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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