Vertigo pathophysiology: Difference between revisions

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Revision as of 17:26, 21 January 2021

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

The normal physiology of vertigo can be understood on the basis of understanding the vestibulo-ocular reflex:

This reflex acts through the activation of vestibular system in order to stabilize gaze during head movement.

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 Causes of Vertigo:


Pathophysiology of Causes of Vertigo^[1]
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.

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

↑ Karatas, Mehmet (2008). "Central Vertigo and Dizziness". The Neurologist. 14 (6): 355–364. doi:10.1097/NRL.0b013e31817533a3. ISSN 1074-7931.

Template:WH Template:WS

[Karatas2008-1] Karatas, Mehmet (2008). "Central Vertigo and Dizziness". The Neurologist. 14 (6): 355–364. doi:10.1097/NRL.0b013e31817533a3. ISSN 1074-7931.

[1]

@@ Line 7: / Line 7: @@
 ==Pathophysiology==
 ===Physiology===
-The normal physiology of [name of process] can be understood as follows:
+The normal physiology of vertigo can be understood on the basis of understanding the [[vestibulo-ocular reflex]]:
-'''Neurochemistry of Vertigo:'''
+*This [[reflex]] acts through the [[activation]] of [[vestibular system]] in order to [[stabilize]] [[gaze]] during [[head]] movement.
-*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===