Publication date: Available online 14 February 2018
Source:Hearing Research
Author(s): Wilhelmina H.A.M. Mulders, Ian L. Chin, Donald Robertson
Noise exposures that result in fully reversible changes in cochlear neural threshold can cause a reduced neural output at supra-threshold sound intensity. This so-called “hidden hearing loss” has been shown to be associated with selective degeneration of high threshold afferent nerve fiber-inner hair cell (IHC) synapses. However, the electrophysiological function of the IHCs themselves in hidden hearing loss has not been directly investigated. We have made round window (RW) measurements of cochlear action potentials (CAP) and summating potentials (SP) after two levels of a 10 kHz acoustic trauma. The more intense acoustic trauma lead to notch-like permanent threshold changes and both CAP and SP showed reductions in supra-threshold amplitudes at frequencies with altered thresholds as well as from fully recovered regions. However, the interpretation of the results in normal threshold regions was complicated by the likelihood of reduced contributions from adjacent regions with elevated thresholds. The milder trauma showed full recovery of all neural thresholds, but there was a persistent depression of the amplitudes of both CAP and SP in response to supra-threshold sounds. The effect on SP amplitude in particular shows that occult damage to hair cell transduction mechanisms can contribute to hidden hearing loss. Such damage could potentially affect the supra-threshold output properties of surviving primary afferent neurons.
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Τετάρτη 14 Φεβρουαρίου 2018
Simulated auditory nerve axon demyelination alters sensitivity and response timing to extracellular stimulation
Publication date: Available online 14 February 2018
Source:Hearing Research
Author(s): Jesse M. Resnick, Gabrielle O'Brien, Jay T. Rubinstein
Since cochlear implant function involves direct depolarization of spiral ganglion neurons (SGNs) by applied current, SGN physiological health must be an important factor in cochlear implant (CI) outcomes. This expected relationship has, however, been difficult to confirm in implant recipients. Suggestively, animal studies have demonstrated both acute and progressive SGN ultrastructural changes (notably axon demyelination), even in the absence of soma death, and corresponding altered physiology following sensorineural deafening. Whether such demyelination occurs in humans and how such changes might impact CI function remains unknown. To approach this problem, we incorporated SGN demyelination into a biophysical model of extracellular stimulation of SGN fibers. Our approach enabled exploration of the entire parameter space corresponding to simulated myelin diameter and extent of fiber affected. All simulated fibers were stimulated distally with anodic monophasic, cathodic monophasic, anode-phase-first (AF) biphasic, and cathode-phase-first (CF) biphasic pulses from an extracellular disc electrode and monitored for spikes centrally. Not surprisingly, axon sensitivity generally decreased with demyelination, resulting in elevated thresholds, however, this effect was strongly non-uniform. Fibers with severe demyelination affecting only the most peripheral nodes responded nearly identically to normally myelinated fibers. Additionally, partial demyelination (<50%) yielded only minimal increases in threshold even when the entire fiber was impacted. The temporal effects of demyelination were more unexpected. Both latency and jitter of responses demonstrated resilience to modest changes but exhibited strongly non-monotonic and stimulus-dependent relationships to more profound demyelination. Normal, and modestly demyelinated fibers, were more sensitive to cathodic than anodic monophasic pulses and to CF than AF biphasic pulses, however, when demyelination was more severe these relative sensitivities were reversed. Comparison of threshold crossing between nodal segments demonstrated stimulus-dependent shifts in action potential initiation with different fiber demyelination states. For some demyelination scenarios, both phases of biphasic pulses could initiate action potentials at threshold resulting in bimodal latency and initiation site distributions and dramatically increased jitter. In short, simulated demyelination leads to complex changes in fiber sensitivity and spike timing, mediated by alterations in action potential initiation site and slowed action potential conduction due to non-uniformities in the electrical properties of axons. Such demyelination-induced changes, if present in implantees, would have profound implications for the detection of fine temporal cues but not disrupt cues on the time scale of speech envelopes. These simulation results highlight the importance of exploring the SGN ultrastructural changes caused by a given etiology of hearing loss to more accurately predict cochlear implantation outcomes.
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Source:Hearing Research
Author(s): Jesse M. Resnick, Gabrielle O'Brien, Jay T. Rubinstein
Since cochlear implant function involves direct depolarization of spiral ganglion neurons (SGNs) by applied current, SGN physiological health must be an important factor in cochlear implant (CI) outcomes. This expected relationship has, however, been difficult to confirm in implant recipients. Suggestively, animal studies have demonstrated both acute and progressive SGN ultrastructural changes (notably axon demyelination), even in the absence of soma death, and corresponding altered physiology following sensorineural deafening. Whether such demyelination occurs in humans and how such changes might impact CI function remains unknown. To approach this problem, we incorporated SGN demyelination into a biophysical model of extracellular stimulation of SGN fibers. Our approach enabled exploration of the entire parameter space corresponding to simulated myelin diameter and extent of fiber affected. All simulated fibers were stimulated distally with anodic monophasic, cathodic monophasic, anode-phase-first (AF) biphasic, and cathode-phase-first (CF) biphasic pulses from an extracellular disc electrode and monitored for spikes centrally. Not surprisingly, axon sensitivity generally decreased with demyelination, resulting in elevated thresholds, however, this effect was strongly non-uniform. Fibers with severe demyelination affecting only the most peripheral nodes responded nearly identically to normally myelinated fibers. Additionally, partial demyelination (<50%) yielded only minimal increases in threshold even when the entire fiber was impacted. The temporal effects of demyelination were more unexpected. Both latency and jitter of responses demonstrated resilience to modest changes but exhibited strongly non-monotonic and stimulus-dependent relationships to more profound demyelination. Normal, and modestly demyelinated fibers, were more sensitive to cathodic than anodic monophasic pulses and to CF than AF biphasic pulses, however, when demyelination was more severe these relative sensitivities were reversed. Comparison of threshold crossing between nodal segments demonstrated stimulus-dependent shifts in action potential initiation with different fiber demyelination states. For some demyelination scenarios, both phases of biphasic pulses could initiate action potentials at threshold resulting in bimodal latency and initiation site distributions and dramatically increased jitter. In short, simulated demyelination leads to complex changes in fiber sensitivity and spike timing, mediated by alterations in action potential initiation site and slowed action potential conduction due to non-uniformities in the electrical properties of axons. Such demyelination-induced changes, if present in implantees, would have profound implications for the detection of fine temporal cues but not disrupt cues on the time scale of speech envelopes. These simulation results highlight the importance of exploring the SGN ultrastructural changes caused by a given etiology of hearing loss to more accurately predict cochlear implantation outcomes.
Graphical abstract
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Persistent hair cell malfunction contributes to hidden hearing loss
Publication date: Available online 14 February 2018
Source:Hearing Research
Author(s): Wilhelmina H.A.M. Mulders, Ian L. Chin, Donald Robertson
Noise exposures that result in fully reversible changes in cochlear neural threshold can cause a reduced neural output at supra-threshold sound intensity. This so-called “hidden hearing loss” has been shown to be associated with selective degeneration of high threshold afferent nerve fiber-inner hair cell (IHC) synapses. However, the electrophysiological function of the IHCs themselves in hidden hearing loss has not been directly investigated. We have made round window (RW) measurements of cochlear action potentials (CAP) and summating potentials (SP) after two levels of a 10 kHz acoustic trauma. The more intense acoustic trauma lead to notch-like permanent threshold changes and both CAP and SP showed reductions in supra-threshold amplitudes at frequencies with altered thresholds as well as from fully recovered regions. However, the interpretation of the results in normal threshold regions was complicated by the likelihood of reduced contributions from adjacent regions with elevated thresholds. The milder trauma showed full recovery of all neural thresholds, but there was a persistent depression of the amplitudes of both CAP and SP in response to supra-threshold sounds. The effect on SP amplitude in particular shows that occult damage to hair cell transduction mechanisms can contribute to hidden hearing loss. Such damage could potentially affect the supra-threshold output properties of surviving primary afferent neurons.
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Source:Hearing Research
Author(s): Wilhelmina H.A.M. Mulders, Ian L. Chin, Donald Robertson
Noise exposures that result in fully reversible changes in cochlear neural threshold can cause a reduced neural output at supra-threshold sound intensity. This so-called “hidden hearing loss” has been shown to be associated with selective degeneration of high threshold afferent nerve fiber-inner hair cell (IHC) synapses. However, the electrophysiological function of the IHCs themselves in hidden hearing loss has not been directly investigated. We have made round window (RW) measurements of cochlear action potentials (CAP) and summating potentials (SP) after two levels of a 10 kHz acoustic trauma. The more intense acoustic trauma lead to notch-like permanent threshold changes and both CAP and SP showed reductions in supra-threshold amplitudes at frequencies with altered thresholds as well as from fully recovered regions. However, the interpretation of the results in normal threshold regions was complicated by the likelihood of reduced contributions from adjacent regions with elevated thresholds. The milder trauma showed full recovery of all neural thresholds, but there was a persistent depression of the amplitudes of both CAP and SP in response to supra-threshold sounds. The effect on SP amplitude in particular shows that occult damage to hair cell transduction mechanisms can contribute to hidden hearing loss. Such damage could potentially affect the supra-threshold output properties of surviving primary afferent neurons.
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Simulated auditory nerve axon demyelination alters sensitivity and response timing to extracellular stimulation
Publication date: Available online 14 February 2018
Source:Hearing Research
Author(s): Jesse M. Resnick, Gabrielle O'Brien, Jay T. Rubinstein
Since cochlear implant function involves direct depolarization of spiral ganglion neurons (SGNs) by applied current, SGN physiological health must be an important factor in cochlear implant (CI) outcomes. This expected relationship has, however, been difficult to confirm in implant recipients. Suggestively, animal studies have demonstrated both acute and progressive SGN ultrastructural changes (notably axon demyelination), even in the absence of soma death, and corresponding altered physiology following sensorineural deafening. Whether such demyelination occurs in humans and how such changes might impact CI function remains unknown. To approach this problem, we incorporated SGN demyelination into a biophysical model of extracellular stimulation of SGN fibers. Our approach enabled exploration of the entire parameter space corresponding to simulated myelin diameter and extent of fiber affected. All simulated fibers were stimulated distally with anodic monophasic, cathodic monophasic, anode-phase-first (AF) biphasic, and cathode-phase-first (CF) biphasic pulses from an extracellular disc electrode and monitored for spikes centrally. Not surprisingly, axon sensitivity generally decreased with demyelination, resulting in elevated thresholds, however, this effect was strongly non-uniform. Fibers with severe demyelination affecting only the most peripheral nodes responded nearly identically to normally myelinated fibers. Additionally, partial demyelination (<50%) yielded only minimal increases in threshold even when the entire fiber was impacted. The temporal effects of demyelination were more unexpected. Both latency and jitter of responses demonstrated resilience to modest changes but exhibited strongly non-monotonic and stimulus-dependent relationships to more profound demyelination. Normal, and modestly demyelinated fibers, were more sensitive to cathodic than anodic monophasic pulses and to CF than AF biphasic pulses, however, when demyelination was more severe these relative sensitivities were reversed. Comparison of threshold crossing between nodal segments demonstrated stimulus-dependent shifts in action potential initiation with different fiber demyelination states. For some demyelination scenarios, both phases of biphasic pulses could initiate action potentials at threshold resulting in bimodal latency and initiation site distributions and dramatically increased jitter. In short, simulated demyelination leads to complex changes in fiber sensitivity and spike timing, mediated by alterations in action potential initiation site and slowed action potential conduction due to non-uniformities in the electrical properties of axons. Such demyelination-induced changes, if present in implantees, would have profound implications for the detection of fine temporal cues but not disrupt cues on the time scale of speech envelopes. These simulation results highlight the importance of exploring the SGN ultrastructural changes caused by a given etiology of hearing loss to more accurately predict cochlear implantation outcomes.
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Source:Hearing Research
Author(s): Jesse M. Resnick, Gabrielle O'Brien, Jay T. Rubinstein
Since cochlear implant function involves direct depolarization of spiral ganglion neurons (SGNs) by applied current, SGN physiological health must be an important factor in cochlear implant (CI) outcomes. This expected relationship has, however, been difficult to confirm in implant recipients. Suggestively, animal studies have demonstrated both acute and progressive SGN ultrastructural changes (notably axon demyelination), even in the absence of soma death, and corresponding altered physiology following sensorineural deafening. Whether such demyelination occurs in humans and how such changes might impact CI function remains unknown. To approach this problem, we incorporated SGN demyelination into a biophysical model of extracellular stimulation of SGN fibers. Our approach enabled exploration of the entire parameter space corresponding to simulated myelin diameter and extent of fiber affected. All simulated fibers were stimulated distally with anodic monophasic, cathodic monophasic, anode-phase-first (AF) biphasic, and cathode-phase-first (CF) biphasic pulses from an extracellular disc electrode and monitored for spikes centrally. Not surprisingly, axon sensitivity generally decreased with demyelination, resulting in elevated thresholds, however, this effect was strongly non-uniform. Fibers with severe demyelination affecting only the most peripheral nodes responded nearly identically to normally myelinated fibers. Additionally, partial demyelination (<50%) yielded only minimal increases in threshold even when the entire fiber was impacted. The temporal effects of demyelination were more unexpected. Both latency and jitter of responses demonstrated resilience to modest changes but exhibited strongly non-monotonic and stimulus-dependent relationships to more profound demyelination. Normal, and modestly demyelinated fibers, were more sensitive to cathodic than anodic monophasic pulses and to CF than AF biphasic pulses, however, when demyelination was more severe these relative sensitivities were reversed. Comparison of threshold crossing between nodal segments demonstrated stimulus-dependent shifts in action potential initiation with different fiber demyelination states. For some demyelination scenarios, both phases of biphasic pulses could initiate action potentials at threshold resulting in bimodal latency and initiation site distributions and dramatically increased jitter. In short, simulated demyelination leads to complex changes in fiber sensitivity and spike timing, mediated by alterations in action potential initiation site and slowed action potential conduction due to non-uniformities in the electrical properties of axons. Such demyelination-induced changes, if present in implantees, would have profound implications for the detection of fine temporal cues but not disrupt cues on the time scale of speech envelopes. These simulation results highlight the importance of exploring the SGN ultrastructural changes caused by a given etiology of hearing loss to more accurately predict cochlear implantation outcomes.
Graphical abstract
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Detection of Arytenoid Dislocation Using Pixel-valued Cuneiform Movement
Publication date: Available online 13 February 2018
Source:Journal of Voice
Author(s): Ashley P. O'Connell Ferster, Michael C. Ferster, Haley Glatthorn, Bartholomew J. Bacak, Robert T. Sataloff
ObjectivesThis study aims to assess utility of pixel-valued movement software in detecting arytenoid dislocation preoperatively.Study DesignThis is a retrospective analysis.MethodsTwenty-seven patients diagnosed with unilateral arytenoid dislocation were included. Diagnosis of arytenoid dislocation was confirmed by lack of vocal fold paralysis on preoperative laryngeal electromyography and by intraoperative findings of cricoarytenoid dislocation. A region-tracking software algorithm developed by Zhuang et al was used to analyze 27 preoperative endoscopic videos of patients diagnosed with arytenoid dislocation. Vector analysis measuring cuneiform movement during inspiration was used as an indirect measure of arytenoid movement. Values were normalized using vocal fold length. Two raters blinded to diagnosis of arytenoid dislocation measured vocal fold length and cuneiform movement on both the dislocated and the nondislocated sides.ResultsA Wilcoxon signed-rank test indicated that the mean pixel-valued cuneiform movement and standard deviation (SD) were greater for nondislocated (159.24, SD = 73.35) than for dislocated (92.49, SD = 72.11) arytenoids (Z = 3.29, P = 0.001). The interrater correlation coefficient was 0.87 for the dislocated side and 0.75 for the nondislocated side. The intrarater correlation coefficient was 0.87 for the dislocated side and 0.91 for the nondislocated side. The receiver operating characteristic curve revealed an area under the curve between 0.76 and 0.83 (95% confidence interval 0.63–0.90). Analysis by the first and second raters revealed misdiagnosis of laterality of arytenoid dislocation in four and six patients, respectively.ConclusionsThe software program developed by Zhuang et al provides a high-degree of precision, with good interrater and intrarater correlation coefficients. However, high rates of misdiagnosis of arytenoid dislocation and the laborious analysis process using this software program make it of limited utility as a clinical diagnostic tool in its present state.
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Source:Journal of Voice
Author(s): Ashley P. O'Connell Ferster, Michael C. Ferster, Haley Glatthorn, Bartholomew J. Bacak, Robert T. Sataloff
ObjectivesThis study aims to assess utility of pixel-valued movement software in detecting arytenoid dislocation preoperatively.Study DesignThis is a retrospective analysis.MethodsTwenty-seven patients diagnosed with unilateral arytenoid dislocation were included. Diagnosis of arytenoid dislocation was confirmed by lack of vocal fold paralysis on preoperative laryngeal electromyography and by intraoperative findings of cricoarytenoid dislocation. A region-tracking software algorithm developed by Zhuang et al was used to analyze 27 preoperative endoscopic videos of patients diagnosed with arytenoid dislocation. Vector analysis measuring cuneiform movement during inspiration was used as an indirect measure of arytenoid movement. Values were normalized using vocal fold length. Two raters blinded to diagnosis of arytenoid dislocation measured vocal fold length and cuneiform movement on both the dislocated and the nondislocated sides.ResultsA Wilcoxon signed-rank test indicated that the mean pixel-valued cuneiform movement and standard deviation (SD) were greater for nondislocated (159.24, SD = 73.35) than for dislocated (92.49, SD = 72.11) arytenoids (Z = 3.29, P = 0.001). The interrater correlation coefficient was 0.87 for the dislocated side and 0.75 for the nondislocated side. The intrarater correlation coefficient was 0.87 for the dislocated side and 0.91 for the nondislocated side. The receiver operating characteristic curve revealed an area under the curve between 0.76 and 0.83 (95% confidence interval 0.63–0.90). Analysis by the first and second raters revealed misdiagnosis of laterality of arytenoid dislocation in four and six patients, respectively.ConclusionsThe software program developed by Zhuang et al provides a high-degree of precision, with good interrater and intrarater correlation coefficients. However, high rates of misdiagnosis of arytenoid dislocation and the laborious analysis process using this software program make it of limited utility as a clinical diagnostic tool in its present state.
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Comparing the Exposure-Response Relationships of Physiological and Traditional Vocal Warm-ups on Aerodynamic and Acoustic Parameters in Untrained Singers
Publication date: Available online 13 February 2018
Source:Journal of Voice
Author(s): Jing Kang, Chao Xue, Adriana Chou, Austin Scholp, Ting Gong, Yi Zhang, Zhen Chen, Jack J. Jiang
ObjectivesThe aim of this study was to quantify the effects of traditional and physiological warm-up exercises and to determine the optimal duration of these methods using acoustic and aerodynamic metrics.MethodsTwenty-six subjects were recruited to participate in both straw phonation exercises (physiological vocal warm-up) and traditional singing exercises (traditional vocal warm-up) for 20 minutes each, 24 hours apart. Phonation threshold pressure (PTP), fundamental frequency, jitter, shimmer, and noise-to-harmonics ratio were measured before the intervention (m0), as well as after 5 minutes (m5), 10 minutes (m10), 15 minutes (m15), and 20 minutes (m20) of intervention.ResultsPTP decreased significantly after straw phonation and reached a minimum value at 10 minutes (P < 0.001) and remained stable in traditional singing exercises. There were significant differences in fundamental frequency and shimmer from m0 to m15 and m20 in the traditional singing group (P = 0.001, P = 0.001, P = 0.001, and P = 0.002, respectively). No significant changes in acoustic parameters were observed after straw phonation.ConclusionsBoth straw phonation exercises and traditional singing exercises are effective for voice warm-up. Straw phonation improves the subjects' fatigue resistance and vocal economy, resulting in a reduced PTP, whereas traditional singing exercises focus on technical singing skills, leading to an improvement of acoustic variables.
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Source:Journal of Voice
Author(s): Jing Kang, Chao Xue, Adriana Chou, Austin Scholp, Ting Gong, Yi Zhang, Zhen Chen, Jack J. Jiang
ObjectivesThe aim of this study was to quantify the effects of traditional and physiological warm-up exercises and to determine the optimal duration of these methods using acoustic and aerodynamic metrics.MethodsTwenty-six subjects were recruited to participate in both straw phonation exercises (physiological vocal warm-up) and traditional singing exercises (traditional vocal warm-up) for 20 minutes each, 24 hours apart. Phonation threshold pressure (PTP), fundamental frequency, jitter, shimmer, and noise-to-harmonics ratio were measured before the intervention (m0), as well as after 5 minutes (m5), 10 minutes (m10), 15 minutes (m15), and 20 minutes (m20) of intervention.ResultsPTP decreased significantly after straw phonation and reached a minimum value at 10 minutes (P < 0.001) and remained stable in traditional singing exercises. There were significant differences in fundamental frequency and shimmer from m0 to m15 and m20 in the traditional singing group (P = 0.001, P = 0.001, P = 0.001, and P = 0.002, respectively). No significant changes in acoustic parameters were observed after straw phonation.ConclusionsBoth straw phonation exercises and traditional singing exercises are effective for voice warm-up. Straw phonation improves the subjects' fatigue resistance and vocal economy, resulting in a reduced PTP, whereas traditional singing exercises focus on technical singing skills, leading to an improvement of acoustic variables.
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Adjustment of the Vocal Tract Shape via Biofeedback: A Case Study
Publication date: Available online 14 February 2018
Source:Journal of Voice
Author(s): Patrick Hoyer, Simone Graf
In this study, an adjustment of the vocal tract shape toward selected sound waves in the frequency range of the first and second formants without phonation is discussed. The sound waves of a loudspeaker in front of the open mouth and amplified by the vocal tract are used as biofeedback signals. It is shown that the resonance amplification of the vocal tract complies with the concept of forced oscillation, with the driver being the sound source and the resonator being the vocal tract. An adjustment toward increased amplification via vocal tract resonance can be related to smaller bandwidths and lower damping. Furthermore, the applied adjustment frequencies are preserved as vocal tract resonances during exhalation and even phonation. This novel form of biofeedback might enrich standard voice training procedures by exercises without phonation.
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Source:Journal of Voice
Author(s): Patrick Hoyer, Simone Graf
In this study, an adjustment of the vocal tract shape toward selected sound waves in the frequency range of the first and second formants without phonation is discussed. The sound waves of a loudspeaker in front of the open mouth and amplified by the vocal tract are used as biofeedback signals. It is shown that the resonance amplification of the vocal tract complies with the concept of forced oscillation, with the driver being the sound source and the resonator being the vocal tract. An adjustment toward increased amplification via vocal tract resonance can be related to smaller bandwidths and lower damping. Furthermore, the applied adjustment frequencies are preserved as vocal tract resonances during exhalation and even phonation. This novel form of biofeedback might enrich standard voice training procedures by exercises without phonation.
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