2014 Vol.9 No.
JOURNAL OF
OTOLOGY
BENIGN PAROXYSMAL POSITIONAL VERTIGO
Johan Bergenius 1, ZHANG Qing 2, DUAN Maoli 2
One of the most common causes of vertigo is Benign
Paroxysmal Positional Vertigo (BPPV), a sensation of
spinning that is caused by a sudden change in head posi-
tion. This type of vertigo was first described by Robert
Barany in the early 1920s [1]. He suggested that BPPV
was caused by abnormal otoliths, also called statoconi-
um or otoconius, a structure in the saccule or utricle in
the vestibular sensory organ of vertebrates. For diagnos-
ing BPPV, Dix and Hallpike developed a test that specifi-
cally elicited nystagmus and vertigo similar to that in BP-
PV patients (the Dix-Hallpike test, DHT1952) [2].
A theory to explain the mechanisms behind the posi-
tioning manoeuvre which evoked this kind of vertigo
and nystagmus was proposed by Schuknecht in 1962 [3].
He found basophilic material on the cupula of the poste-
rior semicircular canal in BPPV patients. According to
his theory, this material made the cupula heavier than the
surrounding endolymph, which consequently makes the
cupula sensitive to gravity.This theory, however, could
not explain the transient symptom of vertigo as a heavy
cupula in the provocating position would remain deviat-
ed as long as the head position is sustained. This would
cause a persistent vertigo and nystagmus.
A new explanation for the transient vertigo in patients
BPPV was put forward by Hall and co-workers and Ep-
ley [4-7]. They suggested that BPPV was caused by parti-
cles floating around in the endolymph. As they are heavi-
er than the surrounding endolymph they are subject to
the influence of gravity. Because of fast head move-
ments or long lasting positions of the head (at sleep)
they will precipitate and assemble in the semicircular ca-
nals (SCC). As the patient makes a head movement in a
direction on the plane of the canal the particles take new
positions. When the number of particles has reached a
Affiliation:
1
Department of Neurotology and Audiology, Department of
Otolaryngology Head and Neck, Department of Clinical Sci-
ence,Intervention and Technology,Karolinska University Hos-
pital in Solna, 17176, Stockholm, Sweden
2
Department of Otolaryngology Head and Neck Surgery,
Second Affiliated Hospital, Xian Jiaotong University, Shan-
nxi, China.
1
critical level they will move like an avalanche inducing
an endolymph movement and a cupula deflection, which
in turn gives rise to vertigo and nystagmus.
Epidemiology
BPPV accounts for 8% of the subjects with moderate
or severe dizziness/vertigo [8]. It may be present in child-
hood but increases with age. The lifetime prevalence is
estimated to be 2%. Its reported that the one-year preva-
lence is 0.5% in 18-39 years old and 3.4% in people over
60-years of age [8]. In a Swedish community sample the
one year prevalence was 5% [9].
BPPV is a recurrent disorder and around two thirds of
the patients have suffered from BPPV during the past 12
months. The average recurrence rate is around 50%. BP-
PV is more common in women than men; and the ratio
of women to man population is 2:1 [8,10].
The lifetime incident of BPPV is almost 10% by the age
of 80 years [11]. Bilateral benign paroxysmal positioning
vertigo is rather rare and accounts for 6% to 26%. Twen-
ty percent patients with BPPV show a multiple position-
al nystagmus indicating a multi-canal BPPV [12].
Ethiology
In the majority of patients, the cause of BPPV is un-
known. Possible causes include head trauma [13,14] or after
viral neuro labyrinthitis [15, 16].There is an increased inci-
dence of BPPV in patients with Menieres disease and or
migraine [17,18].Other causes are vestibular lesions in com-
bination with sudden deafness, aerotitis, blood diseases
(polycythemia), hypertension, hyperlipidaemia and den-
tal surgery and drilling [19]. Occasionally BPPV can occur
Corresponding authors:
DUAN Maoli, Email: Maoli.Duan@ki.se
 2014 Vol.9 No.1
after otitis media or during serous otitis media and after
stapedectomy [12].
Pathophysiology
Particles within the semicircular canal observed during
surgical treatment seem related to BPPV [20,21]. They are
thought to be otoconias (canaliths) which have become
dislodged from the utricular or saccular maculae. Abnor-
mal results have been found in tests of the otolith func-
tion, such as vestibular evoked myogenic potentials
(VEMP) (saccular test) and tests of the subjective visual
horizontal or vertical (utricular test) [22-24]. It has also been
suggested that the particles are waste products which not
have been removed from the endolymphatic system. In
the following text the particles will be named canaliths.
Different types of BPPV
There are essentially two kinds of BPPV; canalolithia-
sis and cupulolithiasis. In canalolithiasis the canaliths are
freely moving within the SCC. In these cases, the vertigo
and nystagmus is transient as it is caused by the move-
ment of canaliths when they take a new position in the
semicircular canal. In 60-80% of the patients the disorder
affects the posterior SCC. The lateral SCC accounts for
approximately 10-20% and the anterior SCC for 1-2 %.
In cupulolithiasis, the canaliths have become attached
to the cupula. As the cupula isloadedwith canaliths, it
has gained a higher specific weight than the surrounding
endolymph and is therefore more sensitive to gravity. As
long as the head is kept in a position where the gravity
influences the cupula the vertigo and nystagmus persists.
This condition usually affects the lateral SCC and occa-
sionally the posterior SCC.
BPPV from the vertical semicircular ca-
nal (canalithiasis)
Table 1
Typical features and diagnostic criteria for BPPV of the posterior SCC
Normal ocular smooth pursuit.
Absence of gaze nystagmus.
Absence of spontaneous vertical nystagmus.
Normal nystagmus suppression.
At Dix-Hallpike test, typical rotatory nystagmus with vertica
component.
Duration of nystagmus seldom more than 30 seconds.
Vertigo and nystagmus starts and stops at the same time.
When sitting up, opposite nystagmus than precipitated during
Dix-Hallpike test.
Repeated Dix-Hallpike manoeuvres reduce nystagmus and vertigo.
2
Diagnosis
The vertigo is typically of intense character and is pre-
cipitated by head movements in the sagittal or horizontal
plane that is in the plane of the affected SCC. In most
cases, there is an earlier history of similar symptoms.
The vertigo often starts in the morning when the subject
turns his or her head in order to get out of the bed. If the sub-
ject stops the head movement and puts the head on the pil-
low again the vertigo goes away. Sometimes the vertigo is
elicited as the subject goes to bed or turns his or her head
sideways in bed in order to reach a book or turn out the
light. Characteristically, the nystagmus in time parallels
the vertigo. Apart from vertigo and nystagmus there are no
concomitant auditory or neurologic symptoms.
The diagnosis of BPPV is made by Dix-Hallpike test.
With the patient sitting upright, the head of the patient is
turned 45 degrees sideways to the tested ear. The posteri-
or vertical SSC is in this way aligned with the gravita-
tional vertical and the largest distance achieved for sedi-
mentation of the canaliths within the posterior SCC is ob-
tained during the manoeuvre. The patient is without
great speed brought backwards so that the head is posi-
tioned under the horizontal plane, head hanging. During
the Dix-Hallpike test the plane of the posterior SCC of
the contralateral ear is perpendicular to the gravitational
vertical (aligned with the gravitational horizontal) so
each posterior SCC has to be tested individually.
When the head movement is completed, nystagmus and
vertigo is elicited simultaneously after a few seconds.
The provoked vertigo and nystagmus increase and then
resolve within a time period of not more than 30 seconds
from onset of nystagmus.
Character of nystagmus
Posterior BPPV: When the patient is submitted to the
Dix-Hallpike test, the canaliths in the posterior SCC
moves ampullofugally. The cupula deviates in the same
direction and this causes an excitatory response. This
gives rise to nystagmus with a vertical and rotatory com-
ponent. The vertical component is directed upwards, to-
wards the forehead of the patient. For the rotatory com-
ponent, the upper poles of the eyes are beating toward
the dependent ear. The nystagmus typically fatigues (a re-
duction in severity of nystagmus) when the maneuver is
repeated.
In case of difficulties to judge the rotatory or vertical
component, the separate parts can be augmented if the
patient directs his or her gaze laterally. In canalithiasis of
the posterior semicircular canal the rotatory component
will be more clearly displayed at lateral gaze towards the
undermost ear. The vertical up beating component is
more pronounced at gaze towards the upper most ears.
 2014 Vol.9 No.1

Anterior BPPV: During the Dix-Hallpike test the oto-
liths move ampullofugally in the anterior SCC.This
causes an ampullofugal deviation of the cupula. The ver-
tical component beats downwards, towards chin. The up-
per poles of the eyes are beating toward the dependent
ear. In canalithiasis of the anterior semicircular canal the
rotatory component will be more clearly displayed at lat-
eral gaze towards the uppermost ear. The vertical up
beating component is more pronounced at gaze towards
the undermost ear.
degrees to non-tested side (1).The turn of the head
should be maintained throughout the whole test proce-
dure. The patient is then moved quickly to a horizontal po-
sition so the affected ear is lowermost (2). This position is
held for approximately 30 seconds. In a second step the pa-
tient is brought quickly through the initial sitting position
to the contralateral side (3). After 30 seconds, the patient
is returned slowly to the sitting position (4).

Treatment

Posterior semicircular canal:Without specific treat-

ment the symptoms usually gradually diminish over a pe-
riod of two and four weeks. However when the patient
does not comply with the vertigo, a repositioning manoeu-
vre is advocated. Vestibular suppressant medications are
not effective as a definitive or primary treatment for BP-
PV.
A technique for a relocation of the particles from the
posterior SCC was designed by Semont (1988) [25] and
Epley (1992) [7]. Both models for treatment are based on
the same assumption that the particles can be moved Figure1 Epley's maneuvre. Using gravity force the particles are re-
positioned from the posterior semicircular canal to the utriculus
through the long arm of the SCC and be repositioned in-
through a series of head movements. For detailed information see
to the utriculus by using the gravity force. The Epley ma- text.
noeuvre is probably the most commonly used (figure 1).
After provocation by the Dix-Hallpike test the patients
head is hold in head hanging position for 20 to 30 sec-
onds or double the time for the duration of nystagmus
(2). From there the patients head is turned 90 degrees
to the other side (3). At the second step there is usually
no vertigo or dizziness. The patient should remain in
that position for about 1 minute. At the third step the
head is further turned so that the patient' head is nearly in
the facedown position the body usually has to move from
the supine position to a lateral decubitus position (4). In
this position the patient may experience vertigo and a
nystagmus with the same direction as elicited by the
Dix-Hallpike manoeuvre. This confirms that the particles
have moved in the expected direction within the posteri-
or SCC. The patient should remain in that position for
about 1 minute. At the fourth step the patient, without Figure2 Semontss maneuvre. Using gravity and centrifugal force
changing the turn of the head, is brought up to sitting po- the particles in the posterior part of the posterior semicircular canal
sition (5). It is advocated that the patient remains seated are moved into the utriculus.For detailed information see text.
for another two or three minutes because there may be ad- In 1980, Brandt and Daroff described repositioning ex-
ditional short spells of vertigo, possibly because of parti- ercises that consisted of rapid lateral head and trunk tilts
cles moving from the SCC to the utriculus. to promote a movement of the canaliths toward the utri-
The treatment method suggested by Epley requires a cle [26]. The patient starts in a sitting position and moves
head hanging position. In older patients or patients with quickly to the right-side lying position, with the head ro-
a sore neck the Semont manoeuvre can be recommended tated 45 degrees and facing upward.This position is
(figure 2). In the Semont repositioning manoeuvre the maintained for 30 seconds after the vertigo has ended.
patient is seated upright with his or her head turned 45 The patient then moves rapidly to a left-side lying posi-

3
 2014 Vol.9 No.1

tion, with the head rotated 45 degrees and facing up-
ward. Patients were advocated to repeat these maneuvers
three times a day for 2 weeks.
Anterior semicircular canal:The recommendations
for treatment of the anterior semicircular canal are ambigu-
ous. In some reports, Epleys repositioning manoeuvre is
recommended to start from the head hanging position with
the unaffected ear down. Others propose that the canaliths
can be migrated out of the canal by a rapid uprising in the
plane of the anterior semicircular canal from an extended
head hanging position acquired after a Dix-Hallpike ma-
noeuvre towards the unaffected ear[12].
Treatment outcome
The positive treatment result can often be recorded
during the ongoing consultation when a renewed Dix-Ha-
llpike test is performed or a couple of days later when
the patient in the evening can go to bed with the head
turned to the affected side without any discomfort. Be-
tween 60% and 90% of the patients with posterior BPPV
experience an immediate relief of vertigo. If residual
symptoms persist a second treatment is advocated.
Recurrence rate is about 80% within the first year af-
ter treatment but decreases over years. However, 50%
have new symptoms of BPPV within ten years. A recur-
rence is more common in women than in men.
For the Brandt -Daroff maneuver, the cure rate has
been reported to amount to 60 % at 3-month follow-up.
Recommendations after treatment
autonomic reactions.
Character of nystagmus
When the patient is in supine position and the head
turned sideways a strictly horizontal nystagmus is elicit-
ed with the fast phase directed to the undermost ear. This
occurs in both side positions. This nystagmus is called
geotropic. Usually it starts without latency as the patient
moves his or her head. The nystagmus is more intense
and with longer duration than in vertical BPPV. The
slightest movement of head may start the nystagmus.
The theory behind geotropic nystagmus is that there
are freely moving canaliths in the lateral semicircular ca-
nal. As a result of head movements in the plane of the lat-
eral SCC the movement of the canaliths causes a cupular
deflection. At head turn to either side in supine position
the canaliths move either towards the cupula or away
from the cupula depending on which side is affected. As
the nystagmus is elicited in both side positions it is some-
times difficult to judge which the affected ear is. Theoret-
ically, it is possible to judge the side by applying
Ewalds second law. This law states that ampullopetal
stimulation (canaliths move towards cupula=ampullope-
tal deviation of cupula) is stronger than ampullofugal
stimulation (canaliths move away from cupula=ampullof-
ugal deviation of cupula) in the lateral semicircular ca-
nal. When the patient is lying on the affected side the
canaliths will move towards the ampulla which results in
a more intense nystagmus than when the patients lays on
the unaffected side.

After treatment, the patient is usually advised not to Treatment

make extensive head movements forwards or backwards.
The patient is not recommended to sleep in horizontal Lateral BPPV is usually performed by means of a
position. These restrictions are usually recommended for barbeque rotationor forced prolonged position. The
the first and second night after treatment. However, re- barbeque rotation starts with the patient in supine posi-
cent studies found that these limitations do not affect the tion with head elevated 30 degrees from the horizontal
recurrence rate. plane. The manoeuvre consist of quickly turning the
head of the patient toward the unaffected side with a 90-,
BPPV from the horizontal semicircular ca- 180-, 270-, and 360-degree rotation performed in steps
nal (canalithiasis) of 90 degrees with 30-second intervals. These move-
ments allow the canaliths to move through the long arm
Diagnosis of the canal into the utricle.
In the third step from 180 degrees to 270 degrees the
Canalolithiasis in the horizontal semicircular canal patient shifts to prone position with the nose down. Pref-
usually causes more intense vertigo compared to canalo- erably the patient bends the head forwards so that the lat-
lithiasis in the vertical semicircular canal. The vertigo eral semicircular canal is a lined with the gravitational
starts when the patient bends his or her head forward or vertical. From the 360 degrees position the patient is
backwards or takes a supine position and moves the head brought upright.
to either side. These symptoms differ from the vertical Another way of treatment is performed in aforced
BPPV where the vertigo is elicited in only one side posi- prolong positionas the patient is recommended to lie
tion of the head. The vertigo is often very intense and re- on the non-effected ear for twelve consecutive hours.
peated positioning procedures will provoke unpleasant
4

Treatment outcome
The natural history of lateral canal BPPV is less well
defined than that of posterior canal BPPV. It is generally
agreed that lateral canal BPPV are prone to more rapid
spontaneous resolution than posterior canal BPPV. The
mean time between the onsets of vertigo in lateral canal
BPPV to spontaneous resolution is within 2-3 weeks. Af-
ter a barbecue repositioning maneuver 80-90 % of the pa-
tients become asymptomatic. 49 T. Imai, M. Ito and N.
Takeda et al., Natural course of the remission of vertigo
in patients with benign paroxysmal positional vertigo,
Neurology 64 (2005), pp. 920-921. View Record in Sco-
pus | Cited By in Scopus (13)
Cupulolithiasis in the lateral semicircular canal
By cupulolithiasis is meant that the canaliths have be-
come attached on the ampullar or canal side of the cupu-
la of the lateral semicircular canal. This makes the cupu-
la heavier than the surrounding endolymph. The cupula
becomes gravy dependent. When a patient with a right
sided cupulolithiasis turns his or her head towards right
in supine position the heavy cupula will persistently devi-
ate away from the ampulla which will cause a decreased
input from the right ear. This will result in a persistent
left beating apogeotropic nystagmus. When the patient is
lying down on his or her left side, the cupula in the right
lateral semicircular canal will deviate towards the ampul-
la. This causes an increased input from the right ear re-
sulting in a right beating apogeotropic nystagmus.
Diagnosis
Dizziness or vertigo is elicited when the patient makes
a horizontal or sagittal head movement. The vertigo pro-
voked by moving the head is usually not as intense as in
canalolithiasis of the lateral semicircular canal. The nys-
tagmus and vertigo persists as long as the head in kept in
lateral position.
Treatment of cupulolithiasis of lateral semicircu-
lar canal
There are no generally accepted principles for treating
cupulolithiasis.The most common treatment procedure is
to detach the particles from the cupula by shaking the
head vigorously in the plain of the lateral semicircular
canals or using a vibrator towards the mastoid bone.
The successful disconnection of the canaliths from the
cupula will show up as a conversion of apogeotropic nys-
tagmus to geotropic nystagmus. The freed canaliths are
then migrated out through the long arm of the lateral
5
2014 Vol.9 No.1
semicircular canal by a barbeque rotation towards the un-
affected ear and also. A variant of liberatory meneouvre
has been suggested by Gufoni and coworkers [26]has
shown a resolution of symptoms in a high percentage of
patients.
Differential diagnosis of BPPV
Vertical BPPV: Very few other diseases meet the sub-
jective and objective symptoms as indicated in table 1.
Patients with BPPV who are initial treatment failures
should be examined for central nervous system disor-
ders. In these cases accompanying signs of central neuro-
logic symptoms are usually at hand.
Horizontal BPPV: In normal subjects positional nys-
tagmus of geotropic or ageotropic type, is rare. If the pa-
tient experiences vertigo or dizziness or headache togeth-
er with positional nystagmus this is clearly pathological.
Positional nystagmus, mostly of the apogeotropic type,
may be a sign of a central nervous system lesion such as
vascular lesions in the cerebellum or inflammatory reac-
tions (MS). However, this is scarce if subjective and ob-
jective symptoms of central nervous system lesions are
absent. In patients with atrophic cerebellar diseases sac-
cadic pursuit eye movements, gaze nystagmus, spontane-
ous vertical nystagmus and impaired nystagmus suppres-
sion is likely to be at hand. In patients with brainstem le-
sions multiple signs of focal nervous disturbances are
highly likely as the nuclei and the pathways to the crani-
al nerves runs very closely to each other.
Geotropic nystagmus after ingestion of alcohol is
called positional alcohol nystagmus (PAN1). When the
alcohol level in blood reaches around 0.4 per mille a geo-
tropic persistent nystagmus will be displayed together
with vertigo when the head is turned to either side in su-
pine position. When blood concentration of alcohol
reaches zero per mille, the nystagmus is reversed and an
apogeotropic nystagmus can be recorded (PAN2).
The theory behind positional alcohol nystagmus is based
on the Buoyancy theory [28]. In the acute phase of alcohol
the concentration the cupula is lighter than the surround-
ing endolymph and when the head is turned to either
side the cupula of the under most ear deviates ampullope-
tally and the cupula on the contra lateral side deviates am-
pullofugally. This causes a nystagmus to the undermost
ear. In PAN2 the cupula is assumed to be heavier than the
surrounding endolymph (mimicking cupulolithiasis).
This causes a persistent apogeotropic nystagmus. It is
important to recognize the patients drinking habits when
a geotropic or apogeotropic nystagmus is recorded.
 2014 Vol.9 No.1

Table2 P-SCC posterior semicircular canal, A-SCC anterior [10] Brandt, Huppert D, Hecht J, Karch C, Strupp N: Benign Par-
semicircular canal, H-SCC Horisontal semicircular canal oxysmal positioning vertigo:A long term follow up (6 - 17 years)
of 125 patients. Acta Otolaryngol 2006 Feb:126 (2):160 - 3.
Nystagmus Paroxysmal Affected side latency [11] Neuhauser HK, von Brevern M, Radtke A, Lezius F, Feldma-
Torsional Affected ear nn M, Ziese T, Lempert T. Epidemiology of vestibular vertigo: a
P-SCC Yes 2-3 s neurotologic survey of the general population. Neurology.2005 Sep
upward down in HP pos.
27;65(6):898-904.
Torsional Unaffected ear [12] Bhattacharyya N et al.Clinical practice guideline: benign par-
A-SCC Yes 2-3 s
down ward down in HP pos. oxysmal positional vertigo.Otolaryngol Head Neck Surg. 2008.
139 (5 suppl 4): S47-81.
H-SCC Horizontal Most intense
Yes [13] Ghilardi PL, Casani A. Benign paroxysmal positional vertigo:
canalithiasis geotrop nystagmus
clinical aspects and medico-legal considerations. Acta Otorhinolar-
H-SCC Horizontal yngol Ital. 1989 Jan-Feb;9(1):79-85.
No Undecided
cupulolithiasis apogeotrop [14] Ahn SK, Jeon SY, Kim JP, Park JJ, Hur DG, Kim DW, Woo
SH, Kwon OJ, Kim JY. Clinical Characteristics and Treatment of
Benign Paroxysmal Positional Vertigo After Traumatic Brain Inju-
Table 3 ry. J Trauma. 2010 May 19. [Epub ahead of print]
[15] Mandal M, Santoro GP, Awrey J, Nuti D. Vestibular neuritis:
Ethiology to BPPV
recurrence and incidence of secondary benign paroxysmal posi-
Idiopathic tional vertigo.Acta Otolaryngol. 2010 May;130(5):565-7.
Vestibular neuritis [16] Harada K, Oda M, Yamamoto M, Nomura T, Ohbayashi S,
Kitsuda C. A clinical observation of benign paroxysmal positional
Head trauma
vertigo (BPPV) after vestibular neuronitis (VN). Acta Otolaryngol
Secretory otitis media Suppl. 1993;503:61-3.
[17] Gross EM, Ress BD, Viirre ES, Nelson JR, Harris JP. Intracta-
Sudden deafness
ble benign paroxysmal positional vertigo in patients with Me-
Aerotitis niere's disease. Laryngoscope. 2000 Apr;110(4):655-9.
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pert T. The interrelations of migraine, vertigo, and migrainous ver-
Blood diseases (polycythaemia)
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Hypertension Ishiyama A, Jacobson KM, Baloh RW. Migraine and benign posi-
Hyperlipidaemia tional vertigo. Ann Otol Rhinol Laryngol 2000;109:377-80.
[19] Lee NH, Ban JH, Lee KC, Kim SM. Benign paroxysmal posi-
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( J Vestib Res. 2010;20(5):391-8. doi: 10.3233/VES-2010-0370. (Received August 12 2013)