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PubMed1995

Hearing loss and cochlear abnormalities in the congenital hypothyroid (hyt/hyt) mouse.

The congenital hypothyroid (hyt/hyt) mouse has been described as having a homozygous recessive mutation of a single locus on chromosome 12 which results in significant endocrine hypofunction and retarded growth. Although a distinct correlation between inherited hypothyroidism and hearing loss in humans exists, there has been no previous evaluation of the auditory system in these mutant mice. We determined hearing thresholds by auditory-evoked brainstem response testing and noted a 40-45 dB elevation in the hyt/hyt mouse compared to littermate heterozygote (hyt/+) animals and normal progenitor controls BALB/cByJ (+/+). Conventional light microscopy was used to examine the general anatomy of the cochlea in these animals, and the surface structure of the organ of Corti was further evaluated with scanning electron microscopy. Heterozygote and normal control mice had no significant abnormalities of the cochlea, however the hyt/hyt mice displayed consistent morphologic abnormalities of the stereocilia on both inner and outer hair cell systems. The surrounding and supporting cells were identified in the cochleas of the hypothyroid mouse and control animals and showed no significant histologic abnormalities. The auditory, histologic, and ultrastructural characterization of this model provides a foundation for evaluating the effects of true inherited hypothyroidism on auditory pathway development.

Animals↗
PubMed1996

Suppression in auditory-nerve fibers of cats using low-side suppressors. III. Model results.

A phenomenological model which simulates auditory-nerve (AN) two-tone suppression was developed. The model uses the output of the outer hair cell (OHC) to control the gain of the cochlear amplifier, which presumably affects only frequencies near the characteristic frequency (CF). Among other things, the model can simulate basic AN suppression patterns including the 1/4 to 1/2 cycle relationships which exist between phase of suppression and phase of excitation to the suppressor (SUP) tone alone (Cai and Geisler, 1996a). Without any changes, it is also able to simulate the experimental low-frequency biasing data and the suppression of CF component by the low-frequency SUP tone in the OHC outputs (Cheatham and Dallos, 1994). These successful simulations of the suppression patterns support the basic assumption in the model, that the saturation of OHC transduction current produces two-tone suppression. However, the amplitude behavior of the model fits that obtained only from AN fibers with high spontaneous rates (and from inner hair cells (IHC)), but not fibers with lower spontaneous rates. It appears, therefore, that other unknown mechanism(s) operating at stages following the IHC potential are important in determining the magnitude of low-side suppression.

Acoustic Stimulation↗
PubMed1996

Frequency-specific identification of hearing loss using transient-evoked otoacoustic emissions to clicks and tones.

Transient-evoked otoacoustic emissions (TEOAE) to clicks and to 500- and 2000-Hz brief tones were measured in 72 normal-hearing and hearing-impaired subjects (86 ears). The TEOAE's reproducibility parameter was used for the analyses. The purpose of the investigation was to determine which stimuli best predicted the presence of sensorineural hearing loss in a frequency-specific manner at 500, 1000, 2000, and 4000 Hz. Analyses of the TEOAEs filtered into frequency-specific bands showed that separation of normal and impaired ears at 1000, 2000 and 4000 Hz was best achieved by TEOAEs evoked by clicks. Identification of hearing loss at 500 Hz was best obtained using 500-Hz tone-evoked TEOAEs filtered using a band centered at 500 Hz. Octave- and half-octave-wide bands identified hearing loss equally well. An analysis sweep time of 20 ms provided slightly better results compared to 30 ms, except for 500 Hz, where the 30-ms sweep time slightly improved the identification of hearing loss. Increases in the audiometric criterion did not yield better test performance once hearing loss exceeded 20 dB HL. The findings from this study suggest that the combination of bandpass-filtered TEOAEs to clicks and TEOAEs to 500-Hz tones identifies with reasonable accuracy ears with sensorineural hearing loss at 500, 1000, 2000, and 4000 Hz.

Acoustic Stimulation↗
PubMed2005

Compression estimates using behavioral and otoacoustic emission measures.

Cochlear compression in normal-hearing listeners was estimated at octave frequencies from 250 to 4000 Hz using a forward-masking paradigm. Temporal masking curves (TMCs) for a 10-dB SL signal were obtained with two maskers -- one equal in frequency to the signal and another an octave below the signal. The ratio of the slope of the off-frequency function to that of the mid-level portion of the on-frequency function was computed as an estimate of the amount of compression at each frequency. Compression was less frequency selective at low frequencies, so an average of the off-frequency slopes at high frequencies (1000, 2000, and 4000 Hz) was used in computing the ratio for each signal frequency. Results indicated strong compression (approximately 0.15-0.30) at all frequencies using the averaged off-frequency slopes, indicating little difference in compression across frequencies. Distortion product otoacoustic emission (DPOAE) input-output (I-O) functions were obtained for each subject at 1000, 2000, and 4000 Hz. The slopes of the DPOAE I-O functions and the psychophysical growth rates were similar to one another, reinforcing the assumption that the forward-masking procedure is providing an estimate of cochlear compression, at least at frequencies from 1000 to 4000 Hz.

Acoustic Impedance Tests↗
PubMed2005

Click-evoked myogenic potentials recorded on alert guinea pigs.

The aim of this study was to establish an animal model of acoustically evoked vestibulo-collic reflex using guinea pigs. A special clamp was applied to restrain the head and body of the guinea pigs, but leaving its four legs free. Each animal underwent vestibular evoked myogenic potential (VEMP) and caloric tests using clip electrode method without general anesthesia or decerebrate surgery. The response rates for the myogenic potentials on the neck of guinea pigs using 100, 90, 80 and 70 dB monaural acoustic stimulation with unilateral recording were 100%, 62%, 50% and 0%, respectively. The mean latencies of the positive and negative peaks for the myogenic potentials were 7.24+/-0.49 and 9.15+/-0.47 ms, 7.09+/-0.43 and 9.28+/-0.42 ms, as well as 7.03+/-0.59 and 9.14+/-0.56 ms, when elicited by 100, 90 and 80 dB acoustic stimulation, respectively. The median (minimum-maximum) peak-to-peak amplitudes were 11.93 (6.14-16.86), 10.99 (5.28-19.40), and 11.17 (5.02-20.72) microV, when elicited by 100, 90 and 80 dB acoustic stimulation, respectively. We found no significant relationship between the stimulus intensity and the mean latencies or peak-to-peak amplitude of the myogenic potentials in guinea pigs. For those treated with gentamicin unilaterally, all guinea pigs showed absent caloric responses on the lesion side, and absent myogenic potentials on the neck when using ipsi-lesional acoustic stimulation, while the hearing was preserved. Hence, the use of gentamicin-treated animals, along with normal controls and auditory brainstem responses, results in convincing results that the recorded myogenic potentials are in fact of vestibular origin.

Acoustic Stimulation↗
PubMed2006

Effects of auditory pathway anatomy and deafness characteristics? (1): On electrically evoked auditory brainstem responses.

The purpose of this study was to distinguish the effects of different parameters on latencies of wave IIIe, wave Ve, and interpeak interval IIIe-Ve of electrical auditory brainstem responses (EABRs). EABRs were recorded from all the intra-cochlear electrodes in eight adult HiRes90K((R)) cochlear implant users. The relationship between latencies and stimulation sites in the cochlea was characterized to assess activity along the auditory pathway. Audiograms before implantation, psychophysics at first fitting and duration of deafness were used to describe the influence of deafness on latencies. A decreasing baso-apical latency gradient was found for waves IIIe and Ve, while the interpeak interval IIIe-Ve remained the same along the electrode array. Electrical stimulation enabling to stimulate various parts of the cochlea at the same time, this could indicate an anatomical way of compensating for the delay the acoustic wave takes to reach the cochlea apex in a non-implanted ear. However, psychophysical levels were also found to increase at the cochlear base showing that the latency gradient could result from an increasing gradient of neural degeneration toward the base. Correlations of EABR latencies with psychophysics, audiometric data and duration of deafness show that factors linked to deafness have indeed an influence on EABR latencies. The possible explanations for the latency shift observed, whether they are anatomical and/or pathological, are exposed.

Adolescent↗
PubMed2006

Does erythropoietin augment noise induced hearing loss?

Noise-induced hearing loss may result from excessive release of glutamate, nitrogen oxide and reactive oxygen species. The effects of these factors on the inner ear may potentially be prevented or reduced by erythropoietin (EPO), as indicated by previously demonstrated neuro-protective effects of EPO upon damage to the central nervous system and the retina. This paper reports three separate trials, conducted to investigate the hypothesis that noise-induced hearing loss is prevented or reduced by erythropoietin. The trials employed three different modes of drug application, different administration time windows and different rodent species. In trial 1, guinea pigs were exposed to 110dB SPL, 4-20kHz wide band noise (WBN) for 8h. EPO was administered to the round window membrane 24h after noise exposure, either sustained by pump for a week or by single dose middle ear instillation. In trial 2, rats were exposed to 105dB SPL, 4-20kHz WBN for 8h. EPO was administered by single dose middle ear instillation 1 or 14h after noise exposure. In trial 3, rats were exposed to 105dB SPL, 4-20kHz WBN for 8 or 3x8h. EPO was injected intraperitoneally 1h before noise exposure. Oto-acoustic emissions and auditory brainstem responses (at 16kHz) were recorded before and after noise exposure in all trials. The noise exposure induced a hearing loss in all animals. In trial 1, no recovery and no improvement of hearing occurred in any treatment group. In trial 2 and 3, a partial hearing recovery was seen. However, the hearing loss of the EPO treated animals was significantly worse than controls in trial 2. In trial 3, the hearing of the EPO treated animals exposed for 3x8h was significantly worse than controls. Thus, surprisingly, the results from 2 of the 3 present trials indicate that erythropoietin may in fact augment noise-induced hearing loss. This is contradictory to the beneficial effect of EPO reported by the vast majority of studies on stressed neural tissues. EPO administration may alter the blood flow dynamics of the cochlear vascular bed during or after noise exposure, by a potential induction of vasoconstriction. This may be the cause of the surprising findings.

Animals↗
PubMed2005

Diagnostic tools in pseudohypacusis in children.

Pseudohypacusis is the term used for a non-organic or functional hearing loss. The mainstay of diagnosis is a lack of consistency in audiological testing. It is usually easier to diagnose in children than in adults, as children are less able to reproduce consistently erroneous results on repeated testing. Nevertheless, the diagnosis is often missed in children, probably due to a lack of awareness of the condition. In a previous study from our department, we highlighted the usefulness of speech audiometry in establishing the diagnosis. However, with the advent of otoacoustic emissions testing, we have changed the emphasis of our testing protocol. Using otoacoustic emissions, the diagnosis of pseudohypacusis can be established quickly and easily.

Adolescent↗
PubMed2004

Sound frequency representation in cat auditory cortex.

Using the intrinsic signal optical recording technique, we reconstructed the two-dimensional pattern of stimulus-evoked neuronal activities in the auditory cortex of anesthetized and paralyzed cats. The average magnitude of intrinsic signal in response to a pure tone stimulus increased steadily as the sound pressure level increased. A detailed analysis demonstrated that the evoked signals at early frames were scaled by the sound pressure level, which in turn indicated the presence of a minimum level of sound pressure beyond which stimulus-related intrinsic signal can be generated. Intrinsic signals evoked significantly by pure tone stimuli of different frequencies were localized and arranged in an orderly manner in the middle ectosylvian gyrus, which indicates that the primary auditory field (AI) is tonotopically organized. The arrangement of optimal frequencies obtained from optical recordings of the same auditory cortex, which were conducted on different days, was highly reproducible. Furthermore, other auditory fields surrounding AI in the recorded area were allocated based on the observed tonotopicity. We also conducted unit recordings on the cats used for optical recording with the same set of acoustic stimuli. The gross feature of the arrangement of optimal frequencies determined by unit recordings agreed with the tonotopic arrangement determined by the optical recording, although the precise agreement was not obtained.

Acoustic Stimulation↗
PubMed2001

Mitosis and apoptosis in postnatal auditory system of the C3H/He strain.

The mouse auditory neurons, hair cells and their supporting cells in the cochlea are considered to be generated mainly in the embryonic days and to be sustained throughout the whole life. In the present study, however, we observed that auditory ganglion cells in the spiral ganglia undergo apoptosis and mitosis in the suckling mouse (1- to 2-week-old C3H/HeJ mice) with a normal auditory system. In spiral ganglia at postnatal days 7 (P7) and 10 (P10), TUNEL (TdT-mediated dUTP nick-end labeling)-positive and morphologically apoptotic ganglion cells were found. Furthermore, by bromodeoxyuridine labeling, mitosis of auditory ganglion cells was found at P10 to P14. In a functional study of auditory brainstem response, we demonstrated that the C3H/HeJ mouse acquires the ability to hear airborne sound at P12 and this is the same time as the opening of their external acoustic meatus (EAM). These results indicate that C3H/HeJ auditory ganglion cells have the ability to proliferate even after opening of the EAM and the initial input of airborne sound. We found that postnatal apoptosis and mitosis after P7 also occurred in the greater epithelial ridge (GER) which is an important organ for maturation of the organ of Corti and is located around the inner hair cells. This indicates that GER cells are not only degenerated but also regenerated until their disappearance around P12. This is the first report on mammals to demonstrate that neuronal mitosis of spiral ganglion cells and that of GER cells occur not only in embryonic and neonatal development but also in postnatal development of the normal auditory system.

Age Factors↗
PubMed1997

Auditory cortical responses in humans with profound unilateral sensorineural hearing loss from early childhood.

We recorded auditory evoked magnetic fields from five patients with profound unilateral sensorineural hearing loss from early childhood, using a 122-channel whole-scalp neuromagnetometer. The stimuli were 50-ms 1-kHz tone bursts delivered to the healthy ear at interstimulus intervals (ISI) of 1, 2, and 4 s. As the normal-hearing controls, four patients had shorter latencies of N100m, the 100-ms response, over the hemisphere contralateral to the stimulation than over the ipsilateral hemisphere. With 1-s ISI, three patients had, instead of N100m, a deflection of opposite polarity at about 100 ms (P100m) after the stimulus onset. A 10-year-old patient had a prominent P100m response, did not produce a clear N100m at any ISI, but had a clear N50m at the 4-s ISI. Four patients had bilateral N200m deflections peaking about 200 ms after the stimulus onset; the fifth patient showed N200m over the right hemisphere. N200m was also observed in the three youngest controls in both hemispheres. The ISI dependence of N100m amplitude and latency was similar in controls and patients. The amplitudes and latencies of N200m did not show any ISI dependence. In patients, the appearance of P100m-N200m deflections of auditory evoked fields, normally present in children, is more pronounced than in controls. The defect apparently delays the development of N100m, possibly by interfering with function of callosal connections.

Acoustic Stimulation↗
PubMed1996

Auditory evoked potentials in aged gerbils: responses elicited by noises separated by a silent gap.

The compound action potential (CAP) and the auditory brainstem response (ABR; waves ii and iv) were recorded in young (4-8 month) and aged (33-37 month) gerbils using a paradigm similar to that used in some psychophysical studies of gap detection (a pair of identical low-pass noises separated by a silent gap). Response amplitudes were analyzed in terms of absolute amplitudes and the 'amplitude ratio' (the amplitude of the response to the second noise of a pair divided by that to the first). Response latencies were analyzed in terms of the absolute latencies as well as the 'latency shift' (the latency of the response to the second noise minus that to the first). Response amplitudes were much smaller in the aged subjects for both the first and second stimuli of a pair. There were minimal changes in amplitude ratios across age for both the CAP and ABR. Absolute latencies were similar between groups for the first stimulus of a pair, but latencies to wave iv were much longer for the aged subjects when the gap was short. Thus, the latency shift for the aged group was much longer for wave iv in the aged compared to the young group, but were similar between groups for the CAP or wave ii of the ABR. The results suggest that there may be changes in coding of temporal information in the auditory brainstem of aged gerbils which are not a direct result of abnormal temporal processing in the auditory periphery.

Acoustic Stimulation↗
PubMed1997

Suprathreshold measures of auditory function in the aging chinchilla.

The purpose of this study was to examine the relationship between aging and suprathreshold auditory function in the chinchilla, a rodent with a relatively long life span and a range of hearing similar to that of humans. Subjects were six 11-12-year-old chinchillas and six young controls. Tests of auditory function utilized evoked potential (EVP) recordings from electrodes implanted in the inferior colliculus and measurements of 2f1-f2 distortion product otoacoustic emissions (DPOAEs). Tests of frequency resolution (EVP tuning curves for a 2 kHz probe tone), temporal resolution (EVP forward masking functions using a 2 kHz probe tone), cochlear non-linearity (remote masking), and a DPOAE 'tone challenge', in which DPOAEs at six frequencies were monitored before and after each of five 1-min exposures to a 2 kHz tone at 80 dB SPL, were performed. The results indicate that aged chinchillas can exhibit deficits in suprathreshold tests of auditory function even when the test stimulus is in a region of relatively normal-hearing sensitivity. The results support the notion that aging, independent of hearing loss, can influence suprathreshold auditory function.

Aging↗
PubMed1998

Masking of tones and speech by Schroeder-phase harmonic complexes in normally hearing and hearing-impaired listeners.

Tone detection and sentence recognition were measured for normally hearing and hearing-impaired listeners using maskers consisting of harmonic series with components summed in positive or negative Schroeder phase. Each task was carried out with the signal set at 60, 70, or 80 dB SPL. For listeners with normal hearing, positive Schroeder-phase complexes masked tones and sentences less than negative Schroeder-phase maskers. In the two experimental tasks, to achieve the same amount of masking, positive Schroeder-phase complexes had to be set as much as 12-15 dB higher than negative Schroeder-phase complexes. Large phase effects were observed on both tasks at all three test levels. The two maskers were more nearly equal in effectiveness in the presence of cochlear damage. The findings support an interpretation that involves differences in the shape of the basilar-membrane waveform generated by each masker and active cochlear processing which enhances the internal signal-to-masker ratio for signals presented in the positive Schroeder masker. This spectral enhancement appears to require nonlinear active gain that is characteristic of normal auditory processing at moderate presentation levels. The results of the sentence recognition task suggest that group differences observed in tone detection transfer fairly directly to speech perception under masking.

Acoustic Stimulation↗
PubMed2006

Mice doubly deficient in the midkine and pleiotrophin genes exhibit deficits in the expression of beta-tectorin gene and in auditory response.

alpha-Tectorin and beta-tectorin are major noncollagenous proteins of the tectorial membrane, which plays a crucial role in the reception of sonic signals in the cochlea. Midkine and pleiotrophin are closely related proteins that serve as growth factors and cytokines. In mice doubly deficient in the midkine gene and pleiotrophin gene, expression of beta-tectorin mRNA was nearly abolished in the cochlea on day 1 and 7 after birth. Expression of alpha-tectorin mRNA was unaffected in the double knockout mice, and expression of beta-tectorin mRNA was not altered in mice deficient in only the midkine or pleiotrophin gene. In newborn wild-type mice, both midkine and pleiotrophin were expressed in the greater epithelial ridge of the cochlea, in which beta-tectorin mRNA was strongly expressed. These results indicate that either midkine or pleiotrophin is required for significant expression of beta-tectorin. In agreement with the view that beta-tectorin is essential for normal auditory function, mice doubly deficient in both midkine and pleiotrophin genes exhibited very severe auditory deficits. We observed that mice deficient in either midkine or pleiotrophin gene were also impaired in their auditory response, but the level of the deficit was generally low or moderate. The present finding illustrates the importance of growth factor expression in the cochlea for auditory function.

Animals↗
PubMed1991

Conductive hearing loss during infancy: effects on later auditory brain stem electrophysiology.

Long-term effects on auditory electrophysiology from early fluctuating hearing loss were studied in 27 children, aged 5 to 7 years, who had been evaluated originally in infancy. For controls (Group A), infant auditory brain stem responses (ABRs) were normal from birth to age 2 years. A second group (Group B) had intermittent conductive hearing loss. A third group (Group C) had more abnormal ABRs during infancy than Group B and more severe and frequent conductive hearing loss. For this follow-up study, all children had normal peripheral hearing at test. ABRs were obtained to monaural and binaural stimuli. Binaural interaction (BI) in the ABR was assessed in difference traces, derived by subtracting summed binaural from summed monaural waveforms. Controls differed from both groups with early hearing loss for wave III and wave V latencies and interpeak I-III and I-V latencies. There was a significant difference in the presence of BI. Eight of 9 A subjects and 8 of 9 B subjects, but only 4 of 9 C subjects, had demonstrable BI. Findings suggest that early fluctuating hearing loss disrupts later auditory brain stem electrophysiology.

Auditory Threshold↗