Positional Dizziness.9

Review Article
Positional Dizziness
Address correspondence to
Dr Terry D. Fife, Barrow
Neurological Institute, 240
West Thomas Road, Suite 301.
Phoenix, Arizona 85013, Terry D. Fife, MD, FAAN, FANS
tfife@email.arizona.edu.
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Products/Investigational Purpose: This article reviews the most common conditions that are caused by changes
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in head or body positions. Practical clinical methods to help distinguish vestibular from
* 2012, American Academy of nonvestibular and central from peripheral vestibular positional dizziness are discussed.
Neurology. This article also reviews the treatment methods of selected canal variants of benign
paroxysmal positional vertigo (BPPV).
Recent Findings: Two recent evidence-based guidelines have established canalith
repositioning maneuvers (Epley and Semont maneuvers) as safe and highly effective
in the treatment of posterior canal BPPV. Recent studies suggest the Gufoni and the
Lempert roll (barbecue) maneuvers are effective in treating lateral canal forms of
BPPV.
Summary: Most cases of positional vertigo are of peripheral vestibular origin and can
be effectively treated by simple positioning maneuvers. This article reviews the variants
of BPPV encountered in clinical practice, including mechanistic cause, differential diag-
nosis, prognosis, and treatment. Generous use of figures is intended to aid in under-
standing the most effective treatment maneuver techniques for the more common
forms of BPPV. Clinicians who can recognize the types of nystagmus associated with
the various canal types of BPPV can usually recognize CNS causes as distinct.
Continuum Lifelong Learning Neurol 2012;18(5):1060–1085.
EVALUATION NONVESTIBULAR POSITIONAL

When a patient reports positional DIZZINESS
dizziness, further clarification of the A number of conditions may cause pa-
history is needed to determine what is tients to report dizziness related to posi-
meant by the term dizziness and what tion changes. Among the most common
is meant by positional. Positional diz- causes of positional dizziness is ortho-
ziness refers to dizziness caused by static hypotension, which patients may
changes in head or body position. Po- notice when they arise from bed or from
sitional vertigo is a subset of positional a chair to stand. A momentary decre-
dizziness in which a sensation of spin- ment in cerebral perfusion pressure may
ning results from a change in head cause a near-faint sensation. Most peo-
Supplemental digital content:
Videos accompanying this ar-
position. Vertigo from any cause is aggra- ple instinctively try to sit, but when the
ticle are cited in the text as vated by head movement. Positional sensation occurs suddenly, it may culmi-
Supplemental Digital Content. vertigo, however, implies that spinning nate in a wilting fall or overt syncope. To
Videos may be accessed by
clicking on links provided in occurs with certain specific types of head confuse matters further, some patients,
the HTML, PDF, and iPad position changes. For example, a patient as in Case 4-1, have two separate kinds
versions of this article; the
URLs are provided in the print with dizziness that occurs upon standing of positional dizziness. Some patients
version. Video legends begin but is absent when lying flat most likely may also experience near faintness due
on page 1081.
does not have positional vertigo but to delayed orthostatic hypotension only
rather has postural dizziness caused sporadically.1 Because they do not feel
by orthostatic hypotension (Case 4-1). dizzy every time they stand, they have
Box 4-1 provides a glossary of terms en- not discerned a connection between
countered in this article. being upright and experiencing dizziness.
1060 www.aan.com/continuum October 2012
Copyright @ American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

KEY POINT
Case 4-1 h Positional vertigo is a

subset of positional
A 71-year-old man presented with several months of episodic spinning,
dizziness in which a
lightheadedness, and imbalance. The most recent episode occurred for
sensation of spinning
about 10 seconds when he got out of bed. He sat down and within
results from a change in
20 seconds felt normal again. In another episode, he was awakened
head position.
from sleep with a rotational feeling. At other times, he had a spinning
sensation for approximately 20 seconds while reaching into an upper
cabinet. His most recent spell was of lightheadedness while standing in
line at a grocery store. A cardiac workup discovered no cardiac
abnormalities. A brain MRI was normal. Laboratory studies, including
complete blood count, electrolytes, and liver enzymes, were normal.
Examination was normal except for paroxysmal positional upbeat and
clockwise cyclotorsional nystagmus with Dix-Hallpike positioning to the
left side. Canalith repositioning was performed. With repeat positioning,
all symptoms and nystagmus were gone. At follow-up 3 weeks later, he
reported continuing episodic dizziness occurring when standing or
walking. The Dix-Hallpike maneuver was normal with no vertigo or
nystagmus. A tilt table study demonstrated gradually declining blood
pressure with nadir of 75 mm Hg systolic at 20 minutes of head-up tilt that
was associated with lightheadedness. Heart rate and rhythm remained
normal throughout the period of declining blood pressure. He was treated
with an adjustment in his antihypertensive medications and low-dose
fludrocortisone with resolution of the lightheadedness.
Comment. This case illustrates how some patients do not recognize
that they are experiencing two distinct types of dizziness. This patient
reported both spinning and lightheadedness, but each occurred in a
different circumstance. Following treatment of the patient’s left-sided
benign paroxysmal positional vertigo (BPPV), he still had dizziness because
of delayed orthostatic hypotension that eluded detection by routine
orthostatic blood pressure measurements but was confirmed by a tilt
table study.
Tilt table testing can be helpful in iden- foramen of Monro, leading to positional
tifying these patients when routine and transient equilibrium problems on
postural vital signs are unrevealing.2 the basis of obstructive hydrocephalus.
Other causes of nonvestibular posi- Cervical dizziness is commonly men-
tional dizziness may include cerebral tioned as a possible concern. At present,
hypoperfusion due to cardiac valvular little scientific clarity is available regard-
stenosis, arrhythmia, and severe heart ing a putative mechanism and diagnostic
failure. Cerebrovascular insufficiency criteria for this entity.3
may infrequently produce such symp-
toms but more often causes TIAs with POSITIONAL VERTIGO
focal neurologic features. Rarely CSF Positional vertigo is a vestibular disorder
hemodynamic problems, such as caused by an inappropriate asymmetry
severe intracranial hypotension as originating either from the labyrinths
with CSF overshunting, may produce (eg, benign paroxysmal positional ver-
postural dizziness and headaches. tigo [BPPV]) or from dysfunctional in-
Rarer yet, CSF flow blockage from a tegration of CNS vestibular inputs (eg,
colloid cyst can periodically block the acute lateral medullary infarct).
Continuum Lifelong Learning Neurol 2012;18(5):1060–1085 www.aan.com/continuum 1061

BOX 4-1 Glossary of Terms
Benign paroxysmal positional vertigo (BPPV): An inner ear vertigo syndrome caused by calcium carbonate
material in a semicircular canal, presumably dislodged from the utricle, that inappropriately stimulates the
ampulla of one of the semicircular ducts by the effect of gravity during certain changes in head position.
Benign positional vertigo (BPV) is used synonymously with BPPV.
Benign paroxysmal vertigo of childhood: A condition unrelated to BPPV consisting of spontaneous attacks
of vertigo in children typically aged 4 to 10 years and generally considered to be an acephalgic
manifestation of migraine. Similar to benign recurrent vertigo.
Benign recurrent vertigo: A condition unrelated to BPPV that causes recurrent spontaneous episodes of vertigo
that are not positional. Most cases are attributable to migraine-associated vertigo.
Canalith (or canalolith) repositioning maneuver: Maneuver described by Epley that consists of a series
of positioning maneuvers intended to move dense calcium debris from within the long arm of the affected
semicircular canal back into the main vestibule; it particularly applies to the treatment of posterior canal
BPPV. The terms canalith repositioning treatment or procedure are often used interchangeably with
canalith repositioning maneuver.
Canalithiasis (or canalolithiasis): Calcium carbonate material free floating or loose in the semicircular duct (canal).
Cupula: The vestibular sense organ of the semicircular canals consisting of a gelatinous structure overlying
specialized hair cells. The nerve impulses generated relate to the degree of deflection of the cupula that
is affected by fluid (endolymph) movement in the semicircular canal. Each canal has its own cupula, and
the bulge in which the cupula resides is referred to as the ampulla.
Cupulolithiasis: Calcium carbonate material adherent to the cupula.
Dix-Hallpike maneuver: A specific maneuver that elicits paroxysmal positional nystagmus and vertigo in
BPPV of the posterior semicircular canal.
Epley maneuver(s): A series of positioning maneuvers originally called canalith repositioning by Epley that
later became known as the Epley maneuver or modified Epley maneuver (if a vibration device on the mastoid
was not used). This term is often used interchangeably with canalith repositioning maneuver or procedure.
Liberatory maneuver: Maneuver described by Semont in 1988 that entails position changes that treat
posterior canal BPPV by moving calcium particles from the posterior canal to the main vestibule.
Mastoid oscillation: Direct application of vibration stimulus to the mastoid process done with the intention
to ‘‘loosen up’’ and enhance movement of canalith material during canalith repositioning maneuvers.
Modified Epley maneuver: Any of the various alterations on the original maneuver described by Epley in 1992.
Nylen-Bárány maneuver: Often used to refer to the Dix-Hallpike maneuver, although the original
description entailed moving the head in differing positions to elicit nystagmus.
Otoconia: Calcium carbonate (calcite crystals) ranging from 5 2m to 25 2m in diameter that is part of the
otolithic membrane of the maculae.
Particle repositioning maneuver: Another name for the canalith repositioning maneuver.
Roll test: Supine head turning to elicit horizontal canal BPPV nystagmus; sometimes referred to as the
supine head-turn test or Lempert head-turn test.
Semicircular canal: One of three (anterior or superior, posterior or inferior, and lateral or horizontal) bony
channels within the labyrinth of the temporal bone. The membranous labyrinth inside this canal is the
semicircular duct. The term canal is often used instead of duct.
Semont maneuver: The maneuver originally called the liberatory maneuver by Semont in his original
publication but that later became called the Semont maneuver.
Utricle: Along with the saccule, a portion of the membranous labyrinth that generates and utilizes otoconia
in their respective maculae to detect linear acceleration. The utricle and saccule are often referred to as
the ‘‘otolith organs’’ of the inner ear.

KEY POINT
The history and examination are of- tagmus is a central abnormality and may h The history and
ten sufficient to distinguish CNS causes intensify with positioning or while su- examination are often
from peripheral vestibular causes of po- pine. Downbeat positional nystagmus sufficient to distinguish
sitional vertigo (Figure 4-1, Table 4-1). can occur with some central lesions but CNS causes from
Central causes of positional vertigo that may occasionally indicate recovery nys- peripheral vestibular
begin suddenly, such as stroke or hem- tagmus after very strong posterior canal causes of positional
orrhage, may be associated with sig- BPPV nystagmus or with the less com- vertigo.
nificant nausea and vomiting. Slowly monly encountered anterior canal var-
progressive or chronic central causes iant of BPPV.4
are often associated with very little
nausea. Nausea is common with most BENIGN PAROXYSMAL
peripheral forms of positional vertigo, POSITIONAL VERTIGO
depending on the severity and dura- Epidemiology
tion of the attack and the patient’s in- BPPV is the most common cause of epi-
nate susceptibility to motion sickness. sodic vertigo in adults, with a lifetime
Head movement in a specific plane prevalence of 2.4%.5 BPPV may occur
triggers peripheral forms of positional secondary to other inner ear conditions,
vertigo such as BPPV, whereas central such as head trauma, Ménière disease,
causes are often affected by less specific vestibular neuritis, and idiopathic sen-
head movements. sorineural hearing loss.6
The nystagmus of BPPV is charac- Head trauma causes BPPV when
terized by specific directional features sudden acceleration or deceleration cre-
(Table 4-2). If positional nystagmus is ates ruptures in segments of the macula.
uncharacteristic of BPPV, a central cause About 13% of patients with traumatic
should be strongly considered (Case 4-2). brain injury report positional vertigo, and
Spontaneous downbeat or upbeat nys- half have BPPV responsive to treatment.7
FIGURE 4-1 Algorithm for evaluating positional vertigo.

CRM = canalith repositioning maneuver; BPPV = benign paroxysmal positional vertigo.

TABLE 4-1 Features Distinguishing Central From Peripheral Causes

of Positional Vertigo
Feature Central Peripheral

Severe nausea + +++
Worse with nonspecific head movement ++ -
Evoked only by specific head movements + +++
(eg, Dix-Hallpike positioning, supine head roll)
Paroxysmal upbeat and torsional nystagmus with - +++
Dix-Hallpike maneuver
Paroxysmal downbeat nystagmus with Dix-Hallpike ++ +
maneuver
Paroxysmal horizontal directionYchanging nystagmus + ++
(geotropic or apogeotropic) evoked by supine
head turning
Persistent downbeat nystagmus in any position +++ -
Nystagmus diminishes (fatigues) with repeat - +++
positioning
Nystagmus resolves following positional - +++
treatment maneuver
BPPV resulting from trauma is usually ap- Labyrinthitis may cause BPPV by in-
parent within 1 week of trauma provided flammatory effects within or near the ma-
the patient has been moving and active cula or by compromise of the vascular
enough to elicit symptoms. BPPV is the supply that leads to dislodgement of
most common vestibular problem fol- otoliths that may fall from the utricular
lowing head trauma. space to that of one of the semicircular
TABLE 4-2 Comparison of Benign Paroxysmal Positional Vertigo by

Canal Type
Canal Estimated Provocative

Type Frequency Maneuver Nystagmus
a
Posterior 81%Y89% Dix-Hallpike Upbeat, torsional with
top pole beating
toward the down ear
Horizontal 8%Y17% Supine roll test Horizontal direction
(Pagnini-McClure) changing
Anterior 1%Y3% Dix-Hallpikea Downbeat,b torsional
(torsional element
not always visible)
a
In posterior canal benign paroxysmal positional vertigo (BPPV), nystagmus is provoked following
Dix-Hallpike positioning with the affected ear down. In anterior canal BPPV, nystagmus is provoked
following Dix-Hallpike positioning with the affected ear up.
b
The observation of downbeat positional nystagmus requires careful assessment to rule out brainstem
or cerebellar lesions.

Case 4-2
A 63-year-old man with a 1-year history of unsteadiness and dizziness
associated with quick head movements underwent Dix-Hallpike
positioning and was found to have nystagmus. He had been seeing a
physical therapist for canalith repositioning treatments. After 10 visits with
the therapist, he had not improved. He had no hearing loss or sensation
of spinning, but low-velocity downbeat spontaneous nystagmus was present.
With Dix-Hallpike positioning to both the right and left sides and in the
straight supine position, the downbeat nystagmus was more prominent.
The rapid movement during positioning produced momentary dizziness.
The remainder of the examination was normal, except for inability to walk
in tandem and mild horizontal gaze-evoked nystagmus.
Comment. This patient had central nystagmus that localizes to the
midline cerebellum or cervicomedullary junction. Further evaluation
confirmed sporadic cerebellar degeneration. The downbeat nystagmus
was accentuated by rapid movement backward. The nystagmus was
uncharacteristic of any form of BPPV because low-amplitude spontaneous
downbeat nystagmus, more prominent when supine, was present. This
case illustrates that the type and direction of nystagmus is important in
determining the cause of positional vertigo.
canals.8 Labyrinthine infarction can also from a different vessel, the posterior
lead to BPPV. The anterior vestibular vestibular artery (Case 4-3).
artery supplies the anterior and hori-
zontal semicircular canals and utricle, Pathophysiology
making it possible to have BPPV even Background anatomy. The vestibular
when no caloric responses occur on system consists of three semicircular
that side, because the posterior semi- canals, the saccule, and the utricle. The
circular canal receives its blood supply canals respond to angular acceleration
Case 4-3
A 52-year-old woman had the onset of vertigo with left-sided hearing loss
that persisted for several weeks but gradually abated. Two months later
she felt much better with only slight unsteadiness when turning her head
quickly. The hearing loss remained unchanged, however. Two months
after the onset of her vertigo, she awoke in the morning with a sensation
of severe spinning when she rolled over in bed to turn off her alarm clock.
This episode was brief, lasting only 30 seconds, but seemed to recur
periodically with bending or tilting her head backward. A brain MRI was
performed with normal results, and formal vestibular testing confirmed
absence of caloric vestibular responses from the left ear. Positional testing,
nevertheless, revealed prominent paroxysmal nystagmus following
Dix-Hallpike positioning to the left side.
Comment. Caloric and rotational chair vestibular tests assess only the
function of the horizontal semicircular canal. Since the posterior canal was
affected in this case, it is an example of selectively damaged vestibular
function. Not all parts of the vestibular apparatus are equally affected by
viral or ischemic events.9

KEY POINT
h Benign paroxysmal circular canal, is composed of special-
positional vertigo occurs ized hair cells that have a kinocilium
when some of the and stereocilia that are imbedded into
dense calcium and covered by a gelatinous material
carbonate crystals from (Figure 4-2). When the head moves in
the utricle dislodge and the plane of the canal, endolymph
fall into one of the moves, thereby deflecting the cupula
semicircular canals. and producing nerve excitation.
The saccule and utricle each con-
tain a macula composed of hair cell
sensory epithelium that is covered by
an extracellular mass of calcium car-
bonate crystals (otoconia) (Figure 4-3).
The otoconial mass consists of thou-
sands of otoconia about 10 Hm long,
held together by beaded filaments and
attached to a gelatinous matrix or so-
Crista ampullaris. The called globular substance that actually
FIGURE 4-2
crista ampullaris is the generates the calcium carbonate crys-
sensory epithelium
structure present in each semicircular tals (calcite). The macules of the saccule
canal. Turning the head causes the and utricle respond to linear acceler-
endolymph fluid within the semicircular
duct to move, which bends the cupula and ation and sustained head tilt relative to
the kinocilia and stereocilia of the hair gravity. Linear acceleration (including
cells. Bending in one direction is excitatory tilt of the head) causes the otoconial
and in the other direction is inhibitory.
mass to move and thereby bend the
kinocilium and stereocilia of the hair
or turning movements of the head. The cells, evoking a change in the firing rate
cupula, the motion sensor for the semi- through the vestibular nerve.
FIGURE 4-3 Macula. The macula is the motion transducer

for the utricle and saccule and consists of hair
cells. Each hair cell has a kinocilium and
stereocilia imbedded in the gelatinous matrix of the otolithic
membrane. The gelatinous material or ‘‘globular substance’’
actually generates the calcium carbonate crystals, referred to
as otoconia.

KEY POINTS
The principal matrix protein in the mechanism is the more common canal- h The movement of the
otoconial membrane is otoconin 90. ithiasis or the less common cupulolithia- calcium carbonate
The otoconial membrane is also com- sis, the resulting excitatory ampullary material stimulates the
posed of type II collagen, glycopro- nerve response is reflected in the eye semicircular canals,
teins, and proteoglycans that maintain movements producing the nystagmus. resulting in brief
the calcium crystal content and hold Abnormalities of the lumen of semi- episodes of positional
it to the sensory epithelium.10,11 As a circular ducts may also be a factor in vertigo.
result of the aging process, trauma, in- some refractory cases of BPPV. High- h The likelihood of
flammation, and perhaps other factors, resolution MRI of the membranous laby- developing benign
calcite crystals may dislodge from the rinth suggests that narrowing, stenosis, paroxysmal positional
otolithic membrane and sink into the or other luminal irregularities may occur vertigo may relate in
endolymph fluid. in some patients with intractable BPPV.13 part to the metabolic
Mechanism. BPPV occurs when some considerations and
of the dense calcium carbonate crystals Diagnosis and Treatment the elastic and adhesive
properties of the
from the utricle dislodge and fall into BPPV usually presents with brief attacks
gelatinous matrix that
one of the semicircular canals. The pos- of spinning vertigo lasting 10 to 30 sec-
generate and maintain
terior semicircular canal is affected in onds, often after turning in bed, getting otoconia within the
most cases of BPPV, most likely because up from the supine position, or bend- maculae.
the opening and positioning of the pos- ing or tilting the head. While vertigo is
h Canalithiasis refers
terior canal are in a gravity-dependent the typical sensation, minimally provo-
to mobile calcium
position. BPPV may also affect the other cative head movements can produce a carbonate debris that
semicircular canals but with lower prev- sensation of floating or disequilibrium, moves within the canal
alence. The movement of the calcium often more prominent in the mornings during certain head
carbonate material stimulates the semi- after getting up from sleep. Some pa- movements, resulting in
circular canals, resulting in brief epi- tients are able to determine that turning stimulation of cupula
sodes of positional vertigo. to one side seems to induce the symp- that in turn causes
The calcium sediment has been tom, and that is often the offending side. vertigo and nystagmus.
observed intraoperatively in patients Relatively few clues from the history
with a history of BPPV.12 BPPV may be can ascertain which canal is affected.
associated with a number of condi- Side-to-side rolling in bed that causes
tions, but most cases are idiopathic.
The likelihood of developing BPPV may
relate in part to the metabolic consid-
erations and the elastic and adhesive
properties of the gelatinous matrix that
generate and maintain otoconia within
the maculae.10
Canalithiasis refers to mobile calcium
carbonate debris that moves within the
canal during certain head movements,
resulting in stimulation of the cupula
that in turn causes vertigo and nystag-
mus related to the affected canal. This
mechanism is the most common and re-
ferred to as canalithiasis (Figure 4-4).
Cupulolithiasis occurs when the
calcium carbonate material becomes FIGURE 4-4 Theoretical mechanism of cupular
displacement in canalithiasis and
attached to the cupula itself, render- cupulolithiasis.
ing it sensitive to gravity. Whether the
Posterior canal. Two techniques

have been found to be effective to evoke
the symptoms and nystagmus in BPPV
related to the posterior canal: (1) the
Dix-Hallpike maneuver (Figure 4-5;
Supplemental Digital Content 4-1,
links.lww.com/CONT/A7) and (2) the
side-lying maneuver (Figure 4-6). Both
maneuvers cause movement of otoco-
nia through the posterior canal as the
patient is moved from the sitting to
the recumbent position. Each maneu-
ver is also the initial step in treat-
ment: the Dix-Hallpike maneuver for
canalith repositioning treatment (CRT)
and the side-lying test for the Semont
Dix-Hallpike maneuver to the right (A) and
maneuver.
FIGURE 4-5 The nystagmus for the posterior canal
left (B) sides to evoke nystagmus in posterior
canal benign paroxysmal positional vertigo. is characterized as a 3- to 10-second
latency, and a fast phase of nystagmus is
predominantly upbeat and torsional
KEY POINTS vertigo in both directions suggests with the top pole rotating toward the
h Cupulolithiasis occurs horizontal canal BPPV but can also downward ear (Table 4-2). This type of
when the calcium occur in patients with bilateral posterior nystagmus often fatigues with repeated
carbonate material
canal BPPV. Hence, the examination is positioning maneuvers. Although a
becomes attached to
the best way to determine which canal small horizontal component frequently
the cupula itself,
rendering it sensitive
or canals are affected. beats away from the downward ear, this
to gravity. The examination, clinical observa- element of the nystagmus is often
tions, and treatment differ for BPPV barely visible but may be seen on eye
h Benign paroxysmal
related to each of the canals and will movement recordings. Such recordings,
positional vertigo
usually presents with
be described separately. however, are rarely necessary.
brief attacks of spinning
vertigo lasting 10 to
30 seconds, often after
turning in bed, getting
up from the supine
position, or bending or
tilting the head.
h The nystagmus for the
posterior canal is
characterized as a
3- to 10 second-latency,
and a fast phase of
nystagmus is
predominantly upbeat
and torsional with the
top pole rotating
FIGURE 4-6 Side-lying test to the right (A) and left (B) sides to evoke nystagmus in posterior
toward the downward ear. canal benign paroxysmal positional vertigo.

Two bedside treatments for posterior maneuver or treatment, or Semont
canal BPPV are very effective and estab- maneuver or treatment) (Figure 4-8,
lished with high-quality evidence.14Y16 Table 4-4; Supplemental Digital Con-
One is the CRT17 (also called particle tent 4-3, links.lww.com/CONT/A9).
repositioning procedure or maneuver, The CRT is the most commonly used
Epley maneuver or procedure, or modi- method for treatment of posterior canal
fied Epley maneuver) (Figure 4-7, BPPV in the United States, whereas the
Table 4-3; Supplemental Digital Con- Semont maneuver is somewhat more
tent 4-2, links.lww.com/CONT/A8). commonly used in Western Europe.
The other is the Semont liberatory Each has minor advantages and disad-
maneuver18 (also called the liberatory vantages, but both are highly effective
FIGURE 4-7 Canalith repositioning maneuver for the right side.

KEY POINT
h Perhaps the TABLE 4-3 A Stepwise Method of Performing the Canalith
most common reason Repositioning Treatment (Epley Maneuver) of the
that the canalith Posterior Semicircular Canal
repositioning treatment
and Semont maneuver b Step 1 Seat the patient on a table positioned so he or she may be taken back to
do not work in patients the head-hanging position with the neck in slight extension. Stabilize the head
with an accurate with your hands and move the head 45- toward the side you will test. Move the
diagnosis is insufficient head, neck, and shoulders en bloc to avoid neck strain or forced hyperextension.
extension of the head. b Step 2 Observe the eyes; hold them open if necessary. Wait for all the
nystagmus to stop and then continue to observe the eyes about half as long
as the nystagmus lasted (usually about 10 seconds after it stops).
b Step 3 Keeping the head back with the neck slightly hyperextended, turn
the head about 90- toward the opposite side and wait 20 to 30 seconds.
Then roll the patient all the way onto his or her side and wait 10 to 15
seconds (step not shown in Figure 4-7).
b Step 4 From this side-lying position, turn the head to face the ground and
hold it there 10 to 15 seconds. No nystagmus should occur. If the patient
reports a little dizziness, it is usually a favorable sign that the particles are
moving and the treatment will be successful.
b Step 5 Keeping the head somewhat in the same position, have the patient sit
up and then straighten the head. Hold onto the patient for a moment because
some patients feel a sudden but very brief tilt when sitting up. This may be
caused by particles affecting the macula as they fall back in the vestibule.
b Repeat After waiting 30 seconds or so, repeat the maneuver. If no
paroxysmal nystagmus or symptom is present during Dix-Hallpike
positioning (steps 1 and 2), then complete the canalith repositioning
treatment. The rate of success is approximately 95%.
when done properly. Perhaps the most- not tilted back at least somewhat, the
common reason that these techniques otoconia may not move through the
do not work in patients with an accurate canal as intended. Severe kyphosis can
diagnosis is insufficient extension of the make the positioning of the head diffi-
head. Particularly for CRT, if the head is cult. In such cases, the maneuver can be
performed on a table in the Trendelen-
burg position or one can try the Semont
maneuver. There appears to be no
compelling indication for mastoid vibra-
tion to enhance effectiveness despite
some early reports that it was helpful or
even necessary.
The Semont maneuver may be diffi-
cult to perform in some older or obese
patients because of the quick sweeping
movement from one side to the other.
For some patients with back pain, how-
ever, the Semont maneuver may be
FIGURE 4-8 Semont liberatory maneuver for treatment of easier to tolerate. It may be used for
right benign paroxysmal positional vertigo.
BPPV of the posterior canal caused
by canalithiasis or for refractory cases

KEY POINTS
TABLE 4-4 Steps in Performing the Semont Liberatory Maneuver h Treatment of posterior
canal benign paroxysmal
b Step 1 Start with the patient sitting on a table or flat surface with head positional vertigo using
turned away from the affected side. either the canalith
repositioning treatment
b Step 2 Quickly put the patient into the side-lying position, toward the
or the Semont maneuver
affected side with the head turned up. Nystagmus will occur shortly after
is established care and is
arriving at the side-lying position. Keep the patient in this position until at
least 20 seconds after all nystagmus has ceased. effective in eliminating
vertigo and nystagmus
b Step 3 Quickly move the patient back up and through the sitting position in more than 90% of
so that he or she is in the opposite side-lying position with head facing down patients.
(head did not turn during the position change). Keep the patient in this
position for about 30 seconds (some experts recommend up to 10 minutes). h The nystagmus of
benign paroxysmal
b Step 4 At a normal or slow rate, bring the patient back up to the sitting position.
positional vertigo is
usually visible if the
patient has any degree
of vertigo. If repeated
presumed to be caused by cupuloli- symptom free are most likely due to dif- treatments do not
thiasis. Treatment of posterior canal ferent otoconia (Case 4-4). produce symptom
BPPV using either the CRT or the Posttreatment instructions. Rela- resolution, the diagnosis
Semont maneuver is established care tively little firm data support any specific should be reconsidered.
and effective in eliminating vertigo and instruction, although many clinicians rec-
nystagmus in more than 90% of ommend keeping the head elevated at
patients.14Y16,19,20 least 30- on the night of the treatment.
Some cases of BPPV are refractory, The recommendation is based on the
but these cases are uncommon. For pa- theoretical possibility of recurrence since
tients who are disabled and deemed the calcium particles are still presumably
surgical candidates, canal plugging can loose in the utricle for a few days after
be considered. This procedure re- treatment. Use of a cervical collar or re-
quires certainty about the side and quiring patients to sleep in a chair is
the canal affected since plugging of the unnecessary.21Y24 Pretreatment with ves-
canal will render that canal nonfunc- tibular suppressant medications is gener-
tional and leave the patient with some ally not required but may be considered
dizziness for several weeks. Most pain patients prone to motion sickness or
tients adapt well to this procedure, but nausea. Sedation does not detract from
performing a destructive procedure for the success rate of the maneuver provided
a benign condition requires that the the patient is alert enough to cooperate.
patient be made fully aware of possible Occasionally, patients report subjec-
complications. tive positional dizziness but no nystag-
Following head trauma, BPPV is ty- mus is visible. Although generally no
pically evident from the first time the harm results from treatment, the diag-
patient is mobilized in a manner likely nosis should be considered suspect un-
to evoke the vertigo. Weeks to a few less nystagmus is seen. The nystagmus of
months may elapse before immobilized, BPPV is usually visible if the patient has
sedated, or unresponsive patients are ac- any degree of vertigo. If repeated treat-
tive enough to be aware of the positional ments produce no symptom resolution,
vertigo, as Case 4-4 illustrates. Recurrent the diagnosis should be reconsidered.
symptoms within 1 day of treatment are BPPV may be an isolated condition
probably due to the same otoconia. Re- or may be recurrent for many years.
currences of BPPV after weeks of being Recurrence rates range from 30% to

KEY POINTS
h Some patients with
benign paroxysmal
Case 4-4
A 58-year-old truck driver fell from the truck, which resulted in closed head
positional vertigo (BPPV)
trauma with loss of consciousness, rib fractures, and a vertebral body
develop anxiety and a
fracture. He was hospitalized and relatively immobile for 1 week. When
sense of loss of control
he was transferred from the intensive care unit and began trying to sit up,
and confidence that
he noted a spinning sensation. Examination confirmed bilateral benign
may account for
paroxysmal positional vertigo (BPPV) that was successfully treated with
prolonged symptoms
resolution of the vertigo. After 1 month of being completely free of
of dizziness even after
vertigo, he awoke with intense spinning that was brief and positional.
successful resolution of
Examination confirmed right BPPV, which was successfully treated.
all signs of BPPV.
Comment. This case illustrates how immobilized patients may have
h Patient education BPPV and not experience symptoms until they recover enough to move
should be a part of the about. BPPV occurs spontaneously but is common with traumatic BPPV.
care of patients with Multiple recurrences of BPPV may also occur, presumably from mechanical
benign paroxysmal injury or degradation of the otoconial mass, for months to 1 year or
positional vertigo, more following trauma.
particularly if an
accompanying element
of anxiety is present.
h Some patients can
50%.25 A small subpopulation may be nystagmus after 1 week. Self-treatment
successfully perform
treatment maneuvers
particularly susceptible to multiple with the Semont maneuver (n = 33)
at home as a recurrences, perhaps based on as yet was successful in 58% of patients; self-
complementary undefined characteristics of the oto- treatment using a modified Epley ma-
approach to in-office conial membrane. The recurrence rate neuver (n = 37) was successful in 95%.
care. increases with age and possibly following Clinicians should be prepared for the
head trauma, although there is dis- likelihood that some patients are un-
agreement on the latter point.6 able to perform these self-treatment ap-
Some patients with BPPV develop proaches on their own.
anxiety and a sense of loss of control Another guide to aid patients in self-
and confidence that may account for treatment is a proprietary plastic device
prolonged symptoms of dizziness even mounted on the bill of a ball cap that
after successful resolution of all signs of shows the movements of a small col-
BPPV.26 Symptoms may be relieved by ored ball moving through fluid that
educating, reassuring, and instructing simulates the intended movement of
the patient about what to do if vertigo calcium particles. Several studies have in-
recurs following successful treatment.27 dicated this treatment to be effective.31
Education should be a part of the care Many clinicians provide photocopies
of patients with BPPV, particularly if of Brandt-Daroff exercises to patients
an accompanying element of anxiety to use for self-treatment of BPPV. This
is present. exercise is quite similar to the Semont
Home self-treatment. Some patients maneuver except that the head is
can successfully perform treatment ma- turned during the change from one
neuvers at home as a complementary side-lying position to the other. Given
approach to in-office care.28,29 Radtke the improved effectiveness of the ma-
and colleagues30 followed 70 patients neuvers described by Semont and
who performed self-administered treat- Epley, there is little need to use these
ments for BPPV using the Semont or exercises any longer.
Epley maneuvers. Success was defined Horizontal canal. Horizontal canal
as complete resolution of vertigo and BPPV represents about 10% to 17% of

KEY POINT
cases of BPPV.32Y35 Horizontal canal of the affected ear, causing the nystag- h The nystagmus of
BPPV is often but not always evoked mus to change to the opposite direc- horizontal canal benign
by the Dix-Hallpike maneuver. The tion. Apogeotropic forms of horizontal paroxysmal positional
nystagmus of horizontal canal BPPV, canal BPPV occur because the calcium vertigo (BPPV), unlike
unlike that of posterior canal BPPV, is particles are located on the other side of that of posterior canal
distinctly horizontal and changes the cupula in the short arm of the canal BPPV, is distinctly
direction with changing head position. and thus, the same movements have horizontal and changes
The best way to diagnose horizontal the opposite effects on the cupula.34 direction with changing
BPPV is by a supine head-turn maneu- A number of treatments have been head position. The
ver (head yaw test or Pagnini-McClure advocated for horizontal canal BPPV, best way to diagnose
horizontal BPPV is by a
test) in which the patient is in the supine including the 360- roll maneuver (also
supine head-turn
face-up position. Turning his or her head called barbecue roll or Lempert ma-
maneuver (head yaw
quickly to the right, look for horizontal neuver), forced prolonged position test or Pagnini-McClure
nystagmus, then turn the head to the (Vannucchi technique), and Gufoni ma- test) in which the
left looking for a change in the di- neuver. It is worth noting that nearly patient is in the supine
rection of nystagmus (Figure 4-9; 90% of cases of apogeotropic horizontal face-up position.
Supplemental Digital Content 4-4, canal BPPV resolved in one study within Turning his or her head
links.lww.com/CONT/A10).35,36 The 7 days and all had resolved by 28 quickly to the right, look
direction-changing nystagmus may be days.37,38 All forms seem to self-resolve for horizontal
either geotropic or apogeotropic.36 The even more often than cases of poste- nystagmus, then turn
latency is often brief, and the duration rior canal BPPV. the head to the left
may be 15 to 60 seconds. This nystag- Determining the affected side. If the looking for a change
in the direction of
mus appears less apt to fatigue with re- horizontal canal BPPV occurred after
nystagmus.
peat positioning; consequently, patients treatment for posterior canal BPPV,
are more likely to become ill with the affected ear is likely to be the same
attempts to fatigue this form of BPPV. ear affected by the posterior canal
Geotropic direction-changing posi- BPPV. In cases where the horizon-
tional nystagmus is the most common tal canal BPPV occurs de novo, other
form of nystagmus in patients with
horizontal canal BPPV. The nystagmus
is right beating upon turning the head
to the right while supine and then left
beating when turning the head back
to the left side. By contrast, apogeo-
tropic positional nystagmus is seen
less often and refers to nystagmus that
is right beating with head turns to the
left while supine and left beating with
head turns to the right. One theory to
explain this is that, in the geotropic
form, calcium particles are in the long
arm of the semicircular duct and turn-
ing to the affected side causes endo- Supine roll test. The patient’s head is moved
FIGURE 4-9
lymph flow toward the ampulla, which rapidly from the straight supine position (1) to the
right side (2). At this point, the eyes are observed
is excitatory, and thus the nystagmus for horizontal nystagmus and the direction and intensity are
beats toward the affected ear. Turning noted. Then the patient is returned to position 1 until nystagmus
subsides, then taken to the left (3) and again the eyes are
the head in the opposite direction observed for the intensity and direction of horizontal nystagmus.
causes endolymph to flow away from The side resulting in the strongest nystagmus is the affected side.
the ampulla, which inhibits the ampulla
KEY POINT
h The use of an Epley or methods are used to determine the sitting position. The successive head
Semont maneuver, side to treat. turns can be done with intervals of 15
intended to treat The supine head-turn maneuver to 20 seconds even when the nystagmus
posterior canal benign (Figure 4-9) is the most commonly continues. Waiting longer does no harm
paroxysmal positional used method for determining which but may lead to nausea, and the shorter
vertigo (BPPV), is horizontal canal is affected. The side interval does not appear to detract from
unlikely to be successful associated with the most severe nys- the effectiveness of the treatment. The
in treating horizontal tagmus is presumed to be the affected goal of this maneuver is to utilize the
canal BPPV. side for the geotropic form and the effect of gravity to move the otoconia
opposite side for the apogeotropic from the long arm of the lateral canal to
form of horizontal canal BPPV. 39 the vestibule.41Y43
Another method advocated by some Gufoni maneuver. In 1998, Gufoni
is the seated supine positioning test, and colleagues44 described a different
which is done by rapidly moving the treatment in which the patient is quickly
patient from the seated to the straight lain from a sitting position to the healthy
supine position. This technique evokes earYdown (for geotropic forms) or to the
nystagmus beating toward the healthy affected earYdown position (for apogeo-
side in the geotropic forms and toward tropic forms) (Figure 4-11; Supplemental
the affected side in the apogeotropic Digital Content 4-6, links.lww.com/CONT/
forms. 34,39 Occasionally, the side A12; Supplemental Digital Content 4-7,
involved remains equivocal; thus, one links.lww.com/CONT/A14).
may simply begin on one side and later Then the head is turned 45- toward
treat the other side. the floor and maintained in that position
The use of an Epley or Semont ma- for 30 to 60 seconds. Then the patient
neuver, intended to treat posterior canal returns to the sitting position. This pro-
BPPV, is unlikely to be successful in cedure may be repeated. Using this
treating horizontal canal BPPV. 40,41 Con- method, 22 of 24 patients achieved reso-
sequently, the approach must be altered lution of symptoms.44 In a comparison
if the nystagmus observed is paroxysmal with forced prolonged positioning,
horizontal and changes direction with both the Gufoni maneuver and forced
changing the head position (ie, direction- prolonged positioning achieved suc-
changing positional nystagmus). cess in more than 80% of patients, but
Roll maneuver. The 360- (barbecue) no statistically significant difference was
roll maneuver (Lempert roll maneu- found between the two methods.45 Re-
ver) (Figure 4-10; Supplemental Dig- cently, a class II prospective random-
ital Content 4-5, links.lww.com/ ized sham-controlled study of 157
CONT/A11) is a commonly used treat- patients with the apogeotropic form of
ment method for horizontal canal horizontal canal BPPV found that the
BPPV. With the 360- roll treatment Gufoni maneuver (PG.001) and head
the patient’s head is positioned with shaking (P=.026) were more effective
the affected ear down, and the head is than a sham maneuver for both imme-
then turned quickly 90- toward the diate improvement and improvement
unaffected side (face up). A series of at 1 month following treatment.46
90- turns toward the unaffected side is A recent class I randomized controlled
then undertaken sequentially until the trial comparing the Lempert (barbecue
patient has turned 360- and is back to roll) to the Gufoni maneuver for the
the affected earYdown position. From geotropic form of lateral canal BPPV
there, the patient is turned to the face- found both maneuvers significantly
up position and then brought up to the more effective than a sham maneuver

FIGURE 4-10 Lempert 360- roll maneuver for the treatment of right horizontal canal benign
paroxysmal positional vertigo with geotropic-type nystagmus.
on the day of treatment and also at it the maneuver of choice for horizontal
1-month follow-up.47 canal BPPV, whether geotropic or apo-
A class III prospective study of 60 geotropic. A growing body of literature
patients with geotropic horizontal canal seems to support this conclusion.
BPPV found that forced prolonged Forced prolonged positioning. This
positioning and the Gufoni maneuver treatment technique was first described
were both more effective in elimination by Vannucchi and colleagues in 1997.50
of nystagmus than a single iteration of a Forced prolonged positioning is per-
roll maneuver.48 formed by having the patient seated
Another class II randomized pro- on a bed or table. He or she is then
spective clinical trial of 147 patients quickly lain down on the affected side;
affected by horizontal canal BPPV (103 then a passive 45- downward rotation
geotropic, 44 apogeotropic) found that of the head is performed. The position
among those with geotropic horizontal is maintained for 12 hours before the
canal BPPV, 44 of 54 patients (81%) patient is returned to the starting position.
treated with the barbecue roll maneu- Some clinicians maintain the position
ver plus forced prolonged positioning only 3 to 5 minutes, but no comparative
were symptom free compared to 54 of studies are available to determine the
58 (93%) treated with the Gufoni minimum time needed to achieve suc-
maneuver.49 The authors concluded cess. In studies using this method, most
that the slightly greater response rate patients reported resolution of symp-
combined with the greater ease of toms, including those with refractory
performing the Gufoni maneuver make horizontal canal BPPV.43Y45 It is ideal

KEY POINTS
h It is ideal to eliminate
all nystagmus or to
convert the more
difficult-to-clear
apogeotropic
nystagmus to the more
treatment-responsive
geotropic nystagmus
form of horizontal canal
benign paroxysmal
positional vertigo.
h Of all the types of
benign paroxysmal
positional vertigo
(BPPV), anterior canal
BPPV seems to resolve
spontaneously most
often, although
horizontal canal BPPV
also resolves within 2 to The Gufoni maneuver is a method of treatment for right-sided horizontal canal
FIGURE 4-11 benign paroxysmal positional vertigo (BPPV) that is geotropic (A) or
4 weeks if not sooner.
apogeotropic (B). A, For the geotropic nystagmus type of lateral canal BPPV, the
h Paroxysmal downbeat patient is taken from the sitting position to the straight side-lying position on the unaffected
nystagmus as may occur side (left in this case) and maintained there for 1 minute. The patient’s head is quickly turned
toward the ground 45- to 60- and held in the position for 2 minutes. The patient then sits
with anterior canal up again with the head held toward the left shoulder until sitting upright again. B, For right
benign paroxysmal horizontal canal BPPV with apogeotropic-type nystagmus, the patient is taken from the sitting
positional vertigo may position to the straight side-lying position on the unaffected side (right in this case) for 1 minute.
Then the patient’s head is quickly turned toward the ground and held in the position for
be mimicked by central 2 minutes. The patient then sits up again with the head held toward the right shoulder
lesions of the brainstem until upright.
or cerebellum.
to eliminate all nystagmus or to convert BPPV seems to resolve spontaneously

the more difficult-to-clear apogeotropic most often, although horizontal canal
nystagmus to the more treatment- BPPV also resolves within 2 to 4 weeks
responsive geotropic nystagmus form if not sooner.38 Paroxysmal downbeat
of horizontal canal BPPV.43,51 With this nystagmus as may occur with anterior
strategy, remission rates of 75% to 90% canal BPPV may be mimicked by central
can be achieved. lesions of the brainstem or cerebellum
Anterior canal. This form of BPPV (Case 4-5). Bertholon and colleagues54
is usually transitory and most commonly reviewed 50 patients with downbeat
seen in the course of treating other positional nystagmus and found that
more common forms of BPPV. Chronic three-fourths had CNS disease; at least
or persistent anterior canal BPPV is rare. some of the remaining one-fourth of
Hence, a careful neurologic examination cases were thought to have a form of
and brain MRI are suggested unless the anterior canal BPPV. If the nystagmus
nystagmus can be made to completely does not completely resolve with the
resolve with positioning treatments. initial positioning treatment, brain
The nystagmus is downbeat with a imaging should be performed.
minor torsional component.42,49,52,53 The Dix-Hallpike and side-lying tests
Of all the types of BPPV, anterior canal used for the posterior canal BPPV can

Case 4-5
A 35-year-old software writer presented with several months of positional vertigo that seemed to
begin after a rear-end motor vehicle collision in which he sustained soft tissue neck pain. The spells
were brief but occurred when he wrestled
with his children and with bending or tilting
his head. On examination he experienced
brief paroxysmal downbeat nystagmus
lasting about 5 seconds with positioning
from sitting to supine whether his head was
turned to the right or left side. Attempts
to treat with canalith repositioning
treatment resulted in no change in the
nystagmus or symptoms. Brain MRI was
obtained (Figure 4-12) and showed a lipoid
tumor of supracerebellar region. An attempt
to surgically resect this lesion was aborted
because of its extensive vascular elements.
The pathologic diagnosis was lipoangioma.
Comment. This patient’s nystagmus was
most suspicious for a central form of
positional vertigo, but after the brain MRI
confirmed a chronic lesion, the question
became whether this lesion was the cause.
Over time and considering its inferior
extension to the nodulus and anterior vermis, FIGURE 4-12 Brain MRI showing an extensive
supracerebellar lipoangioma responsible for
it was concluded to be likely related to the paroxysmal downbeat positional nystagmus
lesion. Any contribution from the motor in Case 4-5. A, Magnetic resonance T1-weighted images.
B, Axial images of brain MRI.
vehicle accident remained a matter of
speculation.
also be used to provoke and diagnose same side.57 Because the torsional ele- KEY POINT
anterior canal BPPV, and the same ment of nystagmus may not be obvious,49 h The same maneuvers
maneuvers used to treat posterior canal the direction of torsional nystagmus used to treat posterior
benign paroxysmal
BPPV can be used to treat anterior canal cannot be used to reliably ascertain the
positional vertigo (BPPV)
BPPV.55 A recent retrospective study of affected ear.
can be used to treat
13 patients is described in one report,56 For rare cases that are refractory to anterior canal BPPV.
but comparison to a control group may treatments used for posterior canal
be particularly important in assessing BPPV, a prolonged forced position
effectiveness for this BPPV variant since procedure with the affected anterior
it seems to have a high rate of sponta- canal in the uppermost position for
neous resolution. several hours should be tried before
The affected side is not always en- any invasive procedure such as canal
tirely obvious. If the paroxysmal down- plugging is considered.58
beat positional nystagmus from anterior
canal BPPV developed in the context of Canal Switch
a ‘‘canal switch’’ during treatment of the Occasionally, freely mobile otoconia
posterior canal BPPV treatment, then moving within the lumen of one semi-
the side of the original BPPV is likely the circular canal can be moved during
the course of treatment, not back to izontal canal, and posterior and anterior
the utricle as intended, but to one of canal.34 They can be recognized based
the adjacent canals. This is possible be- on the maneuver used to evoke the
cause the canals directly communicate nystagmus and the direction of the nys-
with one another. This canal switch tagmus. Treatments are the same as
changes the appearance of nystagmus those used for individual canal types of
from that of the original affected canal BPPV and can be done on the same
to that of the newly affected canal.59,60 visit in some cases or spread over sev-
The most common canal switch is from eral visits with more than 90% response
the posterior to the horizontal and pos- rates.63
terior to anterior canals (Case 4-6).
Multicanalar. In some situations CENTRAL POSITIONAL VERTIGO
more than one canal is affected at the Table 4-5 outlines some of the con-
same time.53,61,62 The most common ditions associated with central positional
circumstance is probably bilateral pos- vertigo, and Figure 4-1 outlines some
terior canal BPPV. This can be diagnosed ways of segregating central from pe-
by the presence of typical nystagmus ripheral causes. Slowly progressive le-
with the Dix-Hallpike or side-lying sions affecting the cerebellum, pontine
maneuvers on both sides. In unilateral tegmentum, and dorsal medulla can
BPPV, the nystagmus is only present on lead to surprisingly mild positional
Dix-Hallpike positioning to the affected disequilibrium. Such conditions may
side, and no nystagmus is evident on be associated with paroxysmal posi-
the other side. Other multicanalar forms tional nystagmus and gaze-evoked nys-
may also occur, the most common be- tagmus or other focal neurologic signs.
ing combinations of posterior and hor- The degree of nausea and severity of
Case 4-6
A 68-year-old woman with 6 weeks of positional vertigo of brief duration
was found to have robust upbeat and counterclockwise torsional
nystagmus with Dix-Hallpike positioning to the right. She was taken
through canalith repositioning and returned to the sitting position. The
examiner repeated Dix-Hallpike positioning to the right to be sure all
the nystagmus had cleared and upon positioning noted prominent
horizontal right-beating nystagmus that persisted for 40 seconds. The
examiner concluded that canal switch from the right posterior to the right
horizontal canal had taken place during the previous maneuver. While
the patient was still supine with the head to the right, her head was then
turned 180- to the left whereupon the left-beat nystagmus occurred.
The patient was then moved in 90- steps to the left (unaffected) side. The
patient went from supine head left to face down, to right ear down,
and then back to straight supine (face up). The patient then sat up.
Repeat Dix-Hallpike maneuver showed no further upbeat or horizontal
nystagmus on either side.
Comment. Canal switch occurs when otoconial debris moves from one
canal to another during the course of canalith repositioning. It is
recognized by a change in the direction of the nystagmus. Upon seeing
this kind of change in nystagmus, the examiner should adapt the
procedure to treat the newly affected canal.

KEY POINTS
TABLE 4-5 Differential Diagnosis of Positional Vertigo h The degree of nausea

and severity of vertigo
b Central positional vertigo with nystagmus are generally less
prominent with slowly
b Cerebellar lesions (eg, tumors, strokes, masses, bleeding) progressive central
b Pontomedullary lesions (eg, lateral medullary infarction) lesions, at least up to
a point.
b Multiple sclerosis
h Acute or more rapidly
b Chiari malformationVoften neck pain; obtain MRI
progressive lesions of
b Cerebellar degenerationVspontaneous downbeat nystagmus, impaired the CNS are often
pursuit, gaze-evoked nystagmus associated with more
b Vertebrobasilar vascular insufficiency intense vertigo or
nausea.
b Subclavian steal syndrome
b Atlantoaxial subluxation
b Drug effects (eg, phenytoin toxicity)
b Peripheral vestibular forms of positional vertigo
b Benign paroxysmal positional vertigo and related variants
b Uncompensated unilateral vestibular loss
b Static positional nystagmus and associated dizziness
b Saccular or utricular positional vertigo
b Alcohol positional vertigo
b Migraine-associated vertigo with a positional component
b Motion sickness
vertigo are generally less prominent be associated with central forms of nys-
with slowly progressive central lesions, tagmus and positional vertigo. Migraine-
at least up to a point. related vertigo can be associated with the
Acute or more rapidly progressive development of nausea, occasionally
lesions of the CNS are often associated with static positional nystagmus that
with more intense vertigo or nausea may build over a period of minutes
(Case 4-7). Neurologic signs that lo- upon assuming certain head positions.64
calize to the brainstem or cerebellum Chiari malformation is usually associ-
are often, but not always, present. ated with occipital headaches and may
The conditions most likely to exhibit be associated with downbeat nystag-
few other clinical signs besides positional mus in the straight head-hanging posi-
vertigo with or occasionally without much tion. Direction-changing positional
nystagmus include cerebellar cavernous nystagmus that does not entirely disap-
malformation, arteriovenous malforma- pear after treatment for horizontal
tion, hemangioblastoma, and small mid- canal BPPV should raise suspicion for
line or paramedian cerebellar lesions. a central lesion, such as a stroke of the
Carcinomatous or lymphomatous menin- cerebellar nodulus.65
gitis can result in positional vertigo but Brain MRI is very helpful in excluding
more commonly results in head motionY structural causes of positional vertigo.
related dizziness. Multiple sclerosis can Peripheral forms of positional vertigo

KEY POINTS
h Central forms of
positional vertigo may
Case 4-7
A 62-year-old man had experienced several weeks of episodic isolated
occasionally elude
vertigo lasting minutes. He then developed severe ataxia, an inability to
detection by a standard
walk, dysarthria, and vertigo that persisted, prompting him to go to the
brain MRI; these include
emergency department. He was found to have pronounced vertigo and
some cerebellar
attempts to sit up in
degeneration
bed or stand elicited
syndromes, atlantoaxial
vomiting. Brain
subluxation,
MRI (Figure 4-13)
vertebrobasilar
revealed a large
insufficiency, chronic
posterior inferior
basilar meningitides,
cerebellar artery
and drug toxicities.
distribution stroke
h Conditions with fixed on the right side.
static injury, such as Comment. This
occurs with stroke, case illustrates how
trauma, and an acute infarct can
hemorrhage, may lead to severe
be amenable to vertigo, nausea, and
habituation physical vomiting. This is less
therapy exercises. FIGURE 4-13 Brain MRI showing an acute stroke on
common with slowly diffusion-weighted images (A) and on axial
fluid-attenuated inversion recovery fast spin
enlarging lesions, echo (B) in the right inferior cerebellum and right lateral
suggesting that medulla in the distribution of the right posterior inferior
plastic properties of cerebellar artery (PICA). The red arrow shows cytotoxic
edema affecting midline cerebellar structures. Green arrows
the CNS may be able show infarction of the right lateral medulla. Blue arrows
to compensate to show infarction of the right cerebellum in the PICA
some extent in distribution.
central vestibular
lesions. Acute central positional vertigo can in some cases produce significant
vertigo and vomiting.
are nearly always associated with a nor- ditions with fixed static injury, such as
mal brain MRI. occurs with stroke, trauma, and hem-
Central forms of positional vertigo orrhage, may be amenable to habitu-
may occasionally elude detection by a ation physical therapy exercises. This
standard brain MRI; these include some therapy is discussed elsewhere in this
cerebellar degeneration syndromes, issue but in essence
atlantoaxial subluxation, vertebrobasilar involves exposure to the kinds of head
insufficiency, chronic basilar menin- movements that aggravate the vertigo
gitides, and drug toxicities. Additional while also working on general balance
studies that are sometimes necessary and ocular motor control.
include CSF studies, vascular imaging Progressive disorders such as meta-
by CT angiography or MR angiography, static tumors, astrogliomas, and carci-
cervical spine radiography or CT, and nomatous meningitis require treatment
drug-level testing. of the underlying condition. Symp-
toms can be managed with vestibular
Treatment Approach suppressants.
Treatment of central positional vertigo Sometimes central positional vertigo
depends on the underlying cause. Con- is related to an unstable condition.

Chiari malformation, defined as more cial interest in the field. Our understand-
than 5 mm of cerebellar tonsillar her- ing of the mechanisms and metabolic
niation below the foramen magnum, predispositions for developing BPPV or
may be associated with positional for having multiple recurrences will also
vertigo. Symptoms of Chiari malforma- likely expand over time.
tion may progress as a result of aging, We will likely see more research
trauma, and degenerative effects on the emerge on selective dysfunction of the
craniocervical junction even though low- utricle and saccule and the role of these
lying cerebellar tonsils are congenital. structures in causing some forms of po-
Chiari malformation is treated by sub- sitional vertigo.
occipital surgical decompression, re-
moving some of the occipital bone to VIDEO LEGENDS
allow more space for the inferior cere- The maneuvers depicted in the follow-
bellum and ensure normal CSF flow. ing videos may need to be modified for
Another unstable condition is vas- some patients with reduced neck flexi-
cular narrowing of the vertebrobasilar bility by turning of the head and should-
system. Vertebral artery narrowing as ers together (en bloc).
the vessel crosses the arch of C1 can
result in vertigo associated with head Supplemental Digital Content 4-1
turning in one direction. Head turning Video demonstrates the Dix-Hallpike
causes some narrowing of the vessel maneuver to the right. This maneuver
and may lead to symptoms of transient should evoke paroxysmal positional nys-
ischemia. Antiplatelet agents, vertebral tagmus for right-sided benign parox-
artery angioplasty, or surgical place- ysmal positional vertigo related to the
ment of a stent are treatment options. posterior semicircular canal. The mir-
Atlantoaxial subluxation is instability of ror image of this maneuver constitutes
C1 (atlas) on C2 (axis) of more than 3 mm a left-sided Dix-Hallpike maneuver.
from the C1 arch and odontoid process. links.lww.com/CONT/A7
This condition often arises due to weak- Reproduced with permission from Fife TD,
ness of the transverse ligament and is Iverson DJ, Lempert T, et al. Practice parameter:
especially associated with rheumatoid therapies for benign paroxysmal positional
vertigo (an evidence-based review): report of
arthritis and Down syndrome. Treat- the Quality Standards Subcommittee of the
ment is surgical fusion of C1 and C2. American Academy of Neurology. Neurology
2008;70(22):2067Y2074.
TRENDS AND FUTURE B 2008, American Academy of Neurology.
DIRECTIONS
Supplemental Digital Content 4-2
Treatment of positional vertigo has
changed significantly during the past Video demonstrates canalith reposition-
20 years, and more patients are receiv- ing treatment for right posterior canal
ing treatment for BPPV. The physical benign paroxysmal positional vertigo
therapy and positioning treatments for (BPPV). The mirror image maneuver can
the more common posterior canal be done for left posterior canal BPPV.
variant of BPPV are now well established links.lww.com/CONT/A8
Reproduced with permission from Fife TD,
and can be successfully used in general Iverson DJ, Lempert T, et al. Practice parameter:
medical practice.66 Treatments are being therapies for benign paroxysmal positional
refined for all other variants of BPPV, vertigo (an evidence-based review): report of
the Quality Standards Subcommittee of the
but due to their infrequency, treatment
American Academy of Neurology. Neurology
for the less common versions of BPPV 2008;70(22):2067Y2074.
will likely be limited to those with a spe- B 2008, American Academy of Neurology.

Supplemental Digital Content 4-3 horizontal canal benign paroxysmal po-

Video demonstrates the Semont liber- sitional vertigo (BPPV). The mirror image
atory maneuver for right posterior canal maneuver can be done for the geotropic
benign paroxysmal positional vertigo variant of left horizontal canal BPPV.
(BPPV). The mirror image maneuver can links.lww.com/CONT/A12
be done for left posterior canal BPPV. Reproduced with permission from Fife TD,
Iverson DJ, Lempert T, et al. Practice parameter:
links.lww.com/CONT/A9 therapies for benign paroxysmal positional
Reproduced with permission from Fife TD, vertigo (an evidence-based review): report of
Iverson DJ, Lempert T, et al. Practice parameter: the Quality Standards Subcommittee of the
therapies for benign paroxysmal positional American Academy of Neurology. Neurology
vertigo (an evidence-based review): report of 2008;70(22):2067Y2074.
the Quality Standards Subcommittee of the B 2012, American Academy of Neurology.
2008;70(22):2067Y2074.
B 2012, American Academy of Neurology. Supplemental Digital Content 4-7
Video demonstrates the Gufoni maneu-
Supplemental Digital Content 4-4 ver for apogeotropic variant of right
Video demonstrates the supine roll horizontal canal benign paroxysmal po-
(Pagnini-McClure) test to determine the sitional vertigo (BPPV). The mirror image
affected side in horizontal canal benign maneuver can be done for apogeotropic
paroxysmal positional vertigo. The side variant of left horizontal canal BPPV.
that induces the most intense horizon- links.lww.com/CONT/A14
tal positional nystagmus is presumed Reproduced with permission from Fife TD,
to be the affected side. Iverson DJ, Lempert T, et al. Practice parameter:
therapies for benign paroxysmal positional
links.lww.com/CONT/A10 vertigo (an evidence-based review): report of
Reproduced with permission from Fife TD, the Quality Standards Subcommittee of the
Iverson DJ, Lempert T, et al. Practice parameter: American Academy of Neurology. Neurology
therapies for benign paroxysmal positional 2008;70(22):2067Y2074.
vertigo (an evidence-based review): report of B 2012, American Academy of Neurology.
2008;70(22):2067Y2074.
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Review Article

Continuum Lifelong Learning Neurol 2012;18(5):1060–1085.

EVALUATION NONVESTIBULAR POSITIONAL

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Case 4-1 h Positional vertigo is a

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BOX 4-1 Glossary of Terms

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FIGURE 4-1 Algorithm for evaluating positional vertigo.

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TABLE 4-1 Features Distinguishing Central From Peripheral Causes

Feature Central Peripheral

TABLE 4-2 Comparison of Benign Paroxysmal Positional Vertigo by

Canal Estimated Provocative

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FIGURE 4-3 Macula. The macula is the motion transducer

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Posterior canal. Two techniques

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FIGURE 4-7 Canalith repositioning maneuver for the right side.

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to eliminate all nystagmus or to convert BPPV seems to resolve spontaneously

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TABLE 4-5 Differential Diagnosis of Positional Vertigo h The degree of nausea

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Supplemental Digital Content 4-3 horizontal canal benign paroxysmal po-

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maneuver vs Epley procedure. Neurology 41. Lempert T, Tiel-Wilck K. A positional

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