• Clinical science

Benign paroxysmal positional vertigo

Abstract

Benign paroxysmal positional vertigo (BPPV) is a disease of the inner ear caused by small particles (otoliths) dislodging and migrating within the endolymph fluid into one of the semicircular canals. When provoked by certain head movements, these particles change position and stimulate the vestibular system, which leads to episodes of vertigo generally lasting less than a minute. Patients are typically aware of what movements trigger symptoms (e.g., quickly lying down or reclining the head). Diagnostic maneuvers that provoke vertigo attacks are used to identify BPPV. Treatment involves carrying out repositioning maneuvers to remove the particles from the semicircular canals.

Epidemiology

  • Most common type of peripheral vestibular vertigo
  • Sex: >
  • Peak incidence: > 60 years of age

References:[1]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

  • Often idiopathic
  • In rare cases, traumatic

References:[1]

Pathophysiology

BPPV is caused by semicircular canal dysfunction.

  • Dislodged particles (otoliths) disrupt the endolymph → stimulation of the hair cells on cupulas → signal sent to the brain through the vestibulocochlear nerve that is disproportional to current positioning and movement → severe vertigo attacks lasting several seconds
  • Canalithiasis: dislodgement of otoliths
  • Cupulolithiasis: displacement of the cupula caused by otoliths during movement:

References:[2]

Clinical features

  • Vertigo attacks
    • Sudden (“paroxysmal”) and recurrent
    • Triggered by certain head movements (“positional”)
    • Lasts several seconds (generally ≤ 1 minute)
    • A propensity to fall towards the healthy side
    • Typically associated with nystagmus (towards the affected side)
    • Sometimes nausea or even vomiting
    • Not associated with hearing or neurological symptoms
  • Common triggers
    • Rolling over in bed, lying down quickly
    • Quick rotation of the head, reclining, etc.
      • Vertigo occurs with a latency of a few seconds

BPPV does not cause any cochlear symptoms: neither hearing loss nor tinnitus!

References:[1]

Diagnostics

Suspected cases are confirmed with provocative diagnostic testing.

  • Dix-Hallpike test
    • The patient sits with their legs extended.
    • The head is rotated by about 45° (affected side facing downwards).
    • The head is then quickly reclined.
    • If right-sided BPPV: rotational nystagmus with a counterclockwise rapid phase occurs after a few seconds. In contrast, left-sided BPPV presents with a clockwise rapid phase.
    • Rotational nystagmus to the opposite side is common when returning to a sitting position.
  • Alternative maneuver:
    • Patient sits sideways wearing Frenzel goggles
    • Tilt patient's head approximately 25° backwards
    • Lie patient on their side
    • Positive test: rotational nystagmus occurs towards the affected side with a 5–15 second delay if the affected ear is pointing down (often accompanied by vertigo and nausea).

References:[3][1]

Differential diagnoses

Consider other diagnoses if attacks last longer than one minute, or if hearing or neurological symptoms (e.g., gait disturbances) are present (see differential diagnoses for vertigo)

The differential diagnoses listed here are not exhaustive.

Treatment

  • First-line
    • Epley repositioning maneuver: removes otoliths from the semicircular canals via the effects of gravity following a targeted movement
      • The patient should sleep upright for three days following the maneuver to avoid irritating the posterior canal.
      • The patient is returned to an upright posture.
      • The entire body is turned to the healthy side.
      • The examiner helps the patient to quickly recline and then tips the head backwards.
      • The patient then sits upright on the examination table.

  • In resistant cases: surgical obliteration of the affected canal

Antivertigo drugs (e.g., dimenhydrinate) are contraindicated in BPPV because they may exacerbate unsteadiness by inhibiting central compensation!

References:[1]

last updated 10/04/2018
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