BPPV: An Examination of Emerging Variations

Have you ever been asked to evaluate an individual with dizziness, only to be left feeling confused by their presentation? Atypical benign paroxysmal positional vertigo (BPPV) may be the source of your uncertainty.

BPPV is the most common peripheral vestibular disorder in adults. BPPV is caused by displaced utricular otoconia (debris) that alters semicircular canal function. It commonly responds to canalith repositioning maneuvers that redirect debris from the involved semicircular canals to the utricle. Free-floating particles (canalithiasis) in the posterior and horizontal canal are well-recognized BPPV variants with clearly definable diagnostic criteria and treatment interventions.

In recent years, literature has proposed emerging variations of BPPV. An understanding of alternative forms of BPPV is critical to accurate identification and effective treatment administration.

Canal Jam

“Canal jam” implies a partial or complete obstruction of the membranous semicircular canal lumen by displaced debris. This obstruction is believed to cause a pressure differential within the canal that creates a sustained displacement of the cupula, which, depending on the location of the obstruction, may be excitatory or inhibitory. It’s theorized that the debris becomes wedged in an area where the semicircular canal is narrow. Most of the literature on canal jam is about the horizontal canal, although there is speculation that it could also involve the anterior or posterior canal.

The primary presenting complaint is positional-type dizziness. Persistent dizziness that is accentuated with head movement may also be reported. Horizontal canal jam can be associated with a positive head impulse test, caloric weakness, unidirectional nystagmus with gaze testing, and direction-fixed nystagmus with positioning tests. Examination findings can mimic acute unilateral vestibular loss.

Nonampullary Arm Posterior Canal BPPV

This refers to debris that is free-floating in the posterior canal near the common crus in the superior portion of the posterior canal. The presenting complaint would commonly be short episodes of positional dizziness. Downbeat nystagmus with a torsional component to the uninvolved ear during Dix-Hallpike testing to the involved ear would be expected. This occurs due to transient utriculopetal displacement of the posterior canal cupula with Dix-Hallpike testing. This condition can mimic the findings expected with anterior canal canalithiasis.

Short-Arm Posterior Canal BPPV

Debris may migrate from the utricle to the “infundibulum,” which consists of a short duct that connects the posterior canal ampulla to the utricle. It is one of the lowest-lying portions of the vestibular labyrinth.

Persistent upbeating nystagmus with a torsional component to the involved ear that is maximized with a Half Dix-Hallpike test to the involved ear would be an anticipated finding with testing. The nystagmus may not reverse in direction when the patient arises to sit following a test.

There may be instances in which short-arm posterior canal BPPV evolves following canalith repositioning maneuvers for long-arm posterior canal BPPV. This complication may account for complaints of imbalance following treatment of long-arm posterior canal BPPV.

Enhanced awareness of emerging and less common forms of BPPV is critical for clinicians specializing in the management of BPPV. Recognition of atypical BPPV can lead to improvements in the efficiency and effectiveness of patient care. To learn more about BPPV, including considerations for evaluation, diagnosis, treatment, check out my series of BPPV and vestibular-focused MedBridge courses.