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Pathophysiology

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

Various pathophysiological mechanisms have been proposed to explain this condition.

  • has been suggested that this condition occurs secondary to damage of the sensory epithelium of the utricle and saccule following trauma (e.g. head injury), chronic infection (often thought to be viral) or vascular disease
  • posterior semicircular canal (PSCC) has been suggested as the main site of the lesion in benign paroxysmal positional vertigo (BPPV) (2)
    • majority of posterior canal BPPV is thought to be caused by 'canalolithiasis' (free-floating particles within a semicircular canal) (2)
    • 'canalolithiasis' hypothesis postulates that otoconial particles or debris from the utricle are trapped in the PSCC and start to move when head position is changed quickly with respect to gravity
      • otocania can be thought of as "ear rocks" - small crystals of calcium carbonate derived from the utricle
      • supported by the direct observation of free-floating endolymph particles in the PSCC during the procedure of occlusion of the PSC
      • the major evidence in favour of the PSCC as the site of the lesion is that the two recommended surgical procedures for BPPV, singular neurectomy which deafferentates the PSCC and occlusion of the PSCC which defunctions it, are effective in treating the positional vertigo
    • the alternative cupulolithiasis (literally, "cupula rocks") theory for pathophysiology for BPPV refers to densities adhered to the cupula of the crista ampullaris.
      • cupulolith particles reside in the ampulla of the semicircular canals and are not free floating
      • is thought to play an important role in lateral canal BPV than in the posterior canal BPV (2)

Notes:

  • based on the canalithiasis theory, BPPV can be treated successfully in most patients by simple physical manoeuvres which are believed to move the displaced otoconia back into the utricule (3)

Reference:


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