ライフサイエンスコーパス: tinnitus

1 omposer is interference from internal noise (tinnitus).

2 ndidate for treating epilepsy and preventing tinnitus.

3 ral processing impairments, hyperacusis, and tinnitus.

4 osed adult rats with behavioural evidence of tinnitus.

5 ed and sleep disturbance are associated with tinnitus.

6 non-auditory neuronal networks, resulting in tinnitus.

7 ies are being developed for the treatment of tinnitus.

8 ound-exposure gap inhibition animal model of tinnitus.

9 he varied neuropsychiatric manifestations of tinnitus.

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

11 egative voltages prevents the development of tinnitus.

12 ng one experienced a transient withdrawal of tinnitus.

13 ablishing the cause of unilateral, pulsatile tinnitus.

14 rained by the heterogeneity of patients with tinnitus.

15 , 8 of the 13 blasted rats exhibited chronic tinnitus.

16 lecules that participate in the induction of tinnitus.

17 at must certainly generate the perception of tinnitus.

18 ompatible with a maladaptive central gain in tinnitus.

19 ther Sham animals or exposed animals without tinnitus.

20 a possible neural correlate of noise-induced tinnitus.

21 ies of the Kv7 channel and the generation of tinnitus.

22 idate the use of animal data in the study of tinnitus.

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

24 neurons in the neural reorganization causing tinnitus.

25 percept and not to an affective reaction to tinnitus.

26 ochlear damage resulting in hearing loss and tinnitus.

27 to objectively measure neural correlates of tinnitus.

28 reporting of outcomes in clinical trials of tinnitus.

29 ral activity, which are neural correlates of tinnitus.

30 ivity in a group of 17 patients with chronic tinnitus.

31 -too-common "musicians' hearing loss" and/or tinnitus.

32 an be correlated with behavioral evidence of tinnitus.

33 vance our understanding of the mechanisms of tinnitus.

34 es, but it is unclear if hearing loss causes tinnitus.

35 somatosensory-auditory processing accompany tinnitus.

36 arrow band noise and behaviorally tested for tinnitus.

37 al spontaneous hyperactivity associated with tinnitus.

38 DCN is correlated with peripheral damage and tinnitus.

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

40 hyperactivity that has been associated with tinnitus.

41 plicate the dorsal cochlear nucleus (DCN) in tinnitus.

42 targets to ameliorate the effects of chronic tinnitus.

43 might suppress abnormal cortical activity in tinnitus.

44 sed animals, especially those that developed tinnitus.

45 nvolved in the generation and maintenance of tinnitus.

46 ing are de facto physiological correlates of tinnitus.

47 esetting of the default prediction to expect tinnitus.

48 th frequency-specific behavioral measures of tinnitus.

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

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

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

52 ned activity in the DCN may underlie central tinnitus.

53 therapeutics that may promote resilience to tinnitus.

54 onal hyperexcitability, such as epilepsy and tinnitus.

55 r outcome measurements in clinical trials of tinnitus.

56 otransmitter dysfunction in the pathology of tinnitus.

57 Tinnitus: [1] effects 50 million individuals, [2] often

58 ulting in a Type-I auditory neural-generated tinnitus; [4] dynorphins participate in central NMDA-rec

59 Tinnitus (40% patients) was significantly correlated wit

60 It has long been known that subjective tinnitus, a constant or intermittent phantom sound perce

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

62 Tinnitus, a phantom auditory sensation, is associated wi

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

64 ue opportunity to study the relation between tinnitus and brain activity.

65 Tinnitus and chronic pain may reflect thalamocortical dy

66 Tinnitus and cochlear damage have been associated with c

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

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

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

70 and were assessed for behavioral evidence of tinnitus and hearing loss immediately after the noise tr

71 in aged animals with behavioral evidence of tinnitus and hearing loss.

72 More specifically, tinnitus and hyperacusis could result from an increase o

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

74 rats with a dose of salicylate that induces tinnitus and hyperacusis-like behavior.

75 elieved to play a major role in debilitating tinnitus and hyperacusis.

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

77 em in an effort to relieve the perception of tinnitus and its impact on one's emotional and mental st

78 ase the perception and emotional salience of tinnitus and loud sounds.

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

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

81 ivity (hyperacusis) to loudness recruitment, tinnitus and non-tinnitus ears were carefully matched fo

82 rved only in noise-exposed mice that develop tinnitus and only in the dorsal cochlear nucleus regions

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

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

85 icating that stress and emotion can modulate tinnitus, and from brain imaging studies showing functio

86 les in the enhancement phase in animals with tinnitus, and in the suppressive phase in exposed animal

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

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

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

90 t develop tinnitus, timing rules in verified tinnitus animals were more likely to be anti-Hebbian and

91 People who experience tinnitus are another important participant group.

92 A total of 60% of the guinea pigs developed tinnitus as indicated by gap-induced prepulse inhibition

93 reflex (ASR) became a popular technique for tinnitus assessment in laboratory animals.

94 correctly apply gap detection techniques for tinnitus assessment in laboratory animals.

95 nough to be replicated, but are critical for tinnitus assessment.

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

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

98 as significantly correlated to the degree of tinnitus behavior, assessed via a loss of gap detection

99 Moreover, in conditions of tinnitus, bimodal integration in DCN is enhanced, produc

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

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

102 Tinnitus can occur when damage to the peripheral auditor

103 ght be effective for that condition, but the tinnitus can persist.

104 f the most common causes of hearing loss and tinnitus, can increase the auditory cortex (AC) response

105 t, unilateral, treatment-resistant pulsatile tinnitus caused by a small dural arteriovenous fistula r

106 onse in vmPFC was positively correlated with tinnitus characteristics such as subjective loudness and

107 Patients presenting with tinnitus commonly have neuropsychiatric symptoms with wh

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

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

110 auditory sensitivity should be increased in tinnitus compared with non-tinnitus subjects.

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

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

113 nnitus intensity in order to measure dynamic tinnitus correlates in individual patients.

114 he predictions of our computational model of tinnitus development, which proposes a possible mechanis

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

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

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

118 acerbate chronic subjective neural-generated tinnitus during periods of heightened stress.

119 and other variables known to be affected in tinnitus (e.g., depression, anxiety, noise sensitivity,

120 ction by examining the loudness functions in tinnitus ears (n = 124) compared with non-tinnitus human

121 s) to loudness recruitment, tinnitus and non-tinnitus ears were carefully matched for hearing loss.

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

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

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

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

126 However, the tinnitus field is changing.

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

128 ndent (BOLD) responses to stimulation at the tinnitus frequency in the ventral striatum (specifically

129 ght be an important underlying mechanism for tinnitus generation.

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

131 Gaze-evoked tinnitus (GET) is a rare form of tinnitus that may arise

132 onnectivity in the lower frequencies for the tinnitus group.

133 bands that is significantly stronger in the tinnitus group.

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

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

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

137 tus was perceived, whereas correlations with tinnitus handicap inventory scores and other variables k

138 Tinnitus has been related to hyperactivity in the centra

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

140 role of the medial geniculate body (MGB) in tinnitus has not been previously addressed, specifically

141 in tinnitus ears (n = 124) compared with non-tinnitus human ears (n = 106).

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

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

144 ic inhibition, have successfully ameliorated tinnitus in animal studies, suggesting that the MGB and,

145 chnique has been successfully used to assess tinnitus in different laboratory animals, many of the fi

146 ic drugs that may prevent the development of tinnitus in humans.

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

148 nection between the somatosensory system and tinnitus in patients we sought to determine whether plas

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

150 Subjects typically describe tinnitus in the deaf ear on the side of the surgery that

151 ies near the pitch of the salicylate-induced tinnitus in the rat).

152 Rare causes of tinnitus include cranial dural arteriovenous fistulas (D

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

154 the first support of this loop hypothesis of tinnitus, independent of the initial experiments that le

155 ci in which we examined the contrast between tinnitus individuals and controls and the difference in

156 n between sound stimuli and resting state in tinnitus individuals.

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

158 in Kv7.2/3 channel activity is essential for tinnitus induction and for the tinnitus-specific hyperac

159 After noise exposure and tinnitus induction, stimulus timing-dependent plasticity

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

161 ted an inverse correlation between perceived tinnitus intensity and auditory cortex gamma oscillation

162 ion, a positive correlation was seen between tinnitus intensity and both delta/theta (6/14 patients)

163 bring about transient changes in spontaneous tinnitus intensity in order to measure dynamic tinnitus

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

165 Tinnitus is a common disorder that often complicates hea

166 Tinnitus is a common medical symptom that can be debilit

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

168 Tinnitus is a phantom sound percept that can be severely

169 Tinnitus is an auditory percept without an environmental

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

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

172 Tinnitus is developed in mice that do not compensate for

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

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

175 Because tinnitus is often accompanied by hearing loss and that h

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

177 Tinnitus is the perception of sound in the absence of a

178 Tinnitus is the phantom perception of sounds occurring i

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

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

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

185 Furthermore, increased tinnitus loudness is represented by increased activity i

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

187 nd raise the possibility that attenuation of tinnitus may be achievable by using an agonist of the ch

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

189 Tinnitus may result from lesions occurring at any locati

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

191 for any otological pathology associated with tinnitus might be effective for that condition, but the

192 timing dependence of bimodal plasticity in a tinnitus model.

193 Contemporary tinnitus models hypothesize tinnitus to be a consequence

194 studying its disruption in hearing loss and tinnitus models.

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

196 ults suggest that the areas described in the tinnitus network are solidly replicable regardless of th

197 article is part of a Special Issue entitled: Tinnitus Neuroscience.

198 article is part of a Special Issue entitled: Tinnitus Neuroscience.

199 article is part of a Special Issue entitled: Tinnitus Neuroscience.

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

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

202 Tinnitus, occurring at least once in a lifetime in about

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

204 One patient reported grade 4 tinnitus, one patient reported grade 4 thrombosis, one r

205 ndent plasticity as underlying mechanisms in tinnitus, opening the way for a therapeutic target.

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

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 Other symptoms included plugging, pruritus, tinnitus, pain, and bleeding.

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

211 lation of GABA(A)Rs, which may be altered in tinnitus pathology, and its key anatomical position in t

212 itory receptors in key circuits to normalize tinnitus pathophysiology.

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

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

215 g functional differences in vmPFC between 20 tinnitus patients and 20 age-matched controls.

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

217 fferences in limbic-related brain regions of tinnitus patients and controls.

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

219 n ventromedial prefrontal cortex (vmPFC), of tinnitus patients compared to controls.

220 this condition is relatively uncommon among tinnitus patients, induction of phantom sounds by a less

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

222 te the somatic-auditory interactions seen in tinnitus patients.

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

224 es are indeed related to the strength of the tinnitus percept and not to an affective reaction to tin

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

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

227 Tinnitus perception depends on the presence of its neura

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 In tinnitus, PET and other functional imaging modalities ha

232 (10-20 kHz), frequencies associated with the tinnitus pitch.

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

234 , permitting robust characterization of core tinnitus processes.

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

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

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

238 geting inhibition, which stems from reported tinnitus-related homeostatic plasticity of inhibitory ne

239 gic inputs, it might be possible to suppress tinnitus-related hyperactivity of fusiform cells using t

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

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

242 Tinnitus-related maladaptive plastic changes of MGB-rela

243 udy proves that PET is a useful modality for tinnitus research and solidifies human tinnitus research

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

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

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

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

248 A major goal of tinnitus research is to find the loci of the neural chan

249 y for tinnitus research and solidifies human tinnitus research itself by confirming previously descri

250 CNS make the MGB a compelling structure for tinnitus research.

251 ional and mental state has become a focus of tinnitus research.

252 orate vmPFC as a region of high interest for tinnitus research.This article is part of a Special Issu

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

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

255 gnificant positive correlation with animals' tinnitus scores.

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

257 Tinnitus severity and hearing loss were correlated posit

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

259 Paresthesias (hands and feet) and tinnitus showed significant three- to four-fold increase

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

261 development of an animal behavioral model of tinnitus, so that neural changes can be correlated with

262 cated for some patients, but availability of tinnitus-specific CBT in the UK is poor.

263 essential for tinnitus induction and for the tinnitus-specific hyperactivity.

264 ing the dorsal cochlear nucleus, we reveal a tinnitus-specific increase in the spontaneous firing rat

265 stable phantom sounds on day 7 and underwent tinnitus spectrum characterization with the earplug stil

266 sponse, respectively, associated with higher tinnitus states.

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

268 The high prevalence of hyperacusis in tinnitus subjects suggests that both symptoms have a com

269 und stimuli, compared with resting state, in tinnitus subjects was the secondary auditory cortex.

270 t the most consistently activated regions in tinnitus subjects, compared with controls, were the left

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

272 d be increased in tinnitus compared with non-tinnitus subjects.

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

274 Gaze-evoked tinnitus (GET) is a rare form of tinnitus that may arise after vestibular schwannoma remo

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

276 Tinnitus, the perception of a phantom sound, is a common

277 Tinnitus, the perception of phantom sound, is often a de

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

279 d noise-exposed animals that did not develop tinnitus, timing rules in verified tinnitus animals were

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

281 on of the AC support a model that attributes tinnitus to a dysrhythmia of the thalamocortical loop, l

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

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

284 ion and why these agents may be effective in tinnitus treatment.

285 o undertake a metaanalysis of PET studies on tinnitus using a coordinate-based technique (activation-

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

287 Tinnitus was evaluated with a gap detection acoustic sta

288 suppressive phase in exposed animals without tinnitus was in contrast to narrow, Hebbian-like timing

289 ess and the percent of time during which the tinnitus was perceived, whereas correlations with tinnit

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

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

292 Furthermore, units from exposed animals with tinnitus were more weakly suppressed than either Sham an

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

294 Hypertension, headache, and pulsatile tinnitus were the most common presenting symptoms of the

295 o the development of a neuronal correlate of tinnitus when auditory nerve activity is reduced due to

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

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

298 sound, is a common symptom in patients with tinnitus, Williams syndrome, autism, and other neurologi

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

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