Dizziness Pete Kang NYU School of Medicine Class of 2001.
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Transcript of Dizziness Pete Kang NYU School of Medicine Class of 2001.
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Dizziness
Pete KangNYU School of Medicine
Class of 2001
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Dizziness: epidemiology
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
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Dizziness: differential diagnosisbroad categories of diseases
Vertigo Near-faint or Presyncope dizziness Psychophysiologic dizziness Hypoglycemic dizziness Disequilibrium Drug-induced dizziness
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Vertigo: subclasses
Acute spontaneous attack Recurrent spontaneous attacks Recurrent episodes of positional vertigo
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Acute spontaneous attack of vertigo
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
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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
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Viral neurolabyrinthitis
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
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Bacterial otomastoiditis w/ labyrinth involvement
Prior infection; bony erosion seen in CT Possible cholesteatoma Possible complication of bacterial meningitis Antibiotics Surgical debridement
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Cerebellar infarct/hemorrhage
Elderly, w/ vascular risk factors
Other focal neurological signs present usually
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Multiple sclerosis
Vertigo is the presenting symptom in 5% of patients w/ MS
Multifocal neurologic symptoms/signs
Characteristic T2-intense lesions in white matter on MRI
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Recurrent, spontaneous attacks of vertigo
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
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Meniere’s disease
Characteristic fluctuating low-frequency hearing loss
Episodic vertigo Roaring tinnitus Ear pressure
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Autoimmune inner ear disease
May mimic Meniere’s disease Signs/symptoms of systemic involvement Elevated ESR, positive ANA’s/rheumatoid
factor Immunosuppression
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Syphilitic labyrinthitis
Similar to Meniere’s disease in signs/symptoms
Positive VDRL and/or FTA-ABS Penicillin, steroids
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Migraine
Vertigo occurs in approximately 25% of migraine patients
Hearing loss infrequent Headaches that meet International Headache
Society criteria for migraine Treat migraine
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Vertebrobasilar TIA
Common cause in older patients w/ risk factors Subclavian steal syndrome Abrupt, last several minutes Other sx’s of posterior circulation Antiplatelet drugs, anticoagulation
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Recurrent, positional vertigo
Transient excitation within the vestibular pathways triggered by change in position
Central vs. Peripheral lesions
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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
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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
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Recurrent, positional vertigo: central lesions
Multiple sclerosis Cerebellar tumors Medulloblastomas Cerebellar atrophy Chiari type I malformation
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Near-faint dizziness or presyncope
“Light-headedness” before losing consciousness or fainting
Reduced blood flow to the entire brain Causes
– Vasovagal– Orthostatic hypotension– Volume depletion– Cardiac arrhythmias, cardiomyopathy, constrictive pericarditis,
aortic stenosis
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Psychophysiologic dizziness
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.)
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Hypoglycemic dizziness
Complication of insulin/sulfonylurea treatment Insulinoma Fasting Postprandial phenomenon (functional
hypoglycemia)
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Disequilibrium
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
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Drug-induced dizziness
Aminoglycosides, cisplatin– Vertigo, disequilibrium– Damage to vestibular hair cells
Antiepileptic– Carbamazepine, pheytoin, primidone– Disequilibrium, intoxication
Tranquilizers– Barbiturates, benzodiazepines, tricyclics– Intoxication
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Drug-induced dizziness
Antihypertensives/diuretics– presyncope
Alcohol– Intoxication CNS depression– Disequilibrium cerebellar toxicity– Positional vertigo change in cupula specific
gravity
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Treatment: medical
Best therapy: treating the underlying disease Indication for symptomatic therapy:
– Illness is not readily treatable– Treatment must be continued for a long period
before improvement– Severe and prolonged vertigo
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Treatment: medical
Acute severe vertigo– Promethazine (antihistamine): sedative (++),
antiemetic (++)– Diazepam: sedative (+++), antiemetic (+)
Nausea & vomiting– Prochlorperazine (phenothiazine)– Metoclopramide (benzamide)
Chronic recurrent vertigo– Meclizine (antihistamine)– Dimenhydrinate (antihistamine)
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Treatment: surgical
Conservative surgery– Shunt surgery (decompress endolymphatic sac)
Effective in ~75% of cases
– Selective section of vestibular division of CN VIII Effective in >90% of cases <10% significant hearing loss
– Abnormal vascular loop at the brainstem insertion of CN VIII
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Treatment: surgical
Destructive surgery– Labyrinthectomy
Complete destruction of the end organ Extremely high cure rate Cost: destruction of all hearing in the involved ear
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Vestibular rehabilitation
Process of compensation Requires:
– Intact vision & depth perception– Normal proprioception– Intact sensation in lower limbs
Graded increase in demand for central compensation of vestibular input