Tinnitus does not require macroscopic tonotopic map reorganization

Langers, Dave R. M.; Kleine, Emile de; Dijk, Pim van

doi:10.3389/fnsys.2012.00002

Cited by 140 publications

(105 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2007) and the transient N1 response known to localize to distributed sources in the region of the auditory parabelt (called here nonprimary auditory cortex, A2). ASSR sources show a coarse but consistent low-frequency anterolateral, high-frequency posteromedial tonotopic organization (Pantev et al, 1996;Wienbruch et al, 2006;Gander et al, 2010a) that reflects the summation of extracellular field potentials across two cochleotopic maps with strong low-frequency anterolateral and high-frequency posteromedial activations in Heschl's gyrus (Langers et al, 2012). In contrast, N1 sources localize to distributed and cytoarchitectonically heterogeneous regions of A2 (Godey et al, 2001) where tonotopy is lacking or not strongly expressed (Schreiner and Cynader, 1984;Langers et al, 2007;Lütkenh€ oner et al, 2003).…”

Section: Introductionmentioning

confidence: 95%

Evidence for differential modulation of primary and nonprimary auditory cortex by forward masking in tinnitus

et al. 2015

View full text Add to dashboard Cite

It has been proposed that tinnitus is generated by aberrant neural activity that develops among neurons in tonotopic of regions of primary auditory cortex (A1) affected by hearing loss, which is also the frequency region where tinnitus percepts localize (Eggermont and Roberts 2004; Roberts et al., 2010, 2013). These models suggest (1) that differences between tinnitus and control groups of similar age and audiometric function should depend on whether A1 is probed in tinnitus frequency region (TFR) or below it, and (2) that brain responses evoked from A1 should track changes in the tinnitus percept when residual inhibition (RI) is induced by forward masking. We tested these predictions by measuring (128-channel EEG) the sound-evoked 40-Hz auditory steady-state response (ASSR) known to localize tonotopically to neural sources in A1. For comparison the N1 transient response localizing to distributed neural sources in nonprimary cortex (A2) was also studied. When tested under baseline conditions where tinnitus subjects would have heard their tinnitus, ASSR responses were larger in a tinnitus group than in controls when evoked by 500 Hz probes while the reverse was true for tinnitus and control groups tested with 5 kHz probes, confirming frequency-dependent group differences in this measure. On subsequent trials where RI was induced by masking (narrow band noise centered at 5 kHz), ASSR amplitude increased in the tinnitus group probed at 5 kHz but not in the tinnitus group probed at 500 Hz. When collapsed into a single sample tinnitus subjects reporting comparatively greater RI depth and duration showed comparatively larger ASSR increases after masking regardless of probe frequency. Effects of masking on ASSR amplitude in the control groups were completely reversed from those in the tinnitus groups, with no change seen to 5 kHz probes but ASSR increases to 500 Hz probes even though the masking sound contained no energy at 500 Hz (an "off-frequency" masking effect). In contrast to these findings for the ASSR, N1 amplitude was larger in tinnitus than control groups at both probe frequencies under baseline conditions, decreased after masking in all conditions, and did not relate to RI. These results suggest that aberrant neural activity occurring in the TFR of A1 underlies tinnitus and its modulation during RI. They indicate further that while neural changes occur in A2 in tinnitus, these changes do not reflect the tinnitus percept. Models for tinnitus and forward masking are described that integrate these findings within a common framework.

show abstract

Section: Introductionmentioning

confidence: 95%

Evidence for differential modulation of primary and nonprimary auditory cortex by forward masking in tinnitus

et al. 2015

View full text Add to dashboard Cite

show abstract

“…None of them had a history of neurological or psychiatric disorders. Subjects' characteristics are listed in Table 1 (Langers et al 2012). Except for the presence of tinnitus in the patient group, all subjects were selected to have normal or near-normal hearing up to 8 kHz.…”

Section: Participantsmentioning

confidence: 99%

Tinnitus- and Task-Related Differences in Resting-State Networks

Lanting

WoźAniak

Dijk

et al. 2016

Advances in Experimental Medicine and Biology

Self Cite

View full text Add to dashboard Cite

We investigated tinnitus-related differences in functional networks in adults with tinnitus by means of a functional connectivity study. Previously it was found that various networks show differences in connectivity in patients with tinnitus compared to controls. How this relates to patients' ongoing tinnitus and whether the ecological sensory environment modulates connectivity remains unknown. Twenty healthy controls and twenty patients suffering from chronic tinnitus were enrolled in this study. Except for the presence of tinnitus in the patient group, all subjects were selected to have normal or near-normal hearing. fMRI data were obtained in two different functional states. In one set of runs, subjects freely viewed emotionally salient movie fragments ("fixed-state") while in the other they were not performing any task ("resting-state"). After data pre-processing, Principal Component Analysis was performed to obtain 25 components for all datasets. These were fed into an Independent Component Analysis (ICA), concatenating the data across both groups and both datasets, to obtain group-level networks of neural origin, each consisting of spatial maps with their respective time-courses. Subject-specific maps and their time-course were obtained by back-projection (Dual Regression). For each of the components a mixed-effects linear model was composed with factors group (tinnitus vs. controls), task (fixed-state vs. resting state) and their interaction. The neural components comprised the visual, sensorimotor, auditory, and limbic systems, the default mode, dorsal attention, executive-control, and frontoparietal networks, and the cerebellum. Most notably, the default mode network (DMN) was less extensive and shows significantly less connectivity in tinnitus patients than in controls. This group difference existed in both paradigms. At the same time, the DMN was stronger during resting-state than during fixed-state in the controls but not the patients. We attribute this pattern to the unremitting engaging effect of the tinnitus percept.

show abstract

“…However, tonotopic reorganizations and altered efferent activity may not be present in all cases of tinnitus. Functional MRIs performed by Langers, de Kleine and van Dijk (2012) indicated that macroscopic tonotopic reorganization is not common for tinnitus patients with normal hearing thresholds 19 . Furthermore, IC neural recordings performed by Bauer et al (2008) revealed significantly increased contralateral IC spontaneous spiking and cross fiber synchrony in chinchillas with tinnitus (as indicated by behavioral paradigms) with no evidence of a tonotopic edge effect or tuning frequency shift 20 .…”

Section: Introductionmentioning

confidence: 99%

“…In the case of tinnitus accompanied by hearing loss, it is believed that tinnitus pitch is either localized in the "edge" frequencies or within the lowest regions of the hearing loss 19 . If tinnitus pitch exists within the lowest portions of the corresponding hearing loss, then theoretically, specific subcortical neural fibers act as the direct factor of tinnitus percept 19 .…”

mentioning

confidence: 99%

“…If tinnitus pitch exists within the lowest portions of the corresponding hearing loss, then theoretically, specific subcortical neural fibers act as the direct factor of tinnitus percept 19 . However, if tinnitus percept exists at the "edge" frequency, alterations of the tonotopic map would be implicated as the primary source of tinnitus percept, possibly supplemented by affected IC tuning curves 19 . Abnormal synchronous neural activity can be detected by specialized clinical tests.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Detailed Analysis of High Frequency Auditory Brainstem Response in Patients with Tinnitus: A Preliminary Study

Pinkl

Wilson

Billingsly

et al. 2017

The International Tinnitus Journal

View full text Add to dashboard Cite

Increased spontaneous activity and aberrant neural synchrony is thought to be the underlying cause of tinnitus. The perceived pitch of tinnitus may be dictated by frequency specific neural fibers of the subcortical pathway, or the projection of altered cortical activity by-way-of tonotopic reorganizations. Subcortical neural activity in relation to tinnitus was characterized using ABR measurements. In the present study, 11 patients (21 ears) with constant tonal tinnitus underwent a two-part experiment. Experiment 1 involved click ABR measurements and included two experimental groups: tinnitus with normal hearing from 2000-4000 Hz (GI) and tinnitus with hearing loss within the range of 2000-4000 Hz (GII). Experiment 2 utilized tone burst ABRs matched to each participant's perceived tinnitus pitch and included two experimental groups: tinnitus with normal hearing at the tinnitus pitch (GIa) and tinnitus with hearing loss at the tinnitus pitch (GIIa). These groups were compared to a control group (GIII) of ten monaurally tested (10 ears) participants with normal hearing thresholds at 250-20000 Hz and no tinnitus. Click ABR results indicate significantly prolonged V-III IPLs for GI and GII and a significantly extended absolute V latency for GII only. Tone burst ABRs matched to tinnitus pitch revealed significantly prolonged absolute latencies and IPLs at three of the seven frequencies for GIIa. ABR threshold seeking was completed and revealed negative eHL values for two of the four different stimuli for GI and GIa and four of the eight stimuli for GII and GIIa. Click ABRs results are suggestive of upper brainstem abnormalities for both groups. While GI demonstrated prolonged V-III IPLs, no significant differences were found for GIa. This suggests that there is no frequency specific subcortical characteristic associated with tinnitus with normal hearing. Frequency specific properties for subcortical activity could not be characterized due to varying results of GIIa.

show abstract

Tinnitus does not require macroscopic tonotopic map reorganization

Cited by 140 publications

References 70 publications

Evidence for differential modulation of primary and nonprimary auditory cortex by forward masking in tinnitus

Evidence for differential modulation of primary and nonprimary auditory cortex by forward masking in tinnitus

Tinnitus- and Task-Related Differences in Resting-State Networks

Detailed Analysis of High Frequency Auditory Brainstem Response in Patients with Tinnitus: A Preliminary Study

Contact Info

Product

Resources

About