3rd Congress of the European Academy of Neurology

Amsterdam, The Netherlands, June 24 – 27, 2017

Hands-on Course 3

Bedside examination of the vestibular and ocular motor

system - Level 2

How to diagnose and treat BPPV

Marco Mandala
Siena, Italy

Email: [email protected]
Conflict of interest: Not received

Introduction

Benign paroxysmal positional vertigo (BPPV) is the most frequent and

treatable vestibular disorder. Every neuro/otologist should become famil-

iar with the positioning manoeuvres for diagnosis and treatment of this

common condition. Diagnostic criteria and treatment for BPPV represent a

key point due to the incidence of the disorders and its possible effects on

quality of life in patients. The diagnostic criteria are well established for

posterior and lateral canal BPPV. The last revision of these criteria that

are part of the International Classification of Vestibular Disorders were

published in 2015. Other recently proposed variants, like anterior canal

BPPV, peripheral positional downbeat nystagmus and apogeotropic

posterior canal BPPV still represent controversial entities.

BPPV is a common syndrome caused in most cases by displaced otoconia in

the semicircular canals, making them gravity sensitive. It is characterised

by brief episodes of vertigo, precipitated by rapid change in head position.

Because of its anatomical position, the posterior canal (PC) is by far the

most frequently involved; less often, otoconial debris enters the horizon-

tal/lateral canal (HC) or move from one canal to another. Anterior canal

(AC) BPPV is exceptional. Bilateral labyrinthine involvement is possible,

especially after head trauma.

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In most cases BPPV is idiopathic, but may follow head trauma or whiplash

injury. Other predisposing factors include vascular inner ear disorders,

acute unilateral vestibulophaty, prolonged inactivity/bed rest, chronic

infection of the middle ear, inner ear surgery, Menière’s Disease, Migraine

and vitamin D deficiency.

The management of BPPV relies on physical therapy, designed to free the

affected canals of otoconial debris by displacing them into the utricle.

Medical therapy is quite useless and vestibular suppressants help only to

attenuate the nausea that often accompanies the vertigo. Surgical

procedures are only used in persistent and incapacitating cases.

Epidemiology

BPPV can appear at any time from childhood to senility, but the idiopathic

form is typically a disease of old age, peaking in the sixth to seventh

decades. More than 95% of all patients are classified as degenerative or

idiopathic (women:men = 2:1), whereas the symptomatic patients (women

: men = 1:1) are most frequently caused by head injury (17%) or vestibular

neuritis (15%). BPPV occurs often after extensive bed rest in connection

with other illnesses or after operations. About 5% of the spontaneous

patients and 10% of the trauma patients show a bilateral, generally asym-

metrical BPPV. The right posterior canal is affected about twice as often

as the left, which might be related to the fact that more people sleep on

their right side.

Patient History

Benign paroxysmal positional vertigo is the most common cause of vertigo,

not only in the elderly, with a lifetime-prevalence around 3%. The

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symptoms are often stereotyped and a reliable diagnosis is often possible

based on patient history: recurrent second-long attacks of rotatory vertigo

triggered by certain head movements. “A few days ago, just seconds after

I got out of bed, I felt the whole room spinning. It was so strong that I had

to sit down again on the bed. I also had severe nausea, and thought that I

must have eaten spoiled food. Lying back in bed, I had another episode of

vertigo. In the following hours, I was only well when I kept my head still,

but if I tried to turn in the bed or to get up, the spinning sensation

returned again. The next day, I got up very slowly but I was again dizzy

when I went to tie my shoes…I called my GP and he suggested that I have

a brain MRI and X-rays of the cervical spine. Now I am better, but every

time I get up or lie down in the bed, I see the room spinning. The spinning

sensation lasts for a few seconds and stops if I’m still. Doctor, do you

think I have a brain tumor?”. Often even the affected ear can be identi-

fied in this way. In most cases, when PC is involved, the episodes of

vertigo occur in the morning, when the patient gets up, and in the eve-

ning, when he goes to bed. It may occur after a delay, when the patient is

already on his feet, and this may cause him to fall over. This is common in

elderly patients, who may suffer fractures because of the fall. Other

triggering movements include hyperextension of the head, looking upward

and bending forward. In patients with HC involvement the vertigo is trig-

gered by rolling onto a side while lying down. Vertigo may be so intense

and triggered by the slightest movement, that patients report a “sponta-

neous” vertigo and not a “positional” one. The vertigo is often accom-

panied by nausea and sometimes vomiting. Autonomic symptoms are more

intense when the HC is involved. Some patients complain also un-

steadiness and a feeling of walking on pillows.

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Symptoms are recurrent, occurring every time the critical movement is

performed, but generally over a limited period which may be a matter of

days, weeks or exceptionally months. There are also borderline cases in

which the vertigo occurs once or twice, and others in which it continues

for years, if not treated. By definition, the syndrome is not associated

with neurological symptoms. BPPV may determine anxiety and psycho-

pathological mechanisms that produce non-organic symptoms. Many

patients conserve a fear of vertigo and avoid certain head movements for

a long time.

The diagnosis of BPPV requires positioning manoeuvres that result in a

canal-specific positional nystagmus of PC, HC, AC, which are affected in

this order of frequency.

Diagnosis of Benign Paroxysmal Positional Vertigo of

the Posterior Canal (PC-BPPV)

Diagnostic criteria:

A. Recurrent attacks of positional vertigo or positional dizziness provoked

by lying down or turning over in the supine position

B. Duration of attacks < 1 min

C. Positional nystagmus elicited after a latency of one or few seconds by

the Dix-Hallpike maneuver or side-lying maneuver (Semont diagnostic

maneuver). The nystagmus is a combination of torsional nystagmus with

the upper pole of the eyes beating toward the lower ear combined with

vertical nystagmus beating upward (toward the forehead) typically

lasting < 1 minute (Figure 1).

D. Not attributable to another disorder

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It can be accompanied by nausea. BPPV is elicited positioning the head or

body toward the affected ear (Fig. 1). Rotatory vertigo and nystagmus

occur after such positioning with a short latency of seconds in the form of

a crescendo/decrescendo course of maximally 30–60 seconds. The beating

direction of the nystagmus is vertical and rotatory; it also depends on the

direction of gaze, is primarily rotatory when gaze is directed to the under-

most ear and mostly vertical (to the forehead) during gaze to the upper-

most ear. In PC-BPPV the nystagmus corresponds to an (ampullofugal)

excitation of the posterior canal of the undermost ear. Generally, the left

ear should be tested before since the right side PC-BPPV is more frequent,

in order to not miss bilateral cases. In patients with bilateral PC-BPPV, PN

is upbeating and torsional toward the lower ear in both Dix-Hallpike

positions.

Fig. 1: Dix-Hallpike manoeuvre for identification of posterior canal

BPPV on the left. The manoeuvre starts with the patient-sitting upright
with the head turned 45 degrees towards the examiner. The patient is
moved to a lateral head hanging position. The lower part of the figure
illustrates the canalolithiasis mechanism (UT=Utriculus, CU=Cupula,
OT=Otoconia).

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Pathophysiology and Therapeutic Principles

The canalolithiasis hypothesis can explain all symptoms of PC position-

al nystagmus. According to this hypothesis, the attacks are induced by

otoconia that move freely in the semicircular canal. The movement of the

conglomerate causes an ampullofugal or ampullopetal deflection of the

endolymph depending on the direction of sedimentation and thus leads to

a stimulation or inhibition of the vestibular hair cells. This model of the

pathomechanism of BPPV can predict the direction, latency, duration and

fatigability of the typical nystagmus, as well as changes in these para-

meters after head manoeuvres.

Latency. There is a latent period between reaching the diagnostic

Dix-Hallpike position and the onset of nystagmus, in most patients in the

range of 2–10 s. Generally shorter in the early stages of the disease, it is

partially explained by the delay in setting the debris in motion.

Direction and plane. These are crucial for the diagnosis. When the

patient is moved to the diagnostic Dix-Hallpike position, otoconial debris

falls from its starting position in the canal toward the ground and away

from the ampulla, so causing an excitatory stimulus and a mixed torsional-

vertical paroxysmal nystagmus consistent with the excitatory connections

of the PC to the vertical extraocular muscles. The fast phase of the ver-

tical component beats towards the forehead (up) and the fast phase of the

torsional component is directed such that the upper pole of the eyes beats

towards the affected lower ear.

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The torsional component may appears more prominent if or when the

patient looks toward the lowermost ear, and the vertical component more

prominent if the patient looks toward the uppermost ear.

Intensity and Duration. Paroxysmal means that PN is rapidly increasing in

intensity and then begins to decay slowly. PN is typically transitory, that

is, it dissipates in 10–40 s because, once the debris reaches the lowest

point in the canal, the cupula returns to the primary position with its time

constant, primarily due to (its) elasticity.

Static Reversal of Nystagmus. In some patients, when PN is particularly

intense, a spontaneous reversal of its direction may occur, without any

change in head position.

Dynamic reversal of Nystagmus. When the patient is returned to the

sitting position, the particles fall back in the opposite direction and cause

an ampullopetal flow, which produces an inhibitory response and a less

intense nystagmus in the opposite direction, i.e. downbeating with the

torsional component directed such that the upper pole of the eyes beats

away from the affected ear.

Fatigability. The particles that form a plug or clump are loosely held

together. During changes in the head position they tend to fall apart.

Small particles cannot cause suction or pressure on the cupula independ-

ently of each other, as does a single clump with a diameter almost filling

the canal. If the patient holds his head still for several hours (e.g., during

sleep), the particles, which had fallen apart before, coalesce into a clump

in the lowest place within the canal and again induce vertigo when the

head position is changed.

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TREATMENT OF PC-BPPV

Liberatory Manoeuvres. The efficacy of liberatory manoeuvres can only

be explained by the canalolithiasis hypothesis, i.e., a clot that moves

freely within the canal. By quickly turning the patient’s head to the op-

posite side, the plug is washed out of the canal and then can no longer

cause any positioning vertigo. Brandt and Daroff in 1980 first devised an

exercise programme, which, by means of simple head positioning, loosens

the heavy degenerative otolithic material and distributes it into other

areas of the labyrinth, where it no longer impairs canal function. The

Semont’s liberatory maneuver is a simplified version of the original treat-

ment suggested by Semont et al. (1988): from a side-lying position by a

tilt of 180° to the opposite side. The liberatory maneuver provokes accel-

eration in the plane of the PC and should provoke the exit of debris from

the canal into the utricle by centrifugal inertia. In 1992, Epley proposed

another liberatory manoeuvre that involved turning the patient from a

supine position into a head-hanging position.

Evidence-based reviews conclude that all manoeuvres are effective and

can be explained by the mechanism of canalolithiasis. The success rate of

the Semont as well as the Epley manoeuvre is around 90% after several

applications (meta-analyses). There is evidence that these manoeuvre

lead to a repositioning of the otoconia to the utricle.

Semont Manoeuvre (Figure 2). According to the liberatory manoeuvre

developed by Semont – even before the mechanism of canalolithiasis was

known. The examiner stands in front of the patient, who is seated on the

examining bed and rotates his head 45° away from the pathological ear.

Then, with a fast and continuous but not violent movement, the patient is

8
brought to a lying position on the side of the pathological ear, with the

head turned 45° up. This position is similar to the Dix-Hallpike diagnostic

position and triggers an episode of vertigo with typical paroxysmal nystag-

mus. The patient is kept in this position for two minutes and then is

quickly turned onto the opposite side, maintaining the head in the same

position in space. At the end of the manoeuvre the patient is lying on top

of his shoulder with the cheekbone in contact with the bed (head 45°

down). This is the liberatory position. The typical response to the libera-

tory manoeuvre is, after a variable latency, another episode of vertigo

and a paroxysmal nystagmus with the same direction of rotation as in the

diagnostic position. This is called liberatory nystagmus which is nearly

always a good prognostic sign (10).

The nystagmus pattern is well explained by the movement of otoconial

debris in the PC. When the patient is moved from the sitting to the

diagnostic position, the debris fall away from the ampulla provoking an

excitatory nystagmus (ampullofugal stimulus). When the patient is brought

to the contralateral, liberatory, position the nystagmus in the same direc-

tion can only be due to a similar ampullofugal stimulus: the debris con-

tinue to move in the canal and are expelled into the utricle.

After 2 minutes the patient is brought to the sitting position with the head

bent slightly forward. In this final position there is not usually any vertigo

or nystagmus. If the liberatory manoeuvre doesn’t cause vertigo and nys-

tagmus or causes a paroxysmal nystagmus beating in the opposite direc-

tion to that seen in the diagnostic position, the manoeuvre was probably

unsuccessful. In these cases it is probable that a new bout of vertigo and

nystagmus will occur in the sitting position.

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The patient can be checked again with Dix-Hallpike test in an hour and

this manoeuvre should be repeated until the patient is symptom-free. The

success rate of the Semont manoeuvre is around over 80-90% with one

treatment and 90-98% after several manoeuvres.

Fig.2: Semont manoeuvre for treatment of posterior canal BPPV on the

left. The procedure is hand-guided by a therapist (not depicted here). All
movements are performed swiftly.

Epley manoeuvre (Figure 3). Epley’s repositioning manoeuvre consists of

a five-position cycle, which has the aim to cause free canaliths to migrate

by gravitation out of the PC through the common crus. The first position

consists in bringing the patient into the Dix-Hallpike provoking position.

Then the patient’s head is slowly rotated 45° towards the healthy ear.

The head and body are then rotated so that the patient is prone with his

head rotated at 180° with respect to the first position. With the fourth

movement the patient is brought up to the sitting position and finally the

head is turned forward with the chin down at 20°.

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The manoeuvre provokes a nystagmus that reflects the direction in which

the canaliths move, that is ampullofugal. Every position is held until the

nystagmus is over and the five position cycle is repeated until no

nystagmus is observed in the last cycle.

Major differences in the efficacy of the manoeuvres proposed by Semont

and Epley do not emerge from the literature. Both manoeuvres are classi-

fied as class A treatment (highly reccomended) according to the evidence

based medicine.

Fig. 3:
Epley’s manoeuvre for treatment of posterior canal BPPV on the left.

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The occurrence of nystagmus (so-called liberatory nystagmus) in the

second step of the Epley manoeuvre indicates that the treatment will be

successful.

The choice of the manoeuvre to be used should depend on which ma-

noeuvre the therapist has experience with or if there are any individual

contraindications. Very obese patients are easier to treat with the Epley

method, while the Semont manoeuvre is suitable for patients with

shoulder-neck problems.

Transient nausea can occur as an adverse effect, above all during

repeated positionings within one sitting (prophylaxis with, e.g., 100 mg

dimenhydrinate or another antivertiginous substance is indicated). About

20–40% of the successfully treated patients experience 1–3 days of light-

headedness or postural vertigo with gait instability (most likely otolith

vertigo) due to the partial repositioning of the otoconia toward the utri-

cle. Occasionally a positional vertigo of the posterior canal converts into

the horizontal or anterior canal variants during treatment.

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Diagnosis of Benign Paroxysmal Positional Vertigo of

the Horizontal Canal (HC-BPPV)

BPPV of the horizontal canal is less frequent than posterior canal BPPV but

is still diagnosed too seldom. The diagnostic criteria for canalolithiasis of

the HC (geotropic variant) are:

A. Recurrent attacks of positional vertigo or positional dizziness provoked

by lying down or turning over in the supine position.

B. Duration of attacks < 1 min .

C. Positional nystagmus elicited after a brief latency or no latency by the

supine roll test (Figure 4), beating horizontally toward the undermost

ear with the head turned to either side (geotropic direction changing

nystagmus) and lasting <1 min.

D. Not attributable to another disorder.

Figure 4. The supine roll test. When the head of the patient is turned on
right side (right HC-BPPV) the geotropic nystagmus in more intense
(ampullopetal stimulus) than when the head is turned to the left.

13
Its key features differ from those of posterior BPPV:

• It can be induced by turning the head along the longitudinal axis of the

supine body (either to the right or to the left). This results in vertigo

with horizontal geotropic nystagmus, i.e. nystagmus beating toward the

ground in either head lateral position. Nystagmus is more intense when

the head is turned to the side of the affected ear since for the lateral

canal, the stronger response is due to an ampullopetal movement of

the cupula.

• The duration of the attacks and the nystagmus is longer than in pc-

BPPV (20-60 s) because of the horizontal canal’s so-called central

storage mechanism of velocity. Positional nystagmus frequently shows a

reversal of direction during the attacks; this corresponds to post-

rotatory nystagmus.

• The positional nystagmus seems less susceptible to habituation with

repeating the diagnostic maneuvers, even though this characteristic is

often difficult to assess, due to nausea or vomiting. The latency of

geotropic paroxysmal nystagmus is usually shorter than that of PC-

BPPV, sometimes with no appreciable latency.

• The supine roll test is quite indispensable for the diagnosis of HC-BPPV

and the affected ear is revealed by the direction toward which the

most intense nystagmus beats. Sometimes, however, it may be difficult

to appreciate a difference between the intensity of the two sides.

Other diagnostic maneuvers, which should be performed before the

supine roll test: the “pseudo spontaneous nystagmus” and the “bow

and lean test” first described by Choung et al., in 2006.

14
If geotropic positional nystagmus is paroxysmal and transitory, diagnosis of

HC-BPPV due to canalolithiasis is virtually certain and no differential

diagnosis is required.

Typical HC-BPPV can also be explained by canalolithiasis, although occa-

sionally the mechanism switches from canalolithiasis to cupulolithiasis.

In the rare form of HC-BPPV due to cupulolithiasis (the so called apogeo-

tropic variant) nystagmus beats horizontally to the uppermost ear with

weaker nystagmus when the head is turned to the affected side. (the

“zero point” of positional nystagmus (beyond which direction changes) can

be determined by turning the patient’s head 10–20° around the longitudi-

nal axis while in the supine position; this is possible because the cupula of

the ipsilateral horizontal canal is then parallel to the gravity vector. In

this way one can also determine which side is affected by horizontal BPPV.

Therapy for horizontal BPPV

The first treatment described, the Barbecue rotation, involves rotations

around the patient’s longitudinal axis while recumbent. In essence this is

an altered version of the Epley manoeuvre. For canalolithiasis the supine

patient is rotated in three 90°-steps around the longitudinal axis toward

the healthy ear. The patient holds each position for 30.

The Force Prolonged Position or Vannucchi manoeuvre (Figure 5) is an

alternative and very simple method: the patient has merely to lie on the

healthy side for as long as possible (12 hours suggested). The patient is

usually instructed to lie down, then to roll onto the side of the healthy ear

and to stay in that position all night, if possible. This should cause the

15
otoconial debris to come out of the canal, by gravitation. If possible we

check the result the next day. This method is particularly helpful in obese

or very symptomatic subjects.

Fig. 5. The force prolonged position for right side HC-BPPV

canalolithiasis. Debris is forced to exit by gravity lying on the left side.

Alternatively one can perform the so-called Gufoni manoeuvre (Figure.

6), with which patients with either a canalolithiasis or a cupulolithiasis

can be successfully treated. The advantage of this manoeuvre is that it is

quick and it clears the labyrinth immediately. From a sitting position, the

patient is simply laid down on the side exhibiting less nystagmus. It is

advisable to create a good deceleration as the head makes contact with

the bed. Afterwards the head is turned 45° downwards. The treatment

should allow the particles to exit the canal under the centrifugal force

created by the rapid deceleration, and by gravitation, when the head is

maintained with the nose down.

The manoeuvre should be repeated two or three times sequentially.

Gufoni’s treatment is a good option when the patient is moderately

16
tolerant to vertigo. Its effectiveness was recently validated in randomized

double blind studies.

Fig. 6: Gufoni manoeuvre for treatment of horizontal canal BPPV

(canalolithiasis on the left or cupulolithasis on the right). Positioning is
guided by a therapist. Each position is maintained for 30 seconds.

Additional treatments for BPPV

Self-treatment. The Epley and Semont manoeuvres as well as the Force

Prolonged Position can be successfully applied by the patient himself. The

treatments can be repeated daily until symptoms have disappeared. A

thorough guidance by personal demonstration and an illustrated instruc-

tion is necessary. The success rates are not as high as when a physician

performs the manoeuvre. Thus the self-therapy can be used in a comple-

mentary way, for example in patients with remaining complaints or fre-

quent recurrences.

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Recurrences after successful liberatory manoeuvres. According to

follow-up observations over an average of 10 years, the recurrence rate in

treated patients totals about 50%. Of these patients 80% have recurrences

in the first year independently of the type of liberatory manoeuvre ap-

plied. Women have a rate of 58% and thus are more often affected than

men who have a rate of 39%.

Additional Medication. Patients who develop severe nausea after a single

manoeuvre can take an antiemetic, e.g. dimenhydrinate (100 mg) half an

hour before undergoing the liberatory manoeuvre. Patients with excessive

anxiety may require premedication with sublingual lorazepam or another

benzodiazepine.

An association between osteoporosis, vitamin D deficiency and BPPV was

described; this can probably also explain the predominance of women

(2:1) in the idiopathic type of BPPV. Therefore, we determine in every

patient vitamin D and if necessary substitute it.

BPPV of the anterior canal (AC-BPPV)

The existence and pathogenesis of canalolithiasis of the AC is still de-

bated. It was suggested that a positional nystagmus from the AC can be

elicited with both Dix-Hallpike maneuvers and even better in the supine

straight-head hanging position, by bringing the patient to the supine

position with the head 30° (or even more) below the earth-horizontal. For

example, in the case of left AC canalolithiasis, the right Dix-Hallpike ma-

neuver or the supine straight-head hanging positioning provokes a

backward rotation of the left AC and the fall of otoconial debris away

from the ampulla. The resulting positional nystagmus is mixed down-

18
beating and torsional with the top pole of the eyes beating towards the

left pathologic ear and with the vertical component prevailing over the

torsional component. The relative frequency of AC-BPPV is low.

Javocino et al. described a liberatory manoeuvre: from a midline head-

hanging position, the patient must bow his head 30 degrees toward the

chest and sit up after 1 minute. This study reported a success rate of 85%

after one single manoeuvre. This high success rate does not correspond to

our experience.

Differential Diagnosis and Clinical Problems

The diagnosis of BPPV can be made on the basis of a typical patient

history (brief rotatory vertigo when turning over or sitting up/lying down

in bed) and the clinical findings. Especially in patients with therapy-

refractory positional vertigo (despite correct positioning exercises), the

following syndromes should be considered in the differential diagnosis:

central positional nystagmus (infrequent), vestibular migraine, bilateral

BPPV, particularly post-traumatic (ca. 10%), BPPV of the horizontal canal

(too rarely diagnosed, see above), and vestibular paroxysmia. Successful

treatment represents the best differential diagnosis with central

vestibular disorders.

Since HC-BPPV may present with spontaneous or “pseudo-spontaneous”

nystagmus, differentiation from acute unilateral vestibular loss is manda-

tory. Apogeotropic variant of HC-BPPV needs differential diagnosis with

central vestibular disorders.

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Central Positional Vertigo/Nystagmus

Central positional vertigo and central positional nystagmus are caused by

infratentorial lesions that affect connections between the vestibular nu-

clei in the medulla oblongata and cerebellar structures close to the mid-

line (vermis). It is important to distinguish between peripheral and central

vestibular disorders, as the Four characteristic forms of central positional

vertigo/ nystagmus can be distinguished, although the symp-toms overlap

and combinations occur: central downbeat nystagmus, in head-hanging

position (with or without accompanying vertigo), typically in lesions of the

nodulus; central positional nystagmus (without vertigo); central paroxys-

mal positional vertigo with nystagmus, typically in nodulus lesions, and

“central position vomiting”.

These central vestibular disorders occur much more seldom than typical

BPPV. However, it can be difficult to distinguish peripheral and central

disorders in an individual patient. The following clinical rules are impor-

tant for diagnosing a central positional vertigo/nystagmus: persisting

positional nystagmus (slow-phase velocity >5°/s) without associated verti-

go; positioning-induced vomiting after single head movements without any

substantial vertigo or nystagmus; positional vertigo with nystagmus of

purely torsional or vertical character (downbeat or upbeat directions); a

purely horizontal direction of nystagmus is typical for HC-BPPV; and posi-

tional nystagmus that does not correspond to the plane of the semicircular

canal stimulated by the head positioning (e.g., torsional nystagmus after

stimulation of the horizontal canal). In clinical practice the latter seems

to be the most important feature by which a central positional nystagmus

can be identified. According to traditional, positional nystagmus beating

toward the uppermost ear or lasting longer than 1 minute indicated a

20
central pathology; this is no longer considered a reliable differentiating

feature, as both features occur with the cupulolithiasis variant of BPPV.

21
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