Timothy C. Hain,
Last edited: 5/27/99. Please read our disclaimer.
Controversial aspects to the Canalith hypothesis
There are several hypotheses that have been put forth to explain Benign Paroxysmal Positional Vertigo (BPPV). The most popular and current is the "canalith hypothesis", in which dizziness is thought to be due to debris which has collected within the long arm of the posterior canal. This debris is tenatively thought to be loose "otoconia", derived from the utricle. Otoconia consits of crystals of calcium carbonate, about 3 microns in diameter, derived from a structure in the ear called the "utricle" (figure1). The utricle may have been damaged by head injury, infection, or other disorder of the inner ear, or may have degenerated because of advanced age. Normally otoconia appear to have a slow turnover. They are probably dissolved and reabsorbed by the "dark cells" of the labyrinth (Lim, 1973, 1984), which are found adjacent to the utricle and the crista. The figure on the right shows an artists conception of this process. The figure on the left shows a high-resolution MRI of the membranous labyrinth, oriented similarly to the drawing to the right (MRI image courtesy of Dr. M. Maffee, University of Illinois, Chicago).
The canalith hypothesis is not accepted by all. Buckingham (1999) recently summarized a large number of puzzling observations. He suggested that loose otoconia displaced by the Epley maneuver (1992), would end up displaced into the utricle, and then move into the lateral canal or the other end of the posterior canal, in the "sump". He also reviewed articles suggesting that normal, non-symptomatic individuals also have loose debris in their canals. Buckinghams reasoning was based on temporal bone sections, which may not reflect the actual anatomy of the membranous labyrinth.
There are also several other older hypotheses. The "cupulolithiasis" hypothesis, originally put forth by Schuknecht, was based on pathological sections of the ear documenting debris adherent to the cupula of the posterior canal. This mechanism should, in theory, cause permanant nystagmus with the Dix-Hallpike maneuver, rather than transient nystagmus.
There also have been references to debris on the ampullary end of the posterior canal, which we will call "vestibulolithiasis". This location of debris might also cause similar symptoms to canalithiasis, but be untreatable with the Epley maneuver. However, the Semont maneuver would logically be effective in this case.
Our present feeling is that canalithiasis explains about 80% of cases of BPPV. There is room also for other mechanisms, and it seems likely that patients may have any or all operant simultaneously.
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