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

SSNHL patients exhibited significantly reduced cerebral perfusion parameters compared to healthy controls.

• The study enrolled 100 patients with SSNHL and 100 age- and sex-matched healthy controls in a prospective case-control design.
• Perfusion parameters assessed included cerebral blood flow (CBF), cerebral blood volume (CBV), and mean transit time (MTT) using dynamic contrast-enhanced magnetic resonance perfusion imaging.
• SSNHL patients showed reduced CBF, reduced CBV, and prolonged MTT compared to controls (all P<0.05).
• Lower peripheral microcirculatory perfusion was also observed in SSNHL patients as measured by laser Doppler flowmetry (P<0.05).

SSNHL patients demonstrated elevated systemic oxidative stress with reduced antioxidant enzyme activity.

• Serum malondialdehyde (MDA) levels were elevated in SSNHL patients compared to controls.
• Superoxide dismutase (SOD) activity was reduced in SSNHL patients compared to controls.
• Glutathione peroxidase (GSH-Px) activity was reduced in SSNHL patients compared to controls.
• All oxidative stress marker differences between groups were statistically significant (P<0.05).

Rat ischemia-reperfusion model reproduced cochlear oxidative stress, apoptosis, and elevated auditory brainstem response thresholds.

• Experimental validation was performed using a rat cochlear ischemia-reperfusion model.
• Ischemia-reperfusion induced increased cochlear oxidative stress and reduced antioxidant enzyme activity in the cochlea.
• Increased apoptotic cell burden was observed in cochlear tissue following ischemia-reperfusion injury.
• Auditory brainstem response (ABR) thresholds were elevated in the ischemia-reperfusion model, indicating functional hearing impairment.

Perfusion-related parameters correlated with oxidative stress markers in SSNHL patients.

• Correlation analyses demonstrated statistically significant associations between perfusion-related parameters (CBF, CBV, MTT) and oxidative stress markers (MDA, SOD, GSH-Px).
• Multivariable regression analysis demonstrated independent associations between perfusion profiles, oxidative imbalance, and hearing thresholds.
• These associations suggest microcirculatory dysfunction and oxidative stress are interrelated rather than independent features of SSNHL.

The pathophysiology of SSNHL involves incompletely understood mechanisms, with microcirculatory dysfunction and oxidative stress identified as contributing but causally unproven factors.

• The authors state that 'causal inference cannot be established' from the current study design.
• The study design was a prospective case-control study combined with an experimental animal model.
• The authors conclude that 'further mechanistic studies are warranted' to establish causal relationships.
• SSNHL is described as 'an otological emergency with incompletely understood pathophysiology.'