Vertigo pathophysiology

It is thought that vertigo is the result of a disruption in the vestibular system. It is identified as peripheral vertigo if the lesion is in the labyrinth or vestibular nerve or central vertigo if the area of disruption originates from the brainstem or cerebellum.

• Vestibular system is part of the inner ear. It is made of the utricle, the saccule, and three semicircular canals.
• The vestibular system along with the visual pathway prevents blurring of vision duringhead movement. This is called the vestibulo-ocular reflex.
• Disruption of the vestibular system can lead to vertigo and associated signs and symptoms.^[1]

• Disruption in the vestibular system results in vertigo. The region of disruption could be peripheral (labyrinth, vestibular nerve) or central (brainstem, cerebellum).
• Pathophysiology Behind Common Causes of Vertigo:

• 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.^[3]
  • 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.
  • Three other neurotransmitters work centrally.
    • Dopamine may accelerate vestibular compensation.
    • Norepinephrine regulates the strength of central responses to vestibular stimulation and mediates compensation.
    • Histamine is only present centrally and its role is unclear. Centrally acting antihistamines are noted to regulate the symptoms of motion sickness and acute vertigo.^[4].
  • 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^[5].
  • GABA inhibits central emesis reflexes.
  • Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.

Vertigo as a symptom has no genetic origin. However, some diseases associated with vertigo can have genetic factors involved:

• Otosclerosis^[6]
• Familial Ménière’s disease
• Familial episodic ataxia
• Vestibular migraine
• Bilateral vestibular hypofunction

Conditions associated with vertigo include:^[7]

• Vestibular neuritis
• HSV oticus
• Meniere disease,
• Labyrinthine concussion
• perilymphatic fistula
• Semicircular canal dehiscence syndrome
• vestibular paroxysmia
• Cogan syndrome
• Vestibular schwannoma
• Otitis media
• Aminoglycoside toxicity
• Recurrent vestibulopathy
• Vestibular migraine
• Epileptic vertigo
• Multiple sclerosis
• brain tumors
• Cerebellar infarction/hemorrhage
• Brainstem ischemia
• chiari malformation
• Parkinson.

There are no gross pathology findings associated with vertigo.

There are no microscopic histopathological characteristic findings associated with vertigo.

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