Benign paroxysmal positional vertigo

Description

Benign paroxysmal positional vertigo is one of the most common forms of peripheral vertigo. Whilst its name may not be the most imaginative or succinct, it accurately describes the syndrome:

  • Benign – the syndrome itself has no direct harmful effects
  • Paroxysmal – vertigo symptoms occur intermittently
  • Positional – symptoms are provoked by certain positions or movements, predominantly changes in position of the head or neck
  • Vertigo – the “room-spinning” type of dizziness experienced by the individual

Read a clinical case of BPPV.


Epidemiology
  • Lifetime prevalence of BPPV is 2.4% (2007)
  • More common in women, with a reported ratio of 2:1(2007)
  • Increased incidence with age

Pathogenesis
  • Caused by canalithiasis – calcium debris within the semicircular canal. These are likely displaced calcium carbonate crystals, or otoconia, from the utricle. This theory was first proposed by Epley.
  • The canalithiasis are denser than the endolymph hence cause inappropriate movement of the endolymph with linear accelerations. This in turn causes in inappropriate activation of the inner ear’s motion sensors resulting in the perception of vertigo and associated nystagmus.
  • Posterior canal is most commonly affected, but anterior and horizontal canals can also be affected and are associated with slightly different clinical manifestations.
  • Idiopathic in 35% of cases, with another 15% of cases related to head trauma and the remainder associated with other vestibular pathologies including Meniere’s disease, neuronitis or surgery (2007)
  • Some cases are thought to be caused instead by cupulolithiasis – crystals that have become stuck or attached to the cupula in one of semicircular canals. This accounts for the more persistent cases of BPPV that do not respond as well to positioning treatments.
  • Another theory is that bone loss such as that in osteoporosis and osteopenia may contribute to the formation of the calcium densities, however evidence is lacking to support this theory.

Clinical features
  • Sudden onset episodic vertigo
  • Provoked by specific movements of the head e.g. turning over in bed, looking up or lying down
  • Usually last 60seconds or less
  • Commonly associated with nausea and vomiting
  • Recurrent episodes over weeks to months

Episodes can be very violent and distressing to the patient and evokes nausea and vomiting in many. Whilst the syndrome itself is benign, if these attacks occur whilst the patient is performing a high-risk activity such as driving or climbing a ladder, indirect harm may result from the unsteadiness caused by the vertigo.


Diagnosis with the Dix-Hallpike test
  • A bedside diagnostic test first described by Margaret Dix and Charles Hallpike
  • With the patient sitting, the neck is extended and turned to 45degrees towards the affected side. The patient is then placed supine rapidly, with the head hanging over the edge of the bed so as the neck is extended. The examiner should support the head and instruct the patient clearly to keep their eyes open, then observe for nystagmus. The patient is kept in this position until 30 seconds has passed if no nystagmus occurs. The patient is then returned to upright, observed for another 30 seconds for nystagmus, and the maneuver is repeated with the head turned to the other side. 
  • Diagnostic features:
    • Latency – onset of nystagmus is typically delayed by a few seconds
    • Transient – vertigo and nystagmus should settle in within 30-60sec
    • Fatiguability – intensity and duration of nystagmus will reduce on repeated testing
    • Nystagmus – Upbeating- torsional nystagmus observed towards the affected side in posterior canal BPPV, the nystagmus should recur in the reverse direction when the patient is returned to an upright seated position
  • The sensitivity of the Dix-Hallpike maneuver in patients with BPPV ranges from 50 to 88 percent(2007)

Horizontal canal BPPV – purely horizontal nystagmus elicited by a head turn whilst supine

Anterior canal BPPV – has similar provoking factors as classic posterior canal BPPV, it can be diagnosed by downbeating-torsional nystagmus on the Dix-Hallpike test but it is much more rare than posterior canal BPPV.

Differentials include postural hypotension, chronic unilateral vestibular hypofunction, vestibular paroxysmia, vestibular migraine, central causes of vertigo or rotational vertebral artery syndrome.


Treatment
  • Conservative management – BPPV is a benign, self-limiting syndrome, with resolution occurring within weeks to months.
  • Symptomatic treatment – persistent nausea and vomiting may require IV hydration and antiemetics e.g. prochlorperazine
  • Particle repositioning maneuvers – with the aim of moving the canaliths out of the posterior semicircular, back into the utricle. These have been shown to be safe and can be effective at resolving BPPV in 50-85% of cases(20142013) with the Epley and Semont maneuvers showing similar efficacy:
  • Around one third of patients will get recurrence (2009)

History
  • 1820 – Purkinje (1787 – 1869) published a long article on vertigo and nystagmus. He carried out experiments partly on himself and partly on mentally sick persons, who, at that time, if they became violent were treated by being rotated in a cage until such time as the nausea thus induced made them quiet and manageable again.
  • 1825 – a physiologist, Jean Pierre Flourens (1794–1867) observed that when a pigeon’s horizontal semicircular canal was destroyed, it went on turning horizontally in a circle.
  • 1861 Ménière (1799–1862) observed vertigo and tinnitus in inner ear disease
  • Magnus Gustaf Retzius (1842–1919) -initiated the anatomical studies of the semicircular apparatus.
  • 1870 – Goltz deduced that the normal function of the semicircular canal apparatus must be to maintain equilibrium if its destruction caused vertigo and imbalance
  • 1874 – Josef Breuer (1842–1925) concluded that the semicircular canal was a sensory organ for the perception of rotary motion and vertigo was the result of abnormal excitation of this sensory organ.
  • 1874 – Ernst Mach (1838 -1916), Austrian physicist and philosopher, established the mathematical equations for rotary movements and identified the semi-circular canal apparatus was responsible for perceiving rotary movement.
  • 1874 – Crum Brown (1838 -1922) also identified semi-circular canals as the sensory organ capable of perceiving vertigo.
  • 1921 Bárány first described this syndrome of episodic vertigo, induced by sudden movement of the head; the vertigo was abrupt in onset and lasted a few seconds.
  • 1952 Dix and Hallpike further describe the syndrome and give it today’s name of “benign paroxysmal positional vertigo”.
  • 1980 Epley published “new dimensions of benign paroxysmal positional vertigo” and subsequent papers outlining the canalith theory and has since been recognized as developing the Epley maneuver to treat the syndrome.
  • Semont Maneuver

Associated Persons

References

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Studied at Univerisity of Cambridge - BA MB BChir. British doctor working in emergency medicine in Perth, Australia. Special interests include primary care and emergency medicine.

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