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Treatment of Benign Paroxysmal Positional Vertigo
Susan J Herdman
PHYS THER. 1990; 70:381-388.
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Clinical Perspective
Treatment of Benign Paroxysmal Positional Vertigo
Peripheral vestibular disorders result in vertigo, disequilibrium, and frequently
nausea and vomiting. The purpose of this article is to describe the physical therapy
management of one of the more common peripheral vestibular disordersAenign
paroxysmal positional vertigo (BPPV).Several dverent approaches have been used
in the treatment of BPPV These approaches are compared, and the criteria used
in choosing the appropriate approach are presented. Case studies are used to illustrate the dzfferent treatment approaches. [Herdman SJ. Treatment of benign paroxysmal positional vertigo. Phys T h e 1990;70:38l-3881
Susan J Herdman
Key Words: Ear, Nystagmus, Otorhinolayngologic diseases, Vertigo, Vestibular
system.
Peripheral vestibular disorders result
in vertigo, disequilibrium, and frequently nausea and vomiting. The
purpose of this article is to describe
the physical therapy management of
one of the more common peripheral
vestibular disorders-benign paroxysmal positional vertigo (BPPV). Several
different approaches have been used
in the treatment of BPPV. In this article, these approaches are compared,
and the criteria used in choosing the
appropriate approach are presented.
Case studies are used to illustrate the
different treatment approaches.
Characterlstlcs of Benign
Paroxysmal Positional Vertigo
The diagnosis of BPPV is based on
certain characteristic clinical
findings.1-3 Patients with BPPV experience vertigo when moved rapidly into
a supine position with the head
turned so that the affected ear is 30 to
45 degrees below the horizontal
(Fig 1). The vertigo occurs with a
latency of 1 to 40 seconds after the
patient has been placed in the provoking position (usually after 1-5 seconds). Patients also develop a characteristic nystagmus, which is torsional
with the eyes directed toward the
affected side and becomes more vertical ("upbeating") when the eyes are
directed away from the affected side.
The vertigo and the nystagmus
increase in intensity and then disappear in 30 to 60 seconds. The
response usually fatigues if the patient
is placed repeatedly into the provoking position, although this is a variable finding, occurring in only 87% of
the cases.3
Rapidly positioning the patient so that
the affected ear is approximately 30
degrees below the horizontal
(Hallpike-Dix maneuver) (Fig 1)
results in an ampullohgal deflection
of the cupula of the posterior canal.
Neurons innervating the ipsilateral
superior oblique muscle and the contralateral inferior rectus muscle are
S Herdman, PhD, PT, is Assistant Professor, Department of Otolaryngology-Head and Neck Surgery,
Johns Hopkins University, 600 N Wolfe St, Baltimore, MD 21205 (USA).
This article was submitted September 18, 1989, and was accepted January 23, 1990,
56 / 381
excited, resulting in a torsional nystagmus. The Hallpike-Dix maneuver
commonly produces the vertigo and
nystagmus of BPPV, but any movement that excites the posterior semicircular canal (eg, tilting the head
back) may trigger a similar, although
smaller, response. In BPPV, it is
unusual for vertigo to be induced by
movements that excite the anterior o r
the horizontal canals such as leaning
forward o r turning the head in a horizontal plane, although horizontalcanal benign paroxysmal vertigo has
been reported.3.4
Patients with BPPV report a fairly characteristic history. Typically, they experience a sudden onset of vertigo
when rolling over in bed. The duration of the vertigo often cannot be
described because the patient quickly
moves out of the provoking position
and then avoids that position for fear
of initiating another episode. They
may complain that other movements
precipitate the vertigo, such as
straightening up after bending over o r
looking up suddenly as when reaching for an object on a high shelf.
Patients may describe a single occurrence of vertigo, o r they may have a
Physical
Therapyllrolume
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70, Number 6/June 1990
long history of episodic vertigo intermixed with periods in which they are
symptom-free. Patients with BPPV typically have periods of remission lasting
from months to years during which
they experience no episodes of
vertigo.
Patients with BPPV also may complain
of disequilibrium, and they may have
abnormal postural responses. Black
and Nashner5 found decreased postural stability in patients with BPPV
and suggested that these patients rely
excessively on visual cues to maintain
balance. A more recent study by
Voorhees6 failed to reproduce this
finding, although Voorhees did find
that patients with BPPV could not use
vestibular cues effectively to maintain
balance. Voorhees6 suggests that the
difference may be related to the comorbidity of head injury in the
patients studied by Black and
Nashner,' which was not true of his
patient sample.
-
Table. Camparisan of Characteristics of Benign Paroxysmal Positional Vertigo
(BPPV) and Central Positional Vertigo
Characterlstlc
BPPV
Central Positional Vertigo
Latency (sec)
none
Duration (sec)
> 60
Fatigues
no
Nystagmus
etiology and age of onset. Patients
with idiopathic BPPV were from 45 to
85 years of age, whereas patients in
the posttrauma group were considerably younger (age 20-45 years).
not always present
Other Causes of
Positional Vertigo
Positional vertigo occurs with lesions
of the central nervous system as well
as with lesions of the peripheral nervous system. The characteristics of
central positional vertigo and BPW,
The etiology of BPPV is often
unknown. Baloh et a13 report that, in
a study of 240 patients with BPPV, a
diagnosis could not be determined in
118 patients. Among the patients in
whom a diagnosis could be made, the
most frequent diagnoses were head
trauma (n = 43) and viral neuronitis
(n = 37). The remainder of the
patients had varied histories including
surgery, Meniere's disease, vertebral
basilar insufficiency, migraine, and
multiple sclerosis. In many cases, the
diagnoses were unrelated to the
BPPV. Gacek7 suggests that some type
of insult (eg, head trauma, infection,
vascular injury) to the labyrinth resulting in degeneration is common to all
cases of BPPV.
Baloh et a13 found that the peak incidence of onset occurred in the sixth
decade of life in the patients in whom
no diagnosis could be made. In
patients with a history of head trauma,
there was no correlation of age to
onset, whereas in those patients with
a history of viral neuronitis, the onset
was usually between the fourth and
sixth decades of life. Semont et ala in
a study of 711 patients with BPPV,
found a different relationship between
Physical TherapyNolume 70, Number
Fig 1. Hallpike-Dix maneuver. Moving the patient rapidly from a sitting to a supine
position with the head turned so that the affected ear is 30 to 45 degrees below the horizontal will stimulate the posterior canal and produce vertigo and nystagmux
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however, are different (Table).9 In
central positional vertigo, the vertigo
begins as soon as the patient is put
into the provoking position; the
response persists as long as the position is maintained, and it does not
fatigue with repeated positional
changes. Central positional vertigo
may occur in a variety of disorders
affecting the brain stem such as
infarct, tumors, and multiple
s c l e r ~ s i sUnfortunately,
. ~ ~ ~ ~ ~ central
positional vertigo does not respond to
the treatments that can be used so
effectively in BPPV. Another type of
positional vertigo that does not habituate occurs when the vestibular nerve
is compressed by blood vessels. This
type of disorder is treated with microvascular decompression surgery.12
Another diagnosis that may be confused with BPPV is cervical vertigo.lj
Cervical vertigo, although poorly
understood, is believed to be due to
inappropriate afferent signals from
joint and spindle receptors.14Animal
studies have demonstrated that unilateral cervical rhizotomies o r the injection of a local anesthetic unilaterally
in the cervical region results in ataxia
or nystagrnus.'3 This effect has been
difficult to demonstrate in human
beings. De Jong and Bles13 report that
patients with cervical vertigo will tend
to fall backward if they extend their
neck while standing with eyes closed.
Because patients with BPW sometimes complain of vertigo induced by
neck extension (head movement from
flexion to extension would excite the
posterior semicircular canals), these
two diagnoses may be confused. In
addition, patients with cervical vertigo
as well as those with BPPV may have a
history of trauma.
Vertigo induced by positional changes
may also occur in patients with perilymph fistula (PLF). In patients with
PLF, there is an abnormal communication between the inner and middle
ears, usually through the round o r
oval window. Patients with PLF typically complain of sudden hearing loss,
vertigo, disequilibrium, and
nausea.15.l6As in BPPV, this disorder
can occur after head trauma, although
there are many other causes such as
stapedectomy and barotrauma.15J7.18
The nystagmus that occurs with positional changes in patients with PLF
may be similar to that seen in patients
with BPPV, although other forms of
nystagmus also 0 c c u r . ~ ~ ~ ~ 9
Pathogenesis
Two different theories-"cupulolithiasis" and "canalithiasis"-relate the
structural relationship of the utricle
and the posterior canal to the vertigo
and nystagmus that occur with specific head movements in patients with
BPPV. Normally, the semicircular
canals respond to head movement but
not to head position (ie, not to the
pull of gravity). Both theories suggest
that structural changes occur in which
one of the posterior semicircular
canals becomes gravity-sensitive,The
characteristics of BPPV (ie, latency,
burst, and duration) can be
adequately explained by both
theories.
Theory l-Cupulollthiasis. This
theory proposes that degenerative
debris from the utricle (probably fragments of otoconia) fall onto the cupula of the posterior canal, making the
ampulla gravity-sensitive.This phenomenon-cupulolithiasis-was
first
described in 1969 by S c h ~ k n e c h t , ~ ~
who found basophilic deposits on the
cupula of the posterior canal in
patients with a history of BPPV. Positioning the head with the affected ear
below the horizontal causes an inappropriate deflection of the cupula of
the posterior canal, presumably
because of its gravity-sensitivity, and
results in vertigo, nystagmus, and nausea. The latency of the onset of the
vertigo and nystagmus is related to
the time required to displace the
gravity-sensitive cupula. The gradual
increase in vertigo and nystagmus is
related to the increased deflection of
the cupula. The gradual decrease in
vertigo and nystagmus that occurs if
the head-hanging position is maintained is due to adaptation.
Theory 2 4 a n a I i t h i a s i s . Hall et
a121propose a somewhat different
theory concerning the mechanical
factors producing BPPV. They suggest
that the degenerative debris is not
adherent to the cupula of the posterior canal but instead is free-floating
in the endolymph. When the head is
moved into the provoking position,
the endolymph, moved by the falling
otoconia, pulls on the cupula, thus
exciting the neurons. The latency of
the response is related to the time
required for the cupula to be
deflected by the pull of the
endolymph. The increase in vertigo
and nystagmus that occurs is related
to the relative deflection of the cupula. The decrease in vertigo and
nystagmus as the position is maintained is due to cessation of
endolymph movement. As with the
cupulolithiasis theory, the HallpikeDix maneuver is most likely to result
in vertigo and nystagmus, although
symptoms may be provoked by other
movements in the plane of the posterior canal. Hall et alzl argue that their
model explains the fatigue of vertigo
that occurs with repeated positional
changes in patients with BPW better
than does the cupulolithiasis model.
They hypothesize that with repeated
movement of the head into the precipitating position, some of the debris
moves out of the posterior canal,
thereby reducing the response.
Treatment
Several approaches have been developed to treat patients with BPW. One
treatment approach is based on the
idea that the debris embedded in the
cupula of the posterior canal can be
dislodged by repeatedly moving the
patient into the position that provokes
the vertigo.22An alternative treatment
approach, the Liberatory maneuver,
moves the patient through a series of
positions in order to float the debris
out of the posterior canal but does
not distinguish between cupulolithiasis and canalithiasis.8 A third
approach, suggested by Norre and De
Weerdt23 and by Tangeman and
Wheeler,24 is based on the concept of
habituating the CNS response to
movement-provoked vertigo.
Treatment 1-Brandt's exercises.
Proposed by Brandt and Daroff,22 this
treatment requires the patient to
Physical TherapyNolume 70, Number 6/June 1990
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Fig 2. Brandt's exercises. The patient moves quickly from the sitting position into the position that produces vertigo. The patient
stays in that position until the vertigo stops and then sits up again. The patient remains in the upright position for 3 0 seconds and
then moves rapidly into the mirror-image position on the other side, maintains that position for 3 0 seconds, and then sits up. The
entire maneuver is repeated until the vertigo diminishes. (Modijied from Brandt and Darofz2)
move into the provolng position
repeatedly, several times a day. The
patient is first positioned sitting and
then rapidly moves into the position
that causes the vertigo (Fig 2). Torsional nystagmus may occur with the
onset of the vertigo. The severity of
the vertigo will be directly related to
how rapidly the patient moves into
the provolng position. The patient
stays in that position until the vertigo
stops and then sits up again. Usually
moving to the sitting position will also
result in vertigo, although this
"rebound effect" will be less severe
and of a shorter duration. Nystagmus,
if it reoccurs, will be in the opposite
direction. The patient remains in the
upright position for 30 seconds and
then moves rapidly into the mirrorimage position on the other side,
maintains that position for 30 seconds,
and then sits up. The patient then
repeats the entire maneuver until the
vertigo diminishes. The entire
sequence is repeated every 3 hours
during the day until the patient has
experienced no episodes of vertigo
for 2 consecutive days. It is not clear
why these exercises result in a
decrease in the vertigo and nystagmus. One explanation is that the
debris becomes dislodged from the
cupula of the posterior canal and
moves to a location where it no
longer affects the cupula during head
movement. A second possibility is that
central adaptation occurs, reducing
the nervous system response to the
signal from the posterior canal.
Brandt and DaroP2 argue against central adaptation as a mechanism for
recovery because many patients
recover abruptly.
Treatment 2-Liberatory maneuver. As with the treatment approach
proposed by Brandt and D a r ~ f fthe
,~~
provolng position must first be
identified.8 The patient is first moved
Physical TherapyNolume 70, Number 6/June 1990
quickly from a sitting position to the
provoking position and kept in that
position for 2 to 3 minutes. He is then
turned rapidly to the opposite eardown position with the therapist
maintaining the alignment of the neck
and head on the body. The patient
stays in this position for 5 minutes.
Typically, nystagmus and vertigo reappear in this position. The patient is
then slowly returned to a seated position. He must remain in a vertical
position for 48 hours (including while
sleeping) and must avoid the provoking position for 1 week following the
treatment. Unlike the exercises suggested by Brandt and Daroff,22 the
Liberatory maneuver usually requires
only a single treatment. It purportedly
works by floating the debris through
the canal system to the common crus.
Treatment 3-Habituation exercises. The exercises of Norre and De
Weerdt23 differ from those described
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384 / 59
by Brandt and DaroP2 in that the provoking positions used are specific for
each patient and are not limited to
the Hallpike-Dix maneuver. In a more
recent article, Norre and Beckers25
describe the specific movements used
to establish the individualized treatments and discuss the results of those
treatments. Tangeman and Wheeler2*
describe the three phases of their
treatment protocol. Phase I is similar
to the Brandt and DaroP2 protocol
and consists of having the patient
move repeatedly into the Hallpike-Dix
position; phases I1 and I11 include a
wide variety of balance exercises that
incorporate eye and head movements
and that seem similar to the
Cawthome-Cooksey exercises advocated for patients with unilateral vestibular hypofunction.26 The inclusion of
specific exercises for balance in these
latter approaches is appropriate for
the treatment of the postural instability sometimes seen in patients with
BPPV. In addition, the patient samples
in these studies included patients with
vestibular hypofunction or patients
with BPPV combined with vestibular
hypofunction who would most likely
also have balance problems.
Treatment Efficacy
Studies on the efficacy of these treatments indicate that both Brandt's
exercises and the Liberatory maneuver facilitate r e ~ o v e r y .The
~ , ~results
~
of these studies are confounded, however, by the high incidence of spontaneous remission in patients with
BPW. Several authors have reported
spontaneous recovery within 3 to 4
weeks627 although Brandt and
DaroP2 suggest that the vertigo may
not disappear for months if left
untreated.
Brandt and DaroP2 studied a series of
67 patients with histories of BPW of 2
days' to 8 months' duration. None of
these patients had evidence of other
neurological or neurotological disease. They reported that 98% of the
patients had no symptoms after 3 to
14 days of exercises. The only patient
who did not respond to treatment
had a PLF requiring surgical repair.
Recurrence of BPPV was minimal,
60 / 385
aEecting only 3% of the patients. In
our experience with a series of 20
patients with BPW treated with exercises similar to those advocated by
Brandt and D a r ~ f f ?the
~ amount of
time until the patients were symptomfree (n = 12) or had at least a moderate reduction in symptoms (n = 7)
was more protracted, extending from
1 week to 6 months. Patients with
only partial recovery complained
most frequently of an intermittent
"swimming" sensation rather than of
true vertigo. One patient experienced
no change in vertigo. These patients
had histories of BPPV ranging from a
few days to 35 years. Possibly, the
longer the history of the disorder, the
more resistant the BPPV is to treatment. We also observed that most
patients requiring a more extended
course of treatment had additional
nervous system disorders that may
have impeded recovery.
Semont et a18 report a series of 711
patients with BPPV treated with the
Liberatory maneuver over an &year
period. It is not clear from their article whether the patients had other
neuro-otological problems. The
authors state that some of the patients
had slightly increased or decreased
responses on caloric testing, but they
did not define their criteria for a normal response. Statistically significant
abnormal responses to caloric testing
have been reported to occur in up to
47% of patients with BPPV.3 Semont et
a18 report a "cure" rate of 84% after a
single treatment and 93% after two
treatments. Again, recurrence of the
symptoms was infrequent (4%). We
have used a similar maneuver (Fig 3)
on a much smaller sample of patients
with BPPV (N = 14). This maneuver
resulted in remission of BPPV in 11
patients; 2 of those patients required
two treatments. The maneuver was
ineffective in 3 patients, one of whom
had multiple sclerosis; whether her
vertigo was due to a peripheral nervous system lesion or a CNS lesion is
not known. Neither the Liberatory
maneuver nor Brandt's exercise
approach ameliorated the symptoms
in these 3 patients.
Fig 3. ModiJied Liberatoy maneuver.
The patient isJirst moved quickly from a
sitting position to the position that provokes the t~ertigoand is kept in that position for 2 to 3 minutes. His head is then
turned to the opposite ear-down position
with the therapist maintaining the alignment of the neck and head on the body.
The patient stays in this position for 5
minutes. The patient is then slowly
returned to a seated position. He must
remain in a vertical position for 48
hours and mztst avoid the provoking
position for I week.
Norre and B e c k e r ~ ~compared
~ ~ ~ 9 the
efficacy of the Liberatory technique
with Habituation exercises. For the
Habituation treatment, patients
repeated the positional changes five
times and performed two or three
sessions each day. In their series of 23
Physical Therapyflolume 70, Number 6/June 1990
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patients treated with the Liberatory
technique, 52% were free of vertigo
after one treatment. Only 32% of the
28 patients treated with Habituation
exercises were free of vertigo at the
end of 1 week, but the remaining
patients reported a decrease in their
symptoms. By the end of 6 weeks, all
28 of the patients treated with Habituation exercises had no vertigo. In
addition, those patients treated with
the Liberatory technique who did not
improve with a single treatment were
switched to the Habituation treatment
protocol, and all except one was free
of vertigo at the end of the 6-week
treatment period. They concluded that
the two treatments were equally effective in the treatment of BPPV.
Guidelines to Treatment of
Benign Paroxysmal
Positional Vertigo
The diagnosis of BPPV is usually made
by a neuro-otologist or a neurologist,
who would then refer the patient for
physical therapy. The physical therapist should examine the patient to
determine 1) what positional changes
produce the vertigo, 2) whether any
balance problems exist that are associated with the BPPV, and 3) whether
other conditions exist that may affect
treatment (ie, neck pain).
Tests to determine the provoking
positions are important in order to
develop the appropriate treatment
protocol and to monitor the progress
of the patient. The latency, duration,
and intensity (scaled 1-5 o r 1-10) of
the vertigo should be documented for
each of the position changes (Fig 4).
It is important to perform the positional changes quickly in order to
provoke a response. Testing must be
performed consistently because a
decreased response, obtained when
the positional change is made too
slowly, may imitate improvement.
Nystagmus is observed using Frenzel
glasses, which magnify the patient's
eyes for the observer. These glasses
prevent the patient from using visual
fixation to suppress the nystagmus.
The direction and duration of the
nystagmus should be noted. Some of
the position changes listed in Figure 4
VERTIGINOUS POSITIONS
Name:-------------- Date:-----------Sitting
turn head to left
turn head to right
tilt head to left
return to upright
tilt head to right
return to upright
bend forward to left
return to center
bend forward to right
return to center
Sitting to supine
roll to left
return to supine
roll to right
return to supine
Left Hallpike-Dix
Return to sitting
Right Hallpike-Dix
Return to sitting
Latency Intensity Duration Symptom
F[g 4. Documentation of latency, intensity, and duration of the responsefor d i j
ferent positional changes. Testing patients to determine what positional changes provoke the vertigo is important in order to develop the appropriate treatment protocol
and to monitor the progress of the patient. Some of the position changes listed should
not result in vertigo or nystagmus in patients with benign paroxysmal positional vertigo
but may result in complaints of vertigo or dizziness in patients with vestibular
hypofunction. (Modifiedfrom Herdman.l4)
should not result in vertigo or nystagmus in patients with BPPV because
the movements do not affect the posterior canal.
For most patients, either Brandt's
exercises o r the Liberatory treatment
approach may be used; however, the
following factors should be
considered:
1. Elderly patients may be less toler-
ant of the Liberatory maneuver
than younger patients, especially if
they move cautiously because of
other conditions such as arthritis.
2. Patients may not wish to stay in an
upright position for the 48 hours
required by the Liberatory maneuver. Bending over may be difficult
for some patients to avoid (eg, parents with small children, patients
required to perform certain workrelated activities).
Physical 'Therapy/Volume 70, Number 6/June 1990
3. Patients, especially those with long
histories of BPPV, may have anxiety
about moving into the provoking
position and may be resistant to
the Liberatory maneuver; Brandt's
exercises may be modified so that
the patient has more control over
the positional change and gradually
becomes less fearful of provoking
the vertigo and nausea. The anxious patient, however, may tend to
move out of the provoking position too quickly when attempting
to perform the exercises without
assistance. The extent of anxiety
patients can experience should not
be underestimated; one patient I
observed with a long history of
BPPV became so fearful of provoking the vertigo that he tied one
arm down at night to keep from
rolling over onto the "bad side."
4. The success of Brandt's exercises
are dependent on the compliance
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386 /61
of the patient. Some improvement
may occur within a few days after
initiating the treatment, but treatment may have to be continued for
extended periods of time. Weekly
clinical visits may help improve the
compliance of the patient, but in
patients with poor compliance, the
Liberatory maneuver may be the
more appropriate choice.
5. Cervical and back pain may preclude the Liberatory maneuver or
may be aggravated by the repeated
positional changes of Brandt's exercises. The positional changes used
in Brandt's exercises may be modified to enable the patient to perform them.
6. There is some risk of neck injury
when performing the Liberatory
maneuver or similar maneuvers.
This risk is small, however,
because the head is turned to the
side before the patient reclines and
because the head is supported at
all times.
7. The patient must "work through"
the vertigo and its accompanying
nausea.14Usually, these complaints
disappear quickly when the patient
is moved out of the provoking
position or as the vertigo
decreases. Repeated positional
changes, as would occur with the
Brandt's exercises, may cause a
prolonged and generalized disequilibrium with persistent nausea.
These effects may be disturbing
enough that the patient stops the
exercises. Patients should be
warned that these effects may
occur and that they are temporary.
Usually, these effects can be controlled by modifying the exercises
(eg, decreasing the repetitions for
a while) or by regulating the time
during the day when the exercises
are performed. These effects may
also be controlled by taking medication, such as Phenergan@,*half
an hour before the exercises are
performed. Brandt's exercises are
usually performed with the eyes
closed to minimize the visuovestibular conflict contributing to the
nausea. Opening the eyes may
result in an increase in the nausea
but may also facilitate adaptation
and therefore recovery.
8. The Liberatory maneuver usually
should not be used in patients with
bilateral BPPV. Bilateral BPW, like
BPPV affecting the labyrinth unilaterally, has been reported in idiopathic cases and after head injury.30
Case Studies
Case 1
The patient was a 50-year-old woman
who was hit by a car 2 weeks previously while crossing a street. At the
time of the accident, she was alert and
oriented as to time, place, and person
but had complaints of cervical pain
and was taken to the emergency
room of the nearest hospital. While in
the radiology department, the patient
had a cardiac arrest and was resuscitated. She was admitted to the intensive care unit but had no other cardiac incidents. While in the intensive
care unit, the patient began to complain of vertigo when she turned her
head to the left. On examination 1
week later, the patient's strength and
sensation were within normal limits,
her cerebellar signs were negative,
and she had no pathological reflexes.
The Hallpike-Dix maneuver to the left
resulted in a "down-beating" and
counterclockwise nystagmus and complaints of vertigo with a latency and
duration consistent with BPPV. Sitting
up resulted in vertigo and nystagmus
(in the opposite direction) that was
less severe and of shorter duration.
Down-beating nystagmus, in contrast
to upbeating nystagmus, is unusual in
BPPV, but it has been reported in 9%
of subjects with BPPV.3 A diagnosis
was made of postconcussional BPW.
The patient was treated with
meclizine and was referred to physical therapy for exercises.
At the time of her initial physical therapy visit, the patient was found to
have vertigo and torsional nystagmus
when placed in either the left o r the
right Hallpike-Dix position. In addition, the patient still complained of
cervical pain and was wearing a cervical collar at the advice of the therapist
who was treating her neck injury. Her
neck rotation range of motion and
neck lateral flexion ROM were
decreased by 20% to the right and
left. Brandt's exercises were used for
treatment of the BPPV because of the
patient's cervical complaints and the
fact that the BPPV was bilateral (Fig 2).
The treatment goal was to eliminate
the vertigo in 8 weeks. Initially, the
patient was instructed to perform the
exercises wearing her cervical collar
as that seemed to minimize her neck
pain. On follow-up visits, the patient
reported a gradual decrease in the
intensity and duration of the vertigo
induced by the positional changes. In
4 weeks, she had no complaints of
vertigo, and nystagmus could not be
observed under Frenzel lenses with
the Hallpike-Dix maneuver to the left;
vertigo and nystagmus occurred with
the Hallpike-Dix maneuver to the
right but were less severe. Seven
weeks after initiation of treatment, the
patient had no complaints of vertigo,
and nystagmus could not be induced
with any positional changes. The
patient was discharged from treatment
with the goal of eliminating the vertigo attained.
Case 2
The patient was a 51-year-old man
who reported a history of intermittent
mild vertigo occurring for several
years. He described a spinning sensation that lasted for only a few seconds
when he rolled from right to left or
when he moved from a supine to a
sitting position. He denied experiencing vertigo o r disequilibrium induced
by movement of the environment,
movement through the environment,
or pressure changes. He was still playing tennis and reported no vertigo
while serving. He denied experiencing falls or unsteadiness.
*Wyeth-Ayerst Laboratories, Div of American Honne Products Corp, PO Box 8299, Philadelphia, PA
19101.
Physical Therapyllrolume 70, Number 6IIJune 1990
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-
On assessment, he was without spontaneous, gaze-evoked, or head-shaking
nystagmus. With movement into the
left Hallpike-Dix position, he complained o f vertigo. A torsional nystagmus was also observed through Frenzel lenses. The latency, burst pattern,
and duration of the vertigo and
nystagmus was consistent with BPPV.
On sitting up, the patient experienced
a second episode of vertigo, although
it was milder than the initial episode.
No other positional changes provoked
the vertigo.
This patient was treated using a modification o f the Liberatoly maneuver
(Fig 3). He tolerated the procedure
well and was instructed to remain
upright for 48 hours and to avoid
lying on the left side for 1 week. At
the end of 1 week, he returned for
reassessment. At that time, the left
Hallpike-Dix maneuver was repeated.
The patient subsequently experienced
no vertigo, and no nystagmus was
observed through Frenzel lenses. The
patient was then discharged from
treatment.
Conclusion
Benign paroxysmal positional vertigo
is a common peripheral vestibular
disorder that can be treated with
physical therapy. This anicle has
reviewed its etiology and pathology
and has described several different
treatment approaches. Suggestions are
made as an aid for clinical decision
making.
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Treatment of Benign Paroxysmal Positional Vertigo
Susan J Herdman
PHYS THER. 1990; 70:381-388.
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