Figure 2.

The current potential management approaches that may be considered based on known and proposed mechanisms of BPPV. H, Histamine; VOR, Vestibular ocular reflex; and VSR, Vestibulospinal reflex. Appropriate canalith repositioning maneuvers (CRMs) to remove the otolith from the semicircular canal provide relief from symptoms and positional nystagmus in up to 92% with ≥1 CRMs (36). Vitamin D deficiency is associated with microcirculatory dysfunction (59, 118). The biologically active form of vitamin D is involved in the upregulation of epithelial Ca2+ channel transporters that helps maintain low endolymph Ca²⁺, retain the capacity to dissolve exfoliated otoconia, and prevent abnormal otoconia (55).^† Betahistine increases local vestibular blood flow (56)^† and is involved in the regulation of intracellular calcium, which helps to reduce/delay otoconial detachment (51).^† Betahistine also facilitates central vestibular compensation by enhancing the rebalancing of the neuronal activity of the vestibular nuclei complexes on both sides (50, 64)^† and (67).^‡ Betahistine also improves brain arousal, a crucial factor for functional recovery/behavioral adaptation, through general upregulation of histamine (15, 50, 58).^† Gaze stabilization and vestibular rehabilitation exercises facilitate central compensation and reduce symptoms of dizziness and vertigo (1, 61).^{‡ †}Evidence from animal studies. ^‡Evidence from clinical studies.