What should be considered by medical personnel?

1. Vertigo• A sense of feeling the environment moving when

it does not. Persists in all positions. Aggravated by head movement.

2. Dysequilibrium• A feeling of unsteadiness or insecurity without

rotation. Standing and walking are difficult.

3. Light headedness/dyzziness• Swimming, floating, giddy or swaying sensation

in the head or in the room.

VISUAL INPUT

PROPRIOCEPTIUAL INPUT VESTIBULAR INPUT

equilibrium

Development of vertigo• Teori Konflik sensoris

Vertigo timbul bila ada gangguan pada salah satu atau lebih dari ketiga sistem tsb pada tingkat resepsi, integrasi atau persepsi

• Teori Neural Mismatch (sensory rearrangement)Vertigo timbul akibat adanya gerakan yang tidak sesuai dengan yang tersimpan dalam memori

Development of vertigo• Teori Sinaps

Penelitian CRF/H (Corticotropin Relesing Factor / Hormon) muncul krn gerakan, stress fisik, psikis (hipotalamus) merangsang locus coeruleus yang menyebabkan terganggunya sistim autonom dan juga menimbulkan panik yang kemudian terjadi desensitisasi reseptor dan penurunan influks Calsium

Vertigo

vestibular non-vestibular

peripheral central psychogenic visual others

Vestibular vertigo

peripheral vestibular central vestibular

central vestibular central ocular motor

• IS TRUE VERTIGO PRESENT?

• ARE THERE ASSOCIATED NEUROLOGIC SYMPTOMS?

• WHAT IS THE PATTERN OF ONSET ?

• WHAT IS THE DURATION OF THE SYMPTOMS?

• HAVE THERE BEEN AUDITORY SYMPTOMS?

Caused of Vertigo Central? Peripheral?

• ARE THERE OTHER ASSOCIATED SYMPTOMS?

• WHAT MEDICATIONS IS THE PATIENT TAKING?

• WHAT IS THE PATIENT’S PAST MEDICAL HISTORY?

• ANY RECENT OR REMOTE HEAD OR NECK INJURY?

Central vestibular disorders• Identifying these is critical

*Common 25% older patients presenting to ER with acute isolated – vertigo have a cerebellar infarction – Life-threatening – The earlier the Dx the better the Px – Severe neurologic sequelae – 1 st, 2nd & 3rd Prevention

*Acta Neurol Scand 91:43–48, 1995

Vertigo

• Peripheral

– CN VIII– Vestibular

apparatus– Labyrinth

• Central– Brainstem

• Vestibular nuclei in medulla and pons

– Cerebellum– Cerebellopontine

angle

Differential Diagnosis

• Peripheral (85-90%)– BPPV (20-50%)– Menier’s disease (vertigo, tinitus, progressing

hearing loss)– Ototoxicity (gentamicin, streptomicin, heavy

metals, chemotherapy, alcohol, salicilat, diphenilhydantoin,etc)

– Vestibular neuritis– Labyrinthitis

• Central (10-15%)– Migraine – Stroke / TIA – Head trauma – Multiple Sclerosis– SOL (Acoustic neuroma, frequently CN7

involvement)

Differential Diagnosis

VERTIGO:

Onset Sudden Slow, gradualIntensity Severe Ill defined/ Often less

intensDuration Paroxysmal, episodic Constant/persistent

Nausea/Diaphoresis Frequent, severe Infrequent

CNS signs Absent Usually present

Tinnitus/hearing loss Can be present Absent

Head position Associated with head position

Constant/non-positional

Imbalance Mild to moderateAble to stand, lean to lesion

Severeunable to stand

Nystagmus Torsional/horizontal Vertical

Nystagmus Fatigable Non-fatigable

PERIPHERAL CENTRAL

Duration of vertigoTime Peripheral CentralSeconds BPPV VB-TIA, aura of

epilepsy

Minutes perilymph fistula VB-TIA, aura of migraine

(Half) hours Meniére disease basilar migraine

Days vestibular neuronitis labyrinthitis

VB stroke

Weeks, Month acustic neurinoma, drug toxicity

multiple sclerosis cerebellar

degenerations

DIAGNOSIS

1. Anamnesis (Taking history)• What the patient means by vertigo• Time of onset• Temporal pattern• Associated signs and symptoms (tinnitus,

hearing loss, headache, double vision, numbness, difficulty of swallowing)

• Precipitating, aggravating and relieving factors• If episodic: sequence of events, activity at

onset, aura, severity, amnesia etc.

2. Physical examination

• Spontaneous nystagmus • Positional nystagmus • Optokinetic nystagmus • Posture and balance control

• Romberg’s test • Blind walking• Bárány’s test

• Stimulations of labyrinth• Caloric test (cold, warm water)• Rotational test

DIAGNOSIS

3. Laboratory examinations and imaging • Electronystagmography• Video-oculography• Audiometry• BAEP• CT• MRI

DIAGNOSIS

BPPV• Commonest cause of vertigo (20-50%)• History taking up to 90% predictive

– Episodic, self limiting, assoc with nausea– Occurs with head movement

• Hallpike test used to clinch diagnosis– Neurological exam normal

• 30-50% resolve spontaneosly• 50% recurrent (no predictive indicators)

BPPV: Pathophysiology

• Degenerative debris from utricle (otoconia)

• Canalithiasis TheoryFloating freely in the endolymph

• Cupulolithiasis TheoryAdhering to the cupula

BPPV diagnosis: Dix-Hallpike manoeuvre (a sensitivity of 82% and a specificity of 71%)

BPPV: therapy• Pharmacology• Position training/vestibular rehabilitation

canalith repositioning technique (CRT).

Semont Brandt-DaroffEpley

EXERCISES REHABILITATION

ANTIVERTIGO• SEDATIVE/TRANQUILIZER, BARBITURAT;

fenobarbital, secobarbital, pentobarbital. ATARAXICOS, droperidol, diazepam, lorazepam, procloperazina

• ALCALOID BELLADONA, atropin, scopolamin• ANTIHISTAMIN, difenhidramin, dimenhidrinat, ciclizin,

meclizina, astemizol• SIMPATOMIMETIC, efedrin, anfetamin, metanfetamin,

metilfenidat• VASOACTIVE, ANTAGONIS CALCIUM, cinarizin,

flunarizin• “AGENT NOOTROPICS”, gingko biloba, codergocrin,

nicergolin, vincamina, piritinol, piracetam

Time for a break

HistamineBetahistine

Betahistine Dihydrochloride2-[2-(methylamino) ethyl] pyridine

• H1 receptor agonist (located on blood vessels in the inner ear) vasodilatation: to an improvement on the microcirculation of the labyrinth and to a reduction in the endolymphatic pressure

• H3 receptor antagonist increases secresi histaminergic neurotrasmission and other neurotransmitters from the nerve endings -> improving the coordination neuronal electrical activity in the vestibular nuclei.

• is transformed, mainly at the hepatic level, in aminoethylpyridine (M1) and hydroxyethylpyridine (M2), then excreted with the urine as pyridylacetic acid (M3)

STUDI TERAPI/daily DURASI VARIABELOUTCOME

Jumlah sampel NILAI p

PERLAKUAN KONTROL

Oosterveld, 1984 • 3 x 12 mg BD• Placebo

6 weeks 24 24 0,004

Deering et al, 1986

•12 mg BD•15 mg cinnarisin

3 months Clinical Global Impression 44 44 0,02

Kinqma et al, 1997

• 16 mg BD• 32 mg BD• 64 mg BD• Placebo

8 hours vestibulo-ocular reflex (VOR) 12 12 < 0,02< 0,00>0,05

Bradoo, 2000 • 48 mg BD daily 6 weeks Frequncy of vertigo 30 - < 0,03

Mira et al, 2003 • 2 x 16 mg BD• Placebo

3 months intensity and duration of vertigo attacks

75(41 MD/34 PPV)

69(40 MD/29 PPV)

< 0,05

Albera et al, 2003

• 48 mg BD daily• 10 mg FL daily

8 weeks Dizziness Handicap Inventory (DHI)

52 52 0,03

Kazmiercsak et al,2004

• 3 x 8 mg BD• 3 x 16 mg BD

120 – 180 days(Mean 132 days)

Vertebrobasiler insufisiensyvisuo-oculomotor and vestibulo-oculomotor reflexes videonystagmography and stabilometry

150 150 0,00050,0005

Solov’eva et 2004

• 3 x 8 mg BD 4 weeks Vestibular respons 39 39 0.00

Hahn, et al 2008 •3 x 12 mg BD•3 x 20 mg cinnarzine + 3 x 40 mh Dimenhirinat

4 weeks Mean vertigo score 33 33 0,013 for cinnarizin+dimenhid

rinat

Hasil studi multi-center, RCT, double blind, Betahistine Dihydrochloride for vertigo

C. DELLA PEPA et al, 2006, ACTA OTORHINOLARYNGOL ITAL 26, 208-215