What is the pathophysiology of migraine-associated vertigo?

Updated: Jun 17, 2021
  • Author: Aaron G Benson, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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In 1992, Cutrer and Baloh developed the most commonly accepted theory regarding the pathophysiology of migraine-associated vertigo. [18] They proposed that episodes of dizziness of a duration similar to that of a migraine aura (< 60min) that are time-locked with the headache most likely have the same pathophysiologic mechanism (eg, spreading wave of depression) as other aura phenomena.

According to the spreading depression theory, some type of stimulus (eg, chemical, mechanical) results in a transient wave front that suppresses central neuronal activity. This depression spreads in all directions from its site of origin. Neuronal depression is accompanied by large ion fluxes, including increases in extracellular potassium (K+) and decreases in extracellular calcium (Ca++). These changes result in a reduction in cerebral blood flow in the areas of spreading depression. However, most patients with migraine-associated vertigo have dizziness independently of the headache.

Cutrer and Baloh suggested that when the dizziness is unrelated to the headache, the dizziness results from the release of neuropeptides (ie, neuropeptide substance P, neurokinin A, calcitonin gene–related peptide [CGRP]). [18] Neuropeptide release has an excitatory effect on the baseline firing rate of the sensory epithelium of the inner ear, as well as on the vestibular nuclei in the pons.

Asymmetrical neuropeptide release results in the sensation of vertigo. When neuropeptide release is symmetrical, the patient feels an increased sensitivity to motion due to an increased vestibular firing rate during head movements.

Cutrer and Baloh also proposed that CGRP and other neuropeptides may produce a prolonged, hormonelike effect as these peptides diffuse into the extracellular fluid. [18] This may explain the prolonged symptoms in some patients with migraine-associated vertigo, as well as the typical progression of persistent spontaneous vertigo, followed by benign positional vertigo and then motion sensitivity.

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