Recurrent Benign Paroxysmal Positional Vertigo: A Microcirculatory and Metabolic Hypothesis of Otoconial Degeneration Supported by Preliminary Clinical Observations

Background: Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular disorder, accounting for approximately 20% - 30% of patients presenting with dizziness in specialized clinics. Although canalith repositioning maneuvers achieve symptom resolution in most cases, recurrence remains a significant clinical challenge, affecting approximately 15% - 30% of patients within the first year and up to 50% during long-term follow-up. Current pathogenetic models primarily attribute recurrent BPPV to age-related degeneration of the otoconial membrane; however, they do not fully explain the strong association between recurrent disease and systemic vascular and metabolic disorders. Objective: To propose a novel pathophysiological hypothesis linking labyrinthine microcirculatory dysfunction, chronic tissue hypoxia, extracellular acidification, and degeneration of the otoconial membrane, and to describe preliminary clinical observations obtained following adjunctive oral alkalinizing mineral supplementation in patients with recurrent BPPV. Methods: A preliminary observational study was performed in approximately twenty patients with recurrent BPPV treated with standard canalith repositioning maneuvers followed by oral alkalinizing mineral supplementation (Alkimo HP？, one sachet twice daily). Clinical outcomes were evaluated according to recurrence of positional vertigo during follow-up and subjective improvement in balance and quality of life. Four representative clinical cases are presented. Results: During the observation period, all patients reported subjective clinical improvement after initiation of supplementation. Several patients remained free of recurrent positional vertigo throughout follow-up, whereas recurrence was observed in some patients after treatment discontinuation. The representative clinical cases consistently demonstrated a reduction in recurrence frequency associated with improved postural stability and quality of life. Conclusions: Microvascular impairment may represent the common biological pathway linking many recognized risk factors for recurrent BPPV, including aging, hypertension, diabetes mellitus, hyperlipidemia, migraine, and chronic sleep disorders. We hypothesize that chronic labyrinthine hypoperfusion induces activation of hypoxia-responsive metabolic pathways, leading to extracellular acidification, alteration of the otoconial extracellular matrix, and increased susceptibility to otoconial detachment. Although preliminary clinical observations are encouraging,