Loudness Perception

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Richard Salvi - One of the best experts on this subject based on the ideXlab platform.

  • Using auditory reaction time to measure Loudness growth in rats.
    Hearing research, 2020
    Co-Authors: Kelly E. Radziwon, Richard Salvi
    Abstract:

    Abstract Previous studies have demonstrated that auditory reaction time (RT) is a reliable surrogate of Loudness Perception in humans. Reaction time-intensity (RT-I) functions faithfully recapitulate equal Loudness contours in humans while being easier to obtain than equal Loudness judgments, especially in animals. In humans, Loudness estimation not only depends on sound intensity, but on a variety of other acoustic factors. Stimulus duration and bandwidth are known to impact Loudness Perception. In addition, the presence of background noise mimics Loudness recruitment; Loudness growth is rapid near threshold, but growth becomes normal at suprathreshold levels. Therefore, to evaluate whether RT-I functions are a reliable measure of Loudness growth in rats, we obtained auditory RTs across a range of stimulus intensities, durations, and bandwidths, in both quiet and in the presence of background/masking noise. We found that reaction time patterns across stimulus parameters were repeatable over several months in rats and generally consistent with human Loudness perceptual data. Our results provide important building blocks for future animal model studies of Loudness Perception and Loudness perceptual disorders.

  • Testing the Central Gain Model: Loudness Growth Correlates with Central Auditory Gain Enhancement in a Rodent Model of Hyperacusis.
    Neuroscience, 2018
    Co-Authors: Benjamin D. Auerbach, Kelly E. Radziwon, Richard Salvi
    Abstract:

    Abstract The central gain model of hyperacusis proposes that loss of auditory input can result in maladaptive neuronal gain increases in the central auditory system, leading to the over-amplification of sound-evoked activity and excessive Loudness Perception. Despite the attractiveness of this model, and supporting evidence for it, a critical test of the central gain theory requires that changes in sound-evoked activity be explicitly linked to perceptual alterations of Loudness. Here we combined an operant conditioning task that uses a subject’s reaction time to auditory stimuli to produce reliable measures of Loudness growth with chronic electrophysiological recordings from the auditory cortex and inferior colliculus of awake, behaviorally-phenotyped animals. In this manner, we could directly correlate daily assessments of Loudness Perception with neurophysiological measures of sound encoding within the same animal. We validated this novel psychophysical-electrophysiological paradigm with a salicylate-induced model of hearing loss and hyperacusis, as high doses of sodium salicylate reliably induce temporary hearing loss, neural hyperactivity, and auditory perceptual disruptions like tinnitus and hyperacusis. Salicylate induced parallel changes to Loudness growth and evoked response-intensity functions consistent with temporary hearing loss and hyperacusis. Most importantly, we found that salicylate-mediated changes in Loudness growth and sound-evoked activity were correlated within individual animals. These results provide strong support for the central gain model of hyperacusis and demonstrate the utility of using an experimental design that allows for within-subject comparison of behavioral and electrophysiological measures, thereby making inter-subject variability a strength rather than a limitation.

  • Salicylate-induced hyperacusis in rats: Dose- and frequency-dependent effects.
    Hearing research, 2017
    Co-Authors: Kelly E. Radziwon, David P. Holfoth, Julia Lindner, Zoe Kaier-green, Rachael A. Bowler, Maxwell E. Urban, Richard Salvi
    Abstract:

    The use of auditory reaction time is a reliable measure of Loudness Perception in both animals and humans with reaction times (RT) decreasing with increasing stimulus intensity. Since abnormal Loudness Perception is a common feature of hyperacusis, a potentially debilitating auditory disorder in which moderate-intensity sounds are perceived as uncomfortable or painfully loud, we used RT measures to assess rats for salicylate-induced hyperacusis. A previous study using an operant conditioning RT procedure found that high-dose sodium salicylate (SS) induced hyperacusis-like behavior, i.e., faster than normal RTs to moderate and high level sounds, when rats were tested with broadband noise stimuli. However, it was not clear from that study if salicylate induces hyperacusis-like behavior in a dose- or frequency-dependent manner. Therefore, the goals of the current study were to determine how RT-intensity functions were altered by different doses of salicylate, and, using tone bursts, to determine if salicylate induces hyperacusis-like behavior across the entire frequency spectrum or only at certain frequencies. Similar to previous physiological studies, we began to see faster than normal RTs for sounds 60 dB SPL and greater with salicylate doses of 150 mg/kg and higher; indicating the rats were experiencing hyperacusis at high salicylate doses. In addition, high-dose salicylate significantly reduced RTs across all stimulus frequencies tested which suggests that a central neural excitability mechanism may be a potential driver of salicylate-induced changes in Loudness Perception and hyperacusis.

  • Early age noise exposure increases Loudness Perception - A novel animal model of hyperacusis.
    Hearing research, 2016
    Co-Authors: Ana'am Alkharabsheh, Senthilvelan Manohar, Richard Salvi, Fen Xiong, Binbin Xiong, Guang-di Chen, Wei Sun
    Abstract:

    The neural mechanisms that give rise to hyperacusis, a reduction in Loudness tolerance, are largely unknown. Some reports suggest that hyperacusis is linked to childhood hearing loss. However, the evidence for this is largely circumstantial. In order to rigorously test this hypothesis, we studied Loudness changes in rats caused by intense noise exposure (12 kHz narrow band noise, 115 dB SPL, 4 h) at postnatal 16 days. Rats without noise exposure were used as controls. The exposed noise group (n = 7) showed a mean 40-50 dB hearing loss compared to the control group (n = 8) at high frequencies (>= 8 kHz) and less hearing loss at lower frequencies. Loudness was evaluated using sound reaction time and Loudness response functions in an operant conditioning-based behavioral task using narrow-band noise (40-110 dB SPL, centered at 2, 4 and 12 kHz). Interestingly, the sound reaction time of the noise group was significantly shorter than the control group at supra-threshold levels. The average reaction time was less than 100 ms in the noise group at 100 dB SPL, which was three times shorter than the control group. Our results indicate that early noise-induced hearing loss leads to a significant increase of Loudness, a behavior indicative of hyperacusis. Our results are consistent with clinical reports suggesting that hearing loss at an early age is a significant risk factor for hyperacusis.

Todd A. Ricketts - One of the best experts on this subject based on the ideXlab platform.

  • The effect of test signal type and bandwidth on the categorical scaling of Loudness
    The Journal of the Acoustical Society of America, 1996
    Co-Authors: Todd A. Ricketts, Ruth A. Bentler
    Abstract:

    Recently several methods for obtaining clinical measures of Loudness growth through the use of categorical scaling (CS) have been proposed for the selection of hearing aids. These methods use differing test signals or suggest frequency‐specific level corrections in an attempt to reflect the Loudness Perception of hearing aid‐processed speech. While some decisions regarding the stimuli utilized for Loudness Perception procedures are based on measured relationships to speech signals, the effect on Loudness Perception of changing signal type and bandwidth (as measured by CS) remains unclear. The relationships between the CS Loudness growth of signals of differing type, (pure tones, noise bands, filtered/temporally inverted/passband speech) and bandwidth were examined for subjects with both normal and impaired hearing. Results suggest that when the bandwidth is similar (e.g., pure tone and 1/3 oct), signal type does not have significant bearing on Loudness Perception. As expected, increasing the bandwidth beyond the critical band affected Loudness growth, as wideband speech stimuli were judged to be significantly louder than narrow‐band speech at equivalent overall sound levels. In this investigation, similar Loudness growth patterns were noted across category ratings for all test signal bandwidths. In contrast, Loudness growth data obtained using an intelligible speech signal [Cox et al., The American Academy of Audiology (1994a)], revealed Loudness growth patterns for speech were fundamentally different than those obtained for tones. Implications for hearing aid fitting strategies are discussed.Recently several methods for obtaining clinical measures of Loudness growth through the use of categorical scaling (CS) have been proposed for the selection of hearing aids. These methods use differing test signals or suggest frequency‐specific level corrections in an attempt to reflect the Loudness Perception of hearing aid‐processed speech. While some decisions regarding the stimuli utilized for Loudness Perception procedures are based on measured relationships to speech signals, the effect on Loudness Perception of changing signal type and bandwidth (as measured by CS) remains unclear. The relationships between the CS Loudness growth of signals of differing type, (pure tones, noise bands, filtered/temporally inverted/passband speech) and bandwidth were examined for subjects with both normal and impaired hearing. Results suggest that when the bandwidth is similar (e.g., pure tone and 1/3 oct), signal type does not have significant bearing on Loudness Perception. As expected, increasing the bandwidth bey...

  • The effect of test signal type and bandwidth on the categorical scaling of Loudness.
    The Journal of the Acoustical Society of America, 1996
    Co-Authors: Todd A. Ricketts, Ruth A. Bentler
    Abstract:

    Recently several methods for obtaining clinical measures of Loudness growth through the use of categorical scaling (CS) have been proposed for the selection of hearing aids. These methods use differing test signals or suggest frequency-specific level corrections in an attempt to reflect the Loudness Perception of hearing aid-processed speech. While some decisions regarding the stimuli utilized for Loudness Perception procedures are based on measured relationships to speech signals, the effect on Loudness Perception of changing signal type and bandwidth (as measured by CS) remains unclear. The relationships between the CS Loudness growth of signals of differing type, (pure tones, noise bands, filtered/temporally inverted/passband speech) and bandwidth were examined for subjects with both normal and impaired hearing. Results suggest that when the bandwidth is similar (e.g., pure tone and 1/3 oct), signal type does not have significant bearing on Loudness Perception. As expected, increasing the bandwidth beyond the critical band affected Loudness growth, as wideband speech stimuli were judged to be significantly louder than narrow-band speech at equivalent overall sound levels. In this investigation, similar Loudness growth patterns were noted across category ratings for all test signal bandwidths. In contrast, Loudness growth data obtained using an intelligible speech signal [Cox et al., The American Academy of Audiology (1994a)], revealed Loudness growth patterns for speech were fundamentally different than those obtained for tones. Implications for hearing aid fitting strategies are discussed.

  • Fitting Hearing Aids to Individual Loudness-Perception Measures
    Ear and hearing, 1996
    Co-Authors: Todd A. Ricketts
    Abstract:

    Objective: The purpose of this study was to compare the prescribed gain, compression ratios, compression thresholds, and the relative predicted speech intelligibility (Speech Intelligibility Index [SII], American National Standards Institute 3.79, proposed) provided by four strategies proposed for selecting hearing aid parameters for low-threshold compression hearing instruments and by a traditional threshold-based hearing aid fitting procedure. The strategies used were Desired Sensation Level Input/Output (DSL TM [i/o]; Cornelisse, Seewald, & Jamieson, 1994), Visual Input-Output Locator Algorithm (VIOLA; Cox, 1994), FIG6 strategy (Killion, Reference Note 2), Ricketts and Bentler strategy (RAB), and a threshold-based hearing aid fitting procedure (National Acoustics Laboratories-Revised [NAL-R]; Byrne & Dillion, 1986). These new strategies have been suggested as alternatives to threshold-based strategies, which do not provide the varying amounts of target gain, as a function of input level, necessary to fit low-threshold compression hearing aids. Design: The electroacoustic prescriptions and the predicted speech intelligibility were calculated across all five fitting strategies for 20 subjects. The threshold and Loudness growth information used for each fitting was reported previously (Ricketts & Bentler, in press). Results: Comparison across prescriptions revealed that the NAL-R strategy (due to the linear gain provided) prescribed the least gain for low-level inputs and the greatest gain for high-level inputs. Gain comparisons across fitting by Loudness (FBL) strategies revealed a more shallow frequency response slope for strategies that require individual measures of Loudness growth (RAB, VIOLA) in comparison with strategies that assumed average data (FIG6, DSL TM [i/o]). SII results revealed greater predicted speech intelligibility for the FIG6 and the DSL TM [i/o] compared with the NAL-R, RAB, and VIOLA. These differences were most apparent in noise backgrounds and least evident when Loudness differences were minimized. Conclusions: It appears that differences in SII scores across the FBL fitting strategies are due, in part, to differences in the Loudness of the output signal. It is assumed that differences in high-frequency shaping may also be a factor. These data do not appear to support the use of additional clinical time to obtain individual Loudness growth measures. However, due to the fact that SII results are based on average performance, it is difficult to predict whether differences across these fitting strategies would be realized in actual measures of speech intelligibility or sound quality on an individual basis.

Wei Sun - One of the best experts on this subject based on the ideXlab platform.

  • Early age noise exposure increases Loudness Perception - A novel animal model of hyperacusis.
    Hearing research, 2016
    Co-Authors: Ana'am Alkharabsheh, Senthilvelan Manohar, Richard Salvi, Fen Xiong, Binbin Xiong, Guang-di Chen, Wei Sun
    Abstract:

    The neural mechanisms that give rise to hyperacusis, a reduction in Loudness tolerance, are largely unknown. Some reports suggest that hyperacusis is linked to childhood hearing loss. However, the evidence for this is largely circumstantial. In order to rigorously test this hypothesis, we studied Loudness changes in rats caused by intense noise exposure (12 kHz narrow band noise, 115 dB SPL, 4 h) at postnatal 16 days. Rats without noise exposure were used as controls. The exposed noise group (n = 7) showed a mean 40-50 dB hearing loss compared to the control group (n = 8) at high frequencies (>= 8 kHz) and less hearing loss at lower frequencies. Loudness was evaluated using sound reaction time and Loudness response functions in an operant conditioning-based behavioral task using narrow-band noise (40-110 dB SPL, centered at 2, 4 and 12 kHz). Interestingly, the sound reaction time of the noise group was significantly shorter than the control group at supra-threshold levels. The average reaction time was less than 100 ms in the noise group at 100 dB SPL, which was three times shorter than the control group. Our results indicate that early noise-induced hearing loss leads to a significant increase of Loudness, a behavior indicative of hyperacusis. Our results are consistent with clinical reports suggesting that hearing loss at an early age is a significant risk factor for hyperacusis.

  • Loudness Perception affected by high doses of salicylate--a behavioral model of hyperacusis.
    Behavioural brain research, 2014
    Co-Authors: Chao Zhang, Elizabeth Flowers, Qiuju Wang, Wei Sun
    Abstract:

    The major side-effects of high doses of salicylate include sensorial hearing loss and tinnitus. Although salicylate decreases cochlear output, it enhances the evoked potentials recorded from the central auditory system (CAS), suggesting an increase to sound sensitivity. However, the Loudness change after salicylate administration has not yet been directly measured. In this study, we established an operant conditioning based behavioral task in rats and measured their Loudness Perception changes before and after high doses of salicylate injection (250 mg/kg, i.p.). We found that high doses of salicylate induced a significant increase to Loudness response in 40% of the rats (out of 20 rats), suggesting a hyperacusis behavior. In another 40% of rats, a rapid increase of Loudness response was detected, suggesting Loudness recruitment. The reaction time of the rats was also measured during the Loudness tests before and after salicylate exposure. The reaction time level functions are highly correlated to the Loudness response functions. Our studies confirmed that increased sound sensitivity, which is commonly seen in patients with tinnitus and hyperacusis, can be induced by high doses of salicylate. This Loudness change induced by salicylate may be related with hypersensitivity in the CAS.

  • Loudness Perception affected by early age hearing loss
    Hearing research, 2014
    Co-Authors: Wei Sun, Chao Zhang, Senthilvelan Manohar, Anand Kumaraguru
    Abstract:

    Abstract Tinnitus and hyperacusis, commonly seen in adults, are also reported in children. Although clinical studies found children with tinnitus and hyperacusis often suffered from recurrent otitis media, there is no direct study on how temporary hearing loss in the early age affects the sound Loudness Perception. In this study, sound Loudness changes in rats affected by perforation of the tympanic membranes (TM) have been studied using an operant conditioning based behavioral task. We detected significant increases of sound Loudness and susceptibility to audiogenic seizures (AGS) in rats with bilateral TM damage at postnatal 16 days. As increase to sound sensitivity is commonly seen in hyperacusis and tinnitus patients, these results suggest that early age hearing loss is a high risk factor to induce tinnitus and hyperacusis in children. In the TM damaged rats, we also detected a reduced expression of GABA receptor δ and α6 subunits in the inferior colliculus (IC) compared to the controls. Treatment of vigabatrin (60 mg/kg/day, 7–14 days), an anti-seizure drug that inhibits the catabolism of GABA, not only blocked AGS, but also significantly attenuated the Loudness response. Administration of vigabatrin following the early age TM damage could even prevent rats from developing AGS. These results suggest that TM damage at an early age may cause a permanent reduction of GABA tonic inhibition which is critical towards the maintenance of normal Loudness processing of the IC. Increasing GABA concentration during the critical period may alleviate the impairment in the brain induced by early age hearing loss.

Kelly E. Radziwon - One of the best experts on this subject based on the ideXlab platform.

  • Using auditory reaction time to measure Loudness growth in rats.
    Hearing research, 2020
    Co-Authors: Kelly E. Radziwon, Richard Salvi
    Abstract:

    Abstract Previous studies have demonstrated that auditory reaction time (RT) is a reliable surrogate of Loudness Perception in humans. Reaction time-intensity (RT-I) functions faithfully recapitulate equal Loudness contours in humans while being easier to obtain than equal Loudness judgments, especially in animals. In humans, Loudness estimation not only depends on sound intensity, but on a variety of other acoustic factors. Stimulus duration and bandwidth are known to impact Loudness Perception. In addition, the presence of background noise mimics Loudness recruitment; Loudness growth is rapid near threshold, but growth becomes normal at suprathreshold levels. Therefore, to evaluate whether RT-I functions are a reliable measure of Loudness growth in rats, we obtained auditory RTs across a range of stimulus intensities, durations, and bandwidths, in both quiet and in the presence of background/masking noise. We found that reaction time patterns across stimulus parameters were repeatable over several months in rats and generally consistent with human Loudness perceptual data. Our results provide important building blocks for future animal model studies of Loudness Perception and Loudness perceptual disorders.

  • Testing the Central Gain Model: Loudness Growth Correlates with Central Auditory Gain Enhancement in a Rodent Model of Hyperacusis.
    Neuroscience, 2018
    Co-Authors: Benjamin D. Auerbach, Kelly E. Radziwon, Richard Salvi
    Abstract:

    Abstract The central gain model of hyperacusis proposes that loss of auditory input can result in maladaptive neuronal gain increases in the central auditory system, leading to the over-amplification of sound-evoked activity and excessive Loudness Perception. Despite the attractiveness of this model, and supporting evidence for it, a critical test of the central gain theory requires that changes in sound-evoked activity be explicitly linked to perceptual alterations of Loudness. Here we combined an operant conditioning task that uses a subject’s reaction time to auditory stimuli to produce reliable measures of Loudness growth with chronic electrophysiological recordings from the auditory cortex and inferior colliculus of awake, behaviorally-phenotyped animals. In this manner, we could directly correlate daily assessments of Loudness Perception with neurophysiological measures of sound encoding within the same animal. We validated this novel psychophysical-electrophysiological paradigm with a salicylate-induced model of hearing loss and hyperacusis, as high doses of sodium salicylate reliably induce temporary hearing loss, neural hyperactivity, and auditory perceptual disruptions like tinnitus and hyperacusis. Salicylate induced parallel changes to Loudness growth and evoked response-intensity functions consistent with temporary hearing loss and hyperacusis. Most importantly, we found that salicylate-mediated changes in Loudness growth and sound-evoked activity were correlated within individual animals. These results provide strong support for the central gain model of hyperacusis and demonstrate the utility of using an experimental design that allows for within-subject comparison of behavioral and electrophysiological measures, thereby making inter-subject variability a strength rather than a limitation.

  • Salicylate-induced hyperacusis in rats: Dose- and frequency-dependent effects.
    Hearing research, 2017
    Co-Authors: Kelly E. Radziwon, David P. Holfoth, Julia Lindner, Zoe Kaier-green, Rachael A. Bowler, Maxwell E. Urban, Richard Salvi
    Abstract:

    The use of auditory reaction time is a reliable measure of Loudness Perception in both animals and humans with reaction times (RT) decreasing with increasing stimulus intensity. Since abnormal Loudness Perception is a common feature of hyperacusis, a potentially debilitating auditory disorder in which moderate-intensity sounds are perceived as uncomfortable or painfully loud, we used RT measures to assess rats for salicylate-induced hyperacusis. A previous study using an operant conditioning RT procedure found that high-dose sodium salicylate (SS) induced hyperacusis-like behavior, i.e., faster than normal RTs to moderate and high level sounds, when rats were tested with broadband noise stimuli. However, it was not clear from that study if salicylate induces hyperacusis-like behavior in a dose- or frequency-dependent manner. Therefore, the goals of the current study were to determine how RT-intensity functions were altered by different doses of salicylate, and, using tone bursts, to determine if salicylate induces hyperacusis-like behavior across the entire frequency spectrum or only at certain frequencies. Similar to previous physiological studies, we began to see faster than normal RTs for sounds 60 dB SPL and greater with salicylate doses of 150 mg/kg and higher; indicating the rats were experiencing hyperacusis at high salicylate doses. In addition, high-dose salicylate significantly reduced RTs across all stimulus frequencies tested which suggests that a central neural excitability mechanism may be a potential driver of salicylate-induced changes in Loudness Perception and hyperacusis.

Chao Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Loudness Perception affected by high doses of salicylate--a behavioral model of hyperacusis.
    Behavioural brain research, 2014
    Co-Authors: Chao Zhang, Elizabeth Flowers, Qiuju Wang, Wei Sun
    Abstract:

    The major side-effects of high doses of salicylate include sensorial hearing loss and tinnitus. Although salicylate decreases cochlear output, it enhances the evoked potentials recorded from the central auditory system (CAS), suggesting an increase to sound sensitivity. However, the Loudness change after salicylate administration has not yet been directly measured. In this study, we established an operant conditioning based behavioral task in rats and measured their Loudness Perception changes before and after high doses of salicylate injection (250 mg/kg, i.p.). We found that high doses of salicylate induced a significant increase to Loudness response in 40% of the rats (out of 20 rats), suggesting a hyperacusis behavior. In another 40% of rats, a rapid increase of Loudness response was detected, suggesting Loudness recruitment. The reaction time of the rats was also measured during the Loudness tests before and after salicylate exposure. The reaction time level functions are highly correlated to the Loudness response functions. Our studies confirmed that increased sound sensitivity, which is commonly seen in patients with tinnitus and hyperacusis, can be induced by high doses of salicylate. This Loudness change induced by salicylate may be related with hypersensitivity in the CAS.

  • Loudness Perception affected by early age hearing loss
    Hearing research, 2014
    Co-Authors: Wei Sun, Chao Zhang, Senthilvelan Manohar, Anand Kumaraguru
    Abstract:

    Abstract Tinnitus and hyperacusis, commonly seen in adults, are also reported in children. Although clinical studies found children with tinnitus and hyperacusis often suffered from recurrent otitis media, there is no direct study on how temporary hearing loss in the early age affects the sound Loudness Perception. In this study, sound Loudness changes in rats affected by perforation of the tympanic membranes (TM) have been studied using an operant conditioning based behavioral task. We detected significant increases of sound Loudness and susceptibility to audiogenic seizures (AGS) in rats with bilateral TM damage at postnatal 16 days. As increase to sound sensitivity is commonly seen in hyperacusis and tinnitus patients, these results suggest that early age hearing loss is a high risk factor to induce tinnitus and hyperacusis in children. In the TM damaged rats, we also detected a reduced expression of GABA receptor δ and α6 subunits in the inferior colliculus (IC) compared to the controls. Treatment of vigabatrin (60 mg/kg/day, 7–14 days), an anti-seizure drug that inhibits the catabolism of GABA, not only blocked AGS, but also significantly attenuated the Loudness response. Administration of vigabatrin following the early age TM damage could even prevent rats from developing AGS. These results suggest that TM damage at an early age may cause a permanent reduction of GABA tonic inhibition which is critical towards the maintenance of normal Loudness processing of the IC. Increasing GABA concentration during the critical period may alleviate the impairment in the brain induced by early age hearing loss.