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Halusinasipendengarandanmekanismenya
MizunoT*

KlinikMikokoro,Nishitenma5-14-2,Kita-ku,Osaka,530-0047danInsutitutdelaPhilosophiePsychiatriquedesserviteursdelaNotre-Dame,Kitashirakawa
higashioguracho23-3,Sakyo-ku,Kyoto,606-8265,Jepang

Penulisyangsesuai: TatsuoMizuno
KlinikMikokoro,Nishitenma5-14-2,Kita-ku,Osaka
530-0047danInsutitutdelaPhilosophie
PsychiatriquedesserviteursdelaNotre-Dame
Kitashirakawahigashioguracho23-3
Sakyo-ku,Kyoto,606-8265,Jepang
Tel:81663611230
E-mail:mizunoclinique@mac.com

Diterima:08Mei2015;Diterima:13Mei2015;Diterbitkan:16Mei2015
Kutipan:MizunoT(2015)HalusinasiPendengarandanMekanismenya.JNeurolDisord3:230.Doi:10.4172/2329-6895.1000230

HakCipta:2015MizunoT.IniadalahartikelaksesterbukayangdidistribusikanberdasarkanketentuandariCreativeCommonsAttributionLicense,yang
mengizinkanpenggunaan,distribusi,danreproduksitidakterbatasdalammediaapapun,asalkanpenulisaslidansumbernyadikreditkan.
ArtikelterkaitdiPubmed(https://www.ncbi.nlm.nih.gov/pubmed/?term=Auditory+Hallucinations+and+Its+Mechanism),ScholarGoogle
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Abstrak
Halusinasi(https://www.omicsonline.org/neurological-disorders.php)pendengaranadalahsalahsatugejalapsikosisyangpalingseringdandapatdiandalkan.
Namun,dasarneurokognitifdanneurofisiologishalusinasipendengarandanverbaltetaptidakjelas.Halusinasiinidiperkirakanberakibatdaripengamatan
tidakteraturterhadapucapandalam.Padaartikelini,sinapsisdanpsikopatologis(https://www.omicsonline.org/open-access/the-importance-of-
psychopathological-assessment-in-patients-withmigraine-2155-9562-1000284.php?aid=51782)Mekanismeuntukhalusinasipendengarandibahas.Halusinasi
pendengaranmungkinterjadikarenakegagalankonektivitassinaptik.Gangguantulangbelakangdisebabkanoleheksitasineuronalabnormalsementaradan
kegagalankonektivitassinaptikakandiamati.KelainanpadaneurotransmisiasamglutamatdanGABAakanmenyebabkanhalusinasimusikal,kesadaran
pendengaranyangmeningkatdan"Leseidolieshallucinosiques"(yanghalusinasitanpadelusi).Denganmenambahkanneurotransmisiabnormaldari
dopamindan/atauserotonin(https://www.omicsgroup.org/journals/selective-serotonin-reuptake-inhibitors-are-they-all-equal-apharmacoepidemiological-
study-2167-1052-1000203.php?aid=75751)KelainanGABAdanglutamat,khayalannyaakanditerapkanpada"Leseidolieshallucinosiques"daniniakanmenjadi
halusinasiparanoid("Leshallucinationsdlirantes").AsamvalproikyangmenghambatenzimdanagonisdegradasiGABAdarireseptorNMDAakanmenjadi
pilihanpertamauntuk"Leseidolieshallucinosiques"segerasetelahonset.Jikapasienmengeluhkangejalaparanoid,antagonisreseptordopamindan
serotoninakandiinginkan.

Katakunci
Halusinasipendengaran;Eksitasineuron(https://www.omicsonline.org/open-access/reversal-of-neuronal-atrophy-role-of-cellular-immunity-in-
neuroplasticity-and-aging-2329-6895-2-170.php?aid=28203);Neurotransmisi;GABA

pengantar
Halusinasipendengaranadalahsalahsatugejalayangpalingseringdandapatdiandalkandaripsikosis(https://www.omicsonline.org/open-
access/acceptance-and-commitment-therapy-compared-to-treatment-as-usual-inpsychosis-a-systematic-review-and-metaanalysis-2378-5756-1000366.php?
aid=73088)[1].Namun,dasarneurokognitifdanneurofisiologishalusinasipendengarandanverbaltetaptidakjelas[2].Halusinasiinidiperkirakan
berakibatdaripengamatanlinglungyangtidakteratur[3].StimulasilangsungataupenyakitdidaerahWernickemenghasilkanhalusinasipendengarandan
verbaltanpapidatosubvokal[4].PenfielddanPerotmelaporkanbahwarangsanganlistrikpadaotakmenghasilkanfenomenasepertihalusinasihalustapi
initidakmenyerupaihalusinasiskizofrenia(https://www.omicsonline.org/scholarly/neurodegenerative-disorders-journals-articles-ppts-list.php)[5].
Selanjutnya,electroencephalogram(https://www.omicsonline.org/open-access/clinical-pattern-of-epilepsy-and-their-electroencephalogram-findings-2155-
9562-1000335.php?aid=64882)permukaandankedalaman(https://www.omicsonline.org/open-access/clinical-pattern-of-epilepsy-and-their-
electroencephalogram-findings-2155-9562-1000335.php?aid=64882)(EEG)padapasienselamahalusinasitidakmenunjukkankelainanyangkonsisten[6,7].
Gejalaskizofrenia[8]

Disini,kitamempertimbangkanbagaimanahalusinasipendengaranterjadisebagaiprosespikiranyangmembeda-bedakan.Gambaranklinisskizofreniadini
akandibahas,tapimungkininimerupakanprosesumumuntukpembubaranmental.Pembubaranmentaldimulaidengankeadaansepertineurosisyang
terdiridarimalaisespsikosomatik.Pasiensecarabertahapmenjadipendiamdantidakaktif.Merekacenderungtinggaldirumahsepanjangwaktu.Gejala
berikutmungkindikenali.Pertama,pengalamanasli(https://www.omicsonline.org/open-access/administration-of-three-autochthonous-bacillus-subtilis-
strains-induceearly-appearance-of-gastric-glands-and-vestiges-of-pylorus-i-2155-9821-1000271.php?aid=70328)dijelaskan.Inimengikutijenispengalaman.

1)Pemikiranyangbagus:Kondisidimanaberbagaipemikiranmenganggurmunculsecaraalami.

2)Ingatanyangmenyenangkan:Adeganyangpernahdialamidimasalaludihidupkankembalidengansendirinyatanpamempedulikansituasisaatini.

3)Gambarfantasilucu:Iniadalahfenomenafantastisyangdikembangkansepertisebuahnarasi.
4)Gambarmusikasli:Suaradanmusikbergemadikepalaseseorang.Halinijugadianggapsebagaihalusinasimusikal.

Keadaankesadarantinggijugadiamatipadapasiendenganskizofreniadini.Tampaknyaterutamadalampengertianpendengaran.

Pasiensensitifterhadapberbagairangsanganpendengaransepeleselainrangsangan(https://www.omicsonline.org/open-access/a-functional-model-of-fast-
action-selection-guided-by-emotional-stimuli-2090-4908-1000132.php?aid=72208)yangdiperhatikan.Masalahnyaharuskeluardalamkehidupansehari-hari
karenakesadaranpendengaranyangmeningkat.

Selainitu,jenisketeganganbahwasesuatuakansegeraterjadidengansendirinya.Inimembuatbingungpasien.Merekamemilikisuasanahatiyang
menegangkandanmembingungkandanperasaansamaruntukdiawasi.

Parapasienterkadangmerasaseolah-olahseseorangberadadisisinyasendiri,dibelakang,atauberadadiatas.
IniadalahkesadaransubstantifJaspers(LeibhaftigeBewutheit)[9].Merekajugamemilikikecurigaanuntukdiamatidandikomentariolehorang-orangdi
sekitar.Inibukankhayalanlukaataupengamatankarenaakanberlaludanmerekatidakbisamempercayainya.Dangangguanpemahamanlangsung,
penilaianatauingatanjugabisadiamati.

Dikatakanbahwakeadaanhalusinasi-paranoidakandiamatidari1-2minggusampaibeberapatahunsetelahkapangejala-gejalayangdijelaskandiatastelah
diamati.

Adakemungkinanbahwagejaladiatastidakspesifikuntukskizofrenia,tapiakanumumdiamatidalamprosespembubaranmental[10].

KlasifikasiHalusinasiPendengaran
Disini,kitaakanmencobamemikirkanapaituilusi.

Esquirol[11]didiskriminasikanantarailusidanhalusinasidaridefinisiambigudenganadatidaknyastimuluseksternal.Diamendefinisikankembali
halusinasisebagai"kepercayaandaripikiranbahwamerekabenar-benardirasakanmeskipuntidakadaobjekeksternaluntukmerangsangpersepsi".

Esquirolmenganggapbahwahalusinasidisebabkanolehpatologigagasandanbukanmasalahmasalah.

Esquirolmenganggapdelusidanhalusinasihampirsamaartinya.

Sebaliknya,Kahlbaum[12]menganggapbahwakegembiraansensorisselalumerupakantitikawalhalusinasi.Danitudialamisebagaihalusinasimelalui
deformasimental.

Tamburini[13]menganggapbahwagejalapsikiatridariepilepsiadalahmodelhalusinasi.Diamemahamihalusinasisebagaisentakanpusatsensorik.
Ball[14]didefinisikanhalusinasisebagai"persepsisansobjet"(persepsitanpaobjek).

Baillarger[15]menganggapbahwaesensihalusinasiadalahhalusinasipsiko-sensorik.Diaberasumsibahwahalusinasisensorikyangburuk(halusinasi
nabati)tidaklengkap.

Jackson[16]difokuskanpadakesamaanantaramimpidanhalusinasi.Diamenganggapbahwamimpidanhalusinasiadalahgejalapositifyangterkait
denganpembubaranmental.Diamenghipotesiskanbahwaperbedaantingkatgangguanpemikirandanpersepsibergantungpadaperbedaantingkat
kekuatanpelepasanneuron.

Jaspers[17]mendefinisikanhalusinasisejatisebagaisatu-satunyapengalamanyangtidakbergantungpadakehendakdandilokalisasididunialuardengan
jelas.Dandiamenyebuthalusinasiyangdekatdenganrepresentasisebagaihalusinasipseudo.Bleuler[18]mendefinisikanhalusinasisebagairepresentasi
yangdiberinilaiperseptualolehsubjek.

Janet[19]mempertimbangkansebagaiberikutberdasarkanpengamatanhalusinasiselamadisosiasi.Pemikirandelusiituberasaldaridisosiasifungsinyata
atauatenuasiketeganganpsikologis.Halusinasiadalahrepresentasiyangdiberinilainyatauntukbahansubjektif[19].

DeClrambault[20]berasumsibahwaadapengalamanutamayangnetraldansensoris(lepetitautomatismemental)didasarsemuahalusinasi.Ini
menjadihalusinasi("automatismemental")ketikatingkatpemrosesandelusionaltertentuditerapkanpadapengalamanyangtidakberartiinidan
berkembangmenjadisistemdelusional.
Ey[21]mempertimbangkankembalihalusinasidenganmengintegrasikanteorihierarkisteoripsikogenikJacksondanJanet.Diamendefinisikankembali
halusinasisebagai"persepsisansobjetpercevoir"(persepsitanpakeberatanuntukdirasakan).Diamengklasifikasikanhalusinasimenjadiduakelompok
besar,"Leshalusinasidlirantes"(yanghalusinasidengandelusi)dan"Leseidolieshallucinosiques"(yangmerupakanhalusinasitanpadelusi).Selainitu,Ey
membagi"leseidories"antara"protegeolie"(yangmerupakangambarelemenpoladasar)dan"phantidolie"(yangmerupakangambarkompositcitra
komposit,miripdenganpengalamanmimpi).

AbnormalitasNeurotransmiterpadaSkizofrenia

Kelainanneurotransmisi(https://www.omicsgroup.org/journals/effect-of-2-nitropropane-on-chemical-neurotransmission-spontaneous-evoked-in-sartorius-
muscle-2167-7700.1000102.php?aid=3391)GABA(-aminobutyricacid)danglutamatdiamatipadaskizofrenia.Dankelainaniniadasejaktahapawal.

AdajugaperubahandalamEEG,yangdianggapmencerminkanneurotransmisiGABAdanglutamatdiotak.
osilasi

EEGdiukurmedanlistrikyangdihasilkanolehpotensisinaptikselpyramidaldikorteksserebral.Sel-selpiramidmenerimaproyeksidariinterneuron
GABAergic.TingkatpenembakannyadiaturmelaluireseptorGABAsinaptik.Bilainidiukurdariruangekstraselular,makaakanmenjadiperubahanpotensial
listriksiklik(,,danosilasi).OsilasiationsdikaitkandenganneurotransmisiGABA.Padaskizofrenia,kelainanosilasiationsdiamati[18].Abnormalitas
enzimsintetisGABA,kelainanGABAtransporterdanabnormalitasreseptorGABAdianggapsebagaipenyebab[22].Padapermulaanskizofrenia,kelainan
osilasiationssudahdiamati[23].Iniberkorelasidengangejalaklinis[24,25].

Ketidakcocokan-negatif(MMN)

MMNadalahsalahsatuevent-relatedpotential.BilaPCP(phencyclidine)yangmerupakanantagonisreseptorNMDA(N-methyl-Daspartate)diresepkanpada
monyetdanMMNdiukurdenganareapendengaranprimer,amplitudoMMNdilemahkandibandingkandengansebelumpemberian[26].Selainitu,
pemberianketaminyangmerupakanantagonisreseptorNMDAtelahdilemahkanamplitudoMMNpadamanusia[27].Fromtheabove,MMNisconsideredto
berelatedwithabnormalitiesofneurotransmissionofglutamate.TheMMNamplitudeinveryearlyphaseofschizophreniaissameashealthyperson.But1.5
yearslater,theamplitudeisattenuatedthantheonsettimeinschizophrenia.ThisMMNamplitudeattenuationwasalsocorrelatedwithgraymattervolume
lossofHeschlsgyrus(partoftheauditorycortex)[28].Thereforethereisapossibilitythatthereisanabnormalityintheneurotransmissionofglutamate
fromimmediatelyafteronsetofschizophrenia.

Case
Thenwedliketoconsiderthemechanismofauditoryhallucinationsthroughcasesthatareconsideredauditoryhallucinationshascausedahardnessof
hearing.Mr.Gwasa69-year-oldJapanesemanwhoworkedasabanker.Hewasneglectfulbecauseofauditoryhallucinationsanddelusionsandoftenmade
mistakesinhiswork,asaresultofwhichhelosthisjobwithinayear.Heconsultedapsychiatrist(https://www.omicsgroup.org/journals/the-role-of-clinical-
psychiatrists-in-forensic-evaluations-of-legal-sanity-jfm-1000102.php?aid=64153)becauseofinsomnia,autism,inexpressivenessandmonologuespeech.At
thetimeofconsultation,hehaddelusionsofpersecutionaswellasauditoryandverbalhallucinationsinwhich11unknownwomenreproachedhimforhis
stubbornnessandtenaciousness.Hecouldnotunderstandthenecessityforhishospitalization.Therefore,hewasadmittedwithoutconsentattheageof23
andwasdiagnosedwithparanoidschizophrenia.Hewasprescribed18mghaloperidol,150mgthioridazinehydrochloride,12mgperphenazineand1200mg
sulpiride.HisEEGwasnormal,andhedidnotcomplainofhearingimpairment.Acomputedtomographyscanoftheheadindicatedslightfrontaland
temporalatrophy(leftdominant).Later,hecomplainedofsuddenhearingimpairment.Accordingtohim,theimpairmentoccurredbecauseofaloudauditory
hallucinationandbecauseanursewhohadcaredforhim3yearsagohadspokentohimmaliciouslyinaloudvoice.Anaudiogramshoweda65-Dbhearing
impairmentonbothsides(thefrequencyofJapaneselanguageisfrom150Hzto1500Hz.Thehearingabilityat5001000Hzwasstudied,andanaveragewas
calculated).AnEEGshowedspikeabnormalitiesatthefrontalandtemporallobes.Althoughconsultationwithanotolaryngologistwasconsideredatthat
time,thehallucinationssuddenlydiminishedandhishearingabilitywasrecovered.Hebelievedthatheregainedhishearingbecausethenurseforgavehim.
Atthistime,hisEEGwasnormalandahearingabilityof35dBonbothsideswasrecordedonanaudiogram.Subsequently,hecomplainedofloudauditory
hallucinationsandhearingimpairment.Atthistime,ahearingabilityof67.5dBonbothsideswasrecordedonanaudiogram.The100mgoflamotriginewas
prescribedinitially.Thehallucinationsdiminishedafter200mgoflamotriginewasprescribed,therebyimprovinghishearingability(35dBonbothsides).The
patienthasnotshownanysignsofimpairmentsincethen.

TheMechanismofAuditoryHallucinations
Psycopathologicallevel
Auditoryandverbalhallucinationshavebeenattributedtoaberrantactivityintheprimaryauditorycortex(Heschlsgyrus)andareusuallytriggeredby
emotionallychargedandstressfulsituations[2].Severalhypotheseshavebeenproposedtoexplainthemechanismofauditoryhallucinations[29].Inthis
study,theexplanationforauditoryhallucinationswasbasedonHenriEyorganodynamism[30],withreferencetotheperceptualexpandedmodelof
Hugdahlshypothesis[29].Inanintegratedcorticalnetwork,theperi-Sylvianregionconnectsventrallywithanteriorpartsofthetemporallobetogenerate
auditoryhallucinationsasperceptualmisrepresentations,withprefrontalregionsfortop-downinhibitorycontrolanddorsallywithparietalregionsfor
attentiontothevoice.Adefiningfeatureofauditoryhallucinationsisastrongattentionshifttowardsthevoice[29].Inschizophrenia,prefrontalcortexforup-
downinhibitorysystemassuperiorfunctionisimpaired(negativesymptom).Andthiscausesareleasefrominhibitionsforthegenerationofauditory
hallucinationsasperceptualmisrepresentationsintheleftperi-Sylvianregionandfortheattentionstowardsthevoiceintheparietalcortex.Thus,the
auditoryhallucinationsaregeneratedandattendedtointhismanner(positivesymptom).Theinnervoiceexperiencedinhealthyindividualscanbeexplained
inthesamemanner.Thefunctiontoinhibitattentiontowardsthevoiceintheparietalcortexworksnormally,whilethattoinhibitthegenerationofauditory
hallucinationsasperceptualmisrepresentationsintheleftperi-Sylvianregionisreleased.Therefore,thefrequencyofinnervoicegenerationmayincreasebut
willnotbeperceivedasanauditoryhallucination.PenfieldandPerotreportedthatelectricalstimulationofthebrainproduceselementaryhallucination-like
phenomena,butthesedonotresembleschizophrenichallucinations[5].Thismaybetheinnervoice.Ourpatienthadauditoryhallucinationsanddelusions
for30yearsandwasdiagnosedwithparanoidschizophrenia.Atrophyoftheperisylvianregionswasobserved.Gaseretal.reportedthattheseverityof
auditoryhallucinationsissignificantlycorrelatedwithvolumelossinHeschlsgyrus[31].ActivationofHeschlsgyrusisobservedduringauditory
hallucinations[32].ThevolumelossinHeschlsgyrusmaydisconnecttheneuralnetworkthatinhibitsauditoryhallucinations.Thedistinguishedfeatureof
thiscasewasthatthesuddenandloudauditoryandverbalhallucinationscausedahearingimpairmentthatdiminishedspontaneously.Thespike
abnormalitiesdetectedinhisEEGduringthesesymptomsdisappearedaftertheloudauditoryhallucinationsdiminished,suggestingthatthehallucinations
mayhavebeencausedbyabnormalexcitationsaroundtheauditoryhallucinationinhibitoryneuralnetwork.
Psychopathologyofthecaselistedaboveisasfollows.

HenriEyclassifiedhallucinationsintotwolargegroups:leshallucinationsdlirantes(hallucinationswithdelusions)andleseidolieshallucinosiques
(hallucinationswithoutdelusions)[21].
Hisauditoryhallucinationswereclassifiedasleshallucinationsdlirantesduringnormaltimes.However,duringtimesofhearingimpairment,theywereles
eidolieshallucinosiques,whichareproducedbyabnormalfiringaroundtheauditoryhallucinationinhibitorynetwork.Thus,leshallucinationsdlirantes
coexistedwithleseidolieshallucinosiqueswithinapatientwithschizophrenia.Infact,thepatientstatedthathewasunabletointerprettheloudvoicesand
evenwonderedabouttheirpresence.
Synapticlevel
About80%oftheneuronsinthecerebralcortexareexcitatoryneurons.Themajorityofexcitatorysynapsesareformedinadendriteasthespinesthatare
mushroom-likestructures[33].Thespinalconnectivestrengthwillvarydependingonthestimulusandsynaptictransmissionefficiencychangesdramatically
[34].

Thereisapossibilitythatforminganabnormalneuralcircuitscauseschizophrenia[35].Lossofvolumeofthegraymatterincerebralcortexwithafocuson
thefrontalandtemporalareahasbeenrepeatedlyreportedinschizophrenia,butthereisnoobviouschangeinglialcellnumberandnumberofneuron[36].

Intheviewofthefactthatthevolumeofcellbodyiscorrelativetothesumofneurites[37,38],thelossofvolumeingraymatterinschizophreniamaybedue
todecreaseasynapticdensity(https://www.omicsonline.org/open-access/resistance-sized-arteries-structure-and-capillary-density-changes-in-glioblastoma-
and-meningioma-peritumoral-brain-tissue-2329-6895.1000106.php?aid=12070)andneurites.Thedegreeofaggravationofschizophreniamaybedependedon
adegreeoffailureofsynapticconnectivity[35].

Atthetimeofonsetofschizophrenia,theabnormalityintheneurotransmissionofglutamicacidandGABAwillbeobserved.Andthedisturbancesofthe
spinemayoccurbythetransienthyperexcitabilityinneurotransmissionpathwaysofglutamateandGABA.
Asaresult,theMMNamplitudeattenuationandabnormaloscillationsmightbeoccurred.

Anditwillcauseamusicalhallucinations,heightenedauditoryawarenessandLeseidolieshallucinosiques(whichishallucinationswithoutdelusions).
Byaddingtheabnormalneurotransmissionofdopamineand/orserotonintoGABAandglutamateabnormalities,thedelusionswillbeappliedtotheLes
eidolieshallucinosiquesanditwillbecomeparanoidhallucinations(Leshallucinationsdlirantes).
Inourcase,thepatientexperiencedLeseidolieshallucinosiquesbecauseanewabnormalGABAandglutamateneurotransmissionwasappliedinastateof
controlledparanoidhallucinations.

PropositionofConcreteRemedyStrategy
ThevalproicacidthatinhibitstheGABAdegradingenzymeandagonistoftheNMDAreceptorwillbethefirstchoiceforLeseidolieshallucinosiquesfrom
immediatelyafteronset.Ifthepatientcomplainstheparanoidsymptoms(https://www.omicsonline.org/open-access/causal-factors-of-anxiety-symptoms-in-
children-2471-2701-1000131.php?aid=75773),thedopamineandserotoninreceptorantagonistwillbedesirable.

Conclusion
Auditoryhallucinationsmightbeoccurredduetoafailureofsynapticconnectivity.

Thedisturbanceofthespineiscausedbytemporaryabnormalneuronalexcitationsandthefailureofsynapticconnectivitywillbeobserved.
TheabnormalityintheneurotransmissionofglutamicacidandGABAwillcauseamusicalhallucinations,heightenedauditoryawarenessandLeseidolies
hallucinosiques(whichishallucinationswithoutdelusions).

Byaddingtheabnormalneurotransmissionofdopamineand/orserotonintoGABAandglutamateabnormalities,thedelusionswillbeappliedtotheLes
eidolieshallucinosiquesanditwillbecomeparanoidhallucinations(Leshallucinationsdlirantes).

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