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.

These results compared favourably with previous reports. A new therapeutic procedure may allow improved results.

In a retrospective study performed at the Otolaryngology, Head and Neck Surgery Department, Pitié-Salpêtrière Hospital, Paris from 1991 to March 2007, we determined surgical procedures for the treatment of tegmen breaches in chronic otitis media. Forty-two cases were examined: 76% corresponded to chronic otitis media with cholesteatoma, and 24% to chronic otitis media without cholesteatoma. Twenty-eight cases were operated using a combined approach, eight cases using a single suprapetrous approach, and six cases using a transmastoid approach. A total of 33% of the cases showed a meningocele or a meningoencephalocele treated through either a combined or a suprapetrous approach. No recurrence or neural/meningeal infectious involvement was found after a mean time of 43 months in the 36 long-term follow-up cases operated through the combined or suprapetrous approaches. Two cases included in the study were a loss to follow-up. Three of the former cases had already been operated for supracentimetric fissure using lower approach. Two out of the six patients operated using lower approach presented post surgery cerebrospinal fluid otorrhea. Combined or suprapetrous approaches seem to be best adapted to the treatment of supracentimetric or recurrent tegmen breaches, as well as to the precise examination and repair of meningeal lesions. Treatment for tegmen breach can be achieved in a single intervention, even when there is an ongoing infection of the middle ear. The mastoid approach should be used only for infracentimetric defects when there is no neural/meningeal lesion.