The Role of Calcium in the Pathophysiology of Vertigo and its Treatment with Flunarizine

Abstract

Vertigo is a complicated symptom caused mainly by a dysfunctional vestibular system, either central or peripheral. Benign paroxysmal positional vertigo (BPPV), vestibular migraine (VM) and posterior circulation ischemia (PCI) are the three common causes of vertigo, all of which are related to abnormal calcium function. As a calcium antagonist, flunarizine has a multitude of mechanisms of action in vertigo treatment. The drug exerts neuroprotective effects on brain, endothelial and hair cells of the inner ear; reduces angiospasm, normalizes blood viscosity, improves the circulation of blood flow to the brain and inner ear; protects and restores injured neuronal or vascular cells from hypoxic-ischaemic damage; accelerates vestibular function recovery and inhibits cortical spreading depression (CSD). Many studies showed flunarizine to be effective especially against vertiginous attacks resulting from BPPV, VM and PCI with few serious side effects, probably due to its multiple mechanisms of action.