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There are types of deafness and tinnitus in which ruptures or massive changes in the ionic permeability of the membranes lining the endolymphatic space [e.g., of the reticular lamina (RL)] are believed to allow potassium-rich endolymph to deluge the low [K+] perilymphatic fluid (e.g., in the small spaces of Nuel). This would result in a K+ intoxication of sensory and neural structures. Acute attacks of Ménière's disease have been suggested to be an important example for this event. The present study investigated the effects of transiently elevated [K+] due to the addition of artificial endolymph to the basolateral cell surface of outer hair cells (OHC) in replicating endolymph-induced K+ intoxication of the perilymph in the small spaces of Nuel. The influence of K+ intoxication of the basolateral OHC cell surface on the transduction was then examined. Intoxication resulted in an inhibition of the physiological repolarizing K+ efflux from hair cells. This induced unwanted depolarizations of the hair cells, interfering with mechanoelectrical transduction. A pathological longitudinal OHC shortening was also found, with subsequent compression of the organ of Corti possibly influencing the micromechanics of the mechanically active OHC. Both micromechanical and electrophysiological alterations are proposed to contribute to endolymph leakage induced attacks of deafness and possibly also to tinnitus. Moreover, repeated or long-lasting K+ intoxications of OHC resulted in a chronic and complete loss of OHC motility. This is suggested to be a pathophysiological basis in some patients with chronic hearing loss resulting from Ménière's syndrome.

Objective To assess the effects of use of personal stereo systems (PS) on hearing by means of the objective measure of transient‐evoked otoacoustic emissions. Participants and setting People aged between 10 and 59 years who had otoacoustic emissions recorded by the National Acoustic Laboratories between 1989 and 1997 were eligible for inclusion. Recordings from participants with hereditary disorders or any form of aural disease (eg, otitis media, otosclerosis, fluctuant hearing loss, Meniere's syndrome, or exposure to ototoxic substances) were excluded. Methods Transient‐evoked otoacoustic emission (TEOAE) records were obtained with a standard 260 repetitions of an 80 dB train of clicks used for recording outer hair cell activity. The measure of otoacoustic emission strength was the Otodynamics IL088 variable Waverepro%. For each participant, all the key factors relating to their hearing history were assessed from patient referral information or from demographic information obtained in writing at the time of recording either in the form of a detailed questionnaire or verbal assessment. Otoacoustic emission data were analysed according to age, industrial noise exposure and personal stereo use. Results Usable otoacoustic emission records were obtained from 1724 people (1066 males and 658 females). Otoacoustic emission strength declined with age, and was significantly lower in males than females, lower in people exposed to industrial noise than those not exposed, and significantly lower in users of personal stereo systems than non‐users. People with both kinds of noise exposure had values which were significantly lower again, indicating an additive effect. Conclusions As only 39 people with PS exposure admitted any hearing problems, decline in otoacoustic emission strength forewarns premature hearing loss in personal stereo users.

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The form of the mammalian cochlear frequency-position map has been well described by Greenwood and empirical values found for its coefficients for a number of species. The apical portion of the mammalian map is spatially compressed relative to the base, and this nonuniformity in the representation of frequency is evidently consistent across species. However, an evolutionary reason for this consistency, encompassing critical band behavior with respect to position, is conspicuously missing. Likewise, the length of the cochlea in any mammal, including echolocating species, is related to body size, but attempts to explain the length in terms of frequency limits, range, or resolution have no general explanation. New insight stems from a hypothesis in which the map curvature may be appreciated as an adaptation for optimal frequency resolution over the auditory range. It is demonstrated numerically that the mammalian curve may be considered a member of a family of curves which vary in their degree of warp. The "warp factor" found to be common across mammals is an optimal trade-off between four conflicting constraints: (1) enhancing high-frequency resolution; (2) setting a lower bound on loss of existing low-frequency resolution; (3) minimizing map nonuniformity; and (4) keeping the whole map smooth, thereby avoiding reflections.