Original Study
Sitting Up Vertigo. Proposed Variant of Posterior Canal
Benign Paroxysmal Positional Vertigo
Darı́o H. Scocco, Iván E. Garcı́a, and Marı́a A. Barreiro
Institute of Neuroscience, Favaloro Foundation University Hospital, Buenos Aires, Argentina
Objective: To describe a variant of posterior canal benign
paroxysmal positional vertigo (BPPV).
Study Design: Retrospective case review.
Setting: Tertiary referral center.
Patients: Fifteen patients with symptoms of BPPV and
oculomotor evidence of activation of posterior semicircular
canal (P-SCC) cupula that arises when sitting up from Dix-
Hallpike maneuver (DH).
Intervention: All patients were examined with videonystag-
mography and underwent brain magnetic resonance imaging
(MRI).
Results: All patients showed up-beating nystagmus with
ipsilateral torsional component when coming up from right
or left side DH. Most patients described vertiginous symp-
toms when sitting up from bed and many described severe
non-positional disequilibrium. Eight patients had been treated
with Epley canalith repositioning maneuver (CRM) at our
clinic for posterior canal BPPV. Four of them were re-tested
Benign paroxysmal positional vertigo (BPPV) is the
most common type of vertigo reported in the general
population (1). The accepted pathophysiological mecha-
nism involves dislodged otoconia from the utricular
macula that enters and flows freely in the semicircular
canals (SSC), on canalolithiasis type BPPV, or otoconial
debris attached to SSC cupula changing its flotation
characteristic in relation to the endolymph, on cupuloli-
thiasis type BPPV (2).
In canalolithiasis, changes in head position elicit
movement of the otoconial debris inside the SCC medi-
ated by gravity. That movement will push or pull the
endolymphatic column as a piston, which ultimately
deflects the cupula to the vestibular or SSC side respec-
tively. Cupula deflection generates a paroxysmal posi-
tional nystagmus whose characteristics will depend on
the involved canal and the direction of deflection. BPPV
Address correspondence and reprint requests to Darı́o H. Scocco,
M.D., 461 Solis St. (C1078AAI), Ciudad Autónoma de Buenos Aires,
Argentina; E-mail: dscocco@ffavaloro.org
Source of Funding: none.
The authors disclose no conflicts of interest.
Supplemental digital content is available in the text.
DOI: 10.1097/MAO.0000000000002157
ß 2019, Otology & Neurotology, Inc.
Copyright © 2019 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
within an hour for CRM effectiveness and the rest, a week
later. Three patients had been diagnosed with BPPV and
were being treated with CRM in other institutions. Four
patients showed these findings but they had not previously
undergone CRM. All patients were treated with CRM
without success, but they resolved their positional vertigo by
means of Brandt Daroff exercises. No patient showed
evidence of central vestibular disorder.
Conclusion: We propose a P-SCC canalolithiasis limited to
the periampullar portion by means of an anatomical restric-
tion of distal movement of the otoconial debris. This
syndrome seems to be more frequent early after CRM of
classical P-SCC canalolithiasis. Close attention to ocular
movement on sitting up after DH on patients is warranted.
Key Words: Benign paroxysmal positional vertigo—
Posterior canalolithiasis—Sitting up vertigo—Vertigo.
Otol Neurotol 40:497–503, 2019.
involves most frequently the posterior semicircular canal
(P-SSC), the horizontal semicircular canal (H-SSC) and
more rarely, the anterior semicircular canal (A-SSC). In
P-SCC canalolithiasis, the Dix-Hallpike provocative
maneuver (DH) triggers an ampullofugal movement of
the otoconial mass with a consequent cupular deflection
in the same direction. In P-SSC, ampullofugal deflection
is excitatory and it generates a nystagmus that is vertical-
torsional, having the linear component of its fast phase
directed upward (to the forehead) and the torsional one
directed with the upper pole of the eye to the lowermost
ear. This nystagmus has typical paroxysmal velocity
profile and generally lasts under 60 seconds. If the patient
sits up after a positive DH, a less intense and inverted
vertical-torsional nystagmus with a downward vertical
component with a torsional component beating toward
the opposite side of the involved ear, secondary to the
inhibitory ampullopetal (towards the vestibule) cupular
deflection, will be noted (3).
Recently, Vannucchi et al. (4,5) have reported a P-SSC
canalolithiasis variant in which DH elicits a vertical-
torsional nystagmus, having a downward vertical com-
ponent with a subtle torsional component towards the
uppermost ear. This pattern is identical to the nystagmus
that would evoke the activation of contralateral A-SSC.
498 D. H. SCOCCO ET AL.

The author suggested that the otoconial debris located in
the non-ampullary arm of P-SSC, near the common crus,
would move towards the ampulla on DH, triggering an
inhibitory, down-beat torsional nystagmus. This nystag-
mus has a long-lasting non-paroxysmal velocity profile.
When the patient comes up, no reverse nystagmus
appears. Proposed pathophysiological mechanism for
these findings suggests that the otoconial debris could
be trapped on distal P-SSC by canal stenosis or a canalith
jam that preclude its movement.
The appearance of vestibular symptoms when coming
up from supine position is a common complaint among
patients in neuro-otological clinics. Many mechanisms
are potentially related to such symptomatology. Explo-
ration of hemodynamic, structural, vascular, central, and
peripheral vestibular causes in those patients is war-
ranted. Büki et al. (6) have proposed a BPPV variant
in which vestibular symptoms arise when sitting up from
DH without oculomotor manifestations but with a pos-
turographic documented anteroposterior truncal oscilla-
tion instead. Authors propose a utricular side P-SSC
canalolithiasis as potential mechanism. We have recently
encountered some patients with vestibular symptoms
when sitting up from DH with oculomotor evidence of
activation of P-SSC cupula. We propose a model that
tries to explain these findings.
(CRM) at our clinic for P-SSC canalolithiasis. Four patients
were re-tested early for CRM effectiveness, less than an hour
after the maneuver and four patients were tested a week after
CRM. Three out of 15 had a history of BPPV and had been
treated with CRM in other institutions between a week and a
month before our examination. However, we lack any docu-
mentation that provides details about the examination findings
or CRM performed. All 15 patients had a personal history
suggestive of recurrent BPPV.
Detailed neurological and neuro-otological history was col-
lected on all patients. All patients were examined by means of
videonystagmography (Chartr, Otometrics, Denmark). Video
recordings of the examination sessions were analyzed retro-
spectively. Gaze with and without fixation, horizontal saccades,
smooth pursuit, optokinetic, spontaneous, and head shake nys-
tagmus were checked. The set of positional maneuvers per-
formed varied among patients given that findings of the
maneuvers gave rise to different repositioning strategies. The
positional maneuvers and the oculomotor findings on each
patient are depicted in Table 1.
All patients but one were followed until they resolved
positional nystagmus and symptoms. All patients underwent
brain magnetic resonance imaging (MRI) to rule out central
origin of atypical positional nystagmus.
Informed consent was obtained in all patients whose video
recordings were used as supplemental digital content.
RESULTS

MATERIALS AND METHODS
At the neuro-otology unit of the Institute of Neuroscience of
the Favaloro Foundation University Hospital, Buenos Aires,
Argentina, during the period that goes from July 2017 to
June 2018, we collected a group of 15 patients that presented
with symptoms when coming up from DH showing an up-
beating nystagmus with torsional component towards the side
of the lowermost ear at DH.
Patients (F9) had a mean age of 66 years. Eight out of 15
had been treated with Epley canalith repositioning maneuver
We will assign the labels ‘‘ipsilateral (i)’’ to the side of
the lowermost ear in the DH that presents with up-beating
torsional nystagmus when coming up, and ‘‘contralateral
(c)’’ to the opposite side. All patients showed up-beating
nystagmus with ipsilateral torsional component when
coming up from right or left side DH (patient cohort
selection criteria). Nystagmus starts after a short latency
and then evidences prolonged slowly crescendo-decre-
scendo velocity profile different from the typical parox-
ysmal P-SSC canalolithiasis. It lasts for approximately

TABLE 1. Demographic information of patients and clinical findings on positional maneuvers

Sex/Age Side DHi "DHi DHc "DHc H-H "H-H HYTc HYTi Y1 Y2 Epley 2 Epley 3 Dx Maneuvre

1 M 70 L No "t #t "t "t "t

2 F 67 L No "t #t "t No "t #t "t
3 F 65 R No "t
4 M 25 R No "t #t "t "t #t #t
5 F 59 R No "t #t No #t "t #t "t "t "t No #t
6 F 88 R No "t #t No #t No No "t No No No
7 F 73 L No "t No "t #t #t
8 F 73 R No "t " # #t #t
9 F 79 L No "t No "t No "t No No #t #t
10 M 61 L No "t No "t
11 M 74 R No "t No No No No No "t
12 M 66 L No "t Right No No Right "t
13 F 62 R No "t No No No "t No No #t #t
14 F 70 R No "t No No No No #t "t #t #t þ
15 M 77 L No "t No "t No #t "t #t #t þ

c indicates contralateral; DH, Dix-Hallpike maneuver; Dx maneuver, diagnostic maneuver; H-H, head-hanging maneuver; HYT, Head Yaw
Test; i, ipsilateral; L, left; No, no nystagmus; R, Right; Y1, Y2, step 1 and 2 of Yacovino maneuver; "t, up-beat torsional nystagmus; #t, down-
beat torsional nystagmus; ", sitting up from.

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 SITTING UP VERTIGO
40 seconds (see Video, Supplemental Digital Content 1,
http://links.lww.com/MAO/A761). We also found up-
beating torsional nystagmus with different frequencies
when performing other positional maneuvers: coming up
from head-hanging maneuver in seven out of 10 patients,
anterior flexion of the neck in the first step of the
Yacovino maneuver in two out of three patients (see
Video, Supplemental Digital Content 2, http://links.
lww.com/MAO/A762), coming up from step one of
the Yacovino maneuver in two out of three patients,
on performing ipsilateral head yaw test (HYTi) in eight
out of 10 patients (see Video, Supplemental Digital
Content 3, http://links.lww.com/MAO/A763). Other
positional maneuvers evoked an opposite direction nys-
tagmus, beating downwards with contralateral torsional
component. This nystagmus had a slower constant veloc-
ity profile either lasting more than a minute or not
stopping at all. We found this type of nystagmus in five
out of 11 patients on contralateral Dix-Hallpike maneu-
ver (DHc) (see Video, supplementary Digital Content 4,
http://links.lww.com/MAO/A764), in four out of 10
patients on contralateral head yaw test (HYTc) (see
Video, Supplemental Digital Content 3, http://links.
lww.com/MAO/A763), in seven out of nine patients
on the second step of ipsilateral Epley maneuver
(Epley2i) and eight out of nine patients on the third step
in the Epley maneuver (Epley3i) (see Video, Supplemen-
tal Digital Content 5, http://links.lww.com/MAO/A765).
All eight patients who had had a documented typical P-
SSC canalolithiasis and were treated in our clinic by
means of the Epley maneuver presented with up-beating
torsional nystagmus after sitting up from the same side,
previously symptomatic, DH.
All patients were treated with P-SSC CRM (Epley
maneuver, Semont maneuver, and demi-Semont maneu-
ver) without success in the immediate retesting. All
patients were prescribed domiciliary Brant-Daroff exer-
cises. Some patients resolved their positional syndrome
at the next control, 7 days after the initial evaluation, but
others persisted for a longer period of time. The median
follow-up until patients resolved this positional nystag-
mus was 1.42 visits. Four patients converted to typical P-
SSC canalolithiasis and one patient to geotropic H-SSC
canalolithiasis. All but one patient were followed until
they resolved positional nystagmus and symptoms. Two
effectively-treated patients of this cohort had ipsilateral
typical P-SSC canalolithiasis recurrence after 2 and 4
months, respectively. They were treated by means of the
Epley maneuver. On the early retest (<1 hour post-CRM)
they developed up-beating torsional nystagmus again,
when sitting up from ipsilateral DH. One patient resolved
this positional nystagmus on the next control after 7 days.
The other patient converted to classical P-SSC canal-
olithiasis that could not be resolved after several CRM
sessions and domiciliary maneuvers.
No patient showed evidence of central vestibular
compromise on the neurologic and oculomotor examina-
tion. MRI imaging did not show any lesion suggestive of
central vestibular or oculomotor compromise.
Copyright © 2019 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.
499
Most patients described vertiginous symptoms when
sitting up from bed and many described severe non-
positional disequilibrium.
DISCUSSION
We find, in this cohort of patients, a vertical-torsional,
up-beating positional paroxysmal nystagmus suggestive
of stimulatory-ampullofugal deflection of the P-SSC
cupula when sitting up from the ipsilateral DH. This
finding is atypical and, as far as we are concerned, has not
been previously reported. Personal history consistent
with positional vertigo in all patients and the performance
of CRM for a documented ipsilateral P-SSC canaloli-
thiasis under 7 days before the findings in eight out of
15 patients, suggest this mechanism. Additionally,
certain maneuvers triggered an inverted down-beating
torsional nystagmus of lesser velocity, suggestive of
inhibitory-ampullopetal deflection of ipsilateral posterior
cupula. Other signs suggestive of central vestibular dys-
function and structural lesions revealed by MRI imaging
were absent. All patients resolved the positional nystag-
mus and symptoms on the follow-up.
We propose a pathophysiological model that could
explain these findings. We propose the presence of a
free-floating otoconial debris on the descending periam-
pullar portion of the P-SCC. This debris might have an
ampullofugal restriction of its movement given some
anatomical features: either the size of the debris prevents
progression of ampullofugal movement through the SCC
or the presence of an anatomical reduction of the SCC
diameter, which may be the result of a partial otolith jam
(7,8) (Fig. 1A). Restrictions on the free debris movement
through SCC have been proposed as a mechanism on
atypical canalolithiasis variants such as apogeotropic
P-SCC (4,5), direction-fixed horizontal canal BPPV
(9,10), and cases of intractable BPPV (11). In this scenario,
a high-acceleration, anterior torsional head movement in
the plane or near the plane of P-SSC, as occurs on sitting up
from DHi, sitting up from head hanging maneuver and on
step one and two of Yacovino maneuver, could provoke
an ampullopetal movement of the debris mediated by
negative inertia force and then a second ampullofugal
movement mediated by gravitational force. The initial
ampullopetal movement could be related with the latency
until the ampullofugal movement of debris ultimately
provoked the stimulatory deflection of the posterior canal
cupula and hence the stimulatory nystagmus pattern. The
crescendo-decrescendo non-typically paroxysmal pattern
of nystagmus could be potentially related to: 1) the soft
descendent slope that periampullar P-SCC region has on
sitting position elicited a slower debris displacement
mediated by gravity than the one of typical P-SSC canal-
olithiasis; 2) the debris could impact on the proposed
stenosis thus generating a partial otolith jam and then
acting as a valve that prevented the free endolymph flux
that was necessary for the cupula to return to its resting
position (Fig. 1A-D, see Video, Supplemental Digital
Content 6, http://links.lww.com/MAO/A766).
Otology & Neurotology, Vol. 40, No. 4, 2019
500 D. H. SCOCCO ET AL.

FIG. 1. Proposed model of posterior cupula deflection on sitting up. A, Right P-SCC on DHi. Free-floating otoconial debris on the
descending periampullar portion with a distal restriction on its displacement. B, Ampullopetal movement of the debris mediated by negative
inertia force on sitting up. C, Posterior ampullofugal movement of the debris mediated by gravitational force evokes an ampullofugal
excitatory cupular deflection. D, Sustained ampullofugal excitatory cupular deflection mediated by a proposed canalith jam valvular
mechanism. P-SCC indicates posterior semicircular canal.

The down-beating nystagmus with inhibitory charac-
teristics seen on DHc (five out of 11 patients), HYTc
(four out of 10 patients), Epley2i (seven out of nine
patients), and Epley3i (eight out of nine patients) could
be explained in the proposed model by gravitational
mediated debris movement towards posterior canal
cupula which is in a lower position in relation to the
periampullar sector of P-SSC on these maneuvers. The
debris movement would trigger an ampullopetal (towards
the vestibule) inhibitory deflection of the cupula. The
prolonged, constant or non-fatigable pattern of the
inhibitory nystagmus could be mediated by a sustained
pressure of the debris located over the posterior
cupula (Fig. 2A-D, see Video, Supplemental Digital
Content 7-9, http://links.lww.com/MAO/A767, http://
links.lww.com/MAO/A768, http://links.lww.com/MAO/
A769).
The up-beating torsional nystagmus suggestive of
stimulatory ampullofugal deflection seen HYTi in six
out of eight patients could be explained, in the proposed
model, by the gravitational mediated ampullofugal debris
movement towards the proposed canal stenosis, which is

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 SITTING UP VERTIGO 501

FIG. 2. Periampullar portion of right posterior canal on positional maneuvers. On A, DHc, Epley2i; B, Epley3i, and C, HYTc gravitational
force pushes the debris towards the cupula, thus exerting an ampullopetal inhibitory deflection. D, On HYTi gravitational force pushes the
debris on ampullofugal direction, thus exerting an ampullofugal stimulatory deflection.

in a lower position in relation to the periampullar sector
of P-SSC on this maneuver (Fig. 2D, see Video, Supple-
mental Digital Content 8, http://links.lww.com/MAO/
A768).
The findings mentioned on the different positional
maneuvers are indicative of the debris being on the
ampullar and not in the non-ampullar arm of the posterior
canal. For example, if the debris were located on the non
ampullary arm of P-SSC, HYTi should eventually elicit
an ampullopetal debris movement with a consequent
inhibitory down-beating torsional nystagmus and HYTc
should eventually elicit an ampullofugal movement on
the debris eliciting a stimulatory up beating torsional
nystagmus; on the contrary we encountered the opposite
findings. On the other hand, on the third step of the Epley
maneuver for the affected ear (Epley3i, contralateral nose
down) we found a consistent, long-lasting or non-fatiga-
ble, inhibitory down-beating torsional nystagmus (differ-
ent from the short liberatory down-beating nystagmus
that sometimes is seen on step 3 or 4 of the Epley
maneuver), which would be difficult to justify if the
debris were located on the non ampullary arm, where it

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502 D. H. SCOCCO ET AL.

should elicit an ampullofugal cupular deflection medi-
ated by an ampullofugal debris movement. Additionally,
the down beating inhibitory nystagmus in nose down
position would be more easily justified if the debris were
located on the ampullary arm where a sustained inhibi-
tory ampullopetal cupular deflection would be expected
(Fig. 2B, videos 5, http://links.lww.com/MAO/A741 and
9, http://links.lww.com/MAO/A745).
The mechanism that should explain the case of patients
that presented with typical PC-BPPV and after CRM
presented with sitting up beating torsional nystagmus
could be that in the original CRM there was a partial
passage (maybe the smaller fragments) of the otoconial
debris throughout the canal, the other part being trapped by
some anatomical feature in the periampullar section. The
distal particles could effectively be removed by CRM but
the bigger ones remains trapped in the ampullary arm.
Findings suggest that head positions that direct the
periampullar portion of P-SSC close to gravitational
vertical are more prone to inducing a cupular deflection.
For example, Epley3i, where the periampullar portion of
the canal is close to vertical, the ampulla being in an
inferior position, is the maneuver that most frequently
evokes an inhibitory nystagmus. On the other hand,
HYTi, where the periampular portion of the canal is
close to vertical, the ampulla being in superior position, is
the maneuver that most frequently evokes a stimulatory
nystagmus. To test this hypothesis, we used an original
maneuver that intends to put the periampullar portion of
the posterior canal close to vertical, initially with the
ampulla being lower with respect to the canal, and then
move the head to put the ampulla vertically above the
canal. The patient’s head is initially positioned at 135
degrees towards the contralateral suspected side (as
Epley3i) and after that the head is rotated 180 degrees
towards de suspected side (resting at 45 degrees to the
suspected side) (Fig. 3, see Video, Supplemental Digital
Content 10, http://links.lww.com/MAO/A770). We have
tested this maneuver prospectively on the last two
patients of our cohort and we have observed an inhibitory
prolonged down-beating/torsional nystagmus in the first
step and an up-beating torsional nystagmus with cre-
scendo-decrescendo velocity profile on the second step,
as expected (see Video, Supplemental Digital Content
11, http://links.lww.com/MAO/A771).
The recurrence of ipsilateral P-SCC canalolithiasis and
the re-appearance of up-beating/torsional nystagmus on
sitting up after CRM in two patients suggest the existence
of an anatomical predisposing factor.
The severe non-positional disequilibrium showed by
many patients could be related to a different vestibular
stimulation pattern from the one in the usual P-SSC
canalolithiasis, which may be evoked by usual daytime
movements. Similar symptomatology is described in
apogeotropic variant of P-SCC canalolithiasis.
The limitations of this work are the small number of
patients in our series and its retrospective design. Future
work involves prospective analysis and follow-up, stan-
dardized examination of positional maneuvers, trial, and
validation of specific CRM and SCC imaging and 3D
reconstruction in search of anatomical irregularities.
CONCLUSION
We describe a positional vertigo syndrome evoked
by sitting up with evidence of stimulation of P-SSC

FIG. 3. Proposed diagnostic maneuver for right periampullar cupulolithiasis. A, Initially the patient’s head is positioned 135 degrees
towards the contralateral suspected side (as Epley3i) evoking an ampullopetal debris movement and a sustained inhibitory cupular
deflection. B, The head is rotated 180 degrees towards the suspected side (resting at 45 degrees) where gravitational force pushes the
debris on ampullofugal direction exerting an ampullofugal stimulatory deflection.

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 SITTING UP VERTIGO
cupula. We propose a posterior canal canalolithiasis
limited to the periampullar portion by means of an
anatomical restriction of distal movement of the oto-
conial debris. This syndrome seems to be more fre-
quent early after CRM of classical PC-BPPV canal, but
we have found that it also occurs weeks after it or even
spontaneously. It is possible that these findings are
transient and less frequent if control examination is
delayed after CRM. This mechanism could account for
vestibular symptomatology on the days following the
performing of therapeutic CRM. Close attention to
ocular movement on sitting up after DH on patients
is warranted.
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