Cupulolithiasis, Canalithiasis and Vestibulithiasis

BPPV (benign paroxysmal positional vertigo) is presently generally accepted to be due to dislodged particles from the utricle.The utricle is one of the two otolith organs. There are several possible sites within the inner ear where particles can accumulate. The purpose of this page is to explain

these terms and give some general orienting information. More detail can be found in Squires et al, 2004, and in Hain et al, 2005
Canalithiasis

This is thought to be the cause of most BPPV. Debris is loose within the fluid filled pathways of the inner ear. When the head is repositioned with respect to gravity, the particles move to the new lowest portion of the inner ear. This causes a "nystagmus", or jumping of the eyes with the following features: Here we are discussing debris in the posterior canal.

A latency between 5-30 seconds. Particles move out of the ampulla (dilated part of inner ear at bottom of picture above). While they are moving, there is no nystagmus. After the particles finish moving, the nystagmus begins. A "burst" of nystagmus, typically lasting 10 seconds. The direction of the burst is about the axis of the canal containing the debris (i.e. upbeating and torsional for the posterior canal). A reversal of nystagmus on sitting Fatigueability (i.e. less nystagmus when the maneuver is repeated, within a short period of time). This is thought to be due to margination.

In theory, there might be canalithiasis involving any of the semicircular canals (or several at once). Each canal produces a different vector of nystagmus --

Posterior canal -- upbeating and twisting towards earth Anterior canal -- downbeating, with variable twisting (torsion) Lateral canal - -side-beating, either always downward (geotropic), or always upward (ageotropic).

Cupulolithiasis

This is thought to be unusual (less than 5%). Here, debris is attached to the cupula of one of the canals. When the cupula is horizontal, there is no nystagmus or dizziness. When the cupula is nonhorizontal (most of the time), there is a constant input from the inner ear and dizziness. The typical nystagmus of cupulolithiasis is thought to have the following features:

No latency Permanent nystagmus, that persists as long as the head is positioned so that the canal being stimulated is not horizontal Weak nystagmus (about 5 deg/sec), directed about the axis of the canal being stimulated. Cupulolithiasis might occur in any canal -- horizontal, anterior or vertical, each of which might have it's own pattern of positional nystagmus (see above). For the lateral canal, the nystagmus is "ageotrophic", meaning that it beats upward with respect to the head position. Reversibility when the head is positioned such that canal is 180 degrees. This is called "direction changing", and is most commonly observed in persons in whom lateral canal BPPV is diagnosed.

Cupulolithiasis was found on pathology of autopsy specimens made by Schuknecht and Ruby in three patients who had BPPV during their lives (Schuknecht 1969; Schuknecht et al. 1973).

Moriarty and colleagues found similar deposits in 28% of 566 temporal bones (Moriarty et al. 1992). If cupulolithiasis is suspected, it seems logical to treat with either the Epley with vibration, or alternatively, use the Semont maneuver. There are no studies of cupulolithiasis to indicate which strategy is the most effective.
Vestibulolithiasis

The prevalence of this condition is unknown. The conjecture is that debris is on the "vestibule" side of the labyrinth, rather than within or on the canal side. Debris might be either attached or loose. If attached, the pattern is identical to cupulolithiasis. Pathologic studies of BPPV have found roughly equal amounts of fixed debris on either side of the cupula (Moriarty et al. 1992), suggesting that loose debris might also be found on either side. If loose, then there should be a mixture of cupulolithiasis and canalithisis (see below). Very little is written on this condition. Loose variant pattern vestibulolithiasis features

For head position where gravity is directed away from vestibule (and towards cupula).

No latency Permanent nystagmus, that persists as long as the head is positioned so that the canal being stimulated is not horizontal AND direction of gravity is towards cupula rather than towards vestibule. Weak nystagmus (about 5 deg/sec), directed about the axis of the canal being stimulated. For the lateral canal, the nystagmus is "ageotrophic", meaning that it beats upward with respect to the head position. Asymmetrical nystagmus o When head is positioned so that debris is pulled off of the cupula, nystagmus dies away in a way similar to canalithisis.

References:

Hain, T. C., T. M. Squires and H. A. Stone (2005). "Clinical implications of a mathematical model of benign paroxysmal positional vertigo." Ann N Y Acad Sci1039: 384-94. Moriarty, B., et al. (1992). "The incidence and distribution of cupular deposits in the labyrinth." Laryngoscope 102(1): 56-9. Schuknecht, H. F. (1969). "Cupulolithiasis." Arch Otolaryngol 90(6): 76578. Schuknecht, H. F., et al. (1973). "Cupulolithiasis." Adv Otorhinolaryngol 20: 434-43. Squires TM, Weidman MS, Hain TC, Stone HA. A mathematical model for top-shelf vertigo: the role of sedimenting otoconia in BPPV. J Biomech, 2004. 37(8): p. 1137-46.

Copyright April 6, 2012 , Timothy C. Hain, M.D. All rights reserved. Last saved on April 6, 2012