Research's Attempt to Objectively Assess Tinnitus

Discussion in 'Research News' started by Frédéric, Jun 21, 2017.

    1. Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      I just wanted to start a thread gathering experiences trying to objectively assess tinnitus (I did not find a thread for this subject in this forum).

      I found this link today :
      http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0179150

      Tinnitus alters resting state functional connectivity (RSFC) in human auditory and non-auditory brain regions as measured by functional near-infrared spectroscopy (fNIRS)

      Abstract

      Tinnitus, or phantom sound perception, leads to increased spontaneous neural firing rates and enhanced synchrony in central auditory circuits in animal models. These putative physiologic correlates of tinnitus to date have not been well translated in the brain of the human tinnitus sufferer. Using functional near-infrared spectroscopy (fNIRS) we recently showed that tinnitus in humans leads to maintained hemodynamic activity in auditory and adjacent, non-auditory cortices. Here we used fNIRS technology to investigate changes in resting state functional connectivity between human auditory and non-auditory brain regions in normal-hearing, bilateral subjective tinnitus and controls before and after auditory stimulation. Hemodynamic activity was monitored over the region of interest (primary auditory cortex) and non-region of interest (adjacent non-auditory cortices) and functional brain connectivity was measured during a 60-second baseline/period of silence before and after a passive auditory challenge consisting of alternating pure tones (750 and 8000Hz), broadband noise and silence. Functional connectivity was measured between all channel-pairs. Prior to stimulation, connectivity of the region of interest to the temporal and fronto-temporal region was decreased in tinnitus participants compared to controls. Overall, connectivity in tinnitus was differentially altered as compared to controls following sound stimulation. Enhanced connectivity was seen in both auditory and non-auditory regions in the tinnitus brain, while controls showed a decrease in connectivity following sound stimulation. In tinnitus, the strength of connectivity was increased between auditory cortex and fronto-temporal, fronto-parietal, temporal, occipito-temporal and occipital cortices. Together these data suggest that central auditory and non-auditory brain regions are modified in tinnitus and that resting functional connectivity measured by fNIRS technology may contribute to conscious phantom sound perception and potentially serve as an objective measure of central neural pathology.
       
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    2. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      An umpteenth study about tinnitus involving an umpteenth part of the brain :

      Amygdala functional disconnection with the prefrontal-cingulate-temporal circuit in chronic tinnitus patients with depressive mood
      https://doi.org/10.1016/j.pnpbp.2017.07.001Get rights and content

      Highlights
      •Depressed tinnitus patients showed disrupted amygdala-cortical FC
      •Amygdala disconnections with prefrontal-cingulate-temporal circuit were observed.
      •Amygdala FC provides new insight into the neural mechanism of depressive tinnitus.

      Abstract

      Chronic tinnitus is often accompanied with depressive symptom, which may arise from aberrant functional coupling between the amygdala and cerebral cortex. To explore this hypothesis, resting-state functional magnetic resonance imaging (fMRI) was used to investigate the disrupted amygdala-cortical functional connectivity (FC) in chronic tinnitus patients with depressive mood. Chronic tinnitus patients with depressive mood (n = 20), without depressive mood (n = 20), and well-matched healthy controls (n = 23) underwent resting-state fMRI scanning. Amygdala-cortical FC was characterized using a seed-based whole-brain correlation method. The bilateral amygdala FC was compared among the three groups. Compared to non-depressed patients, depressive tinnitus patients showed decreased amygdala FC with the prefrontal cortex and anterior cingulate cortex as well as increased amygdala FC with the postcentral gyrus and lingual gyrus. Relative to healthy controls, depressive tinnitus patients revealed decreased amygdala FC with the superior and middle temporal gyrus, anterior and posterior cingulate cortex, and prefrontal cortex, as well as increased amygdala FC with the postcentral gyrus and lingual gyrus. The current study identified for the first time abnormal resting-state amygdala-cortical FC with the prefrontal-cingulate-temporal circuit in chronic tinnitus patients with depressive mood, which will provide novel insight into the underlying neuropathological mechanisms of tinnitus-induced depressive disorder.

      Keywords : Tinnitus Depression Amygdala Functional connectivity Resting-state fMRI
      Source : http://www.sciencedirect.com/science/article/pii/S0278584617301203
       
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    3. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Another article found today :

      Auditory Related Resting State fMRI Functional Connectivity in Tinnitus Patients: Tinnitus Diagnosis Performance
      Minami, Shujiro B.; Oishi, Naoki; Watabe, Takahisa; Uno, Kimiichi; Ogawa, Kaoru
      Otology & Neurotology: Post Author Corrections: November 28, 2017
      doi: 10.1097/MAO.0000000000001626
      Original Study: PDF Only

      Objective:

      The purpose of the present study was to investigate functional connectivity in tinnitus patients with and without hearing loss, and design the tinnitus diagnosis performance by resting state functional magnetic resonance imaging (rs-fMRI).

      Subjects and Methods:

      Nineteen volunteers with normal hearing without tinnitus, 18 tinnitus patients with hearing loss, and 11 tinnitus patients without hearing loss were enrolled in this study. The subjects were evaluated with rs-fMRI, and region of interests (ROIs) based correlation analyses were performed using the CONN toolbox version 16 and SPM version 8. The correlation coefficients from individual level results were converted into beta values.

      Results:

      With a beta threshold of more than 0.2, 91% of all possible connections between auditory-related ROIs (Heschl's gyrus, planum temporale, planum polare, operculum, insular cortex, superior temporal gyrus) in the control group remained intact, whereas 83 and 66% of such connections were present in the hearing loss and the normal-hearing tinnitus group. However, between non-auditory-related ROIs, the rates of intact connections at a beta threshold of more than 0.2 were 17% in the control group, and 16 and 15% in the tinnitus groups. When resting state fMRI positive is defined as less than 9% of all possible connections between auditory-related ROIs with a beta threshold of more than 0.7, the sensitivity and specificity of tinnitus diagnosis is 86 and 74%, respectively.

      Conclusions:

      The associations between auditory-related networks are weakened in tinnitus patients, even if they have normal hearing. It is possible that rs-fMRI can be a tool for objective examination of tinnitus, by focusing the auditory-related areas.

      Address correspondence and reprint requests to Shujiro B. Minami, M.D., Ph.D., National Tokyo Medical Center, National Institute of Sensory Organs, 2-5-1 Higashigaoka, Meguro, Tokyo 152-8902, Japan; E-mail: shujirominami@me.com

      This work was supported by JSPS KAKENHI Grant Number 25462657, and research grants from Suzuken Memorial Foundation and Mitsubishi Tanabe Pharma Corporation.

      The authors disclose no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

      Supplemental digital content is available in the text.

      Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Website (http://journals.lww.com/otology-neurotology).

      Copyright © 2017 by Otology & Neurotology, Inc. Image copyright © 2010 Wolters Kluwer Health/Anatomical Chart Company

      Source: http://journals.lww.com/otology-neu...ated_Resting_State_fMRI_Functional.96841.aspx
       
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    4. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      And this article:

      Objective measurement of subjective tinnitus using the acoustic change complex
      Abstract
      At present, there is no objective method for diagnosing subjective sensorineural tinnitus. Recently, the acoustic change complex (ACC) has been used to evaluate neural detection of sounds. Thus, the present study aimed to examine whether the ACC can reflect cortical detection and discrimination of sounds matched with tinnitus frequencies. We hypothesized that the ACC to change stimuli matched with tinnitus frequencies would be decreased in tinnitus patients because the tinnitus interferes with the perception of acoustic changes. To test the hypothesis, 96 ears of normal-hearing (NH) tinnitus patients and controls were tested. Among the tinnitus patients, 33 ears with a tinnitus frequency of 8 kHz constituted the tinnitus group, and the remaining 63 ears with no experience of tinnitus were allocated to the control group. For the 4 kHz non-tinnitus matched frequency, a subset of tinnitus (n = 17) and NH (n = 47) subjects was tested. The acoustic stimuli were pure tones with a total duration of 500 ms consisting of a 1 kHz tone in the first 250 ms and a second tone of either 8 kHz or 4 kHz in the latter 250 ms. The normalized amplitude of the ACC (naACC) was calculated separately for the amplitude of the N1’-P2’ complex evoked by an 8 kHz or 4 kHz change stimulus and for the amplitude of the N1-P2 complex elicited by the initial 1 kHz background stimulus. Our results showed that the naACC to an 8 kHz stimulus in the tinnitus group was significantly smaller than those to 4 kHz and 8 kHz in normal controls. Additionally, in the tinnitus group, the naACC to 4 kHz was greater compared to 8 kHz. The receiver operating characteristic (ROC) curve analysis conducted for naACC to 8 kHz at UCL revealed a fair degree of diagnostic efficacy. Overall, our results indicated that the ACC to a change stimulus matched with the tinnitus frequency can provide an objective measure of frequency-specific tinnitus.

      Source: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0188268
       
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    5. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      I found this article today
       

      Attached Files:

    6. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Comparisons of auditory brainstem response and sound level tolerance in tinnitus ears and non-tinnitus ears in unilateral tinnitus patients with normal audiograms
      Hyun Joon Shim, Conceptualization, Investigation, Methodology, Validation, Writing – original draft, Writing – review & editing,* Yong-Hwi An, Conceptualization, Methodology, Dong Hyun Kim, Data curation, Formal analysis, Ji Eun Yoon, Data curation, Investigation, and Ji Hyang Yoon, Investigation
      Manuel S. Malmierca, Editor
      Author information ► Article notes ► Copyright and License information ►

      Go to:
      Abstract
      Objective
      Recently, “hidden hearing loss” with cochlear synaptopathy has been suggested as a potential pathophysiology of tinnitus in individuals with a normal hearing threshold. Several studies have demonstrated that subjects with tinnitus and normal audiograms show significantly reduced auditory brainstem response (ABR) wave I amplitudes compared with control subjects, but normal wave V amplitudes, suggesting increased central auditory gain. We aimed to reconfirm the “hidden hearing loss” theory through a within-subject comparison of wave I and wave V amplitudes and uncomfortable loudness level (UCL), which might be decreased with increased central gain, in tinnitus ears (TEs) and non-tinnitus ears (NTEs).

      Subjects and methods
      Human subjects included 43 unilateral tinnitus patients (19 males, 24 females) with normal and symmetric hearing thresholds and 18 control subjects with normal audiograms. The amplitudes of wave I and V from the peak to the following trough were measured twice at 90 dB nHL and we separately assessed UCLs at 500 Hz and 3000 Hz pure tones in each TE and NTE.

      Results
      The within-subject comparison between TEs and NTEs showed no significant differences in wave I and wave V amplitude, or wave V/I ratio in both the male and female groups. Individual data revealed increased V/I amplitude ratios > mean + 2 SD in 3 TEs, but not in any control ears. We found no significant differences in UCL at 500 Hz or 3000 Hz between the TEs and NTEs, but the UCLs of both TEs and NTEs were lower than those of the control ears.

      Conclusions

      Our ABR data do not represent meaningful evidence supporting the hypothesis of cochlear synaptopathy with increased central gain in tinnitus subjects with normal audiograms. However, reduced sound level tolerance in both TEs and NTEs might reflect increased central gain consequent on hidden synaptopathy that was subsequently balanced between the ears by lateral olivocochlear efferents.

      full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5734686/
       
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    7. jer

      jer Member

      Tinnitus Since:
      06/2015
      Cause of Tinnitus:
      Acoustic trauma
      Thank you for continuing to post these. I for one, appreciate it!
       
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    8. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Another article found today: Auditory System Synchronization and Cochlear Function in Patients with Normal Hearing With Tinnitus: Comparison of Multiple Feature with Longer Duration and Single Feature with Shorter Duration Tinnitus

      See attached file
       

      Attached Files:

    9. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      I found this article today but it's about rodents:
      Relationship between Tinnitus and IHC synaptopathy in an animal model
      Hearing loss is often accompanied by comorbidities like tinnitus, a phantom perception of sound which in western civilizations affects up to 15% of the adult population. As studies in rodents could show, tinnitus may not only be a result of hearing loss due to cochlear hair cell damage but can also be a consequence of synaptopathy at the inner hair cells (IHC) already induced by moderate sound traumata (hidden hearing loss, HHL).

      Here we investigate the IHC synaptopathy in our animal model, the Mongolian gerbil, and relate it to behavioral signs of tinnitus in this species. Tinnitus was induced by a mild monaural acoustic trauma which in > 90% of the animals leads to a monaural noise induced hearing loss in the animals, as quantified by brainstem response audiometry. Behavioral signs of tinnitus percepts were detected by GPIAS (gap pre-pulse inhibition of the acoustic startle response) in about two-thirds of the animals. 14 days after trauma the cochleae of traumatized and non-traumatized ears were isolated and inner hair cell synapses were counted within several spectral regions of the cochlea.

      Inner hair cell synaptopathy was only found in animals with behavioral signs of tinnitus, independent of type of hearing loss (HHL or threshold increase). On the other hand, animals with apparent hearing loss but without behavioral signs of tinnitus showed a reduction in amplitudes of auditory brainstem response waves I/II (cochlear nerve and dorsal cochlear nucleus) but no significant changes in the number of synapses at the inner hair cells.

      We conclude – in line with the literature – that hearing loss is caused by damage to the inner and/or outer hair cells, but that the development of tinnitus, at least in our animal model, is closely linked to synaptopathy at the IHC.

      Source: https://www.thieme-connect.com/products/ejournals/html/10.1055/s-0038-1640657
       
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    10. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      I found this article yesterday from Frontiers website. It is strange that this article is not part of the topic "Towards an understanding of tinnitus heterogeneity":

      Deviant dynamics of resting state electroencephalogram microstate in patients with subjective tinnitus
      Yuexin Cai1, 2, 24.jpg Dong Huang3, Yanhong Chen1, 2, 24.jpg Haidi Yang1, 2, Changdong Wang4, Fei Zhao5, 6, Jiahao Liu1, 2, Yingfeng Sun1, 2, Guisheng Chen1, 2, Xiaoting Chen1, 2, Hao Xiong1, 2 and 24.jpg Yiqing Zheng1, 2*
      • 1Department of Otolaryngology, Sun Yat-Sen Memorial Hospital, China
      • 2Institute of Hearing and Speech-Language Science, Sun Yat-sen University, China
      • 3College of mathematics and informatics, South China Agricultural University, China
      • 4School of Data and Computer Science, Sun Yat-sen University, China
      • 5Department of Speech Language Therapy and Hearing Science, Cardiff Metropolitan University, United Kingdom
      • 6Department of Hearing and Speech Science, Xinhua College, Sun Yat-sen University, China
      Given the importance of central reorganization and tinnitus, we undertook the current study to investigate changes to electroencephalogram (EEG) microstates and their association with the clinical symptoms in tinnitus. High-density (128 channel) EEG was used to explore changes in microstate features in 15 subjects with subjective tinnitus and 17 age-matched controls. Correlations between microstate parameters and subjective tinnitus symptoms were also analyzed. An increased presence of class A microstate and decreased presence of class D microstate were found in coverage and lifespan of microstate parameters in the tinnitus patients. Syntax analysis also demonstrated an aberrant pattern of activity, with reduced transitions from Class D to B in tinnitus patients. Moreover, a significant positive correlation of tinnitus loudness with increased lifespan of microstate class C was found. Significant differences in temporal characteristics and syntax of the EEG microstate classes were found at rest between tinnitus patients and the healthy subjects. Our study indicates that EEG microstates may provide a possible valuable method to study large-scale brain networks, which may in turn be beneficial to investigation of the neurophysiological mechanisms behind tinnitus.

      Keywords: EEG, Microstate, dynamics, Tinnitus, Mechanism
      Source: https://www.frontiersin.org/articles/10.3389/fnbeh.2018.00122/abstract
       
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    11. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Audiometric Profiles in Patients With Normal Hearing and Bilateral or Unilateral Tinnitus

      Song, Kudamo*; Shin, Sun, Ae†; Chang, Dong, Sik*; Lee, Ho, Yun*

      Otology & Neurotology: July 2018 - Volume 39 - Issue 6 - p e416–e421
      doi: 10.1097/MAO.0000000000001849
      Audiology
      *Department of Otorhinolaryngology—Head and Neck Surgery, School of Medicine, Eulji University

      †Department of Medical Science, Chungnam National University, Daejeon, Korea

      Address correspondence and reprint requests to Ho Yun Lee, M.D., Department of Otorhinolaryngology—Head and Neck Surgery School of Medicine, Eulji University Medical Center, Eulji University, Dunsan-seoro 95, Seo-Gu, Daejeon 35233, South Korea; E-mail: hoyun1004@gmail.com

      Hypothesis: Patients with subjective nonpulsatile tinnitus and a normal conventional audiogram have more objective audiologic evidence of hidden hearing loss and deafferentation-related pathology than patients without tinnitus.

      Background: The aim of this study was to assess the epidemiologic characteristics and audiologic profiles, including auditory brainstem response (ABR), distortion product otoacoustic emission, and threshold-equalizing noise test results, in patients with tinnitus and a normal audiogram.

      Methods: The test results for 20 patients complaining of nonpulsatile chronic tinnitus were compared with those of 91 subjects with normal hearing and no tinnitus.

      Results: Patients with unilateral tinnitus had higher tinnitus handicap inventory scores than those with bilateral tinnitus (p < 0.05). Threshold-equalizing noise tests were normal in all study participants. In patients with unilateral tinnitus, the ABR and distortion product otoacoustic emission test results were similar to those of controls. In contrast, patients with bilateral tinnitus showed a shortening of latency in wave III of the ABR on the right (p = 0.047) and in wave V on the left (p = 0.024). Logistic regression analysis revealed that enhanced wave III/I (p = 0.018) and V/I (p = 0.012) ratios on the left and poorer pure-tone average on the right were significant risk factors for bilateral tinnitus.

      Conclusion: The mechanism involved in the development of tinnitus may depend on its laterality. Bilateral tinnitusmay be associated with hyperactivity at the level of the cochlear nucleus whereas a higher-order cortical area may be involved in unilateral tinnitus.

      Source: https://journals.lww.com/otology-ne...etric_Profiles_in_Patients_With_Normal.5.aspx
       
    12. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Effects of lifetime noise exposure on the middle-age human auditory brainstem response, tinnitus and speech-in-noise intelligibility
      • a National Acoustic Laboratories, Australian Hearing Hub, 16 University Avenue, Macquarie University, New South Wales, 2109, Sydney, Australia
      • b Department of Linguistics, Australian Hearing Hub, 16 University Avenue, Macquarie University, New South Wales, 2109, Sydney, Australia
      • c The HEARing CRC, 550 Swanston Street, Audiology, Hearing and Speech Sciences, University of Melbourne, Victoria, 3010, Melbourne, Australia
      Received 21 December 2017, Revised 25 May 2018, Accepted 8 June 2018, Available online 12 June 2018
      https://doi.org/10.1016/j.heares.2018.06.003
      Get rights and content
      Highlights

      ABR wave I amplitude negatively correlates with lifetime noise exposure.
      Subjects with tinnitus presented active central gain mechanisms.
      No systematic effect of noise exposure on human auditory evoked activity.
      No clear evidence for noise exposure influencing speech-in-noise performance.
      Central gain and brainstem conduction speed are relevant factors in speech-in-noise.
      Abstract
      Recent animal studies have shown that the synapses between inner hair cells and the dendrites of the spiral ganglion cells they innervate are the elements in the cochlea most vulnerable to excessive noise exposure. Particularly in rodents, several studies have concluded that exposure to high level octave-band noise for 2 h leads to an irreversible loss of around 50% of synaptic ribbons, leaving audiometric hearing thresholds unaltered. Cochlear synaptopathy following noise exposure is hypothesized to degrade the neural encoding of sounds at the subcortical level, which would help explain certain listening-in-noise difficulties reported by some subjects with otherwise ‘normal’ hearing. In response to this peripheral damage, increased gain of central stages of the auditory system has been observed across several species of mammals, particularly in association with tinnitus. The auditory brainstem response (ABR) wave I amplitude and waves I-V amplitude ratio have been suggested as non-invasive indicators of cochlear synaptopathy and central gain activation respectively, but the evidence for these hearing disorders in humans is inconclusive. In this study, we evaluated the influence of lifetime noise exposure (LNE) on the human ABR and on speech-in-noise intelligibility performance in a large cohort of adults aged 29 to 55. Despite large inter-subject variability, results showed a moderate, but statistically significant, negative correlation between the ABR wave I amplitude and LNE, consistent with cochlear synaptopathy. The results also showed (a) that central gain mechanisms observed in animal studies might also occur in humans, in which higher stages of the auditory pathway appear to compensate for reduced input from the cochlea; (b) that tinnitus was associated with activation of central gain mechanisms; (c) that relevant cognitive and subcortical factors influence speech-in-noise intelligibility, in particular, longer ABR waves I-V interpeak latencies were associated with poorer performance in understanding speech in noise when central gain mechanisms were active; and (d) absence of a significant relationship between LNE and tinnitus, central gain activation or speech-in-noise performance. Although this study supports the possible existence of cochlear synaptopathy in humans, the great degree of variability, the lack of uniformity in central gain activation and the significant involvement of attention in speech-in-noise performance suggests that noise-induced cochlear synaptopathy is, at most, one of several factors that play a role in humans' speech-in-noise performance.

      Keywords
      • Noise-induced hearing loss;
      • Cochlear synaptopathy;
      • Hidden hearing loss;
      • Central gain;
      • Speech-in-noise;
      • Cocktail party;
      • Tinnitus
      List of abbreviations
      • ABR: Auditory brainstem response;
      • AI, AIII, AV: Amplitude of waves I, III, and V;
      • AI/AV: Waves I/V amplitude ratio;
      • ANF: Auditory nerve fiber;
      • CAP: Compound action potential;
      • DPOAEs: Distortion product otoacoustic emissions;
      • EEG: Electroencephalogram;
      • HHL: Hidden hearing loss;
      • HL: Hearing level;
      • HL-LF: Hearing loss in low frequencies;
      • HL-HF: Hearing loss in high frequencies;
      • HL-EHF: Hearing loss in extended-high frequencies;
      • IHC: Inner hair cell;
      • LNE: Lifetime noise exposure;
      • LSR: low spontaneous rate;
      • LI, LIII, LV: Latency of waves I, III, and V;
      • LV-LI: Waves I-V interpeak latency;
      • OHC: Outer hair cell;
      • RMSE: Root-mean-square error;
      • SD: Standard deviation;
      • SPL: Sound-pressure level;
      • TE: Test ear;
      • TEA: Test of everyday attention;
      • TIP: TIPtrode placed in the ipsilateral ear canal
      Source: https://www.sciencedirect.com/science/article/pii/S0378595517306287
       
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    13. Samir
      Obedient

      Samir Manager Staff Benefactor Ambassador Advocate

      Location:
      Sweden
      Tinnitus Since:
      12/2016
      Cause of Tinnitus:
      Accoustic trauma
      Nice list of abbreviations! :) I have such list of my own. The trouble with such abbreviations is when there is no consistency and the same abbreviation is used for more than one thing. For example HL can mean Hearing Level as well as Hearing Loss.

      The most difficult one on this list for me is EEG. Electro... encephalo... gram. I always have problems saying this word out loud or even vocalizing it mentally (subvocalization). I'm thankful that there is a globally recognized abbreviation for it. (y)
       
    14. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Disrupted local neural activity and functional connectivity in subjective tinnitus patients: evidence from resting-state fMRI study
      Qi Han, Yang Zhang, Daihong Liu, Yao Wang, Yajin Feng, Xuntao Yin, Jian Wang

      1. Department of Radiology, Southwest HospitalThird Military Medical University (Army Medical University)ChongqingChina
      2. 2.Department of Otolaryngology, Southwest HospitalThird Military Medical University (Army Medical University)ChongqingChina
      Functional Neuroradiology
      First Online: 29 August 2018

      Abstract

      Purpose
      The study aimed to investigate the abnormal alterations of both the intra-regional brain activity and inter-regional functional connectivity (FC) in patients with subjective tinnitus (ST) using resting-state functional MRI (rs-fMRI) methods.

      Methods
      Twenty-five ST patients and 25 normal controls (NCs) were included and underwent resting-state functional magnetic resonance imaging scans. ReHo, fALFF, and seed-based FC were calculated and compared between ST patients and NCs. Meanwhile, correlation analyses were calculated between altered connectivity and clinical data in ST patients.

      Results
      Compared with NCs, ST patients exhibited increased ReHo and fALFF values in the right middle temporal gyrus (MTG), and the ReHo values were also increased in the right cuneus. In contrast, decreased ReHo values in ST patients were observed in the right middle frontal gyrus (MFG) and left cerebellar anterior lobe. Considering these brain areas with altered ReHo and fALFF clusters as seeds, the right MTG (ReHo) exhibited decreased connectivity with the right MFG, lingual gyrus, and left cerebellar posterior lobe, besides, the right cuneus showed decreased connectivity with the right MTG. In ST patients, the decreased FC between the right MTG (ReHo) and the right MFG was also positively correlated with the Tinnitus handicap inventory score (r = 0.675, P = 0.001).

      Conclusion
      The present study revealed that ST patients had altered regional neural activity and inter-regional connectivity in partial auditory and non-auditory brain regions, mainly involving the default mode network and audio-visual network, which could further improve our understanding of the neuroimaging mechanism in ST.

      Keywords
      Fractional amplitude of low-frequency fluctuation Functional connectivity Resting-state functional magnetic resonance imaging Regional homogeneity Subjective tinnitus
      Abbreviations
      ALFF: Amplitude of low-frequency fluctuation
      CNS: Central nervous system
      DMN: Default mode network
      fALFF: Fractional amplitude of low-frequency fluctuation
      FC: Functional connectivity
      FDG: Fluorodeoxyglucose
      FWHM: Full-width at half maximum
      HQ: Hyperacusis questionnaire
      MFG: Middle frontal gyrus
      MTG: Middle temporal gyrus
      NCs: Normal controls
      ReHo: Regional homogeneity

      Source: https://link.springer.com/article/10.1007/s00234-018-2087-0
       
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    15. 85dB T
      Malnourished

      85dB T Member

      Tinnitus Since:
      *
      Cause of Tinnitus:
      *
      Review Article:

      A Brain Centred View of Psychiatric Comorbidity in Tinnitus:
      From Otology to Hodology

      Massimo Salviati,1,2 Francesco Saverio Bersani,2 Giuseppe Valeriani,2
      Amedeo Minichino,2 Roberta Panico,2 Graziella Francesca Romano,2 Filippo Mazzei,1Valeria Testugini,1 Giancarlo Altissimi,1 and Giancarlo Cianfrone1

      1 Department of Sensory Organs, Sapienza University of Rome, Rome, Italy
      2 Department of Neurology and Psychiatry, Sapienza University
       

      Attached Files:

    16. JohnAdams
      Starving

      JohnAdams Member Benefactor Hall of Fame

      Location:
      here
      Tinnitus Since:
      it started.
      Cause of Tinnitus:
      hearing loss
      @Frédéric
      may we have a synopsis of all of this please?
       
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    17. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Wow it is very difficult to have a synopsis since each experience uses a specific tool (MRI, EEG, MEG, ABR...) and targets a specific area of the brain (or a mode). But the protocol remains the same, to highlight one or several differences between a cohort of tinnitus sufferers and a cohort of control subjects. As far as I understood, the main difference is that a system called default mode system (when we are at rest) is no more activated in tinnitus sufferers.
       
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    18. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Reduced sound-evoked and resting-state BOLD fMRI connectivity in tinnitus
      Benedikt Hofmeier, Stephan Wolpert, Ebrahim Saad Aldamer, Moritz Walter, John Thiericke, Christoph Braun, Dennis Zelle, Lukas Rüttiger, Uwe Klose, Marlies Knippera
      https://doi.org/10.1016/j.nicl.2018.08.029Get rights and content

      Highlights
      Tinnitus is linked with reduced rather than enhanced central sound responsiveness.
      Tinnitus allies with reduced sound-evoked BOLD fMRI activity in the auditory cortex
      Tinnitus joins reduced connectivity between lower and higher level auditory regions.
      Tinnitus combines altered connectivities to stress-regulating frontal regions.
      Changed stress-regulating regions in tinnitus may cause blunted cortisol levels.

      Abstract

      The exact neurophysiological basis of chronic tinnitus, which affects 10–15% of the population, remains unknown and is controversial at many levels. It is an open question whether phantom sound perception results from increased central neural gain or not, a crucial question for any future therapeutic intervention strategies for tinnitus.

      We performed a comprehensive study of mild hearing-impaired participants with and without tinnitus, excluding participants with co-occurrences of hyperacusis. A right-hemisphere correlation between tinnitus loudness and auditory perceptual difficulty was observed in the tinnitus group, independent of differences in hearing thresholds. This correlation was linked to reduced and delayed sound-induced suprathreshold auditory brain responses (ABR wave V) in the tinnitus group, suggesting subsided rather than exaggerated central neural responsiveness. When anatomically predefined auditory regions of interest were analysed for altered sound-evoked BOLD fMRI activity, it became evident that subcortical and cortical auditory regions and regions involved in sound detection (posterior insula, hippocampus), responded with reduced BOLD activity in the tinnitus group, emphasizing reduced, rather than increased, central neural gain. Regarding previous findings of evoked BOLD activity being linked to positive connectivities at rest, we additionally analysed r-fcMRI responses in anatomically predefined auditory regions and regions associated with sound detection. A profound reduction in positive interhemispheric connections of homologous auditory brain regions and a decline in the positive connectivities between lower auditory brainstem regions and regions involved in sound detection (hippocampus, posterior insula) were observed in the tinnitus group. The finding went hand-in-hand with the emotional (amygdala, anterior insula) and temporofrontal/stress-regulating regions (prefrontal cortex, inferior frontal gyrus) that were no longer positively connected with auditory cortex regions in the tinnitus group but were instead positively connected to lower-level auditory brainstem regions. Delayed sound processing, reduced sound-evoked BOLD fMRI activity and altered r-fcMRI in the auditory midbrain correlated in the tinnitus group and showed right hemisphere dominance as did tinnitus loudness and perceptual difficulty. The findings suggest that reduced central neural gain in the auditory stream may lead to phantom perception through a failure to energize attentional/stress-regulating networks for contextualization of auditory-specific information. Reduced auditory-specific information flow in tinnitus has until now escaped detection in humans, as low-level auditory brain regions were previously omitted from neuroimaging studies.

      Trial registration: German Clinical Trials Register DRKS0006332.

      Keywords
      Tinnitus, ABR wave, fMRI, R-fcMRI, Cortisol

      Full text: https://www.sciencedirect.com/science/article/pii/S2213158218302705
       
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    19. Greg Sacramento

      Greg Sacramento Member Benefactor Hall of Fame

      Tinnitus Since:
      April 2011
      Cause of Tinnitus:
      syringing and now somatic T dental work
      Many neuro surgeons say on neuro boards that a nerve or group of nerves causes tinnitus. They state it doesn't matter what nerve(s). Mentioned is a nerve(s) can be cut, injured or damaged. Nerve trauma is often caused from toxins, infections or injury. Nerves connect to the lower-level brainstem regions. Discussion talks about how nerves reflect upon hair cell damage.

      It's still to complicated for me to digest.

      Update: I need to add neuro's were talking nerves in the face, neck, face - the head.
       
      Last edited: Sep 5, 2018
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    20. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Eyes and Ears: cross-modal interference of tinnitus on visual processing
      24.jpg Zhicheng Li1, 2, 24.jpg Ruolei Gu3, Xiangli Zeng1*, Min Qi1, Jintian Cen1, Shuqi Zhang1, Jing Gu1 and 24.jpg Qi Chen2*
      • 1Department of Otolaryngology head and neck surgery, Third Affiliated Hospital of Sun Yat-sen University, China
      • 2School of Psychology, South China Normal University, China
      • 3Key Laboratory of Behavioral Science, Institute of Psychology, Chinese Academy of Sciences, China
      The visual processing capacity of tinnitus patients is worse than normal controls, indicating cross-modal interference. However, the mechanism underlying the tinnitus-modulated visual processing is largely unclear. In order to explore the influence of tinnitus on visual processing, this study used a signal recognition paradigm to observe whether the tinnitus group would display a significantly longer reaction time in processing the letter symbols (Experiment 1) and emotional faces (Experiment 2) than the control group. Signal detection and signal recognition, which reflect the perceptual and conceptual aspects of visual processing respectively, were manipulated individually in different conditions to identify the pattern of the cross-modal interference of tinnitus. The results showed that the tinnitus group required a significantly prolonged reaction time in detecting and recognizing the letter symbols and emotional faces than the control group; meanwhile, no between-group difference was detected in signal encoding. In addition, any gender- and distress-modulated effects of processing were not found, suggesting the universality of the present findings. Finally, follow-up studies would be needed to explore the neural mechanism behind the decline in speed of visual processing. The positive emotional bias in tinnitus patients also needs to be further verified and discussed.



      Keywords: Tinnitus, crossmodal, bottom-up attention, Reaction Time, letter recognition, emotional face processing

      Received: 20 Apr 2018; Accepted: 03 Sep 2018.

      Source: https://www.frontiersin.org/articles/10.3389/fpsyg.2018.01779/abstract
       
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    21. JohnAdams
      Starving

      JohnAdams Member Benefactor Hall of Fame

      Location:
      here
      Tinnitus Since:
      it started.
      Cause of Tinnitus:
      hearing loss
      There are progenitor cells in the human auditory nerve that can regenerate.
       
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    22. 85dB T
      Malnourished

      85dB T Member

      Tinnitus Since:
      *
      Cause of Tinnitus:
      *
      Disclaimer: I have no medical training, only pretending here.

      This may be similar to a symptom of severe depression. A delayed reaction to sound is something commonly used to detect a clinical depressive state.

      There are many references to this, here's just one:

      https://www.sciencedirect.com/science/article/pii/0301051181900260
       
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    23. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Changes in the regional shape and volume of subcortical nuclei in patients with tinnitus comorbid with mild hearing loss
      Woo-Suk Tae, Natalia Yakunina, Woo Hyun Lee, Yoon-Jong Ryu, Hyung-kyu Ham, Sung-Bom Pyun, Eui-Cheol Nam

      Brain Convergence Research Center Korea University Seoul Republic of Korea
      Institute of Medical Science, School of Medicine Kangwon National University Chuncheon Republic of Korea
      Department of Otolaryngology Kangwon National University Hospital Chuncheon Republic of Korea
      Department of Otolaryngology, School of Medicine Kangwon National University ChuncheonRepublic of Korea
      Department of Psychology Emory University Atlanta USA
      Department of Physical Medicine and Rehabilitation, College of Medicine Korea University Seoul Republic of Korea

      First Online: 11 September 2018

      Abstract

      Purpose
      Tinnitus, the perception of sound without an external source, is a prevalent disease, but its underlying mechanism has not been fully elucidated. Recent studies have suggested the involvement of subcortical nuclei in tinnitus generation. We investigated changes in the local shape and volume of subcortical nuclei in relation to tinnitus.

      Methods
      The participants included 53 patients with tinnitus and 52 age- and gender-matched normal controls. Individual 3D T1-weighted structural images were obtained using 3-T magnetic resonance imaging. Surface-based vertex analysis (SVA) was performed with automated segmentation of the bilateral caudate nuclei, putamina, nucleus accumbens, thalami, pallidum, hippocampi, amygdalae, and brainstem. The scalar distances from the mean surface and volumes of 15 nuclei were compared between the tinnitus and control groups and correlated with tinnitus handicap score (THI) and tinnitus duration.

      Results
      SVA revealed regional contractions in the accessory basal and lateral nuclei of the right amygdala and expansions in the left medial and right ventral posterior nuclei and lateral dorsal nucleus of both thalami. The surface distances of the right nucleus accumbens were positively correlated with tinnitus duration, while those of the left nucleus accumbens and left hippocampus were negatively correlated with THI.

      Conclusion
      Regional atrophy of the amygdala may indicate self-modulation of emotional response regulation to diminish tinnitus-related emotional distress. Thalamic regional expansion may signify dysfunctional auditory gating in the thalamus, where inhibition of the tinnitus signal at the thalamus level is disrupted due to abnormal changes in the limbic system, ultimately leading to the tinnitus percept.

      Keywords
      Tinnitus Magnetic resonance imaging Surface-based vertex analysis Amygdala Thalamus

      Source: https://link.springer.com/article/10.1007/s00234-018-2093-2
       
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    24. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      A study from Susan Shore and al.:

      Dorsal cochlear nucleus fusiform-cell plasticity is altered in salicylate-induced tinnitus
      David T.Martel, Thibaut R.Pardo-Garcia, Susan E.Shore
      Departments of Biomedical Engineering, University of Michigan, Ann Arbor, Michigan, 48109, United States
      Otolaryngology, University of Michigan, Ann Arbor, Michigan, 48109, United States
      Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan, 48109, United States
      Neuroscience Graduate Program, University of Michigan, Ann Arbor, Michigan, 48109, United States
      Received 2 July 2018, Revised 15 August 2018, Accepted 30 August 2018, Available online 12 September 2018.

      https://doi.org/10.1016/j.neuroscience.2018.08.035Get rights and content

      Highlights
      Stimulus-timing-dependent plasticity is altered in animals administered salicylate.
      Cross-unit synchrony and spontaneous firing rates are increased in animals with salicylate-induced tinnitus.
      Gap-prepulse inhibition of the acoustic startle reflex and an operant conditioning test both indicate animals administered salicylate have tinnitus.
      Salicylate-induced tinnitus and noise-exposure-induced tinnitus could have a similar mechanism.

      Abstract

      Following noise overexposure and tinnitus-induction, fusiform cells of the dorsal cochlear nucleus (DCN) show increased spontaneous firing rates (SFR), increased spontaneous synchrony and altered stimulus-timing dependent plasticity (StDP), which correlate with behavioral measures of tinnitus. Sodium salicylate, the active ingredient in aspirin, which is commonly used to induce tinnitus, increases SFR and activates NMDA receptors in the ascending auditory pathway. NMDA receptor activation is required for StDP in many brain regions, including the DCN. Blocking NMDA receptors can alter StDP timing rules and decrease synchrony in DCN fusiform cells. Thus, systemic activation of NMDA receptors with sodium salicylate should elicit pathological changes to StDP, thereby increasing SFR and synchrony and induce tinnitus. Herein, we examined the action of salicylate in tinnitus generation in guinea pigs in vivo by measuring tinnitus using two behavioral measures and recording single unit responses from DCN fusiform cells pre- and post-salicylate administration in the same animals. First, we show that animals administered salicylate show evidence of tinnitus using both behavioral paradigms, cross-validating the tests. Second, fusiform cells in animals with tinnitus showed increased SFR, synchrony and altered StDP timing rules, like animals with noise-induced tinnitus. These findings suggest that alterations to fusiform-cell plasticity is an essential component of tinnitus, regardless of induction technique.

      Abbreviations
      DCN: Dorsal cochlear nucleus
      SFR: spontaneous firing rate
      StDP: stimulus-timing dependent plasticity
      STDP: spike-timing dependent plasticity
      NMDA: N-methyl-D-aspartate
      VGluT: vesicular glutamate transporter

      Keywords

      Tinnitus
      Stimulus-timing-dependent plasticity
      Dorsal cochlear nucleus
      Fusiform cell
      Salicylate
      Spontaneous firing rate

      Source: https://www.sciencedirect.com/science/article/abs/pii/S0306452218305876
       
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    25. Soren

      Soren Member Benefactor

      Location:
      Denmark
      Tinnitus Since:
      12/2017
      Cause of Tinnitus:
      Loud sound
      And here we are again at the Dorsal cochlear nucleus.
       
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    26. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Even if it concerns guinea pigs:
      Glutamatergic Projections to the Cochlear Nucleus are Redistributed in Tinnitus
      Amarins N.Heering, CalvinWu, Christopher Chung, Michael West, David Martel, Leslie Liberman, M. Charles Liberman, Susan E.Shore
      Kresge Hearing Research Institute, Otolaryngology, University of Michigan, Ann Arbor, MI 48104, USA
      Eaton-Peabody Laboratories, Massachusetts Eye and Ear Infirmary and Department of Otolaryngology, Harvard Medical School, Boston, MA 02114, USA
      Received 11 May 2018, Revised 30 August 2018, Accepted 3 September 2018, Available online 18 September 2018.

      https://doi.org/10.1016/j.neuroscience.2018.09.008Get rights and content

      Highlights

      VGLUT2 puncta density is upregulated in the cochlear nucleus ipsilateral to acoustic.trauma.
      VGLUT1 puncta density is downregulated in the cochlear nucleus contralateral to.acoustic trauma.
      Tinnitus does not correlate with measures of cochlear dysfunction or histopathology.
      VGLUT asymmetries are abolished upon auditory-somatosensory bimodal stimulation. treatment that reversed behavioral tinnitus
      Tinnitus-associated glutamatergic redistribution is likely the result of maladaptive somatosensory compensation
      Abstract
      Tinnitus alters auditory-somatosensory plasticity in the cochlear nucleus (CN). Correspondingly, bimodal auditory-somatosensory stimulation treatment attenuates tinnitus, both in animals and humans (Marks et al., 2018). Therefore, we hypothesized that tinnitus is associated with altered somatosensory innervation of the CN. Here, we studied the expression of vesicular glutamate transporters 1 and 2 (VGLUT1 and VGLUT2) in the CN, which reveals glutamatergic projections from the cochlea as well as somatosensory systems to this brainstem auditory center.

      Guinea pigs were unilaterally exposed to narrowband noise and behaviorally tested for tinnitus using gap-prepulse inhibition of the acoustic startle. Following physiological and behavioral measures, brain sections were immunohistochemically stained for VGLUT1 or VGLUT2. Puncta density was determined for each region of the ipsilateral and contralateral CN.

      Tinnitus was associated with an ipsilateral upregulation of VGLUT2 puncta density in the granule cell domain (GCD) and anteroventral CN (AVCN). Furthermore, there was a tinnitus-associated interaural asymmetry for VGLUT1 expression in the AVCN and deep layer of the dorsal CN (DCN3), due to contralateral downregulation of VGLUT1 expression. These tinnitus-related glutamatergic imbalances were reversed upon bimodal-stimulation treatment.

      Tinnitus-associated ipsilateral upregulation of VGLUT2-positive projections likely derives from somatosensory projections to the GCD and AVCN. This upregulation may underlie the neurophysiological hallmarks of tinnitus in the CN. Reversing the increased ipsilateral glutamatergic innervation in the CN is likely a key mechanism in treating tinnitus.

      Abbreviations
      ABR: auditory brainstem response
      AVCN: anteroventral cochlear nucleus
      CN: cochlear nucleus
      DCN: dorsal cochlear nucleus
      DCN1: molecular layer of the dorsal cochlear nucleus
      DCN3: deep layer of the dorsal cochlear nucleus
      ET: exposed tinnitus
      ENT: exposed no tinnitus
      ETT: exposed tinnitus treated
      GCD: granule cell domain
      GI: gap index
      GPIAS: gap-pre pulse inhibition of the acoustic startle reflex
      icp: inferior cerebellar peduncle
      N: sham-exposed control animals
      PBS: phosphate buffered saline
      PFA: paraformaldehyde
      PVCN: posteroventral cochlear nuclues
      Sp5: spinal trigeminal nucleus
      sp5: spinal trigeminal tract
      TTS: temporary threshold shift
      tz: trapezoid body
      VCN: ventral cochlear nucleus
      VGLUT1: vesicular glutamate transporter 1
      VGLUT2: vesicular glutamate transporter 2
      Keywords
      Auditory
      Cross-modal compensation
      Noise exposure
      Synaptopathy
      VGLUT1
      VGLUT2

      Source: https://www.sciencedirect.com/science/article/abs/pii/S0306452218305979
       
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    27. Greg Sacramento

      Greg Sacramento Member Benefactor Hall of Fame

      Tinnitus Since:
      April 2011
      Cause of Tinnitus:
      syringing and now somatic T dental work
      @Frédéric
      Sp5
      spinal trigeminal nucleus
      sp5
      spinal trigeminal tract
      TTS
      temporary threshold shift
      tz
      trapezoid body

      Susan Shore had discussed this years ago - Basically the cause is muscles spasms of the muscles in back and neck with an open extended jaw or pressure on the jaw when the neck is extended. This is how TMD/tinnitus often happens combined with CN input.
       
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    28. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Tinnitus Impacts on Speech and Non-speech Stimuli
      Omidvar, Shaghayegh*,†; Mahmoudian, Saeid‡; Khabazkhoob, Mehdi§; Ahadi, Mohsen*; Jafari, Zahra||,¶
      Otology & Neurotology: September 19, 2018 - Volume Publish Ahead of Print - Issue - p
      doi: 10.1097/MAO.0000000000002002

      *Department of Audiology, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran
      †Department of Audiology, School of Rehabilitation Sciences, Shiraz University of Medical Sciences, Shiraz
      ‡ENT and Head & Neck Research Center, Iran University of Medical Sciences
      §Department of Medical Surgical Nursing, School of Nursing and Midwifery, Shahid Beheshti University of Medical Sciences
      ||Department of Basic Sciences in Rehabilitation, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran
      ¶Department of Neuroscience, Canadian Center for Behavioral Neuroscience, University of Lethbridge, Lethbridge, Alberta, Canada

      Address correspondence and reprint requests to Zahra Jafari, Ph.D., Department of Basic Sciences in Rehabilitation, School of Rehabilitation Sciences, Iran University of Medical Sciences, Tehran, Iran; E-mail: jafari.z@iums.ac.ir, zahra.jafari@uleth.ca
      This work was supported by Iran University of Medical Sciences (Grant# 93D.3303.320).
      None of the authors have potential conflicts of interest to be disclosed.

      Objective: To investigate how tinnitus affects the processing of speech and non-speech stimuli at the subcorticallevel.

      Study Design: Cross-sectional analytical study.

      Setting: Academic, tertiary referral center.

      Patients: Eighteen individuals with tinnitus and 20 controls without tinnitus matched based on their age and sex. All subjects had normal hearing sensitivity.

      Intervention: Diagnostic.

      Main Outcome Measures: The effect of tinnitus on the parameters of auditory brainstem responses (ABR) to non-speech (click-ABR), and speech (sABR) stimuli was investigated.

      Results: Latencies of click ABR in waves III, V, and Vn, as well as inter-peak latency (IPL) of I to V were significantly longer in individuals with tinnitus compared with the controls. Individuals with tinnitus demonstrated significantly longer latencies of all sABR waves than the control group. The tinnitus patients also exhibited a significant decrease in the slope of the V-A complex and reduced encoding of the first and higher formants. A significant difference was observed between the two groups in the spectral magnitudes, the first formant frequency range (F1) and a higher frequency region (HF).

      Conclusions: Our findings suggest that maladaptive neural plasticity resulting from tinnitus can be subcortically measured and affects timing processing of both speech and non-speech stimuli. The findings have been discussed based on models of maladaptive plasticity and the interference of tinnitus as an internal noise in synthesizing speech auditory stimuli.

      Copyright © 2018 by Otology & Neurotology, Inc. Image copyright © 2010 Wolters Kluwer Health/Anatomical Chart Company

      Source: https://journals.lww.com/otology-ne...s_on_Speech_and_Non_speech_Stimuli.96638.aspx
       
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    29. Greg Sacramento

      Greg Sacramento Member Benefactor Hall of Fame

      Tinnitus Since:
      April 2011
      Cause of Tinnitus:
      syringing and now somatic T dental work
      This is interesting as the frontal and temporal lobes - the Broca area has major influence from the CNS.
       
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    30. AUTHOR
      AUTHOR
      Frédéric

      Frédéric Member Benefactor

      Location:
      Marseille, France
      Tinnitus Since:
      11/19/2012
      Cause of Tinnitus:
      acoustic trauma
      Normal hearing young adults with mild tinnitus: Reduced inhibition as measured through sensory gating
      DOI https://doi.org/10.4081/audiores.2018.214

      Julia Campbell *
      Department of Communication Sciences and Disorders; Central Sensory Processes Laboratory, University of Texas at Austin, Austin, Texas, United States.
      Connor Bean
      Department of Communication Sciences and Disorders; Central Sensory Processes Laboratory, University of Texas at Austin, Austin, Texas, United States.
      Alison LaBrec
      Department of Communication Sciences and Disorders; Central Sensory Processes Laboratory, University of Texas at Austin, Austin, Texas, United States.
      (*) Corresponding Author:
      Julia Campbell | busta.png julia.campbell@austin.utexas.edu

      Abstract

      Decreased central inhibition, possibly related to hearing loss, may contribute to chronic tinnitus. However, many individuals with normal hearing thresholds report tinnitus, suggesting that the percept in this population may arise from sources other than peripheral deafferentation. One measure of inhibition is sensory gating. Sensory gating involves the suppression of non-novel input, and is measured through cortical auditory evoked potential (CAEP) responses to paired stimuli. In typical gating function, amplitude suppression is observed in the second CAEP response when compared to the first CAEP response, illustrating inhibitory activity. Using this measure, we investigated central inhibitory processes in normal hearing young adults with and without mild tinnitus to determine whether inhibition may be a contributing factor to the tinnitus percept. Results showed that gating function was impaired in the tinnitus group, with the CAEP Pa component significantly correlated with tinnitus severity. Further exploratory analyses were conducted to evaluate variability in gating function within the tinnitus group, and findings showed that high CAEP amplitude suppressors demonstrated gating performance comparable to adults without tinnitus, while low amplitude suppressors exhibited atypical gating function.

      Source: https://audiologyresearch.org/index.php/audio/article/view/214
       
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