Benign paroxysmal positional vertigo is the most common vestibular disorder. Canalolithiasis of the posterior semicircular canal is now widely accepted as the biological basis for typical benign paroxysmal positional vertigo. Better understanding of its pathophysiological concepts has led to specific therapeutic strategies, which aim to clear the affected semicircular canal from mobile particles. In this article, the authors have added new insight in the prevention of recurrent benign paroxysmal positional vertigo with vitamin D supplementation.
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• Benign paroxysmal positional vertigo is the most common vestibular disorder, affecting about 10% of the general population at some point during their lives.
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• Canalolithiasis of the posterior semicircular canal is the most common underlying pathophysiology.
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• Several variants have been recognized, reflecting involvement of the posterior, horizontal, or anterior semicircular canal by canalolithiasis or cupulolithiasis.
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• Conservative treatment with specific positional maneuvers is almost always effective at improving or resolving the clinical manifestations.
Historical note and terminology
The first detailed description of benign paroxysmal positional vertigo of the posterior canal was published by Barany in 1921. He described a 27-year-old woman who had experienced attacks of positional vertigo for 2 weeks (06). Barany noted the rotatory-vertical nystagmus, the brief duration of the attacks, and the fatigability with repetition of the provocative maneuver, but he did not recognize the latency of onset and the reversal of nystagmus after moving away from the provoking position. In 1952 Dix and Hallpike supplied the first complete description of the cardinal manifestations of benign paroxysmal positional vertigo (27). In their report, they also described a positioning test, today known as the Dix-Hallpike maneuver, to elicit benign paroxysmal positional vertigo.
Since its first recognition, benign paroxysmal positional vertigo has been considered almost unanimously a peripheral vestibular disorder. However, its pathophysiology has been a matter of debate and an intellectual challenge (66). Barany, as well as Dix and Hallpike, speculated that the dysfunction must involve the otoliths, but they did not propose a specific pathophysiological mechanism (06; 27). In 1962 Schuknecht was the first to provide a pathophysiological concept of benign paroxysmal positional vertigo that explained the clinical features of the disease as a mechanical irritation of the posterior semicircular canal (82). On the basis of pathological studies, he later coined the term “cupulolithiasis,” indicating that heavy particles attached to the cupula would render it sensitive to gravity (83). Later it was noted that several clinical features cannot be explained by the concept of cupulolithiasis, such as the limited duration of the attack even though the provocative head position is maintained, the fatigability on repeated testing, and the lack of nystagmus with slow head tilts (84; 12). This problem was solved when Hall, Ruby, and McClure formulated the concept of “canalolithiasis” (36); this term has become widely accepted. Canalolithiasis has provided the basis for effective treatment (85; 29) and the pathophysiological understanding of all variant manifestations of benign paroxysmal positional vertigo (12; 42).