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Otol."],"published-print":{"date-parts":[[2022,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec id=\"S0022215121002826_sec_a1\"><jats:title>Background<\/jats:title><jats:p>Described just over 20 years ago, superior semicircular canal dehiscence remains a relatively unknown and easily missed cause of dizziness and auditory symptoms.<\/jats:p><\/jats:sec><jats:sec id=\"S0022215121002826_sec_a2\"><jats:title>Objective<\/jats:title><jats:p>This review focused on the origin, presenting symptoms and underlying pathophysiology of superior semicircular canal dehiscence, and the available treatment options.<\/jats:p><\/jats:sec><jats:sec id=\"S0022215121002826_sec_a3\"><jats:title>Main findings and conclusion<\/jats:title><jats:p>The bony dehiscence acts as a \u2018third window\u2019, affecting inner-ear homeostasis, and resulting in hypersensitivity and a vestibular response to lower sound level stimuli. The third window effect explains the pressure- and sound-induced vertigo, oscillopsia, and nystagmus, as well as autophony, conductive hyperacusis and tinnitus. The origin of superior semicircular canal dehiscence is linked to the combination of a congenital or developmental factor, and a \u2018second event\u2019 like head trauma, rapid pressure changes or age-related factors. Computed tomography of the temporal bone and reduced vestibular-evoked myogenic potential thresholds can confirm the diagnosis. Despite only retrospective cohorts, surgery is considered a safe treatment option, targeting mainly vestibular but also auditory symptoms, with transmastoid approaches gaining popularity.<\/jats:p><\/jats:sec>","DOI":"10.1017\/s0022215121002826","type":"journal-article","created":{"date-parts":[[2021,10,7]],"date-time":"2021-10-07T07:09:31Z","timestamp":1633590571000},"page":"284-292","source":"Crossref","is-referenced-by-count":13,"title":["Superior semicircular canal dehiscence: a narrative 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