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The possible contribution of angiitis to the onset of benign paroxysmal positional vertigo (BPPV)

Fumiyuki Goto1, Ken Hayashi, Takanobu Kunihiro

  • 1Department of Otorhinolaryngology, Hino Municipal Hospital, Tokyo, Japan. amifumi@bc5.so-net.ne.jp

The International Tinnitus Journal
|May 26, 2011
PubMed
Abstract

Insights

Oxidative stress and angiitis markers, diacron reactive oxygen metabolites (d-ROM) and vascular cell adhesion molecule 1 (VCAM-1), are elevated in benign paroxysmal positional vertigo (BPPV). Higher levels correlate with longer recovery times.

Area of Science:

  • Neuroscience
  • Vascular Biology
  • Otolaryngology

Background:

  • Benign paroxysmal positional vertigo (BPPV) is a common vestibular disorder.
  • The underlying pathophysiology of BPPV is not fully understood.
  • Oxidative stress and vascular inflammation are implicated in various medical conditions.

Purpose of the Study:

  • To investigate the role of oxidative stress and angiitis in patients diagnosed with BPPV.
  • To evaluate the relationship between specific biomarkers and BPPV recovery duration.

Main Methods:

  • Patients with recent-onset BPPV (within 14 days) were enrolled.
  • Levels of diacron reactive oxygen metabolites (d-ROM) and soluble vascular cell adhesion molecule 1 (VCAM-1) were measured.
  • Prognosis was assessed by the time to resolution of positional nystagmus, with patients performing Brandt-Daroff exercises.

Main Results:

  • Patients with prolonged recovery times exhibited significantly higher levels of d-ROM and VCAM-1.
  • Conversely, patients with shorter remission periods showed lower concentrations of these biomarkers.
  • A positive correlation was observed between elevated d-ROM/VCAM-1 levels and longer BPPV duration.

Conclusions:

  • Findings suggest increased oxidative stress and angiitis, indicated by elevated d-ROM and VCAM-1, in BPPV patients.
  • These results support the involvement of vascular mechanisms in the pathogenesis of BPPV.
  • Identifying these biomarkers may pave the way for targeted pharmacological interventions to manage oxidative stress and endothelial activation in BPPV.

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