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Summary Table

Category	Detail
Risk Factors	Age > 50, female sex, head trauma, prolonged bed rest, post-viral labyrinthitis, osteoporosis, vitamin D deficiency
Etiology	Displaced otoconia (calcium carbonate crystals) migrating into the semicircular canals, most commonly the posterior canal
Patient Presentation	Brief episodes of intense rotational vertigo triggered by changes in head position (rolling over in bed, looking up, bending forward)
Classic Physical Exam	Positive Dix-Hallpike test: upbeat-torsional nystagmus with latency (2-5 seconds), fatigability, and duration < 60 seconds
Key Diagnostic Results	Clinical diagnosis based on Dix-Hallpike maneuver; no labs or imaging required unless atypical features are present
Management	Epley maneuver (canalith repositioning procedure) for posterior canal BPPV; no role for medications as first-line treatment
Keywords	"Vertigo with position change," "rolling over in bed," "brief episodes," "latency and fatigability of nystagmus," "Dix-Hallpike positive"

1. Pathophysiology

BPPV arises from the displacement of otoconia, small calcium carbonate crystals normally embedded in the utricular macula. These crystals become dislodged and migrate into one of the semicircular canals, where they do not belong. The posterior semicircular canal is affected in approximately 80-90% of cases because of its dependent anatomical position relative to the utricle, making it the natural gravitational destination for free-floating debris.

Once inside the canal, the otoconia create abnormal endolymph flow during head movements. When the patient changes head position, gravity pulls the debris through the canal, generating a plunger-like effect on the cupula. This produces a false signal of angular rotation to the brain that does not match input from the other ear, the eyes, or proprioception. The result is a sensory mismatch that the brain interprets as spinning, which is what the patient perceives as vertigo.

This mechanism explains several hallmark features. The latency of 2-5 seconds before nystagmus onset corresponds to the time required for otoconia to settle and begin moving through endolymph after the head is repositioned. The brief duration (typically under 60 seconds) reflects the time it takes for the debris to reach a new resting position and stop generating endolymph flow. Fatigability, the diminishing of symptoms with repeated positioning, occurs because repetitive maneuvers disperse the clumped otoconia, reducing the hydraulic effect with each successive trial.

There are two pathophysiologic subtypes worth understanding. Canalithiasis refers to free-floating otoconia within the canal lumen and accounts for the vast majority of cases. Cupulolithiasis refers to otoconia that become adherent to the cupula itself, which produces a persistent, non-fatigable nystagmus and is less common but more refractory to treatment.

2. Classification and Clinical Manifestation

By Canal Involved

Canal	Frequency	Nystagmus	Test	Key Feature
Posterior canal	~80-90%	Upbeat + torsional (top pole of eye beats toward the affected ear)	Dix-Hallpike	Most common; latency, fatigability present
Horizontal (lateral) canal	~10-15%	Direction-changing horizontal (geotropic or apogeotropic)	Supine roll test (Pagnini-McClure)	Nystagmus changes direction depending on which side the head is turned
Anterior canal	~1-2%	Downbeat + torsional	Dix-Hallpike	Rare; must exclude central causes of downbeat nystagmus before diagnosing

Pathophysiologic Mechanism

Mechanism	Nystagmus Behavior	Duration of Nystagmus	Fatigability	Treatment Response
Canalithiasis (free-floating debris)	Transient, crescendo-decrescendo	< 60 seconds	Yes	Excellent response to repositioning maneuvers
Cupulolithiasis (debris adherent to cupula)	Persistent as long as position is maintained	> 60 seconds	No	More refractory; may require prolonged or modified repositioning

Clinical Features Common to All Variants

Feature	Detail
Trigger	Head position change (not spontaneous)
Duration per episode	Seconds to under 1-2 minutes
Associated symptoms	Nausea, imbalance; no hearing loss, no tinnitus, no focal neurologic deficits
Between episodes	Patient is completely normal
Natural history	Self-limiting in weeks to months; high recurrence rate (~50% within 5 years)

3. Diagnostic Workup

Test	Role	Expected Finding
Dix-Hallpike maneuver	Best initial test and confirmatory test for posterior canal BPPV	Upbeat-torsional nystagmus with 2-5 second latency, duration < 60 seconds, fatigable on repeat
Supine roll test	Best initial test for horizontal canal BPPV	Direction-changing horizontal nystagmus
Audiometry	Not routinely needed	Normal in BPPV; order only if hearing loss is reported to exclude other diagnoses
MRI of the brain	Not routinely needed	Order only if central features are present (see below)

BPPV is a clinical diagnosis. The Dix-Hallpike maneuver serves as both the best initial test and the gold standard for posterior canal involvement. No laboratory test, imaging study, or audiometric evaluation is required when the maneuver produces classic findings.

To perform the Dix-Hallpike test, the patient sits upright on the exam table, and the examiner turns the patient's head 45 degrees toward the side being tested. The patient is then rapidly laid back so the head hangs approximately 20 degrees below the horizontal plane. The examiner watches the eyes for nystagmus. A positive result on the right side means otoconia are in the right posterior canal.

The characteristics of the nystagmus are what confirm the diagnosis and differentiate it from central vertigo. You must look for four features: (1) latency of onset (2-5 seconds after assuming position), (2) limited duration (nystagmus resolves within 60 seconds), (3) fatigability (diminishes with repeated testing), and (4) the direction must be upbeat-torsional with the torsional component beating toward the downward (affected) ear.

If the Dix-Hallpike is negative but clinical suspicion remains, perform the supine roll test to evaluate horizontal canal BPPV. The patient lies supine and the head is turned rapidly to one side, then the other, observing for horizontal nystagmus.

When to image: MRI is indicated when findings suggest a central cause of positional vertigo. Red flags include nystagmus that is purely vertical (downbeat or upbeat without torsion), nystagmus without latency or fatigability, nystagmus lasting longer than 1-2 minutes, direction-changing nystagmus on Dix-Hallpike, and any accompanying neurologic signs such as dysarthria, diplopia, dysphagia, limb ataxia, or severe truncal instability disproportionate to the vertigo.

4. Management and Treatment

Clinical Scenario	Treatment	Details
Posterior canal BPPV (first-line)	Epley maneuver (canalith repositioning)	Series of 5 sequential head positions held 30-60 seconds each; can be performed in clinic or taught for home use
Posterior canal BPPV (alternative)	Semont maneuver	Rapid side-to-side repositioning; similar efficacy
Horizontal canal BPPV (geotropic)	Lempert (BBQ roll) maneuver or Gufoni maneuver	360-degree roll toward the unaffected side
Refractory BPPV (failed multiple repositioning)	Referral to vestibular specialist; consider surgical posterior canal occlusion	Reserved for rare, debilitating cases
Symptomatic relief (adjunct only)	Meclizine 25 mg orally, or dimenhydrinate	Short-term use only; NOT a substitute for repositioning

The Epley maneuver is the first-line treatment for posterior canal BPPV and is the answer the exam is looking for. It works by using gravity to guide the dislodged otoconia out of the posterior canal, through the common crus, and back into the utricle where they can be reabsorbed. The maneuver involves five sequential positions, each held for approximately 30-60 seconds. Success rates after one to three treatments exceed 80-90%.

After the Epley maneuver, some clinicians recommend post-treatment precautions such as sleeping with the head elevated at 45 degrees for 1-2 nights, though evidence for this is limited and guidelines do not strongly endorse it.

Vestibular suppressants such as meclizine or dimenhydrinate should not be used as primary treatment. They do not reposition otoconia and only mask symptoms. Prolonged use actually delays central compensation and worsens long-term balance recovery. If used at all, they should be limited to short-term control of severe nausea or used while awaiting a repositioning session.

Vestibular rehabilitation therapy can be considered as an adjunct for patients with residual dizziness or imbalance after successful repositioning, and for patients with chronic or frequently recurrent BPPV.

For the rare patient who fails all conservative measures and remains severely symptomatic, posterior semicircular canal occlusion is a surgical option. This procedure physically blocks the canal, preventing endolymph flow and eliminating the vertigo. It carries a risk of sensorineural hearing loss and is a last resort.

There is emerging evidence supporting vitamin D and calcium supplementation in patients with recurrent BPPV and documented vitamin D deficiency, as low vitamin D levels are associated with higher recurrence rates. This is increasingly tested as a long-term preventive strategy.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Meniere disease	Both cause episodic vertigo	Meniere episodes last 20 minutes to several hours, are accompanied by fluctuating sensorineural hearing loss, tinnitus, and aural fullness; BPPV episodes last seconds, with no auditory symptoms
Vestibular neuritis	Both cause vertigo without hearing loss	Vestibular neuritis causes a single prolonged episode (days), is not triggered by position changes, and produces spontaneous horizontal nystagmus that does not fatigue; BPPV is brief and positional
Labyrinthitis	Vertigo with an acute onset	Labyrinthitis includes hearing loss (cochlear involvement); BPPV has normal hearing
Central positional vertigo (posterior fossa lesion)	Can produce positional nystagmus	Central nystagmus has no latency, does not fatigue, may be purely vertical, and is accompanied by other neurologic signs (ataxia, cranial nerve deficits)
Vestibular migraine	Episodic vertigo in a younger patient	Episodes last minutes to 72 hours, often associated with headache, photophobia, or phonophobia, and are not reliably reproduced by the Dix-Hallpike test
Orthostatic hypotension	Dizziness triggered by positional change	Symptoms are lightheadedness/presyncope, not true rotational vertigo; triggered by standing up (not head turning); diagnosed by orthostatic vital signs showing a drop in blood pressure
Perilymphatic fistula	Positional vertigo, sometimes post-trauma	Vertigo and hearing loss provoked by straining, coughing, or loud sounds (Tullio phenomenon); history of trauma or barotrauma

6. Traps and High-Yield Pearls

The most common way students get BPPV questions wrong is by confusing it with other causes of vertigo based on duration and triggers. The exam tests whether you can distinguish seconds-long positional vertigo (BPPV) from minutes-to-hours episodes with auditory symptoms (Meniere disease) from a single prolonged episode without positional triggers (vestibular neuritis). The vignette will often include a patient who "gets dizzy when rolling over in bed" or "looking up at a shelf," and the correct next step is the Dix-Hallpike maneuver, not an MRI or audiogram.

A second trap involves management. Students frequently choose meclizine as the treatment for BPPV because it is a familiar vertigo medication. The correct answer is always the Epley maneuver. Medications do not treat the underlying problem. If the question stem describes a patient with classic BPPV and asks for the most appropriate treatment, canalith repositioning is the answer regardless of whether a medication is listed as a choice.

A third pitfall is the negative Dix-Hallpike. If the vignette describes positional vertigo but the Dix-Hallpike is negative, the student must think about horizontal canal BPPV and select the supine roll test rather than jumping to imaging or dismissing the diagnosis.

Finally, watch for vignettes that describe positional nystagmus without latency or fatigability. This pattern should immediately raise concern for a central lesion, and the next step becomes brain MRI, not a repositioning maneuver. The core competency being tested is whether you can differentiate peripheral from central positional vertigo based on nystagmus characteristics alone.

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