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There are two possible pathophysiologic mechanisms that lead to BPPV: canalithiasis or cupulolithiasis (6, 7).
Multicanal BPPV is addressed by treating canalolithiasis before cupulolithiasis and repositioning posterior canal otoliths before horizontal canal otoliths.
Several maneuvers based on cupulolithiasis and canalolithiasis theories have been proposed for BPPV treatment by Brandt, Daroff, Norre, Beckers, and McCabe.4-6 Presently, the most widely used maneuver for the treatment of posterior canal BPPV is the canalith repositioning procedure of Epley.7
BPPV is characterized by a sense of vertigo that arises in certain head positions (2), and the pathophysiology of the disease is based on two major theories: cupulolithiasis (3) and canalithiasis (4).
Benign paroxysmal positional vertigo is the most common etiology of recurrent vertigo and is caused by abnormal stimulation of the cupula by free-floating otoliths (canalolithiasis) or otoliths that have adhered to the cupula (cupulolithiasis) within any of the three semicircular canals.
Steddin, "Current view of the mechanisms of benign paroxysmal positioning vertigo: cupulolithiasis or canalolithiasis?," Journal of Vestibular Research, vol.
Canalithiasis refers to the displacement of otoconia located within the gelatinous membrane in the macula into the semicircular canals, whereas cupulolithiasis defines the adherence of these particles to the cupula of the semicircular canals.
BPV can result from canalolithiasis where the otoconia are freely floating in the duct of the semicircular canal or cupulolithiasis where the otoconia are adherent to the cupula.
The two main hypothesis; which explain the development of BPPV are the cupulolithiasis and canalithiasis theory, which is based on the presence of free- floating debris in the lumen of the canal which is the cause of vertigo4.
Two proposed causes of vertigo are canalithiasis and cupulolithiasis, which are often cited to explain benign paroxysmal positional vertigo (BPPV) in particular.
Canalithiasis and cupulolithiasis are the most likely mechanisms underlying BPPV.
In 1969, Schucknecht proposed another form of this theory named as "cupulolithiasis" and demonstrated the attached otoconia to the cupula of PSCC of the affected side (6-8).