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VERTIGO AND MENIERE’S DISESASE dr. Ida Ayu Sri Wijayanti, M.Biomed, Sp.S Departement of Neurology FMUNUD/Sanglah Hospital Denpasar

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Spinal Cord Injury TJOKORDA GB MAHADEWA, M.D., M.Med., SFNS(jpn), Ph.D.Presented in Block Neuroscience 22th April 2015Suspect Spine Injury ExaminationHigh-Speed CrashUnconscious patient Multiple injuries Neurologic deficit Spinal pain / tendernessExclude other injuries. Palpate all spinous processes. Ask patient to move spine within the pain limits. Inspect motor and sensory function. Look for Horner's syndrome. Torticollis. Screening for Spine and Spinal Cord Injury Conscious PatientPresence of paraplegia/quadriplegia /pentaplegiaPresume spinal instabilityIdentify bony Early neurosurgicalFracture subluxation consult Screening for Spine and Spinal Cord injuryAlert,sober, neurologically normal patient :① If no neck or spine pain or tenderness to palpation or voluntary movement ② If no painful distracting injury ③ Remove C-colar If still no pain or tenderness with voluntary movementNo further spine evaluation or c-spine x-ray necessary ATLS 2014Screening for Spine and Spinal Cord InjuryATLS 2014Alert, sober, neurologically normal patient :Neck or spine pain or tenderness to palpation or voluntary movement ?After removal of c- collar ?If “ yes” to any question Protect c-spine Obtain necessary x-ray examsSensory ExaminationATLS 2014Motor ExaminationATLS 2014 Neurologic Assessment ATLS 2014Neurogenic Shock Hypotension associated with cervical /high thoracic spine injury Bradycardia Treatment : Maintenance fluids, atropine and occasionally vasopressors Spinal “Shock”Neurologic Not hemodynamic phenomenon Occurs shortly after cord injury Flaccidity Loss of reflexes Classification of Injury ATLS 2014Incomplete Any sensation Position sense Voluntary movement in lower extremity Sacral sparing CompleteNo motor / sensory functionNo sacral sparingMay have reflexes Classifications of InjuryATLS 2014 Spinal Cord Syndromes Central cord Posterior cordAnterior cord Brown – SequardComplete transectionMorphology Fracture or fracture / dislocation Spinal cord injury without radiographic abnormality (SCIWORA)Spinal Cord Injury without radiographic evidence of Trauma (SCIWORET)Penetrating Classification of InjuryATLS 2014Morphology Consider unstable if : X-ray evidence of injury Neurologic deficitSevere pain on spine movement or palpation C Spine X-ray GuidelinesATLS 2014 Adequacy Alignment Bony abnormality Base of skull Cartilage , Contours Disc space Soft tissue C – Spine X-rays 10% of patients with a C-spine fracture have a 2nd, associated noncontiguous vertebral column fracture Indentify one abnormality ? Look for another!Radiographic screening of entire spine required in this instance Crosstable lateral film exludes 85% of fracture Additional 2 views exludes most fractures Also may require Swimmers view Ct scan for bony detail Flexion extension views MRI/CT myelogram Other spine X –ray GuidelinesAdequacy Alignment Bony abnormalityCartilage, Contours Disc Space Soft tissue ManagementImmobilization Entire Patient Proper padding Maintain until spine injury excludedAvoid prolonged use of backboard!MANAGEMENTTreat life threatening injuries first Immobilize Appropriate spine imagingDocument examination Definitive treatmentOccipito-Cervical FusionOccipito-Cervical FusionCervical FracturesThoracic FracturesThoracic FracturesStab WoundThoracolumbal FracturesLumbosacral FracturesSacrococcygeal FracturesMedical ManagementEnsure adequate ventilation especially for high level (c-4) quadriplegic Maintain blood pressure Atropine as needed Methylprednisolone (NASCIS III)SteroidsIV Methylprednisolone Proven spinal cord injury Starts within 1st 8 hours from injury only 30

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VERTIGO AND MENIERES DISESASE

VERTIGO AND MENIERES DISESASEdr. Ida Ayu Sri Wijayanti, M.Biomed, Sp.SDepartement of Neurology FMUNUD/Sanglah HospitalDenpasarDEFINITIONChang et al, 2008

DizzinessIs a nonspecific term that describes a sensation of altered spatial orientationAny sensation of discomfort of head.Dizziness has resulted in a classification system with 4 different subtypes

IMBALANCE /DIZZINESS Vertigo

DisequilibriumPresyncopeRotating Spinning

Vestibular spinningSwimming or floating sensatonswayingRocking

NonvestibularVisual, cervicallight-headedA sense of unsteadiness in the lower bodyFeelings in the head are unaffectedRelieved when sitting down Neuropathy, ataxia fallingA feeling offaintness orloss ofconsciousness

Cardiovascular faintingDrachman DA, Hart CW. Neurology 1972;22:3234. Sloane PD et al. Ann Intern Med 2001;134:82332. 4Vertigo is one of four types of dizzinessDizziness can be described as abnormal sensations relating to a persons perception of their body in the environment (Drachman & Hart 1972, Sloane et al 2001). In their influential paper of 1972, Drachman and Hart described four different types of dizziness. These classifications of dizziness subtypes, listed below, are still used today.

Vertigo an illusion of movement typically characterized by feelings of rotationPresyncope a feeling of impending faintDisequilibrium a feeling of unsteadiness, particularly in the lower body, without sensations in the head. It is worse when standing or walking, and is alleviated by sitting down. Other subtypes other feelings of dizziness not encompassed by the preceding definitions. Drachman and Hart described this type of dizziness as ill-defined light-headedness. People have since suggested that this category can include sensations of swimming or floating or feelings of dissociation. Patients falling into this category often have difficulty describing their symptoms.

ReferencesDrachman DA, Hart CW. An approach to the dizzy patient. Neurology 1972;22:32334Sloane PD, Coeytaux RR, Beck RS, Dallara J. Dizziness: State of the Science. Ann Intern Med 2001;134:82332.

Body Balance is Controlled by 3 Sensory Systems:Vestibular, Visual, Proprioseptif Balance dyfunction Imbalance /DizzinessCentral Nervous system Skin,Muscle and joint (Proprioceptive)Postural control via musclesGoebel JA. Otolaryngol Clin North Am 2000;33:48393. Shepard NT, Solomon D. Otolaryngol Clin North Am 2000;33:45569Controls eye movements

Eye(Visual)

Inner ear (vestibular system)5Maintaining balance is dependent on input from a number of sourcesBalance results from a complex interaction of sensory information from several sources. The inner ears, or vestibular system sensory hair cells within the inner ear monitor the position and motion of the head in the environment. The eye visual cues are important in maintaining balance and oculomotor control. Skin pressure receptors provide information about which part of the body is in contact with the ground.Muscle and joint sensory receptors provide information on the position of the limbs in the environment.

Sensory information from all relevant sources is processed in the central nervous system (specifically the brain stem and cerebellum with additional input from the cerebral cortex). The output from this processing controls motor responses relating to eye movements, postural control and perceptual output, allowing the body to navigate in the environment. Contradictory or missing information from any of the sensory systems, or an impairment of the central processing of information can lead to forms of dizziness or imbalance, such as vertigo.

ReferencesGoebel JA. Management options for acute versus chronic vertigo. Otolaryngol Clin North Am 2000;33:48393.Shepard NT, Solomon D. Functional operation of the balance system in daily activities. Otolaryngol Clin North Am 2000;33:45569.

Vestibular LabyrinthPathophysiologyComplex interaction of visual, vestibular and proprioceptive inputs that the CNS integrates as motion and spatial orientation3 semicircular canalsrotational movementcupula2 otolithic organs utricle & sacculelinear accelerationMacula

Cause of VertigoAn imblance of sensory input into the two vestibular nuclei from overactivity or underactivity of either or both sides of labyrinth. The brain interprets such input differences as a sensation of movement. Cont..However, any disturbances to the labyrinth, visual-vestibular interaction centres in the brainstem & cerebellum, and sensory pathway to or from thalamus, can result VERTIGO

VERTIGOVertigo is an erroneous perception of motionof either the subject or the environment.

1. VESTIBULAR VERTIGO Vestibular system2. NONVESTIBULAR VERTIGO Visual, Somatosensory systems

VERTIGOVestibular vs Nonvestibular Vestibular Nonvestibular

Feeling Spinning Swaying, rocking, swimming, floating

Duration of attack Episodic Constant

Trigger Movement of the Stress, hyperventilation, head or body busy environment

Associated symptoms Nausea, vomit, tinnitus, Pale, tachycardy, deafness, oscillopsia parresthesia, syncope

Physiological vertigo (motion stimulation) and pathological vertigo (induced by lesion or stimuli) are characterised by similar signs and symptoms that derive from the functions of the multisensory vestibular system (Brandt and Daroff 1980)

1010

Balance requires information of similar intensity from both vestibular systemsHead movement

Activation of cells in right vestibular systemActivation of cells in left vestibular system

Normally, the input from left and right vestibular system is of similar intensity (e.g. of size 10)

Central nuclei13Balance requires information of similar intensity from both vestibular systemsMovement of the head in any direction leads to movement of sensory hair cells in both left and right semicircular canals. Both vestibular systems (labyrinths) will then send similar information of the same intensity to the central vestibular nuclei located in the brain stem (e.g., information of intensity 10). The central nervous system integrates this information from the left side and the right side, and balance is maintained providing that the information is coherent and similar in intensity.Peripheral vestibular vertigoDysfunction of vestibular apparatus, vestibular nerve5

Central nuclei10

14Peripheral vertigo results from a dysfunction in vestibular system functioningIn peripheral vertigo, the problem is located in one peripheral vestibular system or in the acoustic nerve (nerve number VIII), most often on one single side. This pathology means that there is an imbalance in the intensity of information sent from the vestibular apparatus to the vestibular nuclei in the brainstem. When the difference is important (e.g., an intensity of 5 on one side compared to the normal intensity of 10 on the other side), the central process is not able to compensate or integrate the information, and thus vertigo appears.

Any of the structural components of the peripheral vestibular system may be affected in peripheral vertigo (e.g., the sensory cells, endolymph or local microcirculation). The damage can result from several pathophysiological mechanisms including trauma, infection, and tumor. When a cause can be identified, curative treatments can restore normal balance. However, it can be difficult to establish the exact cause because access to the vestibular apparatus is restricted by their encapsulation in bone.

In the absence of an identifiable cause, or if the patient does not respond to treatment, this type of vertigo may still improve over time as spontaneous, physiological mechanisms adapt to the difference (a compensation process). This mechanism of compensation is reinforced by vestibular rehabilitation exercises but usually takes time, and is often only partially successful.

Central Vestibular Vertigo dysfunction in central processing1010

Central nuclei

15Central vertigo results from a dysfunction in central processingIn central vertigo, the problem lies in the central nervous system, particularly in the vestibular nuclei of the brain stem. Several diseases can be responsible for dysfunction of the central nervous system by altering normal neuronal functioning or the transfer of information between vestibular nuclei. It is important to diagnose these conditions; if vertigo is a symptom of a more severe brain disease, then treatment is imperative.

The process of ageing can also be responsible for central dysfunction. Ageing may cause an excessive loss of neurons in the vestibular nuclei, a local decrease in microcirculation or a local decrease of neuronal metabolism. Changes to neurotransmission and transfer of information between the left and right nuclei can also be a consequence of ageing. These processes (alone or in combination) can result in vertigo. Indeed, vertigo is more frequently observed in older people (Sloane 1989).

In central vertigo the treatment must be focused on the brain. Nootropil is particularly suited for the treatment of central vertigo in aged people because of its activities on microcirculation, neuronal metabolism, neurotransmission and transfer of information inside the central nervous system.

ReferencesSloane PD. Dizziness in primary care: results from the national ambulatory medical care service. J Fam Pract 1989;29:338.

VESTIBULAR VERTIGOPeripheral

2. CentralVertigo of Peripheral origin: causesConditionDetailsBenign paroxysmal positional vertigo (BPPV)Brief, position-provoked vertigo episodes caused by abnormal presence of particles in semicircular canal Menieres diseaseAn excess of endolymph, causing distension of endolymphatic systemVestibular neuronitisVestibular nerve inflammation, most likely due to virusAcute labyrinthitisLabyrinth inflammation due to viral or bacterial infectionLabyrinthine infarctCompromises blood flow to the labyrinthineLabyrinthine concussionDamage to the labyrinthine after head traumaPerilymph fistulaTypically caused by labyrinth membrane damage resulting in perilymph leakage into the middle earAutoimmune inner ear diseaseInappropriate immunological response that attacks inner ear cellsDecreasing frequencyBaloh RW. Lancet 1998;352:18416. Mukherjee A et al. JAPI 2003;51:1095-101. Parnes LS et al. CMAJ 2003;169:681 93. Puri V, Jones E. J Ky Med Assoc 2001;99:31621. Salvinelli F et al. Clin Ter 2003;154:3418. 17Vertigo of peripheral origin: causesPeripheral causes of vertigo typically involve the structures of the inner earBenign paroxysmal positional vertigo: probably the most common cause of vertigo (e.g., Toupet et al 2003). It is characterised by brief, position-provoked vertigo episodes usually caused by freely floating particles in the semicircular canal (Parnes et al 2003). Menieres disease: Accounting for 1015% of vertigo cases (Mukherjee et al 2003), Menieres disease is often associated with hearing loss and tinnitus, and is usually chronic. Menieres disease occurs in the vestibular system and appears to result from distention of the membranous labyrinth and an excess of endolymph. Patients often complain of a feeling of fullness or pressure in the ear (Baloh 1998). Vertigo episodes may result from reversible mechanical dysfunction or from ruptures in the membrane separating the endolymph and perilymph. Vestibular neuronitis: refers to inflammation of the vestibular nerves, that may be the consequence of a virus, or have an ischaemic cause. (Strupp & Arbusow 2001). This type of vertigo is accompanied by nausea, vomiting and disequilibrium. Patients may present with a deep, burning ear pain. Acute labyrinthitis: inflammation of the labyrinth due to viral or bacterial infection. It often follows infections such as acute otitis media, chicken pox, mumps or measles.Labyrinthine infarct: The blood supply to the inner ear originates in the vertebrobasilar system. Infarct or haemorrhage in this system compromises blood flow to the labyrinthine and has a profound effect on labyrinthine function. Labyrinthine concussion: damage to the labyrinthine may occur after head trauma.Perilymph fistula: Leakage of the perilymph from the inner to the middle ear can result following damage to the labyrinth membranes. Such damage may result from head trauma, cholesteatoma, or a pressure altering event (Baloh 1998, Strupp & Arbusow 2001). Autoimmune inner ear disease: in some rare cases autoimmune disorders destroy inner ear cells, which may lead to hearing loss and/or vertigo. The autoimmune disease may only target the inner ear, or the inner ear damage may be a feature of a systemic disorder (Baloh 1998).

ReferencesBaloh RW. Vertigo. Lancet 1998;352:18416.Mukherjee A, Chatterjee SK, Chakravarty A. Vertigo and dizziness a clinical approach. JAPI 2003;51:109101. Parnes LS, Agrawal SK, Atlas J. Diagnosis and management of benign paroxysmal positional vertigo (BPPV). CMAJ 2003;169:681 93.Puri V, Jones E. Childhood vertigo: a case report and review of the literature. J Ky Med Assoc 2001;99:31621.Salvinelli F, Firrisi L, Casale M, et al. What is vertigo? Clin Ter 2003;154:3418.Strupp M, Arbusow V. Acute vestibulopathy. Curr Opin Neurol 2001;14:1120.Toupet M, Rothoft J, Bremaud des Ouilleres L. Prise en charge des plaintes vertigineuses en ORL de ville. Rev SFORL 2004;83:5763.Vertigo of Central origin: causesConditionDetailsMigraineVertigo may precede migraines or occur concurrentlyVascular diseaseIschaemia or haemorrhage in vertebrobasilar system can affect brainstem or cerebellum functionMultiple sclerosisDemylination disrupts nerve impulses which can result in vertigoVestibular epilepsyVertigo resulting from focal epileptic discharges in the temporal or parietal association cortexCerebellopontine tumoursBenign tumours in the internal auditory meatusDecreasing frequencyBaloh RW. Lancet 1998;352:18416. Mukherjee A et al. JAPI 2003;51:1095-101. Salvinelli F et al. Clin Ter 2003;154:3418. Solomon D. Otolaryngol Clin North Am 2000;33:579601. Strupp M, Arbusow V, Curr Opin Neurol 2001;14:1120.18Vertigo of central origin: causesCentral causes of vertigo originate in the central nervous systemMigraine: vertigo may occur separately or with migraines; migraines are one of the most common central causes of vertigo Vascular disease: ischaemia in the vertebrobasilar system can lead to infarction in the brain stem or cerebellum. The resultant reduced blood supply to these areas can result in vertigo symptoms. It should be noted that cerebrovascular disease can also cause peripheral infarctions (structures in the inner ear each have their own blood flow which also originates in the vertebrobasilar arterial system), or a combination of peripheral and central infarctions may occur. Multiple sclerosis: vertigo may be the presenting feature of multiple sclerosis in approximately 5% of cases, and 50% of patients with multiple sclerosis are likely to suffer from vertigo during the course of their disease (Solomon 2000)Vestibular epilepsy: a rare cause of vertigo related to focal epileptic discharges in the temporal or parietal association cortex (Strupp & Arbusow, 2001)Cerebellopontine tumours: a rare cause of vertigo, these are most often benign tumours in the internal auditory meatus.

ReferencesBaloh RW. Vertigo. Lancet 1998;352:18416.Mukherjee A, Chatterjee SK, Chakravarty A. Vertigo and dizziness a clinical approach. JAPI 2003;51:109101. Salvinelli F, Firrisi L, Casale M, et al. What is vertigo? Clin Ter 2003;154:3418.Solomon D. Distinguishing and treating causes of central vertigo. Otolaryngol Clin North Am 2000;33:579601. Strupp M, Arbusow V. Acute vestibulopathy. Curr Opin Neurol 2001;14:1120.

VERTIGOPERIPHERAL vs CENTRALSymptomLikely aetiology Peripheral CentralVertigo episodesMild/mod. Chronic and unremittingSymptom onsetSudden GradualImbalanceMild/mod. SevereNausea, vomitingSevere VaryingAuditory symptomsCommon RareNeurological symptomsRare CommonChanges in mental status/ consciousnessInfrequent SometimesCompensation/resolutionRapid SlowBaloh RW. Otolaryngol Head Neck Surg 1998;119:559. Puri V, Jones E. J Ky Med Assoc 2001;99:31621.19Distinguishing peripheral and central peripheral causes of vertigoVertigo can result from peripheral or central dysfunction. While the overall presenting symptom (e.g., an illusion of rotation) may be the same regardless of the cause, a number of features can provide an indication as to the location of the specific dysfunction. For example, peripheral causes usually result in vertigo of a sudden onset, with nausea and vomiting commonly reported; neurological symptoms and changes in consciousness are rare. In contrast, vertigo due to central causes is more likely to have a gradual onset and a persisting duration accompanied by severe imbalance and other neurological symptoms.

Identifying the underlying aetiology is paramount to appropriate management.

ReferencesBaloh RW. Differentiating between peripheral and central causes of vertigo. Otolaryngol Head Neck Surg 1998;119:559.Puri V, Jones E. Childhood vertigo: a case report and review of the literature. J Ky Med Assoc 2001;99:31621.

Vertigo-CharacteristicsPeripheralCentralOnsetSuddenUsually slowSeverity of VertigoIntenseUsually mildPatternParoxysmalConstantExac. by movement YesVariableAutonomicFrequentVariableLateralityUnilateralUni or bilatNystagmusHorizontorotaryAnyFatigable/FixationYesNoAuditory symptomsYesNoCNS symptomsAbsentPresentApproach to Patients with Vertigo COMPLAINT Mabuk, pusing

Dizziness / Imbalance? Not Dizziness ? Ilusion of motion (+) Ilusion of motion (-)

- Headache - Stress

Ask the patient to describe the symptom ! ! DIZZINESS / IMBALANCE

no VERTIGO ? DYSEQUILIBRIUM, PRESYNCOPE yes

Vertigo type Vestibular or Nonvestibular ?

Etiology - Peripheral ? - Visual ? or or - Central ? - Somatosensory ? Diagnosis

TherapyQuestions for differentiating types of Vertigo Apakah anda terasa mau pingsan ? ( Pingsan / fainting)PRESYNCOPE

Apakah anda merasa kedua tungkai tidak stabil, dan menjadi stabil kalau duduk ? DYSEQUILIBRIUM ( Jatuh / falling)

Apakah lingkungan anda kelihatannya berputar, atau anda sendiri terasa berputar ? - VESTIBULAR VERTIGO ( Berputar / spinning) Apakah merasa lingkungan melayang, atau anda sendiri terasa melayang ? VERTIGO NONVESTIBULAR (Melayang / light-headed) Apakah anda merasa gugup atau cemas ? PSYCHOGENIC ( Melayang / light-headed)Symptoms Accompanying Peripheral DiseaseHearing lossTinnitusAural fullness

Position changes exacerbate the dizzinessLying still lessens the symptoms

Sem in Neurol. 2001;21(4)

Symptoms Accompanying Central Nervous System DiseaseThe sensation may be described in a variety of ways: spinning, tilting, pushed to one side, lightheadedness, clumsiness, or even blacking out.Signs of neural dysfunction, that is, dysarthria, dysphagia, diplopia, hemiparesis, severe localized cephalgia, seizures, and memory lossSem in Neurol. 2001;21(4)Symptoms Accompanying Auditory ComplaintsUnilateral otologic complaint: aural fullness, tinnitus, hearing loss, or distortion.

Frequent causes of unilateral auditory disease with dizziness include:Endolymphatic hydropsPerilymphatic fistulaLabyrinthitisVestibular neuritisSem in Neurol. 2001;21(4)

General Physical & Emotional HealthHypertension, hypotension, atherosclerotic disease, endocrine imbalances, anxietycommon causes of lightheadedness, near syncope, instabilityrarely produce a sense of true vertigo

Medication side effects and excessive caffeine, nicotine, and alcohol intake should be investigated as a source of dizzinessSem in Neurol. 2001;21(4)Routine Full Head & Neck ExaminationImportant for 2 reasons:

Dizzy patients frequently have other ear, nose, throat pathology

Structural problems of the ear, nose, throat at times cause dizziness or indicate a more widespread processSem in Neurol. 2001;21(4)Neuro-otologic examinationVESTIBULOOCCULER REFLEX EXAMINATIONNYSTAGMUSinvoluntary, ritmic, continuous, to and fro or shuttle movement of eyeballs. Shuttle with different speed (Jerky) or same speed (Pendulum), whereas its direction can be horizontal, vertical or mixed. Nystagmus can be seen by naked eyes or Frenzel glasses

Nystagmus Forms1. Spontaneous Nystagmus : Happen by normal eye position without head alternationCharacteristic of spontaneous nystagmus :- No change after fixation possible caused by central vestibular abnormality - Spontaneous nystagmus with vertical, see saw, rotatory direction caused by central vestibular abnormality

332. Gaze Nystagmus :happen when eye glance a side at 30 degree from neutral position. Simple examination by asked the patient to follow movement of fingers examiner - Nystagmus happen bilateral very possible central vestibular lesion. - Nystagmus happen unilateral central or peripheral lesion34Dix-Hallpike ManeuverActionTurn the patient's head 45 degrees to one side while seated and rapidly but carefully have the patient reclineObserve the eyes for nystagmus and, if present, note the following 5 characteristics: Latency, direction, fatigue, habituation (duration), and reversal upon sitting up

InterpretationA positive maneuver is diagnostic for benign position vertigo (posterior semicircular canal).Classical positioning nystagmus:geotropic torsional directionbrief latency (5 to 20 seconds)decline with repeated positioning30 seconds or less durationreversal upon arising

Tests of stance and gaitRomberg testAction:Have the patient stand with feet close together and arms at the side with eyes open and then eyes closed

Observe for the relative amount of sway with vision present versus absent

InterpretationPatients with compensated bilateral vestibular loss stand normally in both eyes-open and eyes-closed Romberg position because of adequate proprioception from the stable support surface.Increase sensitivity with:tandem stance3-inch foam

Gait testWalk 5 m, firstly with the eyes open and then with the eyes closedTandem gait testStart with feet in the tandem position and arms folded against the chest and to make 10 stepsEyes open test of cerebellar functionEyes closed test of vestibular functionAs long as cerebellar and proprioceptive functions intact

Treatment of Vertigo1. Pharmacotheraphy:a. Symptomaticb. Causal2. RehabilitationThe goals of Pharmacotherapy for VertigoElimination VertigoEnhance Vestibular CompensationDecreasing the Neurovegetative SymptomsDecreasing Psychoaffective Symptoms

Symptomatic I. ANTI VERTIGO 1.Vestibular Suppressant a. Ca antagonist: Flunarizin b. Vasodilator : Betahistine c. Tranquilizer : Diazepam, haloperidol, sulpiride, clonazepam d. Antihistamin : Difenhidramine, meclizine untuk mengobati motion sickness

2. CNS stimulant Ephedrin, amphetamin

ContII. ANTI EMETIC 1. Anticholinergic : atropine, scopolamin 2. Antidopaminergic : Prochlorperazine, metoclopramide.

Drug/ Medicine Calcium Entry BlockerRehabilitationBrandt-Daroff Exercisesmethod 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

MENIERES DISEASEMnire DiseaseFirst described in 1861Triad of vertigo, tinnitus and hearing lossDue to cochlea-hydropsUnknown etiologyPossibly autoimmuneAbrupt, episodic, recurrent episodes with severe rotational vertigoUsually last for several hours2 phases early (almost always unilateral and symptoms episodic) and late (symptoms present more or less all the time with episodes of exacerbation consisting of an increased severity of symptoms).Mnire DiseaseOften 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 presentManagementSevere Mnire 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

MATUR SUKSMA