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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