Wideband Acoustic Reflex Growth in Adults With Cystic Fibrosis
| Autor: | Daniel B. Putterman, Angela C. Garinis, M. Patrick Feeney, Lisa L. Hunter, Martha R. Westman |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Adult
medicine.medical_specialty Cystic Fibrosis Otoacoustic Emissions Spontaneous Otoacoustic emission Audiology Cystic fibrosis 03 medical and health sciences Speech and Hearing Animal data 0302 clinical medicine Ototoxicity Evoked Potentials Auditory Brain Stem medicine Animals Humans Auditory system 030223 otorhinolaryngology Acoustic reflex Special Issue: Selected Papers From the 9th Biennial National Center for Rehabilitative Auditory Research Conference medicine.diagnostic_test business.industry Auditory Threshold medicine.disease Reflex Acoustic Cochlea medicine.anatomical_structure Acoustic Stimulation Audiometry Pure-Tone Synaptopathy sense organs Audiometry business 030217 neurology & neurosurgery |
| Zdroj: | Am J Audiol |
| ISSN: | 1558-9137 1059-0889 |
| DOI: | 10.1044/2020_aja-20-00117 |
| Popis: | Purpose Individuals with cystic fibrosis (CF) are often treated with intravenous (IV) aminoglycoside (AG) antibiotics to manage life-threatening bacterial infections. Preclinical animal data suggest that, in addition to damaging cochlear hair cells, this class of antibiotics may cause cochlear synaptopathy and/or damage to higher auditory structures. The acoustic reflex growth function (ARGF) is a noninvasive, objective measure of neural function in the auditory system. A shallow ARGF (small reflex-induced changes in middle ear function with increasing elicitor level) has been associated with synaptopathy due to noise exposure in rodent and human studies. In this study, the ARGF was obtained in CF patients with normal hearing, some of whom have been treated with IV AGs, and a control group without CF. The hypothesis was that patients with IV-AG exposure would have a shallow ARGF due to cochlear synaptopathy caused by ototoxicity. Method Wideband ARGFs were examined in four groups of normal-hearing participants: a control group of 29 individuals without CF; and in 57 individuals with CF grouped by lifetime IV-AG exposure: 15 participants with no exposure, 21 with low exposure, and 21 with high exposure. Procedures included pure-tone audiometry, clinical immittance, wideband acoustic immittance battery, including ARGFs, and transient evoked otoacoustic emissions. Results CF subjects with normal pure-tone thresholds and either high or low lifetime IV-AG exposure had enhanced ARGFs compared to controls and CF participants without IV-AG exposure. The groups did not differ in transient evoked otoacoustic emission signal-to-noise ratio. Conclusion These results diverge from the shallow ARGF pattern observed in studies of noise-induced cochlear synaptopathy and are suggestive of a central mechanism of auditory dysfunction in patients with AG-induced ototoxicity. |
| Databáze: | OpenAIRE |
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