Clin. Otolaryngol.

2002, 27, 392395

The test and treatment methods of benign paroxysmal positional

vertigo and an addition to the management of vertigo due to the
superior vestibular canal (BPPV-SC)
T. RAHKO
The Department of Otorhinolaryngology, Tampere University Hospital, Tampere, Finland
Accepted for publication 18 June 2002
R A H K O T.

(2002) Clin. Otolaryngol. 27, 392395

The test and treatment methods of benign paroxysmal positional vertigo and an addition to the
management of vertigo due to the superior vestibular canal (BPPV-SC)
A review of the tests and treatment manoeuvres for benign paroxysmal positional vertigo of the posterior,
horizontal and superior vestibular canals is presented. Additionally, a new way to test and treat positional vertigo
of the superior vestibular canal is presented. In a prospective study, 57 out of 305 patients visits are reported.
They had residual symptoms and dizziness after the test and the treatment of benign paroxysmal positional vertigo
of the horizontal canal (BPPV-HC) and posterior canal (PC). They were tested with a new test and treated with a
new manoeuvre for superior canal benign paroxysmal positional vertigo (BPPV-SC). Results for vertigo in 53
patients were good; motion sickness and acrophobia disappeared. Reactive neck tension to BPPV was relieved.
Older people were numerous among patients and their quality of life (QOL) improved.
Keywords benign paroxysmal positional vertigo
treatment manoeuvre

Different forms of the benign paroxysmal

positional vertigo
The first to present the clinical description of paroxysmal
positional vertigo was Barany1 in 1921.
The first test for benign paroxysmal positional vertigo is
Hallpikes test for vertigo involving the posterior canal.2 In this
test,thepatientsitshisbacktotheexaminertheheadrotatedtothe
right by 458. The body of the patient is brought straight back. The
head is finally hanging over the border of the examination bed by
308. The examiner waits for 40 s for the torsional nystagmus fastphase responses. It was supposed that the direction of the
nystagmus could differentiate between posterior and superior
benign positional paroxysmal vertigo but, even with this method,
23%of the cases described by Herdman et al.3 remained obscure.
After the test, the patient returns to the sitting position. The test is
repeated as a mirror image to the other side. The theory on the

Correspondence: Tapani Rahko MD, Department of Otorhinolaryngology, Tampere University Hospital, Tampere 33521, Finland
(e-mail: tapani.rahko@tays.fi).

392

BPPV-HC BPPV-PC BPPV-SC BPPV-SC test

BPPV-SC

background of positional vertigo was first presented by Schuknecht4 1969 as cupulolithiasis, the mass of mineral crystals
affecting the cupular cells.
The treatment manoeuvres were described by Epley5 or
Semont et al.6 In Epleys treatment, the patient sits on the
examination bed and the head is lowered to the side of lesion
over the rim hanging 308 rotated to the lesion side by 458. The
position is kept for at least 30 s or until nystagmus is absent.
The head is then rotated to the opposite side by 458 and the
position is held for another 30 s. Thereafter, further rotation
until the head is 458 from the vertical and toward the floor for
12 min. Even longer times have been suggested. The patient
is then elevated to the sitting position.
In the Semont treatment, the patient is lying with the lesion
ear-down. The head is rotated upwards by 458 and the
examiner waits until the nystamus has stopped. The position
is held for 2 or 3 min. Then the patient is swung to the opposite
side holding the head and neck with two hands in position. The
position is kept for 5 min. Then the patient is elevated slowly
to normal position. According to Semont the patient is asked
to keep the head vertical for 48 h.
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Benign paroxysmal positional vertigo 393

McClure7 in 1985 presented the description of benign

paroxysmal positional vertigo, which would be the result of
horizontal canal canalolithiasis. This idea was supported by
the description of the clinical disease by Pagnini et al.8 (1989),
Baloh et al.9 (1993) and Lempert & Tiel-Wilck10 (1996). The
typical description of the disease was the direction-changing
nystagmus according to the position of the patient. The
geotrophic nystagmus is seen as a sign of benign positional
vertigo of the horizontal canal. This was mainly geotropic
and stronger on the affected side. The latency was short.8
The direction of the stronger nystagmus on the supposed
affected side could change direction. The typical phenomenon was the lack of adaptation of the nystagmus in repeated
tests.11
As a pathogenesis, the canalolithiasis theory is mostly
favoured. The head movement stimulates the movement of
the mass of otocones and generates the flow of endolymph in
an ampullopetal or fugal direction. The inversion of the
nystagmus from geotrophic to apogeotrophic would then
happen when gravity would induce the return of the otoconial
mass back in the canal and the flow would be ampullofugal.8
As the basis to the lack of adaptation of the nystagmus,
Steddin & Brandt12 suggested the ostium to the horizontal
canal to be funnel-like on the utricular side. This would
prevent the movement of the otocones or other debris and
it would not leave the canal.
When testing for BPPV-HC, geotrophic or apogeotrophic
nystagmus is recorded with electronystagmography or Frenzel
glasses. This is performed with the patient lying supine and
the head moved to both sides.7
A more sensitive method for benign positional vertigo of
the horizontal canal is the Rahko WRW test.13 In this test, the
patient walks forward and rotates briskly on the rotation
direction foot and returns back. The examiner follows the
reactions of the patient. When the patient rotates, he may not
be able to maintain balance, because walking makes it difficult. This is seen, for example, as staggering or some incomplete or compensatory movement. The acceleration in the
horizontal canal in the rotation direction is stronger than in
earlier positional testing and thus the Rahko WRW test is more
sensitive.
Benign paroxysmal positional vertigo involving the horizontal canal (BPPV-HC) is treated with the Lempert manoeuvre.10 The patient is lying supine. He rotates the head to the
healthy side by 908, then turns to the prone position, the head
is turned nose-down and again the head is turned with the
affected ear down, each phase 30 s. Finally, the patient sits up.
The treatment results have been good.14
With regard to superior canal positional vertigo, Herdman
et al.3 presented in 77 patients, nine patients with superior
(anterior) canal involvement, but in 18 patients the lesion site
was impossible to locate as superior or posterior vestibular
canal. If a quarter of the patients cannot be defined, Hallpikes
# 2002 Blackwell Science Ltd, Clinical Otolaryngology, 27, 392395

test can hardly be regarded as a reliable test in superior canal

positional vertigo.
Honrubia et al.,15 using an infrared video camera and
Frenzels glasses, found four patients with superior (anterior)
canal positional vertigo out of a total of 292 BPPV patients.
Their treatment was a reverse Epley manoeuvre and the
success rate was 50%.
Anyhow, all patients with positional vertigo of the posterior
and/or horizontal canal in our Department did not obtain an
excellent result with Epley, Semont or/and Lempert manoeuvres, although the result was considered good in respect
to the posterior and horizontal canal.
Thus, because of inconstant results by other methods, a test
for superior canal positional vertigo and a manoeuvre for its
treatment was created by the author in May 1999. The results
of these are presented.

Materials and methods

The material consists of patients with benign paroxysmal
positional vertigo of the superior canal; 43 women and 14
men, mean age 49 years, range 2575 years. They were tested
and treated by the author between May 1999 and June 2000 in
The Department of Audiology and Otoneurology, Clinic of
Otolaryngology, Tampere University Hospital. The initial
material consisted of 305 patients, who were treated for
BPPV-HC and BPPV-PC during that period.
All underwent Hallpike and WRW positional vertigo tests.
The necessary treatment manoeuvres were performed. When
the posterior and horizontal canals were free of otoconia, it
was possible to test for the superior canal without the interference of the other canals.
To test for the free otoconia in the superior canal, the patients
were instructed to bow forward 608 and straighten back with
closed eyes quickly. The observer recorded the possible movement of the patient sideways during straightening.
Because the Epley and Lempert manoeuvres are performed
earlier, the otoconia, if present, move in the affected superior
canal and produce a response. The balance system response of
the body is seen as moving sideways to the affected side.
In the case of a positive test result, the treatment manoeuvre
is as follows: the patient lies on the healthy side, the head is
tilted downwards 458, then horizontally, upwards 458 for 30 s
each, and finally the patient sits up and stays there well
supported for at least 3 min. During the course of the manoeuvre, gravity pulls the otoconia downwards in the superior
canal and finally drops them into the utricle. Thus, the
disturbing paroxysmal superior canal stimulation disappears.
After this manoeuvre, the test is repeated to register the
possible effects of the manoeuvre. The sideways movement
disappears if the treatment is successful.
The patients are advised to perform the treatments at home
for a week twice daily, and then again if the symptoms

394 T. Rahko

reappear. An illustration on the movement schedule is given to

the patients.
The patients were called to follow-up visit after 34 weeks,
re-examined and tested.
In total, 20 healthy adults with no history of vertigo served
as control material.

Results
After the Lempert and Epley manoeuvres, the patients in this
study showed a tendency to move sideways in the superior
canal test. The test was performed twice. The intensity of the
movement varied. In 37 cases, the lesion site was the right
superior canal, in the rest the left. The positive test response
was mostly on the same side as the horizontal canal lesion, in
two patients on the opposite side.
The manoeuvre was performed as described above. When
sitting up typically after 24 s the patients experienced vertigo. It lasted a few seconds. The patient sat well supported for
3 min to allow the balance to stabilize. When the superior
canal test was repeated after this, the sideways movement had
disappeared.
As for other symptoms, 25 patients reported on motion
sickness for more than 10 years, and 27 reported acrophobia.
When the patients came to follow-up visit, these symptoms
had disappeared. All the patients had neck tension of varying
degrees before the treatments of different vestibular canals.
The neck tension was relieved when the last manoeuvre was
performed. This happened after sitting up from 24 min. The
head felt lighter according to the patients as well as the gaze
was accurate in head movements.
In the follow-up visit, one patient had developed symptoms
to the opposite side superior canal; 53 patients were symptomfree and three patients had benign positional vertigo of the
superior canal in the follow-up visit but, when the superior
canal manoeuvre was performed, they became symptomless.
They had not performed the manoeuvre at home.
Not one of the 20 healthy control subjects was positive in
this test.

Discussion
The test presented in this paper was constructed to analyse the
role of the superior canal in BPPV. It was apparent that when
the posterior and horizontal canals were treated and patients
still had symptoms, the superior canal should be tested somehow to clarify its role in BPPV.
When the patient in the superior canal test straightens up
briskly from the bowing forward position, the otoconia in the
superior canal, if present, produce a stimulation to cupula
cells. This stimulation causes the movement sideways to the
affected side, because there is no good balance model to
compensate the random superior canal stimulus. Because the

eyes of the patient are closed during straightening up, visual

control cannot help to maintain balance.
The superior canal canalolithiasis treatment manoeuvre is
very simple, but has an effect on the superior canal because the
other canals have been treated.
After the Epley and Lempert manoeuvres, the patient must
walk and move his head for half a minute to eliminate the
earlier balance compensation for the other vestibular canals. If
the superior canal test is made immediately, these compensation mechanisms affect the superior canal test result.
After the treatment manoeuvre, the sideways movement of
the patient was not seen in the repeated superior canal test.
This ensured that the effect of the treatment was real and its
focus was the superior canal.
The patients had subjectively better control of their body;
the swaying and dizziness were absent. When we look at the
age distribution, even elderly patients benefitted from this
manoeuvre.
The superior canal test described in this study is easier to
perform than the method described by Honrubia et al.15 and it
gives a focused approach on the anterior canal after the
elimination of the effect of other canals. Because the superior
canal test presented in this article has larger trajectory and
speed, it produces greater impact to the cells in the superior
canal. This explains its greater sensitivity.
The patients walked typically using visual fixation some
metres in front of them either continuously or intermittently. It
was seen even in the test situation. When the vestibular system
produced inconsistent information, the enhanced visual fixation helped the patients to maintain balance. After treatment
the gait of the patients returned to normal.
Increased neck tension in connection with vertigo is often a
consequence reaction.16 The patient tightens his shoulder and
neck muscles to maintain balance with muscle control. When
the reason for the imbalance is absent, the tension of these
muscles is not needed. When the neck muscle tension
diminishes after the manoeuvres, the head feels lighter.
The disappearance of motion sickness in this patient group
is a logical consequence of the treatment. When the vestibular
canals after the treatments react normally to the movements of
the body, there is no confusion in the balance system.
There is so far no other study of benign positional vertigo,
where canalolithiasis of all three vestibular canals of the
patients are treated.
The disappearance of acrophobia is a real phenomenon in
this material, but the background is open. One possibility is
presented by Brandt17 but, among my patients, 27 with
acrophobia and 25 with motion sickness, not one had medical
history of psychiatric disease.
The test and manoeuvre described above are logical and
give clear and immediate results. The tests and treatments
must be performed in the order described above, otherwise the
last test and manoeuvre do not work.
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Benign paroxysmal positional vertigo 395

It must be emphasized that the scale of the responses of the

patients vary according to age, co-ordination capacity, training, etc. as in all balance tests. Thus, as a clinical method, it
presumes training by the physician.

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