Contralateral modification of transitory evoked otoacoustic emissions

Abstract

In recent publications the influence of contralateral white noise on transient evoked otoacoustic emissions (TEOAE) is discussed with regard on contributions of the efferent auditory system. In the present study the effects have been investigated with regards to middle-ear muscles, efferents and cross hearing. TEOAE to monaural 40-80 dB SPL clicks were recorded in normal-hearing adults under simultaneous presentation of 20-60 dB SPL broadband noise to the contralateral ear. Control runs were performed before, during a short break of, and after contralateral stimulation. The control run before contralateral stimulation was used as a reference. Decrease in TEOAE, and increase in accompanying noise floor, were found to follow the contralateral stimulation. In particular a 1-3 dB decrease was found for contralateral noise levels of 40 and 60 dB SPL, even though the readings at 60 dB only were statistically significant (paired-samples t test, p = 0.05). For both TEOAE and noise floor no systematic dependence on click intensity was seen. The control runs during temporary break and after contralateral noise revealed an increase in both TEOAE and noise floor. As a rule, the TEOAE adapted to the reference within 2-3 min following the cessation of contralateral stimulation, whereas the increased noise floor level was still noted after 10 min. Traditionally, suppressing effects of contralateral stimulation on TEOAE have been attributed to cochlear efferents (CEs). Occasionally, the middle-ear muscle and cross hearing involvement have been considered as well. Substantially, the present results and findings of other workers are inconsistent with the basic knowledge of CE functioning: (I) The decrease in TEOAE under contralateral stimulation is in conflict with an increase in cochlear microphonics and summating potentials observed during activation of CEs: (II) contralateral suppression of TEOAE exhibited no significant dependence on the test-stimulus level while the CEs are known to be efficient in the range of the low signal intensities only, and (III) acoustic activation of the CEs can hardly be expected to reach levels sufficient to influence the TEOAE mechanism. The present findings, i.e. decrease in TEOAE and increase in noise floor level, can more reasonably be explained as being mainly attributable to activation of the middle-ear muscles.