{"title":"Vestibular function analyzed by a video head impulse test in patients with idiopathic sudden sensorineural hearing loss associated with vertigo.","authors":"Daichi Hirokane, Masaya Takumida, Munehiro Shiraishi, Nobuaki Hiraki, Shuji Ishikawa, Hideaki Suzuki, Tsuyoshi Udaka","doi":"10.1080/00016489.2026.2688395","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The vestibular-organ site that is responsible for vertigo-associated idiopathic sudden sensorineural hearing loss (ISSNHL) has not been identified clearly.</p><p><strong>Aims/objectives: </strong>To analyze the function of each semicircular canal (SCC) separately in patients with vertigo-associated ISSNHL.</p><p><strong>Patients/methods: </strong>ISSNHL patients with or without vertigo (<i>n</i> = 19 each) underwent a video head impulse test. Their vestibulo-ocular reflex (VOR) and catch-up saccades (CUS) were recorded.</p><p><strong>Results: </strong>As for the affected side, the VOR gains of the lateral and posterior SCCs were lower in the vertigo group versus the nonvertigo group. The percentage of patients with decreased VOR gains of the posterior SCC and those with CUS (+) for the lateral and posterior SCCs were higher in the vertigo group versus the nonvertigo group. In the vertigo group, the VOR gain was lower in the affected side in all SCCs. The percentage of patients with decreased VOR gains and that with CUS (+) were higher for the posterior SCC in the affected side versus the unaffected side.</p><p><strong>Conclusion/significance: </strong>The posterior SCC was predominantly impaired in patients with vertigo-associated ISSNHL. Considering the vascular anatomy of the inner ear, these results indicate that a microcirculatory disturbance plays a crucial role in the pathophysiology of ISSNHL.</p>","PeriodicalId":6880,"journal":{"name":"Acta Oto-Laryngologica","volume":" ","pages":"1288-1294"},"PeriodicalIF":1.3000,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Oto-Laryngologica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/00016489.2026.2688395","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/7/9 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"OTORHINOLARYNGOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: The vestibular-organ site that is responsible for vertigo-associated idiopathic sudden sensorineural hearing loss (ISSNHL) has not been identified clearly.
Aims/objectives: To analyze the function of each semicircular canal (SCC) separately in patients with vertigo-associated ISSNHL.
Patients/methods: ISSNHL patients with or without vertigo (n = 19 each) underwent a video head impulse test. Their vestibulo-ocular reflex (VOR) and catch-up saccades (CUS) were recorded.
Results: As for the affected side, the VOR gains of the lateral and posterior SCCs were lower in the vertigo group versus the nonvertigo group. The percentage of patients with decreased VOR gains of the posterior SCC and those with CUS (+) for the lateral and posterior SCCs were higher in the vertigo group versus the nonvertigo group. In the vertigo group, the VOR gain was lower in the affected side in all SCCs. The percentage of patients with decreased VOR gains and that with CUS (+) were higher for the posterior SCC in the affected side versus the unaffected side.
Conclusion/significance: The posterior SCC was predominantly impaired in patients with vertigo-associated ISSNHL. Considering the vascular anatomy of the inner ear, these results indicate that a microcirculatory disturbance plays a crucial role in the pathophysiology of ISSNHL.
期刊介绍:
Acta Oto-Laryngologica is a truly international journal for translational otolaryngology and head- and neck surgery. The journal presents cutting-edge papers on clinical practice, clinical research and basic sciences. Acta also bridges the gap between clinical and basic research.