Experience with the Vibrant Soundbridge RW-Coupler for round window Vibroplasty with tympanosclerosis

Usage of the Vibrant Soundbridge (VSB) with round window (RW)-Coupler placement at the RW has been shown to successfully treat mixed hearing loss. Coupling between the VSB's floating mass transducer (FMT) and the RW membrane is difficult in the case of sclerosis in the RW and drilling down the bony lip until the RW membrane can be seen completely can possibly induce a perilymphatic fistula. A 68-year-old woman who had bilateral mixed hearing loss with sclerosis in the RW due to tympanosclerosis underwent a RW-Vibroplasty with a RW-Coupler. Speech discrimination scores in quiet and noise and functional gain with the VSB with RW-Coupler were better than those using a conventional hearing aid. The results of the present case have shown the feasibility of implanting a VSB with RW-Coupler in patients with mixed hearing loss due to tympanosclerosis

Novel Radiographic Measurement Algorithm Demonstrating a Link between Obesity and Lateral Skull Base Attenuation

OBJECTIVES: (1) To describe a validated algorithm for measuring tegmen thickness on computed tomography scans. (2) To compare the tegmen thickness in 3 groups: patients with spontaneous cerebrospinal fluid (CSF) leaks, obese controls, and nonobese controls. STUDY DESIGN: Retrospective review. SETTING: Patients with spontaneous CSF otorrhea often have highly attenuated tegmen plates. This is associated with obesity and/or idiopathic intracranial hypertension (IIH). No evidence exists, however, that objectively links obesity and/or IIH with skull base attenuation. SUBJECTS AND METHODS: This was a retrospective review from 2004 to the present. Patients with spontaneous CSF otorrhea and matched obese (body mass index [BMI] \u3e30 kg/m(2)) and nonobese (BMI/m(2)) controls were selected. Tegmen thickness was measured radiographically. Interrater validity was assessed. RESULTS: Ninety-eight patients were measured: 37 in the CSF group (BMI, 36.6 kg/m(2)), 30 in the obese group (BMI, 34.6 kg/m(2)), and 31 in the nonobese group (BMI, 24.2 kg/m(2)). The CSF group had a significantly thinner tegmen compared to both the obese control (P \u3c .01) and nonobese control (P = .0004) groups. Obese controls had a thinner tegmen than nonobese controls (P \u3c .00001). A significant inverse correlation was detected between skull base thickness and BMI. Signs/symptoms of IIH were most commonly found in the CSF group. Good to very good strength of agreement was detected for measures between raters. CONCLUSION: This is the first study to (1) quantify lateral skull base thickness and (2) significantly correlate obesity with lateral skull base attenuation. Patients who are obese with spontaneous CSF leaks have greater attenuation of their skull base than matched obese controls. This finding supports theories that an additional process, possibly congenital, has a pathoetiological role in skull base dehiscence

Supporting Cell Characteristics in Long-deafened Aged Mouse Ears

Significant sensory hair cell loss leads to irreversible hearing and balance deficits in humans and other mammals. Future therapeutic strategies to repair damaged mammalian auditory epithelium may involve inserting stem cells into the damaged epithelium, inducing non-sensory cells remaining in the epithelium to transdifferentiate into replacement hair cells via gene therapy, or applying growth factors. Little is currently known regarding the status and characteristics of the non-sensory cells that remain in the deafened auditory epithelium, yet this information is integral to the development of therapeutic treatments. A single high-dose injection of the aminoglycoside kanamycin coupled with a single injection of the loop diuretic furosemide was used to kill hair cells in adult mice, and the mice were examined 1 year after the drug insult. Outer hair cells are lost throughout the entire length of the cochlea and less than a third of the inner hair cells remain in the apical turn. Over 20% and 55% of apical organ of Corti support cells and spiral ganglion cells are lost, respectively. We examined the expression of several known support cell markers to investigate for possible support cell dedifferentiation in the damaged ears. The support cell markers investigated included the microtubule protein acetylated tubulin, the transcription factor Sox2, and the Notch signaling ligand Jagged1. Non-sensory epithelial cells remaining in the organ of Corti retain acetylated tubulin, Sox2 and Jagged1 expression, even when the epithelium has a monolayer-like appearance. These results suggest a lack of marked SC dedifferentiation in these aged and badly damaged ears