PENATALAKSANAAN VERTIGO: NON-MEDIKAMENTOSA DAN MEDIKAMENTOSA

HOW TO MANAGE PATIENTS WITH VERTIGO ?Andradi S. Department of Neurology.University of Indonesia, Jakarta

OUTLINES1. Vertigo vs Dizziness 2. Vertigo: - Types - Pathophysiology - Causes3. Approach to Patients with Vertigo - Diagnosis - Treatment

VERTIGO vs DIZZINESS

DIZZINESS : is a balance disorder.

VERTIGO : is one of the types of Dizziness

Body Balance is Controlled by 3 Sensory Systems:Vestibular, Visual, Proprioceptive BALANCE dysfunction Imbalance /DizzinessCENTRAL NERVOUS SYSTEM(Coordination, integration)

Postural control by muscle

Goebel JA. Otolaryngol Clin North Am 2000;33:48393. Shepard NT, Solomon D. Otolaryngol Clin North Am 2000;33:45569Control of eye movement

VISUAL(Eye)

VESTIBULAR (Labyrinth)

PROPRIOCEPTIVE(Muscle, joint, skin)

4Maintaining 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.

BALANCE DISORDER / DIZZINESS Four Types Vestibular Vertigo Non-vestibular VertigoDisequilibriumPresyncopeSensation:SpinningSensation:FloatingSwaying Rocking Sensation:Falling Unstable Disappear when sittingSensasi:FaintingSistem:Vestibular Sistem:VisualProprioseptivePsychogenic Sistem:Spinal Peripheral nerveCerebellarSistem:Cardiovascular

DIZZINESS : Frequency 40% Peripheral vestibular dysfunction 10% Central brainstem vestibular lesion 25% Presyncope or disequilibrium

15% Psychiatric disorder

10% Unknown cause

December 4, 2001, Swedish Family Medicine, Dobrina Okorn, MD

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OUTLINES1. Vertigo vs Dizziness 2. Vertigo: - Types - Causes3. Approach to Management of Patients with Vertigo - Diagnosis - Treatment

VERTIGO Vertigo is an ilusion of movement in which a subject feels him-/herself or the surrounding object is moving.

Two types:I. Vestibular Vertigo ( spinning vertigo / true vertigo) Vestibular dysfunction II. Vertigo Nonvestibular (non-spinning vertigo) Visual dysfunction Proprioceptive dysfunction

VERTIGO VESTIBULAR vs NONVESTBIULAR VESTIBULAR NONVESTIBULAR (vestibular system) (visual & proprioceptive)Sensation Spinning, rotating Swaying, floating, rocking lightheaded

Duration Episodic Constant

Precipitating factor Head or body movement Stress, hiperventilation, cardiac arrhythmia

Associated symptoms Nausea, vomit, tinitus, Paleness, paresthesia, deafness, oscillopsia syncope

VESTIBULAR VERTIGO True Vertigo; Spinning Vertigo

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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 nuclei

12Balance 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 nerve

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Central nuclei10

13Peripheral 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 processing

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Central nuclei

14Central 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 Vertigo Two types1. Peripheral Vertigo Lesion site: - Inner ear (canalis semicircularis, sacculus, utriculus) - N. vestibularis.

2. Vertigo Sentral Lesi site: - Brainstem (nucleus vestibularis) - Serebelum - Talamus - Korteks serebri

VESTIBULAR VERTIGOPERIPHERAL vs CENTRALSymptomPeripheral CentralVertigo episodesMild - severe Chronic and unremittingSymptom onsetSudden GradualImbalanceMild/mod. SevereNausea, vomitingSevere VaryingAuditory symptomsCommon RareNeurological symptomsRare CommonChanges in mental status/ consciousnessInfrequent SometimesCompensation/resolutionRapid Slow

Baloh RW. Otolaryngol Head Neck Surg 1998;119:559. Puri V, Jones E. J Ky Med Assoc 2001;99:31621.

16Distinguishing 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.

CAUSES OF VERTIGO PERIPHERALCanalithiasis (BPPV) 50%Neuritis vestibularis /labyrinthitis 25%Menieres disease 10%TraumaOtotoxic drugs (aminoglycosides) CENTRALVascular (vertebrobasilar stroke) 50%Demyelinating (multiple sclerosis)Drugs (anticonvulsant, alcohol, hypnotic)

17Utricle and saccule detect linear accelerations of the head (ie gravity) -- otoliths are important for determining head position in static conditionssemicircular canals lie in three different planes; the cristae within the canals detect angular acceleration of the head (head turns)

OUTLINES1. Vertigo vs Dizziness 2. Vertigo: - Types - Causes3. Approach to Management of Patients with Vertigo - Diagnosis - Treatment

Approach to Management of Patient with Vertigo

Patient complaint (pusing, mabuk) Step 1 Verify : VERTIGO or NOT? No Yes Headache, stress, step 2 Identify : TYPE of VERTIGO other dizziness Step 3 Establish: DIAGNOSIS / ETIOLOGY

Step 4 Planning THERAPY

STEP 1 and STEP 2 Verifying and Identifying Types of Dizziness QUESTION : 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 bergoyang, atau anda sendiri terasa bergoyang ? VERTIGO NONVESTIBULAR (Melayang / light-headed) Apakah anda merasa gugup atau cemas ? PSYCHOGENIC ( Melayang / light-headed)

STEP 3ESTABLISHING DIAGNOSIS AND ETIOLOGY OF VERTIGO

1. History taking 2. Physical examination a. General PhysicaL Examination b. Routine Neurologic Examination c. Bed-side Neuro-otologic examination

3. Investigations (as indicated) - ENG, EEG, EMG, CTScan, MRI, MRA - Laboratory

1. HISTORY TAKINGSensation- Spinning, rocking, swaying, swimming, light-headed ? Temporal profile - Onset, duration, course. Head/body position - Occurs on lying, turning, rising, sitting up, standing, nodding, bending, head turning Associated symptomsTinnitus, deafness, cranial nerves symptoms, hemiparesis, hemihipesthesia, hemiataxia.Past history - Head injury, stroke, cardiac and pulmonar disorders, CNS infection, ENT diseases, psychiatric disorder. MedicationDrugs that may give rise to dizziness, including garamycin, sedative, tranquilizer.

2. PHYSICAL EXAMINATIONS a. General Physical Examinations Searching for pathology related to current dizziness complaint: - Hypertension, hypotension - Cardiovascular disorder - Pulmonary disease - Malignancy

2. PHYSICAL EXAMINATION b. Routine Neurologic Examination - Mental - Cranial nerves - Motor system - Sensory system - Autonomic system

2. PHYSICAL EXAMINATION c. Bedside Neurootologic Examination I. Otologic examination II. Hearing testing III. Vestibular examination

I. Otologic Examination

External ear

Tympanic membrane

II. Hearing TestingUsing tuning forksFor differentiating conductive and sensorineural hearing loss RINNE test WEBER test

III. VESTIBULAR EXAMINATION 1. Eye Movement Test 2. Examination of Balance and Coordination

1. EYE MOVEMENT TESTS- Aim: to evaluate Vestibulo-ocular Reflex (VOR)- Manifestation: NystagmusExaminations: Spontaneous nystagmus Gazed-evoked nystagmus Head thrust test Head shaking test Dix Hallpike ( for BPPV)

2. EXAMINATION OF BALANCE AND COORDINATIONA. Test for BALANCE 1. Seated : hold out arms and legs, eyes open/eyes closed 2. Stand: Romberg test, sharpened Romberg test 3. Gait : broad-based gait 4. Tandem walking, past-pointing, Fukuda test, Babinski-Weil test.B. Test for COORDINATION (cerebellum) 1. Upper extremity a. Finger- to- nose b. Finger-nose-finger c. Adiadochokinesis d. Rebound phenomen 2. Lower extremity a. Heel-knee-shin b. Repetitive heel tapping c. Rebound phenomenon 3. Ocular dysmetria

THERAPY OF VERTIGO

I. Etiologic Pharmacologic therapy Surgery II. Symptomatic Pharmacologic therapy

III. Rehabilitative Vestibular Rehabilitation Therapy (VRT) IV. Prevention of aggravating factor Diet control Life-style modification V. Physical Conditionng Exercise

32Current management optionsBecause vertigo can result from a range of peripheral and central causes, appropriate treatment requires the identification of the most likely underlying pathology. Once this has been established, the principal aim of treatment must be to treat the underlying problem using surgery, pharmacotherapy, or, in the case of benign paroxysmal positional vertigo, particle repositioning procedures. If this is not possible (for example if a definitive cause cannot be identified) or if treating the cause will take some time, symptoms should be managed using pharmacotherapy, or long-lasting relief instigated by the use of vestibular rehabilitation exercises.

ReferencesBaloh RW. Vertigo. Lancet 1998;352:18416.Mukherjee A, Chatterjee SK, Chakravarty A. Vertigo and dizziness a clinical approach. JAPI 2003;51:1095-101.

I. ETIOLOGIC TREATMENT

TREATMENT OF THE CAUSES OF VERTIGOCAUSE TREATMENTPeripheral Cause BPPVLabyrinthine concussionVestibular rehabilitationMenieres diseaseLow-salt diet, diuretic, surgery, transtympanic gentamicinLabyrinthitisAntibiotics, removal of infected tissue, vestibular rehabilitationPerilymph fistulaBed rest, avoidance of strainingVestibular neuritisBrief course of high-dose steroids, vestibular rehabilitationCENTRAL CAUSEMigraineBeta-blockers, calcium channel blockers, tricyclic amines

Vascular diseaseControl of vascular risk factors, e.g., antiplatelet agentsCPA tumoursSurgery

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

Canalith repositioning manoeuvre (Brandt-Daroff, Epley, Semont

34Treatment is dependent on vertigo typeWherever possible, treatment should be directed at the underlying cause of the disease. This table shows specific treatments that can target certain types of vertigo.

Treatment for Menieres diseases could involve: restriction of salt intake to 12 g daily, diuretics (hydrochlorothiazide, acetazolamide), and surgery if these treatments fail. Recently, transtympanic low-dose gentamicin has been increasingly used. Treatment for migraine could involve: beta-blockers (propranolol 120240 mg/day), calcium channel blockers (verapamil 120240 mg/day), and tricyclic amines (nortriptyline 75100 mg/day).Treatment for vertebrobasilar insufficiency or transient ischaemic attacks could involve aspirin 75330 mg/day or ticlopidine 500 mg/day.

ReferencesBaloh RW. Vertigo. Lancet 1998;352:18416. Goebel JA. Management options for acute versus chronic vertigo. Otolaryngol Clin North Am 2000;33:48393.

II. SYMPTOMATIC TREATMENT

Symptomatic PharmacologicTreatmentI. ANTIVERTIGO 1.Vestibular Suppressant a. Ca antagonist : Flunarizin b. Vasodilator : Betahistine c. Tranquilizer : diazepam, haloperidol, sulpiride, clonazepam d. Antihistamine : Difenhidramine, meclizine. 2. CNS stimulant Ephedrin, amphetamin

II. ANTIEMETIC 1. Anticholinergic : atropine, scopolamine 2. Antidopaminergic: : Prochlorperazine, metoclopramide. 3. Antihistamine: Difenhidramine

III. PSYCHOAFFECTIVE Clonazepam, diazepam for anxiety and panic attack

How to Choose Antivertigo Drug ?

Clinical evidence Drugs with sedative effect may disturb central compensation mechanism

Ideal Drug Effective in suppressing vertigo Non-sedative does not disturb central compensation

Vestibular Suppressant

Ideal Vestibular Suppressant

a. Ca antagonist : Flunarizin b. Vasodilator : Betahistine c. Tranquilizer : diazepam, haloperidol, sulpiride, clonazepam d. Antihistamin : Difenhidramine, meclizine. a, c, d Sedative effect !! b (Betahistine) - No sedative effect !!

III. REHABILITATIVE THERAPY

VESTIBULAR REHABILITATION THERAPY (VRT) TYPES I. Specific VRT for BPPV II. Balance exercises III. Gaze Stabilization Exercises IV. Visual Dependence Exercises V. Physical conditioning exercise

B P P VBenign Paroxysmal Positional Vertigo

Vestibular Rehabilitation Therapy 1. Specific Interventions for BPPV a. Semont maneuver b. Epley maneuver c. Brandt Daroff Exercise

a. Semont Maneuver

30 sec30 sec30 sec b. Epley maneuverOther name: Canalith repositioning Particle repositioning

c. Brandt Daroff maneuver

Time Exercise Duration---------------------------------------------Morning 5 X 10 minNoon 5 X 10 minEvening 5 X 10 min----------------------------------------------Each position 30 sec or vertigo subsides in < 30 secIf Vertigo >30 sec sit up 30 sec other side

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IV. AGGRAVATING FACTORS

PREVENTION OF AGGRAVATING FACTOR

Control of Nutrition and Life-style: Adequate food and diet

Avoid excessive alcohol, tobacco

Medicine: sedative, ototoxic, opioid

Sleeping, working position.

V. PHYSICAL CONDITIONING EXERCISE

Recommend doing one or more of the following, 3 times a week:- Walking on a treadmill (1 mile) - Brisk walking outdoors (1 mile or more) - Riding a stationary bicycle- Swimming

INTEGRATED VESTIBULAR THERAPY

Therapeutic Modalities Options:1. Symptomatic treatment 2. Treatment for Specific Conditions 3. Rehabilitative therapy 4. Prevention of aggravating factor

SINGLE THERAPY or INTEGRATED THERAPY ?

Single TherapyEtiologic or Specific treatment is paramount, but it does not offer the patient a significant improvement or vertigo symptoms resolution when used alone

Symptomatic drug therapy bring improvement in 75.1% of the patients with peripheral vestibulopathies and 39.8% of the patients with central vestibular disorders

Vestibular rehabilitation therapy were efficient in 51.1% of patient when used alone

Diet and feeding habit change improve vertigo in 42.2% patients with vestibulopathies

Gananca et al. Brazilian Journal of Otorhinolaryngology 2007;73(1):12-8

INTEGRATED THERAPY

Integrated Vestibular Therapy (IVT)

A combination therapeutic modalities of Specific Treatment, Symptomatic Treatment, Vestibular Rehabilitaton Therapy, Diet Control and Life-style changes, brought about 96 % of vertigo improvement.

CONCLUSIONS

Balance function depends on the integrity of vestibular, visual and somatosensory systems. Disorder of these system (s) leads to dizziness, which includes 4 types: Vestibular Vertigo, Nonvestibular Vertigo, Presyncope, and Disequilibrium.

Treatment of vertigo includes etiologic, symptomatic, vestibular rehabilitative therapies, dietary and life habit control, and conditioning physical exercise.

Integrated Vestibular Therapy (IVT) proved to bring better resolution of vertigo compared to single therapy

Thank You

Vestibular Rehabilitation Therapy (VRT)Definition VRT is a specific form of physical therapy designed to promote habituation and compensation for deficits related to balance disorders.

VRT is effective in : - Peripheral vestibular hypofunction, unilateral and bilateral - Central balance disorders.

VRT: GOALS GOALS :Improve balance Minimize falls Decrease subjective sensations of dizziness Improve stability during locomotion Reduce overdependence on visual and somatosensory inputs Improve neuromuscular coordination Decrease anxiety and somatization due to vestibular disorientation

BY : improving vestibular function and promoting mechanisms of central adaptation and compensation

NON-MEDICAMENTOUS MANAGEMENTI. REHABILITATIVE THERAPY

VESTIBULAR REHABILITATON THERAPY (VRT)

TYPES OF AND INDICATIONS FOR VRT1. Specific interventions for BPPV 2. General interventions (Cowthorne Cooksey exercise) 3. Fluctuating vestibular problems4. Empirical treatment for situations where the diagnosis is unclear 5. Balance exercise6. Gaze Stabilization Exercise7. Visual Dependence Exercise8. Psychogenic vertigo

TYPES OF AND INDICATIONS FOR VRT

1. Specific interventions for BPPV In doctor office: Epley maneuver and the Semont maneuver At home: Brandt-Daroff exercises Log roll exercises (for lateral canal BPPV)

2. General interventions Cowthorne Cooksey exercise Unilateral loss, such as for vestibular neuritis or acoustic neuroma Bilateral loss, such as for gentamicin toxicity and related conditions

3. Fluctuating vestibular problems To prepare the person for anticipated dizziness rather than to make any permanent change. Meniere's syndrome Perilymphatic fistula

TYPES AND INDICATIONS OF VRT (Contd)4. Empirical treatment for situations where the diagnosis is unclear Post-traumatic vertigo Multifactorial disequilibrium of the elderly - Central vertigo (eg. cerebellar stroke)5. Balance exercise - Standing on heel and toes - Walking to and fro with eyes open qand close - Walking on rubber foam floor5. Psychogenic vertigo Brandt-Daroff exercises for phobic postural vertigo Other situations where there is irrational fear of situations in which balance is challenged

TYPES AND INDICATIONS OF VRT (Contd)6. Gaze stabilization Exercise - Head turning left and right while eyes looking at stationary object.7. Visual Dependence Exercise - Walking in crowded and busy place: market, mall, street, discotique.8. Psychogenic vertigo Brandt-Daroff exercises for phobic postural vertigo Other situations where there is irrational fear of situations in which balance is challenged

a. Semont ManeuverAlso called the liberatory maneuver

The patient is rapidly moved from lying on one side to lying on the other

Roughly an 80% cure rate (Herdman et al, 1993).

Takes about 15 minutes to complete.

Instructions For Patients After Office Treatment (1) (Epley or Semont Maneuvers)

1. Wait for 10 minutes after the maneuver is performed before going home -To avoid "quick spins, brief bursts of vertigo as debris repositions itself immediately after the maneuver. - Don't drive yourself home.

2. Sleep semi-recumbent for the next two nights - Sleep at 45 angle - During the day, keep head vertical

Instructions For Patients After Office Treatment (2) (Epley or Semont Maneuvers)

3. For at least one week, avoid provoking head positions that might bring BPPV on again: - Use 2 pillows when you sleep - Avoid sleeping on the "bad" side - Don't turn your head far up or far down - Be careful to avoid head-extended position - Try to stay as upright as possible. -. Do not start doing the Brandt-Daroff exercises immediately or two days after the Epley or Semont maneuver, unless specifically instructed otherwise by your doctor.

4. At one week after treatment, put yourself in the position that usually makes you dizzy. Position yourself cautiously and under conditions in which you can't fall or hurt yourself..

c. Brandt-Daroff maneuver

1 repetition = maneuver done to each side in turn (4x30 second = 2 minutes) 1 set = 5 repetition (5x2 minute = 10 minutes)

Schedule : 3 sets per day 2 weeks - Morning set : 5 repetitions (10 minutes) - Noon set : 5 repetitions (10 minutes) - Evening set : 5 repetitions (10 minutes) Success rate : 95% Complete relief: mostly after 30 sets ( 10 days) Recurrence: 30% in 1 year may + 1 set per day (Amin et al, 1999).

I. VESTIBULAR REHABILITATON THERAPY

2. General Intervention Cowthorne Cooksey exercise

Cawthorne Cooksey exercisesFor dizziness, unsteadiness or vertigo.

Do one set of exercises in the morning and one set in the evening.

Begin at 5 minutes per set gradually (over several days) extend to 10 minutes.

VRT: Cowthorne Cooksey Maneuver Adaptation exercise

VRT: COWTHORNE COOKSEY ManeuverAdaptation Exercise

NON-MEDICAMENTOUS MANAGEMENT

4. EMPIRICAL TREATMENT

In patients with undiagnosed dizzines (15 - 50%) - Try medications + balance/vestibular rehabilitation program (for 1-2 months)

In patients with central vestibular problems ( eg. cerebellar stroke - Very unlikely to benefit from medication or therapy. May try all possible modalities.

Thank You

Betahistine

HHHHH 1H 1H 3BHBetahistine: - Direct stimulation on H1 receptors - Blocking of H3 receptor (autoreceptor)Relaxation of vascular smooth muscles bloodflow in CNS & inner earBBBB

76Betaserc memblok autoreceptor H3, sehingga mencegah mekanisme kontrol feedback negatif dari histamin,dan merangsang pelepasan histamin relaksasi otot polos vaskular memperbaiki aliran darah pada cns & telinga bagian dalam (PROPHYLACTIC EFFECT)

HHSH 2H 3BBetahistine: Blocking on H3 heteroreceptor in serotoninergic neurone (Brainstem)

SHS Post-synaptic nerveSerotonin has a regulatory effect on vestibular nuclei Sensation of Vertigo

77Betaserc memblok reseptor H3 pada neuron non-histaminergic (heteroreceptors) dan merangsang pelepasa serotonin.Serotonin memiliki efek pengaturan pada inti vestibular penurunan sensasi vertigo (SYMPTOMATIC EFFECT ON VERTIGO)

Betahistine HCL

H3 AutoreceptorH3 Heteroreceptor

Stimulates release of HistamineH1ReceptorRelaxation of vascular smooth musclesH1ReceptorImprovement of bloodflow inCNS and inner earStimulates release of serotoninRegulatory effect onVestibular nuclei Sensation of vertigo

Prophylactic effect (treat the cause)

Symptomatic effec (w/o sedation)

781.) Betahistine does not sedate. It has no antagonistic effects on H1 Receptors which controls wakefulness (sleep patterns and state of alertness). Betahistine stimulates H1 receptors instead of blocking them so pts remain alert. 2) Betahistine has no affinity for H2 Receptors it does not stimulate H2 receptors (which are found in the stomach) to any great extent so betahistine is generally free from gastric side effects. So far no H3 receptors have been discovered in the stomach, which might explain why no indirect H2 effects are seen. 3) Betahistine has specific interaction with H3 & H1 receptors.

4. Latihan Brandt-Daroff: Mulai dengan duduk tegak (posisi 1), lalu ber-gerak Then move into the side-lying position (position 2), with the head angled upward about halfway. ke posisi samping berbaring ( posisi 2), dengan kepala miring ke atas sekitar setengah. An easy way to remember this is to imagine someone standing about 6 feet in front of you, and just keep looking at their head at all times. (6) Cara mudah untuk mengingat ini adalah membayangkan seseorang berdiri sekitar 6 kaki di de-pan Anda, dan dan pertahankan untuk menatap kepalanya setiap saat. Tahan pada setiap posisi berbaring selama 30 detik atau sampai rasa pusing reda, Stay in the side-lying position for 30 seconds, or until the dizziness subsides if this is longer, then go back to the sitting position (position 3). jika hal ini lebih lama, kembali ke posisi duduk ( posisi 3 ).Stay there for 30 seconds, and then go to the opposite side (position 4) and follow the same routine. Menetap selama 30 detik, dan kemudian bergerak ke sisi berlawanan ( posisi 4 ) dan mengikuti rutinitas yang sama.

Epley Maneuver

Lempert roll maneuver7. Lempert roll maneuver untuk BPPV kanalis horizontal kanan.Bila telah ditentukan BPPV gangguan kanalis horizontal kanan, pasien diminta untuk memutar kepala 900 menjauhi sisi lesi pada langkah 1 sampai 5, tahan posisi ini selama 10 30 detik. Dari langkah 5 posisi pasien kembali (6) ke posisi persiapan dengan cepat dan bersamaan dengan gerakan dari wajah menghadap keatas ke posisi duduk (7)

Cawtherne Cooksey exercises

Latihan pada posisi berbaring

Latihan Mata

1. Lihat keatas dan kebawah tanpa menggerakkan kepala.

2. Lihat kekiri dan kekanan tanpa menggerakkan kepala.

3. Latihan konvergensi: konvergensikan kedua mata dengan melihat ujung hidung anda.

Cawtherne Cooksey exercises

Latihan pada posisi berbaring

Latihan Kepala

1.Gerakkan kepala kedepan dan kebelakang pada leher

2.Gerakkan kepala kekiri dan kekanan pada leher

Cowthorne Cooksey exercises

Latihan sambil Berjalan

1. Sambil berjalan lemparkan bola keatas dan menangkapnya.

2. Jalan naik turun anak tangga.

3. Berjalan menglilingi ruang dengan mata terbuka kemudian dengan mata tertutup.

4. Bermain yang mengandung gerakan membungkuk, stretching, dan melempar bola kearah saaran.

Cowthorne Cooksey exercises

Latihan pada posisi Duduk

1. Angkat dan putar bahu kekiri dan kekanan

2. Membungkuk untuk mengambil benda. Duduk dikursi lalu membungkuk untuk mengambil benda di lantai

3. Duduk di meja atau kursi tak bertangan, putar kepala dan badan kekiri dan kekanan.

Cowthorne Cooksey exercises

Latihan dalam posisi Berdiri

1. Duduk di kursi lalu bangun, berulang-ulang. Lakukan mula-mula dengan mata terbuka dan kemudian dengan mata tertutup.

2. Ambil sebuah bola pingpong, dan lemparkan dari tangan satu ke lainnya hingga lintasannya membentuk lengkungan mula-mula perlahan, makin lama makin cepat.Gerakkan mata mengikuti gerakan bola tersebut.

d. Lempert roll maneuver For horizontal semicircular canal

Vestibular Rehabilitation TherapyPatient Selection YES NOStable peripheral /central Patient with unstable lesion (migraine,TIA) vertigo Progressive degenerative processSymptom provide specific Fluctuaing or episodic symptom of activity / stimuli imbalanceIntact cognitive,visual, proprioceptive, cerebellumStop antivertigo prior to VRTAcute vertigo early VRT Chronic: patient who has not recovered after 2-3 months

Conditions NOT Benefit from VRT 1. Low blood pressure

2. Medication reactions (other than ototoxicity)

3. Migraine associated vertigo

4. Transient ischemic attack -- TIA

5. There are some conditions where it is not clear whether rehabilitation is helpful

MODE OF ACTION BETAHISTINE1. Direct stimulation on H1 receptor in the inner ear blood vessel increasing local vasodilation as well as permeability solving the problem of endolymphatic hydrop.

2. Strong H3 receptor (autoreceptor) antagonist and increasing neurotransmitter histamine release at nerve ending in the inner ear more increase in vasodilating effect (Prophylactic effect)

3. Blocking of H3 receptor (heteroreceptor) in serotoninergic neurone Increasing serotonin release in the brainstem, which suppresses vestibular nuclei decreases vertigo (Symptomatic effect)

Betahistine is a weak H1 agonist and strong H3 antagonist

CONTROL OF BALANCE IS DEPENDENT ONVISUAL, SOMATOSENSORY, and VESTIBULAR SYSTEMS

PERIPHERAL NEUROLOGIC-RELATED VERTIGOHOW TO RECOGNIZE ? Site of lesion: N. Vestibularis Characteristics: 1. Vertigo of peripheral type. 2. Often accompanied by hearing symptom. 3. May be associated with symptoms of involvement of neighbouring cranial nerves (Nn V, VII ).

2. PHYSICAL EXAMINATIONB. NEUROLOGIC EXAMINATION Routine Cranial nerves, motor, sensory, and autonomic systems. Bedside Neurootologic examination

CENTRAL NEUROLOGIC-RELATED VERTIGOHOW TO RECOGNIZE ? Site of lesion: brainstem, cerebellum, cerebrum. Characteristics: 1. Vertigo of central type. 2. Often accompanied by symptoms of involvement of neighbouring structures: Brainstem: facial paresthesia,hemihypesthesia, Horners syndrome, dysphagia, hemiataxia. Cerebellum: ataxia, dysarthria, nystagmus, hypotonia Cerebrum: epileptic seizure.

Manifestations of Vestibular Disorder Vestibular disorder

Subjective Objective Vertigo Nystagmus Ataxia

VERTIGO is an illusion of movement either of the person or of objects about the person.

COMPLAINT Mabuk, pusing

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

- Headache - Stress

Ask patient to describe the symptom ! !

DIZZINESS / IMBALANCE

no VERTIGO ? DYSEQUILIBRIUM, PRESYNCOPE yes

Vertigo type

Etiology

Diagnosis

Therapy

The Vestibular System SacculeSemicircular canalsUtricleAmpullaeCochleaVestibular nerve

Sensory hair cells within the inner ear provide information on the position and movement of the head

Otolith organs

Goebel JA. Otolaryngol Clin North Am 2000;33:48393.

103The vestibular system is the dominant sensory input guiding balanceThe dominate input into the balance system is from the vestibular system of the inner ear. This structure consists of the otolith organs (utricle and saccule maculae) and the semicircular canals, each in its own orientation (lateral, posterior and superior) (Goebel 2000; Shepard & Solomon 2000). Each semicircular canal originates from the utricle and terminates in the ampulla. Within each ampulla and otolith organ are a number of sensory hair cells that connect to the vestibular nerve, providing the brain with sensory information pertaining to the position and movement of the head.

Dysfunction of any aspect of the vestibular system will result in abnormal activation of the vestibular nerve, which may lead to 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.

STRATEGY FOR MANAGEMENT OF VERTIGO Complaint (pusing, mabuk etc) VERTIGO ? Not - headache ? Yes - stress ? etc.

Vestibular Nonvestibular - Visual Peripheral Central - Proprioceptive

Etiology Therapy

VESTIBULAR VISUAL SOMATOSENSORY

CENTRALVESTIBULAR PATHWAY

PARIETO- BRAINSTEM SPINAL - MEDULLARY VOMITING CENTRE TEMPORAL - LIMBIC SYSTEM CORTEX

Spatial orientation VOR Posture Vegetative effectsMotion perception

Vertigo Nystagmus Ataxia Nausea, vomit CENTRAL VESTIBULAR PATHWAYTEMPORO-PARIETALCORTEXBRAINSTEMSPINAL-MEDULLARY VOMITING CENTRE - LIMBIC SYSTEM

105

OtakPATOFISIOLOGI VERTIGO Manifestasi Klinis Persepsi VERTIGO Nn III/IV/VI (VOR) NISTAGMUS, OSILOPSIA Nukleus Vestibularis gaster MUAL, MUNTAH Pusat autonom jantung PALPITASI kelenjar keringat KERINGATAN Vestibulospinal ATAKSIA, GANGGUAN POSTUR

BrainstemLabyrin

Medula spinalis

APPROACH TO PATIENTS WITH VERTIGO COMPLAINT (mabuk, pusing) dizziness, cephalgia, stress??? DIZZINESS /IMBALANCE (melayang, muter, tak stabil, mau pingsan) Not VERTIGO ? Other Dizziness type (DISEQUILIBRIUM; PRESYNCOPE) Yes Peripheral VESTIBULAR VERTIGO Vertigo Type Central NON-VESTIBULAR VERTIGO

ETIOLOGY

DIAGNOSIS

THERAPY

A. Test for Balance1. Seated -Sitting, hold out arms and legs, eyes open/eyes closed 2. Stand a. Romberg test b. Sharpened Romberg test 3. Gait - Broad-based gait - Walking sudden stop quick turn walking back 4. Tandem walking 5. Past-pointing test 6. Fukuda stepping test 7. Babinski-Weil test

NYSTAGMUSNystagmus is a constant, involuntary, cyclical movement of the eyeball.Type 1. Pendular (Ocular) nystagmus - Due to disturbance of visual fixation associated with loss of central vision, congenital or acquired. 2. Jerk (Vestibular) nystagmus - Due to disturbance of vestibular system, peripheral or central.

Neurophysiological mechanisms of VertigoThe main neurotransmitters in the vestibular nuclei : Cholinergic H1 histaminergic - Cholinergic system modulates the neural store - Histaminergic system stimulate the vomiting center Vestibular nuclei stimulate the vomiting center via histaminergic (H1) system.

- GABA as inhibitory signals from cerebellar Purkinje cells

- Adrenergic system inhibit vestibular activity.

- Serotonergic pathway, activated by stimuli from the gastrointestinal tract act on the vomiting center

- Dopamine (D2) agonist blocks chemoreceptor trigger zone Chemoreceptor trigger zone in the area postrema acts on the vomiting center

THERAPY OF VERTIGO

I. Information, Counseling, and Reaasurance II. Medicamentous Therapy 1. Etiologic Pharmacotherapy Surgery 2. Symptomatic Pharmacotherapy

III. Nonmedicamentous Therapy 1. Rehabilitative Vestibular Rehabilitation Therapy (VRT) 2. Prevention of aggravating factor Diet control Life-style modification 3. Physical Conditioning Exercise

IV. Treatment of Specific Conditions BPPV, Migrainous vertigo, Menieres disease. Vestibular paroxysmia.

111Current management optionsBecause vertigo can result from a range of peripheral and central causes, appropriate treatment requires the identification of the most likely underlying pathology. Once this has been established, the principal aim of treatment must be to treat the underlying problem using surgery, pharmacotherapy, or, in the case of benign paroxysmal positional vertigo, particle repositioning procedures. If this is not possible (for example if a definitive cause cannot be identified) or if treating the cause will take some time, symptoms should be managed using pharmacotherapy, or long-lasting relief instigated by the use of vestibular rehabilitation exercises.

ReferencesBaloh RW. Vertigo. Lancet 1998;352:18416.Mukherjee A, Chatterjee SK, Chakravarty A. Vertigo and dizziness a clinical approach. JAPI 2003;51:1095-101.

MODE OF ACTION BETAHISTINE1. Direct stimulation on H1 receptor in the inner ear blood vessel increasing local vasodilation as well as permeability solving the problem of endolymphatic hydrop.

2. Strong H3 receptor (autoreceptor) antagonist and increasing neurotransmitter histamine release at nerve ending in the inner ear more increase in vasodilating effect (Prophylactic effect)

3. Blocking of H3 receptor (heteroreceptor) in serotoninergic neurone Increasing serotonin release in the brainstem, which suppresses vestibular nuclei decreases vertigo (Symptomatic effect)

Betahistine is a weak H1 agonist and strong H3 antagonist

HHHHH 1H 1H 3BHBetahistine: - Direct stimulation on H1 receptors - Blocking of H3 receptor (autoreceptor)Relaxation of vascular smooth muscles bloodflow in CNS & inner earBBBB

114Betaserc memblok autoreceptor H3, sehingga mencegah mekanisme kontrol feedback negatif dari histamin,dan merangsang pelepasan histamin relaksasi otot polos vaskular memperbaiki aliran darah pada cns & telinga bagian dalam (PROPHYLACTIC EFFECT)

INFORMATIONS, COUNSELLING, REASSURANCE

H1 agonist dan H3 antagonistH1 dan H2 receptors act mainly at peripheral. Blocking of central receptors will induce sedative effect. H3 which is mainly found centrally is inhibitor of histamine autoreceptor at histaminic nerve terminal, it modulates release of histamine which stimlate release of exitatory neurotransmiter, glutamate and acethylcholine via stimulation of H1 receptor in the brain, thus unlike H1 antagonist which induce sedation, H3 antagonist has no sedative effect.

Vestibular Suppressants

a. Ca antagonist : Flunarizin b. Vasodilator : Betahistine c. Tranquilizer : diazepam, haloperidol, sulpiride, clonazepam d. Antihistamin : Difenhidramine, meclizine. a, c, d sedative effect !! b no sedative effect !!

Okamoto K et al. Theurapetic effectiveness of betahistine on meniere's disease. Medical Treatment 1968;22:5:650* p value < 0.01Merislon 36 mg/day shows significant improvement in symptom score for vertigo1*Betahistine mesylate administered for 2 weeks

Jan

Reliable partner in treating VERTIGO & DIZZINESS

DIAGNOSIS2. Physical examination a. General examination b. Neurologic examinations Routine Bed-side Neuro-otologic testing: - Postural tests - Eye movement tests

H1 agonist dan H3 antagonistH1 dan H2 receptors act mainly at peripheral. Blocking of central receptors will induce sedative effect. H3 which is mainly found centrally is inhibitor of histamine autoreceptor at histaminic nerve terminal, it modulates release of histamine which stimlate release of exitatory neurotransmiter, glutamate and acethylcholine via stimulation of H1 receptor in the brain, thus unlike H1 antagonist which induce sedation, H3 antagonist has no sedative effect.

6. Supine roll test (PagniniMcClure maneuver) untuk menentukan BPPV kanalis horizontal.Pasien dipersilakan duduk kemudian Berbaring terlentang (1). Kepala pasiendiputar ke kanan (2) dengan observasiadanya nistagmus, lalu kembali wajahmenghadap keatas (1). Setelah itu kepala diputar ke sisi kiri (3).Sisi dimana terdapat nistagmus yang menonjol merupakan gangguan kanalissemisirkularis horizontal.

6. Supine roll test (PagniniMcClure maneuver)

Semont maneuverContoh: BPPV pada disfungsi vestibular KANAN (gambar) - Sementara duduk di langkah 1, kepala pasien digerakkan 450 ke sisi kiri - Kemudian pasien dengan cepat pindah ke posisi berbaring seperti digambarkan pada langkah 2. Posisi ini dipertahankan selama 30 detik atau lebih - Elanjutnya pasien cepat dikembalikan ke posisi berbaring berlawanan, tanpa berhenti dalam posisi duduk, atau mengubah posisi kepala relatif terhadap bahu.

b. Epley maneuverNama lain: Canalith repositioning procedure, atau Particle repositioning procedureContoh: untuk BPPV sebelah KANANLangkah 1 dan 2: serupa dengan manuver Dix-Hallpike, pasien dibaringkan pada sisi KANAN dengan posisi kepala menggantung (langkah 2) selama 20 - 30 detikLangkah 3: kepala diputar 900 kerah KIRI, dan ditahan selama 20 30 detik.Langkah 4: kepala diputar lagi 90 ke KIRI, pertahanlkan .selama 30 detik- Langkah 5: Pasien duduk kembali

Information, Counselling, ReassuranceExplains nature of vertigo.Frees from unnecessary fear.Provides information for patient cooperation in therapy and realistic treatment goals.

Take Home Message Therapy of vertigo includes information, counselling and reassurance, etiologic, symptomatic, vestibular rehabilitative therapies, dietary and life habit control, and physical conditioning exercise.

Ideal Antivertigo agent is the one with effective and nonsedative properties. e.g. Betahistine.

Integrated Therapy of all therapeutic modalities proved to bring better resolution of vertigo compared to single therapy with each modality.

BPPV: Benign Paroxysmal Positional Vertigo, BD: Brandt-Daroff Technique, BD-BE: Brandt-Daroff Technique with Betahistine. Betahistine administered until complete recovery. Response to treatment using the criteria of EpleyMayFaster recovery in BPPV patients with Betahistine1n=51Cavaliere M, et al. Benign Paroxysmal Positional Vertigo: a study of two manoeuvres with and without betahistine. Acta Otorhinolaryngol Ital 25, 107-112, 2005.

Reliable partner in treating VERTIGO & DIZZINESS

Cavaliere M, et al. Benign Paroxysmal Positional Vertigo: a study of two manoeuvres with and without betahistine. Acta Otorhinolaryngol Ital 25, 107-112, 2005.

Faster recovery in BPPV patients withBetahistine1BPPV: Benign Paroxysmal Positional Vertigo, LM: Liberatory Manoeuvre, LM-BE: Liberatory Manoeuvre with Betahistine. Betahistine administered until complete recovery. Response to treatment using the criteria of Epley. Apr**n=30

Reliable partner in treating VERTIGO & DIZZINESS

128

Treatment of Specific ConditionsBPPV Positional maneuvers: Brandt Daroff, Epley, Semont. Migrainous vertigoMigraine prophylaxis. Beta-blockers, calcium channel blockers, tricyclic amines Menieres disease Low-salt diet, diuretic, surgery, transtympanic gentamicin Anxiety disorder Antianxiety, cognitive-behavioural therapy.

is effective in patients with various types of vertigo1 The curative effect of both Betahistine Mesylate was satisfactory. Merislon 12mg more effective than Merislon 6mg. Betahistine mesylate administered 1 monthMar

Graph adapted from Zi-ming W, et al. The effect of betahistine mesylate as a treatment to vertigo induced by inner ear ischemia. Chinese Scientific Journal of Hearing and Speech Rehabilition 2007;05-0026-04.

Reliable partner in treating VERTIGO & DIZZINESS

130

decreases frequency and duration of vertigo1Adapted from: Atarashi J., Yamate S. Clinical results with the use of E-220. Modern Clinical Medicine 1968;10:2.Jun

Reliable partner in treating VERTIGO & DIZZINESS

132

is well tolerated1 Doses: 18mg 36mg. Total patients : 2.254 Total Adverse Event : 26 patients (1.15%)Common Adverse Event : Nausea (0.44%) Skin Eruption (0.13%)Japanese Package Insert, July 2009; 8th versionSep

Well tolerated in 99% patients

Reliable partner in treating VERTIGO & DIZZINESS

133

Betahistine HCL

H3 AutoreceptorH3 Heteroreceptor

Stimulates release of HistamineH1ReceptorRelaxation of vascular smooth musclesH1ReceptorImprovement of bloodflow inCNS and inner earStimulates release of serotoninRegulatory effect onVestibular nuclei Sensation of vertigo

Prophylactic effect (treat the cause)

Symptomatic effec (w/o sedation)

1341.) Betahistine does not sedate. It has no antagonistic effects on H1 Receptors which controls wakefulness (sleep patterns and state of alertness). Betahistine stimulates H1 receptors instead of blocking them so pts remain alert. 2) Betahistine has no affinity for H2 Receptors it does not stimulate H2 receptors (which are found in the stomach) to any great extent so betahistine is generally free from gastric side effects. So far no H3 receptors have been discovered in the stomach, which might explain why no indirect H2 effects are seen. 3) Betahistine has specific interaction with H3 & H1 receptors.

2. PHYSICAL EXAMINATIONS a. General Physical Examinations Searching for pathology related to current dizziness complaint: - Anemia - Hypertension, hypotension - Cardiovascular disorder - Pulmonary disease - Malignancy

Rehabilitative TherapyVestibular Rehabilitation TherapyEye-head coordinationRetraining of balanceGait trainingPhysical exercise

ETIOLOGIC THERAPY

TREATMENT OF THE ETIOLOGY OF VERTIGOCAUSE TREATMENTPERIPHERAL CAUSEBPPVCanalith repositioning maneuver (Brandt-Daroff, Epley, SemontLabyrinthine concussionVestibular rehabilitationMenieres diseaseLow-salt diet, diuretic, surgery, transtympanic gentamicinLabyrinthitisAntibiotics, removal of infected tissue, vestibular rehabilitationPerilymph fistulaBed rest, avoidance of strainingVestibular neuritisBrief course of high-dose steroids, vestibular rehabilitationCENTRAL CAUSEMigraineBeta-blockers, calcium channel blockers, tricyclic amines

Vascular diseaseControl of vascular risk factors, e.g., antiplatelet agentsCPA tumoursSurgery

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

138Treatment is dependent on vertigo typeWherever possible, treatment should be directed at the underlying cause of the disease. This table shows specific treatments that can target certain types of vertigo.

Treatment for Menieres diseases could involve: restriction of salt intake to 12 g daily, diuretics (hydrochlorothiazide, acetazolamide), and surgery if these treatments fail. Recently, transtympanic low-dose gentamicin has been increasingly used. Treatment for migraine could involve: beta-blockers (propranolol 120240 mg/day), calcium channel blockers (verapamil 120240 mg/day), and tricyclic amines (nortriptyline 75100 mg/day).Treatment for vertebrobasilar insufficiency or transient ischaemic attacks could involve aspirin 75330 mg/day or ticlopidine 500 mg/day.

ReferencesBaloh RW. Vertigo. Lancet 1998;352:18416. Goebel JA. Management options for acute versus chronic vertigo. Otolaryngol Clin North Am 2000;33:48393.

DRUGS FOR SYMPTOMATIC TREATMENTI. ANTIVERTIGO 1.Vestibular Suppressant a. Ca antagonist : Flunarizin b. Vasodilator : Betahistine c. Tranquilizer : diazepam, haloperidol, sulpiride, clonazepam d. Antihistamine : Difenhidramine, meclizine. 2. CNS stimulant Ephedrin, amphetamin

II. ANTIEMETIC 1. Anticholinergic : atropine, scopolamine 2. Antidopaminergic: : Prochlorperazine, metoclopramide. 3. Antihistamine: Difenhidramine

III. PSYCHOAFFECTIVE Clonazepam, diazepam for anxiety and panic attack

EPLEY Maneuver(For exercise at home)

1. HISTORY TAKINGEstablishing the cause of vertigo (Pt 1)Time courseBPPV: lasts < 1 minute, self-limited, responds poorly to anti-vertigo drugsVascular: single episode lasting minutes to hours; usually due to migraine or to transient ischemia of the labyrinth or brainstem; occasionally Menieres diseaseRecent onset of more prolonged episodes characteristic of vestibular neuronitis, multiple sclerosis, vertebrobasilar ischemia

142History holds the best cluescan occur as single or recurrent episodes that last seconds, hours, days

BPPV: positional changes; looking up while standing; getting up out of bed; can wax and wane over time; spontaneous remission then recur at later date; may be assoc with N/V

1. HISTORY TAKINGEstablishing the cause of vertigo (Pt 2)Associated symptomsVertebrobasilar stroke: diplopia, dysarthria, dysphagia, weakness, numbnessMenieres disease: aural fullness, deafness, tinnitusPsych/Panic attack: palpitations, diaphoresisMultiple sclerosis: vertigo preceded by other neurologic dysfunction

143

1. HISTORY TAKINGEstablishing the cause of vertigo (Pt 3)Prior risk factorsMigraineHTN, DM, smoking, PVD Head injuryPsychiatric illness

144