Dizziness Pete Kang NYU 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 diagnosis broad 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 T 2 -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 pCO 2  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