Evidence map›Paper›PMID 28286099›Full record

ArticleHearing research2017

Tinnitus and hyperacusis: Contributions of paraflocculus, reticular formation and stress.

Yu-Chen Chen, Guang-Di Chen, Benjamin D Auerbach, Senthilvelan Manohar, Kelly Radziwon, Richard Salvi

Open access · hybridAbstract read
In one paragraph

Article in Hearing research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 49 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Yu-Chen ChenDepartment of Radiology, Nanjing First Hospital, Nanjing Medical University, 210006 Nanjing, China; Center for Hearing and Deafness, SUNY at Buffalo, Buffalo, NY 14214, USA.
Guang-Di ChenCenter for Hearing and Deafness, SUNY at Buffalo, Buffalo, NY 14214, USA. Electronic address: gchen7@buffalo.edu.
Benjamin D AuerbachCenter for Hearing and Deafness, SUNY at Buffalo, Buffalo, NY 14214, USA.
Senthilvelan ManoharCenter for Hearing and Deafness, SUNY at Buffalo, Buffalo, NY 14214, USA.
Kelly RadziwonCenter for Hearing and Deafness, SUNY at Buffalo, Buffalo, NY 14214, USA.
Richard SalviCenter for Hearing and Deafness, SUNY at Buffalo, Buffalo, NY 14214, USA.
Women & Children's Hospital of Buffalo · USBuffalo State University · US

Funding

Hyperacusis and Central GainR01DC014693 · NIDCD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SALVI, RICHARD J · 2016 to 2020
$2.3M
Neural Basis of HyperacusisR01DC014452 · NIDCD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SALVI, RICHARD J · 2016 to 2020
$2.0M
Occupational exposure to manganese and noise potentiate hearing lossR01OH010235 · OH · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI ROTH, JEROME ALLAN, SALVI, RICHARD J · 2012 to 2015
$2.0M
The Role of Central Gain Control in Hyperacusis of Diverse OriginF32DC015160 · NIDCD · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI AUERBACH, BENJAMIN D · 2016 to 2018
$183k
NIDCD NIH HHS F32 DC015160NIDCD NIH HHS R01 DC014452NIDCD NIH HHS R01 DC014693NIOSH CDC HHS R01 OH010235
6 · The paper itself

Abstract

Tinnitus and hyperacusis are common and potentially serious hearing disorders associated with noise-, age- or drug-induced hearing loss. Accumulating evidence suggests that tinnitus and hyperacusis are linked to excessive neural activity in a distributed brain network that not only includes the central auditory pathway, but also brain regions involved in arousal, emotion, stress and motor control. Here we examine electrophysiological changes in two novel non-auditory areas implicated in tinnitus and hyperacusis: the caudal pontine reticular nucleus (PnC), involved in arousal, and the paraflocculus lobe of the cerebellum (PFL), implicated in head-eye coordination and gating tinnitus and we measure the changes in corticosterone stress hormone levels. Using the salicylate-induced model of tinnitus and hyperacusis, we found that long-latency (>10 ms) sound-evoked response components in both the brain regions were significantly enhanced after salicylate administration, while the short-latency responses were reduced, likely reflecting cochlear hearing loss. These results are consistent with the central gain model of tinnitus and hyperacusis, which proposes that these disorders arise from the amplification of neural activity in central auditory pathway plus other regions linked to arousal, emotion, tinnitus gating and motor control. Finally, we demonstrate that salicylate results in an increase in corticosterone level in a dose-dependent manner consistent with the notion that stress may interact with hearing loss in tinnitus and hyperacusis development. This increased stress response has the potential to have wide-ranging effects on the central nervous system and may therefore contribute to brain-wide changes in neural activity.

Indexed as

Acoustic StimulationAnimalsAuditory PathwaysBehavior, AnimalBiomarkersCerebellumCorticosteroneDisease Models, AnimalEmotionsEvoked Potentials, AuditoryHearingHyperacusisMaleMidbrain Reticular FormationMotor ActivityPontine TegmentumBiomarkersCorticosteroneSodium SalicylateCorticosteroneHyperacusisParaflocculusReticular formationSalicylateStressTinnitus

Identifiers

PMID28286099
PMCPMC5438778
OpenAlexW2592878232

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.