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VERTIGO
Sensasi dimana penderita merasa dirinya berputar thd sekelilingnya
(vertigo subyektif) atau sebaliknya (vertigo obyektif). Berasal dari kata Vertere art. Berputar
Klasifikasi : 1.Vertigo sentral /kronis 2.Vertigo peripir/ Akut : Vertigo spontan
Vertigo provokasi
Vertigo
Perception of movement illusion of movement Peripheral or Central
Syncope
Transient loss of consciousness with loss of postural tone
Prevalence
1 in 5 adults report dizziness in last month Increases in elderly Worsened by decreased visual acuity, proprioception and vestibular input
Etiologies of Vertigo
BPPV Labyrintitis Acute suppurative Serous Toxic Chronic Vestibular neuronitis Vestibular ganglionitis Mnires 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
Pathophysiology
Vestibular Labyrinth
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)
Sistem Keseimbangan
ada 3 komponen
SENSORIS
1. Sistem Visual (mata) 2. Sistem vestibuler 3. Sistem proprioseptif
PUSAT
MOTORIS
1. Otot Postur ( reflek vestibulospinal) 2. Otot bola mata (refleks vestibulookuler)
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serebellum
N. Vestibularis
LABIRIN
Formatio Retikularis
6.
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Klinis Vertigo
Gejala respon motoris otak : 1. III (Mata) 2. 3. 4. 5.
: rasa berputar , Nistagmus Simpatis : palor ( pucat ), keringat dingin X (Vagus) : mual, muntah Otot postur : jatuh 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 Peripheral Sudden Intense Paroxysmal Yes Frequent Unilateral Horizontorotary Yes Yes May be abnormal Absent Central Usually slow Usually mild Constant Variable Variable Uni or bilat Any / Rotatoir No No Normal Present
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Onset Severity of Vertigo Pattern Exac. by movement Autonomic Laterality Nystagmus Fatigable/Fixation Auditory symptoms TM CNS symptoms
Duration of vertigo
Duration 1. BPPV 2. VBI Seconds, always < 1 min Few minutes, focal neurological signs Varies sec, minutes, hours or days 20 minutes to hours Days Days
1. 2. 3. 4. 5.
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Peripheral Vertigo-Differential
Labyrinthine Disorders Most common cause of true vertigo Five entities 1. Benign paroxysmal positional vertigo (BPPV) 2. Labyrinthitis 3. Mnire disease 4. Vestibular neuronitis 5. Acoustic Neuroma
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Management
Severe Mnire disease may require chemical ablation with gentamicin Attempt Epley maneuver for BPPV Mainstay 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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Etiology of BPPV
Idiopathic in 49% Traumatic in 18% Viral Labyrinthitis in 15% VBI in 5% Menieres in 2% Surgery in 4% Ototoxicity in 2%
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BPPV
Extremely common Otoconia displacement No hearing loss or tinnitus Short-lived episodes brought on by rapid changes in head position Usually a single position that elicits vertigo Horizontorotary nystagmus with crescendo-decrescendo pattern after slight latency period Less pronounced with repeated stimuli Typically can be reproduced at bedside with positioning maneuvers
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1. Semont maneuver
Right ear lat canal PPV
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2. Epley maneuver
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3. Modified Epley
30 SEC.
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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 Serous Acute suppurative Toxic Chronic
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Serous
Adjacent inflammation due to ENT or meningeal infection Mild to severe vertigo with nausea and vomiting May have some degree of permanent impairment
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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: Scarpas 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 Mnire disease Ramsay Hunt Syndrome -Deafness -Facial Nerve Palsy
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Mnire Disease
First described in 1861 Triad of vertigo, tinnitus and hearing loss Due to cochlea-hydrops Unknown etiology Possibly autoimmune Abrupt, episodic, recurrent episodes with severe rotational vertigo Usually last for several hours
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Often patients have eaten a salty meal prior to attacks May occur in clusters and have long episode-free remissions Usually low pitched tinnitus Symptoms subside quickly after attack No 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 Vertigo
Vertebrobasilar Insufficiency Atheromatous plaque Subclavian Steal Syndrome Drop Attack Wallenberg Syndrome Cerebellar Hemorrhage Multiple Sclerosis
Head Trauma Neck Injury Temporal lobe seizure Vertebral basilar migraine Metabolic abnormalities Hypoglycemia Hypothyroidism
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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 TIAs 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
4. Head and Neck Trauma 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
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5. Vertebral Basilar Migraine Syndrome of vertigo, dysarthria, ataxia, visual changes, paresthesias followed by headache Distinguishing 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 Hypoglycemia Suspected in any patient with diabetes with associated headache, tachycardia or anxiety Hypothyroidism Clinical picture of vertigo, unsteadiness, falling, truncal ataxia and generalized clumsiness
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Tes Romberg
Prosedur : 1. Penderita bediri tegak, kaki rapat, mata tertutup dan
tangan menggantung atau 2. Satu kaki di depan kaki lainnya dan tangan ekstensi
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
Kanan Kiri Kiri Kanan
Waktu Nistagmus
Detik
1. 2. 3. 4.
(1 + 3) - (2 + 4) Sensitifitas Ki Ka : ------------------------ X 100 % (1 + 2 + 3 + 4) < 40 dt ( < 20 % ) > 40 dt ( > 20 % ) Normal paresis kanal
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Tes Gait
Prosedur : 1. Penderita berjalan mengikuti garis lurus dg mata
terbuka kemudian tertutup atau 2. Berjalan dimana tumit bertemu dg jari kaki
TES VESTIBULER
Utk menilai sistem vestibuler/ keseimbangan tubuh
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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. b. c. d. e. Diminishes with fixation Unidirectional fast component Can be horizontorotary or vertical Nystagmus increases with gaze in direction of fast component Can be accentuated by head movement
c. Can be horizontorotary or vertical Peripheral 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. b. c. d. e. Does not change with gaze fixation Can be unidirectional or bidirectional Can be horizontal, rotary or vertical Nystagmus increases with gaze in direction of fast component 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 neuroma b. Acute labrynthitis e. Meniere ds c. BPPV c. BPPV will not have associated hearing loss or tinnitus All 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 above Many everyday medications can cause vertigo which is easily reversible if recognized.
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