PEMICU 4 BLOK PENGINDERAAN

Vivian Saputra
405140126
 LI
1. Fisiologi pendengaran & keseimbangan
2. Ggn / infeksi telinga dalam (otosklerosis, labirintitis)
3. Ggn pendengaran (tuli (kongenital, perseptif, konduktif),
presbiakusis, trauma akustik akut)
4. Ggn keseimbangan (BPPV, mabuk perjalanan, Meniere’s
disease, vestibular neuritis)
5. Onkologi THT (Ca nasofaring, tumor laring, angiofibroma
nasofaring juvenile)
FISIOLOGI PENDENGARAN DAN
KESEIMBANGAN
 Telinga
• Telinga luar ,tengah dan dalam
• Bag luar & tengah : menyalurkan gelombang suara dari udara ke telinga
dalam yg berisi cairan ,dimana energi suara mngalamai penguatan dlm
proses ini
• Telinga dalam : 2 sistem senosrik berbeda : koklea ( reseptor u/ gelombang
suara mnjd impuls saraf ),aparatus vestibularis ( sensasi keseimbangan)
• Pendengaran: persepsi energi suara oleh saraf ,terdiri dari 2 aspek:
identifikasi suara & lokalisasinya
• Gelombang suara : getaran udara yg mrambat terdiri dari daerah2
bertekanan tinggi krn kompresi (pemadatan) molekul udara bergantian
dgn daerah bertekanan rendah
Properties of sound wave
 Tipe konduksi
• Konduksi/hantaran suara dri telinga luar ke tlinga dalam lewat 3 jalur:
a) Konduksi osikular : hntaran glombang suara dlm telinga tengah lewat os
auditorius
b) Konduksi udara : hantaran gelombang suara melalui udara dlm telinga
tengah (jika rantai osikular terputus ,konduksi terjd lewat konduksi
udara (sering pd otosklerosis)
c) Konduksi tulang : hantaran glombang suara dalam telinga tengah
melalui tulang (ktika telinga tengah terganggu maka akan terjdi
konduksi tulang)
• Gerakan stapes pd oval window mmicu gelombang tekanan di kompartemen atas ,2 cara
stapes mnyebabkan oval window nonjol ke dalam :
a) Penekanan round window
b) Defleksi mmbran basalis
Awal jalur,gelombang tekanan mendorong maju perilimfe di kompartemen
atasmengelilingi helikotrema kompartemen bawah (t4 mnyebabkan round
window mnonjol keluar mengarah ke rongga telinga tengah u/ mngompensasi
pningkatan tekanan.

Jadi saat stapes bergerak mundur & menarik oval window kearah luar ke tlinga tengah
perilimfe mengalir kearah berlawananround window mnonjol ke dalam
mnghilangkan tekana & tdk mnyebabkan penerimaan suara

• Gelombang tekanan di kompartemen atas disalurkan mbrana vestibularis

tipisduktus koklearis mbran basilaris ( round window mnonjol keluar )
– Transmisi gelombang melalui mmbran basilaris mbran bergerak naik turun /bergetar ( krn
organ corti ada diatas mmbran basilaris maka sel rambut juga ikut getar)
 Peranan telinga dalam
• Gelombang yg merambat
– Titik resonansi : bag mmbran basilaris yg diaktifkan o/ gelombang yg merambat
pd awal ,gelombang yg merambat mmiliki kekuatan yg lemah ,tp saat lewat mmbran basilaris dari bag
dasar mnuju apeks ,gelombang mnjd kuat & titik resonansi mmbran basilaris mnjd kuat
mngaktifkan mbran basilaris
 Jarak antara stapes & titik resonansi berbanding terbalik dgn frekuensi gelomang suara yg mncapai
telinga
 Perambatan yg ditimbulkan suara tinggiberhenti di bag basal koklea
 Glombang yg suara sedang : berhenti tengah jalan
 Gelombang yg ditimbulkan suara rendah: mrambat disluruh mmbran basilaris
• Eksitasi sel rambut: getaran yg mnyebabkan getaran pd membran basilaris dititik resonansi
,mka serabut basilaris,sel batang corti ,sel rambut & lamina retikularis akan bergerak
Sel rambut dalam Sel rambut luar
a) Mngubah gaya mekanis suara (getaran cairan a) Sel rambut luar tdk mmberi sinyal ke otak
koklea )impuls listrik pendengaran ( potensial ttg suara yg datang
aksi dari otak ke kortek serebri) b) Sel rambut luar aktif & cpt berubah
pnjang (sbg respon trhdp prubahan
b) Krn berkontak dgn mbran tektorium yg kaku
stereosilia sel reseptor tertekuk maju potensial membran)elektromotilitas
mundur (ktika mmbran basilar mngubah posisi c) Sel rambut ini memendek saat
trhdp mmbran tektorium) depolarisasi dsb
d) Memfasilitasi gerakan mbran basilaris &
c) Deformasi mekanis maju mundurmbuka & mningkatkan amplitudo serta ketajaman
mnutup sal ion disel rambut suara
d) Berhub dgn serat saraf aferenmmbntuk
n.auditorius (koklearis)
n/b : modif pergerakan mbran basilaris
e) Depolarisasi sel rambut ini (saat mbran basilaris mningkatkan respon sel rambut dalam
terangkat)mningkatkan laju pelepasan ,reseptor sensorik pendegnaran peka
neurotransmitter mningkatkan frekuensi trhdp intensitas suara & dpt mmbedakan
lepas muatan diserat aferen nada suara
 Role of Inner hair cells

1. Stereosilia dari stiap hair cell terorganisasi dalam baris mulai dari rndah ke tinggi
(staircase pattern)
2. Tip linksCAMs ( Cell adhesion molecules)mnghubungkan ujung dari
stereosilia
3. Jika membran basilar terangkat ,kumpulan dari stereosilia akan menekuk
/bengkok ke arah stereosilia yg pling tinggi ,dan melonggarkan tip links nya
4. Tip link yg meregang mmbuka channel kation
5. Endolimfe memiliki konsentrasi tinggi K+ dibanding didalam sel rambut
6. Bbrp channel kation terbuka pd resting hair cell mnyebakan terjadinya
penurunan gradien konsentrasi dari tinggi ke rendah
7. Jika channel kation terbukasmakin banyak K+yg masuk ke dalam
seldepolarisasi (eksitasi) sel rambut)
8. Jika mbran basilar bergerak berlawanantiplinks tdk akan tertekuk lagi &
menutup channelhiperpolarisasi hair cells
9. Sel rambut dalam berkomunikasi via chemical synapse (saraf terminal dari serat
aferen mmbntuk saraf auditori )
10. Jika terjdi depolarisasi sel rambut p’mbukkan pintu Ca2+ mningkatkan
sekresi neurotransmitter
Sound transduction
Auditory Pathway
 Lintasan Auditorius
• Serabut lintasan auditoricabang koklearis
• Bag utama lintasan auditorius:MO,mesensefalon & regio thalamus
• Pusat yg lbh tinggi u/ pndengaran : ada dlm lobus temporalis korteks serebri

1) NEURON URUTAN PER1:

a) Berupa sel bipolar m’bntuk ganglion spiralis (ada dlm modiolus koklea)
b) Dendrit sel bipolartersebar di hair cell organ corti ( sbg saraf aferen )
c) Akson : tinggalin meatus auditorius interna sbg n.koklearismsk ke MO trbagi mnjdi 2
klompok (berakhir pd nukleus koklearis ventralis & dorsalis)

Serabut saraf eferen : nukleus olivarius sup berkhir lgsg pd badan sel

2) NEURON URUTAN KE 2
a) Neuron pd nukleus koklearis ventralis & dorsalis dlm MOmbntuk neuron ke 2
b) Akson neuron urutan ke 2 serbaut mnyilang garis tengah & ke sisi kontralateral korpus
trapezoideus nukleus olivarius sup
-lemnikus lateralis pd sisi yg sama & berakhir pd sisi yg sama
-formasio retikularis

3) NEURON URUTAN KE 3
a) Terletak dalam : nukleus olivarius sup & lemnikus lateralis
b) Berakhir : korpus genikulatum medialis mbntuk pusat auditorius kortikal
Balancing mechanism
GANGGUAN/INFEKSI TELINGA
DALAM
 Otosclerosis
 localized hereditary disorder affecting endochondral
bone of the otic capsule that is characterized by
disordered resorption and deposition of bone
– Clinical otosclerosis
•  lesion that involves stapes bone &
stapediovestibular joint  conductive hearing
impairment
– Cochlear otosclerosis
•  occurrence of pure sensorineural hearing
impairment due to otosclerosis in an ear without
any conductive component to hearing impairment
 Otosclerosis
• Epidemiology
 Otosclerosis
• Etiology
– Genetic predisposition
• Females 2x >, defects in expression of the COL1A1 gene,
type 1 osteogenesis imperfecta
– Measles
• Measles RNA has been found in archival & fresh footplate
specimen with otosclerosis, anti-measles antibody >>
– Autoimmune disease
• Antibodies to type II collagen
– Biochemistry
• As a result of reactivation of the arrested secondary
remodelling process within the cartilaginous rest areas of
the otic capsule
 Otosclerosis
• Histopathology
– Bone of otic capsule is unique  very little remodelling &
contains small region of immature cartilaginous tissue (globuli
interossei)
– Otosclerotic lesions
• Areas of bone resorption, new bone formation, vascular proliferation,
connective tissue stroma (fibroblasts & histiocytes)
• Absence of acute inflammatory cells / PMN
• Blue mantle  areas of the otic capsule that stain more basophilic
• Enlargement of perivascular spaces followed by deposition of
immature bone
• Remodelling continues  production of more mature bone
• Proliferation of blood vessels

• Active (spongiotic)  areas of > cellularity, vascularity (schwartze’s

sign), & bone resorption & formation
• Inactive (sclerotic)  focus consisting mineral bone
 Otosclerosis

Distribution of the lesion  anterior of oval window, round window niche, stapes
footplate, posterior of oval window; walls of internal auditory canal, around
vestibular & cochlear aqueducts, semicircular canal, malleus & incus
 Otosclerosis
• Pathology of conductive hearing impairment
– Expansion of the focus anterior to oval window 
fibrous fixation of footplate (conductive impairment
30-40 dB)
– Diffuse bony ankylosis involving the entire
circumference of the annular ligament  conductive
loss > 40dB
– Bone remodelling  cytokines & angiogenic factors
 deposition of connective tissue & >> vascularity 
fibrovascular proliferative
– Otosclerotic bone can invade the round window niche
 Otosclerosis
• Pathology of sensorineural hearing impairment
– Sensory & neural elements of cochlea & stria
vascularis are intact
– The focus reaches the endosteum of the cochlea 
atrophy of spiral ligament with impairment of
fibrocytes & replacement by an amorphous
eosinophilic substance (hyalinization)
– Cytokines released by remodelling bone  reached
the ligament  disrupt fluid & ion homeostasis within
the cochlea  sensorineural hearing impairment
 Otosclerosis
• Diagnosis
– Otoscopy
• Flamingo flush/schwartz’s sign (vascularity on tympanic membrane of
an active otosclerosis)  rare
• Can also occur when the membrane is abnormal (chronic otitis media)
– Gold standard  surgery
• bone around the oval window may be whiter than normal
• After surgical removal  bony atic wall thicker than normal
– Histological diagnosis
– Pure tone audiometry
• Air-bone gap & Carhart notch
– Radiology
• High resolution CT
 Otosclerosis
• Management
– Fluoridation of drinking water
– Oral fluorides
– Conventional hearing aids
• Effective method of managing conductive hearing
impairment
– Bone-anchored hearing aids
– Surgery
• Stapedectomy & mobilization of the stapes
• Fenestration procedures
• Mobilization of the stapes revisited along with stapedectomy
with prostheses in the later half of 20th century
 Bacterial labyrinthitis
•  inflammation of the labyrinth
– Serous / toxic labyrinthitis
• Sterile inflammation response to the labyrinth to bacterial
toxins & characterized histologically by acidophilic staining of
the perilymphatic fluid
• Result from COM & may be meningitis
– Suppurative otogenic labyrinthitis
• Caused by bacterial invasion to the inner ear & characterized
histologically by collections of PMN in the perilymphatic
spaces at the site of bacterial invasion
• Forming of local precipitate  endolymphatic hydrops 
necrosis of membranous labyrinth + spread to meninges
– Suppurative meningogenic labyrinthitis
• Spread of bacteria from the subarachnoid space into the
labyrinth (via cochlear duct or internal auditory canal
 Bacterial labyrinthitis
• Etiology
– B-haemolytic streptococci, pneumococci, Staphylococci,
Haemophilus inJluenzae, Proteus vulgaris and
Pseudomonas aeruginosa

• Clinical picture
– Acute / subacute onset of hearing loss
– vertigo with malaise and fever in association with an upper
respiratory infection
– Bacterial invasion  inflammation and tissue destruction
(necrosis) with a fibro-osseous reaction  profound
auditory and vestibular functional loss
 Bacterial labyrinthitis
• Clinical course
– Dissemination of infection from middle ear space
(otitis media & cholesteatoma)
– Early stages
• Sensorineural hearing loss, but various cytocochlear
elements (hair cells, spiral ganglion, stria vascularis) are
intact
–  the hearing loss is metabolic in nature
inflammatory cytokines disrupt the integrity of spiral ligament 
ion & fluid maintenance within the cochlea can’t be maintained
the host inflammatory response  hearing loss
– Serous labyrinthitis  reversible hearing loss
– Suppurative labyrinthitis  permanent hearing deficit
 Bacterial labyrinthitis
• Treatment
– Suppurative labyrinthitis
• Antibiotics + steroid
 timely institution can reverse the sensorineural hearing
loss
– Acute labyrinthitis
• Bedrest, IV antibiotics, & sedatives (prochlorperazine)
– Observed carefully for early signs of meningitis
• General condition improved  middle ear & mastoid should
be explored (surgery)
• With suspected labyrinthine fistula  early surgical
management to prevent deterioration of inner ear function
 Bacterial labyrinthitis
• Complication
– Balance disturbance  1st sign of labyrinthine
fistula (invariably into the lateral canal)
• chronic low grade imbalance with/-out detectable
nystagmus, sudden acute vertigo (rare),
• erosion of the bone overlying the lateral canal 
mucosal & squamous epithelial disease
 Viral labyrinthitis
• Clinical presentation
– Upper respiratory infection, associated with an acute
disturbance of auditory and vestibular function with vertigo and
nystagmus (3-5 days)
– Varying degrees of permanent hearing loss

• Histopathology
– restricted to the scala media, vestibular labyrinth, internal
auditory canal
• degeneration of the organ of Corti, early encapsulation of the tectorial
membrane, degeneration of the stria vascularis, and round cell
infiltration of the modiolus and contents of the internal auditory canal
• saccule was degenerated with sloughing of the otolithic membrane
• Cystic degeneration of the hair cells with round cell infiltration
(typical)
GANGGUAN PENDENGARAN (TULI (KONGENITAL,
PERSEPTIF, KONDUKTIF), PRESBIAKUSIS, TRAUMA
AKUSTIK AKUT)
 Hearing loss & deafness
• Hearing impairment is the
inability to hear as well as
someone with normal
hearing.
• Hearing impaired people
can be hard of hearing
(HOH) or deaf.
• If a person cannot hear at
all, then they have deafness
• Hearing impairment may be
inherited, caused by
– maternal rubella or
complications at birth,
– certain infectious
diseases such as
meningitis,
– use of ototoxic drugs,
– exposure to excessive
noise and ageing
 Hearing loss & deafness
• People with hearing loss can benefit from the
use of hearing devices, such as
– hearing aids,
– cochlear implants
– They may also benefit from speech therapy, aural
rehabilitation and other related services
 Age related sensorineural hearing
impairment (presbycusis)
•  mid- to late-adult onset, bilateral, progressive
sensorinerual hearing loss, where underlying cause
have been excluded
• Exclude
– Loud noise exposure
– Underlying medical condition
• Atherosclerosis, DM, hypertension, Paget’s disease, myxoedema
– Intrinsic otological disease
• Otosclerosis, chronic otitis media, Meniere’s disease
– Head injury
– Ototoxic drugs
• Pathology
– External ear
• Cerumen production >>, epithelial migration <<, hair growth >>, potential
collapse of ear canal, enlargement of pinna
– Middle ear
• Stiffening, thinning, loss of vascularity of tympanic membrane
• Arthritic changes & ossification in ossicles & ossicular joints
• Degeneration of middle ear muscles
• Calcification of cartilaginous support of eustachian tube
– Inner ear
• Sensory type  loss of hair cells at the basal end of the organ of corti
• Neural type  degeneration of neuron of the cochlear nerve
• Vascular / metabolic  atrophy of stria vascularis
• Mechanical / cochlera conductive associated with stiffness of cochlear basilar
membrane
• Change of the cochlear duct (intracellular organelles, endolymph composition)
• Mixed
• Other factors
– Genetic
• Homozygotic twins >>
• Ahl genes in mouse chromoseome 10
• Mitochondrial genome mutations / variations
– Environmental
•  not clear
• Ex: noise exposure, cigarette smoking, alcohol use,
systolic blood pressure & blood hyperviscosity
• Symptoms
– High-tone hearing loss over the age of 50 to age-
related changes
– Slow & insidious hearing problem
– Difficulty in hearing, conversation (in the presence of
other background/competing sound)
– May be tinnitus

• Examination
– Pure tone audiogram
•  mild high-tone hearing loss  progressive loss of middle
(1-2 kHz) and low (250 & 500 kHz) frequencies
• Diagnosis
– Over the age of 60
– Normal examination findings
– A symmetrical hearing loss

• Management
– Nonspecific management
• Hearing aids (little benefit if mild high-tone hearing loss)
• Reduction of background noise
• Psychological counselling, lip-reading class
– Specific management
• Hearing aids
• Management of tinnitus
 Noise-induced hearing loss
•  reduction in auditory acuity associated
with noise exposure
– May be
• temporary threshold shift (TTS)
– Hours to days
• permanent threshold shift (PTS)
– Following repeated TTS or following a single episode of noise
exposure
–  maximum reduction in sensitivity to
stimulation in the range 3-6kHz & recovery at
8kHz
• Pathology
– Cochlear function (metabolic & structural changes)
• Recovery from TTS  role of metabolic mechanisms
– Acoustic overstimulation  excessive release of neurotransmitters
associated with transduction function of the cochlea
• Persistance of PTS  structural change mechanisms
– Change to the micromechanical structures within the cochlea
– Apoptosis & necrosis
• Cessation of voice  apoptotic changes in OHC (nuclear
condensation & cell body shrinkage) in 5 min  necrosis in 30 min
– Predisposing factors
• Smoking, DM, cardiovascular disease
• Recreational drugs; ototoxic agents
• Symptoms
– Acustic shock
• Otalgia, tinnitus, hyperacusis, dizzines, headaches, sleep
disturbance, poor concentration (common)
• Neck pain, shoulder pain, panic attacks (less)
– History of hearing difficulties in the presence of
background noise is encountered
• Lack of clarity rather than loss of volume
– Difficulty of the tv being louder than is comfortable for
others
– Telephone conversation may become difficult
– As hearing loss progress  more obvious hearing problem
& frequently have to ask others to repeat themselves
• Examinations
– Pure tone audiogram with both bone & air conduction
• High-tone hearing loss on 4 or 6 kHz with some recovery at 8 kHz
– Tympanometry
• Confirm normal middle ear functioning
– Evoked reflex audiometry
• Objective measure of hearing thresholds  significant asymetry 
MRI to exclude vestibular schwannoma

• Diagnosis
– Clear prolonged history of unprotected exposure to excessive
noise
– No evidence of any other otological pathology
– Audiogram  good preservation of low & mid frequencies,
significant high-tone hearing loss (classical notching 4-6 kHz)
• Managements
– Prevention
• Further noise exposure should be kept away as far as
possible
– Personal hearing protection
• Earplugs, earmuffs, active noise reduction
– Non specific management
• No way to replace the hearing that has been lost
– Mild high-tone hearing lost  hearing aids
• Reduction of background noise
• More severe hearing loss  directed rehabilitation +
psychological counselling
– Specific management
• Hearing aids & tinnitus retraining therapy
TRAUMA AKUSTIK AKUT
 Ossicular chain and associated injuries
• Trauma to the ear fractures of the temporal bone and damage to the
cochlea and facial nerve.
– Lesser trauma results in damage to the ossicular chain.
• The most common lesion identified is dislocation of the incus
• Surgical management:
– Surgical correction of incus  using conventional ossiculoplasty
techniques or repositioning of the incus
– In cases of incus dislocation, repositioning of the incus in its
physiological position is an attractive option and is best achieved using
a posterior attic approach combined with a tympanotomy
• Result
– Physiological repositioning of the incus has the most impressive
results, but good results can also be obtained with conventional
ossiculoplasty techniques.

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 Temporal bone trauman
• Def:
• Physical insult of the temporal bone induced
by impact with a blunt surface or penetrating
missile.

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 Clinical features
• History
– 17% of patients will lose all hearing in the affected ear as a
result of a temporal bone fracture
– conductive hearing loss of greater than 20dB hearing loss
(HL) will occur in 66% of patients if tested for within the first
72 hours
– 17% patients will have a persisting conductive hearing loss
six weeks after sustaining a temporal bone fracture
• Clinical sign
– Adanya bukti penetrating injury pada temporal region
– Otorrhea
– Bruising pd processus mastoid (battle’s sign)
– Lower motor neurone facial nerve palsy

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 Investigation
• Using thin section axial and coronal high
resolution CT scans  diagnostic gold standard
test for the presence or absence of a temporal
bone fracture
• Treatment is usually guided by symptoms and
clinical signs
• MRI
– Identified temporal bone contusion not identified by
CT scanning
– provide evidence of facial nerve injury and
haematoma within the cochlear

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 Investigation
• Hearing assessment
– Crude testing of the hearing is part of the Glasgow Coma
Scale assessment in testing response to verbal commands
• Vestibular assessment
– Unilateral acute vestibular failure will lead to horizontal
beating nystagmus with the quick component away from
the affected ear.
• Facial nerve function
– can be assessed by observing active and passive facial
movements
• CEREBROSPINAL FLUID LEAK
– The best investigation is to submit the suspicious fluid for
beta-2 transferrin analysis.

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 Management
• Prophylactic antibiotics
– Routine antibiotic use for meningitis prophylaxis is not supported
• Lacerations of the external auditory meatus
– Haematorrhoea  hallmarks of a skull base fracture
• usually arises from a laceration of the skin of the external auditory meatus
– Impressive haemorrhage  potential laceration of the jugular bulb or carotid
artery, darah kabur melalui mem tymp yg rusak / fraktur dr tulang temporal
– The perforation is initially treated conservatively with the avoidance of water
or other contaminants.
– Surgery  tympanic membrane perforations, which persist for three months
or more after the initial injury.
• Haemotympanum
– diagnosed by the characteristic appearance of the blue drum and is the major
reason for the conductive hearing impairment found in 41 percent of patients
with a temporal bone fracture
– Spontaneous resolution within 3-6 weeks (pd 72% kasus)

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 • Ossicular disruption with an intact tympanic membrane
– A patient whose conductive hearing loss persists six weeks
post-injury is likely to have sustained damage to the
ossicular chain
– Tympanopalsty
• CSF leak
– occurs in 25–33 percent of patients with a temporal bone
fracture
– Initially conservative  spontaneous resolution within five
days (81%)
– leak persists  lumbar drainage can lead to resolution
– The site of the leak must be identified to facilitate closure.
Fluorescein cisternography is sometimes required to identify
the site.

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

GGN KESEIMBANGAN (BPPV, MABUK PERJALANAN,
MENIERE’S DISEASE, VESTIBULAR NEURITIS)
 Vestibular neuritis
•  disorder in which there is sudden,
spontaneous, isolated, total / subtotal loss of
afferent vestibular input from one labyrinth

• Etiology
– Viral infection of the vestibular nerve
• Latent HSV type 1 infection has been demonstrated in the
vestibular nerve
– Bony canal of superior division of semicircular canal is
longer & narrower  more vulnerable to entrapment
when the nerve is inflammed
• Clinical manifestation
– Acute spontaneous vertigo
• aggravated by head movement, minimized by keeping the
head still & the eyes shut
– Nausea, vomiting
– Postural imbalance
• unsteady when standing  veer towards the side of the
affected labyrinth
– A spontaneous horizontal-torsional nystagmus
– Head impulse test  ‘catch up’ saccades with rotation
of the head toward the affected side
– Rotate towards the affected side when attempting to
march on the spot with their eyes closed
(fukuda/unterberger test +)
• Examination
– Subject visual horizontal test
– Electronystagmography
– Caloric testing
• For demonstratong a canal paresis about 3-4 days after
onset of symptoms

• DD
– Cerebellar infarction
• the head impulse test is (-), CT, MRI
– Labyrinthine infarction
• Hearing loss (+)
– Autoimmune inner disease
– First attack of meniere disease
• Management
– Corticosteroid (methylprednisolone) & antiviral
(NOT valacyclovir)

• Complications
– Acute peripheral vestibulopathy on the opposite
side (bilateral sequential vestibular neuritis)
– BPPV
 MENIERE’S DISEASE
 Gangguan yang ditandai oleh serangan spontan vertigo,
dengan gangguan pendengaran sensorineural yang fluktuasi,
tinnitus, dan kadang” perasaan penuh atau tekanan di telinga.

Etiologi :
• Idiopatik tapi berbagai faktor predisposisi telah diidentifikasi.
faktor” predisposisi menyebabkan produksi berlebihan atau
malabsorpsi endolymph  endolymphatic hipertension 
pembesaran masif labirin membran (hydrops endolimfatik)
 ruptur periodik labirin membran  kebocoran endolymph
kaya potasium ke dalam perilymph  serangan meniere.

Scott Brown’s otorhinolaryngology, 7th edition

 MENIERE’S DISEASE
Manifestasi Klinis
• Serangan berulang vertigo spontan,
mual, muntah
• Gangguan pendengaran frekuensi
rendah, tinnitus & perasaan penuh
di telinga.
• Serangan yg khas memiliki 3 fase ,
yg masing” ditentukan oleh arah
nistagmus spontan :
– Fase irrritatif
Nystagmus Horizontal /
horizontal-torsional , berdetak
ke arah telinga yang terkena
(terakhir <1 jam)
– Fase paretik
Scott Brown’s otorhinolaryngology, 7th edition
Nystagmus berdetak jauh dari
telinga yang terkena (beberapa
jam - 1 atau 2 hari)
– Fase pemulihan
Nystagmus berdetak ke telinga
yang terkena lagi ( berlangsung
sama lamanya dengan fase ke-
2)
• Pada tahap lanjut penyakit 
dapat terjadi drop attacks.
– Pasien jatuh ke tanah tanpa
peringatan & bisa menderita
patah tulang atau luka serius
lainnya.
Ballenger JJ, Snow JB.
Otorhinolaryngology,
Head and neck
surgery. 17th ed.
Canada : Williams &
Wilkin; 2009
 MENIERE’S DISEASE
Diagnosis Diagnosis banding
• Pada tahap awal Penyakit Meniere, • Vestibular neuritis
tes fungsi auditori dan vestibular
 sering normal di antara • Vertigo migrain
serangan.
• Penyakit autoimun telinga
• Seiring perkembangan penyakit 
gangguan permanen fungsi dalam.
auditori & vestibular menjadi jelas
terlihat pada sisi yg terkena.
• Audiogram  semua frekuensi
menjadi terpengaruh sehingga
menyebabkan gangguan
pendengaran sensorineural yang
datar.
• Electrocochleografi  paling
sensitif & spesifik untuk penyakit
Meniere ketika stimulus tone-burst
& click digunakan
Scott Brown’s otorhinolaryngology, 7th edition
 Tatalaksana
• Tujuan utama terapi : untuk – Selective vestibular
menurunan produksi atau neurectomy
timbunan endolymph. – Labyrinthectomy
• Pembatasan sodium yg ketat • Gangguan pendengaran  alat
(sodium di urin <50 mmoL/hari) bantu dengar dapat dibantu
& diuretik  efektif dengan implantasi koklea.
mengurangi frekuensi serangan • Aminoglikosid sistemik
vertigo. (streptomycin & gentamycin)
• Pasien yg terus mengalami
serangan vertigo mungkin
cocok untuk operasi:
– operasi endolymphatic sac
(ES)
Scott Brown’s otorhinolaryngology, 7th edition
Benign paroxysmal positional vertigo
•  disorder characterized by brief attacks of vertigo,
nystagmus, precipitated by certain changes in head
position with respect to gravity

• Etiology
– Gravity, sequestered otoconia  inappropriate stimulation
of the hair cells
• Otoconia find their way into the duct of an SCC (canalolithiasis) or
attach to cupula (cupulolithiasis)  altering endolymphatic fluid
pressure  vertigo & nystagmus
• Otoconia in the posterior-anterior SCC  vertical torsional
nystagmus; lateral SCC  horizontal nystagmus
– Head trauma
– Vestibular neuritis
• Clinical manifestations
– Reccurrent episodes of vertigo following certain
changes in head position with respect to gravity
• Last 10-20 seconds
– Nausea, vomiting
– Remain unwell between attacks & constantly dizzy
– Nystagmus following Dix-Hallpike manoeuvre

• Diagnosis
– Clinical signs & MRI (exclude structural central cause)
• DD
– Migrainous vertigo
– Posterior fossa tumour
– Malformation or degenerative conditions

• Management
– Epley manoeuvre
 Juvenile angiofibroma
•  uncommon, benign & extremely vascular tumour that
arises in the tissues within the sphenopalatine foramen;
locally invasive
– The tumour extends into the nasopharynx, paranasal sinuses,
pterygopalatine & infratemporal fossa
– Larger tumours can involve orbit & cavernous sinus

• Pathology
– Well defined, lobulated, covered by nasopharyngeal mucosa
– Consists of proliferating, irregular vascular channels within a
fibrous stroma
– Tumour blood vessels lack smooth muscle & elastic fibers 
sustained bleeding
• Etiology
– Androgen receptors are present in vascular & stromal
elements of the tumours (75%)
– Vascular endothelial growth factors has been found
localized on both endothelial & stromal cells
– Overexpression of insulin like growth factor II
– Mutations of adenomatous polyposis coli (APC) gene
• Presentation
– Reccurrent severe epitaxes + nasal obstruction
– Early symptoms  swelling of cheek, trismus, hearing loss
secondary to eustachian tube obstruction, anosmia, nasal
intonation
– Invasion of the orbit  proptosis, diplopia, visual loss, facial
pain, headache
– Anterior rhinoscopy
• Abudant mucopurulent secretions in the nasal cavity 
obscure the tumour from vision
– The soft palate often displaced inferiorly by the bulk of tumour
(pink reddish mas that fills the nasopharynx)
• Assessment
– Plain lateral skull radiographic
• Anterior bowing of the
posterior wall of the
maxillary sinus
– CT & MRI

– Stagging system (Fisch)

• Treatment
– Preoperative embolization
• Some tumours acquire blood supply from other vessles
like internal carotid artery
– Preoperative chemotherapy
• Flutamide (nonsteroidal androgen receptor blocker)
– Surgical resection
• Endoscopic endonasal techniques
• Open approaches
• Radiotherapy
NASOPHARYNGEAL CARCINOMA
 Etiology
• genetic factors,
• early latent infection by EBV and its
reactivation and
• exposure to environmental carcinogens.

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 Pathogenesis
• The exact steps involved in the pathogenesis of
NPC are far from clear
• Genetically determined susceptibility
undoubtedly plays a fundamental role, which is
supported by strong epidemiological evidence
• The part played by the EBV, although still
unconfirmed, is likely to be critical
• epidemiological evidence shows that an
environmental carcinogen(s) has a definite role to
play. However, the exact mechanism involved is
much more controversial

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 Clinical findings
• Early tumor  no symptoms • Neurological symptom: headache /
– Jika memberikan gejala  tdk cranial nervesymptoms
spesifik • Tempat metastasis: paru, tulang, hati
– Gejala timbul dr besar dan posisi – Paru  biasanya asymptomatik,
tumordi nasofaring, penyebaran terdeteksi setelaah dilakukan
disekitar nasofaring, dan distant imaging
metastasis – Tulang  localized pain dan dpt di
• Gejala paling sering: benjolan di leher dx dgn bone scan
(unilateral) – Hepatic  jika kecil tdk memberi
• 30% psn dgn nasal symptoms: gejala, jika besar memebri sara tdk
– Bloodstained nasal discharge nyaman pd abdomen
– Nasal obstruction
– Post nasal drip
– frank epistaxis
• 20% psn dgn aural symptoms
– Deafness
– Tinnitus
– Otalgia
– Retract tympanic membrane / otitis
media dgn efusi
Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed
 Diagnosis

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 Examination
• Transoral retrograde nasopharyngoscopy 
cara terbaik melihat nasofaing
• Antegrade nasopharyngoscopy  preferred
dan hrs dilakukan dgn topikal anestesia
– Sumbatan kapas direndam pd 5% cocain solution
dan diletakkan pd dasar hidung

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

 DD
• Rhinosinusitis / nasal polyp
• Sinonasal undifferentiated carcinoma
• Amelanotic melanoma

Scott brown’s otorhinolaryngology, head and neck surgery. 7 th ed

Scott brown’s otorhinolaryngology, head and neck surgery. 7th ed

Other dx tool
• Serology
– Deteksi IgA antibodies to EBV spesific antigen
• Cytology
– Fine needle aspiration cytology  berguna untuk psn dgn pembesaran nodul
mencurigakan tetapi primary tumor tdk terdeteksi
• Imaging
– CT scan  widely used methode for primary tumor evaluation
• accurately demonstrates the tumour mass, including submucosal disease,
and its local extension, and it is preferred by many clinicians to
demonstrate bony erosion of the skull base or vertebral bodies
– MRI  most accurate method of evaluating the primary tumour and its direct
local spread.
• much more sensitive than CT in evaluating marrow infiltration
• due to its much higher cost, MRI is not easily available or affordable,
especially in developing countries where NPC is endemic.
– Ultrasound  its accuracy is very operator dependent.
• FNAC of neck nodes under US guidance is the most accurate method to
diagnose nodal metastases especially in the post-irradiated neck
 Daftar Pustaka
• Sherwood, human physiology
• Scott Brown’s otorhinolaryngology, 7th edition
• Ballenger JJ, Snow JB. Otorhinolaryngology, Head and neck
surgery. 17th ed. Canada : Williams & Wilkin; 2009