Download Dizziness - Pil (Pete) Kang

Dizziness
Pete Kang
NYU School of Medicine
Class of 2001
Dizziness: epidemiology
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1.5% of all hospital admissions
26% of all ED pts stated that they had
experienced “dizziness”
Most common non-pain-related complaint in
the ED
Account for 8 million outpatient visits per year
in the U.S.
Adult > Pediatric
Dizziness: differential diagnosis
broad categories of diseases
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Vertigo
Near-faint or Presyncope dizziness
Psychophysiologic dizziness
Hypoglycemic dizziness
Disequilibrium
Drug-induced dizziness
Vertigo: subclasses
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Acute spontaneous attack
Recurrent spontaneous attacks
Recurrent episodes of positional vertigo
Acute spontaneous attack of
vertigo
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Unilateral loss of vestibular function
Clinical presentation:
– Intense sense of rotation aggravated by head
motion
– World turns slowly toward intact side, then quickly
toward affected side
– Prefers to sit upright w/ head still or to lie w/ intact
side undermost
– Difficulty in standing/walking; may fall toward
affected side
– May have nausea/vomiting, malaise, pallor, diarrhea
Peripheral vs. Central lesions
Peripheral
 Severe nausea/vomiting
 Mild imbalance
 Hearing loss common
 Mild oscillopsia
 No focal signs
 Rapid compensation
Central
 Mod. nausea/vomiting
 Severe imbalance
 Hearing loss rare
 Severe oscillopsia
 Focal signs
 Slow compensation
Viral neurolabyrinthitis
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Most common; >90% of cases in younger age
group w/o major vascular risk factors
Subacute onset; URI ~2 weeks prior
Unilateral caloric paresis, +/- hearing loss
No other focal signs
Symptomatic management, vestibular
rehabilitation
Bacterial otomastoiditis w/
labyrinth involvement
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Prior infection; bony erosion seen in CT
Possible cholesteatoma
Possible complication of bacterial meningitis
Antibiotics
Surgical debridement
Cerebellar infarct/hemorrhage
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Elderly, w/ vascular risk
factors
Other focal neurological
signs present usually
Multiple sclerosis
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Vertigo is the presenting
symptom in 5% of
patients w/ MS
Multifocal neurologic
symptoms/signs
Characteristic T2-intense
lesions in white matter
on MRI
Recurrent, spontaneous attacks of
vertigo
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Sudden, temporary, and large reversible
impairment of resting neural activity in one
labyrinth or its central connections
Lasts from minutes to hours
Restoration of normal neural activity, rather
than compensation
Meniere’s disease
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Characteristic fluctuating low-frequency
hearing loss
Episodic vertigo
Roaring tinnitus
Ear pressure
Autoimmune inner ear disease
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May mimic Meniere’s disease
Signs/symptoms of systemic involvement
Elevated ESR, positive ANA’s/rheumatoid
factor
Immunosuppression
Syphilitic labyrinthitis
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Similar to Meniere’s disease in
signs/symptoms
Positive VDRL and/or FTA-ABS
Penicillin, steroids
Migraine
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Vertigo occurs in approximately 25% of
migraine patients
Hearing loss infrequent
Headaches that meet International Headache
Society criteria for migraine
Treat migraine
Vertebrobasilar TIA
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Common cause in older patients w/ risk factors
Subclavian steal syndrome
Abrupt, last several minutes
Other sx’s of posterior circulation
Antiplatelet drugs, anticoagulation
Recurrent, positional vertigo
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Transient excitation within the vestibular
pathways triggered by change in position
Central vs. Peripheral lesions
Recurrent, positional vertigo:
peripheral vs. central
Peripheral
 Torsional/horizontal
 Latency
 Brief
 Fatigability
 Debris moving in
semicircular canal
Central
 Pure vertical
 No latency
 Persistent
 No fatigability
 Damage to central
vestibulo-ocular
pathways
 Brainstem or cerebellum
Benign positional vertigo (BPV)
Dix-Hallpike test
 2-10 sec latency
 Torsional/horizontal
nystagmus
 Lasts < 30 sec
(fatigability)
 Any deviation from this
must raise suspicion for
a central lesion
Recurrent, positional vertigo:
central lesions
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Multiple sclerosis
Cerebellar tumors
Medulloblastomas
Cerebellar atrophy
Chiari type I malformation
Near-faint dizziness or presyncope
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“Light-headedness” before losing consciousness or
fainting
Reduced blood flow to the entire brain
Causes
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Vasovagal
Orthostatic hypotension
Volume depletion
Cardiac arrhythmias, cardiomyopathy, constrictive pericarditis,
aortic stenosis
Psychophysiologic dizziness
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Associated with panic disorder (lifetime
prevalence of 1.6%)
Hyperventilation  reduce pCO2  cerebral
vasoconstriction  decreased cerebral blood
flow
Onset with specific situations (such as public
places, driving in highways, etc.)
Hypoglycemic dizziness
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Complication of insulin/sulfonylurea treatment
Insulinoma
Fasting
Postprandial phenomenon (functional
hypoglycemia)
Disequilibrium
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Sensation of losing one’s balance without
feeling of illusionary movement or impending
LOC
Unsteadiness standing, walking
Disruption in integration between sensory
inputs and motor outputs
Associated with aging
Drug-induced dizziness
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Aminoglycosides, cisplatin
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Antiepileptic
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Vertigo, disequilibrium
Damage to vestibular hair cells
Carbamazepine, pheytoin, primidone
Disequilibrium, intoxication
Tranquilizers
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Barbiturates, benzodiazepines, tricyclics
Intoxication
Drug-induced dizziness
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Antihypertensives/diuretics
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presyncope
Alcohol
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Intoxication  CNS depression
Disequilibrium  cerebellar toxicity
Positional vertigo  change in cupula specific
gravity
Treatment: medical
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Best therapy: treating the underlying disease
Indication for symptomatic therapy:
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Illness is not readily treatable
Treatment must be continued for a long period
before improvement
Severe and prolonged vertigo
Treatment: medical
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Acute severe vertigo
– Promethazine (antihistamine): sedative (++),
antiemetic (++)
– Diazepam: sedative (+++), antiemetic (+)
Nausea & vomiting
– Prochlorperazine (phenothiazine)
– Metoclopramide (benzamide)
Chronic recurrent vertigo
– Meclizine (antihistamine)
– Dimenhydrinate (antihistamine)
Treatment: surgical
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Conservative surgery
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Shunt surgery (decompress endolymphatic sac)
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Selective section of vestibular division of CN VIII
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Effective in ~75% of cases
Effective in >90% of cases
<10% significant hearing loss
Abnormal vascular loop at the brainstem insertion of
CN VIII
Treatment: surgical
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Destructive surgery
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Labyrinthectomy
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Complete destruction of the end organ
Extremely high cure rate
Cost: destruction of all hearing in the involved ear
Vestibular rehabilitation
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Process of compensation
Requires:
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Intact vision & depth perception
Normal proprioception
Intact sensation in lower limbs
Graded increase in demand for central
compensation of vestibular input