ライフサイエンスコーパス: tinnitus

1 omposer is interference from internal noise (tinnitus).

2 innitus and a parahippocampal cortex related tinnitus.

3 has been proposed for the treatment of tonal tinnitus.

4 ternal sounds and the top-down perception of tinnitus.

5 g-impaired controls presented with simulated tinnitus.

6 mals with and without behavioral evidence of tinnitus.

7 rmore, people with normal audiograms can get tinnitus.

8 headache and non-headache subjects with any tinnitus.

9 sely others with hearing loss do not develop tinnitus.

10 tonic inhibitory networks and thus suppress tinnitus.

11 ral processing impairments, hyperacusis, and tinnitus.

12 ng one experienced a transient withdrawal of tinnitus.

13 , 8 of the 13 blasted rats exhibited chronic tinnitus.

14 nd gaps, which is often considered a sign of tinnitus.

15 reporting of outcomes in clinical trials of tinnitus.

16 eatures include fever, nausea, vomiting, and tinnitus.

17 ing are de facto physiological correlates of tinnitus.

18 esetting of the default prediction to expect tinnitus.

19 th frequency-specific behavioral measures of tinnitus.

20 d with sensorineural hearing loss (SNHL) and tinnitus.

21 o 12 kHz), tests of middle ear function, and tinnitus.

22 s, including epilepsy, neuropathic pain, and tinnitus.

23 ned activity in the DCN may underlie central tinnitus.

24 therapeutics that may promote resilience to tinnitus.

25 k of developing AD/PD increases after having tinnitus.

26 onal hyperexcitability, such as epilepsy and tinnitus.

27 r outcome measurements in clinical trials of tinnitus.

28 otransmitter dysfunction in the pathology of tinnitus.

29 ndidate for treating epilepsy and preventing tinnitus.

30 rther illuminate central interference due to tinnitus.

31 osed adult rats with behavioural evidence of tinnitus.

32 ed and sleep disturbance are associated with tinnitus.

33 non-auditory neuronal networks, resulting in tinnitus.

34 ies are being developed for the treatment of tinnitus.

35 ound-exposure gap inhibition animal model of tinnitus.

36 he varied neuropsychiatric manifestations of tinnitus.

37 sis, is a pervasive complaint of people with tinnitus.

38 are a characteristic of hearing loss, not of tinnitus.

39 ng loss-induced tonotopic reorganization and tinnitus.

40 26% and reached 40% in subjects with severe tinnitus.

41 al sound and a separate top-down pathway for tinnitus.

42 in normal hearing listeners with or without tinnitus.

43 sociated with pathologic adaptation, such as tinnitus.

44 There was an association with tinnitus.

45 reorganization than in hearing loss without tinnitus.

46 prominent in the hearing loss group without tinnitus.

47 yet little is known on how headaches impact tinnitus.

48 ed with tinnitus but does not always lead to tinnitus.

49 d 27 young, normal-hearing listeners without tinnitus (11 females and 16 males).

50 asks between 45 human listeners with chronic tinnitus (18 females and 27 males with a range of ages a

51 -year follow-up period, 398 individuals with tinnitus (3.1%) and 501 control individuals (2.0%) devel

52 Tinnitus (40% patients) was significantly correlated wit

53 stead of reversing it.SIGNIFICANCE STATEMENT Tinnitus, a common and potentially devastating condition

54 Tinnitus, a phantom auditory percept, is encoded by path

55 ntom percepts.SIGNIFICANCE STATEMENT Chronic tinnitus affects 15% of the population worldwide.

56 The mechanism through which tinnitus affects attention is unclear.

57 ests two distinct types of bottom-up related tinnitus: an auditory cortex related tinnitus and a para

58 related tinnitus: an auditory cortex related tinnitus and a parahippocampal cortex related tinnitus.

59 is observation suggests a connection between tinnitus and an incomplete form of central compensation

60 Urinary albumin levels increased, with tinnitus and atrial arrhythmias more common, in the sals

61 rtant factor in the causal mechanism between tinnitus and attention.

62 Tinnitus and chronic pain may reflect thalamocortical dy

63 our understanding of the pathophysiology of tinnitus and connect tinnitus to the neuropsychiatric sy

64 ypertension (n=2 [5%]), insomnia (n=1 [2%]), tinnitus and dizziness (n=1 [2%]), and thrombocytopenia

65 r ear defined by sensorineural hearing loss, tinnitus and episodic vertigo, and familial MD is observ

66 covered an asymmetrical relationship between tinnitus and external sounds: although external sounds h

67 Eighteen participants with tinnitus and fifteen controls completed the Counting Str

68 Our results indicate an association between tinnitus and higher risk of developing AD and PD.

69 Considering that hearing disorders such as tinnitus and hyperacusis have been linked to abnormal an

70 firm the diversity of the personal impact of tinnitus and illustrate a lack of consensus in what aspe

71 of acoustic overstimulation associated with tinnitus and impaired speech perception cause cochlear s

72 o unilateral 14 psi blast exposure to induce tinnitus and measured auditory and limbic brain activity

73 results in the context of current models of tinnitus and methodological constraints.

74 mmation as a therapeutic target for treating tinnitus and other hearing loss-related disorders.

75 r to noise trauma prevents the occurrence of tinnitus and reduction in GABAergic inhibition.

76 findings support a striatal gating model of tinnitus and suggest tinnitus biomarkers to monitor trea

77 istress mediates the relationship(s) between tinnitus and sustained, selective and executive attentio

78 igh-frequency hearing loss, with and without tinnitus, and a control group were included.

79 an include headaches, visual loss, pulsatile tinnitus, and back and neck pain, but the clinical prese

80 He experienced swallowing difficulties, tinnitus, and fecal incontinence, and he had undergone c

81 SFR), correlated with behavioral evidence of tinnitus, and increased synchrony and bursting were asso

82 iving tDCS had higher rates of skin redness, tinnitus, and nervousness than did those in the other tw

83 ual disturbance, additional visual symptoms, tinnitus, and non-perceptional symptoms.

84 ciple neurons of the DCN, in normal hearing, tinnitus, and non-tinnitus guinea pigs.

85 clarify the relations between hearing loss, tinnitus, and tonotopic reorganization.

86 People who experience tinnitus are another important participant group.

87 Auditory phantom percepts such as tinnitus are associated with auditory deafferentation.

88 tus (odds ratio, OR = 2.61) and more so with tinnitus as a big problem (as measured by the tinnitus f

89 jury and sensory deprivation, it can lead to tinnitus as an unwanted side effect.

90 , we provide evidence for a top-down type of tinnitus associated with a deficient noise-cancelling me

91 articipants with tonal and non-blast induced tinnitus at the end of 6 (24.3% vs. 2%, p = 0.05) and 12

92 models of hearing damage, which also produce tinnitus based on behavioral evidence, have identified a

93 tion, and may form the basis of a convenient tinnitus biomarker, which we name Intensity Mismatch Asy

94 triatal gating model of tinnitus and suggest tinnitus biomarkers to monitor treatment response and to

95 the differential effect of hearing loss and tinnitus, both male and female participants with bilater

96 erexposure is a major factor associated with tinnitus but does not always lead to tinnitus.

97 lities of brain activity are associated with tinnitus, but it is unclear how these relate to the phan

98 In summary, tinnitus can be regarded as a maladaptive 'disconnection

99 This is in accordance with the idea that tinnitus can have different generators as proposed in a

100 Tinnitus can occur when damage to the peripheral auditor

101 We propose that tinnitus can only develop after fast auditory fiber acti

102 Patients presenting with tinnitus commonly have neuropsychiatric symptoms with wh

103 roject is described which engages the global tinnitus community (patients and professionals alike) in

104 y and in certain limbic regions of rats with tinnitus compared to age-matched controls.

105 Tonndorf Lecture presented at the 1st World Tinnitus Congress and the 12th International Tinnitus Se

106 c oxide synthase increases when animals have tinnitus (Coomber et al., 2015).

107 Demonstrating "core" tinnitus correlates (processes that are both necessary a

108 n-inhibition balance could influence whether tinnitus develops and its severity if it does.

109 suggests that headaches could contribute to tinnitus distress and potentially its severity.

110 Tinnitus distress was assessed using the Tinnitus Questi

111 he auditory cortex and areas associated with tinnitus distress, including the cingulate cortex.

112 gnificant morbidity, including hearing loss, tinnitus, dizziness, and possibly even death from brains

113 have been widely used to cover up tinnitus, tinnitus does not impair, and sometimes even improves, t

114 contradictory to the widely held assumption, tinnitus does not interfere with the perception of exter

115 firing patterns only in animals that develop tinnitus, driving activity in central brain regions and

116 s of a group of 14 patients with lateralized tinnitus (eight left ear) and 14 controls matched for ag

117 Thus, the neural representation of tinnitus emerges early in auditory processing and likely

118 MGB units in animals with tinnitus exhibited enhanced spontaneous firing, altered

119 There is also evidence that the tinnitus experienced by listeners with clinically normal

120 However, the tinnitus field is changing.

121 ernal sounds, leading to hypotheses such as "tinnitus filling in the temporal gap" in animal models a

122 ope alone, over 70 million people experience tinnitus; for seven million people, it creates a debilit

123 o begin to distinguish neural changes due to tinnitus from those that are due to hearing loss.

124 t caudate and cuneus was correlated with the Tinnitus Functional Index (TFI) relaxation subscale.

125 innitus as a big problem (as measured by the tinnitus functional index, TFI >= 48; OR = 5.63) or seve

126 ings support a prediction resetting model of tinnitus generation, and may form the basis of a conveni

127 lear nucleus (DCN), key brainstem neurons in tinnitus generation.

128 tonotopic maps for the hearing loss without tinnitus group were significantly different from the con

129 ate to the controls and hearing loss without tinnitus group.

130 onnectivity in the lower frequencies for the tinnitus group.

131 bands that is significantly stronger in the tinnitus group.

132 he DCN, in normal hearing, tinnitus, and non-tinnitus guinea pigs.

133 weeks, the paired VNS group improved on the Tinnitus Handicap Inventory (THI) (p = 0.0012) compared

134 ated with the percentage improvements in the Tinnitus Handicap Inventory (THI) scores, and numeric ra

135 48; OR = 5.63) or severe tinnitus (using the tinnitus handicap inventory, THI >= 58; OR = 4.99).

136 Tinnitus has been implied as a "soft" sign of neurodegen

137 Historically, tinnitus has been the poor cousin of hearing science, wi

138 The term "tinnitus" however represents a highly heterogeneous cond

139 Hearing loss is a major risk factor for tinnitus, hyperacusis, and central auditory processing d

140 nts, back pain in 53%, and pulse synchronous tinnitus in 52%.

141 nd gaps, a commonly used behavioral sign for tinnitus in animal models.

142 lpha into AI resulted in behavioral signs of tinnitus in both wild-type and TNF-alpha knockout mice w

143 istress significantly mediated the effect of tinnitus in incongruent trials (TQ: Sobel test t = 1.73,

144 ted the behavioral phenotype associated with tinnitus in mice with NIHL.

145 ogical depletion of microglia also prevented tinnitus in mice with NIHL.

146 hermore, SF0034 prevented the development of tinnitus in mice.

147 -induced hearing loss (NIHL) and its role in tinnitus in rodent models.

148 t synchrony and bursting have been linked to tinnitus in several higher auditory stations but not in

149 Bothersome tinnitus in single-sided deafness (SSD) is particularly

150 enous dilatation, paresthesia, headache, and tinnitus) in the setting of extreme erythrocytosis.

151 We provide an overview of tinnitus, including its types and pathophysiology.

152 tent with this idea, our research shows that tinnitus indeed has different subtypes related to hearin

153 g in the temporal gap" in animal models and "tinnitus inducing hearing difficulty" in human subjects.

154 Months after a tinnitus-inducing sound exposure, gaboxadol-evoked tonic

155 dorsal cochlear nucleus (DCN), the putative tinnitus-induction site, exhibit increased synchrony.

156 ty in the auditory cortex, whereas bottom-up tinnitus instead relates to changes in the parahippocamp

157 andards for outcomes in clinical trials of a tinnitus intervention.

158 Tinnitus is a common disorder that often complicates hea

159 Tinnitus is a phantom sound commonly thought of to be pr

160 Tinnitus is a sound heard by 15% of the general populati

161 Tinnitus is an auditory percept without an environmental

162 Subjective tinnitus is an auditory phantom perceptual disorder with

163 olled for hearing loss and hyperacusis, that tinnitus is associated with a significant reduction in a

164 Vulnerability to noise-induced tinnitus is associated with increased spontaneous firing

165 external sounds can sometimes mask tinnitus, tinnitus is assumed to affect the perception of external

166 We tested the popular, unproven theory that tinnitus is caused by resetting of auditory predictions

167 Tinnitus is developed in mice that do not compensate for

168 Resilience to tinnitus is developed in mice that show a re-emergence o

169 The heterogeneity of tinnitus is likely accounting for the lack of effective

170 havioral paradigm in which the perception of tinnitus is manipulated and accurately reported by the s

171 The interference caused by tinnitus is more likely central in origin.

172 , postsynaptic gain) rises sufficiently then tinnitus is perceived.

173 We demonstrate that top-down related tinnitus is related to a change in the pregenual anterio

174 s large fMRI study, we provide evidence that tinnitus is related to a more conservative form of reorg

175 sult contrasts with the previous notion that tinnitus is related to excessive reorganization.

176 Subjective tinnitus is the conscious perception of sound in the abs

177 an alternative model based on evidence that tinnitus is: (1) rare in people who are congenitally dea

178 work suggests a shift in focus from treating tinnitus itself to treating its comorbid conditions and

179 relationships of GABA inhibitory changes to tinnitus itself, as opposed to other consequences of hea

180 Permanently affecting one in seven adults, tinnitus lacks both widely effective treatments and adeq

181 Regardless of tinnitus laterality, post hoc testing indicated reductio

182 lation of sensory predictions, to unattended tinnitus-like sounds were greater in response to upward

183 As anticipated, we observed tinnitus-linked low-frequency (delta) oscillations [5-9]

184 during short-term modifications in perceived tinnitus loudness after acoustic stimulation (residual i

185 es, and numeric rating scale (NRS) scores of tinnitus loudness and tinnitus perception.

186 ty in the auditory cortex is correlated with tinnitus loudness, we assessed resting-state source-loca

187 As a consequence, treatments for tinnitus may need to enhance the cortical plasticity, ra

188 r, our data suggest that while blast-induced tinnitus may play a role in auditory and limbic hyperact

189 The literature suggests various tinnitus mechanisms, most of which invoke changes in spo

190 posed mice that do not develop tinnitus (non-tinnitus mice), remain unknown.

191 olving attention and central noise in animal tinnitus models but also a shift in focus from treating

192 Contemporary tinnitus models hypothesize tinnitus to be a consequence

193 control that have been described in previous tinnitus models.

194 aluate the association between headaches and tinnitus (n = 1,984 cases and 1,661 controls) and ii) in

195 ic characteristics of tinnitus subjects with tinnitus (n = 660) or without (n = 1,879) headaches.

196 The present data suggest that tinnitus negatively affected masked speech recognition e

197 and the parahippocampus, areas that generate tinnitus, negatively correlated with improvements in lou

198 inst an SSD cohort with no or non-bothersome tinnitus (NO TIN; N = 15) using resting-state functional

199 sound exposed with no behavioral evidence of tinnitus (Non-T).

200 ed in noise-exposed mice that do not develop tinnitus (non-tinnitus mice), remain unknown.

201 It is not known why tinnitus occurs in some cases of hearing damage but not

202 the theory that auditory phantom perception (tinnitus) occurs when a default auditory prediction is f

203 adache was significantly associated with any tinnitus (odds ratio, OR = 2.61) and more so with tinnit

204 , it may be relevant to temporary or chronic tinnitus or to some other aftereffect of long-duration s

205 increased risk of ototoxicity (hearing loss, tinnitus, or both).

206 viduals with tinnitus.SIGNIFICANCE STATEMENT Tinnitus, or ringing in the ears, is a neurologic disord

207 sing deficits that commonly accompany aging, tinnitus, ototoxic drug exposure or noise damage.

208 neurophysiological and integrative models of tinnitus; our results serve as a milestone in the develo

209 We use cross-sectional data from the Swedish Tinnitus Outreach Project to i) evaluate the association

210 th tonotopic maps and response amplitudes of tinnitus participants appear intermediate to the control

211 Tinnitus participants had significantly slower reactions

212 ges in GABAergic function may be markers for tinnitus pathology in the MGB.

213 The proposed framework unites many ideas of tinnitus pathophysiology and may catalyze cooperative ef

214 racranial recordings from an awake, behaving tinnitus patient during short-term modifications in perc

215 We then explain why treatment of the tinnitus patient falls within the purview of neuropsychi

216 als (2.0%) developed AD (P < 0.001), and 211 tinnitus patients (1.7%) and 249 control patients (1.0%)

217 trospective matched cohort study with 12,657 tinnitus patients and 25,314 controls from the National

218 y using the average resting state EEG of 311 tinnitus patients and 256 healthy controls.

219 ith tones may be effective for a subgroup of tinnitus patients and provides impetus for a larger pivo

220 oncentration difficulties are common amongst tinnitus patients in clinical settings and these afflict

221 Many tinnitus patients report difficulties understanding spee

222 We find that chronic tinnitus patients show an abnormal pattern of evoked res

223 nal masking via lexical interference may tax tinnitus patients' central auditory processing resources

224 three months of VNS-tone pairing in chronic tinnitus patients.

225 mulation (VNS) paired with sounds in chronic tinnitus patients.

226 d likely contributes to the formation of the tinnitus percept.

227 Improvements in the NRS scores of tinnitus perception correlated positively with the pre-T

228 g can help patients to achieve reductions in tinnitus perception or to expedite motor rehabilitation

229 s that are both necessary and sufficient for tinnitus perception) requires high-precision recordings

230 scale (NRS) scores of tinnitus loudness and tinnitus perception.

231 internal sounds, and several other puzzling tinnitus phenomena such as discrepancy in loudness betwe

232 und the frequency of a tone that matched the tinnitus pitch, f(T), with fixed ratios relative to f(T)

233 subcortical auditory pathway constitutes a 'tinnitus precursor' which is normally ignored as impreci

234 , permitting robust characterization of core tinnitus processes.

235 Tinnitus distress was assessed using the Tinnitus Questionnaire (TQ), severity of depressive mood

236 mena such as discrepancy in loudness between tinnitus rating and matching.

237 clude routine inquiry for hearing status and tinnitus, referral to audiologists as clinically indicat

238 These tinnitus-related changes in GABAergic function may be ma

239 In summary, we found little evidence of tinnitus-related decreases in GABAergic neurotransmissio

240 Tinnitus-related distress significantly mediated the eff

241 rovement in NF2-related QOL and reduction in tinnitus-related distress were reported in 30% and 60% o

242 ked tonic GABAAR currents showed significant tinnitus-related increases contralateral to the sound ex

243 In agreement with this hypothesis, we found tinnitus-related increases in tonic extrasynaptic GABAAR

244 Tinnitus-related maladaptive plastic changes of MGB-rela

245 uli are symmetrically spaced relative to the tinnitus-related population of abnormally synchronized c

246 Tinnitus-related risk on developing AD/PD followingly wa

247 We demonstrate that top-down related tinnitus relates to a change in the pregenual anterior c

248 eflect on the present and future progress of tinnitus research and treatment and what is needed for t

249 This project seeks to improve future tinnitus research by creating an evidence-based consensu

250 Importantly, this would enhance tinnitus research by informing sample-size calculations,

251 as approved funding to create a pan-European tinnitus research collaboration network (2014-2018).

252 inclusivity and brings together clinicians, tinnitus researchers, experts on clinical research metho

253 Although tinnitus retraining therapy (TRT) is efficacious in most

254 gnificant positive correlation with animals' tinnitus scores.

255 Tinnitus Congress and the 12th International Tinnitus Seminar in Warsaw, Poland, provided an opportun

256 Tinnitus severity and hearing loss were correlated posit

257 Tinnitus severity appeared to especially limit listeners

258 With increasing tinnitus severity, fewer differences were found, the maj

259 plication of this may be that treatments for tinnitus shift their focus toward enhancing the cortical

260 trate a lack of consensus in what aspects of tinnitus should be assessed and reported in a clinical t

261 about hearing difficulty in individuals with tinnitus.SIGNIFICANCE STATEMENT Tinnitus, or ringing in

262 a, otorrhea, otalgia, vertigo, autophony, or tinnitus since her adoption.

263 xperiments, clinical studies, other types of tinnitus sound treatment such as tailor-made notch music

264 Tinnitus, sound perception in the absence of physical st

265 Examining tinnitus-specific changes in single-cell populations ena

266 d provides fairly accurate classification of tinnitus status at the individual subject level.

267 how that auditory sensitivity is enhanced in tinnitus subjects compared with non-tinnitus subjects, i

268 intensity deviants in 26 unselected chronic tinnitus subjects with normal to severely impaired heari

269 nvestigate the phenotypic characteristics of tinnitus subjects with tinnitus (n = 660) or without (n

270 o severely impaired hearing, and in 15 acute tinnitus subjects, but not in 26 hearing and age-matched

271 anced in tinnitus subjects compared with non-tinnitus subjects, including subjects with normal audiog

272 controlled for hearing loss, we establish a tinnitus subtype associated with a deficient top-down no

273 yses, and facilitating the identification of tinnitus subtypes, ultimately leading to improved treatm

274 Existing animal models represent tinnitus that may not be distinguishable from homeostati

275 Tinnitus, the perception of phantom sounds, is thought t

276 When focusing on subjects with tinnitus, the prevalence of headaches was 26% and reache

277 tists, clinicians, and even individuals with tinnitus themselves, who often report hearing difficulty

278 may catalyze cooperative efforts to develop tinnitus therapies.

279 ); sound exposed with behavioral evidence of tinnitus (Tin); and sound exposed with no behavioral evi

280 We contrasted an SSD cohort with bothersome tinnitus (TIN; N = 15) against an SSD cohort with no or

281 nal sounds have been widely used to cover up tinnitus, tinnitus does not impair, and sometimes even i

282 Because external sounds can sometimes mask tinnitus, tinnitus is assumed to affect the perception o

283 Contemporary tinnitus models hypothesize tinnitus to be a consequence of maladaptive plasticity-i

284 dels but also a shift in focus from treating tinnitus to managing its comorbid conditions when addres

285 the pathophysiology of tinnitus and connect tinnitus to the neuropsychiatric symptoms.

286 ional index, TFI >= 48; OR = 5.63) or severe tinnitus (using the tinnitus handicap inventory, THI >=

287 The presence of tinnitus was associated with a reduction in auditory cor

288 Tinnitus was evaluated with a gap detection acoustic sta

289 inhibition of the acoustic startle to assess tinnitus, we recorded spontaneous activity from fusiform

290 Compared with controls, patients with tinnitus were 1.54 times more likely to develop AD (95%

291 PTSD arousal symptoms and tinnitus were directly dependent upon blast exposure, wi

292 the controls, whereas the maps of those with tinnitus were not.

293 Thirty-two patients with debilitating tinnitus were prospectively enrolled, and qEEG data were

294 why some people without hearing loss develop tinnitus, whereas conversely others with hearing loss do

295 physical mechanisms underlying resilience to tinnitus, which is observed in noise-exposed mice that d

296 f auditory system plasticity associated with tinnitus, which may provide a testable assay for future

297 ates of effect and with devices marketed for tinnitus without strong evidence for those product claim

298 essing is gained through sensory experience, tinnitus would not exist in congenital deafness.

299 Headaches have been related to tinnitus, yet little is known on how headaches impact ti

300 ral auditory processing disorders, including tinnitus, yet the changes in synaptic connectivity under