Benign Paroxysmal Positional Vertigo

Terry D. Fife, M.D.

Disclosures

Semin Neurol. 2009;29(5):500-508. 

In This Article

Pathophysiology of Benign Paroxysmal Positional Vertigo

Anatomic Background

The vestibular part of the membranous labyrinth consists of three semicircular canals: the anterior, posterior, and horizontal canals (Fig. 1). These canals detect turning movements of the head. The labyrinth also consists of two otolith structures, the utricle and saccule that detect linear acceleration, including detection of gravity. The cupula is the motion sensor for the semicircular canal, and it is activated by deflection caused by endolymph flow.

Figure 1.

Membranous labyrinth.

The macula of the utricle is the presumed source of the calcium particles that cause BPPV. It consists of calcium carbonate crystals (otoconia) embedded in a gelatinous matrix, into which the stereocilia of hair cells project (Fig. 2). The calcium carbonate crystals are more than twice as dense as endolymph, so move in response to gravity and other accelerative movements. The otoconial membrane consists of a top heavy mass of calcium carbonate crystals overlying an elastic intermediary that makes the macular receptor very sensitive to linear acceleration.[8,9]

Figure 2.

Otolithic membrane of the macula showing the organization of calcium carbonate otoliths.

Mechanistic Basis of BPPV

Benign paroxysmal positional vertigo is caused when otoliths composed of calcium carbonate that originate from the utricular macula dislodge and move within the lumen of one of the semicircular canals. When the calcium carbonate crystals move within the semicircular canal (canalithiasis) they cause endolymph movement that stimulates the ampulla of the affected canal, thereby causing vertigo. The direction of the nystagmus is determined by ampullary nerve excitation in the affected canal by direct connections to the extraocular muscles. Each canal affected by canalithiasis has its own characteristic nystagmus (Table 1). Canalithiasis refers to the freely moving calcium particles within the semicircular canal. Cupulolithiasis refers to the less common circumstance of calcium particles adherent to the cupula itself. A concept of "canal jam" has also been proposed to indicate calcium particles that can sometimes move, but sometimes become stuck within the canal.[10]

The reason for this shedding of calcium crystals from the macula is not well understood. The calcium debris may break off following trauma or viral infections, but in many instances it seems to occur without identifiable illness or trauma. It may have to do with age-related changes in the protein and gelatinous matrix of the otolithic membrane. Patients with BPPV have recently been found to have more osteopenia and osteoporosis than matched controls, and those with recurrent BPPV tended to have the lowest bone density scores.[11] This observation suggests that the spontaneous release of otoconia may parallel bone demineralization in general. It remains to be determined if treatment of osteopenia or osteoporosis impacts on the likelihood of recurrent BPPV.

Canal Variants

Benign paroxysmal positional vertigo may affect the posterior, horizontal, or anterior semicircular canal, and in some cases it may even involve more than one canal at a time. Due to its gravity-dependent position, the most commonly affected semicircular canal is the posterior canal. This accounts for ~85 to 90% of cases of BPPV; therefore, when not otherwise qualified, BPPV generally refers to the posterior canal form of the disorder. The horizontal semicircular canal is positioned within the membranous labyrinth such that it may also be affected by the same mechanism, and accounts for ~10% of cases of BPPV.[7,12] The anterior canal and polycanalicular forms are the least common.[13]

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