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__NOTOC__
__NOTOC__
{{Vertigo}}
{{Vertigo}}
{{CMG}} {{AE}} {{ZMalik}}
{{CMG}}; {{AE}} {{ZMalik}}
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
 
OR
 
It is thought that vertigo 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].


==Overview==
OR
Disruption in the [[vestibular system]] results in vertigo. The region of disruption could be peripheral or central.
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Pathophysiology==
==Pathophysiology==
===Physiology===
The normal physiology of [name of process] can be understood as follows:
'''Neurochemistry of Vertigo:'''
*The neurochemistry of vertigo includes 6 primary [[neurotransmitter]]s that have been identified between the 3-neuron arc that drives the [[vestibulo-ocular reflex]] (VOR). Many others play more minor roles.<ref name="Angelaki2004">{{cite journal|last1=Angelaki|first1=Dora E.|title=Eyes on Target: What Neurons Must do for the Vestibuloocular Reflex During Linear Motion|journal=Journal of Neurophysiology|volume=92|issue=1|year=2004|pages=20–35|issn=0022-3077|doi=10.1152/jn.00047.2004}}</ref>
*Three [[neurotransmitters]] that work peripherally and centrally include:
**[[Glutamate]] maintains the resting discharge of the central vestibular [[neurons]], and may modulate [[chemical synapse|synaptic transmission]] in all 3 neurons of the [[vestibulo-ocular reflex]] system.
**[[Acetylcholine]] appears to function as an excitatory [[neurotransmitter]].
**[[GABA]] is thought to be inhibitory.
*Three other [[neurotransmitters]] work centrally.
**[[Dopamine]] may accelerate vestibular compensation.
**[[Norepinephrine]] regulates the strength of central responses to vestibular stimulation and mediates compensation.
**[[Histamine]] is only present centrally and its role is unclear. Centrally acting [[antihistamines]] are noted to regulate the symptoms of [[motion sickness]] and [[acute]] vertigo.<ref name="pmid18523693">{{cite journal| author=Kuo CH, Pang L, Chang R| title=Vertigo - part 2 - management in general practice. | journal=Aust Fam Physician | year= 2008 | volume= 37 | issue= 6 | pages= 409-13 | pmid=18523693 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18523693  }} </ref>.
*The [[neurochemistry]] of [[emesis]] overlaps with the [[neurochemistry]] of [[motion sickness]] and vertigo.
*[[Acetylcholine]], [[histamine]], and [[dopamine]] are [[excitatory]] [[neurotransmitters]], working centrally on the control of [[emesis]]<ref name="Kerber2009">{{cite journal|last1=Kerber|first1=Kevin A.|title=Vertigo and Dizziness in the Emergency Department|journal=Emergency Medicine Clinics of North America|volume=27|issue=1|year=2009|pages=39–50|issn=07338627|doi=10.1016/j.emc.2008.09.002}}</ref>.
*[[GABA]] inhibits central [[emesis]] [[reflexes]].
*[[Serotonin]] is involved in central and peripheral control of [[emesis]] but has little influence on vertigo and [[motion sickness]].
===Pathogenesis===
*Disruption in the [[vestibular system]] results in vertigo. The region of disruption could be peripheral ([[labyrinth]], [[vestibular]] [[nerve]]) or central ([[brainstem]], [[cerebellum]]).
*Disruption in the [[vestibular system]] results in vertigo. The region of disruption could be peripheral ([[labyrinth]], [[vestibular]] [[nerve]]) or central ([[brainstem]], [[cerebellum]]).
'''Pathophysiology Behind Causes of Vertigo:'''
'''Pathophysiology Behind Causes of Vertigo:'''
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'''Neurochemistry of Vertigo:'''
 
*The neurochemistry of vertigo includes 6 primary [[neurotransmitter]]s that have been identified between the 3-neuron arc that drives the [[vestibulo-ocular reflex]] (VOR). Many others play more minor roles.<ref name="Angelaki2004">{{cite journal|last1=Angelaki|first1=Dora E.|title=Eyes on Target: What Neurons Must do for the Vestibuloocular Reflex During Linear Motion|journal=Journal of Neurophysiology|volume=92|issue=1|year=2004|pages=20–35|issn=0022-3077|doi=10.1152/jn.00047.2004}}</ref>
==Genetics==
*Three [[neurotransmitters]] that work peripherally and centrally include:
[Disease name] is transmitted in [mode of genetic transmission] pattern.
**[[Glutamate]] maintains the resting discharge of the central vestibular [[neurons]], and may modulate [[chemical synapse|synaptic transmission]] in all 3 neurons of the [[vestibulo-ocular reflex]] system.
 
**[[Acetylcholine]] appears to function as an excitatory [[neurotransmitter]].
OR
**[[GABA]] is thought to be inhibitory.
 
*Three other [[neurotransmitters]] work centrally.
Genes involved in the pathogenesis of [disease name] include:
**[[Dopamine]] may accelerate vestibular compensation.
*[Gene1]
**[[Norepinephrine]] regulates the strength of central responses to vestibular stimulation and mediates compensation.
*[Gene2]
**[[Histamine]] is only present centrally and its role is unclear. Centrally acting [[antihistamines]] are noted to regulate the symptoms of [[motion sickness]] and [[acute]] vertigo.<ref name="pmid18523693">{{cite journal| author=Kuo CH, Pang L, Chang R| title=Vertigo - part 2 - management in general practice. | journal=Aust Fam Physician | year= 2008 | volume= 37 | issue= 6 | pages= 409-13 | pmid=18523693 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18523693  }} </ref>.
*[Gene3]
*The [[neurochemistry]] of [[emesis]] overlaps with the [[neurochemistry]] of [[motion sickness]] and vertigo.
 
*[[Acetylcholine]], [[histamine]], and [[dopamine]] are [[excitatory]] [[neurotransmitters]], working centrally on the control of [[emesis]]<ref name="Kerber2009">{{cite journal|last1=Kerber|first1=Kevin A.|title=Vertigo and Dizziness in the Emergency Department|journal=Emergency Medicine Clinics of North America|volume=27|issue=1|year=2009|pages=39–50|issn=07338627|doi=10.1016/j.emc.2008.09.002}}</ref>.
OR
*[[GABA]] inhibits central [[emesis]] [[reflexes]].
 
*[[Serotonin]] is involved in central and peripheral control of [[emesis]] but has little influence on vertigo and [[motion sickness]].
The development of [disease name] is the result of multiple genetic mutations such as:
 
*[Mutation 1]
*[Mutation 2]
*[Mutation 3]
 
==Associated Conditions==
Conditions associated with [disease name] include:
 
*[Condition 1]
*[Condition 2]
*[Condition 3]
 
==Gross Pathology==
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
==Microscopic Pathology==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
 
 


== References ==
== References ==

Revision as of 02:15, 21 January 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Overview

The exact pathogenesis of [disease name] is not fully understood.

OR

It is thought that vertigo 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

Physiology

The normal physiology of [name of process] can be understood as follows: Neurochemistry of Vertigo:


Pathogenesis

Pathophysiology Behind Causes of Vertigo:

Pathophysiology of Causes of Vertigo[4]
Ménière’s disease
Benign paroxysmal positional vertigo
  • Dislodged otoliths stimulate vestibular sense organ.
Acute labyrinthitis
Acute vestibular neuritis
Cholesteatoma
  • Cyst/sac of keratin debris in middle ear.
Otosclerosis
  • Abnormal bone growth in the middle ear.
Perilymphatic fistula
  • Abnormal connection between the middle ear and inner ear.


Genetics

[Disease name] is transmitted in [mode of genetic transmission] pattern.

OR

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

Conditions associated with [disease name] include:

  • [Condition 1]
  • [Condition 2]
  • [Condition 3]

Gross Pathology

On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].


References

  1. ↑ Angelaki, Dora E. (2004). "Eyes on Target: What Neurons Must do for the Vestibuloocular Reflex During Linear Motion". Journal of Neurophysiology. 92 (1): 20–35. doi:10.1152/jn.00047.2004. ISSN 0022-3077.
  2. ↑ Kuo CH, Pang L, Chang R (2008). "Vertigo - part 2 - management in general practice". Aust Fam Physician. 37 (6): 409–13. PMID 18523693.
  3. ↑ Kerber, Kevin A. (2009). "Vertigo and Dizziness in the Emergency Department". Emergency Medicine Clinics of North America. 27 (1): 39–50. doi:10.1016/j.emc.2008.09.002. ISSN 0733-8627.
  4. ↑ Karatas, Mehmet (2008). "Central Vertigo and Dizziness". The Neurologist. 14 (6): 355–364. doi:10.1097/NRL.0b013e31817533a3. ISSN 1074-7931.

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