Background

Benign positional vertigo (BPV) is the most common cause of vertigo. Vertigo is
an illusion of motion (an illusion is a misperception of a real stimulus) and
represents a disorder of the vestibular proprioceptive system.
BPV was first described by Adler in 1897 and then by Brny in 1922; however,
Dix and Hallpike did not coin the term benign paroxysmal positional vertigo until
1952. This terminology defined the characteristics of the vertigo and introduced the
classic provocative test that is still used today. Using positional testing, benign
positional vertigo can readily be diagnosed in the emergency department. Benign
positional vertigo is one of the few neurologic entities the emergency physician can
cure at the patient's bedside by performing a series of simple and safe headhanging maneuvers.
For further information, see Benign Positional Vertigo in the Neurology volume.
Pathophysiology
Benign positional vertigo (BPV) is caused by calcium carbonate particles called
otoliths (or otoconia) that are inappropriately displaced into the semicircular canals
of the vestibular labyrinth of the inner ear. These otoliths are normally attached to
hair cells on a membrane inside the utricle and saccule. Because the otoliths are
denser than the surrounding endolymph, changes in head movement vertically
causes the otoliths to tilt the hair cells, which triggers a nerve that send a signal to
the brain letting the brain know that the head is tilting up or down.
The utricle is connected to the 3 semicircular canals. The otoliths may become
displaced from the utricle by aging, head trauma, or labyrinthine disease. When
this occurs, the otoliths have the potential to enter the semicircular canals. When
they do, they almost always enter the posterior semicircular canal because this is
the most dependent (inferior) of the 3 canals.

Anatomy of the semicircular canals.

According to the canalolithiasis theory (the most widely accepted theory of the
pathophysiology of benign positional vertigo), the otoliths are free-floating within
the canal. Changing head position causes the otoliths to move through the canal.
Endolymph is dragged along with the movement of the otoliths, and this stimulates
the hair cells of the cupula of the affected semicircular canal, causing vertigo.
When the otoliths stop moving, the endolymph also stops moving and the hair cells
return to their baseline position, thus terminating the vertigo and nystagmus.
Reversing the head maneuver causes the particles to move in the opposite
direction, producing nystagmus in the same axis but reversed in direction of
rotation. The patient may describe that the room is now spinning in the opposite
direction. When repeating the head maneuvers, the otoliths tend to become
dispersed and thus are progressively less effective in producing the vertigo and
nystagmus (hence, the concept of fatigability).
Epidemiology
Frequency
United States
The incidence of benign positional vertigo (BPV) is 64 cases per 100,000
population per year (conservative estimate).[1]
International
One study in Japan found an incidence of 11 cases per 100,000 population per year,
but patients were counted only if examined by a subspecialist or at a referral center.
Mortality/Morbidity
The B of BPV stands for benign and designates that the cause of the vertigo is
peripheral to the brainstem and, hence, likely to be benign. However, BPV can be
severely incapacitating to the patient.
Sex
Women are affected twice as often as men.
Age

BPV, in general, is a disease of elderly persons, although onset can occur at any
age. Several large studies show an average age of onset in the mid 50s. Vertigo in
young patients is more likely to be caused by labyrinthitis (associated with hearing
loss) or vestibular neuronitis (normal hearing).
History
When asked about their dizziness, patients with benign positional vertigo (BPV)
characteristically describe that the room or world is spinning. However, other
descriptions, such as rocking, tilting, somersaulting, and the like, are also possible.
All that matters is that an illusion of motion is caused by a misperception of a
stimulus (the otoliths). Diagnosis of BPV is based on a characteristic history and a
positive Hallpike test.
Episodic vertigo may occur with the following head movements:
Rolling over in bed
Lying down
Sitting up
Leaning forward
Turning the head in a horizontal plane
Symptoms of BPV are usually worse in the morning (the otoliths are more likely to
clump together as the patient sleeps and exert a greater effect when the patient gets
up in the morning) and mitigate as the day progresses (the otoliths become more
dispersed with head movement).
Nausea is typically present (vomiting is less common).
A history of head trauma may be present, especially in young patients with BPV.
The head trauma may dislodge the otoliths off the hair cells within the utricle,
allowing them the opportunity to enter the semicircular canals.
Eliciting that the individual episodes of vertigo in BPV last for seconds at a time is
important. Patients may describe that they are having continuous vertigo, when in
reality, they are having repeated episodes (with each episode typically lasting

seconds or less than a minute). Patients with vestibular neuritis and labyrinthitis
have continuous vertigo, often for hours to days.
During the interview, if patient states that the "room is spinning" while the patient's
head is still and prior to any manipulative tests, then it is highly unlikely that the
patient has BPV because the vertigo in BPV lasts for seconds at a time and occurs
only after head movement.
Physical
In addition to the patient's history, a diagnosis of benign positional vertigo (BPV)
is confirmed by a positive Hallpike test (see video below).[2, 3]
Hallpike test. In this example, the right posterior semicircular canal is being tested.
Note that the head extends over the edge of the gurney. The thumb can be used to
help keep the eyelids open since noting the direction of the nystagmus is important.
In this test, the patient is placed in the head-hanging position after turning the head
to the side. After a short delay of a few seconds, nystagmus and reproduction of the
vertigo occurs and typically resolves within 30-60 seconds. The neurologic
examination is otherwise unremarkable.
Nystagmus (an involuntary rhythmic oscillation of the eyes) is described in terms
of the fast-phase component.
Classic nystagmus occurs when the patient's head is dependent and turned to the
affected side.
The nystagmus is torsional or rotatory. In the head-hanging position, the fast phase
should beat toward the forehead (upbeat) and in the same direction as the affected
side (ipsilateral). Although some describe the fast phase in terms of being
clockwise or counterclockwise, most experts avoid this terminology because it can
be unclear if the clock is being viewed from the patient's or physician's perspective.
Nystagmus usually occurs within 10 seconds after positioning but may present as
late as 40 seconds. Hence, if the history is classic, observe the patient for at least
40 seconds while he or she is in the head-hanging position during the Hallpike test.
Duration varies from a few seconds to a minute and parallels the sensation of
vertigo.

Response fatigues if the patient is repeatedly placed into the provoking position
(due to dispersion of the otoliths).
Note: If the patient has a classic history of BPV (after a short delay, the room spins,
but then revolves in 20-30 seconds, and then the rooms spins in the opposite
direction when he or she sits back up) but no nystagmus is seen during the Hallpike
test, most experts would agree to go ahead and treat the patient with the modified
Epley maneuver (see Treatment).
Nystagmus may be blocked by fixation suppression. Most emergency physicians
do not have access to Frenzel lenses or infrared nystagmography that specialists
use to prevent fixation suppression.
One study showed that treating such patients with the Epley maneuver is still
effective (despite the lack of nystagmus). Again, these patients must have a classic
history.
Perform the Hallpike test as follows (Caution: For patients with cervical
spondylosis, it may not be advisable to extend the neck. However, because having
the head dependent is important, the same effect can be achieved if the gurney is
placed in the Trendelenburg position for such patients).
First, warn the patient that symptoms of vertigo will likely be reproduced but will
resolve after a few seconds.
Seat the patient close enough to the end of the gurney so that when he or she lies
supine, the head can extend backward an additional 30-45.
Instruct the patient to keep his or her eyes open because you want to observe the
direction of the nystagmus. The examiner may need to use his thumb to hold the
eyelid open because patients may involuntarily close their eyes even when
instructed to keep them open.
To test the left posterior canal, follow these steps:
Turn the patient's head 45 to the left. This position orients the head such
that the left posterior semicircular canal is going to be in the same plane as
the upcoming head movement (next step). This is the most provocative way
to move the otoliths (if they are indeed in the posterior semicircular canal)
which will result in a positive test.

 With your hands on either side of the patient's head, lay the patient down
until the head is dependent (hanging over the edge of the gurney). Note that
this step does not need to be performed rapidly.
Check for reproduction of symptoms and nystagmus. In most cases, the fast
phase of the nystagmus should be upbeat (toward the forehead) and
ipsilateral (in this example, toward the patient's left).
Return the patient to the upright position. Nystagmus may be observed in the
opposite direction, and the patient may describe that the world is spinning in
the opposite direction.
To test the right posterior canal, repeat the Hallpike test with the head turned 45 to
the right side. In general, if the patient has BPV, only one side should test positive
during the Hallpike test. Although having bilateral posterior semicircular canal
BPV is possible, it is unlikely and should suggest horizontal canal involvement,
vestibular neuritis/labyrinthitis, or a central cause.
Note that almost all patients experience mild dizziness when being brought up
from the head-hanging position to the sitting position. It is important not to confuse
this dizziness (which is more near-syncope in character) with true vertigo.
If the patient's head cannot be extended over the edge of the gurney, 2 additional
options exist. The first is to place the patient in the Trendelenburg position if a
gurney that allows this position is available. The other alternative is to use the sidelying test; the patient sits with his or her legs over one side of the gurney. To test
the left posterior semicircular canal, turn the patient's head 90 to the opposite side
(in this case, the right side). Then, lay the patient on his or her left side. By turning
the patient's head to the right, the left posterior semicircular canal is aligned in the
same plane as the sideways movement. As in the Hallpike test, this will allow the
greatest chance for otoliths to move if they are indeed located in the posterior
semicircular canal.
The neurologic examination findings should be otherwise normal; if not, strongly
consider alternative diagnoses.
Causes
Several disorders affecting the peripheral vestibular system may precede the onset
of benign positional vertigo (BPV).

 Idiopathic (50-60%)
Infection (viral neuronitis)
Head trauma, especially in younger patients
Degeneration of the peripheral end organ
Surgical damage to the labyrinth
Laboratory Studies
No pathognomonic laboratory test for benign positional vertigo (BPV)
exists. Laboratory tests may be performed to rule out other pathology.
Imaging Studies
Currently, no imaging study can demonstrate the presence of otoliths.
Head CT scanning or MRI is indicated if the diagnosis is in doubt.
Other Tests
Although most patients with benign positional vertigo (BPV) have posterior
semicircular canal involvement, some patients have horizontal canal involvement.
This canal should be suspected if the patient has bilateral symptoms during the
Hallpike test. Use the Roll test to formally diagnose horizontal canal BPV, and use
the bar-b-que treatment to treat horizontal canal BPV.
Roll test
Have the patient lie in the supine position on the gurney. Unlike the Hallpike test,
the head does not need to hang over the edge of the gurney.
Turn the patient's head 90 to one side. The patient should experience a
reproduction of symptoms and the presence of horizontal nystagmus. The fast
phase should beat toward the earth (geotropic).
Now, turn the patient's head 180 (or 90 to the opposite side). The patient should
again experience a reproduction of symptoms and the presence of horizontal
nystagmus. The fast phase again beats toward the earth (note that it has changed

direction). This is known as direction-changing nystagmus (nystagmus that

changes direction based on turning the head) and is different from gaze-evoked
nystagmus (which is nystagmus that changes direction depending on where the
patient is looking, as in Dilantin toxicity).
Note that both sides will have nystagmus and a reproduction of symptoms, but one
side will be much more symptomatic (and demonstrate stronger nystagmus) than
the other side. This is considered the involved side.
A positive Roll test should be treated with the bar-b-que treatment (see Treatment
and the video below).
Bar-b-que maneuver. This maneuver is used to treat horizontal canal benign
positional vertigo. In this example, the right horizontal canal is being treated. Each
position should be held at least 20-30 seconds.
Head-thrust test
When the Epley maneuver does not work, it may be because it is being applied
inappropriately to patients with vestibular neuritis and labyrinthitis.
The head-thrust test is used to diagnose vestibular neuritis and labyrinthitis.
In this test, the patient is told to look at the examiner's nose. The examiner places
both his or her hands on the patient's head and rapidly turns it approximately 1015 to one side. If the vestibular apparatus is functioning properly, the patient will
be able to maintain his or her focus on the examiner's nose. If the vestibular
apparatus is not working properly, the patient's eyes will deviate to the side and
then quickly jerk back to view the examiner's nose. This jerking eye movement is
called a saccade and indicates a positive head-thrust test.
Procedures
The Hallpike test, along with the patient's history, confirms the diagnosis of
BPV. See Physical for details of this procedure.
The modified Epley maneuver is used to treat posterior canal BPV (see
Treatment as well as the video below for a demonstration).
Epley maneuver. In this example, the left posterior semicircular canal is
being treated. In this clip, the maneuvers are performed quickly. In a real

patient, each position should be held for at least 30 seconds or until

resolution of the nystagmus and vertigo.
Emergency Department Care
If the history and physical examination are typical, no further evaluation is
necessary, and the emergency physician may proceed with the modified Epley
maneuver described below (see the video below).
Epley maneuver. In this example, the left posterior semicircular canal is being
treated. In this clip, the maneuvers are performed quickly. In a real patient, each
position should be held for at least 30 seconds or until resolution of the nystagmus
and vertigo.
If the history and physical examination findings are atypical, consider other causes
of positional vertigo, which may occur with tumor or infarcts in the posterior fossa.
Contraindications to performing the Epley maneuver include ongoing CNS disease
(ie, stroke or transient ischemic attack [TIA]), unstable heart disease, severe neck
disease (eg, rheumatoid arthritis) or history of cervical spine fracture or surgery,
carotid bruit on examination indicating carotid stenosis, or body habitus preventing
performance of the maneuver.
Further information on diagnosis and treatment guidelines and recommendations
are available from the American Academy of Neurology and the American
Academy of Otolaryngology-Head and Neck Surgery Foundation.[2, 4]
The goal of the Epley maneuver is to move the otoliths out of the posterior
semicircular canal and back into the utricle where they belong.
The success rate of the Epley maneuver is very high (approximately 85-90%).
When it fails, it is the author's experience that it is being incorrectly applied to
patients with vestibular neuritis or labyrinthitis.
Epley maneuver, general guidelines
The head must be in the dependent (head-hanging) position for this maneuver to
work. If the patient does not tolerate this position, put the gurney in the
Trendelenburg position to simulate this head-hanging position.[5]

Maintain each position until the symptoms and nystagmus have disappeared or for
at least 30 seconds.
If the patient cannot tolerate the maneuver because of vomiting or severity of the
vertigo, premedicate with a vestibular sedative, such as 25 mg IV promethazine
(Phenergan).
Epley maneuver steps
Have the patient sit upright on the gurney with the head turned 45 to the affected
side (this was predetermined by using the Hallpike test). Make sure the patient is
sitting far enough back in the gurney so that the head will hang over the edge of the
gurney when the patient is laid back. Make sure the guardrail on the opposite side
has been lowered (the patient will eventually sit up so his or her legs overhang the
edge of the gurney). See the image below.

Epley maneuver. Move the patient back in the gurney

such that when he lies down, his or her head will hang over the edge of the gurney.
Emphasize to the patient to keep his or her eyes open during each position so that
nystagmus can be observed. Lower the guardrails of the gurney on the opposite
side from which the patient's head is turned.
Place your hands on either side of the patient's head and guide the patient down
with the head dependent (as in the Hallpike test). See the image below.

Epley maneuver. Turn the patient's head 45 to the side

that had the most prominent symptoms during the Hallpike test. In this example,
the patient's head is turned 45 to the left. With both hands holding the patient's

head, gently lay the patient down in the supine position with the head hanging over
the edge of the bed. Note: Each maneuver does not need to be performed rapidly.
The Epley maneuver is positional, not positioning.
Rotate the head 90 to the opposite side with the patient's face upward and be sure
to maintain the head-dependent position (head is hanging over the edge of the
gurney).
Ask the patient to roll onto his or her side while holding the head in this position
and then rotate the head so that it is facing downward (tell the patient to look to the
ground). See the images below.

Epley maneuver. Ask the patient to turn onto his or her

shoulder.
Epley maneuver. Guide the patient's head
down so that he or she is looking at the ground. Again, wait for at least 30 seconds.
Raise the patient to a sitting position while maintaining head rotation (This author
finds that sitting the patient up so that he or she is sitting with his or her legs
hanging over the edge of the gurney is easier. This is why the side guardrails need
to be lowered before the procedure is started). See the images below.

Epley maneuver. The patient's head needs to be

regripped again. Then, the patient needs to sit up with the legs hanging over the
side of the gurney (which is why the guardrails need to be lowered before the start

of the procedure).
sitting upright.

Epley maneuver. The patient is now

Simultaneously rotate the head to a central position and move it 45 forward.

The Semont maneuver (liberatory maneuver)
This maneuver is primarily used in Europe. Although it can be used to treat classic
posterior canal BPV, in the United States, it is usually reserved to treat the
cupulolithiasis form of BPV (where the otoliths are not free-floating but instead are
attached to the cupula of the posterior semicircular canal). Because of its somewhat
violent nature (and the fact that most patients with BPV are elderly), the author
does not advocate its use but includes it to be complete.
As in the side-lying test, the patient sits on the edge of the gurney with the head
turned opposite to the involved side. The patient is brought rapidly down onto his
or her side (this serves to dislodge the otoliths off the cupula). The patient is then
rapidly brought to the other side, maintaining the head in the same position (so the
patient's face will be facing the gurney). The patient is then brought to the original
sitting position. See the video below.
Semont maneuver. Generally reserved for the cupulolithiasis form of benign
positional vertigo, in which the otoliths are attached to the cupula of the
semicircular canal. This maneuver has to be performed rapidly to be effective, and

it is not recommended in elderly persons. In this example, the right posterior

semicircular canal is being treated.
Consultations
Neurologic consultation is indicated for cases of positional vertigo and nystagmus
that do not satisfy criteria for BPV. For example, downbeat nystagmus usually
indicates a central cause. Although downbeat nystagmus can also indicate anterior
canal involvement (which is benign), this is extremely rare.
Medication Summary
Medical treatment for benign positional vertigo (BPV) is generally ineffective but
may be used to lessen the symptoms.[4] The natural history of BPV is to resolve
with time as the otoliths eventually dissolve while in the semicircular canals.
The use of vestibular suppressants is based on the sensory conflict theory, in which
sensory input is compared from different systems, and if a conflict exists, then
nausea and vomiting result. Over time, habituation occurs. Several main
neurotransmitters mediate these functions: GABA, acetylcholine, and
histamine/serotonin.
Antihistaminic antiemetics
Class Summary
The antihistaminic antiemetics block the emetic response. For patients with severe
vertigo or vomiting, intravenous promethazine (Phenergan) is the drug of choice;
prochlorperazine (Compazine) is not very useful in this context. Meclizine is given
orally and does not work fast enough to be effective acutely. Most antiemetics have
anticholinergic activity as well.
View full drug information
Promethazine (Phenergan, Anergan, Prorex)

Antidopaminergic agent used to treat emesis. Blocks postsynaptic mesolimbic

dopaminergic receptors in the brain and reduces stimuli to brainstem reticular
system. Also has cross reactivity with the cholinergic receptors.

View full drug information

Meclizine (Antivert, Antrizine, Dramamine)

Decreases excitability of middle ear labyrinth and blocks conduction in middle ear
vestibular-cerebellar pathways. These effects are associated with relief of nausea
and vomiting.
Benzodiazepines
Class Summary
These agents block the GABA receptors and serve as the "brakes" to the system.
Although they can be used acutely in the ED, they are not recommended for longterm use because they interfere with the process of vestibular rehabilitation.
View full drug information
Lorazepam (Ativan)

Sedative hypnotic in benzodiazepine class that has short time to onset and
relatively long half-life. Depresses all levels of CNS, including limbic and reticular
formation, probably through increased action of GABA, a major inhibitory
neurotransmitter.
Anticholinergics
Class Summary
These agents block the conflict signal sites.
View full drug information
Scopolamine (Isopto, Scopace Tablet)

Blocks action of acetylcholine at parasympathetic sites in the smooth muscle,

secretory glands, and CNS. Antagonizes histamine and serotonin action.
Transdermal scopolamine may be most effective agent for motion sickness. Use in
the treatment of BPV is limited by slow onset of action.
View full drug information
Dimenhydrinate (Dimetabs, Dramamine)

Mixture of 1:1 salt consisting of 8-chlorotheophylline and diphenhydramine.

Believed to be useful, particularly in treatment of vertigo. Diminishes vestibular
stimulation and depresses labyrinthine function through central anticholinergic
effects. However, prolonged treatment may decrease rate of recovery of vestibular
injuries.
Sympathomimetic
Class Summary
These agents are useful in reversing soporific effects of vestibular sedatives.
View full drug information
Methylphenidate (Ritalin)

Piperidine derivative most commonly prescribed; efficacy has been

demonstrated in randomized, double-blind, dose-response, and placebocontrolled trials. Stimulates cerebral cortex and subcortical structuresFurther
Inpatient Care
Patients with persistent vomiting or intractable vertigo may require
admission for hydration and vestibular suppressant medication.
Surgical elimination of posterior canal function is restricted to rare cases of
long-standing refractory benign positional vertigo (BPV).

Further Outpatient Care

Head exercise therapy (positional exercises of Brandt and Daroff) that promotes
central accommodation may be helpful for BPV, although most patients have
difficulty tolerating these maneuvers. The patient can perform the following
therapy:
Sit on the edge of the bed near the middle, with legs hanging down.
Turn the head 45 to the right side. Quickly lie down on the left side, with
the head still turned, and touch the bed with a portion of the head behind the
ear.
Maintain this position and every subsequent position for about 30 seconds.
Sit up again.
Quickly lie down to the right side after turning head 45 toward the left side.
Sit up again.
Do 6-10 repetitions, 3 times per day.
If the patient becomes confused about the direction to turn his or her head,
tell the patient his or her nose should always point toward the ceiling.
Inpatient & Outpatient Medications
Meclizine is the most common outpatient medication. This medication is
indicated for vertigo but should not be given for other categories of dizziness
(near-syncope, dysequilibrium, or lightheadedness).
Deterrence/Prevention
Avoid provocative movements and limit activities.
Complications
No complications (eg, neck injury, vertebral dissection) other than vomiting
have been reported from the use of the Epley maneuver.

Prognosis
Benign positional vertigo (BPV) tends to resolve spontaneously after several
weeks or months. An Italian researcher removed the otoliths from an animal,
placed them in a Petri dish full of endolymph, and noted that the otoliths
dissolved in approximately 100 hours.
Patients may experience recurrences months or years later (if the otoliths got
out once, they can do it again).
Variants range from a single, short-lived episode to decades of vertigo with
only short remissions.
A study by Kim et al assessed patients who were discharged home from the
ED with a diagnosis of isolated dizziness or vertigo and determined that
stroke occurs in less than 1 in 500 patients within the first month.[6]
Cerebrovascular risk factors should be considered for individual patients.
Patient Education
For excellent patient education resources, visit eMedicine's Brain and
Nervous System Center. Also, see eMedicine's patient education article
Benign Positional Vertigo.