Objective: The pathogenesis of idiopathic sudden sensorineural hearing loss (ISSHL) remains unknown, but vascular involvement is one of the main hypotheses. The main objective of this study was to investigate the association between ISSHL and cardiovascular and thromboembolic risk factors. Study Design: Multicentric case-control study. Methods: Ninety-six Caucasian patients with ISSHL and 179 sex- and age-matched controls were included. Patients were evaluated on the day of the inclusion and 1 week, 3 weeks and 3 months later. Clinical information concerning personal and familial cardiovascular and thromboembolic risk factors and concerning the ISSHL was collected. Blood samples were collected for genetic analysis of factor V Leiden and G20210A polymorphism in the factor II gene. The severity of the hearing loss was classified as mild (21–40 dB), moderate (41–70 dB), severe (71–90 dB) and profound or total (>90 dB). Hearing improvement was calculated as a relative improvement of hearing thresholds using the contralateral ear as baseline. Results: Systolic blood pressure was higher in patients (130 ± 1.7 mm Hg) than in controls (124 ± 1.1 mm Hg, p = 0.003). The personal/familial history of cardiovascular events was also more prevalent in patients (p = 0.023 and p = 0.014, respectively), whereas no difference was found in the prevalence of personal cardiovascular risk factors (hypertension, diabetes mellitus, hyperlipidemia, smoking habits). There was no correlation between the audiogram type, the hearing outcome and the presence of cardiovascular risk factors. No significant difference was observed in the personal/familial history or in the presence of thromboembolic risk factors. The prothrombin and factor V mutations were uncommon in both patients and controls. The final hearing threshold was only correlated with the severity of the initial hearing loss (p < 0.001), but not influenced by the presence of vertigo, audiogram type, time elapsed from onset of ISSHL to hospitalization or failure of a previous oral therapy. Hearing stabilization was obtained at 21 days in 92% of patients. Conclusion: These results support the theory of vascular involvement as the etiology of some cases of ISSHL. The sole predictive factor of poor final hearing is the severity of the initial hearing loss.

This study assessed the effects of spectral smearing and temporal fine structure (TFS) degradation on masking release (MR) (the improvement in speech identification in amplitude-modulated compared to steady noise observed for normal-hearing listeners). Syllables and noise stimuli were processed using either a spectral-smearing algorithm or a tone-excited vocoder. The two processing schemes simulated broadening of the auditory filters by factors of 2 and 4. Simulations of the early stages of auditory processing showed that the two schemes produced comparable excitation patterns; however, fundamental frequency (F0) information conveyed by TFS was degraded more severely by the vocoder than by the spectral-smearing algorithm. Both schemes reduced MR but, for each amount of spectral smearing, the vocoder produced a greater reduction in MR than the spectral-smearing algorithm, consistent with the effects of each scheme on F0 representation. Moreover, the effects of spectral smearing on MR produced by the two schemes were different for manner and voicing. Finally, MR data for listeners with moderate hearing loss were well matched by MR data obtained for normal-hearing listeners with vocoded stimuli, suggesting that impaired frequency selectivity alone may not be sufficient to account for the reduced MR observed for hearing-impaired listeners.