BPPV Treatment in San Diego - Benign Paroxysmal Positional Vertigo

Deep inside each of your inner ears is a tiny structure called the utricle. Sitting on top of it is a small patch coated with hundreds of thousands of microscopic calcium carbonate crystals, called otoconia. Most people just call them ear crystals. They are supposed to be there. They help your brain sense gravity and head tilt.

The problem starts when a few of those crystals break loose from the utricle and drift into one of the semicircular canals nearby. The semicircular canals are fluid-filled loops that sense head rotation. They are not designed to have crystals floating inside them.

When those loose crystals slide through the canal fluid, the fluid moves in a way it normally would not. The tiny sensors inside the canal read that fluid movement as head rotation and send a signal to the brain saying "you are spinning." Your eyes and body know you are not spinning. Your inner ear is telling the brain that you are. The mismatch is what you feel as vertigo.

That is why BPPV symptoms come in short bursts triggered by specific head movements. Rolling over in bed, looking up at a shelf, or bending down to tie your shoes all shift the crystals in the canal, which produces a brief but intense spinning sensation. Once the crystals stop moving, the spinning fades within a minute or so.

The Epley maneuver and other repositioning techniques work by using head position and gravity to guide those loose crystals out of the canal and back onto the utricle where they belong. When it works, the false signal stops. When it does not, either the crystals did not move, they moved to the wrong place, or the source of the dizziness was never the crystals to begin with.

Our evaluation for BPPV and persistent dizziness goes beyond a single positional test. When patients arrive already having tried the Epley without lasting relief, the assessment needs to cover both peripheral and central components so the actual source of the symptoms becomes visible.

We begin with a full Dix-Hallpike sequence on both sides, performed under controlled conditions with observation of the eye movement patterns that identify which canal is involved. When the presentation suggests horizontal canal involvement, we add the supine roll test, which the Dix-Hallpike alone does not detect. Together those two tests map the peripheral inner ear component.

From there, our clinicians perform oculomotor testing that assesses smooth pursuit, saccades, gaze stability, and the vestibulo-ocular reflex. These are the assessments that identify central vestibular contributions to positional dizziness. When those tests reveal abnormalities, the presentation is not straightforward BPPV and the intervention plan changes accordingly.

We also assess cervical spine contribution. The upper cervical spine feeds dense proprioceptive input into the same brainstem circuits that process vestibular signals, so restriction or dysfunction in the neck can produce dizziness patterns that mimic peripheral vertigo. When cervical involvement is present, it is addressed as part of the overall picture.

If the pattern points toward autonomic involvement such as lightheadedness on standing, that usually belongs to POTS rather than BPPV, and the evaluation shifts accordingly. If the dizziness began after a head injury, post- concussion vestibular dysfunction is a separate pathway that we assess with different testing.

This is a more comprehensive assessment than what an ENT or general practice office typically performs, because most of those settings are designed to confirm or rule out peripheral inner ear pathology and do not include the central vestibular or cervical components.