Subcallosal brain structure: Correlation with hearing threshold at supra-clinical frequencies (> 8 kHz), but not with tinnitus
ABSTRACT This study tested for differences in brain structure between tinnitus and control subjects, focusing on a subcallosal brain region where striking differences have been inconsistently found previously. Voxel-based morphometry (VBM) was used to compare structural MRIs of tinnitus subjects and non-tinnitus controls. Audiograms of all subjects were normal or near-normal at standard clinical frequencies (≤8 kHz). Mean threshold through 14 kHz, age, sex and handedness were matched between groups. There were no definitive differences between tinnitus and control groups in modulated or unmodulated maps of gray matter (GM) probability (i.e., GM volume and concentration, respectively). However, when the image data were tested for correlations with parameters that were either not measured or not matched between the tinnitus and control groups of previous studies, a notable correlation was found: Threshold at supra-clinical frequencies (above 8 kHz) was negatively correlated with modulated GM probability in ventral posterior cingulate cortex, dorsomedial prefrontal cortex, and a subcallosal region that included ventromedial prefrontal cortex and coincided with previously-reported differences between tinnitus and control subjects. The results suggest an explanation for the discrepant findings in subcallosal brain: threshold at supra-clinical frequencies may have differed systematically between tinnitus and control groups in some studies but not others. The observed correlation between (1) brain structure in regions engaged in cognitive and attentional processes and (2) hearing sensitivity at frequencies generally considered unnecessary for normal human auditory behavior is surprising and worthy of follow up.
SourceAvailable from: Yu-Chen Chen[Show abstract] [Hide abstract]
ABSTRACT: Objective. Subjective tinnitus is hypothesized to arise from aberrant neural activity; however, its neural bases are poorly understood. To identify aberrant neural networks involved in chronic tinnitus, we compared the resting-state functional magnetic resonance imaging (fMRI) patterns of tinnitus patients and healthy controls. Materials and Methods. Resting-state fMRI measurements were obtained from a group of chronic tinnitus patients (í µí± = 29) with normal hearing and well-matched healthy controls (í µí± = 30). Regional homogeneity (ReHo) analysis and functional connectivity analysis were used to identify abnormal brain activity; these abnormalities were compared to tinnitus distress. Results. Relative to healthy controls, tinnitus patients had significant greater ReHo values in several brain regions including the bilateral anterior insula (AI), left inferior frontal gyrus, and right supramarginal gyrus. Furthermore, the left AI showed enhanced functional connectivity with the left middle frontal gyrus (MFG), while the right AI had enhanced functional connectivity with the right MFG; these measures were positively correlated with Tinnitus Handicap Questionnaires (í µí± = 0.459, í µí± = 0.012 and í µí± = 0.479, í µí± = 0.009, resp.). Conclusions. Chronic tinnitus patients showed abnormal intra-and interregional synchronization in several resting-state cerebral networks; these abnormalities were correlated with clinical tinnitus distress. These results suggest that tinnitus distress is exacerbated by attention networks that focus on internally generated phantom sounds.
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ABSTRACT: Tinnitus is highly complex, diverse, and difficult to treat, in part due to the fact that the underlying causes and mechanisms remain elusive. Tinnitus is generated within the auditory brain; however, consolidating our understanding of tinnitus pathophysiology is difficult due to the diversity of reported effects and the variety of implicated brain nuclei. Here, we focus on the inferior colliculus (IC), a midbrain structure that integrates the vast majority of ascending auditory information and projects via the thalamus to the auditory cortex. The IC is also a point of convergence for corticofugal input and input originating outside the auditory pathway. We review the evidence, from both studies with human subjects and from animal models, for the contribution the IC makes to tinnitus. Changes in the IC, caused by either noise exposure or drug administration, involve fundamental, heterogeneous alterations in the balance of excitation and inhibition. However, differences between hearing loss-induced pathology and tinnitus-related pathology are not well understood. Moreover, variability in tinnitus induction methodology has a significant impact on subsequent neural and behavioral changes, which could explain some of the seemingly contradictory data. Nonetheless, the IC is likely involved in the generation and persistence of tinnitus perception.Frontiers in Neurology 03/2015; 6:61. DOI:10.3389/fneur.2015.00061
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ABSTRACT: A surprising fact in voxel-based morphometry (VBM) studies performed in tinnitus is that not one single region is replicated in studies of different centers. The question then rises whether this is related to the low sample size of these studies, the selection of non-representative patient subgroups, or the absence of stratification according to clinical characteristics. Another possibility is that VBM is not a good tool to study functional pathologies such as tinnitus, in contrast to pathologies like Alzheimer's disease where it is known the pathology is related to cell loss. In a large sample of 154 tinnitus patients VBM and QEEG (Quantitative Electroencephalography) was performed and evaluated by a regression analysis. Correlation analyses are performed between VBM and QEEG data. Uncorrected data demonstrated structural differences in grey matter in hippocampal and cerebellar areas related to tinnitus related distress and tinnitus duration. After control for multiple comparisons, only cerebellar VBM changes remain significantly altered. Electrophysiological differences are related to distress, tinnitus intensity, and tinnitus duration in the subgenual anterior cingulate cortex, dorsal anterior cingulate cortex, hippocampus, and parahippocampus, which confirms previous results. The absence of QEEG-VBM correlations suggest functional changes are not reflected by co-occurring structural changes in tinnitus, and the absence of VBM changes (except for the cerebellum) that survive correct statistical analysis in a large study population suggests that VBM might not be very sensitive for studying tinnitus.PLoS ONE 03/2015; 10(3):e0115122. DOI:10.1371/journal.pone.0115122 · 3.53 Impact Factor