Limbic‐Visual Disintegration and Salience‐Control Specialization Characterize Tinnitus Network Topology

Subjective tinnitus (ST) has been hypothesized to arise from large‐scale network reorganization, but the affected circuits and their symptom scaling remain unclear. In a normal‐hearing cohort ( N = 114; 57 ST, 57 matched controls), we combined resting‐state fMRI graph topology, ROI‐to‐ROI connectivity, voxel‐based morphometry (VBM), and multivariate modelling using a harmonized 50‐ROI parcellation from the CONN atlas, spanning 15 functional networks. Node‐wise analyses (covarying age, sex, education, and motion; multiple‐comparison control) showed selective, not global, reconfiguration: reduced integration centered on the left posterior parahippocampal gyrus (lower global efficiency and degree), increased segregation/clustering in inferior frontal and anterior insular hubs, longer path length in parahippocampal and frontal regions, and elevated local efficiency in the right amygdala. Network‐based revealed hyperconnectivity in fronto–salience–language–cerebellar circuits and hypoconnectivity across default mode and dorsal attention/temporo‐parietal pathways. Symptom coupling was convergent and dissociable: Higher tinnitus severity/duration tracked reduced integration in medial visual/limbic regions with increased integration/degree in right frontal–temporal opercular nodes, whereas higher anxiety related to increased integration/clustering in subcallosal, cerebellar, and occipito‐limbic territories alongside decreases in putamen. VBM demonstrated widespread white‐matter reductions (inferior frontal, temporal pole, insula, inferior temporal gyrus, and putamen) with more focal gray‐matter effects, and a multivariate GLM confirmed a robust omnibus group difference. These multimodal, symptom‐linked signatures provide strong evidence that ST reflects targeted network reorganization reduced medial temporal/visual–limbic integration accompanied by increased local specialization within salience and control hubs and yield actionable circuit markers for patient stratification and mechanism‐guided treatment targeting.