01/10/2021

Vestibular Disorder

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Dr. Kurnia Kusumatuti,dr., Sp.S(K)
Wardah Rahmatul Islamiyah, dr., Sp.S
Hanik Badriyah H, dr., Sp.S
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TIU
• Can explain “balance” and balance’s disorder

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TIK

• Able to give comprehensive treatment for

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BPPV
• Able to diagnose and give early treatment of
meniere’s disease
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 Balance system

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 Anatomy vestibular system

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 Definition &
Classification

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International Classification of Vestibular

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Disorder (ICVD-I) 2009

• Vestibular disorder:
1. Vertigo
2. Dizziness
3. Vestibulo-visual symptoms
4. Postural symptoms

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vertigo
• thesensation of self-motion (of head/body)
when no self-motion is occurring or the
sensation of distorted self-motion during an
otherwise normal head movement.
•2 type

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Spontaneous vertigo
Triggered vertigo : positional, head-motion, visual-
induced, sound-induced, valsava-induced,
orthostatic induced, other
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Dizziness
• thesensation of disturbed or impaired spatial
orientation without a false or distorted sense of
motion.

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Vestibulo-visual symptoms
• Visualsymptoms that usually result from vestibular
pathology or the interplay between visual and
vestibular systems. These include false sensations of
motion or tilting of the visual surround and visual
distortion (blur) linked to vestibular (rather than
optical) failure.

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Postural symptoms
• balance symptoms related to maintenance of
postural stability, occurring only while upright
(seated, standing, or walking).

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 How to diagnose (ICVD-I)

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How to differentiate vertigo
vestibular and nonvestibular ?

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Vertigo vestibular vs nonvestibular

Symptoms Vestibular Nonvestibular

Sensation spining dizzy
Time Episodik Continue/konstan
Nausea/vomit (+) (-)
Auditory symptoms +/- -

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Triger Head movement Visual object
movement

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Vertigo vestibular peripheral vs central

Symptoms Peripheral Central

Onset abruptly Slowly
Severity Severe benign
Head movement effect ++ +/-
Nausea/vomit/sweating ++ +
Hearing disorder +/- -

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Neurological deficit - +/-

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 examination
Neurotological

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Romberg test
• Without shoes
• Open eyes 30 second
• Close eyes 30 second
• Cerebellum lesion :
patient fall ipsilateral
lesion when open and
close eyes

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• Vestibular lesion or
proprioseptif: patient
fall to one side only
when close eyes

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Sharpened romberg test

• Without shoes
• Open eyes 30 second
• Close eyes 30 second
• Interpretation =
romberg
• False : obesity and
elderly

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Tandem gait
• Without shoes
• eyes staring straight ahead
• Cerebellar lesion: patient fall
to one side
• Vestibular lesion: deviation to
one side

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Fukuda test
• stand in the middle of a room.
• Closeboth eyes and hold your
arms outstretched directly in
front of you. Now, start
stepping in place 50 times
• Abnormal : deviation more

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than 30º or go forward or
backward 1 meter
• Lesionlocation associated to
deviation direction

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Past pointing test
• Examiner finger fixed
(don’t move)
• Open eyes then closed eyes
• Cerebellumlesion:
hypermetri or hypometri

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when open and closed eyes
• Vestibularlesion: patient’s
finger deviation to lesion
site when closed eyes
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Examination to differentiate
central vs peripheral vertigo
• Halmagyi-curthoys/Head impulse test

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• Peripheral vestibular lesion: saccadic
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Gaze nistagmus
• Patient’s
eyes follow examiner’s finger left to right
approximately 30º
• Then up and down direction

Nystagmus Peripheral central

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Direction Unidirectional Bidirectional
type Horisontal + rotatoar Vertical, rotatoar,
horisontal

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 Vertigo management

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 Cowthorn- Cooksey Exercise

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 (SKDI 3A)
Meniere Disease

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Kompetensi 3 A
• Able to diagnose
• Able to give early treatment
• Ableto do referral system (merujuk & rujuk
balik)

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Meniere’s Disease

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Vertigo  Meniere’s Disease

Definition

Clinical syndrome that consists of episodes of spontaneous vertigo

usually associated with unilateral fluctuating sensorineural hearing
loss (SNHL), tinnitus, and aural fullness

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Patofisiologi

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 Pathogenesis

Distension of the
membranous labyrinth or
endolymphatic hydrops is
postulated as a cause of
this condition either due to
excessive production or
impar absorption of
endolymph

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Pathogenesis

Theories behind endolymphatic hydrops :

 Obstruction of endolymphatic duct/sac
 Hypoplasia of endolymphatic duct/sac
 Alteration of absorption of endolymph
 Alteration of production of endolymph
 Autoimmune insult
 Vascular origin
 Viral etiology

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 Diagnostic Criteria of Meniere’s Disease
A. Definite Meniere’s Disease
1. Two or more spontaneous episodes of vertigo, each lasting 20 minutes to 12 hours.
2. Audiometrically documented low-to medium-frequency sensorineural hearing loss in one ear,
defining the affected ear on at least one occasion before, during or after one of the episodes of vertigo.
3. Fluctuating aural symptoms (hearing, tinnitus or fullness) in the affected ear.
4. Not better accounted for by another vestibular diagnosis.

B. Probable Meniere’s Disease

1. Two or more episodes of vertigo or dizziness, each lasting 20 minutes to 24 hours.
2. Fluctuating aural symptoms (hearing, tinnitus or fullness in the affected ear.
3. Not better accounted for by another vestibular diagnosis

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Definition = hidrop endolimfatik idiopatic

• Vertigo
vestibular perifer, duration minimal 20
minutes, no longer than 24 hours
• Hearing loss (fluctuatif, sensorineural hearing
loss progressive)
• Tinitus

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Etiology = unknown
• Familial (5 – 20%)
• Geografis/etnis: Eropa utara + Amerika Utara
• Anomali dan malformation
• Genetic (mutasi gen COCH)
• Autoimune
• Otosklerosis
• Vaskularisasi disorder
• Dysregulation otonom sistem endolymph

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• Alergy inner ear
• tiroid dan glucose metabolism disorder
• Viral infection: herpes simplex, Epstein Barr, CMV
• Traumatic brain injury
• psychological (neurosis)
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Additional examination
• Audiometri : sensorineural hearing loss
• Elektrocochleografi

• confirmation: histopathological postmortem

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Pharmacological treatment
• Betahistin 48 mg/day
• Diuretik
: Hydrochlorthiazide/acetazolamide
50 mg/day
• Steroid:
prednisone 80 mg/hari for 7
daystappering off

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• KCl

• Antihistamin : dipenhidramin injeksi

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Nonpharmacological treatment
• Diet:
Low salt(1.5 – 2 gr/day)
High potassum, high protein
Hidration
Triger : avoid
• Intervention:

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Intratimpanik Injection steroid
Endolymphatic sac-mastoid decompression and/or shunt
intratimpanik Injeksi gentamycin
• Rehabilitation treatment
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Prognosis
• No statement “healing”
• 80 – 90% cases: symptoms reduction

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BPPV
kompetensi 4a

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Kompetensi 4
• Completely and comprehensive treatment

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 VERTIGO  BPPV

Most Common Vestibular

Disorders
BPPV
Disrupting social life and health
condition of patients

One of the most common symptom

that bring px to the hospital

Most Commonly Acute

Vertigo in ER

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 ANATOMY & PHYSIOLOGY
V= Vestibular apparatus,
informs:
• Balance
• Coordination of head,
eye, and body posture

Part of labyrinth
membrane= 3 canals
semicircular
Inner Ear
P= posterior semicircular canal
C= Cochlea
V= Vestibular apparatus 1
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ANATOMY
Labyrinth

Otolith organ

Utriculus Sacculus
Near Canal Semicircular Near cochlea

Planum Planum
horizontal vertical Acceleration detection

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ANATOMY & PHYSIOLOGY
Cupula: motion Utricle & saccule
sensor of Canal contain hair cell &
Semicircular, otoconia/otolith
activated by
endolymph1

1: (Devesahayam PR, 2013) 46

• Canalithiasis :
Partikel yang
terapung bebas
di CS
• Cupulolithiasis
:
Partikel yang
melekat pada
cupula
PATOPHYSIOLOGY OF BPPV

Canalithiasis: Debris / otoconia canal

●

floats freely in the semicircular canal /

endolymph

●
Cupulolithiasis: Otoconia
debris attaches to the cupula

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PATOFISIOLOGI BPPV

Canalith/ Canalith Ab-

Fragment/ Fall from
utricle to
movement normal
Ca in the Endo- Move-
Carbonat Posterior firing
Canal
Posterior lymph ment
crystal Canal from
semicircu- move illusion
Otoconia
lar
Semicircu- terminal
lar neuron

The ampularis nerve is associated with extra ocular muscles 

nystagmus

Density Ca carbonat= 2x endolymph

 Respond to changes in gravity & other acceleration movements

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 Mechanism of Transduction

Bear, MF, Connors, BW, Paradiso, MA : Neuroscience Exploring The Brain Williams & Wilkins, Baltimore, 1996, p. 272-288.

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Signal Transduction [start video at 1:24]

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 Diagnostic Criteria for BPPV
A. Symptoms
1. Attacks of rotatory vertigo or dizziness are induced by changes in the head position relative to
gravity.
2. Short latency, lasts for less than a minute, is characterized by an increase followed by a decrease
in its intensity.
3. The intensity of the vertigo decreases or disappears after repeated head positioning.
4. Not associated with any cochlear symptoms such as hearing loss, tinnitus, or ear fullness.
5. No neurologic symptoms other than vertigo.

B. Signs
1. Torsional nystagmus (upper pole of the eye rotates toward the affected ear, is induced by Dix
Hallpike maneuver.
2. Torsional nystagmus (upper pole of the eye rotates toward the contralateral ear, is induced by Dix
Hallpike maneuver.
3. The nystagmus appears with short latency.
4. Other peripheral and central vestibular diseases causing vertigo are excluded.

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Diagnostic Categories

 Definite BPPV
 To meet all the points in criteria A dan B.
 Probable BPPV
 To meet all the points in criteria A in the history but no
observable nystagmus and no vertigo with any positional or
positioning maneuver, probably because the BPPV is resolved
spontaneously.
 Atypical BPPV
 To meet all the points in criteria A and point 4 in criteria B, but not
any of points 1-3 in criteria B

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Examination for the Diagnosis of BPPV

Dix-Hallpike
Maneuver

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Demonstration
• Reposition maneuver : Eppley maneuver
• Adaptation maneuver : Brandt Daroff
maneuver

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Definition
•B : Benign
•P : Paroxysmal
•P : Positional
•V : Vertigo

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Pathophysiology
• Cupulolithiasis:
Debris (Kalsium karbonat)
otokonia stick to cupula
canalis semicircularis
posterior
• Canalitiasis

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kalsium karbonat cristal move
in canalis semicircularis
(canalitiasis)  endolymph
movement  stimulate
ampula
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 Pathophysiology

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Dix Hallpike manuver
(gold standar – level 1)

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BPPV lateral
– manuver supine-roll test

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Contraindication dix Hallpike dan

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supine roll test

• Stenosis cervical
• Kyphoscoliosis berat
• Limitation range of motion cervical
• Down’s syndrome
• Rhematoid artritis berat
• Radiculopathy cervical

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• Paget’s disease
• Ankylosing spondilitis
• Low back dysfunction
• Spinal cord injury
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 Reposition therapy for BPPV posterior

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Self treatment at home
• Eye closed
• Every movement 30
seconds
• 3x daily, for 2 weeks
• Or 2x daily for 3
weeks

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Reposition for BPPV lateral
• Prolonged Positional maneuver :
sleep with affected ear on top for 12 hours. Efficacy 90%
• Barrel Roll/ Barr B Que maneuver:
sleep supine and rolling to leave affected ear 360 derajad until supine
position again
• Log Roll maneuver (gambar 12):

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1st position : lying with nonaffected area on top
2nd position ; supine position 1 minute
3rd position : lying with nonaffected area on top for 1 minute
4th position ; sitting with knee as a basis and to bow down the head

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 Log Roll Manuver

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Prognosis
• benign : self remision.
• 70patients BPPV canalis posterior self
limiting for 39 days – 6 weeks
• 16patients BPPV canalis lateralis self limting
for 16 days - 2,5 weeks

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 All manuver

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 Thank you

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