Vertigo pathophysiology: Difference between revisions
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*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. | *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. | ||
*Three [[neurotransmitters]] that work peripherally and centrally include: | |||
*Three neurotransmitters that work peripherally and centrally include: | |||
**[[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]]. | ||
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**[[Norepinephrine]] modulates the intensity of central reactions to vestibular stimulation and facilitates 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. | **[[Histamine]] is present only centrally, but its role is unclear. It is known that centrally acting [[antihistamines]] modulate the symptoms of motion sickness. | ||
*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]]. | *[[Acetylcholine]], [[histamine]], and [[dopamine]] are [[excitatory]] [[neurotransmitters]], working centrally on the control of [[emesis]]. | ||
*[[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 19:00, 6 January 2021
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Vertigo Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Vertigo pathophysiology On the Web |
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American Roentgen Ray Society Images of Vertigo pathophysiology |
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Risk calculators and risk factors for Vertigo pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
- 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.
- 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.
- 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.
- GABA inhibits central emesis reflexes.
- Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.