VERTIGO

dr. Ketut Widyastuti, SpS

The Ear

3
Vestibulocochlear Nerve VIII

 Special Sensory
 Provides hearing (cochlear branch) and sense of balance (vestibular branch)
 Damage produces deafness, dizziness, nausea, loss of balance and
nystagmus
Vestibular Labyrinth
 Pathophysiology
Complex interaction of visual, vestibular and
proprioceptive inputs that the CNS integrates as
motion and spatial orientation
 3 semicircular canals
rotational movement
cupula
 2 otolithic organs
utricle & saccule
linear acceleration
Macula
What is vertigo
 Definisi Vertigo
 Vertigo adalah sindroma disebabkan oleh berbagai
penyakit yang mengganggu alat keseimbangan
tubuh (AKT).

 Definisi:
Gerakan sebenarnya atau rasa gerakan
Gerakan linier / sirkuler pada tubuh
penderita atau sekitarnya.
Diikuti gejala vegetatif, psikik dan gejala
lainnya.
Akibat terganggunya AKT.

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 Balance

Patophysiology

Mercado 2013©
Balance Function and Dysfunction
Interaction of Vestibular, Visual and Proprioceptive systems

Skin pressure
Eye receptors
Inner ear
(vestibular system) Muscle and joint
sensory receptors

Central Nervous system

Controls eye Postural control

movements via muscles

Balance
dyfunction
dizziness
Goebel JA. Otolaryngol Clin North Am 2000;33:483–93.
Shepard NT, Solomon D. Otolaryngol Clin North Am 2000;33:455–69
Patophysiology
Alat keseimbangan tubuh (AKT) terdiri atas 3 sistem:

1. Sistem somatosensori (proprioseptif) (15 %)

2. Sistem Visual (30 %)
3. Sistem Vestibuler (55 %)
Semua rangsangan yang diterima reseptor masing-
masing sistem diintegrasikan di batang otak dan
serebelum, sehingga terjadi hubungan fungsional
yang terpadu antara ketiga sistem
 Bila ada gangguan

PERSEPSI KORTEKS
VERTIGO

FUNGSI KESEIMBANGAN
Melalui:
1. Refleks vestibulospinal.
2. Refleks vestibulookuler.

NUKLEUS
INTEGRASI VESTIBULARIS SEREBELUM OLIVA
INFERIOR

NUKLEUS
OKULOMOTORIS

RESEPSI RESEPTOR VESTIBULUM RETINA

(Sistem vestibuler) (Sistem visual)
PROPRIOSEPTI
F
(Sistem somatosensori)
 4 jenis Dizziness

DIZZINESS

Vertigo Vertigo Presyncope Dysequilibium

Vestibular Non-vestibular

Ilusi berputar Ilusi melayang Rasa akan pingsan tungkai tak

stabil

Sistem Sistem Visual, Sistem Sistem

Vestibular Proprioseptif Kardiovaskular Serebelar,
Psikogenik Spinal

“Spinning” “Light-headed” “ Fainting” “Falling”

 Diagnostic
Algorithm

DIZZINESS VESTIBULAR
- Vestibular VERTIGO ETIOLOGY
- Non Vestibular - Peripheral - Peripheral
- Disequilibrium - Central - Central
- Presyncope
 Cortica
Brainstem l Thalamus
Cerebellum
CENTRAL
Vestibula VESTIBULAR
PERIPHERAL r
Nuclei
VESTIBULAR
Vestibular Vestibula
apparatus r
Nerve
Semicircular Otolith
Canal
Angular Linear
acceleration acceleratio
n
VERTIGO VESTIBULER

Dapat dibagi atas:

1. Vertigo vestibuler tipe perifer
yang timbul akibat gangguan susunan vestibularis
bagian perifer (vestibulum dan nervus
vestibularis).
2. Vertigo vestibuler tipe sentral
yang timbul akibat gangguan susunan vestibularis
bagian sentral (nukleus vestibularis, korteks).
 PERBEDAAN KLINIS VERTIGO VESTIBULAR DAN
VERTIGO NON VESTIBULAR

GEJALA VERTIGO VESTIBULAR VERTIGO NON VESTIBULAR

- Sifat Vertigo Rasa berputar Melayang, hilang keseimbangan

- Serangan Episodik Kontinyu

- Mual/muntah (+) (-)

- Gangguan (+)/(- ) (-)

Pendengaran

- Gerakan Gerakan kepala Gerakan obyek visual

Pencetus

- Situasi pencetus (-) Ramai orang, lalu-lintas macet

Vertigo-Characteristics
Peripheral Central
Onset Sudden Usually slow
Severity of Vertigo Intense Usually mild
Pattern Paroxysmal Constant
Exac. by movement Yes Variable
Autonomic Frequent Variable
Laterality Unilateral Uni or bilat
Nystagmus Horizontorotary Any
Fatigable/Fixation Yes No
Auditory symptoms Yes No
CNS symptoms Absent Present
Langkah-langkah
 Langkah 1  vertigo atau bukan
 Langkah 2  tentukan jenis vertigo :
- vertigo vestibular : sentral atau
perifer
- vertigo non vestibular
 Langkah 3  cari etiologi
 Langkah 4  terapi
Anamnesis
1. Deskripsikan secara jelas :
apa yang dimaksud pusing oleh pasien?
2. Bentuk serangan vertigo :
- pusing berputar
- rasa goyang/melayang
3. Sifat serangan vertigo :
- periodik
- kontinu
- ringan atau berat
4. Faktor pencetus atau situasi pencetus :
- perubahan gerakan kepala atau posisi
- situasi : keramaian, emosional
- suara
5. Gejala otonom : mual, muntah, keringat dingin
- berat atau ringan
6. Gangguan pendengaran : tinnitus, tuli
7. Defisit neurologik : hemihipestesi, baal wajah
satu sisi, disfagia, hemiparesis, penglihatan
ganda, ataksia serebelaris
8. Penyakit yang diderita pasien : DM, hipertensi,
kelainan jantung
9. Obat-obatan ; streptomisin, gentamisin,
kemoterapi
10. Tindakan tertentu : temporal bone surgery,
trans-tympanal treatment
Pemeriksaan fisik

 Tanda vital
 Pemeriksaan umum
 Pemeriksaan neurologik
 Pemeriksaan khusus Neuro-otologik
Pemeriksaan khusus Neuro-otologik pada
vertigo
 Test Romberg
 Tes Romberg dipertajam
 Tes Jalan tandem
 Tes Fukuda
 Tes past pointing
 Head thrust test
 Pemeriksaan nistagmus

De jongs, The neurologic examination 2005, Brandt T, vertigo and dizziness, 2009)
Pemeriksaan nistagmus
 Bedside secara sederhana dengan atau
tanpa kaca mata Frenzel
 Head shaking test
 Dix-Hallpike test
 ENG (electronistagmography)
 Tes kalori
Tes Romberg
 Pemeriksa berada di belakang pasien
 Pasien berdiri tegak dengan kedua tangan di
dada, kedua mata terbuka
 Diamati selama 30 detik
 Setelah itu pasien diminta menutup mata dan
diamati selama 30 detik
 Jika pada keadaan mata terbuka pasien
sudah jatuh  kelainan serebelum
 Jika pada mata tertutup pasien cenderung
jatuh ke satu sisi  vestibuler/propioseptif
Tes Romberg di pertajam
 Pemeriksa berada di belakang pasien
 Tumit pasien berada didepan ibu jari
kaki yg lainnya
 Pasien diamati dalam keadaan mata
terbuka selam 30 detik
 Kemudian pasien menutup mata dan
diamati selama 30 detik
 Interpretasi = test Romberg
Distinguishing Characteristics of Peripheral vs. Central Causes of Vertigo

Feature Peripheral vertigo Central vertigo

Nystagmus Combined horizontal and torsional; Purely vertical, horizontal, or torsional

inhibited by fixation of eyes onto object; ; not inhibited by fixation of eyes onto object;
fades after a few days; does not change may last weeks to months
direction with gaze to either side ; may change direction with gaze

Imbalance Mild to moderate; able to walk Severe; unable to stand still or walk

Nausea May be severe Varies

, vomiting

Hearing loss,
tinnitus Common Rare

Nonauditory Rare Common

neurologic
symptoms

Latency following
provocative
diagnostic Longer (up to 20 seconds) Shorter (up to 5 seconds)
maneuver)
Disorder Duration Auditory Prevalence Peripheral or
symptoms central vertigo

Benign paroxysmal Seconds No Common Peripheral

positional vertigo

Perilymphatic fistula (head Seconds Yes Uncommon Peripheral

trauma, barotrauma)

Vascular Ischemia,TIA Seconds to hours Usualy not Uncommon Central or

peripheral

Meniere’s disease Hours yes common peripheral

Syphillis Hours yes Uncommon central
Vertiginous migraine Hours No Common Central

Labyrinthitis Days Yes common peripheral

Vascular Ischemia: Stroke Days Usually not Uncommon Central or
peripheral

Vestibular neuronitis Days No Common Peripheral

Anxiety disorder Variable Usually not Common Unspecified

Acoustic neuroma months yes Uncommon Peripheral

Multiple sclerosis Months no uncommon central

Vestibular ototoxicity months yes uncommon peripheral

TERAPI PENYEBAB VERTIGO
PENYEBAB TERAPI
PERIFER
BPPV Canalith repositioning manoeuvre (Brandt-Daroff, Epley)
Labyrinthine concussion Vestibular rehabilitation
Meniere’s disease Low-salt diet, diuretic, surgery, transtympanic gentamicin
Labyrinthitis Antibiotics, Menghilangkan jaringan yang terinfeksi,
Rehabilitasi Vestibular
Perilymph fistula Bed rest, hindari mengejan
Vestibular neuritis Brief course of high-dose steroids, Rehabilitasi Vestibular

PUSAT/SENTRAL

Migraine Beta-blockers, calcium channel blockers, tricyclic amines

Vascular disease Control of vascular risk factors, e.g., antiplatelet agents

CPA tumours Surgery

Baloh RW. Lancet 1998;352:1841–6. Goebel JA. Otolaryngol Clin North Am 2000;33:483–93.
Integrated therapy

Modalitas terapi kombinasi pengobatan etiologi,

pengobatan simptomatis, terapi rehabilitasi
vestibular, Kontrol diet dan perubahan gaya hidup,
memberikan perbaikan vertigo 96 %.

Gananca et al. Brazilian Journal of Otorhinolaryngology 2007;73(1): 2-8

Obat-obatan Untuk Pengobatan Simptomatik

I. ANTI VERTIGO
1.Vestibular Suppressant
a. Ca antagonist : Flunarizin
b. Vasodilator : Betahistine
c. Tranquilizer : Diazepam, haloperidol,
sulpiride, clonazepam
d. Antihistamin : Difenhidramine, meclizine.

2. CNS stimulant
Ephedrin, amphetamin
Obat-obatan Untuk Pengobatan Simptomatik
lanjutan……..

II. ANTI EMETIC

1. Anticholinergic : atropine, scopolamin
2. Antidopaminergic : Prochlorperazine,
metoclopramide.
 Benign Paroxysmal Positional Vertigo (BPPV)

 Benign: not a very serious or progressive

condition
 Paroxysmal: sudden and unpredictable in
onset
 Positional: comes with a change in head
position
 Vertigo: causing a sense of dizziness.

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Benign Paroxysmal Positional Vertigo
 Extremely common
 Caused by otoconia displacement (calcium
debris) in semicircular canals
 No hearing loss or tinnitus
 Short-lived episodes brought on by rapid
changes in head position
 Horizontorotary nystagmus with crescendo-
decrescendo pattern after slight latency period
 Less pronounced with repeated stimuli
BPPV: Pathophysiology
Degenerative debris from
utricle (otoconia)

Canalithiasis Theory
floating freely in the endolymph

Cupulolithiasis Theory
Adhering to the cupula
Canalolithiasis Theory
 The most widely accepted theory of the pathophysiology of
BPV
 Otoliths (calcium carbonate particles) are normally attached
to a membrane inside the utricle and saccule
 The utricle is connected to the semicircular ducts
 These otoliths may become displaced from the utricle to
enter the posterior semicircular duct since this is the most
dependent of the 3 ducts
 Changing head position relative to gravity causes the free
otoliths to gravitate longitudinally through the canal.
 The concurrent flow of endolymph stimulates the hair cells of
the affected semicircular canal, causing vertigo.

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Posterior SCC
PSCC
Hangs down like the
water trap in a drain
pipe

Allowing the crystals to

settle in the bottom of
the canal.
Causes
 Idiopathic
 Infection (viral neuronitis)
 Head trauma
 Degeneration of the peripheral end organ
 Surgical damage to the labyrinth

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Symptoms
 Starts suddenly
 Associated with change in head position.
rolling over or getting into bed
assuming a supine position.
arising from a bending position
looking up to take an object off a shelf
tilting the head back to shave
turning rapidly.
 Nausea and vomiting.
 There is no new hearing loss or tinnitus.

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Diagnosis
 Lab Studies:
No pathognomonic laboratory test for BPPV
exists. Laboratory tests may be ordered to rule
out other pathology.
 Procedures:
The Dix-Hallpike test, along with the patient's
history, aids in the diagnosis of BPV.

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The Dix-Hallpike test

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Dix-Hallpike test
 Pasien menoleh 45⁰ kesatu sisi, setelah
itu pasien dijatuhkan sehingga kepala
menggantung 15⁰ dibawah bidang datar
 Diamati adakah nistagmus atau tidak
 Kemudian pasien tegak kembali dan
diamati adakah nistagmus atau tidak
 Hal yang sama dilakukan kembali pada
sisi yang lainnya
Dix-Hallpike test
 Pada pemeriksaan Dix-hallpike ini dapat membedakan
kelainan sentral atau perifer
 Nistagmus pada kelainan perifer :
- latensi : 3-10 detik
- lamanya : 10 – 30 detik, atau < 1 menit
- fatigue
- disertai gejala vertigo yang berat
 Pada kelainan sentral :
- nistagmus langsung muncul
- tidak ada fatigue
- gejala vertigo bisa ada atau tidak
(De Jong, the neurologic examination, 2005)
Treatment
 Medications
Antiemetic
Antihistaminic
Anticholinergic
 The Canalith Repositioning Procedure
(CRP)
 Surgery

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Canalith Repositioning Procedure
(CRP )
 The treatment of choice for BPPV.
 Also known as the Epley maneuver,
 The patient is positioned in a series of
steps so as to slowly move the otoconia
particles from the posterior semicircular
canal back into the utricle.
 Takes approximately 5 minutes.

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The Epley Maneuver

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Treatment BPPV
Canalith repositioning (Epley Maneuver)
displaces debris back to vestibule
Patient may need to remain upright for 24
hrs post procedure to prevent recurrence
Contraindications includes: severe carotid
stenosis, unstable heart disease, severe
neck disease (cervical spondylosis or
advanced RA)
Treatment of BPPV
 Initial studies suggested 80% success rate
with Epley Maneuver first time, and 100%
success rate with repeated treatments
 Repeat studies suggested 50-90%
success
 Cochrane Review concluded Epley
Manuver is safe treatment that will likely
improve symptoms of BPPV
 Recurrence rate is about 15% per year
Brandt-Daroff Exercises
 method of treating BPPV, usually used
when the office treatment fails.
 These exercises should be performed
for two weeks, three times per day
for three weeks, twice per day.
 In each time, one performs the maneuver
as shown five times.
 1 repetition = maneuver done to each side
in turn (takes 2 minutes)
Brandt-Daroff Exercises

                                                     
Ménière Disease
 First described in 1861
 Triad of vertigo, tinnitus and hearing loss
 Due to cochlea-hydrops
Unknown etiology
Possibly autoimmune
 Abrupt, episodic, recurrent episodes with
severe rotational vertigo
 Usually last for several hours
Ménière Disease
 Often patients have eaten a salty meal prior
to attacks
 May occur in clusters and have long
episode-free remissions
 Usually low pitched tinnitus
 Symptoms subside quickly after attack
 No CNS symptoms or positional vertigo are
present
Meniere’s disease
 Treatment involves lowering endolymphatic
pressure
 Low salt diet and diuretics (usually dyazide
[HCTZ+triamterene] improve vertigo, but
not tinnitus and hearing loss
 Surgical intervention
Endolymphatic shunt
Ablation of vestibular hair cells by intratympanic
injection of gentamycin
 Treatment of Meniere’s Disease
(Distension of Endolymphatic compartment due to
impaired endolymphatic filtration and excretion)

 Low salt diet ( < 1-2 gm/day)

 Diuretics ( combo HCTZ and Triamterene)
 Surgery in rare cases - ablation of vestibular hair
cells)
TERIMA KASIH