Causes of Benign Paroxysmal Positional Vertigo (BPPV)
BPPV is caused by dislodged calcium carbonate crystals (otoconia) that break free from their normal location in the utricle and migrate into the semicircular canals, where they abnormally stimulate the vestibular apparatus during head position changes. 1, 2
Primary Pathophysiologic Mechanisms
The fundamental cause involves two distinct mechanisms:
Canalithiasis (most common) – Free-floating otoconial particles move from the utricle and collect near the cupula of the affected semicircular canal, creating inertial forces during head movement that cause abnormal cupular displacement, resulting in vertigo and nystagmus. 1, 2, 3
Cupulolithiasis (less common) – Otoconial debris adheres directly to the cupula of the affected semicircular canal, displacing it and producing abnormal vestibular stimulation. 1, 3
The posterior semicircular canal is affected in 85-95% of cases, likely due to its gravity-dependent position when supine, while the lateral (horizontal) canal accounts for 5-15% of cases. 1, 2, 3
Identified Risk Factors and Precipitating Causes
Most cases occur idiopathically – The majority of BPPV cases happen for no identifiable reason. 1
Trauma-related causes:
- Head or neck trauma is a major causative factor, particularly in patients younger than 50 years. 2
- Whiplash injury is recognized as a potential causative factor. 2
- Post-traumatic BPPV is more refractory, requiring repeated canalith repositioning in up to 67% of cases, compared with 14% of non-traumatic BPPV. 3
- Bilateral involvement rarely occurs after trauma. 3
Age-related factors:
- BPPV is significantly more common in older adults over 50 years. 3
- Age-related degeneration of the otoconial membrane may contribute to crystal dislodgement. 3
Associated medical conditions:
- Migraine – Associated with increased BPPV risk. 1
- Other inner ear disorders – BPPV can appear concurrently with Meniere's disease or vestibular neuritis. 1, 3
- Diabetes – Identified as a risk factor. 1
- Osteoporosis – Associated with BPPV development. 1
Prolonged immobilization:
- Lying in bed for extended periods increases risk, including preferred sleep side positioning, post-surgical procedures, and prolonged illness. 1
Critical Clinical Distinctions
When BPPV coexists with other conditions:
- BPPV may coexist with CNS disorders such as multiple sclerosis; patients can exhibit a positive Dix-Hallpike maneuver and respond to standard repositioning maneuvers despite the CNS comorbidity. 3
- When a patient's presentation does not fit a single vestibular entity, consider the coexistence of more than one disorder. 3
Red flags suggesting non-BPPV causes:
- Failure to respond to canalith repositioning procedures after 2-4 attempts should prompt reconsideration of the diagnosis, as the underlying cause may not be BPPV. 3
- Downbeating nystagmus without torsional component, direction-changing nystagmus without head position changes, constant severe dizziness unaffected by position, associated hearing loss, or syncope suggest alternative diagnoses. 3