Introduction Results: Auditory Brainstem Response Results...
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It is well-established that auditory brainstem response (ABR) latency decreases with increasing stimulus level (e.g. Gorga et al., 1988; Neely et al., 1988). However, the physiological mechanisms that underlie this phenomenon are not well-established. Our preferred interpretation is that the level-dependent component of ABR latency stems from cochlear mechanics (Neely et al., 1988). Rasetshwane at el. (2013a) recently demonstrated significant correlations between distortion product otoacoustic emission (DPOAE) input-output functions and loudness growth as estimated using a categorical loudness scaling (CLS) procedure. Because DPOAEs are known to be a byproduct of cochlear amplifier gain, this correlation between the two measures suggests that cochlear mechanics may play a significant role in mediating loudness growth. The goal of the present study was to examine the relationship between ABR latency changes with level and loudness growth. The presence of significant correlations between the two measures would support the existence of a common underlying mechanism, presumably cochlear response growth. Laura D Mueldener 1,2 , Daniel M Rasetshwane 1 , Sara E Fultz 1 , Judy G Kopun 1 , Stephen T Neely 1 Boys Town National Research Hospital 1 ; University of Iowa 2 This work was supported by the NIH-NIDCD grants T35 DC008757 and R01 DC008318 (STN). The authors would like to thank Carissa Allen for her assistance with data analysis. An electronic version of this poster may be viewed using the QR code to the right. Introduction Results: Auditory Brainstem Response Methods Results: ABR and CLS Slope Comparisons Conclusions References & Acknowledgements Gorga, M. P., Kaminski, J. R., Beauchaine, K. A., and Jesteadt, W. (1988). “Auditory brainstem responses to tone bursts in normally hearing subjects,” J. Speech Hear. Res. 31, 87–97. Neely, S. T., Norton, S. J., Gorga, M. P., and Jesteadt, W. (1988). “Latency of auditory brain-stem responses and otoacoustic emissions using toneburst stimuli,” J. Acoust. Soc. Am. 83, 652–656. Neely, S.T. & Rasetshwane, D.M. (2017). “Modeling signal propagation in the human cochlea.” J. Acoust. Soc. Am. 142 (4), 2155-2167. Rasetshwane, D. M., Argenyi, M., Neely, S. T., Kopun, J. G., and Gorga, M.P. (2013a). “Relation of distortion-product otoacoustic emission input-output functions to loudness,” J Acoust. Soc. Am. 134(1), 369–383. Rasetshwane, D. M., Trevino, A.C., Gombert, J.N., Liebig-Trehearn, L., Kopun, J., Jesteadt, W., Neely, S. T., and Gorga, M.P. (2015). “Categorical loudness scaling and equal-loudness contours in listeners with normal hearing and hearing loss,” J Acoust. Soc. Am. 137(4), 1899–1913. Trevino. A.C, Jesteadt, W., and Neely, S.T. (2016). “Development of a multi-category psychometric function to model categorical loudness measurements.” J. Acoust. Soc. Am. 140(4), 2571–2583. • ABR wave V forward latency slope values were consistent with predictions made by Neely et al. (1988). • A mild but significant correlation was present between ABR wave V forward latency slope and CLS slope at 4 kHz. No significant correlations were present for wave V at 1 kHz. Results: Categorical Loudness Scaling Relating auditory brainstem response latency to loudness growth Figure 2. CLS growth functions. The mean (circles and squares) and standard deviation (error bars) of loudness expressed in CUs (upper panels) and phons (lower panels) at 1000 Hz (left) and 4000 Hz (right) are shown. Slopes of linear regressions of the mean data are included in the figure. Slope was calculated for the lower half of each CLS function. Figure 3. Comparison of ABR and CLS slopes. The symbols indicate the CLS lower slope (x axis) and log forward latency slope (y axis) for Wave I (upper panels, red) and Wave V (lower panels, blue) at 1000 Hz (left) and 4000 Hz (right) for each individual participant. The lines represent standard major axis regressions of the data in each panel. Pearson correlation coefficients and associated p-values are displayed in each quadrant. Subjects: Subjects included 20 adults (11 female, 9 male) with normal hearing (mean age = 30.85 years, SD = 8.89). All subjects had pure tone thresholds ≤ 20 dB HL in the test ear at 0.25, 0.5, 1, 2, 3, 4, 6, and 8 kHz, normal middle ear, and no air-bone gaps ≥ 15 dB at octave frequencies 0.25 – 4 kHz. Auditory Brainstem Response Measurements: ABR recordings were obtained across a series of levels (110 – 40 dB SPL) using 1 and 4 kHz toneburst stimuli. Stimuli were presented at a rate of 33/second. Stimulus duration at each frequency (! 0 ) was equal to 4/ ! 0 ms, and stimuli were windowed using a Blackman function. ABR peak latencies were scored and converted to forward latencies using a method based on Neely et al. (1988). Forward latency was defined as the portion of ABR wave latency that is level-dependent and that does not include the nearly constant delay introduced by neural conduction and synaptic transmission. ABR latency-intensity functions (ABR wave latency as a function of stimulus level) were generated for each subject, and slope coefficients were calculated based on linear regressions of the data. Categorical Loudness Scaling Measurements: CLS measurements were obtained using 1 and 4 kHz pure tone stimuli. Pure tones were 1000 ms in duration with a 20 ms rise/fall time. Stimuli were presented to the test ear at a variety of intensities. Subjects were asked to select one out of eleven loudness categories best corresponding to their perception of a given stimulus, with each category having an associated categorical unit (CU). CUs were converted to phons using values based on Rasetshwane et al. (2015). CLS loudness growth functions (loudness perception as a function of stimulus level) were generated for each subject from trial-by-trial responses using a maximum likelihood estimation method described by Trevino et al. (2016). Slope coefficients were obtained for the lower portion of each growth function. Figure 1. ABR latency-intensity functions. The mean (circles and squares) and standard deviation (error bars) of ABR latency (upper panels) and forward latency (lower panels) at 1000 Hz (left) and 4000 Hz (right) are shown. ABR Waves I (red) and V (blue) are superimposed. ABR forward latency was calculated for wave I by subtracting 1ms to account for synaptic delay. Forward latency for wave V was calculated by subtracting 1 ms to account for synaptic delay and 4 ms to account for neural conduction delay. Slopes of linear regressions of the mean data are included in the figure. Neely et al. (1988) estimated wave V forward latency slope as approximately equal to 1.6% per dB. • Results support the existence of a common underlying physiological mechanism between ABR latency level-dependence and loudness growth. • A lack of information in the literature made it difficult to predict the behavior of ABR wave I in Fig. 3. Further research is needed to explain the pattern of ABR-CLS correlation results for wave I in the present study. • These results are consistent with a model for cochlear compression introduced by Neely & Rasetshwane (2017), which proposes that the effect of neural adaptation on level- dependent latency changes is less for higher frequencies than lower frequencies.
Transcript of Introduction Results: Auditory Brainstem Response Results...
It is well-established that auditory brainstem response (ABR) latency decreases with increasing stimulus level (e.g. Gorga et al., 1988; Neely et al., 1988). However, the physiological mechanisms that underlie this phenomenon are not well-established. Our preferred interpretation is that the level-dependent component of ABR latency stems from cochlear mechanics (Neely et al., 1988).
Rasetshwane at el. (2013a) recently demonstrated significant correlations between distortion product otoacoustic emission (DPOAE) input-output functions and loudness growth as estimated using a categorical loudness scaling (CLS) procedure. Because DPOAEs are known to be a byproduct of cochlear amplifier gain, this correlation between the two measures suggests that cochlear mechanics may play a significant role in mediating loudness growth.
The goal of the present study was to examine the relationship between ABR latency changes with level and loudness growth. The presence of significant correlations between the two measures would support the existence of a common underlying mechanism, presumably cochlear response growth.
Laura D Mueldener1,2, Daniel M Rasetshwane1, Sara E Fultz1, Judy G Kopun1, Stephen T Neely1
Boys Town National Research Hospital1; University of Iowa2
This work was supported by the NIH-NIDCD grants T35 DC008757 and R01 DC008318 (STN). The authors would like to thank Carissa Allen for her assistance with data analysis.An electronic version of this poster may be viewed using the QR code to the right.
Introduction Results: Auditory Brainstem Response
Methods
Results: ABR and CLS Slope Comparisons
Conclusions
References & AcknowledgementsGorga, M. P., Kaminski, J. R., Beauchaine, K. A., and Jesteadt, W. (1988). “Auditory brainstem responses to tone bursts in normally hearing subjects,” J.
Speech Hear. Res. 31, 87–97.Neely, S. T., Norton, S. J., Gorga, M. P., and Jesteadt, W. (1988). “Latency of auditory brain-stem responses and otoacoustic emissions using toneburst stimuli,”
J. Acoust. Soc. Am. 83, 652–656.Neely, S.T. & Rasetshwane, D.M. (2017). “Modeling signal propagation in the human cochlea.” J. Acoust. Soc. Am. 142 (4), 2155-2167.Rasetshwane, D. M., Argenyi, M., Neely, S. T., Kopun, J. G., and Gorga, M.P. (2013a). “Relation of distortion-product otoacoustic emission input-output
functions to loudness,” J Acoust. Soc. Am. 134(1), 369–383. Rasetshwane, D. M., Trevino, A.C., Gombert, J.N., Liebig-Trehearn, L., Kopun, J., Jesteadt, W., Neely, S. T., and Gorga, M.P. (2015). “Categorical loudness scaling
and equal-loudness contours in listeners with normal hearing and hearing loss,” J Acoust. Soc. Am. 137(4), 1899–1913.Trevino. A.C, Jesteadt, W., and Neely, S.T. (2016). “Development of a multi-category psychometric function to model categorical loudness measurements.” J.
Acoust. Soc. Am. 140(4), 2571–2583.
• ABR wave V forward latency slope values were consistent with predictions made by Neely et al. (1988).
• A mild but significant correlation was present between ABR wave V forward latency slope and CLS slope at 4 kHz. No significant correlations were present for wave V at 1 kHz.
Results: Categorical Loudness Scaling
Relating auditory brainstem response latency to loudness growth
Figure 2. CLS growth functions. The mean (circles and squares) and standard deviation (error bars) of loudness expressed in CUs (upper panels) and phons (lower panels) at 1000 Hz (left) and 4000 Hz (right) are shown. Slopes of linear regressions of the mean data are included in the figure. Slope was calculated for the lower half of each CLS function.
Figure 3. Comparison of ABR and CLS slopes. The symbols indicate the CLS lower slope (x axis) and log forward latency slope (y axis) for Wave I (upper panels, red) and Wave V (lower panels, blue) at 1000 Hz (left) and 4000 Hz (right) for each individual participant. The lines represent standard major axis regressions of the data in each panel. Pearson correlation coefficients and associated p-values are displayed in each quadrant.
Subjects:Subjects included 20 adults (11 female, 9 male) with normal hearing (mean age = 30.85 years, SD = 8.89). All subjects had pure tone thresholds ≤ 20 dB HL in the test ear at 0.25, 0.5, 1, 2, 3, 4, 6, and 8 kHz, normal middle ear, and no air-bone gaps ≥ 15 dB at octave frequencies 0.25 – 4 kHz.
Auditory Brainstem Response Measurements:ABR recordings were obtained across a series of levels (110 – 40 dB SPL) using 1 and 4 kHz toneburst stimuli. Stimuli were presented at a rate of 33/second. Stimulus duration at each frequency (!0) wasequal to 4/ !0 ms, and stimuli were windowed using a Blackman function.
ABR peak latencies were scored and converted to forward latencies using a method based on Neely et al. (1988). Forward latency was defined as the portion of ABR wave latency that is level-dependent and that does not include the nearly constant delay introduced by neural conduction and synaptic transmission. ABR latency-intensity functions (ABR wave latency as a function of stimulus level) were generated for each subject, and slope coefficients were calculated based on linear regressions of the data.
Categorical Loudness Scaling Measurements:CLS measurements were obtained using 1 and 4 kHz pure tone stimuli. Pure tones were 1000 ms in duration with a 20 ms rise/fall time. Stimuli were presented to the test ear at a variety of intensities. Subjects were asked to select one out of eleven loudness categories best corresponding to their perception of a given stimulus, with each category having an associated categorical unit (CU).
CUs were converted to phons using values based on Rasetshwane et al. (2015). CLS loudness growth functions (loudness perception as a function of stimulus level) were generated for each subject from trial-by-trial responses using a maximum likelihood estimation method described by Trevino et al. (2016). Slope coefficients were obtained for the lower portion of each growth function.
Figure 1. ABR latency-intensity functions. The mean (circles and squares) and standard deviation (error bars) of ABR latency (upper panels) and forward latency (lower panels) at 1000 Hz (left) and 4000 Hz (right) are shown. ABR Waves I (red) and V (blue) are superimposed. ABR forward latency was calculated for wave I by subtracting 1ms to account for synaptic delay. Forward latency for wave V was calculated by subtracting 1 ms to account for synaptic delay and 4 ms to account for neural conduction delay. Slopes of linear regressions of the mean data are included in the figure. Neely et al. (1988) estimated wave V forward latency slope as approximately equal to 1.6% per dB.
• Results support the existence of a common underlying physiological mechanism between ABR latency level-dependence and loudness growth.
• A lack of information in the literature made it difficult to predict the behavior of ABR wave I in Fig. 3. Further research is needed to explain the pattern of ABR-CLS correlation results for wave I in the present study.
• These results are consistent with a model for cochlear compression introduced by Neely & Rasetshwane (2017), which proposes that the effect of neural adaptation on level-dependent latency changes is less for higher frequencies than lower frequencies.
