Craig A. Champlin

Comparison of Auditory Evoked Potentials in Heterosexual, Homosexual, and Bisexual Males and Females

The auditory evoked potentials (AEPs) elicited by click stimuli were measured in heterosexual, homosexual, and bisexual males and females having normal hearing sensitivity. Estimates of latency and/or amplitude were extracted for nine peaks having latencies of about 2–240 ms, which are presumed to correspond to populations of neurons located from the auditory nerve through auditory cortex. For five of the 19 measures obtained, the mean latency or amplitude for the 57 homosexual and bisexual females was different from that of the 49 heterosexual females in a manner that implies a masculinization of the auditory systems of the homosexual and bisexual females. A similar masculinization effect was previously observed for the otoacoustic emissions generated by the cochlea. For five other measures, the mean latency or amplitude for the 53 homosexual and bisexual males was different from that of the 50 heterosexual males in a manner that implies a hypermasculinization of the auditory systems of the homosexual and bisexual males. Hypermasculinization has been reported recently for other physical characteristics of homosexual males. One parsimonious interpretation of these findings is that homosexual males and females both were exposed to higher than normal levels of androgens at some point(s) in development. Data are reported only for the female subjects not using oral contraceptives because those drugs can masculinize certain AEP measures.

Auditory Temporal Resolution in Specifically Language-Impaired and Age-Matched Children:

Recently there has been renewed interest in the auditory processing capabilities of children with specific language impairment. In this study, eight children with specific language impairment and eight nonimpaired, age-matched peers completed a task to assess temporal resolution abilities. Children were asked to detect a tone in three masking conditions wherein the masker contained silent gaps of 0 msec., 40 msec., or 64 msec. in duration. Thresholds were measured in each masking condition at 500 Hz and 2000 Hz. Across the groups, thresholds decreased (improved) significantly as a function of increases in the duration of the gaps. Children in the two groups exhibited remarkably similar thresholds for the three masking conditions. However, children with specific language impairment required a significantly greater number of ascending trials to achieve the threshold criterion than did age-matched children. Results suggest that language-impaired children perceive temporal aspects of acoustic stimuli as well as their normally developing peers. Attentional mechanisms may play an important role in the difficulties they exhibit in auditory processing.

Reductions in overshoot during aspirin use

The overshoot effect was measured before, during, and after the administration of a moderate dose of aspirin. Prior to the drug, detectability of the 6-ms, 3550-Hz signal was 5-11 dB worse when presented 2 ms after the onset of the 200-ms wideband masking noise than when presented 190 ms after masker onset. Following 4 days of aspirin use, detectability in the long-delay condition was unchanged from the predrug value, but (for four of the five subjects) detectability in the short-delay condition was improved by about 4-8 dB. Thus the overshoot effect was markedly reduced by aspirin because the drug partially counteracted the normally poor detectability for signals presented soon after masker onset. This paradoxical improvement in detectability was accompanied by an aspirin-induced loss in detectability of 5-16 dB for a 200-ms sample of that same signal presented in the quiet. Similar paradoxical effects have previously been obtained by inducing a temporary hearing loss with exposure to intense sound. It is presumed that the same basic mechanisms underlie the parallel outcomes. The so-called cochlear amplifier is discussed in this regard, and also the possibility that the known differences in those primary auditory fibers having high and low spontaneous rates may be involved. A supplementary experiment demonstrated that shifting audibility with either a wideband or a narrow-band background noise does not affect the overshoot effect in the same way as does aspirin or exposure to intense sound, further suggesting that the cochlear amplifier must be altered in order for overshoot to be diminished.

Reductions in overshoot following intense sound exposures

Overshoot refers to the poorer detectability of brief signals presented soon after the onset of a masking noise compared to those presented after longer delays. In the present experiment, brief tonal signals were presented 2 or 190 ms following the onset of a broadband masker that was 200 ms in duration. These two conditions of signal delay were tested before and after a series of exposures to a tone intense enough to induce temporary threshold shift (TTS). The magnitude of the overshoot was reduced after the exposure when a TTS of at least 10 dB was induced, but not when smaller amounts of TTS were induced. The reduction in overshoot was due to a decrease in the masked thresholds with the 2-ms delay; masked thresholds with the 190-ms delay were not different pre- and post-exposure. The implication is that the mechanisms responsible for the normal overshoot effect are temporarily inactivated by the same stimulus manipulations that produce a mild exposure-induced hearing loss. Thus the result is the paradox that exposure to intense sounds can produce a loss of signal detectability in certain stimulus conditions and a simultaneous improvement in detectability in other stimulus conditions.

Acute effect of nicotine on non-smokers: I. OAEs and ABRs.

This paper is the first in a series of three investigating the role of cholinergic mechanisms in the auditory system by assessing the acute effects of nicotine, an acetylcholinomimetic drug, on aggregate responses within the auditory pathway. In a single-blind procedure, auditory responses were obtained from 20 normal-hearing, non-smokers (10 male) under two conditions (nicotine, placebo). After the drug session, plasma tests revealed a subjects nicotine concentration. The effects of nicotine on early, exogenous responses of the auditory system (otoacoustic emissions and auditory brainstem potentials) are described in this first paper. Results indicated that transdermal administration of nicotine to non-smokers does not significantly affect cochlear activity but does acutely affect the neural transmission of acoustic information. Overall, otoacoustic emissions were unaffected by transdermal nicotine while wave I of the auditory brainstem response was significantly increased in latency and decreased in amplitude.

Acute effect of nicotine on non-smokers: II. MLRs and 40-Hz responses

This paper is the second in a series of three investigating the role of cholinergic mechanisms in the auditory system by assessing the acute effects of nicotine, an acetylcholinomimetic drug, on aggregate responses within the auditory pathway. In a single-blind procedure, auditory responses were obtained from 20 normal-hearing, non-smokers (10 male) under two conditions (nicotine, placebo). The effects of nicotine on central, mesogenous responses of the auditory system (middle latency and 40-Hz responses) are described in this second paper. Results indicated that transdermal administration of nicotine to non-smokers does significantly affect the central, neural transmission of acoustic information. Na-Pa amplitude and Nb latency of the middle latency response and latency measures of the 40-Hz response were acutely altered by the presence of nicotine.

Acute effect of nicotine on non-smokers: III. LLRs and EEGs.

This paper is the last in a series of three investigating the role of cholinergic mechanisms in the auditory system by assessing the acute effects of nicotine, an acetylcholinomimetic drug, on aggregate responses within the auditory pathway. In a single-blind procedure, auditory responses were obtained from 20 normal-hearing, non-smokers (10 male) under two conditions (nicotine, placebo). The effects of nicotine on long-latency responses of the auditory system and on electroencephalograms are described in this paper. Results indicated that transdermal administration of nicotine to non-smokers significantly affects the afferent and efferent transmission of acoustic information, as well as enhancing cortical activation. Long-latency response amplitudes and electroencephalogram activity (dominant power and frequencies) were altered by acute doses of transdermal nicotine.

Evaluation of distortion products produced by the human auditory system

During the simultaneous monaural presentation of two primary tones, distortion products can be measured acoustically in the ear canal (DPOAEs) and electrically as auditory evoked potentials (DPAEPs). The purpose of this investigation was to elucidate the sources of nonlinearity within the human auditory system responsible for generating quadratic (QDT) and cubic (CDT) difference tones. Measurements of DPOAEs and DPAEPs were obtained from 24 normal-hearing adults (12 male) in conditions with and without presentation of a 60 dB SPL contralateral noise. The effects of primary-tone signal duration and mode of presentation on measurements of DPAEPs were also examined. Results indicated that overall, both acoustic and electric distortion products were suppressed during presentation of a contralateral noise. Increases in the duration of the primary tones caused increases in DPAEP amplitudes. A greater proportion of individuals exhibited DPAEPs with monotic compared to dichotic presentation of the primary tones. The findings of the investigation supported the conjecture that a cochlear nonlinearity produced CDT acoustic and electric distortion products. Evidence concerning the origin of the QDT DPAEP was inconclusive, and contributions from both cochlear and neural nonlinear sources could not be ruled out.

Differences by Sex, Ear, and Sexual Orientation in the Time Intervals between Successive Peaks in Auditory Evoked Potentials

Auditory evoked potential (AEP) data from two studies originally designed for other purposes were reanalyzed. The auditory brainstem response (ABR), middle-latency response (MLR), and long-latency response (LLR) were measured. The latencies to each of several peaks were measured for each subject for each ear of click presentation, and the time intervals between successive peaks were calculated. Of interest were differences in interpeak intervals between the sexes, between people of differing sexual orientations, and between the two ears of stimulation. Most of the differences obtained were small. The largest sex differences were for interval I → V in the ABR and interval N1 → N2 of the LLR (effect sizes > 0.6). The largest differences between heterosexuals and nonheterosexuals were for the latency to Wave I in both sexes, for the interval Na → Nb in females, and for intervals V → Na and Nb → N1 in males (effect sizes > 0.3). The largest difference for ear stimulated was for interval N1 → N2 in heterosexual females (effect size ∼0.5). No substantial differences were found in the AEP intervals between women using, and not using, oral contraceptives. Left/right correlations for the interpeak intervals were mostly between about 0.4 and 0.6. Correlations between the ipsilateral intervals were small; i.e., interval length early in the AEP series was not highly predictive of interval length later in the series. Interpeak intervals appear generally less informative than raw latencies about differences by sex and by sexual orientation.

Otoacoustic emissions, auditory evoked potentials and self-reported gender in people affected by disorders of sex development (DSD)

Both otoacoustic emissions (OAEs) and auditory evoked potentials (AEPs) are sexually dimorphic, and both are believed to be influenced by prenatal androgen exposure. OAEs and AEPs were collected from people affected by 1 of 3 categories of disorders of sex development (DSD) - (1) women with complete androgen insensitivity syndrome (CAIS); (2) women with congenital adrenal hyperplasia (CAH); and (3) individuals with 46,XY DSD including prenatal androgen exposure who developed a male gender despite initial rearing as females (men with DSD). Gender identity (GI) and role (GR) were measured both retrospectively and at the time of study participation, using standardized questionnaires. The main objective of this study was to determine if patterns of OAEs and AEPs correlate with gender in people affected by DSD and in controls. A second objective was to assess if OAE and AEP patterns differed according to degrees of prenatal androgen exposure across groups. Control males, men with DSD, and women with CAH produced fewer spontaneous OAEs (SOAEs) - the male-typical pattern - than control females and women with CAIS. Additionally, the number of SOAEs produced correlated with gender development across all groups tested. Although some sex differences in AEPs were observed between control males and females, AEP measures did not correlate with gender development, nor did they vary according to degrees of prenatal androgen exposure, among people with DSD. Thus, OAEs, but not AEPs, may prove useful as bioassays for assessing early brain exposure to androgens and predicting gender development in people with DSD.