Can Tinnitus Cause Speech-in-Noise Deficits?

Srividya Grama Bhagavan; Valerie Ingalls; Juan Antonio Raygoza Garay; Nilesh Washnik; Ishan Sunilkumar Bhatt

doi:10.1097/AUD.0000000000001836

Studies examining the relationship between tinnitus and speech-in-noise (SIN) perception have produced conflicting results, possibly due to observational study designs and confounders related to aging, hearing loss, and tinnitus-related distress. To address this concern, the present study investigated the relationship between tinnitus and SIN perception using complementary observational and genetic epidemiological approaches across multiple independent cohorts, enabling the identification of converging evidence to clarify this relationship. A total of 216 young adults, including 87 with continuous chronic tinnitus (bothersome tinnitus for >1 y), aged 18 to 37 y, with hearing thresholds (HTs) ≤20 dB HL for 250 to 8000 Hz, participated in the study. Speech perception was evaluated using the Speech, Spatial, and Quality of Hearing scale (SSQ12), QuickSIN, and 3-digit Dichotic Digit Test. Extended high-frequency HTs (up to 16 kHz) were evaluated. A linear mixed-effects model was used to assess the influence of tinnitus on audiological measures while controlling for confounders, including lifetime noise exposure (LNE), firearm use, and a history of recurring ear infections. To obtain causal inference, we employed latent causal variant (LCV) analysis using the summary statistics of genome-wide association studies, followed by functional enrichment analyses to identify shared tissues and pathways between tinnitus and SIN deficits. Multimarker Analysis of GenoMic Annotation was conducted to obtain gene-based statistics. Gene-based gene statistics were integrated with single-cell transcriptomic data from mice cochlear tissues to identify cell types shared between the two phenotypes. Tinnitus was associated with lower SSQ12 scores and poorer dichotic digit test performance, even after statistically controlling for the differences in HTs. Tinnitus severity was negatively correlated with SSQ12 scores. Lifetime noise exposure and firearm use were associated with elevated HTs and lower SSQ12 scores. Tinnitus and SIN deficits revealed significant genetic correlations, but the latent causal variant analysis found no evidence of a causal impact of tinnitus on SIN deficits. The Multimarker Analysis of GenoMic Annotation-based analysis identified several brain tissues, including the frontal cortex, anterior cingulate cortex, cerebellum, nucleus accumbens, caudate, putamen, hippocampus, amygdala, and hypothalamus, that were shared between tinnitus and SIN deficits. Gene ontology terms for synaptic functioning were jointly enriched. No cochlear cell types revealed significant associations with tinnitus and SIN deficits. Tinnitus and SIN deficits are comorbid conditions with a shared genetic basis. Tinnitus is not causally associated with SIN deficits; rather, a shared genetic architecture independently predisposes individuals to both phenotypes. A converging line of evidence from observational and genome-wide association study-based enrichment analyses suggests that a shared genetic basis likely alters synaptic functioning in key brain regions involved in audition, cognition, and emotional regulation. Future studies are necessary to elucidate the shared biological pathways underlying tinnitus and SIN deficits.

Can Tinnitus Cause Speech-in-Noise Deficits?

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