Abstract:Sensory training therapies for tinnitus are based on the assumption that, notwithstanding neural changes related to tinnitus, auditory training can alter the response properties of neurons in auditory pathways. To assess this assumption, we investigated whether brain changes induced by sensory training in tinnitus sufferers and measured by electroencephalography (EEG) are similar to those induced in age and hearing loss matched individuals without tinnitus trained on the same auditory task. Auditory training w… Show more
“…3a, collapsed over the tinnitus and control groups. These topographies and waveforms are similar to those we have observed previously when probing control and tinnitus subjects with 500 Hz and 5 kHz 40-Hz AM stimuli (Roberts et al, 2012;Paul et al, 2014) and normal hearing subjects with 2 kHz 40-Hz AM stimuli (Gander et al, 2010a(Gander et al, , 2010b. Following practices adopted in these previous studies, a Fourier transform was applied to the two-pulse waveforms for each subject.…”
Section: Electrophysiological Recordingmentioning
confidence: 89%
“…Fig. 6b presents typical results from an independent study (Roberts et al, 2012) where subjects were probed at 5 kHz in two EEG sessions separated by about 6 days. These data returned a ratio 18.9 and r ¼ 0.90 (p < 0.0001), indicating that individual differences in ASSR amplitude while large are stable across days and reapplication of the recording sensors.…”
Section: Effects Of Maskingmentioning
confidence: 98%
“…The first analysis assessed differences in age, audiometric hearing loss, and probe sound level between tinnitus and control groups tested at each carrier frequency. Although the mean age of subjects in the control/500 group (43.9 years) was 10.5 years younger than the Roberts et al, 2012). ASSR amplitude is measured as total field power (TFP) at 40 Hz.…”
Section: Effects Of Age Hearing Loss and Sound Level On Brain Respomentioning
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.
“…3a, collapsed over the tinnitus and control groups. These topographies and waveforms are similar to those we have observed previously when probing control and tinnitus subjects with 500 Hz and 5 kHz 40-Hz AM stimuli (Roberts et al, 2012;Paul et al, 2014) and normal hearing subjects with 2 kHz 40-Hz AM stimuli (Gander et al, 2010a(Gander et al, , 2010b. Following practices adopted in these previous studies, a Fourier transform was applied to the two-pulse waveforms for each subject.…”
Section: Electrophysiological Recordingmentioning
confidence: 89%
“…Fig. 6b presents typical results from an independent study (Roberts et al, 2012) where subjects were probed at 5 kHz in two EEG sessions separated by about 6 days. These data returned a ratio 18.9 and r ¼ 0.90 (p < 0.0001), indicating that individual differences in ASSR amplitude while large are stable across days and reapplication of the recording sensors.…”
Section: Effects Of Maskingmentioning
confidence: 98%
“…The first analysis assessed differences in age, audiometric hearing loss, and probe sound level between tinnitus and control groups tested at each carrier frequency. Although the mean age of subjects in the control/500 group (43.9 years) was 10.5 years younger than the Roberts et al, 2012). ASSR amplitude is measured as total field power (TFP) at 40 Hz.…”
Section: Effects Of Age Hearing Loss and Sound Level On Brain Respomentioning
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.
“…According to recent estimations, approximately 50 million people in the US and 70 million people in the European Union are affected by tinnitus [5]. Although previous research and treatment focused on the inner ear, it has since been widely accepted that tinnitus should not 10 be considered as a sole dysfunction of the ear, even though tinnitus is usually preceded by and associated with substantial to minor or even hidden peripheral hearing loss [6,7]. Instead, it has widely been agreed that tinnitus emanates from a perplexing network that includes the inner ear, the auditory pathway, and non-auditory brain areas [8,9,10,11,12].…”
Structural neuroimaging techniques have been used to identify cortical and subcortical regions constituting the neuroarchitecture of tinnitus. One recent investigation used voxel-based morphometry (VBM) to analyze a sample of tinnitus patients (TI, n=257) [1]. A negative relationship between individual distress and cortical volume (CV) in bilateral auditory regions was observed. However, CV has meanwhile been identified as a neuroanatomical measurement that confounds genetically distinct neuroanatomical traits, namely cortical thickness (CT) and cortical surface area (CSA). We performed a re-analysis of the identical sample using the automated FreeSurfer surface-based morphometry (SBM) approach [2]. First, we replicated the negative correlation between tinnitus distress and bilateral supratemporal gray matter volume. Second, we observed a negative correlation for CSA in the left peri-auditory cortex and anterior insula. Furthermore, we noted a positive correlation between tinnitus duration and CT in the left peri-auditory cortex as well as a negative correlation in the subcallosal anterior cingulate, a region collated to the serotonergic circuit and germane to inhibitory functions. In short, the results elucidate differential neuroanatomical alterations of CSA and CT for the two independent tinnitus-related psychological traits distress and duration. Beyond this, the study provides further evidence for the distinction and specific susceptibility of CSA and CT within the context of neuroplasticity of the human brain. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A negative relationship between individual distress and cortical volume (CV) in bilateral auditory regions was observed. However, CV has meanwhile been identified as a neuroanatomical measurement that confounds genetically distinct neuroanatomical traits, namely cortical thickness (CT) and cortical surface area (CSA). We performed a re-analysis of the identical sample using the automated FreeSurfer surface-based morphometry (SBM) approach [2]. First, we replicated the negative correlation between tinnitus distress and bilateral supratemporal gray matter volume. Second, we observed a negative correlation for CSA in the left peri-auditory cortex and anterior insula. Furthermore, we noted a positive correlation between tinnitus duration and CT in the left peri-auditory cortex as well as a negative correlation in the subcallosal anterior cingulate, a region collated to the serotonergic circuit and germane to inhibitory functions. In short, the results elucidate differential neuroanatomical alterations of CSA and CT for the two independent...
“…The results were compared in a unified analysis to the 5 kHz groups reported by Roberts et al [6] which performed the same auditory detection task except for the carrier frequency chosen. In addition, two additional long-latency responses, namely, the N2 transient response (latency ~325 ms) and the auditory sustained response (SR, commencing after N2 and persisting to the end of stimulation), were studied in both groups, to determine whether modulation of these late responses was similarly affected by tinnitus.…”
Age and hearing-level matched tinnitus and control groups were presented with a 40 Hz AM sound using a carrier frequency of either 5 kHz (in the tinnitus frequency region of the tinnitus subjects) or 500 Hz (below this region). On attended blocks subjects pressed a button after each sound indicating whether a single 40 Hz AM pulse of variable increased amplitude (target, probability 0.67) had or had not occurred. On passive blocks subjects rested and ignored the sounds. The amplitude of the 40 Hz auditory steady-state response (ASSR) localizing to primary auditory cortex (A1) increased with attention in control groups probed at 500 Hz and 5 kHz and in the tinnitus group probed at 500 Hz, but not in the tinnitus group probed at 5 kHz (128 channel EEG). N1 amplitude (this response localizing to nonprimary cortex, A2) increased with attention at both sound frequencies in controls but at neither frequency in tinnitus. We suggest that tinnitus-related neural activity occurring in the 5 kHz but not the 500 Hz region of tonotopic A1 disrupted attentional modulation of the 5 kHz ASSR in tinnitus subjects, while tinnitus-related activity in A1 distributing nontonotopically in A2 impaired modulation of N1 at both sound frequencies.
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