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==Overview==
It is thought that vertigo is the result of a disruption in the [[vestibular]] [[system]]. It is identified as [[peripheral]] vertigo if the [[lesion]] is in the [[labyrinth]] or [[vestibular nerve]] or [[central]] vertigo if the [[area]] of [[disruption]] originates from the [[brainstem]] or [[cerebellum]].
 
==Pathophysiology==
==Pathophysiology==
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.  
===Physiology===
*[[Vestibular system]] is part of the inner [[ear]]. It is made of the [[utricle]], the [[saccule]], and three [[semicircular canals]].
*The [[vestibular system]] along with the [[visual]] pathway prevents blurring of [[vision]] during[[head]] movement. This is called the [[vestibulo-ocular reflex]].
*Disruption of the [[vestibular system]] can lead to vertigo and associated [[signs]] and [[symptoms]].<ref> "Vertigo"University of Maryland Medical Center. Retrieved 13 November 2015.</ref>
 
===Pathogenesis===
*Disruption in the [[vestibular system]] results in vertigo. The region of disruption could be peripheral ([[labyrinth]], [[vestibular]] [[nerve]]) or central ([[brainstem]], [[cerebellum]]).
*Pathophysiology Behind Common Causes of Vertigo:
:*
{| class="wikitable"
|+
! colspan="2" | Pathophysiology of Common Causes of Vertigo<ref name="Karatas2008">{{cite journal|last1=Karatas|first1=Mehmet|title=Central Vertigo and Dizziness|journal=The Neurologist|volume=14|issue=6|year=2008|pages=355–364|issn=1074-7931|doi=10.1097/NRL.0b013e31817533a3}}</ref>
|-
![[Ménière’s disease]]
|
*Increased [[endolymph]] volume in [[semicircular canals]].
|-
![[Benign paroxysmal positional vertigo]]
|
*Dislodged [[otoliths]] stimulate vestibular sense organ.
|-
![[Acute]] [[labyrinthitis]]
|
*Inflammation of [[labyrinth]]/ [[viral]] or [[bacterial]].
|-
![[Acute vestibular neuritis]]
|
* Inflammation of [[vestibular]] nerve caused by [[viral]] [[infection]].
|-
![[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.
|}
*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]].
 
==Genetics==
Vertigo as a [[symptom]] has no [[genetic]] origin. However, some [[diseases]] associated with vertigo can have [[genetic]] factors involved:
*[[Otosclerosis]]<ref name="pmid15564430">{{cite journal| author=Davies R| title=Bedside neuro-otological examination and interpretation of commonly used investigations. | journal=J Neurol Neurosurg Psychiatry | year= 2004 | volume= 75 Suppl 4 | issue=  | pages= iv32-44 | pmid=15564430 | doi=10.1136/jnnp.2004.054478 | pmc=1765673 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15564430  }} </ref>
*[[Familial]] [[Ménière’s disease]]
*[[Familial]] [[episodic]] [[ataxia]]
*[[Vestibular]] [[migraine]]
*[[Bilateral]] [[vestibular]] [[hypofunction]]


Three neurotransmitters that work peripherally and centrally include [[glutamate]], [[acetylcholine]], and [[GABA]].  
==Associated Conditions==
Conditions associated with vertigo include:<ref name="pmid16445269">{{cite journal| author=Labuguen RH| title=Initial evaluation of vertigo. | journal=Am Fam Physician | year= 2006 | volume= 73 | issue= 2 | pages= 244-51 | pmid=16445269 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16445269  }} </ref>
*[[Vestibular neuritis]]
*[[Herpes simplex virus|HSV]] oticus
*[[Ménière's disease|Meniere disease]],  
*[[Labyrinthine]] [[concussion]]
*[[Perilymph fistula|perilymphatic fistula]]
*[[Semicircular canal]] [[dehiscence]] [[syndrome]]
*[[Vestibular system|vestibular]] [[paroxysmia]]
*[[Cogan syndrome]]
*[[Vestibular schwannoma]]
*[[Otitis media]]
*[[Aminoglycoside]] [[toxicity]]
*[[Recurrent]] [[vestibulopathy]]
*[[Vestibular]] [[migraine]]
*[[Epileptic]] [[vertigo]]
*[[Multiple sclerosis]]
*[[Brain tumor|brain tumors]]
*[[Cerebellar infarction]]/[[hemorrhage]]
*[[Brainstem]] [[ischemia]]
*[[Arnold-Chiari malformation|chiari malformation]]
*[[Parkinson's disease|Parkinson]].


Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate [[chemical synapse|synaptic transmission]] in all 3 neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. GABA is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections between the cerebellar [[Purkinje cells]] and the lateral vestibular nucleus, and the vertical VOR.  
==Gross Pathology==
There are no [[gross]] [[pathology]] findings associated with vertigo.


Three other neurotransmitters work centrally. [[Dopamine]] may accelerate vestibular compensation. [[Norepinephrine]] modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. [[Histamine]] is present only centrally, but its role is unclear. It is known that centrally acting antihistamines modulate the symptoms of motion sickness.  
==Microscopic Pathology==
There are no [[microscopic]] [[histopathological]] characteristic findings associated with vertigo.


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. GABA inhibits central emesis reflexes. [[Serotonin]] is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.
== References ==
== References ==
{{Reflist|2}}
{{Reflist|2}}
{{WH}}
{{WS}}


[[Category:Neurology]]
[[Category:Neurology]]
[[Category:Otolaryngology]]
[[Category:Otolaryngology]]
[[Category:Primary care]]
[[Category:Needs overview]]
[[Category:Needs overview]]
{{WH}}
{{WS}}

Latest revision as of 21:40, 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

It is thought that vertigo is the result of a disruption in the vestibular system. It is identified as peripheral vertigo if the lesion is in the labyrinth or vestibular nerve or central vertigo if the area of disruption originates from the brainstem or cerebellum.

Pathophysiology

Physiology

Pathogenesis

Pathophysiology of Common Causes of Vertigo[2]
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

Vertigo as a symptom has no genetic origin. However, some diseases associated with vertigo can have genetic factors involved:

Associated Conditions

Conditions associated with vertigo include:[7]

Gross Pathology

There are no gross pathology findings associated with vertigo.

Microscopic Pathology

There are no microscopic histopathological characteristic findings associated with vertigo.

References

  1. ↑ "Vertigo"University of Maryland Medical Center. Retrieved 13 November 2015.
  2. ↑ Karatas, Mehmet (2008). "Central Vertigo and Dizziness". The Neurologist. 14 (6): 355–364. doi:10.1097/NRL.0b013e31817533a3. ISSN 1074-7931.
  3. ↑ 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.
  4. ↑ Kuo CH, Pang L, Chang R (2008). "Vertigo - part 2 - management in general practice". Aust Fam Physician. 37 (6): 409–13. PMID 18523693.
  5. ↑ 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.
  6. ↑ Davies R (2004). "Bedside neuro-otological examination and interpretation of commonly used investigations". J Neurol Neurosurg Psychiatry. 75 Suppl 4: iv32–44. doi:10.1136/jnnp.2004.054478. PMC 1765673. PMID 15564430.
  7. ↑ Labuguen RH (2006). "Initial evaluation of vertigo". Am Fam Physician. 73 (2): 244–51. PMID 16445269.

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