Introduction to Benign Paroxysmal Positional Vertigo: Difference between revisions

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The majority of BPPV occurs in the posterior canals  (85 to 95 percent). 5 to 15 percent occurs in the horizontal canals and 1 to 5 percent occurs in the anterior canals.<ref>Bhattacharyya N, Gubbels SP, Schwartz SR, Edlow JA, El-Kashlan H, Fife T et al. [https://journals.sagepub.com/doi/10.1177/0194599816689667?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed Clinical practice guideline: benign paroxysmal positional vertigo (update)]. Otolaryngol Head Neck Surg. 2017;156(3_suppl):S1-S47.</ref>
The majority of BPPV occurs in the posterior canals  (85 to 95 percent). 5 to 15 percent occurs in the horizontal canals and 1 to 5 percent occurs in the anterior canals.<ref>Bhattacharyya N, Gubbels SP, Schwartz SR, Edlow JA, El-Kashlan H, Fife T et al. [https://journals.sagepub.com/doi/10.1177/0194599816689667?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed Clinical practice guideline: benign paroxysmal positional vertigo (update)]. Otolaryngol Head Neck Surg. 2017;156(3_suppl):S1-S47.</ref>
== Variants of BPPV ==
Two variants of BPPV can be present:
# Cupulolithiasis
# Canalithiasis
=== Cupulolithiasis (i.e. ‘stuck crystals’) ===
* The debris adheres to the cupula of the affected canal, causing the cupula to be gravity sensitive
* Changes in head position cause an inappropriate deflection of the cupula resulting in nystagmus, vertigo, and nausea
* This is a relatively uncommon form of BPPV<ref name=":2" />
=== Canalithiasis (‘free floating crystals’) ===
* This theory better explains the typical characteristics of BPPV
* Otoconia are floating freely within the endolymph of the SCC
* When the head is moved into the plane of the affected canal, the debris moves into the most dependent portion causing movement of the endolymph which deflects the cupula producing vertigo, nystagmus and nausea<ref name=":2" />
The key characteristics of these two variants of BPPV are summarised in Table 1.
{| class="wikitable"
|+Table 1. Characteristics of BPPV variants.<ref name=":1" />
Assessing the Vertical Canals
The Dix-Hallpike (DH) test is used to assess BPPV (primarily the vertical canals).
This test enables the therapist to identify the side of the lesion and frequently the specific canal involved.
* Patient is seated with their head turned 45º toward the test side
* Patient is moved as rapidly (safely) as possible into a supine position with the head extended 20 degrees (CHECK as Bernard says 30 degrees) BPPV CPG
* Have the patient look at your nose and observe his / her eyes for nystagmus - note the direction of the movement, latency, and duration of nystagmus
* Wait until the nystagmus stops and then typically proceed into treatment (see below) if indicated (some therapists will slowly sit the patient up in order to assess the other side, but nausea can be a problem)
* Depending on results, repeat to the other side
!
!Canalithiasis
!Cupulolithiasis
|-
|Latency of onset
|>1 second before the onset of vertigo and nystagmus
|No latency
|-
|Duration
|Vertigo and nystagmus lasts < 60 seconds
|Vertigo and nystagmus persist > 1minute
|-
|Direction of nystagmus
|Characteristic nystagmus depending on which canal is involved
|Characteristic nystagmus depending on which canal is involved
|-
|Fatigability
|Decreased intensity of vertigo and nystagmus with repeated movement of the patient in provoking positions
|Decreased intensity of vertigo and nystagmus with repeated movement of the patient in provoking positions
|}


== References ==
== References ==
[[Category:Course Pages]]
[[Category:Course Pages]]
[[Category:Neurology]]
[[Category:Neurology]]

Revision as of 11:31, 13 June 2021

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Introduction[edit | edit source]

Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo that arises from a peripheral vestibular disorder. It accounts for 20 to 30 percent of all patients seen for vertigo in clinics that specialise in dizziness.[1]

While the overall incidence of BPPV in the general population is around 2.5 percent,[1] it is more common in older adults. Some studies show that 50 percent of older adults have BPPV.[2]

Symptoms tend to be provoked by head movements, such as:[3]

  • Looking up
  • Lying down flat quickly
  • Bending forwards
  • Rolling in bed

BPPV is a biomechanical problem in which one or more of the semicircular canals is inappropriately excited, resulting in vertigo, nystagmus and occasionally nausea.[3] It occurs when there is displacement of calcium-carbonate crystals or otoconia from the utricle into one of the three fluid-filled semicircular canals of the inner ear.[3][4] For more information on the anatomy of the vestibular system, please click here.

Aetiology[edit | edit source]

It is not yet known what causes BPPV. The majority of cases are idiopathic, but it is more likely to recur in older adults.[2]

The two primary theories about its aetiology are that it is:

  1. Related to ischaemia and cardiovascular disease[5]
  2. Related to vitamin D deficiency and calcium metabolism (seasonal variations may be present)[6][7]

Predisposing factors include:

  • Head trauma in all age groups[7]
    • In a younger population head trauma is a leading predisposing factor
  • The recurrence rate may be higher and treatment may not be as effective in a head trauma population[3]
  • Surgical trauma to the inner ear[8]
  • Vestibular labyrinthitis / neuritis[8]
  • Migraines[1]
  • Ischaemia of the anterior vestibular artery and cardiovascular disease[3][9]

The majority of BPPV occurs in the posterior canals  (85 to 95 percent). 5 to 15 percent occurs in the horizontal canals and 1 to 5 percent occurs in the anterior canals.[10]

Variants of BPPV[edit | edit source]

Two variants of BPPV can be present:

  1. Cupulolithiasis
  2. Canalithiasis

Cupulolithiasis (i.e. ‘stuck crystals’)[edit | edit source]

  • The debris adheres to the cupula of the affected canal, causing the cupula to be gravity sensitive
  • Changes in head position cause an inappropriate deflection of the cupula resulting in nystagmus, vertigo, and nausea
  • This is a relatively uncommon form of BPPV[2]

Canalithiasis (‘free floating crystals’)[edit | edit source]

  • This theory better explains the typical characteristics of BPPV
  • Otoconia are floating freely within the endolymph of the SCC
  • When the head is moved into the plane of the affected canal, the debris moves into the most dependent portion causing movement of the endolymph which deflects the cupula producing vertigo, nystagmus and nausea[2]

The key characteristics of these two variants of BPPV are summarised in Table 1.

Table 1. Characteristics of BPPV variants.[3] Assessing the Vertical Canals The Dix-Hallpike (DH) test is used to assess BPPV (primarily the vertical canals). This test enables the therapist to identify the side of the lesion and frequently the specific canal involved.
  • Patient is seated with their head turned 45º toward the test side
  • Patient is moved as rapidly (safely) as possible into a supine position with the head extended 20 degrees (CHECK as Bernard says 30 degrees) BPPV CPG
  • Have the patient look at your nose and observe his / her eyes for nystagmus - note the direction of the movement, latency, and duration of nystagmus
  • Wait until the nystagmus stops and then typically proceed into treatment (see below) if indicated (some therapists will slowly sit the patient up in order to assess the other side, but nausea can be a problem)
  • Depending on results, repeat to the other side
Canalithiasis Cupulolithiasis
Latency of onset >1 second before the onset of vertigo and nystagmus No latency
Duration Vertigo and nystagmus lasts < 60 seconds Vertigo and nystagmus persist > 1minute
Direction of nystagmus Characteristic nystagmus depending on which canal is involved Characteristic nystagmus depending on which canal is involved
Fatigability Decreased intensity of vertigo and nystagmus with repeated movement of the patient in provoking positions Decreased intensity of vertigo and nystagmus with repeated movement of the patient in provoking positions

References[edit | edit source]

  1. 1.0 1.1 1.2 von Brevern M, Radtke A, Lezius F, Feldmann M, Ziese T, Lempert T et al. Epidemiology of benign paroxysmal positional vertigo: a population based study. J Neurol Neurosurg Psychiatry. 2007;78(7):710-5.
  2. 2.0 2.1 2.2 2.3 Balatsouras DG, Koukoutsis G, Fassolis A, Moukos A, Apris A. Benign paroxysmal positional vertigo in the elderly: current insights. Clin Interv Aging. 2018;13:2251-66.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 Tonks B. Benign Paroxysmal Positional Vertigo Course. Physioplus, 2021.
  4. Palmeri R, Kumar A. Benign Paroxysmal Positional Vertigo. [Updated 2020 Jun 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470308/
  5. Zhang D, Zhang S, Zhang H, Xu Y, Fu S, Yu M, Ji P. Evaluation of vertebrobasilar artery changes in patients with benign paroxysmal positional vertigo. Neuroreport. 2013;24(13):741-5.
  6. Jeong SH, Kim JS, Shin JW, Kim S, Lee H, Lee AY et al. Decreased serum vitamin D in idiopathic benign paroxysmal positional vertigo. J Neurol. 2013;260(3):832-8.
  7. 7.0 7.1 Chen J, Zhao W, Yue X, Zhang P. Risk factors for the occurrence of benign paroxysmal positional vertigo: A systematic review and meta-analysis. Front Neurol. 2020;11:506.
  8. 8.0 8.1 Kansu L, Aydin E, Gulsahi K. Benign paroxysmal positional vertigo after nonotologic surgery: case series. J Maxillofac Oral Surg. 2015;14(Suppl 1):113-5.
  9. Li S, Wang Z, Liu Y, Cao J, Zheng H, Jing Y et al. Risk factors for the recurrence of benign paroxysmal positional vertigo: a systematic review and meta-analysis. Ear Nose Throat J. 2020:145561320943362.
  10. Bhattacharyya N, Gubbels SP, Schwartz SR, Edlow JA, El-Kashlan H, Fife T et al. Clinical practice guideline: benign paroxysmal positional vertigo (update). Otolaryngol Head Neck Surg. 2017;156(3_suppl):S1-S47.