Benign Paroxysmal Peripheral Vertigo

Benign paroxysmal peripheral vertigo (BPPV) is one of the most common causes of peripheral vertigo, accounting for as many as 17 to 22 percent of patients presenting to dizziness clinics.5 The incidence of BPPV has been estimated as being as high as 64 per 100,000 per year. 6 This estimate was derived from patients seen only by ear/nose/throat (ENT) specialists, omitting those seen only by primary care physicians. Thus, the incidence may be underestimated. BPPV is defined as a mechanical disorder of the inner ear causing transient vertigo (with autonomic symptoms) and associated nystagmus that is precipitated by certain head movements. The condition was first described by Barany in 1921, and most of the essential clinical features were described by Dix and Hallpike in 1952. 7

The most widely accepted hypothesis to explain BPPV is known as canalolithiasis. According to this hypothesis, BPPV is caused by inappropriate activation of the posterior semicircular canal (typically unilateral) by the presence of free-floating particles or otoconia. The otoconia become displaced from the utricular macula by aging, head trauma, or labyrinthine disease. Because the particles are heavier than the surrounding endolymph, they tend to collect in the long arm of the posterior semicircular canal, the most dependent part of the endolymph system. Once the particles clump in sufficient mass, changes in head position cause gravitation of the particles, which creates a hydrodynamic drag (or plunger effect) on the endolymph, causing the cupula to be displaced. This results in aberrant neural firing, causing both vertigo and nystagmus.

BPPV can occur at any age, but the average age of onset is in the mid-fifties. Women are twice as likely to be affected as men. The onset is sudden, and an attack is typically precipitated by rolling over in bed, assuming a supine position, leaning forward, looking up at the sky or ceiling, or turning the head. Nausea is often present, although vomiting is unlikely because of the transient nature of the symptoms. Because the symptoms fatigue, they tend to be worse in the morning and become less pronounced as the day progresses. Patients may eliminate the offending activities. There is no associated hearing loss or tinnitus and no physical findings on examination of the external auditory canal.

Several findings support a diagnosis of BPPV (TabJe,..223-3). There is a latency period of 1 to 5 s between assuming the offending head position and onset of vertigo and nystagmus. Both the vertigo and nystagmus crescendo to a peak of intensity, then subside within 5 to 40 s. BPPV is diagnosed using the Dix Hallpike position test. Although Nylen and Barany are sometimes credited with discovering the maneuver, Dix and Hallpike clearly published the first description of the test in wide use today.8 When the head is rotated 30 to 45° toward the affected side and the patient is brought to the supine position with the head lying 30° below the level of the examining table, this brings the affected ear into the dependent position. After a latency of 1 to 5 s, this causes rotatory nystagmus with a fast-beating component toward the undermost ear. The nystagmus may reverse direction as the head is returned to the erect position. The response to repeated provocative testing fatigues, causing the vertigo and nystagmus to disappear.8

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