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 to the brain letting the brain know 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.
According to the canalolithiasis theory (the most widely accepted theory of the pathophysiology of benign positional vertigo), the otoliths are free-floating within the semicircular canal. Changing head position causes the otoliths to move through the canal. Endolymph is dragged along with the movement of the otoliths, and this stimulates the hair cells of the cupula of the affected semicircular canal, causing 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).