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Acute Vertigo, Ambulatory Case Conf

Apr 09, 2018

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    VERTIGO

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    IDENTIFICATION DATA

    24 . .

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    CHIEF COMPLAIN

    15 .

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    PRESENT ILLNESS

    15 . 10 .

    3-4

    ,

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    OTHER INFORMATIONS

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    PHYSICAL EXAMINATION

    Abdomen : Soft, Normal contour, Active bowel

    sound, no rebound tenderness, no

    Hepatosplenomegaly

    Ext : no edema , no skin lesion

    LN : no lymphadenopathy

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    NEUROLOGIC EXAMINATION

    Alert, Orientation*III

    CN II : No RAPD, No visual field defect

    CN III, IV, VI : Pupils3mm RTLBE. Full EOM, Horizontalnystagmusto right (cansuppress by fixation)

    CNV : No jaw deviation, Corneal Reflex +ve, CNVII : No facial palsy

    CNVIII : Weber > No lateralization, Rinne > AC> BC Bothsides, Head Thrust-ve

    CN

    IX & X : uvulain

    mi

    dlin

    e. Gag reflex

    +ve CN XI : Normal Trapezius and Sternocleidomastoid motor

    power bothsides

    CN XII : No Tongue deviation

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    COCHLEAR NERVE EVALUATION

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    NEUROLOGICAL EXAMINATION

    No cerebellar sign

    No motor deficit

    No sensoryimpairment DTR 2 + all

    MMSE > 29/30

    No auditory agnosia

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    PROBLEM LISTS

    Acute onset of vertigo

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    VERTIGO

    Latin origin: vertere, to spin

    The illusionthatthe environmentisspinning

    Distinct from dizziness light-headed faintness

    off-balanced feeling

    feeling of floating

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    ANATOMY AND PHYSIOLOGY

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    ANATOMY AND PHYSIOLOGY

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    ANATOMY AND PHYSIOLOGY

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    ANATOMY AND PHYSIOLOGY

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    TYPES OF VERTIGO

    Central vestibular causes (Brainstem or

    cerebellum)

    Peripheral vestibular causes ( Labyrinth orvestibular nerve)

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    CAUSES OF VERTIGO

    CENTRAL

    Cerebrovascular Disease

    Migraine

    Multiple Sclerosis Neurodegenerative Disorders

    Epilepsy

    Inherited Disorders

    Familial BilateralVestibulopathy

    Familial Hearing loss and

    Vertigo

    Familial Ataxia Syndromes

    PERIPHERAL

    Vestibular Neuritis

    BPPV

    Meniers Disease Vestibular Paroxysmia

    Perilymphatic Fistula

    Other Peripheral Disorders

    Drugs Toxins

    Acoustic Neuroma

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    CAUSES..

    Drugs

    Alcohol

    Aminoglycosides

    Anticonvulsants Antidepressants

    Antihypertensives

    Barbiturates

    Cocaine

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    HISTORY

    Timings

    Duration

    Provoking, aggravating factors

    Associated symptoms Risk factors for Cardiovascular disease

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    PHYSICAL EXAMINATION

    General Medical Examination

    General Neurological Examination

    Ocular motor function Facial strength and symmetry

    Observing palatal elevation, tongue protrusion, and

    trapezius and sternocleidomastoid strength

    Coordination (Ataxia, the finger-nose-finger test, the

    heel-knee-shintest, and rapid alternating

    movements)

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    PHYSICAL EXAMINATION

    The Neurotological Examination Ocular Motor Function Testing

    Gaze Testing

    Smooth Pursuit

    Saccades Optokinetic Nystagmus and FixationSuppression ofthe

    Vestibulo-ocular Reflex

    Vestibular Nerve Examination

    Positional Testing

    Fistula Testing

    Gait Assessment

    AuditoryExamination

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    OCULAR MOTOR FUNCTION TESTING

    Nystagmusis characterized by a slow and fast

    phase component and is classified as

    spontaneousspontaneous, gazegaze--evokedevoked, or positionalpositional. The

    direction ofnystagmusis described

    conventionally bythe direction ofthe fastthe direction ofthe fast

    phasephase.

    Spontaneousnystagmus canhave either aperipheral or a central pattern.

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    OCULAR MOTOR FUNCTION TESTING

    Central lesions canmimic a peripheral

    pattern ofnystagmus but peripheral lesions

    cannot cause central patterns ofnystagmus.

    Saccadic intrusions

    Square wave jerks- normal intersaccadic delay

    Saccadic oscillations- do nothave the

    intersaccadic intervalOcular Flutter - Horizontal

    Opsoclonus Vertical or Torsional

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    NYSTAGMUS

    Nystagmus of Central Origin

    May be purely vertical

    May be purelyhorizontal

    May be horizonto-rotary

    May change direction with gaze

    Not diminished by fixation

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    NYSTAGMUS

    Nystagmus of Peripheral Origin

    Horizontal and torsional

    Diminished by fixation

    May fatigue (if elicited byhead movement)

    Doesnot change direction with gaze change

    Diminishes with fixation

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    Cluesto Distinguish Between Peripheral and Central Vertigo

    Clues Peripheral vertigo Central vertigo

    Findings on Dix-Hallpike

    maneuver

    Latency ofsymptoms and

    nystagmus2to 40

    seconds

    None

    Severity of vertigo Severe Mild

    Duration ofnystagmus Usually< 1 minute Usually>1 minute

    Fatigability Y es No

    Other findings

    Postural instability Able to walk;

    unidirectional instability

    Falls while walking;severe

    instability

    Hearing loss or tinnitus Can be present Usually absent

    Other neurologic

    Symptoms

    Absent Usually present

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    SMOOTH PURSUIT AND SACCADES

    Abnormalities ofsmooth pursuit occur asthe result of

    disordersthroughoutthe central nervoussystem and

    with use oftranquilizingmedicines or alcohol and with

    fatigue. Saccades are generated bythe burstneurons ofthe

    pons (horizontal movements) and the midbrain

    (vertical movements).

    Lesions or degeneration ofthese regions leadsto

    slowing ofsaccades

    Ocular dysmetria (Overshootingsaccades) - indicates

    a lesion ofthe cerebellum.

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    VESTIBULAR NERVE EXAMINATION

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    POSITION TESTING

    Dix-Hallpike test

    Positional testing usingthe head-hangingtechnique

    patients with benign positional vertigo will show a

    burst ofnystagmus after a delay of 5 to 10

    seconds, the nystagmus lasts about30 seconds

    The testisnever subtly positive

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    DIX-HALLPIKE TEST

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    PATHOLOGY AND PHYSICAL

    EXAMINATION

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    CHARACTERISTICS OF PERIPHERAL

    VERTIGO

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    CHARACTERISTICS OF CENTRAL

    VERTIGO

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    RED FLAGS OF ACUTE VERTIGO

    Any central neurological symptoms or signs

    New type ofheadache (especially occipital)

    Acute deafness Vertical nystagmus

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    COMMON PRESENTATIONS OF

    VERTIGO

    Acute Severe Vertigo

    Focal neurological symptoms, particularlythosethat can be related to the posterior circulation,

    suggests anischemic strokeischemic stroke If a peripheral vestibular pattern ofnystagmusis

    identified, a positive result onhead thrusttestinglocalizesthe lesionto the vestibular nerve

    Young patient > Vestibular neuritisVestibular neuritisOlder patient > Acute ischemia ofthe vestibular nerve orAcute ischemia ofthe vestibular nerve or

    vestibular labyrinth cannot be excludedvestibular labyrinth cannot be excluded

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    COMMON PRESENTATIONS OF

    VERTIGO

    Acute Severe Vertigo

    Ifhearing loss accompaniesthe episode, Labyrinthitisisthe most likely diagnosis

    Whenhearing loss and facial weakness accompanyacute-onset vertigo, the examiner should closelyinspectthe outer ear for vesicles characteristic ofHerpeszoster (RamsayHuntsyndrome)Herpeszoster (RamsayHuntsyndrome)

    MigraineMigraine canmimic vestibular neuritis, althoughthe

    diagnosis ofmigraine - associated vertigo hinges onrecurrent episodes and lack of progressive auditorysymptoms

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    COMMON PRESENTATIONS OF

    VERTIGO

    Recurrent Attacks ofVertigo

    Meniere's diseaseMeniere's disease isthe likely cause in patientswith recurrent vertigo lasting longer than20

    minutes and associated with unilateral auditorysymptoms

    Transientischemic attacks (TIAs)Transientischemic attacks (TIAs)should besuspected in patients who experience brief

    episodes (minutesin duration) of vertigo,particularly when vascular risk factors are presentand other neurological symptoms are reported

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    COMMON PRESENTATIONS OF

    VERTIGO

    Recurrent Attacks ofVertigo

    The migraine equivalentmigraine equivalent, benign recurrent vertigo,

    is characterized by a history ofsimilar symptoms,

    normal findings on physical examination, family orpersonal history ofmigraine headaches, and typical

    triggers.

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    COMMON PRESENTATIONS OF

    VERTIGO

    Recurrent Positional Vertigo

    Inthe patient complaining of recurrent episodes of

    vertigo triggered by certainhead movements, the

    likely diagnosisis BPPVBPPV

    The historystronglysuggeststhe diagnosis of BPPV

    whenthe positional vertigo is brief (duration less

    than 1 minute), hastypical triggers, and is

    unaccompanied by other neurological symptoms

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    COMMON PRESENTATIONS OF

    VERTIGO

    Recurrent Positional Vertigo

    Central positional nystagmus occurs asthe result ofdisorders affectingthe posteriorposterior fossafossa includingincluding

    tumors,tumors, cerebellarcerebellar degeneration,degeneration, ChiariChiarimalformation, and MSmalformation, and MS

    Following loss of one vertebral arteryloss of one vertebral artery, vertigo orsignificant dizziness after head turnsto the

    direction opposite the intact arterymay develop,because the bonystructures ofthe spinal columncan pinch offthe remaining vertebral artery

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    COMMON PRESENTATIONS OF

    VERTIGO

    Recurrent Positional Vertigo

    Patients withmigrainemigraine asthe cause typically report

    a longer duration ofsymptoms once the positional

    vertigo istriggered, and the nystagmusmay be of acentral or peripheral type

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    DIAGNOSIS

    History

    Physical Exam

    Neurologic Exam

    No Laboratory Investigation Brain Imaging

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    GENERAL TREATMENT PRINCIPLES

    Medication for Acute Vertigo that lasts for few hoursto

    several days

    Medicationshave various combinations of

    acetylecholine, dopamineand histamine receptorantagonism.

    Benzodiazepines enhance GABA action ( GABA is

    inhibitoryneurotransmitter in vestibular system)

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    STRENGTH OF RECOMMENDATION

    The canalith repositioning procedure (Epleymaneuver)is recommended in patients with benignparoxysmal positional vertigo. A

    The modified Epley maneuver also is effective in

    patients with benign paroxysmal positional vertigo. B Vestibular suppressantmedicationis recommended

    for symptom reliefin patients with acute vestibularneuronitis. C

    Vestibular exercises are recommended for more rapidand complete vestibular compensationin patientswith acute vestibular neuronitis. B

    A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus,disease-oriented evidence, usual practice, opinion, or case series.

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    STRENGTH OF RECOMMENDATION

    Treatment with a low-salt diet and diureticsisrecommended for patients with Mnire's disease andvertigo. B

    Effective treatments for vertiginousmigraine include

    migraine prophylaxis (e.g., tricyclic antidepressants,beta blockers, calcium channel blockers), migraine-abortive medications (e.g., sumatriptan), andvestibular rehabilitation exercises. B

    Selective serotonin reuptake inhibitors can relievevertigo in patients with anxiety disorders. Because ofside effects, slow titrationis recommended. B

    A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus,disease-oriented evidence, usual practice, opinion, or case series. See page 1046 for more information.

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    MEDICATIONS

    Meclizine* (Antivert) 12.5 to 50 mg orally every4to 8 hour

    Dimenhydrinate* (Dramamine)25 to 100 mg

    orally, IM, or IV every4to 8 hours Diazepam (Valium)2to 10 mg orally or IV every4to 8 hours

    Lorazepam (Ativan) 0.5 to 2mg orally, IM, or IVevery4to 8 hours

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    MEDICATIONS

    Metoclopramide (Reglan) 5 to 10 mg orallyevery6hours; 5 to 10 mg byslow IV every6hours

    Prochlorperazine (Compazine) 5 to 10 mg orallyor IM every6to 8 hours25 mg; rectally every12hours; 5 to 10 mg byslow IV over 2minutes

    Promethazine (Phenergan) 12.5 to 25 mgorally, IM, or rectally every4to 12hours

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    VESTIBULAR REHABILITATION

    EXERCISES

    These exercisestrainthe brainto usealternative visual and proprioceptive cluestomaintain balance and gait

    Improve postural control duringthe firstmonthafter acute unilateral vestibular lesionsresulting from vestibular neuronitis

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    TREATMENT OF BPPV

    Medications

    Head Rotation Maneuvers : Epley Maneuver

    Contraindication: Severe carotid stenosis,

    unstable heart disease, severe neck disease

    Success rate: 80 % after one treatment, 100%with repeated treatments.

    Recurrence rates: 15% /year, 20% at20months, and 37% at60 months.

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    TREATMENT OF BPPV

    Epleymaneuver

    The patientshead issystematically rotated to move

    the loose particles out ofthe posterior semicircular

    canal backinto the utricle

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    TREATMENT OF BPPV

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    TREATMENT OF VESTIBULA

    NEURONITIS

    Symptom relief using vestibular suppressantmedications, followed by vestibular exercises.

    Vestibular compensations occursmore rapidly

    and more completelyifthe patient beginstwice-daily vestibular rehabilitation exercisessoon after symptom control withmedications.

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    TREATMENT OF MENIERS DISEASE

    Low salt diet ( < 1-2 gm/day)

    Diuretics

    Surgeryin rare cases-

    ablation of vestibularhair cells)

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    TREATMENT OF VASCULAR ISCHEMIA

    TIA /Stroke: BP control, Cholesterol Lowering ,smoking cessation, inhibition of plateletfunction, anticoagulation

    Vestibular suppressantmedications plusminimal head maneuver on first day, theninitiate rehabilitation

    Vestibular stents for symptomatic criticalvertebral arterystenosis

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    THEEND