Effects of aspirin on distortion product otoacoustic emission suppression in human adults: A comparison with neonatal data

Abstract

One of the distortion product otoacoustic emission (DPOAE) paradigms used to study cochlear function is DPOAE (2f1-f2) ipsilateral suppression. Newborns do not have adultlike DPOAE suppression. At 6000 Hz, infants show excessively narrow DPOAE suppression tuning and shallow growth of suppression for low-frequency suppressor tones. The source of this immaturity is not known but the outer hair cell (OHC) is one possible locus. In the present study, DPOAE suppression was measured at f2 = 1500 and 6000 Hz from two groups with impaired OHC function in an attempt to model the observed immaturity in neonates: adults with aspirin-induced OHC dysfunction and subjects with sensorineural hearing loss (SNHL). Their DPOAE suppression results were compared to those obtained from a group of term newborns to address whether infant DPOAE suppression resembles suppression from individuals with known OHC dysfunction. Results indicate that aspirin systematically alters DPOAE suppression in adults at f2 = 6000 Hz, but not 1500 Hz. However, neither aspirin-induced OHC dysfunction nor naturally occurring SNHL produces "neonatal-like" DPOAE suppression at either test frequency. This finding does not support the hypothesis that non-adultlike DPOAE suppression characterizing newborns can be explained by minor impairments or alterations of OHC function.