Dizziness

Pete KangNYU School of Medicine

Class of 2001

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

Dizziness: differential diagnosisbroad categories of diseases

Vertigo Near-faint or Presyncope dizziness Psychophysiologic dizziness Hypoglycemic dizziness Disequilibrium Drug-induced dizziness

Vertigo: subclasses

Acute spontaneous attack Recurrent spontaneous attacks Recurrent episodes of positional vertigo

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

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

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

Prior infection; bony erosion seen in CT Possible cholesteatoma Possible complication of bacterial meningitis Antibiotics Surgical debridement

Cerebellar infarct/hemorrhage

Elderly, w/ vascular risk factors

Other focal neurological signs present usually

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

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

Meniere’s disease

Characteristic fluctuating low-frequency hearing loss

Episodic vertigo Roaring tinnitus Ear pressure

Autoimmune inner ear disease

May mimic Meniere’s disease Signs/symptoms of systemic involvement Elevated ESR, positive ANA’s/rheumatoid

factor Immunosuppression

Syphilitic labyrinthitis

Similar to Meniere’s disease in signs/symptoms

Positive VDRL and/or FTA-ABS Penicillin, steroids

Migraine

Vertigo occurs in approximately 25% of migraine patients

Hearing loss infrequent Headaches that meet International Headache

Society criteria for migraine Treat migraine

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

Recurrent, positional vertigo

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

Multiple sclerosis Cerebellar tumors Medulloblastomas Cerebellar atrophy Chiari type I malformation

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

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.)

Hypoglycemic dizziness

Complication of insulin/sulfonylurea treatment Insulinoma Fasting Postprandial phenomenon (functional

hypoglycemia)

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

Drug-induced dizziness

Aminoglycosides, cisplatin– Vertigo, disequilibrium– Damage to vestibular hair cells

Antiepileptic– Carbamazepine, pheytoin, primidone– Disequilibrium, intoxication

Tranquilizers– Barbiturates, benzodiazepines, tricyclics– Intoxication

Drug-induced dizziness

Antihypertensives/diuretics– presyncope

Alcohol– Intoxication CNS depression– Disequilibrium cerebellar toxicity– Positional vertigo change in cupula specific

gravity

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

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)

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

Treatment: surgical

Destructive surgery– Labyrinthectomy

Complete destruction of the end organ Extremely high cure rate Cost: destruction of all hearing in the involved ear

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