Benign paroxysmal positional vertigo pathophysiology: Difference between revisions

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==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
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 cell|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.
 
OR
 
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
 
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Pathophysiology==
==Pathophysiology==
{| align="right"
|
[[File:Blausen 0329 EarAnatomy InternalEar.png|200px|thumb|left|https://en.wikipedia.org/wiki/File:Blausen_0329_EarAnatomy_InternalEar.png]]
|-
|
[[File:Vestibular system's semicircular canal- a cross-section.jpg|200px|thumb|left|https://en.wikipedia.org/wiki/File:Vestibular_system%27s_semicircular_canal-_a_cross-section.jpg]]
|}
===Physiology===
===Physiology===
The normal physiology of semicircular canals can be understood as follows:
The normal [[physiology]] of [[semicircular canals]] can be understood as follows:<ref name="pmid1925743">{{cite journal |vauthors=Chester JB |title=Whiplash, postural control, and the inner ear |journal=Spine |volume=16 |issue=7 |pages=716–20 |date=July 1991 |pmid=1925743 |doi= |url=}}</ref>
* One of the most important inner ear structures are horizontal, superior (anterior) and posterior semicircular canals.  
* One of the most important [[inner ear]] structures are [[Horizontal semicircular canal|horizontal]], [[Superior semicircular canal|superior]] (anterior) and [[Posterior semicircular canal|posterior semicircular canals]].  
* There is an osseous ampulla at the end of each semicircular canal which consist of ampulla crest, the crista ampullaris, and hair cells.  
* There is an [[osseous ampullae]] at the end of each [[semicircular canal]] which consist of ampulla crest, the [[crista ampullaris]], and [[Hair cell|hair cells]].  
* Semicircular canals are hollow structures with endolymph inside them.  
* [[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 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 [[horizontal semicircular canal]] detects the head movement in the [[transverse plane]] ([[Head-related transfer function|head]] turning to right and left).  
* The superior (anterior) semicircular canal detects head rotational movement in the sagittal plane (head nodding).  
* The [[Superior semicircular canal|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)
* The [[posterior semicircular canal]] detects [[head]] [[rotational]] movement in the [[coronal plane]] ([[head]] touching the [[shoulders]])


===Pathogenesis===
===Pathogenesis===
*The exact pathogenesis of [disease name] is not completely understood.
*It is understood that BPPV is the result of free floating [[calcium carbonate]] crystal formation ([[canalolithiasis]]) inside the [[semicircular canals]].<ref name="pmid21808648">{{cite journal |vauthors=Hornibrook J |title=Benign Paroxysmal Positional Vertigo (BPPV): History, Pathophysiology, Office Treatment and Future Directions |journal=Int J Otolaryngol |volume=2011 |issue= |pages=835671 |date=2011 |pmid=21808648 |pmc=3144715 |doi=10.1155/2011/835671 |url=}}</ref>
OR
*These debris are normally attached to the membrane of utriculus, a gravity-sensitive structures in the [[inner ear]].  
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*Movement of these [[otoconia]] with [[head]] [[movement]] will result in inappropriate stimulation of [[Hair cell|hair cells]] following movement of the [[endolymph]].  
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*The inappropriate impulses to the [[brain]] will result in false [[sensation]] of spinning.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.


*
==Genetics==
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
* The development of idiopathic BPPV may be the result of multiple [[genetic mutations]].<ref name="pmid9870618">{{cite journal |vauthors=Gizzi M, Ayyagari S, Khattar V |title=The familial incidence of benign paroxysmal positional vertigo |journal=Acta Otolaryngol. |volume=118 |issue=6 |pages=774–7 |date=November 1998 |pmid=9870618 |doi= |url=}}</ref><ref name="pmid25135283">{{cite journal |vauthors=Gizzi MS, Peddareddygari LR, Grewal RP |title=A familial form of benign paroxysmal positional vertigo maps to chromosome 15 |journal=Int. J. Neurosci. |volume=125 |issue=8 |pages=593–6 |date=2015 |pmid=25135283 |doi=10.3109/00207454.2014.953157 |url=}}</ref>
 
* 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.
OR
* 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.
 
Genes involved in the pathogenesis of [disease name] include:
*[Gene1]
*[Gene2]
*[Gene3]
 
OR
 
The development of [disease name] is the result of multiple genetic mutations such as:
 
*[Mutation 1]
*[Mutation 2]
*[Mutation 3]


==Associated Conditions==
==Associated Conditions==
Conditions associated with [disease name] include:
Conditions associated with BPPV include:<ref name="CohenKimball2004">{{cite journal|last1=Cohen|first1=Helen S.|last2=Kimball|first2=Kay T.|last3=Stewart|first3=Michael G.|title=Benign Paroxysmal Positional Vertigo and Comorbid Conditions|journal=ORL|volume=66|issue=1|year=2004|pages=11–15|issn=0301-1569|doi=10.1159/000077227}}</ref><ref name="ChuLiu2015">{{cite journal|last1=Chu|first1=Chia-Huei|last2=Liu|first2=Chia-Jen|last3=Lin|first3=Liang-Yu|last4=Chen|first4=Tzeng-Ji|last5=Wang|first5=Shuu-Jiun|title=Migraine is associated with an increased risk for benign paroxysmal positional vertigo: a nationwide population-based study|journal=The Journal of Headache and Pain|volume=16|issue=1|year=2015|issn=1129-2369|doi=10.1186/s10194-015-0547-z}}</ref>


*[Condition 1]
*[[Migraine headache]]
*[Condition 2]
*[[Diabetes mellitus]]
*[Condition 3]
*[[Ménière's disease|Meniere disease]]


==Gross Pathology==
==Gross Pathology==
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
* there is no gross pathology findings with BPPV.


==Microscopic Pathology==
==Microscopic Pathology==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
* On microscopic [[histopathological]] analysis, crystals with combination of a gelatinous matrix and [[calcium carbonate]] are characteristic findings of [[otoconia]] in BPPV.<ref name="pmid21808648" />


==References==
==References==

Latest revision as of 19:25, 22 February 2019

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

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

https://en.wikipedia.org/wiki/File:Blausen_0329_EarAnatomy_InternalEar.png
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

  • 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

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

Gross Pathology

  • there is no gross pathology findings with BPPV.

Microscopic Pathology

References

  1. Chester JB (July 1991). "Whiplash, postural control, and the inner ear". Spine. 16 (7): 716–20. PMID 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. PMC 3144715. PMID 21808648.
  3. Gizzi M, Ayyagari S, Khattar V (November 1998). "The familial incidence of benign paroxysmal positional vertigo". Acta Otolaryngol. 118 (6): 774–7. PMID 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. PMID 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. ISSN 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. ISSN 1129-2369.

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