Aims and objectives: The overall aim of this thesis is to investigate the neural substrates of tinnitus perception using advanced magnetic resonance imaging (MRI) techniques. The main objectives of this thesis dissertation are to (1) identify the impact of tinnitus perception on the quality of life, (2) investigate the morphological alterations in cortical and subcortical brain structures in tinnitus, (3) explore the auditory perception in tinnitus, (4) identify the perfusion pattern changes in tinnitus, (5) investigate the effect of tinnitus perception on brain functional connectivity, (6) explore the microstructure alterations in white matter structures in tinnitus and (7) investigate the relationship between tinnitus handicap scores and brain structure/function. Materials and methods: A total of 34 individuals with tinnitus, 20 healthy controls with mild to moderate hearing loss (MH), and 20 healthy controls with normal hearing (NH) participated in the work presented in this thesis. Pure tone air conduction audiometry was performed to assess the hearing level. Behavior assessments were undertaken of handedness, anxiety and depression, and tinnitus severity. Different MR images were acquired: T1-weighted images, T2-weighted images, functional images (resting-state and task-based fMRI), arterial spin labelling images (ASL) and diffusion tensor imaging (DTI). Different MRI analysis techniques were applied including: voxel and surface based morphometry (VBM and SBM), shape appearance differences, independent component analysis (ICA), and tractbased spatial statistics (TBSS).

Some tinnitus patients have normal hearing on the conventional audiogram. It has been suggested that the presence of a limited area of damaged outer hair cells (OHCs) with intact inner hair cells, which is not detected on the audiogram, results in unbalanced neural activity between Type I and Type II fibers leading to tinnitus. Distortion product otoacoustic emissions (DPOAEs) provided ambiguous data of OHC function in normal-hearing tinnitus patients when compared to non-tinnitus controls. It is known that hearing loss in the extended high frequency (EHF) region may decrease DPOAEs evoked at lower frequencies. Results of EHF audiometry in tinnitus patients are limited. The aim of the study was to evaluate DPOAEs and EHF thresholds in normal-hearing patients reporting unilateral tinnitus in left ear. Thus, each subject acted as their own control. Data were obtained for 25 subjects with bilateral hearing thresholds 3dB. Median audiometric data showed that thresholds in the left ears were significantly higher than those in the right ears at all four EHFs. Mean DPOAE levels of the left ears were lower than those of the right ears in the frequency range above 1 kHz. Additionally, a paired-comparison test of DPOAE levels of each patient’s right and left ear revealed significant differences at 6, and 8 kHz. The results indicate that: 1. OHC impairment in the most basal region reduces contribution to more apically generated DPOAEs; 2. OHC impairment in a limited area, which may be revealed by DPOAEs but not by conventional audiometry, can contribute to tinnitus generation; and 3. patients with unilateral tinnitus and normal hearing on the conventional audiogram are likely to demonstrate hearing loss in the EHF region.

No description available.

This session is developed by, and presenters invited by, Hearing, Balance, Tinnitus – Assessment and Intervention: Adult. This combined mini-series will present both clinical and research findings addressing the auditory and vestibular consequences of traumatic brain injury (TBI). Presenters will elucidate TBI’s effect on auditory processing, vestibular function, and tinnitus with case studies to illustrate management strategies relevant for each of the patient groups.

Konstanz, Univ., Diplomarbeit, 2006.

Konstanz, Univ., Diplomarbeit, 2007.

Thesis (Ph. D.)--Southern Illinois University Carbondale, 2008. / "Department of Pharmacology." Keywords: Aging, Brain-derived, Dorsal cochlear nucleus, Gephyrin, Glycine receptor, Tinnitus. Includes bibliographical references (p. 118-171). Also available online.

Konstanz, Univ., Diss., 2004.

Diss.--Méd.--Iéna, 1669?

Subjective tinnitus is the perception of a sound in the absence of an environmental source, and is thought to derive from maladaptive neuroplasticity that occurs following hearing impairment. However, the underlying structural and functional mechanisms remain unresolved. Our aims were thus to develop a model of trauma-induced tinnitus, and to investigate whether primary auditory cortex played a causal role. We tested ferrets on a gap-in-noise detection task to assess auditory temporal processing, which is impaired in tinnitus and hearing loss. Ferrets displayed robust gap-detection performance, with sensitivity that varied with the frequency content and bandwidth of the acoustic carrier noise, as we also found in human subjects tested on a comparable task. This confirmed the ferret as a relevant model of auditory temporal processing. To investigate hearing-loss-related neuroplasticity, ferrets underwent a partial, unilateral lesion of the spiral ganglion (SG), replicating aspects of otopathology described in tinnitus. Behaviourally, this lesion induced heterogeneous outcomes, with some ferrets displaying temporal processing impairments, and others showing post-lesion adaptation. These behavioural outcomes correlated with features of the auditory brainstem response, indicating a possible predisposition towards adaptation/maladaptation. Anatomical and physiological analysis of auditory cortical cells showed evidence for lesion-related central neuroplasticity that correlated with each animal's behavioural phenotype. We finally sought to determine whether these cortical changes underpinned the behavioural changes described. The optogenetic protein Archaerhodopsin-T was expressed bilaterally in auditory cortical neurons of SG-lesioned ferrets, allowing suppression of neural spiking during behaviour. Only contralesional suppression mediated any substantive behavioural effects, improving the performance of animals with temporal processing impairments, and impairing performance in animals with post-lesion improvements. The mechanistic basis for these effects was shown, through physiological recordings, to derive from optogenetic enhancements in cortical temporal processing. Together, these results suggest that primary auditory cortex plays an important role in mediating deafferentation-related neuroplasticity, suggesting possible strategies for remediation of the maladaptive processing potentially underpinning tinnitus in humans.