Lightheadedness and vertigo pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Lightheadedness and vertigo}} | {{Lightheadedness and vertigo}} | ||
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{{CMG}} | {{CMG}} | ||
==Pathophysiology== | ==Pathophysiology== | ||
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 [[glutamate]], [[acetylcholine]], and [[GABA]]. | 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 [[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. | :*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. | |||
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. | 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]]. | 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== | ||
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Latest revision as of 22:30, 29 July 2020
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Lightheadedness and vertigo Microchapters |
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Differentiating Lightheadedness and Vertigo from Other Symptoms |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
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.