Clin Exp Otorhinolaryngol. 2023 Aug 23. doi: 10.21053/ceo.2023.00486. Online ahead of print.
ABSTRACT
OBJECTIVES: Acute low-tone sensorineural hearing loss (ALHL) is thought to have a different etiology than idiopathic sudden sensorineural hearing loss. We hypothesized that endolymphatic hydrops (EH) in the inner ear organ contributes to ALHL, even in patients without vertigo. This study aimed to evaluate the presence of EH in ALHL and to compare the clinical characteristics of patients with or without EH.
METHODS: We retrospectively reviewed 38 patients diagnosed with ALHL without vertigo from January 2017 to March 2022. EH was measured in all patients using inner ear magnetic resonance imaging (MRI). In addition, we selected patients who showed only mid- or high-frequency hearing loss and had available MRI data as a control group and compared the difference between the ALHL and control groups.
RESULTS: After treatment, the pure-tone average at low frequencies was significantly improved compared with the initial hearing (P<0.001). Hearing recovery was observed in 63.1% of patients; however, the recovery rate did not differ based on treatment method. During the follow-up period, 6 patients (15.8%) progressed to Meniere’s disease, and 18 (47.4%) experienced recurrence. In the ALHL group, the cochlear hydrops ratio on the affected side (0.34 ± 0.09) was significantly higher than on the contralateral side (0.29 ± 0.12, P=0.005), and most patients showed hydrops in the apex area of the cochlea. Compared with the control group (0.25 ± 0.15), the ALHL group showed significantly higher cochlear hydrops ratio (P=0.043). The correlation analysis showed a tendency for hearing thresholds at low frequencies to increase as hydrops ratio increased, although there was no statistical significance.
CONCLUSION: Our study showed that the cochlear hydrops ratio, especially in the apex area on the affected side, was significantly higher in patients with ALHL, indicating that EH in the cochlea contributes to the pathogenesis of ALHL.
PMID:37641856 | DOI:10.21053/ceo.2023.00486
