
Health Dictionary
Reliable, easy-to-read patient information on common medical conditions β written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
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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Physiology
The normal physiology of semicircular canals can be understood as follows:[1]
- One of the most important inner ear structures are horizontal, superior (anterior) and posterior semicircular canals.
- There is an osseous ampullae at the end of each semicircular canal which consist of ampulla crest, the crista ampullaris, and hair cells.
- Semicircular canals are hollow structures with endolymph inside them.
- The movement of endolymph following changing head position will stimulate hair cells to send an impulse to the brain, determining the head position.
- The horizontal semicircular canal detects the head movement in the transverse plane (head turning to right and left).
- The superior (anterior) semicircular canal detects head rotational movement in the sagittal plane (head nodding).
- The posterior semicircular canal detects head rotational movement in the coronal plane (head touching the shoulders)
Pathogenesis
- It is understood that BPPV is the result of free floating calcium carbonate crystal formation (canalolithiasis) inside the semicircular canals.[2]
- These debris are normally attached to the membrane of utriculus, a gravity-sensitive structures in the inner ear.
- Movement of these otoconia with head movement will result in inappropriate stimulation of hair cells following movement of the endolymph.
- The inappropriate impulses to the brain will result in false sensation of spinning.
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
Gross Pathology
Gross Pathology
- there is no gross pathology findings with BPPV.
Microscopic Pathology
Microscopic Pathology
- On microscopic histopathological analysis, crystals with combination of a gelatinous matrix and calcium carbonate are characteristic findings of otoconia in BPPV.[2]
References
References
- β Chester JB (July 1991). “Whiplash, postural control, and the inner ear”. Spine. 16 (7): 716β20. PMIDΒ 1925743.
- β 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.
- β Gizzi M, Ayyagari S, Khattar V (November 1998). “The familial incidence of benign paroxysmal positional vertigo”. Acta Otolaryngol. 118 (6): 774β7. PMIDΒ 9870618.
- β Gizzi MS, Peddareddygari LR, Grewal RP (2015). “A familial form of benign paroxysmal positional vertigo maps to chromosome 15”. Int. J. Neurosci. 125 (8): 593β6. doi:10.3109/00207454.2014.953157. PMIDΒ 25135283.
- β Cohen, Helen S.; Kimball, Kay T.; Stewart, Michael G. (2004). “Benign Paroxysmal Positional Vertigo and Comorbid Conditions”. ORL. 66 (1): 11β15. doi:10.1159/000077227. ISSNΒ 0301-1569.
- β 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.


