Original Editor - Rachael Lowe

Top Contributors - Rachael Lowe, William Jones, Evan Thomas, Jennifer Lohmus and Kai A. Sigel

Clinically Relevant Anatomy

Interior View of Labyrinth

Benign paroxysmal positional vertigo (BPPV) is a specific type of vertigo that is brought on by a change in position of the head with respect to gravity. This disorder is caused by problems in the inner ear. Its symptoms are repeated episodes of positional vertigo, that is, of a spinning sensation caused by changes in the position of the head.[1]

The vestibular system monitors the motion and position of the head in space by detecting angular and linear acceleration. The 3 semicircular canals in the inner ear detect angular acceleration and are positioned at near right angles to each other. Each canal is filled with endolymph and has a swelling at the base termed the ampulla. The ampulla contains the cupula, a gelatinous mass with the same density as endolymph, which in turn is attached to polarized hair cells. Movement of the cupula by endolymph can cause either a stimulatory or an inhibitory response, depending on the direction of motion and the particular semicircular canal[2]. There is a vestibular apparatus within each ear so under normal circumstances, the signals being sent from each vestibular system to the brain should match, confirming that the head is indeed rotating to the right, for example.

Within the labyrinth of the inner ear lie collections of calcium crystals known as otoconia. In patients with BPPV, the otoconia are dislodged from their usual position within the utricle and they migrate over time into one of the semicircular canals (the posterior canal is most commonly affected due to its anatomical position)[2]. When the head is reoriented relative to gravity, the gravity-dependent movement of the heavier otoconial debris (colloquially ear rocks or crystals) within the affected semicircular canal causes abnormal (pathological) fluid endolymph displacement in the affected ear. This fluid displacement will send a signal to the brain indicating that rotational movement is occuring. However, the vestibular apparatus in the unaffected ear will not be transmitting the same signal because there are no loose otoconia triggering the hair cells abnormally. This resultant mismatch in signals coming from the right and left vestibular systems lead to the sensation of vertigo. This more common condition is known as canalithiasis. Vertigo associated with this condition will be of short duration, even if the person with the condition stays in the provocative position, because the endolymph and otoconia will quickly come to a rest so the hair cells will no longer be displaced and triggering the signal to the brain.

In rare cases, the crystals themselves can adhere to a semicircular canal cupula rendering it heavier than the surrounding endolymph. Upon reorientation of the head relative to gravity, the cupula is weighted down by the dense particles thereby inducing an immediate and maintained excitation of semicircular canal afferent nerves. This condition is termed cupulolithiasis. Vertigo associated with this condition will not resolve until the head is moved out of the provocative position because even when the endolymph comes to a rest, the adhered otoconia will continue to displace the hair cells and trigger the signal of movement to the brain.

It can be triggered by any action which stimulates the posterior semi-circular canal which may be:

  • Tilting the head
  • Rolling over in bed
  • Looking up or under
  • Sudden head motion

BPPV may be made worse by any number of modifiers which may vary between individuals:

  • Changes in barometric pressure - patients often feel symptoms approximately two days before rain or snow
  • Lack of sleep (required amount of sleep may vary widely)
  • Stress

Clinical Presentation

  • Symptoms
    • Vertigo: Spinning sensation (not lightheadedness or feeling off-balance.
    • Short duration (Paroxysmal): Lasts only seconds to minutes (usually less than 60 seconds)
    • Positional in onset: Only can be induced by a change in position.
    • Nausea is often associated
    • Visual disturbance: It may be difficult to read or see during an attack due to the associated nystagmus.
    • Pre-Syncope (feeling faint) or Syncope (fainting) is unusual.
    • Emesis (Vomiting) is uncommon but possible.
  • Signs
    • Rotatory (torsional) nystagmus, where the top of the eye rotates towards the affected ear in a beating or twitching fashion.

Diagnostic Procedures

The condition is diagnosed from patient history (feeling of vertigo with sudden changes in positions) and by performing a positional test. Different positional test exist. The exact positional test used to confirm the presence of BPPV will depend on which semicircular canal is involved. The most commonly used test is Dix-Hallpike which assesses involvement of the posterior canal (the most commonly affected semicircular canal).[2] The test involves turning the head 45 degrees to the side being tested and then quickly moving from a seated to a supine position with the head declined 30 degrees below the trunk. The test must be performed quickly to ensure sufficient displacement of the endolymp and otoconia to provoke the expected symptoms. The test is considered positive for canalithiasis of the posterior canal if vertigo is provoked and nystagmus is observed, both of which should be of short-duration for canalithiasis. The direction of the observed nystagmus should be consistent with the canal being assessed. For the posterior canal, nystagmus should be up-beating and torsional in an ipsilateral direction (if testing the affected side. If the left side is affected but the test is performed with the head turned to the right, the nystagmus would be up-beating and torsional to the right).

If the nystagmus and vertigo are sustained, cupulolithiasis should be considered or potentially a more central cause of vertigo. Patient history and other neurological tests can help to rule out a more serious central cause. Any positional tests should be performed within the framework of a more comprehensive vestibular assessment to avoid an incorrect diagnosis of BPPV.


The nystagmus associated with BPPV has several important characteristics which differentiate it from other types of nystagmus.

  • Positional: the nystagmus occurs only in certain positions
  • Latency of onsent: there is a 5-10 second delay prior to onset of nystagmus
  • Nystagmus lasts for 5-30 seconds
  • Visual fixation does not suppress nystagmus due to BPPV
  • Both a rotatory and upbeat vertical components are present
  • The nystagmus beats in a geotrophic (top of the eye towards the ground fashion
  • Repeated Dix-Hallpike maneuvers cause the nystagmus to fatigue or disappear temporarily

Outcome Measures

Dizziness Handicap Inventory (DHI)

Dynamic Gait Index (DGI)

Clinical Test of Sensory Interaction in Balance (CTSIB)

Management / Interventions

Two treatments have been found effective for relieving symptoms of posterior canal BPPV: the canalith repositioning procedure (CRP) (aka Epley manoeuvre) and the liberatory or Semont manoeuvre.[1] The CRP employs gravity to move the calcium build-up that causes the condition. The particle repositioning manoeuvre can be performed during a clinic visit by trained otolaryngologists, neurologists, chiropractors, physical therapists or audiologists. The manoeuvre is relatively simple but few general health practitioners know how to perform it correctly. In the Semont manoeuvre, patients themselves are able to achieve canalith repositioning. Only limited data are available comparing the two treatments and it is not known which is more effective.[1] Different repositioning manoeuvres are required for canalithiasis of the anterior or horizontal semicircular canals or in cases of cupulolithiasis.


Devices such as a head over heels "rotational chair" are available at some tertiary care centers. Home devices, like the DizzyFIX, are also available for the treatment of BPPV and vertigo.

The Epley maneuver (particle repositioning) does not address the actual presence of the particles (otoconia), rather it changes their location. The maneuver moves these particles from areas in the inner ear which cause symptoms, such as vertigo, and repositions them into areas where they do not cause these problems.

Meclizine is a commonly prescribed medication, but is ultimately ineffective for this condition, other than masking the dizziness. Other sedative medications help mask the symptoms associated with BPPV but do not affect the disease process or resolution rate. Betahistine (trade name Serc) is available in some countries and is commonly prescribed but again it is likely ineffective. Particle repositioning remains the current gold standard treatment for most cases of BPPV.

Surgical treatments, such as a semi-circular canal occlusion, do exist for BPPV but carry the same risk as any neurosurgical procedure. Surgery is reserved for severe and persistent cases which fail particle repositioning and medical therapy.

Differential Diagnosis

Ménière's disease - the vertigo spells are not provoked by position change, are episodic, can cause hearing loss and/or tinnitus, and they last much longer (30 minutes to several hours)[2]

Posterior circulation stroke - should be considered if associated numbness and weakness.

Orthostatic (Postural) hypotension - quick or abrupt changes in body position causes increased dizziness or lightheadedness, can confirm by supine blood pressure and standing blood pressure fluctuations to differentiate [2]

Labyrinthitis - inflammatory condition of the endolymph sac within the labyrinthe by immunological, bacterial or viral origin that affects the cochlea and vestibular system of the inner ear through blocking sensory cell signals resulting in hearing loss[2]

Vestibular Neuritis - viral - induced atrophy and inflammation of the vestibulocochlear nerve (Cranial Nerve VIII) and can often lead to development of BPPV in future [2]


Neil Bhattacharyya et al. Clinical practice guideline: Benign paroxysmal positional vertigo. Otolaryngology–Head and Neck Surgery, 2008, 139, S47-S81[1]

Recent Related Research (from Pubmed)

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  1. 1.0 1.1 1.2 1.3 Neil Bhattacharyya, Reginald F. Baugh, Laura Orvidas, David Barrs, Leo J. Bronston, Stephen Cass, Ara A. Chalian, Alan L. Desmond, Jerry M. Earll, Terry D. Fife, Drew C. Fuller, MPH, James O. Judge, Nancy R. Mann, Richard M. Rosenfeld, Linda T. Schuring, Robert W. P. Steiner, Susan L. Whitney, and Jenissa Haidari. Clinical practice guideline: Benign paroxysmal positional vertigo. Otolaryngology–Head and Neck Surgery, 2008, 139, S47-S81
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Lorne S. Parnes, Sumit K. Agrawal and Jason Atlas. Diagnosis and management of benign paroxysmal positional vertigo (BPPV). CMAJ. September 30, 2003; 169 (7)
  3. Physiotutors. Dix Hallpike Test | Posterior BPPV. Available from: https://www.youtube.com/watch?v=7wMvTUPaNPo
  4. Physiotutors. Supine Head Roll Test | Lateral BPPV. Available from: https://www.youtube.com/watch?v=IlrVqmIjGeI
  5. Physiotutors. Modified Epley Maneuver | Posterior BPPV Treatment. Available from: https://www.youtube.com/watch?v=u23Wuj6zVLM
  6. Physiotutors. Semont Liberatory Maneuver | Posterior BPPV Treatment. Available from: https://www.youtube.com/watch?v=dvC1xrks7qc
  7. Physiotutors. Barbecue/BBQ Roll Maneuver | Lateral BPPV Treatment. Available from: https://www.youtube.com/watch?v=6zsfIa_Z8_k
  8. Physiotutors. Gufoni Maneuver | Lateral BPPV Treatment. Available from: https://www.youtube.com/watch?v=uA9ZcKbPAz8