Benign Positional Vertigo in Emergency Medicine

Updated: Mar 21, 2018
  • Author: Andrew K Chang, MD, MS; Chief Editor: Liudvikas Jagminas, MD, FACEP  more...
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Benign positional vertigo (BPV), also known as benign paroxysmal positional vertigo (BPPV), is the most common cause of vertigo. Vertigo is an illusion of motion (an illusion is a misperception of a real stimulus) and represents a disorder of the vestibular proprioceptive system.

BPV was first described by Adler in 1897 and then by Bárány in 1922; however, Dix and Hallpike did not coin the term benign paroxysmal positional vertigo until 1952. This terminology defined the characteristics of the vertigo and introduced the classic provocative diagnostic test that is still used today. Using positional testing, benign positional vertigo can readily be diagnosed in the emergency department. Benign positional vertigo is one of the few neurologic entities the emergency physician can cure at the patient's bedside by performing a series of simple and safe head-hanging maneuvers.

For further information, see Benign Positional Vertigo in the Neurology volume.



Benign positional vertigo (BPV) is caused by calcium carbonate particles called otoliths (or otoconia) that are inappropriately displaced into the semicircular canals of the vestibular labyrinth of the inner ear. These otoliths are normally attached to hair cells on a membrane inside the utricle and saccule. Because the otoliths are denser than the surrounding endolymph, changes in vertical head movement causes the otoliths to tilt the hair cells, which sends a signal informing the brain that the head is tilting up or down.

The utricle is connected to the 3 semicircular canals. The otoliths may become displaced from the utricle by aging, head trauma, or labyrinthine disease. When this occurs, the otoliths have the potential to enter the semicircular canals. When they do, they usually enter the posterior semicircular canal because this is the most dependent (inferior) of the 3 canals, and so gravitational forces will result in most otoliths entering the posterior canal.

Anatomy of the semicircular canals. Anatomy of the semicircular canals.

According to the canalolithiasis theory (the most widely accepted theory describing the pathophysiology of benign positional vertigo), the otoliths are free-floating within the semicircular canal. Changing head position causes the misplaced otoliths to continue to move through the canal after head movement has stopped. As the otoliths move, endolymph moves along with them and this stimulates the hair cells of the cupula of the affected semicircular canal, sending a signal to the brain that the head is turning when it is not.  This results in the sensation of vertigo. When the otoliths stop moving, the endolymph also stops moving and the hair cells return to their baseline position, thus terminating the vertigo and nystagmus. Reversing the head maneuver causes the particles to move in the opposite direction, producing nystagmus in the same axis but reversed in direction of rotation. The patient may describe that the room is now spinning in the opposite direction. When repeating the head maneuvers, the otoliths tend to become dispersed and thus are progressively less effective in producing the vertigo and nystagmus (hence, the concept of fatigability).




United States

The incidence of benign positional vertigo (BPV) is 64 cases per 100,000 population per year (conservative estimate). [1]


One study in Japan found an incidence of 11 cases per 100,000 population per year, but patients were counted only if examined by a subspecialist or at a referral center.


The B of BPV stands for benign and designates that the cause of the vertigo is peripheral to the brainstem and, hence, likely to be benign. However, BPV can be severely incapacitating to the patient.


Women are affected twice as often as men.


BPV, in general, is a disease of elderly persons, although onset can occur at any age. Several large studies show an average age of onset in the mid 50s. Vertigo in young patients is more likely to be caused by labyrinthitis (associated with hearing loss) or vestibular neuronitis (normal hearing).