Tracking white-matter brain modifications in chronic non-bothersome acoustic trauma tinnitus.

Subjective tinnitus is a symptom characterized by the perception of sound with no external acoustic source, most often accompanied by co-morbidities. To date, the specific role of white matter abnormalities related to tinnitus reaches no consensus in the literature. The goal of this study was to explore the structural connectivity related to tinnitus percept per se, thus focusing on a specific population presenting chronic non-bothersome tinnitus of similar etiology (noise induced) without co-morbidities. We acquired diffusion-weighted images with high angular resolution in a homogeneous group of mildly impacted tinnitus participants (n = 19) and their matched controls (n = 19). We focused the study on two subsets of fiber bundles of interest: on one hand, we extracted the acoustic radiation and further included any intersecting fiber bundles; on the other hand, we explored the tracts related to the limbic system. We modeled the diffusion signal using constrained spherical deconvolution. We conducted a deep-learning based tractography segmentation and mapped Apparent Fiber Density (AFD) on the bundles of interest. C, as well as Fractional Anisotropy (FA) and FOD peak amplitude for comparison. Between group statistical comparison was performed along the 27 tracts of interest controlling for confounding hearing loss, tinnitus severity, and duration since onset. We tested a potential correlation with hearing loss, tinnitus duration and tinnitus handicap score along these tracts. In the tinnitus group, we observed increased AFD related to chronic tinnitus percept after acoustic trauma in two main white matter regions. First, in the right hemisphere, in the isthmus between inferior temporal and inferior frontal cortices, in the uncinate fasciculus (UF), and in the inferior fronto-occipital bundle (IFO). Second, in the left hemisphere, underneath the superior parietal region in the thalamo parietal tract and parieto-occipital pontine tract. Between-group differences in the acoustic radiations were not significant with AFD but were with FA. Furthermore, significant correlations with hearing loss were found in the left hemisphere in the inferior longitudinal fasciculus and in the fronto-pontine tract. No additional correlation was found with tinnitus duration nor with tinnitus handicap, as reflected by THI scores. The regions that displayed tinnitus related increased AFD also displayed increased FA. The isthmus of the UF and IFO in the right hemisphere appear to be involved with a number of neuropsychiatric and traumatic disorders confirming the involvement of the limbic system even in chronic non-bothersome tinnitus subjects, potentially suggesting a common pathway between these pathologies. White matter changes underneath the superior parietal cortex found here in tinnitus participants supports the implication of an auditory-somatosensory pathway in tinnitus perception.