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

Disruption in the vestibular system results in vertigo. The region of disruption could be peripheral or central.

Pathophysiology

• 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
Ménière’s disease	Increased endolymph volume in semicircular canals.
Benign paroxysmal positional vertigo	Dislodged otoliths stimulate vestibular sense organ.
Acute labyrinthitis	Inflammation of labyrinth/ viral or bacterial.
Acute vestibular neuritis	Inflammation of vestibular nerve caused by viral infection.
Cholesteatoma	Cyst/sac of keratin debris in middle ear.
Otosclerosis	Abnormal bone growth in the middle ear.
Perilymphatic fistula	Abnormal connection between the middle ear and inner ear.

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.
• 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.