Effects of Cochlear Hearing Loss on the Benefits of Ideal Binary Masking

Author(s):  
Vahid Montazeri ◽  
Shaikat Hossain ◽  
Peter F. Assmann
1999 ◽  
Vol 106 (2) ◽  
pp. 898-907 ◽  
Author(s):  
Brian C. J. Moore ◽  
Brian R. Glasberg ◽  
Deborah A. Vickers

2019 ◽  
Vol 122 (4) ◽  
pp. 1421-1460
Author(s):  
Tony L. Sahley ◽  
David J. Anderson ◽  
Michael D. Hammonds ◽  
Karthik Chandu ◽  
Frank E. Musiek

Acoustic overstimulation (AOS) is defined as the stressful overexposure to high-intensity sounds. AOS is a precipitating factor that leads to a glutamate (GLU)-induced Type I auditory neural excitotoxicity and an activation of an immune/inflammatory/oxidative stress response within the inner ear, often resulting in cochlear hearing loss. The dendrites of the Type I auditory neural neurons that innervate the inner hair cells (IHCs), and respond to the IHC release of the excitatory neurotransmitter GLU, are themselves directly innervated by the dynorphin (DYN)-bearing axon terminals of the descending brain stem lateral olivocochlear (LOC) system. DYNs are known to increase GLU availability, potentiate GLU excitotoxicity, and induce superoxide production. DYNs also increase the production of proinflammatory cytokines by modulating immune/inflammatory signal transduction pathways. Evidence is provided supporting the possibility that the GLU-mediated Type I auditory neural dendritic swelling, inflammation, excitotoxicity, and cochlear hearing loss that follow AOS may be part of a brain stem-activated, DYN-mediated cascade of inflammatory events subsequent to a LOC release of DYNs into the cochlea. In support of a DYN-mediated cascade of events are established investigations linking DYNs to the immune/inflammatory/excitotoxic response in other neural systems.


2004 ◽  
Vol 115 (5) ◽  
pp. 2422-2423
Author(s):  
Enrique A. Lopez‐Poveda ◽  
Christopher J. Plack ◽  
Ray Meddis ◽  
Jose L. Blanco

2003 ◽  
Vol 14 (09) ◽  
pp. 510-517 ◽  
Author(s):  
Susan E. Spirakis ◽  
Raymond M. Hurley

This study investigated the characteristics of hearing loss in children with ventriculoperitoneal (VP) shunted hydrocephalus. Twelve hydrocephalic children with patent VP shunts participated. The etiology of the hydrocephalus was either intraventricular hemorrhage or spina bifida. Audiometric examination included pure-tone air conduction thresholds, tympanometry, contralateral and ipsilateral acoustic reflex thresholds (ARTs), and distortion product otoacoustic emissions (DPOAEs). A unilateral, high-frequency, cochlear hearing loss was found in the ear ipsilateral to the shunt placement in 10 (83%) of the 12 shunt-treated hydrocephalic children. No hearing loss was observed in the ear contralateral to shunt placement. Based on the pure-tone audiometric findings, coupled with the decrease in DPOAE amplitude in the shunt ear, the hearing loss appears to be cochlear in nature. We suggest that cochlear hydrodynamics are disrupted as the result of reduced perilymph pressure, a consequence of cerebrospinal fluid (CSF) reduction due to the combined effects of a patent shunt and a patent cochlear aqueduct. In addition, a concomitant brain stem involvement is evidenced in the ART pattern, possibly produced by the patent shunt draining the CSF from the subdural space, resulting in cranial base hypoplasia.


2002 ◽  
Vol 45 (2) ◽  
pp. 392-402 ◽  
Author(s):  
Sid P. Bacon ◽  
Jane M. Opie

Listeners were asked to detect amplitude modulation (AM) of a target (or signal) carrier that was presented in isolation or in the presence of an additional (masker) carrier. The signal was modulated at a rate of 10 Hz, and the masker was unmodulated or was modulated at a rate of 2, 10, or 40 Hz. Nine listeners had normal hearing, 4 had a bilateral hearing loss, and 4 had a unilateral hearing loss; those with a unilateral loss were tested in both ears. The listeners with a hearing loss had normal hearing at 1 kHz and a 30- to 40-dB loss at 4 kHz. The carrier frequencies were 984 and 3952 Hz. In one set of conditions, the lower frequency carrier was the signal and the higher frequency carrier was the masker. In the other set, the reverse was true. For the impaired ears, the carriers were presented at 70 dB SPL. For the normal ears, either the carriers were both presented at 70 dB SPL or the higher frequency carrier was reduced to 40 dB SPL to simulate the lower sensation level experienced by the impaired ears. There was considerable individual variability in the results, and there was no clear effect of hearing loss. These results suggest that a mild, presumably cochlear hearing loss does not affect the ability to process AM in one frequency region in the presence of competing AM from another region.


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