Microcirculatory Dysfunction and Oxidative Stress in Sudden Sensorineural Hearing Loss: Insights From a Case-Control and Experimental Study

Abstract

Background: Material/Methods: Results: Conclusions: Sudden sensorineural hearing loss (SSNHL) is an otological emergency with incompletely understood pathophysiology. Evidence suggests microcirculatory dysfunction and oxidative stress contribute to cochlear injury; however, their interrelationship remains insufficiently characterized. This prospective case–control study enrolled 100 patients with SSNHL and 100 age-and sex-matched healthy controls. Perfusion-related surrogate parameters, including cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT), were assessed using dynamic contrast-enhanced magnetic resonance perfusion imaging. Peripheral microcirculation was evaluated by laser Doppler flowmetry. Systemic oxidative stress markers malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were quantified in serum. Experimental validation was performed using a rat ischemia–reperfusion model to assess cochlear oxidative stress, apoptosis, and auditory brainstem response thresholds. Compared with controls, SSNHL patients exhibited reduced CBF and CBV, prolonged MTT, and lower peripheral microcirculatory perfusion (all P<0.05). Oxidative stress was increased in SSNHL, reflected by elevated serum MDA levels and reduced SOD and GSH-Px activities. Animal model showed ischemia–reperfusion induced parallel alterations, including increased cochlear oxidative stress, reduced antioxidant enzyme activity, increased apoptotic cell burden, and elevated auditory brainstem response thresholds. Perfusion-related parameters correlated with oxidative stress markers. Multivariable regression analysis demonstrated independent associations between perfusion profiles, oxidative imbalance, and hearing thresholds. SSNHL is associated with unfavorable perfusion-related surrogate parameters and heightened oxidative stress accompanied by reduced antioxidant defenses. Clinical and experimental findings suggest microcirculatory dysfunction and oxidative imbalance are interrelated features of SSNHL-associated cochlear injury. Causal inference cannot be established, and further mechanistic studies are warranted.