PEMICU 4

BLOK PENGINDERAAN
CLARISSA TAN
405120024
FISIOLOGI PENDENGARAN DAN KESEIMBANGAN

• Sound waves = alternating high- and low-pressure re-

gions traveling in the same direction through some
medium (such as air).
• Originates from vibrating object.
• Frequency = pitch
• Higher frequency  higher pitch
• Amplitude = intensity (in dB)
• Higher amplitude  louder
http://www.britannica.com/science/ear/The-
physiology-of-hearing
Fisiologi Pendengaran
https://www.studyblue.com/notes/note/n/uni
t-3/deck/5563686
Hall JE. Guyton and hall textbook of medical physiology. 13th ed.
Philadelphia: Elseviers Saunders; 2015.
Role of the vestibular apparatus
Balancing mechanism
• Apparatus vestibularis
• Kanalis semisirkularis deteksi akselerasi atau deselerasi
kepala rotasional atau angular (saat berhenti berputar,
jungkir balik, atau menengok)
• Organ Otolit
• Utriculus akselerasi dan deselerasi linier arah horizontal (cth.
Berjalan lurus, memiringkan kepala)
• Sacculus keseimbangan dalam gerakan miring kepala yang
menjauhi posisi horizontal (cth. Bangun dari posisi tidur)

Sherwood L. Fisiologi Manusia Dari Sel Ke Sistem (Edisi 6, 2011)

HEARING IMPAIRMENT
• 2 types:
• Sensorineural
• Conductive
 AGE-RELATED SENSORINEURAL
HEARING LOSS
• Mid- to late- adult onset, bilateral, progressive sensorineural
hearing loss, where underlying causes have been excluded.
• Primary factors:
• Loud noise exposure
• Underlying medical conditions (e.g. atherosclerosis, diabetes,
hypertension, Paget’s disease of bone, myxo- edema)
• Intrinsic otological disease (e.g. otosclerosis,
chronicotitismediaandMenie`re’sdisease),headinjury and ototoxic drug
therapies
• 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
• Electron microscope finding:
– In the sensory type, there is loss of hair cells (and of
sustentacular cells) at the basal end of the organ of Corti.
– In the neural type there is degeneration of the neurons of
the cochlear nerve, with resulting cochlear ganglion cell
loss.
AGE-RELATED SENSORINEURAL HEARING
LOSS
S O A P
• High-tone • Pure tone Sensorineural • Nonspecific
hearing loss over audiogram: mild hearing management :
the age of 50 to high-tone Hearing aids (little
age-related hearing loss  benefit if mild high-
changes progressive loss tone hearing loss)
• Slow & insidious of middle (1-2 • Reduction of
hearing problem kHz) and low background noise
• Difficulty in (250 & 500 kHz) • Psychological
hearing, frequencies counselling, lip-
conversation (in reading class
the presence of • Specific
other management:
background/com Hearing aids
peting sound) • Management of
• May be tinnitus tinnitus
NOISE-INDUCED HEARING LOSS
• Definition: reduction in auditory acuity associated with noise
exposure
• Temporary temporary threshold shift (TTS), duration may be from hours to
days
• Permanent  permanent threshold shift (PTS). Occur following repeated TTS,
or following a single episode of noise exposure.
• 'acoustic trauma'  a single exposure to an intense sound leads to an
immediate hearing loss.
• Characteristic notched audiometric  maximum reduction in
sensitivity to stimulation in the range 3-6 kHz, and recovery at 8 kHz.
Scott-Brown’s Otorhinolaryngology Head &
Neck Surgery 7Th Edition page 3548-3555
• Pathology
• Cochlear function (metabolic & structural changes)
• Recovery from TTS  role for metabolic mechanism
1. Metabolic mechanism
• Acoustic overstimulation  excessive release of
neurotransmitters associated with the transduction
function of the cochlea
• Other metabolic cochlear mechanism: outer hair cell
plasma membrane fluidity, role of glucocorticoid receptors,
oxidative stress
2. Structural Mechanism
• Changes to the micromechanical structures of cochlea
• Depolymerization of action filaments in stereocilia 
substrate of TTS
3. Apoptosis and necrosis
Scott-Brown’s Otorhinolaryngology Head &
Neck Surgery 7Th Edition page 3548-3555
• Predisposing factors:
• Ahl gene
• Interaction with age-related hearing loss
• Smoking
• Diabetes and cardiovascular disease
• Blue eyes
• Recreational drug
• Exposure to ototoxic agents
• Dx of hearing loss:
1. Age
2. Noise
3. Idiopathic component

Scott-Brown’s Otorhinolaryngology Head &

Neck Surgery 7Th Edition page 3548-3555
• History:
• Male
• Middle age
• Complaint of
tinnitus
• Woman  acoustic
shock
• History of hearing
difficulties

Scott-Brown’s Otorhinolaryngology Head &

Neck Surgery 7Th Edition page 3548-3555
• Examination
• Investigation: classical audiometric pattern is of a high-tone
hearing loss with a notched appearance centred on 4 or 6
kHz, with some recovery at 8 kHz.
• Tympanometry is helpful to confirm normal middle ear
functioning.
• Individuals in whom a significant nonorganic component
(feigned thresholds) is suspected cortically evoked reflex
audiometry
• Cases of significant asymmetry, MRI to exclude a vestibular
schwannoma
• Loudness discomfort levels are a useful measure of
hyperacusis.

Scott-Brown’s Otorhinolaryngology Head &

Neck Surgery 7Th Edition page 3548-3555
Dx
• a clear and prolonged history of unprotected
exposure to excessive noise,
• no evidence of any other otological pathology
• an audiogram showing good preservation of mid and
low frequencies but a significant high-tone hearing
loss with classical notching at 4-6 kHz

Scott-Brown’s Otorhinolaryngology Head &

Neck Surgery 7Th Edition page 3548-3555
Management
• Prevention: avoiding the excessive noise altogether or, use
of ear protection in the form of earplugs or earmuffs.
• Personal hearing protection: earplugs, earmuffs and
active noise reduction
• Nonspecific management: reduction of background noise
(as far as possible), face-to-face conversation, more
severe hearing loss infrared headphones for use with
television, volume controllable telephones, louder doorbells, often
with an alternative. alerting system such as a flashing light or
vibrating pager system. Lip-readingclasses can be extremely
valuable.
• Specific management: hearing aid
• Claim
Scott-Brown’s Otorhinolaryngology Head &
Neck Surgery 7Th Edition page 3548-3555
NOISE-INDUCED HEARING LOSS
S O A P
Sering: • Pure tone audiogram (konduksi Gangguan Prevention:
• Otalgia udara & tulang) pada 3 & 6 kHz pendengaran • Earplugs
• Tinnitus  untuk mengidentifikasi tuli berupa • Pengurangan
• Hyperacusis konduktif pengurangan volume suara dari
• Dizziness • Tympanometri  untuk ketajaman sumber
• Sakit kepala konfirmasi telinga tengah pendengaran • Penggunaan
• Gangguan berfungsi dgn Normal yang disebabkan proteksi telinga
tidur • MRI pada kasus asimetris yg dengan paparan ditempat kerja yg
• Kurang signifikan, untuk menyingkirkan kebisingan. bising
konsentrasi DD vestibular schwanoma (earmuff/protector
Jarang: • Tinnitus pitch & intensity telinga)
• Nyeri leher matching
• Nyeri pundak • Loundness discomfort levels
• Serangan
panik

Scott-Brown’s Otorhinolaryngology Head &

Neck Surgery 7Th Edition page 3548-3555
IDIOPATHIC SUDDEN SENSORINEURAL HEARING LOSS
(ISSNHL)
TULI KONGENITAL
Congenital permanent bilateral hearing loss
• Risk Factors:
• Three major:
• History of treatment in an NICU or special care abby unit (SCBU) for > 48 hours.
• Family history of early childhood deafness
• Craniofacial anomaly (e.g) cleft palate, abnormalities of pinna & ear canal) associated
with hearing impairment

• Others:
• In utero infection (CMV, herpes, toxoplasmosis or rubella
PEMERIKSAAN

+Serological test : infeksi Rubella atau

CMV
+Genetic screening
TATALAKSANA
• Genetic counselling
• Support and education
• Hearing aid
SYNDROMIC HEARING IMPAIRMENT
 SYNDROMIC HEARING IMPAIRMENT
Autosomal Dominant Hearing Impairment
Branchio-Oto-Renal Syndrome (BOR)
Hearing loss (onset bervariasi), auricular
malformations, branchial arch remnants, renal
anomalies.
Preauricular pits-
https://elementsofmorphology.nih.gov/images/ter
ms/Pit,Preauricular-large.jpg

Branchial fistula-
http://www.surgicalnotes.co.uk/files/imag
es/branchialfistula.jpg
 SYNDROMIC HEARING IMPAIRMENT
Autosomal Dominant Hearing Impairment
Crouzon Syndrome •cranial synostosis, hypertelorism,
exophthalmos, parrot-beaked nose, short upper
lip, hypoplastic maxilla, and a relative mandibular
Prognathism.
•One-third of affected persons have a conductive hearing loss secondary to
external or middle ear abnormalities, and there is frequently an associated
sensorineural component
•Other feature: meningiomas, spinal cord dorsal
root schwannomas, and posterior subcapsular
cataracts
Neurofibromatosis 2 NF2 is a central form of neurofi bromatosis characterized by bilateral vestibular
(NF2) schwannomas
Kriteria Diagnosis :
(1)bilateral internal auditory canal/
cerebellopontine angle tumors;
(2) a first-degree
relative with NF2 and a unilateral eight nerve
tumor;
(3) a first-degree relative with NF2 and
2 of the following: neurofi broma, meningioma,
glioma, schwannoma, or juvenile posterior subcapsularlenticular opacity
 SYNDROMIC HEARING IMPAIRMENT
Autosomal Dominant Hearing Impairment
Stickler Syndrome (STL) •disorder of collagen connective tissue
= hereditary arthro- characterized by marfanoid features, spondyloepiphyseal
ophtamopathy dysplasia, joint hypermobility, midface hypoplasia, severe myopia, and varying
degrees of Robin sequence (cleft palate, micrognathia, and
glossoptosis)
•15% of affected
patients also have a mixed hearing loss
Waardenburg Syndrome Sensorineural deafness and pigmentation defects of the hair, skin, and iris.
(WS). Common to the various WS types
is a defi ciency of melanocytes, which are neural
crest derivatives. pigmentation defects &the high
incidence of deafness, secondary to the loss of
melanocytes from the stria vascularis
 SYNDROMIC HEARING IMPAIRMENT
Autosomal Resessive Hearing Impairment
Pendred Syndrome (PS) •most common syndromic form of deafness,
•Associated with developmental abnormalities of the cochlea,
congenital sensorineural hearing loss, and diffuse
thyroid enlargement (goiter).
•Hearing loss  usually profound
but can be variable in onset, rapidly progressive,
and even unilateral
•Goiter typically presents in mid-childhood, may be at birth.
The thyroid defect involves organifi cation of iodine can be diagnosed by
administering perchlorate, which releases unbound iodide from thyroid
follicular cells
X-linked Syndromic Hearing Impairment
Alport Syndrome (AS) •The deafness was a feature of a previously described familial
nephropathy that caused uremia in males but spared females\
•Considered affected if there are 3 of the following:
(1) a positive family history of hematuria or chronic renal failure;
(2) Electron microscopic renal biopsy evidence of AS;
(3) characteristic eye signs of anterior lenticonus,
white macular fl ecks, or both;
(4) high frequency sensorineural hearing loss
 TULI KONGENITAL (SEBAGAI GENETIC SYNDROME)
S O A P
-Hearing loss + -Pemeriksaan klinis: Branchio-Oto-Renal Hearing aid, support
Terdapat kelainan terdapat kelainan Syndrome (BOR)) to parents.
kongenital lain kongenital
(malformasi aurikular, -Pemeriksaan fungsi
lubang di ginjal
leher/branchial -Audiometri 
fistule, lubang di didapatkan gangguan
preaurikular) pendengaran

Hearing loss+ -Pemeriksaan fisik Pendred Syndrome Hearing aid, support

Terdapat pembesaran -Pemeriksaan fungsi (PS) to parents.
kel.tiroid pendengaranhearin
g loss
-Pemeriksaan
tiroidada goiter
-high frequency -Pemeriksaan ginjal (Alport Syndrome) Hearing aid, support
sensorineural hearing -Pemeriksaan fungsi to parents.
loss+renal pendengaran
impairment
Ballenger’s Otorhinolaryngology 17 (Head and Neck Surgery) chapter 26
 TULI KONGENITAL (INFEKSI IN UTERO)
S O A P
Deafness, ocular -Pemeriksaan fisik: Congenital Rubella Vaksinasi
defects, small head microcephaly, skin
size, intellectual rash, developmental
disability, delay, ocular disorder
developmental delay, (cataract, glaucoma)
maternal infection -Pemeriksaan fungsi
during 1st semester of pendengaran 
pregnancy hearing loss
-Pemeriksaan serologi
untuk Rubella hasil
+
Hearing loss+ loss of -Pemeriksaan fisik Congenital syphilis -Penicillin
vision (cornea : opaque -Identifikasi dan
History of maternal appearance, peg- eradikasi infeksi
syphilis infection shaped upper maternal
(untreated during 1st incisors/Hutchinson’s
or 2nd semester of teeth, 8th canal nerve
pregnancy) deafness
1. Scott Brown Ed 7 Vol 1 Bab 69
2. https://www.nlm.nih.gov/medlineplus/ency/article/001658.htm
LABIRINTITIS
Inflamasi pd labirin (Cochlea,Vestibula,Kanalis
Semilunaris

Serous /
toxic
Labirintitis
suppurative
Klasifikasi
serous
•respon inflamasi steril thdp
toksin bakteri
•Cairan perilymphnya acidofilic
•Dibagi lg mjd :
•Mild serous labyrinthitis 
# perubahan sitologik
•Severe : degenerasi organ
corti
suppurative
•Krn infeksi bakteri ke telinga
dalam
•Kumpulan leukosit PMN di
ruang perilympatic
•Progresif  inflamasi>> 
nekrosis membran labirin
• Etiologi
• Etiologi secara pasti belum jelas
• Viral infections seperti flu (upper respiratory infection)
• Viral (Rubella ,Cytomegalovirus  most common)
• Bacterial infection biasanya karena infeksi telinga tengah
(otitis media,meningitis)
• Komplikasi cholesteatoma
• Gejala klinis
• Nausea
• Vomiting
• Nistagmus
• Sakit kepala
• Tinitus
• Letih
• Unsteady (vertigo)
LABIRINTITIS
• Kepala berubah posisi  cairan mengalir sepanjang vestibula dan canalis
semilunaris  cupula bergerak ketika cairan bergerak/mengalir memicu
rangsang sinyal pada otak (respon diterima dari telinga dalam ,tulang sendi,otot
dan mata) perubahan pada posisi Tubuh

• Pada labirinitis  respon dari telinga dalam berantakan  sinyal telinga dalam
berbeda dengan tulang sendi,otot,mata  GANGGUAN KESEIMBANGAN
(VERTIGO)  hilang dalam beberapa minggu
Patofisiologi
• Early stage dr kedua tipe ini tdpt sensorineural hearing loss tp
struktur kedua koklea lengkap (rambut, sel ganglion,dll)  bukan
sebab anatomis

• Labirinitis  pelepasan sitokin inflamasi  ganggu integritas ligamen

spiral  ganggu homeostatis ion dan cairan di koklea  hearing loss

• Penyebab ketulian pd labirinitis adalah respon inflamasinya, bukan

krn bakterinya
BACTERIAL LABYRINTHITIS
• Disebabkan oleh:
• diseminasi dr telinga tengah pd otitis media/ melalui bony
fistula pd koleostatoma/ otitis media kronik
• bakteri dr subaraknoid  cairan perilymph labyrinth
• pathway bs melalui foramina cribosa pd fundus atau
regio sensori vestibular dan duktus koklear
• hub antara subaraknoid dg aquaduktus koklear 
bakterial/viral meningitis/labirinitis
• gejala : hearing loss akut, vertigo dg malaise, demam
terkait ISPA
secara histologik dpt dibagi jd 3 fase :
• serous labyrinthitis  disebabkan oleh toksin bakteri
(dr otitis media,fistula perilymph, meningitis). Less
severe , generally restored.
• suppurative otogenic labyrinthitis  krn invasi bakteri
ke dlm telinga dalam
• suppurative meningogenic labyrinthitis 
penyebaran bakteri dr subaraknoid melalui
aquaduktus koklear/ kanal auditori internal
VIRAL LABIRINTITIS

Gejala : ISPA + gangguan fungsi pendengaran &

vestibular akut + vertigo & nystagmus (3-5 hr)

Histopatologi:
• degenerasi organ corti
• early encapsulation of the tectorial membrane
• degenerasi stria vascularis
• infiltrasi round cell
• degenerasi kistik sel rambut dg infiltrasi round cell pd
auditory & vestibular labyrinth
• Cytomegalovirus : degenerasi kokleosakular, hydrops
endolymph. Fibrosis, fibro-oseus, ploriferasi epitelia
sensoris & supporting cell, sel sensoris hilang &
degenerasi neuronal
• Mumps : tuli, vertigo
• Herpes Zoster oticus (Ramsay hunt syndrome): rasa
terbakar pd daerah telinga dan wajah. Terdapat
hearing loss, vertigo & paresis facial
• Otosifilis : kongenital / didapat. Akibat treponema
palidum. Gejala : hearing loss tiba2/progresif.
Dg/tanpa gejala vestibular
Tatalaksana
• Antibiotic + steroid
• Terapi yg sesuai dpt memperbaiki tuli sensorineural yg disebabkan
suppurative labyrinthitis
LABIRINTITIS
S 0 A P
1.Telinga Sakit CT-SCAN and MRI Labirintitis - Meclizine
(serious case) - Diazepam
2.Telinga Berbunyi - Do not drive, work
at height or operate
heavy machinery
3.Vertigo - Bed Rest till
dizzines leaves
OTOSKLEROSIS
• Kelainan herediter lokal yg mengenai tulang endokondral pada
kapsula otik berupa gangguan resorpsi dan deposisi tulang
• Lesi terdiri atas : area resorpsi tulang, formasi tulang baru, proliferasi
vaskular, dan stroma jaringan ikat

Scott Brown 7th edition Otorhinolaryngology, Head & Neck

Surgery bab 237e hal 3453-3480
• Clinical otosclerosis : lesi pada stapes atau
stapediovestibular joint dan kerusakan pendengaran
konduktif
• Histologic otosclerosis : lesi tidak melibatkan stapes
atau stapediovestibular joint atau cochlear
endosteum, asimtomatik, hanya dapat di diagnosis
post mortem examination
• Koklear otoskelrosis : kelainan pendengaran sensori
neural tanpa kelainan pendengaran konduktif 
karena hanya mengenai koklear endosteum tanpa
adanya fiksasi stapes

Scott Brown 7th edition Otorhinolaryngology, Head & Neck

Surgery bab 237e hal 3453-3480
• Etiologi:
• Genetik (> sering pd org kulit putih)
• Measles
• Autoimun (humoral autoimmunity to type II collagen)
• Biokimia (hasil reaktivasi proses remodelling sekunder)

Scott Brown 7th edition Otorhinolaryngology, Head & Neck

Surgery bab 237e hal 3453-3480
• Manifestasi klinis
1. Pendengaran terasa berkurang secara progresif
2. Tinitus
3. Kadang vertigo
• Pemeriksaan -> membran timpani utuh
• Tuba biasanya paten dan tidak ada riwayat penyakit/
trauma telinga atau kepala sebelumnya
• Diagnosis diperkuat dengan pemeriksaan audiometri
nada murni dan impedance

Scott Brown 7th edition Otorhinolaryngology, Head & Neck

Surgery bab 237e hal 3453-3480
• Tatalaksana:
• Fluorodation of drinking water
• Fluorides oral
• Hearing aids
• Surgery

Scott Brown 7th edition Otorhinolaryngology, Head & Neck

Surgery bab 237e hal 3453-3480
Otosklerosis
S O A P
Pendengaran Membran timfani Otosklerosis Flouridation of
berkurang secara utuh drinking water
progressive Tuba paten dan Oral Flourides
Tinitus tidak ada riwayat Hearing Aids
Vertigo penyakit/trauma Surgery
telinga
Tidak ada riwayat
penyakit/trauma
kepala
Pemeriksaan
Penunjang :
Audiometri nada
murni dan
tymphanogram
 MENIERE’S DISEASE
• Kelainan yg ditandai dengan serangan vertigo mendadak, terkait dengan kehilangan
pendengaran yg sifatnya fluktuatif, tinnitus, aural fullnes

• Etiologi: idiopatik
• Predisposing factor:
– Endolymph overproduction atau malabsorpsi → HT endolimfatik → pembesaran
labyrinthus membranaceus → endolympatic hydrops
– Kelainan telinga dalam & tulang temporal: sifilis, mumps, Cogan’s syndrome,
trauma, OMSK → gambaran klinis Meniere’s disease → Meniere’s syndrome
o Vertigo spontan bbrp tahun setelah onset hearing loss → delayed
endolymphatic hydrops
o Serangan vertigo bersamaan dgn onset hearing loss pd telinga yg normal →
contralateral delayed endolymphatic hydrops (disebabkan autoimun)
– Ruptur labyrinthus membranaseus → kebocoran perylimph yg kaya potassium ke
perylymph → Meniere’s attack

• Perangsangan awal hair cell menyebabkan peningkatan konsentrasi potassium di

sekeliling permukaan basal → initial irritative phase pada serangan
• Blockade neurotransmitter release → subsequent paretic phase
Clinical Manifestation
• Unilateral
• Reccurent attacks of spontaneus vertigo + mual muntah
• Lateralized low-frequency hearing loss
• Tinnitus
• Aural fullness
• Intensitasnya meningkat selama bbrp menit, berlangsung selama bbrp jam dari onset
• Tinnitus & hearing loss dapat sampai bbrp hari
• Postural imbalance & mual dapat menetap dlm bbrp hari meskipun serangan sudah mereda
• 3 fase tipe serangan (bdsr arah spontaneous nystagmus):
1) Irritative phase → nistagmus horizontal/horizontal torsional; ke arah telinga yg gangguan; < 1 jam
2) Paretic phase → nistagmus menjauhi telinga yg gangguan; bbrp jam, kadang 1-2 hari
3) Recovery phase → nistagmus ke arah telinga yg gangguan, lamanya seperti pd paretic phase
• Later stage : drop attacks (Tumakin/otholitic crisis) → jatuh krn merasa didorong; tdk berhubungan
dgn vertigo & kehilangan kesadaran
Diagnosis
• 2 atau lebih serangan vertigo spontan (masing-masing ≥ 20 menit)
• Hearing loss → cek dgn pure-tone audiogram
• Tinnitus/aural fullnes pd telinga yg gangguan
• Probable Meniere’s disease → ≥2 serangan vertigo, unilateral hearing loss,
tinnitus, aural fullness pd saat bersamaan
• Possible Meniere’s disease → ≥2 serangan vertigo, meskipun tidak ada keluhan
pd pendengaran/tidak menyadari
• Early stage: fungsi vestibular & auditori masih normal, fluctuating low-frequency
sensoryneural hearing loss
• Progresive : kehilangan fungsi vestibular & auditori, flat sensoryneural hearing
loss
• Electrocochleography (sensitif & spesifik)
Management approach
Management
- Tujuan: menurunkan produksi/akumulasi endolymph
• Strict sodium restriction → urinary sodium <50 mmoL/hari
• Diuretik (ES: hipotensi postural & hipokalemi)
• Surgery: pasien dgn continue vertigo attacks yg tidak membaik dgn
obat-obatan
o Endolymphatic sac surgery → me↓ frekuensi, durasi, intensitas
serangan; tapi tidak utk menghentikan & tidak efek utk keluhan
auditori
o Selective vestibular neurectomy →stop vertigo (ES: hearing loss &
facial paralysis)
o Labrinthectomy → stop vertigo (ES: kehilangan pendengaran yg
tersisa di sisi itu)
• Cochlear implanation → utk yg menggunakan alat bantu dengar
• Aminoglikosida sistemik (streptomicin & gentamicin) utk yg bilateral
• Gentamisin intratimpani → utk vertigo yg intractable
 S O A P

• Tinnitus • Pure tone Meniere’s disease • Strict sodium

• Serangan vertigo audiogram restriction
reccurent • electrocochleogr • Diuretik
• Mual muntah aphy • Surgery
• Hearing loss • Cochlear
• Aural fullness implanation
• Postural • Aminoglikosida
imbalance & sistemik
mual dapat • Gentamicin
menetap intratimpani
• Nistagmus
• Drop attack pada
later stage
 BENIGN PAROXYSMAL POSITIONAL
VERTIGO (BPPV)
• Kelainan yang ditandai dengan serangan singkat vertigo, yang di asosiasikan
dengan nistagmus, dengan perubahan posisi kepala.
Etiology
• Inappropriate stimulation of SCC hair cells, by sequestered otoconia.
• Canalolithiasis
• Cupulolithiasis
• Sebagai komplikasi dari trauma kepala atau vestibular neuritis.
Epidemiology
• Occurs 0.5% per year.
• Wanita> pria.
• Rentangan umur 11-84 tahun
• posterior SCC BPPV>15% lateral SCC BPPV.
Clinical Manifestation
• Episode vertigo singkat yang rekuren (10-20 detik) yang muncul saat terjadi
perubahan posisi kepala.
• Provocative manoeuvres : rolling over the bed, getting in or out of bed, pitching
the head towards while bending over, pitching the head backward while looking
up.
• Vertigo yang berat dapat disertai mual dan muntah.
• Nystagmus following Dix-Hallpike manoeuvre.
Diagnosis
• History
• Physical examination
Treatment Prognosis
• Epley Manoeuvre • Most patients  vertigo
• Patient should be instructed lasts several week (self-
to remain upright for 24 limited)
hours after treatment and to
avoid sleeping on the • One recurrence after a
affected side for a week. period of remission
• Severe, intractable lasting weeks, months,
symptoms and not
responding after repeated even years.
manoeuvre  surgery
occlusion of the posterior
SCC.
BPPV
S O A P

• Vertigo singkat • History BPPV • Epley

(10-20 detik) • Physical Manoeuvre
• Vertigo berat examination • Severe 
disertai mual surgery
dan muntah occlusion of
• Nistagmus the posterior
SCC
VESTIBULAR NEURITIS
DEFINITION
• Disorder in which there is sudden, spontaneous, isolated, total or
subtotal loss of afferent vestibular input from one labyrinth
• Synonyms: vestibular neuronitis, labyrinthitis, neurolabyrinthitis and
acuteunilateral peripheral vestibulopathy.

ETIOLOGY
• Viral infection of the vestibular nerve.
VESTIBULAR NEURITIS
CLINICAL MANIFESTATION:
• acute spontaneous vertigo (increases in intensity over a period of hours -- minimized by keeping
the head still and the eyes shut.)
• nausea
• vomiting
• postural imbalance.
• Unsteady and may veer towards the side of the affected labyrinth

CLINICAL SIGNS:
• spontaneous horizontaltorsional nystagmus (unidirectional -- may not be detected on a standard
neurological examination)
• partial or complete ocular tilt reaction towards the affected side
VESTIBULAR NEURITIS
DIAGNOSIS
• Subjective visual horizontal (SVH)
• Electronystagmography.
• Caloric testing (for canal paresis)
• Brain MRI (central cause)

DIFFERENTIAL DIAGNOSIS
• Cerebellar infarction
• Labyrinthine infarction
• Autoimmune inner ear disease
• Meniere’s disease
• Multiple sclerosis
VESTIBULAR NEURITIS
MANAGEMENT OPTIONS
• Corticosteroid
• Antiviral
• Vestibular rehabilitation therapy (postural and visual stability)

COMPLICATIONS
• CVI
• bilateral sequential vestibular neuritis
• Meniere’s disease
VESTIBULAR NEURITIS
S O A P

• Acute • Subjective visual Vestibular • Corticosteroid

spontaneous horizontal neuritis • Antiviral
vertigo • Electronystagmography • Vestibular
• Nausea • Caloric testing rehabilitation therapy
• Vomiting • Brain MRI
• Postural
imbalance
• Unsteady
• Nystagmus
MOTION SICKNESS (MABUK
PERJALANAN)
DEFINISI an unpleasant condition that occurs when persons are subjected
to motion or the perception of motion
associated with travel  most commonly reported form of the
syndrome (sea sickness, travel sickness, space sickness, and
cybersickness)
PATOFISIOLOGI the stimuli applied to the vestibular, visual, and proprioceptive
receptors appear to be in conflict.
*pregnant women, patients with previous vestibular syndromes or
illness, a propensity toward nausea, and patients with a migraine
headache history have increased rates of motion sickness.
GEJALA Nausea, vomiting, generalized feeling of unwellness (malaise),
drowsiness, fatigue, and irritability.
TATALAKSANA •anticholinergic agents (scopolamine)
-sebagai pencegahan + penanganan saat akut
-efek samping yang umum :dry mouth/nose/throat, drowsiness,
loss of visual accommodation, and sensitivity to bright light
•antihistamines (dimenhydrinate [Dramamine]).
•Antiemetik
http://emedicine.medscape.com/article/2060606
Nasopharyngeal carcinoma
• Men > women
• Etiology :
• Genetic factors : the loci involve are the HLA-A, B and DR locus situated on the short
arm of chromosome 6
• EBV
• Environmental carcinogens : inhalants, formaldehide
Histological
• WHO classification :
• Type I squamous cell carcinoma (keratinizing) :
• Well differentiated
• Moderately differentiated
• Poorly differentiated
• Type II nonkeratinizing carcinoma
• Type III undifferentiated carcinoma
• WHO classification  revised :
• Grade 1 – keratinizing squamous cell carcinoma
• Low incidens areas for NPC
• Not associated with EBV infection
• Grade 2 – nonkeratinizing squamous cell or undifferentiated carcinoma
• Places  endemic
• EBV-related  elevated serological titres of anti-EBV Ab
• Grade 1 tumours are less aggressive than grade 2 tumours, also less radiosensitive
• Prognosis for grade 1 tumours is less favourable compared stage to stage with grade 2 tumours
 S O A P
• Early tumour  no • Biopsy Nasopharyngeal Primary treatment :
symptoms • Serology  IgA carcinoma • Radiotherapy 
• Upper neck Ab to the EBV- megavoltage
swelling  spesific antigens external
common unilateral • Cytology  FNAC radiotherapy
• Cervical • Imaging  CT (ERT)
lymphadenopathy scan, MRI, • Chemotherapy
• Nasal symptoms Ultrasound
 bloodstained
nasal discharge,
nasal obstruction,
post-nasal drip or
even epistaxis
• Aural symptoms 
deafness, tinnitus
and otalgia
• Neurological 
headache or
cranial nerve
symptoms
Diagnosis
Staging
Complications of radiotherapy:
• Xerostomia
• Symptom of oropharyngeal mucositis
• Altered taste sensation
• Dermatitis
• Alopecia of the irradiated area
 Tumour of the larynx
S O A P
Horseness Radiology Risk factor : Early glottic cancer:
Dyspnoea • CT scan • Tobacco • Radiotherapy
Stridor • MRI • Alcohol • Open surgery
Foreign body • PET scan • Family history • Endolaryngeal excision (with
sensation • Occupational (asbestos or w/o laser)
exposure)
Haemoptysis Biopsy • HPV infection (high risk
subtype) Early supraglottic cancer:
Neck nodes Endoscopy • Horizontal partial
laryngectomy
Reffered otalgia Diagnosis : • Total laryngectomy
Odynophagia Tumors of the larynx
(benign/malignant) T3 and T4 cancer :
• Operative treatment
• Radiotherapy
• Chemotherapy