Vertigo pathophysiology: Difference between revisions
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**[[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. | **[[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]]. | **[[Acetylcholine]] appears to function as an excitatory [[neurotransmitter]]. | ||
**[[GABA]] is thought to be inhibitory | **[[GABA]] is thought to be inhibitory. | ||
*Three other [[neurotransmitters]] work centrally. | *Three other [[neurotransmitters]] work centrally. | ||
**[[Dopamine]] may accelerate vestibular compensation. | **[[Dopamine]] may accelerate vestibular compensation. | ||
**[[Norepinephrine]] | **[[Norepinephrine]] regulates the strength of central responses to vestibular stimulation and mediates compensation. | ||
**[[Histamine]] is present only centrally, but its role is unclear. It is known that centrally acting [[antihistamines]] | **[[Histamine]] is present only centrally, but its role is unclear. It is known that centrally acting [[antihistamines]] regulates 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. | *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>. | *[[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]]. | *[[GABA]] inhibits central [[emesis]] [[reflexes]]. | ||
*[[Serotonin]] is involved in central and peripheral control of emesis but has little influence on vertigo and [[motion sickness]]. | *[[Serotonin]] is involved in central and peripheral control of [[emesis]] but has little influence on vertigo and [[motion sickness]]. | ||
== References == | == References == | ||
Revision as of 02:02, 7 January 2021
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Vertigo Microchapters |
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Vertigo pathophysiology On the Web |
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Risk calculators and risk factors for Vertigo pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]
Overview
Disruption in the vestibular system results in vertigo. The region of disruption could be peripheral or central.
Pathophysiology
- 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 |
|
| Benign paroxysmal positional vertigo |
|
| Acute labyrinthitis | |
| Acute vestibular neuritis |
|
| Cholesteatoma |
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| Otosclerosis |
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| Perilymphatic fistula |
|
Neurochemistry of Vertigo:
- The neurochemistry of vertigo includes 6 primary neurotransmitters that have been identified between the 3-neuron arc that drives the vestibulo-ocular reflex (VOR). Many others play more minor roles.[2]
- Three neurotransmitters that work peripherally and centrally include:
- Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate 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 present only centrally, but its role is unclear. It is known that centrally acting antihistamines regulates the symptoms of motion sickness and acute vertigo.[3].
- 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[4].
- 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
- ↑ Karatas, Mehmet (2008). "Central Vertigo and Dizziness". The Neurologist. 14 (6): 355–364. doi:10.1097/NRL.0b013e31817533a3. ISSN 1074-7931.
- ↑ 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.
- ↑ Kuo CH, Pang L, Chang R (2008). "Vertigo - part 2 - management in general practice". Aust Fam Physician. 37 (6): 409–13. PMID 18523693.
- ↑ 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.