Baloh and colleagues, in their study of 240 cases of benign positional vertigo, found that 17 percent had their onset within several days or weeks after cerebral trauma and 15 percent after presumed viral neurolabyrinthitis. The significance of these preceding events is unclear, insofar as they did not appear to influence the clinical symptoms or course of the disorder. The provocative suggestion has been made on the basis of small epidemiologic studies such as the one by Jeong and colleagues that osteoporosis is associated with an increased frequency of the disorder.
Sudden changes in position, particularly of the head, may induce vertigo and nystagmus or cause a worsening of these symptoms in patients with all types of vestibular–labyrinthine disease, including Ménière disease and the types associated with vertebrobasilar stroke, trauma, and posterior fossa tumors. However, only if the paroxysm has the special characteristics noted previously—namely, elicitation by change in head position, latency of onset, brevity, reversal of direction of nystagmus on sitting up, fatigability with repetition of the test, and the presence of distressing subjective symptoms of vertigo or its recurrence for months or years without other symptoms—can it be regarded as “benign paroxysmal” in type.
Schuknecht is credited with demonstrating that benign positional vertigo was caused by cupulolithiasis, in which otolithic crystals become detached and attach themselves to the cupula of the posterior semicircular canal. It is now generally believed that the debris, probably detached from the otolith, forms a free-floating clot in the endolymph of the canal (canalolithiasis) and gravitates to the most dependent part of the canal during changes in the position of the head (see Brandt et al).
In 90 percent of cases, the posterior semicircular canal is implicated; the remaining 10 percent are caused by cupulolithiasis in the lateral canal. As mentioned, the conventional maneuver to elicit BPPV may not only fail to induce symptoms in cases of lateral canal cupulolithiasis but the corrective maneuver may even inadvertently produce it. The disorder of the lateral canal is nicely summarized by De la Meilleure and coworkers.
The debris is thought to act by inducing currents on the cupula and triggering an attack of vertigo. Based on this presumed mechanism, several canalith repositioning maneuvers have been devised (Semont et al; Epley), allowing the debris to gravitate out of the semicircular canal and into the vestibule, where it will not induce a current during angular acceleration.