Mechanisms of Vestibular System Damage in Diabetes Mellitus: Implications for Benign Paroxysmal Positional Vertigo Pathogenesis and Recurrence.

BACKGROUND

Diabetes mellitus (DM) is increasingly recognized as an independent risk factor for falls and balance disorders in elderly populations. While diabetic neuropathy and retinopathy are well-established complications, the role of vestibular system dysfunction has been underappreciated. Benign paroxysmal positional vertigo (BPPV), the most common peripheral vestibular disorder, demonstrates markedly increased prevalence and recurrence in diabetic patients, yet the underlying mechanisms remain incompletely understood. Therefore, the aim of the present review was to investigate the mechanism and pathophysiology of vestibular system damage in diabetes and its association with increased risk of BPPV recurrence.

METHODS

We conducted a narrative review by searching PubMed, Scopus, and Web of Science databases using keywords related to diabetes mellitus, hyperglycemia, vestibular system, and BPPV. Our initial search yielded 847 articles; after screening and manual reference review, 12 studies (4,937 total participants) meeting inclusion criteria were selected for detailed analysis. Study designs included histopathological analyses, cross-sectional studies, retrospective cohorts, and one randomized controlled trial.

RESULTS

Evidence identifies four convergent mechanisms: selective saccular hair cell loss, nerve demyelination, disrupted calcium/vitamin D metabolism causing otoconia fragility, and microangiopathy. DM independently predicts BPPV onset (OR 1.5-2.1) and recurrence (>50% vs. 27%), with VEMP latencies correlating with HbA1c levels.

CONCLUSION

Diabetes induces multifactorial vestibular damage, significantly increasing BPPV occurrence and recurrence. Management requires metabolic optimization, vestibular screening with VEMP, vitamin D supplementation, and integration of vestibular rehabilitation.