Otology Seminar
BPPV and the Liberatory Maneuvers
R3 郭士偉 2006/04/11
INTRODUCTION
 Benign paroxysmal positional vertigo (BPPV) is one of the most common
clinical entities encountered in a neurotology clinic
 “benign” distinguish between the types of vertigo caused by peripheral
vestibular ailments and the types of vertigo caused by intracranial neoplasms.
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“paroxysmal” an important and essential characteristic of the disorder: the
vertigo is episodic rather than persistent
“positional” a particular association between a patient’s symptoms and his or
her head position with respect to gravity.
Associated with a characteristic paroxysmal positional nystagmus, which may be
torsional, vertical, or horizontal, and is characterized by findings such as latency,
crescendo and decrescendo, transience, reversibility, and fatigability
HISTORICAL BACKGROUND
 Barany(1921), was the first who provided a clear description of paroxysmal
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vertigo with nystagmus following changes in head position, and attributed it to
otolith disease
Dix and Hallpike (1952) used the descriptive term “benign paroxysmal positional
vertigo” and described a maneuver in order to maximally provoke the attack
Shuknecht (1969) proposed that BPPV resulted from a lesion of the posterior
semicircular canal and he introduced the term cupulolithiasis
Hall (1979) proposed the most convincing theory of canalolithiasis
horizontal canal BPPV was introduced by McClure from the United States and
Cipparrone et al from Italy in 1985
Brandt et al in 1994, anterior canal BPPV was also reported by Herdman et al in
the same year
EPIDEMIOLOGY
 the mean age at onset was 54 years, with a range of 11 to 84 years
 A study in Japan, Mizukoshi et al: 10.7 cases per 100,000 per year
 The percentages of patients who presented to a specialty dizziness clinic who
were found to have BPPV: 17-18%
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Common antecedents of the disorder include vestibular neuronitis (10%) and
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head trauma (20%)
in most patients with benign paroxysmal positional vertigo, no antecedent
association is found.
CLINICAL FINDINGS OF THE POSTERIOR CANAL VARIANT
 The Dix-Hallpike provoking maneuver: diagnose the disease by moving the
patient rapidly from a sitting position to a position of head hanging with each ear
alternately undermost
 beating towards the undermost and affected ear, with a torsional component
clockwise when following leftward movement, or counterclockwise, when
following rightward movement. Typically an upbeating nystagmus component is
superimposed, resulting in a mixed torsional-vertical eye movement.
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Intense vertigo in conjunction with this pattern of nystagmus and the additional
characteristics of a short latency, limited duration, intensity characterized by
crescendo and decrescendo element, reversal on returning to the upright position
and fatigability on repetitive provocation
PATHOGENESIS OF THE POSTERIOR CANAL VARIANT
 Cupulolithiasis
 The existence of basophilic deposits in the cupula of the posterior
semicircular canal has been proved
 Otoconia with a specific gravity greater than endolymph from a
degenerating utricular macula settle on the cupula of the posterior canal
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Latency: inertia of the otoconial mass and the cupula
Fatigability: dispersal of the debris attached to the cupula or even to central
vestibular adaptation
Canalolithiasis
 The degenerative debris are free floating in the endolymph and not adherent
to the cupula.
 These particles, detached from the otoconial layer by degeneration or head
trauma, gravitate into the posterior canal, where they form a plug floating in
its ampullofugal branch.
 Latency: explained by inertia of the clot. The cupula deflection ends when
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the clot reaches its lowest position and accounts for the limited duration of
the nystagmus.
Fatigue: dispersion of the clot particles and reactivation after bedrest is
caused by renewed clot formation.
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REPOSITIONING MANEUVERS OF THE POSTERIOR CANAL VARIANT
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Both the Epley (1992) and Semont (1988) maneuvers inherently require some
degree of torsion, extension, and flexion. Patients who have had strokes or some
sort of paralysis also have a difficult time facilitating the maneuver
John C. Li & John Epley, 2005
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Brandt-Daroff exercises (1980)
THE HORIZONTAL CANAL VARIANT: CLINICAL FINDINGS AND
PATHOGENESIS
REPOSITIONING MANEUVERS OF THE HORIZONTAL CANAL
VARIANT
 Lempert’s Maneuver (barbecue), 1996
Each 90-degree head rotation is performed rapidly within a half second. Head positions are maintained
for between 30 and 60 seconds until all nystagmus has subsided. A. Starting position: supine. B. Head
rotation toward the unaffected ear. C. Body turn from supine to prone while head position is
maintained. D. Head rotation to nose-down position.E. Final head turn to affected-ear-down position. F.
Sitting-up position. X = affected ear (right side); RS = right shoulder.
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FFP (forced prolonged position) maneuver, P. Vannucchi, 1997
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Asprella’s maneuver (1999)
THE ANTERIOR CANAL VARIANT: CLINICAL FINDINGS AND
PATHOGENESIS
 The torsional nystagmic vector is smaller for the anterior than the posterior canal
because the posterior canals are placed at 56° from the sagittal plane whereas the
anterior canals are at 41°
 more down beat than torsional nystagmus is expected from anterior canal BPPV
and more torsional than up beat nystagmus in posterior canal BPPV
 triggering anterior canal BPPV, strict rotation in the canal plane is of relatively
less importance than a final low head down position.
REPOSITIONING MANEUVERS OF THE ANTERIOR CANAL VARIANT
 reverse Epley maneuver (Honrubia V., 1999): 50%
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RAHKO’s maneuver (2002): the patient lies on the healthy side, the head is tilted
downwards 45 degree, then horizontally, upwards 45 degree for 30 s each, and
finally the patient sits up and stays there well supported for at least 3 min. (57
p’ts; one patient had developed symptoms to the opposite side superior canal; 53
patients were symptom-free and three patients had benign positional vertigo of
the superior canal in the follow-up visit but, when the superior canal manoeuvre
was performed, they became symptomless.)
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PFPP(prolonged forced position procedure)- L. Crevits, 2004
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The patient was rapidly moved from sitting to lying supine with the head
bent backwards as far as possible—that is, with the vertex about 60° below
the horizontal. The head was supported in this hanging position for 30
minutes. During this period, the debris were thought to sediment into the
superior part of the anterior canal (now the most dependent) and clot (fig 1).
Then the head was moved quickly forwards, as far as possible—that is, with
the vertex near the vertical. Due to inertia, the canaliths lag somewhat
behind and then move to the common crus of the anterior and the posterior
canals
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