scholarly journals Cochlear Receptor (Microphonic and Summating Potentials, Otoacoustic Emissions) and Auditory Pathway (Auditory Brain Stem Potentials) Activity in Auditory Neuropathy

2001 ◽  
Vol 22 (2) ◽  
pp. 91-99 ◽  
Author(s):  
A. Starr ◽  
Y. Sininger ◽  
T. Nguyen ◽  
H. J. Michalewski ◽  
S. Oba ◽  
...  
2008 ◽  
Vol 123 (4) ◽  
pp. 462-465 ◽  
Author(s):  
T H J Draper ◽  
D-E Bamiou

AbstractObjective:To report the case of an adult patient who developed auditory complaints following xylene exposure, and to review the literature on the effects of solvent exposure on hearing.Case report:The patient presented with a gradual deterioration in his ability to hear in difficult acoustic environments and also to hear complex sounds such as music, over a 40-year period. His symptoms began following exposure to the solvent xylene, and in the absence of any other risk factor. Our audiological investigations revealed normal otoacoustic emissions with absent auditory brainstem responses and absent acoustic reflexes in both ears, consistent with a diagnosis of bilateral auditory neuropathy. Central test results were also abnormal, indicating possible involvement of the central auditory pathway.Conclusions:To our knowledge, this is the first report of retrocochlear hearing loss following xylene exposure. The test results may provide some insight into the effect of xylene as an isolated agent on the human auditory pathway.


2007 ◽  
Vol 97 (2) ◽  
pp. 1775-1785 ◽  
Author(s):  
Keith N. Darrow ◽  
Stéphane F. Maison ◽  
M. Charles Liberman

Cochlear sensory cells and neurons receive efferent feedback from the olivocochlear (OC) system. The myelinated medial component of the OC system and its effects on outer hair cells (OHCs) have been implicated in protection from acoustic injury. The unmyelinated lateral (L)OC fibers target ipsilateral cochlear nerve dendrites and pharmacological studies suggest the LOC's dopaminergic component may protect these dendrites from excitotoxic effects of acoustic overexposure. Here, we explore LOC function in vivo by selective stereotaxic destruction of LOC cell bodies in mouse. Lesion success in removing the LOC, and sparing the medial (M)OC, was assessed by histological analysis of brain stem sections and cochlear whole mounts. Auditory brain stem responses (ABRs), a neural-based metric, and distortion product otoacoustic emissions (DPOAEs), an OHC-based metric, were measured in control and surgical mice. In cases where the LOC was at least partially destroyed, there were increases in suprathreshold neural responses that were frequency- and level-independent and not attributable to OHC-based effects. These interaural response asymmetries were not found in controls or in cases where the lesion missed the LOC. In LOC-lesion cases, after exposure to a traumatic stimulus, temporary threshold shifts were greater in the ipsilateral ear, but only when measured in the neural response; OHC-based measurements were always bilaterally symmetric, suggesting OHC vulnerability was unaffected. Interaural asymmetries in threshold shift were not found in either unlesioned controls or in cases that missed the LOC. These findings suggest that the LOC modulates cochlear nerve excitability and protects the cochlea from neural damage in acute acoustic injury.


2002 ◽  
Vol 111 (5_suppl) ◽  
pp. 29-31 ◽  
Author(s):  
Yvonne S. Sininger ◽  
Patricia Trautwein

Auditory neuropathy (AN) is a term used to describe an auditory disorder in which there is evidence of normal outer hair cell function (otoacoustic emissions and/or cochlear microphonics) and poor function of the auditory nerve (absent or highly distorted auditory brain stem response starting with wave I). Many of these patients have evidence of generalized peripheral nerve disease, leading to an assumption that the peripheral portion of the auditory nerve is the most likely site of lesion. A small group of these patients has received cochlear implants, and the majority of them achieve average to above-average performance. Although this outcome may seem incongruous with neural disease, average performance by patients with AN may be a result of the reintroduction of neural synchrony by electrical stimulation and/or the fact that most deaf patients have poor nerve survival. Although cochlear implants are promising for deaf patients with AN, more study of the disorder is needed.


1995 ◽  
Vol 113 (2) ◽  
pp. P151-P151
Author(s):  
Karen Jo Doyle ◽  
Barbara Burggraaff ◽  
Sharon Fujikawa ◽  
Ju Kim ◽  
Carol MacArthur

1997 ◽  
Vol 116 (6) ◽  
pp. 585-592 ◽  
Author(s):  
Kathleen C. Y. Sie ◽  
Susan J. Norton

Ototoxicity associated with cis-platinum administration commonly presents as hearing loss and tinnitus. The hearing loss is usually an irreversible, high-frequency sensorineural loss. Histologic studies in humans and animals suggest that the outer hair cells (OHCs) are most susceptible to cis-platinum. Evoked otoacoustic emissions (EOAE), as a measure of outer hair cell function, are potentially useful in following ototoxic insults involving OHCs. Distortion-product otoacoustic emissions (DPOAE) test frequency-specific regions of the cochlea and therefore may be particularly well suited for monitoring ototoxic injuries. We measured distortion product otoacoustic emissions, at f2 = 2, 4, 6, 8, 10, and 12 kHz, in gerbils after a single large dose of cis-platinum. Animals treated with saline served as controls. The findings were compared to auditory brain stem evoked response (ABR) thresholds, using tone pips of the same frequencies. The DPOAE and ABR thresholds were measured before treatment and again 2, 5, and 14 days after drug administration. The changes in DPOAE were compared with the changes in ABR. No treatment effect was noted in the 2-day group. Animals treated with c/s-platinum demonstrated significant elevation of DPOAE and ABR thresholds compared with control animals at 5 and 14 days. There was no significant difference between the threshold changes in the 5-and 14-day groups.


2013 ◽  
Vol 133 (5) ◽  
pp. 2803-2817 ◽  
Author(s):  
Daniel M. Rasetshwane ◽  
Michael Argenyi ◽  
Stephen T. Neely ◽  
Judy G. Kopun ◽  
Michael P. Gorga

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