Otosclerosis is a disorder causing a hardening of the middle ear bones which leads to a progressive hearing loss. Internationally renowned experts met in Saas Fee (Switzerland) in 2004 to discuss otosclerosis and stapes surgery, and they have subsequently been invited by the editor to present their findings in this publication. From basic to clinical research, all relevant topics such as epidemiology, genetics, histopathology, molecular biology, and virus etiology are described. Also shown are the mechanics of the middle ear in model and in vivo, audiologic and imaging procedures, and surgical techniques including laser surgery. Further papers discuss advantages and disadvantages of stapes prosthesis, stapedectomy versus stapedotomy, and indications and contraindications of common therapies. Finally postsurgery complications and how to deal with them, short- and long term results, as well as the significance of stapes surgery in training and future developments are presented. This publication will keep the otorhinolaryngologist in clinic and practice up to date on current research and clinical development, but also pathologists, radiologists and virologists will find it inspiring reading.
137 - 145: Superior Semicircular Canal Dehiscence Mimicking Otosclerotic Hearing Loss
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Published:2007
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Book Series: Advances in Oto-Rhino-Laryngology
Saumil N. Merchant, John J. Rosowski, Michael J. McKenna, 2007. "Superior Semicircular Canal Dehiscence Mimicking Otosclerotic Hearing Loss", Otosclerosis and Stapes Surgery, W. Arnold, R. Häusler
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Abstract
A puzzling aspect of middle ear surgery is the presence of an air-bone gap in a smallnumber of cases with no apparent cause. We believe that some of these cases are due tounrecognized superior semicircular canal dehiscence (SSCD). We have now gathered experiencefrom 20 patients with SSCD presenting with apparent conductive hearing loss withoutvestibular symptoms. All affected ears had SSCD on high-resolution CT scan. The commonfindings in these patients were: (1) the air-bone gaps occurred in the lower frequencies below2,000 Hz, and ranged from 10 to 60 dB; (2) bone conduction thresholds below 2,000 Hz weresometimes negative (-5 dB to -15 dB); (3) the acoustic (stapedial) reflex was present; (4)measurement of umbo velocity by laser Doppler vibrometry showed slight hypermobility ofumbo motion; (5) the vestibular-evoked myogenic potential response was present, withthresholds that were abnormally low, and (6) the middle ear was normal at exploratory tympanotomy,including normal mobility of the ossicles and a patent round window niche. Wehave investigated the mechanism of the air-bone gap due to SSCD using a theoretical framework,clinical research data and an animal model (chinchilla). Our research supports thehypothesis that SSCD introduces a ‘third’ window into the inner ear which produces the airbonegap by (1) shunting air-conducted sound away from the cochlea, thus elevating air conductionthresholds, and (2) increasing the difference in impedance between the scala tympaniand scala vestibuli, thus improving thresholds for bone-conducted sound.
