PR BPPV

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Bagaimana mekannisme trauma menyebabkan BPPV ?
Mechanism of BPPV
It is believed that the short, usually intense, episodes of vertigo and nystagmus are caused by two
mechanisms:
(1) Cupulolithiasis: a dislocation of the calcium carbonate crystals which rest on the hair cells of the
saccule and utricle of the inner ear which make them susceptible to the pull of gravity. These "ear stones"
or otoliths become dislodged due to trauma, prior infection (neurolabyrinthitis or "vestibular neuronitis"),
as a normal part of the aging process in 80% of people living between 60 and 80 and just by chance. The
otoliths usually settle on the active part of the posterior semicircular canal and convert the receptor from
one sensitive to acceleration to one sensitive to position and changing of position. The concept of
Cupulolithiasis is bolstered by some histopathology. It is depicted in the following diagram:

The otolith (red, in the insert) has located to the top of a hair cell in the cupula. Exercise therapy is
used
to
move
it
and
eliminate
the
condition
(see
treatment
section).
(2) Canalithiasis: Otoliths or "dense bodies" become located in the canal itself near the cupula, again in a
position to cause symptoms with change in head position. Canalithiasis is depicted in the following
diagram:

The dense bodies (violet) or otoliths (blue squares [depending on your viewer]) are lodged near the
cupula. A series of head position changes can move the material to a non-sensitive portion of the inner
ear (see treatment section).

PR BPPV
Kadhaf
Harie Cipta
Bagaimana mekannisme trauma menyebabkan BPPV

Causes of BPPV
In most cases, BPPV is found in isolation and termed "primary" or "idiopathic" BPPV. This type
accounts for about 50%70% of cases. The most common cause of "secondary" BPPV is head
trauma, representing 7%17% of all BPPV cases. A blow to the head may cause the release of
numerous otoconia into the endolymph, which probably explains why many of these patients
suffer from bilateral BPPV. Viral neurolabyrinthitis or so-called "vestibular neuronitis" has been
implicated in up to 15% of BPPV cases.
Mnire's disease has also been shown to be strongly associated with BPPV. There is large
variation in the literature regarding what proportion of patients with BPPV also have the
diagnosis of Mnire's disease. Estimates range from 0.5% to 31%. Gross and colleagues found
that 5.5% of patients with Mnire's disease had "certain" posterior canal BPPV. The causative
mechanism is not well understood but may be the result of hydropically induced damage to the
macula of the utricle or by partial obstruction of the membranous labyrinth.
Recently, migraines have been found to be closely associated with BPPV. Ishiyama and
colleagues and Lempert and colleagues found an increased incidence of migraine in patients with
BPPV and higher recurrence rates of BPPV after successful positioning in patients with migraine.
It has been suggested that spasm of the inner ear arteries may be a possible causative mechanism,
because vasospasm is well documented in migraines.
Secondary BPPV has also been described after inner ear surgery. The cause is thought to be
linked to utricular damage during the procedure, leading to the release of otoconia.