www.bjorl.org
Brazilian
Journal
of
OTORHINOLARYNGOLOGY
ORIGINAL
ARTICLE
Evaluation
of
peripheral
auditory
pathways
and
brainstem
in
obstructive
sleep
apnea
夽
Erika
Matsumura
a,
Carla
Gentile
Matas
a,
Fernanda
Cristina
Leite
Magliaro
a,
Raquel
Meirelles
Pedre˜
no
a,
Geraldo
Lorenzi-Filho
b,
Seisse
Gabriela
Gandolfi
Sanches
a,
Renata
Mota
Mamede
Carvallo
a,∗aUniversidadedeSãoPaulo(USP),FaculdadedeMedicina,DepartamentodeFonoaudiologia,FisioterapiaeTerapiaOcupacional,
SãoPaulo,SP,Brazil
bUniversidadedeSãoPaulo(USP),FaculdadedeMedicina,LaboratóriodoSono,DivisãodePneumologia,InstitutodoCorac¸ão
(InCor),SãoPaulo,SP,Brazil
Received20April2016;accepted31October2016 Availableonline25November2016
KEYWORDS Obstructivesleep apnea; Hypoxia; Auditorybrainstem response; Hearingtest Abstract
Introduction:Obstructivesleepapneacauseschangesinnormalsleeparchitecture, fragment-ingitchronicallywithintermittenthypoxia,leadingtoserioushealthconsequencesinthelong term.Itisbelievedthattheoccurrenceofrespiratoryeventsduringsleep,suchasapneaand hypopnea,canimpairthetransmissionofnerveimpulsesalongtheauditorypathwaythatare highlydependentonthesupplyofoxygen.However,thisassociationisnotwellestablishedin theliterature.
Objective: Tocompare theevaluationofperipheralauditory pathwayandbrainstemamong individualswithandwithoutobstructivesleepapnea.
Methods:Thesampleconsistedof38adultmales,meanageof35.8(±7.2),dividedintofour groupsmatchedforageandBodyMassIndex.Thegroupswereclassifiedbasedon polysomno-graphy in:control(n=10),mildobstructivesleepapnea (n=11)moderateobstructive sleep apnea(n=8)andsevereobstructivesleepapnea(n=9).Allstudysubjectsdeniedahistoryof riskforhearinglossandunderwentaudiometry,tympanometry,acousticreflexandBrainstem AuditoryEvokedResponse. Statisticalanalyses wereperformedusingthree-factorANOVA, 2-factorANOVA,chi-squaretest,andFisher’sexacttest.Thesignificancelevelforalltestswas 5%.
Results:Therewas nodifferencebetweenthegroupsfor hearingthresholds,tympanometry andevaluatedBrainstemAuditoryEvokedResponseparameters.Anassociationwasobserved betweenthepresenceofobstructivesleepapneaandchangesinabsolutelatencyofwaveV (p=0.03).Therewasanassociationbetweenmoderateobstructivesleepapneaandchangeof thelatencyofwaveV(p=0.01).
夽 Pleasecitethisarticleas:MatsumuraE,MatasCG,MagliaroFC,Pedre˜noRM,Lorenzi-FilhoG,SanchesSG,etal.Evaluationofperipheral
auditorypathwaysandbrainsteminobstructivesleepapnea.BrazJOtorhinolaryngol.2018;84:51---7.
∗Correspondingauthor.
E-mail:renamaca@usp.br(R.M.Carvallo).
PeerReviewundertheresponsibilityofAssociac¸ãoBrasileiradeOtorrinolaringologiaeCirurgiaCérvico-Facial.
https://doi.org/10.1016/j.bjorl.2016.10.014
1808-8694/©2016Associac¸˜aoBrasileiradeOtorrinolaringologiaeCirurgiaC´ervico-Facial.PublishedbyElsevierEditoraLtda.Thisisanopen accessarticleundertheCCBYlicense(http://creativecommons.org/licenses/by/4.0/).
Conclusion:The presence of obstructive sleep apnea is associated with changes in nerve conductionofacousticstimuliintheauditorypathwayinthebrainstem.Theincreasein obstruc-tivesleepapneaseveritydoesnotpromoteworsening ofresponsesassessed byaudiometry, tympanometryandBrainstemAuditoryEvokedResponse.
© 2016 Associac¸˜ao Brasileira de Otorrinolaringologia e Cirurgia C´ervico-Facial. Published by Elsevier Editora Ltda. This is an open access article under the CC BY license (http:// creativecommons.org/licenses/by/4.0/). PALAVRAS-CHAVE Apneiaobstrutivado sono; Hipóxia; Potenciaisevocados auditivosdotronco encefálico; Audic¸ão
Avaliac¸ãodaviaauditivaperiféricaedotroncoencefáliconaapneiaobstrutiva dosono
Resumo
Introduc¸ão:AApneiaObstrutivadoSonoprovocamodificac¸õesnaarquiteturanormaldosono, fragmentando-odeformacrônicacomhipóxiasintermitenteslevando,alongoprazo,asérias consequênciasnasaúde.Acredita-sequeaocorrênciadeeventosrespiratóriosduranteosono comoapneiaehipopneiapodeprejudicaratransmissãodeimpulsosnervososaolongodavia auditivaquesãoaltamentedependentesdofornecimentodooxigênio.Contudo,essaassociac¸ão nãoseencontrabemestabelecidanaliteratura.
Objetivo:Compararosachadosdaavaliac¸ãodaviaauditivaperiféricaenotroncoencefálico entreindivíduosportadoresenãoportadoresdeapneiaobstrutivadosono.
Método: Acasuísticafoicompostapor38adultosdosexomasculino,médiadeidadede35,8 (±7,2);divididosemquatrogruposexperimentaispareadosporidadeeíndicedamassa cor-pórea.Osgruposforamclassificadoscombasenapolissonografiaem:controle(n=10),apneia obstrutivadosonoleve(n=11),apneiaobstrutivadosonomoderada(n=8)eapneiaobstrutiva dosonograve(n=9).Todosossujeitosdoestudonegaramhistóriapregressaderiscoparaperda auditivaeforamsubmetidosàaudiometria,timpanometria,pesquisadosreflexosacústicose PotenciaisEvocadosAuditivosdeTroncoEncefálico. Asanálisesestatísticasforamrealizadas pormeiodeANOVA3-fatores,ANOVA2-fatores,testedeQui-quadradoetesteexatodeFisher. Oníveldesignificânciaadotadoparatodosostestesfoide5%.
Resultados: Nãohouvediferenc¸aentreosgruposparaoslimiaresauditivos,timpanometriae parâmetrosavaliadosdoPeate.Observou-seassociac¸ãoentreapresenc¸adaapneiaobstrutiva dosonoealterac¸ãodalatênciaabsolutadaondaV(p=0,03).Observou-seassociac¸ãoentre apneiaobstrutivadosonodegraumoderadoealterac¸ãodalatênciadaondaV(p=0,01).
Conclusão:A presenc¸adeapneiaobstrutiva dosonoestáassociada àpresenc¸adealterac¸ão naconduc¸ãonervosadoestímuloacústiconaviaauditivaemtroncoencefálico.Oaumento dograudeseveridadedaapneiaobstrutivadosononãopromovepioradasrespostasavaliadas pelaaudiometria,timpanometriaePotenciaisEvocadosAuditivosdeTroncoEncefálico. © 2016 Associac¸˜ao Brasileira de Otorrinolaringologia e Cirurgia C´ervico-Facial. Publicado por Elsevier Editora Ltda. Este ´e um artigo Open Access sob uma licenc¸a CC BY (http:// creativecommons.org/licenses/by/4.0/).
Introduction
Obstructivesleepapnea (OSA)isrecognizedasoneofthe majorcausesofmorbidityandmortality,andisassociated withawiderangeof cardiovascular,metabolic, neurolog-ical, physiological changes, as well as patient cognitive impairments,andhasbeenconsideredasoneofthemajor problemsofpublichealth.1---6 Arecentstudyofadults
per-formed in the metropolitanarea of the city of São Paulo showedthattheprevalenceofObstructiveSleepApnea Syn-drome(OSAS)ishighandincreasing,currentlyaround33%.5
ThepossibilityofOSAinterferingwiththeprocessof gen-erationandtransmissionofnerveimpulsesintheauditory systemisreportedbypreviousstudies,butthisassociation isnotwellestablished,andthereisdoubtastotheactual
effectofOSAonhearing.7,8Inaddition,individualswithOSA
could have serious changes in the mechanisms described above,duetothehyperviscosityofblood plasma9andthe
hypoxiccyclespresentinOSA.10
This study aimed to compare the findings of the eval-uation of the peripheral auditory pathways and of the brainstemamongindividualswithandwithoutOSA.
Methods
This study was approved by the Institutional Ethics Com-mitteeunderprotocolnumber1.437.604,andallvolunteers agreedtoparticipateinthestudybysigningtheInformed Consentbeforeundergoingevaluation.
Table1 PatternofnormalityoflatencyandinterpeakvaluesofBAERforadults,proposedbythemanualofSmartEP---IHS.
WaveI WaveIII WaveV InterpeakI---V
Average(ms) 1.59 3.64 5.57 3.98
Standarddeviation(ms) 0.24 0.17 0.16 0.25
Twovaluesofstandarddeviationareconsideredfortheclassificationofnormallatency. Thesampleconsistedof38adultmalesdividedintofour
groups: control (n=10), mild OSA (n=11), moderate OSA (n=8),and severe OSA (n=9).All of them werematched forageandBodyMass Index(BMI).Allsubjectsunderwent polysomnography.Thiswasfollowedbythefollowing classi-ficationoftheAmericanAcademyofSleepMedicineforthe severityofOSAconsideringtheApneaandHypopneaindex (AHI) per hourof sleep:mild OSA (AHI between5 and 15 eventsperhour ofsleep);moderateOSA (AHIbetween 15 and30eventsperhourofsleep);andsevereOSA(AHI≥30 eventsperhourofsleep).11
The exclusioncriteriaadoptedinthestudy were:Body MassIndex(BMI)greaterthanorequalto40kg/m2,
treat-ment for OSA with continuous positive airway pressure machine(CPAP)orintraoraldevices,heartfailure,diabetes, hypertension,thyroid changes,dyslipidemia,stroke and a historyofriskforhearingloss,includingexposureto occu-pationalnoise.
Conventional threshold tonal audiometry was investi-gatedinthefrequenciesof250---8000HzthroughtheGSI-61 equipment (Grason Stadler, United States) and TDH 50P supra aural headphones (Telephonics, United States). For theinvestigationoftympanometry,thetympanometrycurve ofadmittancewasrecordedwitha226-Hzprobetone,and ipsilateral and contralateral acoustic reflex investigation at frequencies of 500, 1000, 2000 and 4000Hz. Tympa-nometryandacousticreflexes evaluationswereperformed throughtheTitanequipment(Interacoustics,Denmark).The evaluation of Brainstem AuditoryEvoked Response(BAER) was performed using Smart EP (Intelligent Hearing Sys-tems,UnitedStates).Theacousticstimulususedtorecord BAERwastheclickwithrarefiedpolarity(with100-Hzhigh passfilterand3000-Hzlowpass)monoaurallypresentedat 80dBnHLwithtimeofstimulusof0.1ms,andpresentation frequency of 19.1 stimuli per second. In the total, 2048 stimuliwerepresented,withthenumberofartifactsbeing alwayslessthan10%ofthestimulipresented.Thestimulus withcondensedpolaritywasemployedinsituationswhere the amplitudes of the responses showed to be reduced, allowingtheselectionofthebestrouteofwavesforanalysis. Two tracings were recorded toensure wave reproducibil-ity. The values ofabsolute latencies ofwaves I,III and V andinterpeaksI---III,III---VandI---Vinmilliseconds(ms)were identifiedandquantitativelyanalyzed(Figs.1and2).
BAER results wereclassified as normalor abnormalon eachsideoftheear.Thenormalrangeofvaluesofabsolute latenciesofwaves I,IIIandV,andinterpeakI---Vproposed by the Smart EP equipmentmanual --- Intelligent Hearing Systems12(Table1)wasadopted.
Kruskal---Wallisnonparametrictestwasusedtoevaluate the homogeneity among the groups of baseline variables suchasage,BodyMassIndex(BMI)andApneaandHypopnea index (AHI). Models of analysis of variance (ANOVA) of 3 factors13 for audiometry and ipsilateral and contralateral
acoustic reflexes were used. In the models, the factors diseasegroup(Group),earside (Ear)and Frequencywere considered, with the latter two factors being considered with repeated measures. Due to the large number of descriptivelevelsassociatedwiththeFrequencyfactor,the correctionproposedbyGreenhouse---Geisserwasapplied.14
Fortympanometry parameters,TympanometricPeak Pres-sure (TPP), and admittance compensated at the level of thetympanicmembrane(YTM)andBAER(latenciesofwaves
I,III andV andinterpeaks I---III, III---V andI---V), modelsof 2-factorsANOVAwere used.Formultiple comparisonsthe methodproposedbyHolmwasused.15
To verify the association between the degree of OSA severityandthenumberofearswithresponsesoutofnormal standardforlatenciesI,IIIandV,andinterpeakI---V,a non-parametricchi-squaretestwasperformed.ThroughFisher’s exactnonparametrictest,multiplecomparisonswere per-formedofthenumberofearswithresponsesoutofnormal standardforlatenciesI,IIIandV,andinterpeakI---VofBAER of each disease group (mild, moderate and severe), con-frontingthemwiththecontrolgroup.
AllstatisticalanalyseswereperformedusingtheR soft-wareversion3.2.2(RFoundation,UnitedStates)andMinitab 17(MinitabInc.,UnitedStates).Thesignificancelevelforall testswas5%(˛=0.05).
Results
Samplecharacterization
The study included a total of 38 subjects, mean age of 35.3 (±7.1) years and mean BMI of 28.8 (±3.8)kg/m2.
As expected, no significant differences were observed amongdiseasegroups according toage (p=0.08) andBMI (p=0.15).Inaddition,significantdifferencewasfound for AHI(p<0.001),indicatingthatallgroupsinthisstudywere statisticallydifferent.
Audiometry,tympanometryandacousticreflexes
The average hearing thresholds did not differ among the groups (0.22). There was difference only between the frequencies tested in audiometry (p=0.002), with higher frequencies (4, 6 and 8kHz) presenting higher thresholds thanat 3kHz.For tympanometricparameters of TPPand YTM,itwasnotpossibletodetectanysignificantdifference.
Furthermore,thevaluesfortheipsilateralacousticreflexes donotdifferamongthegroups,norinanyotherfactors ana-lyzed.The resultsforthecontralateralacousticreflex,on theirturn,showeddifferenceonlyfortheFrequencyfactor (p<0.001).Thatis,theaverageofthefrequenciesof500, 1000and4000Hzwerehigherthantheaverage frequency of2000Hz.
1.8 1.7 1.6 1.5 1.4 RE
Wave latency I Wave latency III Wave latency V
LE
Control Mild Moderate Severe
RE LE RE LE RE LE RE LE
Control Mild Moderate Severe
RE LE RE LE RE LE RE LE
Control Mild Moderate Severe RE LE RE LE RE LE 1.9 4.2 4.0 3.8 3.6 6.4 6.2 6.0 5.8 5.6 5.4
Figure1 AbsolutelatenciesofwavesI,IIIandV(inmilliseconds)accordingtothesideoftheearandgroup.
RE
Interpeak I-III Interpeak III-V Interpeak I-V
LE
Control Mild Moderate Severe
RE LE RE LE RE LE RE LE
Control Mild Moderate Severe
RE LE RE LE RE LE RE LE
Control Mild Moderate Severe RE LE RE LE RE LE 2.4 2.6 2.8 2.4 2.2 2.0 1.8 4.4 4.3 4.2 4.1 4.0 2.2 2.0 1.8 1.6
Figure2 InterpeaksI---III,III---VandI---V(inmilliseconds)accordingtothesideoftheearandgroup.
Brainstemauditoryevokedpotential
Therewasnostatisticaldifferenceforanyoftheeffectsof interactionbetweenthefactorsGroupandEarintheBAER parametersevaluated. Therewasnosignificant difference forthemaineffectsofthefactorsGroupandEar.Thus,for BAERvariables,therewerenosignificantdifferencesamong
the averages of the groups and among the means of the ears.Therewasnosignificantdifferencebetweenthegroups (p=0.8517).Figs.1and2showtheboxplotgraphicsforthe absolutelatenciesofwavesI,IIIandV,andinterpeaksI---III, III---VandI---V,accordingtothesideoftheearandgroup.
Table2shows thepercentageofchangesfoundineach groupinrelationtotheabsolutelatenciesofwavesI,III,V
Table2 ChangesoflatenciesofwavesI,III,VandinterpeakI---Vforeachearofeachgroupconsideringthenormalvalues providedbySmartEP---IntelligentHearingSystems.
BAERparameters Percentageofchangecomparedtothenumberofearsevaluated p-valuea
Control n(%) MildOSA n(%) ModerateOSA n(%) SevereOSA n(%)
AbsolutelatencyofwaveI 0 0 0 0
---AbsolutelatencyofwaveIII 3(15) 4(18.2) 6(37.5) 2(11.1) 0.23
AbsolutelatencyofwaveV 2(10) 4(18.2) 8(50) 6(33.3) 0.03
InterpeakI---V 1(5) 1(4.55) 5(31.25) 3(16.7) 0.07
p-valueb --- 0.76 0.02 0.17
---aChi-squaretest.
b ComparisonofeachgroupwithOSA(mild,moderateandsevere)withtheControlgrouponlyforabsolutelatencyofwaveVthrough Fisherexacttest.
Table3 SampleagerangeinstudiesrelatingOSAandhearingcomparedtothisstudy.
Studies Agerange
(mean/standarddeviation) Totaln (malen) OSAn (controlN) Moskoetal.,1981 24---40(31±2) 20(12) 6(14) Hoffsteinetal.,1999 13---74(47±12)a 219(156) ---Bernathetal.,2009 30---55(48)b 610(610) 610 Gallinaetal.,2010 24---56(43) 75(51) 45(30) Casaleetal.,2012 25---45(31)b 39(31) 18(21) Sivrietal.,2013 27---66(47±6.23)b 138(96) 78(60) Ballacchinoetal.,2015 14---85(57±13.15) 120(77) c Thometal.,2015 37---74(57) 10(6) 10 Presentstudy 22---54(35.3±7.1) 38 28(10)
a MeanageandstandarddeviationofmaleswithOSA. b MeanageofstudygroupwithOSA.
c SubjectswithriskofOSA. ---,notspecified.
andinterpeakI---V,takingthenormalrange12providedbythe
equipmentusedinthestudy intoaccount.The chi-square testshowedanassociationbetweenthepresenceofOSAand achangeinabsolutelatencyofwaveV(p=0.03). Consider-ingthedegreeofseverityofOSA,Fisher’sexacttestfound theassociationbetweenthepresenceofmoderateOSAand thepresenceofchangeinabsolutelatencyofwaveV.
Discussion
Regarding baseline variables, it is observed that the four studygroupsareproperlymatchedforageandBMI.Theage rangeofthesampleofthisstudywaswide.However,many studies involvingthe hearingof individualswithOSA have alsoincludedsamplesinasimilarway8,9,16andevengreater
thanthatfoundinthisstudy17---19(Table3).
Regarding audiometry,nostatistical differencein audi-torythresholdscausedbythepresenceofOSAwasobserved. Specifically, a subject of the group with severe OSA had mildhearingloss20intheleftear,whoseaverageofhearing
thresholdsof500,1000and2000Hzwas26.66dBHL. More-over,fewindividualshadlowauditorythresholdinisolated frequencies:1individualfromthecontrolgroupand3 indi-vidualsin thegroup withsevere degree of AOS. Asimilar resultwasobservedinanotherstudy,16inwhichthepresence
oflowauditorythresholdwasfound,specificallyincontrol subjectswithoutOSA,andalsowithoutreportingahistoryof hearingloss.Unlikethepresentstudy,anotherstudy18found
thatindividualsathighriskforthepresenceofOSAhad low-eredtonethresholdswhencomparedtocontrol.However, fortheabovestudy,theriskforOSAwasassessedthrougha standardizedquestionnaire,withnopolysomnography diag-nosis.Also,thefactthataverywideagerangewasselected (14---85years)withthepresenceoftinnitusmayhave con-tributed tothe differencein the hearing threshold,since thetwofactorsarestronglyrelatedtothemanifestationof hearingloss.21,22
Regarding tympanometry, the results were considered normalforadults,23,24probablyduetotheexclusioncriteria
adoptedinthisstudy.Thesedatadidnotagreewiththe find-ingsoftheliteraturewheretympanometriccurvesoftypes
BandCwereobservedinsubjectswithmoderateandsevere degreeofOSA.25Thiscanbeexplainedbythefactthatthe
study citedhave included individuals who had undergone septoplastythreemonthsbeforethehearingevaluation.25
BAER examination provides objective information that canbe considered asparametersfor diagnosticpurposes, asfor the structural andfunctional integrity of the audi-torypathwaystothebrainstem,beingwidelyusedclinically, both because it has well-defined generators, and due to thecharacteristicofreproducibility.26Accordingtoastudy,
adultswithOSA have high viscosityofblood plasma, with this hyperviscosity being positively correlated with OSA severity.27 The hyperviscosity and its consequent change
of microcirculation were considered the main causes for changesinBAERinadultswithOSA.9Thesestudiessuggest
thatindividuals whohave OSA disease,when not treated withacontinuous positiveairway pressuredevice (CPAP), forexample,have bloodhyperviscosity.In addition, inter-mittenthypoxia present inadultswithaseveredegree of OSAmayrepresentariskfactorforimpairmentofthe audi-torypathway,andtheseverityand/ordurationofOSAmay contributetothedecreaseofneuronalandvascularfunction oftheauditorypathway.8Therefore,changeswereexpected
intheauditorypathwayinadultswithOSA,accordingtothe diseaseseverity.
Inthisstudy,theanalysisofqualitativedatashowedan associationbetween thepresenceof OSA andachange in absolute latency of wave V of BAER (Table 2). Moreover, considering the multiple comparisons of groups with dis-easecomparedtothecontrol,thegroupwithmoderateOSA showedan association with change in latency of wave V. Althoughnotsignificant,itisimportanttoconsiderthatthe groupwithsevere OSA hadanincreasedpercentage(33%) ofchangeinwaveVlatencycomparedtothecontrol(10%). Likewise,thegroupswithhigherseverityofOSA,moderate andsevere,hadgreateroccurrenceofchangeininterpeak I-Vcomparedtothecontrol.
The study shows that individuals with severe hypox-emiaorhypercapniahavehighprevalenceofabnormalities in BAER.28 Similar results have been reported, showing
increased interpeak I---V in 36.5% of subjects with OSA.16
the group with severe degree of OSA, showing the pres-enceof change in retrocochlear auditory pathways.8 The
sameauthors alsoidentifiedincreased valuesof latencies I,III, V and interpeaks III---V and I---V in severe degree of OSAcomparedtocontrol.8Inanotherstudy,subjectswith
OSAandhyperviscosityshowedimpairedauditorypathway inthebrainstemfromthecaudalportiontothesuperior oli-varycomplex.9Thesechangesmaybepresentasaresultof
reducedbloodflow inthe brainstemregionthat hasbeen observedinpatientswithapneaandthat,therefore,could beexacerbatingtheharmfuleffectsof apneainthe audi-torypathwayofthebrainstem.29Additionally,theresulting
modified microcirculation of blood hyperviscosity appears asthe main cause of changes in BAER in individuals with OSA.9
The reversibility of the change in BAER (latency wave IIInormalized) has been reportedin adultswith OSA who weretreatedandhadbloodviscositynormalized.Thesame authorsspeculatethatpatientswithOSAwithout hypervis-cosity,withresultswithinnormalstandardsinBAER,have effective compensatory mechanisms that balance hypox-emia, hypercapnia, acidosis and altered microcirculation causedduringapnea.
There are studies30,31 that showed discordant results
comparedtothis study,sincenochange wasfound inthe brainsteminindividualswithOSAsyndrome.However,the sameauthors30,31conductedcasestudieswithaconsiderably
smallsamplewithelevenandsixsubjectswithOSA, respec-tively.Thisstudydidnotobserveanydifferenceamongthe valuesobtainedinBAERparametersaccordingtothe sever-ityofOSA.However,thepowerofthestatisticaltestforthe quantitativeanalyses of BAERin this sample of 38 adults was 80% only for large effects, which was considered as alimiting factor.In addition,the presence of thecontrol groupwithchangesinabsolutelatenciesofwaves I,III,V, andinterpeaksI---III,III---V andI---VofBAER,mayhave hin-deredthemorepreciseidentificationthatwouldconfirmthe hypothesisthatOSAinfluencestheauditoryresponsesin dif-ferentgeneratingsites oftheauditorypathway,according tothedegreeofseverityofthedisease.
AstheavailableliteraturethatinvolvesthestudyofBAER inOSA is scarceand shows aneveninconsistent scenario, precluding theestablishment of therealinfluence of OSA in the structural and functional integrity of the auditory pathway,newstudiestoclarifytheassociationofOSAwith thedamageofthe auditorypathwayin thebrainstem are necessary.
Conclusion
The presence of OSA is associated with the presence of changesinnerveconductionofacousticstimuliinthe audi-torypathwayinthebrainstem.TheincreaseinOSAseverity does notpromote theworseningof responses assessedby audiometry,tympanometryandBAER.
Funding
This study received financial support from the São Paulo ResearchFoundation(FAPESP2013/10281-7).
Conflicts
of
interest
Theauthorsdeclarenoconflictsofinterest.
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