Vertigo pathophysiology
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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.