Posterior semicircular canal dehiscence: a morphologic cause of vertigo similar to superior semicircular canal dehiscence

Krombach, Gabriele A.; DiMartino, E.; Schmitz‐Rode, Thomas; Prescher, Andreas; Haage, Patrick; Kinzel, Sylvia; Günther, Rolf W.

doi:10.1007/s00330-003-1828-5

Cited by 82 publications

(44 citation statements)

References 14 publications

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“…Aside from dehiscence of the superior semicircular canal, several other sources of labyrinthine dehiscence can lead to symptoms similar to those in SCDS, including that of the posterior semicircular canal (52, 53), lateral semicircular canal (17, 54), vestibular aqueduct (55), facial nerve (56), internal auditory canal (57), and the carotid canal (58, 59). Merchant and Rosowski synthesized many of these reports and broadly proposed that any dehiscence of the inner ear can lead to an inner ear conductive hearing loss from a third mobile window (60).…”

Section: Etiologymentioning

confidence: 99%

Superior Canal Dehiscence Syndrome: Lessons from the First 20 Years

2017

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Superior semicircular canal dehiscence syndrome was first reported by Lloyd Minor and colleagues in 1998. Patients with a dehiscence in the bone overlying the superior semicircular canal experience symptoms of pressure or sound-induced vertigo, bone conduction hyperacusis, and pulsatile tinnitus. The initial series of patients were diagnosed based on common symptoms, a physical examination finding of eye movements in the plane of the superior semicircular canal when ear canal pressure or loud tones were applied to the ear, and high-resolution computed tomography imaging demonstrating a dehiscence in the bone over the superior semicircular canal. Research productivity directed at understanding better methods for diagnosing and treating this condition has substantially increased over the last two decades. We now have a sound understanding of the pathophysiology of third mobile window syndromes, higher resolution imaging protocols, and several sensitive and specific diagnostic tests. Furthermore, we have a treatment (surgical occlusion of the superior semicircular canal) that has demonstrated efficacy. This review will highlight some of the fundamental insights gained in SCDS, propose diagnostic criteria, and discuss future research directions.

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Section: Etiologymentioning

confidence: 99%

Superior Canal Dehiscence Syndrome: Lessons from the First 20 Years

2017

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“…A postmortem survey of more than 1,000 temporal bones reported the prevalence of superior SCD syndrome in adults at 0.7% [2, 3]. Similar symptoms have been attributed to posterior SCDs [4–6]. …”

Section: Introductionmentioning

confidence: 95%

“…Due to volume averaging and resolution limits, HRCT overestimates the incidence of SCDs, yielding higher numbers than those found in pathological studies [10, 11]. Adult HRCT surveys have found a combined incidence of 2.1–8.6% of posterior and superior SCDs [4, 12]. In patients presenting with symptoms of SCD syndrome, the incidence is greater than 34% [4].…”

Section: Introductionmentioning

confidence: 99%

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Prevalence of radiographic semicircular canal dehiscence in very young children: an evaluation using high-resolution computed tomography of the temporal bones

et al. 2012

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Background Previous studies suggest that semicircular canal dehiscences (SCDs) have a developmental origin. Objective We hypothesized that if SCDs originate during development, incidence of radiographic SCDs in young children will be higher than in adults. Materials and methods Thirty-four temporal bone HRCTs of children younger than 2 years and 40 temporal bone HRCTs of patients older than 18 years were reformatted and re-evaluated for presence of SCD or canal thinning. Results were compared with indications for HRCT and clinical information. Results SCDs were detected in 27.3% of children younger than 2 years of age (superior, 13.8%; posterior, 20%) and in 3% of adults (P≤0.004). Of children with one radiographic dehiscence, 55.6% had multiple and 44% had bilateral SCDs on HRCT. No lateral canal SCDs were present. Thinning of bone overlying the semicircular canals was found in 44% of children younger than 2 years and 2.5% of adults (P<0.0001). Conclusion SCDs are more common on HRCTs of very young children. This supports the hypothesis that SCDs originate from discontinuation of bone deposition/maturation. However, SCDs on imaging do not necessarily correlate with canal dehiscence syndrome and should therefore be interpreted carefully.

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“…4 In another retrospective study, Krombach et al reported complete missing caloric test response only in 2 out of 44 cases of semicircular canal dehiscence. 5 Interestingly, despite minimal caloric function and severe to profound hearing loss, the patient had signs and symptoms of PSC dehiscence. The findings on video-oculography on sound stimulation and pressure stimulation were milder compared to other patients with superior semicircular canal or PSC dehiscence.…”

Section: Discussionmentioning

confidence: 96%

Posterior semicircular canal dehiscence following endolymphatic sac surgery

2012

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Posterior semicircular canal dehiscence is a rare otologic entity which presents with third window signs and symptoms. Petrous apex cholesteatoma, fibrous dysplasia, high riding jugular bulb, and eosinophilic granuloma have been reported to be associated with posterior semicircular canal dehiscence. Here we report a case of development of posterior semicircular canal dehiscence following an endolymaphatic sac surgery for the first time.

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Posterior semicircular canal dehiscence: a morphologic cause of vertigo similar to superior semicircular canal dehiscence

Cited by 82 publications

References 14 publications

Superior Canal Dehiscence Syndrome: Lessons from the First 20 Years

Superior Canal Dehiscence Syndrome: Lessons from the First 20 Years

Prevalence of radiographic semicircular canal dehiscence in very young children: an evaluation using high-resolution computed tomography of the temporal bones

Posterior semicircular canal dehiscence following endolymphatic sac surgery

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