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

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vestibular disorders may have multifactorial patho-

KEY POINTS mechanisms including ischemia [27,28].
 A comprehensive approach integrating detailed
bedside examination and risk estimation strategy is still Diagnostic approach to acute vascular
important for effective diagnosis of acute vascular vertigo
vertigo in the emergency setting.
Posterior circulation strokes are known to have a
 Recognition is required for the newly described features graver outcome than anterior strokes [29]. Even
and causes of acute transient vestibular syndrome, small strokes presenting isolated vertigo in the pos-
combined central and peripheral vestibulopathy, and terior circulation territory have a proportion of large
toxic and metabolic causes of central vertigo.
artery atherosclerosis similar to other stroke sub-
 The features and mechanisms recently identified in types [25]. As large artery atherosclerosis is signifi-
central vestibular disorders would enhance our cantly associated with disability at 3 months after
understanding of the central vestibular function. 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
Misdiagnosis of acute stroke in emergency estimation strategy including ABCD2 scoring system
&&

department [32], and perfusion imaging [8 ,26].

Despite modern imaging technics, patients with
vertigo, because of strokes, have a high chance of VESTIBULAR SYNDROME REQUIRING
& &
misdiagnosis in the emergency department [5 ,6 ]. ADDITIONAL CONSIDERATION WHENEVER
According to a retrospective study performed in APPLYING HEAD IMPULSE TEST,
USA, about 37% of patients with posterior circula- DIRECTION-CHANGING GAZE-EVOKED
tion strokes had an initial misdiagnosis compared NYSTAGMUS, AND TEST OF SKEW
with 16% of anterior strokes (P < 0.001) without a (HINTS)
difference between an academic teaching hospital
& Acute prolonged vestibular syndrome refers to acute
and a regional referral community hospital [5 ].
spontaneous vertigo lasting for more than a day
Furthermore, dizziness–vertigo and nausea–vomit-
[33–35]. Vestibular neuritis and posterior circula-
ing, the most common vestibular symptoms, were
tion strokes are the two most important causes of
associated with two and four folds higher risk of
& acute prolonged vestibular syndrome. It has been
misdiagnosis [5 ]. A recent meta-analysis also
well established that clinical examination, such as
revealed that about 9% of cerebrovascular events
HINTS plus is more sensitive than neuroimaging in
[ischemic strokes, transient ischemic attacks (TIAs),
detecting strokes presenting acute prolonged spon-
and subarachnoid hemorrhages] were missed at
& taneous vertigo [33]. There have been no established
initial presentation [6 ]. This study also found that
tools, however, to securely detect acute vascular
patients with mild transient nonspecific symptoms &&
vertigo lasting less than a day [8 ]. Some disorders
such as dizziness were more likely to be misdiag-
& involving both peripheral and central vestibular
nosed [6 ].
structures also require additional consideration for
&
the diagnosis [9 ,10].
Future risk of strokes in patients with a
diagnosis of peripheral vertigo Acute transient vestibular syndrome
Another study investigated the risk of a stroke in A single-center prospective study investigated the
patients with a diagnosis of ‘peripheral vertigo’ in cause of ATVS, a heterogeneous group of disorders
&&
the emergency department [7 ]. This study found including acute peripheral vestibulopathy and
that the risk for future strokes was apparently higher
&&
strokes [8 ]. The study found strokes or TIAs, docu-
in patients labeled with peripheral vertigo than in mented either with diffusion-weighted MRIs or per-
control patients during a 1-year observation period. fusion imaging, in about one quarter of patients
Especially, the risk for strokes was seemingly ele- with ATVS. Focal neurological deficits and severe
vated within the first 30 days after discharge from cervico-cranial pain were significantly associated
&&
the emergency department [7 ]. This indicates that
&&
with strokes [8 ]. Of note, one-third of patients
TIAs or strokes presenting vertigo may have been with ATVS and resolved symptoms or signs at the
&&
misdiagnosed as peripheral vertigo [7 ]. Otherwise, time of evaluation were found to have strokes or
some proportion of the patients with peripheral
&&
TIAs [8 ]. Thus, we still need a tool to stratify the
vertigo has a vascular cause Indeed, most peripheral risk of strokes in these patients with ATVS [36].

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Central vertigo Choi et al.

Combined peripheral and central &

[9 ]. It should be noted that the HINTS is not perfect
vestibulopathy in detecting AICA infarction involving both periph-
&
Diverse disorders can cause combined central and eral and central vestibular structures [9 ], even
&
peripheral vestibulopathy [9 ]. Of these, anterior though it is very effective for differentiating acute
inferior cerebellar artery (AICA) infarction was the vertigo because of posterior inferior cerebellar artery
most common cause of acute unilateral cases (Fig. 1) 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% bilateral groups (Fig. 2). The study showed that
&
for AICA infarction [9 ,37]. In contrast, Wernike’s the findings from peripheral vestibular involve-
encephalopathy was the most common cause of ment may overshadow those from central lesions
&
acute bilateral group whereas cerebellopontine [9 ]. Thus, careful neurotological examinations in
angle tumors and degenerative disorders were addition to HINTS are still important for these
mostly found in the chronic unilateral and 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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Central vertigo Choi et al.

TOXIC AND METABOLIC CAUSES OF NEW DISCOVERIES IN OLD SYNDROMES

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

nucleus, and may be ascribed to an imbalance in the nystagmus, which represents realigning the axis
NPH-inferior olive–flocculus–vestibular nucleus of eye rotation into the estimated gravity direc-
&&
loop [48 ]. 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
Lateral medulla impaired in about one-third of patients with a
Geotropic positional nystagmus was added to the cerebellar infarction, who mostly have lesions
&
list of nystagmus that may be observed in patients involving the nodulus and uvula [21 ]. As the
with acute or subacute lateral medullary infarction patients with impaired tilt suppression showed
(LMI) [18]. Although the patterns and mechanisms central positional nystagmus more frequently,
of spontaneous and head-shaking nystagmus have the positional nystagmus and impaired tilt sup-
been well established in LMI [50], the incidence pression may share a common pathomechanism.
and mechanism of geotropic positional nystagmus Previous studies also showed that central posi-
requires further elucidation in this classic vestibular tional nystagmus mostly occurs in cerebellar
disorder. lesions, especially whenever the nodulus and uvula
&
Patients with LMI may also show various pat- were involved [52,54 ].
terns of otolithic dysfunction [22]. In 45 patients Transient downbeat nystagmus may occur after
with LMI, tilt of the subjective visual vertical was the horizontal head-shaking [16]. This cross-coupled
most sensitive sign of otolithic dysfunction and was (perverted) nystagmus may be a masked form of
observed in 84%, followed by at least one compo- downbeat nystagmus and is usually found in asso-
nent of the ocular tilt reaction in 64%, abnormal ciation with cerebellar dysfunction. An enhanced
cVEMPs in 29%, and abnormal oVEMPs in 27%. This central processing of the anterior canal signals was
discrepancy in otolithic dysfunction among the suggested as the mechanism [16]. Along with par-
tests suggests different anatomical substrates or oxysmal positional downbeat nystagmus [52], this
dissimilar reciprocal modulation for processing of cross-coupled head-shaking nystagmus appears to
each otolithic signal in central vestibular structures indicate midline cerebellar dysfunction of various
located in the dorsolateral medulla. Delineation of causes [14,16,17].
the structures, however, responsible for processing
of each otolithic signal should be pursued in future
CONCLUSION
studies.
Patients with medullary hemorrhage also Central vertigo may have a diverse clinical spectrum
mostly present with vertigo and headache [51]. In depending on underlying diseases. For proper diag-
a recent study, all 11 patients with medullary hem- nosis and treatment of central vertigo, an approach
orrhage showed spontaneous nystagmus along integrating detailed history taking, careful exami-
with other neuro-otological findings that included nation, and appropriate neuroimaging is essential.
central positional nystagmus, gaze-evoked nys- Recognizing the characteristic findings from dys-
tagmus, ocular lateropulsion, skew deviation, or function of each central vestibular structure would
abnormal HITs. The cause was mostly cavernous enhance our understanding of the central vestibu-
malformation. Thus, neuro-otologic evaluation lar function and lead to better management of
seems important for detecting symptomatic med- central vertigo.
ullary cavernous malformation.
Acknowledgements
J.-Y.C. and S.-H.L. contributed equally to this study as
Cerebellum the first author.
Apogeotropic central positional nystagmus was
described in four patients with a brain tumor [19]. Financial support and sponsorship
As previously reported, apogeotropic positional nys- J.-S.K. serves as an Associate Editor of Frontiers in Neuro-
tagmus refractory to repeated canalith-reposition- otology and on the editorial boards of the Journal of
ing maneuver should be evaluated further for Clinical Neurology, Frontiers in Neuro-ophthalmology,
central diseases, even whenever other neurological Journal of Neuro-ophthalmology, Journal of Vestibular
signs are absent [52]. Research, Journal of Neurology, and Medicine. The other
The vestibulocerebellum, especially the nodulus authors have nothing to disclose. This research was
and uvula, is involved in estimation of the gravity supported by Basic Science Research Program through
direction and generation of the translational VOR by the National Research Foundation of Korea (NRF)
using convergent inputs from the semicircular canals funded by the Ministry of Education, Science and Tech-
and otoliths [53]. Tilt suppression of postrotatory nology (NRF-2016R1D1A1B04935568).

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21. Lee SU, Choi JY, Kim HJ, et al. Impaired tilt suppression of post-rotatory
Conflicts of interest & nystagmus and cross-coupled head-shaking nystagmus in cerebellar lesions:
There are no conflicts of interest. image mapping study. Cerebellum 2017; 16:95–102.
The study showed that lesions involving the nodulus and uvula are associated with
tilt suppression failure of postrotatory nystagmus, perverted head-shaking nys-
tagmus, and central positional nystagmus in patients with a cerebellar infarction.
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