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Canalolithiasis of the superior semicircular canal: An anomaly in benign paroxysmal vertigo

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Abstract

According to the canalolithiasis theory, benign paroxysmal vertigo (BPPV) is caused by gravity-dependent movements of otoconial debris that collects in the endolymph of the posterior semicircular canal. Other parts of the vestibular organ are rarely affected, and it is mainly the horizontal canal that is affected by this atypical form of BPPV. Canalolithiasis of the superior semicircular canal must be considered an anomaly because the superior semicircular canal is the highest point of the vestibular organ and debris normally cannot collect in this special location. Until now, BPPV of the superior canal has mainly been dealt with theoretically in the literature. The authors present three patients with canalolithiasis of the superior semicircular canal and offer direct proof of the condition using high-resolution 3D MRI.
Introductions
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
WAGNER-MANSLAU
Germany
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
filling defect.
Material and methods
-In > 500 patients BPPV
-SSCC involvement only 3 patients (1 male, 2 females)
-Diagnosis of BPPV with Epley’s criteria of
canalolithiasis
-Underwent complete otoneurologic investigation,
including audiometry, caloric irrigation and MRI of
the brain to exclude concomitant neurologic
diseases.
- 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
torsionalnystagmuswhichoccurredwitha latency
of
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.
Audiometry
:showed a minor high-frequency
sensorineural hearing loss on both sides
Caloric irrigation
:revealed a slightly decreased response
on the left side, without the presence of
head-shaking nystagmus.
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
2-mm filling
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.
Case 2
: 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
for hours.
-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.
Audiometry showed
normal hearing on the right side and pancochlear
hearing loss of
70 dB on the left side.
HR
-3D-MRI revealed
a
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
Case 3
- 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
before presentation.
-Putting the head into the right Hallpike position elicited
a counterclockwise rotatory nystagmus which lasted
for
15-20 s and was reversed when the head was
returned to the upright position.
Audiometry showed
nearly normal hearing function in both ears.
The patient had undergone a type I tympanoplasty
12
years previously on the contralateral (left) side
without complications.
For this reason we were suspicious of atypical vertigo
and performed HR
-3D-MRI 2 days after diagnosis
without any further treatment or investigation.
HR-3DMRI
showed a
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
recovered spontaneously
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
Case1 Discussion
-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
cause BPPV.
-We postulate the existence of an “adhesion point
- Caused by traumatization where endolymphatic
particles
can collect (the microfractures creating a ‘‘sticky
endothelium’’.
- 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
labyrinth.
- 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
gentamicin).
-In 2002, Perez et al. reported a patient suffering
from intractable BPPV after gentamicin therapy
for MD.
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
canals’’
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
inner ear.
-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
upright position.
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.
Conclusion
-BPPV of the superior semicircular canal must be
considered an anomaly in canalolithiasis.
-Suspicious of Canalolithiasis of SCC and recommend
the HR-3D-MRI
patients with previous ear surgery or ear disease
(MD, vestibular neuritis, sudden sensorineural
hearing loss, etc.) who present with BPPV on the
contralateral side;
patients with therapy-resistant BPPV.
patients who present with symptoms of BPPV when
in an atypical position.
... Nevertheless, it has been widely demonstrated how pDBN may not rarely occur also in peripheral pathologies (1)(2)(3)8). It can be elicited when the patient is brought into the straight head hanging (SHH) position and/or by Dix Hallpike (DH) maneuvers and it has been mainly related to benign paroxysmal positional vertigo (BPPV) involving the anterior semicircular canal (ASC) (3,(9)(10)(11)(12)(13)(14)(15). Despite detached otoconia, moving inside unusual sites of the labyrinth, represent the assumed underlying mechanism, peripheral pDBN patterns show features classically known as central such as lack of torsional components and long time constant (9,11,15). ...
... Nevertheless, interpretation of pDBN still represent a challenging topic, as patients with ASC-BPPV usually present with atypical positional nystagmus mimicking central pDBN (1)(2)(3)9). In fact, it is rarely evoked only by ipsilateral positioning and it usually exhibits longer time constant compared to typical BPPV-like nystagmus, lacking of both crescendo-decrescendo course and torsional components (3,(9)(10)(11)(12)(13)(14)(15). Moreover, it has been recently hypothesized that the same pDBN could also be generated by particles gravitating through the distal portion of the non-ampullary tract of PSC, close to the common crus [ (16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27); Figures 14A-D]. ...
... Authors have hypothesized that, unlike typical canalolithiasis involving PSC ampullary tract, where particles are free to float along the membranous duct with minimal effect on cupular dynamics during high-frequency testing (75,77), in cases with ASC-BPPV and apogeotropic PSC-BPPV presenting with persistent pDBN debris could alter endolymphatic dynamics and cupular response mechanisms, resulting in high-frequency VOR deficit for the involved canal. This condition is thought to occur whenever otoconia settle in physiological narrow portions of the canal lumen [such as the distal portion of the nonampullary branch of PSC, close to the common crus (20)] or in particular sites of altered canal anatomy due to possible structural changes in SCs orientation (9,13,46) or to acquired stenosis of membranous ducts [as demonstrated for ASC ampullary arm (10,78)] or even to irregularities in membranous walls. Given that hydrodynamic models of fluid-filled SC have demonstrated how a pressure amplification occurs as otoconia enter a narrow section of the canal (79,80), in particular situations it could likely result in an incomplete canalith jam (18,20) leading to impaired ampullary responses for high-frequency range (37). ...
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... BPPV is well accepted as a pathology involving the semicircular canals (canalolithiasis) [4]. While most of the studies have shown the involvement of the posterior semicircular [47,48], some of the studies have also shown the involvement of the horizontal [49] and superior semicircular canals [47,48]. The above studies are testimony to the widespread acceptance of canal involvement among individuals with BPPV. ...
... BPPV is well accepted as a pathology involving the semicircular canals (canalolithiasis) [4]. While most of the studies have shown the involvement of the posterior semicircular [47,48], some of the studies have also shown the involvement of the horizontal [49] and superior semicircular canals [47,48]. The above studies are testimony to the widespread acceptance of canal involvement among individuals with BPPV. ...
... This is in contrast to the origin of the response in case of cVEMP. Saccule is the universally accepted end organ for the origin of cVEMP [9,48,50]. Therefore, it would be erroneous to believe that the pathology in semicircular canals would affect a response which originates from the saccule. ...
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Benign paroxysmal positional vertigo (BPPV) constitutes a major proportion of the population with peripheral vestibulopathies. Although the freely floating otoconia within the semicircular canals is responsible for the symptoms of BPPV, the source of the otoconia debris is mainly believed to be the otolith organs. Therefore, the pathology in either or both the otolith organs appears a logical proposition. Cervical and ocular vestibular-evoked myogenic potentials (cVEMP and oVEMP), being the tests for functional integrity of the otolith organs, appear promising for investigating otolith involvement in BPPV. While recent evidences are suggestive of equivocal findings for cVEMP, there are only a few studies on oVEMP. Additionally, both these potentials have never been explored in the same set of individuals with BPPV. Therefore, the present study aimed to evaluate the functional integrity of the otolith organs through cVEMP and oVEMP in individuals with posterior canal BPPV. Thirty-one individuals with unilateral posterior canal BPPV and 31 age- and gender-matched healthy controls underwent 500 Hz tone-burst-evoked cVEMP and oVEMP. The results demonstrated no significant group difference on any of the cVEMP parameters (p > 0.05). A similar trend was noticed for the latency-related parameters of oVEMP. However, the peak-to-peak amplitude was significantly smaller in the affected ears of individuals with BPPV than their unaffected ears and the ears of healthy controls (p < 0.05). The BPPV group showed significantly higher inter-aural amplitude difference ratio than the healthy controls (p < 0.05). Further, the sensitivity and specificity of oVEMP were also found to be far superior to those of cVEMP. Thus, the outcome of the present study revealed involvement of utricle rather than saccule in posterior canal BPPV, and therefore, oVEMP appears to be better suited to clinical investigation than cVEMP in individuals with posterior canal BPPV.
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Posterior canal benign paroxysmal positional vertigo (BPPV) is the most frequent form of BPPV. it is characterized by paroxysmal positioning nystagmus evoked through Dix-Hallpike and Semont positioning tests. Anterior canal BPPV (AC) is rarer than posterior canal BPPV; it presents a prevalent down beating positioning nystagmus, with a torsional component clockwise for the left canal, counterclockwise for the right canal. Due to the possible lack of the torsional component, it is sometimes difficult to identify the affected ear. An apogeotropic variant of posterior BPPV (APC) has recently been described, characterised by a paroxysmal positional nystagmus in the opposite direction to the one evoked in posterior canal BPPV: the linear component is down-beating, the torsional component is clockwise for the right canal, counterclockwise for the left canal, so that a contra-lateral anterior canal BPPV could be simulated. During a 16 month period, of 934 BPPV patients observed, the authors identified 23 (2.5%) cases of apogeotropic posterior canal BPPV and 11 (1.2%) cases of anterior canal BPPV, diagnosed using the specific oculomotor patterns described in the literature. Anterior canal BPPV was treated with the repositioning manoeuvre proposed by Yacovino, which does not require identification of the affected side, whereas apogeotropic posterior canal BPPV was treated with the Quick liberatory rotation manoeuvre for the typical posterior canal BPPV, since in the Dix-Hallpike position otoliths are in the same position if they come either from the ampullary arm or from the non-ampullary arm. The direct resolution of BPPV (one step therapy) was obtained in 12/34 patients, 8/23 patients with APC and 4/11 patients with AC; canal conversion into typical posterior canal BPPV, later treated through Quick liberatory rotation (two-step therapy), was obtained in 19 patients,14/23 with APC and 5/11 with AC. Three patients were lost to follow-up. Considering the effects of therapeutic manoeuvres, the authors propose a grading system for diagnosis of AC and APC: "certain" when a canalar conversion in ipsilateral typical posterior canal BPPV is obtained; "probable" when APC or AC are directly resolved; "possible" when disease is not resolved and cerebral neuroimaging is negative for neurological diseases. our results show that the oculomotor patterns proposed in the literature are effective in diagnosing APC and AC, and that APC is more frequent than AC. Both of these rare forms of vertical canal BPPV can be treated effectively with liberatory manoeuvres. KEy WorDS: Anterior canal BPPV • Posterior canal BPPV • Apogeotropic posterior canal BPPV • Quick Liberatory Rotation manoeuvre • yacovino manoeuvre riASSUnTo La VPPB da canalolitiasi posteriore è la forma più frequentemente osservata; essa è caratterizzata da un nistagmo parossistico posizionale evocato dal posizionamento di Dix-Hallpike o di Semont con una componente lineare up-beat ed una componente torsionale oraria per il canale posteriore sinistro, antioraria per il canale posteriore destro. La VPPB da canalolitiasi anteriore è più rara per la posizione più alta del canale anteriore ed è caratterizzata da un nistagmo parossistico evocabile nei posizionamenti Head-Hanging, con una componen-te lineare down-beating prevalente rispetto ad una incostante componente torsionale, oraria per il canale sinistro, antioraria per quello destro. La incostante presenza della componente torsionale rende talvolta difficile il riconoscimento del lato malato. Recentemente è stata descritta una variante apogeotropa della canalolitiasi posteriore caratterizzata da un quadro nistagmico evocato invertito rispetto alla canalolitiasi posteriore tipica, e cioè con una componente lineare down-beating ed una componente torsionale antioraria per il canale sinistro, oraria per il canale destro, cosicché può essere simulata una canalolitiasi anteriore controlaterale. In un periodo di 16 mesi, applicando come criteri diagnostici i patterns oculomotori descritti in letteratura, gli Autori hanno identificato, su un totale di 934 casi di VPPB, 23 casi di VPPB da canalolitiasi posteriore apogeotropa (2,5%) ed 11 casi di VPPB da canalolitiasi anteriore (1,1%). La VPPB da canalolitiasi anteriore è stata trattata con la manovra di Yacovino, che non necessita dell'individuazione del lato affetto, mentre la VPPB da canalolitiasi posteriore apogeotropa è stata trattata con la manovra di Rotazione Rapida Liberatoria, basandosi sulla considerazione che gli otoconi, sia che provengano dal braccio ampollare che da quello non ampollare del canale posteriore, nella posizione finale dei test diagnostici si trovino nella stessa parte del canale. La risoluzione diretta della VPPB è stata ottenuta con le manovre terapeutiche utilizzate in 8/23 canalolitiasi posteriori apogeotrope ed in 4/11 canalolitiasi anteriori (one-step therapy), mentre la conversione in una canalolitiasi posteriore tipica, trattata con manovra di Rotazione Rapida Liberatoria, è stata osservata in 14/23 canalolitiasi posteriori apogeotrope ed in 5/11 canalolitiasi anteriori (two-step therapy). Tre pazienti sono stati persi al follow-up. Considerando gli effetti delle manovre terapeutiche, gli Autori propongono un sistema di gradazione della diagnosi di VPPB da canalolitiasi posteriore apogeotropa e di VPPB da canalolitiasi anteriore: "grado certo" quando si ottiene una conversione in canalolitiasi posteriore tipica, "grado probabile" quando si ottiene direttamente la risoluzione della malattia,"grado possibile" quando la malattia non si risolve e la RMN cerebrale non evidenzia segni di patologia neurologica. I nostri risultati mostrano come i patterns oculomotori già descritti in letteratura siano efficaci nella diagnosi di VPPB da canalolitiasi posteriore apogeotropa e di VPPB da canalolitiasi anteriore e che la canalolitiasi posteriore apo-geotropa sia più frequente rispetto alla canalolitasi anteriore. Entrambe le forme rispondono bene alla terapia liberatoria. PArolE ChiAVE: VPPB da canalolitiasi anteriore • VPPB da canalolitiasi posteriore • VPPB da canalolitiasi posteriore apogeotropa • Manovra di rotazione rapida liberatoria • Manovra di Yacovino
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Zusammenfassung Der benigne periphere paroxysmale Lagerungsschwindel (BPPV) ist die häufigste Schwindelform, vor allem im höheren Alter. Die Lebenszeitprävalenz liegt bei 3%. Bei der klinischen Untersuchung sieht man bei den Lagerungsmanövern einen zum unten liegenden Ohr rotierenden und zur Stirn schlagenden vertikalen Lagerungsnystagmus. Die Canalolithiasishypothese, aus vielen Otokonien zusammengesetzte Agglomerate, kann alle Symptome und Befunde erklären. Der Nystagmus entspricht einer ampullofugalen Erregung des betroffenen hinteren vertikalen Bogengangs des unten liegenden Ohrs. Über 90% aller Fälle sind idiopathisch, also degenerativ, während die symptomatischen Fälle am häufigsten auf ein Schädeltrauma, Neuritis vestibularis und M. Menière zurückgeführt werden. Der seltenere BPPV des horizontalen Bogengangs wird durch Kopfdrehung um die Körperlängsachse im Liegen ausgelöst. Unbehandelt persistiert der BPPV bei etwa 30% der Patienten. Therapie der Wahl sind entweder das Semont- oder Epley-Manöver. Beide Manöver sind gleichermaßen wirksam, und die Heilungsrate liegt bei über 95% innerhalb weniger Tage. Das jährliche Rezidivrisiko des BPPV liegt bei etwa 15 bis 30%. Im Verlauf kommt es bei ca. 50% der Patienten zu einem Rezidiv, das auf die gleiche Art erfolgreich behandelt werden kann.
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Der benigne paroxysmale Lagerungsschwindel (BPLS) ist die häufigste vestibuläre Erkrankung und macht in Spezialambulanzen für Schwindelerkrankungen etwa 20% der Diagnosen aus. Die Ursache der Störung liegt nach neueren Befunden in einer sog. Kanalolithiasis des hinteren vertikalen Bogengangs. Frei bewegliche Partikel, die in den Endolymphschlauch des Bogengangs geraten sind, führen dort bei Lagewechsel zu einer unphysiologischen Endolymph-Strömung und Reizung des vestibulären Sinnesepithels. Das Verständnis der pathophysiologischen Grundlage führte zur Entwicklung spezifischer Lagerungsmanöver, die den Kopf in der Ebene des betroffenen Bogengangs rotieren, um ihn von den frei flottierenden Partikeln zu befreien. Die nach Epley und Semont benannten Manöver führen nach einmaliger Anwendung bei etwa 60% der Patienten zu sofortiger Beschwerdefreiheit, bei mehrfacher Anwendung erreicht die Erfolgsrate nahezu 100%.
Article
A strong paroxysmal positional horizontal nystagmus accompanied by symptoms similar to those of paroxysmal positional vertigo (PPV) can be observed in a small fraction of patients who have positional vertigo. This nystagmus may be a lateral canal variant of PPV. We evaluated nine patients who had episodes of prolonged, intense positional vertigo provoked by lateral movements of the head while in the supine position. The nystagmus appeared as horizontal and was directed toward the uppermost ear (ageotropic) when the head was rotated to either side (bidirectional). The duration of nystagmus lasted more than 1 minute in all the cases, although it presented a progressive decrease in the velocity of the slow component. The clinical and electronystagmographic features of this syndrome lead us to propose a different form of horizontal canal PPV associated with a paroxysmal positional ageotropic and bidirectional nystagmus, probably caused by a “heavy cupula” as a result of deposits of extraneous bodies (otolithic?) or by a cupula denser than the endolymph.
Article
Der benigne paroxysmale Lagerungsschwindel (BPLS) ist die hufigste vestibulre Erkrankung und macht in Spezialambulanzen fr Schwindelerkrankungen etwa 20% der Diagnosen aus. Die Ursache der Strung liegt nach neueren Befunden zumeist in einer so genannten Kanalolithiasis des hinteren vertikalen Bogengangs: Frei bewegliche Partikel, die in den Endolymphschlauch des Bogengangs geraten sind, fhren dort bei Lagewechsel zu einer unphysiologischen Endolymphstrmung und Reizung des vestibulren Sinnesepithels. Das Verstndnis der pathophysiologischen Grundlage fhrte zur Entwicklung spezifischer Lagerungsmanver, die den Kopf in der Ebene des betroffenen Bogengangs rotieren, um ihn von frei flottierenden Partikeln zu befreien. Die nach Epley und Semont benannten Manver fhren nach einmaliger Anwendung bei etwa 60% der Patienten zu sofortiger Beschwerdefreiheit, bei mehrfacher Anwendung erreicht die Erfolgsrate nahezu 100%. Heutzutage ist der BPLS die am besten behandelbare Ursache fr vestibulren Schwindel.Benign paroxysmal positional vertigo is the most common vestibular disorder, accounting for about 20% of referrals in specialized dizziness clinics. Nowadays, canalolithiasis of the posterior semicircular canal has been widely accepted as the biological basis for typical benign paroxysmal positional vertigo as it is compatible with all clinical features of the disorder. Better understanding of its pathophysiological concepts has led to specific therapeutic strategies, which aim to clear the affected semicircular canal from mobile particles. After a single maneuver both Epleys and Semonts procedures lead to complete recovery in about 60% of patients and in nearly 100% when performed repeatedly. These positioning maneuvers have made benign paroxysmal positional vertigo the most successfully treatable cause of vertigo.
Article
High resolution magnetic resonance imaging (HR-MRI) and computed tomography (HR-CT) of the inner ear are becoming more important for the diagnosis of peripheral vestibular lesions. Modern HR-MRI techniques allow visualization of detailed anatomic features of the vestibulo-cochlear regions as well as pathologic findings in the inner ear such as, neoplastic lesions (e.g., small intracanalicular acoustic neuromas), anomalies causing vertigo and hearing loss (e.g. Mondini’ s-malformation, perilymph fistula, vestibular paroxysmia), and inflammatory diseases (e.g., Cogan’s syndrome, labyrinthitis, zoster neuritis). HR-CT is still the first examination that should be performed in patients with middle ear diseases (e.g., tumor, infection), trauma (e.g. temporal bone fractures), or fibro-osseous diseases. Although the imaging of the vestibulo-cochlear system has dramatically improved, there are still several peripheral vestibular disorders that cannot be visualized so far, e.g., benign paroxysmal positioning vertigo, idopathic vestibular neuritis or Menière’s disease.
Article
Benign paroxysmal vertigo (BPV) is a disorder of the vestibular labyrinth. The clinical features can be explained by an abnormality in the posterior semicircular canal. Under the influence of gravity, a density differential between the endolymph and the cupula will cause displacement of the cupula when changes in head position occur. The presence or absence of fatiguability is a useful test as it helps define etiology, prognosis, and therapy. At the risk of adding yet another classification of nystagmus to the literature, we submit that division of BPV into two types (fatiguable and nonfatiguable) will simplify and rationalize the management of this common complaint.
Article
Findings of large basophilic staining deposits on the cupula of the posterior semicircular canal ampulla have been used in part to explain the clinical phenomenon of benign positional vertigo (BPV). Although it is generally agreed that cupulolithiasis may involve other canal ampullae, the precise nature, distribution, and origin of these deposits remains unclear. In order to provide a better understanding of this finding, a series of 566 temporal bone specimens from the Ear Pathology Research Laboratory at the University of Toronto were reviewed. The results from this survey and speculations concerning the nature and formation of these deposits are discussed.
Article
The Canalith Repositioning Procedure (CRP) is designed to treat benign paroxysmal positional vertigo (BPPV) through induced out-migration of free-moving pathological densities in the endolymph of a semicircular canal, using timed head maneuvers and applied vibration. This article describes the procedure and its rationale, and reports the results in 30 patients who exhibited the classic nystagmus of BPPV with Hallpike maneuvers. CRP obtained timely resolution of the nystagmus and positional vertigo in 100%. Of these, 10% continued to have atypical symptoms, suggesting concomitant pathology; 30% experienced one or more recurrences, but responded well to retreatment with CRP. These results also support an alternative theory that the densities that impart gravity-sensitivity to a semicircular canal in BPPV are free in the canal, rather than attached to the cupula. CRP offers significant advantages over invasive and other noninvasive treatment modalities in current use.