Roland Duclaux

Effect of contralateral auditory stimuli on active cochlear micro-mechanical properties in human subjects.

The present study investigates the possibility that contralateral auditory stimulation along medial efferent system pathways may alter active cochlear micromechanics and hence affect evoked oto-acoustic emissions in humans. A first experiment, involving 21 healthy subjects showed reduction of oto-acoustic emission amplitude under low intensity contralateral white noise (from 30 dB SPL, 10 dB SL, upwards). The effect is found for intensities below the acoustic reflex threshold (85.2 dB HL). A second experiment, involving 10 of the above 21 subjects, sought to rule out any technical artefact. Recording was again carried out, but after sealing of the contralateral ear with a silicon putty plug. No contralateral intensity effect on oto-acoustic emission amplitude was found for contralateral intensities below 65 dB SPL. In subjective perception terms (dB SL) an effect was found under sealing when the sound reached or passed above the 10 dB SL level. These two findings confirm the preceding experiment. The third experiment investigated the role of transcranial transmission of the contralateral auditory stimulus. 16 subjects having total unilateral deafness and one healthy ear were tested by the same procedure as above. No fall-off in oto-acoustic emission amplitude was found for contralateral stimuli equal to or less than 80 dB SPL. There is thus a contralateral auditory stimulus effect on active cochlear micromechanics. The most appropriate explanation involves the medial cochlear efferent system, excited at brainstem level via the afferent auditory pathways. Alteration of active cochlear micromechanics seems promising at a basic level, pointing, as it does, to an interactive cochlear functioning which can be investigated by simple, non-intrusive, objective techniques which can be used with human subjects. We have here a model for functional exploration of the medial olivocochlear efferent system.

Vestibular Evoked Myogenic Potentials in Humans: a Review

The human vestibule has preserved an ancestral sound sensitivity and it has been suggested that a reflex could originate from this property, thus inducing cervical muscle microcontractions secondary to strong acoustic stimulations. This reflex is assumed to originate in the saccule, the afferent pathways being either the vestibulocochlear nerve or the inferior vestibular nerve, and the efferent pathways the vestibulospinal tract. Averaging these muscular responses allows vestibular evoked myogenic potentials (VEMPs) to be obtained. The responses consist of two alternatively positive and negative successive waves (p13-n23, p33-n43). The characteristics of this reflex are defined in the literature as follows: it has been established that VEMP amplitude depends on muscular tension. All studies give concording evidence that in healthy subjects the first component of VEMP is more consistent than the second. Binaural stimulation is always responsible for responses of greater amplitude than those obtained from monaural stimulation. Following monaural stimulation, however, VEMPs are either of greater amplitude on the muscle ipsilateral to the stimulation or of the same amplitude on both muscles. There is consensus in the literature demonstrating that VEMP amplitude depends on stimulus intensity: the threshold of VEMP occurrence is clearly above auditory level but varies from one individual to the next. In the 1970s, recordings performed in cases of specific audiovestibular defects suggested that the reflex receptor could be the saccule. More recent studies suggest that the cochlea too could be involved in the response. Likewise, while a number of studies tend to demonstrate that VEMPs depend on vestibular integrity, others suggest that afferent pathways could be of both cohlear and vestibular origin. Finally, while it has been suggested that VEMP efferent pathways travel through the vestibulospinal tract, whether it is the lateral or the medial vestibulospinal tract that is concerned remains to be clarified. A few points regarding VEMP receptors and afferent and efferent pathways call for further investigation. They are inaccurate for use in routine vestibular examination. Once precise receptor localization and pathways are clarified, VEMP recording will provide both a straightforward non-invasive exploration of each vestibule independently and an attractive method by which to explore otolithic receptors and vestibulospinal pathways.

Myogenic Vestibular-Evoked Potentials in Normal Subjects: A Comparison Between Responses Obtained from Sternomastoid and Trapezius Muscles

Brief intense clicks cause short latency microcontraction of cervical muscles. Several studies have supported the hypothesis that these microcontractions are of vestibular origin. Averaging these muscular responses enables us to obtain myogenic vestibular evoked potential (MVEP). The receptor of these responses is thought to be the saccule, afferent pathways being the vestibular nerve and efferent pathways the vestibulospinal tract. However, discrepancies are reported with regard to results obtained in healthy subjects: some authors obtained symmetrical response to monaural clicks whereas others obtained responses of greater amplitude on the muscle ispilateral to stimulation. These discrepancies may be due to the presence of different recording sites (inion, sternomastoid or trapezius muscles). The aim of this study was to clarify MVEP results in healthy subjects, using a simple non-traumatic method, and to compare the results obtained on sternomastoid (SM) and trapezius muscles (TRP). Sixteen normal hearing healthy subjects were involved. Latencies and amplitude of both SM and TRP muscle were reproducible in the same subject. Patterns of response were similar to those obtained in previous studies. Following binaural and monaural stimulations, latencies of MVEP were symmetrical on both muscles and amplitudes tended to be greater on muscles contralateral to stimulation, which conflicts with previous results in the literature. Whatever the type of stimulation, latencies of responses obtained on SM were significantly shorter (mean = -3.8 ms), and amplitudes lower (mean = -7.1 microV), than those obtained on TRP. Binaural stimulation resulted in responses of greater amplitude compared to monaural (mean = 0.45 microV). Given the intrasubject reproducibility of the responses, these methods allow MEVP to be recorded in a standardized and reproducible way.

Development of cochlear active mechanisms in humans differs between gender

Despite onset of function early during the third term of gestation, the human auditory system demonstrates continued maturation, thought previously to occur primarily at the neural level. The electromotile properties of outer hair cells appear to contribute substantially to hearing sensitivity and frequency selectivity and lead to the generation of otoacoustic emissions (OAEs). This report demonstrates continued development of cochlear active mechanisms (i.e. end-organ level) after onset of cochlear function, as reflected by OAEs. Significant gender differences also are reported, corresponding to recently observed intersex differences in cochlear length and precursory to gender differences observed in the adult.

Hemispheric asymmetry of late auditory evoked response induced by pitch changes in infants: influence of sleep stages

Late auditory evoked potentials (LAEPs) have been recorded in response to a 1000 Hz standard (occurrence 80%) or a 2000 Hz deviant (occurrence 20%) tone on the left (T3) and right (T4) temporal scalp in 6-week-old full-term newborns during pure quiet or active sleep states. Sleep states were premanently controlled by polygraphic recording including EEG, EOG, EMG, EKG and respiratory movements. During quiet sleep LAEPs consisted of a clear polygraphic response: N1-P2-N2-P3. Mean latencies ranges on T3 and T4 were: N1 = 28-70 ms; P2 = 343-407 ms; N2 = 966-1178 ms; and P3 = 1461-1492 ms. During active sleep LAEPs consisted of a N1-P2-N2 response. Mean latency ranges on T3 and T4 were: N1 = 36-79 ms; P2 = 278-304 ms; N2 = 555-620 ms. N2 latency was significantly shorter in AS than in QS. Amplitude of the N1-P2-N2 complex was significantly lower during active sleep. In response to standard stimuli, mean amplitudes and latencies of the LAEP were similar on T3 and T4 during active or quiet sleep states. In response to deviant stimuli mean amplitude of the N1-P2-N2 complex was significantly higher and mean latencies of N1 and N2 were significantly shorter on T3 during quiet sleep. No significant difference was observed during active sleep. These results confirm that sleep stages have a considerable influence on cortical auditory pathways. The auditory message is amplified during quiet sleep and inhibited during active sleep. Therefore sleep states need to be controlled to analyze LAEPs in young children.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of hyperthermia on cochlear micromechanical properties in humans

We investigated the effect of body temperature on transient evoked otoacoustic emissions (TEOAEs) in humans. Hyperthermic conditions were obtained in adults in a climatic chamber. During hyperthermia up to an average temperature of 38.4 degrees C, significant falls were found in total amplitude and peak values of TEOAEs: by 1.3 dB SPL/degree C and 2.3 dB/degree C, respectively. This inhibition affected all spectrum components equally. These findings indicate that the outer hair cell micromechanical activity that is presumed to be measured by TEOAEs is not independent of variations in body temperature. The reduction found in hyperthermia suggests that temperature-dependent mechanisms are involved in the generation of TEOAEs.

Cochleovestibular Afferent Pathways of Trapezius Muscle Responses to Clicks in Human

Brief intense clicks cause short-latency cervical muscles microcontractions which are supposed to be of vestibular origin. Averaging these microcontractions allows myogenic vestibular evoked potentials (MVEP) to be obtained. MVEP from the trapezius muscles were investigated in normal subjects, cochleovestibular nerve-damaged patients and patients with a vestibular or a cochlear lesion. Muscular responses were recorded on right and left trapezius by averaging from surface electrodes following right and left monaural 100 dB hearing level click stimulation. In normal subjects, responses to monaural stimuli were bilateral, of equal amplitude and latency in left and right trapezia. Normal response consisted of four consecutive waves, labelled p13, n23, p32 and n40 according to their polarity (p, positive; n, negative) and mean peak latency in msec. In total unilateral cochleovestibular damaged patients, auditory stimulation of the affected side gave no MVEP either ipsilateral or contralateral to the stimulation. In the case of selective cochlear lesion, stimulation of the affected side gave MVEP which was present on ipsilateral and contralateral trapezius muscles. The four successive waves were present with a normal latency; however, amplitude was lower than that obtained after stimulation of the healthy ear. In the case of selective vestibular lesion, the four waves of MVEP were again present with normal latency but with reduced amplitude. Responses were present on both the ipsilateral and contralateral trapezius muscle. It is concluded that normal MVEP recorded on the trapezius muscles are bilateral and consist of four waves, the amplitude of which could depend on the simultaneous stimulation of both cochlear and vestibular afferents. In the case of unilateral cochlear and/or vestibular impairments responses were present on both ipsilateral and contralateral trapezius muscles. Latencies had normal values but amplitudes were reduced. MEVP recorded on trapezius muscles were absent in the case of total cochleovestibular damage.

Effect of anesthesia on transient evoked otoacoustic emissions in humans: a comparison between propofol and isoflurane

The influence of general anesthesia (GA) on auditory brainstem responses (ABRs) has been widely studied in humans whereas few studies have been devoted as yet to its effect on cochlear micromechanical properties. This study was aimed at evaluating: (1) the effect of GA on transient evoked otoacoustic emissions (TEOAEs) in humans (n=10), and (2) to compare the effects induced by two different anesthetic agents: propofol (n=5) and isoflurane (n=5). The TEOAEs were continuously monitored together with hemodynamic patterns describing various measures of blood pressure. (1) The GA induced a decrease in TEOAE amplitude and TEOAE amplitude was significantly correlated with the hemodynamic patterns. (2) Both anesthetic agents were responsible for a decrease in TEOAE during the first 20 min of recording. Under propofol, TEOAE amplitude increased after 20 min whereas under isoflurane TEOAEs continued to decrease. Under propofol, TEOAE amplitude was correlated with blood pressure changes in a highly significant manner, whereas under isoflurane TEOAE levels were completely independent of such hemodynamic patterns. These results infer that (1) the GA induced a decrease in TEOAE amplitude, and that (2) TEOAE changes induced by propofol could depend on the concomitant hemodynamic changes whereas isoflurane could be responsible for TEOAE changes depending on both, hemodynamic changes and its own pharmacological properties.

Sympathetic nerve regulation of cochlear blood flow during increases in blood pressure in humans.

Abstract The purpose of this work was to show that regulation of the blood flow to the cochlea by the sympathetic nervous system occurs in humans at the level of the cochlear microcirculation during increases in blood pressure and that its involvement depends on the pressure level. Eight anaesthetized patients undergoing tympanoplasty for hearing disease took part in a pharmacological protocol of stimulation and inhibition of the autonomic nervous system (ANS) to provide variations in systolic blood pressure (BPS) and cochlear blood flow (CBF). The CBF was measured by laser-Doppler flowmetry. Changes in autonomic nerve activity were brought about by changes in baroreceptor activity (BR) initiated by the injection of an α adrenergic agent before and after sympathetic and parasympathetic blockade. The CBF variations (δCBF) were plotted against BPS increases at each stage of the ANS inhibition. The BR diminished significantly after α blockade, after α and β blockade, and after α and β blockade and atropine, by 50% (P < 0.01), 29% (P < 0.05), and 95% (P < 0.001) respectively. The BPS increased significantly (P < 0.01) by 36 (SD 9)%, 47 (SD 1)%, and 67 (SD 16)% respectively. The CBF response to an increase in BPS exhibited two opposing variations in the patients: CBF decreased significantly in one group, and increased significantly in the other group. In both groups, δCBF decrease and δCBF increase, respectively, were significant after ANS blockade; even so the decrease and increase, respectively, levelled off at BPS around 160 mmHg before ANS blockade. For BPS below 160 mmHg, correlations between δCBF and BPS were significant before inhibition and after inhibition of ANS. For BPS above 160 mmHg, BPS and δCBF were not correlated before inhibition of ANS, and were significantly correlated after inhibition of ANS. For BPS below 160 mmHg, CBF response to the BPS increase was the same before and after ANS blockade, i.e. ANS control did not predominate; even so, for BPS above 160 mmHg, the CBF response to BPS increase was different before and after ANS blockade: CBF varied significantly after ANS blockade as it varied for BPS below 160 mmHg, while it remained constant before ANS blockade that elicited ANS control of CBF. In conclusion, sympathetic nerve regulation via its vasomotor tone at the level of cochlear microcirculation occurred markedly when the blood pressure was above 160 mmHg; the autonomic nervous system would appear to control the cochlear blood flow against large variations in blood flow in response to hypertensive phenomena.

Otoacoustic emissions and brainstem auditory evoked potentials in children with neurological afflictions

Findings are reported for evoked otoacoustic emissions (EOAEs) recorded from 22 children with neurological afflictions, whose brainstem auditory evoked potentials (BAEPs) were pathological on at least one side (41 ears explored). Our results confirmed that EOAEs are always present in children and infants having normal BAEPs. Absence of EOAE (n = 22) was almost always related to middle ear or cochlear damage with BAEPs indicating diagnoses, respectively, of transmission damage (n = 7) or endocochlear damage (n = 16). Conversely, for BAEP diagnoses of retrocochlear damage (n = 12), EOAEs were always present. EOAEs associated with BAEPs, therefore, appear to offer a well-adapted technique for precise etiological diagnosis of childhood hearing loss. When no wave is identifiable by BAEP recording, EOAE presence indicates retrocochlear damage.