Influence of the individual DPOAE growth behavior on DPOAE level variations caused by conductive hearing loss and elevated intracranial pressure.

OBJECTIVES

Minor conductive hearing loss (CHL) can compromise the evaluation of the inner ear function with distortion product otoacoustic emissions (DPOAE). Elevation of the intracranial pressure (ICP) is also expected to alter the middle ear (ME) sound transmission. An impaired ME sound transmission leads to an attenuation of the DPOAE primary tone levels (L1 and L2) during forward transmission and of DPOAE levels (LDP) during backward transmission. The effect of the attenuation of L1 and L2 is complex and might have unexpected effects on DPOAE levels. In this work, CHL- and ICP-induced alterations of LDP versus L1 growth functions (constant L2 and increasing L1) are investigated. The first aim of this study is to explain how alterations of ME sound transmission can affect DPOAEs and to characterize the dependency of DPOAE level alterations on L2,L1 combinations and on the individual shape of LDP versus L1 growth functions. The second aim is to identify analogies between CHL- and ICP-induced alterations of DPOAEs and to discuss implications for a potential noninvasive ICP monitoring.

DESIGN

This study focuses on general theoretical considerations, supported by selected experimental observations in different species and simulations. DPOAEs were measured in guinea pigs before and after induction of a CHL (1 ear) and during increased ICP (1 ear), and in humans during changes of the postural position to alter the ICP (4 ears).

RESULTS

In both CHL and elevated ICP, DPOAE levels are not only reduced, but LDP versus L1 growth functions exhibit a shift to higher L1. The absolute DPOAE level alterations strongly depend on the L2,L1 combinations and the individual shape of the LDP versus L1 growth functions. In steeper LDP versus L1 growth functions, the DPOAE level alterations exhibit a larger variation. DPOAE levels can even increase. The largest variation can be found in ears with a nonmonotonic DPOAE growth behavior. An example of a guinea pig ear is presented with a nonmonotonic DPOAE growth behavior and a CHL of 4 dB, where the DPOAE level alterations varied between -32 and +9 dB depending on L1.

CONCLUSIONS

The data enable a more comprehensive view of DPOAE level alterations during CHL and elevated ICP. The observations also explain the problem that DPOAE and ICP alterations do not correlate linearly. An evaluation of the shift of the LDP versus L1 growth function along the L1 axis provides a potential tool to improve both the assessment of the inner ear function in the presence of a CHL and noninvasive ICP monitoring with DPOAEs.