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Neurologic Manifestations of Benign Positional Vertigo


Benign paroxysmal positional vertigo (BPPV) is probably the most common single cause of vertigo in the United States. Estimates indicate that at least 20% of all patients who present to the physician complaining of vertigo have benign paroxysmal positional vertigo. However, because benign paroxysmal positional vertigo is misdiagnosed frequently, this figure may not be completely accurate and is probably an underestimation. As benign paroxysmal positional vertigo can occur concomitantly with other inner ear diseases (eg, a patient may have Ménière disease and BPPV concurrently), statistical analysis may be skewed toward lower numbers.

Benign paroxysmal positional vertigo was described first by Ménière in 1921. The characteristic nystagmus and vertigo
associated with positioning changes were at that time attributed to the otolithic organs. Dix and Hallpike in 1952 became the namesakes for the provocative positional test still used today to identify benign paroxysmal positional vertigo. They further defined the classic nystagmus and went on to localize the pathology to the affected ear during provocation.


Defining benign paroxysmal positional vertigo is complex because, as our understanding of its pathophysiology has evolved, so has its definition. As more interest is focused on benign paroxysmal positional vertigo, new types of positional vertigo have been discovered. What was previously lumped together as benign paroxysmal positional vertigo is now subclassified on the basis of the offending semicircular canal (posterior semicircular canal vs lateral semicircular canal). These groups are divided further into canalithiasis and cupulolithiasis depending on pathophysiology. Benign paroxysmal positional vertigo is defined as an abnormal sensation of motion that is elicited by certain critical provocative positions. The provocative positions usually trigger specific eye movements (eg, nystagmus). The character and direction of the nystagmus is specific to the part of the inner ear affected and the underlying pathophysiology.

Although some controversy exists regarding the 2 pathophysiologic mechanisms, canalithiasis and cupulolithiasis, agreement is growing that the 2 entities actually coexist and account for different subtypes of benign paroxysmal positional vertigo. However, classic benign paroxysmal positional vertigo is best explained by canalithiasis. In canalithiasis (literally, canal rocks) the particles reside in the canal portion of the semicircular canals (in contradistinction to the ampullary portion). These densities are considered to be free-floating and mobile, and to cause vertigo by exerting a force. Cupulolithiasis (literally, cupula rocks), on the other hand, refers to densities adhering to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the semicircular canals and are not free-floating.

Classic benign paroxysmal positional vertigo is the most common variety of benign paroxysmal positional vertigo. It involves the posterior semicircular canal and is characterized by the following: geotropic nystagmus with the problem ear down, predominantly rotatory, fast phase toward undermost ear, latency (ie, a few seconds), and limited duration.

For related information, see the Medscape Reference article Dizziness, Vertigo, and Imbalance.

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