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

Hearing Research, 43 (1990) 251-262

25t

Elsevier H EARES 01314

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

1.2, D a v i d

T. K e m p 3, E v d y n e Veuillet t, R o l a n d D u c l a u x

2,

Annie Moulin and Alain Morgon f L ~ , ~ M r c d'F~pl~r~tions Fonctiannelles Neurosensorieiles, Pavilion U, H~pital Edouard Herriot, Lyon, France. 2 Lab,~gratoire de Physiologie Sensorieile, Facult~ de M~decine Lyon Sud, Pierre Benite, France and J Functional ,4aalysis Sectio~ Audiology Departmen~ tnstituve of Laryngolo~ and Otology. London, U.K (Received 3 April 198% accepted 6 September 1989)

The present study investigates the possibility that contralateral auditory stimulation along medial efferent system pgtn*,vays may alter active cochlear micromechanics and hence affect evoked oto-acoustic emissions in humans. A first exFerimen~ invoh-~ng 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 experime~L involving 10 of the above 21 subjects, sought to rule out any techrdcal artefact. Recording was again carried ont, but after sealing of the contralateral ear with a sificon putty plug. No contralateral intensity effect on oto-acoustic e m i ~ o n amplitude was found for contralateral intensifies 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 file preceding eaperin~ent. The third experiment investigated the role of transeranial tran~qrfission of the contralaterai auditory stimulus. 16 sabj~ts ha~ng total unilateral deafness and one healthy ear were tested by the same procedure as above. No fall-off in olo-acoustic emission amplitude was found for contralateral stimuli equal to or less than 80 dB SPL, There is thus a eontralateral auditory stimulus effect on active cochlear m i c r o m ~ The most appropriate explanation involves the medial cochlear efferent system, excited at brainstem level via the afferent auditory pathways. Alteration of active cochlear ~ a n i c s seems promising at a basic level, pointing, as it does. to an imeracti~e cochlear functioning which can be invest/gated by simpte~ non-intrusive, objective techniques which can be used with human subjects. We have here a model for functional exploration of the tmxlial olivocochtear efferent system. Oto-acoustic emission; Olivocochlear efferent: Contral~teral sound; Cochlear micromedmnics

Introduction The cochlear organ of Corti receives centrifugal pathways, from the Central Nervous System. the function of which is still almost unknown. Following Rasmussen's (1946) discover), of the olivocochlear bundl~ two distinct efferent system.~ ha~e been shown to exist (Warr and Guinan, 1978~, one basically contralateral medial system largely involved in the innervation of the outer hair c.dls of the organ of Corti (prc~synmptic ending); and a Correspondence to: L. C o l l , ,

Laboratoir¢ d'Ea#orations Fonctionndles Neurosensoriell¢~, PaviLion U, Hbpital Edotmrd Humor. Place d'ArsoavaL 69374, Lyoch France.

0378*5955/90/$03,50 © 1990 Elsevier Science Publisbers B.V,

basically ipsilateral lateral system synapsing with the cochlear afferent neuron dendrites near to the inner hair cells (post-synaptic ending). The effect of section and of electrical stimulation (either overall or limited to the median system) of the olivoc,.x:hlear bundle has mainly been i n v e s t i ~ in terms of cochlear microphonic potential variations (BonD.is ¢t al., 1987bL cochlear frequency selectivity (Bonfils et aL, 1986a, b, 1987ag spon~neons auditor2/ nerve electro-physiological response changes (Giff0xd and Guinaa~ 1983, 1987; Guinan and Gifford, 1988a. b) auditory nerve tcslxmse to noise (Winslow and Sachs, 1987) and on temporary threshold shifts (Rajah, 1988a, b) Stimulation of the crossed olivocoeMcar efferent

252

system also affects mechanical cochlear phenomena as measured by distortion products (Mountain, 1930) and receptor potential in inner hair cells under accompanying low intensity acoustic stimulation (Brown et al. 1983). Taken together, these studies show an inhibition effect of the efferent system. The exact role of this system with respect to hearing remains, however, undefined. Indeed, the section experiments are open to criticism: Methodologically, the operation is not easy and fails to be fully selective for the efferent system (particularly in experiments involving median section of the floor of the 4th ventricle). The same is true for the electrical stimulation experiments, which moreover give rise to problems of interpretation due to stimulus artefacts. Section and stimulation experiments are global in nature and fail to allow specific investigation of r~eurons in terms of cochlear input. Finally and obvmusly, none of these procedures can be applied to human studies. Buno's (1978) work represents a new approach to the role of the efferent system. He demonstrated a change in spontaneous auditory nerve activity in cats under low-intensity contralateral acoustic stimulation. One can thus think in terms of a "pathway" in which the contralateral auditory afferent neurons synapse at brainstem level with the olivocochiear efferent bundle fibres. A similar interpretation may explain the results of Folson and Owsley (1987) who demonstrated a fall in composite action potential amplitude (Art) with simultaneous contralateral pure sound stimulation in a human study. It seems logical to account for these effects in terms of cochlear efferent system action on auditory afferent electrophysiological response. However, these studies fail to distinguish between a possible direct (lateral efferent system) action on the afferent pathways and indirect action effecting the or~,~an of Corti. Recording ore-acoustic emissions may represent a means of evaluating a direct effect of the efferent system on the organ of Corti. The medial efferent system synapses directly onto the outer hair cells of the organ of Corti. New, these cells show active mechanical phenomena (Hock et al., 1986) and are involved in the production of oreacoustic emissions. The question therefore arises as to whether contralateral auditory stimuli could, via the medial efferent system, affect the micro-

mechanics of the cochlea and, hence, affect evoked oto-acoustic emissions. Our present research shows a fall in oto-acoustic emission amplitude under contralateral white noise. This effect is independant of the acoustic reflex and does not come from bone-transmission of the contralateral white noise. Our findings here represent a proof of a reciprocal interaction between the two organs of Corti in human subjects and so of a medial efferent system effect in humans.

Method

Subjects The study involved 37 subjects: 21 healthy (age 19-45 year old, mean = 28.7, SD = 7.2; 6 male, 15 female) with no history of auditory patholc,~;y and having normal audiometric functions (less than 10 dB HL loss between 250 Hz and 8000 Hz per octave on pure tone audiogram and presence of middle ear reflexes); and 16 patients (age 6-52 years, mean = 26.1, SD = 13.6; 9 male, 7 female) having total unilateral deafness originating from a history of mumps. On the affected side, these patients had no subjective auditory response for any of the intensifies employed on audiogram at frequencies of between 250 and 8000 Hz (per octave); the audiogram of the unaffected side was normal (it showed less than I0 dB hearing loss at octave frequencies between 250 and 8000 Hz).

Audiometry Tonal audiometry was conducted in a soundproof room using a Madsen DA I!1 audiometer: Hearing threshold was measured at 250, 500, 1000, 2000, 4000 and 8000 H.z.

Acoustic Reflex Recordings The acoustic reflex threshold in response to contralaterai white noise stimuli was measured for all healthy subjects, using an Amplaid 702 impedancemeter. This reflex was present in all control subjects (threshold mean--86.67 dB SL; SD-2.05), but absent in unilaterally deaf subjects.

EOAE recordings Transient evoked oto-acoustic emissions ( E O ~ ) were recorded and analysed using the method proposed by Bray and Kemp (1987), In

2,~3 this study the 'non-linear' difference method wa~ not employed since change in responses belween only two conditions was needed. Also the lower levels of stimulation did not require the middle-ear artefact rejection facility. The probe comprised a Knowles 1843 microphone and BP 1712 transmitter embedded in a plastic ear plug. The stimulus was a non-filtered click of 80 ~ts duratior~. Click-rate was 50 c.p.s, and post-stimulus analysis time was 20 ms. The number of responses to be averaged was set at 600. A pass:e~and of 500 Hz-6000 Hz was employed; stimulus presentation, data recording, averaging and spectrum analysis were carried out using otodynamic II.988 software and hardware. Stimulus level in the outer ear canal was measured by the 1I-.088 and adjusted to obtain a peak reception level of 63 dB SpL ( + 3 dB). Contralateral acoustic stimulation Contralateral acoustic stimulation was via an Amplaid 455 stimulator and a T D H 49 earphone. Stimulus was broad-band white noise (band-width: 50-8000 Hz). Intensity ranged between 0 and 50, 70 or 80 dB SPL, according to the study. Procedure For each healthy" subject, measurements were made of tonal auditory threshold, acoustic r~flex threshold, oto-acoustie ewdssion with or without contralateral white poise, and subjective perception threshold for contralateral white noise. The same me~_nuremcnts were taken for the patientgroup, with the exception of acoustic reflex threshold. Retx~rdings were all made with the subi~=t lying down. For healthy subjects, the EOAE probe was introduced into the right ear and white noise sent into the ~eft ear through the T D H 49 earphone held on a headphone-set. For the unilateral total deafness patients, EOAE was recorded from the healthy ear, during continuous auditory stimulation (white noise) to the other ear. A few pre-test EOAE trials were conducted for each subject to dc~rmine file el~'k inten~ty re~ quired to obtain meatus stimulation of 63 ± 3 dB peak equivalem SPL. Three types of experiment were ~ a e t e d . The first involved 21 healthy subjec~ Following audiogram and acoustic reflex testing, EOAEs were

recorded with and without continuous contralateral white noise stimulation ranging from 5 to 50 dB SPL by 5 dB SPL stages. EOAE was recorded for all 10 intensity levels, and 4 recordings were made without such contralaterat stimulus. The 14 recordings were made in random order. The subjective perception threshold of the contralateral white noise was measured concomitantly. The second experiment involved 10 of these 21 healthy subjects (age 22-45 years, mean = 30.411 SD = 6; 2 male, 8 female). EOAEs were recorded from the right ear after sealing the Deftear with a silicon putty plug. Lefthand auditory stimuli in this case ranged from 5 to 70 dB SPL by 9 dB ~PL stages, plus 4 recordings made without eontralateral stirmdation, order being randonx Subjective perception thresholds for white noise were measured for the 10 subjects. The third experiment involved 16 patients having unilateral total deafness. EOAEs were recorded from the healthy ear with or without contraiateral stimulus. The contralaterat auditory stimulus was white noise, intensity ranging from 5 to 80 dB SPL by. 5 dB SPL stages, with 4 extra recordings made without such ¢ontralateral stimulation. Measuremem and statiszics In all cases, EOAE amplitude was measured in dB SPL within the whole analyzed sample time. This measurement concerned either a window of between 3 and 20 ms for a frequency band of 0-6000 Ha, or various windows and bands. The windows of analysis used were 5-10 ms, 10-15 ms and 15-20 ms_ The frequency bands used were 0-1000 Hz, t000-2000 Hz 2000-4000 Hz and 4000-,6000 Hz~ R~ults for each experimental situation were compared by analysis of variance for repeated measurements. C ~ n of EOAE amplitude in relation to contralateral stimulus intensity was made by a Student's t test, using residual variance and the a m b e r of ~ of f ~ e ~ m of the r e , dual variance, ~malysis concerned EOAE .amplitude in r e l a t i ~ to eoa~alateral stimulus intensity in dB SPL for all 3 experinaents, and also in relatioa to contralaterai sdmulus intensity in dB SL (obtained aecocding to the subjects" s u b j e ~ v e perception thtexh~k~ ~or

254 white noise) for the first 2 experiments. The mean value for the 4 recordings without contralateral stimulus was expressed as a reference value equal to 0 d~. T h e Snedecor F test was used to compare the variances of EOAE intensity in the control and unilateral total deafness groups.

Results First experiment: effect of contralateral stimulus on evoked oto-acoustic emission. Fig. 1 shows a typical subject, The mean acoustic reflex threshold for the 21 subjects was 85.2 dB H L (SD = 10.3). EOAE amplitude decreased significantly under increasing contralateral stimulation: F(10,200)= 22.36(P < 0.0001) (Fig. 2). The t test showed that

EOAE amplitude was significantly reduced under contralateral stimulation (at the 0.0001 level) at 30 dB SPL, 35 dB SPL, 40 dB SPL, 45 dB SPL and 50 dB SPL compared to that found without contralateral stimulation. N o dilference was found for intensities lower than 30 dB SPL. The mean white noise perception threshold was 24.8 dB SPL (SD = 5.4). Data analysis in terms of contralateral stimulus intensity Ln dB SL (intensity of white noise in dB SPL minus white noise perception threshold) showed a significant effect of stimulation on EOAE amplitude: F(17,136) = 12.96(P < 0.0001). EOAE amplitude was significantly reduced (at the 0.001 level) when contralateral stimulation was equal to or greater than 10 dB SL (compared to EOAE intensity at minus 15 dB SL) (Fig. 3).

C~ble~ ksl~e

X4

Fig. I. Evoked otoaoouslJc emissions and specb-al analysis of a typ/cal subject in absence of a 50 dB white noise contralatelral stimulus (Trace A) or in pr~eno~ of ll~s noise(Trace B). The lowe~ trace is the di~al ~abslra~ion of the two highest traces Lnd has a scale expanded by a factor of four. T ~ freq~'~j spcclza on the right axe from the traces on O~ l~b (T'~ lime period is the whole 20 ms smz',ple time). The real zrcsp(m~ is shov~ in outlined plots and lhe random ~ in solid plots.

25~

0.5

m

"o

0

O

S

II[]] [ ] ~t

*rims i

•

o.

E Q e Jm

cO

-0.5

[I O

m

O

ee

O "1

"

L 0

I. 5

i

I

I.

I

J

10

15

20

25

30

Contralatoral

stimulation

.... 1

J__

35 40 (dBSPL)

J

I

45

50

Control subjects Fi& 2. Relative amplitude of EOAE according to the contralateral stimu~tion (in dB SPL) in ~he control groep (mean± SD)~ The means that it reached sla~sticai s/~mf'w.an~ at the O.05 |e~l.

By spectrum analysis, without contralateral stimulation EOAE amplitude was greater for windows 5-10 ms and 10-15 ms (Fig. 4). Under contralateral stimulation, a significant differeno~ was found for the 5-10 and 10-15 ms ( P < 0.0001 ) and 15-20 ms windows ( P < 0.05). As for windows 5-10 and 10-15 ms, diffcrenc~ were significant, as compared to EOAE Lqtensity without contralateral stimulus, for con. trilateral stimuli of 40 dB SPL for the 5-10 and 10.-15 ms windows ( P < 0.001). Differences were also significant for 45 dB ¢ontralat~al stimuli for the 5-10 and 10-15 ms window~ And for a 50 dB SPL contralateral stimuhts~ significant differences were found for the 5-10 and 10-15 ms windows (at the 0.0001 level). in terms of frequency. EOAEs without con. tralatersl stimulus were of greater amplited¢ for

*

the 1000-2000 Hz and 2000-4000 Hz b~nds~ With contralateral stimulus, no stimulus cheer was found on OAE a ~ l i t u d e for the O-1000 Hz band nor for the 4000-6000 Hz band. However, significant d i f f e r e r ~ were found for the 1000-2000 Hz band and for the 2000~4000 Hz band (at the 0.0001 level). As regard~ 'C,w1000-2000 Hz window, significant differences, as compared to recorcfins;s without contralaterat stimulus, were f o v ~ for intensitiesof 40 dB S P L 45 dB SPL ~nd 50 dB SPL (al the 0.0001 ~ ) . Likewise. ~a the 20D0-~O0 Hz window, si~[w..ant differences were fotmd at 45 dB SPL and 50 dB SPL {~t the 0.001 level). (Fi& 5). Second ex ~ : m e , ~ : sea~,g of ower ~ o r y ca~m~ to 0~1£. The tO healthy s u ~ t s invotved were drawn from :he ~ cm~cemed in

cosur~I~d

256 10

oo~-1 g H z • I-2

iIi.ii

0.5

Q ¢¢

-

-_

KHx

• 2-4

gttz

• 4-6

KH~

-

•

•

•

c

--

o

! 40

I 4S

; 50

:Q

-

0

i i

~eL

~

- ~
Q

-S -0,5

-10

-1 t . . . . . I ,.

-20

I~ ,,

-15

-10

I

.....

-5

0

I

I

5

10

Fig. 3. Relative amplitude of EOAE according so the contralateral stimulation (in dB SL) in the control group (mean ± 1 SD}. The data were o b m i ~ d from the same rims wl~ch were originally plotted in clB SPL. * See Fig. 2 legend.

the first experiment and conformed to group norms (Fig. 6 shows a typical subject) No signifY:ant difference was found in analysis concerning contralateral wl'dte nois: intensities identical tc those u ~ d in the previous study 0-50 dB SPL for contralateral stimuli). However, a significant dif¢r~

0 I0-11t ¢~ • 1S+20 mU

f~

o

0

5

iO

'tl

2@

C~mt~elattt~t~

©~

26

~

~14.as

3S

40

t 10

i 15

i 20

,I 25

I 30

i 35

Control Subjects

20

eohtralatera! sttm~)at|~n (dBSL) Cont¢ot a~blects

+ 5-I0

t S

Co.tralot~ral stlm4d4t~n (dSSL)

t. . . . . . . !

15

t 0

!

I

4S

SO

t ~

Fig, 4, F.OAE amplitude for 5-10 ms, IO-l$ ~ argt 15-20 ms windows according m the conlcalateral stimulat/oq in dB SPL.

Fig. 5. EOAE amplitude for 0--1 kHz. 1 - 2 kHz, 2 - 4 kHz and 4 - 6 kHz frequency bands according to the contralatcral stiJ,mlat/on in dB SPL. * See Fig. 2 legend.

ferenc¢ was found in the case of contralateral stimulus intensities of between 0 and 70 dB SPL: FO4A26) = 3 . 6 4 ( P < O.001). Significant differences were found with respect to stimulus intensity for contralateral stimuli of 65 dB SPL and 70 dB SPL (at the 0.001 level). In the same subjects without sealing, a significant diff~-ence in EOAE amplitude was found in relation to contralateral stimulus intensity: F(10,gQ) = 15.38 ( P < 0.001). Significant diff~ences at the 0.01 level were found for intensities of 30 dB SPL, 35 dB SPL, 40 dB SPL, 45 dfi SPL and 50 dB SPL (Fig. 7). The effect of the p~ceived ¢ontralateral white noise leccl on the amplitude of the EOAE may he measured in dB SL. Significant contralateral stimulus effects wcr¢ found: without sealing, F(8.64) ,= 8 . 1 6 ( P < 0.0001); and with sealing, F(CL55)*, 4.8(P < 0.0001 )~ In both c a s ~ EOAE amplitude was significantly weaker at 10 dB SL and 15 dB SL than at 0 dB $ L {Fig. 8).

Third experimcm: study of total unilateral ~ n e s s patients Fi& 9 shows a typical subject, EOAE amplitude in the healthy ear was unaffected by

I

[

~,~

~

!

FiS~ 6. EOAE and spectra] analys~s of a Z y p ~ ~ i*~ absen~ o f ~ ~ dB ~ * e ~ ~ r t t r ' ~ t e r ~ ~t~tts ( T r ~ A) ~ in presence of this ~ (Trace B), wid~ se...z~ of ~ outer ~ , ~ ~. TI~ I~es~ Ua~e i* ~he 4 ~ J ~ ~ z b ~ x e t ~ ~ U~ t ~ t ~ t

contrala~cra] ~ i (intensity from ~ to 80 dB SPL): F(16~40) ,~ O. 53, NS. {Fif~ I0)~

These ~ b ~ t s f,ited to p e e v e the ~ , :ralatera! szimettts whatever its itltensity ( ~ 0 and ~ d8 Sl~), The s t ~ a ~ d e v l a ~ of the EOAE ampSrude w e ~ ~ f i c a m l y Oeater in the u.ilateral~y deaf group than in the ~etrol group (firsz expertmere). The EOAE emplip~e was ~ ~ 1 o~!y for ~ ~ v e d contraitt~M s t ~ , ~ t t ~ r ~ ( ~ $, IO, I ~ 20 dB SPL),

0

!

| |

T. ~ e

~

c.f EOAE ~

t0 ~

~.

The first ~ t ~_,et~ a ~treleterat auditory s t i m ~ effect on EOAE am-

plitud¢, a~,laimng ~/8rtif~.ance as ~ t as the contr~atera| stira~u~ i n t ~ t y is equal to or greater than 30 dB SPL. The ~ subjective perception Ihresl~d here is 24.8 dB S P L With respect to tl~ white noise p ~ : e p t ~ ~.hresbo~ the effect attains s t a ~ [ s ~ s/gn~ficance from 10 dB SL. The e~f~t may be described a~ an cver-grea'~ r e d u c t ~ of EOAE ~ t u d e as contralaterai stimulus intensity inc~..uses from 10 dB SL. Closer

o

analysis reveals that this di~q~en_~ ~ more partitively EOAEs with ft~eencies in the 1 ~ to 4000 Hz b~tnd. T ' ~ ~ be a~counted for by the fa~t that most EOAE~ are represented in this bargL and more prec/sd~ in the 1000--2000 Hz ~nge. The ~ffe~ is clearer on analysis of the 5 - I 0 ms w~dow ~ on that of 10-15 ms, This may

F'~ 8. R~lati~ aml~i|tg~e of EOAE a~o~rd~ng~ ~h¢ o ~ t~alatef~tstimt~latioa~ dB SL wi~h~and w i ~ { .~¢~I/t~of t ~

. . . . . . . . . . . . .

_~

__

r ~ t ~ i T - ~ i

"~

~,

~

.

.

.

.

.

i

I

0+5

I

£

It

i. qli

It

-O+S

-1

i__.+.i_,

0

S

i

~ i ......

io

~S

1 tO

+

i i+i

i

~0

.. _ l . . . . . i ......... j : SS 40 iS

u~-ti+lt

~

1.....-, i = + So S~

i +

SO

_L+_.

Ct

J.,,. ....... !_+_+_J IS eO

#0

ttmml

(m+~ ± l SOl+

i~t~ ~m+~ are ma,m~y premmt itt tt~: 5+ lO tin++ Our remit~ show a whi~ PPm~ ~+~.:t m++tiicii m y bring the ~i¢l~lit sy~,d~ into play tO i i b l t EOAI~ e,+'otiit irrom il~ c o m ~ ¢+m++O t t ~ a p l ~ e x p l , n i l i ~ mithi be; a l ~ b ~ licitnical a+rlelaci, an ~ i i ¢ r~ ~fe~+ or a bone ~ n ~ ~ i m t ~ out mmy such m,tef~i; ~ ¢¢mimtaimmt ~ ~ ~ of EOAE ~ l i i m ~ ¢ ~ for c ~ m ~ stim~ up to 50 dB sr"L ~ ~ ~ probI ~ (molably, a i r - ~ ) + Moreover+ that llm +d+t~m,t mmmitP~l+ minter mmiimt l ~ i m ~ t i m

lim~ wl d~ m. ~ I~.i~ lot i . m m ~ The ~ m ~

m+l~ ~ M ~

,$ml,il+ ~ mint i . of tie order of iO ~ S L cot ~

our ftmt+

low imtmmt~ at whk+k EOAE

cc+m¢~m~A F m + t ~ , tim ~ +oi~ acoustic ~ chr~..~,~ld is markedly ~ t e ~ r t h ~ dB SPL (m~ximuzn ~ + y ~ ia elm+ t r + I m ~ m i m u t ~ m tot tt~e he~xhy ~.,~+~c ltmlp)+ l++m.~+ c',m~iilPmalimmof middi+ ~ sure d o ~ miniitaly+ii ~ d i m cm + + c~ ~ ~E and a mbsumtial pre.m'¢ (700 ram) needed to ~ ~ ~L But n ' d ~ rnusc~ c c ~ ~ s cannm be ~ y ml~ "l'be~ may be ~ ~ ~ b~ ~ p~tu~ To ~ oul any lmlii+liural + l i ~ nmorimi to a, ~ l~l+o. ~

~ mvcdv~ . o ~ I ~ m m ' + i mmmmmiion~

pmmmmo~

m amm~

in ~ . m c i m ~ ~ t ~

T~~oi

io++all

260

any effect at the to+ted intensities argues against any tranm+r,~nial transmis+sion of the contralateral stimulus. Our research here shows the contralateral inhibitory message to be a neural phenomenon originating in the cochlea which excites the medial cochlear efferent system brainstem level. When an acoustic stimuIus attains audibility, it excites the ¢<~hlear neurons. The superior d/vary complex receives auditory affetents, particular|y to the lateral Sul~rior olivary nucleus (LSO) and the medial o | i ~ nucleus (M$O)+ It may be assumed that the efferent system projecting onto the con. tralateral cochlea is excited at this same level. Indeed, the medial olivocochlear efferents originate in medial nuclei of the superior olivary complex (Wart+ 1986). Furthermore, certain efferent neurons have been shown to respond to auditor) stimuli (Fex, 1962+ 1965; Cody and Johnstone+ 1987). The efferent system wig,hi be stimulated in this area by auditory afferents. The medial efferent system, c o n s i s t e d inhibitory ( W ~ h o l d , 1980, projects directly onto the outer hair cells of the organ of Corti (Warr and Guinam 1978)+ It can thus he imagined that mch stimuli reduce o u t ~ hair ce~t contr~tioas and hence ~ evoked O A E amp~i|~sd~+ Co~mi~teral auditory sttmula+ lion thus acts upon the active micromechan~ of the cochhm. There are other arguments letting to prove interaction in the acrid+ales of the two cochleae+ Dedson et al. (1987) showed that unilateral extracochlear electrical stimu~tion of the round window ia guinea-pigs led Io bilateral i n c ~ in the number of synapfic vesicle+ at the cochlear efferent endings+ Also the co,blear action IXamtial temporary t,hrgshold shift(YI'S) is reduced by contralateral acoustic stimulation (Ra.~n and Johngone~ 198~)+ The effect on ~ of a binaural acoustic stimulation looks like the effect of ¢]~iri¢~d stimulation of efferent fibres ( ~ and Jolms~one+ 19~) l~ao's (1978) studies show complex interact/oa betwee~ the t~o au~tory s y s ~ ~nilary a~titory nerve fibre respoases ckxmmsing ~nder ¢ontralalg~aJ pur~ souml stimu~tion bat ~.ng ~ contmlamral white noise m/muh+ tkon+ Warren and L ~ 0989a. b) did not flintthislastn~uh showing a ~ of units by contralatcr~ broad.~,~gl while noise+ Our study

was limited to evoked oto+acoustic emissions+ but spontaneous oto-aconstic emissions (Mort et al., 1989) and distortion products (Puel et ai., 1989) are also altered by conlralateral auditory stimulation. The unilateral deafness group shows no recipr+ncal interaction but a greater variabRity in EOAE amph+mdes than the control group. One may suggest that efferent fibres play a role in absence of contralateral stimulation linked to the ipsilateral stimulation+ The cffe¢¢nt system might modulate the contraction+ of the outer hair cells+ Absem:e of such a modulation could explain the variability in the unilateral deafness group. Alteration of active cocl~dear m2~'onmchanics seems promising at a basic level It points to an interactive cocbdear functioni_ng which can be investigated by simple, non-intrusive objective ruthtuques which can be used with human subjects. We have here a model for functional exploration of the medial efferent system+ Admm~edg~ The authors wish to thank Mrs A. Vidal for a~ting the manum~pc Rel~eaees Altm:imler.R.A. and Fe~ J. (1986) F_.ffePemneurotramanitler~ In: R+ A1tg~-.aler.R+ Bobbin and D. Hoffman+ (Edge, Nea.,~+olo~ of H ~ The cochlem ga-mm P0~s New+

ttm~fi~ P_ Remond, M.C+ ~ mad ~ 23"]-283. +ec~k+m d

l%jol+ R. (lg~m) P . 3 f ~ I fmqaeac-+~ ~ t y + Hear. Res. 24+

the medgal effemm tracts ( ~

and mm-

cgmm~ Im~ of ti~ medial olivo-gocldc~ Immdlc+ Hmr.

km+/h, P~ Rmmmml+ ~ + and Pajol.Ro(19S+Po)v a ~ cm~c= ~

pom~

ae~ ~

+n~t

t ' / ~ s m the ¢aehlca. Hear+ Reg 31g ~6+I-272+

~m:lmiq~ m/++atmleto+/alam ~ ~m

~r. £ aaa~ml+2L

M.C,+ 1~e+tmLA+L ~ t Mast& ILl+ (19~3) I n ~

~ l £ ~ a t ear sound stimulation. Exp. N e ~ 59. 6 2 ~ Canto~. B., Borg, E. and, F~cL A (lggS) P~o~e~-do~~

a~,dcrossedoT~vo-cocMe~b c ~ e s ~ m u | a ~ ~ r

cocMc~r

lx~d. J.L~ ~ h i ~ r ~ G. a ~ l~q~L R~ q[t989) Active Hear. Rcs. 197-200. Cody, A.R. and .Iolmston~, B~M. Ct9~/2) A ~ c . ~ y ¢~ok~ ~ty of ~ © ~ e ~ m ncmxmsin th~ g ~ p/g cocht¢~ Dod,o ~ H.C., Watlil~, J.IL. Bamm~o LIL, D ~ , F~E ~m~ F o u n ~ ~ . (19~/) ~ ef'~ts of ~ ~ m a~l

F¢~, J. (1961) Amlitory a~ivit~ ia ~ t r i [ ~ ¢oddmr t i l ~ s ou ca¢ A s m @ ~ a f ~

amt o m m p ~ ~ t m . #,ct,

F~

~mn~gal sysaea~ I! ~ . ~

J. (196S) Audhory a c ~ y ia ~ cod/lear f~m~sia ~ A stm~ of n ! ~

Flock, A~ Fl0cL B. and Ul(eadahL M. ( I ~ ) ~ s m s o~ ia oa~r kaircdh and a possibleswacm~a~ bas~s. Arch. ~ n ~ 243. 83-90. Folsom, R.L and Owsk~. ILM. (1987) ~ a~-~a l ~ q ~ m tioa Acta ~ . ( S ~ d L ) 103, 2~-26.~o CfiffotcL M.L and Guma~, lJ. Jr. (19¢g~)F.~¢ctsof ~ ~ ~mdl~ stimalatioa oa cat ~ rm~

179--194. s a ~

~ ~f~at ~oti~ ~ on cm ~b~rs. I Rat~le~d fmgaioa~ Him. R ~ ~,

9T-Ill. Cmiam~ JJ. Jr. amt Cmfford, M.L (19~b) Eff~g~t~o~ ,t¢c~rg~1

! l~-t2g. K*mp, D.T. (1978) S~inm~l~l ~ ~ the baama ~ sysam~ ~. A ~ . 1386-1391.

by ~ ~_tioa ~. 229-~12.

I~ ~.

w~i~*a A~. C~..

of the coauah.icml ~r. ~ r .