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Abstract
Keywords
- positional vertigo
- paroxysmal vertigo
- dizziness
- canalolithiasis
- cupulolithiasis
Benign paroxysmal positional vertigo (BPPV) is the most common and the most
effectively treated vestibular disorder. The prevailing pathomechanism is canalolithiasis, which is otoconia falling in one of the semicircular canals where they move in
response to changes of the head position, triggering excitation of the vestibular
receptors of the affected canal. In the majority of patients with BPPV, the posterior
canal is affected by canalolithiasis and there are two highly effective therapeutic
maneuvers for treatment. About 20% of patients present with lithiasis of the horizontal
or anterior canal. The author focuses on recent advances in diagnosis and treatment of
the more rare variants of BPPV.
Epidemiology
Benign paroxysmal positional vertigo is the most common
cause for vertigo, particularly in the elderly. A populationbased survey in Germany found a lifetime prevalence of
3.2% in women and 1.6% in men and a cumulative incidence
reaching almost 10% at the age of 80 years.^ The point
prevalence of BPPV in unselected geriatric populations has
been found to be around 10%.'''^ In childhood, the disorder
is exceedingly rare. In dizziness clinics, approximately one
out of five patients presents with BPPV.
In idiopathic BPPV, women outnumber men by ~2:1. This
preponderance of female sex is less evident in BPPV after head
trauma and peripheral vestibular disorder.^
Pathophysiology
Benign paroxysmal positional vertigo is caused by otoliths
that are dislodged from the utricular macula and fall into a
semicircular canal. These particles are composed of calcium
carbonate and have a density higher than endolymph. In the
most common condition (canalolithiasis), the otoconia are
mobile within the canal and changes of the head position in
the plane of the affected semicircular canal causes them to
move to the most dependent point of the canal. The resulting
inappropriate endolymph flow activates hair cell receptors,
provoking attacks of positional vertigo and nystagmus.^ More
rarely, otoconia are attached to the cpula of a semicircular
canal and render it sensitive to gravity (cupulolithiasis).^ The
hypothesis of canalolithiasis and cupulolithiasis is supported
by an animal model.^ The most convincing proof for canalolithiasis is provided by the efficacy of positioning maneuvers, which aim to clear the affected canal from mobile
particles.
Diagnosis
Most patients present with the typical history of short attacks
of vertigo precipitated by turning in bed, lying down from
sitting, sitting up from lying, and extending the neck to look
up. Patients are usually aware that certain head movements
can provoke attacks of vertigo and often develop strategies to
DOI http://dx.doi.org/
10.1055/S-0033-1354590.
ISSN 0271-8235.
von Brevern
Fig. 1 (A,B) Dix-Hallpike maneuver for provocation of benign paroxysmal positional vertigo of the left posterior canal. Below, a model of the
undermost posterior semicircular canal is shown. When the patient lies down, the particles move away from the cpula within the canal. The
resulting endolymph flow causes an unphysiologic activation of the posterior canal and leads to paroxysmal vertigo and torsional-vertical
nystagmus. (UT, utricle; CU, cpula; OT, otoconial debris) (From von Brevern M, tempert T. Benign paroxysmal positional vertigo. Nervenarzt
2004;75:1027-1036. With permission of Springer + Business Media).
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Direction of nystagmus
Canalolithiasis:
Horizontal, geotropic, and transient in both lateral supine
positions
Cupulolithiasis:
Horizontal, apogeotropic, and persistent in both lateral
supine positions
Rarely, torsional-vertical positional nystagmus as described above, but lasting longer than 1 minute may be
observed in the Dix-Hallpike maneuver. In the absence of
other neurologic signs, this finding may indicate cupulolithiasis of the posterior canal. Typically, the intensity of
nystagmus is strongest with the head resting slightly raised
from supine ("half Dix-Hallpike maneuver"), thus with the
affected cpula in an earth-horizontal position to be maximally deflected by the gravitational
Benign Paroxysmal Positional Vertigo of the
Horizontal Canal
Table 2 Identification of the affected side in benign paroxysmal positional vertigo of the horizontal canal
Maneuver
Canalolithiasis
Cupulolithiasis
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eye movement recording is not available, rendering identification of the affected side in clinical practice unreliable.^ ^^^^"^^ The positional downbeating nystagmus in
BPPV of the anterior canal may show no latency and no
crescendo-decrescendo time course, and rarely reverses
direction when sitting up from the provoking position.^^'^^
It is important to bear in mind that positional downbeat
nystagmus is most commonly due to central vestibular dysfunction, presenting usually with additional neurologic
signs.^^ Hence, the diagnosis of BPPV of the anterior canal
requires a meticulous neurologic examination. In addition,
brain MRI should be performed in those cases refractory to
treatment.
Treatment
Treatment of canalolithiasis aims to induce the displacement
of the otolithic debris through the open end of the affected
semicircular canal into the utricular cavity where they no
longer produce positional vertigo. The therapeutic aim in
V.
Fig. 2 (A-E) Epiey maneuver for treatment of benign paroxysmal positional vertigo of the left posterior canal, consisting of a set of five successive
head positions that are hand-guided by the therapist. The head rotations are performed rapidly and the time interval between each step is
30 seconds or until nystagmus subsides. The vertex of the head is kept tilted downwards throughout the rotations in the supine position. A
positional nystagmus appearing in the second and third head position and beating in the same direction with respect to the head indicates
successive movement of the particles toward the utricular cavity and predicts a favorable outcome. (From von Brevern M, Lempert T. Benign
paroxysmal positional vertigo. Nervenarzt 2004;75;1027-1036. With permission of Springer + Business Media).
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Fig. 3 Semont maneuver for treatment of benign paroxysmal positional vertigo of the left posterior canal. The maneuver is hand-guided by a
therapist who is not depicted for the sake of clarity. All movements are performed rapidly. The head is kept turned 45 degrees away from the
affected ear throughout the maneuver. (From von Brevern M. Lempert T. Benign paroxysmal positional vertigo. Nervenarzt 2004:75:1027-1036.
With permission of Springer + Business Media).
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Fig. 4 (A-C) Roll maneuver for treatment of canaloiithiasis of the left horizontal canal. The supine patient is rotated 270 degrees in rapid steps of
90 degrees in the plane of the horizontal semicircular canal toward the healthy side. The time interval between each step is 30 seconds or until
nystagmus has subsided. (From von Brevern M, Lempert T. Benign paroxysmal positional vertigo. Nervenarzt 2004:75:1027-1036. With
permission of Springer + Business Media).
Prognosis
Most recurrences occur in the first year after treatment with a
recurrence rate in canalolithiasis of the posterior canal of
15%peryear^''^
Patients often ask for strategies for the prevention of BPPV.
Postural restrictions for one to several days after successful
treatment of BPPV of the posterior canal (including not lying
on the affected ear, sleeping upright, and wearing a cervical
collar) slightly reduce the recurrence rate.^^ However, these
restrictions are unpleasant for patients and not recommended by many experts. A daily routine of Brandt-Daroff
exercises or self-application of the modified Epley maneuver
by the patient does not avoid recurrence of BPPV of the
posterior
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