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PubMed · 6500824

Sedation in brainstem response audiometry.

C C Baranak·R R Marsh·W P Potsic
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Abstract

In many children, sedation is virtually essential for reducing myogenic interference during brainstem response (BSR) audiometry. The most widely accepted sedative for young children is chloral hydrate. Children who are tired before the sedation is given fall asleep much more quickly with sedation, and in turn, require fewer doses of chloral hydrate. Instructing the parents to keep the child tired has produced significant increases in percent of those sleeping after the first dose (z = 2.08, P less than 0.05).

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AudiometryAudiometry, Evoked ResponseBrain StemChildChloral HydrateHumansHypnotics and SedativesJournal Article

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BibTeXRIS

C C Baranak, R R Marsh, W P Potsic. 1984. Sedation in brainstem response audiometry.. https://doi.org/10.1016/s0165-5876(84)80025-7

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PubMed1995

Patterns of evoked otoacoustic emissions associated with acoustic neuromas.

Evoked otoacoustic emissions (OAEs) are assumed to reflect healthy outer hair cell function. Over the past few years, evoked OAEs have been shown to be useful as indicators of cochlear hearing loss. Because basic studies have shown that OAEs are extremely sensitive to cochlear anoxia and hypoxia, as well as to the adverse effects of many inner ear diseases, it is possible that these objective tests can provide some insight into the fundamental basis of the hearing loss exhibited by patients with acoustic neuromas. The primary aim of the present study was to examine the effects of acoustic neuromas on the amplitudes of evoked OAEs and to compare these findings with tumor-induced hearing levels. To this end, tests of behavioral audiometry, distortion-product otoacoustic emissions and transiently evoked otoacoustic emissions were performed on 44 patients with verified acoustic neuromas. The results demonstrated that the majority of ears with acoustic neuromas displayed one of two distinct patterns of evoked OAEs: a cochlear pattern or a noncochlear pattern. Although behavioral hearing thresholds were higher with larger tumors, OAE levels exhibited no clear relationship to tumor size. The present findings support the notion that acoustic neuromas may cause hearing impairment according to two types of influence that act at different levels of the peripheral auditory system. The tumor's cochlear effect on evoked OAE activity is most likely caused by an indirectly mediated compromise of the organ of Corti's vascular supply. It is probable that the direct pressure of the tumor on the eighth cranial nerve is responsible for the observed noncochlear effects.

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