Jeffery T. Lichtenhan

A new auditory threshold estimation technique for low frequencies: proof of concept.

Objectives: Presently available nonbehavioral methods to estimate auditory thresholds perform less well at frequencies below 1 kHz than at 1 kHz and above. For many uses, such as providing accurate infant hearing aid amplification for low-frequency vowels, an accurate nonbehavioral method to estimate low-frequency thresholds is needed. A novel technique was developed to estimate low-frequency cochlear thresholds based on the use of a previously reported waveform. It was determined how well the method worked by comparing the resulting thresholds to thresholds from onset-response compound action potentials (CAPs) and single-auditory-nerve (AN)- fibers in cats. A long-term goal is to translate this technique for use in humans. Design: An electrode near the cochlea records a combination of cochlear microphonic (CM) and neural responses. In response to low-frequency, near threshold-level tones, the CM is almost sinusoidal whereas the neural responses occur preferentially at one phase of the tone. If the tone is presented again but with its polarity reversed, the neural response keeps the same shape, but shifts ½ cycle in time. Averaging responses to tones presented separately at opposite polarities overlaps and interleaves the neural responses and yields a waveform in which the CM is canceled and the neural response appears twice each tone cycle, that is, the resulting neural response is mostly at twice the tone frequency. The resultant waveform is referred to as “the auditory nerve overlapped waveform” (ANOW). In this study, ANOW level functions were measured in anesthetized cats from 10 to 80 dB SPL in 10 dB steps using tones between 0.3 and 1 kHz. As a response metric, the magnitude of the ANOW component was calculated at twice the tone frequency (ANOW2f). The ANOW threshold was the sound level where the interpolated ANOW2f crossed a statistical criterion that was higher than 95% of the noise floor distribution. ANOW thresholds were compared with onset-CAP thresholds from the same recordings and single-AN-fiber thresholds from the same animals. Results: ANOW and onset-CAP level functions were obtained for 0.3 to 1 kHz tones, and single-AN-fiber responses from cats. Except at 1 kHz, typical ANOW thresholds were mostly 10 to 20 dB more sensitive than onset-CAP thresholds and 10 to 20 dB less sensitive than the most sensitive single-AN-fiber thresholds. Conclusions: ANOW provides frequency-specific estimates of cochlear neural thresholds over a frequency range that is important for hearing but is not well accessed by nonbehavioral, objective methods. Results suggest that with further targeted development, the ANOW low-frequency threshold estimation technique can be useful both clinically in humans and in basic-science animal experiments.

Click- and chirp-evoked human compound action potentials

In the experiments reported here, the amplitude and the latency of human compound action potentials (CAPs) evoked from a chirp stimulus are compared to those evoked from a traditional click stimulus. The chirp stimulus was created with a frequency sweep to compensate for basilar membrane traveling wave delay using the O-Chirp equations from Fobel and Dau [(2004). J. Acoust. Soc. Am. 116, 2213-2222] derived from otoacoustic emission data. Human cochlear traveling wave delay estimates were obtained from derived compound band action potentials provided by Eggermont [(1979). J. Acoust. Soc. Am. 65, 463-470]. CAPs were recorded from an electrode placed on the tympanic membrane (TM), and the acoustic signals were monitored with a probe tube microphone attached to the TM electrode. Results showed that the amplitude and latency of chirp-evoked N1 of the CAP differed from click-evoked CAPs in several regards. For the chirp-evoked CAP, the N1 amplitude was significantly larger than the click-evoked N1s. The latency-intensity function was significantly shallower for chirp-evoked CAPs as compared to click-evoked CAPs. This suggests that auditory nerve fibers respond with more unison to a chirp stimulus than to a click stimulus.

Effects of Low-Frequency Biasing on Otoacoustic and Neural Measures Suggest that Stimulus-Frequency Otoacoustic Emissions Originate Near the Peak Region of the Traveling Wave

Stimulus-frequency otoacoustic emissions (SFOAEs) have been used to study a variety of topics in cochlear mechanics, although a current topic of debate is where in the cochlea these emissions are generated. One hypothesis is that SFOAE generation is predominately near the peak region of the traveling wave. An opposing hypothesis is that SFOAE generation near the peak region is deemphasized compared to generation in the tail region of the traveling wave. A comparison was made between the effect of low-frequency biasing on both SFOAEs and a physiologic measure that arises from the peak region of the traveling wave—the compound action potential (CAP). SFOAE biasing was measured as the amplitude of spectral sidebands from varying bias tone levels. CAP biasing was measured as the suppression of CAP amplitude from varying bias tone levels. Measures of biasing effects were made throughout the cochlea. Results from cats show that the level of bias tone needed for maximum SFOAE sidebands and for 50% CAP reduction increased as probe frequency increased. Results from guinea pigs show an irregular bias effect as a function of probe frequency. In both species, there was a strong and positive relationship between the bias level needed for maximum SFOAE sidebands and for 50% CAP suppression. This relationship is consistent with the hypothesis that the majority of SFOAE is generated near the peak region of the traveling wave.

Temporary hearing loss influences post-stimulus time histogram and single neuron action potential estimates from human compound action potentials

An analytic compound action potential (CAP) obtained by convolving functional representations of the post-stimulus time histogram summed across auditory nerve neurons [P(t)] and a single neuron action potential [U(t)] was fit to human CAPs. The analytic CAP fit to pre- and postnoise-induced temporary hearing threshold shift (TTS) estimated in vivo P(t) and U(t) and the number of neurons contributing to the CAPs (N). The width of P(t) decreased with increasing signal level and was wider at the lowest signal level following noise exposure. P(t) latency decreased with increasing signal level and was shorter at all signal levels following noise exposure. The damping and oscillatory frequency of U(t) increased with signal level. For subjects with large amounts of TTS, U(t) had greater damping than before noise exposure particularly at low signal levels. Additionally, U(t) oscillation was lower in frequency at all click intensities following noise exposure. N increased with signal level and was smaller after noise exposure at the lowest signal level. Collectively these findings indicate that neurons contributing to the CAP during TTS are fewer in number, shorter in latency, and poorer in synchrony than before noise exposure. Moreover, estimates of single neuron action potentials may decay more rapidly and have a lower oscillatory frequency during TTS.

Large endolymphatic potentials from low-frequency and infrasonic tones in the guinea pig

Responses of the ear to low-frequency and infrasonic sounds have not been extensively studied. Understanding how the ear responds to low frequencies is increasingly important as environmental infrasounds are becoming more pervasive from sources such as wind turbines. This study shows endolymphatic potentials in the third cochlear turn from acoustic infrasound (5 Hz) are larger than from tones in the audible range (e.g., 50 and 500 Hz), in some cases with peak-to-peak amplitude greater than 20 mV. These large potentials were suppressed by higher-frequency tones and were rapidly abolished by perilymphatic injection of KCl at the cochlear apex, demonstrating their third-turn origins. Endolymphatic iso-potentials from 5 to 500 Hz were enhanced relative to perilymphatic potentials as frequency was lowered. Probe and infrasonic bias tones were used to study the origin of the enhanced potentials. Potentials were best explained as a saturating response summed with a sinusoidal voltage (Vo), that was phase delayed by an average of 60° relative to the biasing effects of the infrasound. Vo is thought to arise indirectly from hair cell activity, such as from strial potential changes caused by sustained current changes through the hair cells in each half cycle of the infrasound.

Influence of hearing sensitivity on mechano-electric transduction

This study examined the relation between the extent of permanent hearing loss and the change in a third-order polynomial transducer function (PTF) representing mechano-electric transduction (MET). Mongolian gerbils were exposed to noise for 1 to 128 h. A control group received no exposure. The cochlear microphonic (CM) was recorded from a round-window electrode and stapes velocity was recorded with a laser Doppler vibrometer in response to Gaussian noise. A nonlinear systems identification procedure provided the frequency-domain coefficients of the PTF and their associated coherence functions. In the control group, the PTF in the high frequencies was dominated by linear and cubic terms. In noise-exposed animals, the magnitude of these terms decreased with increasing threshold, suggesting a progressive decrease in the receptor currents through basal hair cells. Moreover, the linear coherence increased and the cubic coherence decreased, indicating that MET in the cochlear base became linear. In the low frequencies, noise exposure altered the group delay of the CM, demonstrating a redistribution of hair-cell currents. The low-frequency PTF was characterized by an increase in the contribution in the quadratic term. With increasing threshold, the slope of the PTF decreased and the saturation for positive CM was eliminated.

How Does Wind Turbine Noise Affect People

The essence of the current debate is that on one hand you have the well-funded wind industry 1. advocating that infrasound be ignored because the measured levels are below the threshold of human hearing, allowing noise levels to be adequately documented through A-weighted sound measurements, 2. dismissing the possibility that any variants of wind turbine syndrome exist (Pierpont 2009) even when physicians (e.g., Steven D. Rauch, M.D. at Harvard Medical School) cannot otherwise explain some patients’ symptoms, and, 3. arguing that it is unnecessary to separate wind turbines and homes based on prevailing sound levels.

Amplitude modulation of audible sounds by non-audible sounds: Understanding the effects of wind turbine noise

Our research has suggested a number of mechanisms by which low-frequency noise could bother individuals living near wind turbines: causing endolymphatic hydrops, exciting subconscious pathways, and amplitude modulation of audible sounds. Here we focus on the latter mechanism, amplitude modulation. We measured single-auditory-nerve fiber responses to probe tones at their characteristic frequency in cats. A 50 Hz tone, which did not cause an increase in spontaneous firing rate (i.e., was not audible to the fiber when presented alone) was used to amplitude modulate responses to the probe tone. We found that as probe frequency decreased, a lower level of the low-frequency non-audible tone was needed to achieve criterion amplitude modulation. In other words, low-frequencies that are coded in the cochlear apex require less low-frequency sound pressure level to be amplitude modulated as compared to higher-frequencies that are coded in the cochlear base. This finding was validated, and extended to lower frequenci...

Direct administration of 2-hydroxypropyl-beta-cyclodextrin into guinea pig cochleae: Effects on physiological and histological measurements

2-Hydroxypropyl-Beta-Cyclodextrin (HPβCD) can be used to treat Niemann-Pick type C disease, Alzheimer’s disease, and atherosclerosis. But, a consequence is that HPβCD can cause hearing loss. HPβCD was recently found to be toxic to outer hair cells (OHCs) in the organ of Corti. Previous studies on the chronic effects of in vivo HPβCD toxicity did not know the intra-cochlear concentration of HPβCD and attributed variable effects on OHCs to indirect drug delivery to the cochlea. We studied the acute effects of known HPβCD concentrations administered directly into intact guinea pig cochleae. Our novel approach injected solutions through pipette sealed into scala tympani in the cochlear apex. Solutions were driven along the length of the cochlear spiral toward the cochlear aqueduct in the base. This method ensured that therapeutic levels were achieved throughout the cochlea, including those regions tuned to mid to low frequencies and code speech vowels and background noise. A wide variety of measurements were made. Results were compared to measurements from ears treated with the HPβCD analog methyl-β-cyclodextrin (MβCD), salicylate that is well known to attenuate the gain of the cochlear amplifier, and injection of artificial perilymph alone (controls). Histological data showed that OHCs appeared normal after treatment with a low dose of HPβCD, and physiological data was consistent with attenuation of cochlear amplifier gain and disruption of non-linearity associated with transferring acoustic sound into neural excitation, an origin of distortion products that are commonly used to objectively assess hearing and hearing loss. A high dose of HPβCD caused sporadic OHC losses and markedly affected all physiologic measurements. MβCD caused virulent destruction of OHCs and physiologic responses. Toxicity of HPβCD to OHC along the cochlear length is variable even when a known intra-cochlear concentration is administered, at least for the duration of our acute studies.

Efferent inhibition strength is a physiological correlate of hyperacusis in children with autism spectrum disorder

Autism spectrum disorder (ASD) is a developmental disability that is poorly understood. ASD can influence communication, social interaction, and behavior. Children with ASD often have sensory hypersensitivities, including auditory hypersensitivity (hyperacusis). In adults with hyperacusis who are otherwise neurotypical, the medial olivocochlear (MOC) efferent reflex is stronger than usual. In children with ASD, the MOC reflex has been measured, but without also assessing hyperacusis. We assessed the MOC reflex in children with ASD by measuring the strength of MOC-induced inhibition of transient-evoked otoacoustic emissions (TEOAEs), a noninvasive physiological measure that reflects cochlear amplification. MOC activity was evoked by contralateral noise. Hyperacusis was assessed subjectively on the basis of the childrens symptoms. We found a significant correlation between hyperacusis scores and MOC strength in children with ASD. When children were divided into ASD-with-severe-hyperacusis (ASDs), ASD-with-not-severe-hyperacusis (ASDns), and neurotypical (NT) groups, the last two groups had similar hyperacusis and MOC reflexes, whereas the ASDs group, on average, had hyperacusis and MOC reflexes that were approximately twice as strong. The MOC inhibition of TEOAEs averaged larger at all frequencies in the ASDs compared with ASDns and NT groups. The results suggest that the MOC reflex can be used to estimate hyperacusis in children with ASD and might be used to validate future questionnaires to assess hyperacusis. Our results also provide evidence that strong MOC reflexes in children with ASD are associated with hyperacusis and that hyperacusis is a comorbid condition and is not a necessary, integral part of the abnormal neural processing associated with ASD.NEW & NOTEWORTHY Children with autism spectrum disorder (ASD) are a heterogeneous group, some with hyperacusis and some without. Our research shows that hyperacusis can be estimated in children with ASD by using medial olivocochlear (MOC) reflex measurements. By establishing that an objective measure correlates with attributes of hyperacusis, our results enable future work to enable subtyping of children with ASD to provide improved individualized treatments to at-risk children and those without adequate language to describe their hyperacusis symptoms.