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11
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Positional Testing and Treatment
Richard A. Clendaniel
introduCtion
The first detailed description of positional vertigo was
supplied by Bárány in 1921 (Lanska & Remler, 1997),
in which he noted several of the key characteristics of
benign paroxysmal positional vertigo (BPPV): mixed
vertical and torsional nystagmus, the brief duration of
the nystagmus and vertigo, as well as the decreased
response, or fatigability, of the nystagmus and vertigo
with repetitive provocations. In 1931 and 1950, Nylén
(1931, 1950) described a series of tests positions used
for the assessment of positional nystagmus. While
Nylén included many positions in his tests, none of
which were analogous to the currently accepted provocative test for BPPV, he did make a clinically important marked distinction between positional nystagmus
and positioning nystagmus. The positional tests are
performed slowly, taking five seconds to move the
patient 90 degrees, and the resulting nystagmus is
thought to be due to the position of the head in space,
compared with the positioning tests, which are performed rapidly, and the resulting nystagmus is due to
the movement of the head into a specific position. Based
on this distinction, BPPV is technically benign paroxysmal positioning vertigo (Brandt, 1990). The purposes
of this chapter are (1) to describe the different test procedures for positional and positioning nystagmus, (2)
identify the various interpretations of the test results,
and (3) provide guidance for the treatment of the various forms of BPPV.
Positional nystagmus
The purpose of the positional test battery is to determine
if head position in the gravitational field has any effect
on the production of nystagmus. In these tests, the head
is brought slowly into different positions, the static position is maintained, and the eye movements are recorded
and analyzed. These tests are performed with vision
blocked, although one can allow for vision to determine
if the patient can visually suppress the nystagmus. There
is variability among vestibular testing labs as to which
positions are used, although the following eight positions are typically assessed: sitting with head turned to
the right and with head turned to the left; supine; supine
with head turned to the right and with head turned to
the left; right and left side lying; and the pre-irrigation
position. If there is no cervical spine pathology, pain, or
limited range of motion, then the following positions
can be assessed before placing the patient in the pre-irrigation position: supine, head hanging with the cervical
spine not rotated, rotated to the left, and rotated to the
right. Shepard and Telian (1996) suggested the following criteria for determining whether or not the observed
spontaneous (sitting with the cervical spine in neutral)
and positional nystagmus are clinically significant:
n Slow component eye velocity (SCV) in any
position is greater than 5 deg/sec
n SCV less than 6 deg/sec and persistent in 4 or
more positions
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n
SCV less than 6 deg/sec and sporadic in all of
the tested positions
n Direction-changing nystagmus within a given
head position
If there is a spontaneous nystagmus with vision
blocked while the patient is seated, then to have a
pathological positional nystagmus, the observed positional nystagmus should be greater than the spontaneous nystagmus. If there is not an increase in the SCV,
then the nystagmus observed in the different positions
is simply a manifestation of the underlying spontaneous nystagmus.
Interpretation of Positional Nystagmus
Positional nystagmus may be observed secondary to
both peripheral vestibular and central causes (Harrison
& Ozsahinoglu, 1972; Sakata, Ohtsu, Shimura, & Sakai,
1987) and can be seen in indviduals with normal vestibular system function (Barber & Wright, 1973). General considerattions for the interpretation of positional
nystagmus will be discussed here, especially as the
findngs relate to positional nystagmus from a peripheral cause. However, since positional nystagmus due to
a central cause may be observed in both the positional
and positioning tests, the interpretation of both positional and positioning nystagmus due to central causes
will be discussed in more detail later in this chapter.
Positional nystagmus may be seen following a unilateral vestibular loss, especially in more acute or uncompensated stages. The nystagmus is horizontal, either
geotropic (beating toward the ground), or apogeotropic
(beating away from the ground). Generally the pattern
of nystagmus will remain direction fixed in the positional tests, or will be either geotropic or apogeotropic in the positional tests. The nystagmus observed in
these cases is thought to be due to the interaction of the
changing otolithic input with the asymmetrical semicircular canal (SCC) input, or may be due to a reduction in the suppression of the asymmetric SCC activity.
Since the geotropic or apogeotropic nystagmus in the
positional tests may also be observed in cases of horizontal SCC BPPV, or as a result of a central disorder,
the interpretation of the test results can be challenging.
As will be discussed later, individuals with horizontal SCC BPPV will develop geotropic or apogeotropic
nystagmus with the position changes and are very
symptomatic with the change in position. Conversely,
individuals with positional nystagmus as a result of
unilateral vestibular loss are either asymptomatic or
have mild symptoms. In these cases, the intensity of the
symptoms may aid in the determination of the cause
of the nystagmus. Isolated geotropic or apogeotropic
positional nystagmus may be due to a central lesion,
but in the absence of other oculomotor abnormalities,
this nystagmus is generally thought to be attributable
to a peripheral cause.
Cervicogenic Nystagmus
While cervicogenic dizziness and cervicogenic nystagmus are rare occurrences, the positional tests allow for
evaluation of this condition. Nystagmus generated by
the cervical spine would be expected to be provoked by
head position relative to the body, regardless of head
position in space. For example, if the cervical rotation
to the right were to cause nystagmus, then one would
expect to see the nystagmus in sitting with head turned
to the right, supine with head turned to the right, and
with head hanging with head turned to the right. At the
same time, one would not expect to see nystagmus in sitting, right side lying, or in the head hanging positions.
POSITIONING NYSTAGMUS
Unlike the tests for positional nystagmus, the tests
for positioning tests are designed to determine if the
sudden change in head orientation relative to gravity
produces nystagmus and elicits symptoms. When the
position change elicits vertigo and specific patterns of
nystagmus, the patient can be diagnosed with BPPV.
BPPV is one of the most common causes of dizziness,
in some studies (Kroenke, Hoffman, & Einstadter, 2000)
accounting for 16% of all cases of dizziness. In clinics
specializing in the treatment of dizziness, BPPV is diagnosed in close to 30% of individuals (Neuhauser, Leopold, von Brevern, Arnold, & Lempert, 2001). Estimates
of the one-year incidence of BPPV range from 0.01 to
2.4%, with a lifetime prevalence of 2.4% (Froehling et
al., 1991; Mizukoshi, Watanabe, Shojaku, Okubo, &
Watanabe, 1988; von Brevern et al., 2007). Fortunately,
BPPV is easily diagnosed with relatively simple clinical
tests and is, generally, effectively treated with various
treatment maneuvers.
It wasn’t until 1952 that Dix and Hallpike (1952)
described the technique that we know as the Dix–
Hallpike test. In addition, Dix and Hallpike confirmed
the key characteristics of BPPV described earlier by
Bárány and identified two other key characteristics of
BPPV: (1) the latency to the onset of the nystagmus and
11. PositionAl tEsting And trEAtmEnt 227
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vertigo and (2) the reversal of the nystagmus when the
patient sits up. They labeled this “positional vertigo
of the benign paroxysmal type” and felt that it was
caused by an irritative lesion of the peripheral vestibular system. Dix and Hallpike further postulated that it
was irritation of the utricle that was responsible for the
signs and symptoms of BPPV.
The utricular origin of BPPV was a matter of
debate for several years. In the early 1960s, Schuknecht
(1962) modeled a gravity-dependent movement of
loose otoconia that caused stimulation of the posterior
SCC ampulla, producing the nystagmus and vertigo
observed in BPPV. However, the model was anatomically incorrect and did not fit with the known physiology of the hair cells within the posterior SCC. This
hypothesis was revised based in part on the finding of
deposits attached to the cupula, as well as to fit with
the known anatomy and physiology of the vestibular
system. The revised hypothesis (Schuknecht & Ruby,
1973), cupulolithiasis, proposed that the otoconia were
attached to the cupula of the posterior SCC, making
the cupula gravity dependent, which would cause the
cupula to deflect in a direction that excites the hair cells
in the posterior SCC during the provocative tests. This
hypothesis, while explaining the direction and latency
of the observed nystagmus in BPPV, does not explain
the typical short duration of the nystagmus.
Hall, Ruby, and McClure (1979) proposed an
alternative mechanism behind BPPV, canalolithiasis
(commonly called canalithiasis today), in which the
displaced otoconia, or canaliths, are freely mobile
within the semicircular canal. This model accounts for
all the characteristics of typical BPPV: latency, duration,
direction of the nystagmus, reversal of the nystagmus,
and fatigability. They also recognized a second form of
BPPV where the canaliths are attached to the cupula,
giving rise to nystagmus of prolonged duration.
There is some physical evidence to support these
hypotheses. Schuknecht (1973) did observe granular
deposits adherent to the cupula of the posterior SCC in
temporal studies of individuals who had a history of
BPPV. Others (Parnes & McClure, 1992) have observed
mobile particulate matter within the endolymph of the
posterior SCC during canal plugging surgical procedures for BPPV, lending some anatomical support for
canalithiasis. In addition, one study (Welling et al.,
1997) evaluated the particulate matter removed from
one posterior SCC under electron microscopy and
reported that the material appeared consistent with
degenerating otoconia. There are, however, studies that
raise some questions about canalithiasis and cupulolithiasis. Kveton and Kashgarian (1994) reported finding
particulate matter in the posterior SCC of individuals
who had no symptoms of BPPV. Moriarty and colleagues (1992) conducted temporal bone studies and
measured the frequency and size of deposits on the
cupulae of over 1,000 semicircular canals. They found
deposits on close to 22% of the cupulae. The clinical
histories were available for most of the patients, and
there was no history of BPPV. Based on these findings,
the significance of the deposits and particulate matter
is unclear.
etiology
There are few large series studies assessing the cause of
BPPV. In the two studies (Baloh, Honrubia, & Jacobson,
1987; Katsarkas & Kirkham, 1978), the most common
etiology was idiopathic, accounting for 49% and 66%
of the cases. BPPV secondary to head trauma was the
next most common cause, accounting for 18% of the
patients in both studies. BPPV was seen secondary to
viral neurolabyrinthitis in 2% and 15% of the patients,
respectively, in the two studies and secondary to vertebrobasilar insufficiency in 1% and 5% of the cases. Miscellaneous disorders, including Meniere’s, migraine,
otosclerosis, and other ear disorders, were associated
with BPPV in 12.5% and 13% of the patients in the two
studies. Baloh and colleagues (1987) found that across
all diagnostic groups the ratio of females to males was
1.6:1. While BPPV can be seen across all age ranges, it
is unusual to see BPPV in children, and the idiopathic
form of BPPV most frequently occurs in individuals in
their 60s (Baloh et al., 1987).
While the earlier studies proposed that BPPV was
due to stimulation of the posterior SCC, BPPV can
be seen in the anterior and horizontal SCCs as well.
Several studies (Herdman, Tusa, & Clendaniel, 1994;
Korres et al., 2002; Prokopakis et al., 2005) have documented the occurrence rate of BPPV affecting the different semicircular canals. All three studies found that
the posterior SCC was the most commonly affected
canal, accounting for 83% to 91% of the identified
cases. The study by Korres and colleagues (2002) as
well as the study by Prokopakis and colleagues (2005)
found that horizontal SCC BPPV accounted for 8%
and 10% of the cases, respectively, and that anterior
SCC BPPV accounted for only 1% and 2% of the cases.
In the study by Herdman and colleagues (1994), the
prevalence of anterior SCC BPPV, 15%, was greater
than horizontal SCC BPPV, 2%. In this study, there
were a substantial number of individuals with BPPV
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who were not included in the analysis because the
pattern of nystagmus, and the affected semicircular
canal, could not be ascertained secondary to either
eye closure during the nystagmus or a vertical component that could not be determined. This may have
affected the observed distribution of the affected semicircular canals.
CLINICAL PRESENTATION
Individuals suffering from BPPV experience brief, but
often intense, symptoms of vertigo associated with
changes in head orientation relative to gravity. These
individuals commonly complain of vertigo associated
with lying down, rolling over in bed, and sitting up
from a reclined position. They will often note symptoms of vertigo with bending over and with looking
up for objects on a high shelf, prompting the name
“top-shelf vertigo” (Squires, Weidman, Hain, & Stone,
2004). In addition to the symptoms of vertigo, individuals with BPPV typically also experience symptoms of
nonspecific dizziness, lightheadedness, imbalance, and
nausea (Baloh et al., 1987; Blatt, Georgakakis, Herdman, Clendaniel, & Tusa, 2000; Bloom & Katsarkas,
1989; von Brevern et al., 2007).
Before describing the clinical tests for BPPV, it is
important to keep two facts in mind. (1) What is critical
in the testing (and treatment) of BPPV is the position of
the head in space, not the position of the head relative
to the patient’s body. The tests that we will describe
can be modified to accommodate individuals who
have restricted cervical and trunk mobility. (2) The pattern and duration of the elicited nystagmus will indicate which of the semicircular canals is affected and
whether it is a case of canalithiasis or cupulolithiasis.
For both the canalithiasis and cupulolithiasis models of
posterior semicircular canal BPPV, the provoking test
will cause excitation of the posterior SCC hair cells,
which will result in a mixed up-beating and torsional
nystagmus, with the torsional nystagmus beating
toward the affected ear. In cases of anterior SCC BPPV,
the provoking test will cause excitation of the anterior
SCC hair cells, leading to a mixed down-beating and
torsional nystagmus, again with the torsional nystagmus beating toward the affected ear. BPPV affecting
the horizontal SCC will produce a horizontal nystagmus. For horizontal SCC canalithiasis, when the displaced otoconia are located in the posterior aspect of
one horizontal SCC, the provoking test will evoke nystagmus beating to the right when the head is turned
to the right, and to the left when the head is turned to
the left. In both cases, the nystagmus will beat toward
the ground and is referred to as geotropic nystagmus.
In cases of horizontal SCC cupulolithiasis as well as
canalithiasis where the displaced otoconia are located
in the anterior arm of the horizontal SCC, the provoking test will cause the opposite pattern of stimulation
to the hair cells and produce left-beating nystagmus
when the head is turned to the right and right-beating
nystagmus when the head is turned to the left. In both
cases, the nystagmus will beat away from the ground
and is referred to as apogeotropic nystagmus. The elicited pattern of nystagmus in the provocative tests is
summarized in Table 11–1.
Ta ble 11–1. Elicited Nystagmus in BPPV by Semicircular Canal
Involvement
Affected Semicircular Canal Right Left
Posterior
Anterior Down-beating
Horizontal
Canalithiasis
Cupulolithiasis and anterior
arm canalithiasis
* Indicates that BPPV on one side will produce nystagmus with provocative test
to both sides.
Up-beating
Right torsion
Right torsion
Geotropic*
Ageotropic*
Up-beating
Left torsion
Down-beating
Left torsion
Geotropic*
Ageotropic*
11. POSITIONAL TESTING AND TREATMENT 229
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Testing for BPPV
The classic test for BPPV is the Dix–Hallpike test,
originally described in 1952 (Dix & Hallpike, 1952). To
perform this test the patient starts sitting on a treatment table with his neck rotated 45 degrees to one side
(Figure 11–1A). This neck rotation places the ipsilateral
posterior SCC in the sagittal plane, which will be the
plane of the movement during the test. This will also
place the ipsilateral posterior SCC in a gravity-dependent position when the patient is supine, which should
maximize the effect of gravity on the displaced otoconia
within the semicircular canal. The clinician can stand
either facing the patient (as shown in Figure 11–1A), or
behind the patient. The clinician will guide and assist
the patient into lying supine with neck now in 20 to
30 degrees of extension (Figure 11–1B). The position
change from sitting to supine should be performed relatively quickly, over the course of a couple of seconds.
This position is maintained and the clinician monitors
the patient’s symptoms and eye movements, looking
for nystagmus. The test can be performed in room
light or with vision blocked using Frenzel goggles
(either optical or video). Patients typically cannot suppress the nystagmus associated with BPPV, so Frenzel
goggles are not required; however, the Frenzel goggles
will make it easier to observe the nystagmus. There is
typically a short latency to the onset of the nystagmus
and vertigo once the patient is in the supine position,
but in some cases the latency can be prolonged, so
when performing the Dix–Hallpike test, it is recommended that the patient be kept in the supine position
for 30 seconds. Once the nystagmus and symptoms
have stopped, or after the 30 seconds in the test position. The patient is assisted to a seated position (Figure
11–1C). Again, the clinician will monitor the patient
for symptoms and nystagmus. Patients who have
BPPV will often develop symptoms and nystagmus on
A B
Figure 11–1. The Dix–Hallpike test on the right. A. Patient sits lengthwise on the treatment table. The clinician rotates
the patient’s neck 45 degrees to the right. B. The patient lies down quickly, assisted by the clinician, and extends
their neck approximately 30 degrees. The undermost ear, in this case the right ear, should be below the level of the
patient’s shoulder. The clinician monitors the patient’s symptoms and eye movements. continues
230 BALANCE FUNCTION ASSESSMENT AND MANAGEMENT
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C
figure 11–1. continued C . The clinician maintains the
45 degrees of neck rotation and assists the patient back
into a sitting position, again monitoring for symptoms
and nystagmus.
coming back to a seated position, so it is critical that
the clinician maintains contact and guards the patient
after the patient sits up. The test is then repeated
with the neck rotated 45 degrees to the other side. If
the patient has limited cervical extension, the test can
be modified by having the patient lie on an inclined
table, with the head of the table lower than the foot of
the table.
Another test is the side-lying test, described
by Cohen (2004) as an alternative to the traditional
Dix–Hallpike test for individuals with limited mobility, especially cervical extension. To perform this test,
the patient starts sitting on the treatment table with
her neck rotated 45 degrees away from the side to be
tested. The clinician will assist and guide the patient
into a side-lying position on the side to be tested (Figures 11–2A and B). Like the Dix–Hallpike test, this
movement is performed rapidly, and then the clinician
monitors the patient for provocation of symptoms and
nystagmus. The clinician will then assist the patient
back to a seated position, maintaining the cervical rotation during the movement. Once upright, the patient
rotates her neck to neutral and the clinician monitors
the patient for nystagmus and symptoms. The test
is then repeated for the opposite side with the neck
rotated in the opposite direction. Rotating the patient’s
neck 45 degrees to one side will place the contralateral posterior semicircular canal in the frontal plane,
which will be the plane of the movement during the
test. This again places the posterior SCC in a gravitydependent position when the patient is side lying and
should maximize the effect of gravity on the displaced
otoconia within the semicircular canal. Cohen (2004)
found no statistical difference between the side-lying
and Dix–Hallpike tests in the initial study.
While the Dix–Hallpike test is thought to primarily test the posterior and anterior semicircular canals,
patients with horizontal semicircular canal BPPV may
have a positive Dix–Hallpike test. The Roll test is a
positioning test designed to specifically assess for horizontal canal BPPV. This basis of this test was discussed
briefly by McClure (1985) and then formally described
by Pagnini, Nuti, and Vannucchi (1989). To perform
this test, the patient starts sitting on the treatment table
with the neck in neutral. The patient then lies supine,
with the head elevated approximately 30 degrees,
which places the horizontal SCC in an earth vertical
orientation. The clinician will then assist the patient
in rotating their neck 90 degrees to one side (Figures
11–3A and B). Like the Dix–Hallpike test, this movement is performed rapidly through the available range
of cervical rotation. If the patient has limited cervical
rotation, then the patient can simply roll to one side.
The clinician monitors the patient for provocation of
symptoms and nystagmus. The patient will then rotate
their neck to a neutral position. This process will then
be repeated to the other side (Figure 11–3C).
What constitutes a positive, or abnormal, positioning test? One can make the diagnosis of BPPV when the
positioning test induces vertigo and nystagmus that
meet the following criteria:
1. Vertigo and nystagmus that is consistent with
stimulation of the posterior SCC (mixed up-beating and torsion), the anterior SCC (mixed downbeating and torsion), or horizontal SCC (horizontal
nystagmus, geotropic or apogeotropic, when testing both sides),
2. A latency (generally less than five seconds) to the
onset of the symptoms and nystagmus once the
patient is in the testing position,
11. POSITIONAL TESTING AND TREATMENT 231
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A B
figure 11–2. The side-lying test for the right. A. Patient sits on the treatment table. The clinician rotates the patient’s
neck 45 degrees to the left. B.
side bends their neck to bring their head to the table.
movements.
symptoms and nystagmus.
The clinician will then assist the patient back up to a seated position. Again monitoring the patient’s
3. Paroxysmal vertigo and nystagmus (duration less
than one minute, displaying an increase and then
decrease in intensity), and
4. Fatigability of the nystagmus and vertigo with
repeated testing (Bhattacharyya et al., 2017; Furman & Cass, 1999).
The patient lies down quickly on their right side, assisted by the clinician, and extends
The clinician monitors the patient’s symptoms and eye
The elicited pattern of nystagmus is critical for
determining the affected semicircular canal. For the
posterior SCC, the diagnosis is usually straightforward,
as the Dix–Hallpike test on the affected side will generate the expected pattern of nystagmus, and the Dix–
Hallpike test on the healthy side will be negative (no
nystagmus or vertigo). The clinical presentation of ante-
From a clinical perspective, the fatigability of the
nystagmus and symptoms is often not tested, as the
patients will typically be treated following the diagnosis of BPPV. The duration of the nystagmus shows
some variability. The nystagmus associated with horizontal SCC canalithiasis may last longer than one minute secondary to the velocity storage system. In cases of
cupulolithiasis affecting any of the semicircular canals,
the nystagmus may persist as long as the individual
remains in the provoking position.
rior SCC BPPV is not as clear. There are reports in the
literature that for anterior SCC BPPV, the Dix–Hallpike
test will be positive when the neck is rotated away from
the affected ear (Kim, Shin, & Chung, 2005), toward the
affected ear (Bertholon, Bronstein, Davies, Rudge, &
Thilo, 2002; Crevits, 2004), and with cervical rotation
in both directions (Bertholon et al., 2002). The variability of the provocative test is due to the orientation of
the anterior SCC during the testing. For example, when
performing the right Dix–Hallpike test, the left anterior
A
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B
figure 11–3. Roll test for horizontal SCC BPPV. A. The
patient starts in supine with the neck flexed approximately 30 degrees. B. The clinician assists the patient
in rotating their neck 90 degrees to the right.
cian monitors the patient’s symptoms and nystagmus.
Then the patient will return their neck to neutral rotation.
C.The clinician assists the patient in rotating their neck
90 degrees to the left, again monitoring the patient’s
symptoms and nystagmus.
their neck to neutral rotation.
Then the patient will return
The clini-
C
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SCC is in the plane of the movement and ends up in an
earth vertical orientation. Canaliths within that canal
could then fall away from the ampulla, leading to excitation of the hair cells with a resultant down-beating,
left torsional nystagmus. If one were to perform the left
Dix–Hallpike in this same patient, the left anterior SCC
would not be aligned with the movement or end up
in an earth vertical orientation. However, due to the
cervical extension in the Dix–Hallpike, the left anterior
SCC will tilt below horizontal. Again, canaliths within
the canal could then fall away from the ampulla, leading to excitation of the hair cells, again with a resultant
down-beating, left torsional nystagmus. The clinician
must base the determination of the affected anterior
SCC on the direction of the torsional nystagmus, not
on the side of the provocative Dix–Hallpike test.
The horizontal SCC poses additional diagnostic
challenges. Due to the orientation of the horizontal
SCCs during the provoking tests, one horizontal SCC
will be stimulated with tests to both sides. The elicited
nystagmus will either be geotropic or apogeotropic
with positioning tests to both sides. Geotropic nystagmus is attributed to canalithiasis of the horizontal SCC
(Baloh, Jacobson, & Honrubia, 1993; McClure, 1985).
Apogeotropic nystagmus may be caused by either
cupulolithiasis of the horizontal SCC or by a variant of
canalithiasis where the canaliths are located in the anterior arm of the horizontal SCC near the cupula (Baloh,
Yue, Jacobson, & Honrubia, 1995; Fife, 1998; Nuti,
Vannucchi, & Pagnini, 1996; Steddin & Brandt, 1996).
Determination of the affected ear may be made based
on the intensity of the elicited nystagmus and symptoms. For horizontal SCC canalithiasis, it is hypothesized (McClure, 1985; Pagnini et al., 1989) that the
direction of the head rotation that elicits the greatest
nystagmus and symptoms is the affected side. This is
based in part on Ewald’s second law (Baloh, Honrubia,
& Konrad, 1977), whereby an excitatory stimulus generates a greater response than an inhibitory stimulus
of equal magnitude. The observed response asymmetry may also be due to the distance between the canaliths and the cupula, as well as the diminished effect as
the canaliths move out of the canal into the utricular
space (Baloh et al., 1993). For horizontal SCC cupulolithiasis and the anterior arm variant of canalithiasis,
the positioning tests will generate cupular deflections
opposite to those induced by typical horizontal SCC
canalithiasis. Thus, a positioning test to the involved
side will lead to inhibition of the hair cells of that canal,
and a decreased response compared with the response
elicited by the positioning test to the unaffected side
(Baloh et al., 1977; Steddin & Brandt, 1996).
Another test to determine the affected horizontal
SCC is the Bow and Lean test described by Choung,
Shin, Kahng, Park, and Choi (2006). Once the direction
of the nystagmus, geotropic or apogeotropic, has been
determined, the Bow and Lean test can be performed.
The patient starts seated upright. To perform the “bow,”
the patient will flex her/his cervical and upper thoracic
spine to bow the head 90 degrees. Once in this position,
the clinician will determine the direction of the elicited
nystagmus. After the patient returns to an upright,
seated position, the “lean” component of the test is performed by having the patient extend neck and trunk to
lean the head back 45 degrees. Again, the clinician will
determine the direction of the elicited nystagmus. For
patients with horizontal SCC canalithiasis, the nystagmus elicited with the bow will beat toward the affected
ear, and the nystagmus elicited with the lean will beat
away from the affected ear. For example, consider
right-sided, horizontal SCC canalithiasis. The “bow”
will cause the canaliths to fall toward the ampulla in
ampullopetal stimulation, leading to excitation of the
hair cells in the right horizontal SCC, which will elicit
nystagmus beating to the right (toward the affected ear).
The “lean” will cause the canaliths to fall away from the
ampulla in ampullofugal stimulation, leading to inhibition of the hair cells in the right horizontal SCC, which
will elicit nystagmus beating to the left (away from the
affected ear). For patients with horizontal SCC cupulolithiasis, the opposite pattern is seen; the nystagmus
elicited by the bow will beat away from the affected ear,
and that elicited by the lean will beat toward the affected
ear. As an example, consider right-sided, horizontal SCC
cupulolithiasis. The “bow” will cause the canaliths to fall
away from the ampulla in ampullofugal stimulation,
leading to inhibition of the hair cells in the right horizontal SCC, which will elicit nystagmus beating to the
left (away from the affected ear). The “lean” will cause
the canaliths to fall toward the ampulla in ampullopetal
stimulation, leading to excitation of the hair cells in the
right horizontal SCC, which will elicit nystagmus beating to the right (toward the affected ear). In the initial
study (Choung et al., 2006) of 11 patients with horizontal
SCC BPPV, there was agreement between the Bow and
Lean test and the intensity of the nystagmus in determination of the affected side in 50% of the cases. There
were 3
determine an intensity difference, but there were clear
findings with the Bow and Lean test. Likewise, there
were 3 patients who had no nystagmus in the Bow and
Lean test. There was disagreement between the two testing methods in 7 patients. In all 7, treatment based on
the results of the Bow and Lean test was successful.
patients in whom the investigators could not
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