Auditory evoked cortical magnetic field (M100—M200) measurements in tinnitus and normal groups

Jacobson, Gary P.; Ahmad, B. K.; Moran, John; Newman, Craig W.; Tepley, N.; Wharton, Jeanne A.

doi:10.1016/0378-5955(91)90152-y

Cited by 53 publications

(30 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Other neuromagnetic studies, however, failed to support these findings [Jacobson et al, 1991;Saermark and Mikkelsen, 1993]. Contrary to earlier reports [Shiraishi et al, 1991;Attias et al, 1993], Attias et al [1996a] found, in a standard oddball target detection paradigm in tinnitus patients, significantly prolonged latencies for the auditory non-target ERP waves N 1 , N 2 and P 3 and for the auditory target ERP wave P 3 .…”

Section: Event-related Potentials (Erp) or Fieldscontrasting

confidence: 51%

Tinnitus and Event-Related Activity of the Auditory Cortex

Hoke

Mühlnickel²,

Roß³

et al. 1998

Audiol Neurotol

View full text Add to dashboard Cite

A neuromagnetic study in tinnitus patients and normal-hearing controls was performed with a modified contingent negative variation (CNV) paradigm. While the warning stimulus S1 was a tone burst at an intensity well above threshold, the imperative stimulus S2 was presented at a near threshold intensity because, in the majority of cases, the perceived loudness of tinnitus is very close to the threshold for a pure tone of the same frequency. Subjects had to respond to S2 by pressing a button until its offset was detected. In this case, instead of the usual sudden cut-off of the CNV after the perception of S2, a slow negative deflection develops, the post-imperative negative variation (PINV). Its initial portion probably indicates the development of a second initial CNV because the subject had to attend also to the offset of S2. The neuromagnetic data were analysed both in the time domain and in the frequency domain (short-time spectral analysis of the classical EEG bands). The time domain waveform as well as the spectrotemporal patterns of the MEG bands exhibited deviations from the normal pattern in several tinnitus subgroups, depending on the characteristics of tinnitus (tonal vs. noisiform, monaural vs. binaural) and on the stimulation conditions (tinnitus side vs. non-tinnitus side).

show abstract

Section: Event-related Potentials (Erp) or Fieldscontrasting

confidence: 51%

Tinnitus and Event-Related Activity of the Auditory Cortex

Hoke

Mühlnickel²,

Roß³

et al. 1998

Audiol Neurotol

View full text Add to dashboard Cite

show abstract

“…Hoke et al, 1989;Jacobson et al, 1991;Attias et al, 1993), and occasionally even the same group fails to replicate their own earlier findings (e.g. Weisz et al, 2007a;Kahlbrock and Weisz, 2008).…”

Section: Discussionmentioning

confidence: 83%

“…Using MEG or EEG, an abnormally elevated response to external sounds (hyperexcitability) has also been shown to co-occur with TI (e.g. Hoke et al, 1989;Noreña et al, 1999;Kadner at al., 2002), but such hyperexcitability has been reported at frequencies unrelated to the dominant TI pitch and a number of studies have failed to replicate these results (Jacobson et al, 1991;Colding-Jorgensen et al, 1992;Attias et al, 1993), suggesting that this abnormal activity is unlikely to underpin the TI percept. The main focus of our review discusses the evidence for the three mechanisms, linking the animal models to current perspectives from human neuroimaging.…”

Section: The Neural Mechanisms Of Timentioning

confidence: 99%

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

2009

View full text Add to dashboard Cite

In this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power. AbstractIn this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power.

show abstract

“…When the data of this study were analyzed for N1 amplitude (Diesch et al, 2012), N1 amplitude decreased with increasing carrier frequency in both groups but did not differ significantly between the groups (a finding that was interpreted to suggest that ASSR responses in tinnitus do not reflect attention). Overall, prior research comparing N1 responses between tinnitus and normal hearing subjects have produced an unclear picture with some studies reporting increases in N1 amplitude or N1 loudness growth functions in tinnitus subjects compared to controls for tones presented near the edge of the tinnitus (hearing loss) region (Dietrich et al, 2001;Noreña et al, 1999;Hoke et al, 1989), while other studies have reported either decreases in these variables at frequencies in the TFR (Sereda et al, 2013) or below or near the audiometric edge (Kadner et al, 2002;Lee et al, 2007), or no changes at all in N1 amplitude in tinnitus subjects compared to controls (Jacobson et al, 1991;Jacobson and McCaslin, 2003;Diesch et al, 2012;Sereda et al, 2013).…”

Section: Previous Studies Of Assr and N1 Responses In Tinnitus And Rimentioning

confidence: 93%

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

Auditory evoked cortical magnetic field (M100—M200) measurements in tinnitus and normal groups

Cited by 53 publications

References 11 publications

Tinnitus and Event-Related Activity of the Auditory Cortex

Tinnitus and Event-Related Activity of the Auditory Cortex

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

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

Contact Info

Product

Resources

About