64 channel linear recording electrode array Search Results


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Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG <t>electrodes</t> and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.
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Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG <t>electrodes</t> and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.
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Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG <t>electrodes</t> and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.
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Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG <t>electrodes</t> and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.
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Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG <t>electrodes</t> and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.
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Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG <t>electrodes</t> and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.
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plexon inc linear electrode array plexon 24 channels
Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG <t>electrodes</t> and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.
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Image Search Results


Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG electrodes and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.

Journal: bioRxiv

Article Title: The human pupil and face encode sound affect and provide objective signatures of tinnitus and auditory hypersensitivity disorders

doi: 10.1101/2023.12.22.571929

Figure Lengend Snippet: Increased central gain is not correlated tinnitus or sound sensitivity burden A) Cartoon denotes a stage of central auditory processing (e.g., the auditory cortex) with excitatory projection neurons (red) and inhibitory interneurons (cool colors). In this model, disinhibition of excitatory neurons promotes elevated, hypersynchronous firing in silence (the purported generator of the phantom sound) and a steeper growth in spiking with sounds of increasing intensity (i.e., excess central gain, the purported generator of loudness hyperacusis). Hyperactive auditory projection neurons feed into downstream centers of limbic processing and autonomic regulation but, as distal upstream precipitator, excess central gain is less predictive of individual differences in psychoaffective burden than autonomic affective markers. B) Top: Cartoon denotes the 64-channel array of scalp EEG electrodes and activity from a central electrode corresponding to the increasing intensity of a 40Hz amplitude modulated tone. Note that EEG amplitude is synchronized to the amplitude modulation rate. Bottom : Spectrogram plots the amplitude of synchronized EEG activity across frequencies and time as the amplitude modulated 2kHz tone slowly increases and decreases across a 70 dB range. Note the rise and fall of the 40Hz envelope following response (EFR) amplitude as a function of time/sound intensity. C) EFR growth as a function of sound intensity relative to the 2kHz audibility threshold measured for each participant (i.e., the sensation level, SL). NT and DH are neurotypical and disordered hearing participants, respectively. Central gain was measured as the change in neural response over a 25 dB change in sound level. D) Hyperacusis and tinnitus severity for all participants based on Hyperacusis questionnaire (HQ) and Tinnitus Handicap Index (THI) scores, respectively (N = 35/35 NT/DH). Circles denote individual participants. Marginal distributions for each group are shown as normalized density functions. All participants can provide a meaningful HQ score but only participants with tinnitus can provide a meaningful THI value. E) Central gain is significantly elevated in DH participants (two-sample t-test, p = 0.009, N = 36/33 NT/DH). Density functions display the central gain measure for each participant (individual circle) and sample mean (vertical lines). F) Central gain is not correlated with hyperacusis severity (Pearson R = 0.16, p = 0.19, N = 68). Shaded region denotes the 95% confidence interval. Solid line denotes linear fit. Circles denote individual participants. G) Central gain is not correlated with tinnitus severity (Pearson R = 0.13, p = 0.52, N = 22). Plotting conventions as per e. Note that THI values are limited to participants with tinnitus.

Article Snippet: EEG recordings were performed with a 64-channel array of scalp electrodes and insert earphones (EarTone 3A) connected to an electrically isolated digitizer and signal processor (BioSemi ActiveTwo, Cortech Solutions Inc.).

Techniques: Activity Assay