VERTIGO

DIAGNOSIS AND MANAGEMENT

Dr Aris Catur Bintoro, SpS(K)

Bag/KSM Neurologi, FK Undip/RSUP Dr Kariadi
Semarang

7 Maret 2021
Outline

 Epidemiology
 Anatomy & Physiology
 Diagnosis
 Management
 EPIDEMIOLOGY

 Vertigo and dizziness in the general population are among the

most frequent symptoms in medical practice, :
 lifetime prevalence of 17.0–30.0% (1)
 annual prevalence of 16.7–27.0% (2)

 In a study of dizziness on 2064 of working-age people in the

community, results (3)
 over 20% suffered in the previous month
 6% had dizziness that lasted more than 5 years

1. Murdin L, Schilder AG. Epidemiology of balance symptoms and disorders in the community: a systematic
review. Otol Neurotol. 2015;36: 387–392
2. Neuhauser HK, Radtke A, von Brevern M, Lezius F, Feldmann M, Lempert T. Burden of dizziness and vertigo in the
community. Arch Intern Med. 2008;168: 2118–2124. 10.1001/archinte.168.19.2118
3.Yardley L, Owen N, Nazareth I, Luxon L. Prevalence and presentation of dizziness in a general practice community
sample of working age people. Br J Gen Pract. 1998;48: 1131–1135
 In a large German epidemiological population‐based study,
 the lifetime prevalence of vestibular vertigo was estimated
at 7.4% → medical cosultation 5,8% (Nauhaser 2005).
 Estimates of the prevalence of significant vertigo impacting
on daily life range 3%-10% (Murdin 2015)

1. Neuhauser HK, von Brevern M, Radtke A, Lezius F, Feldmann M, Ziese T et al. Epidemiology of
vestibular vertigo: a neurotologic survey of the general population. Neurology. 2005;65: 898–904.
10.1212/01.wnl.0000175987.59991.3d
2. Murdin L, Schilder AG. Epidemiology of balance symptoms and disorders in the community: a
systematic review. Otol Neurotol. 2015;36: 387–392
 Fisiologi Keseimbangan

Korteks Lobus Temporalis

Persepsi

Talamus

Batang otak /serebelum

Integrasi/ koordinasi/ Komparasi

Vestibular Visual Somatosensori

Sistem arteri Vertebrobasiler
 Diagnosis

Langkah-langkah yang harus ditempuh dalam tata

laksana penderita vertigo :
- Memastikan keluhan sebagai vertigo
- Memastikan jenis dan letak lesi
- Mencari penyebab
-Memantau terapi

→ ditegakkan berdasar anamnesis, pemeriksaan fisik,

laboratorium elektrofisiologis dan radiologis
 Anamnesis
 Bentuk : melayang, berputar, tujuh keliling, rasa naik perahu
 Keadaan yang memprovokasi : perubahan posisi kepala &
tubuh, keletihan, dan ketegangan.
 Profil waktu : apakah timbulnya akut atau perlahan-lahan,
hilang timbul, paroksismal, kronik, progresif atau membaik.
 Adanya gangguan pendengaran yang menyertai. (lesi di alat
vestibuler atau non vestibuler → gangguan pendengaran)
 Penggunaan obat-obatan: streptomisin, kanamisin, salisilat,
dll
 Vertigo Vestibuler VS Non Vestibuler

PERBEDAAN VESTIBULER NON VESTIBULER

rasa berputar rasa melayang, goyang,
sifat vertigo
(true vertigo) sempoyongan
sifat serangan episodik kontinyu
mual muntah (+) (-)
gang. pendengaran (+)/(-) (-)
situasi pencetus (-) ramai, macet, pasar, sibuk

letak lesi sistem vestibuler sistem visual, propioseptif

 Vertigo Vestibuler PERIFER vs SENTRAL

VERTIGO VESTIBULER
PERIFER SENTRAL
Bangkitan vertigo mendadak lebih lambat
Intensitas berat ringan
Pengaruh gerakan kepala (+) (-)
Gejala otonom (++) (+)/(-)
Gangguan pendengaran (+) (-)
Tanda fokal otak (-) (+)
Terus menerus atau intermiten ?
• Vertigo intermiten dan posisional sugestif untuk BPPV
• Vertigo kontiniu sugestif untuk akut vestibulopati perifer, neuritis
vestibular, labirintitis, atau lesi serebelum

Onset
• Onset mendadak : BPPV, Stroke
• Onset progresif gradual : tumor, demielinisasi

Gejala penyerta
• Kurang pendenganran, tinnitus sugestif pada neuronitis vestibuler,
labirintitis, peny. Meniere
• Demam dan nyeri telinga sugestif pada labirintitis bakterialis
 Vertigo sentral → gejala neurologik lain dan gejalanya
ditandai dengan:
 Onset sering bertahap
 lebih ringan dibandingkan vertigo perifer
 perubahan posisi → sering tdk berpengaruh

 Vertigo sentral → penyakit serebrovaskuler (cari

faktor risiko : hipertensi, atrial fibrilasi, riwayat stroke
sebelumnya, usia lanjut )
 Kelainan sentral dapat hanya sebagai gait ataxia
kronik maupun episodik tanpa disertai vertigo.
 Vertigo of Central Origin: Causes

Condition Details
Migraine Vertigo may precede migraines or occur concurrently
Release of neuropeptide P subst , neurokinine A,
calcitonin gen relatef factor (CGRP) → excitacion to
sensory epilthel inner ear & nucl n vestibularis
Vascular disease Ischaemia or haemorrhage in vertebrobasilar system
can affect brainstem or cerebellum function
Multiple sclerosis Demylination disrupts nerve impulses which can
result in vertigo
Vestibular Vertigo resulting from focal epileptic discharges in
epilepsy the temporal or parietal association cortex
Cerebellopontine Benign tumours in the internal auditory meatus
tumours

Baloh RW. Lancet 1998;352:1841–6. Mukherjee A et al. JAPI 2003;51:1095-101. Salvinelli F et al. Clin Ter 2003;154:
341–8. Solomon D. Otolaryngol Clin North Am 2000;33:579–601. Strupp M, Arbusow V, Curr Opin Neurol 2001;14:11–20.
 Vertigo of Peripheral origin causes

Condition Details
Benign paroxysmal Brief, position-provoked vertigo episodes caused by
positional vertigo abnormal presence of particles in semicircular canal
(BPPV)
Meniere’s disease An excess of endolymph, causing distension of
endolymphatic system
Vestibular neuronitis Vestibular nerve inflammation, most likely due to virus
Acute labyrinthitis Labyrinth inflammation due to viral or bacterial infection
Labyrinthine infarct Compromises blood flow to the labyrinthine
Labyrinthine Damage to the labyrinthine after head trauma
concussion
Perilymph fistula Typically caused by labyrinth membrane damage
resulting in perilymph leakage into the middle ear
Autoimmune inner ear Inappropriate immunological response that attacks inner
disease ear cells

Baloh RW. Lancet 1998;352:1841–6. Mukherjee A et al. JAPI 2003;51:1095-101. Parnes LS et al. CMAJ
2003;169:681– 93. Puri V, Jones E. J Ky Med Assoc 2001;99:316–21. Salvinelli F et al. Clin Ter 2003;154:341–8.
Pemeriksaan Fisik

 Nistagmus
 Tes Romberg
 Past Pointing Test
 Dix – Hallpike
 Tes Kalori
 Saraf-saraf Kranial
 Fungsi Motorik dan Sensorik
NYSTAGMUS
HORIZONTAL

NYSTAGMUS
VERTICAL
 Nistagmus Perifer Nistagmus Sentral
• Horisontal • Vertikal, torsional, horizontal
• Unidireksi • Bidireksi
• Dapat Lelah • Tidak dapat Lelah
• Berkurang dengan fiksasi • Menetap dengan fiksasi
• Terlambat mengikuti • Dapat mengikuti stimulus dg
stimulus cepat
Tes Romberg Tes Romberg dipertajam /
Tandem gait
 Pemeriksa harus mengidentifikasi Cerebellar Sign

• Identifikasi Bicara (pasien dengan lesi serebellar cenderung

memecah frasa menjadi beberapa suku kata)
• Nistagmus
• Pronator Drift : Mata tertutup, tangan terbentang ke depan
supinasi. Akan terlihat upward drift pada salah satu tangan
yang sugestif lesi serebelar
• Rebound Test
• Finger-to-nose test, knee-heel
• Rapid Alternating Movement
• Gait atau truncal ataxia
VERTIGO Perifer
Benign Positional Vertigo (BPPV)
• Penyebab vertigo paling umum. Lebih banyak terjadi pada wanita, insiden
paling tinggi pada usia 50-60 tahun
• Akibat otolit pada kanalis semisirkularis
• Onset mendadak dengan episode singkat vertigo osisional yang
berlangsung selama kurang lebih 30 detik yang akan membaik apabila
tidak ada gerakan
• Tanpa disertai dengan kurang pendengaran
• Nistagmus horizontal
• Manuver posisional seperti Epley : hasil perbaikan
• Pengobatan suportif : anti emetic

Vestibular Neuronitis
• Kemungkinan diakibatkan oleh virus (HSV atau Zoster) mengikuti “Flu
like illness”
• Onset dalam beberapa jam, membaik dalam hitungan hari
• Vertigo tetap muncul saat kepala dalam posisi stasioner
• Nistagmus horizontal
• Pengobatan : antiemetic dan antihistamin
Vertigo perifer

Labirintitis
• Mungkin diakibatkan oleh viral atau bacterial (berasal dari Otitis Media)
• Kurang lebih sama dengan vestibular Neuronitis akan tetapi disertai
keluhan tinnitus atau kurang pendengaran
• Pasien tampak toxic appearance dan membutuhkan rawat inap untuk
Antibiotik Intravena

Penyakit Meniere
• Sering muncul pada manusia paruh baya, sebagai akibat berkurangnya
resorbsi endolimfe
• Vertigo episodic yang berlangsung selama 30 menit hingga 24 jam
• Nistagmus horizontal, jerky dapat disertai dengan mual, muntah dan
berkeringat
• Tinnitus yang unilateral dan low pitched
• Tatalaksana termasuk membatasi konsumsi garam dan kafein, diuretic
tiazid
Head Impulse, Nistagmus, Test of Skew (HINTS)

Head Impulse
• Menilai refleks vestibulo-okuler.
• Hasil abnormal (positif) mengindikasikan adanya vertigo perifer
• Hasil normal (negative) mengindikasikan adanya penyebab sentral
Nistagmus
• Menilai lirikan pasien saat kepala dalam kondisi statis.

Test of Skew
• Juga dikenal sebagai alternating cover test.
• Pasien duduk berhadapan dengan pemeriksa, salah satu mata pasien
ditutup, penutup mata dipindahkan secara bergantian terhadap dua
mata. Akan terlihat mata berusaha kembali ke posisi normal
Pemeriksaan Penunjang
 BAEP (Brainstem Auditory Evoked Potential)
 Audiometri
 CT Scan / MRI
 Laboratorium : darah lengkap, profil lipid,
 X Foto Servikal
 EEG (Electroensefalografi)
 EMG (Electromiografi)
 TREATMENT OF VERTIGO

CURRENT TREATMENT OPTIONS

1. Symptomatic
● Pharmacotherapy

2. Treatment of Specific condition (Etiology)

● Pharmacotherapy
● Particle repositioning procedure (in BPPV)
● Surgery

3. Rehabilitative
● Vestibular Rehabilitation Therapy

4. Prevention of aggravating factor

● Diet control
● Life-style changes

Baloh RW. Lancet 1998;352:1841–6. Mukherjee A et al. JAPI 2003;51:1095-101.

1. Symptomatic Treatment

I. ANTIVERTIGO
Vestibular Suppressant
1. Ca channel blocker : Flunarizin
2. Histaminic : Betahistine
3. Antihistamin : Difenhidramine, sinarisin

II. ANTIEMETIC
Proklorperazine, metoclopramide.

III. PSYCHOAFFECTIVE
Clonazepam, diazepam for anxiety and panic attack
 GOLONGAN JENIS OBAT ESO EKSTR
SEDASI PRMDL
Ca Entry Flunarizine , dosis : 1 x 5-10 mg/hr. + +
Blocker
GOL OBAT
Antihistamin Cinnarizine , dosis : 3 x 25mg/hr. + +
Dimenhidrinat , dosis : 3 x 50 mg/hr. + -
Antikolinergik Scopolamine , dosis : 3x 0,6 mg + -
Atropin. dosis : 3x 0,4 mg - -
Histaminik Betahistin , dosis : 3 x 8 mg/hr. 1x + +
24 mg
Fenotiazine Chlorpromazine , dosis : 3 x 25 +++ +++
mg/hr
Benzodiazepine Diazepam, dosis 3 x 2-5 mg/hr +++ -

Simptomatik Metoclopropamid (Primperan),

otonom dosis : 3 x 10 mg/hr
2. Treatment for Specific Conditions
PERIPHERAL VERTIGO
● BPPV
Canalith repositioning manoeuvre (Brandt-Daroff, Epley, Semont
maneuvre)
● Meniere’s disease
Low-salt diet, diuretic, surgery, transtympanic gentamicin
● Labyrinthitis
Antibiotics, removal of infected tissue, vestibular rehabilitation
● Vestibular neuritis
Steroids, vestibular rehabilitation
● Labyrinthine concussion
Vestibular rehabilitation
● Perilymph fistula
Bed rest, avoidance of straining
2. Treatment of Specific Conditions

CENTRAL VERTIGO

Migraine
Beta-blockers, calcium channel blockers, tricyclic amines,
anticonvulsants

Vascular disease
Control of vascular risk factors, antiplatelet / antikogulan
agents

CPA tumours
Surgery
Specific Treatment for BPPV

1. Office Treatment
● Epley maneuver
● Semont maneuver

2. Home Treatment
● Brandt-Daroff Exercises
Epley Maneuver
3 min

3 min

30 sec
Other name:
• Canalith repositioning
• Particle repositioning
B. Semont Maneuver
C. Lampert Roll Maneuver
Brandt-Daroff maneuver

Time Exercise Duration

-----------------------------------------
Morning 5X 10 min
Noon 5X 10 min
Evening 5X 10 min
-----------------------------------------
Vestibular Rehabilitation Therapy (VRT)

VRT is a specific form of physical therapy designed to

promote habituation and compensation for deficits related to
balance disorders.
VRT is effective in unilateral and bilateral peripheral vestibular
hypofunction as well as from central balance disorders.

Integrated Therapy
Integrated Vestibular Therapy (IVT)
A combination therapeutic modalities of Etiologic
Treatment, Symptomatic Treatment, Vestibular Rehabilitaton
Therapy, Diet Control and Life-style changes, brought about
96 % of vertigo improvement.
 MODE OF ACTION BETAHISTINE
Betahistine adalah H1 agonis lemah dan H3 antagonis kuat.

1. Efek stimulasi langsung (agonist) H1 reseptor pada

pembuluh darah di telinga dalam
→ meningkatkan vasodilatasi lokal dan permeabilitas
→ membantu mengatasi permasalahan dengan hidrop
endolimfatik.

2. Efek antagonis H3 reseptor kuat dan meningkatkan

neurotransmiter yang dikeluarkan oleh nerve ending
ditelinga dalam → meningkatkan efek vasodilatasi
pada telinga dalam.
Juga meningkatkan neurotransmiter serotonin pada
batang otak yang akan menghambat vestibular nuclei.
 1.) Betahistine does not sedate. It has no antagonistic effects
on H1 Receptors which controls wakefulness (sleep patterns
and state of alertness). Betahistine stimulates H1 receptors
instead of blocking them so patients remain alert.

 2) Betahistine has no affinity for H2 Receptors → it does not

stimulate H2 receptors (which are found in the stomach) to any
great extent so betahistine is generally free from gastric side
effects. So far no H3 receptors have been discovered in the
stomach, which might explain why no indirect H2 effects are
seen.

 3) Betahistine has specific interaction with H3 & H1 receptors.

 Betahistine HCL

H3 Heteroreceptor H3 Autoreceptor

Stimulates release
of Histamine
Stimulates release
of serotonin H1 H1
Receptor Receptor

Regulatory effect on
Relaxation of vascular smooth
Vestibular nuclei
muscles

Improvement of bloodflow in
↓ Sensation of vertigo CNS and inner ear

Symptomatic effec (w/o sedation) Prophylactic effect (treat the cause)

 Betahistine on H1 receptors and H3
Autoreceptors (Blood Vessels of the inner ear)
H B

H3

H1 H1

Relaxation of vascular smooth muscles→ ↑ bloodflow in CNS & inner ear

Betahistine on H3 Heteroreceptors
(Brainstem)
H
S B

H3

Serotonin has a
regulatory effect on H
vestibular nuclei →

↓ Sensation of
Vertigo

Post-synaptic nerve
H2
Vestibular Suppression
The Higher The Dose, The Greater The Efficacy
Betahistin 2 x 24 mg
Author & Betahisti Treatme Reduced frequency of
Years of Study ne nt vertigo episodes
dose/day Duration change over
(mg) (months betahistine (%)
)
Canty 1981 32 2 -44%
Mira 2003 32 2 -63%
Fraysse 48 2 -93%
1991
Bradoo 48 1 -97%
2004
Authors' conclusions: Low quality evidence suggests that in patients
suffering from vertigo from different causes there may be a positive effect of
betahistine in terms of reduction in vertigo symptoms. Betahistine is generally
well tolerated with a low risk of adverse events. Future research into the
management of vertigo symptoms needs to use more rigorous methodology
and include outcomes that matter to patients and their families.
Results: Clinical improvement was observed in 80/262 (30. 5%) of patients treated
with betahistine and 43/252 (17. 1%) of control patients. Betahistine significantly (p<0.
0001) improved tinnitus in treated individuals.
Conclusions: The daily dosage of 48 mg of betahistine during 120 consecutive days
is useful to reduce or eliminate tinnitus in patients with vestibular disorders.
Conclusion

This observational study found that treatment of vestibular vertigo with betahistine
(dosed at 48 mg/day) appeared to be effective in reducing vertigo-associated symptoms
in a routine outpatient clinical setting.
The VIRTUOSO results showed that the effectiveness of betahistine treatment
persisted for 2 months after cessation of treatment, which may suggest that betahistine
may facilitate lasting vestibular compensation.
Future controlled trials are required to confirm this observed compensatory effect.
Betahistine was well tolerated when administered at 48 mg/day for 2 months, and
should be considered as a good therapy option by physicians treating vertigo.
 Take Home Message

 Treatment of vertigo :
symptomatic, specific, vestibular rehabilitative therapies, and
dietary and life habit control.

 Integrated VestibularTherapy proved to bring better

resolution of vertigo compared to single therapy
with each modality.
 Betahistine →the higher the dose, the greater the
efficacy
TERIMA KASIH
 Betaserc memblok autoreceptor H3, sehingga
mencegah mekanisme kontrol feedback negatif dari
histamin,dan merangsang pelepasan histamin →
relaksasi otot polos vaskular → memperbaiki aliran
darah pada cns & telinga bagian dalam
(PROPHYLACTIC EFFECT)
 Betaserc memblok reseptor H3 pada neuron non-
histaminergic (heteroreceptors) dan merangsang
pelepasan serotonin.
 Serotonin memiliki efek pengaturan pada inti
vestibular → penurunan sensasi vertigo decreases
(SYMPTOMATIC EFFECT ON VERTIGO)