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Tinnitus is a condition where affected patients experience a persistent sound in one or both ears or in the head. 14% of adults suffer from chronic tinnitus, whereas 50% of all adults experience tinnitus in a silent environment (1). Apart from an objective Tinnitus in which an underlying physiological condition can be found, in a subjective tinnitus no source can be detected. The formation and the way how and why this disabling experience sustains remain unclear. We aim to add new findings to the current knowledge about the pathogenesis of tinnitus. While tinnitus often originates in the periphery, mechanisms of the central auditory pathway and of the auditory cortex have also been shown to be important in its generation, maintenance, and persistence. Changes in the homeostatic plasticity increasing the central gain are suspect to be part of the pathogenesis (2).
We focus on these mechanisms by researching the role of inhibition modulated by neurotransmitters in the auditory cortex in tinnitus patients. Earlier studies showed promising results in GABA concentration deficits in the auditory cortex of tinnitus patients (3-6). With our research we will extend those observations in that we will analyse the concentration and role of several different neurotransmitters in the auditory cortex and adjacent regions and how they differ in tinnitus vs. healthy subjects. Additionally, we will further explore neuroanatomical features and their influence on tinnitus. We use magnetic resonance spectroscopy (MRS) to analyse metabolites in the auditory cortex of our subjects. MRS is an innovative and promising approach that is based on the well-established magnetic resonance imaging (MRI) technology. MRS allows to inspect different tissues for the presence and concentration of numerous metabolites. Furthermore we analyse the neuroanatomic features in our subjects using MRI (7). To assess the hearing abilities of our subjects several hearing-tests will be applied.
This all-embracing approach is new to the research of the role of metabolic changes in tinnitus and the insights gained will help to further understand the pathophysiology of tinnitus. If an inhibitory deficiency turns out to be responsible for causing or maintaining tinnitus a pharmacological or similar neuromodulatory intervention could be developed for a treatment.
1. Shargorodsky J, Curhan GC, Farwell WR. Prevalence and characteristics of tinnitus among US adults. Am J Med. 2010;123(8):711-8.
2. Sedley W. Tinnitus: Does gain explain? Neuroscience. 2019.
3. Sedley W, Parikh J, Edden RA, Tait V, Blamire A, Griffiths TD. Human Auditory Cortex Neurochemistry Reflects the Presence and Severity of Tinnitus. J Neurosci. 2015;35(44):14822-8.
4. Brozoski T, Odintsov B, Bauer C. Gamma-aminobutyric acid and glutamic acid levels in the auditory pathway of rats with chronic tinnitus: a direct determination using high resolution point-resolved proton magnetic resonance spectroscopy (H-MRS). Front Syst Neurosci. 2012;6:9.
5. Cacace AT, Silver SM. Applications of magnetic resonance spectroscopy to tinnitus research: initial data, current issues, and future perspectives. Prog Brain Res. 2007;166:71-81.
6. Cacace AT, Hu J, Romero S, Xuan Y, Burkard RF, Tyler RS. Glutamate is down-regulated and tinnitus loudness-levels decreased following rTMS over auditory cortex of the left hemisphere: A prospective randomized single-blinded sham-controlled cross-over study. Hear Res. 2017.
7. Scott-Wittenborn N, Karadaghy OA, Piccirillo JF, Peelle JE. A methodological assessment of studies that use voxel-based morphometry to study neural changes in tinnitus patients. Hear Res. 2017;355:23-32.
