Effects of Presbycusis and Other Types of Hearing Loss on Auditory Brainstem Responses

1986 ◽  
Vol 15 (4) ◽  
pp. 179-185
Author(s):  
Ulf Rosenhall ◽  
Kai Pedersen ◽  
Mats Dotevall
Keyword(s):  
Hearing Loss ◽  
Auditory Brainstem ◽  
Auditory Brainstem Responses

Hearing recovery from deafness caused by bromate intoxication

2018 ◽  
Vol 132 (11) ◽  
pp. 1039-1041 ◽  
Author(s):  
J Suzuki ◽  
Y Takanashi ◽  
A Koyama ◽  
Y Katori
Keyword(s):  
Hearing Loss ◽  
Sensorineural Hearing Loss ◽  
Pure Tone ◽  
Pure Tone Audiometry ◽  
Auditory Brainstem ◽  
Sensorineural Hearing ◽  
Auditory Brainstem Responses ◽  
Common Symptom ◽  
Hearing Recovery ◽  
Continuous Haemodiafiltration

AbstractObjectivesSodium bromate is a strong oxidant, and bromate intoxication can cause irreversible severe-to-profound sensorineural hearing loss. This paper reports the first case in the English literature of bromate-induced hearing loss with hearing recovery measured by formal audiological assessment.Case reportA 72-year-old woman was admitted to hospital with complaints of profound hearing loss, nausea, diarrhoea and anuria after bromate ingestion in a suicide attempt. On admission, pure tone audiometry and auditory brainstem responses showed profound bilateral deafness. Under the diagnosis of bromate-induced acute renal failure and sensorineural hearing loss, continuous haemodiafiltration was performed. When dialysis was discontinued, pure tone audiometry and auditory brainstem responses showed partial threshold recovery from profound deafness.ConclusionSevere-to-profound sensorineural hearing loss is a common symptom of bromate intoxication. Bromate-induced hearing loss may be partially treated, and early application of continuous haemodiafiltration might be useful as a treatment for this intractable condition.

Auditory Brainstem Responses in a Case of High-Frequency Conductive Hearing Loss

1985 ◽  
Vol 50 (4) ◽  
pp. 346-350 ◽  
Author(s):  
Michael P. Gorga ◽  
Jan K. Reiland ◽  
Kathryn A. Beauchaine
Keyword(s):  
Hearing Loss ◽  
High Frequency ◽  
Conductive Hearing Loss ◽  
Auditory Brainstem ◽  
Intensity Function ◽  
Auditory Brainstem Responses ◽  
Normal Limits ◽  
Interpeak Latency ◽  
Lower Limits ◽  
Conductive Hearing

Click-evoked auditory brainstem responses were measured in a patient with high-frequency conductive hearing loss. As is typical in cases of conductive hearing loss, Wave I latency was prolonged beyond normal limits. Interpeak latency differences were just below the lower limits of the normal range. The Wave V latency-intensity function, however was abnormally steep. This pattern is explained by the hypothesis that the slope of the latency-intensity function is determined principally by the configuration of the hearing loss. In cases of high-frequency hearing loss (regardless of the etiology), the response may be dominated by more apical regions of the cochlea at lower intensities and thus have a longer latency.

Auditory Brainstem Responses in Noise-Induced Permanent Hearing Loss

1988 ◽  
Vol 27 (1) ◽  
pp. 36-41 ◽  
Author(s):  
G. Almadori ◽  
F. Ottaviani ◽  
G. Paludetti ◽  
M. Rosignoli ◽  
L. Gallucci ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Brainstem ◽  
Auditory Brainstem Responses

Auditory Brainstem Responses in Ears with Hearing Loss: Case Studies

1981 ◽  
Vol 10 (4) ◽  
pp. 247-254 ◽  
Author(s):  
C. D. Bauch ◽  
D. E. Rose ◽  
S. G. Harner
Keyword(s):  
Hearing Loss ◽  
Case Studies ◽  
Auditory Brainstem ◽  
Auditory Brainstem Responses

scholarly journals miR-153/KCNQ4 axis contributes to noise-induced hearing loss in a mouse model

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Qin Wang ◽  
Wei Li ◽  
Cuiyun Cai ◽  
Peng Hu ◽  
Ruosha Lai
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Noise Exposure ◽  
Auditory Brainstem ◽  
Sensory Epithelium ◽  
Outer Hair Cells ◽  
Broadband Noise ◽  
Hek293 Cells ◽  
Auditory Brainstem Responses ◽  
Luciferase Reporter

AbstractDamage to the cochlear sensory epithelium is a key contributor to noise-induced sensorineural hearing loss (SNHL). KCNQ4 plays an important role in the cochlear potassium circulation and outer hair cells survival. As miR-153 can target and regulate KCNQ4, we sought to study the role of miR-153 in SNHL. 12-week-old male CBA/J mice were exposed to 2–20 kHz broadband noise at 96 dB SPL to induce temporary threshold shifts and 101 dB SPL to induce permanent threshold shifts. Hearing loss was determined by auditory brainstem responses (ABR). Relative expression of miR-153 and KCNQ4 in mice cochlea were determined by Real-Time quantitative PCR. miR-153 mimics were co-transfected with wild type or mutated KCNQ4 into HEK293 cells. Luciferase reporter assay was used to validate the binding between miR-153 and KCNQ4. AAV-sp-153 was constructed and administrated intra-peritoneally 24- and 2-h prior and immediately after noise exposure to knockdown miR-153. The KCNQ4 is mainly expressed in outer hair cells (OHCs). We showed that the expression of KCNQ4 in mice cochlea was reduced and miR-153 expression was significantly increased after noise exposure compared to control. miR-153 bound to 3′UTR of KNCQ4, and the knockdown of miR-153 with the AAV-sp-153 administration restored KCNQ4 mRNA and protein expression. In addition, the knockdown of miR-153 reduced ABR threshold shifts at 8, 16, and 32 kHz after permanent threshold shifts (PTS) noise exposure. Correspondingly, OHC losses were attenuated with inhibition of miR-153. This study demonstrates that miR-153 inhibition significantly restores KNCQ4 in cochlea after noise exposure, which attenuates SNHL. Our study provides a new potential therapeutic target in the prevention and treatment of SNHL.

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