White Matter Changes in Cases with Unilateral Idiopathic Sudden Sensorineural Hearing Loss Indicated by Diffusion Tensor Imaging Based on Tract-Based Spatial Statistics

BACKGROUND: To characterize alterations in white matter microstructure in cases with idiopathic sudden sensorineural hearing loss (SSNHL) through tract-based spatial statistics applied to diffusion tensor imaging (DTI), elucidating both early-stage and chronic neuroanatomical alterations. METHODS: All cases underwent high-resolution conventional magnetic resonance imaging and DTI. Diffusion data preprocessing was performed using the FMRIB Software Library, including corrections for eddy currents and head motion, brain extraction, and normalization to standard space. Tract-based spatial statistics was employed to undertake voxel-wise whole-brain analysis of fractional anisotropy (FA), mean diffusivity (MD), and radial diffusivity across 3 groups: left-sided idiopathic SSNHL, chronic left-sided sensorineural hearing loss (SNHL), and healthy control (HC). Additionally, in the SNHL group, correlation analysis of regional DTI metrics with clinical variables was implemented, involving disease duration, interaural latency difference, and auditory brainstem response thresholds. RESULTS: Relative to the HC group, the left SNHL group exhibited remarkably diminished FA values in the bilateral internal capsules, superior corona radiata, and left external capsule. Concurrently, elevated MD values were noteworthy in the body of the corpus callosum, left external capsule, bilateral internal capsules, and corona radiata. Radial diffusivity values were escalated in the corpus callosum body, bilateral superior corona radiata, and left external capsule, suggesting compromised microstructural integrity. CONCLUSION: Both idiopathic SSNHL and chronic SNHL cases demonstrated discernible white matter abnormalities, implicating a disruption in major commissural and projection fiber tracts. Notably, cases with prolonged auditory deprivation exceeding 2 years exhibited microstructural signatures consistent with axonal degeneration and progressive demyelination.