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D
figure 11–9. continued C. The clinician then assists
and guides the patient into right side lying, keeping
the neck in 0 degrees of rotation. The patient remains
in this position for 30 to 60 seconds, or until the nystagmus stops. Note, the treatment can be performed by
simply rotating the neck 90 degrees, which makes the
subsequent position change a bit more involved. D. The
patient then rolls over into prone and props up on their
elbows. The clinician will support the patient’s head in
some flexion to place the horizontal SCC in an earth vertical orientation. The patient again remains in this position for 30 to 60 seconds, or until the nystagmus stops.
E. The patient can get up from this position, or can roll
another 90 degrees onto their left side and sit up from
a side lying position.
E
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this position for 30 to 60 seconds until the nystagmus
stops. From this position, the clinician will guide and
assist the patient to rotate the entire body to assume a
prone-on-elbows position. The patient’s neck remains
in neutral relative to rotation but assumes some flexion to place the horizontal SCC in an earth vertical
orientation (Figure 11–9D). The clinician should take
care in the placement of the patient’s hands to ensure
appropriate support of the patient’s head. One hand
will typically be supporting the patient’s forehead,
while the other hand is placed on the patient’s occiput.
Again, the patient will remain in this position for 30
to 60 seconds until the nystagmus stops. At this point
the patient has completed 270 degrees of rotation, and
the canaliths should have exited the horizontal SCC.
A patient who is able can get up from this position.
There are several methods that can be used: (1) the
patient can rise up on hands and knees and rock back
to sit on the heels; (2) the patient can rise up on hands
and knees, rotate the lower trunk to one side and drop
the pelvis to the treatment table, and then sit up from
that position; or if mobile, (3) the patient, from the
prone-on-elbows position, can rotate the lower trunk
so that the pelvis and legs are in essentially a side-lying
position, and then push up from the prone-on-elbows
position. The other, and often simpler, alternative
is to have the patient rotate the entire body another
90 degrees into the side-lying position (to complete
360 degrees of rotation; Figure 11–9E), and then sit up
from that position.
Regardless of the method used to get the patient
into a seated position, the provider should maintain
contact with the patient once sitting, just in case the
patient develops vertigo with the final position change.
Also, as with the CRP for the posterior SCC, the provider is simply guiding the patient’s head through the
movements.
Gufoni Maneuver for Geotropic Nystagmus. This
treatment was first published in English in a 2001
manuscript written by Appiani, Catania, and Gagliardi
(2001). In this article the authors credit the technique to
Gufoni in a 1999 Italian manuscript written by Asprella,
Libonati, and Gufoni. Hence there is some confusion in
the literature regarding the naming of the technique,
and it has been called both the Appiani maneuver and
the Gufoni maneuver. The current suggested terminology, based on the clinical practice guidelines (Bhattacharyya et al., 2017), is the Gufoni maneuver for
geotropic nystagmus. The premise of this technique
is similar to other treatments of canalithiasis, which is
the use of gravity to move the canaliths through the
affected horizontal SCC.
To perform the treatment, the patient starts in sitting on a treatment table. The clinician faces the patient
and assists and guides the patient into a side-lying position on the unaffected side (Figures 11–10A and B). The
patient remains in this position for 30 seconds. In this
position, gravity should cause the canaliths to migrate
posteriorly in the horizontal SCC. After the 30 seconds,
the clinician rotates the patient’s neck 45 to 60 degrees,
bringing the nose down toward the treatment table
(Figure 11–10C), which should cause the canaliths to
migrate out of the horizontal SCC and into the utricular
space. The patient remains in this position for an additional one to two minutes and is then brought back to
a seated position. Once the patient is upright, the neck
is brought back to a neutral position (Figure 11–10D).
Forced Prolonged Positioning (FPP)
This treatment was described by Vannuchi, Giannoni,
and Pagnini (1997) as an alternative treatment for horizontal SCC canalithiasis. This is a treatment that the
patient will perform on their own at home. The patient
starts by lying on the affected side for 30 to 60 seconds
until the vertiginous symptoms stop, during which
the canaliths should migrate to the most lateral aspect
of the horizontal SCC. The patient then slowly rolls
through supine onto the unaffected side and remains in
this position for 12 hours. The patient can get up to eat,
etc., but then returns to bed to continue the treatment.
Outcomes
There is evidence to support the use of the PRMs in the
treatment of horizontal SCC canalithiasis that generates geotropic nystagmus in the positioning tests. Nuti
et al. (1998) found that 71% of the 36 patients treated
with the CRP for horizontal SCC canalithiasis had resolution of their signs and symptoms. Likewise, Kim and
colleagues (2012) found a statistically significant difference in the resolution of signs and symptoms following the CRP for the horizontal SCC canalithiasis
compared with a sham treatment. In the same study,
they also reported a similar statistically significant difference in the resolution of signs and symptoms following the Gufoni maneuver for geotropic nystagmus
compared with a sham treatment. They found no difference between the resolution rates for CRP for the
horizontal SCC canalithiasis and the Gufoni maneuver for geotropic nystagmus treatments. Mandalà and
colleagues (2013) also found a statistically significant
difference between the Gufoni maneuver for geotropic nystagmus (88.9%) compared with a sham treatment (8.6%). Results of the FPP treatment appear to be
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C D
figure 11–10. The Gufoni maneuver for left horizontal SCC canalithiasis. A. The patient starts sitting on the treatment
table, with their neck in neutral. B. The patient lies down quickly on their right side. The clinician maintains the neutral
neck position. The patient remains in this position for 30 seconds. C. The patient rotates their neck 45 to 60degrees
to the right (nose down position) and remains in this position for 1 to 2 minutes. D. Maintaining the neck rotation,
the patient sits back up. Once upright they can bring their neck back to a neutral position.
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beneficial as well. In the original study, 22 of 29 patients
with horizontal SCC canalithiasis had resolution of
their signs and symptoms following one treatment
session (Vannuchi et al., 1997). Nuti and colleagues
(1998) reported a 76.2% success rate (n = 63) with the
FPP treatment. Recent meta-analyses (Buzzell, Frank,
Williams, Goode, & Clendaniel, 2014; Fu et al., 2019)
showed that CRP for the horizontal SCC canalithiasis,
the Gufoni maneuver for geotropic nystagmus, and
FPP were all effective methods of treating horizontal
SCC BPPV with geotropic nystagmus.
Horizontal Semicircular Canal BPPV
with
Apogeotropic Nystagmus
As discussed previously, the finding of bilateral apogeotropic nystagmus during the positioning tests is
consistent with either horizontal SCC cupulolithiasis or
canalithiasis with the canaliths located in the anterior
arm of the horizontal SCC. There are different treatment procedures that have been proposed based on the
presumed location of the otoconia. One treatment is
based on the possibility that the otoconia are attached
to the utricular side of the cupula. The other treatment
is based on the possibility that the otoconia are on the
canal side of the cupula, either attached to the cupula
or located in the anterior arm of the horizontal SCC.
Since it is not possible to determine if the otoconia are
located on the utricalar or canal side of the cupula, the
clinician should try one technique, and if that is unsuccessful, try the other technique. In the case of otoconia located on the canal side of the cupula, one would
expect that the elicited nystagmus will be persistent in
cupulolithiasis and of a shorter duration in the anterior
arm canalithiasis.
Gufoni Maneuver for Apogeotropic Nystagmus
This treatment was described by Casani, Vannucci,
Fattori, and Berrettini (2002) as a method of treating horizontal SCC cupulolithiasis; in the article the
authors reference the technique to an Italian publication by Gufoni and colleagues in 1998. Hence there is
some confusion in the literature regarding the naming
of the technique, and it has been called both the Casani
maneuver and the Gufoni maneuver. The current
suggested terminology, based on the clinical practice
guidelines (Bhattacharyya et al., 2017), is the Gufoni
maneuver for apogeotropic nystagmus.
To perform the treatment when the otoconia
are thought to be located on the utricular side of the
cupula, the patient will start sitting on the treatment
table with the neck in neutral. The clinician will hold
on to the patient’s head and rapidly guide the patient
into a side-lying position toward the affected ear. The
patient remains in this side-lying position for 30 seconds. The clinician will then rapidly rotate the patient’s
neck 45 to 60 degrees nose down toward the table. The
patient remains in this position for one to two minutes
and then sits upright (Figure 11–11).
To perform the treatment, when the otoconia are
thought to be on the canal side of the cupula or located
in the anterior arm of the horizontal SCC, the patient
will start sitting on the treatment table with neck
in neutral. The clinician will hold on to the patient’s
head and rapidly guide the patient into a side-lying
position toward the affected ear. The patient remains
in this side-lying position for 30 seconds. The clinician will then rapidly rotate the patient’s neck 45 to 60
degrees nose up from the table. The patient remains
in this position for one to two minutes and then sits
upright (Figure 11–12). This treatment is designed to
transform the initial condition into the typical posterior
arm horizontal SCC canalithiasis, and if the treatment
was successful, on retesting the clinician will observe
geotropic nystagmus. This can then be treated with
either the Gufoni maneuver for geotropic nystagmus,
CRP for the horizontal SCC, or FPP.
Other Treatments
Kim and colleagues (2012) described a procedure which
essentially combines vibration applied to the mastoid
and CRP for the horizontal SCC. The procedure is
designed to treat horizontal SCC cupulolithiasis for
otoconia that are attached to either side of the cupula.
While there are no RCTs of this treatment, the investigators reported that 76 of 78 patients experienced a
resolution of their signs and symptoms, and the mean
number of treatments was 2.1. Other treatments have
been proposed for the treatment of presumed horizontal SCC cupulolithiasis, such as head shaking and FPP
lying on the affected side. There is insufficient data to
support these treatments at this time.
Outcomes
There is mixed evidence to support the use of the
Gufoni maneuver for apogeotropic nystagmus. Casani
and colleagues (2002) reported that 6 of 9 patients
(66.7%) with presumed horizontal SCC cupulolithiasis
had resolution of their signs and symptoms following
one or two treatments. A similar study (Oh et al., 2009)
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figu re 11–11. The Gufoni maneuver for apogeotropic
nystagmus from left horizontal
patient starts sitting on the treatment table, with their
neck in neutral. B. The patient lies down quickly on their
left side. C. After 30 seconds, the clinician rapidly rotates
the patient’s neck 45 to 60 degrees to the left (nose
down position). The patient remains in this position for 1
to 2 minutes and then sits back up. Once upright they
can bring their neck back to a neutral position.
SCC cupulolithiasis. A.T he
C
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B
figure 11–12. Gufoni maneuver for apogeotropic nystagmus from left horizontal
rior arm horizontal
sitting on the treatment table, with their neck in neutral.
B. Assisted by the clinician, the patient lies down quickly
on their left side. The patient remains in this position for
30 seconds. C. The clinician then rotates the patient’s
neck 45 to 60 degrees to the right (nose up). The patient
remains in this position for one to two minutes and then
sits back up. Once upright they can return their neck to
a neutral position.
SCC canalithiasis. A. The patient starts
SCC cupulolithiasis or ante-
C
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demonstrated less impressive results: 17 of 84 individuals (20.2%) had resolution of the signs and symptoms
following one treatment. Ciniglio Appiani et al. (2005)
reported on 16 patients, all of whom showed a transition from apogeotropic to geotropic nystagmus in
the provoking tests following treatment. A recent
RCT (Kim et al., 2012b) demonstrated that the Gufoni
maneuver was more successful than a sham treatment:
45/52 (86.5%) compared with 22/49 (44.9%), respectively, for the treatment of presumed anterior arm horizontal SCC canalithiasis.
CENTRAL POSITIONAL NYSTAGMUS
AND CENTRAL POSITIONAL VERTIGO
While BPPV is a common finding that is relatively
easy to diagnose and treat, there are causes of positional nystagmus and positional vertigo that are due to
either abnormalities within the central nervous system
or other peripheral vestibular conditions. These conditions will not respond to the interventions described
for the treatment of BPPV. The goal of this section is
to help the clinician identify the signs and symptoms
of positional nystagmus and positional vertigo that are
not consistent with BPPV and are suggestive of other
disorders.
Central Positional Nystagmus
Two types of central positional nystagmus have been
identified, central positional nystagmus without vertigo (CPN) and central positional nystagmus with
vertigo (CPV) (Harrison & Ozsahinoglu, 1972; Sakata,
Ohtsu, Shimura, & Sakai, 1987). CPN is characterized
by nystagmus that persists as long as the head is held
in the provoking position (Harrison & Ozsahinoglu,
1972). The nystagmus is typically in one direction (vertical, horizontal, or torsional), unlike the mixed vertical torsional nystagmus seen in posterior and anterior
semicircular canal BPPV. Central positional nystagmus
may be seen in elderly patients when they are supine.
The elicited nystagmus is typically vertical. In the
absence of other findings on the examination, the CPN
is thought to be benign. In other individuals, CPN may
be seen in conjunction with either up-beating or down
beating-spontaneous nystagmus while the patient is
seated. The CPN in these cases is typically greater than
the spontaneous nystagmus observed in sitting.
The down-beating spontaneous nystagmus and
CPN have been associated with a variety of central
disorders, including Chiari malformation, multiple
sclerosis, olivopontocerebellar atrophy, and brainstem
infarction (Baloh & Spooner, 1981). These patients had
other oculomotor signs such as impaired smooth pursuit and impaired VOR cancellation. The actual pathophysiology causing the down-beating nystagmus is not
well understood at this point, but it is thought that the
down-beating nystagmus results from an imbalance
between the anterior and posterior SCC pathways.
Recall that the SCC inputs are separated at the level
of the vestibular nuclei into vertical (pitch), horizontal
(yaw), and roll pathways. A lesion that causes either
an increase in the central anterior SCC pathways or a
decrease in the central posterior SCC pathways would
lead to down-beating nystagmus.
The up-beating spontaneous nystagmus and CPN
have been associated with central disorders such as
tumor, stroke, and multiple sclerosis affecting the brachium conjunctivum or the ventral tegmental tract
(Fisher, Gresty, Chambers, & Rudge, 1983). Many of
these patients also had findings of abnormal smooth
pursuit. The presumed pathophysiology for the upbeating nystagmus is thought to be the opposite of that
for the down-beating nystagmus. The up-beating nystagmus is due to a higher level of neural activity in the
central posterior SCC pathways relative to the central
anterior SCC pathways.
Given the lack of symptoms of vertigo with the
positional tests, the unidirectionality of the positional
nystagmus, and the other oculomotor findings, it
should not be difficult for the clinician to differentiate
between CPN and BPPV.
Central positional nystagmus with vertigo can
present with persistent positional induced nystagmus and vertigo. In this type of CPV, the nystagmus is
down-beating without a torsional component, the nystagmus and vertigo persist as long as the head is in the
provoking position, and the nystagmus and vertigo do
not fatigue, nor do they habituate with repeated testing. This pattern of CPV has been attributed to cerebellar tumors or to hemorrhage dorsolateral to the fourth
ventricle (Brandt, 1990; Harrison & Ozsahinoglu, 1975).
Unlike CPN, CPV may present in a manner
remarkably similar to BPPV. Central positioning nystagmus with vertigo is often characterized by brief
episodes of positioning vertigo and nystagmus, which
has been called pseudo-BPPN (Buttner, Helmchen, &
Brandt, 1999; Sakata et al., 1987). Based on clinical and
experimental studies, there is a large degree of overlap
in the signs and symptoms associated with BPPV and
CPV. For example, the latency to the onset of nystagmus in cases of CPV has been reported to be between
0 and 5 seconds (Gregorius, Crandall, & Baloh, 1976;
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Jacobson, Butcher, Newman, & Monsell, 1995; Watson, Barber, Deck, & Terbrugge, 1981). The pattern of
nystagmus in CPV can take a variety of forms. Findings from clinical studies have reported pure vertical
(down-beating or up-beating), pure torsional, pure
horizontal, and mixed vertical and horizontal patterns
of nystagmus (Barber, 1984; Gregorius et al., 1976; Kattah, Kolsky, & Luessenhop, 1984; Kim, Yi, & Lee, 2012;
Sakata et al., 1987). The duration of the elicited nystagmus and symptoms is typically relatively brief (5 to 60
seconds) and mimics that seen in BPPV (Barber, 1984;
Gregorius et al., 1976). Fatigability of the response to
repeated testing within a short time frame, although
not always tested in the clinic, is a hallmark of BPPV
and may also be seen in individuals with CPV (Gregorius et al., 1976; Kattah et al., 1984). However, fatigability of the response is not seen in all patients with CPV
(Gregorius et al., 1976; Sakata et al., 1987). As can be
seen from these studies, in terms of latency, duration,
and fatigability, there are marked similarities between
BPPV and CPV. There do appear to be differences in
the patterns of elicited nystagmus; however, downbeating torsional nystagmus could be due to anterior
SCC BPPV or CPV, and horizontal nystagmus could be
due to horizontal SCC BPPV or CPV. While the other
patterns of nystagmus seen in CPV do not fit with the
classical descriptions of the nystagmus seen in BPPV,
the nystagmus seen in individuals with BPPV may not
appear to fit the pattern of mixed vertical and torsional
nystagmus seen in posterior and anterior SCC BPPV.
For example, the lateral position of the eye in the orbit
will accentuate either the vertical or the torsional component of the nystagmus, which may make it difficult
to determine if the nystagmus is mixed vertical and torsional, pure vertical, or pure torsional. Also, lid closure
or rapid blinking may make it difficult to assess the
pattern of nystagmus. Either scenario would increase
the difficulty in making an accurate diagnosis.
The presence of other neurologic findings and
symptoms would not be expected in cases of BPPV.
Associated symptoms, such as sudden hearing loss,
tinnitus, fainting sensations, progressive imbalance,
and vomiting have been reported in individuals with
paroxysmal positioning vertigo of central origin (CPV)
(Dunniway & Welling, 1998; Shoman & Longridge,
2007). An abnormal oculomotor exam is often seen in
individuals with CPV (Buttner et al., 1999). The presence of other neurologic signs and symptoms, however, is not a requirement for CPV. There are numerous
reports of individuals with CPV and no other signs or
symptoms (Barber, 1984; Gregorius et al., 1976; H. A.
Kim et al., 2012; Watson et al., 1981). The similarities
and differences between BBPV, CPV, and CPN are summarized in Table 11–2.
ta ble 11–2. Common Features of Peripheral and Central Positional Vertigo and Nystagmus
Features BPPV CPV CPN
Latency 1–15 0–5 0
Duration 5–60 seconds (longer in
horizontal canal and in
cupulolithiasis)
Direction of
nystagmus
Symptoms Vertigo Vertigo No vertigo
Fatigability Typical Possible No
Nausea and
vomiting
Associated
neurological signs
and symptoms
In the plane of the
stimulated canal. Most
commonly mixed
up-beating and torsion,
may be down-beating and
torsion, or horizontal
Unusual with a single test;
may develop with repeat
testing
None None, cerebellar signs, or
5–60 seconds Persistent as long as the
head is in the provoking
position
Pure vertical, pure torsional,
or horizontal
More frequently seen with a
single test
oculomotor signs
Typically pure down beat,
may be pure up-beat or
horizontal
No
None, spontaneous
nystagmus, or oculomotor
abnormalities
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Various causes of CPV have been reported in the
literature, including cerebellopontine angle tumors,
lesions affecting the cerebellar vermis or the fourth
ventricle, and an infarction of the cerebellar nodulus
(Dunniway & Welling, 1998; H. A. Kim et al., 2012;
Shoman & Longridge, 2007). A more common form
of CPV is migrainous vertigo and positional nystagmus. Spontaneous, positional, or a combination of
spontaneous and positional nystagmus can be seen
during an acute migraine with associated symptoms
of dizziness (von Brevern, Zeise, Neuhauser, Clarke, &
Lempert, 2005). In these cases the nystagmus can be
vertical, horizontal, or torsional and may change with
different positional tests. In patients with a history of
migrainous vertigo who were assessed when they were
asymptomatic, 12% to 28% (depending on the time of
assessment) demonstrated significant positional nystagmus (Radtke, von Brevern, Neuhauser, Hottenrott,
& Lempert, 2012).
Other Causes of Positional
Nystagmus/Vertigo
Vertebrobasilar insufficiency (VBI) has been reported
to produce episodic bouts of vertigo and nystagmus
(Grad & Baloh, 1989; Strupp et al., 2000). These findings have been seen in both positional testing as well
as in sitting with cervical rotation. Symptoms associated with VBI would be dependent of the position of
the head on the trunk (neck position), rather than the
position of the head in space (positional testing). Consequently, nystagmus and vertigo seen in the Dix–Hallpike test should be reproducible in sitting with cervical
extension and rotation, if the cause of the signs and
symptoms were due to VBI. Vertiginous symptoms are
common in cases of VBI, but isolated episodes of vertigo in VBI are controversial, with conflicting reports
as to the incidence of this finding (Gomez, Cruz-Flores,
Malkoff, Sauer, & Burch, 1996; Wityk et al., 1998).
Perilymphatic fistula and superior canal dehiscence can make the membranous labyrinth susceptible
to pressure changes such as Valsalva maneuvers or the
Dix–Hallpike test, where the head is hanging below the
horizontal plane. These conditions are typically accompanied by hearing loss. The production of nystagmus
and symptoms are not dependent on the position of
the head in space and can often be reproduced in an
upright (seated) position with the Valsalva maneuver.
As discussed previously, positional nystagmus
may be seen following a unilateral vestibular loss.
The nystagmus is horizontal (geotropic or apogeotropic), and generally the pattern of nystagmus will
remain constant (geotropic or apogeotropic) in each
Dix–Hallpike or Roll test. Thus the nystagmus may
appear similar to horizontal SCC BPPV (canalithiasis
or cupulolithiasis). Whereas individuals with horizontal SCC BPPV are very symptomatic, individuals with
positional nystagmus as a result of unilateral vestibular
loss are either asymptomatic or have mild symptoms.
The nystagmus observed in these cases is thought to
be due to the interaction of the changing otolithic input
with the asymmetrical SCC input, or a reduction in the
suppression of the asymmetric SCC activity.
Summary
There are causes of positional vertigo and nystagmus
that are not due to BPPV. The challenge to the clinician is
to identify the cause of the positional vertigo, such that
appropriate treatment can be initiated. There are differences in the clinical presentation of the various causes
of positional vertigo, but at times it may be difficult
to determine whether the positional vertigo is due to
BPPV or another cause, such as CPV. The latency, duration, and symptoms may be very similar in cases of
BPPV and CPV. There are generally differences in the
pattern of elicited nystagmus in BPPV and CPV. The one
consistent difference between BPPV and CPV is that
BPPV will respond to maneuvers such as the canalith
repositioning maneuver or Semont maneuver, while
CPV will not respond to these treatments. If the presumed BPPV is not responding to the therapeutic maneuvers, the clinician should be suspicious of possible CPV.
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