Timothy C. Hain, MD Page last modified: June 18, 2009
|Figure 1: schematic of inner ear showing structures thought important to the canalithiasis hypothesis.||Figure 2: 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).|
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 tentatively thought to be loose "otoconia", derived from the utricle. Otoconia consist of crystals of calcium carbonate, about 3-6 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 evidence for the canalithiasis hypothesis is now overwhelming. Nevertheless, strangely enough, it 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, which we feel is incorrect, 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.
At this writing (1/09), there is overwhelming placebo controlled evidence that the canalith repositioning maneuvers are very successful.
In retrospect, when one goes back and looks at some of the older literature -- one must think -- what on earth was going on ? How could these respected researchers get it wrong, and say the wrong thing so forcefully ? Perhaps the most striking of these papers was that of Brian Blakely, who wrote in 1994 (after studying 38 subjects), "All patients in both experimental and control groups, in this study experienced substantial improvement. Although the maneuver is safe it does not have treatment benefit for benign positional vertigo". Perhaps it was bad luck, or perhaps Dr. Blakely did not use an effective maneuver (his description of the maneuver is somewhat difficult to follow). Certainly this paper shows the danger of blindly insisting on "evidence based treatment", especially when it contradicts the evidence of ones experience.
Similarly, Buckingham's comments that the CRP maneuver is physically impossible, is contradicted by the clear objective evidence that the CRP maneuver works very very well.
While most authors now feel that BPPV treatments work by moving debris out of the canal and into the vestibule, there are two other ideas in the literature.
Habituation -- basically the brain getting used to dizziness - was the first mechanism proposed for utility of these exercises. It seems reasonable to us that some part of the improvement may indeed be due to habituation.
Another potential mechanism is acceleration of the natural process of dissolution of debris. Repeated exercises may "shake things up", and cause debris to dissolve (Sato, 2003).