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Benign paroxysmal positional vertigo pathophysiology

Introduction

Overview

Overview

It is understood that BPPV is the result of free floating calcium carbonate crystal formation (canalolithiasis) inside the semicircular canals. Movement of these otoconia with head movement will result in inappropriate stimulation of hair cells following movement of the endolymph. In some studies it was demonstrated that people with BPPV in their first degree family are at more risk of development of the disease themselves. One of the theories behind the familial aspect of BPPV is that these families might have less adhesive gelatinous matrix of the utricular macula which predisposed them to BPPV. On microscopic histopathological analysis, crystals with combination of a gelatinous matrix and calcium carbonate are characteristic findings of otoconia in BPPV.

Pathophysiology

Pathophysiology

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https://en.wikipedia.org/wiki/File:Vestibular_system%27s_semicircular_canal-_a_cross-section.jpg

Physiology

The normal physiology of semicircular canals can be understood as follows:[1]

Pathogenesis

    Genetics

    Genetics

    • The development of idiopathic BPPV may be the result of multiple genetic mutations.[3][4]
    • In some studies it was demonstrated that people with BPPV in their first degree family are at more risk of development of the disease themselves.
    • One of the theories behind the familial aspect of BPPV is that these families might have less adhesive gelatinous matrix of the utricular macula which predisposed them to BPPV.
    Associated Conditions

    Associated Conditions

    Conditions associated with BPPV include:[5][6]

    Gross Pathology

    Gross Pathology

    • there is no gross pathology findings with BPPV.
    Microscopic Pathology

    Microscopic Pathology

    References

    References

    1. ↑ Chester JB (July 1991). “Whiplash, postural control, and the inner ear”. Spine. 16 (7): 716–20. PMIDΒ 1925743.
    2. ↑ 2.0 2.1 Hornibrook J (2011). “Benign Paroxysmal Positional Vertigo (BPPV): History, Pathophysiology, Office Treatment and Future Directions”. Int J Otolaryngol. 2011: 835671. doi:10.1155/2011/835671. PMCΒ 3144715. PMIDΒ 21808648.
    3. ↑ Gizzi M, Ayyagari S, Khattar V (November 1998). “The familial incidence of benign paroxysmal positional vertigo”. Acta Otolaryngol. 118 (6): 774–7. PMIDΒ 9870618.
    4. ↑ Gizzi MS, Peddareddygari LR, Grewal RP (2015). “A familial form of benign paroxysmal positional vertigo maps to chromosome 15”. Int. J. Neurosci. 125 (8): 593–6. doi:10.3109/00207454.2014.953157. PMIDΒ 25135283.
    5. ↑ Cohen, Helen S.; Kimball, Kay T.; Stewart, Michael G. (2004). “Benign Paroxysmal Positional Vertigo and Comorbid Conditions”. ORL. 66 (1): 11–15. doi:10.1159/000077227. ISSNΒ 0301-1569.
    6. ↑ Chu, Chia-Huei; Liu, Chia-Jen; Lin, Liang-Yu; Chen, Tzeng-Ji; Wang, Shuu-Jiun (2015). “Migraine is associated with an increased risk for benign paroxysmal positional vertigo: a nationwide population-based study”. The Journal of Headache and Pain. 16 (1). doi:10.1186/s10194-015-0547-z. ISSNΒ 1129-2369.

    Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.