Vertigo pathophysiology

	Vertigo Microchapters
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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:

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.^[1]
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 only present centrally and its role is unclear. Centrally acting antihistamines are noted to regulate the symptoms of motion sickness and acute vertigo.^[2].
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^[3].
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).

Pathophysiology Behind Causes of Vertigo:


Pathophysiology of Causes of Vertigo^[4]
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

↑ 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.
↑ 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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[Angelaki2004-1] 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.

[pmid18523693-2] Kuo CH, Pang L, Chang R (2008). "Vertigo - part 2 - management in general practice". Aust Fam Physician. 37 (6): 409–13. PMID 18523693.

[Kerber2009-3] 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.

[Karatas2008-4] 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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