Incidence, characteristics, and neuroanatomical substrates of vestibular symptoms in supratentorial stroke

Abstract

The incidence and characteristics of acute vestibular symptoms, responsible structures, and lateralization of the causative lesions in supratentorial stroke remain unknown. This study aimed to determine the incidence, clinical features, and anatomical correlation of acute vestibular symptoms in supratentorial stroke. We performed a prospective, multicenter, observational study that had recruited patients with supratentorial stroke from the neurology clinics of referral-based four university hospitals in Korea. All patients received a constructed neuro-otological evaluations, and neuroimaging. We analyzed the incidence of acute vestibular symptoms, abnormal ocular motor and vestibular function tests, and stroke lesions. Of 1301 patients with supratentorial stroke, 48 (3.7%) presented with acute vestibular symptoms, and 13 of them (1%) had the vestibular symptoms in isolation. In patients with acute vestibular symptoms, abnormal findings included spontaneous nystagmus (5%), impaired horizontal smooth pursuit (41%), and abnormal tilt of the subjective visual vertical (SVV) (20%). Video head impulse and caloric tests were normal in all the patients. There was no clear correlation between acute vestibular symptoms and involvement of specific vestibular cortex. In patients with unilateral stroke, there was also no lateralization of the causative lesions of acute vestibular symptoms (left vs. right; 52 vs. 48%), even in patients with vertigo (left vs. right; 58 vs. 42%). This study demonstrates that the incidence of acute vestibular symptoms in supratentorial stroke is 3.7%, with being isolated in 1%. The widespread lesions responsible for acute vestibular symptoms implicate diffuse multisensory cortical–subcortical networks in the cerebral hemispheres without a lateralization.

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Journal of Neurology
https://doi.org/10.1007/s00415-023-11566-9
ORIGINAL COMMUNICATION
Incidence, characteristics, andneuroanatomical substrates
ofvestibular symptoms insupratentorial stroke
Ji‑YunPark1· Jae‑HwanChoi2· Jee‑HyunKwon1· YoungCheolWeon3· Suk‑MinLee4· HyoJungKim5·
SeoYoungChoi4· Eun HyeOh2· HyunAhKim6· HyungLee6· Ji‑SooKim7· Kwang‑DongChoi4
Received: 25 October 2022 / Revised: 6 January 2023 / Accepted: 9 January 2023
© The Author(s), under exclusive licence to Springer-Verlag GmbH Germany 2023
Abstract
The incidence and characteristics of acute vestibular symptoms, responsible structures, and lateralization of the causa-
tive lesions in supratentorial stroke remain unknown. This study aimed to determine the incidence, clinical features, and
anatomical correlation of acute vestibular symptoms in supratentorial stroke. We performed a prospective, multicenter,
observational study that had recruited patients with supratentorial stroke from the neurology clinics of referral-based four
university hospitals in Korea. All patients received a constructed neuro-otological evaluations, and neuroimaging. We ana-
lyzed the incidence of acute vestibular symptoms, abnormal ocular motor and vestibular function tests, and stroke lesions.
Of 1301 patients with supratentorial stroke, 48 (3.7%) presented with acute vestibular symptoms, and 13 of them (1%) had
the vestibular symptoms in isolation. In patients with acute vestibular symptoms, abnormal findings included spontaneous
nystagmus (5%), impaired horizontal smooth pursuit (41%), and abnormal tilt of the subjective visual vertical (SVV) (20%).
Video head impulse and caloric tests were normal in all the patients. There was no clear correlation between acute vestibular
symptoms and involvement of specific vestibular cortex. In patients with unilateral stroke, there was also no lateralization
of the causative lesions of acute vestibular symptoms (left vs. right; 52 vs. 48%), even in patients with vertigo (left vs. right;
58 vs. 42%). This study demonstrates that the incidence of acute vestibular symptoms in supratentorial stroke is 3.7%, with
being isolated in 1%. The widespread lesions responsible for acute vestibular symptoms implicate diffuse multisensory
cortical–subcortical networks in the cerebral hemispheres without a lateralization.
Keywords Supratentorial stroke· Acute vestibular syndrome· Vestibular hemispheric dominance· Vestibular cortex
Introduction
While acute unilateral lesion involving the labyrinth, the ves-
tibular nerve, the vestibular nuclei, or the brainstem circuitry
causes typical vestibular syndromes due to a vestibular tone
Ji-Yun Park, Jae-Hwan Choi, Hyun Ah Kim and Kwang-Dong Choi
contributed equally to this work.
* Hyun Ah Kim
kha0206@dsmc.or.kr
* Kwang-Dong Choi
kdchoi@pusan.ac.kr
1 Department ofNeurology, University ofUlsan College
ofMedicine, Ulsan University Hospital, Ulsan, Korea
2 Department ofNeurology, Pusan National University
School ofMedicine, Research Institute forConvergence
ofBiomedical Science andTechnology, Pusan National
University Yangsan Hospital, Yangsan, Korea
3 Department ofRadiology, University ofUlsan College
ofMedicine, Ulsan University Hospital, Ulsan, Korea
4 Department ofNeurology, Pusan National University
Hospital, Pusan National University School ofMedicine
andBiomedical Research Institute, College ofMedicine, 179,
Gudeok-Ro, Seo-Gu, Busan602-739, Korea
5 Research Administration Team, Seoul National University
Bundang Hospital, Seongnam, Korea
6 Department ofNeurology, Keimyung University School
ofMedicine, 1095, Dalgubeol-Daero, Dalseo-Gu,
Daegu42601, RepublicofKorea
7 Dizziness Center, Clinical Neuroscience Center,
andDepartment ofNeurology, Seoul National University
Bundang Hospital, Seongnam, SouthKorea

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imbalance [1–3], unilateral cerebral hemispheric lesions
infrequently give rise to acute vestibular symptoms [4–12].
Studies using functional MRIs, cytoarchitectonic mapping,
and cortical stimulation have shown that the vestibular cor-
tex comprises a network of several distinct and separate tem-
poroparietal areas with its core region, the parietoinsular
vestibular cortex (PIVC) [13–18]. The PIVC is located in
the posterior insula and retroinsular region, and includes the
parietal operculum. Structural and functional studies also
disclosed the vestibular dominance in the right hemisphere
in right-handers and in the left hemisphere in left-handers
[14, 19–21]. Only a few studies have previously explored
acute vestibular symptoms in rather a small number of
patients with hemispheric lesions, [4–6, 8] but could not pro-
vide consistent results on the incidence of vestibular symp-
toms, responsible structures, and hemispheric dominance.
Therefore, we conducted a large prospective study to
determine the incidence and clinical characteristics of
acute vestibular symptoms in supratentorial stroke. We also
attempted to define the neuroanatomical substrates respon-
sible for the vestibular symptoms and lateralization of the
causative lesions.
Methods
Subjects
We performed a multicenter, prospective, observational
study that had consecutively recruited patients with
supratentorial stroke presenting acute vestibular symptoms
(7days from the symptom onset) from the neurology clin-
ics of four university hospitals in Korea between August
2018 and December 2019. The stroke was documented by
computed tomography or magnetic resonance imaging of the
brain during the acute phase. The inclusion criteria were as
follows: (1) acute vestibular symptoms including dizziness,
vertigo, and unsteadiness based on the classification of ves-
tibular symptoms defined by The Committee of the Barany
Society in 2009 [22], and (2) stroke involving the supraten-
torial brain structures only. Patients were excluded if they
had inability to explain vestibular symptoms due to impaired
cognitive function or dysphasia, transfer to another hospital
during evaluation, declination or inability to undergo MRIs,
a history of neurologic diseases that could influence cogni-
tive function, and declination to participate in the study.
Neuro‑otological evaluation
Each patient had a general neurological and a specialized
neuro-otological examination including HINTS plus (Head
Impulse, Nystagmus, Test of Skew, and acute hearing loss
detected by finger rubbing) by the authors. Spontaneous,
gaze-evoked, head shaking, and positional nystagmus,
saccades, and smooth pursuit were measured using three-
dimensional video-oculography. We also performed vestib-
ular function tests including bithermal caloric tests, video
head impulse tests (HIT), and subjective visual vertical
(SVV) tests. Detailed methods and normative data of each
test have been described elsewhere [23].
Bithermal caloric tests were performed by irrigating the
ears for 25s alternatively with 150mL of cold (30°C) and
hot (44°C) water. Nystagmus was recorded binocularly
with video-oculography. Vestibular function was calculated
using Jongkees’ formula, and caloric paresis was defined
by a response difference of 25% or more between the ears.
The VOR during head impulse testing was quantita-
tively assessed using a video-based equipment (SLMED,
Seoul, Korea). The patient was instructed to look at a distant
(1.5m) target while seated. After calibration of eye position,
the examiner applied a series of horizontal head impulses
in each direction in a random order. Vertical head impulses
were also applied along the left anterior–right posterior
canal plane and the right anterior–left posterior canal plane.
At least 20 valid impulses with head velocities between 100
and 250°/s were required for each canal. The VOR gain was
calculated as the ratio of the area under the entire eye-veloc-
ity response relative to the area under the entire head-veloc-
ity response stimulus. Corrective catch-up saccades (CS)
were defined as the saccades in the opposite direction of the
head rotation that reached the peak acceleration before (cov-
ert) or after (overt) the head stopped moving. We defined an
abnormal HIT response when the mean VOR gains exceeded
the mean ± 2SD obtained from 31 normal controls [normal
gains for the horizontal canals (HCs) = 0.85–1.02, for the
anterior canals (ACs) = 0.91–1.06, for the posterior canals
(PCs) = 0.88–1.05], or when there were corrective catch-up
saccades.
The SVV tilt was measured by seating the patient upright
in a dark room and asking to align a rod (80cm long and
0.3cm wide). The rod was presented randomly at various
angles from the vertical at a distance of 130cm from the
patient’s eyes. The SVV tilt was determined by calculating
the average of five adjustments. The SVV tilt was considered
abnormal when it exceeded normal values of healthy con-
trols (− 3.0° to 3.0° in both eyes; a negative value indicates
a counterclockwise rotation).
Neuroimaging andlesion analysis
We used stroke protocol brain CT and MRIs, including
axial T2, fluid-attenuated inversion recovery image, DWI,
and angiography, performed on a 3.0-T MRI unit (Verio;
Skyra, Erlangen, Germany). The DWI parameters were
as follows: repetition time = 5160 ms; echo time = 69
or 117ms; matrix = 192 × 192; field of view = 22 cm;

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section thickness = 4mm, and intersection gap = 0.8mm.
The reference of standard for an ischemic stroke diagnosis
was a confirmation of acute stroke with DWI.
We performed lesion analysis in 45 patients after
excluding 1 with hemorrhagic stroke and 2 with bilateral
strokes. Diffusion- and T1-weighted images were spa-
tially normalized with SPM8 (www. fil. ion. ucl. ac. uk/ spm/
softw are/ spm8). Using the MRIcron (www. mccau sland
center. sc. edu/ mricro/ mricr on), overlap images were then
obtained for each group using lesion density plots [24].
We flipped the regions of interest in patients with left-
sided lesions and displayed them on the right side.
Results
Clinical features
During the study period, 1,301 patients with acute supraten-
torial stroke were initially recruited after excluding 50 who
had decreased mentality or dysphasia (n = 37), transfer
to another hospital during admission (n = 5), a history of
neurologic diseases that could influence cognitive function
(n = 4), and declination to participate in the study (n = 4).
Of these 1301 patients, 48 (3.7%) presented with acute ves-
tibular symptoms, and isolated vestibular symptoms with-
out focal neurologic signs were present in 13 (1%). In this
study, 48 patients were selected for analysis (Fig.1, mean
age, 63 ± 13years; ranging from 38 to 87years; 58% male).
Fig. 1 Study flow diagram

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Forty-six patients were right-handed, and the remaining 2
were left-handed, as assessed by the Edinburgh Handedness
Inventory [25]. The average score on NIHSS was 2.4 rang-
ing from 0 to 8.
Table1 summarizes the demographic and clinical char-
acteristics, and the results of neuro-otological evaluations
of 48 patients with acute vestibular symptoms. Patients
developed mainly acute dizziness (42%), vertigo (33%),
or unsteadiness (25%). The vestibular symptoms lasted
for seconds to minutes (19%), hours (14%), or days (67%).
Accompanying neurological signs were hemiparesis or limb
ataxia (58%), visual field defect (8%), paresthesia (2%), and
dysarthria (2%). Only three patients (6%) experienced auto-
nomic symptoms of nausea or vomiting. None had pusher
syndrome.
Of the 48 patients, 44 underwent ocular motor and ves-
tibular function tests which was obtained within 7days from
the symptom onset in 91%, and within 2weeks in all. vHITs
and caloric tests were normal in all the patients, while ocular
motor and/or other vestibular function tests were abnormal
in 19 (43%). Abnormal ocular motor and vestibular function
tests included impaired horizontal smooth pursuit in 18 (2
ipsilesional, 1 contralesional, and 15 bilateral), weak (< 3°)
spontaneous horizontal nystagmus only without fixation in
2 (1 ipsilesional and 1 contralesional), subtle apogeotropic
positional nystagmus in 1, and abnormal SVV tilt in 9 (8
contraversive and 1 ipsiversive). Nine patients with abnor-
mal SVV tilt presented with mainly dizziness (n = 5), vertigo
(n = 3), and unsteadiness (n = 1).
Neuroimaging results
Acute supratentorial strokes included 47 ischemic and 1
hemorrhagic strokes (46 unilateral and 2 bilateral strokes).
Stroke lesions affected various cortical and subcortical areas
associated with vestibular information processing (Fig.2).
There was no clear correlation between acute vestibular
symptoms and involvement of the vestibular cortex, even in
16 patients with vertigo (Fig.3). Involvement of core ves-
tibular cortical regions distributed within the insular or pari-
etal opercular cortices was present in only 10% of patients,
whereas approximately half had lesions affecting the sub-
cortical white matter or structures (Fig.2). In patients with
unilateral stroke, there was also no hemispheric dominance
of acute vestibular symptoms (left vs. right; 52 vs. 48%),
even in patients with vertigo (left vs. right; 58 vs. 42%).
Characteristics ofpatients withisolated vestibular
symptoms
Thirteen patients with isolated vestibular symptoms devel-
oped mainly vertigo (54%), dizziness (23%), or unsteadi-
ness (23%), which lasted for seconds to minutes (31%),
hours (8%), or days (62%) (Table2). In all the 13 patients,
vHITs and caloric tests were normal. Ocular motor and/or
other vestibular function tests were abnormal in six patients
(38%) including impaired bilateral horizontal smooth
pursuit (n = 5), weak ipsilesional spontaneous nystagmus
(n = 1), and abnormal contraversive SVV tilt (n = 1). Since
most of the patients (92%) did not show spontaneous nys-
tagmus, HINTS plus examination could be not applicable.
One patient with weak spontaneous nystagmus showed nor-
mal head impulse tests without skew deviation, suggesting
stroke.
Except for 1 patient with hemorrhagic stroke, 12 had
supratentorial ischemic stroke (11 unilateral and 2 bilat-
eral) (Fig.4). A composite of lesion distribution did not
reveal any correlation between acute vestibular symptoms
and affected structures, even in patients with vertigo (Fig.3).
There was no hemispheric dominance of acute vestibular
symptoms (left, 55 vs. right, 45%) or vertigo (left, 60 vs.
right, 40%) in patients with unilateral stroke.
Table 1 Clinical characteristics and abnormal vestibular findings
in 48 patients with supratentorial stroke presenting acute vestibular
symptoms
VOG video-oculography; vHITs video head impulse tests; SVV sub-
jective visual vertical
a Of the 48 patients, 44 received neuro-otological evaluations
Patients with acute
vestibular symptoms
(n = 48), %
Acute vestibular symptoms
Vertigo 33
Dizziness 42
Unsteadiness 25
Duration
Seconds to minutes 19
Hours 14
Days 67
Accompanying neurological signs
Hemiparesis or limb ataxia 58
Visual field defect 8
Paresthesia 2
Dysarthria 2
Neuro-otological evaluationsa
VOG
Spontaneous nystagmus 5
Impaired smooth pursuit 41
Positional nystagmus 2
Bithermal caloric tests, abnormal 0
vHITs, abnormal 0
Pathologic SVV tilt 20

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Discussion
The present study demonstrated that 3.7% of supratentorial
stroke presented with acute vestibular symptoms, and 1.2%
developed vertigo. Our results are somewhat different from
those of previous studies which reported the incidence of
vestibular symptoms ranging from 1.2 to 40%, and vertigo
from 0 to 9% in hemispheric stroke [4–6, 8]. These vari-
able incidences would be attributed to the discrepancy in the
study design, sample size, and contents of vestibular symp-
toms. To reduce bias affecting on the incidence of acute ves-
tibular symptoms, we conducted a prospective multicenter
study recruiting a large number of consecutive patients.
We incorporated analysis of three representative vestibu-
lar symptoms of vertigo, dizziness, and unsteadiness, while
most of earlier studies included a great variety of vestibular
symptoms which might increase the incidence.
Unilateral injuries to the right cerebral hemisphere lead to
hemi-spatial neglect [26–28]. The analysis of imaging data
in patients with neglect revealed the overlap of the corti-
cal areas involved with the vestibular cortical areas, imply-
ing that the mechanism of visuo-spatial neglect is probably
elicited by a vestibular tonus imbalance [13, 26–28]. Stud-
ies using functional MRIs, cytoarchitectonic mapping, and
cortical stimulation showed an area located deep within the
Sylvian fissure at the junction of the posterior parietal oper-
culum with the insular/retroinsular region (OP 2) as the core
human vestibular cortex [14–18]. Investigation of the human
vestibular cortex as identified by caloric stimulation reported
a strong right hemispheric dominance of the vestibular
multisensory cortex areas, regardless of the stimulated side
[14, 19–21]. Similarly, structural lesions studies revealed
that vestibular infarctions along the vestibular pathways
cause compensatory mechanisms within the cortical–sub-
cortical network (i.e., a reorganization) with volumetric
increases in vestibular parietal opercular multisensory and
(retro-) insular areas with right-sided preference [29, 30].
In these studies, distinct vestibular signs could be related
to specialized areas which means that there is evidence for
a symptom- and sign-related distribution of affected areas
within the vestibular and ocular motor networks. Small
clinical studies also exhibited that cortical strokes affect-
ing the right (dominant) hemisphere (in right-handed indi-
viduals) are more likely to cause vestibular symptoms than
left hemispheric strokes [4–6]. However, our data are not in
agreement with the results of previous explorations. We did
not find any significant correlation between acute vestibu-
lar symptoms and involvement of specific vestibular cortex,
even in patients with vertigo. Involvement of core vestibu-
lar cortical regions distributed within the insular or pari-
etal opercular cortices was present in only 10% of patients,
whereas approximately half had lesions affecting subcortical
white matter or structures including basal ganglia, thalamus,
and internal capsule. Moreover, there was no lateralization
of the causative lesions for acute vestibular symptoms or
vertigo in supratentorial stroke. Our results suggest that any
lesion of widespread cortical–subcortical vestibular net-
works including the PIVC and other multisensory (visual,
vestibular, and somatosensory) cortex areas responsible for
spatial orientation can give rise to acute vestibular symptoms
Fig. 2 Distribution of stroke
lesions. BG basal ganglia; PL of
IC = posterior limb of internal
capsule

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without a lateralization. A recent report also showed that
there is no single vestibular cortex for acute vestibular symp-
toms [6]. Indeed, none of the patients with unilateral insular
stroke did not reveal vestibular symptoms, a deficit in the
perception of verticality, or any further vestibular otolith
deficits [31]. The vestibular sense is special in that bilateral
activation has to be integrated into a global percept of body
orientation and self-motion by the interaction with other
sensory (visual, somatosensory, etc.) systems [27]. Low
incidence of vertigo in the PIVC lesion would be explained
by structural and functional disconnection. In most of the
published ten cases with rotational vertigo, disconnections
of interhemispheric connections via the corpus callosum and
interhemispheric connections via the arcuate fascicle were
present, but spared in lesions of the PIVC without vertigo
[32].
Most of our patients presenting vestibular symptoms
had a high incidence of accompanying neurological signs
Fig. 3 Lesion overlay map shows the stroke lesions in 45 patients
with unilateral supratentorial infarction presenting acute vestibular
symptoms (A) including 14 with acute vertigo (B), 10 with isolated
vestibular symptoms (C), and 5 with isolated vertigo (D) on a 2mm
brain atlas. The color scale represents the number of subjects that
had a lesion in the represented area on the map. All four groups have
lesions widespread across the cortex or subcortex with no clear corre-
lation between acute vestibular symptoms and involvement of specific
vestibular cortex

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including hemiparesis and visual field defect, highlighting
the need for a detailed neurologic evaluation in any patient
with vertigo, dizziness and unsteadiness. Only 6% of the
patients experienced autonomic symptoms of nausea or vom-
iting, which might be a distinction with infratentorial stroke.
Remarkably, our study disclosed that 1% of supratentorial
stroke can present isolated vestibular syndrome without
any other neurological signs. A recent study also reported
8 patients (1.2%) with chief complaints of acute isolated
vestibular symptoms among 668 with hemispheric infarction
[5]. Although the incidence is low, the diagnosis of stroke in
this group remains a challenge when only based on the find-
ings of bedside examination. Since most of patients in our
and a previous study did not show spontaneous nystagmus,
HINTS plus examination could not be applicable. Alterna-
tively, we found abnormal horizontal smooth pursuit eye
movement or subjective visual vertical tilt in approximately
40% of our patients with isolated vestibular symptoms, sug-
gesting that detailed ocular motor and vestibular evaluations
would be informative for the suspicion of stroke.
Our study has potential limitations. Since this study
was based on the data from tertiary stroke referral centers,
the results from this study may not be applied to the com-
munity hospitals or the ambulatory care units. A selec-
tion bias should be considered in interpreting the results.
Because this study did not include all patients presenting
with isolated vestibular symptoms, patients with supraten-
torial stroke who refused to image might have been missed
in our study, and this may have decreased the incidence
of isolated vestibular symptoms. Furthermore, we did not
repeat MRIs in patients with isolated vestibular symptoms
who received MRIs within 24h from the symptom onset.
Therefore, some patients may have escaped the diagno-
sis of stroke. Actually, in patients presenting with minor
ischemic stroke, MRI including DWI may initially miss
stroke in up to 21% [33, 34]. The abnormalities of smooth
pursuit eye movement are very important in evaluation of
patients with supratentorial stroke presenting acute dizzi-
ness. However, from the practical viewpoint, this is dif-
ficult, as older age group often have vision impairment
(refractive issues, cataracts, macular degeneration, and
glaucoma) that could contribute to abnormal pursuit.
Table 2 Characteristics of 13 patients with isolated vestibular symptoms
L left; R right; SVV subjective visual vertical; CR corona radiate; WM white matter; STG superior temporal gyrus; IPL inferior parietal lobule;
IFG inferior frontal gyrus; IC internal capsule; B bilateral
Sex/age Vestibular symptoms Duration Abnormal neuro-otological
findings
Lesion side Lesion site
1 M/39 Vertigo Days (–) L Putamen and CR
2 M/78 Unsteadiness Days Impaired horizontal
smooth pursuit, bilateral
L Putamen and CR
3 M/68 Dizziness Days Impaired horizontal
smooth pursuit, bilateral
L Subcortical WM of STG
4 F/83 Dizziness Days Contralesional SVV tilt R IPL
5 F/50 Vertigo Seconds–minutes Impaired horizontal
smooth pursuit, bilateral
L IFG and subcortical WM
6 M/41 Dizziness Seconds–minutes (–) R Precentral gyrus
7 F/59 Vertigo Days (–) R Medial thalamus
8 F/55 Vertigo Hours (–) R Posterior limb of IC
9 M/68 Unsteadiness Days Impaired horizontal
smooth pursuit, bilateral
R Ri
10 M/56 Unsteadiness Days Ipsilesional SN,
impaired horizontal
smooth pursuit, bilateral
L Ri
11 F/50 Vertigo Seconds–minutes (–) L IFG
12 M/54 Vertigo Seconds–minutes (–) B R postcentral gyrus and L occipital lobe
13 F/78 Vertigo Days (–) B R posterior limb of IC and L IFG

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Author contributions Drs. J-YP and J-HC wrote the manuscript and
analyzed and interpreted the data. Drs. J-HK, Y-CW, S-ML, H-JK,
S-YC, EHO, HL, and J-SK contributed to interpretation of the data
and revision of the manuscript. Drs. K-DC and H-AK conducted the
design and conceptualization of the study, interpretation of the data,
and drafting and revising the manuscript.
Funding There is no funding source.
Data availability The data that support the findings of this study are
available on request from the corresponding author. The dataare not
publicly available due to privacy or ethical restrictions.
Declarations
Conflicts of interest Drs. Ji-Yun Park, Jae-Hwan Choi, Jee-Hyun
Kwon, Young Cheol Weon, Suk-Min Lee, Hyo Jung Kim, Seo Young
Choi, Eun Hye Oh, Hyun Ah Kim, and Kwang-Dong Choi have no
disclosures. Dr. Hyung Lee serves on the editorial boards of the Re-
search in Vestibular Science, Frontiers in Neuro-otology, and Current
Medical Imaging Review. Dr. J-S Kim 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, and Journal of Vestibular Research, Journal of
Neurology and Medicine.
Fig. 4 MRI lesions of 11 patients with unilateral stroke presenting isolated vestibular symptoms

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Ethical approval This study followed the tenets of the Declaration of
Helsinki and was approved by the Institutional Review Board of par-
ticipating hospitals (approval no. 2110-006-107). Informed contents
were obtained after the nature and possible consequence of this study
had been explained to participants.
References
1. Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker
DE (2009) HINTS to diagnose stroke in the acute vestibular
syndrome: three-step bedside oculomotor examination more
sensitive than early MRI diffusion-weighted imaging. Stroke
40:3504–3510. https:// doi. org/ 10. 1161/ STROK EAHA. 109.
551234
2. Newman-Toker DE (2016) Missed stroke in acute vertigo and
dizziness: it is time for action, not debate. Ann Neurol 79:27–
31. https:// doi. org/ 10. 1002/ ana. 24532
3. Fetter M (2016) Acute unilateral loss of vestibular function.
Handb Clin Neurol 137:219–229. https:// doi. org/ 10. 1016/ B978-
0- 444- 63437-5. 00015-7
4. Dieterich M, Brandt T (2015) Why acute unilateral vestibu-
lar cortex lesions mostly manifest without vertigo. Neurology
84:1680–1684. https:// doi. org/ 10. 1212/ WNL. 00000 00000
001501
5. Eguchi S, Hirose G, Miaki M (2019) Vestibular symptoms in
acute hemispheric strokes. J Neurol 266:1852–1858. https:// doi.
org/ 10. 1007/ s00415- 019- 09342-9
6. Man Chan Y, Wong Y, Khalid N, Wastling S, Flores-Martin A,
Frank LA, Koohi N, Arshad Q, Davagnanam I, Kaski D (2021)
Prevalence of acute dizziness and vertigo in cortical stroke. Eur
J Neurol 28:3177–3181. https:// doi. org/ 10. 1111/ ene. 14964
7. von Brevern M, Süßmilch S, Zeise D (2014) Acute vertigo due
to hemispheric stroke: a case report and comprehensive review
of the literature. J Neurol Sci 339:153–156. https:// doi. org/ 10.
1016/j. jns. 2014. 02. 005
8. Anagnostou E, Spengos K, Vassilopoulou S, Paraskevas GP,
Zis V, Vassilopoulos D (2010) Incidence of rotational vertigo in
supratentorial stroke: a prospective analysis of 112 consecutive
patients. J Neurol Sci 290:33–36. https:// doi. org/ 10. 1016/j. jns.
2009. 11. 015
9. Park KM, Shin KJ, Ha SY, Park J, Kim SE (2014) Isolated
rotational vertigo due to internal capsular infarction. J Neu-
roophthalmol 34:61–63. https:// doi. org/ 10. 1097/ WNO. 00000
00000 000088
10. Naganuma M, Inatomi Y, Yonehara T, Fujioka S, Hashimoto Y,
Hirano T, Uchino M (2006) Rotational vertigo associated with
parietal cortical infarction. J Neurol Sci 246:159–161. https://
doi. org/ 10. 1016/j. jns. 2006. 02. 012
11. Nakajima M, Inatomi Y, Yonehara T, Hirano T, Uchino M
(2012) Rotational vertigo associated with putaminal infarction.
J Stroke Cerebrovasc Dis 21:912.e919–910. https:// doi. org/ 10.
1016/j. jstro kecer ebrov asdis. 2011. 12. 008
12. Kim JM, Mun SK, Yoo IH, Lopez C, Kim JS (2018) Vertigo
and impaired pursuit eye movements in a small medial superior
temporal infarction. J Neurol 265:2740–2742. https:// doi. org/
10. 1007/ s00415- 018- 9023-4
13. Mazzola L, Lopez C, Faillenot I, Chouchou F, Mauguière F,
Isnard J (2014) Vestibular responses to direct stimulation of the
human insular cortex. Ann Neurol 76:609–619. https:// doi. org/
10. 1002/ ana. 24252
14. Dieterich M, Brandt T (2018) The parietal lobe and the vestibu-
lar system. Handb Clin Neurol 151:119–140. https:// doi. org/ 10.
1016/ B978-0- 444- 63622-5. 00006-1
15. Frank SM, Greenlee MW (2018) The parieto-insular vestibu-
lar cortex in humans: more than a single area? J Neurophysiol
120:1438–1450. https:// doi. org/ 10. 1152/ jn. 00907. 2017
16. Brandt T, Dieterich M (1999) The vestibular cortex. Its loca-
tions, functions, and disorders. Ann N Y Acad Sci 871:293–312.
https:// doi. org/ 10. 1111/j. 1749- 6632. 1999. tb091 93.x
17. Lopez C, Blanke O, Mast FW (2012) The human vestibular
cortex revealed by coordinate-based activation likelihood esti-
mation meta-analysis. Neuroscience 212:159–179. https:// doi.
org/ 10. 1016/j. neuro scien ce. 2012. 03. 028
18. Eickhoff SB, Weiss PH, Amunts K, Fink GR, Zilles K (2006)
Identifying human parieto-insular vestibular cortex using fMRI
and cytoarchitectonic mapping. Hum Brain Mapp 27:611–621.
https:// doi. org/ 10. 1002/ hbm. 20205
19. Bense S, Bartenstein P, Lochmann M, Schlindwein P, Brandt T,
Dieterich M (2004) Metabolic changes in vestibular and visual
cortices in acute vestibular neuritis. Ann Neurol 56:624–630.
https:// doi. org/ 10. 1002/ ana. 20244
20. Dieterich M, Kirsch V, Brandt T (2017) Right-sided domi-
nance of the bilateral vestibular system in the upper brainstem
and thalamus. J Neurol 264:55–62. https:// doi. org/ 10. 1007/
s00415- 017- 8453-8
21. Fasold O, von Brevern M, Kuhberg M, Ploner CJ, Villringer A,
Lempert T, Wenzel R (2002) Human vestibular cortex as identi-
fied with caloric stimulation in functional magnetic resonance
imaging. Neuroimage 17:1384–1393. https:// doi. org/ 10. 1006/
nimg. 2002. 1241
22. Bisdorff A, Von Brevern M, Lempert T, Newman-Toker DE
(2009) Classification of vestibular symptoms: towards an
international classification of vestibular disorders. J Vestib Res
19:1–13. https:// doi. org/ 10. 3233/ ves- 2009- 0343
23. Choi JH, Oh EH, Choi SY, Kim HJ, Lee SK, Choi JY, Kim
JS, Choi KD (2022) Vestibular impairments in episodic ataxia
type 2. J Neurol 269:2687–2695. https:// doi. org/ 10. 1007/
s00415- 021- 10856-4
24. Rorden C, Fridriksson J, Karnath HO (2009) An evaluation of
traditional and novel tools for lesion behavior mapping. Neu-
roimage 44:1355–1362. https:// doi. org/ 10. 1016/j. neuro image.
2008. 09. 031
25. Oldfield RC (1971) The assessment and analysis of handedness:
the Edinburgh inventory. Neuropsychologia 9:97–113. https://
doi. org/ 10. 1016/ 0028- 3932(71) 90067-4
26. Brandt T, Strupp M, Dieterich M (2014) Towards a concept of
disorders of “higher vestibular function.” Front Integr Neurosci
8:47. https:// doi. org/ 10. 3389/ fnint. 2014. 00047
27. Kirsch V, Keeser D, Hergenroeder T, Erat O, Ertl-Wagner B,
Brandt T, Dieterich M (2016) Structural and functional connec-
tivity mapping of the vestibular circuitry from human brainstem
to cortex. Brain Struct Funct 221:1291–1308. https:// doi. org/ 10.
1007/ s00429- 014- 0971-x
28. Karnath HO, Dieterich M (2006) Spatial neglect—a vestibular
disorder? Brain 129:293–305. https:// doi. org/ 10. 1093/ brain/
awh698
29. Conrad J, Habs M, Ruehl RM, Boegle R, Ertl M, Kirsch V,
Eren OE, Becker-Bense S, Stephan T, Wollenweber FA, Duer-
ing M, Dieterich M, Zu Eulenburg P (2022) Reorganization of
sensory networks after subcortical vestibular infarcts: a longi-
tudinal symptom-related voxel-based morphometry study. Eur
J Neurol 29:1514–1523. https:// doi. org/ 10. 1111/ ene. 15263
30. Conrad J, Habs M, Boegle R, Ertl M, Kirsch V, Stefanova-
Brostek I, Eren O, Becker-Bense S, Stephan T, Wollenweber F,
Duering M, Zu Eulenburg P, Dieterich M (2020) Global multi-
sensory reorganization after vestibular brain stem stroke. Ann
Clin Transl Neurol 7:1788–1801. https:// doi. org/ 10. 1002/ acn3.
51161

Journal of Neurology
1 3
31. Baier B, Conrad J, Zu Eulenburg P, Best C, Müller-Forell W,
Birklein F, Dieterich M (2013) Insular strokes cause no ves-
tibular deficits. Stroke 44:2604–2606. https:// doi. org/ 10. 1161/
STROK EAHA. 113. 001816
32. Conrad J, Boegle R, Ruehl RM, Dieterich M (2022) Evaluating
the rare cases of cortical vertigo using disconnectome map-
ping. Brain Struct Funct 227:3063–3073. https:// doi. org/ 10.
1007/ s00429- 022- 02530-w
33. Oppenheim C, Stanescu R, Dormont D, Crozier S, Marro B,
Samson Y, Rancurel G, Marsault C (2000) False-negative dif-
fusion-weighted MR findings in acute ischemic stroke. AJNR
Am J Neuroradiol 21:1434–1440
34. Lövblad KO, Laubach HJ, Baird AE, Curtin F, Schlaug G, Edel-
man RR, Warach S (1998) Clinical experience with diffusion-
weighted MR in patients with acute stroke. AJNR Am J Neuro-
radiol 19:1061–1066
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