Incidence of semicircular canal dehiscence in Singapore
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Semicircular canal dehiscence is a congenital syndrome that mainly affects the superior and, less commonly, the posterior semicircular canals. The diagnosis of superior semicircular canal dehiscence syndrome depends on the demonstration of a very small defect in the bony wall of the superior semicircular canal. Any amount of intact bone present excludes the diagnosis. The study will give an approximation of the incidence of semicircular canal dehiscence in Singapore. No specific data regarding the number of such cases exist currently. Retrospective review of CT scans of the temporal bone performed at our institution between January 2005 and July 2007 revealed a total of 10 such cases over this period, comprising 8 males and 2 females, with all cases involving the superior semicircular canal. Almost all of the patients scanned had evidence of previous or existing cholesteatoma. Three patients had bilateral superior semicircular canal dehiscence (all males), with an almost equal number of semicircular canal dehiscence on both sides for both sexes. Our study shows no significant advantage to obtaining reformatted oblique sagittal images for all temporal bone studies, unless the visualized walls show questionable defects. In these cases, reconstructed images are probably advantageous and should be obtained and reviewed.Keywords:
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Abstract Objectives To present a histopathological case of a 91‐year‐old woman who was diagnosed with superior semicircular canal dehiscence postmortem. Methods The patient was a registered donor with the National Temporal Bone Donor Program at the NIDCD National Temporal Bone, Hearing and Balance Pathology Resource Registry. Computed tomography imaging was performed on each temporal bone. The temporal bones were decalcified with ethylenediaminetetracetate and embedded in celloidin, and tissue sections were stained with hematoxylin and eosin. Horizontal sections were taken through the left temporal bone, and vertical sections were taken through the right temporal bone. Results Histopathological sections taken through the right temporal bone demonstrated no bone between the membranous wall of the superior semicircular canal and the middle fossa dura. There was no histopathological evidence of superior semicircular canal dehiscence in the left temporal bone; however, a small dehiscence would not be identified on horizontal sections. Microcavitations were observed in the common crus of the left temporal bone. Conclusion This reports describes the case of a woman who was diagnosed with superior semicircular canal dehiscence postmortem. The presence of microcavitations in the temporal bone is consistent with osteoclastic activity, which may play a role in the development of superior canal dehiscence.
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To illustrate that posterior semicircular canal dehiscence can present similarly to superior semicircular canal dehiscence.The symptomatology initially presented as probable Menière's disease evolving into a mixed conductive hearing loss with a Carhart notch-type perceptive component suggestive of otosclerosis-type stapes fixation. A small hole stapedotomy resulted in a dead ear and a horizontal semicircular canal hypofunction. Recurrent incapacitating vertigo attacks developed. Vestibular evoked myogenic potential (VEMP) testing demonstrated intact vestibulocollic reflexes. Additional evaluation with high resolution multidetector computed tomography (MDCT) of the temporal bone showed a dehiscence of the left posterior semicircular canal.Besides superior semicircular canal dehiscence, posterior semicircular canal dehiscence has to be included in the differential diagnosis of atypical Menière's disease and/or low tone conductive hearing loss. The value of performing MDCT before otosclerosis-type surgery is stressed. VEMP might contribute to establishing the differential diagnosis.
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Abstract Objective: The objective of this study was to describe the operative management of posterior canal dehiscence. Methods: A transmastoid approach to and plugging of the posterior canal was performed for posterior semicircular canal dehiscence (PSCD). Results: Postoperatively, the patient exhibited improvement in conductive hearing loss and vestibular symptoms. Conclusions: PSCD can cause symptoms identical to that of superior semicircular canal dehiscence. Successful PSCD plugging can be performed without visualization of the actual area of dehiscence.
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We describe the clinical evaluation and operative management of posterior semicircular canal dehiscence caused by a high jugular bulb.We performed a retrospective case report.The patient had clinical and audiometric findings consistent with semicircular canal dehiscence and imaging findings that demonstrated erosion of the posterior semicircular canal by a high jugular bulb. Resurfacing of the eroded canal provided resolution of the vestibular symptoms without damage to the inner ear.Dehiscence of the posterior semicircular canal can cause clinical and audiometric findings similar to those of superior semicircular canal dehiscence syndrome. Resurfacing of the area of dehiscence can successfully relieve the vestibular symptoms. In the case of dehiscence of the posterior canal from a high jugular bulb, resurfacing may offer advantages over canal plugging for definitive management.
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The objective of this study was to evaluate the characteristic symptoms of and treatments for lateral semicircular canal dehiscence (LSCD) and posterior semicircular canal dehiscence (PSCD) and its proposed mechanism. A dehiscence acquired in any of the semicircular canals may evoke various auditory symptoms (autophony and inner ear conductive hearing loss) or vestibular symptoms (vertigo, the Tullio phenomenon, and Hennebert sign) by creating a "third mobile window" in the bone that enables aberrant communication between the inner ear and nearby structures. A PubMed search was performed using the keywords lateral, posterior, and semicircular canal dehiscence to identify all relevant cases. Our data suggest that PSCD, although clinically rare, is most likely associated with a high-riding jugular bulb and fibrous dysplasia. Patients may experience auditory manifestations that range from mild conductive to extensive sensorineural hearing loss. LSCD is usually associated with chronic otitis media with cholesteatoma.
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