EFFECT OF CONTRALATERAL ACOUSTIC STIMULATION ON ACTIVE COCHLEAR MICROMECHANICAL PROPERTIES IN HUMAN-SUBJECTS - DEPENDENCE ON STIMULUS VARIABLES

Outer hair cells (OHCs) have active micromechanical properties that are thought to be the origin of evoked otoacoustic emissions (EOAEs). In the present study, click-evoked otoacoustic emissions were recorded in humans with or without various contralateral acoustic stimulations. A previous study, concentrating on contralateral stimulation with broadband noise, had shown a decrease of the EOAE amplitude in humans. Results support a role for the efferent system in cochlear mechanics; indeed, medial efferent neurons of the olivocochlear bundle terminate on the OHCs. To obtain a better understanding of the medial efferent system functioning in humans, the present study looked at the contralateral suppressive effect as a function of stimulus parameters. The study of the input-output function of the EOAE amplitude with and without a 50-dB SPL contralateral broadband noise showed that the suppressive effect was equivalent to a mean reduction of 3.77 dB. For the EOAEs to tone pips, the contralateral suppressive effect was strongest when the contralateral ear stimuli were narrow bands that were centered around the central EOAE frequency. This frequency specificity disappeared for contralateral narrow band noise levels > 50 dB SPL. The contralateral suppressive effect was also observed with transient contralateral sounds (nonfiltered clicks). Significant reductions of the EOAE amplitude were seen with contralateral click levels as low as 17.5 dB SL. Above this level, the EOAE amplitude decreased as the contralateral stimulus level increased. This effect was still present in subjects without any stapedial reflex, but absent in total unilateral hearing-loss subjects. Therefore this suppressive effect is unlikely to be due to alteration of the middle ear function or to transcranially conducted sound. When the contralateral interclick interval exceeded 14.2 ms, the suppressive effect was smaller. With contralateral stimulus level maintained subjectively constant, the effect was found to disappear when the interclick interval was >49.9 ms. A saturation of the contralateral suppressive effect was observed for click rates >70/s (interclick interval <14.2 ms). Our study confirms and specifies the contralateral sound suppression effect on cochlear mechanisms in humans, assessing the equivalent reduction, showing a frequency specificity and extending these findings to contralateral transient sounds. Any influence of the acoustic crosstalk was eliminated. A role played by middle ear muscles cannot be absolutely ruled out but is not necessary to produce such a contralateral suppressive effect (the effect being found in subjects after surgical removal of the stapedius muscle) and could not explain the frequency specificity. The cochlear phenomenon, of a decrease in the ipsilateral EOAE amplitude when the contralateral cochlea was stimulated, may be helpful in protecting the ear in noisy environments.