Vertigo pathophysiology
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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
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] | |
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| Ménière’s disease |
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| Benign paroxysmal positional vertigo |
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| Acute labyrinthitis | |
| Acute vestibular neuritis |
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| Cholesteatoma |
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| Otosclerosis |
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| Perilymphatic fistula |
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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.
Genetics
Vertigo as a symptom has no genetic origin. However, some diseases associated with vertigo can have genetic factors involved:
- Familial Ménière’s disease
- Familial episodic ataxia
- Vestibular migraine
- Bilateral vestibular hypofunction
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.
- ↑ 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.