Effect of anesthesia on transient evoked otoacoustic emissions in humans: a comparison between propofol and isoflurane

Ferber-Viart, C.; Preckel, Marie-Pierre; Dubreuil, C.; Banssillon, V.; Duclaux, R.

doi:10.1016/s0378-5955(98)00064-1

Cited by 23 publications

(25 citation statements)

References 29 publications

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“…Isoflurane has been shown to suppress the amplitude of evoked otoacoustic emissions (Ferber-Viart et al, 1998), which is in agreement with the suppressive effect on the CM found in this study. Isoflurane's effects on the ABR have been reported previously and the present results are for the most part consistent with these reports, but there are some differences.…”

Section: Discussionsupporting

confidence: 92%

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Effects of isoflurane on auditory evoked potentials in the cochlea and brainstem of guinea pigs

2010

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Section: Discussionsupporting

confidence: 92%

“…Effects of isoflurane on the auditory nerve and cochlear responses using direct CAP recordings have not yet been reported. Isoflurane was shown to suppress the amplitude of evoked otoacoustic emissions, indicating an effect on cochlear hair cells (Ferber-Viart et al, 1998).…”

Section: Introductionmentioning

confidence: 95%

Effects of isoflurane on auditory evoked potentials in the cochlea and brainstem of guinea pigs

2010

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“…Isoflurane has complex central effects, inhibiting both excitatory glutamatergic and inhibitory GABAergic systems (Franks 2008). Most studies report reduced amplitude of evoked activity (Ferber-Viart et al 1998; Heneghan et al 1987; Santarelli et al 2003), reduced steady-state-driven activity (Cheung et al 2001; Plourde et al 1998), and otoprotection from high-level exposure (Chung et al 2007; Kim et al 2005). The permanent ipsilateral threshold elevation in the present study remains to be explained.…”

Section: Discussionmentioning

confidence: 99%

Bilateral Dorsal Cochlear Nucleus Lesions Prevent Acoustic-Trauma Induced Tinnitus in an Animal Model

Brozoski

Wisner

Sybert

et al. 2011

JARO

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Animal experiments suggest that chronic tinnitus (“ringing in the ears”) may result from processes that overcompensate for lost afferent input. Abnormally elevated spontaneous neural activity has been found in the dorsal cochlear nucleus (DCN) of animals with psychophysical evidence of tinnitus. However, it has also been reported that DCN ablation fails to reduce established tinnitus. Since other auditory areas have been implicated in tinnitus, the role of the DCN is unresolved. The apparently conflicting electrophysiological and lesion data can be reconciled if the DCN serves as a necessary trigger zone rather than a chronic generator of tinnitus. The present experiment used lesion procedures identical to those that failed to decrease pre-existing tinnitus. The exception was that lesions were done prior to tinnitus induction. Young adult rats were trained and tested using a psychophysical procedure shown to detect tinnitus. Tinnitus was induced by a single unilateral high-level noise exposure. Consistent with the trigger hypothesis, bilateral dorsal DCN lesions made before high-level noise exposure prevented the development of tinnitus. A protective effect stemming from disruption of the afferent pathway could not explain the outcome because unilateral lesions ipsilateral to the noise exposure did not prevent tinnitus and unilateral lesions contralateral to the noise exposure actually exacerbated the tinnitus. The DCN trigger mechanism may involve plastic circuits that, through loss of inhibition, or upregulation of excitation, increase spontaneous neural output to rostral areas such as the inferior colliculus. The increased drive could produce persistent pathological changes in the rostral areas, such as high-frequency bursting and decreased interspike variance, that comprise the chronic tinnitus signal.

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“…Santarelli et al (2003) reported increased latency and decreased amplitude of several ABR peaks after isoflurane administration. Ferber-Viart et al (1998) compared the effect of isoflurane and propofol on otoacoustic emissions, but hearing threshold consequences were not examined. It has also been shown that isoflurane attenuates cochlear evoked responses (Stronks et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

A comparison of the effects of isoflurane and ketamine anesthesia on auditory brainstem response (ABR) thresholds in rats

Ruebhausen¹,

Brozoski²,

Bauer³

2012

Hearing Research

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Effect of anesthesia on transient evoked otoacoustic emissions in humans: a comparison between propofol and isoflurane

Cited by 23 publications

References 29 publications

Effects of isoflurane on auditory evoked potentials in the cochlea and brainstem of guinea pigs

Effects of isoflurane on auditory evoked potentials in the cochlea and brainstem of guinea pigs

Bilateral Dorsal Cochlear Nucleus Lesions Prevent Acoustic-Trauma Induced Tinnitus in an Animal Model

A comparison of the effects of isoflurane and ketamine anesthesia on auditory brainstem response (ABR) thresholds in rats

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