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Biomedical subjects

E G Pasanen

Publications and source records attributed to E G Pasanen.

14 recordsLinked to original sources

An automated procedure for identifying spontaneous otoacoustic emissions.

An algorithm is described for objectively identifying and measuring spontaneous otoacoustic emissions (SOAEs) using the spectrum that results from transformation of the acoustic waveform measured in the outer ear canal. Prior to spectral analysis, the rms level is calculated for successive short segments of the waveform and only the weakest 25% of the segments are retained for the spectral analysis [the quietest 150 when using 16k-point fast Fourier transforms (FFTs)]. The resulting initial spectrum is scanned for peaks (potential SOAEs) which are then deleted from the spectrum. New values are estimated for the deleted values using linear extrapolations from frequency ranges on either side of the deleted values. The end result is a smoothed spectrum devoid of all local peaks. The initial spectrum is then compared peak-by-peak with the smoothed spectrum, and those peaks having differences that exceed an objectively determined decision criterion are identified as likely SOAEs. The effects of varying some of the important parameter values of the algorithm are described, and the sensitivity of the procedure is evaluated by measuring the detection rate for a Lorentzian peak of known amplitude added to a spectrum otherwise devoid of SOAEs.

Cochlea↗

Spontaneous otoacoustic emissions in heterosexuals, homosexuals, and bisexuals.

Click-evoked otoacoustic emissions (CEOAEs) were previously shown to be significantly less strong in homosexual and bisexual females than in heterosexual females. Here it is reported that the spontaneous otoacoustic emissions (SOAEs) of those same 60 homosexual and bisexual females were less numerous and weaker than those in 57 heterosexual females. That is, the SOAEs of the homosexual and bisexual females were intermediate to those of heterosexual females and heterosexual males. The SOAE and CEOAE data both suggest that the cochleas of homosexual and bisexual females have been partially masculinized, possibly as part of some prenatal processes that also masculinized whatever brain structures are responsible for sexual orientation. For males of all sexual orientation, the SOAEs were less numerous and weaker than for the females, and there were no significant differences among the 56 heterosexual, 51 homosexual, and 11 bisexual males. All subjects passed a hearing screening test. When all SOAEs above 3000 Hz were excluded (as a control against incipient, undetected hearing loss) the same results were obtained as with the full range of data (550-9000 Hz). The differential use of oral contraceptives by the heterosexual and nonheterosexual females also could not explain the differences in their OAEs.

Adult↗

Comparison of the auditory systems of heterosexuals and homosexuals: click-evoked otoacoustic emissions.

Click-evoked otoacoustic emissions (CEOAEs) are echo-like waveforms emitted by normal-hearing cochleas in response to a brief transient. CEOAEs are known to be stronger in females than in males. In this experiment, the CEOAEs of homosexual and bisexual females were found to be intermediate to those of heterosexual females and heterosexual males. A parsimonious explanation is that the auditory systems of homosexual and bisexual females, and the brain structures responsible for their sexual orientation, have been partially masculinized by exposure to high levels of androgens prenatally. No difference in CEOAEs was observed between homosexual and heterosexual males.

Acoustic Stimulation↗

Changes in otoacoustic emissions in a transsexual male during treatment with estrogen.

Otoacoustic emissions (OAEs) were monitored in two human males undergoing estrogen treatment prior to sex-reversal surgery. In one subject, multiple spontaneous emissions (SOAEs) appeared where none had been evident previously. One reasonable interpretation is that (in this male, at least) androgens normally produced a suppressive effect on the cochlear mechanisms responsible for SOAEs, and that the decline in androgen levels produced by the estrogenic drug led to a reduction in that suppression.

Acoustic Stimulation↗

Additional findings on heritability and prenatal masculinization of cochlear mechanisms: click-evoked otoacoustic emissions.

A previous demonstration of a substantial genetic contribution to the expression of spontaneous otoacoustic emissions (SOAEs) is here extended to an aspect of click-evoked otoacoustic emissions (CEOAEs). CEOAEs were measured in the same twins and non-twins used for the SOAE heritability study. The stimuli were 100-microsecond clicks presented a nominal rate of 2/s; the emitted waveforms from 50 clicks were summed, and a 20-ms sample of that averaged waveform (beginning 6 ms after click presentation) was subjected to spectral analysis. The total power in the spectrum from 1 to 5 kHz in this temporal segment of the CEOAE waveform was used as the primary dependent variable. This overall power was significantly greater in female and right ears than in male and left ears, but the difference between dark- and light-eyed subjects was not significant. The overall power in the two left, and two right, ears of monozygotic co-twins was more highly correlated than in dizygotic co-twins, and structural modeling indicated that about 65-85% of the individual variation in the expression of CEOAE power could be attributed to genes-essentially the same heritability estimate as obtained previously from the SOAE data. Within-subject correlations between CEOAE power and number of SOAEs ranged from about 0.3 to 0.7, suggesting that these two forms of otoacoustic emission may depend upon somewhat different aspects of the same underlying mechanism and, thus, that heritability estimates based on one measure are not completely redundant to those from the other. While the average spectral power of the CEOAEs in opposite-sex dizygotic (OSDZ) females was smaller than that in same-sex dizygotic (SSDZ) females- and thus approached the value for males-the difference did not achieve statistical significance. Thus, the evidence for a prenatal masculinizing effect was less definitive in these CEOAE data than in the SOAE data obtained from the same subjects. An interpretation that accounts for both the CEOAE and SOAE results is that the strength of the so-called cochlear amplifiers is under genetic control that is to some extent mediated and/or modified through prenatal exposure to androgens. The indicated direction of effect is that weak cochlear amplifiers result when prenatal androgen levels are high. Under this view, then, androgen level contribute both to the sex differences observed in otoacoustic emissions and the prenatal masculinizing effects observed in opposite-sex twins, and they may be a factor in individual differences in OAE expression as well. Additionally it is shown that, although the powers of the CEOAE waveforms were reasonably highly correlated for the two ears of subjects in all groups, and across MZ co-twins, cross-correlations on the fine structures of those same pairs of CEOAE waveforms were essentially zero-presumably owing largely to the synchronizing of (different) SOAE frequencies in the ears being compared.

Acoustic Stimulation↗

Otoacoustic emissions and quinine sulfate.

A moderate dose of quinine sulfate, administered to three young adult males, reduced or eliminated various forms of otoacoustic emission (OAE). The individual differences in response to the drug were substantial, but a number of generalizations did emerge. The time courses of onset and recovery were considerably more rapid than for the parallel effects produced by aspirin. Most spontaneous otoacoustic emissions (SOAEs) were eliminated within 7 h of the first 325-mg dose (about 3 h after the second dose). Most SOAEs showed partial or complete recovery about 24 h after the last dose, although considerable instability often remained. The functions relating the magnitude of a distortion-product OAE (DPOAE) to the sound-pressure level (SPL) of the primary tones producing it were displaced toward higher primary levels and became lower sloped following quinine administration. The magnitudes of SOAEs, DPOAEs, and nonlinear peaks in the click-evoked spectra declined and recovered with grossly similar time courses, but there were some partial dissociations. The ability of a DPOAE to suppress an SOAE lying about 50 Hz below it either increased slightly or remained about constant through the drug episode, even though the magnitudes of both DPOAE and SOAE were changing. On several occasions, increases in SOAE magnitude of as much as 10-20 dB were observed during the first 15-30 min of an SOAE measurement period (an initializing effect). Psychophysical measures revealed hearing losses of as much as 20 dB at some frequencies in some subjects. Several short-lived "enhancements" of OAEs are discussed relative to similar quinine-induced effects reported in an animal model.

Acoustic Stimulation↗

Wavelet-type analysis of transient-evoked otoacoustic emissions.

A transient-evoked otoacoustic emission (TEOAE) is a sound originating in the cochlea in response to a brief acoustic stimulus, such as a click. The response is typically a weak (25 dB SPL maximum) signal that lasts 20-40 ms. Analysis of TEOAEs is promising as a noninvasive technique for understanding cochlear function and as a diagnostic tool in identifying hearing loss. A TEOAE database was collected on many subjects, some of which were administered quinine to study the effect of the drug on TEOAE. Historically, FFT techniques have not worked well on TEOAE data because of the nonstationary nature of the signals. We have used a wavelet-like approach in analyzing the data by employing a set of equal-bandwidth filters, which have revealed the emission energy to be concentrated in the 800-2000 Hz range. This type of analysis is shown to be useful in examining the time progression of different frequency bands of the click-evoked emissions in subjects who took quinine.

Acoustic Stimulation↗

Partial dissociation of spontaneous otoacoustic emissions and distortion products during aspirin use in humans.

Otoacoustic emissions (OAEs) of two types--spontaneous and evoked distortion products--were studied before, during, and following a period of aspirin use. As previously reported, aspirin consumption uniformly reduced the spontaneous OAEs (SOAEs) to unmeasurable or extremely low levels. Aspirin consumption also reduced the amplitude of the evoked distortion products (EDPs) but did not eliminate them entirely. The amplitude of the EDP and its change with aspirin consumption were related to both the proximity of the EDP to the frequency of the SOAE and to the level of the primaries producing the EDP. At low primary levels, even with the SOAE absent (due to aspirin consumption, or suppression), EDPs near the SOAE frequency were 10-20 dB higher than when they were 100 Hz away from the SOAE frequency.

Acoustic Stimulation↗

Aspirin-induced hearing loss as a model of sensorineural hearing loss.

Performance in forward-masking, temporal-integration, and gap-detection tasks was measured in five normal-hearing subjects before and during a five-day period of aspirin use. The drug regimen was 3.9 g per day, taken in four equal doses at 6-h intervals. In the subjects showing substantial temporary hearing loss induced by the aspirin, (1) forward masking declined at about a normal rate as the masker-to-signal interval was increased, (2) the temporal-integration functions were flatter than normal, and (3) detection of a temporal gap was worse than normal at low sound-pressure levels (SPLs) but was essentially normal at levels above about 60 dB SPL. These aspirin-induced changes in performance are similar to the differences observed between normal listeners and listeners with mild sensorineural hearing loss. Thus, temporary, aspirin-induced hearing loss offers promise as a model condition for sensorineural hearing loss. The advantages offered by this model include all those typically attributed to within-subjects experimental designs, as well as the ability to manipulate the amount of hearing loss. Its primary disadvantages are that the hearing loss is not asymmetrically distributed toward the high-frequency region, as it typically is with sensorineural deafness, and there are large individual differences in the amount of temporary hearing loss induced by fixed doses of aspirin.

Adult↗

Binaural detection at high frequencies with time-delayed waveforms.

Recent research has demonstrated that the binaural system can utilize ongoing interaural time differences for lateralization at high frequencies as well as at low frequencies. The requirement is that the signal be complex so that the time difference appears as a delay in the envelope of the waveform at one ear. Reported here are several masking experiments that examine detection performance with time-delayed signals or maskers. In the first experiment, the signal was a 50-Hz band of noise centered at 4000 Hz that was time delayed by different amounts on different blocks of trials; the masker was similar band of noise, presented diotically. Large masking-level differences (MLDs) were obtained for some values of time delay, but the MLDs did not increase monotonically within time delay as they should were envelope time delay the basis for detection performance. Subsequent experiments in which the masker was time delayed and the signal was a diotic, high-frequency tone, revealed that detectability follows the autocorrelation function, and that MLDs as large as 24 dB can be obtained at 4000 Hz at time delays corresponding to negative values in the autocorrelation function. Examination of the signal-plus masker waveforms in these conditions reveals that ongoing interaural differences in level and cycle-by-cycle time exist in those conditions that yield MLDs. Since the time differences are small by usual standards, the basis for detection performance in these conditions appears to be the ongoing interaural level differences. In a final experiment, lateralization performance was measured for a time-delayed, complex waveform in the presence of maskers of various intensities. The results show that subjects are able to extract information about the time delay in the envelope even when the signal is added to a masker of equal intensity or greater. Thus, at the small signal-to-noise ratios used in our detection experiments, extraction of envelope time information was impossible, but also unnecessary, for detection was accomplished on the basis of another cue--most likely the ongoing interaural level differences.

Auditory Perception↗

Binaural beats at high frequencies.

Binaural beats have long been believed to be audible only at low frequencies, but an interaction reminiscent of a binaural beat can sometimes be heard when different two-tone complexes of high frequency are presented to the two ears. The primary requirement is that the frequency separation in the complex at one ear be slightly different from that in the other--that is, that there be a small interaural difference in the envelope periodicities. This finding is in accord with other recent demonstrations that the auditory system is not deaf to interaural time differences at high frequencies.

Auditory Pathways↗

Temporary hearing loss induced by combinations of intense sounds and nonsteroidal anti-inflammatory drugs.

Intense sounds were delivered to 11 subjects with normal hearing both before and during administration of standard doses of four nonsteroidal anti-inflammatory drugs. After four days of aspirin treatment (3.9 g daily), the subjects' resting hearing levels raised by about 10 dB. Administration of intense sounds that had previously been shown to produce about 12 dB of temporary hearing loss added increments of 10 to 15 dB to the aspirin-induced hearing loss. That is, the total temporary hearing loss produced by aspirin plus exposure to intense sound was about 10 to 15 dB greater than that produced by exposure to the intense sound alone. A similar effect was observed for sodium salicylate. After similar administrations of sulindac (400 mg per day) and diflunisal (750 mg per day), there was no corresponding increase in the sound-induced hearing loss. Under certain reasonable assumptions about underlying mechanisms, these findings suggest that persons taking moderate doses of aspirin or sodium salicylate may be at increased risk of noise-induced hearing loss.

Adult↗