In 1980, Epley published his theories regarding canalithiasis. [3] He thought that the symptoms of BPPV were much more consistent with free-moving densities (canaliths) in the posterior SCC rather than fixed densities attached to the cupula. While the head is upright, the particles sit in the PSC at the most gravity-dependent position. When the head is tilted back supine, the particles are rotated up approximately 90° along the arc of the PSC. After a momentary (inertial) lag, gravity pulls the particles down the arc. This causes the endolymph to flow away from the ampulla and causes the cupula to be deflected. The cupular deflection produces nystagmus. Reversal of the rotation (sitting back up) causes reversal of the cupular deflection and thus dizziness with nystagmus beating in the opposite direction.
This model can be compared with pebbles inside a tire. As the tire is rolled, the pebbles are picked up momentarily and then tumble down with gravity. This tumbling triggers the nerve inappropriately and causes dizziness. Reversal of the rotation obviously causes reversal of the flow and reversal of the dizziness direction.
Canal densities would better explain the delay (latency), transient nystagmus, and reversal on return to upright than would cupular densities. This supports canalithiasis rather than cupulolithiasis as the mechanism for classic BPPV.
The canalithiasis theory received further corroboration by Parnes and McClure in 1991 with the discovery of free densities in PSC at surgery.
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The patient is placed in a sitting position with the head turned 45° towards the affected side and then reclined past the supine position.
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The patient is then brought back up to the sitting position.
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Next, the patient is rolled 180° from the affected side to the opposite side. Note that the position of the head is 45° toward the affected side before the roll. The head winds up facing down, 180° away from the starting position.
