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Sensasi dimana penderita merasa dirinya berputar thd sekelilingnya

(vertigo subyektif) atau sebaliknya (vertigo obyektif).
Berasal dari kata Vertere art. Berputar

Klasifikasi :
1.Vertigo sentral /kronis
2.Vertigo peripir/ Akut :
Vertigo spontan
Vertigo provokasi
( PPV / BPPV ) ... 20 30 %
VERTIGO
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Vertigo
Perception of movement
illusion of movement
Peripheral or Central

Syncope
Transient loss of consciousness with loss of postural tone
Prevalence
1 in 5 adults report dizziness in last month
Increases in elderly
Worsened by decreased visual acuity,
proprioception and vestibular input

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Etiologies of Vertigo
BPPV
Labyrintitis
Acute suppurative
Serous
Toxic
Chronic
Vestibular neuronitis
Vestibular ganglionitis
Mnires
Acoustic neuroma
Perilymphatic fistula
Cerumen impaction
CNS infection (TB, Syphillis)
Tumor (Benign or Neoplastic)
Cerebellar infarct
Cerebellar hemorrhage
Vertebrobasilar insufficiency
AICA syndrome
PICA syndrome
Multiple Sclerosis
Basilar artery migraine
Hypothyroidism
Hypoglycemia
Traumatic
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Vestibular Labyrinth
Pathophysiology

Complex interaction of visual, vestibular and
proprioceptive inputs that the CNS integrates as
motion and spatial orientation.

3 semicircular canal .....
rotational movement (cupula)

2 otolithic organs utricle & saccule
........ linear acceleration (Macula)
Sistem Keseimbangan
ada 3 komponen



1. Sistem Visual (mata)
2. Sistem vestibuler Formatio retikularis
3. Sistem proprioseptif (SSP)
(kulit, otot, sendi)


1. Otot Postur ( reflek vestibulospinal)
2. Otot bola mata (refleks vestibulookuler)

SENSORIS
PUSAT
MOTORIS
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MEKANISME KESEIMBANGAN SISTEM
VESTIBULARIS
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N. Vestibularis






Bola mata Palor Laring Otot postur
(Nistagmus) Keringat dingin Diafragma
Klj. Ludah
GIT
LABIRIN
Nukleus
Vestibularis
Korteks
cerebri
serebellum
Formatio
Retikularis
N.III
Simpatis
N. X
Kornu ant.
Medula sp.
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Evaluation of the vertigo
1. What type of dizziness is it?
2. How long does it last? Continuous or episodic
3. Spontaneous or positional
4. Duration of vertigo if episodic
5. Are there otologic symptoms?
6. Are there focal neurological symptoms?

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Otologic Symptoms of the Vertigo
Hearing Loss: progressive, sudden
Tinnitus: continuous or episodic
Aural fullness
Ear pain, or chronic drainage
History of ear surgeries/infection

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Neurological Symptoms of Vertigo
Vertigo if secondary to cerebrovascular insufficiency is
indicative of posterior circulatory problems
Visual loss
Loss of consciousness
Weakness especially if on one side
Incoordination as if drunk, esp if in spells
Difficulty swallowing
Slurring of the speech

Klinis Vertigo
Gejala respon motoris otak :

1. III (Mata) : rasa berputar , Nistagmus
2. Simpatis : palor ( pucat ), keringat dingin
3. X (Vagus) : mual, muntah
4. Otot postur : jatuh
5. Telinga : tinitus, pendengaran menurun


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Dix-Hallpike Maneuver
Dix-Hallpike maneuver (used to diagnose benign paroxysmal positional vertigo).
This test consists of a series of two maneuvers: With the patient sitting on the
examination table, facing forward, eyes open, the physician turns the patient's
head 45 degrees to the right (A). The physician supports the patient's head as the
patient lies back quickly from a sitting to supine position, ending with the head
hanging 20 degrees off the end of the examination table. The patient remains in
this position for 30 seconds (B). Then the patient returns to the upright position
and is observed for 30 seconds. Next, the maneuver is repeated with the patient's
head turned to the left. A positive test is indicated if any of these maneuvers
provide vertigo with or without nystagmus.
Differential of Vertigo
Peripheral Central
Onset Sudden Usually slow
Severity of Vertigo I ntense Usually mild
Pattern Paroxysmal Constant
Exac. by movement Yes Variable
Autonomic Frequent Variable
Laterality Unilateral Uni or bilat
Nystagmus Horizontorotary Any / Rotatoir
Fatigable/Fixation Yes No
Auditory symptoms Yes No
TM May be abnormal Normal
CNS symptoms Absent Present
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Duration of vertigo
Duration

1. BPPV Seconds, always < 1 min

2. VBI Few minutes,
focal neurological signs

1. Migraine Varies sec, minutes, hours or days
2. Menieres 20 minutes to hours
3. Vest.neuritis Days
4. Stroke Days
5.

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Peripheral Vertigo-Differential
Labyrinthine Disorders
Most common cause of true vertigo
Five entities
1. Benign paroxysmal positional vertigo
(BPPV)
2. Labyrinthitis
3. Mnire disease
4. Vestibular neuronitis
5. Acoustic Neuroma

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Management
Severe Mnire disease may require chemical ablation with
gentamicin
Attempt Epley maneuver for BPPV
Mainstay of peripheral vertigo management are antihistamines
that possess anticholinergic properties
-Meclizine -Diphenhydramine
-Promethazine -Droperidol
-Scopolamine

For neurovegetatif symptom ....... Anti emetic


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Pharmacotherapy

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Epley Maneuver

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Positional Vertigo
/
PPV / BPPV
Sudden attacks of vertigo precipitated by certain head positions.
Rolling over in the bed, reaching for an object from the top shelf, washing
the hair
Vertigo is of short duration ( < 1min )

Etiology:
Litiasis theory, originally describe by Schucknecht in1974
Degeneration of the salt-like crystals (otoliths) in the utricle which
break free and float into or attach to semicircular canals.
Proprioceptive mismatch btw the general proprioception (from muscles,
ligament and joints) and special proprioception (from maculae and
cristae); spino-cerebello-vestibular circuitry.

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Etiology of BPPV in 240 patients (Baloh et al., 1987)

Idiopathic in 49%
Traumatic in 18%
Viral Labyrinthitis in 15%
VBI in 5%
Menieres in 2%
Surgery in 4%
Ototoxicity in 2%

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BPPV
Extremely common
Otoconia displacement
No hearing loss or tinnitus
Short-lived episodes brought on by rapid changes in head
position
Usually a single position that elicits vertigo
Horizontorotary nystagmus with crescendo-decrescendo pattern
after slight latency period
Less pronounced with repeated stimuli
Typically can be reproduced at bedside with positioning
maneuvers

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Two main types

Dix-Hallpike maneuver elicited
Head hyperextension and rotation to AS
Induced typical horizontal-rotatory geotropic
(towards the ground) nystagmus
Nystagmus appears some seconds delay
Habituation phenomena
MacClure maneuver elicited
Pt supine, rolling the head from side to side
Pure horizontal geotropic and ageotropic nystagmus

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Treatment for PPV
Semont maneuver
Epley maneuver
Personal maneuver for PPV elicited by Dix-
Hallpike positioning ( Epley modified)

Lempert maneuver horizontal
semicircular lithiasis
post. Semicircular
canal lithiasis
80~90%effective

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1. Semont maneuver
Right ear lat canal PPV
1. Head turn towards left
side(SS)
2. Lying on R side, head is
rotated upward 105,
3mins
3. Lying on L side, head is
rotated downward 195,
3 mins
4. Slowly sit-up

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2. Epley maneuver
Left ear post. Canal PPV
Each stage wait 30 s

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3. Modified Epley
Left ear BPPV
30 SEC.

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4. Lempert maneuver
Right ear PPV

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Labyrinthitis
Associated hearing loss and tinnitus
Involves the cochlear and vestibular systems
Abrupt onset
Usually continuous
Four types of Labyrinthitis
Serous
Acute suppurative
Toxic
Chronic

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Serous
Adjacent inflammation due to ENT or meningeal infection
Mild to severe vertigo with nausea and vomiting
May have some degree of permanent impairment

Acute suppurative labyrinthitis
Acute bacterial exudative infection in middle ear
Secondary to otitis media or meningitis
Severe hearing loss and vertigo
Treated with admission and IV antibiotics

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Chronic
Localized inflammatory process of the inner
ear due to fistula formation from middle to
inner ear

Most occur in horizontal semicircular canal

Etiology is due to destruction by a
cholesteatoma

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Vestibular Neuritis
Subacute onset of vertigo, often with nausea and vomiting
Suspicion for viral cause but evidence for ischemic causes
Sudden onset vertigo that increases in intensity over several
hours and gradually subsides over several days
Mild vertigo may last for several weeks
May have auditory symptoms
Highest incidence in 3
rd
and 5
th
decades
Temporal bone histopathology: Scarpas ganglion neuronal
loss

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Vestibular Ganglionitis
Usually virally mediated-most often VZV

Affects vestibular ganglion, but also may affect multiple ganglions

May be mistaken as BPPV or Mnire disease

Ramsay Hunt Syndrome
-Deafness -Vertigo
-Facial Nerve Palsy -EAC Vesicles

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Mnire 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

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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

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Acoustic Neuroma
Peripheral vertigo that ultimately develops central manifestations
Tumor of the Schwann cells around the 8
th
CN
Vertigo with hearing loss and tinnitus
With tumor enlargement, it encroaches on the cerebellopontine
angle causing neurologic signs
Earliest sign is decreased corneal reflex
Later truncal ataxia
Most occur in women during 3
rd
and 6
th
decades

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Central Vertigo
Vertebrobasilar Insufficiency
Atheromatous plaque
Subclavian Steal Syndrome
Drop Attack
Wallenberg Syndrome
Cerebellar Hemorrhage
Multiple Sclerosis
Head Trauma
Neck Injury
Temporal lobe seizure
Vertebral basilar migraine
Metabolic abnormalities
Hypoglycemia
Hypothyroidism

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Most commonly will also have:
-Dysarthria -Ataxia -Facial numbness
-Hemiparesis -Diplopia -Headache
Tinnitus and hearing loss unlikely
Vertical nystagmus is characteristic of a (superior colliculus) brain stem
lesion
Up to 30% of TIAs are VBI with pontine symptoms and a focal
neurologic lesion

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2. Cerebellar Hemorrhage
Neurosurgical emergency

Suspected in any patient with sudden onset headache, vertigo,
vomiting and ataxia

May have gaze preference

Motor-sensory exam usually normal

Gait disturbance often not recognized because patient appears
too ill to move

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3. Multiple Sclerosis
Vertigo is presenting symptom in 7-10%
Thirty percent develop vertigo in the course of the disease
May have any type of nystagmus
Internuclear ophthalmoplegia is virtually pathognomonic
Onset during 2
nd
to 4
th
decade
Rare after 5
th
decade
Usually will have had previous neurological symptoms
Due to damage to the inner ear and central vestibular nuclei, most
often labyrinthine concussion
Temporal skull fracture may damage the labyrinth or eighth
cranial nerve
Vertigo may occur 7-10 days after whiplash
Persistent episodic flares suggest perilymphatic fistula
Fistula may provide direct route to CNS infection
4. Head and Neck Trauma

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5. Vertebral Basilar Migraine
Syndrome of vertigo, dysarthria, ataxia, visual changes, paresthesias
followed by headache
Distinguishing features of basilar artery migraine
-Symptoms precede headache
-History of previous attacks
-Family history of migraine
-No residual neurologic signs
Symptoms coincide with angiographic evidence of intracranial
vasoconstriction

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6. Metabolic Abnormalities
Hypoglycemia
Suspected in any patient with diabetes with associated
headache, tachycardia or anxiety

Hypothyroidism
Clinical picture of vertigo, unsteadiness, falling, truncal
ataxia and generalized clumsiness
DD vertigo sentral dg peripir
VERTIGO SENTRAL VERTIGO PERIPIR
1. Onset
2. Durasi
3. Perubahan posisi
4. Jenis Nistagmus
5. Gejala kranial
(kesadaran turun)
6. Gejala vestibuler
(tinitus, gg. Pend.)
7. Gejala vegetatif
(mual, muntah)
Pelan-pelan
Lama
Tidak terpengaruh
Nistagmus Rotatoir

Positip

Negatip

Negatip
Mendadak
Tidak lama
Terpengaruh
Nistagmus horisontal

Negatip

Positip

Positip
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Tes Fungsi Vestibuler
Macam Tes Vestibuler/Keseimbangan

1. Tes Romberg
2. Tes Kalori
3. Tes Gait
4. Tes Elektronistagmusgrafi
5. Tes Barany
6. Tes Rotasi
Tes Romberg

Prosedur :
1. Penderita bediri tegak, kaki rapat, mata tertutup dan
tangan menggantung atau
2. Satu kaki di depan kaki lainnya dan tangan ekstensi



Penderita goyang atau jatuh ke satu sisi


Lesi vestibuler baru pada sisi yg sama
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Tes fungsi vestibulum
UJI KALORI

Prosedurnya :

1. Posisi pasien : tidur telentang dg kepala flexi 30 atau
duduk dg kepala ekstensi 60
2. Irigasi telinga dg air es 5 cc selama 20 dt (cara Kobrak)
Lamanya nistagmus : 120 - 150 dt (normal)
< 120 dt (paresis kanal)
3. Irigasi telinga dg air 30 dan 44 sebanyak 250 cc,
selama 40 dt. (Cara Dick & Hall Pike)
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Kesimpulan :
No.

Telinga Suhu Arah
Nistagmus
Waktu
Nistagmus
1.
2.
3.
4.
Kiri
Kanan
Kiri
Kanan
30 C
30C
44C
44C
Kanan
Kiri
Kiri
Kanan
Detik




(1 + 3) - (2 + 4)
Sensitifitas Ki Ka : ------------------------ X 100 %
(1 + 2 + 3 + 4)

< 40 dt ( < 20 % ) Normal
> 40 dt ( > 20 % ) paresis kanal
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Tes Gait
Prosedur :
1. Penderita berjalan mengikuti garis lurus dg mata
terbuka kemudian tertutup atau
2. Berjalan dimana tumit bertemu dg jari kaki


Jalannya cendrung ke satu sisi/jatuh


Lesi vestibuler pd sisi yg sama
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TES VESTIBULER
Utk menilai sistem vestibuler/ keseimbangan tubuh
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Tes Fungsi Saraf Kranial
Saraf I : tes penciuman
Saraf II : tes penglihatan
Saraf III,IV, VI : penderita disuruh memandang ke
segala arah, apakah timbul nistagmus
Saraf V : tes sensitifitas refleks wajah / refleks
kornea
Saraf VII : apakah ada perot
Saraf VIII : tes audiometri dan vestibulum
Saraf IX : apakah faring simetris
Saraf XI : tes mengangkat bahu
Saraf XII : apak ada deviasi lidah
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1.Nystagmus due to peripheral causes has all of the following features excep

a. Diminishes with fixation
b. Unidirectional fast component
c. Can be horizontorotary or vertical
d. Nystagmus increases with gaze in direction of fast component
e. Can be accentuated by head movement

c. Can be horizontorotary or vertical
Peripheral nystagmus is typically horozonto-rotary, not pure horizontal or rotary
and is definitely not vertical.

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2. Nystagmus due to central causes has all of the following features except:
a. Does not change with gaze fixation
b. Can be unidirectional or bidirectional
c. Can be horizontal, rotary or vertical
d. Nystagmus increases with gaze in direction of fast component
e. Can be dramatically accentuated by head movement.
e. Can be dramatically accentuated by head movement
Vertigo and nystagmus produced by central causes does not significantly worsen
with head movement

3. All of the following will have hearing loss and tinnitus associated with the vertigo
except:
a. Vestibular neuronitis d. Acoustic neuroma
b. Acute labrynthitis e. Meniere ds
c. BPPV
c. BPPV will not have associated hearing loss or tinnitus
All of the other responses will have hearing loss and tinnitus to varying degrees




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5. All of the following have been implicated in causing vertigo except:
a. Loop diuretics e. Fluoroquinolones
b. Anticonvulsants f. All of the above
c. Aminoglycosides
d. NSAIDS

F All of the above
Many everyday medications can cause vertigo which is easily reversible if recognized.

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