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Benign Paroxysmal Positional Vertigo

Author: John C Li, MD; Chief Editor: Arlen D Meyers, MD, MBA more...
Updated: May 06, 2016

Background

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frequently misdiagnosed, this figure may not be completely accurate and is probably
an underestimation. Since BPPV can occur concomitantly with other inner ear
diseases (for example, one patient may have both Mnire disease and BPPV at
once), statistical analysis may be skewed toward lower numbers.
BPPV was first described by Barany in 1921. The characteristic nystagmus and
vertigo associated with positioning changes were attributed at that time to the
otolithic organs. In 1952, Dix and Hallpike performed the provocative positional
testing named in their honor, shown below. They further defined classic nystagmus
and went on to localize the pathology to the proper ear during provocation.

The patient is placed in a sitting position with the head turned 45 towards the affected side
and then reclined past the supine position.

BPPV is a complex disorder to define; because an evolution has occurred in the

understanding of its pathophysiology, an evolution has also occurred in its definition.
As more interest is focused on BPPV, new variations of positional vertigo have been
discovered. What was previously grouped as BPPV is now subclassified by the
offending semicircular canal (SCC; ie, posterior superior SCC vs lateral SCC) and,
although controversial, further divided into canalithiasis and cupulolithiasis
(depending on its pathophysiology). (A literature review by Anagnostou et al
indicated that approximately 3% of all BPPV cases consist of the anterior canal
variant of the condition.[1] )

BPPV is defined as an abnormal sensation of motion that is elicited by certain critical

provocative positions. The provocative positions usually trigger specific eye
movements (ie, nystagmus). The character and direction of the nystagmus are
specific to the part of the inner ear affected and the pathophysiology.
Although some controversy exists regarding the 2 pathophysiologic mechanisms,
canalithiasis and cupulolithiasis, agreement is growing that the entities actually
coexist and account for different subspecies of BPPV. Canalithiasis (literally, "canal
rocks") is defined as the condition of particles residing in the canal portion of the
SCCs (in contradistinction to the ampullary portion). These densities are considered
to be free floating and mobile, causing vertigo by exerting a force. Conversely,
cupulolithiasis (literally, "cupula rocks") refers to densities adhered to the cupula of
the crista ampullaris. Cupulolith particles reside in the ampulla of the SCCs and are
not free floating.
Classic BPPV is the most common variety of BPPV. It involves the posterior SCC
and is characterized by the following:
Geotropic nystagmus with the problem ear down
Predominantly rotatory fast phase toward undermost ear
Latency (a few seconds)
Limited duration (< 20 s)
Reversal upon return to upright position
Response decline upon repetitive provocation

Because the type of BPPV is defined by the distinguishing type of nystagmus,

defining and explaining the characterizing nystagmus are also important.

Nystagmus is defined as involuntary eye movements usually triggered by inner ear

stimulation. It usually begins as a slow pursuit movement followed by a fast, rapid
resetting phase. Nystagmus is named by the direction of the fast phase. Thus,
nystagmus may be termed right beating, left beating, up-beating (collectively
horizontal), down-beating (vertical), or direction changing.

If the movements are not purely horizontal or vertical, the nystagmus may be
deemed rotational. In rotational nystagmus, the terminology becomes a bit more
loose or unconventional. Terms such as clockwise and counterclockwise seem
useful until discrepancies regarding point of view arise: clockwise to the patient is
counterclockwise to the observer. Right versus left terminology is poorly descriptive
because as the top half of the eye rotates right, the bottom half moves left.

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ground), then the nystagmus is geotropic. If the head is turned toward the left, then
geotropic nystagmus is a counterclockwise rotation. This term is particularly useful in
describing BPPV nystagmus because the word geotropic remains appropriate
whether the right or the left side is involved.
These 2 terms are useful only when the head is turned. If the patient is supine and
looking straight up, these terms cannot be used. Fortunately, the nystagmus
associated with BPPV usually is provoked with the head turned to one side. The
most accurate way to define nystagmus is by terming it clockwise or
counterclockwise from the patient's point of view.

Pathophysiology

To understand pathophysiology, an understanding of normal SCC anatomy and

physiology is necessary. Each inner ear contains 3 SCCs oriented in 3 perpendicular
planes; the SCCs mediate spatial orientation. Each canal consists of a tubular arm
(crura) that sprouts from a large barrellike compartment, much like the handle of a
coffee mug sprouts from the mug. Each of these arms has a dilated (ampullary) end
located near the top or front portion that houses the crista ampullaris (nerve
receptors).
The crista ampullaris has a sail-like tower, the cupula, that detects the flow of fluid
within the SCC. If a person turns suddenly to the right, the fluid within the right
horizontal canal lags behind, causing the cupula to be deflected left (toward the
ampulla, or ampullopetally). This deflection is translated into a nerve signal that
confirms the head is rotating to the right.
In simple terms, the cupula acts as a 3-way switch that, when pressed one way,
appropriately gives the body a sensation of motion. The middle or neutral position
reflects no motion. When the switch is moved the opposite way, the sensation of
motion is in the opposite direction.

Particles in the canal slow and even reverse the movement of the cupula switch and
create signals that are incongruous with the actual head movements. This mismatch
of sensory information results in the sensation of vertigo.

Cupulolithiasis theory

In 1962, Harold Schuknecht, MD, proposed the cupulolithiasis (heavy cupula) theory
as an explanation for BPPV. Via photomicrographs, he discovered basophilic
particles or densities that were adherent to the cupula. He postulated that the
posterior semicircular canal (PSC) was rendered sensitive to gravity by these
abnormal dense particles attached to or impinging upon the cupula.
This theory is analogous to the situation of a heavy object attached to the top of a
pole. The extra weight makes the pole unstable and thus harder to keep in the
neutral position. In fact, the pole is easily prone to "clunk" from one side to the other
depending on the direction it is tilted. Once the position is reached, the weight of the
particles keeps the cupula from springing back to neutral. This is reflected by the
persistent nystagmus and explains the dizziness when a patient is tilted backward.

Canalithiasis theory

In 1980, Epley published his theories regarding canalithiasis.[2] He thought that the
symptoms of BPPV were much more consistent with free-moving densities
(canaliths) in the posterior SCC rather than fixed densities attached to the cupula.
While the head is upright, the particles sit in the PSC at the most gravity-dependent
position. When the head is tilted back supine, the particles are rotated up
approximately 90 along the arc of the PSC. After a momentary (inertial) lag, gravity
pulls the particles down the arc. This causes the endolymph to flow away from the
ampulla and causes the cupula to be deflected. The cupular deflection produces
nystagmus. Reversal of the rotation (sitting back up) causes reversal of the cupular
deflection and thus dizziness with nystagmus beating in the opposite direction.

This model can be compared with pebbles inside a tire. As the tire is rolled, the
pebbles are picked up momentarily and then tumble down with gravity. This tumbling
triggers the nerve inappropriately and causes dizziness. Reversal of the rotation
obviously causes reversal of the flow and reversal of the dizziness direction.
Canal densities would better explain the delay (latency), transient nystagmus, and
reversal on return to upright than would cupular densities. This supports
canalithiasis rather than cupulolithiasis as the mechanism for classic BPPV.
The canalithiasis theory received further corroboration by Parnes and McClure in
1991 with the discovery of free densities in PSC at surgery.

Epidemiology
Frequency

United States

In one study, the age- and sex-adjusted prevalence of BPPV was 64 per 100,000.
Other studies corroborate this finding.

Race

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The sex distribution seems to indicate a predilection for women (64%).

Age

BPPV seems to have a predilection for the older population (average age, 51-57.2
y). It is rarely observed in individuals younger than 35 years without a history of
antecedent head trauma.
Clinical Presentation

Contributor Information and Disclosures

Author
John C Li, MD Private Practice in Otology and Neurotology; Medical Director, Balance Center
John C Li, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and
Neck Surgery, American Neurotology Society, American College of Surgeons, American Medical Association,
American Tinnitus Association, Florida Medical Association, North American Skull Base Society
Disclosure: Received consulting fee from Synthes Power Tools for consulting.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.

Peter S Roland, MD Professor, Department of Neurological Surgery, Professor and Chairman, Department of
Otolaryngology-Head and Neck Surgery, Director, Clinical Center for Auditory, Vestibular, and Facial Nerve
Disorders, Chief of Pediatric Otology, University of Texas Southwestern Medical Center; Chief of Pediatric
Otology, Childrens Medical Center of Dallas; President of Medical Staff, Parkland Memorial Hospital; Adjunct
Professor of Communicative Disorders, School of Behavioral and Brain Sciences, Chief of Medical Service,
Callier Center for Communicative Disorders, University of Texas School of Human Development
Peter S Roland, MD is a member of the following medical societies: Alpha Omega Alpha, American Auditory
Society, The Triological Society, North American Skull Base Society, Society of University Otolaryngologists-Head
and Neck Surgeons, American Neurotology Society, American Academy of Otolaryngic Allergy, American
Academy of Otolaryngology-Head and Neck Surgery, American Otological Society
Disclosure: Received honoraria from Alcon Labs for consulting; Received honoraria from Advanced Bionics for
board membership; Received honoraria from Cochlear Corp for board membership; Received travel grants from
Med El Corp for consulting.
Chief Editor
Arlen D Meyers, MD, MBA Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado
School of Medicine

Arlen D Meyers, MD, MBA is a member of the following medical societies: American Academy of Facial Plastic
and Reconstructive Surgery, American Academy of Otolaryngology-Head and Neck Surgery, American Head and
Neck Society
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for:
Cerescan;RxRevu;SymbiaAllergySolutions<br/>Received income in an amount equal to or greater than $250
from: Symbia<br/>Received from Allergy Solutions, Inc for board membership; Received honoraria from RxRevu
for chief medical editor; Received salary from Medvoy for founder and president; Received consulting fee from
Corvectra for senior medical advisor; Received ownership interest from Cerescan for consulting; Received
consulting fee from Essiahealth for advisor; Received consulting fee from Carespan for advisor; Received
consulting fee from Covidien for consulting.
Additional Contributors
Michael E Hoffer, MD Director, Spatial Orientation Center, Department of Otolaryngology, Naval Medical Center
of San Diego

Michael E Hoffer, MD is a member of the following medical societies: American Academy of Otolaryngology-Head
and Neck Surgery
Disclosure: Received royalty from American biloogical group for other.
Acknowledgements
John Epley, MD Director, Portland Otologic Clinic

John Epley, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and
Neck Surgery, American Medical Association, and Oregon Medical Association
Disclosure: Nothing to disclose.

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