DEFINITION

VERTIGO is an illusion of movement either of the person or of objects about the person. It is one of the manifestations of vestibular disorder.

Vestibular disorder

Subjective Vertigo

Objective Nystagmus Ataxia

INCIDENCE OF VERTIGO
(Brandt 2002) 5-10% of all patients seen by general practitioners 10-20% seen by neurologists & otolaryngologist

The Ear

The Inner Ear

(horizontal)

SUPERIOR
Endolymphatic sac

Semicircular canals Anterior vertical Posterior vertical Horizontal

ANTERIOR

POSTERIOR

LOCATION OF VESTIBULAR & COCHLEAR DIVISIONS OF THE INNER EAR

endolymph

Crus commune

Semicicular canals Anterior vertical perilymph Horizontal Posterior vertical

BONY & MEMBRANOUS LABYRINTH

Bony labyrinth is bounded by petrous portion of the temporal bone. Membranous labyrinth contains organ of hearing (cochlea) & equilibrium (utricle, saccule, & semicircular ducts). Bone & membranous labyrinth filled with perilymph, membranous labyrinth filled with endolymph)

Ampullary crista

Semicircular canal
Angular acceleration

A. The ampullary crista contains the hair cells. The hair bundles of the hair cells extend into the cupula, which stretches from the crista to the roof of the ampulla B. The cupula is displaced when the head moves, & the hair cells are also displaced

Endolymph flow

HAIR CELLS IN THE VESTIBULAR LABYRINTH TRANSDUCE MECHANICAL STIMULI INTO NEURAL SIGNALS

Axis of hair cells

Ampulla

(Move clockwise because of inertia)

Horizontal canals

Depolarization (excitation)

Hyperpolarization (inhibition)

Because of inertia, rotation of the head in a counterclockwise direction causes endolymph to move clockwise. This reflects the stereocilia in the left canal in the excitatory direction & excites the afferent fibers on this side. In the right canal the hair cells are hyperpolarized & afferent firing there decreases.

PATOFISIOLOGI
Sindroma vertigo (SV) I. Teori Konflik Sens. Oleh Norre (1978)
Konflik masukan sens pusat AKT bingung. Kanan kiri. Vestib visus propriosep. Keluaran pusat AKT abnormal. Korteks : vertigo Motorik : deviasi posisi tegak, berjalan, dll. Otonom : pucat, peluh, mual & muntah. Visual : nistagmus.

II. Teori MG Gaudry (1991)

Garis besar = konflik sensoris. Lebih rinci dan luas gejalanya. Teori I & II tidak menjelaskan adaptasi.

III. Teori Neural Mismatch dari Reason (1975)

SV timbul gerakan baru lama. Adaptasi rearrangement masukan sensoris baru = lama sensory rearrangement Kegunaan klinisnya ?

Neural Mismatch

Sensory Rearrangement

PATOFISIOLOGI SV
IV. Teori Sinap
Stres CRF Switch SS simp SS Parasimpatis Vertigo, pusat, peluh Switch SS Simpatis SS Par Mual & muntah. Stres berulang Switch berulang progressive Ca Channel Closure influks Ca NT respon adaptasi (+).

CLASSIFICATION OF VERTIGO (Brandt 2002)

Physiological stimulation
Height vertigo Motion sickness

Pathological dysfunction
Labyrinthine & vestibular nerve disorders (peripheral) Central vestibular disorders (central)

----------------------------------------------------------------Syndrome Manifestation ----------------------------------------------------------------- Spatial orientation & motion perception Vertigo Vestibulo-Ocular reflex Nystagmus Posture Ataxia Autonomic Nausea, vomiting, anxiety

Syndromal manifestations of vertigo (Brandt 2002)

CLASSIFICATION OF PHYSIOLOGICAL VERTIGO & VESTIBULAR DISORDERS WITH THEIR ORIGIN AT DIFFERENT SITES WITHIN PERIPHERAL OR CENTRAL VESTIBULAR STRUCTURES (Brand & Daroff, 2002)

Visual input

equilibrium

Proprioceptiual input

Vestibular input labyrinths.

RE-AFFERENCES

EXPECTED AFFERENCES

---------------CENTRAL STORE ----------------

NEURAL MISMATCH CONCEPT OF VERTIGO AND MOTION SICKNESS (Brandt 2002)

OCULOMOTOR SYSTEM

HIGHER CENTERS CEREBELLUM

END ORGAN

VESTIBULAR NUCLEI RETICULAR FORMATION

END ORGAN

inhibition

AUTONOMIC SYSTEM MOTOR SYSTEM

Communication between the vestibular system & other system of centers in the CNS (Durrant 1982)

CN VIII

Labyrinth Vertigo

(Vestibular portion)

Cerebellum

Brainstem
Vestibular nuclei

CAUSES OF VERTIGO

FREQUENCY OF DIFFERENT VERTIGO SYNDROMES (Brandt 1989-1999)

-------------------------------------------------------------------------------------------------------------------Diagnosis Frequency n % ------------------------------------------------------------------------------------------------------------------- Benign paroxysmal positional vertigo (BPPV) 533 17.6 Somatoform phobic postural vertigo 434 14.3 Central vestibular syndromes with vertigo 364 12.0 Peripheral vestibulopathy (vestibular neuritis) 263 8.7 Basilar migraine, vestibular migraine 241 7.9 Menieres disease 200 6.6 Bilateral vestibular failure 89 2.9 Psychogenic vertigo (without 2) 89 2.9 Vestibular paroxysmia (neurovascular cross compression) 63 2.1 Perilymph fistula 7 0.3 Various rare vertigo syndrome 112 3.7 Unknown etiology 132 4.3 Central vestibular syndromes (without vertigo) 396 13.0 Other disorders 115 3.8

DD PERIPHERAL VS CENTRAL VERTIGO (Finestone 1982)

-------------------------------------------------------------------------------------------------------------Symptome Peripheral Central ------------------------------------------------------------------------------------------------------------- Hallucination of movement Definite Less definite Onset Usually paroxysmal Seldom paroxysmal Intensity Usually severe Seldom severe Duration Usually short Longer Influence of head position Frequent Seldom Nystagmus Present Present or absent Autonomoc nervous system Definite Less intense or absent Tinnitus Frequently present Seldom present Deafness Frequently present Seldom present Disturbs of consciousness Seldom present More frequently present Other neurologic signs Usually absent Frequently absent --------------------------------------------------------------------------------------------------------------

SPINNED
PERIPHERAL CENTRAL
Sudden (Onset) Positional Intensity Nausea/Diaphoresis Nystagmus Ear (hearing loss) Duration CNS signs

Yes Yes Severe Frequent

Torsional/horizontal

Slow, gradual No Ill defined Infrequent Vertical Absent

Can be present

Paroxysmal (< 1 min) Constant Absent Usually present

Carvalho et al. CTU , Oct, 2004

CAUSES OF PERIPHERAL VERTIGO (Finestone 1982) ---------------------------------------------------- Ear Acute otitis media Chronic otitis media Mastoid infection, acute & chronic Cholesteatoma Local trauma Foreign body or impacted cerumen Menieres syndrome Benign paroxysmal positional vertigo (BPPV) Vestibular neuronitis Ototoxic drugs Otoslerosis Motion sickness Psychogenic

CAUSES OF CENTRAL VERTIGO (Finestone 1982) --------------------------------------------------Vertebrobasilar insufficiency Stroke (cerebellar) Tumors, cerebellar or brainstem, primary or metastatic Degenerative disease of CNS (eg M.S.) Head trauma Psychogenic Epilepsy Migraine equivalent

Pemeriksaan khusus Neuro-otologik pada vertigo Tes Romberg Tes Romberg dipertajam Tes Jalan tandem Tes Fukuda Tes Past Pointing Head thrust test Pemeriksaan nistagmus

Pemeriksaan nistagmus
Bedside secara sederhana dengan atau tanpa kaca mata Frenzel Head shaking test Dix-Hallpike test ENG Tes kalori

Tes Romberg
Pemeriksa berada di belakang pasien Pasien berdiri tegak dengan kedua tangan di dada, kedua mata terbuka Diamati selama 30 detik Setelah itu pasien diminta menutup mata dan diamati selama 30 detik Jika pada keadaan mata terbuka pasien sudah jatuh kelainan serebelum Jika pada mata tertutup pasien cenderung

Tes Romberg di pertajam

Pemeriksa berada di belakang pasien Tumit pasien berada didepan ibu jari kaki yg lainnya Pasien diamati dalam keadaan mata terbuka selam 30 detik Kemudian pasien menutup mata dan diamati selama 30 detik Interpretasi = tes Romberg

Tes jalan tandem

Pasien diminta berjalan dengan sebuah garis lurus, dengan menempatkan tumit di depan jari kaki sisi yg lain secara bergantian Pada kelainan serebelar pasien tidak dpt melakukan jalan tandem dan jatuh kesatu sisi Pada kelainan vestibular pasien akan mengalami deviasi ke sisi lesi

Test fukuda
Pemeriksa berada di belakang pasien Tangan diluruskan ke depan, mata pasien ditutup Pasien diminta berjalan ditempat 50 langkah Tes fukuda dianggap abnormal jika deviasi ke satu sisi > 30 atau maju/ mundur > 1 meter Tes fukuda ini menunjukkan lokasi kelainan disisi kana atau kiri

Tes past pointing

Pada posisi duduk, pasien diminta untuk mengangkat satu tangan dengan jari mengarah keatas Jari pemeriksa diletakkan didepan pasien Pasien diminta dengan ujung jarinya menyentuh ujung jari pemeriksa beberapa kali dengan mata terbuka Setelah itu dilakukan dengan cara yang sama dengan mata tertutup

Test past pointing

Pada kelainan vestibular ketika mata tertutup maka jari pasien akan deviasi kearah lesi Pada kelainan serebelar akan terjadi hipermetri atau hipometri

Head thrust test

Pasien diminta memfiksasikan mata pada hidung / dahi pemeriksa Setelah itu kepala digerakkan secara cepat ke satu sisi Pada kelainan vestibular perifer akan dijumpai adanya sakadik

Pemeriksaan nistagmus
Pasien diminta mengikuti jari pemeriksa kekiri atau kanan 30 nistagmus horisontal Pasien diminta mengikuti jari pemeriksa kearah atas dan bawah nistagmus vertikal Nistagmus disebutkan berdasarkan komponen cepat sedangkan komponen lambat menunjukkan lokasi lesi

Head shaking tes

Pasien di gerakkan kepala kekiri dan kanan 20 hitungan Kemudian diamati adanya nistagmus horisontal dan vertikal

Dix-Hallpike test
Pasien menoleh 45 kesatu sisi, setelah itu pasien dijatuhkan sehingga kepala menggantung 15 dibawah bidang datar Diamati adakah nistagmus atau tidak Kemudian pasien tegak kembali dan diamati adakah nistagmus atau tidak Hal yang sama dilakukan kembali pada sisi yang lainnya

 Pada pemeriksaan Dix-hallpike ini dapat membedakan kelainan sentral atau perifer Pada kelainan perifer : - latensi : 3-10 detik - lamanya nistagmus: 10 30 detik, atau < 1 menit - fatigue - disertai gejala vertigo yang berat

Dix-Hallpike test
Pada kelainan sentral : - nistagmus langsung muncul - tidak ada fatigue - gejala vertigo bisa ada atau tidak

Pemeriksaan penunjang
Sesuai dengan etiologi Pemeriksaan : - laboratorium : stroke, infeksi - EEG : vestibular epilepsi - EMG : neuropati - EKG : CVD - TCD : CVD LP : infeksi CT Scan/ MRI : stroke, infeksi, tumor

MENIERES DISEASE (MD)

TRIAD: (Colletti 2000) - Vertigo spells + nausea vomiting - Fluctuating but progressive hearing loss - Tinnitus INCIDENCE: 7.5 160 per 100.000 persons. PATHOPHYSIOLOGY: (Strupp 2006) Too high production or too low absorption of endolymph (endolymph hydrops). endolymph pressure causes periodic rupturing or leakage opening of nonselective stretch-activited ion channels of the membrane separating endolymph from perilymph space.

Pathophysiology of Menieres Disease

Pathophysiology: Newer theories
Multifactorial inheritance Immune-mediated phenomena Association of allergies

Study by Gottschlich et al.

50% meeting criteria have antibodies to 70-kD heat-shock protein 70-kD HSP implicated in AI-SNHL

2 VARIANTS OF MENIERES DISEASE (MD) (Colletti 2000)

Cochlear MD : Fluctuating aural fullness Sensorineural hearing loss Tinnitus No vertigo Vestibular MD: Menieres episodes of vertigo without cochlear symptoms

BPPV
B = Benign
Not a brain tumor Can be severe and disabling V = Vertigo An illusion of motion The room is spinning Other descriptions Rocking Tilting Somersaulting Descending in an elevator

P = Paroxysmal
Episodic, not persistent Helpful feature in the differential diagnosis

P = Positional
Occurs with position of head Turning over in bed Looking up Bending over

BPPV
CHARACTERISTIC HISTORY - If you turn the head - After a few seconds delay, vertigo occurs - Resolves within 1 minute if you dont move - If you turn your head back, vertigo recurs in the opposite direction - Incidence : 60-70 yrs (F:M = 2:1)

2 CAUSES OF BPPV
Most common cause Dysfunction of posterior SCC (semicircular ch.) Cupulolithiasis vs. Canalithiasis Cupulolithiasis
Calcium deposits embedded on cupula in ampulla PSCC becomes dependent on gravity

Canalithiasis
Calcium debris (otoconia) displaced into PSCC Does not adhere to cupula in ampulla

Canalolithiasis Theory
Canalolithiasis theory is the most widely accepted theory of the pathophysiology of BPPV 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.

Canalolithiasis Theory
BPPV is generally thought to be due to otoconia (crystals of ca-carbonate) in the utricle displaced to semicircular canals. The utricle is damaged by head injury, infection, degeneration in old age. Otoconia is dissolved naturally or reabsorbed by dark cells of the labyrinth. (Timothy C.Hain 2007)

Otoconia =
(small crystals of calcium carbonate)

ATYPICAL BPPV (Timothy C. Hain 2007)

Horizontal canal BPPV Anterior canal BPPPV Cupulolithiasis Vestibulolithiasis Multicanal patterns

Causes
Idiopathic Infection (viral neuronitis) Head trauma Degeneration of the peripheral end organ Surgical damage to the labyrinth

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.

Diagnosis
Lab Studies:
No pathognomonic laboratory test for BPPV exists. Laboratory tests may be ordered to rule out other pathology.

Imaging Studies:
Head CT scan or MRI.

Procedures:
The Dix-Hallpike test, along with the patient's history, aids in the diagnosis of BPPV.

Vestibular Neuritis
Sudden onset of peripheral vertigo Usually without hearing loss Period of several hours - severe Lasts a few days, resolves over weeks Inflammation of vestibular nerve presumably of viral origin Spontaneous, complete symptomatic recovery with supportive treatment Treatment aimed at stopping inflammation

Vestibular Neuritis
Ariyasu et al.
20 patients: double-blinded, crossover Methylprednisolone vs. placebo 90% decrease in vertigo within 24 hours vs. 30% of placebo group Placebo switched to steroid after 24 hours with decrease in vertigo over next 24 hours 16 patients receiving steroid with resolution had normal ENG within one month

VERTIGO SENTRAL
CVD BATANG OTAK MENINGITIS TUMOR EPILEPSI VESTIBULER MIGREN BASILER TRAUMA KEPALA DAN LEHER VERTIGO OKULER

CVD BATANG OTAK

INFARK PENDARAHAN 5% DARI CVD KLINIS INFARK : - SUMBATAN KECIL : VERTIGO RINGAN BERAT DEFISIT NEUROLOGIS TAK JELAS - A. SEREBELLI POSTERIOR INFERIOR : SIND. WALLENBERG - A. SEREBELLI ANT. INF : VERTIGO DISARTRIA, DISFASIA, STRABISMUS PARESTESI MUKA GANGGUAN SIST. PIRAMIDAL - SUBCLAVIAN STEAL SYNDROM VERTIGO DROP ATTACK - SPONDILOSIS CERVICALIS

CVD BATANG OTAK

PERDARAHAN TERSERING DI PONS INSIDENS 5 12% DARI CVD PERDARAHAN BIASANYA FATAL GEJALA POKOK YANG PERTAMA TIMBUL : 1. VERTIGO 2. NYERI KEPALA 3. KESADARAN MENURUN

MENINGITIS
MENINGITIS OTOGENIK MENINGITIS TBC MENINGITIS REKURENS MENINGITIS MALIGNA KLINIS : - DEMAM - NYERI TENGKUK - GRM (+) - VERTIGO - OTONOM : MUAL, MUNTAH, HIPERHIDROSIS, PUCAT, LEMAH, LESU DIAGNOSTIK : - PEMERIKSAAN LCS - MRI

TUMOR
GANGGUAN KESEIMBANGAN DAN GANGGUAN VERTIGO SANGAT DITENTUKAN OLEH LOKASI TUMOR, YAITU: 1. DAERAH FOSSA POSTERIOR (SEREBELUM DAN BATANG OTAK) 2. LOBUS TEMPORALIS DIAGNOSTIK : 1. BERDASARKAN GAMBARAN KLINIK 2. TES AUDIOLOGIK 3. TEST VESTIBULER 4. BRAINSTEM EVOKED RESPONS AUDITORY (BERA) 5. CAIRAN SEREBRO SPINAL 6. CT SCAN DAN MRI + KONTRAS

VESTIBULAR EPILEPSY
- DEFINISI : 1. VE ADALAH SUATU SINDROMA VERTIGO KORTIKAL YANG TERJADI AKIBAT ADANYA DISCHARGE FOKAL DARI LOBUS TEMPORALIS ATAU KORTEK ASOSIASI VERTIGO ( BALOH ) 2. VE ADALAH KEJANG PARSIAL SEDERHANA ATAU KOMPLEK DIMANA GEJALA YANG MENONJOL ADALAH VERTIGO (YOUNG) - EPID : 1% DARI KEJANG - ETIOLOGI : 1. IDIOPATIK 2. SIMPTOMATIK : - NEOPLASMA - TRAUMA KEPALA - VASKULER - INTOKSIKASI OAE KLINIS : 1. KEJANG PARSIAL / UMUM 2. VERTIGO 3. KESADARAN MENURUN

MIGRAIN BASILER
ADALAH MIGRAIN DENGAN AURA YANG JELAS BERASAL DARI BATANG OTAK ATAU DARI KEDUA LOBUS OKSIPITALIS GEJALA : - GANGGUAN LAPANGAN PANDANGAN - DISARTRIA - VERTIGO - TINNITUS - PENDENGARAN MENURUN - ATAKSIA - DIPLOPIA - PARESTESI DAN PARESE BILATERAL - KESADARAN MENURUN DIAGNOSTIK : 1. MEMENUHI KRITERIA MIGRAIN + AURA 2. ADA 2 GEJALA KLINIS DIATAS

TRAUMA KEPALA DAN LEHER SINDROM VPT

- BPPV TK. RINGAN - VERTIGO AKUT KOMOSIO LABYRIN - SINDROM NEURO BERAT AKIBAT TK. BERAT DENGAN VERTIGO DAN ATAKSIA - BAROTRAUMA DAN LEDAKAN - TRAUMA IATROGENIK - TRAUMA PSIKOLOGIS TRAUMA LEHER (WHIPLASH INJURY) : 1. TERPUTUSNYA INPUT PROPIOSEPTIK 2. ISKEMI 3. KERUSAKAN BATANG OTAK YANG LUAS AKIBAT PEREGANGAN 4. AKSELERASI/DESELERASI DAPAT MENGELUARKAN OTOKONIA

OCULAR VERTIGO
AKIBAT KETIDAKCOCOKAN VISUAL VESTIBULAR KARENA :
KELAINAN REFRAKSI PARESIS OKULOMOTOR

KELAINAN REFRAKSI : - AWAL PENGGUNAAN KACAMATA : 1. KOREKSI ASTIGMAT 2. PERUBAHAN DIOPTRI - KACAMATA DIOPTRI TINGGI - POS. OP KATARAK IMBALANS OTOT EKSTRA OKULER LESI VESTIBULAR DAN SSP : - OSILOPSIA

CURRENT TREATMENT OPTIONS

1.Treat the underlying cause
Pharmacotherapy Particle repositioning procedure (in BPPV) Surgery

2. Symptomatic
Pharmacotherapy

3. Rehabilitative
To promote long-lasting neural reorganisation Vestibular rehabilitation exercises
Therapeutic option Depends on the type and cause of vertigo
Baloh RW. Lancet 1998;352:18416. Mukherjee A et al. JAPI 2003;51:1095-101.

CURRENT TREATMENT OPTIONS

1.Treat the underlying cause 2. Symptomatic 3. Rehabilitative

Therapeutic option Depends on the type and cause of vertigo

Baloh RW. Lancet 1998;352:18416. Mukherjee A et al. JAPI 2003;51:1095-101.

TREATMENT OF THE CAUSE OF VERTIGO CAUSE TREATMENT

PERIPHERAL CAUSE
BPPV Labyrinthine concussion Menieres disease Labyrinthitis Perilymph fistula Vestibular neuritis Canalith repositioning manoeuvre (Brandt-Daroff) Vestibular rehabilitation Low-salt diet, diuretic, surgery, transtympanic gentamicin Antibiotics, removal of infected tissue, vestibular rehabilitation Bed rest, avoidance of straining Brief course of high-dose steroids, vestibular rehabilitation

CENTRAL CAUSE
Migraine Vascular disease CPA tumours Beta-blockers, calcium channel blockers, tricyclic amines Control of vascular risk factors, e.g., antiplatelet agents Surgery

Baloh RW. Lancet 1998;352:18416. Goebel JA. Otolaryngol Clin North Am 2000;33:48393.

CURRENT TREATMENT OPTIONS

1.Treat the underlying cause 2. Symptomatic 3. Rehabilitative

Therapeutic option Depends on the type and cause of vertigo

Baloh RW. Lancet 1998;352:18416. Mukherjee A et al. JAPI 2003;51:1095-101.

SYMPTOMATIC TREATMENT
ANTIVERTIGO I. Vestibular Suppressant
1. Ca antagonist : Flunarizin 2. Vasodilator : Betahistine 3. Tranquilizer : diazepam, haloperidol, sulpiride 4. Antihistamin : Difenhidramine, meclizine. 5. CNS stimulant: ephedrin, amphetamin

II. Antiemetic
1. Anticholinergic : atropine, scopolamine 2. Phenotiazine : Prochlorperazine, metoclopramide. Side effects: sedation, extrapyramidal.

CURRENT TREATMENT OPTIONS

1.Treat the underlying cause 2. Symptomatic 3. Rehabilitative

Therapeutic option Depends on the type and cause of vertigo

Baloh RW. Lancet 1998;352:18416. Mukherjee A et al. JAPI 2003;51:1095-101.

VESTIBULAR REHABILITATION EXERCISE

Mechanism: neural learning and neural reorganization. Aim: to promote adaptation and compensation of the nervous system Particularly useful when:
Medical therapy is ineffective Patients have poor central integration or motor function

Baloh RW. Lancet 1998;352:18416. Goebel JA. Otolaryngol Clin North Am 2000;33:48393. Konnur MK. J Postgrad Med 2000;46:2223. Mukherjee A et al. JAPI 2003;51:1095101.

 Perform vestibular rehabilitation early Favour active retraining Modify rehabilitation programs to suit individual patients Examine patients in a standardized environment Use static and dynamic test Avoid drug with sedative effect
Lacour M,Durr.Med.Research and Opinion vol 22. No.9,2006,1651-1659

INSIGHT FOR THE REHABILITATION OF PATIENTS WITH VESTIBULAR DEFICIT

MANAGEMENT OF VERTIGO (Brandt 2002)

--------------------------------------------------- Pharmacologic therapies Physical therapies Surgical interventions ----------------------------------------------------

PHARMACOLOGIC THERAPIES FOR VERTIGO (Brandt 2002)

-------------------------------------------------------------------------------------------------------------------Therapy Vertigo -------------------------------------------------------------------------------------------------------------------Vestibular suppressant Acute peripheral & vestibular nuclei lesions, Prevention of motion sickness Antiepileptics Vestibular epilepsy, vestibular paroxysmia (disabling positional vertigo), paroxysmal dysarthria & ataxia in MS), other central vestibular paroxysms, superior oblique myokymia Beta-blockers Basilar migraine (vestibular migraine; benign recurrent vertigo) Betahistine Menieres disease Antibiotics Infection of the ear & temporal bone Ototoxic antibiotics Menieres disease (meniere drop attacks) Corticosteroids Vestibular neuritis, autoimmune inner ear disease Baclofen Downbeat or upbeat nystagmus or vertigo Acetazolamide Familial periodic ataxia or vertigo --------------------------------------------------------------------------------------------------------------------

Symptomatic Pharmacotherapy
Predominant targeted vestibular neurotransmitters:
Cholinergic Histaminergic GABA neurotransmitters - negative inhibition

Vomiting center transmitters:

Dopaminergic (D2) Histaminergic (H1) Serotonergic

Multiple classes of drugs effective

Symptomatic Pharmacotherapy
Anticholinergics - scopolamine, meclizine Antihistaminergic - dimenhydrinate Gamma-aminobutyric acid enhancing (GABA-ergic) agents - lorazepam, valium Anti-dopaminergic - droperidol

Symptomatic Pharmacotherapy
Some drugs of the antihistamine class are useful for symptomatic control of vertigo Have anti-motion sickness properties in large part due to inhibition of vestibular system H1 histaminergic neurotransmitters Examples include dimenhydrinate (Dramamine) and promethazine (Phenergan) Also suppress the vomiting center

PHYSICAL THERAPIES FOR VERTIGO (Brandt 2002)

--------------------------------------------------------------------------------Deliberate manoeuvres Benign paroxysmal positioning vertigo (BPPV) Vestibular exercises Vestibular rehabilitation, central compensation of acute vestibular loss, habituation for prevention of motion sickness, improvement of balance skills (eg in the elderly)

Neck collar Cervical vertigo (fiction or reality?) ---------------------------------------------------------------------------------

SURGICAL INTERVENTIONS FOR VERTIGO (Brandt 2002)

------------------------------------------------------------------------------------------------------------Decompression of VIIIth nerve Acoustic tumor or cyst Decompression of vertebral artery Rotational vertebral artery occlusion Ampullary nerve section Benign paroxysmal postioning vertigo (BPPPV) canal plugging Endolymphatic shunt Menieres disease Vestibular nerve section or Intractable Menieres disease labyrinthectomy Surgical patching Perilymph fistula ------------------------------------------------------------------------------------------------------------

COMMONLY USED ANTIVERGINOUS & ANTIEMETIC DRUGS (1) (Brandt 2002)

------------------------------------------------------------------------------------------------------Drug Dosage Action ------------------------------------------------------------------------------------------------------Anticholinergics Muscarinic Antagonist - Scopolamine 4-6 x 0.6mg po or (transderm) Transderm 1 q 3 days Antihistamines - Dimenhydrinate 4-6 x 50 mg po/4-6x im (dramamine) 100 mg supp q8-10h - Meclizine 4-6 x 25mg po (antivert,bonine) - Promethazine 4-6 x 15-50 mg po/ im (phenergan) 4-6 x supp Histamine (H1) Antagonist Muscarine Antagonist Histamine (H1) Antagonist
Muscarine Antagonist

Histamine (H1) Antagonist Muscarine Antagonist

COMMONLY USED ANTIVERGINOUS & ANTIEMETIC DRUGS (2) (Brandt 2002)

------------------------------------------------------------------------------------------------------Drug Dosage Action ------------------------------------------------------------------------------------------------------Phenothiazine -Prochlorperazine 4-6x5-10 mg po/4xim Muscarine Antagonist 2 x 25 mg supp Dopamine (D2) Antagonist Butyrophenone -Droperidol 2 x 2.5 5 mg im Muscarine A. (inapsine) Dopamine (D2) Antagonist Benzodiazepines -Diazepam 5-10 mg po, 2-4 x im GABAA agonist (valium) 4-6 x 1V -Clonazepam 3 x 0.5 mg GABAA agonist --------------------------------------------------------------------------------------------------------

Treatment
Medications The Canalith Repositioning Procedure (CRP) Surgery

Medications
Antiemetic Antihistaminic Anticholinergic

Canalith Repositioning Procedure ( CRP )

The treatment of choice for BPPV, 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.

The Epley Maneuver

Debris deposited In utricle. Patient experiences relief

If vertigo affects the R. ear, turn head to the right

Debris in PSCC

Inner ear (right side)

Hold for 30 seconds Utricle Anterior ) Posterior ) SCC Lateral ) Crista ampullaris Anterior Lateral

Posterior PSCC Inverted

Debris Hold for 30 seconds Settling debris causes nystagmus

The Epley Maneuver

Contraindications
Unstable heart disease High grade carotid stenosis Severe neck disease Ongoing CNS disease (TIA/stroke) Pregnancy beyond 24th week gestation (relative)

Furman JM, Cass SP. N Engl J Med 1999;341:1590-96

Brandt-Daroff Exercises
Timothy C. Hain 2007)

Method of treating BPPV, usually used when the office treatment fails. These exercises should be performed for two weeks, three times per day for three weeks, twice per day. In each time, one performs the maneuver as shown five times. 1 repetition = maneuver done to each side in turn (takes 2 minutes)

Brandt-Daroff Exercises (Timothy C.Hain 2007)

Time Exercise Duration --------------------------------------------Morning 5X 10 min Noon 5X 10 min Evening 5X 10 min ---------------------------------------------

EXERCISE THERAPY (Todd 2004)

Patient begins in sitting position & then rapidly to the side, placing the head on the bed or table remains there until vertigo subsides & then returns to sit, remaining there until vertigo subsides. The maneuvre is repeated toward the opposite side.

Surgery
Singular neurectomy Vestibular Nerve Section Posterior Canal Plugging Procedure

POSTERIOR CANAL PLUGGING PROCEDURE

(Timothy C. Hain 2007)

USA : low-salt diet, diuretic, intratympanic injection of gentamycin and corticosteroid (Strupp 2006), systemic streptomycin (Colletti 2000). Europe: betahistine (Strupp 2006) Longterm medical treatment (Colletti 2000) Na restriction 2 g/day (the endolymph sac is rich in K & expands at the expense of Na-rich perilymphatic system); Bananas & orange juice to K intake; Acetazolamide (diuretic) is based on the localization of carbonic anhydrase in the dark cells & stria vascularis. Supressant drugs: cinnarizine, promethazine, diazepam. Betahistine 3 X 16 mg for 3 months. Surgical treatment for disabling MD (Colletti 2000) Endolymphatic sac decompression, endolymphatic shunt, labyrinthectomy, selective vestibular neurectomy + betahistine after operation for adaptive compensation. Vestibular neurectomy is to date the surgical treatment of choice.

TREATMENT OF MENIERES DISEASE (MD)

Newer Treatment of Menieres Disease

Immunosuppressive agents gaining favor
Systemic and intra-tympanic glucocorticoids Cyclophosphamide Methotrexate

Shea study - intractable Menieres

48 patients intra-tympanic dexamethasone 66.7% elimination of vertigo 35.4% improvement in hearing (>10dB and/or 15% change in word recognition score)

VESTIBULAR MIGRAINE (Strupp 2006)

Recurrent attacks of vertigo, ataxia of stance & gait, visual disorders, other brainstem symptoms, occipitally located head pressure, pain, nausea, vomiting.

Treatment:
Prophylactic as for mIgraine with aura: betablockers (metroprolol, propanolol), valproic acid for 3-6 months. Tricyclic antidepressants; zolmitriptan; topiramate migraine vertigo with auditory symptoms; lamotrigine 1 X 100 mg more marked effect on vertigo.