Contralateral suppression of transient-evoked otoacoustic emissions in humans: intensity effects.

Transient evoked otoacoustic emissions (TEOAEs) were recorded to clicks presented at peak sound pressures of 50, 55, 60, 65 and 70 dB while continuous contralateral white noise was varied from 10 dB below to 10 dB above the click level. Suppression increased predictably with suppressor noise level for any given click level. However, when the suppressor noise level was held constant, suppression was greater for lower click levels.

Contralateral suppression of non-linear click-evoked otoacoustic emissions.

Click-evoked otoacoustic emissions from nominal 80 dB pSP (peak sound pressure) 80-microseconds pulses presented at 50 pulses per second were collected from the right ears of eleven normal hearing subjects using an ILO88 Otodynamic Analyzer in the non-linear mode. Clicks, pure tones, and narrow bands of noise were then presented to their left ears through insert earphones. The 80-microseconds contralateral clicks ranged in intensity from 80 dB pSP in 5 dB steps down to 60 dB pSP but data on only 10 of the subjects were collected successfully.

Does type I afferent neuron dysfunction reveal itself through lack of efferent suppression?

We present here two patients and three control subjects to demonstrate the clinical utility of studying evoked otoacoustic emissions and their contralateral suppression, as an aid to the delineation of afferent neuron dysfunction and possible lack of efferent suppression. The key patients here who fail to show contralateral suppression of their very robust otoacoustic emissions, concomitantly show paradoxically absent auditory brainstem responses (ABRs) and absence of middle ear muscle reflexes despite normal audiograms in the 2 kHz region and normal tympanograms. One of these patients has nearly normal pure tone sensitivity up to 3 kHz.

Lowering extracellular chloride concentration alters outer hair cell shape.

In general, increasing external K+ concentration, as well as exposure to hypotonic medium, induces a shortening of outer hair cells (OHCs) accompanied by an increase in width and volume. One possible mechanism suggested for these changes is a movement of Cl- and/or water across the cell membrane. We therefore examined the role of Cl- in OHC volume maintenance by testing the effect of decreasing extracellular Cl- concentration on OHC length and shape.