Besides typical symptoms and signs (including pulsatile tinnitus, hyperacusis, pressure/sound-induced torsional nystagmus, conductive hearing loss and lowered thresholds of air-conducted VEMPs) an analysis of the relevant literature reveals a certain clinical polymorphism induced by superior canal dehiscence (SCD). In addition to asymptomatic persons or subjects with SCD presenting exclusively with cochlear symptoms (only partly explained by the so-called “near-dehiscence syndrome”), SCD cases mainly presenting with atypical/refractory/recurrent positional vertigo and/or Meniere-like vertigo spells have been recently described. Moreover, if surgical occlusion of the superior canal (SC) results in symptoms control inducing a selective SC hypofunction, clinicians my sometimes accidentally detect a reduced SC VOR gain in asymptomatic patients with wide-sized dehiscence. These findings led authors to propose the occurrence either of a natural SC plugging (complete or incomplete) by middle fossa dura prolapsing into the canal lumen or a dispersion of mechanical energy through the dehiscence. Typical and atypical scenarios is presented. A subsample of patients from the personal series with a complete otoneurologic assessment (audiometry, VOG eye recording, air/bone-conducted cervical/ocular VEMPs, video head impulse test) is selected to explain these emerging theories on possible pathomechanisms.
Course created on December 17, 2021
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Learning Outcomes
- After this course, participants will be able to identify Superior Canal Dehiscence Syndrome according to the most recent criteria.
- After this course, participants will be able to discuss the current use of the available diagnostic tests to detect signs consistent with SCD.
- After this course, participants will be able to identify atypical scenarios associated with SCD.
Agenda
| 0-5 Minutes | Introduction of the speakers |
| 5-10 Minutes | Definition and pathomechanisms of the third mobile windows |
| 10-15 Minutes | Definition, clinical presentation, epidemiology and etiology of SCD |
| 15-30 Minutes | Diagnostic work-up and diagnostic criteria of SCD |
| 30-45 Minutes | Surgical therapy, postoperative findings in SCD, and overview of unusual clinical pictures of SCD |
| 45-60 Minutes | Near-dehiscence syndrome and variability of SCD anatomy |
| 60-70 Minutes | Spontaneous auto-plugging process of SCD and endolymphatic hydrops |
| 70-75 Minutes | SCD and BPPV |
| 75-90 Minutes | Debate and questions |
Reviews
270 ReviewsPresented By
Andrea Castellucci
MD
BACKGROUND: 2008: Medical Degree at the University of Bologna, Italy 2009-2014: Residency in Otolaryngology, Head & Neck Surgery at the ENT & Audiology Unit of the University of Bologna, Italy. Grown-up in the otologic and neurotologic group of the ENT Unit of the University Hospital of Bologna directed by prof. Giovanni Carlo Modugno. 2014-2015: Research Assistant at the ENT & Audiology Unit of the University of Bologna, Italy
CURRENT OCCUPATION Since 2015 ENT consultant dedicated to Otology and Neurotology at the ENT Unit of Santa Maria Nuova Hospital, AUSL – IRCCS in Reggio Emilia, Italy. Head of the Vestibular outpatient unit in Reggio Emilia, working in collaboration with Emergency and Neurology Department for the treatment of acute vestibular syndromes. Good knowledge in modern vestibular testing (calorics, skull vibration, vHIT, and VEMPs). Author and co-author of journal articles and book chapters in national and international literature. Presenter in national and international meetings.
CURRENT RESEARCH ACTIVITIES in Reggio Emilia and in collaboration with other Centers in Italy and in Switzerland: SSCD, near-dehiscence syndrome, how SSCS can mimic other pathologies and differential diagnosis o Selective canal hypofunction at the vHIT and correlation with other vestibular findings and underlying pathologies Positional DBN due to vertical canal BPPV, complete and incomplete canalith jam and the use of vHIT for differential diagnosis. Minimum stimulus strategy for HSC-BPPV diagnosis MD mimicking acute vestibular loss and differential diagnosis with vHIT and VEMPs. Dissociation between calorics and vHIT and correlation with underlying pathologies.
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