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PubMed1992

The human frequency-following response (FFR): normal variability and relation to the click-evoked brainstem response.

The frequency-following response (FFR) was recorded from twenty human subjects (11 female and 9 male) over a frequency range of 128-832 Hz in order to study the normal variability of this evoked potential and its dependence on age and sex. Moreover the relation of the FFR to the click-evoked brain stem response (BER) was analyzed in order to contribute to the FFR source discussion. The FFR had a maximum amplitude of about 400 nV and a latency of about 6.4 ms for stimulus frequencies around 350 Hz; the inter-individual variance of the best frequency and of the shape of the frequency function was considerable. Large second harmonics were seen in the FFR to stimuli below about 200 Hz. The FFR amplitude tended to be larger in younger subjects, whereas no such effect was found for the BER. No significant sex effect was found for the FFR amplitude, whereas the BER waves IV and VI were larger for females than for males. There were no correlations between FFR and BER latencies. Significant correlations were found between the amplitudes of the FFR and BER components II, III and IV, but not of waves V and VI. The results support the notion that the FFR and the BER reflect different mechanisms. Moreover the results do not favor the common hypothesis that the inferior colliculus is the major source of the scalp-recorded human FFR, but rather point to lower brainstem levels.

Acoustic Stimulation↗
PubMed1993

Temporal integration and oscillatory responses of the human auditory cortex revealed by evoked magnetic fields to click trains.

We recorded neuromagnetic evoked responses from the right auditory cortex of 7 healthy adults with a 24-channel planar SQUID gradiometer. The stimuli were 200-ms click trains presented at rates of 40, 80, 160 and 320 Hz, with interstimulus intervals (ISIs) of 1 and 4 s. The transient N100m response to the train onset depended on the click rate: the peak latency shortened to the same extent as the interval between successive clicks decreased in trains with rates from 40 Hz to 320 Hz. The N100m amplitude increased simultaneously, saturating at rates of 160-320 Hz. The mean N100m latency was slightly longer with the 1-s than with the 4-s ISI for all click rates. The systematic changes of the N100m amplitude and latency according to click rate demonstrate the importance of temporal integration for N100m generation, and imply an integration time of 20-25 ms. The 20- and 40-Hz click trains also elicited oscillatory 40-Hz responses 80-250 ms after the train onset. The 40-Hz responses were more resistant than N100m to changes of the ISI, and their sources slightly differed from those of N100m. These two responses evidently reflect different aspects of auditory processing.

Acoustic Stimulation↗
PubMed1993

Interrelation of spontaneous and evoked otoacoustic emissions.

The interrelation of spontaneous otoacoustic emissions (SOAEs) that can be synchronised by acoustic stimuli and transiently evoked otoacoustic emissions (TEOAEs) was studied in different experiments in normal ears. Click evoked TEOAEs mixed with synchronised SOAEs were investigated in time windows of 102.4 ms. Frequency spectra were obtained from the whole time window, the first and second half and from each quarter separately. Synchronised SOAEs recorded by time domain averaging show exactly the same frequencies in the TEOAE spectra of all analysed time window quarters compared to SOAEs recorded by frequency domain averaging. Moreover, synchronised SOAEs can influence the response shape of the TEOAE additionally. This is shown in long lasting responses exceeding the inter stimulus interval (ISI). In this case superimposing of consecutive single responses takes place and the shape of the averaged response depends on the exact ISI value used. These effects were investigated by varying the ISI in steps of 0.1 ms. The ISI variation has more pronounced effects on the response shape at short ISI values (50 ms) and low stimulus levels (10 dB HL). Thus the wave form changes are not accompanied by a change of the frequency content poor phase cancellation takes place. This is confirmed by simulated phase interaction. It is suggested that the phase of an already synchronised SOAE has significant effects on the re-synchronisation of the SOAE by the next click. Both influences should be considered in TEOAE recordings if synchronised SOAEs are present.

Acoustic Stimulation↗
PubMed1993

Pure-tone masking profiles for human auditory brainstem and middle latency responses.

Several studies have compared the frequency selectivity of waves I and V of the auditory brainstem response (ABR) in humans, however little is known about the frequency selectivity of the middle latency response (MLR). Simultaneous recordings of ABRs and MLRs to 60 dB peSPL 2000-Hz probe tones were obtained in the presence of 0.5, 1.0, 1.41, 2.0, 2.83 and 4.0 kHz maskers presented at 40, 60, and 80 dB SPL. ABR/MLR iso-intensity masking profiles showing the percentage of the unmasked amplitudes as a function of frequency were constructed for ABR peak V-Vn and MLR peaks Na-Pa and Nb-Pb at each masker intensity. No significant differences were found between the frequency selectivity of the ABR and MLR, and the effects of masking on the amplitudes of these responses were similar. These results are consistent with the suggestion that frequency tuning is similar up to the level of the primary auditory cortex.

Acoustic Stimulation↗
PubMed1993

Binaural interaction in auditory evoked potentials: brainstem, middle- and long-latency components.

Binaural interaction occurs in the auditory evoked potentials when the sum of the monaural auditory evoked potentials are not equivalent to the binaural evoked auditory potentials. Binaural interaction of the early- (0-10 ms), middle- (10-50 ms) and long-latency (50-200 ms) auditory evoked potentials was studied in 17 normal young adults. For the early components, binaural interaction was maximal at 7.35 ms accounting for a reduction of 21% of the amplitude of the binaural evoked potentials. For the middle latency auditory evoked potentials, binaural interaction was maximal at 39.6 ms accounting for a reduction of 48% of the binaural evoked potential. For the long-latency auditory evoked potentials, binaural interaction was maximal at 145 ms accounting for a reduction of 38% of the binaural evoked potential. In all of the auditory evoked potentials binaural interaction was long lasting around the maxima. The binaural interaction component extends for several milliseconds in the brainstem to tens of milliseconds in the middle- and long-latency components. Binaural interaction takes the form of a reduction of amplitude of the binaural evoked potential relative to the sum of the monaural responses, suggests that inhibitory processes are represented in binaural interaction using evoked potentials. Binaural processing in the auditory pathway is maximal in the time domain of the middle-latency components reflecting activity in the thalamo-cortical portions of the auditory pathways.

Acoustic Stimulation↗
PubMed1995

Responses of neurons in the inferior colliculus of the rat to interaural time and intensity differences in transient stimuli: Implications for the latency hypotheses.

Although the sensitivity to interaural intensity differences (IIDs) of neurons receiving excitatory - inhibitory binaural input (EI neurons) has been examined in numerous studies, the mechanisms underlying this sensitivity remain unclear. According to the 'latency hypotheses' neuronal sensitivity to IIDs reflects sensitivity to differences in the timing of ipsilateral and contralateral inputs that are produced as a consequence of the effects of intensity upon latency. If the latency hypothesis is correct, a neuron's responses over any given IID range should be predicted by its responses to the interaural time differences (ITDs) that are 'equivalent' to the IIDs tested, in the sense that they produce the same changes in the relative timing of inputs. This prediction from the latency hypotheses were examined by determining the sensitivity of EI neurons in the inferior colliculus of anesthetized rats to IIDs and ITDs in click stimuli, under conditions that allowed 'equivalent' ITDs to be estimated. In approximately 10% of the 41 neurons tested, the IID-sensitivity function was a perfect or near-perfect match to the equivalent-ITD function, indicating that IID sensitivity could be entirely accounted for in terms of sensitivity to intensity-produced neural time differences, as asserted by the latency hypothesis. For the majority of neurons, however, sensitivity to equivalent ITDs accounted only partially for the characteristics of the IID-sensitivity function; other features of the function in these cases appeared to reflect the operation of an additional factor, most probably the relative magnitude of the inputs from the two ears. Although the conclusions are qualified by the fact that one of the assumptions on which the estimation of equivalent ITDs was based was probably not satisfied for some neurons, the results suggest that intensity-produced changes in both the magnitude and the timing of excitatory and inhibitory inputs shape the IID sensitivity of most EI neurons.

Acoustic Stimulation↗
PubMed2006

Strain background effects and genetic modifiers of hearing in mice.

Genetic modifiers can be detected in mice by looking for strain background differences in inheritance or phenotype of a mutation. They can be mapped by analyses of appropriate linkage crosses and congenic lines, and modifier genes of large effect can be identified by positional-candidate gene testing. Inbred strains of mice vary widely in onset and severity of age-related hearing loss (AHL), an important consideration when assessing hearing in mutant mice. At least 8 mapped loci and a mitochondrial variant (mt-Tr) are known to contribute to AHL in mouse strains; one locus (ahl) has been identified as a variant of the cadherin 23 gene (Cdh23(753A/G)). This variant also was shown to modify hearing loss associated with the Atp2b2(dfw-2J) and Mass1(frings) mutations. The hearing modifier (Moth1) of tubby (Tub(tub)) mutant mice was shown to be a strain variant of the Mtap1a gene. Human hearing modifiers include DFNM1, which suppresses recessive deafness DFNB26, and a nuclear gene that modulates the severity of hearing loss associated with a mitochondrial mutation. Recently, a variant of the human ATP2B2 gene was shown to exacerbate hearing loss in individuals homozygous for a CDH23 mutation, similar to the Atp2b2(dfw-2J)-Cdh23(753A/G) interaction affecting hearing in mice. Because modifier genes and digenic inheritance are not always distinguishable, we also include in this review several examples of digenic inheritance of hearing loss that have been reported in both mice and humans.

Age Factors↗
PubMed2004

Protection of auditory function against noise trauma with local caroverine administration in guinea pigs.

Glutamate is the most likely neurotransmitter at the synapse between the inner hair cell and its afferent neuron in the peripheral auditory system. Intense noise exposure may result in excessive glutamate release, binding to the post-synaptic receptors and leading to neuronal degeneration and hearing impairment. The present study investigated the protective effect of caroverine, an antagonist of two glutamate receptors, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, on noise-induced hearing loss. Two different doses of caroverine were applied onto the round window membrane with gelfoam, followed by one-third-octave band noise centered at 6.3 kHz (110 dB SPL) for 1 h. Auditory brainstem responses were measured at regular time intervals afterwards. Caroverine was found to offer significant protection of the cochlear function against noise-induced hearing loss.

Animals↗
PubMed2005

The effect of different noise types on the speech and non-speech elicited mismatch negativity.

The effect of different types of real-life noise on the central auditory processing of speech and non-speech sounds was evaluated by the means of mismatch negativity and behavioral responses. Subjects (19-34 years old; 6 males, 4 females) were presented, in separate conditions, with either speech or non-speech stimuli of approximately equal complexity in five background conditions: babble noise, industrial noise, traffic noise, wide band noise, and silent condition. Whereas there were no effects of stimuli or noise on the behavioral responses, the MMN results revealed that speech and non-speech sounds are processed differently both in silent and noisy conditions. Speech processing was more affected than non-speech processing in all noise conditions. Moreover, different noise types had a differential effect on the pre-attentive discrimination, as reflected in MMN, on speech and non-speech sounds. Babble and industrial noises dramatically reduced the MMN amplitudes for both stimulus types, while traffic noise affected only speech stimuli.

Acoustic Stimulation↗
PubMed2001

What has MMN revealed about the auditory system in schizophrenia?

Evidence that deficits in early auditory processing occur in schizophrenia was first provided by an ERP study demonstrating that mismatch negativity (MMN) to duration increments is reduced in medicated patients. Our subsequent research, which is reviewed in this paper, demonstrates that duration MMN reduction cannot be attributed to neuroleptic medication, and is specific to schizophrenia. It is not dependent upon the nature of the task used to distract attention away from the auditory modality. Most importantly, a reduced duration MMN in schizophrenia is a replicable result, having been observed in multiple independently-selected groups of patients from two separate laboratories. It also occurs in unaffected first-degree relatives of patients, suggesting that it may be a vulnerability marker of the disorder. The most intriguing questions however, relate to what underpins the reduced MMN to duration increments in schizophrenia and therefore, what it reveals about the nature of the auditory system deficit in this disorder. Three hypotheses are considered here: a pervasive problem in auditory sensory memory; a specific impairment in duration processing; or an abnormality within the window of temporal integration, coincident with the early phase of auditory sensory memory. Our data so far offer preliminary support for the third hypothesis only, although the possibility of a more broadly defined deficit in temporal processing restricted to brief or rapidly-presented auditory stimuli is canvassed.

Acoustic Stimulation↗
PubMed1995

Significance of auditory brain stem response and gadolinium-enhanced magnetic resonance imaging for idiopathic sudden sensorineural hearing loss.

Previous studies tried to correlate prognosis and response to oral corticosteroids in patients with idiopathic sudden sensorineural hearing loss to such factors as the age of the patient, presence of vertigo, shape of the audiogram, or severity of the hearing loss. However, temporal bone histopathologic evidence shows that idiopathic sudden sensorineural hearing loss may be caused by cochleitis or cochlear nerve neuritis. Herein we report results of a retrospective study of 96 consecutive patients with idiopathic sudden sensorineural hearing loss who were evaluated with auditory brain stem responses and gadolinium-enhanced magnetic resonance imaging. Results of the auditory brain stem response and magnetic resonance imaging were correlated with hearing outcome. Follow-up was available for 65 patients: 14 with abnormal and 51 with normal auditory brain stem responses. The overall rate of hearing recovery or improvement was 65% in the normal auditory brain stem response group compared with 43% in the abnormal auditory brain stem response group (p = 0.07). Among the 38 patients treated with a tapering course of oral corticosteroids, the recovery or improvement rate was 83% for those with normal auditory brain stem responses and 56% for those with abnormal auditory brain stem responses (p < 0.05). Of the 27 patients who did not receive steroid therapy, the improvement rate was 41% in those with normal auditory brain stem responses and 20% in those with abnormal auditory brain stem responses (p = 0.09). Magnetic resonance imaging with gadolinium was obtained on all 14 patients with abnormal auditory brain stem responses but on none with normal auditory brain stem responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed2000

Neural plasticity in the mouse inferior colliculus: relationship to hearing loss, augmented acoustic stimulation, and prepulse inhibition.

C57BL/6J (C57) and DBA/2J (DBA) mice exhibit progressive high-frequency hearing loss. Extracellular recordings of responses of neurons in the inferior colliculus (IC) evoked by 70-dB SPL tones indicated that normal tonotopic organization was greatly disrupted in both strains: still-audible lower frequencies (4-12 kHz) evoked responses in a large percentage of recording sites in ventral tonotopic regions that normally respond strongly to high frequencies only. To relate the IC responses to an auditory behavior, prepulse inhibition (PPI) was measured using 70-dB tones as prepulses. As high-frequency hearing loss progressed in C57 mice, prepulses of 4-12 kHz elicited stronger PPI, and this was significantly correlated with changes in the percentage of IC recording sites responding to 70-dB tones (the neural pathway for PPI includes the IC). The analysis was extended to DBA mice that had been exposed to an augmented acoustic environment (AAE) - a procedure that improves PPI. In these mice, a higher percentage of IC recording sites responded to 70-dB tones, and this was correlated with improved PPI. The data suggest that responses of IC neurons reflect both hearing loss-induced plasticity and changes induced by exposure to an AAE, and these neural changes are correlated with the magnitude of PPI.

Acoustic Stimulation↗
PubMed2001

Functional development of the inferior colliculus (IC) and its relationship with the auditory brainstem response (ABR) in the tammar wallaby (Macropus eugenii).

To discover the developmental relationship between the auditory brainstem response (ABR) and the focal inferior colliculus (IC) response, 32 young tammar wallabies were used, by the application of simultaneous ABR and focal brainstem recordings, in response to acoustic clicks and tone bursts of seven frequencies. The IC of the tammar wallaby undergoes a rapid functional development from postnatal day (PND) 114 to 160. The earliest (PND 114) auditory evoked response was recorded from the rostral IC. With development, more caudal parts of the IC became functional until age about PND 127, when all parts of the IC were responsive to sound. Along a dorsoventral direction, the duration of the IC response decreased, the peak latency shortened, while the amplitude increased, reaching a maximum value at the central IC, then decreased. After PND 160, the best frequency (BF) of the ventral IC was the highest, with values between 12.5 and 16 kHz, the BF of the dorsal IC was the lowest, varying between 3.2 and 6.4 kHz, while the BF of the central IC was between 6.4 and 12.5 kHz. Between PND 114 and 125, the IC response did not have temporal correlation with the ABR. Between PND 140 and 160, only the early components of the responses from the ventral and central IC correlated with the P4 waves of the ABR. After PND 160, responses recorded from different depths of the IC had a temporal correlation with the ABR.

Acoustic Stimulation↗
PubMed2003

Aging and the processing of sound duration in human auditory cortex.

Age-related declines in coding the fine temporal structure of acoustic signals is proposed to play a critical role in the speech perception difficulties commonly observed in older individuals. This hypothesis was tested by measuring auditory evoked potentials elicited by sounds of various durations in young, middle-aged and older adults. All stimuli generated N1 and P2 waves that peaked at about 104 and 200 ms post-stimulus onset. The N1 amplitude increased linearly with increases in the tonal duration in young, middle-aged, and older adults. The P2 amplitude also increased linearly with signal duration, but only in young and middle-aged adults. The results demonstrate that the N1 and P2 waves can resolve duration differences as short as 2-4 ms and that normal aging decreases the temporal resolving power for processing small differences in sound duration.

Adult↗
PubMed1997

Effects of interaural intensity and time disparity on transient evoked otoacoustic emissions.

Monaural and binaural 11/s, 65 dB pe SPL clicks with interaural time and intensity disparities known to affect central auditory processing were used to study contralateral suppression of transient evoked otoacoustic emissions (TEOAEs) in 10 subjects (20 ears). Psychophysical assessment of sound lateralization induced by the same stimuli was also conducted. TEOAEs were recorded to monaural (ipsilateral to the OAE recording probe) and to binaural clicks when clicks to the contralateral ear were synchronous and symmetrical in intensity, or, in the binaural intensity disparity conditions, synchronous but 10 dB higher or 10 dB lower in the ear contralateral to the OAE recording probe. When interaural time disparities were studied, the clicks to the contralateral ear were of the same intensity throughout, but 400 micros earlier or 400 micros later than to the ear with the probe. The TEOAE components at 13-15.8 ms showed suppression, relative to monaural responses, under all binaural conditions. This contralateral suppression did not correlate with the psychophysical findings. Suppression effects were more pronounced with binaural disparity than with binaurally symmetrical clicks. Thus, although contralateral click intensity was the same with time disparities, suppression was paradoxically enhanced compared to the binaurally symmetrical stimulation. To explain these results we propose that two factors are involved in TEOAE suppression with binaural clicks: (1) contralateral intensity and (2) interaural disparity (time or intensity). The latency of the suppressions observed, the effect of interaural disparity on these suppressions, coupled with the anatomical origin of the crossed efferent fibers and the disparity sensitivity of the superior olivary complex (SOC), all suggest SOC involvement in these TEOAE suppressions.

Acoustic Stimulation↗
PubMed2004

The selectivity of neurons in the auditory zone of the mouse midbrain to the direction of movement of a spectral notch in wide-band noise.

A series of noise signals was synthesized with spectral notches whose central frequencies moved regularly along the frequency range (from low frequencies to high and from high frequencies to low), imitating movement of the sound source in the vertical plane. The spike responses of neurons in the inferior colliculus of the mouse (Mus musculus) to noise signals changed as the spectral notch moved relative to the excitatory and inhibitory areas of the receptive fields of the neurons and depended on the notch width. Disinhibition reactions in the inhibitory zones were more marked when a frequency notch in the inhibitory zone was followed by a frequency notch in the excitatory part of the response. It is suggested that the selectivity of neurons to the direction of movement of the spectral notch in a noise signal is based on the interaction of the excitatory and inhibitory inputs. The overall set of neuron responses can provide information on the movement of the sound source in acoustic space.

Acoustic Stimulation↗