scholarly journals eABR THR Estimation Using High-Rate Multi-Pulse Stimulation in Cochlear Implant Users

2021 ◽  
Vol 15 ◽  
Author(s):  
Ali Saeedi ◽  
Ludwig Englert ◽  
Werner Hemmert
Keyword(s):  
Phase Locking ◽  
Correlation Coefficients ◽  
Auditory Brainstem ◽  
High Rate ◽  
Absolute Difference ◽  
Growth Functions ◽  
Brainstem Response ◽  
Response Thresholds ◽  
Phase Locking Value ◽  
Pulse Stimulation

We estimated the electrically-evoked auditory brainstem response thresholds (eABR THRs) in response to multi-pulses with high burst rate of 10,000 pulses-per-second (pps). Growth functions of wave eV amplitudes, root mean square (RMS) values, peak of phase-locking value (PLV), and the lowest valid data point (LVDP) were calculated in 1-, 2-, 4-, 8-, and 16-pulses conditions. The growth functions were then fitted and extrapolated with linear and exponential functions to find eABR THRs. The estimated THRs were compared to psychophysical THRs determined for multi-pulse conditions as well as to the clinical THRs measured behaviorally at the rate of 1,000 pps. The growth functions of features showed shallower growth slopes when the number of pulses increased. eABR THRs estimated in 4-, 8-, and 16-pulses conditions were closer to the clinical THRs, when compared to 1- and 2-pulses conditions. However, the smallest difference between estimated eABR THRs and clinical THRs was not always achieved from the same number of pulses. The smallest absolute difference of 30.3 μA was found for the linear fittings on growth functions of eABR RMS values in 4-pulses condition. Pearson’s correlation coefficients (PCCs) between eABR THRs and psychophysical THRs were significant and relatively large in all but 16-pulses conditions. The PCCs between eABR THRs and clinical THRs, however, were smaller and in less cases significant. Results of this study showed that eABRs to multi-pulse stimulation could, to some extent, represent clinical stimulation paradigms, and thus in comparison to single pulses, could estimate clinical THRs with smaller errors.

Glutathione Ester But Not Glutathione Protects Against Cisplatin-Induced Ototoxicity in a Rat Model

2003 ◽  
Vol 14 (03) ◽  
pp. 124-133 ◽  
Author(s):  
Kathleen C.M. Campbell ◽  
Deb L. Larsen ◽  
Robert P. Meech ◽  
Leonard P. Rybak ◽  
Larry F. Hughes
Keyword(s):  
Auditory Brainstem Response ◽  
Outer Hair Cell ◽  
Tone Burst ◽  
Auditory Brainstem ◽  
Control Group ◽  
Brainstem Response ◽  
Group A ◽  
Direct Administration ◽  
Response Thresholds ◽  
Para Determinar

Glutathione (GSH) provides an important antioxidant and detoxification pathway. We tested to determine if direct administration of GSH or GSH ester could reduce cisplatin- (CDDP) induced ototoxicity. We tested eight groups of five rats each: a control group, a group receiving 16 mg/kg ip CDDP infused over 30 minutes, and six groups receiving either GSH or GSH ester at 500, 1000, or 1500 mg/kg intraperitoneally 30 minutes prior to 16 mg/kg CDDP. Auditory brainstem response thresholds were measured for click and tone-burst stimuli at baseline and 3 days later. Outer hair cell (OHC) loss was measured for the apical, middle and basal turns. The 500 mg/kg GSH ester reduced hearing loss and OHC loss, but protection decreased as dosage increased, suggesting possible toxicity. GSH was not significantly protective. The best GSH ester protection was less than we have previously reported with D-methionine. El glutatión (GSH) brinda una importante vía antioxidante y de cetoxificación. Realizamos una prueba para determinar si la administración directa de GSH o del éster de GSH podía reducir la ototoxicidad inducida por cisplatino (CDDP). Hicimos una evaluación en ocho grupos de cinco ratas cada uno: un grupo control, un grupo que recibió CDDP intraperitoneal a 16 mg/kg en una ínfusión durante 30 minutos y seis grupos que recibieron intraperitonealmente GSH o el éster de GSH a 500, 1000 o 1500 mg/kg, 30 minutos antes del CDDP a 16 mg/kg. Se midieron umbrales de respuestas auditivas del tallo cerebral tanto para clicks como para bursts tonales, al inicio y 3 días después. La pérdida de células ciliadas externas (OHC) fue establecida a nivel de las vueltas apical, media y basal. La dosis de 500 mg/kg de éster de GSH redujo la hipoacusia y la pérdida de OHC, pero la protección disminuyó conforme la dosis se incrementó, sugiriendo una posible toxicidad. EL GSH no resultó significativamente protector. El mejor efecto protector del éster de GSH fue menor que el previamente reportado con D-Metionina.

Effects of noise exposure on neonatal auditory brainstem response thresholds in pregnant guinea pigs at different gestational periods

2016 ◽  
Vol 43 (1) ◽  
pp. 78-86
Author(s):  
Chihiro Morimoto ◽  
Kazuhiko Nario ◽  
Tadashi Nishimura ◽  
Ryota Shimokura ◽  
Hiroshi Hosoi ◽  
...  
Keyword(s):  
Auditory Brainstem Response ◽  
Guinea Pigs ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Brainstem Response ◽  
Response Thresholds

Comparison of Electrically Evoked Whole-Nerve Action Potential and Electrically Evoked Auditory Brainstem Response Thresholds in Nucleus CI24R Cochlear Implant Recipients

2002 ◽  
Vol 13 (08) ◽  
pp. 416-427 ◽  
Author(s):  
Marcia J. Hay-McCutcheon ◽  
Carolyn J. Brown ◽  
Kelly Schmidt Clay ◽  
Keely Seyle
Keyword(s):  
Action Potential ◽  
Cochlear Implant ◽  
Auditory Brainstem Response ◽  
Electrode Array ◽  
Auditory Brainstem ◽  
Electrode Arrays ◽  
Direct Stimulation ◽  
Nerve Action ◽  
Brainstem Response ◽  
Response Thresholds

In this study, differences between electrically evoked whole-nerve action potential (EAP) and electrically evoked auditory brainstem response (EABR) measurements within Nucleus CI24R cochlear implant recipients were evaluated. Precurved modiolus-hugging internal electrode arrays, such as the CI24R, are designed to provide more direct stimulation of neural elements of the modiolus. If the electrode array is closer to the modiolus, electrically evoked and behavioral levels might be lower than were previously recorded for the straight electrode array, the CI24M. EAP and EABR growth functions and behavioral levels were obtained for 10 postlingually deafened adults. Results revealed no significant differences between EAP and EABR threshold levels, and these levels were not significantly lower than those obtained using the CI24M.

scholarly journals N-Methyl-D-Aspartate Receptors Involvement in the Gentamicin-Induced Hearing Loss and Pathological Changes of Ribbon Synapse in the Mouse Cochlear Inner Hair Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Juan Hong ◽  
Yan Chen ◽  
Yanping Zhang ◽  
Jieying Li ◽  
Liujie Ren ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Brainstem ◽  
Ribbon Synapse ◽  
Synaptic Ribbons ◽  
Pathological Changes ◽  
Inner Hair Cell ◽  
Ribbon Synapses ◽  
Brainstem Response ◽  
Mature Mouse ◽  
Response Thresholds

Cochlear inner hair cell (IHC) ribbon synapses play an important role in sound encoding and neurotransmitter release. Previous reports show that both noise and aminoglycoside exposures lead to reduced numbers and morphologic changes of synaptic ribbons. In this work, we determined the distribution of N-methyl-D-aspartate receptors (NMDARs) and their role in the gentamicin-induced pathological changes of cochlear IHC ribbon synaptic elements. In normal mature mouse cochleae, the majority of NMDARs were distributed on the modiolar side of IHCs and close to the IHC nuclei region, while most of synaptic ribbons and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) were located on neural terminals closer to the IHC basal poles. After gentamicin exposure, the NMDARs increased and moved towards the IHC basal poles. At the same time, synaptic ribbons and AMPARs moved toward the IHC bundle poles on the afferent dendrites. The number of ribbon synapse decreased, and this was accompanied by increased auditory brainstem response thresholds and reduced wave I amplitudes. NMDAR antagonist MK801 treatment reduced the gentamicin-induced hearing loss and the pathological changes of IHC ribbon synapse, suggesting that NMDARs were involved in gentamicin-induced ototoxicity by regulating the number and distribution of IHC ribbon synapses.

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