Objective: In a common cavity (CC) deformity, the cochlea and vestibule are confluent to form a single cavity without internal architecture, and distribution of auditory neuronal tissue is unclear. The purposes of this study are to reveal the spatial distribution of auditory neuronal tissue in CC deformity using electrically evoked auditory brainstem response (EABR) during cochlear implantation.
Study Design: Retrospective case review.
Setting: Cochlear implant (CI) center at a tertiary referral hospital.
Patients: Five patients with CC deformity who underwent cochlear implantation and intraoperative EABR testing.
Main Outcome Measures: Spatial distribution of electrodes that elicited an evoked wave V (eV) in EABR testing was evaluated in each CC deformity.
Results: Electrically evoked auditory brainstem response testing demonstrated that electrodes attached on the inner wall of the anteroinferior cavity of the CC deformity successfully elicited a reproducible eV in all cases, and the latency of each eV was an approximately 4 ms, which is similar to those reported in patients without an inner ear malformation. Interestingly, in Case 1 with the lowest percentage of eV-positive electrodes (31.8%), CI-aided audiometric thresholds were changed, depending on the frequency allocation to eV-positive electrodes in the programming. Cochlear implant-mediated facial nerve stimulation was observed in 3 of 5 cases, and results of EABR testing were useful for optimizing the device program to decrease facial nerve stimulation without sacrificing CI-mediated auditory performance.
Conclusion: The results of EABR testing suggested that auditory neuronal elements are distributed to the anteroinferior part of CC deformity, mainly around or near the inner wall of the cavity. In cases with CC deformity, EABR testing is useful to achieve the optimal electrode array placement and to adjust programming parameters of the implanted device, which might be essential to maximize CI outcomes and to decrease facial nerve stimulation.
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http://dx.doi.org/10.1097/MAO.0000000000000375 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Department of Neurobiology, Harvard Medical School, Boston, MA 02115.
The sense of hearing originates in the cochlea, which detects sounds across dynamic sensory environments. Like other peripheral organs, the cochlea is subjected to environmental insults, including loud, damage-inducing sounds. In response to internal and external stimuli, the central nervous system directly modulates cochlear function through olivocochlear neurons (OCNs), which are located in the brainstem and innervate the cochlear sensory epithelium.
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Department of Otolaryngology at Unfallkrankenhaus Berlin, Charité Medical School, University of Berlin, 12683 Berlin, Germany.
Background: Previous studies have shown that multiple post-traumatic irradiations of the cochlea with near-infrared light (NIR) can significantly reduce noise-induced hearing loss. However, a single NIR pre-treatment was shown to have the same effect. Extending the pre-treatment time did not result in any further reduction in hearing loss.
View Article and Find Full Text PDFNeurosci Res
January 2025
Department of Cell Physiology, Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan. Electronic address:
Sensorineural hearing loss causes cell death in central auditory neurons, but molecular mechanisms of triggering this process are not fully understood. We report here that loss of afferent activity promotes cell death by facilitating proBDNF-p75NTR signals in cochlear nucleus of chicks around hatch. RNA-seq analyses revealed up-regulation of genes related to proBDNF-p75NTR-JNK signals as well as apoptosis at the nucleus within 24hours after unilateral cochlea deprivation.
View Article and Find Full Text PDFNat Commun
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Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
While animals readily adjust their behavior to adapt to relevant changes in the environment, the neural pathways enabling these changes remain largely unknown. Here, using multiphoton imaging, we investigate whether feedback from the piriform cortex to the olfactory bulb supports such behavioral flexibility. To this end, we engage head-fixed male mice in a multimodal rule-reversal task guided by olfactory and auditory cues.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Pharmacology and Therapeutics, University of Florida, Gainesville, FL, USA.
Assembly of actin-based stereocilia is critical for cochlear hair cells to detect sound. To tune their mechanosensivity, stereocilia form bundles composed of graded rows of ascending height, necessitating the precise control of actin polymerization. Myosin 15 (MYO15A) drives hair bundle development by delivering critical proteins to growing stereocilia that regulate actin polymerization via an unknown mechanism.
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