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P8' Diagnosis and TreatJnent of
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Benign Paroxysmal
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~ Positional Vertigo
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3 Susan J. Herdman, Ph.D., P.T.
Professor
3 Division of Physical Therapy
Department of Orthopaedics and Rehabilitation
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University of Miami School .of Medicine
Miami, Florida
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Ronald J. Tusa, M.D., Ph.D.

Professor

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Bascom Palmer Eye Institute
Departments of Ophthalmology and Neurology
University of Miami School ofMedicine
Miami, Florida
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medical

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Table of Contents
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r Introduction ......................................... 1
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3 Review of Semicircular Canal Function ................... 2
3
Pathophysiology of BPPV .. ........................... 6

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Posterior and Anterior Canal BPPV .... ~ ................. 8
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Horizontal Canal BPPV .............................. 18
;Slit

=- Summary ................... ; ..................... 22

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Illustrative Cases .................................. . 23

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Acknowlectgement .................................. 25
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s References ......................... ............... 26

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INTRODUCTION
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=-=-- INTRODUCTION

Benign paroxysmal positional vertigo (BPPV) is the most common

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peripheral vestibular disorder.u Nearly all patients with this disorder pre-
sent with the complaint of episodic vertigo, most of them report that their

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vertigo is provoked by head movement, and some can specifY the exact head
movement that causes their symptoms. BPPV occurs in adults of all ages,
but is most common in middle-aged and elderly individuals. It is uncom-
mon in children, 2J and has never been reported in a child under the age of
3' 11 years. 3 BPPV occurs spontaneously in most patients, but may follow

=-\ head trauma, labyrinthitis, or ischemia in the distribution of the anterior

vestibular artery.3 .

Diagnosis ofBPPV is made by provoking and observing an abnormal

:51' nystagmus response of the semicircul<rr -canals. Three differel!t provoking
maneuvers are used--the Dix-Hallpike maneuver, the sidelying maneuver,
:!1' and the roll maneuver. For many years it Was believed that all cases Df
:8 BPPV were caused by cupulolithiasis of the posterior semicircular canals_
Now we know that most cases of BPPV are caused by canalithiasis {not
:II cupuiolithiasis) and that sometimes the anterior or horizontal canal (not the
posterior canal) is involved:'8 Distinctions among these various types of
:8' BPPV can be made only by careful observatjon of the patient's nystagmus
response to the provocative maneuver, and these observations are greatly
::fl aideJ by the use of an infrared video. eye movement monitor -.,..,;ith video
recording capabilities.
:tl Spontaneous remission of BPPV is common, but for those patients in
whom the disorder persists, the symptoms can be annoying, disruptive, and
:!1 often lead to significant changes in normal activities. There are three effec-
:at tive treatments for BPPV--the canalith repositioning treatment (CRT), the
Liberatory maneuver, and Brandt-Daroff exe1;cises. These treatments are

=-::8 safe and simple, and they provide immediate relief of symptoms for many
patients. Each treatme1_1t works bes{ for a specific type ofBPPV, so it is nec-
essary io identifY the involved canal and type of pathology in order to select

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the appropriate one.
In the fol_fowing sections, we review semicircular canal function and t.~e
pathophysiology ofBPPV and then describe the diagnosis and treatment of
each specific type of BPPV.

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a. 1

 DIAGNOSIS AND TREATMENT OF BENIGN PAROXYSMAL POSITIONAL VERTIGO

REVIE\V OF SEMICIRCULAR CANAL FUNCTION

A semicircular canal can be visualized as a continuous ring of fluid.

called endolymph, that is blocked by a flexible plug, called the cupula. The
cupula pen cis whenever there is a difference in pressure of the endolyT.nph
across it. The hairs of the receptor cells, called hair cdls. are imbedded in
the cupula, and these hairs bend whenever the cupula bends. Hair cells are
directionally polarized, that is, they are excited when their hairs are bent in
one direction and inhibited when their hairs are bent in the other direction.
All hair cells of a given cupula are polarized in the same direction.
Semicircular canals ar:e_designed to respond to angular accelerations of
the head. There a~c six semicircular canals. three in each labyrinth (Figure
"I). These six canals function as three pairs lying in mutually perpendicular
planes, with each pair max:imally sensitive to angular accelerations in its
own plane.

Excite left horizontal canal ~ ~ Excite right horizontal ::anal .

inhibit right horizontal canai (/7 _.-
~ f:fb;tleft horironJal can~

Left antc:ior canai---+-- Right anterior canal

Left horizontal canal Right horizontal canal
left posterior canal--t-- Right posterior canal

Excite left posterior canal Excite right posterior canal

inhibit right anterior canal inhibit left anterior canal

Figure I. Orientation ofthe semicircular canals and their responses to angular accelera-
t{ons of!he head. Note that the size ofthe canals is great~v e-wggerated.

The first pair consists of the left and riglzt horizontal canals, which lie
_in the horizontal plane when the person is upright with head inclined for-
ward by about 30 deg. The horizontal canals respond maximally to leftward
and rightward.angular accelerations of the head. When the head undergoes
angular acceleration in this plane, the movement of endolymph in the hori-
zontal canals lags the movement of the canal walls, causing differential

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::t REVIEW OF SEMICIRCULAR CANAL FUNCTION

::!1 pressure across their cupulae, which are located in the most anterior portion
::t of the canaL This differential pressure causes both cupulae to bend oppo-
site the direction of motion. \Vhen head acceleration is to the right, both
~ cupulae bend to the left, causrng the hair ceiis in the right horizontal canal
to be excited and those in the left horizontal canal to be inhibited. When
:2 head angular acceleration is to the left, both cupulae bend to the right, caus-
ing the hair cells in the left horizontal canal tci be excited and those in the
~ right horizontal canal to be inhibited.
The second pair consists of the right anlerior and ltifi posterior canals,
:3 which lie in the plane shown in Figure I. The cupula of the anterior canal
is located in its most anterior portion, and the cupula of the posterior canal
::3 is located in its most posterior portioiL Forward acceleration of the head
~ toward the right shoulder causes the cupulae of both canals to bend in the
opposite directi<?n, inducing excitatien of the hair cells in the right anterior
::::. canal and inhibition of those in the left posterior canal. Bacl.rward acceler-
ation over the left shoulder causesexci~tion of the hair cells in left posteri-
:3. or canal and inhibition of those in the right anterior canaL
The third pair consists of the lift anterior and right posterior canals
:I (Figure I). Forward acceleration of the head toward the left shoulder caus-
es excitation of the hair cells in the left anterior canal and inhibition of those
~ in the right posterior canaL Head acceler<!tion in the opposite direction
causes the opposite stimulation pattern.
:S The general rule is that the hair cells in the leading ear are excited and
=t those in the trailing ear are inhibited.
The canal stimulation induced by these head movements provokes com-
:s peJisatoiy eye movements, which are mediated by the vestibulo-ocular reflex
and designed to keep the eyes IIXed on a visual target Figure 2 shows each
:s of the six h~d movements described above (first colum'1) . . and the corre-
sponding compensatory eye movement (:::ecor.d column). For hor.zontal
:I canal stimulation, the relationship between head and eye movement is sim-
ple. Rightward heaq movement (causing excitation of hair cells in ihe right
:I horizontal canal and inhibition of those in the left horizontal canal) induces
a leftward compensatory eye movement Leftward head movement (caps-
:s ing excitarion ofhaid::ells in the !eft horizontal canal and inhibition oftbose
in the right horizontal canal) induces a rightward compensatory eye move-
=-:I ment.
For anterior and posterior canal stimulation, the relationship is more
complex because the direc.tion of eye movement depends on the direction of
:!1 the person's gaze. For a forw:rrd head m?vem.ent toward the right shoulder

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 DIAGNOSIS AND TREATMENT OF BENIGN .PAROXYSMAL POSITIONAL VERTIGO

Compensatory 'Eye Movement Nystagmus Fast Phases

Head Movement
(center gaze) (center gaze)

Rightward Leftward

Leftward Rightward

Forward toward Upward and Downward and

right shoulder leftward torsional rightward torsional

Backward over
left shoulder
Downward and
rightward torsional
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Upward and
tettward torsional

Forward toward Upward.and

left shoulder rightward torsional

.. ' Backward over . Downward and Upward and

right shoulder leftward torsional rightward torsional

Figure 2. Eye movement responses to head movements. Note that 1he direction of c:ve
movement is designated re the patient (not the exah;iner). A righr.rard ~ve movement is
toward the patients right. A lift>vard eye movement is toward the patients left. An
upward eye moement is toward the patients forehead. A downward eye movement is
toward the pmient s cheeks. A right>vard torsional eye movement is rotation ofThe eyes
about the visual a.-cis with the superior poles of the eyes moving toward !he patielll s right.
A leftward torsional eye movement is rotation ofthe eyes about the visual a.>:is with the
superior poles of the eyes moving toward the patients left.

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~ REVIEW OF :SEMICIRCULAR CANAL FUNCTION

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(causing excitation of hair cells in the right an:teri{)[ canal and inhibition of
:!~' those in the left posterior canal) with the persn:n gazing to the right (parallel
to the }>lane of those canals), the compensail:n:y eye movement would be.
~ upward. For the same head movement with the person gazing to the leff
~\ (perpendicular to the plane of those canals). the compensatory eye move-
ment would be leftward torsional, that is, the: eye$ would rotate about the
:;S visual axis with the superior pole of the eyes, moving toward the patient's
left. With the person gazing straight-ahead {45 deg to the plane of those
:I canals), the compensatory eye movement is :a mixture of the two--upward
and leftward torsional. For a backward head movement over the left shoul-
:I der (causing excitation of hair cells in the left posterior canal and inhibition

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of those in the right anterior canal) with the person gazing straight ahead,
the compensatory eye movement is downwamand rightward torsionaL For
a forward head movement toward the left shoulder (causing excitation of
hair cells in the left anterior canal and inhibitiQn of those in the right poste-
rior canal) with the person gazing straight ahead, the compensatory eye
:!1 movement is upward and rightward torsionaL For a head movement in the

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3 opposite direction (causing excitation of hair ceiis in the right posterior
canal and inhibition of those in the left anteP.or canal) with the person gaz-
ing straight ahead, the compensatory eye mmrement is downward and left-
ward torsional. The general rule is that compensatory eye movements are
:1 opposite the direction of head movement.
These compensatory eye movements occur when the person performs
;!I natural head movements in normal everyday life. When head movements
are stronger and/or more prolonged (as might occur in an amusement park
:;1 ri.de), the person has nystagmus, as showrn in Figure 2 (third column).
Nystagmus is a back and forth eye moverocnt with distinct slow phases,
;!t which are the compensatory eye movements generated by canal stimulation,

s and fast phases (or beats), which are saccades in the opposite direction. By
convention, the direction of nystagmus is designated according to the direc-
tion of the fast pkses.. The general rule is tml nystagmus fast phases are in
:1 the same direction as the head movement.
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 DIAGNOSIS AND TREATMENT OF BENIG?-< PAROXYS!'.-IAL POSITIONAL \"ERTIGO

PATHOPHYSIOLOGY OF BPPV

It is widely beEeved that two types of pathology-canalithiasis an<;l.

cupulolithiasis-can cause BPPV:
-In cana!ithiasis, otoconia or other debris are presumed to be floating
freely in the endolymph of one of the canals,~ as-sho\Yn in Figure 3. If the
head is positioned so that the involved canal is vertical and then rotated
quickly in the plane of that canal, the otoconia fall to the lowest position in
the canal, moving endolymph along with them. This movement of
endolymph deflects the cupula of that canal, cai.lSing hair cell stimulation
and th.erefore inducing nystagmus and v:ertigo. This response usually begins
after a short latency due to inertial drag of the endolymph. It usually sub-
sides in less than a minute as the otoconia settle in the lowest portion of the
canal and differential pressure across the cupula dissipates. No one has
actually witnessed these events occurring in the semicircular canal, but this
scenario does explain our clinical observations and freely moving debris has
been visualized through a microscope in patients in whom the membranous
labyrinth has been exposed during surgery. 10 Canalithiasis is the cause of
BPPV in most patients.
In cupuloWhiasis, otoconia or other debris are presumed to adhere to the
cupula ofthe semicircular canal, making it gravity-sensitive/ 1 as shown in

A B

Canaliths Rotation

Figure 3. The mechanism of canalithiasis. A. position of canaliths brjOre canal rotation:

B, movements ofcanaliths and deflection of the cupula after canal rotation. Note that the
amount of cupula deflection is greatZv exaggerated.

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PATHOPHYSIOLOGY OF BPPV

A B

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=- Cupu!ollt'ls
Rotation

Figure 4. The medzanism ofcupulolithiasis. A, bifore canal rotation,. B, after canal

rotation. Note that the amount ofcupula deflection is greatly exaggerated.

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Figure 4. Rotation of the canal deflects the cupula, inducing nystagmus and
vertigo, but this time the response is persistent because the cupula remains
deflected due to the weight of the otoconia upon iL Eventually the nystag-
mus and ver!:igo subside, presumably due to ~entral vesti_bular adaptation. 12
Cupulolithiasis is an uncommon cause ofBPPV
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 DIAGNOSIS AND TREATMENT OF BENIGN PAROXYSMAL POSITIONAL VERTlGO

POSTERIOR AND AJ.'l"TERIOR CANAL BPPY

.Provocative maneuver
Diagnosis of posteriQr and anterior canal BPPV is made by provoking
and observing an abnormal nystagmus and vertigo response froni. the
involved semicircular, canal. The examiner may choose either one of two
maneuvers-the Dix-Hallpike maneuver or the sidelying maneuver-to
provoke the abnormal response. We prefer to use the Dix-:Hallpike maneu-
ver because it places the patient's head in perfect pos!tion for treatment with
CRT.
\Vhen performing the provocative maneuver, the examiner should visu-
ally observe: the patient's nystagmus responses with the. patient wearing
Frenzel's glasses in a darkened room or, better yet, record it with an infrared
video system, which allows simultaneous viewing by multiple examiners
and yields a permanent record for later review. ENG is not suitable for
recording these responses because the tracing is often disfigured by move-
ment and eye blink artifact Furthermore the nystagmus has a prominent
torsional component that is not detected by ENG.
The Di:r:-Hal!pike maneuver3 consists of two brisk movements-.-a right
Dix-Hallpike maneuver in the plane of the left anterior/right posterior canals
(Figure 5A) and a left Di:x-Hallpike maneuver in the plane of the right ante-
rinr/left posterior canals (Figure 5B). To perform the right Dix-Ha!lpike
maneuver, begin with the patient sitting on the examination table with the
head turned 45 deg to the right. Then quickly bring the patient's body
straight back (keeping the head turned 45 deg to the right) until the head is
hanging over the edge ofthe examination table by 20-30 deg. Wait at least

Figure 5. Ti1e Dix-f{allpike maneuver. A. right Dix-Hallpike manell\e1: B. lefi Dix-

Hallpike maneuver.

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::. POSTER10RANb ANTERIOR CANAL BPPV

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:I Figure 6. The sidelying maneuver: A, right sidelyingmaneuver; B, lefi sidelying maneuver:

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40 sec for an abnormal response (described belcw) to appear. If it does,
:1 m~ r the re se for at least 1 min or until it subsides. Then initiate
tr atment with CRT ~scribed below) if you wish. If no abnormal response
:I ppears or if.Yoo-elef! riot to treat, bring the patient slowly back to a sitting
:!I position. {f!len perform tleft Dix-Hallpike maneuver ,vith the patient's
head tumM 45 deg to the eft. Again wait at least 40 sec for an abnormal
:t :espo~se to appear. If it <J , monitor the re~ponse and then initiate tr~at-
n nt 1fyou . Ifn<Yf'esponse appears or 1fyou elect not to treat, bnng
:1 thioati:nt-slowly back to a sittinr; po~ition. ,
Th~elying maneuver also consists of two brisk movements-the
:s right sidelying maneuver in the plane of the left anterior/right posterior
canals (Figure <SA) and the left ~idelying maneuver in the plane of the right
:1 anterior/left posterior canals (Figure 6B). To perform the right sidely~1g
maneuver, begin with the patient sitting on the ex~nation table \.vith the
:S . legs over the-side and the head turned 45 deg to the left..Then quickly hr:ing
the patient down -onto the right side. Wait at least 40 .sec for an abriorillal
:I response to appear. If it dQfs, monitor th~ response.. Then bnng the patient
slowly back to a sitting pos~tion. Then perform the left sidelying maneuver,
$ this time bringing the patient quickly down onto the left side with the head
:.'I turned 4 5 deg to the? right (in the plane of the right anterior/left p6sterior
cana"ls). Again wait at.least 40 sec for ap. abnormal response to appear. If
:I it does, monitor the response. Then bring the patient slowly back to a sit-
ting position.
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 DIAGNOSIS AND TREATMENT OF BENIGN PARO?c'YSMAL POSITIONAL VERTIGO

Abnormal responses
Normal persons have a fe_w beats of nystagmus during these backward
movements, but no nystagmus after these movements have been co~pleted.
Patients with BPPV have a burst ofnystagmus after one or more of these
m~vements, which. is the hallmark of the disorder. Usually-this nystagmus
is delayed in onset, sometimes by as much as 40 sec. The nystagmus is also
transient. It usually subsiqes within a minute or less if the cause is canalithi-
asis, but can persist for much longer if the cause is cupulolithiasis. The nys-
tagmus is always accompa.'1ied by vertigo, usuai!y intense vertigo, which
follows the same time course as the nystagmus_
The examiner can identifY the specific canal involved by. noting the
direction of 't~e fast phases of the abnormal nystagmus response. With the
pa~ient's eyes looking straight ahead, "-

d torsional fast phases denote right posterior canal

2. upward, leftward t rsional fast phases denote left posterior canal

. BPPV, j .
_downwaRi;-flghtward orsional fast phases denote right anterior canal
BPP~
4. o~~ard, leftward;orsiDnal fast phases denote left anterior canal
B''l('K~

Note that an abnormal response is provoked most readily by a Dix-

Hallpike or sidelying maneuver performed in the plane of the involved
canal, but .it can also be provoked by a m_aneuver in another plane.
Note also that, if the nystagmus response is very strong, it may by fol-
lowed by secondary nystagmus with fast phases in the opposite direction.
Secondary nystagmus is caused by adaptation within the central vestibular
system.
Note also that, when returned to the sitting position following a positive
response, the patient usually has another bout of nystagmus and vertigo.
This response is just like the original one, except that it is usually weaker
and the nystagmus fast phases are in the opposite direction. It is due to
-canaliths dropping back toward the cupula.
Most cases of BPPV involve the posterior canaL In a study of 77 con-
secutive patients with BPPV, Herdman et aL..~ found that 49 patients (64%)
had posterior canal involvement, 9 patients (12%) had anterior canal

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:::. POSTERIOR AND AA'TERTOR CANAL BPPV

:t involvement, and that in 18 patients (23%), they were unable to detennine

:3 which canal-posterior or anterior-\\'aS inv-olved. One patient had hori-
zontal canal involvement
~ Sometimes the Dix-Hallpike or sidelying maneuver provokes central
positional nystagmus. Usually this nystagmus is downbeating. If so, it may
:J be due to cerebellar degeneration, Chiari malformation, or a sc;lective lesion
involving the cerebellar flocculus or the medial longitudinal fasciculus in
~ the floor of the fourth ventricle. This type of central positional nystagmus

:s can be distinguished from anterior canal BPPV because it is purely dmvn

beating (without a torsional component), persistent, and not accompanied
by vertigo (although the patient may complain of mild lightheadedness).
:I Provocative maneuvers can also provoke upbeating central positional nys-

=-:I tagmus, but this is uncommon. 14

Sometimes the Dix-H;:r.Ilpike or sidelying maneuver provokes horizontal
nysta~~tagmus could be either !he patient's spontaneous or
po~{(onal nystagmus o~t could be evidence of horizontal canal BPPV. If
::1 hofontal nystagmus is PJ;:Ovoked, the examiner should i~ediately per-
fo:r the rorl~-describe~low).
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Treatment ~
.Ar""e maneuvers are
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treat BPPV-C::RT,'516 the Liberatory maneu-

ver, ; ;~ BrandM:Jai.Qf[e-x-erctses. 1
1
~ CRT should be performed immediately after the Dix~Hallpike maneuver

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has provoked an abnormal resp-onse ths.t the examiner has identified as
canalithiasis in either the posterior or anterior canal of the undermost ear. In
that case, t.1.e patient is not retUrned to the sitting position, but rather the
patient's head is rotated in an attempt to slide the canaliths out of the semi-
:t circular ca;J.al and into the utricle, where they can no longer cause s~ymp
toms. If the right posterior canal is involved, the right CRT would~ appro-
:5 priate. The patient begins in the Dix-Hallpike position that provoked the
response (Figure 7A). The h~d is held iil this position for 1-2 min. Then
:S the head is lowered and rotated slowly toward the left side and briet1y held
in this position (Figure 7B). Then tb.e patient is rolled to a sidelying posi-
:5 tion with the head. turned 45 deg leftward and dovmward toward the floor
(Figure 7C). Finally the patient is slowly returned to the sitting position,
::5 with the head still pitched forward and turned to the left (Figure 7D ). After
this treatment, the patient is fitted with a soft collar and told not to bend
:3 over, lie back, or tilt the head for the rest of the day. The patient is also asked
to sleep sitting up that night and the ne}:t ?Tid f4en not to sleep on the affect-
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 DIAGNOSIS AND TREATMENT OF BENIGN PAROXYSMAL POSITIONAL VERTIGO

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A B c D

Figure 7. Right CRT. A, right head hanging position; B, leftward roll; C. jz1rther left-
ward roll; D, sitting up.

ed ear until follow-up assessment 5 days later.

The same maneuver would be appropriate for patients with canalithiasis
of the right anterior canal.
For ~-ith canalithiasis of the left anterior or posterior canals, the
lejj RT would be~ropriate (that is, the patient would begin in the left
ead~hanging position ~ rol~ed to the right before sitting up)._
F1gure 8 shows what WI( think happens when we perform th1s maneuver
on a patien~~alithia~is of the right pos'terior canaL When the patient
is in the sitting position, thb canaliths lie in the lowest part of the posterior
to
canal next the cupula (9lgure 8A). When the right DLx-Hallpike maneu-
ver is perfo'irn.~-~-s;anali!hs slide down away from the cupula (Figure
. B). As they slide, they move endolymph along with them, deflecting the
" exciting the canal receptors, and provoking vertigo and nystagmus
cupula,
with upward, rightward torsional fast phases. This response subsides as the
canaliths settle again in the lowest part of the canal. When the head is low,-
ered and rolled to the left, the canaliu~s slide around the top of the canal
(Figure 8C). The patient again has vertigo and nystagmus with upward,
rightward torsional fast phases, indicating that canaliths are continuing to
move .in the desired direction, that is, away from the cupula. (If the nystag-
. mus fast phases were in the opposite direction, this would indicate that
canaliths were moving backward toward the cupula.) Finally, when the
patient is brought to the sitting_ position, canaTiths drop through the common
crus into the utricle, where they' can no longer cause vertigo.
A key to the success of this maneuver seems to be in getting the head
nearly upside down (Figure 8C) so that canaliths will slide around the top of
the canaL Herdman et al. 19 found that if patients were merely rolled onto the
contralateral side before returning to sitting, the remission rate was only 50

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POSTERIOR AND ANTERIOR CANAL BPPV

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3 Figure 8. Movement ofcanaliths in the right posterior canal during the right Dix~
Hal/pike maneuver and right GRT. A, sitting with head wnzed rightward; B, right head
3 hanging position; C, lefMard roll; D, sitting up.

::5 percent, whereas if they '.Vere rolled onto the contralateral side \vith head
turned 45 deg. toward the iloor before sitting up, the remission rate was.83
::5 percent
One study of the efficacy of CRT for patients with posterior can;1l BPPV
:!1 rep0rted that 70 percent of27 patients in the treated group had no nystag-
:1 mus when evaluated one week after treatment compared to none of 23
patients in the untreated control group.20 A second double-blind, controlled
:t study/ 1 in which CRT was compared to a placebo maneuver, showed a sig-
nificant difference in outcome between the two groups. Ninety percent of
:I patients treated with CRT had full remiss~ on o_f symptoms compared to only

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 DIAGNOSIS AND TREATMENT OF BENIGN PAROXYS~fAL POSITIONAL VERTIGO

27 percent of patients in the control group. The remission of symptoms fol-

lowing CRT appears to be due to the maneuver itself, not to the period dur-
ing which the subjects stay upright 22 Epler has suggested using vibration
over the mastoid bone during the treatment to facilitate the movement oft.;e
debris, but a comparison of studies in which vibration \'(as used with stud-
ies in which vibration was not used shows no difference in outcome.'9-:!l.:!.!.~
Only preliminary work has examined the efficacy of CRT in patients .\vith
anterior canal canalithia<>is. Tusa et aF7 reported an 88 percent remission
rate in 17 patients with anterior canal BPPV following one treahnent.
Occasionally CRT causes complic~tions .. Sometimes sanaEths move
into another canal.28 \Ve found that _in 19 patients who failed treatment,
canaliths had moved into a different canal in 5 patients. Another complica-
tion is neck stiffuess and muscle spasm from keeping the head upright for a
to
prolonged period after treatment. Patients should be advised take off the
soft collar and to move the head horizontally periodically. Pre-existing neck
problems may also preclude the neck extension required during the actual
treatment. We use a tilt table to avoid having to extend the neck. Finally,
some patients experience seyere vertigo and motion sickness (including
nausea and vomiting) during the testing and treatment These patients
should be asked to sit quietly for a period of time before leaving the clinic.
The Liberatory maneuve7; developed by Semont, 17 is also designed to
remove otoliths or other debris from the semicircular canaL The exact form
of the maneuver depends upon which semicircular canal-anterior or pos-
terior-has been identified as the one involved.
If the examiner has determined that the right posterior canal is involved,
the right Liberatory maneuver should be performed. The maneuver begins
with the patient sitting on the examination table with heaCi turned 45 deg to
the left (Figure 9A). The patient is then moved quickly to the right sidely-
ing position with head hanging down toward the right shoulder (Figure 98).
After 1 min, the patient is moved quickly through the initial sitting position
to the left sidelying position with head still turned 45 deg to the le.ft (Figure
9C). The patient is held in this position for 1 min and then returned slowly
to the sitting position (Figure 9D). The patient is then placed in a soft col-
lar and given the same instructions as descrjped above for CRT.
If the right anterior canal is involved, the. maneuver is the same as above,
except that it is performed with the patient's head turned to the right
If th'e left posterior canal is involved, the left Liberatory maneuver
should be performed (that is, the patient is first moved to the left sidelying
position, then to the right sidelying position) with head turned to the right.

14
 ... ,
r-
;"

~ POSTEmDR AND ANTERIOR CANAL BPPV

~
A 8

i!'
r
~
~ c

-
15 ~~ .
-
:-'

~'

=-~
Figure 9. Right Liberatory maneuver with head tumei to the left_ A, sitting; B, moving
to right side{ving position; C. moPing to left side(vingjiosition; D, sitting up.

=-
=a If the left anterior canal is involved, the left Liberatory maneuver is
formed with the head turned to left.
Semont et al. 17 and others have reported e.ure' rates of70 to 84 percent
~ after a single Liberatoiy maneuver and 93 percent after two maneuvers. 26 32
A recent study examined the effectiveness -af this maneuver on a series of
:;1 patients using the patients as their own controF6 First the patients were
treated with the Liberatory man.euver on the1'lJ1ajfocted side. None ofthein

*
:5
reported any relief from their vertigo. Then; they were told to keep their
heads upright for 48 hours, indudirig sleeping in a sitting position. Again,
at the end of 7 days, all of them were still :symptomatic. Th.~n they were

treated usin:g the Liberatory maneuver on the affected side: At the end of7
days, all of them were symptom-free.
Brandt-Daroffexe,;-cises18 are generally ped'Drmed by the pati"nt at home
without the aid of a' therapist (Figure 10). The patient is asked to move

quickly from sitting to lying down on the side that provokes vertigo (\\rith
head turned away from that side) and stay there for at least 30 sec, then to
sit up quickly and stay there for at least 30 sec, then to lie down quickly on

the opposite side"(with head turned away from that side) and stay there for

:-.:: . 15

 DIAGNOSIS AND TREATMENT OF BENIGN PAROXYSMAL POSITIONAL VERTIGO

A B

D E F

Figure 10. Brandt-Daroffexercise.. A, sitting with headtumed to the left; B, ~ving

on the right side; C. sitting up; D, turning head to the right; E, lying down on the left
side; F, sitting up.

at least 30 sec, and then to sit up quickly again. Tne patient performs this
routine 10-20 times, three times a day, until vertigo ~s absent for two days in
a row.
Remission of symptoms following treatment with Brandt-Daroff
exercises has been reported to be as high as 98 percent 18 Presuma~Iy
remission occurs because the exercises throw otoconia off the cupula and
out of the semi.circular canal, where they no longer cause symptoms, but it
also possible that repeated provocation of symptoms causes central vestibu-
lar habituation.
We prefer to treat posterior and anterior canal BPPV due to canalithiasis
with CRT, and because most cases are due to canalithiasis, we use CRT most
of the time. We also use the Libera tory maneuver, but only for the occa-
sional patient with BPPV due to cupulolithiasis. where an attempt to dis-
lodge otoconia from the cupula seems indicated. We use Brandt-Daroff
exercises only for patients with mild residual symptoms, because most
patients will not faithfully perform this routine if it induces severe vertigo.
We use medications in the treatment of BPPV, but only to relieve the nausea
that can accompany vertiginous episodes. Short-acting medications, such

16
:(

::1 POSTERIOR AND ANTERIOR CANAL BPPV

:a
as phenergan, can be given prior to treatment .in those patients with severe
::$ nausea or emesis. Surgical treatments, such as vestibular nerve section, sec- /
tion of the singul<n nerve and occlusion of the affected cana}/9-31 are rarely: /
:::8 used because BPPV is successfully managed in most patients with CRT, the
,, '

Liberatory maneuver, or exercises.

:3
:I

=
:;I
l
:::Q
::rJ
~
~

:rJ
;:Q
::g
::II
~
~
~

=
=
:I

=
= 17
::3
 DIAGNOSIS AND TREATMENT OF BENIGN PAROXYSMAL POSillONAL VERTIGO
ec
e:
HORIZONTAL 'CANAL BPPV ~ =
@:

I
Provocative maneuver
If either the Dix-Hallpike maneuver or sidelying maneuver provokes
horizontal nystagmus, the examiner should proceed inunediately to the roll ~
maneuve~; shown in Figure 11 (top row). c;::
To begin, place the patient in the supine position with nose upward and
the neck flexed about 30 deg so the plane of the horizontal canals is verticaJ c:L
\
(Figure llA). Then tum the patient's head quickly to the right-ear-down
position (Figure 11 B) and wait. at least 40 sec for an a~normal response c:
(described below) to appear. If it qoes, monitor the response for at lea.St I I
m_in or until it subsi~e~~ Then bring the patient's head slowly back to the c:
nose-up position (Figure 11 C). Then tum the patient'~ head quickly to the l
left-ear-down position (Figure liD) and waitatleast40 sec for an abnormal ~
response to appear. If it does, monitor the response for at least 1 min or until
it subsides. Finally bring the patient's head slowly back to the nose-up posi- ~I
tion (Figure liE).
Cf
A B c D E e:p
\
Sf
.
Sf
-==I
~u~ou 'canaJiths
ec=
eI
e:::
0~ 0~ov
0

e:::I
ad=
~
. .
Figure 11. Roll maneuver for horizontal cmwl BPPV. A, nose up; B, rightward roll to
right ear down position; C, nose up; D, leftward roll to left ear down position; E, nose
up. Top row, movement of the patients head;. middle row, movement ofcanaliths and
deflection ofthe cupula in the right horizontal canal; bottom row, deflection ofthe cupula
due to cupulolithiasis in the right horizontal canal. Note that the deflection ofthe cupula
ad= l
is greatly exaggerated.
c:
18 -.:::
Ff I
~

~ HORIZONTAL CANAL BPPV

~
"When performing this maneuver, the examiner should visually observe
:IJ the patient's nystagmus responses v.rith t."'Ie patient weanng Frenzel's glasses
in a darkened room or record it with an in.<tred video system. ENG can
=* also be used to record.these responses if recording is done with the patient's-
vision obscured.
~
Abnormal responses
~ Normal persons have a few beats of nystagmus during the quick right-
ward and leftward head movements, but no nystagmus after these move-
~ ments have been completed.
Patients with horizontal canal BPPV have two bursts ofnystagmus, one
~ following the rightward head movement and one following .the leftward
~ head movement. These two nystagmus responses are usually transient,

=
although- each may last for several minutes. Each response is accompanied
by vertigo, usually intense vertigo, which follows the same time courre as
the nystagmus. One response is always more intense than the other. Ifa nys-
::lQ tagmus response is particularly intense, it may be followed by a secondary
nystagmus response in the opposite direction.
~ The examiner can determine which horizontal canal is involved by not-
ing the relative intensities of these two nystagmus responses and the direc-
~ tions of their fast phases.
Usually the fast phases are geotropic (that is, rightward afterihe right-
~ ward head movement and leftward after the leftward head movement). If so,

=
~
we presume the patient has canalithiasis of the horizontal canal that is
undermost during the more intense nysta.:,a:mus response.
Figure I 1 (middle row) shows what we think happens when \Ve perform
the roil maneuver on a pa!}ent with canalithiasis ofthe right horizontal
::C canaL . When the patient is in the nose-up position, the C<UJ.aliths lie in the
lowest part oft11e horizontal canaL V/hen the patient's head is rolled quick-
:c ly to the nght, the canaliths slide down toward the cupula. P..B they slide,
they push endolymph toward the cupula, deflecting the cupula, exciting the.
:C hair cel.Is, and provoking vertigo and nystagmus with rightward tast phases.

:c "When the head is rolled to the left, the canaliths slide away from the cupu-
h, this time deflecting 1'the cupula in the opposite direction, inhibiting the
:c. canal receptors, and provoking vertigo and nystagmus with lefuvard fast
phases. The excitatory response is stronger than the inhibitory response, and
we think this is because the caniliths move a greater distance.
:IP Sometimes the fast phases of these nystagmus responses are ageotropic
:Ql (that is, leftward after the rightward head J?Overp.ent and rightward after the

~ 19

:B
 .J;
OIAGNOSIS .:-.NO TREATMENT OF BENIG::--1 PAROXYSMAL POSITIONAL VERTIGO
e::_I
-
e}=
leftward head movement). If so, then we presume the patient has cupu-
lolithiasis of the horizontal canal that is undermost during the more intense c::
nystagmus response.
FigUre 11 (bottom row) shows what we think happens when we perform ~
the roll maneuver on a patient y.rith cupulolithiasis of the right horizontal
canaL When the patient is in the nose-up position, the otoliths are attached
c:
to the cupula. \v'hen the patient's head is rolled quickly to the right, the =!:I
weight of t..~e otoliths deflects the cupula, iiL~ibiting the hair cells and pro-
voking vertigo and nystagmus with leftward fast phases. \Vhen the patient's c:i
head is rol!ed to tbe left, the we;ght of the otoliths deflects the cupula in the
opposite diJ;ection, thi~ time exciting the canal receptors" provoking vertigo IE=
a.."'ld nystagmus with righhvard fast phases.
I
Sometimes the examiner sees spontaneous or positional nystagmus
when performing the roll maneuver. These types of nystagmus are easily
"T
distinguished from horizontal canal BPPV. Spontaneous nystagmus is per- -=f
sistent and invariant in different head positions. Positional nystagmus varies
in intensity and/or direction in different head positions, but is persistent and
invariant in a given head position. Spontaneous and positional nystagmus
-== I
'e::::
are both nonspecific evidence of vestibular dysfunction, either peripheral or
centraL e:=II
Treatment e:::I
A modification of CRT_ can be used to treat patients with horizontal
. canal BPPV due to canalithiasis (that is, patients with geotropic nystagmus e:::
responses).3u~ The patient begins in thesupine position with the affected I
ear down, shown (for right horizontal canal involvement) in Figu;e 12 (top
e:::
row). The patient's head is slowly rolled leftward to the nose-up position
and held there for about 15 sec or until any vertigo stops. Then the head is
ed:
rolled leftward until the affected earis uppermost and held there for 15 sec '~
or until vertigo stops. Then the head and body together are rolled leftward
to the nose-do'wn po~ition and held there for 15 sec..Finally, the head and .d:
~
body together are rolled leftward to the original position with the affected
ear undermost After 15 seconds, the patient slowly sits up, keeping the
head level or pitched down by 30 deg. Thd'patient is fitted with a soft col-
lar and given the same in.:,"trtlctions as described above for CRT for anterior ad:
or posterior canal BPPV. Figure 12 (bottom row) shows what we think hap-
pens when we perform this treatment The canaliths slide out of the canal e:::
and into the utricle, where they no longer cause symptoms.
For patients with canalithiasis of the left horizontal canal, the appropri-

20
:a
::$ HORIZO"NiAL C.-\NAL BPPV

:s A 8 c 0 E
:a ~ ~

~ ~
::8
::J (J) v
v
~

::IP

* "'"
u~~ou
. 'canaliths

:Q Figure 12 Modified CRTfqr canalithiasis ofthe right horizontal canal. A, right ear
dOl~'n;B. lefMard roll to nose up position; C. leftward roll to liifi ear dawn position; D,
::Q leftward roll to nose doH'll position; E, lefMard roll to right ear do>m position. Top raw.
movement ofthe patients head; bottom row, movement ofcanaliths in the right horizontal
~ canal.

:. ate maneuver would be the opposite of the -one shown in Figure 12 (that is,
the patient would begin with the left ear undermost and rolled to the right).
:u The Brandt-Daroff exercises can be modi[led for treatment of patients
with horizontal canal BPPV due to cupulolithiasis (that is, patients with
::8 ageotropic nystagmus responses). Such patients would be asked to perform
rapid back-and-forth movements in the plane of the horizontal canal while
:I' supine. This treatment would be expected to dislodge otoconia from the
:a cupula.
As yet evidence of the efficacy of these treatments for horizontal canal
:I BPPV is only anecdotaL

:il
:t
*
:8
:1

*::1 21

=-
 I
.d;:
DIAGNOSIS AND TREATMENT OF BENIGN PAROX'{Stv1AL POSITIONAL VERTIGO
~
SUMMARY

BPPV is a corinnon disorder, and it can be treated by sate and simple

-==
~
procedures that bring immediate relief in many patients.: As we have seen.
there are various types of treatment Selection .of the appropriate type of t::i
treatment depends upon identification"- of the type or' pathology involved,
and sur;h identification depends upon careful observation of.the patient's
c=
nystagmus response to the provocative maneuver. The following t3:ble pro- tg:
vides a summary of the various types of patho!ogy, their identifYing fea- i
tures, and their treatmen~s. c:
Summary Table -==I
Type of pathology IdentifYing features of nystagmus
response to provocative maneuver
Treatment
~
Canalithiasis of . ; Upward & rightward torsional fast Right CRT e:::I
right posterior canal
Cupulolithiasis of
right posterior canal
Canalithiasis of
phases, < 1 min response duration
Up-..yard & rightward torsional fast
phases, > 1 min response duration
Upward & l9ftward torsional fast
Right Liberatory
wJbead turned left
Left CRT
-=
e:::
I
I
left posterior canal
Cupulolithiasis of
phases, < I min response duration
Upward & Jefhvard torsional fast Left Liberatory
e::::I
lclt posterior canal phases, > 1 min response duration wJbead turned right
c:
Canalithiasis of Downward & rightward torsional Right CRT I
right anterior canal fast phases, < 1 min response
e::::
Cupulolithiasis of
right anterior canal
Downward & rightward torsional
fast phases, > 1 min response
Right Liberatory
wJbead turned right .e
Canalithiasis of
left anterior canal
Downward & leftward torsional
fast phases, < 1 min response
Left CRT
ed:
Cupulolithiasis of
left anterior canal
Downward & leftward torsional
fast phases, > 1 min response
Left Liberatory
w/be<Jd turned left e
Canalithiasis of
right horizontal canal
Horizontal, geotropic fast phases,
s'"..ronger right ear down
Modified CRT
Qeftward roll)
"t::
Cupulolithiasis of
right horizontal canal
Horizontal, ageotropic fast phases,
stronger right ear doWh
Modified Brandt-
Daroff ed: i

Canalithiasis of
left horizontal canal
Horizontal, geotropic fast phases,
stronger left ear down
Modified CRT
(rightward roll)
e:::
Cupulolithiasis of
left horizontal canal
Horizontal, ageotropic fast phases,
stronger left ear down
Modified Brandt-
Daroff
.e:::
22
-==
e:::
~
=1:
~ ILLUSTR.A.Tl\'E CASES

~
ILLUSTRATIVE CASES
::1:
Most cases of BPPV are straight forward, but some cases are a more
::8 complex, as illustrated by the following:
A case of bilateral response to the Dix-HaUpike maneuver
~
The patient is a 56-year-old male \vith complaints of intermittent verti-
~ go. The patient also has a degenerative cererellar disorder. Testing was
performed using an infiared camera system to wrevent fixation suppression
~ of nystagmus and to video-record the nystagmus. The left Dix.:.Hallpike
maneuver provoked nystagmus \Vith dmmwaro and leftward torsional fast
~
phases after a latency 9f 5 sec. Concurrent with the nystagmus, he com-
~ plained of slight vertigo. The vertigo lasted 35 seconds, but his nystagmus
pc;rsisted for more than one minute: The right Dix-Hallpike maneuver pro-
~ voked a fulminate nystagmus with upward fust phases, accompanied by
severe vertigo. This nystagmus lasted more than 90 sec. -When he returned
~ to a sitting position, he developed ~ystagmus with doWI!Ward'tlst phases.
Bo.th the left and right Dix-Hallpike manem:ers provok~ nystagmus and
;s. . vertigo. The nystagmus \vas. more vigorous a:nxfhe was more symptomatic
after the right Dix-Hallpike ma~euver. TI1is snggests that he may have had
~ involvement of both the right posterior canal _!i!nd left anterior canal.. It is
more likely, however, that his signs and symptoms were caused solely by the
~ right posterior canal involvement. Some movement of the debris may have
occurred when ti1e left Dix-Hallpike maneuver \Vas performed because of
~
the orientation of his labyrinth or because ofrlle head orientation during the
:s test The persistence of his nystagmus suggests -cupulolithiasis or may
refleCt a central lesion, although the fact that it had upward. fast phases with
:a right ear undermost and downward fast phases with left eai- undermost is not
congruent with a central lesion. . :- .
:s Because the patient had more seYere compfaints associate~~with the light
side, .he was fi_rsf tr~ated for right posterior <Cai:lai cupuloEthiasis using the
::e Liberatory maneuver. On reassessment one week later, the patient had no

:a nystagmus or vertigo .
...
A case of posterio1 canal BPPVfollowed hy horizontal canal BPPV
The patient is a 2 !-year-old female in ~<hom the right Dix-Hallpike
maneuver provoked nystagmus \\'ith up\vant and rightward torsional fast
::8 phases. C0ncurrent with the nystagmus. she had complaints ofvenigo. TI1e
~- latency of onset of the nystagmus \\as 28 see _and the..duration of the nys-

:8 23

:t
 DIAGNOSIS AND TREATiv!ENT OF BENIGN PAROXYSMAL POSITIONAL VERTIGO
c::=
- I

tagmus and vertigo was 20 sec. The patient was treated for right posterior c::=
canal canalith~asis using CRT. Three days later, the patient called with com-
plaints of severe vertigo and imbalance. She was s~n in the clinic that day
~
and it was noted that she needed assistance to walk safely. She stated that
she had been symptom-free following the tr~atment until the first time she ~
lay down on her right side. cg:
On examination, she had no spontaneous or gaze-holding nystagmus.
She had no nystagmus following horizontal or vertical head shaking. The eg:
right Di."'{-Ha1lpike maneuver provoked nystagmus with rightward fast
phases, accompanied by vertigo, after a latency of 49 sec. The nystagmus e:::
a.r:1d vertigo lasted for 30 sec. Then the nysbgmus ~eversed direction and
c::ontinued for another minute. The left DL"'{-Hallpike maneuver provoked e::
nystagmus with leftward fast phases accompanied by mild vertigo. g:::::
This patient initially had posterior canal canalithiasis. It appears that the
free-floating canaiiths may have moved into the horizontal canal when she g::::
first lay down after treatment. She now has a geotropic nystagmus with ver-
tigo, worse on the right, indicating right horizontal canal canalithiasis.
Although the nystagmus and vertigo were provoked in the DL"'{-Hallpike
c:::
maneuver, it would have been appropriate to test her also using the roll test. a:::
1
A case of superior vestibular artery infarct
a::= I
The patient is a 72-year-old female with complaints of episodic and brief
vertigo. The patient states that several years ago, she had vertigo lasting for a= '

. several days. Examination using an infrared camera system revealed no

spontaneous or gaze-holding nystagmus. Horizontal head shaking resulted v:=
in a right beating nystagmus that reversed. She had, no vertical head shak-
ing induced nystagmus. The right Dix-Hailpike maneuver did not pmvoke
ed:
nystagmus or vertigo. The left Dix-Hailpike maneuver provoked nystagmus e:::
with upward fast phases; accompanied by vertigo, that lasted for 12 sec.
The right beating nystagmus following horizontal head shaking suggests
a left horizontal canal paresi;;. The patient's response to the left Dix-
Hallpike maneuver is consistent with left posterior canal canalithiasis. The
combination of horizontal canal paresis with posterior canal BPPV occurs
-
~

'e:::
1

with a superior vestibular artery infarct. This artery supplies the horizontal ra:::
. and anterior canals and the utricle. The arterial supply to the posterior canal
is by the inferior vestibular artery. Presumably, debris from the utricle float- 1!:::::
ed into the still functioning posterior canal.
e.:::

24
-==
-.:::::
'F=

ACKJ.'l"OWLEDGEME:\T
ACKNOWLEDGEME!'-'T

Supported by NIDCD Grant DC-031% .

:$

=-:a
:s
:It
=-
~

=-:8
:e
:e
=-
:a
:e
::e 25

:w
 DIAGNOSIS AND TREATMENT OF BENIGN PAROXYSMAL POSmONAL VERTIGO l
~
REFERENCES ~
L Mizukoshi K, Watanabe Y, Shojaku H, et R.I.: Epidemiological studies ~

~
on benign paroxysmal positional vertigo. Acta Otolaryngol (Stockh)
1988: Suppl 447; 67-72.

2. Froehli...'lg DA, Silverstein MD, Mohr DN, et al: Benign positional 19:
vertigo: Incidence and prognosis in a population-based study in @::
Olmsted county, Minnesota. Mayo Clirr Proc 1991; 66: 596-601.

3. Baloh RW, Hon.'Llbia

. V, Jacobsvn K: Benign positional vertigo; c=
Clinical and oculographic features in 240 cases. Neurology 1987; 37:
371-378. . . -==
4. Herdman SJ, Tusa RJ, Clendaniel RA: Eye movement signs in verti-
-==
cal canal benign paroxysmal positional vertigo. In: Contemporary
Ocular Motor and Vestibular Research: A Tribute to David A. -==
5.
Robinson. A F Fuchs, T Brandt, U Buttner and D Zee (eds). Thieme,
Stuttgart 1994; 385-3.87:

McClure J: Horizontal canal BPV. J OtolaryngoL 1985; 14:30-35.

-=
e:::
6. Baloh RW, Jacobson K, Honrubia V: Horizontal semicircular canal e::
variant ofbenign positional vertigo. Neurology 1993;43: 2542-2549.
e:::
7. De la Meilleure G, behaene I, Depondt M, Damman W, Crevits L,
Vanhooren G: Benign paroxysmal positional vertigo of the horizon- e::
tal canal. J Neurol, Neurosurg, P~ych 1996; 60:68-71.

8. Nuti D, Vannucchi P, Pagnini P: Beni~ Paroxysmal Positional

e:::
Vertigo of the Horizontal Canal: A form of canalithiasis with variable e:::
clinical features. J Vestib Res 1996; 6: 173-184.

9. Hall SF, Ruby RR, McClure J: The mechanisms of benign paroxys-

e:::
mal vertigo. J OtolaryngoL 1979;8: 151-158. e:::
10. Parnes LS, McClure JA: Free-floaring Endolymph Particles: A new
operative finding during posterior semicircular canal occlusion.
e::::
Laryngoscope 1992; 102: 988-992. e::=
1 L Schuknecht HF: Cupulolithiasis. Arch Otolaryngol. 1969;90: 765-
778. -==
e::
26 e:::
F
~
~ REFERENCES

~
12. Boumans LJJM, Rodenburg M and MaasAJJ: Gain of the adaptation
~ mechanism in the human vestibula-ocular reflex system. ORL 1988
50:319-329. ,
:&
13. Dix MR, Hallpike CS: Pathology, symptomatology and diagnosis of
~ certain disorders of the vestibular system. Proc Roy Soc Med 1952;
45: 341-354. .
~
14. Fisher A, Gresty M, Chambers B, Rudge P: Primary position upbeat-
~ ing nystagmus: A variety of central positional nystagmus. Brain.
1983; 106: 949-964.
~
15. Epley JM: New dimensions of benign paroxysmal positional vertigo.
~ Otolaryngol Head Neck Stirg 1980; 88: 599-605.

16. Parnes LS, Price-Jones RG: Particle repositioning maneuver for

~ benign paroxysmal positional vertigo. :Ann Otol Rhino! Laryngol
~ 1993; 102: 325-331.
I 7. Semont A, Freyss G, Vitte E: Curing the BPPV with a Liberatory
:& maneuver. Adv Otorhinolaryngol 1988; 42: 290-293.
~ I 8. Brandt T, Daroff RB: Physical therapy for benign paroxysmal posi-

s tional vertigo. Arch OtoiaryngoL 1980; l 06:484-485.

19. Herdman SJ, Tusa RJ, Zee DS, Proctor LP, Mattox DE: Single treat-
~ ment approaches to benign paroxysmal positional vertigo. Arch
Otolaryngol Head Neck Surg. 1993;119: 450-454.
$

20. Li JC: Ma_stoid oscillation: a critical factor for success in t.i.e canalith
repositioning procedure. _Otolaryngol Head Neck Surg 1995; 112:
670-675.

*
$
21. Lyim S, Pool A, Rose D, Brey R, Suman V: Randomized trial of the
canalith repositioning procedure. Ot61aryngol Head Neck Surg 1995;
113: 712-720. .
:$ 22. Massoud EAS, Ireland DJ: Post-treatment Instructions in
:s Nonsurgical Management of benign Paroxysmal Positional Vertigo.
L Otolaryngoll996; 25: 121-125.
:s
:s
:s 27

:e
DIAGNOSIS AND TREATMENT OF BENIGN PAROXYSMAL POSITIONAL VERTIGO

-23. J;:pley JM: The ca:rialith repositioning procedure: for treatment of

benign paroxysmal positional vertigo. Otolaryngol Head Neck Sttrg.
1992; 107:399-404.
24. Harvey SA, Hain TC, Adamiec LC: Modified Liberatory maneuver:
Effective treatment for benign paroxysmal positional vertigo.
Laryngoscope 1994; 104: 1206-1212.
25. Welling DB, Barnes DE: Particle repositioning maneuver for benign
paroxysmal positional vertigo. Laryngoscope 1994~ 104:946-949.
26. Ireland D. TheSemont mWleuver: Proceedings of the XVIth Barany
Society Meeting, Prague Czechoslovakia 1994; 367-370. .
27. Tusa RJ, Herdman SJ: Assessment ~d treatment of anterior canal
Benign Paroxysmal Positional Vertigo using the analith
Repositioning Ma.11euver (CRi\11). Am Acad Neurology (ANN) Abstr
Neurology 1997; 48: A384..
28. Herdman SJ, Tusa RJ: Complications of the carialith repositioning
procedure. Arvh Otolaryngol HeadNeckSurg 1~96; 122:281-286.
29. Gacek RR: Singular neurectomy update. Ann. Otol. Rhino!.
Laryngol. 1982;91:4~9.
30. Gacek RR: Techniques and results of singular neurectomy for the
management of benign paroxysmal positional vertigo. Acat
Otolaryngol (Stockh) 19~5; 115: 154-157.
3 L Parnes LS, McClure JA: Posterior semicircular canal occlusion for
intractable benign paroxysmal positional vertigo. Ann Otol Rhino!
LaryngoL 1990; 99:330. .
32. Pagnini P, Vannucchi P, Viani C: La riedtlcazione vestibolare: Aspetti
clinici e reseltati. Giomate Italiane de Otoneurologia 1989; 8: 81-94.
33. Lempert T, Tiel-Wilck K: A Positional Maneuver for Treatment of
Horizontal-Canal Benign Positional,. Vertigo. Laryngoscope 1996;
106:476-478. .
34. Herdman SJ: Physical Therapy in the tr~atment of patients \Vith
Benign Paroxysmal . Positional Vertigo. Neurology Report, 1996;
20:46-53.

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