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REVIEW

CURRENT
OPINION Central vertigo
Jeong-Yoon Choi a,b, Seung-Han Lee c, and Ji-Soo Kim a,b

Purpose of review
This review considers recent advances in central vertigo in terms of clinical and laboratory features and
pathophysiology.
Recent findings
Strokes presenting dizziness–vertigo are more likely to be associated with a misdiagnosis in the emergency
setting. The risk of future strokes after discharge is higher in patients diagnosed with peripheral vertigo than
in control patients. Strokes and transient ischemic attacks account for one-quarter of acute transient
vestibular syndrome. Diagnosis of acute combined central and peripheral vestibulopathy such as anterior
inferior cerebellar artery infarction requires additional consideration whenever applying the HINTS (head
impulse test, direction-changing gaze-evoked nystagmus, and test of skew). Heat illness and metronidazole
have been recognized as new causes of central vestibulopathy. Some new findings have also been added
to the clinical and laboratory features of central vertigo.
Summary
Central vertigo is a heterogeneous group of disorders with diverse clinical spectrums. An integrated
approach based on understanding of clinical features, laboratory findings, speculated mechanisms, and
limitations of current diagnostic tests will lead to better clinical practice.
Keywords
central vertigo, dizziness, vestibular disorders

INTRODUCTION and laboratory aspects of central vertigo [16–19,

& &

Central vestibular dysfunction is one of the leading 20 ,21 ,22].

causes of vertigo and is mostly because of strokes,
intracranial tumors, metabolic conditions, and par-
oxysmal or degenerative disorders [1,2]. Vestibular
migraine may be also considered of a central origin
[3]. Central vertigo especially requires early diagnosis
and proper treatments, given its potentially serious
diseases and grave prognosis. In addition, detailed
evaluation of central vertigo can enhance our under-
standing on how the central vestibular system func-
tions to guarantee our daily activities [4].
We will start this review with recent studies on
diagnostic efficacy and prognosis of acute dizziness–
& &
vertigo in the emergency setting [5 ,6 ,7 ]. This
would lead us to recognize limitations of our current
practice for acute vascular vertigo. Then, we will
discuss acute transient vestibular syndrome (ATVS)
and combined central and peripheral vestibulop-
athy that require additional consideration for diag-
nosis whenever applying the HINTS (head impulse
test, direction-changing gaze-evoked nystagmus,
&& &
and test of skew) [8 ,9 ,10]. The characteristics
and prognosis of central vertigo of toxic and meta-
& &
bolic causes are the next topic [11 ,12 ,13–15].
Lastly, we will summarize recent findings in clinical
IDENTIFICATION OF ACUTE VASCULAR
VERTIGO
Dizziness or vertigo is the most common presenting
symptom of posterior circulation strokes, which
accounts for about 20% of all ischemic strokes
[23]. Though isolated dizziness–vertigo had been
considered unusual in central lesions including
strokes [24], recent advances in clinical neuro-
otology and neuroimaging have contradicted this
long belief [25,26].
&&
a
Dizziness Center, Seoul National University Bundang Hospital,
b
Department of Neurology, Seoul National University College of Medi-
cine, Seoul National University Bundang Hospital, Seongnam and
c
Department of Neurology, Chonnam National University Medical School,
Chonnam National University Hospital, Gwangju, Korea
Correspondence to Ji-Soo Kim, MD, PhD, Dizziness Center, Department
of Neurology, Seoul National University College of Medicine, Seoul
National University Bundang Hospital, 173-82 Gumi-ro, Bundang-gu,
Seongnam-si, Gyeonggi-do 463-707, Korea. Tel: +82 31 787 7463;
fax: +82 31 719 6828; e-mail: jisookim@snu.ac.kr
Curr Opin Neurol 2017, 30:000–000
DOI:10.1097/WCO.0000000000000511

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Neuro-otology
KEY POINTS
 A comprehensive approach integrating detailed
bedside examination and risk estimation strategy is still
important for effective diagnosis of acute vascular
vertigo in the emergency setting.
 Recognition is required for the newly described features
and causes of acute transient vestibular syndrome,
combined central and peripheral vestibulopathy, and
toxic and metabolic causes of central vertigo.
 The features and mechanisms recently identified in
central vestibular disorders would enhance our
understanding of the central vestibular function.
Misdiagnosis of acute stroke in emergency
department
Despite modern imaging technics, patients with
vertigo, because of strokes, have a high chance of
& &
misdiagnosis in the emergency department [5 ,6 ].
According to a retrospective study performed in
USA, about 37% of patients with posterior circula-
tion strokes had an initial misdiagnosis compared
with 16% of anterior strokes (P < 0.001) without a
difference between an academic teaching hospital
& Acute prolonged vestibular syndrome refers to acute
and a regional referral community hospital [5 ].
Furthermore, dizziness–vertigo and nausea–vomit-
ing, the most common vestibular symptoms, were
associated with two and four folds higher risk of
& acute prolonged vestibular syndrome. It has been
misdiagnosis [5 ]. A recent meta-analysis also
revealed that about 9% of cerebrovascular events
[ischemic strokes, transient ischemic attacks (TIAs),
and subarachnoid hemorrhages] were missed at
& taneous vertigo [33]. There have been no established
initial presentation [6 ]. This study also found that
patients with mild transient nonspecific symptoms
such as dizziness were more likely to be misdiag-
& involving both peripheral and central vestibular
nosed [6 ].
Future risk of strokes in patients with a
diagnosis of peripheral vertigo
Another study investigated the risk of a stroke in
patients with a diagnosis of ‘peripheral vertigo’ in
&&
the emergency department [7 ]. This study found
that the risk for future strokes was apparently higher
in patients labeled with peripheral vertigo than in
control patients during a 1-year observation period.
Especially, the risk for strokes was seemingly ele-
vated within the first 30 days after discharge from
&&
the emergency department [7 ]. This indicates that
TIAs or strokes presenting vertigo may have been
&&
misdiagnosed as peripheral vertigo [7 ]. Otherwise,
some proportion of the patients with peripheral
vertigo has a vascular cause Indeed, most peripheral
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vestibular disorders may have multifactorial patho-
mechanisms including ischemia [27,28].
Diagnostic approach to acute vascular
vertigo
Posterior circulation strokes are known to have a
graver outcome than anterior strokes [29]. Even
small strokes presenting isolated vertigo in the pos-
terior circulation territory have a proportion of large
artery atherosclerosis similar to other stroke sub-
types [25]. As large artery atherosclerosis is signifi-
cantly associated with disability at 3 months after
strokes [30], we need to improve identification of
vertigo with a risk of strokes, which can be achieved
with an integrated approach using detailed neuro-
otological examination such as HINTS plus [31], risk
estimation strategy including ABCD2 scoring system
&&
[32], and perfusion imaging [8 ,26].
VESTIBULAR SYNDROME REQUIRING
ADDITIONAL CONSIDERATION WHENEVER
APPLYING HEAD IMPULSE TEST,
DIRECTION-CHANGING GAZE-EVOKED
NYSTAGMUS, AND TEST OF SKEW
(HINTS)
spontaneous vertigo lasting for more than a day
[33–35]. Vestibular neuritis and posterior circula-
tion strokes are the two most important causes of
well established that clinical examination, such as
HINTS plus is more sensitive than neuroimaging in
detecting strokes presenting acute prolonged spon-
tools, however, to securely detect acute vascular
&&
vertigo lasting less than a day [8 ]. Some disorders
structures also require additional consideration for
&
the diagnosis [9 ,10].
Acute transient vestibular syndrome
A single-center prospective study investigated the
cause of ATVS, a heterogeneous group of disorders
including acute peripheral vestibulopathy and
&&
strokes [8 ]. The study found strokes or TIAs, docu-
mented either with diffusion-weighted MRIs or per-
fusion imaging, in about one quarter of patients
with ATVS. Focal neurological deficits and severe
cervico-cranial pain were significantly associated
&&
with strokes [8 ]. Of note, one-third of patients
with ATVS and resolved symptoms or signs at the
time of evaluation were found to have strokes or
&&
TIAs [8 ]. Thus, we still need a tool to stratify the
risk of strokes in these patients with ATVS [36].
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Central vertigo Choi et al.

Combined peripheral and central &

vestibulopathy
Diverse disorders can cause combined central and
&
peripheral vestibulopathy [9 ]. Of these, anterior
inferior cerebellar artery (AICA) infarction was the
most common cause of acute unilateral cases (Fig. 1)
[9 ]. It should be noted that the HINTS is not perfect
in detecting AICA infarction involving both periph-
&
eral and central vestibular structures [9 ], even
though it is very effective for differentiating acute
vertigo because of posterior inferior cerebellar artery
infarction from vestibular neuritis [33–35]. Indeed,

FIGURE 1. Acute unilateral combined central and peripheral vestibulopathy in anterior inferior cerebellar infarction. (a)
Moderately reduced head impulse gain for the right horizontal canals (ipsilesional) whereas normal or mildly decreased gain
for the other canals. (b) Direction changing gaze-evoked nystagmus, more intense during leftward (contralesional) gaze. (c)
Right caloric paresis indicating a peripheral vestibular damage. (D) Diffusion-weighted MR image showing an acute ischemic
stroke involving the right flocculus.

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Neuro-otology

the false negative rate of HINTS was about 17–29%
&
for AICA infarction [9 ,37]. In contrast, Wernike’s
encephalopathy was the most common cause of
acute bilateral group whereas cerebellopontine
angle tumors and degenerative disorders were
mostly found in the chronic unilateral and
bilateral groups (Fig. 2). The study showed that
the findings from peripheral vestibular involve-
ment may overshadow those from central lesions
&
[9 ]. Thus, careful neurotological examinations in
addition to HINTS are still important for these
chimeric disorders.

FIGURE 2. Chronic unilateral combined central and peripheral vestibulopathy in a cerebellopontine angle tumor. (a) The
head impulse tests showing bilateral gain reduction, more for the ipsilesional (left) horizontal and anterior canals. (b) Direction
changing gaze-evoked nystagmus with a prominent rebound nystagmus on resuming the straight-ahead gaze after leftward
(ipsilesional) gaze. (c) Left caloric paresis indicating a left peripheral vestibulopathy. (d) A vestibular schwannoma
compressing both peripheral and central vestibular structures on gadolinium-enhanced T1-weighted MRI.

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TOXIC AND METABOLIC CAUSES OF
CENTRAL VERTIGO
Several studies have identified toxic and metabolic
causes of central vertigo. It is important to recog-
nize these conditions because some of them
may be reversible with a prompt and appropriate
intervention.
Central vestibulopathy after heat stroke
Dizziness and vertigo are common symptoms of
heat illness. A recent study described details of
clinical and laboratory features in delayed vesti-
&
bulopathy after heat strokes [11 ]. In this study,
three patients recovered from acute heat stroke
developed vertigo about a week after the heat
exposure. Findings at that time included sponta-
neous downbeat nystagmus, gaze-evoked nystag-
mus, abnormal head impulse tests (HITs),
position-induced or head shaking-induced down-
beat nystagmus. Given the previous observations
on loss of cerebellar Purkinje cells and cerebellar
atrophy in patients with heat stroke, [38], these
findings suggest vestibulocerebellar dysfunction as
a mechanism of delayed vestibulopathy after heat
&
exposure [11 ].
Metronidazole-induced central
vestibulopathy
Metronidazole may cause cerebellar dysfunction
&
[12 ]. The MRIs of patients with metronidazole
intoxication consistently showed cerebellar lesions
involving the deep cerebellar nuclei. The brainstem,
corpus callosum, and other brain areas may be addi-
tionally involved [39]. A study reported bilateral
impairments of the vestibulo-ocular reflex (VOR)
during caloric test and HITs along with gaze-evoked
nystagmus in a patient with metronidazole toxicity.
The findings may be ascribed to either central or
combined central and peripheral vestibulopathy
[15]. Even though the exact mechanism is still
unknown, altered thiamine pathway is considered
responsible for this metronidazole-induced vestibul-
&
opathy [12 ].
Other conditions
Cerebellar atrophy and associated ocular motor
findings were described in X-linked adrenoleuko-
dystrophy and in b-fluoroethyl acetate (rodenticide)
intoxication [13,14]. Pregabalin may also cause
reversible vertigo and downbeat nystagmus espe-
cially whenever administered with other antiepilep-
tic drugs [40].
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Central vertigo Choi et al.
NEW DISCOVERIES IN OLD SYNDROMES
Over the years, several studies have defined distinct
oculomotor and vestibular findings in lesions cir-
cumscribed to specific vestibular structures in the
brainstem and cerebellum.
Medial longitudinal fasciculus
Lesions involving the medial longitudinal fasciculus
(MLF) give rise to various oculomotor and vestibular
abnormalities in addition to internuclear ophthal-
moplegia (INO; Fig. 3) [41]. Previous studies have
described upbeat or jerky seesaw nystagmus [42],
contraversive ocular tilt reaction and subjective
visual vertical tilt [43], impairment of the vertical
VOR and vertical smooth pursuit [41], and abnormal
ocular vestibular-evoked myogenic potentials
(oVEMPs) and cervical vestibular-evoked myogenic
potentials (cVEMPs) [44]. Recent studies docu-
mented a prominent loss of the angular VOR gain
during HIT for the contralesional posterior canal in a
larger number of patients with INO because of a
&&
stroke or multiple sclerosis [45 ,46]. These studies
reaffirmed the finding of a previous study on a single
patient with INO [47], and strongly suggest that the
signals from the anterior canal have additional
ascending routes other than the MLF whereas the
posterior canal signals mostly pass up through the
MLF. Relative sparing of the horizontal VOR with
greater catch-up saccade impairment for the adduct-
ing than abducting eye suggest that an extra-MLF
pathway, such as the ascending tract of Deiters, also
mediates the horizontal VOR, but not adducting
&&
horizontal saccades [45 ,46]. Associated limb and
truncal ataxia in INO localizes the lesion at the level
of pontomesencephalic junction, probably because
of damage of the brachium conjunctivum or mes-
&
encephalic locomotion center near the MLF [20 ].
Nucleus prepositus hypoglossi
The nucleus prepositus hypoglossi (NPH), located
in the midline of the upper medulla and lower pons,
functions as a neural integrator mostly for horizon-
tal eye motion [41]. Lesions involving the NPH
show a unique ocular motor syndrome comprised
of ipsilesional-beating spontaneous nystagmus,
horizontal gaze-evoked nystagmus more intense
on looking toward the ipsilesional side, impaired
pursuit more to the ipsilesional side, central pat-
terns of head-shaking nystagmus, contralateral eye
deviation, and decreased VOR gain during contrale-
&&
sional HIT [48 ]. These findings are in contrast with
ocular motor findings observed in lesions involving
the nearby structure [49], the medial vestibular
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FIGURE 3. Head impulse vestibulo-ocular reflexes in a patient with internuclear ophthalmoplegia. (a) Limitation of adduction
in the left eye during rightward gaze. (b) Vestibulo-ocular reflexes measured at the right eye show a moderate gain reduction
during the ipsilesional (left) horizontal head impulses, a prominent decrease of the head impulse gain of the vestibulo-ocular
reflex for the contralesional (right) posterior canal, and a milder gain reduction during the head impulse tests for the
contralesional (right) anterior canal. (c) Fundus photography showing clockwise (contralesional) ocular torsion. (d) An acute
ischemic stroke involving the left medial longitudinal fasciculus on diffusion-weighted MRI.

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nucleus, and may be ascribed to an imbalance in the
NPH-inferior olive–flocculus–vestibular nucleus
&&
loop [48 ].
Lateral medulla
Geotropic positional nystagmus was added to the
list of nystagmus that may be observed in patients
with acute or subacute lateral medullary infarction
(LMI) [18]. Although the patterns and mechanisms
of spontaneous and head-shaking nystagmus have
been well established in LMI [50], the incidence
and mechanism of geotropic positional nystagmus
requires further elucidation in this classic vestibular
disorder.
Patients with LMI may also show various pat-
terns of otolithic dysfunction [22]. In 45 patients
with LMI, tilt of the subjective visual vertical was the
most sensitive sign of otolithic dysfunction and was
observed in 84%, followed by at least one compo-
nent of the ocular tilt reaction in 64%, abnormal
cVEMPs in 29%, and abnormal oVEMPs in 27%. This
discrepancy in otolithic dysfunction among the
tests suggests different anatomical substrates or
dissimilar reciprocal modulation for processing of
each otolithic signal in central vestibular structures
located in the dorsolateral medulla. Delineation of
the structures, however, responsible for processing
of each otolithic signal should be pursued in future
studies.
Patients with medullary hemorrhage also
mostly present with vertigo and headache [51]. In
a recent study, all 11 patients with medullary hem-
orrhage showed spontaneous nystagmus along
with other neuro-otological findings that included
central positional nystagmus, gaze-evoked nys-
tagmus, ocular lateropulsion, skew deviation, or
abnormal HITs. The cause was mostly cavernous
malformation. Thus, neuro-otologic evaluation
seems important for detecting symptomatic med-
ullary cavernous malformation.
Cerebellum
Apogeotropic central positional nystagmus was
described in four patients with a brain tumor [19].
As previously reported, apogeotropic positional nys-
tagmus refractory to repeated canalith-reposition-
ing maneuver should be evaluated further for
central diseases, even whenever other neurological
signs are absent [52].
The vestibulocerebellum, especially the nodulus
and uvula, is involved in estimation of the gravity
direction and generation of the translational VOR by
using convergent inputs from the semicircular canals
and otoliths [53]. Tilt suppression of postrotatory
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Central vertigo Choi et al.
nystagmus, which represents realigning the axis
of eye rotation into the estimated gravity direc-
tion, is attained by this function, and resection of
the nodulus and uvula abolishes this phenomenon
in monkeys [53]. In humans, tilt suppression is also
impaired in about one-third of patients with a
cerebellar infarction, who mostly have lesions
&
involving the nodulus and uvula [21 ]. As the
patients with impaired tilt suppression showed
central positional nystagmus more frequently,
the positional nystagmus and impaired tilt sup-
pression may share a common pathomechanism.
Previous studies also showed that central posi-
tional nystagmus mostly occurs in cerebellar
lesions, especially whenever the nodulus and uvula
&
were involved [52,54 ].
Transient downbeat nystagmus may occur after
horizontal head-shaking [16]. This cross-coupled
(perverted) nystagmus may be a masked form of
downbeat nystagmus and is usually found in asso-
ciation with cerebellar dysfunction. An enhanced
central processing of the anterior canal signals was
suggested as the mechanism [16]. Along with par-
oxysmal positional downbeat nystagmus [52], this
cross-coupled head-shaking nystagmus appears to
indicate midline cerebellar dysfunction of various
causes [14,16,17].
CONCLUSION
Central vertigo may have a diverse clinical spectrum
depending on underlying diseases. For proper diag-
nosis and treatment of central vertigo, an approach
integrating detailed history taking, careful exami-
nation, and appropriate neuroimaging is essential.
Recognizing the characteristic findings from dys-
function of each central vestibular structure would
enhance our understanding of the central vestibu-
lar function and lead to better management of
central vertigo.
Acknowledgements
J.-Y.C. and S.-H.L. contributed equally to this study as
the first author.
Financial support and sponsorship
J.-S.K. serves as an Associate Editor of Frontiers in Neuro-
otology and on the editorial boards of the Journal of
Clinical Neurology, Frontiers in Neuro-ophthalmology,
Journal of Neuro-ophthalmology, Journal of Vestibular
Research, Journal of Neurology, and Medicine. The other
authors have nothing to disclose. This research was
supported by Basic Science Research Program through
the National Research Foundation of Korea (NRF)
funded by the Ministry of Education, Science and Tech-
nology (NRF-2016R1D1A1B04935568).
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Neuro-otology
Conflicts of interest
There are no conflicts of interest.
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