2019
DOI: 10.1080/14992027.2019.1660812
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A review of auditory gain, low-level noise and sound therapy for tinnitus and hyperacusis

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Cited by 28 publications
(25 citation statements)
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“…This suggests that objective markers for either tinnitus or hyperacusis may have indeed been identified. Keeping this in mind, numerous previously controversial findings of either reduced or enhanced central auditory responses in tinnitus (27,47,67) may find a rational explanation. Also, previous studies that included tinnitus patients with unilateral and bilateral tinnitus and only found tinnitus characteristics in the sub-chronical group (28) may reconsider the findings in the context of the present study.…”
Section: Differences In Neural Correlates Behind T-group and Th-groupmentioning
confidence: 99%
“…This suggests that objective markers for either tinnitus or hyperacusis may have indeed been identified. Keeping this in mind, numerous previously controversial findings of either reduced or enhanced central auditory responses in tinnitus (27,47,67) may find a rational explanation. Also, previous studies that included tinnitus patients with unilateral and bilateral tinnitus and only found tinnitus characteristics in the sub-chronical group (28) may reconsider the findings in the context of the present study.…”
Section: Differences In Neural Correlates Behind T-group and Th-groupmentioning
confidence: 99%
“…The heterogeneity of tinnitus may explain why there is no one effective treatment for all patients and the outcomes of a given therapeutic intervention are highly variable. Patients might use various non-specific methods to cope with tinnitus including sound or music therapies [9][10][11], cochlear implantation [12], psychological therapies [13][14][15][16][17][18][19], brain stimulation [20][21][22], or neurofeedback training [23,24]. No effective pharmacological treatment for this condition is yet available.…”
Section: Introductionmentioning
confidence: 99%
“…A possible theory accounting for reduced slow-wave activity together with increased gamma over the temporal areas in tinnitus patients is the thalamo-cortical dysrhythmia model [29,45] in which tinnitus relates to persistent gamma activity in the auditory cortex due to auditory deafferentation. In the deafferented state the dominant resting-state alpha rhythm (8)(9)(10)(11)(12) decreases to a theta rhythm (4)(5)(6)(7). As a result, GABA-mediated lateral inhibition is reduced, inducing gamma band activity in regions adjacent to the deafferented theta (called PLOS ONE an edge effect, 40).…”
Section: Introductionmentioning
confidence: 99%
“…The exact pathophysiological mechanism(s) responsible for tinnitus and hyperacusis remains enigmatic. However, many researchers believe tinnitus emerges from excessive spontaneous neural activity [87][88][89][90] and hyperacusis results from enhanced sound-evoked neural activity [90] triggered by excessive/aberrant central gain control mechanisms [91][92][93]. Central gain functions in a homeostatic manner, attempting to centrally compensate for a reduced neural output peripherally (i.e., cochlea afferent fibers).…”
Section: Tinnitus and Hyperacusismentioning
confidence: 99%