the EDs to avoid
misdiagnosis of potentially harmful diseases like
cerebrovascular events. The clinical diagnosis is
based on symptom features, such as triggers, dura-
tion of symptoms, history of dizziness, as well as a
comprehensive clinical vestibular, ocular motor,
and postural exam. Diagnostic index tests (like
HINTS, TriAGeþ, CATCH2) may help to estimate
the risk for a central pathology. A consensus process
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is desirable to harmonize the existing index tests
and validate them prospectively. Neuroimaging by
MRI has limited sensitivity in the acute situation,
especially for small lesions, and therefore has to be
applied and interpreted with caution.
Acknowledgements
We thank Katie Göttlinger for copyediting the article.
Financial support and sponsorship
The study was performed as a project of the German
Center for Vertigo and Balance Disorders (DSGZ) (grant
number 01 EO 0901) with the support of the German
Federal Ministry of Education and Research (BMBF) and
the German Foundation for Neurology (Deutsche Stif-
tung Neurologie).
Conflicts of interest
There are no conflicts of interest.
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