Acute endolymphatic hydrops generated by exposure of the ear to non-traumatic low-frequency tones.

Alec N. Salt

Abstract

It has been reported that low frequency sounds presented at high, but non traumatizing levels induce temporary hyperacusis in humans and animals. One explanation proposed for this finding is that the basilar membrane operating point may be disturbed by an endolymph volume change. This possibility was investigated using volume and flow markers applied to the endolymphatic space of guinea pigs. The markers tetramethylammonium or hexafluoroarsenate were iontophoresed into endolymph and their concentrations were measured with ion selective microelectrodes placed apically and basally to the site of iontophoresis during exposure to low frequency tones. Marker concentration changes were interpreted quantitatively using a finite element model of the endolymphatic space, which allowed the specific experimental conditions to be simulated. Changes of endolymph cross sectional area and flow that gave rise to observed concentration changes were derived. Stimulation with a 200 Hz tone at 115 dB SPL for 3 min produced large changes of marker concentration, consistent with the induction of transient endolymphatic hydrops and a basally directed displacement of endolymph. Marker concentration changes were compared with changes in endocochlear potential and action potential (AP) thresholds to tones at 2, 4 and 8 kHz for a range of exposure frequencies and levels. For 200 Hz stimulation, AP hypersensitivity occurred at stimulus levels below those inducing endolymph volume disturbances. Endolymph volume changes are thought to be the result of, rather than the cause of, changes in operating point of the cochlear transducer. The observation that auditory threshold changes are minimal under conditions where substantial endolymphatic hydrops is present is relevant to our understanding of the hearing loss in patients with Meniere’s disease.
 

This study was supported by the National Institutes of Health through the National Institute on Deafness and other Communication Disorders, Grant number DC01368


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