Benign paroxysmal positional vertigo (BPPV) (mechanism of disease)

This is a flowchart on BPPV, covering the etiology, pathophysiology, and manifestations.
ADDITIONAL TAGS:
Risk factors / SDOH
Cell / tissue damage
Structure / motion
Benign paroxysmal
positional vertigo
Medicine / iatrogenic
Infectious / microbial
Biochem / metabolic
Immunology / inflammation
Signs / symptoms
Tests / imaging / labs
Neurological pathology
Genetic / hereditary
Flow physiology
Pathophysiology
Etiology
Manifestations
Free-floating otoconia (calcium carbonate crystals) and debris are dislodged
Otoconia and debris from the acoustic macula enter the semicircular canals
Canalithiasis
Changing head position (or other gravitational forces)
Disruption of endolymph dynamics
Abnormal stimulation of the vestibular apparatus → abnormal stimulation of the vestibulocochlear nerve
Otoconial debris that has adhered to the cupula of the affected semicircular canal
↑ sensitivity of the semi- circular canal
Cupulolithiasis
Chronic or refractory BPPV
Idiopathic
Possibly secondary to degeneration of the acoustic macula?
Risk factors:
Female sex
Increased age
Low vitamin D
Osteopenia/osteoporosis
Triggers:
Rolling over in bed
Bending forwards
Suddenly jerking the head to look up or down
Lying down, reclining, or standing up quickly
Quick rotation of the head relative to gravity
Head injury
Prior otologic surgery
Vestibular neuritis
Meniere disease
Migraine
Episodic vertigo: “room spinning”; Paroxysmal, recurrent episodes; Lasts seconds ( 1 min); Triggered by head movement (positional) after latency period
+/- nystagmus
+/- nausea and vomiting
Risk of falls → subsequent injury
+ Dix-Hallpike maneuver
Fractures (e.g., Colles fracture, hip fracture)
Dislocations (e.g., hip dislocation)
Traumatic brain injury (e.g., hemorrhagic stroke, concussion)
Depression
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