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Vertigo

Abdul Gofir
RS Sardjito/FK-UGM

Anatomic and Physiologic


Components of Balance
Vestibular labyrinth, vestibular
nuclei
Visual CN III, IV, VI
Proprioceptive upper cervical
ms and joints

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Timothy 2006

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Patofisiologi

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NORMAL PROCESSING
Vestibular system
Visus
Propiocepsis

Sensory information
= coordinated
CENTRA = known pattern
Oculomotor centra
Stabilization of visual field
Muscles of the body
Static and kinetic equilibrium
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ABNORMAL PROCESSING
Vestibular system
Visus
Propiocepsis

Sensory information
=abnormal
stimuli
=Excesive
=Discordant information

CENTRA
ALARM
WARNING

= unknown patern

NEUROVEG.
CENTRA

Oculomotor centra: NISTAGMUS


Muscles : DEVIATION

CORTEX

BECOMES CONSCIOUS
AFFECTIVE COMPONENT

VERTIGO
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PATOFISIOLOGI VERTIGO
Reseptor
Mata
Vestibuler
Propioseptik

Pengelola data
Saraf Pusat

Efektor
Otot skelet
Mata
Leher
Badan
Anggota gerak

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VERTIGO TEORY
1. Sensoris Conflict
Rangsangan di atas ambang fisiologis
Banjir informasi

2. Neural mismatch
Comparator - memori

3. Ketidakseimbangan saraf otonomik

Akibat rangsangan gerakan parasimpatis

4. Neurohumoral

Akibat rangsangan gerakan CRF (dr.hipotalamus)


ss.sym strs.hrmn
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Receptor

Central Nervous System

Sign & Simptom

Cerebral cortex
Hypothalamus
Retina

Vestibular
Cerebellum
Pituitary

Motion
stimuli

Vestibular
Apparatus

Vestibular
Nuclei
CTZ

Somatosensory
Receptors

Autonomic
centres

Vomiting centre

KONFLIK SENSORIS

NAUSEA
Dizziness
Somnolence
Headache
Depression
Performancedecrement
Increased
Secretion of
ADH, ACTH,
GH, PRL
SWEATING
PALLOR
Decreased Gastric
motility,
Cardiovasculer &
Inspiratory changes

VOMITING
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Neural Mismatch

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Sensory Rearrangement

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NEUROHORMONAL

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Head Acceleration

Head angular Velocity

Endolymph Displacement

Cupular Angle

Cilia Bending
Receptor Cell Potential
Synaptic Action
Generator Potential
Primay Afferent
Action Potentials
CNS
Perception

VOR

Posture

Ket:
CNS: Central Nervous System
VOR: Vestibulo Ocular Reflex
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STRESS

Behavioral Changes

CIRCADIAN RYTHMS

SSP

HIPPOCAMPUS
CORTEX

5-H-T GABA
(+)
Ach (-)
(+)
LO

(+)

?
IL

CRF

(-)

LYMPHOCYTES

PITUITARY

CSS
ADR.MED

(-)

ACTH

ACTH

A
N
T
I
G
E
N
S

(-)

ADR CORTEX
STEROIDS

Multiple Physiological Responses/Pathology

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IMUNOLOGICAL
RESPONSES
IMUNOSUPRESSION

KETERANGAN:

5 HT
: Serotonin
Ach
: Acetyl Cholin
GABA
: Gama Amino Butyric Acid
CSS
: Central Sympathic System
ADR.MED
: Adrenal Medula
(+)
: Exitatory
(-) : Inhibitory
CRF
: Corticotropin Releasing Factor
ACTH : Adreno Corticotropic Hormon
ADR. Cortex : Adrenal Cortex

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Cervicogenic Vertigo

Hx of neck trauma, muscle spasm


Limited cervical ROM
Positive chair rotation test (Fitz-Ritson)
Patients may complain of dysequilibrium
(tilt) more than rotational vertigo
Overstimulation of upper cervical
proprioceptors
May overlap BPPV or Menieres disease

Vertigo Perifer

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Benign Paroxysmal
Positional Vertigo (BPPV)

Inner ear problem that results in short


lasting, but severe, room-spinning vertigo.
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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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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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
first noticed in bed, when waking from sleep.
Any turn of the head bring on dizziness.
Patients often describe the occurrence of
vertigo with

tilting of the head,


looking up or down (top-shelf vertigo)
rolling over in bed.

nausea and vomiting.


There is no new hearing loss or tinnitus.

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Diagnosis

Lab Studies:

Imaging Studies:

No pathognomonic laboratory test for


BPV exists. Laboratory tests may be
ordered to rule out other pathology.
Head CT scan or MRI.

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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Treatment
Medications
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.
The patient is instructed to wear a neck brace for 24 hours and
to not bend down or lay flat for 24 hours after the procedure.
One week after the CRP, the Dix-Hallpike test is repeated.
If the patient does experience vertigo and nystagmus, then the
CRP is repeated with a vibrator placed on the skull in order to
better dislodge the otoconia.

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The Epley Maneuver

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Clinical Trial
Ruckenstein (2001) Therapeutic efficacy of the Epley
canalith repositioning maneuver. Laryngoscope

Eighty-six patients
74% of cases that were treated with one or two
canalith repositioning maneuvers had a resolution of
vertigo as a direct result of the maneuver.
A resolution attributable to the first intervention was
obtained in 70% of cases within 48 hours of the
maneuver.
An additional 14% of cases that were treated had a
resolution of vertigo.
Only 4% of cases (three patients) manifested BPV
that persisted after four treatments.

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Differential Diagnosis
Ataksia Vestibuler
Ataksia Serebellar
Beberapa hariLebih permanen
minggu kemudian
lenyap
Vertigo
Vertigo (-)
Jatuh ke satu sisi
(-)
Tampak deviasi bila
(-)
menunjuk
Dipengaruhi posisi
(-)
kepala

BAEP / BERA

ABR
Auditory Brainstem Response

Latency:
Latency is the time from the stimulation
onset to the peak point of a wave. The
waveforms are called wave I, wave II,
wave III, wave IV, wave V, wave VI and
wave VII in order of appearance. The
waves I, III and V are stable and have
large amplitude. Depending on the
patient, the peaks of the waves II, IV
and V may not be obtained. The wave II
may have an equivocal waveform and
the waves IV and V may make a fused
waveform.

Inter peak latency (IPL):

By observing the difference in latency


between the wave I and III, between the
wave III and V, and between the wave I
and V. The function of the auditory
pathway can be examined

BAEP

A delayed I-III IPL indicates


abnormality between the periphery
and the medulla.
Long III-V IPL indicates abnormality
between the medulla and the
midbrain.

Peripheral or Central
Cause?
Central

Peripheral

Labyrinth or
vestibular nerve
dysfunction
Recurrent
Nystagmus-horizontal
Position change
Moderate to severe
vertigo

Cerebellum or
brain stem
dysfunction
Continuous
Nystagmus-vertical
Mild vertigo
Non-positional
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CHARACTERISTICS OF PERIPHERAL
AND CENTRAL VERTIGO

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Central Vestibular
Disorders

Brain stem lesion


Basilar artery
migraine
TIA
Stroke
MS
Cerebellar lesions

Metastatic Tumor
Meningioma

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Peripheral Vestibular Disorders

BPPV
Labrynthitis
Menieres disease
Acoustic Neuroma
Motion sickness
Cervicogenic
Perilymphatic
fistula

Vestibular
neuronitis
Semicircular canal
infection
Semicircular canal
water penetration

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Acute Dizziness: Important


Emergency Room
Considerations

Characteristics of peripheral vertigo and


dizziness
Characteristics of vertigo and dizziness of
central origin
Recognizing stroke syndromes that may
present with dizziness as a prominent
feature
Treatment considerations in dizziness of
central origin
Treatment of peripheral vestibular
dysfunction
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Serious vertigo that is disabling


Ataxia out of proportion to vertigo
Vertigo longer than 4 weeks
Changes in hearing
Vertical nystagmus
Focal neurological signs
Systemic disease or psychological origin

Australian Family Physician Vol. 31, No 8, August 2002

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Head and Neck


Nystagmus

Oscillation of eyes on attempted fixation


Fast component is the direction of the nystagmus
and is towards the side of the lesion
Test in 4 directions
Must be sustained for more than a few beats

Dysarthria

Slurred or scanning speech


Usually bilateral lesion
Baby hippopotamus or East Register Street is
opposite West Register Street

Cerebellar Hemorrhage

Sudden vertigo and nausea


Vomiting associated with a headache
Inability to stand
Nystagmus, nuchal rigidity, facial
paralysis, ataxia, dysrythmia, small
reactive pupils

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Acoustic Neuroma

Mild but constant hearing loss


Dizziness with possible tinnitis
Gradual onset
Benign schwannoma of 8th CN
Other CN findings as tumor grows
Surgical excision

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Pengobatan

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1. PENGOBATAN KAUSAL
Kebanyakan kasus vertigo tidak diketahui
sebabnya, kalau penyebabnya diketahui
pengobatan kausal merupakan pilihan utama
2. PENGOBATAN SIMPTOMATIK
Pengobatan ini ditujukan pada dua gejala
utama yaitu rasa vertigo ( berputar,
melayang ) dan gejala otonom (mual,
muntah) Gejala yang paling berat pada
vertigo vestibuler fase akut, menghilang
beberapa hari karena ada kompensasi Back

Terapi Simptomatik / Obat


Anti Vertigo
1)
2)
3)
4)
5)
6)
7)
8)

Ca entry Blocker
Antihistamin
Antikolinergik
Monoaminergik
Bensodiasepin
Antidopaminergik
Histaminik
Antiepileptik
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Mekanisme kerja obat anti


vertigo

CALCIUM ENTRY BLOCKER

Mengurangi aktivitas eksitatori SSP dengan menekan


pelepasan glutamat dan bekerja langsung sebagai
depresor labirin, bisa untuk vertigo perifer dan sentral.
Obat : Flunarisin (Silum)

ANTIHISTAMIN
Efek antikolinergik dan merangsang inhibitori
monoaminergik, akibatnya inhibisi nervus vestibularis.
Obat : Sinarisin
( Merron ), dimenhidrinat (Dramamine), prometasin
(Phenergan), meclizine, cyclizine
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ANTIKOLINERGIK
Mengurangi eksitabilitas neuron dengan
menghambat jaras eksitatori kolinergik ke nervus
vestibularis, mengurangi firing rate dan respon
nervus vestibularis terhadap rangsang. Obat :
Skopolamin, atropin

MONOAMINERGIK
Merangsang jaras inhibitori-monoaminergik pada
n. vestibularis sehingga eksitabilitas neuron
berkurang.
Obat : Amphetamine, efedrin

BENZODIAZEPIN
Menurunkan resting aktiviti neuron

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ANTIDOPAMINERGIK (FENOTIASIN)
Bekerja pada CTZ dan pusat muntah di medula
oblongata. Obat : Clorpromazin (largactil),
proclorperazine (Stemetil), Halloperidol (Haldol)

HISTAMINIK
Inhibisi neuron polisinaptik pada nervus
vestibularis lateralis. Obat : betahistin

ANTIEPILEPTIK
Karbamasepin, fenitoin pada temporal lobe
epilepsi dengan gejala vertigo
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Flunarizine

Calcium entry blocker

Mengurangi aktivitas eksitatori SSP


dengan menekan pelepasan glutamat

Meningkatkan aktivitas NMDA spesifik


channel

Depresor labirin

Dosis satu tablet sehari, tablet pagi


tablet malam
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Lanjutan

Efek samping mengantuk dan rasa


lemas yang sifatnya sementara.
Kontra indikasi belum diketahui.
Keamanan penggunaan pada wanita
hamil,ibu menyusui,dan anak belum
diketahui.

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Betahistine

Analog histamin
Meningkatkan aliran darah
a.vertebrobasiler
Memperbaiki mikrosirkulasi telinga
dalam
Menghambat neuron polisinaptik
Dosis 1 tablet 3 kali sehari
Hati-hati pada penderita gastric ulcer,
asma bronchiale, pheochromocytoma
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Drug-Induced Dizziness

Drugs that cause hypovolemia or


decrease blood pressure
(antihypertensives, tricyclics,
psychotropics, muscle relaxants)
Ototoxic drugs (ASA, aminoglycosides)
NSAIDs (including COX2 inhibitors)
Alcohol - postural hypotension with high
levels, vertigo when levels decline
Zweig, MD
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Eaton, 2003
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Dysequillibrium
Is a feeling that a fall is
imminent and is characterized
by unsteadiness or imbalance
that occurs only when erect and
primarily involves the trunk and
lower extremities rather than
the head; the sensation
diappears when sitting
or2003lying
Eaton,
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VERTIGO

DEFINISI:
Vertigo adalah perasaan penderita
merasa dirinya atau dunia berputar

ETIOLOGI

1. Otologi:

24-61% kasus

Benigna Paroxysmal Positional Vertigo (BPPV)

Meniere Desease
Parese N VIII Uni/bilateral
Otitis Media

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2. Neurologik

23-30% kasus
Gangguan serebrovaskuler batang otak/
serebelum

Ataksia

karena neuropati
Gangguan visus
Gangguan serebelum
Gangguan sirkulasi LCS
Multiple sklerosis
Malformasi Chiari
Vertigo servikal

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3. Interna:
+/-

33% karena gangguan kardio


vaskuler

tekanan darah
Aritmia kordis
Penyakit koroner
Infeksi
Hipoglikemia
Intoksikasi Obat: Nifedipin,
Benzodiazepin, Xanax,
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RISK FACTORS FOR


TIA AND STROKE

High Blood Pressure (2)


Elevated cholesterol (especially LDL)
Smoking (1.7-2.3)
Family history of stroke or heart attack
Age (male > 45, female > 55)
Overweight
Sedentary life style
Diabetes Mellitus (2.7)
Collagen Vascular disease
Heart problem such as atrial fibrillation (1.5) or old infarction (2.7)
elevated homocysteine
(Whisnant et al., 1996)