Benign paroxysmal positional vertigo (BPPV) constitutes a major proportion of the population with peripheral vestibulopathies. Although the freely floating otoconia within the semicircular canals is responsible for the symptoms of BPPV, the source of the otoconia debris is mainly believed to be the otolith organs. Therefore, the pathology in either or both the otolith organs appears a logical proposition.
Timothy C. Hain, MD
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”. 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, which are found adjacent to the utricle and the crista.
The canalith hypothesis is not accepted by all. R. Buckingham recently summarized a large number of puzzling observations. He suggested that loose otoconia displaced by the Epley maneuver, 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.
Anatomical and theoretical observations on otolith repositioning for benign paroxysmal positional vertigo.
To determine if there is an anatomic basis for the assumption that loose, “rogue” otoliths presumed to arise from the utricular macula and theorized to cause benign paroxysmal positional vertigo (BPPV) by impinging on semicircular canal ampullae could be returned to their original site by a series of changes in the position of the head called particle repositioning maneuvers (PRMs). Further, if such otolith movement were possible, once they were replaced into the utricle, would they adhere to the utricular macula?
A study of cross-sections of the temporal bone shows that loose macular otoliths after PRMs would tend to fall into the lumen of the utricle. Once the patient assumes the erect position, however, repositioned otoliths would tend to fall into the near or utriculopetal side of the cupula of the posterior semicircular canal, which opens directly into the inferior portion of the utricle, and could cause labyrinth stimulation and BPPV by the same mechanism of misplaced otoliths on the opposite or far side of the cupula. Loose otoliths in the utricle could also stimulate the horizontal ampullae.
Particle repositioning maneuvers do not remove or fix otoliths in any specific site in the labyrinth. Repositioning of loose otoliths onto the original site in the macula of the utricle, which lies superiorly in the vestibule, could not be accomplished by any of the repositioning maneuvers. If otoliths were to be repositioned on the utricular macula, there is no evidence that the otoliths would adhere to the macula when the patient assumes the erect position. The good results obtained by physiotherapeutic procedures suggest that some other mechanism than repositioning of otoliths is responsible for the relief of BPPV.