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Overshoot measured physiologically and psychophysically in the same human ears.

ABSTRACT: A nonlinear version of the stimulus-frequency otoacoustic emission (SFOAE) was measured using stimulus waveforms similar to those used for behavioral overshoot. Behaviorally, the seven listeners were as much as 11 dB worse at detecting a brief tonal signal (4.0 kHz, 10 ms in duration) when it occurred soon after the onset of a wideband masking noise (0.1-6.0 kHz; 400 ms in duration) than when it was delayed by about 200 ms, and the nonlinear SFOAE measure exhibited a similar effect. When either lowpass (0.1-3.8 kHz) or bandpass noise (3.8-4.2 kHz) was used instead of the wideband noise, the physiological and behavioral measures again were similar. When a highpass noise (4.2-6.0 kHz) was used, the physiological and behavioral measures both showed no overshoot-like effect for five of the subjects. The physiological response to the tone decayed slowly after the termination of the noise, much like the time course of resetting for behavioral overshoot. One subject exhibited no overshoot behaviorally even though his cochlear responses were like those of the other subjects. Overall, the evidence suggests that some basic characteristics of overshoot are obligatory consequences of cochlear function, as modulated by the olivocochlear efferent system.

SUBMITTER: Walsh KP

PROVIDER: S-EPMC2923227 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature

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Overshoot measured physiologically and psychophysically in the same human ears.

Walsh Kyle P KP Pasanen Edward G EG McFadden Dennis D

Hearing research 20100427 1-2

A nonlinear version of the stimulus-frequency otoacoustic emission (SFOAE) was measured using stimulus waveforms similar to those used for behavioral overshoot. Behaviorally, the seven listeners were as much as 11 dB worse at detecting a brief tonal signal (4.0 kHz, 10 ms in duration) when it occurred soon after the onset of a wideband masking noise (0.1-6.0 kHz; 400 ms in duration) than when it was delayed by about 200 ms, and the nonlinear SFOAE measure exhibited a similar effect. When either ...[more]

PMID: 20430072

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Project description:ObjectivesTo determine whether suprathreshold measures of auditory function, such as distortion-product otoacoustic emissions (DPOAEs) and auditory brainstem responses (ABRs), are correlated with noise exposure history in normal-hearing human ears. Recent data from animal studies have revealed significant deafferentation of auditory nerve fibers after full recovery from temporary noise-induced hearing loss. Furthermore, these data report smaller ABR wave I amplitudes in noise-exposed animal ears when compared with non-noise-exposed control animals or prenoise exposure amplitudes in the same animal. It is unknown whether a similar phenomenon exists in the normal-hearing, noise-exposed human ear.DesignThirty normal-hearing human subjects with a range of noise exposure backgrounds (NEBs) participated in this study. NEB was quantified by the use of a noise exposure questionnaire that extensively queried loud sound exposure during the previous 12 months. DPOAEs were collected at three f2s (1, 2, and 4 kHz) over a range of L2s. DPOAE stimulus level began at 80 dB forward-pressure level and decreased in 10 dB steps. Two-channel ABRs were collected in response to click stimuli and 4 kHz tone bursts; one channel used an ipsilateral mastoid electrode and the other an ipsilateral tympanic membrane electrode. ABR stimulus level began at 90 dB nHL and was decreased in 10 dB steps. Amplitudes of waves I and V of the ABR were analyzed.ResultsA statistically significant relationship between ABR wave I amplitude and NEB was found for clicked-evoked ABRs recorded at a stimulus level of 90 dB nHL using a mastoid recording electrode. For this condition, ABR wave I amplitudes decreased as a function of NEB. Similar systematic trends were present for ABRs collected in response to clicks and 4 kHz tone bursts at additional suprathreshold stimulation levels (≥70 dB nHL). The relationship weakened and disappeared with decreases in stimulation level (≤60 dB nHL). Similar patterns were present for ABRs collected using a tympanic membrane electrode. However, these relationships were not statistically significant and were weaker and more variable than those collected using a mastoid electrode. In contrast to the findings for ABR wave I, wave V amplitude was not significantly related to NEB. Furthermore, there was no evidence of a systematic relationship between suprathreshold DPOAEs and NEB.ConclusionsA systematic trend of smaller ABR wave I amplitudes was found in normal-hearing human ears with greater amounts of voluntary NEB in response to suprathreshold clicks and 4 kHz tone bursts. These findings are consistent with the data from previous work completed in animals, where the reduction in suprathreshold responses was a result of deafferentation of high-threshold/low-spontaneous rate auditory nerve fibers. These data suggest that a similar mechanism might be operating in human ears after exposure to high sound levels. However, evidence of this damage is only apparent when examining suprathreshold wave I amplitude of the ABR. In contrast, suprathreshold DPOAE level was not significantly related to NEB. This was expected, given noise-induced auditory damage findings in animal ears did not extend to the outer hair cells, the generator for the DPOAE response.

Project description:BACKGROUND: Propofol is widely used for both short-term anesthesia and long-term sedation. It has unusual pharmacokinetics because of its high lipid solubility. The standard approach to describing the pharmacokinetics is by a multi-compartmental model. This paper presents the first detailed human physiologically based pharmacokinetic (PBPK) model for propofol. METHODS: PKQuest, a freely distributed software routine http://www.pkquest.com, was used for all the calculations. The "standard human" PBPK parameters developed in previous applications is used. It is assumed that the blood and tissue binding is determined by simple partition into the tissue lipid, which is characterized by two previously determined set of parameters: 1) the value of the propofol oil/water partition coefficient; 2) the lipid fraction in the blood and tissues. The model was fit to the individual experimental data of Schnider et. al., Anesthesiology, 1998; 88:1170 in which an initial bolus dose was followed 60 minutes later by a one hour constant infusion. RESULTS: The PBPK model provides a good description of the experimental data over a large range of input dosage, subject age and fat fraction. Only one adjustable parameter (the liver clearance) is required to describe the constant infusion phase for each individual subject. In order to fit the bolus injection phase, for 10 or the 24 subjects it was necessary to assume that a fraction of the bolus dose was sequestered and then slowly released from the lungs (characterized by two additional parameters). The average weighted residual error (WRE) of the PBPK model fit to the both the bolus and infusion phases was 15%; similar to the WRE for just the constant infusion phase obtained by Schnider et. al. using a 6-parameter NONMEM compartmental model. CONCLUSION: A PBPK model using standard human parameters and a simple description of tissue binding provides a good description of human propofol kinetics. The major advantage of a PBPK model is that it can be used to predict the changes in kinetics produced by variations in physiological parameters. As one example, the model simulation of the changes in pharmacokinetics for morbidly obese subjects is discussed.

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Overshoot measured physiologically and psychophysically in the same human ears.

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Overshoot measured physiologically and psychophysically in the same human ears.

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