Review Article
Primary Care
1590
·
November 18, 1999
The New England Journal of Medicine
B
ENIGN
P
AROXYSMAL
P
OSITIONAL
V
ERTIGO
J
OSEPH
M. F
URMAN
, M.D., P
H
.D.,
AND
S
TEPHEN
P. C
ASS
, M.D., M.P.H.
From the Department of Otolaryngology, University of Pittsburgh
School of Medicine, Pittsburgh (J.M.F.); and the Department of Otolaryn-
gology, University of Colorado Health Science Center, Denver (S.P.C.). Ad-
dress reprint requests to Dr. Furman at the Department of Otolaryngology,
University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, or at
furman@pitt.edu.
©1999, Massachusetts Medical Society.
ANY patients consult their doctors because
of dizziness or poor balance. Dizziness is
nonspecific; it may result from a disorder
of almost any organ system. Thus, the differential di-
agnosis for such patients is broad and should in-
clude medical, neurologic, and otologic causes. Ver-
tigo, which is the illusory sensation of motion of either
oneself or one’s surroundings, may be a component
of a patient’s dizziness.
Benign paroxysmal positional vertigo is one of the
most common types of vertigo.
1,2
This condition pre-
sents as dizziness or vertigo of sudden onset that is
provoked by certain changes in head position. The
most common provocative movements are rolling over
in bed, bending over, and looking upward. Although
benign paroxysmal positional vertigo has long been
recognized,
3,4
only more recently has its underlying
pathophysiology been clarified and substantiated.
5-7
Free-floating particulate matter within the posterior
semicircular canal of the vestibular labyrinth has been
observed in vivo in several patients with this disor-
der.
7,8
This finding led to the development of an in-
novative bedside treatment in which the free-floating
particles are moved from the posterior semicircular
canal to another location within the vestibular laby-
rinth.
9
Such maneuvers usually provide the patient
with immediate, and often long-lasting, relief from
vertigo.
9-11
Despite the seemingly simple and straightforward
pathophysiology and treatment of benign paroxysmal
positional vertigo, the diagnosis and treatment of this
condition can be challenging. Patients may present
with some but not all of the characteristic features of
M
typical benign paroxysmal positional vertigo, and there
are several variants. There are several types of maneu-
ver to treat the condition.
TERMINOLOGY
“Benign paroxysmal positional vertigo” is the term
most commonly used to describe a disease with a
characteristic clinical presentation believed to be
caused by free-floating particles within the posterior
semicircular canal. Vertigo is an important feature of
this condition. The word “benign” is used to distin-
guish between the types of vertigo caused by pe-
ripheral vestibular ailments and the types of vertigo
caused by intracranial neoplasms. In fact, however,
benign paroxysmal positional vertigo can be a severe,
disabling problem or a nagging nuisance responsible
for constant frustration. The term “paroxysmal” re-
flects an important and essential characteristic of the
disorder: the vertigo is episodic rather than persistent.
The use of the word “positional” implies a particular
association between a patient’s symptoms and his or
her head position with respect to gravity. However,
the symptoms associated with benign paroxysmal po-
sitional vertigo are elicited by a particular rotational
movement of the head rather than by the final posi-
tion of the head.
A characteristic feature of benign paroxysmal po-
sitional vertigo is an accompanying nystagmus. In the
most common form of the condition, the position-
ally provoked nystagmus contains both torsional and
vertical components. The nystagmus associated with
benign paroxysmal positional vertigo has led some
authors to use the term “benign paroxysmal position-
al nystagmus.”
12
PATHOGENESIS
Our understanding of the pathogenesis of benign
paroxysmal positional vertigo has improved dramat-
ically because of intraoperative observations of ag-
glomerated, free-floating particulate matter in the en-
dolymph of the posterior semicircular canal
7,8
(Fig.
1A). These observations substantiated what were pre-
viously only hypotheses that the movement of intra-
labyrinthine debris underlies most cases of the con-
dition.
5,6
Earlier writings, notably by Schuknecht,
13
postulated that debris adhering to the cupula, rather
than free-floating debris in the semicircular canal,
was responsible.
14
However, the action of free-float-
ing debris is the currently accepted pathophysiologic
mechanism for typical benign paroxysmal positional
vertigo. On the basis of electron-microscopical exam-
ination of particles obtained during surgery (Fig. 1B),
the free-floating debris has been postulated to arise
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PRIMARY CARE
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·
1591
from within the vestibular labyrinth. The particles
are most likely calcium carbonate crystals (otoliths)
that are normally attached to a membrane within the
utriculus, one of two gravity-sensitive structures in the
inner ear.
8
The exact mechanism by which free-floating debris
leads to paroxysmal vertigo and nystagmus is un-
known, but presumably the movement of the debris
causes alterations in endolymphatic pressure and thus
cupular deflection. Also, several studies have reported
postmortem data that indicate that a small percent-
age of patients without an antemortem diagnosis of
benign paroxysmal positional vertigo have debris in
the semicircular canals.
15-17
Despite this uncertainty, all the clinical manifesta-
tions of benign paroxysmal positional vertigo can be
explained by a transitory movement of agglomerat-
ed debris within the posterior semicircular canal.
5,6,18
Moreover, this pathophysiologic process is consis-
tent with the epidemiologic features of the condi-
tion, since head trauma is a frequent antecedent of
benign paroxysmal positional vertigo,
4
presumably
because of the dislocation of otoliths from the utricu-
lus, which then migrate to the posterior semicircular
canal, the most dependent structure in the vestibular
labyrinth.
CLINICAL MANIFESTATIONS
AND EVALUATION
Many patients report dizziness; they may also have
vertigo. In some disorders, including benign paroxys-
mal positional vertigo, vertigo is the most prominent
symptom. In other disorders, however, the vertigo is
less prominent, and dizziness, lightheadedness, and
dysequilibrium may better characterize the patients’
symptoms. Patients with dizziness may also have im-
paired balance. In some neurologic disorders, poor
balance may be present without dizziness. Table 1 lists
the most common causes of vertigo. Benign paroxys-
mal positional vertigo, Meniere’s disease, migraine,
vertebrobasilar insufficiency, and panic disorder are
associated with recurrent vertigo. They can be distin-
guished from one another by various characteristic
symptoms. Benign paroxysmal positional vertigo is
provoked by a change in position and lasts for sec-
onds. In Meniere’s disease, the vertigo occurs sponta-
neously, lasts for minutes to hours, and is accompanied
by unilateral hearing loss and tinnitus. Migraine-
associated vertigo is highly variable in duration and
usually precedes or is accompanied by headache. The
vertigo in vertebrobasilar insufficiency is associated
Figure 1.
Free-Floating Particles in Patients with Benign Paroxys-
mal Positional Vertigo.
Panel A shows debris (arrow) in the posterior semicircular canal
as observed intraoperatively (photograph courtesy of Dr. Lorne
Parnes). Panel B shows a scanning electron micrograph of an
intralabyrinthine particle, obtained during surgery. The debris
is thought to consist of calcium carbonate crystals that origi-
nate in the utriculus of the vestibular labyrinth. Reprinted from
Welling et al.,
8
with the permission of the publisher.
B
A
T
ABLE
1.
C
OMMON
C
AUSES
OF
V
ERTIGO
.
Otologic disorders
Benign paroxysmal positional vertigo
Meniere’s disease (endolymphatic hydrops)
Vestibular neuronitis (labyrinthitis)
Neurologic disorders
Migraine-associated dizziness
Vertebrobasilar insufficiency
Panic disorder
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1592
·
November 18, 1999
The New England Journal of Medicine
with brain-stem symptoms such as diplopia, dysar-
thria, and facial numbness. Vertigo is sometimes a
symptom of a panic attack. Vestibular neuronitis usu-
ally causes a single episode of vertigo that may last as
long as one or two days.
The most prominent symptom of benign paroxys-
mal positional vertigo is vertigo that occurs in bed
when a patient rolls into a lateral position.
3
Vertigo
also commonly occurs when the patient is gazing
upward (e.g., to place an object on a shelf ) or bend-
ing forward (e.g., to tie his or her shoes). The initial
onset of vertigo is often associated with nausea, with
or without vomiting. Because few patients have pre-
viously had sudden, unexpected vertigo of such in-
tensity, the symptoms may be frightening and may
lead to an immediate visit to the emergency room.
Typically, each episode of vertigo lasts only 10 to 20
seconds. The natural history has not been well char-
acterized, but it appears that benign paroxysmal po-
sitional vertigo is usually a self-limited disorder that
may be present for several weeks or even years, with
remissions and recurrences occurring unpredictably.
Most patients quickly learn to avoid the provocative
head movements. This avoidance of movements that
provoke vertigo is understandable but, ironically, tends
to prolong the course of the condition.
Some patients with benign paroxysmal positional
vertigo have a more widespread balance disorder.
4,19
A unilateral reduction in the function of the hori-
zontal semicircular canal is found in many patients.
In addition, the condition often follows head trauma
or vestibular neuronitis. In these patients, labyrin-
thine dysfunction usually affects more than just the
posterior semicircular canal, which is the portion of
the inner ear affected in benign paroxysmal position-
al vertigo. Thus, positionally provoked vertigo may
be part of a constellation of symptoms that includes
gait instability and dysequilibrium during rapid head
movements.
A diagnosis of benign paroxysmal positional verti-
go can be established definitively through the Dix–
Hallpike test
3
(sometimes erroneously called the Bá-
rány or Nylen–Bárány test), as illustrated in Figure 2.
The diagnostic criteria (Table 2) include the occur-
rence during the Dix–Hallpike test of a characteristic
mixed torsional and vertical nystagmus with the up-
per pole of the eye beating toward the dependent
ear and the vertical nystagmus beating toward the
forehead. The nystagmus typically begins after a 1-to-
2-second latency, lasts for 10 to 20 seconds, and is
associated with a sensation of rotational vertigo. Af-
ter the patient returns to the seated position, nys-
tagmus is again observed, but the direction of nystag-
mus is reversed. Although no longer recommended
as a diagnostic maneuver, because it may interfere with
the immediate bedside treatment of benign paroxys-
mal positional vertigo, repetition of the Dix–Hall-
pike test results in a reduction in the intensity of ver-
tigo and nystagmus. Observation of the patient’s eye
movements during the Dix–Hallpike test can be im-
proved through the use of specialized equipment to
reduce visual fixation. However, because visual sup-
pression of torsional nystagmus is minimal,
20
the nys-
tagmus typically associated with the disorder can, in
most cases, be observed directly.
A question that often arises when assessing a patient
with benign paroxysmal positional vertigo is whether
there is a need for further specialized evaluation. In
general, patients with this condition, especially patients
who respond favorably to bedside treatment, do not
require further specialized evaluation. However, pa-
tients with abnormal findings on neurologic examina-
tion, those with atypical positional nystagmus, those
who do not respond to bedside treatment, and those
whose dizziness or dysequilibrium cannot be attrib-
uted entirely to benign paroxysmal positional verti-
go should undergo further specialized evaluation.
21,22
EPIDEMIOLOGY
Benign paroxysmal positional vertigo has been said
to be the most commonly recognized vestibular dis-
order
1
; in one cohort of patients, the mean age at
onset was 54 years, with a range of 11 to 84 years.
4
Froehling et al. estimated that the incidence is as high
as 107 cases per 100,000 population per year.
23
How-
ever, these authors did not require that patients meet
strict diagnostic criteria. A study in Japan in which
patients were considered to have benign paroxysmal
positional vertigo only if they had nystagmus during
a Dix–Hallpike test found an incidence of 10.7 cases
per 100,000 per year.
24
In two other studies, the
percentages of patients who presented to a specialty
dizziness clinic who were found to have benign par-
oxysmal positional vertigo were in nearly complete
agreement, with 17 percent in one study
25
and 18 per-
cent in the other.
11
Common antecedents of the dis-
order include vestibular neuronitis and head trauma.
In our experience, there is an association with vestib-
ular neuronitis in 10 percent of patients and with head
trauma in 20 percent of patients. Similarly, Baloh et
al. reported that 15 percent of cases of benign par-
oxysmal positional vertigo followed neurolabyrinthi-
tis and 18 percent followed head trauma.
4
However,
in most patients with benign paroxysmal positional
vertigo, no antecedent association is found.
4
OTHER DISORDERS
Although the vast majority of patients who present
with paroxysmal positionally provoked vertigo asso-
ciated with transitory nystagmus have benign parox-
ysmal positional vertigo, a small fraction of patients
have other disorders. The most common, horizontal-
canal benign positional vertigo, is a disorder thought
to be caused by free-floating debris in the horizontal
rather than posterior semicircular canal.
26-29
Infrequently, patients with paroxysmal positional-
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PRIMARY CARE
Volume 341 Number 21
·
1593
Figure 2.
The Dix–Hallpike Test of a Patient with Benign Paroxysmal Positional Vertigo Affecting the Right Ear.
In Panel A, the examiner stands at the patient’s right side and rotates the patient’s head 45 degrees to the right to align the right
posterior semicircular canal with the sagittal plane of the body. In Panel B, the examiner moves the patient, whose eyes are open,
from the seated to the supine right-ear-down position and then extends the patient’s neck slightly so that the chin is pointed slightly
upward. The latency, duration, and direction of nystagmus, if present, and the latency and duration of vertigo, if present, should
be noted. The red arrows in the inset depict the direction of nystagmus in patients with typical benign paroxysmal positional ver-
tigo. The presumed location in the labyrinth of the free-floating debris thought to cause the disorder is also shown.
45°S
agitta
l body
plane
Utriculus
Posterior-canal
ampulla
Particles
Posterior
canal
Superior
canal
A
B
Posterior
canal
Superior
canal
Utriculus
Gravity
Gravity
Vantage
point
Vantage
point
Gravity
Gravity
Posterior-canal
ampulla
Particles
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1594
·
November 18, 1999
The New England Journal of Medicine
ly provoked symptoms have an underlying disorder
of the central nervous system rather than an ailment
of the peripheral vestibular system.
12,21,22,30
In rare in-
stances, patients with tumors of the posterior fossa
present with vertigo and nystagmus that are indistin-
guishable from those found in benign paroxysmal
positional vertigo.
22
TREATMENT
The treatment currently recommended for benign
paroxysmal positional vertigo is based on a bedside
maneuver introduced by Epley.
9
The purpose of the
maneuver, shown in Figure 3, is to relocate free-
floating debris from the posterior semicircular canal
into the vestibule of the vestibular labyrinth, where
it presumably adheres, thus no longer causing verti-
go on movement of the head. The maneuver takes
advantage of the fact that the free-floating debris has
a density that exceeds that of the surrounding endo-
lymph. As a result, the debris can be moved within
the labyrinth noninvasively through a sequence of
head orientations with respect to gravity. Severe neck
disease, a high-grade carotid stenosis, and unstable
heart disease are contraindications to the maneuver
shown in Figure 3. Two reports have described a
heels-over-head rotational chair designed to control
T
ABLE
2.
D
IAGNOSTIC
C
RITERIA
FOR
B
ENIGN
P
AROXYSMAL
P
OSITIONAL
V
ERTIGO
.
Vertigo associated with a characteristic mixed torsional and vertical nystag-
mus provoked by the Dix–Hallpike test
A latency (typically of 1 to 2 seconds) between the completion of the Dix–
Hallpike test and the onset of vertigo and nystagmus
Paroxysmal nature of the provoked vertigo and nystagmus (i.e., an increase
and then a decline over a period of 10 to 20 seconds)
Fatigability (i.e., a reduction in vertigo and nystagmus if the Dix–Hallpike
test is repeated)
Figure 3.
Bedside Maneuver for the Treatment of a Patient with
Benign Paroxysmal Positional Vertigo Affecting the Right Ear.
The presumed position of the debris within the labyrinth dur-
ing the maneuver is shown in each panel. The maneuver is a
three-step procedure. First, a Dix–Hallpike test is performed
with the patient’s head rotated 45 degrees toward the right ear
and the neck slightly extended with the chin pointed slightly
upward. This position results in the patient’s head hanging to
the right (Panel A). Once the vertigo and nystagmus provoked
by the Dix–Hallpike test cease, the patient’s head is rotated
about the rostral–caudal body axis until the left ear is down
(Panel B). Then the head and body are further rotated until the
head is face down (Panel C). The vertex of the head is kept tilted
downward throughout the rotation. The maneuver usually pro-
vokes brief vertigo. The patient should be kept in the final, face-
down position for about 10 to 15 seconds. With the head kept
turned toward the left shoulder, the patient is brought into the
seated position (Panel D). Once the patient is upright, the head
is tilted so that the chin is pointed slightly downward.
Utriculus
Posterior-
canal ampulla
Particles
A
B
C
D
Superior
canal
Utriculus
Posterior-canal
ampulla
Posterior
canal
Superior canal
Vantage
point
Posterior
canal
Superior
canal
Posterior canal
Superior canal
Gravity
Gravity
Gravity
Vantage
point
Vantage
point
Vantage
point
Particles
Gravity
Particles
Particles
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