Vertigo pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate [[chemical synapse|synaptic transmission]] in all 3 neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. 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 VOR. | *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 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. | **[[glutamate]], [[acetylcholine]], and [[GABA]]. | ||
**Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate [[chemical synapse|synaptic transmission]] in all 3 neurons of the VOR arc. | |||
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. | **Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. | ||
**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 VOR. | |||
*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. | |||
== References == | == References == | ||
Revision as of 18:56, 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, acetylcholine, and GABA.
- Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate synaptic transmission in all 3 neurons of the VOR arc.
- Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses.
- 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 VOR.
- 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.