A. Moulin

Interrelations between transiently evoked otoacoustic emissions, spontaneous otoacoustic emissions, and acoustic distortion products in normally hearing subjects

Active cochlear mechanisms and especially outer hair cells seem to be involved in oto-acoustic emissions (OAEs) genesis. This study sought to investigate basic characteristics of spontaneous otoacoustic emissions (SOAEs), click-evoked otoacoustic emissions (TOAEs) and interrelations between SOAEs, TOAEs and 2f1-f2 and 2f2-f1 distortion product OAEs (DPOAEs) in 135 normally hearing subjects. A gender effect was shown on TOAEs and DPOAEs amplitude, and is attributed to the higher incidence of SOAEs in women (58%) than in men (22%). Moreover, SOAEs presence seems to mask the age effect found, especially at high frequency components, on TOAEs amplitude. A general influence of SOAEs on TOAEs and DPOAEs is shown, especially at frequencies ranging from 1 kHz to 3 kHz, collecting more than 66% of the SOAEs peaks recorded. Lastly, correlations between TOAEs frequency band amplitude and 2f1-f2 DPOAEs amplitude, shows frequency specificity, at least at low frequencies (i.e., from 0.5 to 2 kHz) in agreement with previous works suggesting that the 2f1-f2 DPOAEs generation site is at the geometric mean of the primaries. The same correlations calculated with 2f2-f1 DPOAEs amplitude show frequency specificity at low frequencies i.e., at 800 Hz and 1600 Hz. 2f2-f1 DPOAEs in humans are shown to be generated near the 2f2-f1 frequency region on the cochlear partition.

Effect of contralateral sound stimulation on the distortion product 2f1−f2 in humans: Evidence of a frequency specificity

The frequency characteristics of the suppression by contralateral stimulations, of the cubic 2f1-f2 distortion products (DPOAEs), were studied during 63 sessions performed in 39 humans with normal hearing. Each session consisted of exposure to five successive series of randomized contralateral NBN frequencies centered between 0.25 and 8 kHz, while measuring 2f1-f2 set at one of the four studied frequencies, i.e., 1, 2, 3 or 5 kHz. For each value of 2f1-f2, analysis of variance and Students t-test were used in order to indicate and, if necessary, to localize, a possible significant frequency specificity. Results showed that the suppression exerted on 2f1-f2 DPOAEs by contralateral sound stimulation, is frequency specific, at least for middle frequencies of 1 and 2 kHz. The frequency specificity is specially marked when 2f1-f2 = 1 kHz with contralateral NBN central frequencies around 1 kHz. When 2f1-f2 = 2 kHz, central frequencies which induced a significant suppressive effect include frequencies around 2 kHz and also lower frequencies around 1 kHz. These observations support the interpretation that the suppression of the DPOAE is mediated by the medial olivo-cochlear efferent system.

Distortion Product Otoacoustic Emissions and Sensorineural Hearing Loss

As other types of otoacoustic emissions, distortion product otoacoustic emissions (DPOAEs) allow the exploration of the active cochlear mechanisms known to take place in the outer hair cell system. Most authors consider that 2f1-f2 DPOAEs are generated in a cochlear region corresponding to the geometric mean (GM) of the primary frequencies. To verify the relevance of this hypothesis in clinical practice, DPOAEs were recorded at seven different frequencies, ranging from 0.5 to 4 kHz, in 81 hearing-impaired patients and in 24 normally hearing subjects. To test the hypothesis that DPOAEs reflect the hearing threshold at the frequency of the GM rather than at the 2f1-f2 frequency, this study compares the 2f1-f2 frequency and the GM of the primaries to the frequency of hearing loss. DPOAEs can be used to explore a large range of frequencies, especially at high frequencies, but responses at low frequencies are less reliable due to noise contamination. Secondly, DPOAEs can be recorded in ears that have a hearing threshold as high as 65 dB HL at the frequency corresponding to the GM of the primaries. Finally, DPOAE recordings show frequency specificity: i.e., hearing loss at a specific frequency correlates best with DPOAEs whose GM of primary frequencies corresponds to the frequency of the hearing loss. However, this frequency specificity is still unsatisfactory and decreases as the levels of primaries increase above 60 dB SPL. Moreover, DPOAE amplitude is too variable to predict hearing loss at a particular frequency, whereas DPOAE threshold allows a correct prediction of abnormal auditory threshold in more than 80% of the cases at frequencies above 1 kHz.

Is the test of medial efferent system function a relevant investigation in tinnitus

The present results are drawn from preliminary observations made in 28 patients suffering from unilateral, permanent, non-pulsatile tinnitus, who were systematically submitted to an investigation of their otoacoustic emissions in both ears. Spontaneous otoemissions (SOAE) were carefully looked for, before recording of transient evoked otoemissions (TEOAE). The effectiveness of the medial olivo-cochlear efferent system (MOC) was also tested. The comparison between TEOAE input/output curves obtained with and without contralateral stimulation allowed a global assessment of the functioning of MOC. Additional information relating to the MOC functioning at the precise frequency of tinnitus and/or around it, was available from the comparison of analogous curves obtained using distortion product otoacoustic emissions (DPOAE) instead of TEOAEs. The results show that: (1) when the amplitude of otoacoustic emissions differs between the two ears, the tinnitus is generally lateralized on the side where amplitude was the lowest, which seems to be related to a greater hearing loss; (2) no general law concerning tinnitus can be drawn from the global testing of MOC functioning; the only result is that the slope of TEOAE input/output function appears as a deciding factor for efficiency of MOC, the least efficiency almost always occurring on the side where the slope is greater, and (3) even in the case of proved global effectiveness of MOC activation, there is, at least in the vicinity and in at least one ear, a part of the cochlea where its functioning is altered. A better comprehension of the mechanisms underlying this symptom will probably come from exhaustive exploration of individual cases rather than a rougher investigation of large samples in which different aetiologies are likely to be mixed.

Influence of spontaneous otoacoustic emissions (SOAE) on acoustic distortion product input/output functions : does the medial efferent system act differently in the vicinity of an SOAE ?

Otoacoustic emission (OAE) generation mechanisms reside in the active micromechanical properties of the organ of Corti, and especially in the outer hair cells (OHCs). OHCs are strongly innervated by medial efferent olivo-cochlear fibres. Decrease of the intensity of transiently evoked otoacoustic emissions (TOAEs) and modification of spontaneous otoacoustic emissions (SOAEs) during acoustic stimulation of the contralateral ear have already been shown in humans. Similar results were obtained in guinea pigs with a decrease of 2F1-F2 acoustic distortion products (DPOAEs) and a suppression of the effect with sectioning of the floor of the fourth ventricle. The present study sought to investigate the influence of contralateral auditory stimulation on DPOAEs recorded in humans. It shows a decrease in DPOAE intensity for all frequencies, at levels above 45 dB SPL of contralateral broad band noise. This effect was found at levels of contralateral BBN well below the acoustic reflex threshold, and in subjects without acoustic reflex. Moreover, the influence of transcranial transmission could be ruled out since no effect was found when contralateral BBN applied to the altered ear of totally unilaterally deaf patients. Thus, the contralateral acoustic stimulation effect on DPOAEs provides a new means of functional exploration of the medial efferent system in humans. The effect obtained is more ample at low primary frequency levels. Moreover, as DPOAEs are known to be stronger and to show more irregular input/output function patterns in the vicinity of an SOAE, the influence of contralateral auditory stimulation was studied for DPOAEs recorded at 10 Hz, 50 Hz and 150 Hz from an SOAE frequency.

Otoacoustic emissions and persistent tinnitus after acute acoustic trauma.

Objectives: To follow up the auditory status of military personnel after an acute acoustic trauma and to identify the possible predictive value of hearing thresholds and otoacoustic emissions during the first 24 hours after the acoustic trauma.

Evoked and spontaneous otoacoustic emissions : a comparison of neonates and adults

Evoked otoacoustic emissions (EOAEs) and spontaneous otoacoustic emissions (SOAEs) were compared between neonates and adults. Several differences were seen for EOAEs: (i) the occurrence of EOAEs was significantly greater in adults than in neonates, and in neonates it increased with extra-uterine age; (ii) the high frequency EOAE intensity was greater in neonates than in adults; (iii) the EOAE intensity was significantly greater in neonates than in adults. No age-related differences for SOAEs were found: (i) age was not significantly related to the presence/absence of SOAEs in neonates or adults; (ii) the occurrence of SOAEs was, however, significantly greater in females than in males in both neonates and adults.

Contralateral auditory stimulation and otoacoustic emissions: a review of basic data in humans.

The influence of contralateral auditory stimulation on otoacoustic emissions (OAE), spontaneous OAE, evoked OAE and acoustic distortion products, can be summarized as follows: (1) alteration (mainly a decrease) of OAE amplitude; (2) alteration of response spectrum (upward shift frequency of SOAE); (3) alteration of phase; (4) effect dependent on intensity of contralateral stimulation; (5) effect inversely dependent on intensity of ipsilateral stimulation; (6) frequency specificity of the suppressive effect. Involvement of the medial olivocochlear bundle is highly probable but one cannot exclude a double pathway including also the acoustic reflex.

Traumatismos sonoros agudos

Los traumatismos sonoros agudos se deben a la exposicion subita de la coclea a una presion acustica excesiva, que supera sus capacidades de tolerancia. Tanto si se debe a ruidos de impulso como a ruidos continuos de corta duracion, las alteraciones auditivas que se producen pueden ser definitivas, incluso en caso de exposicion unica y aislada. Las lesiones cocleares provocadas por los traumatismos sonoros agudos son tanto mecanicas como metabolicas y, segun la cantidad de energia que haya penetrado en el oido interno, las alteraciones auditivas pueden ser reversibles, con elevacion temporal de los umbrales, o irreversibles, con una hipoacusia definitiva. La sintomatologia clinica es bastante tipica, con la asociacion de acufenos, hipoacusia e hiperacusia dolorosa. La magnitud de la perdida auditiva observada en la primera exploracion siempre se debe interpretar en funcion del periodo de tiempo que haya transcurrido desde el traumatismo sonoro agudo, porque las posibilidades de recuperacion disminuyen a medida que pasa el tiempo desde el accidente inicial. En las primeras horas posteriores al traumatismo sonoro agudo, las otoemisiones acusticas parecen tener un mayor valor pronostico que la audiometria tonal, sobre todo en lo referente a la evolucion de los acufenos. La precocidad del tratamiento sigue siendo un principio esencial, pues la recuperacion de los umbrales auditivos es mayor cuando el tratamiento se inicia pronto despues del accidente. Se han propuesto muchos tratamientos, con un papel destacado de la corticoterapia. El respeto de las medidas de proteccion auditiva individual durante las actividades de riesgo sigue siendo la mejor prevencion de estos accidentes cocleares.

Traumi sonori acuti

I traumi sonori acuti sono il risultato dell’esposizione brutale della coclea a una pressione acustica eccessiva che supera le sue capacita di tolleranza. Che siano da rumori impulsionali o da rumori continui di breve durata, le lesioni uditive indotte possono essere definitive, anche per un’esposizione singola e isolata. Le lesioni cocleari generate da traumi sonori acuti sono sia meccaniche sia metaboliche e, a seconda della quantita di energia penetrata nell’orecchio interno, le lesioni uditive possono essere reversibili, con un aumento temporaneo delle soglie, o irreversibili, con una perdita uditiva definitiva. La sintomatologia clinica e abbastanza stereotipata e associa acufeni, ipoacusia e iperacusia dolorosa. L’entita della perdita uditiva constatata al momento del primo esame e sempre da interpretare in funzione del tempo trascorso dal trauma sonoro acuto, poiche le possibilita di recupero si riducono a mano a mano che ci si allontana dall’incidente iniziale. Nelle prime ore dopo il trauma sonoro acuto le otoemissioni acustiche sembrano avere un valore prognostico maggiore dell’audiometria tonale, specialmente per quanto riguarda l’evoluzione degli acufeni. La precocita della gestione rimane un principio essenziale, dato che il recupero delle soglie uditive e tanto maggiore quanto piu rapidamente e intrapreso il trattamento dopo l’incidente. Sono state proposte diverse terapie, con un posto privilegiato per la corticoterapia. Il rispetto delle misure di protezione uditiva individuale durante le attivita a rischio rimane la migliore prevenzione di questi incidenti cocleari.