Hearing research
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The neuroscience of tinnitus represents an ideal model to explore central issues in brain functioning such as the formation of auditory percepts, in addition to opening up new treatment avenues for the condition in the long-term. The present review discusses the origin and nature of tinnitus-related neural activity. First, we review evidence for the hypothesis that tinnitus is caused by the central nervous system changes induced by sensory deprivation, even when hearing loss is not visible in the audiogram. ⋯ Instead, we propose that tinnitus may arise from functional alterations at multiple levels which promote abnormal propagation of neural activity throughout the network involved in auditory perception. In this context, functional coupling within and between central auditory structures may be especially important to consider. Investigating how sensory deprivation affects functional coupling between areas, which might be reflected in changes in temporal coherence of intrinsic ongoing activity patterns, may give critical insights into the mechanisms of tinnitus.
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Brain stimulation is an important method used to modulate neural activity and suppress tinnitus. Several auditory and non-auditory brain regions have been targeted for stimulation. This paper reviews recent progress on auditory cortex (AC) stimulation to suppress tinnitus and its underlying neural mechanisms and stimulation strategies. ⋯ This hypothesis may explain why different types of stimulation can induce tinnitus suppression. Depending on the tinnitus etiology, MGB-TRN-Gating may be different in levels and dynamics, which cause variability in tinnitus suppression induced by different gain controllers. This may explain why the induced suppression of tinnitus by one type of stimulation varies across individual patients.
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The functional organization of cortical and subcortical networks can be altered by sensory experience. Sensory deprivation destabilizes neural networks resulting in increased excitability, greater neural synchronization and increased spontaneous firing in cortical and subcortical neurons. This pathological activity is thought to generate the phantom percept of chronic tinnitus. ⋯ We also recently demonstrated that VNS modulates synchrony and excitability in the auditory cortex at least in part by activation of muscarinic acetylcholine receptors, suggesting that acetylcholine is involved in the mechanism of action of VNS. These results suggest that pairing sounds with VNS provides a new avenue of treatment for some forms of tinnitus. This paper discusses neuromodulation as treatment for tinnitus with a focus on the potential value of pairing VNS with sound stimulation as a treatment of chronic tinnitus.
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Hearing is critical to the performance of military personnel and is integral to the rapid and accurate processing of speech information. Thus, noise-induced hearing loss (NIHL) represents a severe impairment that reduces military effectiveness, safety, and quality of life. With the high levels of noise to which military personnel are exposed and the limited protection afforded by hearing conservation programs, it should be no surprise that annual Veterans Affairs disability payments for tinnitus and hearing loss exceeded $1.2 billion for 2009 and continue to increase. ⋯ Such an understanding may provide insight to who is at risk for each condition, allow aggressive hearing protection measures in those individuals most at risk, and create areas for treatment for those already suffering from the conditions. The current review will address the scope of the problems of NIHL and tinnitus for the military, discuss the noise environments in which military personnel operate, describe the hearing conservation measures currently in place, and the challenges those programs face. Some recent breakthroughs in NIHL research will be discussed along with some challenges and directions for future research on NIHL and tinnitus.
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The present study uses a systems engineering approach to delineate the relationship between tinnitus and hyperacusis as a result of either hearing loss in the ear or an imbalanced state in the brain. Specifically examined is the input-output function, or loudness growth as a function of intensity in both normal and pathological conditions. Tinnitus reduces the output dynamic range by raising the floor, while hyperacusis reduces the input dynamic range by lowering the ceiling or sound tolerance level. ⋯ The active loudness model suggests that tinnitus is a result of increased central noise, while hyperacusis is due to increased nonlinear gain. The active loudness model also generates specific predictions on loudness growth in tinnitus, hyperacusis, hearing loss or any combinations of the three conditions. These predictions need to be verified by experimental data and have explicit implications for treatment of tinnitus and hyperacusis.