BPPV - -where do the otoconia go after canalith repositioning maneuvers ?

Timothy C. Hain, MD Page last modified: April 23, 2010

Normal anatomy of the inner ear. In maneuvers, otoconia are repositioned from the canals back into the vestibule (area holding the utricle). This diagram's perspective is of the right inner ear, from straight lateral.	Otoconia are made of limestone mixed together with a protein matrix (40% by volume).

In the canalith repositioning maneuvers, it is thought that otoconia, possibly attached to protein matrix, are repositioned from the semicircular canals back into the vestibule. Experience has shown that once this is accomplished, in most persons, the "cure" usually is stable after a day or two of caution.

The explanation for this stability was attributed to a "garbage disposal" system in the inner ear. In particular, it was thought that otoconia are reabsorbed by the "dark cells" of the labyrinth (Lim, 1973, 1984), which are found adjacent to the utricle and the crista, although this idea is not accepted by all (see Zucca, 1998, and Buckingham, 1999).

Logically, if there were no "garbage disposal" system in the inner ear, loose otoconia would accumulate and the ear would "petrify". Although normal subjects on autopsy do indeed have considerable depositions in their inner ear (Moriarty et al, 1992)., there does appear to be a "disposal" system in animals (e.g. Parker et al, 1965). On the other hand, there are also dark cells around the ampullae of the semicircular canals. As BPPV routinely persists for weeks to months without treatment, if the dark cells are responsible for recovery, it would seem that this would happen with or without exercises.

As BPPV rarely occurs at intervals greater than a few days post head-injury, this is also evidence for some sort of a natural "garbage disposal" system in the inner ear.

An alternative explanation was put forward by Otsuka (2010). In animal experiments, they observed that loose otoconia "stick" to the maculae of the utricle. Once stuck, then they are no longer movable and cannot cause BPPV. This seems to us to be a reasonable idea, and could be true in parallel with the "dark cell" hypothesis regarding disposition.

Post-BPPV dysequlibrium -- multifactorial ?

• If repositioned otoconia "stick" to the macula as suggested by Otsuka, one would also think that they might distort the normal anatomy of the utricle, and might provide a mechanism for post-BPPV dysequilibrium.
• Post-BPPV dysequilibrium might also be related to utricular damage (Hong et al, 2008) -- otoconia being lost from the utricle.
• Adaptive changes to BPPV might need to be undone
• Finally, debris might changing the pressure within the inner ear by obstructing the endolymphatic duct. In other words, BPPV might lead to hydrops. From the diagram above, it would seem particularly likely to occur if one slept with the "bad ear up" after the maneuver, which is indeed the usual instruction, as the endolymphatic duct opening is dependent in this sleeping position. Whether or not BPPV sometimes leads to hydrops, rather than being sometimes caused by Meniere's disease, is so far unstablished. In these persons, one would expect to find hearing changes (low frequency loss) and aural fullness.

Whatever the mechanism, in these persons it may be reasonable to undertake a course of generic vestibular rehabilitation, as they may still need to compensate for a changed utricular mass or a component of persistent vertigo caused by cupulolithiasis.

References:

• Buckingham RA. Anatomical and theoretical observations on otolith repositioning for benign paroxysmal positional vertigo. Laryngoscope 109:717-722, 1999
• Epley JM. The canalith repositioning procedure: For treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1992 Sep;107(3):399-404.
• Hong SM and others. Subjective visual vertical during eccentric rotation in patients with benign paroxysmal positional Vertigo. Otology and Neurology, 2008. 1167-1170.
• Lim DJ (1984). The development and structure of otoconia. In: I Friedman, J Ballantyne (eds). Ultrastructural Atlas of the Inner Ear. London: Butterworth, pp 245-269.
• Moriarty, B., et al. (1992). "The incidence and distribution of cupular deposits in the labyrinth." Laryngoscope 102(1): 56-9.
• Otsuka K and others. Model experiments of otoconia stability after canalith repositioning procedure of BPPV. Acta Oto-Laryngological, 2010, early Online, 1-6.
• Parker EE, Covell WP, von Gierke HE. Exploration of vestibulra damage in gunea pigs following mechanical stimulation. Acta Otolaryngol (Stockh) SUppl 239: 1-59, 1968
• Parker EE, Von Gierke HE, Covell WP. Preliminary studies of vestibular damage in guinea pigs following high acceleration. In: The role of the vesitbular organs in the exploration of space. Nasa-Sp-77, 183-194, 1965
• Ross MD, Peacor D, Johnsson LG, Allard LF (1976) Observations on normal and degenerating human otoconia. Ann ORL 85:310-326
• Zucca G, Valli AS, Valli P, Perin P, Mira E. Why do benign paroxysmal positional vertigo episodes recover spontaneously ? J. Vest Res, 8, 4, 325-329, 1998.