Vertigo pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
*Disruption in the [[vestibular system]] results in vertigo. The region of disruption could be peripheral or central. | *Disruption in the [[vestibular system]] results in vertigo. The region of disruption could be peripheral ([[labyrinth]], [[vestibular]] [[nerve]]) or central ([[brainstem]], [[cerebellum]]). | ||
*Pathophysiology of some causes of vertigo: | |||
:* | |||
{| class="wikitable" | |||
|+ | |||
! colspan="2" | Pathophysiology of 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]] | |||
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*Inflammation of [[labyrinth]]/ [[viral]] or [[bacterial]]. | |||
|- | |||
![[Acute vestibular neuritis]] | |||
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* Inflammation of [[vestibular]] nerve caused by [[viral]] [[infection]]. | |||
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![[Cholesteatoma]] | |||
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*Cyst/sac of [[keratin]] debris in middle ear. | |||
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![[Otosclerosis]] | |||
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*Abnormal bone growth in the middle ear. | |||
|- | |||
![[Perilymphatic fistula]] | |||
| | |||
*Abnormal connection between the middle ear and inner ear. | |||
|} | |||
*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> | *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> | ||
Revision as of 19:26, 6 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
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 of some causes of vertigo:
| Pathophysiology of Causes of Vertigo[1] | |
|---|---|
| Ménière’s disease |
|
| Benign paroxysmal positional vertigo |
|
| Acute labyrinthitis | |
| Acute vestibular neuritis |
|
| Cholesteatoma |
|
| Otosclerosis |
|
| Perilymphatic fistula |
|
- 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 for the commissures of the medial vestibular nucleus, the connections between the cerebellar purkinje cells and the lateral vestibular nucleus, and the vertical vestibulo-ocular reflex.
- 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[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.