Atypical paroxysmal vertigo is a rare occurrence, with
incidence of 1-20%.
-The best known and commonest type is PC-BPPV.
-BPPV of the superior semicircular canal has mainly dealt
with hypothetically and until now there has been no
convincing proof of its existence.
-The reason is the fact that the PSCC is the most dependent
part of the vestibular organ in both upright and supine
positions and endolymphatic debris is sensitive to gravity.
-For these reasons, involvement of SSCC (highest point) must
be considered an anomaly in BPPV.
Canalolithiasis of the superior
semicircular canal : An anomaly in
benign paroxysmal vertigo
BRUNO SCHRATZENSTALLER, CAROLA
Acta Oto-Laryngologica, 2005;124:1055-1062
HR 3D MRI
-The authors present three patients with canalolithiasis
of the superior semicircular canal by direct proof
using high-resolution 3D MRI.
-Excellent visualization of the inner ear fluid spaces
- The investigation of malformations, traumatic
lesions and inflammatory processes, and for the
detection of intralabyrinthine tissue formations
- Pathological processes are recognized either as an
anomaly of the configuration of the inner ear or as a
Material and methods
-In > 500 patients BPPV
-SSCC involvement only 3 patients (1 male, 2 females)
-Diagnosis of BPPV with Epley’s criteria of
-Underwent complete otoneurologic investigation,
including audiometry, caloric irrigation and MRI of
the brain to exclude concomitant neurologic
- Major concern of anatomical and pathological sites of
semicircular canal ; T2-weighted images, slice
thickness 1 mm.
Case reports 1
: Thepatientwasa 39-year-old male who complained
of brief attacks of rotatory vertigo when turning his
head over his right shoulder in a sitting position.
-triggered a fast-beating counterclockwise pure
5-10 s and lasted for 15 s.
-The nystagmus was accompanied by a severe
spinning sensation and reversed its direction upon
repositioning the head.
-This positional vertigo had occurred immediately after
a skull trauma 4 years previously.
:showed a minor high-frequency
sensorineural hearing loss on both sides
:revealed a slightly decreased response
on the left side, without the presence of
Conventional X-rays, cranial CT and MRI revealed no bone
fractures or brain damage and cerebral angiography and
basic neurological investigations proved to be normal.
HR-3D-MRI ; revealed an infraction or impression in the
right posterior semicircular canal and a
defect in the right superior semicircular canal. left
inner ear showed no abnormalities.
To date, it has not been possible to cure this
patient by means of any physical maneuvers.
Normal Lt. inner ear
Traumatic impression of Lt PSCC, a 2 mm. filling defect
at the top of the SSCC.
: A 58-year-oldfemalepresentedwiththetypical
symptoms of BPPV on both sides, from which she
had been suffering for many years.
Ten years previously
she had been diagnosed with
Meniere’s disease (MD) on the left side, at which time
she suffered from severe pancochlear hearing loss
and recurrent attacks of vertigo and vomiting lasting
-Local gentamicin treatment applied via a ventilation
tube in the left tympanic membrane had been
successful and the attacks of MD ceased;
- However, some years later she developed incurable
positional paroxysmal vertigo on both sides.
The Dix/Hallpike maneuver
a counterclockwise torsional nystagmus on the
right side and a clockwise torsional nystagmus on
the left side, with reversal on both sides when the
patient was returned to a sitting position. On each
side the nystagmus was accompanied by a
sensation of vertigo, which lasted for
20 s on the
right side and
25 s on the left.
Caloric irrigation ; a malfunction on the left side.
normal hearing on the right side and pancochlear
hearing loss of
70 dB on the left side.
3.6-mm long occlusion of the left superior
semicircular canal and a
1.7-mm filling defect in the
left posterior semicircular canal whereas the right
side showed no abnormalities.
Two years later ; no significant changes
- 55-year-old female presented with a history of brief
attacks of rotational vertigo when turning her
head to the right side while lying in bed.
The vertigo had occurred for the first time 3 days
-Putting the head into the right Hallpike position elicited
a counterclockwise rotatory nystagmus which lasted
15-20 s and was reversed when the head was
returned to the upright position.
nearly normal hearing function in both ears.
The patient had undergone a type I tympanoplasty
years previously on the contralateral (left) side
For this reason we were suspicious of atypical vertigo
and performed HR
-3D-MRI 2 days after diagnosis
without any further treatment or investigation.
2.2-mm filling defect in the superior
semicircular canal of the left side, with no
pathological changes in the right labyrinth.
No treatment was necessary as the patient
3 days after diagnosis.
The defect in the left semicircular canal was no
longer visible in a control HR-3D-MRI scan carried out
2 weeks later.
a 2.2 mm long filling defect of SSCC
-Explain BPPV attack in the position
-An ampullofugal deflection of the cupula of
the right superior canal provoked by
dislodged particles moving down from the
top of the non-ampulated arm,
The top of the SCC is the most unlikely
-We postulate the existence of an “adhesion point”
- Caused by traumatization where endolymphatic
can collect (the microfractures creating a ‘‘sticky
- Furthermore, the preceding skull trauma may have
caused increased shedding of otoconia.
Case 2 discussion
- Repeated hydropical distension is supposed to
cause damage both to the maculae, causing
increased shedding of otoconia, and to the
canal endothelium, resulting in stenosis,
occlusions or adhesions as a consequence of
loss of the resiliency of the membranous
- Local application of gentamicin may have
caused further damage, not only to the macula
organs but also to the canal endothelium,
making it easier for loose debris to adhere
inside the canal walls.
-Vyslonzil reported an increased incidence of
otoconial deposits in the posterior canal in
sections of patients who had been treated with
streptomycin (an aminoglycoside like
-In 2002, Perez et al. reported a patient suffering
from intractable BPPV after gentamicin therapy
Parnes and McClure (for cupulolithiasis) and later
Epley (for canalolithiasis) postulated that, in
BPPV, if the superior canal was affected on
one side this would result in the same
symptoms as if the posterior canal of the
opposite side was affected.
Epley used the term ‘‘complementary semicircular
As HR-3D-MRI showed no pathology in the right
vestibular organ but a long filling defect in the left
superior semicircular canal, we conclude that the
affected left superior semicircular canal is ‘‘masking’’
the symptoms of typical BPPV in the right ear.
Epley’s postulate of complementary semicircular canal
causing identical symptoms (affected with canalolithiasis)
Case 3 discussion
:This patient presented with symptoms of
typical BPPV on the right side but had
undergone a tympanoplasty on the left side.
:HR-3D-MRI revealed a 2.2-mm filling defect in
the left superior semicircular canal.
The onset of BPPV following middle ear
surgery, even years later, has frequently
been reported in the literature and is
thought to be due to traumatization of the
-The mechanism ;the symptoms of
canalolithiasis of the right posterior canal
‘‘masking’’ an affected left superior canal.
- Even after increased release following
macula damage, loose otoconia cannot
collect in the superior semicircular canal
and should leave the canal lumen as soon
as the patient gets up from a lying to an
Therefore, as expected,
HR-3D-MRI showed the formation of a solid
clot. As there was no endothelial damage to
make the intracanalicular endothelium
adhesive, this condition must be most unstable.
As confirmed by the spontaneous
remission of symptoms and the absence of
pathologic findings on a control MRI scan.
-BPPV of the superior semicircular canal must be
considered an anomaly in canalolithiasis.
-Suspicious of Canalolithiasis of SCC and recommend
patients with previous ear surgery or ear disease
(MD, vestibular neuritis, sudden sensorineural
hearing loss, etc.) who present with BPPV on the
patients with therapy-resistant BPPV.
patients who present with symptoms of BPPV when
in an atypical position.