Published online: 14.01.

2020

Vertigo Due to Vascular Mechanisms

Hyun Ah Kim, PhD1,
Hyung Lee, MD, PhD1,
Ji-Soo Kim, MD, PhD2,3

1 Department of Neurology, Keimyung University Dongsan Hospital,
Daegu, South Korea
2 Department of Neurology, Seoul National University College of
Medicine, Seoul, South Korea
3 Dizziness Center, Clinical Neuroscience Center, Seoul National
University Bundang Hospital, Seongnam, South Korea
Address for correspondence Ji-Soo Kim, MD, PhD, Department of
Neurology, Seoul National University Bundang Hospital, 173-82 Gumi-
ro, Bundang-gu, Seongnam-si, Gyeonggi-do 13620, South Korea
(e-mail: jisookim@snu.ac.kr).

Semin Neurol

Abstract Isolated dizziness and vertigo due to vascular mechanisms are frequently misdiagnosed
as peripheral vestibulopathy or vestibular migraine. For diagnosis of strokes presenting

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with an acute prolonged ( 24 hours) vestibular syndrome, findings on clinical
examination, such as HINTS (negative head impulse tests, detection of direction-
changing gaze-evoked nystagmus, and presence of skew deviation), are more sensitive
than findings on neuroimaging. Since HINTS alone cannot securely detect anterior
inferior cerebellar artery strokes, additional attention should be paid to the patients
with unexplained hearing loss in addition to acute prolonged vestibulopathy. For
diagnosis of transient (< 24 hours) spontaneous vestibular syndrome due to vascular
Keywords mechanisms, the presence of associated craniocervical pain and focal neurological
► dizziness symptoms/signs is the clue. Even without these symptoms or signs, however, vascular
► vertigo imaging combined with perfusion- and diffusion-weighted MRI should be performed in
► stroke patients with multiple vascular risk factors or a high ABCD2 score (age, blood pressure,
► infarction clinical features, duration of symptom, and presence of diabetes).

Pitfalls in Diagnosing Vertigo Due to

Vascular Mechanisms
When vertigo occurs as a symptom of vertebrobasilar ischemia
or posterior circulation strokes, it is usually associated with
other neurological symptoms or signs.1 Thus, isolated dizziness
or vertigo due to vascular mechanisms may be easily misdiag-
nosed as peripheral vestibulopathy or vestibular migraine.2–4
Furthermore, the findings of vertigo due to vascular mecha-
nisms can mimic those of peripheral vestibular disorders.5,6
Diagnosis of transient vascular vertigo is more challenging
because the diagnosis should be mostly based on the symptoms
reported by the patients.
The traditional approach based on defining the category of
dizziness [vertigo (vestibular), presyncope (cardiovascular),
disequilibrium (neurological), and nonspecific (psychiatric/
metabolic)] may lead to misdiagnosis of dizziness or vertigo
due to vertebrobasilar ischemia or posterior circulation


These authors contributed equally to this work.
strokes.2,7,8 Instead, an alternative diagnostic approach seems
practical: (1) acute prolonged ( 24 hours) vestibular syndrome
that mostly requires a differentiation between inflammatory
disorders involving the inner ear and strokes, and (2) transient
(< 24 hours) spontaneous vestibular syndrome that necessi-
tates distinction between transient ischemic attacks (TIAs)
involving the vertebrobasilar territories and other episodic
vestibular syndromes including vestibular migraine, Meniere’s
disease, and dizziness/vertigo due to psychiatric disorders.
Transient dizziness or vertigo may be rarely triggered by head
motion causing compression of the vertebral artery, likewise in
rotational vertebral artery syndrome.8
Acute Prolonged Vestibular Syndromes Due
to Vascular Mechanisms
Vestibular neuritis and posterior circulation strokes are the
two leading causes of acute prolonged vestibular syn-
drome.9–11 Features of the clinical examination, such as

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Vertigo Due to Vascular Mechanisms Kim et al.

head impulse test (HIT), detection of direction-changing gaze-

evoked nystagmus, and test of skew (HINTS), are more sensi-
tive than that of neuroimaging in identifying strokes that
present with acute prolonged spontaneous vertigo.9 Among
HINTS, negative HIT is most sensitive for the diagnosis of acute
spontaneous vertigo due to strokes.9 Accuracy of bedside HIT
may be affected by the experience of examiner,12 and the
presence of spontaneous nystagmus during the acute period
may also interfere accurate interpretation of bedside HIT.
Furthermore, bedside HIT hardly detects covert saccades
generated during head movements.13 Quantitative HITs using
video-based equipment can improve the sensitivity and spec-
ificity for differentiation of strokes from vestibular neuri-
tis.14,15 Indeed, various patterns of responses have been
documented using video HITs in central vestibulopathy, which
include normal, positive, hyperactive, and cross-coupled head
impulse signs (►Table 1).15 Thus, while negative HITs mostly
Brainstem Strokes
Lateral Medullary Infarction
Isolated vertigo may occur when there is stroke affecting the
root entry zone of the eighth cranial nerve, the vestibular
nucleus, or the pontomedullary junction.30–34 Because the
root entry zone of the eighth cranial nerve has a rich network
of anastomotic vessels,35,36 the likelihood of focal infarction
in that area is extremely low in clinical practice. Focal
infarction or ischemia of the vestibular nuclei can cause
isolated vertigo and nystagmus that may mimic acute
vestibular neuritis.32–34 In this case, even the HITs and caloric
tests may be positive, especially when the medial vestibular
nucleus is affected. Vertigo in lateral medullary infarction
(LMI) is usually accompanied by other neurological symp-
toms or signs, but small infarcts restricted to the lateral
medulla can produce vertigo without other localizing symp-

indicate a central lesion in acute prolonged vestibular syn-
drome,16 positive HITs are not necessarily indicative of a
peripheral lesion. Accordingly, other central signs, such as
direction-changing nystagmus and skew deviation, should be
carefully sought in patients with acute prolonged vestibular
syndrome and positive HITs. Especially, anterior inferior cere-
bellar artery (AICA) strokes involving the inner ear or the root
entry zone of the eighth nerve in the brainstem can cause
positive HITs and can be easily misdiagnosed as peripheral
vestibular disorders when based on the findings of HINTS
alone (►Fig. 1).17 Thus, additional attention should be paid to
the patients with unexplained hearing loss in addition to acute
prolonged vestibulopathy (e.g., HINTS Plus).18
Even after the introduction of HINTS, which is known to be
more sensitive than diffusion-weighted MRIs in detecting
strokes presenting with acute prolonged vestibular syn-
drome,9,16 misdiagnosis of vertigo due to vascular mecha-
nisms remains considerable, especially in emergency care
settings.2–4,19,20 Therefore, studies should use an integrated
approach by combining the features of dizziness/vertigo,
accompanied neurological symptoms and signs, presence of
vascular risk factors, and findings of ocular motor examina-
tion.21–29 In addition to HINTS, vertical nystagmus, perverted
head-shaking nystagmus, asymmetrical oculomotor dysfunc-
tion, and severe postural instability with falling are the
common signs of central vestibular dysfunction.
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toms or signs.37
Patients with LMI frequently exhibit spontaneous, gaze-
evoked, and head-shaking nystagmus.38 In LMI, the patterns
of spontaneous nystagmus are diverse. Typically, horizontal
nystagmus beats away from the lesion side,38–40 especially
when the vestibular nerve root or the caudal lateral parts of
the vestibular nuclei are involved.41 In contrast, the nystagmus
may be ipsilesional when the superior vestibular nucleus or the
rostral portion of the medial vestibular nucleus is damaged.41
The vertical component is usually upbeat, and the torsional
nystagmus may be ipsi- or contralesional.38–40 Later, spontane-
ous nystagmus may change directions.38 Gaze-evoked nystag-
mus is observed in most patients and is mostly horizontal.42 The
horizontal component of head-shaking nystagmus is ipsile-
sional in most patients.38 Even in patients with contralesional
spontaneous nystagmus, horizontal head-shaking induces ipsi-
lesional nystagmus.38 Head-shaking nystagmus may also be
unusually strong or perverted.38 About one-third of patients
with acute or subacute LMI have positional geotropic
nystagmus.43
Patients with LMI may also have otolithic dysfunction.
Most patients with LMI show at least one component of the
ocular tilt reaction (OTR) or subjective visual vertical (SVV)
tilt, which is almost always ipsiversive when observed.44
Nevertheless, less than a third of patients have abnormal
ocular and cervical vestibular-evoked myogenic potentials

Table 1 Head impulse findings in lesions involving the central vestibular structures

Lesion Ipsilesional Contralesional

Bedside Quantitative Bedside Quantitative
Vestibular nucleus Positive Positive Normal Positive
Medial longitudinal fasciculus Normal or positive Normal or positive Normal or positive Normal or positive
Nucleus prepositus hypoglossi Normal Normal Positive Positive
Flocculus Normal or positive Normal or positive Positive Positive
Tonsil/Nodulus/Uvula Normal Normal Normal Normal
Diffuse cerebellum Normal, hyperactive Normal, hyperactive Normal, hyperactive Normal, hyperactive
or cross-coupled or cross-coupled or cross-coupled or cross-coupled

Seminars in Neurology
 Vertigo Due to Vascular Mechanisms Kim et al.

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Fig. 1 A patient with vertigo due to infarction in the right anterior inferior cerebellar artery territory (A) shows right hearing loss (B), left beating
spontaneous and direction-changing gaze-evoked nystagmus (C), decreased gains of the vestibulo-ocular reflex for right semicircular canals
during video head impulse tests (D), and right caloric canal paresis (E). H, horizontal position of the right eye; V, vertical position of the right eye;
AC, anterior semicircular canal; HC, horizontal semicircular canal; PC, posterior semicircular canal; SPV, slow phase velocity. In C, upward
deflection indicates rightward and upward eye movements.

(VEMPs).44 Abnormal ocular VEMPs are more common in
patients with the OTR than those without (38 vs. 6%),
whereas abnormal cervical VEMPs are not correlated with
the presence of OTR.44 This discrepancy in impaired proc-
essing of otolithic signals suggests different anatomical sub-
strates and/or dissimilar reciprocal modulation to process
signals from the utricle and saccule in central vestibular
structures located in the dorsolateral medulla.44
Patients with LMI frequently have an ocular deviation
toward the lesion side without limitation of eye motion
(ipsipulsion), hypermetric saccades to the ipsilesional side
and hypometric saccades away from the lesion side, and
oblique misdirection of vertical saccades.45,46 Ocular ipsi-
pulsion in LMI has been explained by damage to the climbing
fibers from the contralesional inferior olivary nucleus to the
dorsal vermis.47 Activation of the Purkinje cells following
dysfunction of the climbing fibers in the lateral medulla
would suppress the ipsilateral fastigial nucleus generating
the ipsilateral bias of the eye movements.45
LMI may disrupt the descending vestibulospinal tracts
and cause a prominent imbalance, making the patient tend
to fall to the ipsilesional side. Tilting or leaning or veering to
the lesioned side when patients are upright is common.45
Axial lateropulsion correlates with SVV tilt, that is, more
pronounced lateropulsion in patients with greater SVV tilt.42
Medial Medullary Infarction
Medial medullary infarction (MMI) involving the nucleus pre-
positus hypoglossi (NPH) shows a unique pattern of eye move-
ment abnormalities: ipsilesional spontaneous nystagmus;
horizontal gaze-evoked nystagmus, more intense on looking
toward the ipsilesional side; central patterns of head-shaking
nystagmus; reduced smooth pursuit tracking especially ipsile-
sionally; and static contralateral ocular deviation.48 The vesti-
bule-ocular reflex (VOR) gain of HITs tends to be reduced for the
contralesional horizontal canal, whereas the gains increase for
both anterior canals. These findings may be accounted for by
imbalance within the circuit connecting the inferior olive, NPH,
flocculus, and vestibular nuclei.48
Upbeat nystagmus occasionally occurs in MMI and has been
attributed to dysfunction of the perihypoglossal nuclei (NPH,
nucleus of Roller, nucleus intercalatus).49 Development of

Seminars in Neurology
Vertigo Due to Vascular Mechanisms Kim et al.
hemi-seesaw nystagmus in patients with bilateral MMI may
involve VOR pathways from both anterior semicircular
canals.50 Since the medial longitudinal fasciculus (MLF) is a
midline structure that carries signals from the vestibular to the
ocular motor nuclei, upbeat nystagmus in unilateral lesions
may result from damage to decussating fibers from both
anterior semicircular canals at the rostral medulla.50 In the
caudal medullary lesions, the nucleus of Roller and the caudal
subgroup of the PMT cells, which are involved in the processing
of vertical eye position through their projections to the
cerebellar flocculus, may be other neural substrates for upbeat
nystagmus.49,51
The OTR with an isolated unilateral MMI is contrale-
sional.50,52–54 The contralesional OTR in MMI indicates a
unilateral injury of the graviceptive brainstem pathways
from the vestibular nuclei after decussation, which occurs at
the pontomedullary junction. In MMI, damage to the climbing
fibers before decussation also causes ocular contrapulsion.52,53
Abnormal cervical VEMPs are seen on the lesioned side in about
one-half of patients when the infarction extends to the dorsal
tegmentum.
Strokes involving the MLF cause a variety of ocular motor
and vestibular abnormalities in addition to internuclear
ophthalmoplegia (INO).55–57 Among these, upbeat, seesaw
nystagmus, and contraversive OTR and SVV tilt and
impairment of the vertical VOR may occur as well as abnor-
mal cervical and ocular VEMP responses.55–57 Ten patients
with INO due to strokes showed a prominent decrease in the
VOR gain for the contralesional posterior canal during HITs.55
The MLF may serve as the pathway for high acceleration VOR
from the contralateral posterior canal. The associations and
dissociations of the vestibular dysfunction in these patients
indicate variable combinations of damage to the vestibular
fibers ascending or descending in or adjacent to the MLF even
in strokes causing isolated unilateral INO.
Complaints of vertigo are uncommon in infarcts of the
midbrain occurring in only 14% and the vertigo is transient in
those patients (< 1 day).58 Short-lived vertigo in patients
with midbrain strokes is usually associated with lesions of
the caudal tegmentum. Nonvertiginous dizziness such as
swaying or rocking occurs more in infarction affecting the
rostral midbrain near the diencephalon.58
Cerebellar Strokes
Posterior Inferior Cerebellar Artery Territory Infarction
Vertigo is a common symptom in patients with strokes of the
cerebellum, especially in the territory of medial posterior
inferior cerebellar artery (mPICA).6,11,59 PICA infarctions
may mimic vestibular neuritis.6 The isolated prolonged
spontaneous vertigo mimicking vestibular neuritis in mPICA
infarctions may occur by several mechanisms. First, the
mPICA (but sometimes AICA) may supply the nodulus of
the archicerebellum.60 The nodulus has heavy connections
with the ipsilateral vestibular nucleus and also receives
direct projections from the labyrinth.61,62 Second, dysme-
tria, the major finding of cerebellar lesions, may be minimal
or absent in small infarctions in the territory of mPICA.6,63,64
Seminars in Neurology
Third, gaze-evoked nystagmus, a common sign of central
vestibulopathy, may be absent in PICA infractions.6,63–67
Finally, hearing loss, which is generally considered a periph-
eral sign, commonly accompanies AICA strokes, but not PICA
strokes.68 The prominent cerebellar signs such as severe
truncal ataxia and gaze-evoked nystagmus help greatly in
localization.6 Perverted head-shaking (mostly downbeat)
and positional downbeat nystagmus that are also helpful
signs localizing to central vestibular dysfunction are found in
only half of patients with cerebellar infarction.69
Spontaneous ipsilesional nystagmus in PICA infarctions
may be due to disinhibition of the ipsilesional medial and
superior vestibular nuclei, caused by damage to the inhibitory
nodulovestibular fibers.65–67 Patients with cerebellar strokes
of the nodulus and uvula may exhibit positional nystagmus
(apogeotropic nystagmus when the head is turned to either
side while supine, and downbeat nystagmus in straight head-
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hanging position),70–73 transient downbeat nystagmus after
horizontal head-shaking (perverted nystagmus),69,74,75 and
diminished tilt suppression of the post-rotatory nystagmus.75
Tonsillar lesions are more likely associated with impaired
smooth pursuit rather than vestibular dysfunction.76
A patient with unilateral tonsillar infarction showed mild
ipsilesional spontaneous nystagmus only in darkness, a small
contraversive SVV tilt in the absence of OTR, and impaired
ipsilesional smooth pursuit but normal VOR responses.76
Anterior Inferior Cerebellar Artery Territory Infarction
The vestibular dysfunction in AICA territory infarction is usually
a combination of peripheral (i.e., unilateral canal paresis) and
central (i.e., asymmetrically impaired smooth pursuit, gaze-
evoked nystagmus) vestibulopathy (►Fig. 1).77,78 These find-
ings can be explained by irrigation of the peripheral and central
vestibular structures by AICA.79 The majority of patients with
AICA infarcts show unilateral vestibular hypofunction to caloric
stimulation, which suggests that the vertigo is from dysfunction
of the peripheral vestibular structures, at least in part. On the
other hand, some patients showed normal caloric responses,
indicating that vertigo in these patients may be caused by
ischemia involving the central vestibular structures.
Acute vertigo and unilateral hearing loss are the most
common presentations of AICA territory infarction.78 Isolated
labyrinthine infarction (internal auditory artery infarction)
causes acute vertigo and sudden hearing loss in isolation.80
Because the internal auditory artery is a branch of AICA,
labyrinthine infarction is usually associated with an additional
infarction in the brainstem or cerebellum of the AICA territory.68
A recent report showed that 11 out of 12 patients (92%) with
AICA infarction had labyrinthine infarction,68 which may be
clinically diagnosed with sudden sensorineural hearing loss on
pure tone audiogram (PTA) and canal paresis to standardized
bithermal caloric tests.81–83 Because the inner ear is not readily
visualized on routine MRIs, a definite diagnosis of labyrinthine
infarction is not possible unless a pathological study is per-
formed. Labyrinthine infarction should be considered in older
patients with a sudden onset of unilateral deafness and vertigo,
particularly when there is a history of stroke or known vascular
risk factors.84

AICA infarctions can cause OTR and SVV tilt.85,86 Since AICA
infarctions uniformly produce contralateral ocular torsion
when the caloric responses are normal, the peripheral vestib-
ular structures appear to play a crucial role in determining the
direction of ocular torsion in AICA territory infarctions.86
Likewise, the peripheral vestibular structures in the inner
ear seem responsible for abnormal VEMP responses in AICA
territory infarctions, as abnormal VEMPs are mostly observed
in patients with canal paresis and acute hearing loss.87
Isolated floccular infarcts occur rarely because the floccu-
lus is supplied by a branch from the AICA that also supplies
the dorsolateral pons and inner ear.88,89 Acute unilateral
flocculus infarction shows spontaneous nystagmus beating
toward the side of the infarct, impaired ipsilesional smooth
pursuit, contraversive OTR and SVV tilt, and increased VOR
gains during lower frequency stimulation and decreased
VOR gains during higher frequency stimulation.88 Another
patient report with isolated flocculus infarction also had
such findings, but ipsilesional caloric paresis, reduced VOR
gain only for the contralesional horizontal canal during HITs,
and a complete contraversive OTR.89 The caloric responses
became normal within a few weeks, but the abnormal HITs
persisted for months in that patient.89
Unilateral strokes of the middle cerebellar peduncle may
cause acute vertigo, imbalance and spontaneous horizontal-
torsional nystagmus, gaze-evoked nystagmus, OTR, abnormal
HITs, and symmetrically reduced pursuit tracking.90
Superior Cerebellar Artery Territory Infarction
The rostral cerebellum is supplied by the superior cerebellar
artery (SCA) and consequently does not have substantive
connections to vestibular structures and therefore infarcts in
the SCA territory rarely produce vertigo.79,91 The lower
incidence of vertigo in SCA infarctions may be a useful
clinical distinction from PICA or AICA infarctions in patients
with acute vertigo and limb ataxia.79,91 According to a recent
study, however, approximately half of patients with an
isolated SCA territory cerebellar infarction presented with
true vertigo with spontaneous nystagmus mainly beating to
the lesion side or gaze-evoked nystagmus.92 The ipsilesional
spontaneous nystagmus in SCA infarctions may result from
damage to the anterior cerebellar lobe that transmits the
vestibular outputs to the fastigial nucleus.92
Spontaneous Episodic Vestibular Syndrome Due to
Vascular Mechanisms
Spontaneous episodic vestibular syndrome is defined
when the spontaneous vestibular symptoms and signs
resolve within 24 hours.22 Spontaneous episodic vestibular
syndrome may be a manifestation of TIA involving the
vertebrobasilar territory. Vertebrobasilar TIAs93 typically
occur abruptly and usually lasts several minutes. A single-
center prospective study showed a high prevalence of
strokes in spontaneous episodic vestibular syndrome
(27%).22 Of the patients with vertigo due to vertebrobasilar
ischemia/infarction, 62% had a history of at least one
isolated episode of vertigo, and 19% developed vertigo as
the initial symptom.93
Vertigo Due to Vascular Mechanisms Kim et al.
In vertebrobasilar TIAs, the HINTS may not be applicable
because the symptoms and signs often subside by the time of
detailed neurological examination (73%). Thus, detecting acute
vascular vertigo lasting less than a day is more challenging.22
Associated craniocervical pain and focal neurological
symptoms/signs are useful clues for strokes in spontaneous
episodic vestibular syndrome.22 Since unilateral cerebellar
hypoperfusion is associated with stenosis or occlusion of the
ipsilateral vertebral artery in approximately 80% of patients
with the spontaneous episodic vestibular syndrome, vascular
imaging including MR or CT angiography combined with
diffusion-weighted imaging may be informative (►Fig. 2).22
Patients with vertigo and three or more risk factors showed a
5.51-fold higher risk for strokes (95% CI: 3.10–9.79; p < 0.001)
than those without risk factors.94 Patients with a higher ABCD2
score (age, blood pressure, clinical features, duration of symp-
tom, and presence of diabetes),95 a clinical prediction tool to
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assess the risk of strokes after a TIA, showed a higher risk of
strokes compared with those with a lower ABCD2 score.96
Triggered Episodic Vestibular Syndrome Due to
Vascular Mechanisms
Vertigo may occur during head rotation or tilt due to com-
pression of the vertebral artery.97–101 In this instance,
patients usually have a hypoplastic or stenotic vertebral
artery on one side and the contralateral dominant vertebral
artery is compressed or occluded mostly at the atlantoaxial
junction when the head is rotated away from the side of
intact vertebral artery (►Fig. 3).97 Oculographic analyses of
nystagmus triggered during the episodes, revealing various
patterns.98,99 Initially, nystagmus is downbeat sometimes
with some horizontal or torsional nystagmus in either
direction. Some patients show reversal of the nystagmus
during the episode, and absent or markedly diminished
responses on immediate retrial of head rotation (habitua-
tion).99 The structures affected by ischemia that may cause
the vertigo and nystagmus may be either the inner ear98,100
or the inferior cerebellum.101,102 Surgical decompression or
stenting is most optimal in younger patients with frequent
attacks and severe vertebral artery compression during the
attacks.99
Conclusions
Isolated dizziness or vertigo due to vascular mechanisms is
not common, but when it occurs it can easily lead to
misdiagnosis. Vestibular neuritis and posterior circulation
strokes are the two leading causes of acute prolonged
vestibular syndrome. Although HINTS is more sensitive
than diffusion-weighted MRIs in detecting strokes present-
ing with acute prolonged vertigo, even HINTS is imperfect
because a positive HIT response may infrequently be seen
with central lesions too, especially with AICA strokes. What
remains is that HINTS is a useful tool but needs to be
combined with a careful history and physical examination
of limb coordination, speech articulation, and features of
nystagmus. Imaging is also needed at times to distinguish
vertigo due to infarction from vertigo due to inner ear
Seminars in Neurology
Vertigo Due to Vascular Mechanisms Kim et al.

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Fig. 2 A patient with isolated recurrent vertigo shows normal diffusion-weighted MRI (A), but multifocal stenosis in the left distal vertebral
artery (B). Perfusion is decreased in the medial portion of the inferior cerebellum (C). Video-oculography documented right beating
spontaneous nystagmus mostly without fixation in darkness (D).

Fig. 3 In a patient with vertigo during leftward head turning, magnetic resonance (A) and cerebral (B) angiography disclose dominant left vertebral artery
(VA) and hypoplastic right VA that terminates in the posterior inferior cerebellar artery without connection to the basilar artery. In the leftward head-turned
position, cerebral angiography documents a complete occlusion of right VA at the level of C1–C2 junction (C, arrow). Video-oculography (D) recorded a
gradual build-up of right beating horizontal–torsional and downbeat nystagmus several seconds after leftward head turning (a). The nystagmus reverses its
direction on resuming neutral head position (b). EH, horizontal position of the left eye; EV, vertical position of the left eye; ET, torsional position of the left eye.
Upward deflection in each recording indicates rightward, upward, and clockwise (upper poles of the eyes toward right ear) eye motion.

Seminars in Neurology

dysfunction. Vertebrobasilar TIAs are even more challenging
as key signs are usually gone by the time of evaluation.
Finally, triggered vascular causes of vertigo, while rare,
should prompt evaluation of the vertebral arteries for com-
pression with neck turning.
Authors’ Contributions
H.A.K. and H.L. wrote the manuscript.
J-S.K. designed and conceptualized the study and revised
the manuscript.
Sources of Funding
This study was supported by Basic Science Research
Program through the National Research Foundation of
Korea (NRF) funded by the Ministry of Education, Science
and Technology (no. NRF-2016R1D1A1B04935568).
Conflict of Interest
H.A.K. and H.L. report no disclosure. 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.
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