4. Vertigo

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1 PENATALAKSANAAN VERTIGO PENATALAKSANAAN VERTIGO

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penatalaksanaan VERTIGO

Transcript of 4. Vertigo

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PENATALAKSANAAN VERTIGO

PENATALAKSANAAN VERTIGO

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PENATALAKSANAAN VERTIGO

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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 /kronis2.Vertigo peripir/ Akut : Vertigo spontan Vertigo provokasi ( PPV / BPPV ) ... 20 – 30 %

VERTIGO

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VertigoPerception of movementillusion of movementPeripheral or Central

SyncopeTransient loss of consciousness with loss of postural tone

Prevalence1 in 5 adults report dizziness in last monthIncreases in elderlyWorsened 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 Ménière’s 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 LabyrinthPathophysiology

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)

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Sistem Keseimbanganada 3 komponen

1. Sistem Visual (mata) 2. Sistem vestibuler Formatio retikularis3. Sistem proprioseptif (SSP) (kulit, otot, sendi)

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

SENSORISPUSAT

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. XKornu ant.

Medula sp.

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Evaluation of the Evaluation of the vertigo 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 Otologic Symptoms of the Vertigoof 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 SymptomsNeurological Symptoms of Vertigo 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

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Klinis Vertigo

Gejala respon motoris otak :

1.III (Mata) : rasa berputar , Nistagmus2.Simpatis : palor ( pucat ), keringat dingin3.X (Vagus) : mual, muntah4.Otot postur : jatuh5.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.

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Differential of Vertigo

PeripheralPeripheral CentralCentral OnsetOnset SuddenSudden Usually slowUsually slow Severity of VertigoSeverity of Vertigo IntenseIntense Usually mildUsually mild PatternPattern ParoxysmalParoxysmal ConstantConstant Exac. by movement Exac. by movement YesYes VariableVariable AutonomicAutonomic FrequentFrequent VariableVariable LateralityLaterality UnilateralUnilateral Uni or bilatUni or bilat NystagmusNystagmus HorizontorotaryHorizontorotary AnyAny / Rotatoir / Rotatoir Fatigable/FixationFatigable/Fixation YesYes NoNo Auditory symptomsAuditory symptoms YesYes NoNo TMTM May be abnormalMay be abnormal NormalNormal CNS symptomsCNS symptoms AbsentAbsent PresentPresent

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Duration of vertigo Duration of vertigo

Duration

1.BPPV Seconds, always < 1 min

2. VBI Few minutes, focal neurological signs

1.Migraine Varies sec, minutes, hours or days2.Meniere’s 20 minutes to hours3.Vest.neuritis Days4.Stroke Days5.

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Peripheral Vertigo-Differential

Labyrinthine DisordersMost common cause of true vertigoFive entities

1. Benign paroxysmal positional vertigo (BPPV)

2. Labyrinthitis3. Ménière disease4. Vestibular neuronitis5. Acoustic Neuroma

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Management

Severe Ménière disease may require chemical ablation with gentamicinAttempt Epley maneuver for BPPVMainstay 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% Meniere’s in 2% Surgery in 4% Ototoxicity in 2%

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BPPV

Extremely commonOtoconia displacementNo hearing loss or tinnitusShort-lived episodes brought on by rapid changes in head positionUsually a single position that elicits vertigoHorizontorotary nystagmus with crescendo-decrescendo pattern after slight latency periodLess pronounced with repeated stimuliTypically can be reproduced at bedside with positioning maneuvers

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Two main types

Dix-Hallpike maneuver elicitedHead hyperextension and rotation to ASInduced typical horizontal-rotatory geotropic (towards the ground) nystagmusNystagmus appears some seconds delayHabituation phenomena

MacClure maneuver elicitedP’t supine, rolling the head from side to sidePure horizontal geotropic and ageotropic nystagmus

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Treatment for PPV

Semont maneuver Epley maneuverPersonal 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

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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

SerousAcute suppurativeToxicChronic

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SerousAdjacent inflammation due to ENT or meningeal infectionMild to severe vertigo with nausea and vomitingMay have some degree of permanent impairment

Acute suppurative labyrinthitisAcute bacterial exudative infection in middle earSecondary to otitis media or meningitisSevere hearing loss and vertigoTreated 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 3rd and 5th decades Temporal bone histopathology: Scarpa’s 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 Ménière disease

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

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Ménière Disease

First described in 1861Triad of vertigo, tinnitus and hearing lossDue to cochlea-hydrops

Unknown etiologyPossibly autoimmune

Abrupt, episodic, recurrent episodes with severe rotational vertigoUsually last for several hours

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Often patients have eaten a salty meal prior to attacksMay occur in clusters and have long episode-free remissionsUsually low pitched tinnitusSymptoms subside quickly after attackNo 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 8th 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 3rd and 6th decades

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Central VertigoVertebrobasilar Insufficiency Atheromatous plaque Subclavian Steal Syndrome Drop Attack Wallenberg SyndromeCerebellar HemorrhageMultiple Sclerosis

Head Trauma Neck Injury Temporal lobe seizure Vertebral basilar migraine Metabolic abnormalities

HypoglycemiaHypothyroidism

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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 TIA’s 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 2nd to 4th decade Rare after 5th 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 headacheDistinguishing 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

HypoglycemiaSuspected in any patient with diabetes with associated headache, tachycardia or anxiety

HypothyroidismClinical picture of vertigo, unsteadiness, falling, truncal ataxia and generalized clumsiness

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DD vertigo sentral dg peripir

VERTIGO SENTRAL VERTIGO PERIPIR

1. Onset2. Durasi3. Perubahan posisi4. Jenis Nistagmus5. Gejala kranial

(kesadaran turun)6. Gejala vestibuler

(tinitus, gg. Pend.) 7. Gejala vegetatif

(mual, muntah)

Pelan-pelanLamaTidak terpengaruhNistagmus Rotatoir

Positip

Negatip

Negatip

MendadakTidak lamaTerpengaruhNistagmus horisontal

Negatip

Positip

Positip

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Tes Fungsi Vestibuler

Macam Tes Vestibuler/Keseimbangan

1.Tes Romberg2.Tes Kalori3.Tes Gait4.Tes Elektronistagmusgrafi5.Tes Barany6.Tes Rotasi

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Tes Romberg

Prosedur :1.Penderita bediri tegak, kaki rapat, mata tertutup dan

tangan menggantung atau2.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.

KiriKananKiriKanan

30 “C30”C44”C44”C

KananKiriKiriKanan

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 atau2.Berjalan dimana tumit bertemu dg jari kaki

Jalannya cendrung ke satu sisi/jatuh

Lesi vestibuler pd sisi yg sama

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TES VESTIBULERUtk 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 verticalPeripheral 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 bidirectionalc. Can be horizontal, rotary or verticald. Nystagmus increases with gaze in direction of fast componente. 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 neuromab. Acute labrynthitis e. Meniere dsc. BPPVc. BPPV will not have associated hearing loss or tinnitusAll 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 aboveMany everyday medications can cause vertigo which is easily reversible if recognized.

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