ArticleFrontiers in neuroscience2026
Altered cognitive performance is associated with auditory cortex functional connectivity in patients with unilateral sensorineural hearing loss.
Article in Frontiers in neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sensorineural hearing loss (SNHL) has been suggested to be closely associated with cognitive decline, yet the underlying neural mechanisms remain largely unclear. This study sought to explore the potential association between cognitive function and auditory cortex functional connectivity in patients with unilateral sensorineural hearing loss (USNHL) and investigate the possible neural mechanisms underlying subtle cognitive decline. Sixty patients with moderate-to-severe USNHL (disease duration ≥3 years; 30 with right-sided USNHL and 30 with left-sided USNHL) and 30 age-matched normal-hearing controls were enrolled; all participants underwent Montreal Cognitive Assessment (MoCA) and oddball paradigm electroencephalography, mismatch negativity (MMN) amplitude and latency were compared, and standardized low-resolution electromagnetic tomography (sLORETA) combined with partial Granger causality (PGC) was applied to analyze directional functional connectivity among the superior temporal gyrus (STG), inferior frontal gyrus (IFG), parahippocampal gyrus (PHG), and posterior cingulate cortex (PCC), with correlation and serial mediation analyses conducted. Relative to controls, USNHL patients exhibited lower MoCA scores, reduced MMN amplitude, prolonged latency, decreased left STG → IFG/STG → PHG/PHG → PCC connectivity and enhanced left IFG → STG connectivity; left IFG → STG connectivity was negatively correlated with MoCA attention scores, whereas left PHG → PCC connectivity was positively correlated with MoCA memory scores, with more prominent abnormalities in patients with severe USNHL. Serial mediation analysis suggested that the link between hearing loss severity and cognitive alterations might be mediated by two domain-specific serial pathways, both initiated by prolonged MMN latency: an attention pathway (MMN latency → enhanced left IFG → STG connectivity) and a memory pathway (MMN latency → reduced left PHG → PCC connectivity), and USNHL patients displayed left hemispheric lateralization of PGC alterations. These findings imply that enhanced left IFG → STG and weakened left PHG → PCC connectivity may be related to attention and memory alterations respectively, which may represent neural correlates of cognitive decline in middle-aged adults with USNHL.
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