The discovery that aspirin consumption can abolish spontaneous otoacoustic emissions [D. McFadden and H.S. Plattsmier, J. Acoust. Soc. Am. 76, 443–448 (1984)] provides a technique for further exploring the relation between otoacoustic emissions (spontaneous and evoked) and psychoacoustic threshold microstructure. Spontaneous emissions, delayed evoked emissions, synchronous evoked emissions, and threshold microstructure in four subjects were monitored before, during, and after consumption of 3.9 g of aspirin per day (three 325‐mg tablets every 6 h) for 3 or 4 days. The changes in spontaneous emissions are consistent with the findings of McFadden and Plattsmier except that one spontaneous emission appeared to plateau at a reduced level above the noise floor during the last day and a half of the 3‐day period of aspirin consumption. Evoked emissions and threshold microstructure were also reduced by aspirin consumption but persisted longer and recovered sooner. In most instances, the initial change in threshold microstructure was a trend to increased sensitivity (reduced thresholds), with a greater increase near threshold maxima than at threshold minima. Further reduction in the levels of the evoked emissions was accompanied by the eventual decrease in sensitivity (elevation of all thresholds).

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