ORIGINAL ARTICLE

Multiple positional nystagmus suggests multiple canal involvement in

benign paroxysmal positional vertigo
JOSE A. LOPEZ-ESCAMEZ, MARIA I. MOLINA, MARIA J. GAMIZ, ANTONIO J.
FERNANDEZ-PEREZ, MANUEL GOMEZ, MARIA J. PALMA & CRISTOBAL ZAPATA
Otology and Neurotology Group, CTS495, Department of Surgery, Hospital de Poniente de Almer a, El Ejido, Almer a, Spain
Abstract
Conclusion. Video-oculography demonstrates a higher occurrence of atypical positional nystagmus in patients with benign
paroxysmal positional vertigo (BPPV). This includes anterior and horizontal canal variants and multiple positional
nystagmus, suggesting combined lesions affecting several canals. Objective. To analyse the video-oculographic findings of
positional tests in patients with BPPV. Material and methods. Seventy individuals with symptoms of BPPV and positional
nystagmus were included in this study. The diagnosis was based on a history of brief episodes of vertigo and the presence of
positional nystagmus as confirmed by video-oculographic examination during the Dix/Hallpike test, the McClure test or
the head-hanging manoeuvre. Patients were treated by means of different particle repositioning manoeuvres according to
the affected canal (Epleys manoeuvre for the posterior or anterior canals and Lemperts manoeuvre for the lateral canal)
and the effectiveness was evaluated at 7 and 30 days. Results. Twenty-nine individuals (41.43%) presented an affected
unilateral posterior canal. Fifteen patients (21.43%) presented a pure horizontal direction-changing positional nystagmus
consistent with a diagnosis of horizontal canal BPPV. Twelve individuals (17.14%) presented a unilateral down-beating
nystagmus, suggesting possible anterior canal BPPV. In addition, 14 patients (20%) showed multiple positional nystagmus
during the examination corresponding to simultaneous multi-canal BPPV, 5 had bilateral posterior canal BPPV and 2
presented a positional down-beating nystagmus in both left and right Dix/Hallpike manoeuvres and the head-hanging
manoeuvre, which is highly suggestive of anterior canal BPPV. However, seven individuals showed positional horizontal and
vertical side-changing nystagmus that could not be explained by single-canal BPPV. These patients with multiple positional
nystagmus showed changing patterns of positional nystagmus at follow-up.
Keywords: Benign paroxysmal positional vertigo, vestibular system, vestibular testing, video-oculographic examination
Introduction
Benign paroxysmal positional vertigo (BPPV) is the
commonest vestibular disorder for which there is an
easy and effective therapy [1]. It is characterized by
spells of vertigo and nystagmus of short duration
that are elicited by turning the head in the plane of
the affected semicircular canal. There are three
clinical variants, the most frequent of which involves
the posterior canal [2]. The diagnosis of posterior
canal BPPV is based on the observation of a
torsional, up-beating nystagmus during the Dix/
Hallpike (DH) test [3]. The nystagmus is geotropic
(ear-dependent), being clockwise on the left side and
anticlockwise on the right side [4].
BPPV is probably a mechanical disorder of the
semicircular canals and two mechanisms (canalithia-
sis and cupulolithiasis) explain the features of the
positional nystagmus (geotropic or apogeotropic,
latency, duration and fatigue). According to the
accepted hypothesis for explaining the positional
nystagmus, vestibular lithiasis can theoretically affect
each of the three semicircular canals. According to
this hypothesis, high-density particles either free-
float in the canal (canalolithiasis) or adhere to the
cupula of the crista ampullaris (cupulolithiasis).
When they accumulate and reach a critical mass
they can induce an ampullofugal deflection of the
cupula if they move away from the cupula in the DH
manoeuvre and produce an excitatory response.
Correspondence: Jose A. Lopez-Escamez, Otology and Neurotology Group, CTS495, Department of Surgery, Hospital de Poniente de Almer a, Ctra de
Almerimar s/n, ES-04700 El Ejido, Almer a, Spain. Tel: /34 950 022653. E-mail: jalopeze@cajamar.es
Acta Oto-Laryngologica, 2005; 125: 954/961
(Received 27 January 2005; accepted 21 April 2005)
ISSN 0001-6489 print/ISSN 1651-2551 online # 2005 Taylor & Francis
DOI: 10.1080/00016480510040146
The characteristics of the induced nystagmus vary
considerably in patients diagnosed with typical
BPPV. In some cases the positional nystagmus is
mixed with vertical and torsional components,
whereas in others it is almost purely torsional or
vertical. Other cases present a pure horizontal
direction-changing nystagmus, either geotropic or
ageotropic, which has been reported to correspond
to canalolithiasis or cupulolithiasis of the horizontal
canal, respectively [5]. These variations may be
partly explained by the direction of gaze: the
nystagmus appears more torsional when the patient
gazes towards the affected side and more vertical
when he/she gazes in the opposite direction [6].
However, the direction of gaze alone cannot explain
these variations. Two other observations support the
concept of multiple positional nystagmus. First,
positional nystagmus can be demonstrated by differ-
ent manoeuvres; this occurs for bilateral posterior
canal BPPV, which is characterized by a torsional
up-beating nystagmus that can be provoked by both
left and right DH tests. It is also the case for
horizontal canal direction-changing nystagmus [7]
and could be observed in cases of positional down-
beating nystagmus in the DH test and the head-
hanging manoeuvre, suggesting anterior canal BPPV
[8]. Second, in our experience, some patients show a
changing positional nystagmus during follow-up,
despite an initially effective treatment. This may be
due to migration of the canaliths from a posterior
canal to the horizontal canal during repositioning;
however, these relapses occur several months or
years after particle repositioning. It is speculated
that some individuals present a relapsing clinical
course and that vestibular lithiasis can be observed in
any semicircular canal, sometimes affecting several
canals at once [9].
In this study we performed a systematic recording
of positional nystagmus using video-oculography in
patients with BPPV in order to characterize the
direction of the nystagmus during positional tests
and to identify patients with multiple positional
nystagmus.
Material and methods
Patients
We studied a series of 70 individuals with BPPV
between January 2003 and December 2004. Clinical
diagnosis was carried out by means of positional
testing: the DH test and the head-hanging man-
oeuvre were used for the posterior and anterior
canals, respectively and lateral turning of the head
in de cubito was used for the lateral canal. Physical
examination was performed in all individuals and
included examination of the ears, Rinne and Weber
tests, pure-tone audiometry (250/8000 Hz) and a
basic neurotologic examination (oculomotor test,
saccades, head-impulse test, cranial nerve examina-
tion and Romberg, Barany and Fukuda tests). Only
those patients who demonstrated a positional nys-
tagmus associated with vertigo on physical examina-
tion were included in the study.
Exclusion criteria
Patients with abnormal otoscopic findings (i.e.
perforation of the tympanic membrane, active infec-
tion of the ear) or those with a cognitive or
psychiatric disorder were excluded because of pro-
blems with performing the caloric test.
Video-oculographic examination
The video-oculographic (VOG) recording included
spontaneous nystagmus in the primary position of
the eye, positional testing (the DH test for the lateral
canal and the head-hanging manoeuvre for the
anterior canal) and water bithermal caloric testing.
The DH test was considered positive for posterior
canal BPPV if nystagmus was recorded when the
patient was in an appropriate position, had a
characteristic latency, duration and fatigue and was
reversed when the patient sat up [3]. A minimum of
six repeated beats in the same direction were
required as evidence of positional nystagmus. The
differential diagnosis between posterior and anterior
canal involvement was based on the direction of the
vertical component of the fast phase of the nystag-
mus response during the DH test, which is upward
in cases of posterior canal involvement and down-
ward in cases of anterior canal disease. Horizontal
canal BPPV was identified by means of horizontal
direction-changing positional nystagmus. The video
camera was mounted in a mask contralateral to the
side used for the DH test to reduce its movements
during the head-hanging manoeuvres. A caloric test
was performed in each subject using a Variotherm
Plus water irrigator (Atmos, Berlin, Germany), with
a water flow rate of 250 ml/20 s at 308C and 448C,
with an interval of 10 min between successive
irrigations. All irrigations were performed in de
cubito with the head 308 above the horizontal plane.
The recording of eye movements was performed
using a 2D VOG system with an infrared charge-
coupled device (CCD) camera attached to a rubber
mask (SMI, Berlin, Germany) to analyse the eye
response. The recording time was 60 s for sponta-
neous nystagmus and 120 s for the caloric response.
The maximum slow-phase velocity (SPV) was de-
termined by the software and SPV values were
Multiple positional nystagmus in BPPV 955
compared with normal values obtained in our
laboratory. The parameters for the discrete analysis
of the nystagmus were as follows: minimum accel-
eration 5008/s
2
; minimum velocity of the fast phase
508/s; minimum amplitude of the fast phase 18;
minimum amplitude of the slow phase 18; and
maximum SPV 50 ms. The criteria for diagnosis of
BPPV during positional testing were the observation
of (i) up-beating nystagmus for the posterior canal
during the DH test; (ii) horizontal direction-chan-
ging nystagmus for the lateral canal during the DH
or roll test; and (iii) down-beating nystagmus during
the DH test or the head-hanging manoeuvre. All
individuals with down-beating nystagmus were eval-
uated by means of gadolinium-enhanced cranial
MRI to rule out central nervous system (CNS)
disease [9].
Written information was made available to the
patients and informed consent was obtained from all
of them after explaining the purpose of the study.
The Ethical and Research Committee of the hospital
approved the study.
The positional treatment given to the patients
varied according to the canal affected. If it was
suspected that multiple canals were affected, the
treatment started with the canal that elicited a strong
positional nystagmus and vertigo. The particle
repositioning manoeuvre (PRM) or Epleys modified
manoeuvre without a mastoid oscillator were used
for the posterior and anterior canals; the Lempert
manoeuvre was used for the lateral canal. Individuals
were recommended to avoid rapid turning of the
head and were allowed to sleep in de cubito. Patients
were evaluated at 7 and 30 days post-treatment;
if they presented a positional nystagmus, the PRM
or Lempert manoeuvre were repeated up to four
times. Non-responding individuals were treated by
means of a Semont manoeuvre and finally with
Brandt /Daroff exercises. After 30 days, patients
were re-examined every 1 or 2 weeks until both
positioning vertigo and nystagmus had completely
disappeared.
Statistical analysis
Descriptive statistics are presented as means and
SDs. ANOVA was used to test differences in
horizontal and vertical components of the SPV,
latency, duration and number of beats of the
positional nystagmus. p B/0.05 was considered sig-
nificant.
Results
There were 70 individuals in the BPPV group (30
males, 40 females; mean age 57.159/13.93 years;
median 57 years; range 20/81 years). In our series,
29 individuals (41.43%) presented a unilateral up-
beating nystagmus during the DH test, indicating an
affected posterior canal (PC). Fifteen patients
(21.43%) presented a pure horizontal direction-
changing positional nystagmus during the DH or
McClure manoeuvres, consistent with a diagnosis of
horizontal canal (HC) BPPV. Two cases presented
ageotropic nystagmus and the null point, i.e. that
beyond which the nystagmus changed direction, was
identified, corresponding to cupulolithiasis of the
HC. Twelve individuals (17.14%) presented a uni-
lateral down-beating nystagmus during the DH or
head-hanging manoeuvres, suggesting possible ante-
rior canal (AC) BPPV (Table I).
Multiple positional nystagmus in BPPV patients
Fourteen patients (20%) showed multiple positional
nystagmus (MPN) during the examination, corre-
sponding to simultaneous multicanal BPPV. Five of
these cases had bilateral PC BPPV; two patients
presented a positional down-beating nystagmus in
both left and right DH tests and the head-hanging
manoeuvre, suggestive of bilateral AC BPPV. How-
ever, nine individuals showed positional horizontal
and vertical side-changing nystagmus that could not
be explained by a single-canal stimulation. These
cases did not show spontaneous nystagmus, with the
exception of patient No. 4, who had a spontaneous
up-beating nystagmus.
Table I presents the horizontal and vertical com-
ponents of the SPV, latency, duration and number of
beats of nystagmus observed during the positional
test. The maximum SPV of the vertical component
was :/338/s (range 13/818/s) for PC BPPVand 258/
s (range 14/378/s) for AC BPPV. The maximum
SPV of the horizontal component was 168/s (range
4/888/s) for HC BPPV. There were no significant
differences in SPV, latency, duration or number of
beats of nystagmus between unilateral and bilateral
PC BPPV. Moreover, there were no differences in
latency among PC, AC or HC BPPV. However,
significant increases in the duration and number of
beats of the positional nystagmus were observed for
HC BPPV, when compared with AC or PC BPPV
(p/0.001).
Patients with MPN also showed changing patterns
of positional nystagmus at follow-up, probably due
to canalith mobilization during treatment. Table II
presents the VOG parameters for each patient with
MPN on the DH test. Patients Nos. 10, 12, 53, 57
and 66 presented MPN, one of whom had a
positional down-beating nystagmus, suggesting AC
involvement.
956 J. A. Lopez-Escamez et al.
Clinical features
The time course of BPPV was variable (range 1
month to 29 years). The right ear was affected in 38
individuals, the left ear in 19 and both sides in 13
(right:left ratio 2.0). Sixty patients presented idio-
pathic BPPV (86%) and 10 cases had BPPV after
minor head trauma (14%). Twenty-three individuals
(33%) had vascular disease (arterial hypertension).
Moreover, 23/70 patients presented sensorineural
hearing loss (35/70 dB). The clinical features for
each canal variant of BPPV are shown in Table III.
Spontaneous nystagmus and caloric testing
Spontaneous nystagmus was found using vestibulo-
ocular testing in 10/70 individuals (2 with PC, 3 with
AC, 3 with HC and 2 with MPN BPPV). A
bithermal caloric test was performed in 58/70
individuals with BPPV. Twelve patients either re-
fused to perform the test or were unable to finish
it because of nausea and vomiting. Canal paresis
(/25%) was found in 16/58 cases, and a directional
preponderance (/25%) in 11/58. Overall, 20/58
individuals (34% cases) presented an abnormal
caloric test (Table IV). The occurrence of vestibular
abnormalities was as follows: 10/29 for PC, 5/12 for
AC, 6/15 for lateral canal (LC) and 6/14 for MNP
BPPV.
Effectiveness of positional treatment
Fifty-six of the 70 patients (80%) did not present
vertigo and the positional test was negative at 30
days. However, 11 cases presented a positional
nystagmus with persistence of BPPV episodes at 30
days (4 with PC, 3 with AC, 3 with HC and 4 with
MPN BPPV).
Discussion
This study provides VOG information consistent
with multiple-canal positional nystagmus and sug-
gests that several canals can be affected in some
cases of BPPV. We found that atypical positional
nystagmus is not a rare observation and that it can
be demonstrated in /50% cases of BPPV. Positional
nystagmus corresponding to AC (down-beating
nystagmus) or HC (horizontal direction-changing
nystagmus) lithiasis was observed in 17% and
21% of cases, respectively, suggesting that these
findings are underdiagnosed in clinical practice,
because VOG examination is not used during posi-
tional tests.
Positional nystagmus can occur in normal subjects
in total darkness due to the necessity of visual and
vestibular inputs in order to stabilize the eyes after a T
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Multiple positional nystagmus in BPPV 957
positional change [10]. However, the SPV for
positional nystagmus in normal subjects ranges
from :/2.58/s [11] to 58/s and it exceeds 118/s in
only 5% of individuals [12]. The SPVof the vertical
and horizontal components of positional nystagmus
recorded among our patients was higher than this
and was associated with vertigo. Thus, when evalu-
ating positional nystagmus in an individual patient,
not only the presence but also the magnitude of
simultaneous symptoms must be taken into account
when evaluating pathologic findings. In our series,
all the patients presented vertigo and positional
nystagmus.
The estimated occurrence of HC BPPV is 2/16%
of cases of BPPV [13]. It appears to occur more
often than was originally described [14]. Patients
aged /50 years are more prone to develop the
disease, which is compatible with the proposed
theory of utricular degeneration. The patient can
get up or lie down with minimal complaints, but
turning the head to either side in the supine position
usually provokes intense vertigo, which is more
pronounced on the pathological side [15]. The
positional nystagmus is horizontal (without a vertical
component), and usually beats towards the lower-
most ear. Although the nystagmus is characterized
by a short latency, there were no significant differ-
ences in latency between nystagmus originating from
the PC or HC in our series. However, the duration of
the nystagmus and the number of beats observed
were significantly higher in the HC than in the PC or
AC variants.
AC BPPV has been reported to occur in 1/19% of
cases of BPPV [16]. In this variant of BPPV, the
direction of the fast phase of the nystagmus is down-
beating and torsional when the patient is moved into
the DH position. This implies excitation of the AC
of the lowermost ear during the DH manoeuvre,
because debris in the anterior arm of the canal shifts
to the most lowest position by gravity, producing
movement of the endolymph and excitation of the
cupula. This results in a torsional, down-beating
nystagmus [17]. A bilateral positional down-beating
nystagmus triggered by the DH manoeuvre was
Table II. Patients with MPN on DH test.
Vertical component Horizontal component
Patient No. DH test Direction
Maximum
SPV (8/s) Direction
Maximum
SPV (8/s) Latency (s) Duration (s)
No. of beats
of nystagmus
4 L Up 59.8 / / 5 28 30
R / / R 24.7 3 57 36
10 L Down 6.6 R 16.5 1 56 53
R Down 15.8 R 6.3 3 43 11
12 L / / L 9.0 10 28 16
R Down 12.0 R 6.8 2 7 10
15 L Up 62.6 L 13.7 2 22 32
R / / L 17.4 1 40 40
40 L Up 92.6 R 3.9 4 19 40
R / / R 10.1 6 54 50
51 L Up 44.1 L 13.6 5 55 26
R / / / / / / /
53 L Down 20.2 L 47.8 4 58 52
R Up 13.6 L 8.3 5 58 39
57 L Down 17.3 L 61.7 11 14 12
R / / L 40.3 12 43 14
66 L Down 21.3 L 8 4 48 21
R Down 22.3 R 28 3 46 12
Table III. Clinical features of each canal variant of BPPV.
Canal type n
No. of
males/females
Age range
(years)
Vertigo history;
n (%)
Head trauma;
n (%)
Time course
(years)
Vascular
disease; n (%)
Hearing loss;
n (%)
Headache;
n (%)
Posterior 29 16/13 37/80 8 (28) 3 (10) 2/12 7 (24) 8 (27) 10 (34)
Lateral 15 5/10 27/70 6 (40) 2 (13) 1/15 5 (33) 4 (26) 8 (53)
Anterior 12 4/8 20/80 3 (25) 3 (25) 0.25/29 7 (58) 3 (25) 3 (25)
Multiple 14 5/9 28/73 3 (21) 2 (14) 1.67/5 4 (28) 8 (57) 4 (28)
958 J. A. Lopez-Escamez et al.
observed in 2 cases (patients Nos. 8 and 35), and it
was difficult to localize the affected side. This
therefore confirms that head rotation is unlikely to
be critical for particle mobilization in AC lithiasis
[8]. The only difference between left and right DH
manoeuvres is that during a contralateral DH
manoeuvre the head rotates in the plane of the
affected AC, whereas during an ipsilateral DH
manoeuvre the head rotates orthogonally to the
plane of the canal. Ten individuals in our series
had positional down-beating nystagmus as a result of
a straight head-hanging manoeuvre. It has been
argued [8] that rotation of the head in the canal
plane is of less relevance than the final low head-
down position for provoking particle displacement.
Prior to a DH manoeuvre, the head is rotated 458 in
the horizontal plane, so the head cannot reach such
a low vertex position as with the head-hanging
manoeuvre. This additional head angle may be
crucial for provoking AC BPPV, as the ampullary
segment will approach a vertical down-pointing
position. Although cervical ankylosis or obesity can
make the head-hanging manoeuvre difficult, we
should perform it in patients with BPPV and a
negative DH test in order to rule out a positional
down-beating nystagmus.
Although positional down-beating nystagmus is
found in patients with CNS disease, particularly
those with posterior fossa lesions [18], no patient in
our series had an Arnold/Chiari malformation or
multiple system atrophy [19]. However, none of the
individuals with positional down-beating nystagmus
in our series showed any abnormalities in cranial
MRI.
Our higher rates of LC and AC involvement
can be explained by the use of video-oculography,
as many cases of positional horizontal and down-
beating nystagmus are probably missed by visual
observation. In addition, it is possible that posi-
tional nystagmus may be inhibited by ocular
fixation under direct examination, but this phenom-
enon is unlikely to occur with Frenzel glasses or in
darkness. Moreover, some individuals only refer
weak vertigo, despite persistent beating, and the
positional test may be considered negative by the
examiner.
Hayashi et al. [20] analysed the axis of rotation of
the eyeball using an infrared CCD camera and an
algorithm in order to study positional nystagmus
during the DH test in 13 patients with unilateral
BPPV. They found that the patients could be
classified into two groups based on the rotational
Table IV. BPPV individuals with abnormal caloric tests or spontaneous nystagmus.
Patient No. Canal Spontaneous nystagmus Canal paresis (%) Directional preponderance (%)
1 RP L / /
6 RP / 27 L 25 L
18 LP / 51 R 31 R
20 RP / 49 L 31 L
29 LP R / 49 R
30 RP / 46 L /
45 RP / / 33 R
50 RP / 30 R /
59 RP
60 LP / 33 L /
2 RA L / /
8 RA L 36 L 54 L
34 LA L 26 L /
35 LA / / 37 R
64 RA / 32 L /
14 RH / 35 R /
21 RH R / /
28 LH Up / /
31 RH Down 34 L 32 L
43 RH / / 25 R
44 RH / 29 L /
4 MPN Up N.A. N.A.
10 MPN / 38 L /
53 MPN Up / /
57 MPN / 35 L /
66 MPN / 68 L 30 L
67 RP/LP / 38 L 42 L
RP/right posterior; LP/left posterior; RA/right anterior; LA/left anterior; RH/right horizontal; LH/left horizontal; MPN/
multiple positional nystagmus; N.A. /not available.
Multiple positional nystagmus in BPPV 959
axis of the nystagmus. In one group, the axis of
rotation was vertical to the plane containing the
posterior semicircular canal on the affected side; in
the other group, the axis of rotation was clustered
around the naso-occipital axis, which was probably
due to simultaneous stimulation of all three semi-
circular canals. The observation in this study of
positional nystagmus in different positional tests
which cannot be explained by single-canal stimula-
tion supports the hypothesis of multiple-canal in-
volvement [9].
Interestingly, we also found that BPPV more
frequently affects the right ear (right:left ratio 2.0).
This finding was also described in a recent meta-
analysis of 3426 patients [21], which yielded a
right:left ratio of 1.41 (95% CI 1.37/1.45). Sleeping
position seems to be involved in the pathophysiology
of BPPV, as many patients experience attacks when
moving in bed [2]. It has been shown [22] that the
side affected by BPPV correlates with the preferred
sleeping position in patients with PC BPPV, and it is
possible that BPPV predominantly involves the right
ear because most persons prefer the right lateral
supine position for sleeping [21].
Our caloric test findings are similar to those
observed in patients with PC BPPV [2,23]. Sponta-
neous nystagmus and a directional preponderance
were found in 10/70 and 11/58 cases, respectively.
These individuals were considered to have incom-
plete physiologic compensation [24]. Central com-
pensation starts by way of cerebellar inhibition of the
asymmetric activity at the vestibular nuclei. This
allows the brain to reorganize neuronal connections
in such a way that a symmetric spontaneous activity
can be restored at the vestibular nuclei. In our series,
canal paresis was observed in 16/58 cases with
BPPV. Therefore, the vestibular caloric response in
patients with BPPV can vary from normal to canal
paresis, although different signs of incomplete com-
pensation can be observed. These findings suggest
that there are several degrees of vestibular dysfunc-
tion, which are probably related to the extent of the
lesion. This may also influence the relapsing course
of the disease as the causes that facilitate the
shedding of otoconia from the utricular macula
(i.e. ischemic, metabolic, sleeping position) probably
persist.
Conclusions
Video-oculography demonstrated the occurrence of
atypical positional nystagmus in 59% of patients
with BPPV. This includes AC, HC and MPN
variants of BPPV, and suggests that several canals
can be affected simultaneously in BPPV.
Acknowledgements
This study was funded by research project No. FIS
PI021394 from the Instituto de Salud Carlos III.
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