BPPV (Benign Paroxysmal Positional Vertigo)

BPPV and repositioning maneuvers

BPPV occurs when calcium carbonate crystals (otoconia) dislodge from the otoconia layer and travel into the semicircular canals. If they are freely floating in the SCC, we refer to this as canalithiasis. If they adhere to the cupula, we refer to this as cupulolithiasis. Posterior canal is most commonly affected, but anterior and lateral canals (15%) are also affected to a lesser degree. Average onset is at 57 and women are twice as affected as men. BPPV may follow head injury, viral neurolabyrinthitis, labyrinthine ischemia and prolonged or unusual head positioning. 

Patients describe brief episodes of spinning, or vertigo, when turning their head abruptly, changing positions in bed, looking upwards or backing their vehicle up. People can often identify the head position and tend to avoid activating it. 

Clinical examination is performed after taking a careful history by rotating the patient’s head 45 deg to one shoulder, while keeping their eye open, and laying them backwards so that their head is hanging off the edge of the examiners table about 120 deg from upright. This is known as the Dix-Hallpike Maneuver. Expect a latent period from 2 seconds to 30 seconds before vertigo, nausea and nystagmus occurs. It is helpful to reduce fixation via frenzy lenses or VNG testing. 

In posterior canal assessment, you are looking for a slow phase down and towards the nose with mixed upbeat and torsional nystagmus as the top poles of the eyes beat toward the ground. You may see more torsion when looking towards the affected ear, more vertical when looking towards the unaffected ear. It should lessen with the position after 30-60 seconds as the otoliths settle. Repeat this test as it should habituate, which is diagnostically important as central lesions do not dissipate.

Horizontal canal BPPV is tested by bringing the patient supine and rotating head 90 degrees to one side or the other. You are testing both canals in one position, so it is important observe whether the eyes are beating in a geotropic or apogeotropic pattern. Geotropic indicates affected ear is down, apogeotropic indicates affected ear is up. So, the nystagmus is greater towards the affected ear, which is synonymous with Ewald’s second law- ampulla movement in the excitatory direction elicits a brisker nystagmus than the opposing ampulla movement in the inhibitory direction. It is less susceptible to habituation through repeated testing (VSM is the culprit). 

Anterior canal BPPV can be determined by the direction of the eye beating during dix-hallpike maneuver. They will be downbeat with the torsional component beating towards the affected ear with the affected ear up. This represents the relationship between canals, for example RALP. In our clinic we test the patient in the actual anterior canal with VNG goggles to allow for more accuracy. 

Treatment of these conditions is via repositioning maneuvers that relocate the otoconia out of the SCC and into the drainage system, it is a 3 part maneuver and patient is held in each position until nystagmus has dissipated before moving onto the following position. Patient is instructed to sleep in a reclined position that evening, staying as upright as possible for the remainder of the day to ensure drainage. 

It is important to understand that peripheral and central conditions may overlap and can be confused for one another. The hallmark for BPPV is positional induced and it is fatiguable. Peripheral abnormalities usually improve with fixation. If not in normal presentation of canals, consider CNS issues that can manifest as BPPV similarities are MS, cerebellar tumors, infarction, hematoma, vertebral artery compromise, brainstem ischemia or head injury.