OBJECTIVE: Benign paroxysmal positional vertigo (BPPV) is the most common peripheral cause of vertigo. It can be defined as transient vertigo induced by rapid changes in head position associated with a characteristic paroxysmal positional nystagmus. The aim of this study was to search for the possible role of oxidative stress and inflammatory mediators in the pathogenesis of BPPV. MATERIALS AND METHODS: Total antioxidant status as well as paraoxonase, tumor necrosis factor alpha, interleukin (IL) 6, and IL-1β levels were evaluated in peripheral venous serum samples of 30 BPPV and 30 control patients. RESULTS: Total antioxidant status levels were lower in the BPPV group than in the control group (p=0.008). After Epley's repositioning maneuver in the vertigo group, there was a statistically significant decline in IL-1β levels at the first and third month visits (p=0.014 for first month and p=0.013 for third month). CONCLUSION: Our findings suggested that IL-1β and oxidative stress contributed to the pathogenesis of BPPV.
OBJECTIVE:Benign paroxysmal positional vertigo (BPPV) is the most common peripheral cause of vertigo. It can be defined as transient vertigo induced by rapid changes in head position associated with a characteristic paroxysmal positional nystagmus. The aim of this study was to search for the possible role of oxidative stress and inflammatory mediators in the pathogenesis of BPPV. MATERIALS AND METHODS: Total antioxidant status as well as paraoxonase, tumor necrosis factor alpha, interleukin (IL) 6, and IL-1β levels were evaluated in peripheral venous serum samples of 30 BPPV and 30 control patients. RESULTS: Total antioxidant status levels were lower in the BPPV group than in the control group (p=0.008). After Epley's repositioning maneuver in the vertigo group, there was a statistically significant decline in IL-1β levels at the first and third month visits (p=0.014 for first month and p=0.013 for third month). CONCLUSION: Our findings suggested that IL-1β and oxidative stress contributed to the pathogenesis of BPPV.