Table 2.

Table summarizing each of the three possible scenarios accounting for different patterns of pDBN in BPPV and vHIT measurements with corresponding hypothetical pathomechanisms.

	Oculomotor findings	VOR-gain for the affected SC on vHIT	Assumed underlying mechanism	Endolymphatic flows
				Low-frequency	High-frequency
Regular canalolithiasis	Transient paroxysmal pDBN in DH or SHH, usually reversing in upright	Usually normal	Debris are free to float along the SC	Preserved as debris can move in both directions along the canal	Preserved as debris neither aggregate nor occlude the canal lumen, thus do not impair cupular responses
“Incomplete” (or “functional” or “positional”) canalith jam	Persistent pDBN in DH or SHH, rarely reversing in upright	Slightly reduced	Otoliths are partly entrapped in a narrower canal tract, partially plugging the affected SC lumen	Likely preserved as otoliths, despite partly blocked, are allowed to slowly move toward the cupula in DH or SHH	Impaired as otoliths likely prevent high acceleration flows dampening head impulse responses (behaving as a “low-pass filter”)
Complete canalith jam	Spontaneous DBN, slightly increasing in DH and SHH	Greatly reduced	An otolith clot is completely entrapped within a narrower tract of the canal, entirely plugging the affected SC lumen	Impeded due to a continuous endolymphatic pressure constantly displacing the cupula of the affected SC	Impeded due to a continuous endolymphatic pressure constantly displacing the cupula of the affected SC

BPPV, benign paroxysmal positional vertigo; DBN, downbeat nystagmus; DH, Dix Hallpike; pDBN, positional downbeat nystagmus; SC, semicircular canal; SHH, straight head hanging; vHIT, video-head impulse test; VOR, vestibulo-ocular reflex.