Vertigo pathophysiology: Difference between revisions

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Revision as of 17:39, 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]

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.

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.

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.

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 only present centrally and its role is unclear. Centrally acting antihistamines are noted to regulate 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.

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

Conditions associated with vertigo include:^[5]

There are no gross pathology findings associated with vertigo.

There are no microscopic histopathological characteristic findings associated with vertigo.

↑ 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.
↑ Labuguen RH (2006). "Initial evaluation of vertigo". Am Fam Physician. 73 (2): 244–51. PMID 16445269.

@@ Line 96: / Line 96: @@
 ==Microscopic Pathology==
-On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
+There are no [[microscopic]] [[histopathological]] characteristic findings associated with vertigo.
 == References ==