Background: Tinnitus is a phantom perception of sound in the ears or head without any external source. Individuals with tinnitus often have trouble understanding speech-in-noise (SIN). SIN deficits refer to difficulties understanding speech against background noise. Previous studies investigating SIN deficits in individuals with tinnitus revealed mixed results. Genetic variants associated with tinnitus and SIN deficits was identified by recent genome wide association study (GWAS). The present study investigated SIN deficits in individuals with tinnitus and conducted complementary analyses using GWAS summary statistics to identify tissues and molecular pathways shared between the two phenotypes.

Methods: 216 normal hearing (hearing thresholds ≤20 dB HL for 250-8000 Hz) young adults (87 with chronic tinnitus) aged 18-37 years participated in the study. Speech, Spatial, and Quality of Hearing scale (SSQ12) and QuickSIN were used to evaluate SIN perception. Extended high-frequency audiometry and dichotic digit test (DDT) were performed. A linear mixed model (LMM) was used to identify the influence of tinnitus on audiological measures while controlling the effects of confounders. GWAS summary statistics for SIN deficits were obtained from open resources (N=453,482, Ncases=171,586). MAGMA-based gene set enrichment analysis was performed on GWAS summary statistics. The results for SIN deficits were compared with published reports of tinnitus to identify shared enrichment result.

Results: Significantly elevated hearing thresholds, lower SSQ12, and poorer DDT scores were obtained for young adults with tinnitus. Tinnitus severity was correlated with SSQ12. Elevated hearing thresholds and lower SSQ12 were associated with high lifetime noise exposure (LNE) and firearm use. Several brain tissues, such as the brain cortex, frontal cortex, nucleus accumbens, cerebellum, anterior cingulate cortex , caudate, amygdala, hippocampus, putamen, and hypothalamus, were identified by MAGMA based analysis, which was shared between tinnitus and SIN deficits. Outer hair cells were associated with tinnitus but revealed a modest association with SIN deficits.

Conclusion: Results suggests that young adults with chronic tinnitus experience significant SIN deficits. Self-reported auditory-cognitive measures could be more sensitive than performance-based measures for evaluating SIN perception. The shared enrichment of genomic signals points toward the central origin of SIN deficits in normal-hearing young adults with tinnitus.